Board II Review

Medicine
1. Dsecription Infectious disease An infection is the detrimental colonization of a host organism by a foreign species. In infection, the infecting organism seeks to utilize the host's resources in order to multiply at the expense of the host. The infecting organism, or pathogen, interferes with the normal functioning of the host and can lead to chronic wounds, gangrene, loss of an infected limb, and even death. The host's response to infection is inflammation. Top 3 single agent disease killers are: HIV/AIDS, TB, and malaria. Childhood diseases include pertussis, poliomyelitis, diphtheria, measles, and tetanus. Tropical diseases include trypanosomiasis, Chagas disease, schistosomiasis, leishmaniasis, lymphatic filariasis, and onchocerciasis. Calor, rubor, dolor, tumor and loss of function. Constitutional s/s: chills, malaise, loss of appetite and GI distress fever 102 F (must do blood cultures to r/o sepsis) CBC left shift where there is an increase in immature neutrophils and the total WBC countis elevated above 10,000 Low platelet count (>150,000) ABGs that show acidosis, and abnormal Creatinine and BUN that shows early kidney disease Variable by the infecting organism, location of the infection and extent HIV antiviral agents 1. Nucleoside reverse transcriptase inhibitors: Slows or prevents the formation of DNA copies of HIV in infected cells All can causes fatal lactic acidosis, fat redistribution and hyperlipidemia Drugs Description/MOA Indication Contraindications Dose Zidivudine Ist line DOC HIV, pregnanst women-given after the 13-14th wk of gestation, 200mg po tid (AZT) or PO and Parenteral reduces transmission to the fetus from 26%-8% (Retrovir) Anemia, neutropenia, N/V, headaches, fatigue, confusion myopathy and toxic hepatitis Stavudine Used as a 2nd line substitute Similar to AZT 40 mg po bid (D4T-Zerit) for AZT, often combied with DONT COMBINE W/AZT ddI or 3TC Peripheral neuropathy Didnosiine Used in combination with Combination drug 200mg po bid (ddI-Videx) AZT or D4T More toxic, causes peripheral neuropathy, pancreatitis, GI disturbances, lactic acidosis and retinal depigmentation Lamivudine Used in combination with Combination drug, also effective for HBV 150mg po bid (3TC-Epivir) AZT or D4T Less toxic and better tolerated with less side effects Zalcitabine Used in combination with Combination drug only, never used alone N/A (ddC-Hivid) AZT or D4T Least potent, causes peripheral neuropathy, rash, stomatitis, esophageal ulceration, pancreatitis and fever Combinations: Zalcitabine lamivudine (Combivir) 1 tab po bid 2. Non-nulcleoside reverse transcriptase inhibitors Used synergistically with nucleoside Rx: resistance develops too rapidly if used alone Comon side effects: rash, fever, nausea and headache Preparations o Nevirapine (Viramune) 200mg po tid o Delaviradine (Rescriptor) 400mg po tid 3. Protease inhibitors Actions: : prevents cleavage of protein precursors essential for HIV maturation inhibition of the infection of new cells and replication Problems: o Can cause increased bleeding and hyperglycemia chemical diabetes Preparations o Sanquanavir (Invirase) Highly active against HIV including AZT resistant strains, well tolerated 600mg po tid o Ritonavir (Norvir) well absorbed and produces high levels in the serum and lymph nodes. Common side effects: N/D/D, parasthesis, altered taste and renal failure 600mg po bid o Indinavir (Crixivan) 800mg po qid

Epidemiolgy Clincal presentation Labs Treatment

o o o o

Nelfinavir (Viracept) 750mg po tid Aprenavir (Agenerase) Lopinivir Opinivir/ ritonavir (Kalestra) fixed dose combination

DOC for tx of HIV in adults: 2 nucleoside inhibitors and 1 protease inhibitors o Combivir and nelfanivir (1200mg) 2 nucleoside inhibitors and 1 non-nucleoside inhibitors o Combivir and delaviritide (Rescriptor) Drugs for Tuberculosis Mycobacterium TB cultures take two weeks or longer Most commonly prescribed drug regimen o Rifampin 600mg and isoniazid 300mg in a single daily dose for 18mon conventional therapy o 9 months is the short course of treatment 5% relapse rate is acceptable

Empirical Tx: anti-mycobacterial therapy: Initial 4 drug combo ***TQ o Isoniazid Rifampin o Pyrazinamide Ethambutol or streptomycin (if INH resistant) Then INH and rifampin w/o pyrazinamide for the next 6mo Isoniazid **TQ Description Isonicotinic acid hydrazide 1952-synthetic bacteriocidal MOA Interferes with cell wall mycolic acid synthesis in the bacteria Indications Cornerstone of TB tx: all forms of TB and TB prophylaxis Pharmacology Rapidly and completely absorbed po, Contraindications Previous isoniazid associated hepatic injury Warnings Severe and fatal hepatitis, monitor and interview pts monthly, and run LFTs, enzymes are elevated in 10% of patients 10-20% of pts have 4-5X normal discontinue trt Often pyridoxine deficiency (VitB6) is major s/e resulting in peripheral neuropathy Dose Adults: 300mg po qd single dose Rifampin MOA Indications Pharmacology Contraindications Susceptible Organisms Warnings Rx interactions Preparations Dose

Bacteriocidal-blocks RNA polymerase and protein synthesis Staph, MAC (AIDS), H. flu, meningitis (in children) used with dapsone in leprosy PO only, well absorbed from GI; 600mg dose will yield 7mg/ml (peak serum conc) Hepatotoxic-alcoholics and preexisting liver problems are most prone Coagulase po/neg staph, Neisseria, H. flu, Cl difficile, useful in pts with Legionnaires Disease who have fialed to respond to erythromycin, may be combined with nafcillin or vancomycin in the tx of chronic staph osteomyelitis Hepatotoxic; GI disturbances; skin rash; thrombocytompenic purpura, may turn body fluids a red-orange and may permanently stain contact lenses or implants + cytoP50 will decrease the effectiveness of co-administered drugs: protease inhibitors, BCP, warfarin, quinidine, zidovudine, itraconazole, fluconazole, and ketokonazole Combo with Rifampin Rifamate 600mg po qd along with Isoniazid

B. Neurologic disorders 1. Peripheral neuropathies Peripheral causes of peripheral neuropathy D A N G T H R A P I S T

Diabetic-Alcoholic-Nutritional-Guillame Barre-Toxic-Herditary-Reccurrent-Amyloidosis-Porphyria-Infectious- Systemic-Tumor 1. Diabetic peripheral neuropathy

Capasaicin to target substance P, Baclophen, m relaxants, TCAs, anti-seizure meds (Tegretol), GABApentin,(post herpetic neuraligia req titrations up) OD: dizziness, drowsiness, alters ability to drive and use heavy machinery. Excreted unaltered no kidney stress Neurontin 900mg/d (normal dose) initially, (1 tab) 300mg/d then (2 tabs) 600mg/d then 900mg/d (3 tabs) If Neurontin doesnt work, use amytriptiline 25mg w/pm dose + DOPA and NE receptors Diabetic Peripheral Neuropathy Peripheral neuropathy is an all too frequent complication of diabetes affecting sensory, motor and autonomic neurons of the peripheral nervous system and the organs these neurons innvervate. Hyperglycemia and the duration of the disease appear to be the primary factors in its development. Distal symmetrical polyneuropathy is the most common type of neuropathy in diabetics. It develops insidiously may affect the small sensorimotor nerve fibers, large sensorimotor nerve fibers or both. Small, unmyelinated C fibers are composed of autonomic and sensory axons that transmit thermal perception and sympathetic function. These are affected early in the disease process. Patients present with prominent paresthesias and autonomic nervous system dysfunction recognized by the presence of orthostatic hypotension, resting tachycardia and distal anhydrosis. Large myelinated axons include both motor and sensory nerves. They conduct proprioception, light touch, vibratory and pain sensations. Symptoms of large fiber involvement include tingling, burning, numbness, allodynia or deep lancinating pain. Sensory ataxia may occur as a result of diminished vibratory and proprioceptive sense. Sensory changes do not always correlate with nerve conduction deficits. Deep tendon reflex responses are attenuated or absent and there may be distal motor weakness. The neuropathy develops in a length-dependent fashion, progressing from distal to proximal in a stocking and glove distribution. Progression of nerve injury leads to the loss of protective threshold or the ability to detect small objects or stimuli resulting ultimately in the neurotrophic or insensate diabetic foot. This is the cause of diabetic ulceration in up to 85% of patients. The exact pathophysiology of nerve damage in diabetes remains unclear. A number of theories exist which include the polyol pathway, microcirculation complications secondary to the stimulation of protein kinase and the non-enzymatic glycosylation of proteins throughout the body. The polyol pathway has long been implicated. Peripheral nerve tissue does not require insulin for glucose uptake. Hyperglycemia results in increased cellular glucose levels within nerve tissue which require an alternative catabolic pathway to be cleared. Via oxidative reactions, glucose is converted to sorbitol and sorbitol converted to fructose. Initially it was believed that the accumulation of sorbitol and fructose lead to osmotic stress resulting in nerve injury. However, it is now thought that it is the oxidative stress resulting from the breakdown of intraneural glucose that metabolically compromises neurons and leads to nerve damage. Functional loss of axons seems to occur as a length-dependent loss result in an initial distal neuropathy Intracellular hyperglycemia stimulates the activation of protein kinase C or PKC. This enzyme facilitates the transfer of phosphate groups from a donar molecule. Although there are many isoenzymes of protein kinase C, the beta-2 form has been implicated as the mediator of microvascular damage. These elevated levels of protein kinase C beta-2 result in increased basement membrane matrix protein deposition, leukocyte activation and smooth muscle proliferation and contraction. This process results in decreased endoneural blood flow resulting in nerve damage. Exposure of proteins to high levels of glucose initiates a multi-step process resulting in non-enzymatic glycosylation of these proteins - referred to as advanced glycation end-products or AGEs. Proteins, lipids and nucleic acids are all affected with resultant alteration of metabolic function. The large protein complexes may also be difficult for the body to clear resulting in AGE accumulation in susceptible tissues. Interaction with collagen in endoneural vessel walls thickens the walls compromising microcirculation to the nerves. The wide reach of diabetic neuropathy therefore results in many changes in the lower extremity. Sensory involvement results in a loss of protective threshold and the development of a neurotrophic foot. It is recognized early on as a loss of protective threshold and dorsal column involvement characterized by a loss of vibratory and position sense. This is the most prominent factor in the development of foot ulceration and the clinical path to lower extremity amputation. Motor involvement affects initially the intrinsic musculature of the foot leading to what is sometimes referred to as an intrinsic minus foot. Atrophy of the intrinsic musculature results in digital contractures, plantar prominence of the metatarsals and abnormal distribution of the normal weight bearing load with ambulation. In advanced neuropathy a drop foot may develop secondary to anterior compartment muscle wasting in the lower leg. The gastrocsoleus complex, having lost its antagonistic muscle group, then gains mechanical advantage resulting in ankle joint equinus. This deformity adds further to the weight bearing load borne by the forefoot placing the patient at even greater risk for forefoot ulceration. Autonomic nervous system involvement in the lower extremity results in a profound vasodilation of all vessels to the lower extremity and sudomotor changes. The foot will present clinically as warm, erythematous and dry. Increased vascular flow to the foot results in demineralization of bone; it is literally washed away. This is a major contributing factor to the pathogenesis of Charcot joint disease. Medical treatment for diabetic peripheral neuropathy must first start with rigid glucose control and patient education regarding the risks and hazards associated with nerve damage. Superficial nerve pain can be managed with capsaicin creams. Deeper nerve pain may be managed with tricyclic anti-depressants medications such as amytriptyllene or anti-seizure medications such as gabapentin. Muscle relaxants may provide relieve of deep pain. Disease modifying drugs that would modulate the pathogenesis of neuropathy are in clinical trials and will open a new frontier in the prevention of neuropathic complications in the diabetic. Treatment in the lower extremity should be directed towards preventing ulceration. Accommodative shoe gear is indicated in all patients who have lost protective threshold. A laminated plastizote and poron insole provides the ability to off-load plantar prominences and provide absorption of abnormal shearing forces. Often an extra-depth shoe will provide ample room for the diabetic foot, however, if severe foot deformities are present, custom molded shoes are indicated. Physical therapy is an important adjuvant therapy in the diabetic with treatments directed towards increasing the patients balance and muscular strength. 2. Alcoholic The cause of alcoholic neuropathy is controversial but may be because of the toxic effect of alcohol on nerve tissue. It is likely also associated with nutritional deficiencies and may be indistinguishable from nutritional-related neuropathies such as beriberi.

Treatment

Beriberi Thiamine essential co-factor in CHO catabolism areas w/ most enzymatic activity in brain resulting in high Gl-demand greatest risk Description Deficiency in thiamine (vitamin B1) There are two major manifestations of thiamine deficiency: cardiovascular disease (wet beriberi) and nervous system disease (dry beriberi and Wernicke-Korsakoff syndromewhich is alcohol-related brain damage affecting language and thinking). Both types are most often caused by excessive alcohol consumption. Epidemiology Beriberi has become rare in the US b/c most foods are now vitamin-enriched contains adequate amounts of thiamine. Clinical Symptoms of dry beriberi include pain, tingling, or loss of sensation in hands and feet, muscle wasting with loss of function presentation or paralysis of the lower extremities, and potential brain damage and death. Treatment 100 mg IV of thiamine should be administered parenterally along w/ Mg (which is necessary for thiamine metabolism) if response to the thiamine is noted, it should be repeated daily during the acute phase of the diseasecerebellar ataxia will generally improve but recovery may be incomplete Korsakoffs Syndrome Usually occurs as a chronic sequelae to Wernickes syndromeconsists of memory loss, confusion and confabulation, it is associated with lesions in the mammillary bodies of the hypothalamus; its presence is recognized when after appropriate thiamine and magnesium treatment, all other symptoms return to normal with the exception of persistent memory lossas many as 20 to 25% of patients with Korsakoff amnesia do not improve with treatment The most common symptoms are numbness, tingling, burning feet, or weakness. In severe cases, however, the autonomic nerves (those that regulate internal body functions) may be involved. Prolonged heavy use of alcohol, or alcoholism that is present for 10 years or more indicates high risk for alcoholic neuropathy 2. Nutritional Restless Leg Syndrome Ekboms Syndrome Description def of zinc or folate, vitB12 neuropathy-some studies advocate iron deficiency as an underlying etiology Epedemiology <10% of the population are affected, and there seems to be an autosomal dominant inheritance pattern Clinical The m.c s/s is a recurrent, persistent urge to wiggle and move associated w/fibromyalgia. It may be described as presentation uncomfortable, crawling, painful, grabbing sensations, primarily in the LE- 20% of pts also have s/s in the UE. Pts may suffer with periodic limb movements of sleep (PLMS) Treatment Ca/Mg supplements have been found to be useful, vitE may also help at least 400 IU/day is recommended, and the patient Vitamins should be advised to eliminate caffeine and tobacco. Moderate exercise may be helpful but strenuous night time exercises Mod! Activity may actually exacerbate the symptoms, motor activity, particularly walking, will relieve the symptoms regular exercise before bedtime may be helpful for some patients but most biofeedback and relaxation techniques fail to affect a cure the most effective treatment may be pharmacological dopaminergic drugs are the most effective agents: DOC is dopamine agonist pergolide (antiparkinsons drug) dopaminergic agents that BZDsaid in m relaxation and sleep induction, Anticonvulsantsquiet the opiods severe Drugs
work in CNS be careful will lead to tolerance levodopa/carbidopa 25/100 mg tid hs may be effective the controlled release preps may be a bit more beneficial involuntary mvmts cloazepam may be effective if the others fail to relieve the s/s symptomatic relief sedating anti-histamines like diphenhydramine

3. Guillame Barre Syndrome Landrys Ascending Paralysis Description rare entity characterized by symmetrical motor and sensory paresis; Schwann-cell surface membrane targeted acute segmental inflammatory demyelinating polyneuropathy; Etiology unknown; believed to be 2o to a disturbance of the immune syndrome; most frequent antecedent infection is Campylobacter jejuni, a major cause of gastroenteritis; infecting organism induces both humoral and cell mediated immune responses d/t molecular mimicry react with ganglioside surface components of peripheral nerves Epidemiology leading cause of acute flaccid paralysis in western countries; incidence is 1.5/100,000 Pathologic edema of the nerve degeneration of axons and their myelin sheaths Wallerian degeneration; evaluation of cerebrospinal Changes fluid increased protein w/ few monocytes Clinical onset variable; usually the distal limbs are first involved with weakness developing either acutely (within days) or subacutely Features and (within four weeks) symptoms are roughly symmetrical loss of tendon reflexes; autonomic nervous system is variably Course of the involved; motor weakness accompanied by sensory disturbance from mild hypoesthesia to profound absence Disease course of the disease varies; paralysis of the legs, arms, breathing muscles and face may occur; abnormal sensations and weakness; 75% reach maximum disease progression within two weeks, 92% within three weeks and 94% within four weeks; brief plateau phase, improvement begins with gradual resolution of the paralysis over weeks to months; mild cases complete recovery in 1-2 mths; severe cases recovery in 1-2 yrs. Attacks may recur; Treatment plasma phoresis along w/ immunomodulation via infusions of IgG shorten the duration of the disease; helps support the molecular mimicry theory; corticosteroids administered during the acute paralytic phase but their efficacy is difficult to determine; Mx of paralysis is palliative - ~33% of patients require intubation and assisted ventilation; limbs treated by supporting splints to prevent contracture; passive and active exercises used to maintain joint range of motion 4. Toxic-drugs

Heart or blood pressure medications : Amiodarone Hydralazine Perhexiline Drugs used to fight cancer : Vincristine, Cisplatin Drugs used to fight infections : Metronidazole (Flagyl) Nitrofurantoin, Thalidomide (used to fight leprosy) INH (isoniazid) used against tuberculosis Drugs used to treat skin conditions (Dapsone) Anticonvulsants (Phenytoin) Anti-alcohol drugs (Disulfram) Drugs to fight HIV Zidovudine (Retrovir, formerly AZT) Didanosine (Videx) Stavudine (Zerit) Zalcitabine (Hivid) Ritonavir (Norvir) Amprenavir (Agenerase) Drugs to lower cholesterol Lovastatin (Mevacor) Indapamid (Lozol) Gemfibrozil (Lopid)

Toxic-environment
Pollutant Arsenic Description Clinical Signs and Symptoms Medical use is essentially Affects GIT and the nervous system presents as a painful polyneuropathy nonexistent in the 90s with the skin changes occur concomitantly white striae in the fingernails (Mees bands) exception of the management of TX of acute poisoning: emesis and/or gastric lavage, osmotic cathartics (BAL-chelating trypanosomiasis. agent) present in depilatories and some pesticides, it is unlike the barium sulfate used in XR exams, it can lower serum K resulting in the clinical picture of periodic paralysis vasculopathy caused by a protein-containing edematous fluid surrounding abnormally Treatment permeable capillariesthe capillaries b/c engorged and develop endothelial proliferation (BAL) and (EDTA) for chelation and thrombi in focal necrosiscortical neuronal necrosis occurs Supportive: ventilation and Signs and Symptoms seizure control convulsive seizures generalized or focal paralysis may follow these seizures oral penicillamine (with supplemental any type of neurologic sign may develop cerebellar ataxia, hemiplegia or decerebrate pyridoxine) may suffice in milder rigidity, lethargy, delirium and coma cases of lead poisoning It is dangerous in three forms inorganic salts, metallic mercury (occurring primarily from inhalation Treatment of mercurial vapors) and organomercurials (BAL), however, it is not Symptoms of Inorganic Salts and Mercury Vapor Exposure effective in chronic poisoning, increase neurologic complication: tremors and personality changes, tremor of the limbs or postureurinary excretion with holding increases w/voluntary mvmt the administration of Symptoms of Organomercurial Exposure: paresthesias of the limbs, visual, dysarthria, tremors and penicillamine incoordinationw/ large exposure, spastic weakness is followed by coma or death (permanent) neurotoxicity is reversible resulting in tremor, ataxia, dysarthria and brisk DTRs behavioral changes are the first clinical sign: the dz further develops to widespread damage to the basal ganglia resulting in parkinsonismthe rigidity and hypokinesia can be managed with L-dopa Neuropathy

Barium Lead

Mercury (Mad Hatter Syndrome)

Lithium Manganese [Urate]p

5.

Hereditary Herditary Motor and Sensory Neuropathies Characteristics CMT histologically demonstrates segmental demyelination and hypertrophic neuropathy; demonstrates neuronal degeneration and characterized by the onset of distal lower limb weakness Dejerine Sottas Dz hypertrophic neuropathy onion bulb Refsums disease lipid storage disorder associated w/ increased excretion of phytanic acid; connected to CMT Dz b/c syndromes have overlapping sensory & spinal cord pathologies. symptoms repeated attacks & remissions of distal motor and sensory loss in the hands and feet; absent pain and temperature sense; decreased vibratory sense; associated with retinitis pigmentosum; clinical findings enlarged nerve sheathes resembling Dejerine-Sottas Dz; spastic paraplegia optic atrophy and hypertrophic neuropathy typical of type I clinical picture of type I & has the additional complication of retinitis pigmentosum

Type Type I Type II Type III Type IV

Type V Type VI Type VII

Description Classification Dyck & Lambert 1968 Incidence Onset Clinical Findings clinical s/s Diagnosis Treatment

Peroneal Muscular Atrophy Charcot-Marie-Tooth Disease begins as slowly progressive Dz in feet & legs and spreads to the hands and forearms over several years; characterized by atrophy of peroneals and intrinsic musculature of the hands and feet Charcot-Marie-Tooth 1 - demyelinating form characterized by Charcot Marie-Tooth 2 - neuronal form degeneration of the posterior columns of the spinal cord, loss of anterior characterized by axonal degeneration of the peripheral horn cells and degeneration of the spinocerebeallar tracts; slow nerve nerve; onset is later in life with no enlargements of the conduction velocities and changes (onion bulbs) on biopsy peripheral nerves highly variable; m > f; Afro-Americans exempt from CMT; onset b/t 515 yrs; pts not b/c seriously impaired until the 4th decade muscular atrophy is symmetrical and distal; peroneals & intrinsic muscles of the feet affected 1st lose ability to evert the foot; invertors exhibit its mechanical advantage unopposed early symptoms of varus or high arched foot; atrophy spread to anterior calf: TA, EHL, EDL muscles to digits cavus deformity & eventual clawing of the digits; Finally, posterior group atrophy; plump thigh, slender legs with claw toes ostrich or stork legs or inverted champagne bottle w/ symptoms of LMN disease +ve family history; prolonged nerve conduction velocity in involved motor nerves early stages - passive stretching exercises; strengthening exercises to beef up wasting muscles advanced cases - surgical intervention to correct fixed deformities tendon transfer; use of Vitamin E

Other hereditary disorders

Riley-Day Syndrome AKA Familial Dysautonomia Clinical Presentation Roussy-Levy Syndrome Hereditary areflexic dystasia Friedreichs Ataxia AKA Hereditary spinocerebellar ataxia Complete indifference to pain; present from birth; autosomal recessive trait in Ashkenazi Jews; high prevalence of breech presentation, weak/absent suck and poor tone; difficulty feeding in the neonatal pd increasing the risk of aspiration pneumonia. 40% of pts react to stress either physiologic/emotion w/ constellation of s/s termed the dysautonomia crisis characterized by increased HR, sweating and emotional lability; mentality is dull normal; emotional lability, temper tantrums, self-mutilation, thermal regulation is poor, excessive sweating and postural hypotension are usual findings; absent or hyporeflexic DTR; indifference to all pain; trophic ulcers on lower extremity d/t indifference to noxious stimuli a forme fruste of Charcot-Marie-Tooth Dz; familial pes cavus & extension of the digits; absent deep tendon reflex responses; prolonged nerve conduction velocity of involved motor groups; positive Rombergs sign Onset early childhood; rare; autosomal dominant trait; Clinical Presentation static tremor of the hands most common inherited ataxias; involves spinocerebellar tracts, the corticospinal tracts & posterior columns; anterior motor horn cells are normal Onset - males = females; autosomal recessive gene; b/t ages 5-15yrs; Dz d/t protein frataxin which is normally in the CNS heart & pancreas; have AbN high Fe in cardiac tissue reacts w/ O2 to produce free radicals detrimental to neural and muscular tissues; cerebellar signs develop first; initially unsteady gait; tendency to stagger, fall & unable to make sudden turns; delayed motor milestones slowly progressive scoliosis in thoracic region; (mc 80-90% of all cases); LE Findings: feet display a symmetrical cavus foot deformity; muscle imbalance is an important factor; peroneal muscle weakness is mc; foot affected first; wide base unsteady gait; sensory findings loss in position & vibratory sense & 2 pt discrimination; touch, pain & temp preserved absent DTR, +ve Rombergs sign; heel to shin ataxia present speech explosive slurred and staccato; cardiac failure is cause of death paresthesias and shooting or lightning-like pains in extremities wheelchair confinement at 20 yrs, paraplegia and decreased life expectancy Onset infancy; poor walking and inability to run Clinical: all sensory modalities affected; anesthesias to light touch & pinprick in a stocking-glove distribution; proprioception is lost +ve Rombergs sign. Muscles coarse muscle fibrillations like those in CMT Dz & slowly progressive muscle weakness. Reflexes diminished or absent deep tendon reflexes; impaired papillary response to light Tx accommodative care aimed at preventing injury 2o to sensory loss; insensate foot measures should be taken education & Rx like a diabetic; night splinting & passive muscle stretching useful to prevent development of contractural deformities

Dejerine-Sottas Syndrome AKA progressive hypertrophic polyneuritis

6.

Infectious

Tuberculosis/Leprosy Can result in multiple nerve palsies Neurosyphillis Etiological agent: T. Pallidum, occurs in 25% of pts with 3o syphilis, diagnosis is by FTA-ABS or RPR. TX: PCN G Cryptoccocus Neoformans A yeast passed to humans via pigeon vectors can produce a subacute meningitis Poliomyelitis RNA virus, clinical dz state starts as a flu, followed by meningitis and then flaccid paralysis of the limbs and trunk. Tx: vaccine Herpes Zoster Has a dermatomal distribution of vesicles and demonstrates segmental weakness and pain for years Lyme disease Neurologic s/s: meningeal irritation w/ cranial neuritis, motor or sensory radiculoneuritis, mononeuritis multiples and chorea

Meningitis
Bacterial Causes: H. Flu, N. meningitides, diagnosis is confirmed by lumbar puncture and tx: PCN G or ampicillin +Brudzinski and Kernig sign Coccidioidomycosis SW: Valley fever or Dessert rheumatismTransmitted via dust particles. Delayed hypersen. Sequelae persistent arthralgia, Coccidiomycosis and pleuritic pain.Erythema multiforme or nodosum. Disseminated: Granulomas, of the skin, bones, joints, adrenals, and CNS. Cryptococcosis Pigeons are the vectors.Pneumonitis proceeds dissemination to CNS-meningitis, cystic gelatinous masses in the gray Cryptococcus Neoformans matter, no pus. Can disseminates also to skin, bone, liver and other viscera

Histoplasmosis Histoplasma Capsulatum Dsecription Epidemiolgy Clincal presentation Diagnosis Wound management

Associated with bat and starling guano. Molds and dust are inhaled. (granulomatous) Benign pulmonary Lymphadenopathy and Splenopathy Disseminated RES disease infects macrophages -> CNS fatal meningitis

Tetanus
Dz caused by the toxin of Clostridium tetani that affects the central nervous system, sometimes resulting in death. Tetanus causes 5 deaths/yr in U.S and internationally, reports show up to 1 million cases/yr, mostly in developing countries. The spores germinate, releasing active bacteria that multiply and produce a neurotoxin called tetanospasmin. Tetanospasmin selectively blocks inhibitory nerve transmission from the spinal cord to the muscles, allowing them to go into severe spasm, which begins w/mild spasms in the jaw (trismus), neck muscles, and facial muscles. Stiffness rapidly develops in the chest, back, abdominal muscles, and sometimes the laryngeal muscles (which interferes with breathing). Tetanus antibody test Previous immunization history Non tetanus prone wound Tetanus prone wound Uncertain or <3 yrs prior tetanus Td0.5cc IM No TIG TIG (250mg) units IM at other site immunizations Td0.5cc IM <10 yrs since last dose >3 yrs prior tetanus immunizations Nothing TIG (250mg) units IM at other site

8. Systemic hypothyroidism; LE edema from various etiologies compression of nerve under the laciniate ligament 9. Tumor space occupying lesions schwannoma or fibroma create pressure on the nerve Entrapment neuropathies Def - subgroup of compression neuropathies occurring secondarily to: gradual constriction of anatomic structures about a nerve, or chronic compression of the nerve against an adjacent unyielding fibrous or skeletal structure onset of s/s - insidious & mild; motor and sensory changes painful; pain referred along the n. distribution Dx - electromyography and NCVS identifying and localizing the lesions Tx - surgical decompression Principle Lower Extremity Nerves of the Lumbar Plexus Contains anterior rami of the first three lumbar spinal nerves, L1, L2 and L3 as well as a portion of L4
Nerve Lateral Femoral Cutaneous Nerve L2 & L3 SENSORY Femoral Nerve L2, L3 & L4 SENSORY & MUSCULAR Saphenous Nerve SENSORY ONLY Course Injury or Entrapment 1st sensory branch of the lumbar plexus Course: emerges from the lateral border of the psoas major; courses forward along the brim of the pelvis to the lateral end of the inguinal ligament. Enters the thigh through a tunnel formed by the lateral attachment of inguinal ligament & ASIS; 12cm inferior it bifurcates into an anterior and posterior branch anterior branch - supplies skin over the lateral/anterior surface of the thigh posterior branch lateral/posterior thigh Course: exits vertebral canal lateral edge of the psoas muscle musuclar innervation to both the psoas and iliacus muscles exits the pelvis by passing underneath the inguinal ligament, lying just lateral to the femoral artery and vein Sensory branches - skin of the anterior thigh and medial calf Muscular branches pectineus, Sartorius, quadriceps femoris Movements Under Control of the Femoral Nerve: iliopsoas hip flexion; pectineus flexion of the thigh; quadriceps femoris extension of the leg at the knee largest and longest sensory branch of the femoral nerve; innervates skin over the medial aspect of the thigh, leg and foot; Course: accompanies the femoral artery in the femoral triangle descends & diving medially under the sartorius muscle; as courses inferiorly infrapatellar branch supplies the medial aspect of the knee terminal branch courses inferiorly along w/ greater saphenous vein, supplying sensation to the medial aspect of the calf; at medial malleolus continues anteriorly with the greater saphenous vein, supplying sensation to the medial foot; ends at level of the first metatarsal phalangeal joint Injury/Entrapment: injured mostly by laceration; entrapped as it exits the subsartorial (Hunters) canal proximal to the knee no motor weakness b/c nerve has no motor branches **may be injured when the GSV is harvested for CABG surgery formed within the psoas muscle; Course; - enters pelvis immediately anterior to the sacroiliac joint through the obturator canal bifurcating into an anterior and posterior division anterior branch adductor longus, brevis and the gracilis posterior branch obturator externus and half of the adductor magnus sensory fibers supply cutaneous sensation to the upper medial thigh & anastomose with the saphenous nerve Movement; adductor longus; adductor brevis & gracilis(+Internal Rotate leg) Adducts thigh obturator externus External Rotation thigh & adductor magnus muscle Adducts, Flex & Extend Thigh

Obturator Nerve L2, L3 and L4 nerve roots SENSORY & MUSCULAR

Principle Lower Extremity Nerves of the Sacral Plexus

Superior (L4 S1) & Superior Gluteal muscular innervation to gluteus medius, minimus and tensor fascia lata Inferior Gluteal Inferior gluteal innervation to gluteus maximus (L5 - S2) Nerves Muscular Movements; superior gluteal nerve abduction and internal rotation of the thigh; inferior gluteal nerve MUSCULAR extension, abduction and external rotation of the thigh Sciatic Nerve Comprised of peroneal portion from the posterior division of the anterior rami, & tibial portion from anterior divisions of the L4 - S2 anterior rami. Course: exits pelvis through the greater sciatic foramen both portions course inferiorly; the peroneal component MUSCULAR supplies short head of the biceps femoris and a portion of adductor magnus, the tibial branch gives off short muscular branches in the posterior thigh; hamstring muscles in lower third of the thigh, it divides into separate and distinct peroneal and tibial nerves. Dz Sciatica - pain down entire lower limb; Tibial Nerve sciatic nerve bifurcated within the popliteal fossamedial popliteal nerve tibial nerve; motor innervation to the muscles of AKA posterior both the superficial and deep sural muscle groups. Courses inferiorly through the popliteal fossa, it gives off muscular tibial nerve branches to the medial and lateral heads of the gastrocnemius & soleus. In superior calf: motor innervation to deep posterior SENSORY & group - tibialis posterior, flexor hallucis longus and flexor digitorum longus; enters foot: passes through a space between the MUSCULAR medial malleolus and the flexor retinaculum; under the flexor retinaculum, splitting into the medial and lateral plantar nerves; after giving off the 1st small calcaneal branch. medial plantar nerve enters foot courses along with the medial Lateral plantar nerve enter the foot laterally to heel plantar artery; supplies motor innervation to 4 muscles (LAFF) and lateral plantar surface; motor innervation to all other the ABH, FDB,FHBand the1st lumbricale & Cutaneous intrinsic muscles of the foot & sensory innervation on innervation of medial distal 2/3 of plantar foot, plantar of digits 1lateral aspect of the sole and to the lateral aspect of the 3 & medial side of 4th digit fourth and entire fifth toe

Injury and Entrapment of Tibia Nerve Proximal Tarsal Tunnel Syndrome - entrapment of medial and lateral branches of tibial nerve (dependent upon the level of the bifurcation); occurs as it courses beneath the laciniate ligament (flexor retinaculum); factors contributing to entrapment include: Anatomic Flexor retinaculum has deep fibrous septa which blend with the periosteal covering of the medial side of the calcaneus, NVS passing through the laciniate ligament gets attached to some of these septa Vascular Medial and posterior tibial nerves are normally well supplied with arterial blood. They regenerate easily & are extremely susceptible to ischemic injury or arterial insufficiency Tarsal Tunnel Syndrome; enlargement or varicosities of venous system w/i the tarsal tunnel; application of ankle tourniquet venous engorgement Tarsal Tunnel Syndrome Biomechanical compression entrapment of medial & lateral plantar nerves as they enter the foot; seen in pts w/ enlarged ABH muscle bellies or osteophytic spurring of the medial arch of the foot; pronation syndromes extreme PF & adduction of the talus during ambulation, enlarged navicular tuberosities d/t osseous impingement and anomolous insertion of the posterior tibial tendon. Clinical C/O burning or overall tiredness in the foot; pain that rotate proximally = "Valleix phenomenon" Presentation Symptoms - reproduced with percussion of the posterior tibial nerve at the level of the laciniate ligament Diagnosis electro-diagnosis is quite useful; may be normal even when syndrome is present; distal latency(millisecs) is evaluated for medial and lateral plantar nerves; uses surface electrodes & invasive probes are not necessary Represents time required for the stimulus to travel to the end point; a delay in conduction is presented by a greater latency value; indicative of derangement of conductivity of the nerve distal latency of medial plantar nerve -abnormal > 6.1 ms of lateral plantar nerve abnormal > 6.7 milliseconds to perform the nerve conduction studies: PTN stimulated just proximal to the laciniate ligament w/ stimulating electrode; recording electrodes are placed over terminal end point of the respective nerves - the ABH muscle belly to test the medial plantar nerve and the abductor digiti quinti to test the lateral plantar nerve; Treatment Surgical decompression Distal Tarsal Tunnel Syndrome - refers to isolated entrapment of any of the distal segments of the posterior tibial nerve. medial plantar nerve = "jogger's foot" isolated involvement occur 2o to compression of the nerve as it courses into the plantar aspect of the foot b/t the navicular tuberosity & abductor hallucis muscle belly Lateral plantar nerve 1st branch to abductor digiti minimi quinti = "Baxter's nerve"; entrapment between quadratus plantae and ABH muscle is associated w/ chronic heel spur syndrome and is the most common type of distal tarsal tunnel syndrome o pain present for up to a year & traditional Mx for heel spur syndrome has failed to relieve their symptoms; gives classic H/O of post-static dyskinesia but also C/O increased pain following prolonged standing; describe an "afterburn" - continued burning discomfort at rest following a period of prolonged standing

Common Peroneal Nerve L4 L5-S1 SENSORY MUSCULAR

Superficial Peroneal Nerve AKA the musculocutaneous nerve SENSORY MUSCULAR

Deep Peroneal Nerve AKA anterior tibial nerve SENSORY MUSCULAR

Sural Nerve SENSORY Only

Course: branches laterally from the sciatic trunk within the popliteal fossa; becomes superficial at level of the popliteal fossa infero-laterally around the head of the fibula; upon entering the leg gives off the small recurrent nerve which supplies sensation to patella bifurcates into superficial and deep peroneal nerves; Injury or Entrapment: vulnerable to external compression injuries neuropraxia can result from simply crossing the legs; c/o paresthesias and hypesthesias; weakness of anterior muscle group. entrapment - more unusual; occur 2o to constriction with resultant demyelination at the fibrous tunnel arising at the origin of the PL on the fibula; after wrapping around the head and neck of the fibula, the CPN dives underneath the PL coursing between them muscle bellies of the peroneus longus and brevis Diagnosis nerve conduction studies; radiculopathy of L5 EMG aberrations in gluteal & paraspinal muscle groups; More proximal lateral (peroneal component) trunk of the sciatic nerve EMG aberrations of the biceps femoris; clinical signs of injury include weakness of the TA and extensor hallucis muscles resulting in the classic dropfoot deformity supplies motor innervation to the peroneus longus and peroneus brevis eversion & plantarflexion of the foot; Course: descends inferiorly between the peroneal muscles dividing inferiorly into the medial and intermediate dorsal cutaneous nerves; sensory branches anterior to extensor retinaculum, supplying the antero-lateral aspect of the lower half of the leg and the dorsum of the foot and toes; most common nerve injured in the footInjury and Entrapment - occurs as it exits the fascia w/i the calf approximately 10 cm above lateral malleolus. intermediate dorsal cutaneous nerve (AKA Lemonts nerve) located over the dorsal aspect of the foot coursing just medial to the sinus tarsi; severe inversion ankle injuries stretched nerve & injury; medial dorsal cutaneous nerve traumatized or even severed w/surgical procedures which address the 1st MC joint Diagnosis: 3 clinical tests performed to reproduce the pts s/s & to confirm the dx local infiltration of anesthesia should eliminate symptoms; 1) pressure may be applied to the area where the nerve pops through the superficial fascia while pt dorsiflexs and everts the foot against resistance - this maneuver will put the nerve on stretch; 2) foot passively placed into PF and inversion, placing the nerve on stretch, 3) direct percussion of the nerve with the foot held in plantarflexion and inversion Treatment; consists of education regarding properly fitting shoe gear; cortisone injection at the level of entrapment; surgical decompression with release of the nerve and its branches; complete compartmental fascial release if conservative management fails; favorable results from isolated decompression are quite variable supplies motor innervation to TA, EDL, EHL, peroneus tertius and EDB responsible for dorsiflexion & frontal plane movement; cutaneous innervation of small wedge of skin on dorsal surface of lateral hallux and medial aspect of the second toe Injuries or Entrapment = Anterior Tarsal Tunnel SyndromeBlunt trauma occurs as it courses anterior to the ankle; entrapped under the extensor retinaculum or irritated by the superior edge of the inferior extensor reticulum; tarsal spurs compress the DPN over the anterior ankle; maximum point of contact with anterior tarsal tunnel syndrome occurred at the dorsal talonavicular joint. Clinical Findings: symptoms unequivocal; c/o of paresthesias over the dorsum of the foot with numbness in the first intermetatarsal space; nocturnal pain relieved by movement of the foot; d/t motor innervation to EDB wasting of the muscle belly and this area should be palpated and examined for any signs of decreased strength or atrophy Diagnosis: distal motor latencies w/ nerve conduction studies >7milliseconds (normal is 5 milliseconds); provocative testing reproduce symptoms on PF of the ankle and concomitant extension of the toes; palpating the nerve at level of the anterior ankle just medial to the dorsalis pedis artery Arises from union of medial sural cutaneous nerve (from tibial nerve) and sural communicating branch (from common peroneal nerve); originates inferior to the popliteal fossa. Course: b/t bellies of the gastrocnemius, winding inferiorly and distally, posterior to the fibular malleolus; cutaneous innervation to postero-lateral aspect of the distal leg and lateral aspect of the foot; terminal branches divide into a lateral and medial branch: largermedial branch supplies cutaneous innervation to the dorsal skin of the base of the fourth metatarsal; communicates with the intermediate dorsal cutaneous nerve, smaller lateral branch innervation to lateral aspect of the fifth digit; terminal branches provide branches to the tarsal joints; one of the most easily accessible sensory nerves of foot & considered to be the nerve of choice for biopsy - minimal residual anesthesia. Injury and Entrapment: injury occurs at level of the ankle minimal sensory deficit to lateral aspect of the foot Etiology - iatrogenic causes include slip of the hand during excision of a retrocalcaneal spur, excision of an os trigonum or Shepards fracture(Fx of lateral tubercle of the posterior process of talus caused by compression of bone b/t the posterior malleoli and calcaneal tubercle), calcaneal osteotomies and lateral ankle stabilization procedures; Entrapment 2o to fibrosis following a lateral inversion ankle injury;

Joplins Neuroma compression injury or entrapment of medial plantar digital proper nerve; symptoms - numbness and pain infero-medial to the first metatarsal -phalangeal joint; distal involvement with neuritic symptoms radiating along the plantar medial aspect of the hallux; frequently seen in conjunction with valgus bunion deformity and a medial hallux interphalangeal joint tyloma etiology: pronation syndrome apropulsive gait with medial roll-off during propulsion fibrosis of the nerve; massage over the nerve after Sx to prevent entrapment Other Nerve Conditions in the Foot Medial calcaneal nerve entrapment - seen in conjunction w/ infra-calcaneal heel spur syndrome; nerve irritated 2o to abnormal foot pronation and/or anomolous anatomy (a large abductor hallucis muscle belly, insertion of the medial slip of the plantar fascia more superiorly upon the calcaneus)

symptoms - reproduced with percussion of this branch of the posterior tibial nerve; Housers neuroma - first plantar intermetatarsal nerve Heuters neuroma - second plantar IM nerve Mortons neuroma - third plantar intermetatarsal nerve Islens neuroma - fourth plantar IM nerve

2. CNS disorders, including diseases of the spinal cord

Description Deep Tendon Reflex Responses Although diminished or augmented, DTR responses are assoc with LMN or UMN lesions respectively; they may also provide information regarding the sensory innervation to a muscle To elicit a normal deep tendon reflex response all five components of the reflex arc must be in tact. These are: an intact afferent sensory nerve a functional synapse at the spinal cord level an intact motor nerve an intact and functional neuromuscular junction a competent muscle Deep tendon reflex responses are graded as follows: 4+ Brisk - associated w/clonus 3+\ hyper-reflexic 2+ average 1+low normal - hypo-reflexic 0 absent if the reflex response is absent, the examiner should repeat the percussion using recruitment or what is called the Jendrassik maneuver the patient is asked to interlock his hands in front of his chest, and just prior to percussion The integrity is dependent upon spinal nerves L3 and L4 and ellicited on a slightly extended knee Integrity is dependent upon spinal nerves S1 and S2 a reflex response is present when the foot responds in PF

Patellar DTR Achilles DTR

Pathologic reflex responses that elucidates UMN disease 1-Babinski sign: normal if age <2yrs; stroke lateral plantar foot proximal to distal then across ball of foot; positive if extension/doriflex of great toe and flex/fanning of lesser toes; response is slow as compared to plantar withdrawal response from tickling 2-Chaddocks sign: stroke lateral foot from above lat mall moving distally 3-Oppenheim sign: use thumb and index finger as caliper to squeeze tibial crest applying pressure P>Distal 4-Gordons sign: squeeze posterior calf NOTE: all above positive if hallux extend/dorsiflex 5-Rossolimos sign: tap balls or distal pulps of digits; positive if toes PF/flex CNS Disorders 1. CNS disorders
Infections of the CNS demyelinating CNS diseases Description Characteristics Clinical Presentation Histology Progressive Multifocal Viralencephalitis Focal and relentlessly extensive neurologic symptoms and signs due to multifocal Leuckoencephalopathy polyoma JC virus lesions in the cerebral hemisphere, Demylination with viral inclusions CMV Occurs in the fetus or the Severe brain destruction Subacute encephalitis w/CMV inclusions Periimmunosuppressed i.e., AIDS pts microcephaly in fetuses ventricular necrosis-calcification Cerebral T. gondii most common in AIDS pts Subacute, evolving, focal or diffuse neurological symptoms with multiple Toxoplasmosis abscess formation Multiple sclerosis Relapsing, remitting course, classic triad: SIN Scanning speech, Intention tremor and Nystagmus Tabes Dorsalis Degeneration of Dorsal columns d/t tertiary syphilis, associated w/ Charcot joints & Argyll Robertson pupils

Anterior Motor Horn Diseases Dz that cause selective damage that affects voluntary movement & rarely attack other pathways within the spinal cord.
Poliomyelitis Caused by three distinct viruses that actually target the anterior horn cells of the brain stem and spinal cord; immunization has ended epidemics; transmission via respiratory secretions or via fecal contamination; Symptoms H/A malaise and myalgias flulike symptoms; low-grade fever; nuchal rigidity; muscle tightness in hamstrings, thighs and neck; lower motor neuron weakness or paralysis gradual tightening and muscle spasm; muscle weakness develops in asymmetrical and scattered distribution Skeletal deformities occur 2o to disruption of normal agonist-antagonist balance of involved muscle groups; develops yrs after the initial viral infection & is the result of expansion of the territories of the remaining functional motor units; pts c/o increased deterioration of previously involved muscles involves the lateral columns and anterior gray matter which are closely connected within the spinal cord; ALS involves voluntary motor system involving degeneration of the corticospinal tracts and the alpha motor neurons; presents with both upper and lower motor neuron disease. Symptoms dependent upon the degree of UMN and LMN involvement; rate of weight loss is prognostic factor for survival; recent data suggest that hypermetabolism of muscular tissue is associated with the disease process, and maintaining a high fat diet may prolong survival rate

Post Polio Syndrome Amyotrophic Lateral Sclerosis

Cerebral Palsy
Description Cerebral palsy is a group of disorders characterized by loss of movement or loss of other nerve functions. These disorders are caused by injuries to the brain that occur during fetal development or near the time of birth. Mental retardation may be present in up to 60% of all patients with cerebral palsy

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Etiology

Epidemiology Clinical presentation

Spastic CP (Pyriamidal)

Dyskinetic (athetoid) CP Ataxic CP Hypotonia Rigidity Tremor Mixed foot deformities Treatment

Cerebral palsy is caused by injury to the cerebrum (the largest portion of the brain, which is involved with higher mental faculties, sensations, and voluntary muscle activities). Cerebral palsy may pccure prenatal, natal and postnatally occuring during early infancy as a result of illnesses (encephalitis, meningitis, herpes simplex infections, and so on), head injury that results in subdural hematoma, blood vessel injuries, and many others. Some form of CP is reported to occur in between 1.5 to 7.5 of every 1,000 live births and in the US the prevalence has been reported to be between 390 and 590/100,000; it occurs with greater incidence in the lower birth weight infant The classical finding of CP is spasticity which may affect a single limb, one side of the body (spastic hemiplegia), both legs (spastic diplegia) and both arms and legs (spastic quadriplegia). In addition, there may be partial or full loss of movement, sensory abnormalities, and defects of hearing and vision. Speech abnormalities are common and seizures may occur Classifications of cerebral palsy include spastic, dyskinetic, ataxic, and mixed + Babinksi sign 50% of cases Further calssified into: monoplegia - 1% of all CP - involved only one limb, hemiplegia 30% of all CP - involved an arm and leg on the same side of the body (usually the arm is more affected than the leg, diplegia/paraplegia - 20% of all CP - represents paralysis of the legs, diplegia also affecting the arms, but to a lesser extent than the legs, quadraplegia - 13% of all CP - involves all four limbs equally, and double hemiplegia - quadriplegia in which the arms are more severely involved than the legs all of these conditions involve abnormalities in motor coordination and a scissored gait. Extrapyramidal or Dyskinetic Varieties of Cerebral Palsy Affects about 20%. It involves development of abnormal movements (twisting, jerking, or other movements) this variety of CP results from a lesion in the basal ganglia and post natal kernicterus is the most common etiology Involves tremors, unsteady gait, loss of coordination, and abnormal movements. It affects about 10%. Occurs secondary to cerebellar dysfunction inability to control the rate, range, direction and force of fine motor movements, primary incoordination of movement or balance is observed, compensation for this balancing difficulty is a wide base of gait 5% of all cases of CP this results from a lesion in the motor cortex and it is manifest by decreased or absent muscle tone 5% of all cases of CP this results in lead pipe or cog wheel rigidity and resistance to motion is greatest with slow stretch 1% of all cases of CP this results in rhythmic, alternating movements occurring either at rest or during voluntary movement The remaining 20% are classified as mixed, with any combination of the above symptoms. equinus , pes varus , pes cavus, forefoot equinus and metatarsus adductus Physical and occupational therapy. Botox - this is used to temporarily relax spastic muscles it is a protein exotoxin derived the Clostridium botulinum - a gram-positive, spore-forming anaerobe. It exerts its effect at the neuromuscular endplate by preventing the exophytic release of acetylcholine, the toxin will then functionally denervate the muscle resulting in a flaccid paralysis. Within a few months, the muscle develops new acetylcholine receptors and the paralytic effects are reversed. These toxic effects are limited to the peripheral nervous system

2.

Cerebellar disorders The Cerebellar Examination

The cerebellum is responsible for the smooth coordination of voluntary, skilled movements, it contributes to the maintenance of normal posture, balance and unconscious proprioception It contributes to vestibular function helping to maintain equilibrium, and a cerebellar lesion generally results in awkwardness and uncoordination of volitional movements Heel-Knee Test This assesses the integrity of the EPS or spinocerebellar tract it is the most reliable test of cerebellar function in the LE Patting This assesses the integrity of the extrapyramidal or spinocerebellar tract; the pt is asked to pat his foot repetitively against the Test floor, to alternately tap the heel then the toe against the floor or asked to maintain the heel against the floor and abduct, the adduct the foot Rombergs This test assesses a patients proprioception that is, the ability to sense where one is in sense and time: proprioception is Test carried on two tracts conscious proprioception on the dorsal columns and unconscious proprioception on the spinocerebellar Damage Eyes Open Eyes Closed Cerebellar and Dorsal Columns sway Sway Cerebellar Only steady sway Clinical 0 = absent no evidence of contractility 1 =trace evidence of slight contracture no joint motion Muscle 2 =poor complete ROM w/ gravity eliminated 3 = fair complete range of motion against gravity Testing 4 =good-complete ROM against gravity w/ some resistance 5 =normal-complete ROM against gravity w/full resistance Movement disorders with cerrebellar lesions: Asthenia is present - this is exhibited by muscles tiring easily. Hyporeflexia is a concomitant finding shown by a decrease in deep tendon reflex responses

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dysmetria is present - this is a loss of the ability to gauge distance, speed or power or movement a patient may typically "overshoot" a desired point or stop before it is reached speech is slurred, jerky or explosive in nature nystagmus is usually present with cerebellar lesions intention tremor occurs with initiation of voluntary movement that often intensifies as the goal is neared

3.
Description Etiology Epidemiology Clinical presentation Treatment

Basal Ganglia disorders-responsible for fine movements, composed of subthalamic nucleus and substantia nigra Huntingtons chorea

Chronic progressive degenerative CNS disease of adult life characterized by choreic involuntary movement, progressive dementia and psychiatric and behavioral disturbances and this abnormality is confined to the brain and in advanced cases shown extensive atrophy of the cerebral cortex, basal ganglia and cerebellum Assoc w/ a defect in chromosome 4 this gene codes for a protein called huntingtin that is found in neurons throughout the brain its normal function is unknown and the greater number of copies, the more likely the patient is to develop the disease Transmitted via an autosomal dominant pattern with virtually complete penetrance it occurs in from 4 to 7/100,000 It affects both men and women equally, however, a head tremor may be more frequent in women and it is generally present in the older population by age 65 Athetosis- is occurs frequently in the hands and face; hemmiballisms-this is a dramatic condition characterized by wild flinging or circling movements of the limbs (lesion associated with the subthalamus) Essential tremor and choreoathetotic gait haloperidol and phenothiazines may suppress the chorea, but it is rarely possible to suppress of al the involuntary movements and it may subside with low levels of alcohol, propranolol at doses from 60-240 mg/day may reduce the tremor in roughly 75% of patients, beta-2 receptor antagonists are more effective than beta-1 receptor antagonists Sydenham's Chorea aka St. Vitus Dance Sydenham's chorea is considered a major diagnostic sign of rheumatic fever and it can occur up to six months following a Group A beta-hemolytic streptococcal infection (Streptococcus pyogenes) and it is an indication to initiate prophylactic antibiotic therapy to prevent subsequent development of other manifestations of rheumatic fever result from autoantibodies resulting from the strep infection which attack specific areas in the brain it occurs most commonly between ages 5 to 15 with peak incidence at age 8 and it is more common in girls The onset is usually insidious and the child may exhibit nervousness with emotional lability (irritable and/or anxious), aimless involuntary movements, impaired coordination and muscular weakness with reduced muscle tone. Over time, this condition progresses and involuntary movements, sudden jerks and flinging movement of the limbs occur. The movements are worse when trying to repress thsm and disappear while sleeping Traditional treatment of placing the child in a dark room to minimize external stimulus may suffice in mild cases phenothiazines or haloperidol can effectively control the chorea although valium is more practical anti-microbial therapy of the underlying etiology is essential generally a course of penicillin or erythromycin if penicillin-allergic the condition will usually resolve in 3 to 6 weeks Parkinsons disease (PARK)

Description Etiology Epidemiology Clinical presentation Treatment

Pathology Epidemiology Clinical presentation Treatment

most common pathologic feature is the loss of the dopaminergic neurons originating in the substantia nigra the mean onset is between 55 to 60 years of age; 1% of the US population over 50 years of age are affected about 50,000 new cases are diagnosed each year and the incidence does not appear to be changing with time the classic features are the insidious onset of tremor, rigidity, bradykinesia and disturbances in gait and posture Pill rolling resting tremor one of the most common presenting signs; Akinesiaa lack or poverty of movement and Cogwheel ridgidity shuffling festinating gait ; bradykinesia - a slowness and fatiguing of voluntary movement all of these symptoms progress in severity leading to "masked facies" and disabling postural difficulties levodopa - the most effective: a combination of levodopa and carbidopa (Sinemet) is usually used dopamine agonists, amantadin, anticholinergics selegiline: a selective inhibitor of type B-monoamine oxidase which does not stop the progression but has been shown in clinical trials to delay the need for levodopa therapy COMT inhibitors which include entacapone and tolcapone: COMT is an enzyme that breaks down levodopa in the periphery and when given in conjunction with levodopa, COMT inhibitors may increase CNS delivery of dopamine

Wilson's disease in the juvenile patient, symptoms characteristic of parkinsonism may occur it is the result of is a defect in copper-binding ceruloplasmin leading to accumulation of copper in the tissues clinical findings include signs and symptoms of basal ganglia dysfunction and hepatic cirrhosis there is a pathognomonic appearance of copper at the periphery of the cornea (Kayser-Fleischer rings) the children may exhibit arm flapping, schizophrenic behavior and multiple movement disorders treatment is with D- penicillamine which facilitates the removal of the excess body copper

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Upper motor neuron damage

Lower motor neuron damge

4.
Pathways The Dorsal Columns

Spinal Cord diseases Spinal Cord Neuronal Pathways

Damage Produces IPSILATERAL Loss of conscious proprioception, light touch, vibratory and position sense CONTRALATERAL loss of Pain and temp CONTRALATERAL loss CONTRALTERAL loss of motor control

Spinothalamic Tracts Spinocerebellar Tract Corticospinal Tract (Pyramid)

Description Sensory Information Pathway fasciculus gracilis carries receptors in and about taken by ascending vibratory and position sense fibers: impulses from lower thoracic, joints, bones, periosteum, fibers enter the spinal cord and ascend on the ipsilateral lumbar and sacral dorsal roots (i.e. skin, muscles and same side at the level of the brain stem fibers cross the lower extremities) connective tissue over or decussate to the thalamus & relayed to other fasciculus cuneatus carries conscious proprioception; parts of the body; some fibers carrying light touch impulses from the upper thoracic light touch, vibratory and decussate just after ascending only one to two and cervical dorsal roots (i.e. the position sense vertebral levels beyond their entry sparing of light upper extremities) touch sensation with unilateral spinal cord lesion; ascending pain and sensory fibers enter the spinal cord ascend no more than 1 2 vertebral levels before temperature decussating into the contralateral side of the cord fibers ascend up to the cord to the pain and temperature thalamus or relay center of the brain cerebral motor cortex. unconscious pathway of unconscious proprioceptors in the spinocerebellar tract remains ipsilateral proprioception and ascending fibers remain within the cord on the side of entry; the spinocerebellar tract enters the stereognosis cerebellum via the superior and inferior peduncles primary motor pathway exiting the cerebral cortex descends to the brainstem decussating at the junction of the (descending track) responsible for voluntary motor brainstem and spinal cord to provide contralateral motor input; control synapses in the anterior motor horn of the spinal cord

Damage to the corticospinal tract produces pyramidal disease, and outside of the pyramid extra pyramidal disease symptoms (EPS), i.e. Cerebral Palsy.
Spinal Radiculopathy Def. Radiculopathy pathology pertaining to the spinal nerve roots as they exit the spinal column through the vertebral foramina; vertebral foramina is a limited space and subject to impingement by bony spurs, tumors or protruding (herniated) vertebral discs. Frequent causes of lower extremity radiculopathy include: disc herniation, degenerative joint disease and other arthritides affecting the spine, congenital anomalies, acute trauma, repeated mechanical strain, infections and neoplasms;

Radicular Pain*pain follows the distribution of he nerve involved

Spinal cord evaluation of radicuopathy Neris sign: pt takes small steps with knees semi-flexed to prevent stretching of the nerve root Minors sign: when pt rises from seated position, pt places wt on unaffected side with one hand on his back Lumbar lordosis or thoracic kyphosis Pseudoclaudication relieved by flexing spine Straight leg raise test: pt supine and hip passively flexed with knee in full extension; should be nonpainful Lasegues test: reproduction of pain when pts leg is elevated less than 30 degrees and foot dorsiflexed Bowstring test: to differentiate root pain from hip pain; pt is supine, hips in full extension, if nerve pain then when knee is flexed pain goes away Gaenslens test: differentiate lumbosacral from sacral iliac pain; pt supine with one leg in full extension and the other is lowered off the side of the table; the twisting of the pelvis causes sacro-iliac pain Valsalva maneuver: dx space-occupying lesion or herniated disc; b/l compression of jugular vns result in increase intra-spinal pressure and reproduces radicular pain EMG studies Spinal Dysraphisms Def all forms of developmental abnormalities occurring in the midline of the back failure of spinal column to close 2o to faulty development of vertebrae. Normally vertebral column should be closed by 4th intrauterine week; bony canal should be closed by the 12th intrauterine week; defects occur most commonly in the lumbosacral spine incidence 0.05 to 0.25 per 1000 births Prevention: prenatal screening for AFP may demonstrate levels in neural tube defects 20% incidence of false positives folate prevents neural tube defect

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Condition Spina Bifida Occulta Spina Bifida with Meningocele or Meningmyelocele

Tethered Cord Syndrome Anterior Cord Synd Brown-Squard syndrome*** Central cord syndrome Conus medullaris syndrome Cauda equina syndrome

Characteristics Incomplete closure of one or more of vertebral arches only in the sacral region; occurs in 10 25% of population; posterior arches of L5 & S1 are most common; asymptomatic; an incidental finding on radiographic imaging Occurs 2o to faulty closure of the vertebral arches + involvement of meninges (meningcele) or spinal cord itself (meningomyelocele); the spinal column defect is associated w/ a sac-like protrusion of skin and meninges the nature of the clinical symptoms will depend upon the degree and the level of the deformity in the sacral spine Clinical Symptoms Dematological Manifestations Symptoms unitlateral; decreased lumbosacral hypertrichosis (localized overgrowth of hair) at base of the spine; proprioception & cutaneous sensorium; capillary angioma or naevus flammeus most common findings associated with decreased lower extremity DTR with spina bifida; lumbosacral dermal sinus serve as a pathway for infection & concomitant weakness & atrophy of the leg present as meningitis; midline lumbosacral subcutaneous lipoma firm & muscles foot pathology valgus, varus and gritty fat bound together by septal fibers present at the base of the spine cavovarus deformities & gait disturbances. *lumbosacral skin appendage skin tag which resemble a tail Involves traction on the conus medullaris & is associated with a tight filum terminale progressive neurological deterioration in the lower spinal cord; occur 2o to diastematomyelia (division of spinal cord into two segments within the sagittal plane) d/t bony or cartilaginous island projecting from the posterior vertebral arches into the spinal cord; Involves variable loss of motor function; pain and/or temperature sensation, with preservation of proprioception Involves a greater ipsilateral loss of proprioception and motor function, with contralateral loss of pain and temperature sensation. Involves a cervical lesion, with greater motor weakness in the upper extremities than in the lower extremities. Sensory loss variable; more likely to lose pain and/or temperature sensation than proprioception and/or vibration. Dysesthesias (sensation of burning in hands or arms) esp in UE; Sacral sensory sparing exists. Sacral cord injury with or without involvement of the lumbar nerve roots; characterized by areflexia in bladder, bowel, and lower limbs (motor & sensory loss in LE is variable). Injury to the lumbosacral nerve roots; characterized by areflexic bowel and/or bladder, with variable motor and sensory loss in the lower limbs. B/c is a nerve root injury rather than a true Spinal Cord injury the affected limbs are areflexic; caused by a central lumbar disk herniation;

Diseases of the musculature and neuromusclular junction

X-linked Muscular Dystrophies It is caused by mutations in the gene for dystrophin (deletions) Duchenne Muscular Dystrophy Becker Muscular Dystrophy Most common 1:10,000 Least common Most severe: Fatal at 20 years old Least severe: Not fatal 5 years old onset Later in childhood or adolescence No dystrophin Some, but altered dystrophin size Primarily affects walking due to extensive involvement of the pelvic muscles. Pseudohypertrophy-replacement and Slower progression Cardiac infiltration of the muscle cells by fat. Can affect systemic muscles of the heart cause of death disease is less common Pathognomonic for this disease is Gowers sign where the affected child rises from a sitting position by climbing on her legs Limb-Girdle Heterogenous autosomal muscular dystrophies that affect specific muscle groups, specifically the proximal muscles of the trunk muscular and lower limbs. Mutations of the sarcoglycan complex (transmembrane proteins of the sarcolemma that interact with dystrophies dystrophin) are the cause of these diseases. Myotonic Autosomal dominant trait, m.c. seen in adults that causes a myotonia (sustained involuntary contraction) of a muscle group. Dystophy The disorder tends to increase in severity and appear at younger ages in successive generations Anticipation. S/s: Cataracts, Frontal balding, Cardiomyopathy, Decreased IgG and Abnormal GTT FacioSlowly progressive, autosomal dominant inherited disorder; involves muscles of facial expression and the proximal upper extremities; M scapulohu = F; intact intellectual function; onset 3rd & 4th decade better prognosis meral Clinical Sym - characteristic weakness of facial, shoulder girdle and proximal arm muscles; inability to whistle, sullen, expressionless Muscular appearance noted w/I 1st decade; weakness of serratus anterior, trapezium & rhomboid muscles winging of scapular & sloping Dystrophy shoulders; muscles that abduct the glenohumeral jt remain strong; biceps & triceps affected later w/ deltoid spared; foot drop - early in Dz 2o to peroneal & anterior tibial muscle weakness; Eventually lose ability to ambulate w/o assistance; cardiac & respiratory involvement rare; exophthalmos with (N) thyroid function; mild but labile hypertension common Dx CK levels - normal or slightly elevated; EMG and muscle biopsy mixed features of myopathy and neuropathy Tx - generally palliative; AFO for foot drop; scapular stabilization to decrease scapular winging; Limbautosomal recessive 60%; proximal muscular weakness starting w/ legs or arms progresses to all extremities; onset 2nd - 3rd decade; Girdle minimal facial involvement; hypertrophy of calf muscles < 1/3 of pts; ambulation continues for 20 yrs after the initial diagnosis; cardiac Dystrophy involvement may congestive heart failure or arrhythmias; respiratory failure may occur after 30 yrs; Dx - elevated CK not as high as Duchenne's; EMG consistent w/ myopathy; muscle biopsy not specific Tx PT; Breathing exercise Diseases of the NMJ: Myasthenia Gravis Description and Characteristics Autoimmune disorder caused by the production of autoantibodies to the Ach receptor on the motor end plate. Associated with thymic hyperplasia or thymoma

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NB Toe walking - <2yrs (N); other causes of toe walking: CP spastic paralysis; MD muscular contractures <2 bad C. Cardiovascular disorders 1. Major cardiac
Symptoms Pressure, squeezing Impending doom N/V, diaphoreses (sweating) Chest pain Location Time Arm, Jaw 15 min Similar - angina >15 min Causes CAD ischemia Angina may precede Treatment Nitroglycerin

Angina Pectoris Myocardial Infarction

Dissecting aneurysm Pleurisy Esophagitis GERD Tietzes Pericarditis Gallbladder Cholecystitis

Nitrates, ASA, B-blockers, Ca+ antagonists, heparin, thrombolytic tx, PCTA Sharp, knife-like, severe, ripping Generalized >15 min varies stroke Surgery and prevention Sharp pain associated with respirations Generalized >15 min Pleuritis, can be seenControl infection pneumonia Heart burn, dyspepsia (burning) Generalized Assoc with hiatal hernia Medication, surgery Sharp, costochondritis, tender at Chest wall Days wks Inflam. of costocondral Benign, assoc with pressure points joints anxiety Sharp Generalized varies Inflam. between the visceral and pericardium Sitting up and forward Diagphragmatic pain at the right costal Upper abdomen, varies margin shoulder Infection, UTI, gallstones Surgery, control infection

Description Causes Symptoms and signs Treatment

Congestive heart failure Inability of the heart to pump a sufficient amount of blood throughout the body, or requiring elevated filling pressures in order to pump effectively. The pooling of blood leads to congestion in body tissue. Genetic family hx of CHF, infection, alcohol ingestion, anemia, thyrotoxicosis, arrhythmia, and hypertension. The usual heart irritants can make CHF deadly: arterial plaque, stress, smoking, old age, no/little excercise, overworked heart, and obesity. Pulmonary edema, peripheral edema, rales heard on chest auscultation, an enlarged or pulsatile liver, and JVD. Symptoms of decompensated heart failure include dyspnea on exertion, orthopnea (dyspnea that increases upon lying down), fatigue and paroxysmal nocturnal dyspnea. DO NOT use pneumatic compression devices. Treating the signs and symptoms of CHF involves maintaining a euvolemic state diuretic agents, vasodilator agents, and positive inotropes. Delaying the progressionACE inhibitors, beta blockers, and aldosterone antagonists.

Antianginal drugs NO increases cGMP, predominate venodilator to reduce CVP, will be degraded by organic hepatic nitrate reductase if taken orally, will also increase HR and CO Very short acting Amyl nitrate, short acting isosorbide dinatrate (sublingual tablets), intermediate acting isosorbide mononitrate, and long acting transdermal nitrate Ca channel blockers Dighydropyridines: Nefedipine, does not effect AV conduction, Befridil acts on fast Ca channels and predisposed to ventricular arrhythmias and torsade de points ..dipines B blockers Not a vasodialator, not useful in the tx of prinz metals or vasospastic angina Nitrates Antidysrythmiacs Class Ia Quinidine cinchonism high anticholinergic activity, can be used for all arrhythmias; Procainamide local anesthetic, esterNa channel blocker low anticholinergic activity, vent arrhythmias only and Disopyramide - high anticholinergic activity, vent arrhythmias only Class 1b: Weak Na Lidocaine, vent arrhythmias only, used in ischemic arrhythmias ; Phenytoin, vent arrhythmias only, used to treat digitalis toxicity channel blockers Tocainide/mexiltine Class 2 Beta blockers vent arrhythmias only, can also be used to tx digitalis induced arrythmias Class 3 K channel blocker-refractory treatment, can be used for ventricular arrhythmias: Amiodarone, Btretylium, Sotolol Class 4 L-type Ca channel blockers-Verapamil Hypertension A medical condition where the blood pressure is chronically elevated. Persistent hypertension is one of the risk factors for strokes, heart attacks, heart failure and arterial aneurysm, and is a leading cause of chronic renal failure. HTN >140/90 and In patients with diabetes mellitus or kidney disease studies have shown that blood pressure over 130/80 mmHg should be considered a risk factor and may warrant treatment Systolic Diastolic BP Stage 1 140-159 90-99 Stage 2 160-179 100-109 Stage 3 180-209 110-119 Stage 4 >210 >120

Description

Staging

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Essential HTN Risk factors in development of HTN Secondary HTN

Pathophysiology

Complications

Diagnostic evaluation Treatment

Types No identifiable etiology Age Over time, the number of collagen fibres in artery and arteriole walls increases, making blood vessels stiffer and w/ the reduced elasticity comes a smaller cross-sectional area in systole, and so a raised mean arterial blood pressure. High salt intake, Sedentary lifestyle, Tobacco smoking , Alcohol abuse,High levels of saturated fat in the diet. Obesity In obese subjects, losing a kilogram of mass generally reduces blood pressure by 2 mmHg, Stress, Low birth-weight, DM Identifiable etiology Renovascular disease (atherosclerosis, fibromuscular dysplasia(, intrinsic renal disease, hyperaldosteronemia, Cushings disease, coarctation of the aorta, drugs (especially oral contraceptives) 1. Inability of the kidneys to excrete sodium, resulting in natriuretic factor being secreted to promote salt excretion with the side-effect of raising total peripheral resistance. 2. An overactive renin / angiotension system leads to vasoconstriction and retention of sodium and water. The increase in blood volume leads to hypertension. 3. An overactive sympathetic nervous system, leading to increased stress responses. Cerebrovascular accident (CVAs or strokes) Myocardial infarction (heart attack) Cardiomyopathy (heart failure due to chronically high blood pressure) Hypertensive retinopathy - damage to the retina nephropathy - chronic renal failure due to chronically high blood pressure HTN is rarely severe enough to cause symptoms. These only surface with a SBP> 240 mmHg and/or a diastolic blood pressure over 120 mmHg. These pressures without signs of end-organ damage (such as renal failure) are termed accelerated hypertension. When end-organ damage is possible or already ongoing, but in absence of raised intracranial pressure, it is called hypertensive emergency. Malignant hypertension (or accelerated hypertension) is distinct as a late phase in the condition, and may present with headaches, blurred vision caused by increased intracranial pressure and end-organ damage. Kidney function: Serum creatinine and BUN are elevated, urinalysis (proteinuria), elevated K+, EKG, and CXR Lifestyle modification with weight loss and diet. The aim of treatment should be blood pressure control (<140/90 mmHg,). Each added drug may reduce the SBP by 5-10 mmHg, so often multiple drugs are necessary to achieve blood pressure control.

Antihypertensives
Diuretics Mannitol, Carbonic anhydrase inhibitors Loop diuretics o Types: Fursosemide-Lasix o Adverse effects: causes an increase is K loss Thiazide diuretics o Adverse effects K sparing diuretics o Types: Spirinolactone, Amiodarone o Adverse effects Beta blocker Decreases HR, CO, and SBP S/E hypoglucose, hyperTGs, may ppt CHF and angina A2 agonists Clonidine, a-methyldopa (do LFTS, prodrug) does not cause reflex tachycardia A antagonists Phentolamine and Phenoxybenzamine (non-selective) used in the tx of pheochromocytoma .zocinselective will cause reflex tachycardia and 1st dose syncope Post-ganglionic sympatholytics Reserpine, Guanadrel Direct vasodialators Apresozide, hydralazine, Minoxidil ( hirsutism) Diozozide, Nanitroprusside, nitroglycerin infusion Ace inhibitors -prils- cough and hyperkalemia via its inhibition of aldosterone that causes hypoK and hyperNa Ca channel blockers Decreases TRP, CO, and HR, vasodialator Angiotensin receptor antag -artansblocks the angiotensin 2 receptor, has no cough

2.

Arterial, venous, lymphatic

Review of arterial and venous testing

Duplex ultrasound 8-10MHz of U/S Triphasic-faster Q wave form resembles a teepee, biphasic-may be normal in pts with DM, monophasic-slower Q-indicates significant abnormality Plesmography Check the microvascular status, uses UV ligh to create wave form s that are similar to Doppler. Pulse volume recording Measures the actual volume passing through a specific area MRA Contraindicated with a pacemaker, hardware. OK in pts with renal dz b/c no dye is used ABI Wagner in 1979 Normal-09-1.2 Intermittent Claudication-05-0.8 >0.45 indicates healing potential TBI >0.6 low risk, <0.2 severe risk *more reliable than ABIs Digital pressures Normal-70-110mmhg, <30-40mmhg indicates poor healing Segmental pressures Thigh, AK, BK, ankleSuspect occlusion is gradient is >20-30 between 2 levels TCPO2 Wyss, Harrington and Burgess JBJS 1988 Normally 30-40mmhg

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Normal clotting
1. Hemostasis: prevention of bleeding Primary hemostasis blood vessels and the platelets Secondary hemostasis Coagulation proteins 2. Prevention of thrombosis Naturally occurring anticoagulants and platelet inhibitors. Cellular injury vessel vasoconstriction platelet adhesion stabilization and reinforcement of the plug by the intrinsic and extrinsic systems fibrinolysis Phases of the classic theory of coagulation Phase 1: Generation of tissue thromboplastin (Factor III) intrinsic pathway Phase 2: Activation of thrombplastin-end product of intrinsic and extrinsic pathways The final common pathway begins with the activation of Factor X Phase 3: Conversion of prothrombin to thrombin by Factor Xa Phase 4: Conversion of fibrinogen into fibrin, by thrombin, which is stabilized by factor XIII Coagulation factor of Human Blood Factor Synonym Deficiency I (Fibrinogen) Afibrinogenemia II (Prothrombin) Hypoprothrombinemia III (tissue thromoboplastin) IV Calcium ions Hypocalcemia V Labile factor Accelerator globulin Procaccelerin parahemophilia VII Stable factor, Proconvertin or Prothrombin conversion accelerator-SPCA Hypoconvertenemia VIIIa AHF Antihemophilic factor Classic hemophilia VIIIb vWF Von Willebrand disease IX (plasma thromboplastin component-PTC) Christmas factor Hemophilia B-Christmas disease X Stuart Factor Stuart Stuart def XI plasma thromboplastin antecedent-PTA PTA def XII Hagemon factor Glass contact factor Hagemon trait XIII fibrin stabilizing factor Fibrinase XIII def Kallekrein pre-kininogen Fletcher factor HMW kininogen Fitzgerald factor Reactions of the extrinsic pathway are initiated by contact of blood with injured tissue Intrinsic Pathway III + VII VIIa activates X Xa Extrinsic Pathway XII XIIa by surface contact XI XIa IX IXa + VIIIa XXa Xa II IIa Fibrinogen Fibrin clot!! Plasmin Plasminogen t-PA (clot breakdown) Regulation of hemostasis: Natural anticoagulants Antithrombin III: Inhibits thrombin (IIa), VIIa, Xa, IXa, kallekrein and plasmin by forming stable complexes with theses enzymes Heparin Slows the conversion of II IIa Potentiates ATIII Decreases platelet activity and adhesiveness Preventing activation of IX and VII Coagulation studies 1. Platelet count 150,000-400,000/mciro liter 2. Lee-White clotting time (whole blood coagulation time) 6-10 min 3. Bleeding time (finger stick) 1-4 min 4. Prothrombin Time: 11-13s guide for coumadin therapy International normalized ratio Recommended INR ranges Situation INR Prevention of venous thrombosis 2-3 Treatment of venous thrombosis 2-3 Treatment of PE, TIA, and Afib 2-3 Prevention of recurrent DVT 2-3 Treatment post MI 2-3 Prevention of stroke, with reduced mortality and recurrence 3-4.5 Prevention of embolism 2.5-3.5 Mechanical heart valves 2-3

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Tissue heart valves 5. PTT 25-35s used a guide for heparin therapy (pts should have a PTT 1.5-2.5x normal) 6. Fibrinogen 200-400mg/dl 7. Coagulation Factor assays: II, V, VII, IX, X, XI, XII Anticoagulants: Indications: venous thrombosis, DVT, PE, Afib with embolism, MI, and surgical prophylaxis Contraindications: allergy active bleeding, CNS surgery, eye surgery, GI ulceration, severe HTN, pregnancy, L&D, use with caution with liver and pancreatic disease Types: Heparin: LMWH-enoxaprin (Lovenox) and Coumadin-(-) the prod. of VitK dependent factors: II, VII, IX, X Antiplatelet-type drugs 1. ASA : (-) COX, decreasing TXA2, causing decreased platelet aggregation/increased vasodilatation 2. PDE inhibitors Persantine-PDE III inhibitor decreases [cAMP] which leads to decreased platelet aggregation Pletal (clopidrel) PDE III inhibitor decreases [cAMP] which leads to decreased platelet aggregation 3. Ticlid-250mg po bid 4. Trental (pentoxyfilline)-alters the rheology of RBCs (increases flexibility, decreases blood viscosity by decreasing RBC aggregation, decreasing elevated plasma levels of fibrinogen, also releases plasminogen activators thereby promoting fibrinolysis Fibrinolytic therapy Prevent thrombosis and provide a rapid return to normal Q, physiologic and hemodynamic states, thereby preventing end organ damage 27% reduce the mortality of MI Treatment within 6 hours of MI; ideally within -1 post MI First Generation Plasminogen activators: (no longer used) Streptokinase and Urikinase Second generation (fibrin target specific, no systemic plasminogen activation): t-PA (activase) DIC condition in which clotting and hemorrhage occur simultaneously within the intravascular compartment: Overall pathology: Unrestricted coagulation occurs affecting all systems thrombotic events rapid consumption of clotting factors (trying to destroy the clots) bleeding Associated with three pathologic process 1) Endothelial cell damage (burns, brain injury, surgery, MI) causing the 2) Release and activation of tissue thromboplastin which activates the coagulation cascade 3) And direct activation of X (snakes, venoms) involves most often the extrinsic system Treatment Remove the offending agent Restore the appropriate balance between coagulation and fibrinolysis Maintain organ viability Fluid replacement Antibiosis as needed FFP, platelet concentration Heparin, when thrombotic events are present: cyanosis, coldnessetc Athersclerosis Obliterans (ASO) of the lower extremity Plaques tend to occur on the posterior aspect of the LE arteries , m/c bifurcation sites. Other areas: common femoral a, distal superficial a at Hunters canal and the tibioperoneal trunk, Q to distal tissues is maintained thorough collateral vessels Clinical Intermittent claudication Rest pain Ischemic ulceration and gangrene Manifestations Ischemic neuropathy Disuse atrophy Muscular weakness and joint stiffness Laboratory studies NIVAs, Blood chemistry: Fasting sugar, lipid profile, HbA1c, CBC, LFts, kidney and serum chemistries Cardiac testing: 12 lead EKG if surgery is being considered, stress testing, Plain X-ray films of the LE particularly if lesions are present, Arteriogram if intervention is considered Differential Atherosclerosis, Throboangitis obliterans, Takayasus arteritis, Giant cell arteritis, arterial embolism, chronic pernio, popliteal Diagnosis artery entrapment, fibromuscular dyplasia, Cystic adventitial disease of the popliteal a, atheromatous emboli, ergotamine use, phlegmasia cerula dolens, lumbar canal stenosis, degenerative joint disease of the jip and back, arthritis Treatment Lifestyle modifications: d/c smoking, diet control. Exercise tx: Increase collateral Q, decrease blood viscosity, (+) oxidative metabolism in the skeletal m, and improves rheorrheology. Pharmocologic tx: 3 goals: 1) Increase walking distance 2) Decrease the need for surgical revascularization or endovascular therapy3) Prevent the progression of atherosclerosis and reduce cardiac and CV mortality and morbidity. Trental-pentoxyfylline (400mg ot id), Pletal-cilostazol and Antiplatelet drugs ASO drugs: Ticlid, ASA, Persantine Surgical treatment: Lumbar sympathetctomy, aortoiliac-femoral, profunda femoris, femorropopliteal, and femorotibial reconstruction, endovascular Description

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therapy (PTA, stent placement) amputation Some hospital order/prescriptions for acute arterial occlusion 1. Pain: Demorol 100mg IM q4h prn pain or 25-50mg IV q4h prn pain 2. Prevent thrombus extension: Heparin bolus 5000-20,000 U followed by 2000-5000 U/h infusion a. May dose by weight: 80 U/kg IV bolus the 18 U/kg/hour infusion 3. Long-term anticoagulation: Coumadin 5mg po qd x 2-4 days then adjust to INR of q2-3 or PT (2-2.5x control)

Chronic venous insufficiency

Definition Patho-physiology: Long-standing incompetence of the perforating communicating veins of the LE that drain 90% its blood. The middle perforators are located just proximal and extend 7-10 cm above themedial malleolus The basic underlying pathologic mechanism in chronic venous insufficiency is venous hypertension. The proteins polymerize forming sclerosis of the surrounding tissue (lipodermatosclerosis-gives the leg an inverted champagne bottle resemblance). The RBCs break down and the hemoglobin oxidizes brownish hemosiderin staining of the skin. The build-up of toxins and metabolites leads to changes as visible dry, scaly dermatitis. Activated WBCs (cell trapping theory) release their proteolytic enzymes, superoxide radicals and cytokins leading to skin breakdown and ulcers 1) Edema: This may be the first manifestation of early CVI. 2) Venous dilation and varicosities 3) Leg pain: The most frequent type of pain is limb heaviness or ache which occurs after prolonged standing (involvement of the superficial venous system) but can also show a deep venous insufficiency venous claudication that is felt as a bursting or cramping pain (related to an iliofemoral venous obstruction) or pain associated with valvular incompetence that is felt as sudden heaviness or ache that is quite debilitating.
Grade I II III S/S Physical findings Mild swelling, heaviness, vein dilation Ankle edema < 1cm Dilated superficial veins; Normal skin and subQ Moderate-heavy swelling, heaviness, Ankle edema > 1cm Multiple dilated veins varicosities, skin changes Incompetent perforating veins, mild pigmentation and mild liposclerosis Severe swelling, calf pain, with Edema> 2cm, Multiple dilated veins, Incompetent perforating veins (severe), or w/o claudication multiple vein varicaosities, marked skin pigmentation, severe liposclerosis and the presence of an ulcer

Clinical findings

Clinical Classification

Diagnosis NIVA*

Biphasic Trendelenberg or retrograde filling test to assess the competence of the perforators and saphenofemoral valve. The Perthes test to examine the patency of the perforating valves
Duplex scanning imaging is the test of choice in evaluating venous disease. It is highly sensitive, noninvasive, and readily available. Augmentation on distal compression No augmentation on distal release No augmentation on proximal compression Augmentation on proximal release

Treatment Nonsurgical

The cornerstone for control of CVI is the control of venous hypertension external compression. The amount of pressure at the ankle should be between 30 and 40 mmHg, decreasing gradually to 12 to 17mmHg below the knee (sustained pressure). Sclerotheraphy-success is dependent upon producing an inflammatory response in a limited section of a vein (SotradecalSTD: Soidum tetradecyl sulfate 3% and monolate: monoehtanolamine oleate Radio-Frequency Endovenous Occlusion-Closure aternative to saphenofemoral ligation and/or stripping

DEEP VEIN THROMBOSIS INTRODUCTION o Deep venous thrombosis (DVT) is common among hospitalized patients characterized by the formation of thrombi in the leg veins; fatal pulmonary embolism (PE), particularly because it is under recognized and misdiagnosed o Most thrombi in leg are small & asymptomatic, confined to the deep veins of the calf, 20% KIM and extend into proximal deep veins of the thigh, that presents as a painful, swollen leg/arm or asymptomatic o Two major complications - pulmonary embolism and post-phlebitic syndrome. o Incidence uncertain; 300,000 - 600,000 hospitalizations each year in the U.S. for venous thromboembolism; 200,000 people die each year of DVT and its complications; PE was 3rd most frequent cause of death in the U.S. >70% of patients who die of PE are not suspected of having it before death. Predisposing risk factors of DVT I am clotted Immobility/inactivity Longevity of surgery Estrogen Atrial fibrillation/ age Obesity DVT history Morbidity/ MI/malignancy Tobacco/tourniquet Coagulable state Tumor/trauma

1. Immobilization: o risk for pre-operative; intra-operative and post-operative situations & inactivity after discharge;

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high risk - in the paralyzed limb & post-CVA patient; patients w/ incapacitating cardiac & pulmonary disease (COPD); healthy patients during long airplane rides or automobile trips 2. Surgery o Greatest risk - patients undergoing orthopedic procedures (hip, knee, or pelvic surgery); neurosurgery & major abdominal or pelvic surgery for malignancies; o Thrombogenic factors associated with surgery release of tissue thromboplastin; stasis from immobilization, & a reduction of the fibrinolytic system activity 3. Age o Patients >60yrs @ highest risk for developing DVT decreased activity due to systemic disease, venous dilation (venous stasis) common in the elderly patient; decreased fibrinolytic activity; o DVT also in pediatric population due to central venous lines (iatrogenic cause) 4. Malignancy o DVT in unusual anatomical locations & develop thrombi resistant to anticoagulation therapy; o May develop into phlegmasia cerulea dolens (venous gangrene); o Patients w/ neoplasms of the lung, GI tract, UG tract, breast, and intracranial tumors greatest risk for thrombosis Phelmasia cerulean dolens Phlegmasia alba dolens Venous gangrene Milk leg Pain, blue discoloration, marked edema Pale or white leg caused by extensive iliofemoral signs of arterial insufficiency, these patients compression secondary to profound edema or venous often have an underlying malignancy and many thrombosis-associated with pregnancy (post-partum) will require an amputation 5. Obesity o Impairs fibrinolytic activity & promotes greater inactivity an increased frequency of DVT in obese pts (who weigh more than 20% above standard) 6. Pregnancy o DVT d/t decreased fibrinolytic activity during the 3rd trimester, early labor & before placental detachment; o Release of tissue thromboplastin at the time of placental separation, venous stasis resulting from venous dilation, mechanical pressure of the uterus on the Inferior Vena Cava during the 3rd trimester and during delivery. 7. BCPs, increased estrogen o Produces venous dilation, decreased functional levels of antithrombin III & decreased fibrinolytic activity vasoconstriction that lead to clot formation DVT Pathology Venous thrombi form in areas of the venous system where the blood is naturally stagnant (stasis) around the valvular system, and start in the tibial veins and the soleal sinuses popliteal & femoral veins. Propagates in the direction of Q by addition of successive layers of cellular components & fibrin and when the thrombi reach large vein of the thigh, it is loosely attached to the vein walls; increasing the potential for detachment & embolization. Fate of the thrombus - if thrombus does not embolize resolved by canalization, organization, or lysis by fibrinolytic sys, reestablishing the balance btwn thrombosis/ fibrinolysis. PATHO-GENESIS Virchows triad: endothelial damage, venous stasis, and hypercoagulability (increase activation of clotting factors). CLINICAL edema, warmth, erythema, pain (50%), tenderness: palpable firm cord (75%), night cramps, and + Homans sign (pain in the FEATURE calf with passive DF of the ankle /foot); positive in 33% of cases, and >50% false positives. Significant thrombosis may be present w/ minimal findings. Unusual presentation of DVT Phlegmasia AIba Dolens & Phlegmasia Cerelea Dolens dDx OF DVT Muscle aches, muscle tears Arterial insufficiency Bakers cyst Arthritis Neurogenic pain Cellulitis Myositis Lymphangitis Panniculitis Vasculitis Fibrositis Gout Fibromyalgia Superficial phlebitis varicose veins May-Thurner syndrome Extrinsic compression within the pelvis Dx Because clinical findings are notoriously unreliable in DVT, the dx should always be established by an objective invasive or noninvasive test. Contrast venography is the gold standard, most reliable technique for the detection of DVT that is confirmed as an intraluminal filling defect however, procedure puts patients at risk for a DVt Real time (duplex) u/s most accurate NIVA for dx of proximal DVT but less reliable in detecting small isolated thrombi. Impedance plethysmography (IPG) is a NIVA; high sensitivity & specificity in the diagnosis of proximal DVT (proximal and popliteal veins), & insensitive to infrapopliteal occlusions. A hand-held continuous-wave Doppler for examining venous flow in the groin, popliteal fossa, and posterior tibial veins. MRAcould dx either thrombosis or compression of the vein. 97% sensitivity; 95% specificity for dx of IFDVT; MRA has 100% sensitivity & NPV & a specificity of 98.5%. D-dimers: commonly found in circulation when a thrombus is present; increased focus on D-dimer assays, which are rapid, non-invasive/ inexpensive; since D-dimers are also found in other dz states (e.g. cancer, CHF, inflammation) not specific. o Treatment of DVT A painful, swollen leg and a positive duplex scan initiate therapy for DVT; a swollen, painful limb w/ a questionable or negative duplex scan requires a venogram for adequate criteria to initiate treatment. Patients w/ DVT hospitalized and anticoagulated o Obtain a coagulation profile and routine labs (CBC, BCP-7, UA, LFTs)

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Heparinize w/ bolus of 5,000 - 10,000 U, followed by a continuous infusion adjusted to a PTT of 1.5 - 2 x control (1,000 - 15,000 U/h). Heparin dosing based on patient weight (80 U/Kg of actual body weight by bolus followed by 18 U/Kg/h infusion) may achieve therapeutic anticoagulation more rapidly without an increased risk of bleeding o Recall that heparin does not break down the clot, it gives the patients fibrinolytic system time to break clot down o Heparin Reversal Protamine sulfate 10-50mg slow IV infusion over 10min; 1mg/100U of heparin o PTT should be checked 4h after initiation of therapy until therapeutic anticoagulation is achieved, and then q6 - 8h. o Administer local heat (AK pads) and analgesia as needed. o Complete Bed Rest (dont want to mobilize the clot); and elevation of the LE for the 1st 48 - 72h. Coumadin may be initiated on admission to prevent PE (it takes 3-5d to start working). Pt will eventually be discharged with po Coumadin. Dose: 10 mg P.O. qd x 2-3d, subsequent daily doses are adjusted to therapeutic INR of 2-3 or a PT of 1.5-2 x control. o Reversal of Coumadin: o INR > 6 < 10 w/ no serious bleeding vitK: 0.5-1 mg IV or if the INR > 10 < 20 vitamin K 3 - 5 mg IV o if rapid reversal is required d/t serious bleeding or the INR > 20 - vitamin K 10 mg IV o Re-check INR in 6hrs, in cases of severe hemorrhage who require rapid reversal FFP 2 -4 units o Other treatment modalities include: Low-molecular-weight heparin (LMWH): Lovenox (enoxaparin) 1mg/kg q12h; Fragmin o Thrombolytic therapy t-PA, Thrombectomy, Vena cava interruption (Greenfield filter) Note: untreated DVT 25% PE & 35% will be fatal. PREVENTION of DVT: The basis for prevention is effective prophylaxis, which is now available to most non-surgical and surgical patients. TYPE OF OPERATION OR Condition PROPHYLAXIS Abdominal or thoracic surgery Heparin 5000 U SQ ql2h starting 2 h preoperatively AND / OR pneumatic compression stockings Eye surgery or neurosurgery; open prostatectomy Pneumatic compression stockings Orthopedic surgery; hip or knee replacement LMWH 30 mg ql2h or pneumatic compression stockings OR adjusted doses of heparin SQ to prolong PTT 1-3 sec OR warfarin beginning the night of surgery General medical patients including stroke and MI Heparin 5,000 U SQ ql2h AND / OR pneumatic compression stockings LYMPHEDEMA Definition Introduction Lymphedema is defined as the accumulation of fluid (lymph) in any part of the body, m.c in the extremities but also in the lower abdomen, the scrotum, the external genitalia, and the face. Lymphedema is caused by the inability of the lymphatic system to remove lymph from the interstitial space, which causes stasis and accumulation of the lymph. In the lower extremities the lymphatic channels are located in the superficial (subcutaneous) and deep compartments. The deep lymphatic system follows the deep veins: tibial, popliteal and femoral. The superficial system, which is more important and carries 80% of the lymph from the lower extremities, is located along the GSV.The 2 systems (superficial and deep) join at the level of the groin and transport the lymph to the thoracic duct, which empties into the left jugulosubclavian venous junction.
(congenital familial or Milroys disease) Birth or early in life Secondary results from obstruction of the lymphatic channels secondary to mechanical occlusion due to tumors or metastasis or fibrosis from radiation (radiation fibrosis), Hodgkins disease, sarcomas, and neoplasms of bone. And is caused by an inflammatory process in which the lymphatic channels become obstructed USA: streptococcus World: W. Bancrofti Other: influenza, typhoid, pneumonia, malaria, and other systemic disease. Lymphedema precox Obstructive (most common) Inflammatory Before age 25 (9-19 years) Abrupt onset (hallmark) Recurrent lymphangitis cellulitis Notice puffiness around the foot Men prostate CA m.c. cause acute onset, chills, high temp. Red (dorsum) and ankle, painless, nonWomen ovarian CA and post streaks on the feet, LEs, thighs pitting edema w/ no signs of ulceration radical mastectomy (lymphadenopathy). Diffuse cellulitis Lymphedema tardae After age 35 and a portal of entry on the foot

Classifications

Clinical Picture Diagnosis Treatment Complications of lymphedema

Enlargement of the extremities or affected body part; the swelling is painless and is more resistant to pitting when compared with edema of venous nature, and the extremity is of normal color. The dx is based on clinical presentation and clinical findings. The presence of s/s indicating venous insufficiency, DVI, systemic edema, arterial insufficiency, and allergic causes of edema should be ruled-out. Pulses are present. Her notes: TQ: Tx for patient includes: Lasix, HTZ, surgery, outpatient compression therapy*, hospital intermittent compression pumps (immobilized with DVT prophylaxis of 5-10ku (immobile). No cure Malignant lymphangiosarcoma will develop from chronic distorted and enlarged lymph channels. This is usually seen as a bluish cutaneous area resembling a bruise, which eventually enlarges and produces satellite lesions. The central portion of the lesion may ulcerate. This condition should be treated aggressively w/ wide radical excision and chemotherapy. It should be mentioned that no effective chemotx exists and the condition is easily blood-borne causing metastasis elsewhere. Because of this, amputation, followed by radiation tx is often favored over radical excision and chemotherapy.
Stage I Mild: Reversible edema Pitting Reveresed by elevation Normal at waking Stage 2 Moderate: Spontaneous irreversible Need tretment to decreases swelling Pitting takes longer time to resolve Spongy tissue Stage 3 Severe: Lymphoclastic elephantiasis Non-pitting edema Hard, fibrous connective tissue, Limb is very large and swollen

Clinical Stages Lypmhedema

21

*Contraindications to Compression tx: CHF, DVT, active infection, renal failure, metastatic or ischemic disease

3.

Vasomotor

REFLEX SYMPATHETIC DYSTROPHY (RSD) AND CAUSALGIA Represents of group of disorders and wide number of terms or syndromes employed to describe them Current term is Chronic Pain Syndrome Two major types: o Causalgia-chronic pain syndrome associated with nerve injury, defined as burning pain (allodynia) and exaggerated subjective response to pain (hyperpathia) usually in the hand or foot after partial injury of a nerve or one of its major branches. Caused by entrapment neuropathies, stroke, radiculopathies, arthroscopy, neoplasms, a/v thromboses and drug use (rifampin, isonizid and barbiturates) Evidence of SNS over activity and the pain can be stopped with SNS blockers or sympathectomy o RSD- chronic pain syndrome not associated with nerve damage Description RSD is a commonly misdiagnosed condition characterized by severe pain, tenderness, limitation of motion, favoring of one limb, and autonomic dysfunction. Etiology The precipitating causes of RSD can be grouped into traumatic, non-traumatic, and idiopathic. About 60% of the causes of RSD are posttraumatic, can be iatrogenic. Minor or trivial trauma is the most common precipitating factor About 25% are associated w/ non-traumatic conditions such as failure to rehabilitate after stroke, MI, or thrombophlebitis, can also be assoc w/metabolic bone dz, neoplasm, cervical OA and HSV and other 15% are idiopathic. Patho-physiology: Current theories: two different mechanisms: altered sympathetic outflow and regional neurogenic inflammation Clinical Picture PAIN OUT OF PROPORTION to the inciting injury or event (reactive hyperemia, muscle weakness, incoordination, tremors, muscle spasms, cyanosis, livedo reticularis in the contralateral limb, dystrophic changes in the skin and nails, contractures.) More common in patients 40-60 years but can also occur in children and the elderly Diagnosis Plain radiographs of the involved extremity may show patchy osteopenia, termed Sudeks atrophy this is an inconsistent Based on finding that may occur also with disuse or immobilization syndromes. Thermography can detect temperature changes preceding trauma between the limbs, but this test is non-specific. Three-phase bone scan is specific for RSD, but sensitivity varies from 50% to 90%. Nerve conduction velocity studies may be performed, if nerve involvement is suspected. Treatment Goals of therapy: pain control (Narcotics), early join mobilization prevention of contractures, and capsular retraction (physical therapy), and depression or anxiety (TCAs). Sympathetic nerve blockade (medical Phenoxybenzamine or surgical decompression is a popular treatment modality for RSD. Therapeutic blocks can be performed by injection of local anesthetics into the lumber sympathetic ganglia for LE RSD Oral corticosteroids (Predinone 60-80 mg qid for 2wks and then tapered/discontinued by the 3- 4th wk to avoid HPA axis suppression). Amputation (rare) is required to control pain, eradicate infection, or improve function; however, the recurrence of RSD in the stump is common. Steinbroker (clinical stages of RSD) Duration Description 3-6 months Pain, hypersensitivity, swelling, and vasomotor changes that lower or raise the temperature of the extremity, giving a dusky purple appearance and causing dependent rhubor. II Another 3 Characterized by persistent pain, disability and atrophic skin changes. The skin is cool, sweaty, livido reticularis Dystrophic months and cyanosis are present; diffuse osteopenia on x-rays. Edema is increased. III Atrophic Many years Atrophy of the subQ; pain is burning, throbbing and may decrease over stage 2 and may spread proximally. SNS activity is decreased from stage 2, marked loss of function: irreversible impairments-muscle atrophy, contractures, joint rigidity. The skin is cyanotic and edema is less from stage 2. Stage I Acute

Vasospastic diseases
Raynauds Disease Description Cutaneous color changes, produced by reversible spasm of arterioles/ small arteries brought on by exposure to cold or emotional upset. Triphasic sequence of color changes that is well-demarcated White (pallor) ischemia, often the only color change Blue venous congestion and cyanosis Red reactive hyperemia, may present with a throbbing pain, most commonly tingling and burning pins and needles Pathophysiology Heightened vasomotor tone and increased blood viscosity due to increased fibrinogen levels Clinical picture Vasopastic attacks of the fingers (sparing the thumbs) mainly (50%), less than half have attacks of the toes, and only a few with attacks of only the toes. The nose, face, ears and chest can also be affected.Pulses are present and normal unless underlying disease exists Diagnosis Allen and Brown classification in the Dx of Primary Raynauds Vasospastic attack precipitated by cold or stress -Bilateral involvement of the extremities Absence of gangrene, or if present limited to the skin of the fingers -No evidence of underlying disease A history of symptoms for at least 2 years Supported by measurement of ANA (indicates the presence of a systemic diease is present-is normally high in the very young

22

Treatment

and old), ESR (helpful but non-specific normal in the primary, elevated in the secondary form) With no limb-threatening vasospam conservative therapy with heparin and bed rest

Secondary causes of Raynauds phenomenon CREST syndrome: Calcinosis, Raynauds Phenomenon, Esophogeal motility abnormalities, Scelerodactyly, Telengectasias Distal ulcerations, arthralgias, arthritis, an pulmonary and renal vasculature involvement Autoimmune disease. Photosensitivity, butterfly patterned(malar) rash, arthralgia or arthritis, seizures, psychosis, alopecia, pericarditis and nephritis, anemia, thrombocytopenia and leukopenia Immune mediated disorder of exocrine sweat glands Keratoconjunctivitis sicca (dry eyes), Xerostemia (dry mouth) and dry vagina in women Symmetrical muscle weakness, arthritis and arthralgias, an erythemetous skin rash (polymyositis), dysphagia, dysarthria and pulmonary fibrosis. Heliotrope of purple discoloration of the upper eyelids is characteristic of dermatomyositis. Elevated CPK and aldolase Mixed connective tissue disease Joint, muscle, pulmonary and renal involvement. Swelling of the dorsum of the hands and fingers with sausage shaped appearance of the digits. Rheumatoid arthritis Raynauds phenomenon as well as focal ischemic lesions with microinfarctions of the perilungal area and digital pulp. Treatment of Raynauds phenomenon: 1. Conservative: Reassurance that the disease is benign, avoid cold and smoking, minimize stress 2. Drug therapy a. Calcium channel blockers (SE: dizziness, flushing, palpitations, edema, dyspepsia and pruritis) i. Nifidipine 10-20mg tid slow release preparations are better tolerated ii. Dilitiazem 30-120 mg tid b. Sympatholytic agents (postural LBP, decreased HR, lethargy, depression, and impotence) i. Reserpine 0.25-0.5 mg qd ii. Guanethedine 10-50 mg qd c. Alpha-adrenoreceptor antagonists (nausea, palpitations, dizziness, fatigue, diarrhea, edema, dyspepsia, rash) i. Prazocin 2-8 mg qd ii. Methyldopa 1-2 mg qd iii. Phenoxybenzamine 10-30 mg qid iv. Tolazoline 25-100 mg qd Scleroderma(Systemic sclerosis) Connective tissue disease SLE Connective tissue disease Sjogrens syndrome (SS) Polymyositis and Dermatomyositis

A. 1.

Rheumatologic disorders

Myopathies (primary and secondary)

Muscular Dystrophies progressive dz where the pattern of weakness of the muscle determines the dx
Myopathies Inflammatory Myopathies:Dermatomyositis, Polymyositis and inclusion body myositis Skeletal muscle breakdown and elevation of [CPK] and [aldolase] characterize these autoimmune disorders (anti-Jo 1 antibody) diagnostic markers Primary Idiopathic Polymyositis Description 1/3 of all inflammatory myopathies; F>M 2:1; distal muscles are spared in 75% of the cases; Clinical Presentation Proximal limb weakness esp. hips and thighs; difficulty arising from a chair, pain described as "aching" type in buttocks, thighs and calves tender w/ deep palpation; dysphagia; morning stiffness, fatigue, anorexia, weight loss and fever; arthralgias; muscle atrophy, contractures & decreased DTR's Primary Idiopathic Dermatomyositis Description > 1/3 of all the immune myopathies; skin changes may precede muscle involvement; Skin Changes localized or diffuse erythema; maculopapular eruption or scaling; an exfoliative dermatitis; classic heliotrope rash on eyelids, bridge of the nose and cheeks (butterfly or "malar" distribution periobital area); periungual erythema; Photo sensitivity; poikiloderma; shawl sign; Gottron's sign - pink to violaceous scaling typically over the knuckles, elbows and knees; Raynaud's phenomenon Secondary Polymyositis or Dermatomyositis with Neoplasm Description Pt of a paraneoplastic syndrome; 20% (6-60%) of Dz; muscle/ skin changes are indistinguishable from above Presentation Dz processes; m.c. associated malignancies - lung, ovary, breast, gastrointestinal tract and myeloproliferative disorders; The mc type of malignancy is the same that is most typical for the pt's age and sex; Diagnosis Most time serum CK levels elevated; normal CK levels on serial testing in pt w/ symptoms of myositis suggests increased likelihood of malignancy; Bad prognosis: Childhood Polymyositis & 8 to 20% of these processes; clinical or pathologic evidence of vasculitis in skin, muscles, gastrointestinal Dermatomyositis Associated w/ Vasculitis tract and other organs; necrotizing lesions of skin may be present; ischemic infarction of the kidneys, GI tract and even the brain have been reported Polymyositis or Dermatomyositis Assoc. Overlapping Dz process with scleroderma, rheumatoid arthritis and mixed connective tissue disorders; Dx

23

w/ Connective Tissue Dz

difficult.

Endocrine and Metabolic Myopathies

Thyroid Disorders Parathyroid Disorders hyperthyroidism muscle weakness; hypothyroidism weakness & pain; CK elevated 10x normal even w/ minimal muscular involvement; adults have muscle hypertrophy with cramps (Hoffmann's syndrome) hyperpPTH muscle weakness and atrophy; pts c/o muscle "pain" d/t underlying bone disease; hyperreflexia hypopPTH present w/ neuromuscular involvement; tetany; serum CK elevated DDx - polymyositis considered; hyporeflexia or areflexia; presence of Chvostek's sign (spasm of the facial muscles elicited by tapping the facial nerve in the region of the parotid gland) & Trousseau's phenomenon (spasmodic contractions of muscles provoked by pressure upon the nerves that supply them) endogenous elevations of glucocorticoids severe muscle weakness and wasting acromegaly associated with muscle enlargement; weakness of pan-hypopituitaryism d/t coexistent adrenal or thyroid insufficiency severe malabsorption may vitamin E deficiency myopathy; vitamin D deficiency d/t decreased intake or decreased absorption associated w/ renal disease may chronic muscle weakness; pain most likely reflects the underlying bone disease;

Adrenal Disorders Pituitary Disorders Vitamin Deficiency

2.

Arthridities

Synovial Fluid Analysis Joints normally have small amt of synovial fluid & depends on the size of the joint; the fluid collected using aseptic technique and placed in a sterile, heparinized tube (green top) or EDTA; examination for the presence of microorganisms and crystals is the most critical part of the analysis; most findings are non-specific and can be found in a number of disease entities; fluid is inspected for viscosity, color and appearance Microscopic examination total number of cells present, the type of cells and the presence and type of crystals Chemical analysis mucin clot test, synovial fluid glucose and protein determinations, and immunologic studies (rheumatoid factor, antinuclear antibodies, complement,etc.) Microbiologic studies, including a Gram stain and cultures

Condition
Normal Osteoarthritis Traumatic Arthritis SLE Rheumatoid arthritis Gout (acute) Pseudogout Bacterial arthritis (acute) Tuberculous arthritis

Color/Clarity
yellow/clear yellow/clear yellow to bloody/ clear to bloody yellow/clear to slightly cloudy yellow/cloudy yellow/cloudy yellow/clear yellow to bloody/ cloudy to purulent yellow/cloudy

Viscosity
high high high decr low low low low low

Total WBC -%PMN

0-200/l (0-25%) 200-2000/l (0-25%) 200-5000/l (0-50%) 2000-5000/l (25-50%) 5000-50,000/l (50-90%) 5000-50,000/l (50-90%) 5000-50,000/l (35-85%) >50,000/l (90-100%)

Formed Elements
none collagen fibrils cartilage fragments & RBCs LE cells cholesterol crystals (occ) urate crystals CA pyrophosphate crystals bacteria on gram stain gram stain 20% positive cultures 80-90% positive

2000-100,000/l (30-90%)

Infectious Arthritis
Etiology Clinical Presentation Septic arthritis occurs m.c. in infant b/c metaphyseal vessels penetrate the growth plate. In adults, growth plate is closed four types: hematogenous, direct extension, implantation and post-surgical acute changes are non-specific, consistent w/ localized edema and loss of soft tissue planes; begins as synovial infection contamination of the joint fluid and space HOW? Bacteria in synovium incite host defense mechanism releasing enzymes and toxins, attracting neutrophils; synovial fluid production & pressure increases local ischemia, interfering with cartilage nutrition; then chondrolytic enzymes are released, rapidly destroying articular cartilage; the joint space becomes widened d/t increased fluid content and pressure w/i infected joint; late changes in septic jt osteoporosis appears in the subchondral bone d/t synovitis hyperemia; cartilage is rapidly destroyed by this process beginning either in the center of the joint or at the periphery where impingement by the synovial lining occurs; by the time cartilage is destroyed, radiographic changes in subchondral bone are evident and the infection has advanced from the joint cavity into the bone; 30-50% of bone matrix must be destroyed before it is seen radiographically chronic changes develop if the infection is left untreated joint space become narrowed, with irregularity of the subchondral

24

Manifestation

bone surfaces; sequesta (dead bony fragments) develop btwn the borders of the joint space ankylosis of the involved joint Rash

Identifying the Cause (gonococcal vs non-gonococcal arthritis) in infants, Staphylococcus aureus is responsible for most septic joints in children younger than two years, Haemophilus influenzae causes half of the cases following an upper respiratory tract infection in children over two years of age, Staphylococcus aureus is most common in adults and the elderly, 1/2 of the cases are causes by Staphylococcus aureus and the other half by streptococci and gram-negative bacilli Staphylococcus - most common following joint aspiration or injection; it may be accompanied by gram-negative bacilli and anaerobes Staphylococcus aureus, streptococci, gram-negative bacilli are associated with injection of coagulation factors in hemophiliacs polyarticular arthritis is most commonly caused by Staphylococcus aureus in patients with rheumatoid arthritis, hemophilia or immuno-suppression mycobacterial infectious are on the rise primarily as a result of HIV and immuno-suppressed patients Mycobacterium marinum is seen in patients involved in aquatic hobbies candidal organisms can reach joints via direct injection or hematogenous spread Sporothrix schenckii (sporotrichosis) is an occupational disease affecting gardeners Salmonella ssp. have been isolated from sickle cell patients and those with systemic lupus erythematosus Pseudomonas auringinosa may be most common in patients with IVDA along with MRSA Staphylococcus epidermidis is most common in the early infection of prosthetic joints whereas other gram positive cocci may be associated with late infections Gonococcal arthritis Lovers heel Gonococcal arthritis is an infection, usually of a single joint (in 90% to 95% of cases) that occurs with gonorrhea. Migratory polyarticular arthritis involving several joints in rapid succession and then settles in one or two. Must culture all mucus membranes, is not usually cutures in synovial fluid analysis Neisseria gonorrhea It affects women more frequently than men (4:1) and its highest incidence is among sexually active adolescent girls. There is also increased risk during menstruation and pregnancy. Single joint arthritis follows dissemination of the gonococcal infection and is associated with symptoms of fever, chills, multiple joint aches (arthralgia), and rashes (1-mm to 2-cm red macules). This episode may end as a single joint becomes infected. The most commonly involved joints are the large joints such as the knee, wrist, and ankle.

Description Etiology Epidemiology Clinical presentation

Treatment: Patient Profile sexually active young adults* Microorganism Neiserria gonorhoeae Adult Antibiotic Regimen Ceftriaxone sodium (Rocephin), 1-2 g IV or IM/day, then cefuorxime (Ceftin), 500 mg PO q12h or ciprofloxacin (Cipro), 500 mg q12h x 7 days plus Doxycycline (Vibramycin, Doryx) 100 mg q12h Nafcillin sodium (Unipen) 1-2 g IV q4h x 2-4 wks, then PO x 2-4 wks

Children >2 yr and adults who have polyarticular infection or are immunocompromised Elderly persons, children and immunocompromised persons (Enterococcus species) Neonates, children < 2 years, elderly persons, patients with SLE and IVDA**

Staphylococcus aureus

Group A streptococci Non-group A streptococci

Aqueous penicillin G, 1-2 million U IV q4h Ampicillin, 1-2 g IV q4h plus gentamicin (Garamycin) 1 mg/kg IV q8h Third-generation cephalosporin or gentamicin, 1 mg/kd IV q8h plus Nafcillin, 1-2 g IV q4h

Gram-negative bacilli

25

Lyme disease
Description Lyme disease is caused by the bacterium Borrelia burgdorferi (a sphirochete) and is transmitted to humans by the bite of infected blacklegged ticks (ixodes diamini) Clinical presentation Typical symptoms include fever, headache and fatigue. It is a multi-systemic condition involving the skin, nervous system, joints and heart Stages of the disease Stage 1 Erythema chronicum migrans usually occurs within seven to ten days of the tick bite it begins as a patch or macule of erythema , and it will expand over the following days to form a large annular lesion the central portion of the lesion may become extremely erythematous and indurated, vesicular or necrotic it may develop multiple rings and is warm to the touch w/i days, pts with hematogenous spread will lead to secondary annular skin lesions at sites remote from the initial innoculation Stage 2 Early Disseminated Disease the cardiac and neurological stage this stage demonstrated disseminated involvement of the nervous system, along with musculoskeletal symptoms it generally occurs three to 10 weeks after exposure to the bacterium Neurologic s/s are suggestive of meningeal irritation w/ cranial neuritis, motor or sensory radiculoneuritis, mononeuritis multiples and chorea. About 8% of pts develop cardiac involvement and the m.c. abnormality is fluctuating degrees of AV block cardiac involvement usually lasts only a few weeks but may recur within several months after the infection Stage 3 Disseminated Disease - intermittent or chronic arthritis and neurological stage arthritis is the hallmark of late disease and may occur years after the initial disease process this stage will demonstrate severe progressive arthritis, encephalomyelitis, chronic fatigue syndrome, ataxic gait, spastic paresis and polyradiculopathy and the arthritis is characterized by intermittent attacks of oligoarticular symptoms of the large joints occurring most commonly in the knees TX amoxicillin is the DOC for early disease 500-1000 mg 3xd for 10-14d in early disease and up to 28d in disseminated disease doxycycline 100 mg p.o. bid for 14 to 21 days not recommended for children less than 8 years of age Ceftriaxone (Rocephin) DOC for CNS involvement or persistent arthritis 2 grams IV qg for 14 to 21 days

Tuberculosis
Dsecription Epidemiolgy Joint and bone involvement Diagnosis Treatment infection caused by Mycobacterium tuberculosis, which m.c affects the lungs (pulmonary TB) but can also affect the CNS (meningitis), lymphatic system, circulatory system (Miliary tuberculosis), genitourinary system, bones and joints. TB is one of the most deadly and common infectious diseases today, infecting 2 billion people or 1/3 of the world's population. 9 million new cases of active dz, resulting in two million deaths, occur annually, mostly in developing countries. Potts disease is a presentation of extrapulmonary TB that affects spine; a kind of tuberculous arthritis of the intervertebral jts. Also called tuberculous spondyloarthropathy. It is most commonly localized in the thoracic portion of the spine. Tuberculin test (PPD) Rifampin 600mg and isoniazid 300mg in a single daily dose for 18mon conventional tx: 9 mo is the short course of tx M.c resistance isoniazid although there are isolates w/resistances to multiple drugs, preventative tx is only effective w/ INH Empirical Tx: anti-mycobacterial therapy:Initial 4 drug combo : INH Rifampin Pyrazinamide Ethambutol or streptomycin (INH resis) Then INH & rifampin w/o pyrazinamide for next 6mo

Viral arthritis
Description Etiology Treatment Presents as a self-limiting mild inflammatory nondestructive arthritis that lacks suppuration-usually begins as a migrating polyarthralgia that rarely lasts for more then 6 weeks Hep B, Mono, rubella, mumps and parvovirus Conservative regmen of rest and NSAIDS Seronegative spondyloarthropathies (RAPE) 1. Reiter's Syndrome or Reactive Arthritis referred to as reactive arthritis believed to be precipitated by a bacterial infection in the genital, urinary or gastrointestinal tracts; dependent on histocompatability antigens, some individuals respond by the development of reactive arthritis chronic form of arthritis characterized by - classic clinical triad or inflammation of the genital, urinary or gastrointestinal systems urethritis, conjunctivitis and inflamed joints (arthritis) chiefly in young men with an HLA-B27 genotype (positive in 60 to 75% of patients); preceded by a bout of non-gonococcal urethritis (often caused by chlamydia, Shigella flexneri, Salmonella ssp, Yersinia ssp. and Campylobacter fetus) Keratoderma Blenorrhagicum is the cutaneous manifestation of Reiters syndrome

26

2. Anklosing Spondylitis Description Chronic inflammatory arthritis that affects the sacroiliac joint and to a lesser extent the rest of the spine. Signs and symptoms Onset -15-35yrs, M>F 10:1, lower back pain, kyphosis, recurrent acute iritis in 1/3 of patient Diagnosis Increased ESR, +HLA-B27, +Schoebers test. X-ray: bamboo spine Treatment PT and NSAIDS 3. Psoriatic Arthritis - five clinical patterns exist: asymmetric distal interphalangeal joint involvement with nail damage (16% of cases) Arthritis mutilans with radiographic picture is similar to rheumatoid arthritis but RA is NOT at distal ends; osteolysis of the phalangeal and tapering or "whittling" of the phalanges, "cupping" of proximal ends of the phalanges that results in telescoping metacarpals (5%) of the involved digit bony anklysosis, osteolysis of the metatarsals and paravertebral ossification destructive changes have a predilection for the DIPJ and PIPJ w/ relative sparing of the MPJ Symmetric polyarthritis-like rheumatoid affect the small joints of the hands and feet, wrists, ankles, knees and elbows; there is a high frequency arthritis, with claw hands (15%) of DIPJ involvement and a tendency for ankylosis of the DIPJ & PIPJ digital involvement will lead to a "claw" or "paddle" deformity of he hands Oligoarthritis with swelling and this is the most common initial manifestation and is present in two-thirds of the patients: affects one large tenosynovitis of one or a few hand jts joint (such as the hip or knee) and 1 or 2 IPJs with concomitant edema - of the hand or foot; DIPJ arthritic (70%) changes are characteristic of the disease & occur with almost always concomitant nail plate involvement ankylosing spondylitis alone or with peripheral arthritis (5%) Treatment of Arthritis Associated with Psoriasisrest, splinting, passive motion; intramuscular corticosteroid injection may be useful and utilization of NSAIDS Management of Psoriasis short doses that do not create a sunburn may be effective in clearing plaques topical steroids are usually applied directly on the skin bid if less than 10% of the skin is involved, it is acceptable to initiate treatment with high dose, fluorinated corticosteroids; these agents may be particularly effective on pedal lesions Use rule of 9s; Be careful for HPA axis suppression; 2-3x increase in fasting insulin; increase PMNs Calcipotriene synthetic version of vitamin D3 (NOT same as vitamin D dietary supplementation); MOA - inhibits the proliferation of fibroblasts and keratinocytes. Foot lesions - about 60% of patients have a good response w/i 4 mths (it is not (Dovonex) recommended for use on the face) Efficacy - calcipotriene is as effective as corticosteroids w/o the potential risk of atrophy of the subcutaneous fat. S/E - burning, itching and skin irritation (10 to 15% of patients), and erythema, dry skin, peeling, rash, dermatitis and worsening of psoriasis (1 to 10% of patients) Coal Tar may be applied directly to the skin and is available in several strengths; may be combined w/ ultraviolet B (UVB) phototherapy; adv: fewer S/E than topical steroids; Disadv - very messy (strong odor and a tendency to stain clothing) - utilized in the cream form to treat chronic psoriatic lesions; should not be used in acute or active eruptions Disadv- not always successful & may cause skin irritation and discoloration to both skin and clothing. Anthralin One preliminary study found that topical use of vitamin E was able to protect against this side effect. Wont work as quickly as glucocorticoids but have fewer S/E; may be irritating to the skin and should not be used in skin folds. Topical Retinoids (Retin A) Sunlight Cortico-steroids UVB Phototherapy PUVA Therapy The "narrow band" part of the ultraviolet spectrum band that is most helpful for psoriasis. Some physicians may elect to begin therapy with this modality rather than topical medications; treatments are usually given three times a week for two to three months and in conjunction w/ other treatments such as coal tar or anthralin and salicylic acid; the "Goeckerman" treatment combines application of coal tar ointment and UVB phototherapy. PUVA therapy - introduction of a phototoxin enhances dose of 10 to 30 mg. Of 8-methoxypsoralen (Oxsoralen-Ultra) followed by the use of high-intensity long wave UV 2 hours earlier. psoralen will make the skin more sensitive to the long-wave ultraviolet therapy; maintenance treatment must be continued indefinitely; risk of enhanced carcinogenesis is proven particularly SCC and melanoma suspensions of triamincinolone are frequently used (triamcinolone acetonide (Kenalog) suspension 10 mg/ml may be diluted with distilled sterile water to a concentration of 5 mg/ml; good method for treating small lesions; very effective form of therapy; one injection will usually produce clearing at the injection site; good results are obtained with psoriatic nails by injecting traimcinolone into the region,of the matrix and lateral nail fold; injections may be repeated once a month one must use caution to prevent fat atrophy at the injection site particularly important with plantar psoriasis methotrexate, cyclosporine - suppresses the immune system resulting in a slower turnover of skin cells , hydroxyurea may be combined with methotrexate, cyclosporine, UVA and UVB therapies, Dapsone 100mg bid for 3 wks may be effective; followed by 100 mg/day for 1wk. S/E must be seriously considered.new anti--TNF antibody - infliximab - effective in

Intralesional therapy

Systemic Therapy

27

clearing psoriatic plaques ; 5 mg/kg 3xd - 82% responded; 10 mg/kg 3xd, 91% responded; placebo control, 18

4. Enteropathic arthritis (UC and Crohns disease) Description Rheumatologic manifestations seen in about 15-20% of pts with IBD Signs and symptoms Asymmetric, nondestructive and transient arthritis. Flares tend to parallel flares of the underlying bowel disease. Commonly involes the knee, ankles, elbows and wrists, GI abnormalities Treatment PT and NSAIDS

Osteoarthritis
Description Osteoarthritis is the most common joint disorder. The chronic disease causes the cartilage to wear away, leading to pain and stiffness. It can also cause bone spurs, to grow around the joints. OA is classified as primary or secondary. Primary OA occurs without any type of injury or identifiable cause. Secondary OA is osteroarthritis due to another disease or underlying condition. The most common causes of secondary OA are metabolic conditions, such as acromegaly, problems with anatomy, injury, or inflammatory disorders like septic arthritis. Symptoms of osteoarthritis usually appear in middle age and are present in almost everyone by the age of 70. Before the age of 55 it occurs equally in both sexes. However, after 55 it is more common in women. Gradual/ subtle onset of deep aching jt pain worse after exercise or WB, often relieved by rest. Bouchard nodes-at the PIPJ and Heberden nodes at the DIPJ. X-ray: assymetrical joint space narrowing NSAIDS, COX 2 inhibitors, steroids, glucoamine chondroitin,

Epidemiology Clinical Presentation Treatment

Collagen vascular diseases that lead to arthritis 1.

Description Onset/incidence Signs and symptoms

Systemic Lupus Erythematosus

A chronic remitting, relapsing inflammatory and often febrile multisystem disorder of connective tissue. 15-35yrs, W>M (10:1) Joint pain in 90% is an early manisfestation. Photosensitivity, Malar rash, arthralgia seizures, psychosis, alopecia, anemia, thrombocytopenia and leucopenia +ANA, arthritis of predominantly small joints, myopathies, preicarditis/pleuritis, glomerulonephritis, interstial lung disease, seizures and cognitive impairment. Autoimmunity Type III, non-specific Ab against ANA, anti-dsDNA, anti-Smith and anti-histone antobodies with the formation of LE bodies, causes Libman Sacks Endocarditis (valvular vegetations found on both sides of the mitral valve MS) Drugs that can causes SLE: HIPP Hydralazine, INH, Phenytoin and Procanamide Increased ESR, +ANA, decreased Hgb, WBC and platelets Systemic steroids, antimalarials (chloroquine), immunosuppressants, avoid sunlight

Diagnosis Treatment

2. Scleroderma
Description Onset/incidence Signs and symptoms Diagnosis Treatment A systemic disorder of the c/t characterized by induration, thickening and tightness of skin. Leads to migratory polyarthritis 30-40s, W>M (4:1) CREST syndrome: Calcinosis, Raynauds Phenomenon, Esophogeal motility abnormalities, Scelerodactyly, Telengectasias HTN, arthralgias of small/large jts, flexion contractures, swelling of hands and feet. Skin thickening/induration, +ANA Symptomatic

3. Sjogrens syndrome or Sytemic Sclerosis

Description Onset/incidence Signs and symptoms Diagnosis Treatment Chronic Immune mediated disorder of exocrine glands resulting in decreased secretions W>M (9:1), ages 40-60s, often associated with RA Keratoconjunctivitis sicca (dry eyes), Xerostemia (dry mouth) and dry vagina; corneal ulcerations salivary or lacrimal gland enlargement, autoimmune thyroiditis, interstial nephritis and interstial lung disease Mild anemia, leukopenia, +RA Symptomatic

4. Dermatomyositis/polymyositis
Description Onset/incidence Signs and symptoms Diagnosis Chronic progressive inflammatory disease of skeletal muscle characterized by symmetrical weakness of the limb girdles, naeck and pharynx usually associated with pain and tenderness. Polyarthritis occurs in 1/3 of pts. W>M 2:1 If associated with skin lesions (Dermatomyositi- Heliotrope of purple discoloration on upper eyelids is characteristic) and Gottrons sign (flat toped violaceus papules over the dorsal aspect of the knuckles) Symmetrical m weakness and arthritis and arthralgias, dysphagia, dysarthria and pulmonary fibrosis and proximal nail fold telegectasias Elevated CPK and aldolase, muscle biopsy, abnormal EMG, elevated creatine (>200mg) in a 24hy urine specimen

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Treatment

Steroids

Rheumatoid Arthritis Chronic (long-term) disease that causes inflammation of the joints and surrounding tissues. The cause of rheumatoid arthritis (RA) is unknown. It is considered autoimmune disease. The body's immune system normally fights off foreign substances, like viruses. But in an autoimmune disease, the immune system confuses healthy tissue for foreign substances. As a result, the body attacks itself. Epidemiology RA can occur at any age. It usually occurs in people between 25 and 55. Women> Men Clinical Presentation Onset gradually w/fatigue, morning stiffness (>1 hr), widespread muscle aches, loss of appetite, and weakness. Eventually, jt pain appears, when the joint is not used for a while, it can become warm, tender, and stiff. Symmetrical sweeling of the wrists, MCPJs, PIPJs, of the hands but spares the DIPJs Swan neck deformity- (hyperextension of the PIPJ w/flexion of the DIPJ) Boutoneirre deformity (flexion of the PIPJ w/hyperextension of the DIPJ) Feltys Syndrome RA, Splenomegaly , Leuckocytompenia, Lymphadenopathy and weight loss Diagnostic testing Rh Factor RF is an antibody that attaches to a substance in the body called immunoglobulin G (IgG), forming a molecule known as an immune complex. This immune complex can activate various inflammatory processes in the body. + in 70-80% Description Etiology

DMARDS
Drug Hydroxychloroquine sulfate (Plaquenil) Contraindication Dose Allergy to any 4-aminoquinoline 200mg po bid for compound, hemolysis in G6PD, prolonged period, often Adverse reactions: mainly GI 8.5%, N ab combined with slow dose pain and diarrhea cortisone and NSAIDS Warnings: psoriasis, porphyria, Chloroquine retinopathy irreversible damage, need eye exams q 6-12 mo and baseline visual fields Sulfasalazine Prodrug ASA (stays), and sulfapyrazine RA, UC, juvenile RA Allergy to sulfa drugs, salycilates, 500mg bid to 2.0g daily (Azulfidine) (absorbed) in the colon by bacteria. Decreases psoriasis, anklosing pediatrics and porphyria in divided doses (delayed the prod of inflam cytokines (IL-1 and TNF) spondylitis Adverse reactions: nausea, diarrhea, 1.5% release enteric-coated and of IgM RA factor have agranulocytosis tabs) Methotrexate Inhibits the dihydrofolate reductase #1 for refractory RA, Children, pregnancy/lactation, Etohism, Oral 2.5mg tabs or (MTXenzyme, immunosuppressive, neoplastic diseases: liver dysfunction, blood dyscrasias, bone injection usually 10Rheumatrex) decreases IL-2 prod, ameliorate s/s of choriocarcinoma, marrow hypoplasia, agranulocytosis and 15mg once weekly joint inflam but no (-) of bone erosion. chorioadenoma, hydatiform anemia. BLACK BOX: fatal, check for Response is quicker than Plaquenil moles, epidermoid pancytopenia (bone marrow suppression), 3-6weeks carcinomas, lung cancer, renal/liver and lung disease (hypersentivity psoriasis pneumonitis) Gold Gold suppresses/prevents arthritis and RA and Uncontrolled DM, HTN, CHF, renal or Oral: Aurofin 29% gold 3mg compounds synovitis (not a cure or remission), is taken up psoriasis hepatic disease, agranulocytosis, anemia or caps bid Crysotherapy by macs resulting in (-) of phagocytosis and hemorrhage disorders, pregnancy. IM: Aurothioglucose, 50% gold, lysozomal enzyme activity, decreases the [RA Warnings: Pancytopenia, renal disease, 10mg test 1st week then weekly factor] and Igs, decreases synovial inflam, hypersent, diarrhea (50%) run CBC, UA injections 25-50mg up to 1g retards cartilage and bone destruction, occurs prior to and q 2wks. reevaluate in 3-6mo slowly within 6-8wks to 3-8mo, use with Pruritic rash, stomatitis, and proteinuria are Gold Na thiomalate NSAIDS and cortisone the most common 50% gold Leflunomide Oral isoxazole, immnosupressive, a pyrimidine RA only!!! Pregancy and lactation 100mg tab qd x 3d then (Arava) synthesis inhibitor, as effective as the previous Warning: hepatotoxic, run LFTs, risk of 20mg qd two in decreasing s/s, radiographic progression lymphoproliferative disorders is increased ANTI-VIRAL Adverse reactions: Diarrhea, alopecia, rash, increased liver enzymes TNF (-) Cytokine, present in high [ ] in RA in the synovium, causes inflam and immune response IL-1/ IL-6, (+) chemotaxis, neoangenesis and joint destruction. 1. Etharcept Immunomodulator, recombinant DNA protein (TNF Methotrexate refractory Infection and sepsis 25mg SQ 2x week (Embrel) recptor+ IgG), inhibits the binding of TNF to cell surface RA 2. Infliximab (Remicade) Human recombinant IgG Ab which binds to TNFa and inhibits its binding. Given IV Asathioprine Metabolized to 6-mercaptopurine analog used Prevent refection of Pregnancy. Adverse reaction: very toxic, 50mg tabs and 100mg IV (Imuran) as cytotoxic agent, interferes with Adenine and renal transplant, not a causes pancytopenia, allergy Guanine synthesis. Suppresses T-cell fx, Ig 1st line DMARD syn and IL-2 prod Cyclosporine Immunosuppressive response to Il-2 Prophylaxis of organ Increases susceptibility to infection, risk of lymphomas, very toxic, (Sandimmune) Not a first line DMARD, when used for RA, rejection, kidney, nephrotoxic, nausea, extensively metabolized by P450 use oral solution, and often combined with liver, heart, uses with Levels will increase: erythromycins, fluconazole; decrease: rifampin, MTX CCS, RA barbiturates, dilantin Penicillamine Lowers IgM level; depresses T-cells; Not a Chelating agent (Cu Very toxic, nephrotoxic, very often causes 125mg or 250mg in a (Cupramine) first line DMARD, when used for RA removal) in Wilsons rash, pancytopernia single daily dose MOA/ Description Anti-malarial drug, 2nd line tx for RA Immunosuppressive, interferes with APC action, binds histocombatibility Ags and alter their recognition by T-cells, decreases leukocyte chemotaxis, stablize lysozomal membranes, may take up to 6 mo for a clinical response Indication Mod to severe RA DOC for discoid SLE, and malaria

29

Disease

Juvenile Rheumatoid arthritis

Description Onset/incidence Signs and symptoms Classification Diagnosis Treatment Not a life long disorder, usually fades with age <16yrs, W>M (4:1) Usually involves the knees, elbows, ankles or neck-often associated with fever and skin rash 1. Polyarticular (40%) 2. Pauciarticular (40%-accociated with iridocyolitis 3. Stills disease (20%)-assoc w/ systemic manifestations (splenomegaly and generalized adenopathy Negative RA, however +ANA Same as RA, including ASA and other anti-inflammatory modalities

Neurotrophic Joint Disease or Charcot Joint Changes

French theory Neurovascular theory: concomitant loss of SNS results in bounding pulses & increased osseous circulation resulting in demineralization of involved bones German theory Neurotraumatic theory secondary to the loss of jt proprioception allowing jts to undergo extremes in ROM and pressures resulting in pathologic fractures

Common etiologies: 1) tabes dorsalis 2) DM 3) Syringomyelia Hypertrophic Charcot Joint Disease Types
Description VIP to recognize early The most common variant, characterized by deformity and proliferative or dense osseous rx w/ subsequent coalescence or healing concomitant loss of SNS results in bounding pulses & increased osseous circulation resulting in demineralization of involved bones, fractures assoc w/ this process are healed by an exuberant repair process (reconstruction and coalescence)sequelae include bone deposits, jt disruption, collapsed arches (rocker bottom foot) and shortened digits
Stage of Development initial destructive phase characterized by jt laxity, subluxation, osteochondral fragmentation & debris formationa synovial biopsy at this stage reveals osseous debris embedded in a thickened synovium (pathognomonic for initial Charcot jt changes) Stage of Development Bony changes consistent w/exaggerated form of osteoarthritis, generalized demineralization, cartilaginous fibrillation, and loose body formation these changes occur primarily in the solid bones of the tarsus and can mimic osteomyelitis. It is important to identify and rule out any potential nidus of bone infection Stage of Coalescence characterized by marked absorption of the fine debris and subsequent fusion of the larger joints Stage of Coalescence presence of sclerotic bone (AVN) periosteal new bone formation, subchondral sclerosis and the formation of marginal osteophytes Stage of Reconstruction this is an attempt to restore the joint architecturerevascularization and remodeling of bone and bony fragments occur Stage of Reconstruction greater definition of bony contours adequate reconstruction of affected bones or ankylosis of involved bones a poor prognosis is indicated by the continuation of joint destruction

Eikenholtz Stages

X-ray

dDx: OM, bone tumor, DVT cellulites

Clinical s/s

Red, hot, swollen foot

Treatment Acute charcot

NWB!

Description

X-ray changes Clinical Features of the Acute

There is a higher incidence in pts who have had DM on an average of 12 to 18 yrs important to correlate the probability of Charcot joint disease w/the duration of the diabetes realize that in order for Charcot to occur, adequate circulation is necessary the majority of the patients have unilateral foot involvement, are in their 5/6th decades, & are in a state of poor gl-control. Patients will present w/markedly swollen foot it is erythematous, quite warm to the touch and demonstrates anhidrosis. It is usually painless, although about 10% of patients may complain of some discomfort pulses will be bounding. PE of the foot may reveal a rocker bottom subluxation of the midtarsal region w/subluxations of the MPJs, and palpation of the jt will reveal some degree of hypermobility and crepitus. Most common affected joint Lis Franc joint. Infection can play a role in pathogenesis of the dz, and neuropathic ulcers may overlie or appear directly adjacent to the affected joint Prevention of further trauma by the cessation of WB: cast immobilization may be indicated but should not be applied until the edema assoc w/ the development phase has subsided (this is usually one to two weeks after the onset of the disease process)use of total contact cast w/ or w/o WB, CROW boot - Charcot Restraint Orthotic Walker use of a bone stimulator may aid in the reparative process, long term tx should include appropriate use of accommodative footwear molded shoes will support the misshapen foot as well as prevent ulceration but should not be fabricated until the end stage of the process has occurred Diabetic Osteolysis or Atrophic joint disease a less common variety is that of bone resorption, this occurs, theoretically, in response to a hyperemia of the maximally dilated b/v to the foot; it is believed that the sudomotor and vasomotor dysfunction may contribute to the characteristic diabetic osteolysis seen in the metatarsals and phalanges (often referred to as a pencil-cup deformity or mortar-pestle type deformity) the bones are literally washed away and present with characteristic pencilling of the metatarsals tubular bones of the metatarsals and toes will develop atrophic bone changes, these occur secondary to reabsorption of the metatarsal heads and shafts pencilling or hourglass resorption of the phalangeal diaphyses will also occur
Neuropathic Absent or diminished: DTRs Pain and vibration proprioception Skeletal Rocker bottom foot, crepitus midtarsal subluxation, digital Cutaneous neurotrophic ulcer hyperkeratosis

Vascular Bounding pulse Erythema Swelling Warmth

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Charcot

anhidrosis or hyperhidrosis

subluxation; hypermobility

infection

Frykberg-Anatomic Classification of Charcot I. Forefoot/MTP II. Midfoot/LisFrancs joint III. Tarsal/ Choparts joint IV. Ankle joint, STJ V. Calcaneus E. Metabolic and endocrine disorders 1. Diabetes Mellitus
Etiology Description Screening tests It is a disease of insulin action (insulin resistance), insulin secretion or both Epidemiology >16 million are afflicted w/ DM6th leading cause of death in US, leading cause of ESRD, amputations and blindness. Family hx of DM, obesity >120% of desired body weight, pregnant women, HTN or hyperlipidemia, members of a high-risk group (African Americans, Hispanics, or Native Americans) FBS-no food or beverage 8 hrs before testing >115mg/dl (non-pregnant adult) >130mg/dl (child) Confirmatory testing: RPG >200mg/dl with classic s/s, FBS>126mg/dl and OGTT>200mg/dl HbA1c (test semi-annually) < 7.0% Blood pressure : <130/80 LDL cholesterol (q 2yrs) < 100 Foot exam (annually) Types Characteristics: 10% of all DM pts, onset at any age (75% before age 18), abrupt onset, and HLA associations Pathogenesis-progressive autoimmune destruction of beta islet cells in the pancreas Clinical Presentation-diagnosis is made after 90% of the cells have been destroyed Polydyspsia, polyuria, polyphagia, (PPP) weight loss, blurred vision and fatigue prone to ketoacidotic coma Treatment-requires insulin Characteristics-insulin resistance/action and secretion Pathogenesis-genetic defect in insulin action resulting from abnormalities in glycogen synthesis or in glucose transport Clinical Presentation-aging, obesity and genetics can lead to insulin resistance and s/s similar to Type 1 DM not prone to ketoacidotic coma because endogenous insulin is usually sufficient to prevent it Treatment-reverse underlying insulin resistance and impaired cell function Normalizing body wt, serum lipid levels, prevent micro and macrovascular complications, Insulin can be utilized Gestational diabetes treated with insulin b/c it does not cross placenta and Impaired glucose tolerance Micro/macroangiopathy, peripheral and autonomic neuropathy, retinopathy, impaired immunity, nephropathy, increased atherosclerosis, HTN, abnormalities in lipoprotein metabolism and periodontal dz Nicrobiosis Lipoidica Diabeticorum: well circumscribed, hard, depressed, waxy, yellow-brown, atrophic patches tx with intralesional triamcinolone acetonide, use of dipyridamole (Persantine) 225 mg and aspirin one gram per day and pentoxyfylline (Trental) 400 mg, t.i.d. - has also been shown to be effective Diabetic Dermopathy (Shin spots) m.c Generalized Granuloma Annulare: a ring of small, firm, flesh-colored or red papules tx with intralesional triamcinolone acetonide Periungual Erythema: dilation of the capillary loops secondary to microvascular disease Diabetic Dermopathy (Shin Spots): hyperpigmentation and retracted atrophic scars present on the shins; histologically demonstrate red blood cell extravasion and capillary basement membrane thickening Diabetic Bullosis or Bullous Diabeticorum: a spontaneous non-inflammatory blistering which occurs spontaneously in a fairly symmetrical distribution Acanthosis Nigricans: warty pigmentation of the skin, occurs most commonly in the axillae, marker for heterogenous group of endocrine disorders - insulin resistance is the marker, possible association with malignant neoplasm, achrocordons will alleviate with tx of underlying malady Candida infections Treatment Thiazides, loop diuretics, B-blockers, and phenytoin will inhibit secretion and corticosteroids, growth hormone, estrogen and catecholamines will inhibit insulin action Lispro: rDNA origin, human insulin analog: Soluble & rapidly absorbed Onset: 15 min, Peak: 30-70 min, duration 2-3hrs Regular: crystalline zinc (pump use) Soluble & rapidly absorbed Onset: <1hr, Peak: 2-3hrs, duration: 3-6hrs NPH: Neutral Protamine Hagedorn: Onset: <2-4hr, Peak: 4-10 hrs, duration: 10-16 hrs Lente: semilente, lente, ultralente

Treatmetn goals Type 1

Type 2

Other types Complications Cutaneous manifestations of DM

Insulin

31

 Altered to slow absorption, peak and duration similar to NPH, available in long-acting form(Ultralente) Premixed insulin 70/30 70% NPH w/ 30% Regular & 75/25 75% NPL with 25% Lispro premixed (humalog insulin pen) Oral hypoglycemic agents 1. Sulfonylureas: stimulates production of endogenous insulin by blocking K+ channels. Will lower HgbA1c by 1-2% o 1st generation (chlorpropamide) Highly bound to serum albumin therefore may compete for binding sites with other drugs and may potentiate ADH which will lead to water retention, ankle edema and hyponatremia cardiovascular events o 2nd generation restores sensitivity of Beta cell to glucose; less likely to interact with other drugs b/c of non-ionic nature Glypizide-Glucotrol 5mg qd Glimeperide-Amaryl 1-4 mg qd Glyburide-Diabeta 5-20mg qd o Complications: hypoglycemia 2. Biguanides-decreases hepatic Gl- production and intestinal absorption, may enhance glucose utilization in muscle and adipose, and works synergistically with the sulfonylureas Metformin (Glucophage) 500mg bid o contraindicated in pts with renal dz, can lead to lactic acidosis and gastric upset, renal disease, does not lead to hypoglycemia o Discontinue use with contrast, in the presence of renal dz will cause binguanide induced lactic acidosis (50%) mortality rate 3. Alpha-glucosidase inhibitors-delays digestion of CHOs and delays glucose absorption via competitive reversible inhibition of pancreatic amylase and intestinal alpha glucoside hydrolase enzymes intestinal gas, with no increase in insulin secretion o Contraindicated in patients with IBD, UC or bowel obstruction and pts with liver dz Ascarbose (Precose) 50-100mg tid ac Miglitol (Glyset) 50-100mg tid ac 4. Meglitinides:+[insulin] blocks K+ channel Repaglinide (Prandin) 5. Thiazolidinediones-decreases insulin resistance at peripheral receptor site, only active in the presence of insulin insulin sensitizers will not increase insulin secretion, therefore no chance of hypoglycemia: Contraindications monitor LFTS and CHF risk Rosiglitazone (Avandia) 4-8mg qd Pioglitazone (Actos) 15-45 mg qd Gout A familial metabolic disease characterized by hyperurecemia, and resultant deposition of monosodium urate monohydrate in the tissues, joint and the kidneys. Causes recurrent episodes of acute monoarticular arthritis Etiology: Primary: Failure to excrete the urate is the number one cause (under-secretors). Also the increase in the concentration of hypoxanthine precursors(over-producers) increased urate o Lack of uricase enzyme (urate allantoin) high purine foods urate that is normally degraded in the gut by bacteria and excreted renally. Secondary: Renal failure, diuretics (particularly the thiazides), leukemia/polycythemia, psoriasis, hypothyroid, metabolic acidosis, mono, Pb poisoning, Lesch-Nyhan Syndrome, PRPP excess, G6Pdef Epidemiology: Disease of adult me w/a peak incidence of the 5th decade. Most common cause of inflammatory arthritis in men over 30 in women estrogen is protective to promote urate excretion. Dx: [uric]p, 24 urine test to check for overproduction >700mg/24h or undersecretion <700mg/24h, uric acid analysis in the synovial fluid for (-) birefringent crystals. XR findings include rat bite erosions and Martels sign overhanging margins. Clinical Presentation: acute, red hot, swollen joint, most commonly the 1st MPJ (Podagra) hallux limitus. Goal of tx: Reduce serum urate level below the level of the saturation point to suppress precipitation of urate. o Normal UA = 2.5-7 female and 3-8mg% male ([UA] should not be the end all and be all of the diagnosis) dDx: cellulitis, charcot, OA, DVT, RA, Reiters syndrome Treatment: Drug MOA/ Description Indication Contraindication Dose Colchicine Inhibits poly chemotaxis Rapidly Pregnancy, allergy, Max 10 tabs Fatal as low as 7.0mg and phagocytosis of urate absorbed increases intestinal Dose: 0.6mg po qh x 5 doses BEST DRUG (-) histamine release from great for motility, N/V, abdominal Inpatient: 2mg IV in 20ml NS over 10 min then FOR GOUT mast cells. Inhibits LTB4 acute gout pain, diarrhea in toxic an additional 1 mg in 6hrs if needed, no more synthesis pain doses than 4mg in 24hrs Indomethacin Most potent inhibitors of Anti-inflam and Not for chronic administration PO drug only COX, shifts the pathway to acute gout GI toxicity =4 take with food Acute gout: 50 mg tid twice the the lipoxygenase side anti-inflammatory dose Uricosurics MOA: block Potentiate the urinary excretion of urate acidifies the Chronic DONT USE WITH ASA the renal tubular absorption urine and can cause urolithiasis and renal colic which gout with recurrent May accentuate the action of the of urate can be buffered by Na bicarb po, decreases plasma acute attacks anticoagulants i.e, coumadin urate, new tophi formation, and size of old tophi (undersecretors) 1. Sulfinpyrazone Active peptic ulcer disease, blood dycrasias and agranulocytosis Dose: 100-200 mg bid 1st week and then 200-400mg bid maintenance 2. Probenicid Benzoic acid deriv., renal tubular blocking agent, inhibits the 500mg tabs, start with tab (250mg) bid the

32

(Benemid) 3. ColBenemid

tubular secretion of PCN Combination of colchicines 0.5mg and probenecid 0.5g

1st week, then 500mg bid for maintenance Chronic gout only One tablet bid

Chronic gout maintenance: Allopurinol (Zyloprim) Xanthine oxidase inhibitor (hypoxanthine xanthine urate; end product of purine metabolism, leaving us with high [hypoxanthine and xanthine] ok because excreted 10x greater than urate w/o urolithiasis problems and low [urate] Indications (over-producers) Best for patients with renal gouty nephropathy, urate stones, decrease in renal function Contraindications Shellfish and alcoholics Dose 100mg and 300mg tablets Dose: titrate 100-300 mg/day in single dose MOA Description Symptoms Onset Diagnosis Treatment Pseudogout (Calcium pyrophosphate dehydrate, CPPD) Associated with chronic or acute inflammatory arthritis, can be caused by deposition of Calcium pyrophosphate dehydrate crystals in the joint Similar to gout but tends to run longer course (reaches maximum severity at 1-3 days and resolves in 1 week or longer. The knees are often involved (50%) followed by the ankles, wrist and shoulder. Assoc w/ high grade fever Risk increases with age, trauma, pts hospitalized for other medical condition and those with metabolic dz (HypoTH, HyperTH, gout and amyloidosis) Microscopic examination of the joint aspiration reveals rhomboid crystals that are positively birefringent, and on X-ray will see calcifications of the articular cartilage or meniscus Immobilization, NSAIDS and analgesis

Adrenal Disease Adrenal glands are triangular-shaped glands located on top of the kidneys. They are composed of 2 parts. 1) The adrenal cortex which is responsible for the production of the glucocorticoids (cortisol), mineralcorticoids (aldosterone) and the androgens (estrogen and testosterone) 2) The adrenal medulla which is responsible for the production of the catecholamines Function of hormones Aldosterone Regulated by RAAS to increases Na resorbtion and K excretion in the Kidney to balance BP. Cortisol (anti-insulin) This hormone is involved in the response to stress; it increases BP and [glucose] and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning, and lower levels in the evening, several hours after the onset of sleep. Epinephrine Plays a central role in the short-term stress reactionthe fight-or-flight response. It increases heart rate and elevates the blood sugar level by increasing glycogenolysis in the liver, and lipolysis in fat cells. Adrenal Disorders of hyperfunction Cushings Causes increased cortosol, aldosterone and the sex hormoes. Clinical features include: central obesity, moon facies, abdominal Syndrome striae, weakness, hirsutism, and osteoporosis. Other s/s include persistent HTN (due to the aldosterone-like effects) and insulin resistance, leading to hyperglycemia, hyperkalemia and many develop frank DM. Untreated Cushing's syndrome heart dz and increased mortality. Conns Disease Primary hyperaldosteronism Addisons Autoimmune primary chronic adrenocortical deficiency leading to decreased production and secretion of the adrenal hormones Disease (hypocortisol) secondary to deficiency in ACTH hyperkalemia and nyponatremia Pheochromocytoma Tumor of the adrenal medulla causing excessive production of catecholamines which induces hypertension. Follows rule of 10: 10% are located outside of the adrenal gland, 10% are bilateral, and 10% are malignant. Description Paraneoplastic Syndrome Benign neuroendocrine tumor that can secrete hormones/proteins that directly affect the fx of specific organ systems Indirect effect of proteins and hormones over secreted wreaking havoc on the bodys homeostasis This tumor is neuroendocrine in origin (carcinoid tumor) Tumors that secrete PTH High [Ca2+] Tumors that secrete ACTH Cushings Syndrome Parathyroid disease PTH has 2 major fx: to maintain plasma [calcium] and to regulate the rate of bone remodeling. A rise in plasma calcium decreases PTH release, a drop is plasma calcium stimulates PTH release regulatory system is dependent upon two additional factors, catecholamines - which stimulate PTH to release vitD which decreases PTH release. In a calcium depleted state, PTH will cause a decrease in osseous mineralization and an increase in bone remodeling. Acts on the kidney and the bone to maintain Calicium balance A disorder of mineral and/or bone metabolism caused by increased and incompletely regulated secretion of PTH. it leads to hypercalcemia and osteitis fibrosa cystica, kidney stones and bone fractures. Disorder of mineral metabolism resulting from def secretion of PTH hypocalcemia. Clinically, it may present with s/s of tetany and/or a seizure disorder however, it has no consequence for bone density. This is a disorder of mineral metabolism in which the end-organ is unresponsive to the action of PTH. This

Description Clinical Presentation Type: Small cell carcinoma of the lung

Description

Hyperparathyoidism Hypoparathyoidism Pseudo-

33

hypoparathyroidism

unresponsiveness generally stems from the kidney and not the bone alteration in mineral metabolism will result in skeletal abnormalities and pts will present with hypocalcemia and if long standing will be of short statue, mildly obese with shortening of one or more of the metacarpal or metatarsal bones.

Thyroid disease
Description The thyroid gland is located in the base of the neck on both sides of the lower part of the larynx and upper part of the trachea. The gland produces TH in response to stimulation by TSH from the pituitary gland. TH acts throughout the body to regulate metabolism and increase iodine- esential trace element used in the production of thyroxine/ triiodothyronine Diagnostic screening Thyroid function tests: Elevation of Free T4 test Serum TSH T3 Hyperthyroidism Autoimmune activation of TSH receptors which leads to a feedback inhibition Antithyroid meds, radioactive iodine or sx Gravess disease of TH s/s: Weight loss, Increased appetite, Nervousness, Goiter, HTN, to remove the thyroid replacement TH opthalmapathy and dermopathy. Restlessness , Heat intolerance , Increased must be taken for the rest of the person's sweating , Fatigue , Frequent bowel movements , Menstrual irregularities life. Distal neuropathy w/ brisk DTRs Hypothyroidism Autoimmine disorder, results in cretinism in infancy and myxedma in adults A def of TH may develop at a later time. Hashimoto (increased [mucoploysaccharides] in ct to edematous thickening of the Replacement therapy with thyroid hormone Thyroiditis skin) Most common cause of goitrous hypothyrodism; s/s: Intolerance to (levothyroxine) is given if the hormone is cold , wt gain - mild , Fatigue, Constipation , Enlarged neck or presence of deficient or may be given if there is goiter, Dry skin, Hair loss, Small or atrophic thyroid gland (late in the disease), evidence of mild thyroid failure (such as Heavy and irregular menses, Difficulty concentrating or thinking, joint elevated TSH), also known as subclinical stiffness. Distal neuropathy w/ delayed DTRs hypothyroidism

Renal
Function: Maintanence of water and electrolyte balance, removal of metabolic wastes, VitD metabolism and BP regulation via RAAS

Renal failure
Description Etiology Acute renal failure Arises over 2hrs to weeks, and is m.c. in pts with comorbid conditions. GFR falls to 10-20% of normal. ARF s/s do not appear until renal fx has fallen to 10% of normal. Prerenal: hypovolemia, decreased CO, renovascular disease, renal vasoconstriction, impairment of RAAS via angiotensinconverting enzyme inhibitors or NSAIDS Intrinsic renal-glomerulomephritis, acute tubular necrosis (ischemic insult, nephrotoxic drugs ie aminoglycoside/antibiotic), interstitial nephritis or tubular obstruction Myoglobinuria -- this condition may be caused by rhabdomyolysis , alcohol abuse , a crush injury, or seizures or Infections such as acute pyelonephritis or septicemia, post-surgical, sepsis and shock Postrenal-ureteral obstruction, bladder neck problems, urethral obstruction (secondary to enlarged prostate) Intravascular overload, metabolic acidosis, anemia, hyperK+, uremic syndrome (pericarditis, uremic frost, asterixis, uremic fetor Elevated BUN and Creatinine Correction of the fluid and electrolyte imbalance and the underlying cause. Occassionally long term dialysis in needed. Chronic renal disease Can develop fom ARF but more often a complication of a chronic systemic disease. S/s do not appear until renal function has fallen to 10-15% of normal function, at 30-40% of the normal GFR, biochemical evidence can be seen. DM, HTN, glomerulomephritis, interstial nephritis, polycytic kidney disease Uremia, fluid and electrolyte imbalance, endocrine/metabolic disorders (hypertriglyceridemia, VitD def, hyperPTH, osteomalacia, or impotence) CV disorders, GI disturbances, dermatological disorders, hematologic/immunologic abnormalities and neurologic disorders (peripheral neuropathy) Fatigue, peripheral edema, hyperpigmentation, asterixis, PN, and altered mental status Determine underlying cause, hemnodialysis or peritoneal dialysis renal transplant, diet modification, protein, fluid and NA restriction

Complications Diagnosis Treatment Description Etiology Etiology s/s Treatment

Glomerular disease
Description Heterogeneous dzinjury to the glomerulus. Nephritis (inflam) or nephrosis (abnormal permeability of the glomerular membrane Acute glomerulonephritis Abrupt onset of hermaturia, proteinuria, and acute renal failure salt and water retention, HTN and edema Rapidly progressive Glomerulonephritis that advances to ESRD in days to weeks. Most commonly occurs in the setting of AGN but can be glomerulonephritis drug-induced. The key pathologic finding is th extensive formation of extracapillary crescents over of the glomeruli. Nephritic syndrome Proteinuria in excess of 3.5g/d hypoalbuminemia, edema and hyperlipidemia. Chronic glomerulonephritis Slowly progressive glomerular dz that leads to ESRD over a pd of mo-yrs. Most important cause in US is DM. Good pastures Autoimmune disorder against collagen is present in the alveoli (tiny air sacs in the lungs) and in the glomeruli (the filtering syndrome units of the kidney). These antibodies are called anti-glomerular basement membrane antibodies (or anti-GBM antibodies). Polycystic kidney Inherited disorder (autosomal dominant). In early stages of the disease, the cysts enlarges the kidney and interfere with fx, disease resulting in chronic high blood pressure and kidney infections. The cysts may cause the kidneys to increase production of erythropoietin resulting in too many red blood cells, rather than the expected anemia of chronic kidney disease. Other Wegeners granulomatosis and SLE nepritis

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Bone Metabolic Bone diseases

Avascular or aseptic necrosis associated with Gaucher disease, alcohol abuse and corticosteroids Overall loss of bone itself-loss of the calcified and osteoid component assoc with Vit D def and inactivity Loss of mineralization (calcified component only) with pitting of the calcified portion of the bone Acquired condition secondary to excessive production of growth hormone after skeletal maturity, when excess growth hormones are produced before skeletal maturity, the condition is referred to as gigantism and it is associated with a high incidence of impaired sugar tolerance. About 18% of all patients with acromegaly have insulin resistant diabetes mellitus. Thyroid acropachy Rare sequelae of thyroid gland ablationperiostitis of feet bones occur a rectangular appearance to these bones Macrodactyly this is a congenital problem and is present from birth Vit C deficiency Scurvy Most of the bone is reactive and woven with vascular fragility hemorrhage VitD deficiency Loss of mineralization (calcified component only) with hyperplasia of the cartilage in the growth plate Osteitis fibrosis cystica Secondary hyperPTH- Loss of mineralization as well as destruction of the bone overactive osteoclastic activity caused by prolonged hypoCa produces the characteristic brown tumors (Von recklinghausen dx of bone) Pagets disease Triphasic polyaustotic collage of matrix madness with concurrent/simultaneous activation of osteoblastic and Osteitis deformans osteoclastic activity may have a metastatic malignancy and can lead to osteosarcoma that occurs in the elderly Achondroplasia M.c. disease of the growth plate, (autosomal dominant) w loss of endochondral ossification- only membranous ossification Pyogenic OM Staph aureus is responsible for 80-90% Tuberculous OM Potts disease-spread of TB from the lung to the vertebral medulary cavity Osteonecrosis Osteoporosis Osteomalacia Acromegaly

Osteomyelitis
Description Pathophysiology Areas of dead bone (sequestrum) surrounded by reactive bone (involucrum) denotes inflammation and infection metabolic by-products of the bacteria and associated anti-inflammatory rxs decrease local pH breakdown of trabeculae and removal of bone matrix & Ca+ salts [demineralization seen radiographically as radiolucency] *infection spreads via Haversian and Volkmann channels vascular channels occluded bone necrosis and osteocyte death pus formation within channels raises the intraosseous pressure & compromises blood flow sequestra localized segments of necrotic bone become fragmented. *infection violates the outer cortex; if intracapsular septic arthritis; if subperiosteal suppurative material abscess formation & proliferative periosteal reaction/lifting known as involucrum; - highly suggestive of chronic OM *bone infection may s/t involvement as infection "breaks through" the periosteum or jt capsule drainage & spread AKA cloaca Infectious pathogens Staphylococcus aureus is the m.c. pathogen & Staphylococcus epidermidis is associated with joint implants and bone hardware, Pseudomonas aeruginosa is the most common pathogen in osteomyelitis secondary to a puncture wound Diagnostic screening Radiographic Sequestra, involucrum; cloaca not seen for 10-14 days Bone Scans Technitium-99: uptake by osteoblast and hydroxyapatite crystals; tri-phasic (non-specific for OM) Blood flow-immediate Blood pool- after 5 minutes Delayed- after 4 hours Gallium-67: binds WBCs, plasma proteins, lactoferrin; good for neoplasms/ inflam; image for infxn taken 6-24hrs; image for tumors taken 24-72 hrs Indium-111: binds to WBCs cytoplasm components; best for infection dx; Ceretec HMPAO- binds WBCs-4th phase Definitive dx Definite-bone biopsy and bone culture Treatment: Decompression, drainage, debridement, dressing, drugs Conservative IV antibiotic tx is indicated and continued for 4-6weeks and can often be accomplished on an out-patient basis osteomyelitis of the phalanges usually responds well to anti-microbial therapy alone Surgical imperative when necessary and is indicated in acute osteomyelitis when there has been no response after 48 to 72 hours of antimicrobial tx radical debridement and removal of fixation devices is recommended Classification schemes of OM Waldvolgel Hemotogenous OM 19%most common in pediatrics/ pts over 50, affects metaphyseal bone because in the pediatric pt: OM secondary to contiguous focus47% (the most common type seen in podiatry) Post-op contiguous OM (w/in 1 month of surgery) OM associated with vascular insufficiency 34% Chronic or Recurrent Buckholtz: Based on mechanism of action (7 types) 1. Wound induced OM 2. Mechagenistic OM 3. Physeal OM 4. Ischemic limb disease 5. Combination OM (I-IV) 6. Osteitis with septic arthritis 7. Chronic OM Cierny and Anatomic type Physiologic type Mader 1. Meduallary OM 5. Good immune system and delivery

35

2. 3. 4.

Superficial OM Localized OM Diffuse OM

6. Compromised locally or systemically 7. No treatment b/c treatment is worse than the disease

Benign bone lesion

Solitary Bone Cyst (Unicameral Bone Cyst) PAINLESS Aneurysmal Bone Cyst

Description

Bone tumors Characteristics and Radiographic Findings

m.c cystic lesion of foot m.c occurs calcaneus usually asymptomatic unless pathologic fx occurrence possibly secondary to low grade inflammatory process 1st and 2nd decade (young adults) M:F2:1 occurs in distal ends of long bones "fallen fragment" sign no appreciative periosteal rx initial tx may include aspiration and introduction of acetated glucocorticoids (case study reports resolution of cyst with introduction of 240 mg of DepoMedrol) Painful lesion assoc w/focal swelling, pain and tenderness expansile lesion blood filled sinusoidal cavities w/in cyst may appear quite aggressive and difficult to distinguish from a sarcomatous lesion of bone. Incidence: 20-30 but may appear in younger and older people. generally solitary Description PAINFUL classically associated w/ relief of pain by aspirin tumors produce PGs & night pain PAINFUL uncommon accounts for 1% of all primary bone tumors to trauma locally aggressive, Incidence and Location generally affects long bones m.c in the calcaneus and talus affects young adults - primarily 2nd0 yrs predilection for long tubular bones, neural arches of vertebral column peak incidence 2nd decade

Benign Bone tumors Osteoid Osteoma Osteoblastoma

Description

Characteristics and XR Findings

Treatment

Malignant bone forming tumor: Osteosarcoma Primary malignant tumor of the foot, m.c primary malignant bone tumor. May arise from pre-existing Paget's lesion 50-70 y/o bimodal peak, whereas the primary tumor is m.c. in the younger population (3rd mc malignancy in pediatrics) may arise from soft tissue s/s pain, swelling, limitation of ROM, pyrexia PAINFUL Pathognomonic XR findings: sunburst periosteal reaction delicate rays of periosteal bone formation and Codman's triangle periosteal reactiontriangular elevation of periosteum dDX: OM tumor possesses lytic foci: MRI and CT useful to delineate bounds of tumor cortical bone destruction (may actually be disrupted)motheaten" bone destruction may possess dense sclerosis in center of lesion, may possess an extraosseous mass, soft tissue ( Increase in ALP and leuckocyosis) Pre-op chemo to shrink the tumor, but radical excision imperative5 yr survival rate w/ resection only and not amputation essentially zero Symes amputation - if fat pad of heel and dorsal skin are uninvolved, BKA - if tarsal bones are involved, Rotationoplasty Marrow Tumors Affecting Bone Incidence and Location

Tumors Ewings Sarcoma

Description

Characteristics arises from medullary cavities possessing a diaphyseal location motheaten or mottled XR appearance onion skin periosteal reaction generalized osteoporosis scattered punched-out" osteolytic hypercalcemia may be present secondary to bone destruction poorer prognosis

Multiple Myeloma

malignant primary bone tumor PAINFUL w/ palpable swelling constitutional s/s dramatic: anemia of chronic disease fever and leukocytosis highly metastatic& expansile radical amputation 4th m.c malignant bone tumor in footsurpassed by: multiple myeloma osteosarcoma Chondrosarcoma 2nd m.c. primary malignant bone tumor in foot incidence in foot is 5.3% peak incidence - 5 to 15 yr m.c in whites than blacks/ Asians due to unregulated growth and proliferation of clonal (overproduction of either intact monoclonal Igs (IgG, IgA and rarely IgD) or light chains only) plasma cellsdisplays diffuse, plasma cell infiltration in bone marrow (check for Jones protein in the urine*UA) constitutional signs such as bone pain, infections, anemia and renal insufficiency predominates w/skeletal destruction. 1 of the most common if not the most common malignant bone tumors in foot mortality w/in 3 yr onset in middle and old age90% pts > 45yrs, m.c in blacks M>F Incidence/ Location Characteristic findings

Benign Cartilaginous Tumors Enchondroma

usually occur in 3-4th decade chondrosarcoma VIP may develop; Syndromes Associated with Enchondroma: multiple enchondromatosis Ollier's dx or multiple enchondromatosis whemangiotosis Marfucci's syndrome Chondroblastoma (Codman's tumor) Occurs: 10-20 years - predilection for epiphysis usually seen when growth plate is open. Rare tumor Chondromyxoid Fibroma Can affect any age group but m.c in 3rd decade may undergo malignant transformation

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Osteochondroma Subungual Exostosis

2nd-3rd decade cartilaginous cappotential to transform 50% of bone tumors, may correlate w/ trauma; m.c on hallux frequently located underneath nail plate m.c. in adolescent females fibrocartilaginous cap

Malignant Cartilagenous tumor: Chondrosarcoma

Description malignant tumor usually arising from within the bonemay arise from a preexisting cartilaginous tumor metastasize (primarily to the lungs) six subgroups of chondrosarcoma exist: Incidence and Location predilection for long tubular bones, rarely arise in foot, M>F, usually seen in 3rd to 6th decade, Most commonly found in the tarsal bones 42.1% - 5 cases (26.2%) in calcaneus Characteristic XR Findings thick radiolucent defect, present w/i the medullary cavity of bone; may involve soft tissue extensive size may result in pathologic fracture, possesses speckled calcification Treatment radical excision with adequate resection of uninvolved osseous margins and surrounding soft tissue amputation monitor for metastasis (generally pulmonary but may involve liver, kidney, brain) Miscellaneous Tumors Tumors Description Incidence and Location Characteristics and XR Findings Treatment Giant Cell Tumors rare tumors typified by foot lesions seen in lytic lesion surgical curettage, packing with bone chips-bone multinucleated type metatarsals and tarsal bones soap grafting may be required radiation tx must giant cells PAINFUL (especially calcaneus) bubble" monitor these as tumor growth is unpredictable arises from the synovial lining occur m.c along dDX: Ganglionic cyst marginal excision, very low of tendon sheaths PAINLESS the dorsal surface and PVNS, must recurrence rate-implantations of the AKA benign fibrous of the foot about aspirate-but will not tumor into surrounding soft tissue histiocytomas fibroxanthomas the ankle suck out anything may be difficult to treat may arise from any synovial acute synovitis aspiration of the joint synovectomy is the ideal TOC, recurrence tissue occurs m.c around jts but will produce a brownish, bloody and satellite lesions are incredibly common may involve the tendon sheaths appearing fluid dDx: hematoma radiation tx not recommended in the foot Insidious onset, s/t sarcomas usually present as PAINFUL tri-phasic scan will often radical excision of lesions on the plantar aspect of the footdDX: frequently demonstrate increased uptake involved area with mistaken for a fibroma when occurring on the bottom of the in all 3 phases secondary to wide margins foot and a ganglionic cyst when occurring on the dorsum if periosteal inflam of adjacent needle aspiration fails to produce fluid, excision bone these are geographic, multiGenerally btwn 5-20 yrs often an incidental finding, Nada-Curretage with bone lobulated, lytic lesions common occurs w/i metaphyseal bone or at the metaphysealpacking if >50% of self healing lesion epiphyseal junction. Epiphysis is never affected. diameter is involved

Giant Cell Tumor of Tendon Sheath

Pigmented Villonodular Synovitis Synovial Sarcoma

Non-Ossifying Fibroma

F. Hematologic disorders-including anemias and leukemias Leukemias-neoplasms of the bone marrow

Hairy cell Leukemia m>w 2% of the leukemias Acute myelogenous leukemia m>w Chronic myelogenous leukemia 7% to 20% cases Acute lymphocytic anemia Uncommon caused by the abnormal growth of B cells. Average age of onset is 55.S/s: Weakness, Fatigue, Weight loss , Easy brusing or bleeding , Recurrent infections and fevers, Excessive sweating (especially at night), Swollen lymph glands, and Early satiety. Treatment chemotherapy, Interferon and the removal of the spleen may improve blood counts may be required. Malignant disease of the bone marrow in which hematopoietic precursors are arrested in an early stage of development 2 disease processes. First, the production of RBCs markedly decreases, which results in varying degrees of anemia, thrombocytopenia, and neutropenia. Second, the rapid proliferation of these cells, along with a reduction in their ability to undergo apoptosis, results in their accumulation in the bone marrow, blood, and, frequently, the spleen and liver. Symptoms of bone marrow failure are related to anemia, neutropenia, and thrombocytopenia. In fact, MI may be the 1st presenting symptom of acute leukemia in an older patient. Treatment: Chemotherapy, bone marrow transplant and radiation therapy. A myeloproliferative disorder characterized by increased proliferation of the granulocytic cell line without the loss of their capacity to differentiate. Consequently, the peripheral blood cell profile shows an increased number of granulocytes and their immature precursors. It causes rapid growth of myeloid precursors in the bone marrow, peripheral blood, and body tissues. The disease can occur in adults (usually middle-aged) and children. Symptoms: W/i 5 yrs, in most people, the dz progresses to a "blast crisis. Treatment: Chemotherapy, bone marrow transplant and radiation therapy. Progressive, malignant dz characterized by large numbers of immature WBCs that resemble lymphoblasts. These cells can be found in the blood, the bone marrow, the lymph nodes, the spleen, and other organs. In ALL, the malignant cell loses its ability to mature and differentiate. The person becomes susceptible to bleeding; DIC and infection. Symptoms:, Fatigue, , Bone and joint pain or tenderness , Foot pain over small joints of the foot , Lymphadenopathy and Fever Treatment: Chemotherapy, bone marrow transplant and radiation tx. 80% of childhood leukemia ages 3 -7 and 20% of adult

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Chronic lymphocytic anemia Megaloblastic anemias

M of the WBCs characterized by a slow, progressive increase of these cells in the blood and the bone marrow.Causes, incidence, and risk factors CLL affects the B lymphocytes and causes immunosuppression, failure of the bone marrow, and invasion of malignant cells into organs.Usually the symptoms develop gradually. (90% of cases are found in people over 50).

Characterization of Anemias Folate or B12 deficiency B12 binds with IF and subsequently absorbed in the ileum a decrease in B12 is referred to as pernicious anemia and is often caused from atrophy of the gastric musosa which results in decreased intrinsic factor secretion it may occur possibly secondary to an Ab reaction against the gastric parietal cells this more commonly occurs in the elderly (>60 year of age) folate is absorbed in the upper small intestine - a def of folate manifests more quickly as body stores only last a few months drug tx may cause folate def phenytoin, anti-metabolites (especially MTX), Bactrim, and pyrimethamine Clinical Features: glossitis and a variety of GI s/s (indigestion, bloating, anorexia, diarrhea) the neurologic disease points to a B12 def and not a folate deficiency alone (degeneration of the dorsal and lateral columns - the legs affected more severely than the arms) Microcytic Severely anemic patients will often be symptomatic at rest and unable to tolerate significant exertion when the [Hgb] falls below Anemias 7.5 g/dl these include iron-deficiency, siderolastic and the thalassemias they collectively represent a decrease in the availability or synthesis of one of the3 major constituents of the Hgb molecule iron, porphyrin and globin Physical findings pallor is the m.c. feature, tachycardia (d/t increase in resting CO), a wide PP, vertigo and HA Lab Findings: Low serum Fe and ferritin and high Total iron binding concentration (TIBC) Anemia of chronic inflammatory process of greater >1 mo will often cause an anemia and typically, the Hgb will be between 9-11 g/dl; primarily d/t defective RBC prodand secondarily d/t abnormal incorporation of Fe into the RBCs (> 50% of normal) Chronic Disease Hemolytic anemia is a condition of an inadequate number of circulating RBCs caused by premature destruction of red blood Hemolytic cells. There are a number of specific types of hemolytic anemia, which are: anemias 1. acute blood loss - generally obvious 2. splenomegaly - spleen 3x its normal size this occurs m.c w/ portal HTN, chronic infections and myeloproliferative disorders 3. hemolytic disorders - concomitant findings generally include an elevated indirect (unconjugated) bilirubin levels -congenital hemolytic anemias include disorders of the cell membrane, hemoglobinopathies and red cell enzyme deficiencies -hereditary spherocytosis - and hereditary elliptocytosis 4. hemoglobin abnormalities- Hemoglobin SS (sickle cell anemia), Hemoglobin SC, Hemoglobin S-beta thalassemia, Hemoglobin C -a mild to moderate anemia do not use a tourniquet on these patients 5. G6P def -disorder asymptomatic unless pts subjected to oxidant injury-X-linked transmission, affects 2-3% of the world population antimalarials, sulfonamides, nitrofurantoin, phenacetin, aspirin drug causes occurs when the corrected reticulocyte count is not elevated and is a primary marrow disease affecting all cell lines Anemia of 1. aplastic anemia - the marrow is primarily hypocellular Decreased RBC 2. Human parvo virus B19 (HPV) pts present with a nonspecific viral syndrome (fever, malaise, headache, myalgia and a Production fleeting rash 3. fifth disease in children is the m.c inciting factor is and is augmented in persons with a pre-existing hemolytic anemia 4. the anemia of chronic renal failure declining erythropoietin production by the kidneys with shortened red cell survival 5. patients with hypothyroidism and liver disease usually have a normocytic anemia

G. Immunologic disorders-allergic and sensitivity reactions and immunosuppressive states Allergic and sensitivity reactions
Types I-Immediate II-Cytotoxic III-Immune complex Description of s/s Anti-body Anaphylactoid allergy, asthma, eczema, hay fever, IgE urticaria, rhinitis and food. ATOPY this is an antibody-dependent cytotoxic hypersensitivity, IgG where the IgG binds to an antigen in the BM phagocytosis, killer cell activity or complement mediated lysis vasoactive amines are released by platelets, basophils and N/A mast cells which cause endothelial cell retraction and therefore, increase vascular permeability serum sickness Protective cell (s) Mast cells macrophage, neutrophils, eosinophils and killer cells platelets, basophils and mast cells and continuous C3a and C5a activity Examples Anaphylaxis Immune Hemolytic Anemia leukocytoclastic vasculitis, autoimmune disorders

38

IV-Delayed

Antigens are trapped in macrophage and cannot be cleared, N/A CTLs, macrophages and T cells then elaborate cytokines which mediate a vast range of inflammatory responses Immunosuppressive states

allergic contact dermatitis and graft rejection

Primary Immunodeficiencies X-linked agammaglobulinemia Defect of Btk protein kinase for B-cell maturation recurrent pyogenic infections Digeorge Syndrome Thymic hypoplasia poor defense against viral and fungal infections SCIDS Purine salvage deficinecy- Def in adenine deaminase enzyme, combined B and T cell deficiency -recurrent infections Wisckott Aldrich Syndrome X-linked instability of the platelet and lymphocyte associated glycoprotein which reduces their life span low platelet, B/T cells Tx: BM transplant s/s: thrombocytopenia and eczema H. Respiratory disorders, including asthma, COPD, and emphysema Diseases of the lungs Obstructive Disease of the airway, due to an increase in resistance to air flow owing to partial or complete obstruction of the respiratory tubes. Major conditions of COPD syndromes characterized by dyspnea (difficulty breathing) and are accompanied by chronic or recurrent obstruction to airflow. Emphysema Smoking Destruction of bronchiole wall w/o obvious fibrosis Pink puffers-tend to over ventilate to remain well oxygenated Chronic Smoking Exhibits squamous metaplasia Persistent cough w/sputum production for at least 3mo in 2 consecutive years bronchitis Slight increase in goblet cells Blue bloaters- barrel chested and dyspneic, breathe through pursed lips with Severe cases may cause obliteration of slow forced expirations Thick mucinous plugs and submucosal gland bronchiole lumina-bronchiolitis obliterans hypertrophy occlude bronchi (same as in asthma). Asthma Hyperactive airways leading to reversible bronchco-constriction; Over distended lungs Marked goblet cell hyperplasia, Bronchi are occluded by thick mucinous plugs. Curshman spirals in the epithelium caused by the plugs shedding epithelium and charcot layden crystals Bronchiectasis Caused by tumors, foreign bodies, chronic bronchitis, congenital, cystic fibrosis and necrotizing pneumonia Permanent abnormal dilation of the bronchi and bronchioles Restrictive lung disease Decreased expansion of lung parenchyma with decreased total lung capacity. Can be caused by infections, pneumonitis, Pneumoconicosis, or lung rx to inhalation of mineral dust i.e., asbestosis, sarcoidosis Sarcoidosis Disease of unknown cause Lung fibrosis and cor pulmonale. Involves, bilateral hilar lymph nodes. Histologically: Noncasseating granulomas, laminated calcium secretions Asbestos Silicates that form fibers. Assoc with bronchogenic carcinoma and mesotheliomas (malignant neoplasms of mesothelial origin Pneumonia Bacterial: Staph, Strep, H. influenzae, P. aeruginosa, and coliform bacteriaBronchopneumonia (patchy consolidation) Pneumococcus *most common* Lobar pneumonia (entire lobe) Tuberculosis (M. Tuberculosis) Primary TB- Ghon complex parenchymal subpleural lesion and enlarged casseous lymph nodes. Secondary TBcollection of granulomas in tissue, pleura + lymph nodes, characterized by Langerhan giant cells

Definition Risk factors Clinical features Nonspecific & INCONCLUSIVE! (DDx)

PULMONARY EMBOLISM Defined as a thrombotic occlusion of the pulmonary arteries. CHF, Ml, COPD, pregnancy, prolonged immobilization, previous hx of PE, history of DVT, marked obesity, malignancy, estrogen use, surgery in the last 3 months, or lower extremity trauma. Common symptoms - dyspnea, pleural pain, apprehension/anxiety cough, hemoptysis, sweats, and syncope. Common Signs - tachypnea >16 breaths/min - fast & shallow w/ rales; tachycardia or pulse rate >100b/min, T0 >100.4, phlebitis or DVT, cardiac gallop, and diaphoresis. Presence or absence of any s/s does not confirm or exclude the diagnosis of PE; Diagnosis of PE is based on - clinical suspicion, ancillary laboratory data, & results of specific diagnostic studies. In patients without prior cardiopulmonary disease S & S are clues to the diagnosis; in patients with H/O heart or lung disease S & S are mistaken for manifestations of the underlying disease. Respiratory disorders - asthma, COPD, pneumonia, spontaneous pneumothorax, and pleurisy Cardiac disorders Ml, pericarditis Musculoskeletal disorders - muscle strain, rib fracture, costochondritis, herpes zoster Intra-abdominal Disorders that irritate the diaphragm or stimulate breathing Hyperventilation syndrome - mimic PE; Dx of exclusion.

Supplementary Tests that show PE: Arterial blood gases, 12-lead EKG, CXR, Dx confirmed or excluded only with more sophisticated tests, such as ventilation-perfusion lung scan (V-Q scan) or pulmonary angiography.

39

ABGs,

Pa02 < 80 mm Hg in 80% of patients with PE; 5% of patients with PE - Pa02 >90 mm Hg. The presence of an increased alveolar-arterial (A-a) gradient is more sensitive (95%) for PE pH: 7.35-7.45 PaCO2: 35-45mmhg PaO2: 80-100mmhg HCO3: 22-28meq O2 sat: 95-98%(a) 60-85% (v) BE: 0+/-2mmol 12-lead EKG S1Q3T3 Prominent S in Lead 1 ST depression in Lead 2 Prominent Q in lead 3 Inverted T in lead 3 Pattern on the EKG is highly suggestive of PE present only in 12% CXR Hamptons Hump wedge shaped pleural-based infiltrates; Westermark large lung lucency in area of embolus; Other supplemental tests CBC (R/O DDx), PT, PTT (anticoagulation). Enzymes Triad associated with PE - HyperLDH, hyperbilirubinemia and hyper SGOT. * KNOW* Venography Helpful; In PE - radiographic evidence of DVT - 90% pts; clinical signs - 33% pts. V-Q scan Very sensitive test for PE & completely normal study rules out the disorder. Pulmonary angiography Is gold standard for diagnosing PE and is a much more specific test than the V-Q scan. Angiogiaphy more potential complications, esp. in elderly patients; needed to confirm the Dx if the V-Q scan demonstrates equivocal results medium or low probability for PE in at risk pts. TREATMENT of PE Initial stabilization anticoagulation with heparin, and thrombolytic therapy in extreme cases, cardiac monitoring, noninvasive blood pressure device, pulse oximetry monitor, IV line. Administer O2 pulse oximetry 95% Rx hypotension (500-1,000 ml of NS IV bolus) Crystalloid IV fluids Unresponsive hypotension & absence of hypovolemia Rx w/ Dopamine 2 - 5 mcg/Kg/min & titrated to maintain a systolic blood pressure of 90 mm Hg. Full heparinization: Heparin IV bolus of 10,000 to 20,000 U, continuous drip of 1,000 U/h adjusted using PTT, aiming for 1.52x control. o Contraindications to anticoagulation - active internal bleeding, uncontrolled severe hypertension, recent trauma, recent surgery, recent stroke, intracranial or intraspinal neoplasm. Heparin Rx prevents embolization of existing clots so further embolization of formed clots & shock most commonly occur w/in 4h of initial symptoms. Pts w/ clinical instability should be admitted to ICU; Stable pts may be admitted to telemetry bed; Pts stable & beyond this initial highrisk period are admited to a non-monitored bed. Inferior vena cava interruption considered in: Green field filter o Pts in whom anticoagulation is absolutely contra indicated (i.e. active bleeding, immediate postoperative period, neurosurgical patients, severe diastolic hypertension); o Massive pulmonary emboli with hemodynamic compromise, esp. w/ evidence of residual thrombus in a lower extremity, o Pts w/ compromised cardiac or pulmonary function who may not survive a recurrent event, o Patients undergoing pulmonary embolectomy. Systemic thrombolytic therapy with streptokinase, urokinase or t-PA hastens the resolution of the clot but has not yet been shown to reduce mortality. o Thrombolytic therapy considered in Rx of pts w/ (1) Acute massive embolism, hemodynamically unstable & are not prone to bleeding (2) Pt w/ persistent hypotension despite medical Mx Pulmonary embolectomy should be considered in the rare patients w/ confirmed emboli (angiographically) & remain in shock despite thrombolytic therapy and supportive care; or in whom thrombolytic therapy is contraindicated. I. Behavioral disorders, including depression, abuse, and anger disorders and their effects on patient compliance

Depression

Depression may be described as feeling sad, blue, unhappy, miserable, or down in the dumps True clinical depression is a mood disorder in which feelings of sadness, loss, anger, or frustration interfere with everyday life for an extended time. Depression is generally ranked in terms of severity -- mild, moderate, or severe. The degree of your
depression, which your doctor can determine, influences how you are treated. Symptoms of depression include Trouble sleeping or excessive sleeping A dramatic change in appetite, often with weight gain or loss Fatigue and lack of energy Feelings of worthlessness, self-hate, and inappropriate guilt Extreme difficulty concentrating Agitation, restlessness, and irritability Inactivity and withdrawal from usual activities Feelings of hopelessness and helplessness Recurring thoughts of death or suicide Treatment: SSRIs, TCAs, MOAIs Consider in children with recurrent fractures

Abuse
Mania Bipolar disorder :

Anger disorders tx with anti-depressants and Lithium

Constant exicitability Characterized by pds of (mania) alternating w/ pds of depression-"mood swings" btwn mania and depression can be very abrupt.

J. Emergency Medicine, including common medical emergencies and CPR

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Description Etiology and Pathology Incidence Recognition Management

Office Emergencies Vasovagal Reaction (Syncope) Syncopy is defined as the sudden loss of postural tone and consciousness with subsequent spontaneous recovery Transient LOC stimulated by fear/ pain, where the heart b/c overstimulated by the vagus n an ANS mediated response HR and therefore, CO to compensate for the CO, the peripheral vasculature vasoconstricts to help maintain perfusion of the brain patients < 40 y/o are at risk for a vasovagal reaction, patients who are sitting rather than lying down are more susceptible multiple needle sticks may increase the risk and lengthier procedures increase risk patients may complain of nausea, feeling hot or cold, may shiver or even vomit PE include: pallor, diaphoresis, bradycardia, hypotension, mydriasis (full-pupil dilation) LOC and reflex tachycardia Supportive Trendelenberg position (recumbent, supine with legs elevated) to reassure patient; monitor BP and PP, ammonium salts, oxygen (flow rate 2 to 4 liters/minute) as a very last resort - atropine (if bradycardia does not respond to palliative care)- 0.4 mg IM or IV, or ephedrine 15 25 mg IM or IV Insulin Shock or Hypoglycemic Crisis

Description

Recognition

Management

low BS it is defined by a serum glucose level of < 50 mg/dl in men, < 45 mg/dl in women and < 40 mg/dl in children the CNS or ANS are most sensitive to low {Gl-]p insulin shock hypoglycemia secondary to either too much insulin or insulin taken without food, too much exercise may also precipitate hypoglycemia and alcoholic beverages may cause blood sugar to drop early symptoms: CNS changes are observes w/ weakness, faintness, blurry vision, poor concentration and personality changes CVS manifestations: palpitations; GI s/s: nausea, hunger and belching and ANS effects manifest as diaphoresis, nervousness Late s/s: headache, altered mental status such as confusion and mood changes, with eventual coma or seizure Treatment should not be withheld while awaiting laboratory studies! do a Gl- finger stick to ascertain [Gl-]p and if conscious, give orange juice or soda (6 oz), candy or a gl pill (three gl tablets are recommended) If demonstrating altered mental status or the patient is unconscious, administer IV gl- 20 to 50 cc of 50% dextrose solution. Inject slowly until the patient begins to react. Hyperglycemia or Diabetic Coma Characterized by increased thirst and urination usually for one to several days: polyphagia, polydipsia, polyuria patient may have N/V and abdominal pain, an overall feeling of weakness or fatigue and dehydration: Kussmaul breathing - heavy, labored, rapid, deep breathing immediate transport to the hospital so that glucose levels must be brought under control and for patient to be hydrated Insuilin Sliding scale 150-200 201-250 251-300 301-350 351-400 401-450 >450 O units 2 Units 4 Units 6 units 8 units 10 units 12 Units

Description Management

Description Recognition

Management

Seizures seizures are generally associated with epilepsy or drug toxicity and are characterized by an abrupt, transient change in the general nervous system may demonstrate motor, sensory, autonomic and/or psychic changes, and most patients will experience an aura prior to a seizure grand mal seizure signs of CNS over stimulation and muscle spasms LOC with profound muscle spasms, patient may become pale or cyanotic w/possible loss of bladder or bowel control Following a seizure, a period of sleep (post ictal depression frequently occurs)- must observe for status epilepticus which is a dangerous condition with seizures will occur one right after the other preventing the patient from recovering in between. Protect the patient and allow the seizure to run its course: following the seizure check for vomitus in the airway, keep the head turned to the side; if a patient goes into status epilepticus, administer diazepam, 5 to 10 mg IV slow push or dilantin 300 mg IV and administer oxygen. Transport pt to ER ASAP. Epinephrine Reaction recognized by restlessness, agitation, "pounding" HA, HR and palpitations, where pt may c/o chest pain and have an elevated BP toxic effects can be managed with an alpha and a beta blocker, a rapid acting vasodilator such as the nitrates may also be effected and demerol - 12.5 to 25 mg IV

Description Management

41

Description Recognition Management

Hypertensive Crisis Serious consequences if DBP elevates >140 mm/Hg retinal hemorrhage, vascular necrosis and impaired renal fx w/hematuria acutein BP, HA, visual changes, papilledema, ringing in the ears and coma supportive the goal is to drop the patients DBP to between 90-100 mm/Hg: elevate head, ASA for headache Clonidine central it is administered p.o. with a dose of 0.2 mg initially followed by 0.1 mg qh up to a 0.8 mg sympatholytic maximum onset of action is between half an hour and 2 hours and lasts for 6-8 hours, sedation with clonidine is prominent and rebound hypertension may occur Hydralazine arteriolar dosage is 10-20 mg IV, onset in 10-30 minutes and lasts for 2-4 hour - importantly this vasodilator medication may cause myocardial infarction or angina The main use of this medication is for pregnant individuals nifedipine 10 mg sublingually; may repeat in 30 minutes in the hospital setting, nitroprusside may be administered Management if asthma is occurring secondary to an extrinsic trigger, utilize 0.3 to 0.5 mg of epinephrine 1:1000 every 5 to 15 minutes for up to 3 doses (use the epinephrine with some caution as it will increased both the blood pressure and heart rate) administer an albuterol inhaler (a bronchodilator) deliver oxygen (2 to 4 liters/minute)

Asthma and Bronchospasm Acute Asthma Attack bronchospasm with concomitant angioedema wheezing this may occur secondary to a hypersensitivy reaction or may be triggered by anxiety or other emotional stress a patient with a history of asthma will generally recognize the oncoming symptoms and know to loosen their clothing and use their inhaler this should be a reversible process and with proper management will not lead to respiratory arrest

Description

Manifestations of Lidocaine toxicity

Incidence Recognition

Treatment

Lidocaine Toxicity toxicity will occur 2 to an overdose of the local anesthetic and high [local anesthetic] manifest with CNS and CVS effects Rxs occur 2 to direct IV administration or by use of excessive ats of local anesthetic resulting in rapid systemic absorption other factors precluding to toxicity include the speed of injection, CO, pCO2, and idiosyncratic sensitivity and the presence of concomitant disease processes A true toxic reaction must differentiate this from a hypersensitivity reaction to the local patients are most often sensitive to the PABA preservative in local anesthetics. Ampules of local can be purchased that do not contain preservative CNS due to the initial inhibition of the excitatory neurons inhibition of both inhibitory and excitatory neurons as the effects process develops first phase considered to be excitatory and include tingling, numbness, mental status changes and biphasic ultimately, seizures second considered a depressive state and is recognized by the onset of LOC with respiratory depression phase or arrest CVS effects at high levels can lead to re-entrant arrhythmias licodaine is commonly associated with sinus higher [lidocaine] tachycardia where as bupivacaine may lead to ventricular tachycardia and fibrillation as local anesthetics are used in many settings, it is likely that many rxs are not reported with an epidural, the prevalence is 0.2% CNS signs may range from a feeling of sleepiness to a feeling of being intoxicated, and the patient may also complain of dizziness and numbness as toxicity further takes hold, the pt may c/o of tinnitus, have difficulty focusing and become agitated and anxious as levels continue to , the patient may develop a metallic taste in his mouth, demonstrating an RR and begin twitching in the extremities this twitching may evolve to seizures if levels remain high, seizures give way to respiratory depression - possible arrest and CVS depression in patients premedicated with benzodiazapenes or barbiturates, cardiovascular depression may be the first sign of toxicity a useful mnemonic for treating these reactions is SAVED Stop injection, Airway, Ventilate, Evaluate circulation and Drugs give O2 via nasal cannula or a face mask at 100%. If this is not possible, intubation may be required, monitor vitals anticonvulsant drugs should be administered as indicated one may use either a benzodiazapene or a barbiturate diazepam 5 mg -10 mg or thiopental 50-100 mg can be administered succinylcholine may also be effective, however, will require a controlled airway and controlled ventilation if BP remains depressed for > 30 minutes, give a vasopressor (for example, 20 mg methoxamine - Vasoxyl IM or ephedrine 20 mg IM) ephedrine will elevate both BP & HR, whereas, methoxamine (which affects -receptors only) will elevate only BP w/ no effect on HR ventricular arrhythmias should be managed with bretylium initiate EMS prn

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Types and compensatory mechanisms for shock Etiology and treatment Tx: ABCs Loss of preload. Loss of approximately >1/5 the normal blood volume Cause: bleeding external, Fluid replacement-at bleeding, internal, or from hypovolemia. In general, larger and more rapid blood volume losses result in least 20ml/kg more severe shock symptoms. Loss of contractility occurs whenever the heart is unable to pump enough blood for the Restore strength of pump +beta needs of the body. Caused by disorders of the heart muscle, the valves, or the heart's receptors electrical conduction system. Dopamine 2-20mcg/kg/min or dobutamine 3-20 mcg/kg.min Loss of afterload or a decrease in 0.3 to 0.5 mg of epinephrine 1:1000 subQ q15min prn, and establish IV access and systemic vasculature resistance run normal saline wide open owing to increase in vasodilatory deliver oxygen 6 liters/minute, diphenhydramine 25 to 50 mg IM, dexamethasone 8 mechanisms from histamine. mg IM or Solu-cortef (hydrocortisone) 200 mg IV aminophylline 250-500 mg IV given slowly, monitor vitals and activate EMS prn Fnctional loss of preload, afterload and contractility Identify and correct etiology

Hypovolemic Cardiogenic

Anaphylactic

Septic and Neurogenic

Compensatory Mechanisms of shock

aroreceptor reflexes (respond to small changes in vascular tone/pressure) o located in the carotid sinus and aortic arch, stimulation causes decreased vagal tone, which increases heart rate decreases coronary resistance (improves myocardial oxygen supply) increased sympathetic tone, which causes venoconstriction constriction of blood reservoirs (increasing circulating blood volume) spleen - dogs skin and skeletal muscle - humans Chemoreceptor o located locally in tissue beds o sense hypoxia (due to inadequate blood flow in peripheral tissues), and cause further vasoconstriction respiratory stimulation - improves venous return (pump model), also helps compensate for acidosis Cerebral Ischemia (Cerebral Perfusion Pressure<40mmHg) o activates sympathoadrenal system (more potent than Chemo or Baroreceptor mechanisms) o increased catecholamine release from both adrenal gland and sympathetic nerves (can also get vagal stimulation which is counterproductive) Reabsorption of tissue fluids o decreased mean arterial pressure o arteriolar constriction } All lead to decreased hydrostatic pressure o decreased venous pressure in capillaries, leading to increased resorption of fluid15ml/kg/hour, o up to 1l/hour can be reabsorbed in adult sized patients When Hydrostatic Pressure > Osmotic Pressure: Filtration Osmotic Pressure>Hydrostatic: Reabsorption Endogenous Vasoconstrictors o Epinephrine and Norepinephrine released from adrenal medulla and sympathetic nerves cause vasoconstriction and increased cardiac output o Vasopressin (Antidiuretic hormone) released from posterior pituitary potent vasoconstrictor o Renin (from decreased renal perfusion) leads to angiotensinogen production eventually yielding angiotensin - a very potent vasoconstrictor Renal Conservation of Water

o o

43

Aldosterone release stimulated by vasopressin Causes Na reabsorption in distal tubules Water follows the sodium

Facts about CPR

1. 2. 3. 4. 5. 6. Check for responsiveness. Shake or tap the person gently. See if the person moves or makes a noise. Shout, "Are you OK?" Call 911 if there is no response. Shout for help and send someone to call 911. If you are alone, call 911 even if you have to leave the person. Carefully place the person on his or her back. If there is a chance the person has a spinal injury, two people are needed to move the person without twisting the head and neck. Open the airway. Lift up the chin with 2 fingers. At the same time, push down on the forehead with the other hand. (head-tilt chin lift or jaw thrust if suspected neck injury) Look, listen, and feel for breathing. Place your ear close to the person's mouth and nose. Watch for chest movement. Feel for breath on your cheek. If the person is not breathing: a. Cover the person's mouth tightly with your mouth b. Pinch the nose closed c. Keep the chin lifted and head tilted d. Give 2 slow, full breaths If the chest does NOT rise, try the chin lift-head tilt again, and give 2 more breaths. Look for signs of circulation -- normal breathing, coughing, or movement. If these signs are absent, begin chest compressions. Perform chest compressions: a. Place the heel of one hand on the breastbone -- right between the nipples. b. Place the heel of your other hand on top of the first hand. c. Position your body directly over your hands. Your shoulders should be in line with your hands. DO NOT lean back or forward. As you gaze down, you should be looking directly down on your hands. d. Give 15 chest compressions. Each time, press down about 2 inches into the chest. Give the person 2 slow, full breaths. The chest should rise. Continue cycles of 15 chest compressions followed by 2 slow, full breaths. After about 1 minute (four cycles of 15 compressions and 2 breaths), re-check for signs of circulation. Repeat steps 11 and 12 until the person recovers or help arrives.

7. 8. 9.

10. 11. 12. 13.

For a child (1-8yrs) steps 9-13 are different

9. Perform chest compressions: a. Place the heel of one hand on the breastbone -- just below the nipples. Make sure your heel is not at the very end of the breastbone. b. Keep your other hand on the child's forehead, keeping the head tilted back. c. Press down on the child's chest so that it compresses about 1/3 to 1/2 the depth of the chest. d. Give 5 chest compressions. Each time, let the chest rise completely. These compressions should be FAST with no pausing. Count the 5 compressions quickly: "a, b, c, d, off." Give the child 1 slow, full breath. The chest should rise. Continue cycles of 5 chest compressions followed by 1 slow, full breath. After about 1 minute, check again for signs of circulation. At this time, if the child still does not have normal breathing, coughing, or any movement, leave the child to call 911. Repeat steps 11 and 12 until the child recovers or help arrives.

10. 11. 12. 13. 14.

For an infnat (>1yr) steps 9-13 are different 9. Perform chest compressions: a. Place 2-3 fingers on the breastbone -- just below the nipples. Make sure not to press at the very end of the breastbone. b. Keep your other hand on the infant's forehead, keeping the head tilted back. c. Press down on the infant's chest so that it compresses about 1/3 to 1/2 the depth of the chest. d. Give 5 chest compressions. Each time, let the chest rise completely. These compressions should be FAST with no pausing. Count the 5 compressions quickly: "a, b, c, d, off." 10. Give the infant 1 slow, full breath. The chest should rise. 11. Continue cycles of 5 chest compressions followed by 1 slow, full breath.

44

12. After about 1 minute, check again for signs of circulation. 13. At this time, if the infant still does not have normal breathing, coughing, or any movement, leave the infant to call 911. 14. Repeat steps 11 and 12 until the infant recovers or help arrives.

K. Dermatology 1. Diagnosis A. Histopathological studies

Gram staim KOH test Dermatophyte test medium Gram-positive bacteria (purple) and gram-negative bacteria (pink) Scrape the scale from a lesion and apply 10-20% KOH. KOH dissolves kertin so that the skin, nail or hair shaft becomes clear. Examine under the microscope for the presence of fungal hyphae which can be seen growing in epithelial cells Cultures require 10d to grow, Medium will turn red if dermatophytes are present, however, a false positive may be seen w/saprophtes, so the colonies must be examined. Dermatophytes have powdery white colonies; saprophytes have shiny colonies that may be brown, white, black or green in color.

B.
Auspitz sign Diascopy Nikolsky sign Shave biopsy Punch biopsy Excisonal biopsy Tzank test Woods Light

Lab studies and special procedures

Pin point bleeding that occurs when the scales of a psoriatic lesion are removed Glass slide test-press a clear glass against the lesion and look for blanching. Dialated capillaries (erythema) will blanch, hemorrhagic lesions (pupura) will not An epidermal detachment produced by lack of skin cohesion, seen in bullous diabeticorum Suited to lesions confined to the dermis ie seborrheic keratosis or molluscum contagiousum Method of choice for most inflammatory or infiltrative disease-produces a full thickness specimen Method of choice for diagnosis and removal of dermal and subQ cysts and tumors (epidermal cysts and lipomas) use for melanoma and lesions too big to punch out >8mm in diameter Used to diagnose viral disease-HSV, VSV and molluscum contagiosum A black light w/ 360nm of wavelength filtered through glass used to dx certain infections by causinf different colors to fluoresce. Erythrasma-C. Minutissimum coral red, T capitus (M. canis bright green, P aeruginosa green, T versicolor yellow gold

2.
Gram Stain Culture and Sensitivity Blood cultures CBC w/diff

Infections
Laboratory testing in the diagnosis of Infection Extremely important for initial antibiotic choice; GP Blue, GN Red Aerobic and anaerobics should be ordered for clinically infected wounds Fungal, and acid fast cultures Ziehl Neelson is widely used for acid fast staining DO NOT culture superficial wounds, sinus tracts or ulcers that do not appear to be infected. Deep cultures are best and should be taken before the patient is places on antibiotics Must be done if bacteremia is suspected or hematogenous OM is diagnosed. 3 cx should be taken from 3 sites, 10-30min apart Leukocytosis occurs in the presence if acute infection Dohle bodies-remnants of RER RNA which appears as a light blue stained area in a neutrophils cytoplasm; may represent cytoplasms cytoplasmic failure to mature d/t infection Toxic granulation-stress response to infection: dark blue-black granules in a neutrophils cytoplasm Shift to the left-release of immature band cells from bone marrow in response to infection Eosiniphilia may be observed when parasites are observed in infectious process or may be 2o to allergy WBC 4.5-11.0 103 / l o Neutrophils 57-67%: Segs 54-62% and Bands 3-5% Lymphocytes 23-33% o Monocytes 3-7% Eosinophils 1-3% Basophils 0-1% RBCs 3.5-5.5 million cells/mcL Hemoglobin Male 14.0-18.0 Hemoglobin Female 12.0-16.0 Hematocrit Male 40-54% Hematocrit Female 36-48% Platelets 150,000-400,000/ cubic millimeters Leukocytes 5,000-11,000 per cubic millimeter Non specific indicator for inflammation, may be useful to follow course of infectious dz w/ Ab use Normal value: Male: 15 Female: 16 Non specific indicator for inflammation (more sensitive than ESR) Normal value: <0.8

Normal values:

ESR CRP

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Infectious organisms Parasitic

Cutaneous larvae migrans ,Ancylostoma braziliense Toxoplasmosis Gondii Leshmenia (mucocutaneous leishmaniasis). Sarcoptes scabeii Scabies Hookworms Creeping eruption the larvae burrow into the skin, causing an Tx: with topical thiabendazole 10% aqueous intense inflammatory response that follows their progress beneath the solution is good for mild infection in the early skin and leads to severe itching. A visible path that marks the migratory stages and oral thiabendazole is available in trail of the larvae is often seen. chewable 500 mg tables. Protozoans Infants may show signs of CNS disorders, enlargement of the liver Medications: include: pyrimethamine, sulfonamide and spleen, blindness, and mental retardation. drugs, folate clindamycin, and bactrim. It can affect the mucous membranes with a wide range of Antimony-containing compounds are the principal appearances, most frequently ulcers. It may cause skin lesions that medications used to treat leishmaniasis. These include: resemble those of other diseases including cutaneous tuberculosis, meglumine antimonate /sodium stibogluconate syphilis, leprosy, skin cancer (basal cell carcinoma), and fungus. Other drugs that may be used include: The skin may become grayish, dark, dry, and flaky. pentamidine /amphotericin B Arthropoda Characteristic variety of lesions: macules, 3 major tx: lindane 1%, crotamiton (not rec for children or pregnant women) papules, vesicles, pustules, bullae, nodules and sulfur ointment 5% - all topical, oral ivermectin (15-200mg/kg) has also and scaling plaques been shown to be effective against scabies

Bacterial
Description virulence factors MRSA Type Bullous Impetigo Impetigo Neonatorum Scalded Skin Syndrome (Ritter's Dz, Dermatitis Exfoliative Neonatorum) Deep Folliculitis or Furunculosis Connective Tissue Infections Secondary to Staphylococcal Infections Catalase + GPC occurring m.c in grape-like clusters-staphylococcal pyodermas are characterized by purulence, pustules and bullae with a narrow rim of erythema Coagulase, Protein A in its cell wall - this protein will bind to the Fc portion of IgG preventing it from binding to complement teichoic acids present in the staphylococcal cell wall may stimulate antibody production against them SBE exfoliatin - a protein produced by staph with phage group II in its genome staphylococcal scalded skin syndrome resistant to common staph antibiotics: meticillin, oxacillin, nafcillin, cepahlosporins, imipenem and beta lactams and it is no more virulent than other forms of Staph, if it is the pathogen causing an infection, it is more difficult to treat vancomycin is the DOC Description/Location Clinical Presentation Treatment usually caused by Group II coagulase-+ a vesicle that rapidly evolved into a large warm compresses, neomycin or staph, which is PCNresistant fragile bullae ruptured bullae resembles mupirocin; mild cloxacillin, p.o. 50exfoliatin, is responsible vesicular or a second degree burn. Rare regional 100 mg/kg/day q6h and widespread cases bullous presentation lymphadenopathy and these lesions heal amoxacillin 100-200 mg/kg/day q6h IM -occurs in neonate, infants- young kids without scar formation or IV infants and young children and after >12 hrs of generalized Must r/o TEN that generally occurs in older kids/ adults rarely in immuno-compromised erythema, large flaccid and is a result of a rxn to meds which cause sub-epidermal adults bullae appear and then the blister formation (i.e. it is a FT slough occurring w/i the it is a febrile, rapidly evolving, epidermis will begin to peel basement membrane zone) oxacillin, 100-200 mg/kg/day q6h generalized desquamative off in large sheets there is in equal doses IM or IV and tx must be maintained for 10 days disease a positive Nikolsky's sign cloxacillin, p.o.50-100 mg/kg/d q6h A furuncle is a tender, warm moist compresses and topical anti-microbial agents systemic anti-microbial tx is boil; a carbuncle erythematous, appropriate for individuals with chronic or extensive problems or in areas which are very is simply two or nodule sensitive more confluent after few days cloxacillin, p.o. 0.5-1 g q6h dicloxacillin, p.o. 250-500 mg q6h furuncles with and may develop a nafcillin, 0.5-2g 16h IM or IV PCNallergy: erythromycin, p.o. 250-500 separate "heads" "yellow head" mg q6h systemicAb tx should be continued for months in individuals with chronic disease Is an acute or chronic purulent, tender and painful swelling PNA with appropriate wound care w/ appropriate soaking about the nail plate that occurs secondary to a separation of instructions could be: 2 tablespoons of epsom salts in 1 qt of the eponychial fold from the nail plate and usually caused lukewarm or tepid water or 1/4 vinegar in one qt of (acetic acid soak) by trauma; the condition is exacerbated by increased covering the wound with a telfa-type bandaid is generally adequate, moisture and causative agents not only include occasionally oral antibiotic therapy may be necessary, a staphylococcus, but also Pseudomonas aeruginosa and penicillinase-resistant antibiotic such as dicloxacillin would be streptococcus appropriate Nikolsky's sign involves the superficial layers of skin slipping free from the lower layers with slight pressure and is seen in TEN and pehphigus vulgaris as well

Pyogenic Paronychia

46

Type Streptococcus pyogenes GAS

Description GPC typically arranged in chains betahemolysis

Streptococcus agalactiae GBS

Types of relevant pathogenic Streptococcus (obligate aerobic GPC) Virulence Factors collagenase and hyaluronidase facilitates spread of the bacteria through the connective tissue stroma of the skin., and contribute to the development of cellulitis.M-protein in the cell wall - this is an anti-phagocytic factor Causes a type 3 hypersensitivity reaction (acute glomerulitis and RF) and because of this, we must be aggressive with antibiotics for at least 10d to achieve the lag phase kill of this organism, streptolysin O - this is a hemolysin that is antigenic and inactivated by oxidation; the antibody to it ASO (antibody steptolysin O) - can be measured and is an important diagnostic indicator of RF normal found in the female genital tract but may cause an opportunistic infection

Type acute glomerulonephritis

rheumatic fever scarlet fever

Connective Tissue Infections Secondary to Streptococcal Pyogenes Infections Description/Incidence Clinical Presentation Occurs more commonly in children 2-3 weeks after a skin S/S: HTN, edema of the face & ankle and "smoky" urine, edema infection and may occur in up to 10% of patients with a usually resolves within 5-10 days and blood pressure usually streptococcal pyoderma. In children, must do a UC&S returns to normal within 2-3 weeks, gross hematuria usually urine findings consistent with sub-acute glomerulonephritis disappears within 1-3 weeks, the [C3]is normal by 6-8 wks after are the presence of red bleed cells, red cell casts and protein onset in more than 95% of pts occurs more commonly it presents with fever, migratory polyarthritis and carditis which results in myocardial and valvular following a strep pharyngitis damagelaboratory findings include elevated ASO titres and erythrocyte sedimentation rate is an erythematous skin eruption an erythemogenic toxin causes a mild inflammatory response that leads to dilation of blood most commonly associated with vessels, therefore the scarlet rash the presence of a strawberry tongue, with skin group A strep It generally follows changes that resemble sand paper, the characteristic exanthem consists of a fine an episode of strep pharyngitis erythematous, punctate eruption that appears within 1-4 days following the onset of the illness this rash usually lasts for four to five days, then resolves with fine scaling

Generally: streptococcal infections wide rim of spreading erythema, necrosis, lymphangitis, lymphadenopathy and fever; purulence is not a common feature

Type Nonbullous Impetigo

Ecthyma Erysipelas

Cellulitis

Ascending Lymphangitis
Necrotizing Fasciitis 50 and 60 y/o

Cutaneous infections caused by group A Streptococcus Description/Location Clinical Presentation Treatment Impetigo bacterial infection in the upper Honey colored stuck-on crusts lymphtopical Bactroban (mupirocin) epidermis beta-hemolytic streptococcus are adenopathy is often a secondary finding these For lymphadenopathy PCN generally the etiologic factor although staph will usually heal w/o scar formation if pedal 250-500mg qid X 7d for adults may also be recovered highly contagious edema and/or hypertension occur in this 56mg/kg/day divided for children individuals suspect glomerulohephritis Erythromycin in PCN allergy A bacterial infection lower epidermis. Vesicle pustule with a wide rim of induration deep lesions require PCN and must r/o with a slightly elevated advancing margin on erythema ulcer. lymphadenopathy pseudomonas in those lesions occurring generally occurs and healing results in a depressed atrophic scar in the groin or axilla Involves superficial dermis and is always caused by strep. It is common on the legs/face and very frequently will arise from venous stasis dermatitis pruritus, burning, and tenderness are typical complaints.prodrome of malaise, chills, and high fever that often begin before the onset of the skin lesions. Always associated inflam, including warmth, edema, and tenderness and there may be lymphatic involvement manifested by overlying skin streaking and regional lymphadenopathy tx leaves a permanent hyperpigmentation involves the deep dermis Sudden tender and warm erythematous and hard plaque that enlarges Penicillin and erythromycin from a break in the skin peripherally. Prodrome: fever, chills, tachycardia malaise, regional 250-500 mg p.o. qid and cellulitis Staphy aureus, adenopathy. Characteristic Lesion Well-defined vesicular and bullous clindamycin in penicillinP aeruginosa, H. flu, lesions with plaques that may show petechiaelong range sequelae allergic patients parenteral Cryptococcus neoformans from erysipelas & cellulitis damage to the lymphatic drainage administration may be C. perfringens system w/ lymphedema and even elephantiasis necessary to prevent septicemia Secondary to an acute inflammation of the subcutaneous lymphatic channels, occurs secondary to a tx involves identification of GAS infection, an abrasion, wound or cellulitis. Red, irregular, warm, tender streaks (follows course the etiologic factor ad the of GSV) developing on the skin and extending proximally from the break in the skin, working its way appropriate anti-microbial towards the regional lymph nodes that often tender and enlarged. A prodrome is secondary finding therapy and wound care
rapidly spreading necrosis of subQ m.c GAS and strains that cause NF produce streptococcal pyrogenic exotoxins which are directly toxic , and w/ strep super-antigen (SSA release of cytokines that produce clinical signs such as LBP mortality rate is very high 75% the LE is among the areas most commonly involved and is found commonly in individuals with preexisting or co-morbid conditions Types of NF based of the etiologic organisms I the presence of both anaerobic (the most common being Bacterioides fragilis) and facultative anaerobic bacteria II the presence of GAS alone or w/ Staph III clostridial myonecrosis or gas gangrene skeletal muscle infection assoc w/ recent sx or trauma. Diagnostic Criteria no muscle involvement/destruction or major vascular occlusion w/mod to severe systemic toxicity and mental disorientation, with high bilirubin levels Clinical Recognition(dDx: cellulites) Prodrome: Febrile and tachycardia, Edematous, warm limb Upon necrosis of the subQ deep fasciectomy is indicated with radical debridement parenteral Ab tx - PCN still remains the DOC for strep mediated disease HBO provides adjuvant tx with appropriate wound care regiment w/ or w/o delayed primary closure

47

Gram-Negative Skin Infections Pseudomonas Aeuriginosa P. aeurginosa these organisms are GNR which are strict aerobes and they are able to grow in water containing only trace nutrients, ie tap water virulence factors approximately 10% of the pop carry it as a normal part of the colon flora likes to infect burns , patients w/ an absolute neutrophil count of >500 and pts who are immuno-compromised are at risk produces an exotoxin A - which (-) eukaryotic protein synthesis pigments pyocyanin, blue purulence and pyoverdin (fluorescein) - a yellow-green pigment that fluoresces under UV light Types of cutanuous Pseudomonas infections Description/Location Clinical Presentation Treatment Opalescent, tense, grouped vesicles surrounded by pink to violaceous halos. The vesiclesb/c aminoglycoside with an hemorrhagic and violaceous, as vesicles rupture round ulcers w/ necrotic black centers.The anti-pseudomonal PCN presence of these vesicles along suggest the diagnosis DIC, altered mentation GNR sepsis Green Nail frequently seen in patients distal onycholysis with a striking PNA & I&D Topical polymixin B and 1% acetic Syndrome whose hands and feet are often greenish discoloration, frequently assoc acid (vinegar) soaks 2-4x a day in water or wet areas w/ paronychia of the adjacent nail folds G(-) dont like vinegar G(+)dont like salty Pseudomonal most lesions occur on the trunk and LE pruritic follicular, maculo-papular, this is generally a self-limiting process Folliculitis - Hot generally occurs 1 to 4 days after bathing in vesicular or pustular lesions that will leave w/in seven to 14 days Tub Folliculitis a hot tub, whirlpool or public swimming symptoms include marked swelling, 1% acetic acid compresses, gentamycin pool Prodrome: sore throat, HA, fever & redness and a sensation of heat cream and if widespread malaise Flouroquinolone Cipro is a great drug; it has better staph coverage and will kill Pseudomonas Type Ecthyma Gangrenosum Description Bacteroides fragilis non-spore forming, gram-negative rods, and although these organisms are part of the normal skin flora, Bacteroides sp. is the most common cause of serious anaerobic infections infections usually require a break in the mucosal membrane and are generally not communicable both bacteroides and facultative anaerobes are often present in skin infections - the facultative bacteria utilizing the available oxygen and enhancing the living conditions for the strict anaerobes likes to co-habitate when bacteroides is present as a pathogen, antimicrobial should include coverage for both these bugs and the most likely facultative anaerobe they are co-habitating with The polysaccharide capsule of Bacteriodes sp. is its most powerful virulence factor members of Bacteroides fragilis are resistant to penicillins, first-generation cephalosporins and aminoglycosides metronidazole is the drug of choice with cefoxitin, clindamycin and chloramphenicol as alternative

infection

Virulence Factors and Treatment

Other miscellaneous soft tissue infections

Erythrasma Myonecrosis Gas gangrene Cat scratch disease Chlamydia Lymphopathia venereum Interdigital infection caused by C. minitissimus, eval w/ woods lamp Povidone/iodine soaks and oral erythromycin Muscle fails to display the 4 Cs Prompt debridement is necessary. Amputation of an arm or leg may be indicated to control contractility, capillary bleeding, the spread of infection. Antibiotics, preferably penicillin-type, should be given. Initially, color and consistency. Caused by this is given IV Analgesics may be required to control pain. Hyperbaric oxygen has been Clostridium tried with varying degrees of success. Bacillus Henselai : systemic symptoms include fever, malaise, anorexia and generally antibiotic therapy is not necessary headacherarely serious sequelae develop resulting in bacillary angiomatosis; the and Zithromax is the agent of choice when skin and lymph nodes are often infected subcutaneous skin-colored or red antibiotic intervention is indicated papules The dz starts as a painless ulcer on the male genitalia or in the female genital tract. As the Tetracycline, 500 mg by mouth, organism spreads, the inguinal (groin) lymph nodes swell, b/c tender, and may rupture and 4xd for 3 weeks drain through the skin. These enlarged nodes are called buboes. Doxycycline, 100 mg by mouth, The skin above the lymph node is often swollen (edematous) and red. These areas may 2xd for 3 weeks appear to heal, but the pt will have repeated episodes of lymph node swelling and drainage. Erythromycin, 500 mg by mouth, The pt may also have systemic s/s including fever, decreased appetite, and malaise. 4xd for 3 weeks Superficial pitting in the sratum corneum on the soles of the feet giving rise to a mothTopical or oral erythromycin eaten appearance, associated with hyperhydrosis and bromhydrosis result of keratolytic enzymes from Corynebacterium or Micrococcus sedentarius Antibody inducing pseudomembranous collitis Metronidazole 500mg po tid or vancomtcin po 500 mg qid

Pitted keratolysis C. Difficile

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Syphilis T. Pallidum
Description Clinical Presentation Treatment

eruptions are symmetrical, superficial, transient macular roseolas develop into maculopapular or papular eruptions; distributed over face, shoulders, flanks, palms and soles and anogenital regions; lesions on soles are highly suggestive of syphilis

Characteristic Lesions macular lesions < one centimeter in diameter; light pink color becomes brownish red depending on amt of pigmentation in the patient's skin; papular lesions - raw ham color or a coppery tint Development of Lesions develops insidiously appearing six to eight weeks after the chancre; develops rapidly and is pronounced a few days after onset; may last a few hours or several months; the earliest eruptions is macular

penicillin - drug of choice for all stages of syphilis; single intramuscular injection of 2.4 million units of penicillin G benzathine and 8 daily intramuscular injections of 600,000 units of penicillin G procaine penicillin allergic pts - tetracycline or erythromycin orally 500 mg every six hours for 15 days a Jarisch-Herxheimer reaction may occur following the initial dose of penicillin; occurs in 90% of patients with seropositive primary or secondary syphilis; consists of shaking chills, fever, malaise, sore throat, myalgia, headache, tachycardia and exacerbation of the inflammatory reaction at involved sites; occurs six to eight hours after injection

Podiatric Manifestations of syphilis Macular eruptions early macular eruption are "ham-colored macules" on the soles of the foot; most common presentation of all syphilids; pruritis in 10 - 20%; symptoms absent or eruptions self-limiting and disappear spontaneously after a few days or weeks; occasionally sequelae of macular syphilid livedo reticularis

Papular eruptions m.c of the papular eruptions is the lenticular papular syphilid; fully developed lesions are ham or coppery colored or dusky yellowish red on the soles; papules range from 25 mm; slightly palpable with a deep firm infiltration distributed on the face and flexor surfaces of the arms and lower legs; occasionally appear on the trunk; Ollendorf's sign present - exquisite tenderness to direct touch or a papule with a blunt probe

Diagnosis of Syphillis Treponema pallidum isolated from skin lesions; early lesions are teeming with spirochetes; a positive STS (Serologic Tests for Syphilis) - strongly reactive; VDRL is most commonly utilized test VDRL becomes positive w/i 5 - 6 wks after infection; remains highly positive throughout the secondary phase although HIV+ infection patients may be seronegative RPR may be utilized, if positive followed by VDRL tests generalized lymphadenopathy may be present; nodes are enlarged not tender possessing a hard, rubbery feel - "shoddy" nodes Viral HPV Type 1 Type 2 Type 4 Description Characteristic lesions Treatment the lesions are very deep palmoplantar lesions and may causes an endophytic, painful, solitary wart which appears as a be described as myrmecia or type I or inclusion warts hyperplastic hyperkeratotic epidermal lesions extremely resistant to therapy, about 10% of immunodeficient patients, mosaic warts or Topical acid preparations papillomaviridiae can transform from a benign wart into a SCC "group" warts Effudex-mosiac flat wartts capillary loops of the dermis elongate and are responsible for the causes smaller, multiple, punctate, hyperkeratotic "pinpoint" bleeding seen upon debridement plantar warts, Other Cutaneous viral infections

49

Varicella Zoster HSV-III Description Eruption is generally accompanied by local itching, tenderness or pain, and it is more commonly referred to as "shingles" Physical Findings hyperesthesia to light touch typically occurs throughout the involved neurotome, muscle weakness may accompany an outbreak, affecting the muscles of the involved neurotome (for example, quadriceps weakness may occur w/ L2 involvement, and abdominal m weakness with T10 to L1 involvement) attacks vary widely in their intensity but rarely last for more 3-4wks post zoster neuralgia may occur in 10 to 25% of older individuals when they do not receive systemic corticosteroid therapy : capsaicin cream, which is available in 0.25 and 0.75% strengths available OTC and utilized in the initial txt of post herpetic pain2nd line tx would include gabapentin followed by amytriptylline Characteristic several groups of vesicles on an erythematous and edematous base, onset is rapid with fever and neuralgic pain after an Lesion incubation period of 7-12 days, and the eruption usually appears in patches of various sizes as the vesicles dry up, some become hemorrhagic or necrotic and may ulcerate and slough bullous lesions have been reported in pts wi/ CA Lab Findings in all Tzanck smear shows multinucleated giant cells and within and at the sides of the vesicles in a herpes eruption are large, HHV Attacks swollen cells called "balloon cells" these balloon cells represent degenerated and swollen prickle cells, and acidophilic inclusion bodies are seen within the nucleus of the cells Mitigating Factors in Stress/emotional factors may induce the virus to proceed along the course of a peripheral nerve to terminate, epidermal All Herpes Attacks manifestations, and prodromal symptoms are typically reported as anorexia, malaise and low grade fever Treatment Famvir Undergoes biotransformation into the active metabolite penciclovir which is believed to inhibit viral DNA synthesis and

Famciclovir Zovirax

replication: dosage: 500 mg by mouth every eight hours for seven days treatment should be initiated within the first forty-eight hours of the onset of the attack reduces the duration of the lesions, and patients should also experience less pain dosage: 800 mg by mouth five times daily for seven to ten days Undergoes biotransformation to acyclovir. Its advantage over acyclovir is that although it is more expensive, it is more convenient Dosage: 1000 mg p.o. every eight hours for seven days local applications of heat are recommended, and administration of analgesics may be useful to diminish the symptoms associated with the acute neuralgia systemic administration is extremely useful in patients over 50 - oral prednisone is acceptable but anti-viral medications are more likely to shorten the severity and duration of the attack

acyclovir Valtrex

Valacyclovir Other

Name Molluscum Contagiosum

Description Characteristic Lesion caused by members of the pox virus group and the papules range from 2 to 5 mm in diameter, are unbilicated and contain a caseous plug histologically, the prickle cell layer (stratum spinosum) contains cytoplasmic inclusions referred to as molluscum bodies (or HendersonPaterson bodies)

Treament Best accomplished by curettage and if the lesion rests on a particularly sensitive location, local infiltration of an anesthetic agent may precede curettage. Other forms of tx may use of topical salicylic acid and CO2 laser ablation

this disease process is Course of Disease: viral implantation generally occurs on buccal mucosa spreading to the regional produced most frequently lymph node w/i 24 hrs incubation is generally 3- 6 d, prodrome is self-limited, resolving in 5 to 7 by Coxsackie virus type A days Characteristic Lesions: small vesicles that are surrounded by a red halo on the buccal mucosa, 16 - an enterovirus tongue, soft palate and gingivae lesions on the hands and feet begins as red papules. Tx: acyclovir Herpes it occurs most frequently at or near a mucocutaneous jx and in the course of a few days, the lesions oral or IV acyclovir Simplex rupture and the dried serum forms a flaky crust w/ Concomitant Regional Lymphadenopathy (Zovirax) appears to Virus the lesions tend to heal w/oscarring and two recognized strains: HSV-1 and HSV-2 be the only effective HSV- 1 is frequently a less severe and less frequency recurring stain of the virus cold sore tx it is a selective a presentation of herpes simplex, herpes gladiatorum, may occur often in young wrestlers, it occurs substrate for and secondary to skin to skin contact during the sport inhibitor of herpes HSV-2 is frequently more severe and assoc w/ venereal transmission virus DNA polymerase 80 -90% of pts presenting with a first episode of genital herpes present with the HSV-2 strain Dose: 200 mg orally 5x daily for 7-10d HSV and herpes zoster are vesiculating skin lesion associated with cutaneous nerves and 1/3 of Erythema Multiforme is caused by herpes virus Fungal

Hand-FootAnd-Mouth Disease

50

Cutaneous mycosis Etiology Clinical Manifestation Laboratory Diagnosis Treatment Epidemiology Prevention T. Pedis Trichophyton Interdigital T. Pedis Chronic KOH prep of skin scrapings Topical imidazoles, Ciclosporix Olamine, rubrum most hyperkaratotic moccasin Culture: DTM, SabouraudTopical &oral allylamines, Tolfnaftate. common foot/Dry Ti. Pedis Vesicular Dextrose Agar Bacteriologic Oral Griseofulvin Dermatophytid media to r/o C. minutissimum Ketoconazole an dHygiene T. Corporis Microsporum Round to oval erythrematous rings KOH prep of skin scrapings Focal: Topical imadizoles and Ringworm canis (zoophilic) or patches, Raised, scaly inflamed, Culture: DTM, SabouraudTopical allyamines T. Mentagraph. borders with quiescent centers Dextrose Agar Disseminated: Oral griseofulvin T. Tonserans May be vesicular or pustular And oral ketoconazole + topicals T. Capitis T. Hair breakage or loss , autoinoculated from feet KOH prep of skin scrapings Topical imadizoles Tonserans Kerion-boggy lesion that may b/c superinfected Culture: DTM, Sabouraudand allyamines Dextrose Agar T. Cruris T. Rubrum Pruritic rash KOH prep of skin scrapings Topical: imadizoles allyamines Jock itch T. mentagrophytes Centrally papular or pustalar Culture: DTM, SabouraudTolnafate, Undecylenic acid E. floccosum and discolored. Maceration Dextrose Agar Steroids. Oral fluconazole for C. Albicans when moist severe disease T. Barbae Beard itch T. Rubrum T. mentagrophytes T. verucosum Pruritic follicultis KOH DTM/ Sabouraud and Dextrose T. Unguim T. Rubrum T. mentagrophytes Discolored nail plates, can extend to the underlying KOH onychomycosis E. floccosum C. Albicans nail matrix and nail bed onycholysis DTM/ Sabouraud and Dextrose Diaper rash Napkin rash C. Albicans Yeast Maceration does not spare the folds KOH DTM/ Sabouraud and Dextrose Superficial mycosis Etiology Epidemiology Malassezia Furfur Exophiala wernicki Piedraia hortae Trichosporon beigelii Clinical Manifestation Treatment Prevention Most lesions are on the upper body: Limited to the Selenium sulfide shampoos and scrubs Fine scaly lesions with or w/o pruritis superficial Oral ketokonazole, Topical imidazole, May be hypo or hyperpigmented stratum corneum Topical cyclosporix olamine Brown to black macular lesions Mold visible in stratum corneum Surgical or chemical intervention on palmar and plantar Hard, black nodules, scalp hair shaft. Involves the hair shaft only Griseofulvin Topical antifungals Soft, white- brown nodules on hair shafts Involves the hair shaft only Griseofulvin Topical antifungals Subcutaneous mycosis Sporotrichosis Spororothrix Schenkii Saprophyte Etiology Epidemiology Clinical Manifestation Asymptomatic infections. Painless papule developing after the traumatic inoculation ulceration. Lymphangitis and lymphadenopathy Lymphotogenous spread to the joints, eyes, lungs, and CNS Fonsecaea May result in elephantiasis lymphadenitis, firbrosis and pedrosoicongestion, Wart-like growths and cauliflower-like nodules. Lymphadenopathy and abscesses along lymphatic tracts Psedallescherichia boydii (USA) Philaphora species Madurella mycetomatis and M. grisea; Acremonium spp Treatment Prevention Potassium iodide for simple cases. Systemic itraconazole Amphitericin B for disseminated cases Pathology

Tinea or Pityriasis versicolor Tinea Nigra Black Piedra White Piedra

Chromoblastomycosis

Eumycotic mycetoma Differential dx: Bacterial derived eubacterial actimycotic mycetoma

Small isolated lesions: Cryosurgery Larger lesions: Itraconazole, AmphitericinB Ketoconazole, 5Flourocytosine Madura foot or hands; Large tumor No established protocollike lesions draining sinuses Surgery + itroconazole yielding granular pus. Persistent Miconazole infection may be deforming Sulfones and sulfonamides

51

N. American Blastomycosis dermatiditis Coccidioidomycosis Coccidiomycosis

Etiology Epidemiology Transmitted via inhalation and contaminated soil SW: Valley fever or Dessert rheumatism Transmitted via dust particles Pigeons are the vectors.

Clinical Manifestation

Systemic Mycosis Laboratory Diagnosis

Cryptococcosis Cryptococcus Neoformans Histoplasmosis Histoplasma Capsulatum Paracoccidiomycosis S American Blastomycosis

Asso: bat and starling guano. Molds and dust are inhaled. Latin America Dust and inhalation M>F

Granulomatous and suppurative Yeast-broad based thick disease in the lungs, bones, skins, walled blastoconidia mucosa testis, epididymis and prostate glands Incub: 1-3 weeks Symptomatic: Fever, malaise, Disseminated pulmonary or meningitis: myalgis, dry cough (10-21 days) Fluconazole, Itraconazole, Amphitericin B via Delayed hypersen. Sequelae persistent arthralgia, IV Ketoconazole and pleuritic pain. Amd Erythema multiforme or Severe Menigitis: nodosum. Amphitericin B + (synergistic) Flucytosine Disseminated: Granulomas, of the skin, bones, Children: Metronidazole, Fluconazole joints, adrenals, and CNS. Pneumonitis proceeds dissemination Non-meningeal to CNS-meningitis, cystic gelatinous Amphitericin B + (synergistic) Flucytosine masses in the gray matter, no pus Itraconazole Can disseminates also to skin, bone, Meningitis liver and other viscera Amphitericin B + (synergistic) Flucytosine (granulomatous)Benign pulmonary Thermally dimorphic Itraconazole, Amphitericin B Lymphadenopathy and Splenopathy Spiny microconidia via IV Ketoconazole Disseminated RES disease infects Knobby macroconidia macrophages: CNS fatal meningitis Granulomatous lesions in the lungs, Thermally dimorphic Itraconazole, Amphitericin B with lymphatogenous spread to Thick walled yeasts with via IV Ketoconazole mucosa of the mouth, nose and multiple narrow-based URT. Can disseminate to the skin, blastoconidia ships wheel GI, liver and other viscera.

Treatment Prevention Itraconazole, Amphitericin B via IV Ketoconazole

*Amphotericin B is widely used for fungal meningitis and is synergistic along with Flucytosine Etiology Epidemiology Clinical Manifestation Treatment Prevention Aspergillosis 2nd most common Mycotoxicosis: Hepatotoxicity, and Invasive Aspergillosis Amphitericin B + A. fumigas Nosocomial infections hepatocellular CA rifampin: itraconazole, Caspofungin, and aflavotoxins Cases predisposed by Allergic Aspergillosis Voiconazole underlying respiratory disease Aspergilloma-Fungus ball Aspergilloma: Itraconazole and/or surgery or persons on anti-neoplastic Invasive Aspergillosis-necrotizing Allergic aspergillosis:Corticosteroids and antibitotic agents pneumonia Candidiasis Most common fungal human Superficial Oropharangeal/Esophageal: Clotrimazole troches (lozenges) or Monaliasis pathogen and the most Disseminated Nystatin washes; Severe infection: Fluconazole, Itraconzaole, frequently isolated; Blood Nephritis, endocarditis, Ketoconazole, Amphitericin B swish and swallow borne-IV devices or drug use pneumonia, hepatitis, and Caspofungin for refractory monoliasisSystemicAmphitericin B and surgery DIC Oral thrush + Flucytosine, itraconazole/ Ketoconazole Pnemocytosis Only in neonates & Interstitial pneumonia Trimethoprim + sulfamethoxazole + prednisone Pnemocystic immunosuppressed IN AIDS-pneumonitis Clindamycin & Primaquine; Trimethoprim & Dapsone carinii AIDS defining and pneumonia with Atavaquone; Pentamidine + prednisone; HIV prophylaxis: disease foamy exudate Trimethoprim + Dapsone, Sulfamethoxazole & Pentamidine

3.

Dermatoses A. Eczematous

Type Urticaria

Eczema

Specific Allergic and Reactive Dermatoses Description/Cause Characteristic Lesion Clinical Presentation Treatment acute urticaria is generally a type I hypersensitivity it is characterized by the most cases of urticaria are self-limited systematic treatment reaction histamine-mediated by mast cell activation classic wheal and flare and of short duration in extremely can include fixed IgE common offending agents include latex gloves, reaction, very pruritic symptomatic areas of cutaneous administration of oral animal proteins and food stuffs edema antihistamines histologically, the acute stage: vesicles, blisters, bullaesevere pruritis emotional factors and psychologic stress Topical hallmark of all subacute stage:redness, scaling and fissuring, skin is exacerbate all forms of eczema, fatigue or glucoeczematous eruptions is parched or burned moderate pruritis overexertion, gustatory factors such as corticoids spongiosis chronic stage: lichenification moderately pruritic caffeine, tea, tobacco and alcohol

52

Type Pompholyx Dyshidrotic Eczema Dyshidrosis Lamellar dyshidrosis Keratolysis Exfoliativa

Dyshidroses derived from the fact that the skin may be red and wet with perspiration Description Characteristic Lesion Clinical Presentation Treatment it may occur in intraepidermal vesicular the symptoms characteristically consist of pruritis and corticosteroids, hyperhidrotic eruption localized to the palms, burning Transient: lesions are often on the sides of the drying agent feet the process soles and interdigital spaces fingers and may be arranged in clusters or coalesce to form K+ does not involve it is exacerbated by both bullae that are filled with clear to straw-colored permanganate the sweat ducts psychological/physical stress: fluidnegative for the presence of any fungi or bacteria erythromycin characterized by the superficial initially, it will appear as tiny pinhead-sized white spots that 5% tar in gel (Estar Gel absence of any exfoliative tend to spread peripherally and as the spots spread, the mild emollient usually inflammatory changes dermatosis central horny layer ruptures and peels off and the skin may suffices and small dose it may represent a affecting the take on a flaky appearance from desquamation of the 20 to 30 mg of disorder of adhesion of palms and superficial stratum corneum must r/o Tenia triamcinolone acetonide the stratum corneum soles (Kenalog ) IM

Dishydroses continued
Type Asteototic Dermatitis xerotic eczema, winter itch and eczema craquele Nummular Eczema M>F 60-70y/o discoid eczema Description dehydration of the skin secondary to a decrease in the surface lipids of the skin which leads to an increase in skin water loss generally presents with dry skin and is more common in the winter Characteristic Lesion xerotic eczema will show a condensed or packed appearance to the outer keratin layer Clinical Presentation skin will present with redness, very fine superficial cracking and fine flakes (ddx: Keratolysis Exfoliativa) that it is very pruriticmost commonly it is occurs on the anteriolateral aspects of the shins in the elderly population LE are the most common site the symptoms include severe paroxysma pruritis lesions tend to become colonized with Staphylococcus aureus the lesions may become lichenified Treatment topical corticosteroid ointments with 24- to 48-hour occlusion with polyethylene or Unna-boot are the treatment of choice for the rapid resolution of asteatotic dermatitis. Systemic causes (thyroid, AIDS, malignancies, etc.) for dry skin should be ruled out in persistent cases potent topical steroid creams applied once or twice daily may be useful, antibiotics may be indicated if bacterial infection ensues with empiric initiation of antistaphylocccal spectrum drugs mild sedatives and tranquilizers may help with the itching (ddx: lichen simplex chronicus) intralesional injection of triamcinolone suspension is quite effective done only if there are no signs of secondary infection, high potency topicals such as betamethasone dipropionate (Diprolene ) or clobetasol propionate (Temovate ) may be used but only for initial therapy occlusion is occasionally helpful with Cordran Tape

Lichen Simplex Chronicus neurodermatitis circumscripta F>M Prurigo Nodularis

Erythema Nodosum young women during the spring or autumn

clinical appearance of the coinshaped lesions often occurs concomitantly with venous stasis dermatitis; it can be associated with the Koebner phenomenon resulting in multiple linear streaks the onset of this linear excoriations may be predilection for the extremities process is generally present with time, the especially the wrists and insidious; stress and lesion becomes thickly ankles (particularly the ankle anxiety may tend to lichenified, scaly and flexure) as well as the back exacerbate the elevated with accentuated and sides of the neck symptoms skin lines this is considered a variant of it may present as a single or multiple lesion frequently on the LE on the extensor surfaces of the cryosurgery or intralesional lichen simplex chronicus that are generally pea-sized but may be as feet; the pruritis is the most prominent feature cortisone injections may be characterized by discrete or large as 2 cm in diameter and the nodules and is commonly paroxysmal effective multiple hyperkeratotic are erythematous or brownish, indurated and when the disease process becomes chronic, warty nodules may be dome-shaped in appearance An inflammatory Assoc w/ streptococci (a URT infection in the onset of an attack is typically heralded by (PRODROME) Tx underlying process resulting in children), drug rx and sarcoidosis may also be constitutional symptoms ; during the 1st week, lesions are abnormality delayed hypersensitivity assoc w/Trichophytin ssp, and cat-scratch fever. firm, indurated and tender do not suppurate or develop into salicylates reaction w/involvement The generally fairly mild lesions begin as red, ulcerations, lesions generally persist for 1-2wks, having a PCN of the larger cutaneous tender, smooth nodules that are usually tendency to occur in crops they undergo slow involution erythromycin to tx b/v symmetrically distributed on the anterior shins and resemble an ecchymotic bruise the Strep

B.

Papulosquamous

Common papulosquamous diseases that occur in the foot: Psoriasis, Syphilis, Pityriasis rosea, Dermatophytoses Psoriasis Description chronic, inflame dz predilection for the scalp (50%), nails, extensor surfaces, elbows, knees and sacral region; There is one variation inverse psoriasis, occurs on the intertriginous areas; symmetrical bilaterally; Characteristic rounded, circumscribed, erythematous, scaling grayish white or silvery white, imbricated and lamellar scales; Lesion nummular or coin-sized lesions common (dDx: nummular eczema, seborrehic dermatitis and superficial BCC Incidence M=F onset 27yrs; aggravated by emotional stress (40%)of pts; affect all races uncommon in blacks; 1 2% of the population have psoriasis; western European or Scandinavian descent 3%; 25% of pts have arthritis involvement; Clinical The chief features of psoriasis include: tendency to recur; tendency to persist; Presentation Koebner reaction commonly seen as well with Nummular Eczema Auspitz sign occurs because of the severe thinning of the epidermis over the tips of the dermal papillae; Woronoff ring concentric blanching of the erythematous skin at the periphery of a healing psoriatic plaque; Munro abscesses (small collections of neutrophils in the stratum corneum); No bacteria present. Severe psoriasis linked with an increased risk of lymphoma and non-melanoma skin malignancies Characteristic nail numerous >10 pits 1 mm tan oval spots 2 to 4 mm in diameter oil spots onycholysis heaped-up crusts accumulated beneath changes the free nail edges may become secondarily infected with C. albicans

53

Generalized Pustular Psoriasis (von Zumbusch): severe & sometimes fatal; sudden onset w/ formation of lakes of pus periungually, on the palms and soles and w/I the psoriatic plaques S/s: pruritis and intense burning causes extreme discomfort; fever; fetid odor exists; episode triggered by iodides and salicylates; Rx etritinate is the drug of choice Uncommon papulosquamous diseases that occur in the foot: Description Clinical Presentation Treatment Lichen Planus an inflammatory pruritic disease of the skin & mucous membranes hypertriamcinolone 60 mg IM is safer and pigmentation , Koebners Elementary Lesion: possesses grayish puncta or more effective oral prednisone 40 to 50 Adults streaks, Wickhams striae, which form a network over the surface of the papule mg retinoids DMARDS, griseofulvin Lesions in the foot Characteristic Lesion Oral Mucosa occurs in about 25% of patients; generally 125 mg twice daily for three to six occur more commonly located on the buccal mucosa; silvery-white pinhead sized papules mistaken for months has also been reported in cases on the sides leukoplakia , and CA rarely develops; this is more likely if the oral lesions ulcerate w/ oral mucosa erosion and ulceration, Characteristic Nail Changes: occurs in 10% of patients; pterygium formation is dapsone and metronidazole (500 mg/day distinctive of LP. May lead to obliteration of the entire nail and is generally a for up to 60 days) have both been permanent change; longitudinal grooving, ridging and splitting; a peculiar reported to be efficacious calcipotriene midline fissure may occur may also be effective Pityriasis rosea pruritic exanthema acute round or oval salmon-colored lesions which arrange rash irritated by soap so wash with onset lesions rapidly spread in a Christmas tree pattern on the trunk (Chevron water only B/c skin eruption makes the 15 and 40 and then spontaneously appearance, like Zoster)begins with a single herald skin extremely dry, use emollient F>M disappear in 3-8wks or mother patch and mild prodrome of fever, creams pruritius - corticosteroid lesions affect the etiology unknown although malaise, HA arthralgias: secondary lesions appear 2lotions, creams or sprays and trunk more often in a a viral origin is suspected 21d after the appearance of the herald patch and the antihistamines UVB sunlight may be dermatomal secondary to human herpes palms and soles are rarely affected; lesions are helpful, i triamcinolone 20 to 40 mg distribution virus 6 or HH7 pruritic 25% of the time is generally self-limited IM Papular Purpuric Gloves and most commonly associated with a symmetrical, sharply demarcated, purpuric or tender edema & erythema of Socks Syndrome parvovirus B19, however may the hands & feet progress gradually to purpuric papules and petchiae young adults children occur secondary to coxsackie B6 taking on the appearance of a bruise dermatologic signs may be it occurs most frequently in the and CMV; has also been associated accompanied by systemic symptoms of anorexia, fever and arthralgias will spring and summer months with HHS-6 usually resolve spontaneously in 1-2 weeks no treatment Pityriasis Rubra Pilaris small follicular papules most important diagnostic feature -emollient creams Lac reddish brown, pinhead sized lesion topped by a central horny plug w/I which Hydrin 12% cream or male = female incidence there is a hair, evolves to orangy-red or salmon-colored (yellowish-pink) scaly Carmol 40 isotretinoin is the affects all races plaques with well defined borders that are frequently interrupted by characteristic treatment of choice in adultislands of normal skin. Follicular lesions eventually disappear and leave onset, type I given over chronic skin disease often affect the widespread dry, scaly erythroderma which may have an orange hue and on the several months in a dose of 1 scalp first; appearance of palms and soles lesions coalesce to form a confluent hyperkeratotic 2 mg/kg/day, vitamin A in exaggerated gooseflesh erythroderma and hyperkeratosis of the palms and soles has a tendency to doses of 150,000 to 300,000 only subjective symptoms may be fissure; referred to as keratodermic sandal Nail Changes dull, rough, thickened, vitamin E 400 units 2mild pruritis brittle and striated; distal yellow-brown discoloration; subungual hyperkeratosis 3xd IM Kenalog, 60 - 80mg splinter hemorrhages; rarely pitted (in contrast to psoriatic nails)

C.
Erythema Multiforme Bullosum StevensJohnson Syndrome Erythema Multiforme Major M> F 2:1 Porphyria Cutanea Tarda

Bullous

Epidermolysis Bullosa Acquisita

occurs on the Large bullae on an erythematous base, Concommitant systemic therapy is generally limited to supportive palms and soles subungual hemorrhage has been reported, there is measures and systemic corticosteroids, for erythema pruritis is generally often a prodrome of URT s/s and most mild cases are multiforme minor, a short 2 to 3 week course of absent associated with an underlying infection of HSV prednisone starting as 30-40 mg/day is often given a more severe and fatal version it is a mucocutaneous disorder heralded by the acute remove the underlying etiology of erythema multiforme bullosa, and abrupt onset of a fever of 39 to 40 C, headache, early ccs tx is the DOC up to 1.5 to 2 constitutional s/s develop these malaise and a sore throat: presence of an mg/kg/day of prednisone in one daily include a rapid, weak pulse, rapid erythematous, pruritic cutaneous eruption, vesicles on dose has been recommended RR and jt pains, stomatitis in as the lips, tongue and buccal mucosa and these lesions triamcinolone acetonide may be early and conspicuous symptom progress to pseudomembranous exudation and administered 1 mg/kg IM dose, if may often follow an infection of ulceration eating and drinking becomes difficult if there is a poor response to herpes simplex or M. pneumoniae not impossible prednisone after 3 to 4 days an acquired abnormality of include fragility of the skin and bulla formation of the sun-exposed areas(esp. hands) porphyrin metabolism; skin lesions sporadic, non-familial form mc b/t 40- 60, 20% of pts have h/o diabetes mellitus and chronic occur secondary to blister formation; alcoholism; ulceration of the leg not common; pseudoporphyria drug induced or acquired as accumulation -porphyrinogens PCT fairly common; etiologic factors chronic alcohol abuse and contraceptive steroids are common; Target - women on oral contraceptives; Location the dorsum of the foot and shins Location lesions occur in areas with a proclivity for minor trauma hands, feet, knees and elbows; acquired immunobullous disorder presence of antibodies against the type VII collagen within the basement membrane; associated with multiple myeloma, amyloidosis, inflammatory bowel disease and diabetes mellitus; characteristic lesion is a sub-epidermal bullae which develops at the dermal-epidermal junction;

54

4.
Kyrles Disease hyperkeratosis follicularis M=F onset is b/t 30 60 yrs of age Dariers Disease Keratosis Follicularis M=F 4 y/o heat and stress

Systemic relationships A. Genodermatoses

Central keratin plugs or cones that may develop in a widespread small papule with a central silvery scale distribution pattern. The cone projects into dermis & is >1.5 cm often surrounded by a zone of comprised of necrotic cellular debris and degenerated c.t m.c erythema; may remain stationary for associated with chronic renal failure and dialysis; elevated years; the palms and soles are generally phosphorus level; DM alcoholic cirrhosis, congestive heart spared failure, or may occur alone dominantly inherited genodermatosis -lesions on hands are most common but may - characterized by hyperkeratotic papules in seborrheic also involve the feet; small pits on the palms regions & various nail abnormalities and soles are very characteristic punctuate -chronic disease process- occurs secondary to a genetic keratoses mutation that affects desmosomal assembly and cell to - first appear as skin-colored papules which cell adhesion; mutation codes for the SERCA enzyme or develop into persistent yellowish brown, pump (SarcoEndoplasmic Reticulum Calcium-ATPase) greasy papules; that is required to transport calcium within the cell - Symptoms pruritis, but appearance of - desmosomes cannot assemble properly without adequate lesions is the major morbidity in the amounts of calcium; resultant loss of desmosomes, disease breakdown of desmosome keratin intermediate filament -nail changes very specific there are white attachment and perinuclear aggregates of keratin and red longitudinal bands & nail ridges; a Vintermediate filaments shaped nick at the free margin of the nail is the most pathognomonic nail finding A rare disease frequently assoc w/ GI Consists of large ulcers with characteristic purple diseases (ulcerative colitis or Crohns overhanging edges which develop rapidly from pustules and dz) Exact etiology is unknown tender nodules, particularly on the lower legs, abdomin and face -high dose ela tx of Retin-A and vitamin E may be benefit generally palliative with the use of emollient creams -dermabrasive creams (Retin-A) may sometimes be utilized

Pyoderma Gangrenosum

Systemic steroids

B.

Vascular disorders (nodose, lesions, pigmented purpuric eruptions, vasculitides, livedo reticularis, etc)
Systemic Necrotizing Vasculitis

Vasculitis PAN Periarteritis Nodosa

Churg Strauss

Clinical Manifestation Laboratory features Unknown etiology; 2X common in men. (30% Hep B), Constitutional s/s are present Characterized by focal inflammatory lesions.The lungs are usually spared Cutaneous manifestations are palpable purpura, infarctive ulcers of varying sizes and livedo reticularis *TQ Multiple mononeuropathies are the most typical neurologic manifestation and occur in more than 50% of all patients. Nerves diffuse polyneuropathy Kidney Renovascular HTN GI acute abdomen with hematemesis or melena, Liver increased LFTs, Heart; coronary arteritis CHF A.K.A allergic granulomatosis and angiitis. Eosinophilia Involvement of the lungs Decerased renal funct Triad of: asthma, eosinophilia, pulmonary infiltrates and CXR patchy nodular vasculitis. infiltrates Cutaneous findings include petichiae, purpura, or ulcerations Biopsy extramural Peripheral multiple mononeuropathies microgranulomas with Abdominal involvement. eosinophilic infiltrates Eosinophilic granulomatous involvement of the GI and urinary ddX: TB tracts or prostate is diagnostic

Diagnosis Progressive & fatal

asthma dDX: Lofflers syndrome. Hypersensitivity vasculitis, Wegeners

Treatment Prednisone 1mg/kg day Prednisone and cyclophosp hamide (2mg/kg/da y) More responsive to corticosteroids than PAN

Eosinophilic All vasculitides weaken the vessel wall and can cause dilatation and aneurysm formation. Giant cell (medium to large vessels) arteritis Clinical Manifestation Laboratory features Diagnosis Treatment Chronic vasculitis of the aorta and its branches and is most common in Normocytic, normochromic anemia young women of Asian descent.Also known as pulseless disease, Elevated ESR and thrombocytosis idiopathic medial aortopathy involving the AA. Erythema EKG may reveal ischemic pattern (high ST nodusum-like vasculitis lesion may occur over the legs. BP difference segment, T wave inversion **TQ) of >10 mmHG are found in most patients. HTN in 40% and bruits. CXR-widening of the thoracic aorta Temporal arteritis It is associated with polymyalgia rheumatica (PMR) The ESR tends to be +biopsies mural CorticoVasculitis Takayasus arteritis

55

dDx: Wegeners Takayasus

>50yrs, W>M Common manifestations of vascular high averaging about involvement include HA, tenderness over the temples, 80-100 mm/ hr jaw claudication, visual loss, diplopia, cough, sore throat, (westergren and the aortic arch syndrome (pulseless disease). Visual High CRP, High LFTs loss usually results from retinal ischemia secondary to Elevated factor 8 and involvement of the ophthalmic or posterior ciliary arteries. IL-6 *Do not use ccs for very long (-) HPA axis and can cause Cushionoid syndrome Hypersensitivity Vasculitides (small vessels-aterioles, venules)

lymphocyes macrophages, giant cells, fragmented IEL. May need to biopsy contralateral side

steriods most effective Prednisone

Vasculitis Hyper-sensitivity Vasculitis

HSP

Clinical Manifestation Treatment Reactions to drugs are the most common Onset is usually abrupt and occurs after exposure to the etiologic agent. Palpable purpura is the m.c. clinical manifestation. Transient arthralgias frequent, and systemic symptoms may be present Rx to medication that occurs quickly PCN, Iodine Rx to medication that occurs in 7-14 days serum sickness reactions It is a hypersensitivity vasculitis. Affects young pts (18y/o or younger) It affects small vessels of the skin, GI, Joints, and Kidneys. It is preceded by an acute respiratory condition *TQ. (Given a case about a boyhad previous. Resp. condition) Patients present with abdominal pain due to GI ischemia, glomerulonephritis. Purpura, and rash involving the extensor surface of the lower legs and feet, across the buttocks, and extensor surfaces of the UE. Treatment: eliminate the cause prednisone. Wegeners Granulomatosis HSP

Know causes of palpable purpura 1. PAN 2. Hypersensitivity vasculitis Vasculitis CNS Vasculitis Clinical Features

Other Vasculitides Clinical Manifestation Laboratory features Diagnosis Treatment Uncommon Men > women. Very little is known of the pathogenesis, but Dx is difficult Angiograms, biopsies may be helpful 25% of cases have been associated with lympholenticular neoplasms, Consider a pt w/CNS s/s but are difficult to perform also been associated with herpes zoster, HTLV-III virus, and HIV especially if they have a infection. Focal neurological deficits, seizures, and cranial nerve HSV infection, lymphoma dDX: Behcets syndrome, PAN , SLE, involvement are common. or illicit drug use Hodgkins lymphoma Wegeners Uncommon More common in young men. Proteinnuria, hematuria, RCB casts. Prednisone and Granulo-matosis It is often considered a triad of necrotizing granulomatous Biopsies show leukocytoclastic vasculitis cyclophosphamide vasculitis of the tissues of the lower respiratory tract + ANCA pneumocystis carinii *TQ, and focal and segmental glomerulonephritis; Usually associated with thromboembolic pneumonia (PCP) *TQ arthritis also. Pain over the sinus areas and purulent episodes generally a complication of bloody nasal discharge are typical upper respiratory CXR reveals cavitations and infiltrates immunosuppresion, not just symptoms. Nasal pr oral mucosal ulcerations are early (Classic) of Wegeners findings. Destructive changes lead to a saddle-nose dDx: fungal (histoblasma and deformity. (Classic). Cutaneous findings include blastomycosis) /bacterial infections, Churgnodules, purpura and ulcerations Strauss, Kawasaki Disease A.K.A musculocutaneous lymph node syndrome (MLNS)*TQ It affects infants and children < 5y/o and consists of skin and mucous membrane eruptions, fever, lymphadenopathy, polyarteritis of varying severity and multi-system involvement. Erythema Its an acute vasculitis of immune-mediated origin characterized by inflammatory nonAntecedent exposures to a NSAIDS, topical nodosum suppurative cutaneous and subcutaneous lesion of the extremities. toxin or drug (ASA, PCN systemic steroids, Males> females. Classically lesions are located on the anterior lower leg. sulfa or infections (fungi, antimicrobial They are pink, tender, red or violacous flat-topped papuples. strep) therapy Erythema Acute immune-mediated vasculitis characterized by cutaneous and subcutaneous Ddx: Associated with TB antimicrobial Induratum lesion on the posterior aspect of the lower legs. lymphangitis, therapgy (isonizid The lesions are often ulcerated deep-seated nodules red to bluish, painful, lymphadenopathy, and TB. and rifampin) indolent Other Vasospastic diseases Description Unknown etiology-caused by dysfunction of the SNS causing excessive vasomotor tone of the arterioles at ordinary room temp Painless but peripheral coldness and cyanosis/blueness of the distal extremities, occasionally the face and ears Diagnosis/ Treatment Female patient with persistent coldness and cyanosis of the fingers and hands of many years duration. Conservative tx: protect from cold, optionally sympathectoy when severe, small doses of reserpine and guanethedine

Acrocyanosis

56

Livedo Reticularis

Intensified by the cold and relieved by warming Types: Cutis memorata Livedo reticularis idiopathica Livedo reticularis sympathomatica Amantidine HCL a benign form and is not a reason for stopping the medication (anti-viral) Skin of the hands and feet become very red and warm, assoc w/ burning and itching. Pts respond to discomfort when the feet are covered while sleeping.

Erythromelalgia

Mottling and blotching of the skin of the extremities, reddish blue discoloration More intense mottling, persists despite change in temperature Mottling persists, there is evidence of some other disease that affects the vascular system (SLE) It usually affects both sexes and pedal edema may occur, disappears 2-6 weeks after the drug is discontinued Primary or seconday: Primary occurs in myeloproliferative disorders, HTN, CVI, DM, SLE and RA. Tx: ASA and methlysergide

C.
Description Classification

Ulcers Pressure ulcers

Ulcers from excess pressure or shear, moisture or friction forces 1989, the National Pressure Ulcer Advisory Panel NPUAP Stage I: non-blanchable erythema of intact skin; pre-ulcerative state Stage II:a partial thickness skin loss of epidermis and/or dermis; a superficial ulcer presents as abrasion, blister or shallow crater Stage III: a FT skin loss; damage or necrosis of subQ tissue; extend down to but not through underlying fascia Stage IV: Ft skin loss with extensive destruction, tissue necrosis or damage to muscle, bone, tendons or jt capsules; Daignosis Norton Scale Assess 5 parametersPhysical condition, Mental condition, Activity, Mobility, ContinenceScored 1 4 High Risk 16 Treatment Off loading

Venous Ulcers
Description Clinical history Treatment Dysfunction of the valves in the superficial to deep venous systems, loss of adequate muscular calf-pump action and obstruction ie DVT Large pitting edematous exteremities with variable hemosidderin deposition and leakage of serosanguinous fluid. 1st s/s dilated long saphenous vein +varicosities and telengectasias Compression therapy. ABI Diagnosis Therapy 8.0-1.0 Venous High compression 0.5-0.8 Mixed Low compression <0.5 Arterial None
Prominent veins without Edema (very light) 8 15mmHg (light) 16 20mmHg Lipodermatosclerosis (Class 2) 30 40mmHg Venous edema Lymphedema (Class 1) 20 30mmHg (Class 3) Over 40mmHg

Arterial ulcers
Description Secondary to ischemia via P VD, lesions must be revascularized to heal. Smoking is the worse preventable risk factor associated with occlusive arterial disease. Intermittent claudication and rest pain are the two classic symptoms of arterial peripheral vascular disease (PVD). Clinical Presentation Punched out lytic lesion, cyanotic surrounding with no evidence of inflammation. Rest pain, gangrene, and arterial ulcer are the three situations when you MUST refer the patient to a vascular surgeon. Treatment Revascularization

Diabetic ulcers
Description Treatment Major Risk Factors: Peripheral neuropathy (PN), Peripheral arterial disease (PAD), and Infection The combination of this triad leads to gangrene and amputation. (However, both PN and PAD can be independent factors that lead to amputation). Off-loading, prophylactic surgery

D.
Necrobiosis Lipoidica Diabeticorum (NLD)

Metabolic disorders
Diabetic Dermopathies Description/Classic Lesion Occurrence well circumscribed, hard, occurrence of lesions in DM does not depressed, waxy, yellow- correlate w/ [gl] control in DMoccurs in brown, atrophic patches, 3/1000 DM patients, 3x m.c in young (2-3 hemosidderin deposition decade) F> the pts with this dz have DM, remaining ,abnormal gl tolerance curve is Treatment intralesional injection of triamcinolone be careful of fat pat atropy dipyridamole (Persantine) 225 mg and ASA1g/d tx must be continued for up to 3-4 mo b/f results are achieved

57

Generalized Granuloma Annulare similar to NLD Diabetic Dermopathy (Shin Spots)

Diabetic Bullosis or Bullous Diabeticorum Periungual Erythema Carotenodermia

Candida Infections

often present pentoxyfylline (Trental) 400 mg, t.i.d. ring of small, may or may not be assoc w/ DM; m.c in F lesions are generally asymptomatic firm, fleshpast middle age; localized form occurs m.c intra-lesional injections of triamcinolone acetonide colored or red in young adult females and it is m.c on the the disseminated variety may respond to dapsone, papules lateral/ dorsal surfaces of the hands and feet isotretinoin, hydroxychlorogquine and niacinamide early lesions are round to oval, flatthe m.c cutaneous manifestation of diabetes M>F 2:1 hyperpigmentation and topped, red, scaly papules to macules retracted atrophic scars present on the shins; histologically demonstrate RBC become eroded, the lesions eventually extravasion and capillary basement membrane thickening and lesions clear or heal with epidermal atrophy demonstrate impaired healing and post-inflammatory hyperpigmentation, and or hyperpigmentation these lesions are present in up to 50% of all DM pts a non-inflammatory blistering which occurs spontaneously in a fairly symmetrical distribution lesions usually develop overnight abruptly is DM pts usually on the feet and lower legs, there is little or no pain or discomfort, and the bullae are from several mm to several cm in diameter. Tx: after rupturing or de-roofing, these bullae leave a deep painless ulcer lesions will resolve spontaneously over a period of 2-5 weeks usually without scarring dilation of the capillary loops secondary to microvascular disease yellowish discoloration of the skin w of the 50% Dm who have if the yellow pigmentation persists after greatest intensity on the palms and carotenemia-10% have carotenosis carrots are omitted, the patient should also solesthe sclera remain ddx: commonly associated with refrain from ingesting excessive amounts of jaundice there may be night blindness hypoTH other colored fruits and vegetables intertriginous areas are particularly Candida albicans is the m.c cause, the DM pt Castellani , imidazole AB susceptible , and the interdigital areas and particularly susceptible 2o to the glysosylation are also useful as well and nail folds are frequently affectedthese of collagen brittle skin Nail Changes: a Naftin gel, IM triamcinolone eruptions may be quite pruriticthe candidal paronychia results in chronic fourth interdigital space is most inflammation of the nail fold and is common in commonly involved the diabetic Acanthosis Nigricans warty pigmentation of the skin, occurs most commonly in the axillae, can occur in the flexural creases of the lower extremity, symmetrically distributed hyperpigmented (2o to hyperkeratosis and not actual melanin deposition) elevated lesions. Marker for heterogenous group of endocrine disorders - *TQ insulin resistance is the marker possible association with malignant neoplasm Type I may precede (18%) or accompany (60%) or follow (22%) internal cancer most commonly associated with adenocarcinoma especially of the GI tract most
Malignant Acanthosis Nigricans often stomach Type II Familial Acanthosis nigricans extremely rare and is present at birth, inherited in an autosomal dominant manner Type III M.c. variety, presents as a grayish, velvety thickening of the skin,side of the neck, axillae and groins occurs in obesity with or without endocrine disorders, occurs in various well-recognized insulin resistant states

Description

Types

Characteristics Clinical Appearance Treatment

greater insulin resistance and raised insulin levels type A syndrome linked w/genetic defects in receptor fxor post receptor pathwaysmay show hyperandrogenism type B syndrome circulating antibodies to the insulin receptor, excess GF, presence of acrochordons (skin tags) histologically resembles verruca, hyperkeratosis and acanthosis together with a mild degree of hyperpigmentation dermal papillae are evenly elongated, where the pidermis assumes a serrated and papillomatoses configuration will usually resolve with identification and treatment of the underlying systemic malady Lac-ydrin 12% lactic creams may help soften lesions, Carmol-40% urea cream may also be effective, daily application of Retin-A cream of geloral isotretinoin or Accutane can be used but the lesions recur when treatment is stopped chronic leg ulcers are very common; 25 appear to be of the venous stasis type ulcer; Location lower leg, usually around the 75% of patients have leg ulcers; more malleoli; simply defined edges and bases with granulation tissue; highly resistant to common in older age group healing; Hb must be maintained above 10g/100ml for ulcers to heal associated ulcers occur both in the homozygous and heterozygous forms w/ varying degrees of severity; thalassemia major (Cooleys anemia) leg ulcers uncommon; in thalassemia minor- b/c no hemolytic process, ulcers never occur; in intermediate forms of thalassemia, - leg ulcers in 5% of patients; - < 2% develop ulcers; ulcers heal very quickly following a splenectomy; polycythemia vera - blood viscosity & platelet numbers; risk for thrombophlebitis & ulcers act like a characteristic of venous stasis and venous insufficiency occurs in 3% of patients with toxic diffuse goiters; characteristic lesions firm, non-pitting, irregular swellings, nodules or plaques; flesh colored & waxy; ulcerations uncommon characterized by acute necrotizing ulcerations of the leg; borders begin as erythematous papulonodules enlarge rapidly rolled and vegetating; considered pathognomonic for underlying into plaques 2 -12cm diameter; active border deeply chronic ulcerative colitis,;due secondary to regional enteritis, violaceous red; central portion necrotic/ulcerated; halo gastric ulcer, empyema and chronic debilitating infections; lesions of erythema surrounds the lesions; Location - lower extremely painful part of the leg, they can occur anywhere on the body

Sickle Cell Anemia Thalassemia hereditary spherocytosis Pretibial Myxedema Pyoderma Gangrenosa

58

Marjolins Ulcer

refers to malignant changes that occur in a chronic non-healing wound; associated with burn scars and other pre-existing lesions; dysplasia of skin cells in the chronic wound develops resulting in the development of squamous cell carcinoma

59

E.
Allergic Contact Dermatitis

Drug reactions
locale, pattern morphology (papules, vesicles or bullae) of the lesions presence of spongiosis this can be confirmed via a biopsy or Tzanck smear the most common contact allergens include nickel, plants (Rhus genus), preservatives, perfumed, topical medications and occupational agents

identification of the offending agent!!! Patch testing acute short course of systemic corticosteroids (Medrol) and oral anti-histamine chronic the above including topical NSAIDS acute eruption generally results about 48 that work by inhibiting calcineurin which is an hours after exposure lesions may have important mediator of interleukin induction and characteristic linear or geographic forms T-cell activation ie lesions are edematous red papules 1. tacrolimus (Protopic ) inhibit expression developing into vesicles and bullae when the of high-affinity receptors for igE and dendritic reaction is severe enough cell presentation of antigens to lymphocytes chronic exposure results in minimal primary 2. pimecrolimus (Elidel ) lesions with secondary changes such as this does not affect the sensitization phase of the lichenification, pigment changes, allergic contact process, but it does inhibit the hyperkeratosis, excoriation and fissuring effector phase Nonhousewifes eczema typically the patient clinical consequences are desiccation, scaling and fissuring which then progresses to an Allergic or ccurs most frequently will present with eczematous dermatitis. Histopathology demonstrates acute inflammation in the outer Irritant in individuals who do itching papules or most layers of the dermis with extension into the epidermis and healing generally occurs Dermatitis wet work vesicles with no residual scars. SPARES THE INTERDIGITAL SPACES Photo-contact reaction to substance in the skin and UB light (longwave UV 320 400 ng UVA) psoralens present in many types of plants Dermatitis always occurs on sun-exposed skin, common causes are aftershave and PABA it is fairly rare Drug Eruption Cutaneous the most antibiotics are the most common cause of these eruptions in the hospital discontinuation of the reaction to common setting common locations include the trunk, arms, legs and feet the offending drug drugs presentation palms and soles are generally spared systemic corticosteroids is the eruptions may last for one to two weeks may be used in severe morbilliform less common presentations include: acenform (dDX: acne vulgaris), cases but are of exanthematou lichenoid (dDx: Lichen Planus), photosensitivity, vasculitis and questionable efficacy s eruption vesticulobullous reactions

a type IV delayed hypersensitivity reaction allergic dermatitis is mediated by the Langerhans cells, T lymphocytes and Tcell lymphokines be non-protein in nature solublehaptens

Type Erythema Multiforme M> F 40 y/o

Description viewed as a hypersensitivity syndrome therefore, an underlying antigenic stimulus should be suspected 20% of all cases occur in children

Toxic Epidermal Necrolysis Lyells Syndrome

Characteristic Lesion Clinical Presentation Treatment manifests not only in the lesions may be macular, elanom, nodose, vesicular or bullous; annular, circinate the skin but in the or iris-shaped symptoms may include urticaria, pruritis may be persistent mucous membranes evolution is rapid, generally over 12 to 24 hours main sites of Some etiologies include: bacterial infections , viral infections may be the most predilection in the frequently encountered etiology. As many as 1/3 of all cases may be associated with lower elanoma it the herpes virus, but may also occur with the Asian flu, infectious mononucleosis, include the legs and measles, mumps, coxsackie viruses, echoviruses and poliomyelitis dorsum of the feet mycotic infections ,collagen vascular diseases - may occur in association with erythema iris, , is found systemic lupus erythematosis chiefly on the ankles drugs include allopurinol, antipyrine, arsenic, barbiturates, bromides, dapsone, digitalis, dilantin, gold salts, hydralazine, iodides, mercurials, penicillin, penicillamine, phenytoin, elanoma ital, salicylates, sulfonamides, tetracycline, tolbutamide and trimethoprim-sulfamethoxazole characterized by widespread blistering of the in full blown cases of TEN, steroids should be withheld because it is generally skin that is so severe that it has the appearance agreed that the benefits of steroid therapy if any would be observed only in of a widespread scalding burn the early stages of a slowly evolving case of TEN it is believed to be an idiosyncratic, dose once a large area of the dermis is uncovered (greater than 20%), the supposed independent, drug-induced reaction advantages of steroid are outweigh be its drawbacks to rapidly calculate the amount of total body surface involved, use the rule of nines it is differentiated from scalded skin syndrome treatment of the skin lesions is essentially that of treatment of second degree (which is caused by staphylococcus) by the burns. It may include: analgesias for pain relief, silver nitrate solution level of skin cleavage with in TEN is at the followed by a dexamethasone-neomycin erosol spray and cholesterinized dermal-epidermal junction i.e. a fullpetrolatum thickness slough of the epidermis silvadene (silver sulfadiazine) cream is also however, when it is applied over large open areas, there is a risk of granulocytopenia. Also, if the 20-50% of the body can be involved sulfonamides are suspected in the etiology of TEN, it should obviously be the pathogenesis is unclear but T-cell avoided. involvement, specifically the CD8+, appear there are some reports that plasmaphoresis may be useful plasma exchange within the blister fluid should prove beneficial by removing the offending drug or its metabolites

60

F.

Hair, pigment and other disorders (see other derm lesions)

Nevi

Description

20 to 50% of melanomas develop in a pre-existing nevus development of a new nevus over the age of 35 should alert the physician to possible melanoma Types Junctional Nevus it is evenly pigmented flat and well-circumscribed; color is frequently dark where nests of melanocytes are located in the basal layer of the epidermis it is very common in children; very rare in adults over 50 years old, and it is the most likely pre-existing nevus to develop into a melanoma Compound Nevus common in adolescents and comprise the majority of pigmented lesions in children, generally <1cm and ranges in color from brown to black and hairs may be presentoccasionally a depigmented, whitish ring develops around a compound nevus resulting n the so-called halo nevus rarely transform into malignant melanoma Intradermal Nevus this nevus is usually small less than one centimeter with regular edges, more common in adults the giant, progressive nevus or bathing trunk nevus is a variation of either the intradermal or compound nevus, and transformation of these giant progressive lesions may be as high as 10% Atypical or macular lesions that may be present in great numbers and may be up to 6 mm or greater in diameter, they possess a cobblestone Dysplastic Nevi surface with a variable mixture of tan, brown, red or pink coloration with typically have ill-defined bordersatypical mole syndrome is an autosomal dominant familial disorder placing an individual at greater risk to develop malignant melanoma at an early age Blue Nevi Regarded as a failure of melanocytes from the neural crest to arrive at the dermo-epidermal junction. The melanocytes are found in the lower dermis giving refraction of light at this level gives rise to the blue color

5.
Type Leiomyoma more common in adults than children angioleiomyomas are F>M, 2:1

Tumors A. Benign

Leiomyosarcoma Glomus Tumor

Piezogenic Papules

Xanthoma

Lipoma

Soft Tissue Tumors Description Characteristic Lesion Clinical Presentation Treatment benign tumor arising from quite painful such that pain is generally the presenting when lesions become symptomatic, smooth muscle symptoms chief complaint surgical excision is indicated are exacerbated by cold this pain is believed to be secondary to impingement they possess numerous blood weather - "goose bump" of vascular or neural structures vessels with thick muscular walls conditions, lesions arising composed of poorly defined lesions are fixed within the skin, but are freely from venous or arterial smooth muscle moveable over subcutaneous fat smooth muscle are often recurrence rate with resection is angiomyomas are usually solitary nodules referred to as they occur most commonly on the lower extremity it rare angioleiomyoma usually presents as a skin colored nodule (dDX above) malignant variant of a smooth muscle they have a tendency to metastasize and can they are managed with excision, tumor be quite deadly radiation and chemotherapy glomus tumors are benign neuroarterial lesions appear skin-colored to slightly dusky surgical excision when complete, lesions composed of vascular channels blue, it is generally constantly tender and relief of symptoms is immediate surrounded by nerve fibers they arise exquisitely painful with paroxysmal recurrence if possible with from the AV shunts exacerbation incomplete resection these are herniations or they typically occur on the medial and lateral NONE the patient should be counseled protrusions of the plantar aspects of the heel pad abd these lesions occur regarding weight loss, biomechanical control of subcutaneous tissue through in patients who are extremely obese, foot function and/or change in weight bearing the connective tissue striae of excessively pronate or stand for long activities the plantar fat pad periods of time these occur secondary to the deposition of tuberous xanthomas may develop as slow growing yellow papules or nodules lipids in the skin as a result of they affect the knees, elbows and extensor surfaces of the extremities hyperlipidemia, primary lesions are indurated and have a tendency to coalesce hyperlipoproteinemias, familial tendinous xanthomas are smooth and attached to tendons, ligaments and deep fascia hypercholesterolemia and familial these occur frequently on the tendo achilles hyperbetalipoproteinemia subcutaneous tumors composes lesions are generally asymptomatic unless impinging surgical excision is generally curative of fat tissue skin overlying a on surrounding vascular or neural elements intralesion triamcinolone acetonide lipoma may exhibit dimpling if the lesions is larger than 10 cm in diameter, it injections atrophy of fat when pulled (resembling should be resected - particularly when occurring liposuction cellulite) on the thigh - for biopsy and potential malignancy NOT EASY TO REMOVE

61

Type Acrochordons M=F common in 60% population

Periungual Fibroma Kernan's Tumor occurs in the early teens Acral Fibrokeratoma average age 40 years Dermatofibroma occur adults rarely in children

Plantar Fibromatosis Ledderhose's Syndrome

Synovial or Myxoid Cysts Digital Mucin Cysts F>M Ganglionic Cyst

Soft Tissue Cysts Description Characteristic Lesion Clinical Presentation Treatment small, flesh to dark brown colored, sessile, they increase in number when the most lesions can be "clipped" away pedunculated, papillomatouc lesions patient is gaining weight without the need for anesthesia and on the plantar surface of the foot, these lesions tend are frequently associated with cauterization of the base can be to become flattened and are generally seborrheic keratosis and possess a accomplished with electrodesiccation or asymptomatic unless there is some type of external statistical correlation with colonic other techniques recurrence following irritation and lesions may be up to 1 cm polyps this treatment is unusual these lesions may become large enough to disrupt the these are associated with tuberous generally no treatment is required entire nail bed sclerosis 50% of the time unless lesions become symptomatic firm, smooth flesh-colored growth protruding from the remainder of the time, lesions radical excision of the tumor, the nail folds and lesions bleed easily when irritated: are believed to be secondary to underlying nail bed and matrix is friable previous nail surgery or minor recommended these lesions have a symptoms may occur secondary to shoe gear irritation trauma high recurrence rate classically, it presents as a smooth, dome-shaped papule that is due to their predominantly acral simple shave excision and asymptomatic and is usually solitary, it is characterized as a location, trauma is thought to be cautery, surgical excision or benign, acquired pinkish, hyperkeratotic, hornlike projection a precipitating factor it usually ablation this projection usually emerges from a collarette of slightly occurs on the digits but may occur recurrence rate is rare on the palms and soles elevated skin which an important differentiating factor also known as fibroma durum, principle locations include the lower NONE, surgical excision of symptomatic nodulus cutaneous, subepidermal extremities, above the elbow, or on the lesions may result in residual nodular fibrosis, sclerosing sides of the trunk, it is reddish brown and hyperpigmentation - patient's often find this hemangiomait is a common nodular occasionally has a slightly scaly or velvety more objectionable than the original lesion skin lesion and these lesions are appearing surfacediagnosis may be aided intralesional injection of short acting occasionally pruritic by the "dimple sign" - that is upon corticosteroid (dexamethasone phosphate squeezing the lesion from side to side, it may occur secondary to an 4 mg/cc) may be helpful may actually involute insect bite or minor trauma the skin is freely moveable Assoc w/ Dupuytren's accommodative directed towards off-loading , intralesional injection of over the lesion, occurs as a contracture of the triamcinolone acetonide, slerosing solution; wide surgical excision (margins slowly enlarging nodules palmer fascia or > 0.5 cm) with partial fasciectomy may be necessary on the sole - most Peyrone's disease, May recurrence rate of these lesions is >65% with recurrence, resection of common on the medial infiltrate through the the entire plantar fascia is recommended, make sure you put in a band of the plantar plantar fascia drain to prevent hematoma fascia focal accumulations of OA is sometimes present in the high rate of recurrence lesions will often refill within eight mucin in the dermis or dorsal adjacent joint , they are usually weeks, concomitant injection of a small amount of aspect of the distal phalangeal noninflamed, solitary, skincorticosteroid may be helpful or proximal nail folds: colored or bluish nodules, and some recommend "multiple" needlings consisting of up PSEUDO-CYSTS, lesions over with DIPJ lesions, the nail plate to 10 punctures with aspiration of the contents DIPJ may arise from herniation may demonstrate longitudinal surgical excision may be effective with careful of tendon sheath grooving or ridging dissection of both the cyst and its stalk they are herniations of occur commonly over NONE unless the lesions are symptomatic, aspiration and subsequent injection the joint linings and the wrists and ankle, of a corticosteroid may be effective and aspiration may need to be repeated often associated with heel or dorsum of the several times. 4% alcohol sclerosing agent may be successful following exostoses most foot and along the aspiration of the fluid contents. surgical excision may be necessary, albeit common of all lesions dorsal of the foot often frustrating due to the high recurrence rate and when surgical resection affecting the joint and from the extensor required, the entire lining of the cyst should be removed along with joint structures tendon sheathes identification and ligation of the stalk

62

B.
Type Eccrine Poroma F>M >40 y/o Pyogenic Granuloma granuloma telangiectaticum most frequently in children Seborrheic Dermatitis

Premalignant

Lesions Mimicking Malignancies/Pre-Malignant Lesions Description and Characteristic Lesion Clinical Presentation Treatment a benign tumor of the intraepidermal portion of he eccrine sweat duct most commonly on the enbloc surgical excision a slightly protruding fleshy mass generally pink to reddish in color that sides and soles of the when present on the plantar may appear to be slightly lobulated or verrucous foot surface of the foot proud flesh, and it is dull red in color ioccurs on exposed nail fold lesions often respond well to isotretinoin shelling and friable may form at the site of an surfaces of the body and out the lesions with a curette, smaller lesions may respond to injury, on very rare occasions, these the sole of the foot or cauterization following removal with silver nitrate sticks lesions may occur subcutaneously and nail fold of a toe or may stain the skin and mask erythemalesions when are then referred to as lobular capillary finger are also common simply resected without ablation of the base, have a high hemangiomas sites and the lesion incidence of recurrence common, usually generally undergoes remissions and exacerbations and may be accentuated/ aggravated selenium sulfide targets the scalp, by:Parkinson's disease, AIDS ,diabetes mellitus, especially in obese patients, sprue (Selsun), tar, zinc eyebrows, eyelids, (celiac disease) and epilepsy may also increase the incidence of seborrhea. Incidence: pyrithionate and nasolabial creases, the disease process is generally not seen before puberty hormonal influence Presence resorcin shampoos lips, ears, sternal of a lipophilic, pleomorphic fungus Malassezia ovalis responded well to 2% for cases of the area, axillae, ketoconazole cream. scalp umbilicus, groins lesions are also exacerbated by emotional stress and have been induced by the and gluteal crease neuroleptic drugs (haloperidol and droperidol) Actinic or Solar occur on sun exposed areas of the body and frequently in fair elderly Liquid N2 lesions on the back and face, in the presence Keratosis individuals may give rise to SCC and mimics Bowens disease and of broad, extensive lesions - topical 5-fluorouracil and it SCC that arise are well recognized as non-aggressive w/ an excellent has a tendency to "seek out" the lesions - even those which prognosis Characteristic Lesion: lesions are commonly 1 to 2 cm, are are not clinically apparent generally multiple, discrete, flat or elevated, verrucous or keratotic, CO2 laser ablation and oral etritinate is quite effective red, pigmented or skin colored patches or scales prophylaxis against future lesions is imperative with the use of total UV blocking sunscreens Cutaneous occur most frequently on the face and scalp generally a benign condition, these lesions excisional biopsy with histopathologic Horn - Cornu are generally precipitated by UV radiation exposure and have a superimposed lesion examination of the underlying lesion to Cutaneum (often seborrheic keratosis, verruca vulgaris, angioma) 50 to 60% of the time, malignant insure adequate removal and appropriate Peak: 60 and 70 lesions at the base of the horn occur 16 to 20% of the time frequently SCC although therapy for underlying malignant lesion years of age occasionally it will be a basal cell carcinoma if present. Characteristic Lesions: skin colored, horny excrescences Keratoacanthoma Arise from a viral origin and histologically they may be quite difficult to the scar from careful surgical excision is differentiate from SCC though they have the potential to transform into SCC. often more cosmetic than allowing the middle age to Incidence: Occurs very common on the shins and calves in women (ddx of AD lesion to resolve on its own and lesions on elderly and EN) Clinical Appearance: the initial lesion is a smooth, cone-shaped red papule the plantar surface of the foot should always and may resemble molluscum contagiosum or verruca vulgaris and telangiectasias be excised may course through the lesion, lesions develop quickly and it possesses a central injection therapy of 5-fluorouracil :1 keratin-filled plug which may become crusted and the initial rapid growth period is injection/week for 3 consecutive wks then followed by a stationary period for two to six weeks where the lesion will then is spontaneously regress over 2 to 8 months - spontaneous involution that will heal intralesional injection of triamcinolone with a residual, fibrous scar

63

C.

Malignant

Basal Cell Carcinoma Description Lesions often arise historically from actinic activity and it is believed by many to arise from pluripotential cells within the basal layer of the epidermis or follicular structures. The tumors usually arise from the epidermis and occasionally arise from the outer root sheath of a hair follicle, specifically from hair follicle stem cells residing just below the sebaceous gland duct. BCC is considered the most common of all malignancies in man, however, it is very uncommon in the foot, and the disease process is characterized by chronicity - growing slowly, therefore the lesions are characteristically asymptomatic PAINLESS nodular - which is most common pigmented cystic sclerosing or morpheaform superficial nevoid Central Depression: bleeding, crusted and gradually enlarging ulceration, Translucent Borders may actually appear to be "rolled" in w/ telangectasias: Diagnostic highest among middle-aged and elderly people who have a history of considerable sun exposure, and it is actually the most common tumor of light-complexioned people
Pigmented Basal Cell Carcinoma Sclerosing or Morpheaform BCC Superficial Basal Cell Carcinoma Biopsy and Excision Electrosurgery curettage Mohs Surgery Cryosurgery 5-Fluoro-uracil (Efudex )

6 Types Characteristic Lesion Incidence Variants

TX

Topical agents

Imiquimod (Aldara )

Slow developing light to dark brown lesions that mimic melanoma (d/t considerable pigmentation), more common in darker skinned, and pigmentation persists post-treatment Waxy sclerotic plauque mimicking scleroderma or a scar with no rolled in borders, ulceration or crusting, and the most difficult to treat. Telengectasias are the most prominent Erythematous scaly plaques with telengectasias that mimics psoriasis, has a threadlike raised border and appears as a flat growth with no tendency to ulcerate. May correlate with the ingestion of arsenic over a long period of time. If the lesion is 5 to 7 mm in diameter, elliptical excision with margins of 2 to 5 mm is the procedure of choice and with excision of tumors less than 2 cm - a 4 mm margin of surrounding, healthy appearing tissue is acceptable. > 1.5 cm in diameter, and in the hands of an experienced operator, this method is probably superior to all others High cure rate. Treatment of choice for sclerosing BCC. DisAdv: It is time consuming. > 1.5 cm in diameter, but it is a blind approach and it is difficult to tell if all the lesion has been removed (-) DNA syn by blocking methylation of deoxyuridylic acid and inhibiting thymidylate synthetase and therefore, cell proliferation apply bid x 3 wks, only 5% strength is recommended; therapy might be required for up to 10-12 wk the cream is applied to the lesion and an additional 1 cm of surrounding skin and left on 8hrs; tx is repeated 5 d/ week for 6 wks

1. Why is metastasis so rare in basal cell carcinoma? growth of the lesion is dependent upon the underlying connective tissue stroma and most reported metastases are secondary to incomplete excision or because of long-term neglect Squamous Cell Carcinoma Description Etiology Incidence Characteristic Course Metastasis It is the second m.c skin cancer comprising 20% of all nonmelanotic skin cancers; 20% m.c in blacks than BCCs. Most common in the elderly d/t cumulative solar insult. Most common type of squamous cell carcinoma is sun induced, and 60% arise from the site of a previous actinic keratosis. M>F 3:1 incidence is far less than that of basal cell carcinoma Superficial, discrete (freely moveable unlike the fixed BCC) lesion that is flesh-colored containing telengectasias These lesions may be painful and tender even when small and 50-60% occur on the head and neck, followed by the hands and forearms, upper trunk and lower legs presentation in the foot is often atypical a history of blistering sunburns and frequent sun exposure is routinely elicited and may grow rapidly over 6mo -1 year skin biopsy specimens must reach at least the depth of the mid-dermis to allow for determination of the presence or the absence of invasive disease SCC arising from burn scars, chronic ulcers and radio-dermatitis (Marjolins ulcers) are generally more aggressive with incidences of metastases reported between 20 to 30% when metastasis occurs, the five-year cure rate is 34% and recurrence and metastasis typically occurs w/in a three year time from of initial treatment
Prevention excisional removal emphasized with the use of sunscreens most ideal with good margin control in well differentiated lesions less than 2 cm in diameter may be treated with surgical excision with a cure rate of approximately 99% elliptical excision is acceptable with margins of 4 to 6 mm Moh's sx technique it is used when tissue to be removed must be kept an a minimum cyrotherapy curettage are reserved only for the most superficial lesions, and it is generally reserved for in situ and actinic keratotic lesions desiccation radiation Is mainly used as a treatment in patients who cannot tolerate or wish to avoid surgery

Treatment

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Bowen's Disease - Squamous Cell Carcinoma in Situ Description Characteristic Lesion Incidence Treatment an intraepidermal SCC in a classic windblown appearance in situ disease connotes a superior prognosis regardless of treatment modality, and untreated, these lesions may become invasive podiatric appearance may be atypical (examples of such cases include a presentation initially mistaken for a "wet" fungal infection and another mistaken for a heloma durum) highest incidence in older white men and arise on primarily sun-exposed surfaces simple elliptical excision, Mohs surgery is recommended for larger lesions

Malignant Melanoma Discussion Description most arise from a pre-existing nevus, often present from birth, but a small number arise de novosurvival rate can be as high as 90% for early detected lesions Metastases Early lymphatic spread with late hemotogenous spread, therefore it is imperative to examine local lymph nodes when there is an index of suspicion as lymphadenopathy may be an early sign of metastasis where lymph nodes become hard and discrete skin is the primary metastatic site, and the CNS metastasis is the most common cause of death Incidence melanoma is not common in darker races, correlation btwn levodopa tx in Parkinson's disease and the onset of melanoma A - asymmetry - this is present when, if the lesion is bisected, the halves are not identical Clinical B - border irregularity - this is suggestive if the border is scalloped, raggedy or uneven Recognition
C - color variation - more than one shade of pigment warrants concern D - diameter - greater than 6 mm may suggest malignance S - surface - surface irregularities - nodular, warty, unevenness in general one should consider biopsy if one or more of these signs are present

Classification Systems for Melanoma

Breslow's Classification this system is a measure of invasion in mm of thickness and thickness of the lesion correlates with prognosis Stage 1 tumors (localized disease without regional node involvement) are listed as follows*: Stage 1 < 0.76 mm > 98% five year survival Stage 2 0.76 to 1.49 mm 87 to 94% five year survival Stage 3 1.50 to 3.99 mm 66 to 83% five year survival Stage 4 > 4.0 mm < 50% five year survival

Clark's Levels of Cutaneous Invasion this micro-staging classification is based on the level of penetration of the melanoma through the skin Clark's levels do not impose a prognostic outcome Level I melanoma located above the basement membrane of the epidermis; these lesions are essentially in situ and present no re year survival Level II melanoma invades through the basement membrane into the papillary dermis - 95% five year survival Level III melanoma characterized by widening of the melanoma cells which fill the papillary dermis down to its interface with the reticular dermis; there is no invasion of the reticular dermis - 82% five year survival Level IV melanoma penetrates into the reticular dermis - 71% five year survival Level V melanoma penetrates into the subcutaneous tissue - 49% five year survival Because each classification system has its followers, overlap of the two systems is defined below: Breslow Group I (0.65mm) compares to Clark's level II (down to but not penetrating the papillary dermis) Breslow penetration greater than 1.5 mm correlates with Clark's levels IV and V Clark's level III falls between 0.65 and 1.5 mm of thickness Prognosis of these lesions may also relate to other factors: survival rate is more favorable in women, individuals less than 50 years of age and for tumors on the extremity (excluding those on the hands and feet) the five year survival rate inpatients with nodal spread is about 36% and drops to 5% with distant metastasis 1. What is Dermoscopy a noninvasive method that allows the in vivo evaluation of colors and microstructures of the epidermis, the DE junction and the papillary dermis not visible to the naked eye.

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Type Lentigo Maligna Melanoma in Situ Amelanotic Melanoma Superficial Spreading Melanoma Acral Lentiginous Melanoma

Nodular Melanoma

Types of Melanomas Clinical features Incidence % Treatment begins as a tan macule that becomes irregular M=F 60's- 70's 5% photographed first and w/variegated coloring .The lesion will exhibit a radial predilection for sunthen thorough surgical growth over a period of 5- 20 years, and then may become damaged skin excised vertically invasive that is nodular melanoma as the Moh's surgery is again hallmark of its vertical invasion is demonstrated useful in this situation this differs from all the other melanomas only in its lack of pigment Surgical excision with sentinel node the lesions may be pink, erythematous or flesh-colored but otherwise mimic exactly the biopsy; Decarbazine (DTIC) pigmented lesion and is often mistaken for a pyogenic granuloma Temozolomide and vaccines lesions grow much characterized by radial growth: it is multicolored and possesses not only M=F 50's 70% more rapidly than different shades of tan but variegated black, red, brown, blue and white; the possesses no those of lentigo border is often notched, characterized by areas of focal regression and/or predilection for maligna with radial asymmetric growtheasy bleeding, erosion or ulceration is a sign of sun-exposed skin growth only 1-5 years malignancy and heralds metastases female shins M=F 50's 10% involves not only acral but volar structures, that is, the palms and soles m/c site of melanoma notable predilection exists for the distal phalanges of the toes and fingerssubungual lesions foot - 60% have generally fall into this category plantar or subungual radial growth rate lies midway between lentigo maligna and superficially spreading melanoma "Hutchinson's most common type in blacks, Hispanics and American Indians melanotic whitlow" Clinical Features: an irregular, enlarging black macule on the palm, sole, digital pulp or nail fold or where the thumb and bed is virtually diagnostic; a black discoloration of the proximal nail fold at the end of a pigmented hallux are more streak (melanonychia striata) is ominous and may signal a melanoma of the nail matrix frequently involved early lesions may appear simply as a light brown, dark brown or black discoloration & late lesions than the other digits may become nodular & ulcerative; metastasis to the axillary and epi-trochlear nodes develop in late stages of the disease and are common lesions may arise without any clinically apparent preceding radial growth M>F 2:1 15% Clinical Features these lesions tend to invade the dermis very rapidly,they maybe frequently predilection for sun30% misdiagnosed - resembling blood blisters or hemangiomas and older lesions become papillary, exposed areas fungoid or ulceratedbleeding is generally a late sign and coal black or sepia colored spots may appear as if sprayed about the lesion Description Hutchinson as a melanotic freckle

6. 7.

Special disorders of nails and appendages of skin (see other derm lesions) Treatment (see each lesion)

Organisms that cause gas in tissues: BECKSS Bacteroides, E.Coli, Clostridium, Klebsiella, Streptococcus, Seratia, Staph

Pharmocology revisitied
Antibiotics The Natural PCNs: PCN G and PCN V MOA Metabolism Indications Disadvantages Most susceptible pathogens PCN resistance methods Drug rx Bind regulatory enzymes (PBPs-transpeptidase, carbaxypeptidase, endopeptidase) responsible for the peptide linkages involved in peptidoglycan syninhibit cross-linking of the peptidoglycan. Works on actively dividing cells bacteriacidal Minimally, excreted primarily unchanged by the kidneys. Use of probenicid will increase levels of PCN; Exception is nafcillin, oxacillin, cloxicillin and ureidopenicillins which have biliary excretion. Pts with renal impairment dosages do not have to be adjusted Simple and inexpensive drug that has a broad spectrum of bactericidal activity DOC for strep viridans, pharyngitis, primary syphilis, recurrences of rheumatic fever, endocarditis, pneumococcal or meningococcal meningitis PCN G is difficult to get drug to site of infection, because it is very unstable in the acidic PH; Increasing resistance to both: MRSA Gram +: Streptococcus pneumoniae, GBS, streptococcus viridans, anaerobic streptococcus, neisseria, and some bacteroides species. Actinomyces, clostridia, listeria, pasturella, diphtheria, syphilis, Lyme, rat-bite fever, and anthrax. Variable activity against gram (-) Staphylococcus aeurus and epidermis produce B-lactamases which destroy both PCNs B-lactamase (eg S. aureus) Chromosomal mediated resistance (Baceroides, Klebsiella, Legionella) Plasmid mediated B-lactamase resistance (Staph, hemophilus, neisseria, E. coli) DO NOT USE GRISEOFULVIN with PCN allergy

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Drug PCN G Benzylpenicillin PCN V

MOA/ Description Not acid stable, no blactamase resistance must give IM/IV only Acid stable, no blactamase resistance PO ONLY, Units of PCN V: 125mg = 200,000

Advantages Low cost, excellent tissue penetration and therapeutic index Absorbed 60% after po dose on an empty stomach, T1/2 (2hrs)

Disadvantages 10% hypersensitivity, degraded in gastric acid, poorly absorbed Better than PCN G

Forms Crystalline (aq) rapid for continuous IV, T1/2 30min Procaine/PCN G-equimolar conc of both, longer T1/2 IM use 1-3xd Benzathine PCN G-IM long acting, T1/2 (1wk), lasts 34wks, DOC for syphilis Potassium salt: Pen VK or V-cillin K Dose: 250mg-1g 4-6x day Indicated: throat, respiratory and soft tissue infections 1.0g = 1,600,000 units

250mg = 400,000units

500mg = 800,000

The Aminopenicillins: Ampicillin, Amoxicillin, and Becampicillin Presence of an amino group on the beta side chain of the pcn nucleus extends coverage to include some gram-negative bacteria, readily destroyed by staph penicillinase Aminopenicillins Indications Gram-positive susceptible pathogens Gram-negative susceptible pathogens PCN allergy? Otitis media, sinusistis, bronchitis, AHA recommended for the prophylaxis of bacterial endocarditis: 2.0g po 1 hour before procedure and 1.5g po 6hrs after the procedure All of PCN G, including, streptococcus faecalis and non penicillinase producing staphylococcus H. Influenza, E.Coli, Proteus mirablis, shigella, salmonella, N. gonorrhea, NO coverage against pseudomonas, Klebsiella, Enterobacter and Bacteroides Clindamycin 600mg: 2-300mg tabs

Aminopenicillin preparations Drug Description Contraindications; Warnings Dose Ampicillin First 80% develop rash 500mg q6h, can give IV or IM Amoxicillin DOC for endocarditis prophylaxis, (long surgical procedures), absorption is 2x greater than 250mg po q8h or tid (Amoxil) ampicillin, po levels approach IM levels Bacampicillin (Spectrobid) Prodrug-hydrolyxed to amoxixillin, and absorption levels about the same; NO advantages, expensive Penicillinase-Resistant Penicillins: Methicillin, cloxacillin/Doxacillin, Nafcillin/oxacillin Indicated for the DOC for penicillinase producing staph and also effective for penicillin-sensitive pneumococci and streptococci S Aureus/epidermidis are resistant to these penicillins and are called methicillin-resitant staphylococci or MRSA theses are also resistant to cephalosporins, imipenem, and meopenem. Also has no coverage for S. faecalis (enterococcus) or gram negatives (both anaerobic or aerobic) o The DOC for these species is Vancomycin +/- rifampin+/- gentamicin All are highly protein bound, most have hepatic metabolism and biliary excretion contraindicated in patients with liver failure Drug Description Indications Contraindications; Warnings Dose Methicillin No longer marketed in the 1st anti-staph bCauses interstitial Must give q4h (Staphcillin) US, not acid stable, short lactamase stable pcn nephritis 1-2g IV PB q4h T1/2, low plasma binding PARENTERAL ONLY NEPHROTOXIC Cloxacillin Doxacillin Isoxazole pcns, well Diclox higher blood Cloxacillin 250-500mg qid absorbed, the most preferred [ ] PO ONLY Diclox: 250mg q6h Nafcillin and Oxacillin Oral absorption is erratic, Better for staph and Pts on coumadin 4-12g/day or 2g q4h must be given IV, 90% strep than methecillin which are also protein bound, need higher PARENTERAL ONLY highly protein plasma levels bound The Carboxypenicillins: Carbenicillin, indanyl carbenicillin, ticarcillin o o o o o o Indicated for the treatment of UTIs, osteomyletis (pseudomonas) Susceptible organisms: excellent for gram-negative bacillary eg Haemophilus, Neisseria, E. Coli, Psedomonas, Proteus, shigella, salmonella (about the same as ampicillin) NO coverage for enterobacter, morganella, Providencia and all are destroyed by b-lactamases Act synergistically with aminoglycosides against pseudomonas TnT (Ticarcillin and Tobramycin) generally used IV, IM/po doses fail to achieve adequate serum/tissue levels adequate for pseudomonas Know the 3 Problems with carbenicillin and indanyl carbenicillin o Contain 4.7meq of salt and full doses of 12-30g qd may precipitate CHF fluid retention (CHF) and hypokalemia o Both bind ADP receptor sites on platelets preventing normal aggregation and therefore prolong bleeding time o Hypokalemia

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Drug Carbenicillin (Geopen) Indanyl carbenicillin (Geocillin) Ticarcillin (Ticar)

Description The first with antipseudomonal activity Is acid stable and well absorbed 4x more active than carbenicillin

Indications IV/IM PO ONLY UTI and prostatitis Pseudomas

Contraindications; Warnings Platelet aggregation, hypokalemia and CHF Not for systemic infection Platelet aggregation, hypokalemia and CHF

Dose 1-2g dose q4h generally given with 1g of probenicid

The Uerido penicillins: Azlocillin, Mezlocillin, Piperacillin o o o o o Derivatives of ampicillin, and are destroyed by b-lactamases All dosed at 8-16g IV and are usually combined with an aminoglycoside Excreted differently than PCN o 20-3-% via hepatobiliary system, do not have to adjust for renal disease Indications: For serious gram negative infection; parental only Similar in spectrum as ticarcillin, but better coverage for streptococcus, some enterococci, B. Fragilis and Klebsiella Pneumonia Contraindications; Warnings Not absorbed orally, must be given IV Not absorbed orally, must be given IV Not absorbed orally, must be given IV Dose 8-16 g IV 8-16 g IV 8-16 g IV

Drug Azlocillin (Azlin)

Description 8-16 X more active than carbenicillin for pseudomonas, but is less active for Proteus Mezlocillin (Mezlin) Comparable to Ticar against Psedomonas Piperacilin The most active pcn, the DOC for pseudomonas, excellent (Piperacil) against strept, Neissria, Haemophilus, and Bacteroides

B-lactamase inhibitors combinations: Augmentin, Timentin, Unasym and Zosyn Due to the structural similarity to the basic PCN molecule, structure, these inhibitors have a high affinity and irreversible binding to many bacterial b-lactamases and thus prevent the enzyme hydrolysis of the co-administered penicillin Indications: o For the empirical treatment of infections causes by penicillinase producers o Extends the spectrum of activity to include Staph aureus. H. influenza, B. fragilis and gram negative bacteria B-lactamase inhibitors o Clavulonate PO ONLY (-) Richmond Sykes class II, III, IV and V as well as S. aureus and some anaerobes. o Does not inhibit class I or chromosome mediated resistance as in Pseudomonas, Seratia, Enterobacter, and Citrobacter species o Sulbactam IV only, an inhibitor of Class I or chromosome mediated b-lacatamases: Is synergistic with penicillin o Tazobactam Low level of binding to PBP, (-) Richmond Sykes class II, III, and IV penicillinases/cephalosporins. o Does not inhibit class I or chromosome mediated resistance as in Pseudomonas, Seratia, Enterobacter, and Citrobacter species o Drug Augmentin Timentin Unasym #1 Zosyn Combination KNOW Amoxillin 250-500mg and Clavulonate 125 mg PO Indicated for Otitis media, soft tissue infections, UTI Ticarcillin 3gms and Clavulonate 0.1-0.2g IV/IM Ampicillin 1-2g and Sulbactam 0.5-10g Piperacillin 2.25g and Tazobactam 250mg Dose 875 mg po q8h Hospital order: 3.1 or 3.2q q4h IV 3.0g in total 2.25mg; 3g/375mg; 4g/500mg Dose: q6h slow IV over 30 min

The Cephalosporin Family Introduction MOA Spectrum of activity Metabolism Produced by the fungus Cephalosporium acremoium Differs from pcns by the presence of the dihyrothiazine ring that gives more resistance to b-lactamases rather than the 5membered thiazolidine ring of pcn Inhibits cell wall synthesis, peptidoglycan coss-linking, bacteriocidal, Can be used for penicillin sensitive patients, broader spectrum than PCNs but is variable in each generation Liver inactive lactone, then excreted by the kidney, Cefoperazone is metabolized and excreted exclusively by the liver can use in patients with renal disease; None are highly protein bound probenecid will prolong activity

Cephalosporin generations-as we go from the 1st 4th generation the more effective the gram-negative killing First Generation PEK o All have similar spectrum of activity, active against many gram + cocci (not enterococcus or MRSA), E.coli, K. Pneumoniae, Proteus mirabilis (20% of hospital acquired are resistant)

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o o o

No activity against serratia, enterobacter, proteus (indole postive), pseudomonas, Bacteroides fragilis, Neisseria Absorption: PO-best absorption on empty stomach, good synovial fluid level but does not pass BBB (not good for meningitis) Better for strep and staph than subsequent generations Dose 250-500mg qid 500mg po bid 250mg q8h 250mg po q 6h Give q4h Give q4h Hospital order: start IV with D5Q to KVO then give Ancef 1.0g IV PB 30 min b/f surgery Post op- Ancef 1.0g IV PB stat then q6h X 6 doses

First Generation cephalosporins: Drug Description Cephalexin (Keflex) PO, good absorption, peak blood level 15-20 ug/ml, broad spectrum Gr+/Cefadroxil (Duricef) PO, longer T1/2 Cefaclor (Ceclor) PO, more active against gram negatives i.e., H. influenza, E.coli and proteus spp Cephradine (Velosef) PO/IM/IV Cephalothin (Keflin) IM/IV short T1/2 (30-40min) Cephapirin (Cefadyl) IM/IV short T1/2 (30-40min) Cephalozin IM/IV DOC for surgical prophylaxis; staph osteo (good (Ancef, Kefzol) bone penetration), good for staph, strep, E.coli, and some Klebsiella, preffered due to long T1/2

Second Generation Cephalosporins HENPEK Generally indicated for lower or URI, UTI, GI, GU, STDs, skin and skin structure, and bone joint infections Better than 1st gen at gram negative (E.coli, H. flu, Neisseria, Moraxella, Enterobacter and Klebsiella Excellent for strep and staph, but may not be better than 1st generations Drug Cefuroxime axetil (Ceftin) Cefpodoxime (Vantin) Loracarbef (Lorabid) Cefprozil (Cefzil) Cefuroxime (Zinacef) Cefmetazole (Zefazone) Cefotetan (Cefotan) Cefamandole (Mandole) Cefonicid (Monocid) Cefoxitin (Mefoxin) Ceforanide (Precef) Description PO, poor absorption, best taken with food, higher GI upset, longer T Not indicated for joint or bone infections PO, (tabs and suspension) Not indicated for joint or bone infections PO, Not indicated for joint or bone infections PO, indicated for pharyngitis, otitis, bronchitis, skin/sin structure IM/IV enters CSF, indicated for joint or bone infections Not indicated for joint or bone infections IM/IV, better for gr- E.coli, proteus, enterococcus, better for staph except MRSA), and strep. Problem: contains the MTT side chain but rarely causes decreased PT levels, run PT, give VitK, long T (4hrs) IM/IV, Contains the MTT side chain, not as effective for gr+ than 1st gen, not active against bacteroides, or pseudomonas. Better for proteus, enterobacter, H flu. Problem: short T IM/IV, long T , can give qd, increased serum binding and decreased tubular secretion, decreased gr+, may be used for surgical prophylaxis IM/IV, has a methoxy group attached to b-lactam ring b-lactamase resistance, decreased gr+ activity, better for Klebsiella, E. coli, proteus, serratia, than other 1st gen or 2nd gen, also good for B. fragilis and Neisseria IM/IV Dose 250-500mg po BID 200mg po bid 200mg po bid 250mg q12 tabs/susp 1.0g q8h 2.0g q8h IV 1-2g q12 h 1g q4-8 h

1-2g q6-8h

Third Generation Cephalosorins IM/IV/PO Good for gr+ and gr-, even better for gr- aerobes eg Enterobacter, Proteus vulgaris, Serratia, Morganella Wide range of anaerobic and aerobic activity Generall 3rd gen are not the DOC for gr+, not as good as 1st or 2nd gen Excellent for GBS, S. pneumoniae, H. flu, Neisseria Good b-lactamase resistance May not be as good for aneraobes eg Bacteroides as Mefoxin

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Third generation cephalosporins Drug Description Cefixime (Suprax) PO, indicated for pharyngitis, otitis, bronchitis, not indicated for skin/ skin structure or bone/joint infections, long T Ceftibuten (Cedax) PO, same as cefixime but with poor staph activity Cefotaxime (Claforan) IM/IV, good conc in CSF, good for pseudomonas, better for gr+ and best of group for the staph/strep, excellent resistance to cephalosporinases, least nephrotoxic Cefoperazone (Cefobid) IM/IV-has MTT side chain, not indicated for bone infectins, not good for gr+, excellent for pseudomonas, enerobacter, E. coli, Klebsiella, long T Ceftazidine (Fortaz) IM/IV, one of the best for Pseudomonas, and enterobacter, poor activity against gr+ and anaerobes, good conc in the CSF, can be used with Vancomycin Ceftizoxime (Cefizox) IM/IV, good for gr-, longer T not for enterococcus Ceftriaxone (Rocephin) IM/IV, longest T , (qd) excellent spectrum for gr+/-, not good for Pseudomonas, enterococcus, bacteroides frgalis Fourth generation cephalosporin: Cefepime (Maxipine) 1. 2. More active against gr- bacilli IM/IV only Clostridium difficile may be resistant

Dose 400 mg qd 400 mg qd 1-2g IV q8h 2gm q8h 1.0g q8h q12h qd

MTT side chain: Nmethylthiotertraszole group at position 3 causes Dusulfam reaction with ethanol ingestion increased plasma levels of acetaldehyde causes N/V, tachycardia, dyspnea and sweating Prolonged bleeding due to hypothrombinemia ie interferes with VitK production of depended factors 1st generation 2nd generation 3rd generation Moxlactam Cefotetan Cefmandole Cefmetazole Cefoperazone Miscellaneous Beta Lactam Antibiotics for very severe infections

1. Imipenem and cilastin (Primaxin) Prototype of the thienamycin class of antibitotics cllaed the carbapenems, antibiotic produced by streptomyces cattleya (soil organism) Owing to its small size the molecule can gain access to the periplasmic space of a gr- cell wall Absorption and Metabolism Shirt T (1hr) Spectrum of action Largest of any other antibiotic, against all gr+/- bacteria: Susceptible organisms GBS, S. pneumoniae, S. faecalis, S. epidermidis, Enterobacter, Neisseria, Pseudomonas (including the species resistant to PCN and aminoglycosides) Also good for anaerobes eg B. Fragilis, no coverage against MRSA, clamydia, mycoplasma Contraindications May cause seizures Dose IM/IV only combined with Cilastatin* Dose: 500mg 2g q6-8h IV Cilastatin is a dihydropeptidase inhibitor with no antimicrobial activity to prevent to rapid hydrolysis by the kidney Description 2. Others Drug Azotreonam (Azactam) Description Dose Parenteral only, monobactam, isolated from Chromobacterium violaceum, blocks bacterial CW synthesis (inhibits 500-1/2q q8h, PBP-3) Good for gram negative aerobes only eg E.coli, serratia, Pseudomonas, enterobacter, proteus, morganella adjust dose w/ Must combine with Clindamycin (good for gr+ anaerobes) and an antistaph PCN Creatinine Indicated for UTI, LRI, skin/skin structure infections, intraabdominal and gyn infection clearance Meropenem (Merrem) A perenteral carbapenem similar to imipenem with the same spectrum of activity Ertapenem (Ivanz) Reserved for life threatening infection, activity against all GP/GN ex: Pseudomonas and anaerobes 1g IV q24h Quinolones: The Carboxy flouroquinolones o Action: Bacteriocidal: inhibit protein synthesis by binding DNA gyrase which is necessary for DNA replication o Pharm: Good bone penetration, even exceeding aminioglycosides, po good and near complete absorption (95%) requires dosage adjustment for renal failure o Susceptible organisms: Predominantly GN aerobes, DOC for OM o Contraindications: do not uses in children and in pregnancy (articular cartilage damage), do not use in pts on Theophylline, will increase its [ ] and toxicity o Adverse rx: Tendon ruptures, nephrotoxicity, CNS disturbances, photosensitivity rx o 2nd-4th generation with increasing activity in GP organisms, anaerobes, useful as intermediary agents in polymicrobial involvement such as DM foot infections o Preparations:

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o o o o

2nd gen: Ciprofloxacin (Cipro-po/IV) 3rd gen: Levofloxacin (Levaquin) 4th gen: Gatifloxacin (Tequin) 4th gen : Moxifloxacin (Avelox)

500-750mg q12 or 400mg slow IV over 60 min q12h 750mg po qd or 500mg slow IV over 60 min qd 400mg slow IV over 60 min qd 400mg slow IV over 60 min qd

Aminoglycosides: Good for gram negative aerobes, IV only Chemical: Defined by the presence of amino sugars linked by a glycoside bond to an aminocyclitol ring, all contain an amino and a iltrate group o Action: Bacteriocidal-block protein synthesis by interrupting the transmission of genetic information at the 30s ribosome effective against enteroccoccus + a PCN o Toxicity: Ototoxic d/t damamge to the 8th cranial nerve (irreversible) nephrotoxic (if mild is reversible and occurs 5 days to several weeks after initiating antibiotic) and NM blockade 3-5% of the symptoms, high pitch iltrate dose and duration related Pharmacology: Not normally absorbed from the GI tract, well absorbed after IM injection, peak serum levels normally 30-90min after IM injection; does not pass CEF or eye. Initiate therapy w/loading dose to attain a therapeutic serum levels o Synergistic with PCN antipseudomonal pcnase resistant pcns o Not metabolized and excreted via the glom iltrate, excrete proportional to renal function o Aminoglycoside Preparations Streptomyces griseus used in selected cases of TB, plague, Tuleremia, brucellosis, also for strep endocarditis if due to S. faecalis or viridans Gentamicin (Garamycin) Peak: 4-10 ug/ml Trough: 2 ug/ml DOC for GN infections, 95% success with Pseudomonas Kanamycin (Kantrex) Used for TB, replaced by gentamycin Tobromycin Peak: 8-10 Trough: 2-4 More active than gentamycin for pseudomonas, less nephrotoxic Neomycin Most toxic of the group; used for intestinal and intraoperative irrigation Netilmicin A derivative of gentamycin, less nephro and ototoxic, less active against Pseudomonas Amikacin (Amikin) Peak: 20-30 ug/ml Trough: 10ug/ml Used when other organisms are resistant to other aminoglycosides Spectinomycin Long t1/2, permits a one time dose Streptomycin Discussion of peaks and troughs: o o o Macrolides Action: Primarily bacteriostatic or cidal dependent on condentration; blocks protein synthesis by blocking at the 50s ribosomal unit Toxicity: relative safe, only s/e is epigastric distress and nausea. Transient ototoxicity can occur at high doses of erythromycin along with hepatic toxicity Drug interaction: Erythromycin is known to decrease hepatic cytP450 and thus decrease the metabolism of other drugs, increasinf their toxicity: anticoagulants (increased bleeding), digoxin( can cause sudden cardiac death), triazolam, theophyllines, statins 1-2g IM only in divided doses 3 Ivmg/kg/day in 3 equal doses IM/IV q8h 1.5g IV/IM in 2-3 equal doses 3 Ivmg/kg/day in 3 equal doses IM/IV q8h

1.5-2mgkg IV/IM in q12h 8- 15mg/kg/day IV/IM in 2-3 equal doses

Azithromycin (Zithromax)

PO, indicated for the tx of urethritis, cervicitis, pharyngitis, otitis; active against Z-pack Tabs 2 (500mg) day 1 then 1 qd days mycoplasma, Legionella, Strept, Chlamydia pneumonias, and AIDS associated 2-5 take on an empty stomach: Al, Mg mycobacterium avian infection antacids, dairy and Ca interfere w/absorption Clarithromycin PO, similar to azithromycin with shorter T1/2, more active against GP, less against GN, 250-500mg po q12h (Biaxin) used for MAC and H. Pylori in stomach ulcerations. Fewer s/e than erythromycin Dirithromycin (Dynabec) Enteric coated Once daily dosing 500mg po qd Troleandomycin (TAO) Really good for Strep, can cause cholestatic jaundice 250-500mg po qid Erythromycin Should not be used in pts with hepatic dysfunction since it accumulates in the liver 250mg q6h Can cause prolonged cardiac repolarization associated with torsade de pointes Tetracyclines Action: bacteriostatic, inhibits 30s ribosome Contraindications: DO not give to children or pregnant females, will cross the placenta anc cause depression and abnormalities in bone growth or with pts with renal dz o Adverse rx: Skin rashes, photosensitivity, N/V/D, overgrowth of yeast and brownish/black discoloration of tongue o Susceptible organisms: Broad spectrum of g-/g+ DOC for rocky mountain spotted fever, typhus, Chlamydia and mycoplasma. Staph is resistant Preparations: o Tetracycline (Achromycin, Sumycin) 250-500mg po bid-qid o o

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o o

Doxycycline (Vibramycin) Minocycline (Minocin)

100 mg po qd-bid DOC for Lyme dz 100mg po bid

Vancomycin GP anaerobic organisms only! Parenteral use po for enterocolitis only Description Glycopeptide derived from Streptomyces Nocardia MOA Bacteriocidal and inhibits cell wall synthesis, alters baterial membrane permeability and DNA synthesis Toxicity Red man syndrome: too rapid infusion will cause histamine release characteriszed by generalized erythema, chills, fever, drop in BP antidote: Benedryl; Ototoxic and nephrotoxic(reversible) Spectrum MRSA, GP organisms, pseudomembrenous colitis d/t C. diff PMMA beads can be impregnanted with Vancomycin Dose 500 mg IV q6h or 1.0g IV q12h or 500 mg po qid for C. Diff Pharm Peak: 30-40ug/mol Trough: 5-10ug/mol Anti-anerobes: Metronidazole and Clindamycin Clindamycin (Cleocin) Description Usually used in allergies to PCN MOA Inhibits the protein synthesis of bacteria by binding to 50s ribosomal subunit bacteriastatic, must double cover Adverse rx Diarrhea, pseudomembranous colitis Spectrum GP and anerobes, fulminant group of GAS infections such as NF, MRSA and some GN organisms Dose 300mg po q8-12h or 600-900mg IV q12h Pharm PO/IV/IM, good absorption po with long t1/2 Metronidazole (Flagyl) Description Extensive use in the tx of anaerobes including Bacteroides and Clostridial infections MOA Binds to nitroreductase enzyme, inhibiting creation of bacterial DNA Adverse rx Nausea, vomiting, cramps and epigastric distress Spectrum DOC for C. diff induced pseudomembranous colitis500mg po q6h slow infusion over 60 minutes Dose 1.0g IV then 500mg q8h Pharm Disulfram-like rx with alcohold/t accumulation of acetylaldehyde Miscellaneus Antibiotics Sulfonamides (-) folate metabolism Bactrim Description Trimethoprim + Sulfamethoxazole MOA Competitive antagonist of PABA Adverse rx High risk of thrombocytopenia, leukopenia Spectrum PEEK: Proteus, E. coli, Enterococcus, Klebsiella Trimethoprim Inhibits dihydrofolate reductase Sulfamethoxazole Inhibits dyhydropterate synthetase Drugs used in the treatment of MRSA Lets talk a little bit about MRSA, there is a community acquired and hospital acquired MRSA. The hospital acquired MRSA is significantly more resistant than the community acquired strain. Vancomycin Hospital acquired MRSA 1g IV q12h slow infusion over 60 min Bactrim* Community acquired MRSA Synercid Quinupristin/Dalfopristin 500mg IV q8h IV only Synergistically block bacterial ribosomal protein synthesis, indicated for VREF, 150mg quinopristin/500mg dalfopristin MRSA, MRSE. Adverse rx: thrombophlebitis, and potent inhibitor of cytP34A Daptomycin Rifampin* Community acquired MRSA Zyvox Inhibits 30s ribosome (bacteriostatic) Indicated for VRE, MRSA, MRSE, weak 600mg q12h IV infused over 40-120 min inhibitor of MAOI increase BP w/ tyramine, take care with epi, ephedrine and 400-600 mg po q12h SSRIs. High risk of thrombocytopenia. IV=po absorption Minocycline A tetracycline, oral alternative to Vancomycin 100mg po bid *used in combination Topical Antibacterials (Sulfonamides) Drug MOA Indications Contra-indications Side Effects Warnings Silvadene Bacteriostatic-gr+/gr-, yeast Burns- 1st, 2nd and 3rd Allergy to Pts with G6Pase def severe Silver sulfadiazine cr & pseudomonas degree sulfonamides fatal hemolytic anemia 20g and 50g

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Topical Antibiotics Drug MOA Indications Contra-indications Side Effects Chloramphenicol Bacteriostaic, a protein Ophthalmic us, Tx of skin infections caused by E. Coli, Bone marrow suppression, Cream Chloromycetin- synthesis inhibitor Stap/Strep, neisseria Heomophilus, moraxella, DOC: Salmonella aplastic anemia 1% cr, oint, or solution (oral) Corticosporin Steroid responsive dermatoses with secondary bacterial infections, TB or other fungal lesions of the skin and allergy paronychia, bacterial pyoderma to aminoglycosides (neomycin) Gentamycin sulfate Amionoglycoside; Binds the 30s ribosome inhibiting protein synthesis. Good for Gram negative Ototoxicity and 1% cr/oint infections: Ecthyma, impetigo, staph/Strep, Gram neg: Klebsiella, E. Coli, Aerobactor nephrotoxicity Neosporin ointment Topical triple antibiotic First Aid, cuts, burs, abrasions Allergy to aminoglycosides (neomycin) Mupirocin Inhibits bacterial protein synthesis Infections caused by MRSA (b-lactamase producers), S. Not for ophthalmic use Bactroban 2% oint/cr by binding to isoleucyl transferepidermiditis, S. saprophyticus, GBS, and Strep. pyogenes Burning, stinging, pain, RNA synthetase itch Griseofulvin Non-HIV antifungals Causes shrinkage and stunting of fungal hyphae; inhibits fungal mitosis, binds keratin and has a greater affinity for diseased tissueT (24hr) metaobolized in the liver to 6-methylgriseofulvin and excreted in the kidney CNS occasional headaches, lethargy, confusion, vertigo fatigue, blurred vison SKIN photosensitivity and urticaria GI N/V/D heartburn and gas LIVER hepatotoxic HEMATOLOGIC neutropenia, but basophilia and monocytosis RENAL albumenemia Activates cytP450 decreases activity, ie with BCPs, do not use in PCN allergies Blocks ergosterol synthesis via inhibting fungal cytP450, indicated for superficial (dermatophytosis, candidal and P. versicolor) and systemic Blastomycosis, Histoplasmosis, Aspergillosis fungal infections(refractory to Amphotericin B) DONT USE THIS DRUG too hepatotoxic CHF and ventricular dysfunction (-) cytochrome P450. Contraindicated in pts with CHF and pregnant women Oral allylamineBlocks squalene epoxidase which is necessary for the synthesis of ergosterol. Onycomycosis due to Trichophyton rubrum/ mentagrophytes ONLY. Adverse rx: Severe skin reactions (Steven-Johnson Syndrome) and Cholestatic hepatitis 12% headache, N/V, fatigue. DO NOT GIVE IF PTS HAVE ANY LIVER OR RENAL IMPAIRMEN Fatal hepatotoxicity and Jaundice Systemic oral antifungal. Inhibits fungal cytoP450 sterol C-14 alpha demthylation- disseminated candidal infections (usually seen in pts with DM and renal disease) Has been associated with severe fatal hepatic toxicity; jaundice or simple transient elevations in liver enzymes (-) cytochrome P450. DOCfor cryptococcal meningitis.

Itraconazole (Sporanox) Terbinifine HCL (Lamisil) 250 mg po qd x 12 weeks Fluconazole (Diflucan) 100-400mg po qd Tolfinate (Tinactin) Ketoconazole 200-400mg po qd

Imidazole, impairs the synthesis of ergosterol*, Must run baseline LFTs** Biphasic T , elimination 2 and 8hrs Sytemic fungal infections: Hepatotoxic 1:10,000 may be irreversible, can be fatal and blocks adrenal steroid synthesis with possible gynecomastia Miconazole IV, intrathecal or bladder infusion NOT USED PO Severe systemic fungal infections, Vericonazole IV triazole related to Difulcan Invasive aspergillosis and refractory Scedosporium apiospermum Nystatin Alters PM permeability in bacteriaOral and intestinal candidiasis, Not active against bacteria Amphotericin B Topical (cr, lotion, ointment) and IV only NOT GIVEN PO causes increased permeability of the fungal PM due to binding and interfering with the ergosterol Large number of side effects-anaphylaxis, thrombopenia, flushing, pain, convulsion, chills, fever, phlebitis, headache, anemia, anorexia, decreased renal function Flucytosine Synergistic with amphotericin B Monitor blood levels, hepatic, renal and hematologic values, can cause bone marrow suppression Serious infections of Candida, Cryptococcus (septicemia, pulmonary, meningitis, or UTI *Ergosterol is necessary for the stability of the fungal cell membrane Opiates Allergy to codeine: STUD Stadol, Tolwin, Ultram, Darvon General characteristics of all Opiates Action: o Centrally acting opiod receptor blockade (mu, kappa, and sigma) in the limbic system, thalamus, hypothalamus, mid-brain, medulla, hippocampus, and spinal cord. o Produces sedaton (lethargy, deep sleep, mood changes, euphoria, dysphoria); miosis (except Demerol mydriasis), constipation, N/V, Indications: Moderate to severe pain Contraindications: acute EtOhism, asthma, head injuries, respiratory depression, affects rate of respiration, not depth: use with caution with pts with emphysema, obesity, smokers (>2ppd), anoxia Metabolism: Liver to undergo glucoronide conjugation tachyphylaxis

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Natural Opiate Alkaloids Drug Morphine Sulfate IM/subQ/po/ suppository Codeine (methylmorphine) Description Origin: Papaver Somniferum Pure mu receptor blocker Analgesic and anti-tussive (1015mg) Less tachyphylaxis Dose 10 mg IM q4-6h sub Q; po-MS-contin 15-200mg (less potent due to 1st pass effect) 12-64mg Preparations MSIR (immediate relief) 15 and 30mg tabs and caps q 4-6h MSIR oral solution 10 & 20mg/5ml MSContin (continuous relief) 15,30,60,100,200mg q12h (bid) RMS (rectal MS) 5,10,20,30mg Generally added to drug combinations

Synthetic Derivatives of the Opiates Drug Hydromorphone (Dilaudid) CIII Hydrocodone CII (Vicodin, Lortab) Oxymorphone CII (Numorphan) Oxycodone HCL Percodan/Percocet/Tylox Oxycontin/ Oxyfast CII As compared to others 10x as potent, same analgesia, resp. depression, and anti-tussive effects. Less nausea, constipation, and sedation as MS Less euphoria, resp depression, contipation, N/V, and analgesia than Dilaudid Parenteral only in 1.5mg/ml. Allergy to sulfites, Greater nausea, respiratory depression, and phys dependency than MS or dilaudid 1st codeine derivative that is equal to MS and Dilaudid in analgesia, greater constipation, nausea and phys dependence than dilaudid or vicodin, NSAIDS Dose Moderate to severe pain: 1-2mg IM/subQ or 3.0mg suppost 1-4mg po q 4-6h prn Mild-moderate pain Max dose: 10 mg IM q4-6h Moderate to severe pain 1-1.5mg IM/ rectal suppository q4 prn pain = 10mg MS OxyIR oral caps 5mg (i cap q6h)

Non-narcotic analgesics
1. ASA demonstrates Zero order kinetics ASA Anti-inflammatory, antipyretic, pain,antiplatelet: TIA and MI, and cataract toxemia prophylaxis Analgesic dose: (650mg-2 tablets) 9-18 tablets Fatal dose: 10-30g Headache, muscle aches, fever, pain, caution with barbiturates, hydantoins, rifampin, sulfinpyrazone that slow down APAP metabolism Fever >6mo, mild to mod pain, dysmenorrhea RA, OA (-) PG synthetase Short term tx (<5d) of mod to severe pain (-) PG synthetase and platelet aggregation Centrally acting, binds to opiate receptors, not an NSAID/Opiate NO RENAL TOXICITY Asthma, porphyria, allergy, gastric ulcers Uricosuric effects: low doses increase plasma acid urate gout, whereas high doses are uricosuric S/S of toxicity tinnitus, headache, dizziness, hyperventilation, N/V, diarrhea, acid-base imbalance due to salicylate stimulation of the respiratory center of the medulla hyperventilation respiratory alkalosis, drug interaction as ASA is highly protein bound Ethoism, allergy Adverse reactions: glossitis, skin rash, Toxicity: Hepatotoxic at 10-15g (30-46 tabs) Antidote Mucomist (acetylcystine) Fatal dose: 25g Allergy to ASA, gastritis, bleeding, perforation. Renal toxicity (papillary necrosis) Can use with coumadin May combine w/ narcotics not with other NSAIDS interstitial nephritis, renal failure, hyperkalemia, death, and resp. depression pregnancy, MAOIs Seizure risk increased, alcoholics, & w/ CNS depressants or respiratory depression. Causes an (-) of NE, 5Ht uptake antidepressant
30 min

APAP

3-4 hrs

Ibuprofen-OTC Ketorolac Tro-methamine Tramadol HCL Ultram Rx 50mg tabs

2 hrs

Nonsteroidal Anti-inflamamtory Drugs (NSAIDS) 1. 2. 3. 4. 5. 6. 7. An important MOA of NSAIDS is(-) histamine release from mast cells (-) COX 1 (-) Thromboxane formation in platelets to interfere with aggregation (-) COX 2 (-) Prostacyclin production in the endothelium Ketoprophen (Orudis)and Diclophenac (Voltaren) also block the LIPO pathway (-) LTB4 pain mediator NSAIDS are all weak acids Classic triad of NSAID OD nasal polyps, asthma and allergic rhinitis Inhibition of PGE2 reduce renal Q, decr GFR and Na and H2O excretion, increase renin release interstitial nephritis,

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8. Gastric mucosa injury is due to (-) of the cytoprotective PGE1. 15-20% will develop symptoms of gastric upset 9. Etodolac (Lodine) Nabumetone (Relafen), Sulindac (clinoril) are the least GI toxic. 10. Which NSAID causes peripheral neuropathy Fenoprophen Acetylsalicylic Acid Description Salsalate (Disalclid) long T1/2 insoluble in stomach, absorbed in SI safer w/PUD patients, Choline Magnesium Trisalate Allergy, use w/caution in renal failure, erosive gastritis or PUD, does not affect platelet aggregation, (Trilisate) can be used on someone taking coumadin Diflunisal (Dolobid) (not indic for gout) Propionic Acid derivatives little antiplatelet effect; less GI upset = 2, do not combine with ASA Fenoprophen Ca(Nalfon) Anti-inflammatory potency = ASA, shortest T1/2 (2 hrs)Can cause peripheral neuropathy Ibuprophen(Motrin, Ruffin) T 1/2 (2-3hr) Alopecia, More nephrotixic tid, Lowest mucosal injury Naproxen (Anaprox) Longer T 1/2 (12-15 hrs) can be used in kids juvenile RA. Naproxen induced hepatitis can give to pts w/ renal failure Ketoprophen(Orudis, Oruvail) Not a good NSAID, better for pain Oxaprozin (Daypro) Slow onset but longer duration: T (42-50hrs)Weakest, good for OA and long term tx Indole derivatives KNOW Indomethacin(Indocin) Renal sparing drug Potency is 10-40x ASA Sulindac (Clinoril) Prodrug, not active until metabolized in the liver into sulfide Renal sparing drug Little GI (=1) Tometin sulfate (Tolectin) potency > ASA, less than indomethacin and Butazolidin Children with RA Pyrazolon Derivatives-Most hepatotoxic, GI toxicity = 4 Phenylbutazone(Azolid) long T 1/2 50-100 hours Aplastic anemia, agranulocytosis Oxyphenbutazone(Tandearil) Metabolite of phenylbutazone, long T 1/2 (several days) Phenyl Methanthrine Deriv Meclofenemate Na (Meclomen) GI toxicity = 3, takes three weeks to see therapeutic results Mefanamic Acid (Ponstel) Anti-inflammatory potency = 1.5x phenylbutazone; GI toxicity = 1, well absorbed with half-life of 3-4 hours. Oxicams Piroxicam (Feldene) Long T1/2 (30-86hrs), 3-5 hrs to reach peak plasma level; highly protein bound GI toxicity = 3, excretion entirely renal Phenylacetic Acid Derivatives Diclofenac Na (Voltaren) Peak plasma levels in 2-3 hrs (long onset), T1/2 (2hrs); blocks the LTB4 pathway good analgesic and mod potent anti-inflam. Renal Sparing Drug GI toxicity = 2 Hepatotoxic, run LFTs Diclofenac Na/ misoprostol (Athrotec) Combination of Voltaren and misoprostol (PGE1) Cytotec will cause spontaneous abortions Diclofenac K (Cataflam) Fast-acting, immediate release with peak plasma levels in 1 hour. Indicated for acute trauma Etodolac (Lodine) intermediate half-life (7hrs) Analgesic equivalence: GI ulceration with toxicity = 0-1 Renal: papillary necrosis, NaphthylkanoneProdrug, long serum half-life (20-30hrs); GI toxicity = 0, moderate potent anti-inflammatory; preferential COXNabumetone (Relafen) 2 inhibitor, 99% protein bound not for acute inflammation b/c a very high dose is needed COX-2 inhibitors MOA Indications Contraindications Celecoxib (Celbrex) Blocks the inducible COX 2 enzyme at sites OA and RA Not a good analgesic, most common SE are nausea, of inflammationdoes not affect platelet dyspepsia and diarrhea Allergy to sulfonamides, or aggregation or bleeding time ASA asthma, urticaria Rofecoxib (Vioxx) Better analgesic than celebrex, about as OA, acute pain Asthma, urticaria, or allergy to ASA, do effective as ibuprophen and naproxen dysmenorrhea not give to children Meloxicam (Mobic) Similar to above OA Asthma, urticaria, or allergy to ASA Vadecoxib (Bextra) Good analgesic, anti-inflammatory, as RA, DTJ, OA BEST effective as naproxen dysmenorrhea

Laboratory Medicine Revisited

Serological Evaluation Clinical Laboratory Medicine is important to appreciate that a diagnosis is not made on labs alone, however, once a differential impression is made, labs often act to confirm or rule out a specific disease entity. A vast majority of these studies have their basis deeply routed in many of the major biochemical pathways in the body. A general understanding of the processes unique to different cell types and organ systems is essential. I. Liver Function Tests intrahepatic disease or damage to hepatocytes can be evaluated with serum enzymes - LDH, SGOT/AST, SGPT/ALT and GGT as well as the prothrombin time (production of the vitamin K dependent clotting factors.)

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Tests for Intrahepatic damage Clinical Significance LDH -- Lactate Dehydrogenase * normal concentrations of LDH isomers in the blood is in descending order: *found in many tissues mainly - liver, kidney, LDH2 > LDH1 >LDH3 >LDH4 >LDH5 - almost exclusively in liver hepatocytes. Increase myocardium and muscles, facilitates the intrahepatic damage LDH1/LDH2--Both LDH1 and LDH2 associated w/ the myocardium. In the conversion of lactic acid (the end product of normal, healthy heart, there is prevalence of LDH2 >LDH1; following a MI damaged tissues anaerobic glycolysis) to pyruvic acid * LDH1 release LDH1 into the bloodstream disrupting the normal ratio between the two. A LDH flip and LDH2 - very high in myocardial tissue and occur, LDH1 > LDH2. LDH1/LDH2 ratio normally < 1(~0.5 to 0.75), becomes > 1- useful RBCs, LDH5 - very high is skeletal muscle aid in the diagnosis of MI; occurs in over 95% of patients with an acute MI; Other causes & liver; total circulating LDH levels increase in false flip - hemolytic anemia, megaloblastic anemia, pernicious anemia (erythrocyte any disease process resulting in cell destruction disorders), renal disorders & some muscular dystrophies, congestive heart failure (CHF) Ubiquitous enzyme may have LDH1 & LDH5 d/t the right heart back-up" into the liver hepatomegaly d/t increased venous pressure SGOT - Serum Glutamate Oxaloacetate Transaminase/ AST-Aspartate Aminotransaminase enzyme is present primarily within the mitochondria of body tissues esp liver and heart; responsible for the transamination reaction between aspartate and alpha-ketoglutamic acids in amino acid catabolism; reaction requires pyridoxine (Vitamin B6) Can be used to determine liver damage d/t ETOH * liver - SGOT elevates with hepatocyte damage; markedly elevated w/ hepatitis and other chronic liver diseases; cirrhotic liver- SGOT levels may be elevated 2-fold > SGPT b/c alcohol is more directly toxic to mitochondria; *an SGOT (AST)/ SGPT (ALT) ratio > 2:1 strongly suggests alcholic liver damage *cardiac - SGOT is released into the plasma with myocardial damage; elevation of AST in conjunction with other cardiac components (CK, LDH flip and troponins) are consistent with myocardial injury *Hepatic - SGPT parallels SGOT w/ liver damage except in the case of alcoholic liver disease; rises in the aminotransferases (ALT) parallel the extent of hepatocellular damage; ALT rises earlier & higher than AST *Cardiac - SGPT elevate w/ acute myocardial infarction, not to the extent of SGOT & is not used as a marker for MI's

SGPT -- Serum Glutamate Pyruvate Transaminase/ALT - Alanine Aminotransferase *enzyme catalyzes the amino group between alanine and alpha-ketoglutamic acid. much more specific for liver damage than AS; present primarily in the cytosol of the hepatocytes Gamma-Glytamyl Transpepidase - GGT Liver - is a microsomal enzyme induced by alcohol and particularly sensitive in detection of large amt present in the renal tubular epithelium chronic alcohol consumption; a good marker for and is significantly elevated in hepatobiliary and in the liver disease - obstructive jaundice and infiltrative disease of the liver Renal GGT does not serum or liver;monitored in urine to assess specific renal tubular damage

Name LDH1 LDH2

Composition HHHH 17-27%

Main Location

Elevated mainly in: myocardial infarction, hemolytic anemia megaloblastic anemia, muscular dystrophy Myocardial infaraction, carcinomatosis, myelocytic leukemia, hemolytic anemia, muscular dystrophy myelocytic leukemia, pulmonary infarction Pancreatitis, carcniomatosis Hepatitis, congestive heart failure, Kidney pulmonary infarction, cirrhosis Hepatitis, congestive heart failure, Pulmonary infarction, cirrhosis GGT 2-65 IU/L

Myocardium, red blood cells Myocardium, red blood cells, Brain Brain, kidney, lung Liver, skeletal muscle, brain, Liver, skeletal muscle

HHHM 27-37%

LDH3 LDH4 LDH5

HHMM 18-25% HMMM 3-8% MMMM 0-5%

Summary of Reference Values of Liver Enzymes

LDH 38 - 62 U/L SGOT/AST 11-32 IU/L SGPT/ALT 3-30 IU/L

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II. Extrahepatic Liver Damage Elevation of alkaline phosphatase, bilirubin and cholesterol suggest the presence of extrahepatic disease, notably biliary obstruction. Enzymes Clinical Significance Alkaline Phosphatase/ALP *two isoenzymes:- 1)present in the liver which is heat stabile and 2)the other in bone which is heat labile at 56%C (bone burns) and heat fractionation is actually used to help identify the source of AL; enzyme most often measured to indicate bile duct obstruction *enzyme functions to remove phosphate groups from proteins and other molecules; degree of phosphorylation of biologic compounds responsible for their own inherent activities (as enzymes) or structural interactions with other molecules (as in membranes) * high levels of ALP present in rapidly dividing or otherwise metabolically active cells Bilirubin overall increase in serum bilirubin is indicative of biliary * bilirubin - derived primarily from the catabolism of hemoglobin - & also a disease breakdown product of myoglobin, cytochromes, catalase and eroxidase *elevation in direct (conjugated) biliary obstruction. *reaction occurs w/i Kupffer cells of liver utilizing the cytochrome P-450 enzymes to d/t lack of serum albumin, RBC hemolysis, hepatitis and breakdown heme biliverdin bilirubin Gilberts symdrome *in normal healthy individual, the serum has small amount of (indirect) *elevation of indirect (unconjugated) hepatocyte unconjugated bilirubin d/t hemolytic processes, but no(direct) conjugated bilirubin damage or in hemolytic anemiasd.t lymphoma (DC: direct:conjugated) the van den Bergh test is used to differentiate b/t direct and *transported in an inactive form bound to albumin. When there is a lack of albumin indirect bilirubin or an excess of bilirubin (e.g. from hemolysis), free bilirubin levels build up in the *normal elevation of bilirubin may occur in patients with body; free or indirect bilirubin diffuses freely through the blood-brain barrier & Gilberts syndrome elevation in unconjugated, indirect body tissues (yellow discoloration) jaundiced patient - kernicterus bilirubin d/t a transport defect in the sinusoidal membrane *for excretion, bilirubin is conjugated to bile in liver; free bilirubin through of the hepatocyte; condition exacerbated by fasting; fenestrated sinusoidal membrane hepatocytes conjugated w/ glucuronic acid hemolysis benign elevation of unconjugated indirect bile canaliculi excreted in feces; this is referred to as "conjugated" direct bilirubin bilirubin Summary of Reference Values of Liver Enzymes that determine extrahepatic liver damage ALP bilirubin 0.1 - 1.2 mg/dL 25-165 Cholesterol: cholesterol is synthesized in all body tissues, but in higher amts within the liver; made from precursor, acetyl-CoA and undergoes a lengthy process resulting in the four ring compound; synthesis is regulated by the intake of exogenous cholesterol a biofeedback at the synthetic level of HMG CoA reductase (beta-hydroxy-beta-methyglutaryl reductase) step; abnormalities in cholesterol are considered to be nutritional or genetic, but liver function may be a factor Hyperlipidemia: National Cholesterol Education Program (NCEP) proposed treatment goals based on levels of low-density lipoprotein (LDL) cholesterol recommendations - evaluate total cholesterol and high-density lipoprotein (HDL) cholesterol levels in all adults 20 yrs & older increasing importance is assigned to the HDL levels b/c of its protective function treatment decisions - based on the LDL levels, however, HDL levels should be considered in selecting drug therapy patients with triglyceride levels greater than 1000 mg/dL should generally be treated to prevent the risk of pancreatitis guidelines used to assess the risk of coronary heart disease include: Serum cholesterol desirable level <200mg/dL LDL/HDL ratio low risk 0.5-3.0 borderline risk 200-239 mg/dl moderate risk 3.0-6.0 high risk >240 mg/dl high risk >6.0 High density lipoproteins low risk >60 mg/dl Cholesterol/ low risk 3.0- 4.4 moderate risk 35-60 mg/dl HDL ratio average risk 4.4-7.1 high risk <35 mg/dl moderate risk 7.1-11.0 high risk >11.0 Low density lipoproteins desirable level <130 mg/dl Serum triglycerides 10-190 mg/dl borderline risk 130-159 mg/dl high risk >160 mg/dl

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Renal Function Tests

Clinical Significance

BUN - Blood Urea Nitrogen Iincreases With severe renal disease the upper limit of acceptable BUN is urea is the end product of amino group removal" in the very narrow; degradation of amino acids; urea cycle occurs in liver urea is Elevations of - 25 or (25%) of nephrons are already seriously released into the blood stream freely filtered by the glomerulus mg/100ml damaged (normal is 8-22mg/dl) and d/t concentration diffuses back into the loop of Henle intraelevation in serum BUN Classic glomerular injury renal cycling *the ratio of reabsorbed urea:secreted urea (60^% decrease Severe liver damage & reflects the liver's decreased ability to reabsorbed: 40% secreted); urea is not an ideal index of in BUN synthesize urea. This is seen with poisoning and hepatitis (drug glomerular function b/c there are many non-renal events that affect or virally induced). its concentration Creatinine Creatinine used as an indicator of Creatinine is most sensitive indicator of glomerular filtrationend product of creatine metabolism; glomerular filtration and dosing of creatine-PO3 is the storehouse" w/in muscle which provides additional ATP; released when creatinemedication cleared renally. Creatinine Cockroft/Gault Equation: Basically this secreted. It is a nearly ideal biologic product to measure glomerular filtration rate. normal BUN:creatinine ratio is approximately 10:1 ratio increase >15:1 pre-renal pathology, reduced equation is used to determine the dose of muscle mass, compromised renal function; high-protein diet, tissue destruction & myopathies drugs in those individuals with renal failure assoc w/ Cushings syndrome, compartment syndrome Cystatin-C** NEW proposed as an endogenous serum marker for early assessment of changes in glomerular filtration; a basic low molecular mass protein with Normally cystatin C is not found in detectable levels in excreted urine; elevated levels correlate with 120 amino acid residues; freely filtered by decreased glomerular filtration rate; more reliable marker than serum creatinine which may be glomerulus & almost completely reabsorbed misleading in the obese, elderly & malnourished patients; remains unchanged by pregnancy, time of day ; catabolized by the proximal tubular cells (diurnal variation), infection, and neoplastic states; not affected by body mass, diet or drugs, sex or acute inflammatory states Uric Acid- end product of purine (adenine and guanine) nucleic acid metabolism Not a useful indicator of any renal function; serum uric acid levels excreted via the kidney and transported in an inert form bound to albumin. Free have direct correlation to precipitation of uric acid crystals in urate is filtered by the kidney, secreted and resorbed joints. National Kidney Foundation recommendations for classification of kidney disease based on glomerular filtration rate together S Description GFR tage 1 Normal or Increased GFR >90 mL/min/1.732 2 Mildly decreased GFR 60 - 89 mL/min/1.732 3 Moderately decreased GFR 30 - 59 mL/min/1.732 4 Severely Decreased GFR 15 - 29 mL/min/1.732 5 Kidney Failure <15 mL/min/1.732 Clinical Significance or uric acid Of all arthritides, gout has the highest predilection for the joints of the foot. Statistically, 90% of all acute gouty attacks involves (1) first metatarsal phalangeal joint (aka podagra) & 15% >1 foci of involvement; (2) soft tissue & (3) the ankle joint; gouty arthritis can occur in any joint of the body; so if you see red, hot, swollen 4th MPJ still think gout or joint sepsis; primarily a male disease, only 5% in females b/c Estrogens play a protective role preventing the precipitation of gouty crystals; gout attacks the foot and tophi forms on ear lobes b/c at lower temperatures uric acid is less soluble; Solubility of uric acid - 37 C - 6.8 mg%; 30C - decreases to 4.5 mg%;Temperature of the normal ankle joint - approx 29C .: crystalization occurs more readily. Positive joint aspiration yielding uric acid crystals positive diagnosis of gout; on light microscopy - see a needle-like crystal piercing WBC. With a color compensator, the crystal appears negatively birefringent, i.e. Visualization of these crystals is required for the absolute diagnosis of gout. recent evidence suggest that elevated serum uric acid levels in middle aged men strong predictor of future cardiovascular death; levels in upper 1/3 had a >2.5 fold increased risk of death from cardiovascular disease; why uric acid appears to correlate with cardiac death is unclear, it may simply circumstantial or a result of processes leading to cardiovascular injury PO3 is utilized by the muscle; is filtered completely by the kidney, it is not reabsorbed & only a trace alter the dose of drugs.

IV.

Electrolytes
Hyper / Hypo Hyponatremia - serum sodium is 135 mEq/L vary from subtle changes in mentation to profound neurologic abnormalities including generalized convulsions; causes: over hydration triad of low serum Na, low hematocrit and low BUN, diuretics , secretion of inappropriate levels of ADH2.o to CNS diseases, trauma and neoplastic conditions; adrenal failure; aldosterone deficit prevent reabsorption Na-K and Na-H exchange in the distal convoluted tubules Hypernatremia seen in excessive loss of water to sodium or increase in total Na extra-renal profuse sweating and diarrhea - especially in children; renal losses d/t osmotic diuresis, ie diabetes insipidus

Ion Sodium (Na) *major cation in extracellular fluid & principal osmotic particle outside the cell; freely filtered at the glomerulus - 70% of the amount filtered is reabsorbed; changes in extracellular sodium concentration increases or decreases in the osmolality of the extracellular fluid which will affect the distribution of body water

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Potassium major intracellular cation - only 2% of total body potassium is extracellular; *elevated & depressed serum potassium may have profound effects on the neuromuscular system apathy, weakness and paralysis *myocardial effects serious arrhythmias

hypokalemia can occur when total amount of K in the body is normal; movement from extra intracellular fluid occurs in akalemia and insulin therapy.Causes: serum levels become depleted; loss of gastrointestinal fluid d/t vomiting/diarrhea, renal losses most commonly d/t diuretics;the presence of U-wave on EKG is suggestive of hypokalemia - this is an upright wave at directly follows the T-wave hyperkalemia occurs in acute and chronic renal failure; prevent artifactual hyperkalemia by collecting specimen in a heparinized tube prevent the release of K from the platelets as clotting occurs; a hemolyzed specimen elevate the serum potassium secondary to the high concentration of potassium within RBCs d/t hemolysis Peaked T-waves on the ECG Chloride major extracellular anion Hypochloridemia: gastrointestinal losses, diabetic ketoacidosis, mineral-corticoid excess, *slight post prandial depletion of serum chloride 2o to salt-losing renal diseases, compensated respiratory acidosis, and metabolic alkalosis secretion of hydrochloric acid by the parietal cells of hyperchloridemia 2o to losses from the lower gastrointestinal tract in diarrhea; renal the stomach during digestion tubular acidosis and mineral-corticoid deficiency & some hyperPTH Total CO2: formation of CO2 during metabolism dissociation of H2CO3 production of HCO3 reabsorbed by the proximal tubules; total CO2 determinations, pH and PCO2 measurements in evaluation acid-base disorders and the management of acute MIs

Anion Gap
normal value - 12-18 meq/l in adults Normal Anion Gap = [Na+ + K+] - [Cl- + HCO3-] increased ( >17 mmol/l) - indicates significantly increased concentrations of unmeasured anions; 2o to uremia, ketotic states e.g. diabetes, alcoholism or starvation, lactic acidosis; ingestion of toxins - methanol, salicylate, ethylene glycol; increased plasma proteins as with dehydration decreased anion gaps (<10 mmol/l) occur from Li+ intoxication, hyperMgt, multiple myeloma, polyclonal gammopathy and polymyxin B therapy Serum Proteins: All are synthesized in the LIVER Protein Clinical Significance Total Serum Protein: serum protein - made up primarily of globular proteins comprised of albumin low serum protein (approx. 55-60% & H20 soluble); the globulins which include the immunoglobulins, lipoproteins, causes: failure of the liver hepatocytes fibrinogen, hemoglobin, the cytochromes and most cellular enzymes; serum proteins - readily available to synthesize adequate serum proteins, a source of stored protein that can be catabolized in starvation, provide insight into a patients nutritional leaky" glomerular filtration apparatus status. Functional uses: important plasma buffers d/t free carboxyl and amino groups; necessary for proteins filtered through the maintenance of plasma oncotic pressure; depletion of plasma proteins fluid loss into the interstitium podocytes or basement membrane. renal release of angiotensin increased aldosterone and ADH creating additional fluid retention. Albumin*plasma albumin concentration is important for the same decreased serum albumin - indicates decreased ability of the liver to synthesize physiologic reasons as serum protein, has a large body pool and a albumin or an increased rate of albumin excretion due to damage of the glomerular half-life of 20 days; albumin has more specific role in the blood filtration apparatus good marker of the severity of chronic liver disease; good acting as transport protein for many things carried" by albumin indicator of a patients overall nutritional status but it is relatively insensitive to include, uric acid, Vit C., fatty acids, bilirubin, numerous short term changes in nutritionhypoalbuminemia ascites and expanded antibiotics, including tetracycline, the penicillins, and sulfa drugs, plasma volume; serum concentrations affected by the patient's hydration and renal aspirin and many of the sedative hypnotics function; when pool is depleted, it takes 14 days to return to normal Prealbumin preferred marker for protein malnutrition *less affected by * prealbumin production decreases after 14 days of consuming a diet that liver disease than other serum proteins a distinct marker for protein provides only 60% of required proteins; with nutritional supplementation, synthesis b/c liver production will be maintained until late-stage liver prealbumin levels should rise 2 g/dl/day; prealbumin levels are not disease so can be measured & monitored *hydration status does not affect accurate in acute alcoholics. If serum albumin < 3.5 order a prealbumin levels Prealbumin** TQ Serum Transferrin Causes for increase TIBC: iron deficiency anemia, pregnancy, oral transferrin - half-life is about 1 wk respond more quickly to changes in contraceptives and possibly hepatitis nutritional status & is desirable marker; determined by 2 site enzyme serum ferritin - sensitive indicator of iron deficiency; increase with many immuno-assay; measuring total iron binding capacity is equivalent to chronic disorders, including inflammation, infection, viral hepatitis and measuring transferring total iron binding capacity (TIBC) is determined malignancy. by saturating transferrin with iron, removing the unbound iron and then Causes for decreased TIBC: reduced protein synthesis, nephrosis or other measuring the iron in the infiltrate direct loss; increased catabolism (secondary to malignancy or starvation).

V.

VI.

Bone Metabolism Tests

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Tests commonly ordered - alkaline phosphatase, serum calcium and serum phosphorus. Serum calcium and phosphorus levels are dependent greatly on the level of circulating parathyroid hormone.

Tests
Alkaline Phosphatase * released by osteoblasts when they are actively secreting bone matrix *diffuses freely into the bloodstream and elevated levels may be indicative of osteoblast activity

Clinical Significance
pronounced elevation (5x or more) will occur in bile duct obstruction, biliary cirrhosis, osteitis deformans (Pagets disease), osteogenic sarcoma and hyperparathyroidism moderate elevation (3-5x normal) can occur in, granulomatous or infiltrative diseases of liver, infectious mononucleosis, metastatic tumors in bone, metabolic bone diseases (rickets, osteomalacia) slight elevation (up to 3x normal) can occur in viral hepatitis, cirrhosis, healing fractures, pregnancy and normal growth patterns in children hypocalcemia - secondary to aklalosis, renal failure & hypoparathyroidism hypercalcemia - secondary to acidosis and "CHIMPS" - cancer, hyperthyroidism, iatrogenic causes, multiple myeloma, parathyroidism and sarcoidosisTQ hypercalcemia depressed neuromuscular excitability with anorexia, drowsiness, nausea, polyuria and
polydipsia (increased urine flow & increased thirst) d/t high calcium levels which affect the kidneys ability to concentrate urine (i.e. increased calcium levels lead to increased urinary excretion of more dilute urine).

Calcium most abundant cation calcium & phosphorus are considered together in routine clinical evaluations; The kidneys are important in the regulation of calcium; with renal failure- calcium levels fall & phosphate levels rise

Phosphorus these ions are in flux continually controlled by the action of parathyroid hormone ( vitamin D and calcitonin) PTH elevates calcium levels by increasing the resorption of calcium from bone and suppressing loss into the urine, vitamin D decreases Calcium levels by promoting its absorption by the intestine and accelerates turnover of the minerals in bone; phosphorus is necessary for every insulin-mediated transfer of gl- into a cell

Elevated serum phosphorus - healing bone fracture & some bone tumors. Severe hypophosphatemia - DM d/t renal manifestations o (DM Ketoacidosis)

VII.

Evaluation of Muscle
Clinical Significance cardiac elevations - if the CK-MB band is elevated during the 48 hours post event and the LDH isoenzyme pattern is flipped, a reliable diagnosis may be made rises in the serum within 2 to 8 hours of an acute MI; serial measurements taken q2-4 hrs for 12hrs after the onset of symptoms will be indicative of myocardial injury if values are increasing;

Tests Creatine Kinase:elevations occur with any type of muscle damage; CK enzyme levels first to elevate in acute injury; muscular dystrophies - serum CK elevates as much as 200-fold (normal being 0-12 units/ml); three isoenzymes: = BB or CK1 - high percentage in the brain - ~90% MB or CK2 - about 20% in cardiac muscle MM or CK3 80% in cardiac muscle; exists in a high % in skeletal muscle - 99% - the remaining small percentage is in the MB form. Pathological Increases MB isoenzyme - w/ myocardial injury & muscular dystrophy - 15 to 40%;** MM isoenzyme - elevated with skeletal muscle injury BB isoenzyme - seldomly encountered clinically; associated w/ brain necrosis, large intestine necrosis and Reye's syndrome

normally, CK will drop within 1 - 3 d following the incident; if values stay elevated - indicative of reinfarction or extensive myocardial damage myoglobin found in both skeletal and cardiac muscle; very sensitive indicator of muscle injury; rise in myoglobin will elevate even before the CKMB circumstantial evidence as skeletal muscle injury will also cause it to elevate troponin I structural components of cardiac muscle; highly specific for myocardial injury; begin to increase w/i 3-12 hrs after injury; troponin I and T remain elevated for 5 - 9 d; troponin T - remains elevated for up to 2 wks; continued elevation make them of little value in reinfarction Aldolase becomes elevated - following skeletal muscle disease or injury; secondary to metastatic carcinoma (especially liver), glycolytic enzyme granulocytic leukemia, megaloblastic anemia and hemolytic anemia; B/c of a wide range elevating factors it is not useful involved in the except for the evaluation of inflammatory disease of the muscle (e.g. dermatomyositis Grotons lesions) & are elevated metabolism of glucose early in pts who later develop muscular dystrophy; An increase in CK-MM with aldolase is indicative of skeletal muscle distributed in all tissues injury ** Elevations of the MB band are consistent with cardiac injury even though there is more of the MM band in cardiac tissue. The MB isoenzyme is "more unique" to cardiac muscle than any other tissue type. **characteristic pattern of elevation of serum markers associated with myocardial disease** TIMELINE 024 hours 24-days troponin levels peak at 72 hours & remains elevated for 10-14 days; but high levels of troponin (w/i 24hrs) and CK(w/i 2-8 hrs) are extent of elevation is not as striking as AST- the second enzyme to rise earliest to rise after myocardial injury pattern of normal AST and elevated LDH within 1-2 days after an episode of the LDH flip occurs where levels of LDH1 > LDH2 ; occurs chest pain suggests pulmonary infarction within 12-24 hrs and is present w/i 38 hrs in 80% of patients

VIII.

Evaluation of Pancreas

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Amylase 2 major sources & exists as 2 isoenzymes - pancreatic or P-form & salivary or S-form acute pancreatitis serum level elevate 4-6x above normal; rise within 6 - 24 hrs & return to normal in 48 - 72 hrs despite continued presence of pancreatic disease; no correlation b/t severity of the disease and the amount of amylase elevation; elevations in serum amylase - almost always secondary to pancreatic sources; o morphine elevation in serum pancreatic amylase o bone marrow ablation and exposure to nuclear reactor accidents (i.e. 2o to ionizing radiation) elevation of salivary amylase pronounced elevations in amylase (>5x normal) occur with acute pancreatitis, pancreatic pseudocyst and the administration of morphine moderate elevations in amylase (3-5x normal) occur with pancreatic carcinoma, mumps or a salivary gland infection and with a perforated peptic ulcer

Lipase elevated serum lipase is diagnostic for acute pancreatitis almost exclusively in the pancreas; technically more difficult measure than amylase which is why amylase is ordered more commonly; not cleared by the urine and remains elevated in the serum much longer than amylase an elevation in serum lipase may occur following the administration of heparin as a result of the release of lipase from the vascular endothelial membranes

IX. Evaluation of Serum Glucose * The ambient temperature at which the blood sample is kept will affect the rate of glycolysis; refrigerator temperatures - glucose will remain stable for several hours; room temperatures - loss of 1-2% of glucose per hour Use fluoride-containing (gray top) tubes which inhibit glycolysis to circumvent this problem Fasting Plasma Glucose: the best indicator of overall glucose homeostasis and the best screening test for diabetes; fasting - no food or beverage for 8 hrs before testing; diagnose diabetes by fasting plasma glucose - above 126 mg/dl (7mmol)on 2 or more occasions; blood glucose finger stick utilized for easy monitoring; drugs - glucocorticoids and nicotinic acid hyperglycemia Casual Plasma Glucose above 200 mg/dl (11.1 mmol) - pathognomonic of diabetes mellitus; when elevated, a fasting plasma glucose or glucose tolerance test should be performed on a different day Oral Glucose Tolerance Test: Diagnostically useful when fasting or postprandial blood levels are equivocal; useful if there is a good reason to suspect diabetes eg. an obese pt w/ a + family history or in pt w/ unexplained vascular, neurologic or infectious illness; standard glucose load should be 75 grams; baseline blood glucose is taken and the glucose load is administered; 2 hrs after the load, plasma glucose should return to the fasting level ; persistent elevation at two hours is abnormal mild elevation at two hours but return to normal at three hours suggests slightly impaired glucose metabolism but not overt diabetes; Advancing age declines in speed of glucose clearance; in a non-diabetic patient with a negative family history, levels routinely elevate 6 mg/dl for every decade over 30 years of age. Glycosylated Hemoglobin - A1C test: test is a valuable tool in monitoring glucose control; the beta chain of Hb acquires & irreversibly binds a glucose moiety when plasma glucose levels are elevated resulting in "glycosylated" Hb; glycosylation does not affect O2 carrying potential but it does reflect periods of glucose control in the preceding two to three months; normal individuals have 3 to 6% of their hemoglobin glycosylated in the form of A1c; HbA1c levels >10 signal necessity for better glucose control; Test should be done q3mths Glycosylated Albumin NEW, check more short term glucose control (window into the past 2 weeks) b/c albumin has a serum T1/2 in the circulation of about 17-20d, amt of glycosylated albumin reflects hypergl- periods w/i the previous few wks; < 8% may be normally glycosylated Diagnosis of Diabetes Mellitus Fasting glucose: >126 mg/dl - diabetes o 100 - 126 mg/dl - glucose impaired o <100 mg/dl - normal Casual glucose: >200 mg/dl on two separate occasions plus symptoms of diabetes Glucose tolerance: >200 mg/dl two hours after a 75 gram glucose challenge - diabetes o 140 199 mg/dl two hours post challenge glucose impaired o <140 mg/dl normal

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Other Test C-peptide Measurements: the secretory rate of C-peptide to insulin is 1:1; however, the ratio in serum is 5-15:1; 50% of insulin is removed on its initial passage through the liver, however, hepatic removal of the C-peptide is negligible; measured at times to evaluate the residual function of the islet cells in the pancreas; diabetics w/ no residual islet function are considered to be "brittle" and are frequently quite difficult to control; Brittle diabetics produce no insulin Normal to high levels Type 2 and absent to low levels Type 1 C-Reactive Protein CRP: an acute phase reactant; demonstrates a rapid rise in response to acute disease and a rapid clearance once the stimulus has abated most sensitive indicator of inflammation regardless of etiology and a useful marker in the evaluation of the efficacy of empiric therapy with infectious diseases & recently, CRP levels have been used as a screening tool for future coronary events levels should decrease if risk decreases; currently, there is no definitive guidelines for ascribing risk categories, however, widely acceptable values are: CRP levels < 1 mg/L low risk CRP levels from 1-3 mg/L average risk, and CRP levels > 3 mg/L high risk Homocysteine plasma homocysteine is a useful predictor of CV morbidity and mortality; elevated levels atherosclerosis via: damage to the arterial intimal cells via direct toxicity; interference with clotting factors & oxidation of low density lipoproteins; blood is drawn after a twelve hr fast normal: 5 15 mol/L moderate risk 16 30 mol/L intermediate risk 31 100 mol/L severe risk > 100 mol/L Complement Measurements C3 reference values: 75 - 175 mg/dl; C4 reference values: 14 - 45 mg/dl *most abundant complement proteins in the serum; consists of a series of proteins that work to "complement" the work of antibodies in destroying bacteria; circulate in the blood in an inactive form; *levels of serum complement proteins can be related to autoimmune disease activity low levels indicate depletion of complement proteins secondary to their activation Ag-Ab reactions, colleen vascular and c.t. diseases normal or high levels indicate disease regression or response to therapy Carcinoma and Ulcerative colitis Synovial Fluid Analysis Joints normally have small amt of synovial fluid & depends on the size of the joint; normally b/t 0.1 - 3.5 ml unless there is a joint effusion; the fluid collected using aseptic technique and placed in a sterile, heparinized tube (green top) or EDTA; the use of other anticoagulants may cause artifacts during microscopic analysis examination for the presence of microorganisms and crystals is the most critical part of the analysis; most findings are non-specific and can be found in a number of disease entities; fluid is inspected for viscosity, color and appearance Microscopic examination - total number of cells present, the type of cells and the presence and type of crystals Chemical analysis - mucin clot test, synovial fluid glucose and protein determinations, and immunologic studies (rheumatoid factor, antinuclear antibodies, complement,etc.) Microbiologic studies, including a Gram stain and cultures

Surgery, anesthesia, hospital protocol

A. General Anesthesia-a reversible state of unconsciousness produced by anesthetic agents, with loss of sensation of pain over the whole body. The order of descending depression of the CNS during anesthesia is: cortical and psychic centers basal ganglia and cerebellum medullary centers spinal cord TRIAD OF ANETHESIA: UNCONSCIOUSNESS, ANALGESIA AND MUSCLE RELAXATION
Class 1 Class 2 Class 3 Class 4 Class 5 E ASA classification for Anesthesia Normal Healthy-no known diseases Mild Systemic Disease Severe systemic disease (not incapacitating) Incapacitating Systemic disease (is a threat to life) Moriboud patient who is not expected to live with or without surgery Emergency Operation

Anesthesia staging Stage 1-Amnesia and analgesia -plane 1: preanalgesia, memory and sensation intact -plane 2: partial amnesia and analgesia -plane 3: total amnesia and analgesia Stage 2: Delirium

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-unconsciousness, mydriasis, irregular breathing, involuntary movement Stage 3: Surgical anesthesia -plane 1: Sleeping, faint lid reflex, eyeball centrally fixed, regular breathing -plane 3: partial intercostal paralysis, tachycardia, hypotention, hypotonia -plane 4: complete intercostal paralysis and respiratory arrest, requires artificial ventilation Stage 4: Medullary paralysis, respiratory and cardiac failure -plane 1: Reversible respiratory paralysis -plane 2: Irreversible cardiovascular and respiratory arrest Malignant hyperthermia- a condition characterized by acute idiopathic muscle over activity and increases in oxygen demand. The skeletal muscle goes into spasm, and the first signs are: Tachycardia Tachypnea ventricular arrhythmias Acidosis Sweating Arrhythmia Cyanosis Hypoxemia Muscle rigidity fever (late s/s/) Hyperkalemia Causes: Reduction of Ca uptake by the SR necessary for cessation of muscle contraction Tx: Sodium Dantrolene 2.5 mg/kg (may repeat up to 10mg/kg) Suspect in pts with Familial hx of MH Muscular dystrophy Pts on halothane and succynylcholine Mallampati classification of the soft palate Class I Visualization of the soft palate, fauces, uvula, anterior and posterior pillars. Class II Visualization of the soft palate, fauces and uvula. Class III visualization of the soft palate and the base of the uvula Class IV soft palate is not visible at all What is trismus masseter muscle spasm Thyromental distance-thyroid motch to mental protuberance of the mandible should be larger than 6.5cm 1.
Volatile liquids Chloroform Diethyl ether

Types of anesthetics: Inhalation agents

Advantages Disadvantages rapid induction/ recovery, nonflammable, good m relaxation No longer in use, Disadvantages: Myocardial depression, hepatotoxic Reliable signs of anesthesia depth, respiration stimulated, No longer in use, prolonged induction, recovery, irritating to mucous bronchodilator, circulation not depressed, good muscle relaxation, membranes of upper airway, dangerous in patients w/full relatively safe stomachs(emetic) flammable and explosive NO Little effect on the HR, myocardial contractility, respiration, BP, liver Least potent. O2 100% must be given at termination of sx to prevent or kidney metabolism. Rapid induction and recovery, non-irritating, diffusion hypoxia. No muscular relaxation, possible bone marrow bronchodilator, non-emetic, intense analgesia compatible w/epi. depression, and fatal agranulocytosis from prolonged administration or Very high MAC* exposure. Increased risk of spontaneous abortion with prolonged use Hydrogenated Flourocarbons Halothane Most potent, lowest MAC, Rapid smooth induction and Myocardial depression, may trigger malignant hyperthermia, recovery, pleasant smell, non-irritating, non-emetic, nonarrhythmia-producing drug, sensitizes the myocardium to the flammable, bronchodilator may be safely used in action of catecholamines, Halothane hepatitis, postoperative asthmatics shivering decreases HR Isoflurane Rapid induction and recovery, non-irritating, bronchodilator, Depresses the cardiovascular system, shivering post-op, possible non-emetic, non-flammable, good muscle relaxant, maintains acute or delayed liver injury (less likely than Enflurane or Halothane) stable cardiac rhythm, compatible w/epinephrine Enflurane Pleasant smell, rapid induction/ recovery, non-irritating, Myocardial depressant, smooth muscle relaxant, increase hypotension bronchodilator, maintains ability of CV system, nonemetic, w/increase depth of anesthesia, CNS irritant, may cause seizures! compatible w/epinephrine Nephrotoxic and hepatotoxic Methoxyflurane Most potent, least volatile anesthetic, Great margin of safety, No longer in use, Prolonged induction of anesthesia and prolonged good m relaxant, nonflammable recovery Nephrotoxic MAC-minimum alveolar concentration (the higher the value the least potent the agent)

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2.
Ischemic heart disease Smokers Pts with liver disease Alcoholics Pts with renal disease Pts with DM Gouty patient Pts with sickle cell The rheumatoid patient Chronic steroid use Diuretic use

Perioperative conditions and medication cessations

Wait at least 6 months after before elective surgery Must perform a pulmonary function test, arterial blood gases, Post-op complications atelectasis Succinylcholine, muscle relaxants and halothane are contraindicated in these patients Must perform LFTs and Kidney functions tests muscle relaxants and enflurane are contraindicated in these patients Anesthesia masks hypoglycemia Give morning insulin, use 5% IV dextrose, consider NPO status Discontinue chlorpropramide and oral hypoglycemic medications Sx can precipitate attack, use colchicine 0.5mg 3xd for 2-3d prior to surgery and 4-5d post-op Avoid tourniquet use, and repiratory depressants-use local anesthetics Reduce MTX therapy, do cervical spine X-ray Increase steroid therapy, continue 2 days postoperatively otherwise LBP and CV collapse may occur Causes hypokalemia will lead to prolonged non-depolarizing muscle relaxant activity digitalis toxicity, heart irritability. Abnormal K+ will cancel surgery Continue these medications Continue these medications-may produce HBP, angina and arrythmias if discontinued Continue these medications Continue these medications Discontinue these medications 3-6 days pre-op, coumadin is highly plama bound and may potentiate depressant effect Discontinue ASA 2-3 weeks prior to surgery

Arrythmia medications Hypertensive medications Psychotropic medications Bronchodialators Anticoagulants

Pre-op considerations

No solid foods for a minimum of 5 hours, no liquids for 3 hours. Decrease gastric fluids and acidity with Tagament 300mg IV (histamine 2 antagonist) and Reglan 10mg IV (Dopamine antagonist Conscious Sedation Sedative/hypnotic and opiod are titrated slowly. Balance btwn sedation/ amnesia yet patient can maintain own airway. LOC evaluated by a simple motor response squeeze my hand Discharge Vital signs w/in 20% of pre-op for 30 min, afebrile, BP stable supine/standing, orientedx3, no bleeding through bandage, circulation to toes intact, pain controlled w/oral analgesics, tolerate foods by mouth, able to void, sensation and motor return to epidural limbs, can ambulate with assistance Re-admit post-op 4 reasons Uncontrollable pain, untrollable nausea, medical monitoring is needed, dizziness, weakness, can not ambulate

B. Regional Anesthesia 1. Spinal Anesthesia- Should be considered whenever general anesthesia poses greater risk Contraindications Location Side effects and complications Hypovolemia, anticoagulant tx, peridural Local anesthetic medication is Hypotension caused by sympathectomy hematoma, spinal compression, asthma, injected in the epidural space just Late complications include: postural HA, COPD, obesity, pre-existing NMD, DJS, below L2 into the dural sac. It is meningitis, spinal neuraligia, cauda equine local/systemic sepsis or the debilitated host unlike an epidural which injects syndrome and epidural hemotoma just outside the sac. 2. Local Anesthesia blocks Saphenous nerve-the only nerve at the ankle that comes from the femoral nerve, lies medial to the greater saphenous vein PTN-branch of the sciatic, lies in the posterior compartment above the lacinate ligament Sural-made up of branches from the tibial and common peroneal nerves DPN-les between the EHL and Anterior tibial tendons Superficial peroneal-becomes superficial 7-8cm above the ankle Ankle Block Deep peroneal Intermediate dorsal cutaneus nerve Medial dorsal cutaneus nerve Sural nerve Saphenous nerve Posterior tibial nerve Digital block 2 dorsal digital proper nerves 2 plantar digital proper nerves Hallux block 1st dorsal digital proper nerve Deep peroneal nerve 1st-2nd plantar digital proper Mayo Deep peroneal Intermediate dorsal cutaneus nerve Medial dorsal cutaneus nerve Medial plantar nerve Saphenous nerve Mini-Mayo LCDN4th common dorsal4th common plantar 3. Techniques of local anesthesia Local Anesthetics: weak bases that may exist as non-ionized/ionized molecules: Two anesthetic types:

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Ester-ester linkage is metabolized in plasma by Psedocholinesterase (short T1/2), w/high potential for allergenicity d/t PABA Amide-metabolized by the microsomal enzyme system of the liver (long T1/2)-no cross allergenicity with esters Characteristics Actions
Completely reversible, low system toxicity Action confined principally to nerve tissue Short onset time, sufficiently long duration Soluble in saline and water Sterilizable & compatible with vasoconstrictor drugs Non-irritating to tissues Stabilizes the axonal membrane By stabilizing the nerve membrane, these drugs prevent Na and K exchange in action potential depolarization. The threshold for excitation increases with the [ ] of the anesthetic, because it inhibits the ability of the nerve membrane to alter its permeability to the larger NA ion. This is a NON-DEPOLARIZING block and prevents the generation and conduction of nerve impulses (sensory>motor)

The ester group of local anesthetics

Drug Cocaine Tetracaine (Pontocaine) Procaine (Novocain) *Chloprocaine (Nesacaine) Vaso-constrictive Topically active Yes Yes Yes Used for spinals Yes NO -NO Max dose w/epi 150kg 100 mg 1000mg 1000 mg Dose 2mg/kg bw 1mg/kg bw 10mg/kg bw Onset Intermediate Slow <15 minutes long acting Rapid 2-5 min Slow 6-12 minutes Duration Short-20-60 min 2-3hours Slow metabolism Short 30-60 min Short 30 min Toxicity Potency High 10x > procaine coke Low Safest

Drug Lidocaine Lidocaine W/ epi Bupivicaine (Marcaine) Mepivicaine (Carbocaine)

Max dose 300-350mg 500mg 175mg 225mg w/epi 500mg 400mg w/epi

The amide group of local anesthetics Onset Duration Very rapid <2 1-2 hours-shortest minutes Very rapid Duration is doubled 24 hours 2mg/kg/ body Intermediate 4 hours-longest, 12h weight 5 minutes w/epi, 24h as analgesic 7mg/kg bw Rapid Short (max 400) 2-5 minutes 1-2hour Epinephrine Dose 4.5mg/kg body weight 7mg/kg bw

Toxicity Potency Comparable to procaine Comparable to procaine No children <12 yrs Do not use w/ renal dz

Advantages: o Reduces the vascularity locally at the site of injection o Reduces the absorption rate of the local anesthetic o Permits higher allowable single dose of local anesthetic to be used o Increases the duration of action of the block o A 1:1000 solution contains 1mg/ml of epinephrine o A 1: 200,000 solution contains 0.5mcg/ml of epinephrine Contraindications/cautions: o -should not be used for infiltration around end arteries, can lead to tissue necrosis-should use diluted epi at the digits o -use cautiously in pts with hyperPTH, arteriosclerotic dz, CVD, HBP, and PVD o -can create reactive hyperthermic reaction o -should be avoided in pts using Halothane, since halothane sensitizes the myocardium in the presence of exogenously administered catecholamine Conversion 1% solution has 10mg/cc, the maximum dose can be calculated in ccs as % solution converted mg/cc = max ccs or Max mg Special cases for lowering maximum dose 1. Elderly-1/2 or less of adults dose 2. Pediatric a. Clarks rule: used for children >1 yr Weight of child in lbs x Adult dose 150 C. Intravenous sedation = 20mg/cc xylocaine plain = 15ccs 300mg

Adjusted dose

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Intravenous anesthetics used first b/c of rapid distribution. Then intubation is used to control breathing and then inhalation agents are used. Inhalation agents are not used first because will cause muscle relaxation and cessation of breathing. A disadvantage of IV anesthetics is the inability to quickly reverse the effects, therefore side effects can be unexpectedly severe All are highly protein bound by albumin (over 80% except ketamine 12% which causes it to be so nephrotoxic because only nonprotein bound molecules are renally cleared) Lipid solubility, molecular size and state of ionization (only non-ionized molecules freely diffuse) determine effectiveness
Induction Agent Most commonly used induction agent Induction dose 3-6mg/kg Ultra-short acting Barbiturate Onset <30s Extravascular injection can produce tissue necrosis/arterial injection spasm Duration 5-10min Neuroleptic drugs Propofol Cleared by liver at a much faster rate, time from emergence to full recovery Induction dose 1.5-2.5mg/kg Diprivan following induction dose is more rapid than any other IV anesthetic agent Onset 15-45s Duration 5-10min Inovar Analgesia, sedative Anti-emetic, anti-convulsant, and anti-adrenergic effects-LBP 0.05 Fentanyl citrate + 2.5mg droperidol Chloral hydrate One of the oldest and best hypnotics and a very good alternative to barbiturates Induction dose 0.5-1g po in the elderly or children Ketamine Hypnotic, analgesia and amnestic effects. Hallucinogen produces Induction dose 1-2mg/kg body wt IV over 1 min dissociative amnesia. Common in Kids emergence frequently assoc w/ Duration: 10-15min of sleep and anesthesia, 40min bad dreams. No myocardial depression, -useful in traumas where BP drops of analgesia per single dose Etomidate Can be used safely in cardiac and asthmatic patients Muscle relaxants Description Compounds that block the transmission of neural impulses between motor nerve endings and muscle fibers. Major site of action at the cholinergic and nicotinic receptors at the motor end plate. Only effects skeletal muscle and not the smooth muscle of the gut. Depolarizing Succinylcholine-2 acetylcholine molecules chemically linked, Onset in 60s, short duration (3-5min)-must be broken down by agents combines reversibly with postjunctional cholinergic-nicotinic plasma pseudocholinesterases, will not respond to receptors opening Na channels. Most commonly used to acytelcholinesterase inhibitors (pyrodistimine, neostigmine, facilitate tracheal intubation-May cause malignant hypothermia edrophonium) recovery depends on washout of agent from MEP Non-depolarizing Long acting (>60min)- curare, pancuronium, pipecuronium Agents combine reversibly with postjunctional cholinergic-nicotinic agents Inter acting (30-60min)-atracurium, gallmaine, vecuronium receptors without opening Na channels, reduces the number of Short acting(<30min) Mivacurium receptors accessible to acetylcholine molecules by the motor nerve. Reversed by aceytlcholnesterase inhibitors and atropine 1.2mg Thiopental Pentathol

What is the MOA of death by narcotic respiratory depression What anesthetic can be safely used in cardiac and asthmatic patients Etomidate
Sedatives Hydroxazine Benzodiazepines Sedatives and hypnotic agents Used before surgery to relieve anxiety and tension-cerebral cortex depression Pentobarbitol and Secobarbital Has sedative, antihistamine, antiemetic and bronchodilating properties, but is Vistaril used primarily for sedative properties. Excellent in pts w/hx of bronchial asthma Onset(min ) Duration (min) Long duration of action. Preanesthesia sedation, used for Midazolam (Verded) 1-5 10-30min sedative, hynoptic, amnesia sedation during local anesthesia. No CV side effects, mild Diazepam (Valium) immediate 15-30min anti-anxiety, sedative, amnesia respiratory depression; Antidote Flumazenil 0.2mg/kg
Lorazepam 60-120 min

Morphine

Meperidine (Demorol) Fentanyl (Sublimaze) Narcan Phenothiazines

Opiods-analgesic but no amnesia, or anesthesia Analgesia only. Antidiarrheal=constipation. Other s/e: Nausea, itching and urinary retention. Dose 10mg q3h (subQ, IM or IV) Hallmark of OD pinpoint pupil constriction. Asthmatics react poorly to MSO4 b/c of PCA pump DOC (5mg/hr) histamine release smooth m constriction which will lead to LBP, counteracted by histamine onset: 20 min, duration 4-7hrs antagonists hepatic disease increases duration Will not decrease HR. M.C orthopedic med: Combine with Vistaril (antianxiety, Dose 100mg q3h (IM,SubQor PO) Poor po sedative, anti-histamine) 25 or Phenergan 12.5-25 to counteract nausea absorption Produces depression of ventilation which is short in duration, intraoperative Onset-almost immediate Reversed by narcotic antagonist (Naloxone 0.4-2.0mgq2-3min) Short acting (30 min); Analgesia, sedative Opiod antagonist, will promptly reverse respiratory depression of opiods 100ug acts in 2 min Tranquilizers Preanesthetic medication b/c of their sedative, antiemetic, antihistaminic and Thorazine 15-25mg temperature regulating effects. May produce post-op LBP and lethargy Compazine 5-10mg Phenergan 25-50mg

D. Surgical Principles

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1. Wound Healing: The entire wound healing process is a complex series of events that begins at the moment of injury and can continue for months to years. Phases of Wound Healing
Phases Inflammatory Phase Duration Immediate to 2-5 days Principal cell Platelets and Neutrophils Hemostasis Vasoconstriction Platelet aggregation-d/y exposure of the platelets to vWF8 in the damaged endothelium End result is activation of X which activates thrombin which converts fibrinogen to fibrin which forms the clot. Inflammation Histamine Vasodilation and Phagocytosis via Neutrophils and macrophages(which appear in the 1st 5 days and have a long 7-10 d life span) Proliferative Phase Remodeling Phase 2 days to 3 weeks 3 weeks to 2 years Macrophages Fibroblasts Contraction (0.6-0.7mm/day) New collagen forms Wound edges pull together to reduce defect-tension on the which increases tensile wound stimulates production of collagen, therefore excessive strength to wounds tension should be avoided and steristrips used whenever possible By 1 month, the tensile Epithelialization Crosses moist surface strength has increased by Cell travel about 3 cm from point of origin in all directions -rate 40-50% of migratory movement is proportional to the pO2 which is highest under HBO condition Scar tissue is only 80 Neoangenesis -Granulation Fibroblasts lay bed of collagen, percent as strong as fills defect, produces new capillaries- occurs at the same time as original tissue migration and is under the influence of GFs released by MACs. The wound reaches 35% of its original strength by day 14Scar revision should be at this time the tensile strength of the wound=tensile postponed for 1 yr strength of the suture that can now be removed Activated macrophages are the most important inflammatory cells involved in wound healing because they are the only cells able to tolerate the low oxygen levels at the wound edge and thay are involved in: Wound debridement-accomplished by the production and secretion of proteinases, such as collagenases Ingestion of bacteria and cell debris Capillary formation-neovascularization Antigen processing/presentation

Factors that influence wound healing Age Inadequate perfusion Infection Edema Poor nutrition Vitamin and Trace Element deficiencs VitA def can interfere w/wound healing, and may reverse wound healing problems assoc w/ steroid use VitC scurvy-is important in the enzymatic synthesis of collagen Steroid and Cytotoxic medications Steroids slow protein synthesis when given exogenously, interfere with capillary budding, slow fibroblast proliferation as well as the rate of epitheliazation Cytotoxic drugs inhibit cellular proliferation and slows wound healing but not prevent it Radiation-leads to reduction in perfusion b/c of cellular destruction Diseases which are associated with or predispose to chronic wounds Diabetes Mellitus Deposits in the arteries interfere with tissue perfusion DM neuropathy leads to reduced sensation and gait abnormality Metabolic problems lead to a reduction in nutrients available for wound healing Impaired phagocytosis seen as part of the disease spectrum on diabetics lead to increase in bacterial infections, subsequent tissue destruction and abnormal immune response Venous Stasis disease Collagen Vascular Diseases Treatment of Non-healing wounds-see wound management Bone healing Primary bone healing Secondary bone healing (Callus) Fracture reduction Six phases Fracture stabilization-bypasses the Hematoma formation-btwn fx fragments (1-3d) Hematoma organization-inflammation (3-10d) formation of a fibrocartilagenous fibrocartilagenous callus-osteoclastic phagocytosis of necrotic bone with osteoblastic differentiation into callus with simultaneous bone cartilage low O2 tension or fracture instability or bone-high O2 tension/stability (10d-6wks) formation via Haversian remodeling primary bone callus-condensation of fibrocartilagenous callus into bone that bridges fracture interface (6Preservation of fragment vascularity 10weeks) primary bone callus absorption-new bone remodeling into 2o bone callus (2.5-4mo) remodeling-alteration of bone in response to applied forces Wolfs Law

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Inadequate fracture healing Cause Description Treatment Delayed union Inadequate fracture Fx has not healed in a reasonable period immobilization, NWB, revisional sx, reduction and/or bone grafting, refixation or Non-union Weber and Cech classification 8-9months of non-healing: immobilization, overly employment of Electrical bone Hypertrophic (Vascular/reactive) Elephants foot, Horses aggressive surgery growth stimulation-creates an hoof, Oligotrophic (periosteal stripping) or electronegative polarity in the Atrophic (Avascular/Nonreactive)-no bone callus injury, OM, and local collagen- promotes bone growth Without gap, Butterfly fragment, Gap, can determine vascular compromise differences with bone scan Pseudoarthosis When a non-union involves a fibrocartilagenous interface between the fracture fragments creating a type of new jointpainful Bone grafting Main functions: promote osteogenesis, immobilization, bone replacement Advantages Disadvantages autogenous Material of choice, immunologically compatible, highest success Second surgical site Limited quantity rate Stress fracture at the surgical site Allogenic Allograft- living tissue transfer; Alloimplant- non-living tissue Less effective incorporation Absence of osteoconduction transfer, No 2nd surgical site, incorporated via osteoconduction Immunogenic risk Increased expense Osteoconduction-bone graft functions as a scaffold or conduit for migration of new bone as it replaces necrotic old bone Osteoinduction-BMP acts as an inducer substance. Description Advantages Disadvantages Cortical Dense, few viable cells, gives stability, never revascularizes, Stronger to maintain Slower graft incorporation, less does not facilitate osteogenesis, used w/ fixation devices, position, more stable fixation osteogenesis, less fenestration of graft is helpful, , has Haversion systems possible osteoconduction Cancellous Less Dense, many viable cells, fills defects, immediate Faster incorporation, No structural stability, easilt revascularization, facilitates osteogenesis via osteoconduction increased osteogenesis, distorted position, difficult to and osteoinduction, radioopaque when healing, has no osteoconduction fixate Haversion systems Techniques of bone grafting Onlay Uses a large autogenous cortical bone graft to brideg a non-union Inlay Formation of a slot or window in which bone graft is placed Sliding Create a graft from the shaft of the long bone, slide across non-union or arthrodesis site Papineau Described for the tx of OM: excise necrotic bone, cancellous bone grafting, skin coverage designed for rapid revascularization Cartilage healing Description of cartilage Hyaline cartilage consists of chondrocytes within a glycosominoglycan matrix along with type II collagen fibers responsible for maintaining compressive forces Fibrocartilage contains type I cartilage responsible for maintaining tensile forces No direct blood supply, however it requires synovial fluid for nutrition on its superficial/articular surface Healing Limited chondrocyte mitosis and for the most part, metaplasia of mesenchymal stem cells into fibrocartilage or near hyaline cartilage Tendon healing Substrate/Inflammatory Phase 0-14 days Inflammation and fibroblastic splinting with the majority of the tissue strength due to the sutures. Fibroproliferative Phase Week 3 Marked increase in fibroplasia and at this time moderate collagenation strength can sustain gentle passive motion or isometric exercises (brace or cast) Maturation Phase >4 weeks Collagen realignment and remodeling yielding moderate (not full) strength. Gradual progressive strengthening will occur w/subsequent passive/active exercises

Nerve Healing Seddons classification

Neuropraxia Axonotmesis Neurotmesis slight damage to nerve with transient loss of conductivity; esp in motor fibers; Wallerian degeneration (breakdown of the myelin sheathes around nerve) into lipid material does not occur axons are damaged, but the structural framework of the nerve remains intact; axons distal to injury undergo Wallerian degeneration Tinel's sign can be utilized to monitor regeneration of the damaged nerve Internal structural framework of the enclosed axons are divided, torn or destroyed; Wallerian degeneration occurs in the distal segment bulbous neuroma.

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Sunderlands degrees of nerve injury: 1st Conduction deficit with some demyelination; axon is completely intact. deficit is transient repairs itself w/i Overlaps neuropraxia hours; an irritable phase which presents with pain, paresthesias and hyperesthesias; Mechanism of injury compression type of injury - Normal nerve function is eventually restored; 2nd Axon or nerve fiber is severed but the endoneurium remains intact. Nerve undergoes wallerian degeneration & Overlaps axonotomesis regeneration occurs at 1-2 mm/d& depends on presence of an intact endoneural tube. Tinel's sign b/c advancing edge of regenerating nerve fiber is initially unmyelinated & very sensitive to minimal mechanical stimuli. 3rd Damage to axon and fascicles with some degree of scarring in the endoneurium. Regeneration occurs Fourth degree nerve The axon, endoneurium and perineurium are disrupted-complete scarring of the endoneurial tubes. No regeneration injury is possible. Axonal attempts at repair neuroma-in-continuity develops 5th Complete transection of the nerve. 6th Added by Susan Mackinnon - 1988. It describes a combination of nerve injuries within one single nerve. 2. Wound Management Wound Debridement 1. Goal A. B. C. D.

Preserve granulation tissue (pink) Debride fibrin tissue (white, yellow, or green tissue) Debride necrotic tissue (black wound) Exceptions: Stable healing ulcer with dry eschar 1. Dry eschar does not require debridement 2. Debridement indications a. Edema or erythema , Fluctuance , Discharge

Debridement Autolytic

Enzymatic

Mechanical

Surgical Biological

Description Advantages: Disadvantages: Autolysis uses the body's own enzymes Very selective, with no damage to Not as rapid as surgical and moisture to re-hydrate, soften and surrounding skin. The process is safe, debridement. finally liquefy hard eschar and slough. using the body's own defense Wound must be monitored closely Autolytic debridement is selective; only mechanisms to clean the wound of for signs of infection necrotic tissue is liquefied, and can be necrotic debris. Effective, versatile and May promote anaerobic growth if achieved with hydrocolloids, hydrogels easy to perform. Little to no pain for the an occlusive hydrocolloid is used and transparent films. patient Chemical enzymes are fast acting products that produce Fast acting w/ Expensive, Requires a prescription. slough of necrotic tissue. Some enzymatic debriders are minimal or no Application must be performed carefully only selective, while some are not. Papainureas: Panafil damage to to the necrotic tissue. May require a specific and Accuzyme, and collegenases: Santil, healthy tissue. secondary dressing Inflammation/ discomfort may occur Allowing a dressing to proceed from moist to wet, Low Non-selective and may traumatize healthy or healing tissue then manually removing the dressing causes a cost Time consuming, Can be painful to patient form of non-selective debridement. Hydrotherapy can cause tissue maceration. Also, waterborne Hydrotherapy is also a type of mechanical pathogens may cause contamination or infection. Disinfecting debridement. additives may be cytotoxic. Sharp surgical debridement and laser Fast and Selective Painful to patient. Costly, especially if an operating debridement under anesthesia are the fastest Can be extremely room is required. Requires transport of patient if methods of debridement. effective operating room is required. Maggots Selective to necrotic tissue Unsightly, not widely used

Plastic surgery Explanation of grafting: who, when, where, and how Split-thickness (dermal) grafts
Thin Intermediate Thick Thickness (inches) 0.008-0.012 0.012-0.016 0.016-0.020 Description Require less nourishment initially, will take readily with high success rate. Graft contraction and durability is a problem. Will heal in 7-9 days Similar to thin and thick Graft is more durable w/less contraction. Requires less nourishment initially w/lower success rate. Will heal in 14-20 days

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Full thickness Flaps All of the dermis and some fat which decreases the survivability of the graft b/c fat will seal the basement membrane which relies on the subdermal capillary plexus to oxygenate the base of the graft. Will heal by granulating from the edges Types Punch flaps, rotational flaps, local arterial flaps, myocutaneous flaps Local flaps (minimum of epidermis, dermis and sybQ) Advancement flaps Moved directly forward to fill a defect without rotation or lateral movement Transposition flaps Rectangular in shape with rounded edges, can be rotated 90o Rotation flaps Designed when a pie shaped triangle defect is created to remove a lesion or preexisting defect Z-plasties Type of rotation flap that is used to lengthen an existing scar and to reorient them along lines of minimal tension- an optimal 60o orientation will theoretically gain 75% length V-Y or Y-V advancement to lengthen or shorten along the scar axis Island flaps where the only link between the cutaneous flaps and its bed is the NV bundle Myocutaneous flaps Types Lattisamus dorsi, gastrox, TA, ABH, ABDM fibula, FDB posterior and plantar heel Description Phases of flap healing Plasmatic Phase 24-48 hours Fibrin anchor layer, nourishment diffusion where the stratum basale survives Inosculation 48h-4days Vascular buds from the wound cause new b/v to form. The graft will pink up and lymphatic drainage will begin Reorganization Months Connective tissue remodeling w/reinnervation in 1-2 years 3. Perioperative emergencies Hyponatremia Hypokalemia Hyperkalemia Hypoxemia Hypothermia Post op N/V Pulmonary Aspirations 120-125meq/l <3.5meq/l Complications of Anesthesia Confusion, anorexia, lethargy, N/V, coma Give insulin if d/t hyperglycemia and seizures If hypotonic-tx w/isotonic saline Respiratory arrest with <2meq/l, cardiac arrhythmias, renal effects Give K+

EKG changes: Spiked T waves, ST segment depression, Prolonged PR intervals, QRS widening, prolonged QT intervals

Caused by renal failure, administration of blood, K+ PCNs, salt substitutes Tx: CaCl2, NaHCO3, glucose and insulin Reduction in O2 supply to a tissue below physiologic levels. PaCO2 Tx by compensatory mechanisms: Hyperventilation, is the most important regulator of ventilation pulmonary redistribution, increased CO, increased [Hgb] Decreases VO2 and CO2 production. Dysrhythmias at 28C, Vfib/asytole <28C, HR/CO decreases as temp falls EKG changes: sinus bradycardia, prolonged PR, QT interval, widened QRS complex. Tx: Warming of patient Prevent with : Metoclopramide 10-20mg IV, Droperidol 0.63-1.25 mg IV, Cimetidine 200mg po/IV, Ranatidine 150mg po or 50mg IV, Scopolamine 1.5mg transdermal patch Due to passive regurgitationand seen more in the unconscious, obese, pregnant, and patients with full stomachs. Adult/ infants > 6 months must be NPO for 6 hrs (food) clear liquids may be taken up to 2hrs Fever Wind Water Wound Wonder drug Caused by possible DVT or PE Do a CXR to r/o Prevent with heparin or LMWH Occurs post-operative (days) Atelectasis from the anesthesia, aspiration Use incentive spirometer or intra-op Occurs perioperatively, during pneumonia, Malignant hyperthermia give NA Dantrolene surgery Dehydration, constipation Give NS 100 Occurs post-operative (hours) Possible sepsis Do a UA, blood cultures Occurs post-operative (hours-days) NSAIDs, phenobarbitols, phenytoin discontinue Occurs post-operative (hours)

Walk Walk Wind Water Wound Wonder drug

Incentive spirometry is designed to mimic natural sighing or yawning by encouraging the patient to take long, slow, deep breaths. This is accomplished by using a device that provides patients with visual or other positive feedback when they inhale at a predetermined flow rate or volume and sustain the inflation for a minimum of 3 seconds.The objectives of this procedure are to increase transpulmonary pressure and inspiratory volumes, improve inspiratory muscle perfor-mance, and re-establish or simulate the normal pattern of pulmonary hyperinflation.When the procedure is repeated on a regular basis, airway patency may be maintained and lung atelectasis prevented or reversed.

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4. Surgical Hemostasis Indications Contraindications Tourniquet etiquette To exert enough pressure on the arterial Q to a limb to produce a bloodless field. Open fractures of a leg Post traumatic hand reconstruction Severe crush injuries Elbow surgery (w/excess swelling) Severe hypertension Diabetes mellitus With skin grafts in which all bleeding points must be readily distinguished Compromised vascular circulation or in the presence or an arterial graft Sickle cell disease (relative contraindication) as severe pain could result Nerve injury and post-tourniquet increases in Ca Carefully exsanguinate, frequent irrigation is recommended to prevent tissue drying. In the presence of malignant tumors, painful fx, or infection esmarch exsanguination must not be done, only elevate limb for 3-5min is acceptable ankle: 100+SBP thigh 275-350mmhg +SBP max 500mmhg 2 hrs should not be exceeded w/ releasing the tourniquet for 15-20min before reinflating at which time the limb should be elevated about 60 degrees with study pressure on the incision

Complications Precautions Pressure setting Inflation time

Other types of hemostasis

5. Surgical anatomy Incisions Anatomical landmarks should be identified, should be long enough to avoid excess traction on the wound margins Should be parallel to RSTL 5. Biomaterials and fixation techniques General classification of sutures includes natural and synthetic, absorbable and nonabsorbable, and monofilament and multifilament. Synthetic materials cause less rx, and the resultant inflammatory rx around the suture material is minimized. Absorbable sutures are applicable to a wound that heals quickly and needs minimal temporary support. Their purpose is to alleviate tension on wound edges. The newer synthetic absorbable sutures retain their strength until the absorption process starts. Nonabsorbable sutures offer longer mechanical support. Monofilaments have less drag through the tissues but are susceptible to instrumentation damage. Infection is avoided w/monofilament, unlike the braided multifilament, which potentially can sustain bacterial inocula. Absorbable Suture Plain gut Chromic gut Vicryl (polyglactin 910) Monocryl (Poliglecaprone) PDS (polydiaxone) Type Natural multifilament Natural multifilament Synthetic monofilament Synthetic monofilament Synthetic monofilament Description Digested by bodys own enzymes-more reactive than synthetic Rapidly absorbed, tensile strength maintained 7-10d, Completely absorbed 70 d Chromic Nacl solution to resist bodys enzymes, prolonging absorption over 90d 75% of original tensile strength remain at day 14 Absorption complete btwn days 56-70 by hydrolysis Tensile strength- 60% at 7d, 30% 14d, original strength lost 21d, completely absorbed at 91-119 day 70% of original tensile strength remain at day 14, absorption minimal until about 90 dayscompletely absorbed at 6 months

KIM-that the less reactive the suture, the less risk that it may potentiate infection (synthetic, monofilament and non-absorbable sutures are the least reactive i.e. prolene)
Non-absorbable Suture Ethilon Nurolon Mersilene Ethibond Excel Prolene (polypropelene) Dermabond 2-octylcyanoacrylate Steri-strips Staples Type Description Monofilament Nylon Low tissue reactivity, more pliable when wet 9-0, 10-0 for microsurgery Braided nylon Coated to improve handling Multifilament polyester Minimal tissue reaction, most acceptable for vascular synthetic processes Polyester braided Coated with polybutalate Relatively biologically inert, recommended for use where minimal suture rx is desired, ie w/ infection Other closure technique Sterile liquid topical adhesive, indicated to repair low tension lacerations and surgical incisions. In 3 min provides the same strength as healed tissue at 7 days with traditional closure. Resists bacterial contamination and will peel in 5-10 days. Use of surgical adhesives can simplify skin closure in that certain problems inherent to suture use can be avoided. Problems (eg, reactivity, premature reabsorption) can occur with sutures and lead to an undesirable result, both cosmetically and functionally. Hypoallergenic adhesive reinforced with polyester filaments for added strength Staples provide a fast method for wound closure and have been associated with decreased wound infection rates. Staples are composed of stainless steel, which has been shown to be less reactive than traditional suturing material. The act of stapling requires minimal skin penetration, and, thus, fewer microorganisms are carried into the lower skin layers. Staples are more expensive than traditional sutures and also require great care in placement, especially in ensuring the eversion of wound edges. However, with proper placement, resultant scar formation is cosmetically equivalent to that of other techniques.

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What type of closure technique produces the least amount of tissue reaction staples Number of days a suture should remain Face and neck 2-5 days Dorsum 7 days Plantar 10-14 days Retention site 3wks-6wks Types of suture techniques Continuous interlocking stitch Simple interrupted Mattress-everts skin edges a. Horizontal b. Vertical E. Podiatric Surgery 1. Foot Procedures Nail Procedures Nail Pathology nails can indicate systemic diseases Anonychia No nail; congenital anomaly: ischemia, toxins, Raynauds, Dariers Dz, Lichen planus, subungal neoplasms fungus, psorias, trauma Paronychia Infection + IGTN; mc staphylococcus, candida, Beaus Lines Transverse ridges 0.1-.5mm wide x 0.1mm deep in nail plate; d/t sudden arrest in Fx of nail plate- infection - typhus, syphyllis, leprosy, DM, psoriasis, vascular Dz, ACTH, hyperthyroidism, alopecia, exfoliative dermatitis Clubbed Bulbous deformity of terminal phalanges, convex hard thick nails; Lovibonds angle > 160o; Eti congenital heart defects, respiratory ailments lung ca, emphysema, SBE, cirrhosis of liver Darier White Dz Red & white longitudinal streaks on nail; Mees Lines Horizontal striations on nail d/t arsenic & thallium poisoning Eczema Atopic & contact dermatitis nail colour yellow, green, gray or black Glomus Tumor Neoplasm of arteriovenous shunts in nail beds (glomus bodies) purplish tumor & pain. Keratocantoma Subungal ulcerated lesion resembles squamous cell carcinoma Leukonychia White Transverse striations, spots or total nail psoriasis, toxic metal poisoning, scleroderma, leprosy, anemia, cancer, Hodgkins Dz, Dariers DzAtrophy Lichen planus Malignant Melanoma Acral Lentiginous melanoma most dreadful; melanotic whitlow elevation of nail Periungal Fibroma Acquired or congenital associated w/ tuberous sclerosis, mental retardation, seizures, adenomasebaceum Colour Changes in nail are also disease markers Blue Red Green Black/Brown Cyanosis Cancer Pseudomonas Candida

Yellow Addisons Dz, DM

White

White Lines

Normal Heredity, Arsenic Anemia of chronic Dz Addisons Dz anemia, poisoning or Nephrotic Syndrome Junctional nevi, fungal drug toxicity melanoma infection Ingrown Toe nails Etiology - biomechanics is m.c. cause, compression by 2nd digit, excessive pronation, nail cutting, trauma >> foreign body rx & infection Surgical Procedures Chemical Matrixectomies -Indications - Onychocryptosis, onychomycosis, onychauxis, onychogryphosis, onycholysis, incurvated -Contraindications infection (if longer than 2wks R/O osteomyelitis), vascular compromise,uncontrolled blood glucose Type Applications Neutralizer Advantages Recurrance Rate Phenol 89% Phenol X 3 for 30 seconds each No neutralizer Flush Alcohol Phenol longer shelf life, cost less than NaOH 5-10% d/t old phenol, inadequate application or not removing enough nail Removal of the nail matrix is integral to prevent recurrence Sodium Hydroxide - 1980 10% NaOH X 2 15 seconds each Neutralizer 5% acetic acid Less drainage, faster healing Low

White Spots Injury psoriasis

White & pink

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Surgical Matrixectomies cold steel indicated for chronic reoccurring IGTN, failed chemical procedures and nail pathology Inverse L shaped incision excision of nail, matrix & hypertrophic ungual labia; suture Bilateral frost; Mendelsohn & smith suturing of nail edge is removed along with matrix and bed; Snip nail fold wedge to the bone; sutured Removes nail plate & matrix w/o shortening; Focused on nail matrix; excised skin over base of nail bed proximal to lunula & matrix; skin flap advanced & sutured to distal nail bed. Terminal Symes Removal of entire nail plate, bed & matrix, resect of distal phalanx & close defect with plantar skin flap. Disadv- shortens digit, bulbous terminal stub, sloughing of flap, scar, epidermoid cyst, nail spicules Kaplan Stressed removal of both nail matrix and nail bed, H incision carried out at two tissue depths Suppan Frees the eponychial fold & removes the nail, allow visualization of proximal nail matrix, cut lateral & anterior borders and removed proximal attachment Complications Reccurence, excessive drainage, excessive bleeding, poor technique destruction, infection, exuberant granulation tissue, insufficient amount removed, soft tissue migration upward to dorsum of toe Frost 1950 Whitney 1968 Winograd 1929 Zadik Digital Surgery Functions of the digits: stabilization, balance, kinetics, deceleration of foot & assist with propulsion; Goal of surgery relieve symptoms & preserve function. Anatomy Review: Intrinsic Muscles - (med to lat in transverse plane) Abductor hallucis, Adductor hallucis, 1st dorsal interossei, 2nd dorsal interossei, 1st plantar interossei, 3rd dorsal interossei, 2nd plantar interossei, 4th dorsal interossei, 3rd plantar interossei, abductor digiti minimi Etiology of Digital deformities Flexor Stabilization 90% Extensor Substitution 10% Flexor Substitution MC cause of hammer toe; Abnormal STJ Tight gastrocnemius or soleus ankle joint Rarest; d/t weak gastroc & soleus pronation foot pronated in stance phase; equinus or pes cavus foot Equinus gait. calcaneus gait; Flexors substitute to Calcaneal eversion FF abduction Flexors Assist ankle DF in swing phase; Anterior assist ankle PF @ heel off. Overpowers gain mechanical advantage (FDL tight) & over muscles gain a mechanical advantage the interossei. Supinated foot in late powers weaker interossei hammer toe & over powers lumbricales PF metatarsals stance phase straight toe adductovarus 5th digit. as digits contracts contraction adductovarus Flexors> interossei Extensors>lumbricales **Gastrocnemius equinus mc cause Abnormal STJ pronation & hypermobile flat feet mc cause Flexor stabilization mc cause Hammer toe Pathology: Normally when FDL pulls tight flexes the PIPJ & extends MPJ. To correct this PIPJ arthrodesis is performed to change the function of the FDL when FDL pulls tight it now flexes the MPJ & correct the contracted deformity. Indications for surgery: digital contractures impaired function, plantar calluses and pain Surgical consideration Kelikian push-up Test helps determine if deformity is flexible soft tissue procedure or rigid osseous procedure.

Mallet Toe Hammer Toe Claw Tow 1jt; PF of DIPJ; Tx - arthroplasty at DIPJ w resection 2 jts DF of MPJ & PF of PIPJ; Tx 3jts DF MPJ, PF of PIPJ & DIPJ; of the head of middle phalanx resection of the head of proximal phalanx Tx - arthroplasty at both PIPJ and DIPJ Soft Tissue Indication reducible/flexible deformity Procedures Extensor Tenotomy at PIPJ or DIPJ (flexor not often done b/c it sacrifices digital purchase) reduces MPJ Tenectomy cutting tendon and taking out a section extensor hood release cutting the extensor expansion medially and laterally from MPJ to PIPJ reduces MPJ capulotomy cutting MPJ capsule and plantar plate Extensor tendon lengthening and transfer reduces MPJ Flexor tenotomy reduces IPJ Flexor tendon transfers FDL or FDB to proximal phalanx - reduces both PIPJ & MPJ; derotational skin plasty flexor tenotomy for mallet toe and flexor tendon transfer for claw toe & hammer toe are ONLY soft tissue procedures used by themselves for completely reducible deformities; Sequential Hammer Extensor Tendon & hood release(Kelekian push-up test) PIPJ arthroplasty (Kelekian push-up test) MPJ toe Release capsular release (med, lat & dorsal) (Kelekian push-up test) Plantar Plate release w/ maglammery elevator, (Kelekian push-up test) PIPJ arthrodesis fixated w/ 0.045 K-wire for 6-8 wks.

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Arthroplasty Post 1897 Arthrodesis

Interdigital Corn Helloma molle Adductovarus 5th Digit = overlapping 5th toe

Complications of digital surgery

Osseous Procedure Indication semi-flexible deformity; shortens toe and relaxes soft tissue, Dorsal linear incision, transverse tenotomy at level of PIPJ medial & lateral collateral ligaments severed; bone resected at the flare of the bone using rongeur, saw or osteotome. Tendon re-approximated with absorbable sutures vicryl & skin closure with nylon. Indication: failed arthroplasty, flail toe, transverse IPJ deformity, hammer, claw or mallet toe; converts toe rigid lever Types: End to End fusion(Selig) resect cartilage on both bones down to sub-chondral bone & fused with K-wire, screw, or absorbable pin; Peg in hole fusion proximal phanlanx fashioned into peg w/ dorsal cortex intact & base of middle phalanx fashioned into hole to accept peg; fixation not required, very stable w/ high union rate. V-arthrodesis fashion bone into V & fixate; Lambrinudi fusion of PIPJ & DIPJ for claw toe; Resection of base of proximal phalanx NEVER do this! b/c creates instability & lose attachments of intrinsic muscles, cannot act as rigid lever. indicated in bone tumors, RA, OA, OM, or salvage Boney exostosis on the base of 4th proximal phalanx and head of proximal phalanx of 5th rub together; Tx reduction/excision of hypertrophied bone from mostly 4th interdigital space Etiology base of proximal phalanx removed, intrauterine position, tailors bunion procedure , short EDL, hammer toe repair; Presents with keratotic lesion over PIPJ, adduction, contracture of capsule, medial contracted EDl, subluxed MPJ; Tx skin incision - derotational skin V-Y or Z plasty; incision proximal lateral to distal medial;,soft tissue release and lengthening of EDL, capsulotomy, plantar plate release, Bone arthroplasty resection of 5th met head + lateral middle hemi-phalangectomy, abductory wedge resection of phalanx, k-wire fixation. Eg Lapidus extensor Tenotomy w transfer of distal stump under proximal phalanx and attach to abductor digiti quint; Kelikian syndactyly of 4th & 5th after capsule release and arthroplasty of 5th toe; Wilson dorsal V-Y skin plasty & extensor Tenotomy and lengthening Mc - persistent edema , recurrence of the deformity, residual pain, excessive stiffness; less common - sausage digit, floating toe with metatarsalgia, infection, decreased sensation, numbness, blue toe, Floppy digit; malunion/nonunion, implant failure , vascular impairment. B. Lesser Metatarsal Surgery

Anatomy: mets 1 & 5 have individual axis of motion; not 2-4; Blood supply to mets Nutrient artery, metarphyseal and periosteal; normal declination of met 15o IPK Etiology 2-4th met Biomech RF varus, FF varus/valgus, Hammer Toe >> retrograde plantar flexin, atrophy or displacement of plantar fat pad, long or short met, sagittal plane mis alignment Abnormal declination angle, plantar flexed position, hypermobility , abnormal shaped plantar condyle; 5th MET - Biomech RF varus, rigid FF varus/valgus; sagittal plane misalignment plantar flexed 5th met & cuboid, DF 4th met, congenital long 5th met or short 4th met, Abnormal bone shape & size prominent lateral plantar condyle, fat pad atrophy Verucca plantaris (pinpt bleeding w/ skin lines around lesion occur in non wt bearing areas; inclusion cysts; cicatrix; foreign body. Dx Xrays w/ lesion marker & lateral to evaluate metatarsl parabola problem if 2mm longer or shorter Reduce the lesion at time of surgery; Percutaneous Metaphyseal sliding osteotomy capital fragment dorsiflexed, cut is dorsal distal to plantar proximal, must fixate. V osteotomy @ anatomical neck >> transversae and frontal plane correction& stability, apex distal; DFWO @ anatomical neck or base, shortens met, must fixate; McKeever peg in hole , shortens; Chevron double V osteotomy, shortens; Met head resection; plantar condylectomy Transfer lesions, dorsal bump/met elevation, floating or flail toe, nonunion, dislocation of met head, edema, recurrence

DDx Treatment

Complications Taylors Bunion Etiology Description

Uncompensated FF/RF varus, Congenital PF or DF 5th ray, Abnormal STJ pronation, idiopathic, lateral deviation or wide 5th met. Rotation of lateral plantar tubercle into lateral position; increased IM angle; increased lateral deviation angle; large round dumbbell shaped 5th met head,; arthritic changes >> exostosis at 5th MPJ; Combination of the above. XR evaul IM angle normal 6.47; pathologic 8.71 positional; Lateral deviation angle normal 2.64, pathologic 8.05 structural; Conservative Treatment padding, wider shoes, NSAIDS, steroid injections reduce callus Surgical Normal IM & Lat Deviation >> resect lateral prominence; Reverse Hohmann transverse osteotomy at the level of the metatarsal treatment neck w/ medial displacement of capital fragment; oblique osteotomy from distal lateral to proximal & medial w/ displacement of capital fragment proximally & medially (reverse wilson); Modified Mitchell step down osteotomy Reverse Austin 2mm medial transposition; McKeever partial met head resection; Davis removal of lateral eminance (reverse silver); Devries removal of lateral plantar chondyle; Weil transverse osteotomy from surgical neck dorsal distal to plantar proximal phalanx to condyles. Allows proximal sliding to increase joint space & improve digital alignment. Shortens or lengthens. Fixated with screw/pin. Normal IM High Lat Deviation >> Neck procedures Mercado medially based closing wedge osteotomy at met neck, Yancy mid shaft medially based closing wedge osteotomy, Kelikian partial met head resection - 2/3 & syndactylization of 4th & 5th toes; High IM >> Base procedures Gerbert -proximal diaphyseal closing wedge osteotomy, Rappaport - transverse base wedge resection using hinge axis guide, Bishop opening base wedge osteotomy w/bone graft. **excessive 5th met head resection laxity of internal cubic content of the jt further varus or adductovarus malalignment of 5th toe & more retrograde pressure on the 5th met head**

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Other lesser metatarsal surgery Splay Foot Widening of the entire foot in transverse plane; greatest deformity >>> High IM, for 1st & 2nd + 4th & 5th; surgical repair focused on the IM angles. This is accomplished via closing base wedge osteotomy of the 1st metatarsal with AO fixation & distal oblique osteotomy of 5th metatarsal with k-wire fixation. Freibergs Etiology trauma, ischemia, prominent plantar metatarsal head w/ excessive loading; Epi - mc women 3x >men; age 13 S & S pain in MPJ, edema, limited ROM, palpable jt irregularities dorsally, adjacent MPJ hyperkeratosis; Infraction Dx Xrays jt space widening 3-6 wks after symptoms; increased density of subchondral bone, sclerotic rim, loose spicules of bone, flatteningof met head w/ osteophytic lipping , jt space narrowing, soft tissue swelling, bone margins sclerotic Tx g oal - prevent further damage & displacement of MPJ; initially casting & cortisone shots; Later implant arthroplasty; metatarsal head remodelling (splinting 3 mths), cancellous bone grafts to restore contour of met head, Rotational osteotomies rotates the lower aspect of the met head dorsally after a section of damaged cartilage has been excised allowing the plantar cartilage to articulate w/proximal phalanx. Smile Classification (JBJS 1957) I. Fx of ischemic epiphysis II. Fx of the subchondral plate III. Collapse of central met head with plantar cartilage intact IV. Collapse of central met head with non-intact plantar cartilage forming loose bodies V. Complete flattening of the metatarsal head Friebergs Infraction I. No DJD, cartilaje intact II. Periarticular spurs, cartilage intact III. Severe DJD, loss of cartilage IV. Epiphyseal dysplasia with severe met head involvement C. Hallux Surgery

HAV Anatomy review: Muscles EHL, EHB, FHL FHB, Adductor Hallucis, Abductor Hallucis Ligaments Medial & lateral collateral ligs, Tibial & fibular sesamoidal lig, intersesamoidal ligament, deep transverse intermetatarsal ligament, Blood Supply 1st dorsal and plantar met arteries & the superficial branch of medial plantar artery; nutrient artery is 2.7cm from MPJ on lateral side. Biomechanics: Flexible FF valgus & gastrocnemius equinus bilateral abnormal pronation in adducted foot during propulsive phase of gait 1st MPJ DF d/t hypermobility & inverts; hypertrophy of the dorso-medial metatarsal head. Lateral subluxation of hallux d/t weakening of p. longus & DF of met with transverse head of adductor pulling on hallux and enhancing its lateral migration Sesamoids migrate laterally to change abductory forces on the hallux causes boney adaptation on plantar met head and wearing down of the cristae. Stages of HAV I subclinical subluxation of 1st MPJ; seen on XR only w/normal IM & HA II Abduction of hallux force on 2nd met and clinical s/s of HAV III Met primus adductus deformity; early increase in IMAon xray; advanced inc IM clinically; 1 finger breath separation b/t jt IV Clinical subluxation /dislocation of 1st MPJ; Hallux over-riding the 2nd toe

Structural Positional Combined

Types of Deformity PASA or DASA Abnormal PASA & DASA Normal PASA OR DASA Abnormal

PASA + DASA = HAA PASA + DASA < HAA PASA + DASA > HAA

Congruent lines parallel Deviated/Subluxed {lines intersect outside the jt deviated} Deviated/Subluxed {lines intersect within the jt subluxed}

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Important Radiological Angles in the evaluation of HAV Angle MA How to Measure Normal Value (degrees) Line perpendicular to bisection of lesser tarsus, representing bisection of of 2nd met; Bisection of lesser tarsus by 15, >15 in a median point b/t 1st cuneioform & navicular and median point of cuboid connect lines and draw a perpendicular rectus foot line which forms and angle with bisection of 2nd met Engles Angle formed b/t bisection of medial cuneiform & 2nd met shaft- another measurement of MA 24 IM Bisection of lines of 1st & 2nd mets; To determine the effect of met adductus on Normal in a rectus foot 8-12 the deformity subtract 15 from MA and add it to the IMA; structural deformity adducted foot 8-10 HA Lines bisecting met & proximal phalanx; represents transverse plane deviation of hallux 0-15 HAI Line bisecting proximal & distal phalanges of hallux 0-10 PASA Angle between a line perpendicular to shaft bisection and line depicting effective cartilage. Represents the 0-8 articular cartilage deviation on the head of the 1st met. Increase of this angle represents articular cartilage adaptation to deviated hallux in transverse plane DASA Line drawn perpendicular to effective articular cartilage of base of proximal phalanx & line representing dorsal 0-8 longitudinal bisection of the shaft of proximal phalanx. Structural adaption of shaft of proximal phalanx to base MPD Measure of relative length b/t 1st & 2nd mets; + or -- 2mm TSP Position measured by relating the position of tibial sesamoid to 1st met bisection 4 or greater is abnormal & 1-3 dictates removal of the fibular sesamoid position Lateral 1st Met Sagittal plane relationship of 1st met to bisection of talus; line bisecting 1st met is below or above talar 15 20 position bisection plantarflexed or dorsiflexed 1st met. Clinical Evaluation Non-Weight bearing H/o of recalcitrant pain, age of onset of symptoms and failure of conservative tx shoe modification, orthoses and steroid injection; 1st Ray ROM normally 10mm 5mm up & 5mm down - ? increase or decrease, crepitus or other degenerative jt changes; 1st MPJ DF normal > 65-75o & PF >15o; Axis of motion of 1st ray Tracking hallux can be placed in corrected position but drifts back into abnormal position during motion. This is d/t lateral soft tissue adaptation and joint axis deviation. Track bound inability to place hallux into corrected position d/t severe jt axis deviation and articular/boney adaptation; laxity of 1st MC joint; Bunion location dorsomedial mc, medial or dorsal (hallux limitus or met primus elevatus) Skin lesions keratoma, erythema, bursa Goals of Sx pain free congruent joint, IM < 10o, good ROM, normal TSP, acceptable cosmetic results Anatomic Dissection 1. Dissection and Hemostasis 2. Plantar lateral release a. Deep tranverse intermetatarsal ligament b. Conjoined Adductor Hallucis tendon c. Fibular Sesmoidal Ligament d. Lateral head of the FHB e. Plicae attaching proximal surface of sesmoid apparatus to met neck and joint capsule f. Fibular sesmoidectomy 3. Medial dissection and exostectomy 4. Osteotomy 5. Adductor tendon transfer to derotate the sesmoids 6. Medial Capsuloraphy Hinge Axis Guide used for base procedures; K-wire placement to assist with manipulation of the sagittal plane correction & length of 1st met. For PF dorsal medial to plantar lateral; Neutral straight toward 2nd toe; DF plantar medial to dorsal lateral; Lengthen perpendicular to long axis of bone; Maintain length perpendicular to2nd met, Shorten slightly proximal Soft Tissue Procedures Positional procedure indicated for correction of soft tissue component of HAV; Sliver 1923 resect the medial eminence of 1st met head, lateral capusulotomy and medial capsulorraphy McBride1928 resection of dorso-medial eminence, lateral capusulotomy with removal of fibular sesamoid, transfer of the conjoined tendon of the ADH and lateral head of FHB to dorsolateral aspect of 1st met head. Usually modified & sesamoid removed Hiss resection of eminence, lateral capusulotomy, and transfer AHB from plantar to medial to 1st met sutured into hole at base of proximal phalanx to strengthen the medial capsule. Akin Osteotomy medial closing wedge osteotomy done in the proximal phalanx; proximal corrects DASA; distal HIA; central shortens and derotates the hallux. Maintain lateral cortex and fixate w/ staple, K-wire or screws; rarely used alone, as adjunct.

Proximal Phalanx

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Procedure Austin 1962 Reverdin 1881 ReverdinGreen 1977 Reverdin-Laird 1988 ReverdinTodd

Capital Procedures for HAV Description/osteotomy Correction Indicated for IM <15o; Horizontal V chevron osteotomy performed in the center of the met head Unicorrectrional IM, with a 60o between arms for transverse plane correction only. Head shifted laterally. Able to Bicorrectional-normalizes IM lengthen/shorten; Potential complications: limited 1st MPJ ROM, lack of toe purchase, chronic & PASA, Corrects met edema, hallux varus, adductus, excessive shorteningtransfer metatarsalgia, ANV of 1st met head. elevatus, shortens/lengthens Angulated osteotomy performed in metaphyseal bone, medial wedge of bone removed. 1st cut-1cm PASA only proximal and parallel to the articular surface; 2nd cut-perpendicular to the shaft Lateral cortex is intact. Potential complications: sesmoidal damage and OA Horizontal L osteotomy, avoids sesamoid trauma; Initial cut is made parallel to the WB surface being PASA only sure to exit just proximal to articular surface of the 1st MTJ; Plantar shelf-Lateral cortex intact Lateral cortex is cut allowing lateral translation of the capital fragment Potential complications: PASA and mild IM transfer metatarsalgia, dislocation of capital fragment, intrarticular fracture correction Allows plantarflexion of the met head, same as Reverdin Laird with penetration of the plantar cortex to PASA mild IM allow sagittal place correction; Unstable osteotomies; Fixation k-wire, screws; post-op NWB

Peabody Hohmann 1921 Wilson DRATO 1971 Mitchell 1958

Neck Procedures for HAV Same as Reverdin- except osteotomy is done at the anatomical neck Trapezoidal osteotomy (base oriented medially) to correct sagittal and transverse plane abnormalities, through and through; shortens 1st met and decompress MPJ; fixation & NWB Shortens and lateral displaces head; Oblique osteomy oriented distal-medial to proximal-lateral.Through and through. Capital fragment is shifted proximally & laterally or dorsally & plantarly along osteotomy. Fixation & NWB Derotational Angulated Transpositional Osteotomy: Distal osteotomy-perpendicular to the long axis of the 1st met, through and through; proximal osteotomy-angled proximal medial to distal lateral; DF capital fragment to place the articular cartilage in a more functional position attempting to increase DF at the 1st MPJ Oblique angulated osteotomy to PF met head, is similar to Hohmann ex: lateral cortex strut intact with step off after a medial wedge of boneis removed; capital fragment slid laterally; Indicated for long 1 st met, will significantly shorten

PASA only IM and PASA IM PASA, IM, abnormal met declination IM <15o

Shaft Procedures for HAV Modified Austin, performed in the center of the met head; Long dorsal arm allows for 2 screw fixation IM Unable to swivel capital fragment to correct PASA Scarf 3 cuts from medial-lateral through met shaft /diaphyseal resembling a Z. Distal cut dorsal; proximal cut IM up to 18o, lengthens or 1983 plantar, avoids possibility of scoring sesmoids, easier to fixate *Trough effect* shortens, PASA Ludloff 1918 Oblique osteotomy oriented dorsal proximal to plantar distal & exit distal to met head; can swivel for IM and PASA PASA correction Mau 1926 Oblique osteotomy oriented plantar proximal to dorsal distal exiting proximal to met cuneioform joint; IM opposite to ludloff; Adv. versatile, both capital fragment can be elevated, depressed, lengthen, shorten, adducted or abducted; Fixation & NWB required; Disadv done in diaphyseal bone poor healing Labrinudi PF wedge osteotomy IM Kalish
*Trough effect-dorsal segment of the cortical bone of the Z wants to sink into the plantar segment when screws are tightened down

Base Procedures for HAV Created approx 1.5cm distal to 1st MC joint no shortening; Distal segment is rotated until the desired correction is IM attained may be fixated slightly dorsi or plantarflexed; 2 screw fixation NWB 6-8 wks Juvara Oblique closing base wedge osteotomy from proximal-medial to distal-lateral, proximal cortical apex is IM 1919 maintained, fixation with 1 or more screws. Type A-corrects transverse plane; Type B1-corrects transverse/sagittal Type B2- corrects sagittal, transverse, and long/short 1st met Type C1-sagital correction only Type C2-sagitall and long/short 1st met Loison-balacesu Osteotomy described as being at a point just distal to the insertion of the PL. Base lateral w/medial cortical apex intact IM Logroscino Short 1st metReverdin &Trethowan; Long 1st met Reverdin & Loison-balacesu Fixated w/kwire, screw staples IM, PASA Sagittal Logroscino Waterman and Labrinudi IM, PASA Trethowan opening base wedge osteotomy with medial wedge of bone allograft or auto graft pushes over the met to correct IM; IM, PASA soft tissue correction, adductor release & medial capsule reefing; NWB 10-12 wks; Modified Cotton opening medial cuneiform procedure indicated for short 1st ray in juveniles, graft >> lateral & plantar migration IM, PASA Of distal met shaft; fixation staples or K-wire Fixation: Normally bunions are fixated with 2.7 cortical screw using OA lag screw technique. Osteopenic bone/osteoporosis can be fixated with crossed K-wires Crescentic

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Complcations of HAV Sx staking of met head & producing hallux varus, hammered hallux, longitudinal fractures , sesamoiditis, fracture of articular cartilage, unstable osteotomy, non or delayed union, damage to neurovasculator structures, elevatus and hallux rigidus, over or under correction, disuse osteoporosis, infection, AVN, fixation problems Joint Replacement Indications inflammator arthritidies (RA; Degenerative arthrosis d/t osteochondral fractures, osteochondritis dissecans, congenital deformity, trauma, brachymetatarsi, fkail toe, floating toe, revisional Sx Types Swanson flexible hinge , Sgarlato double stem cup implant, swanson condylar implant Technique Lazy S incision over MPJ Linear or U capsulotom ; extensor/flexor tenotomies & or plantar plate release, boney resection of met head, ream medulary canals , ck fit, flush & assemble implant; wound closure Contraindications Severe osoteoporosis, prior jt infection w/I 6mths, allergic reaction to implant material, medically compromised Complications implant instability & pistoning , implant failure, foreign body reaction, osteochondritis dissecans, dendritic synovitis, infection, chronic edema, Fx of proximal phalanx

Hallux Limitus Definition of hallux limitus/rigidus - Limitus-dimished ROM at 1st MPJ; Rigidus-absent ROM at 1st MPJ, less than 10 o of DF. DF is normally 65o-75 o, PF = 40 o What are the etiologies of Hallux limitus (most common) - . Hypermobile 1st ray, long 1st ray, 1st met elevatus, DJD, neoplasms, trauma, sepsis, iatrogenic, short 1st ray, NMD, systemic arthridities, AVN, foreign bodies (implants) Classification scheme of Hallux Limitus Drago, Olaff and Jacobs Regnauld 1. Functional limitus 1. Development 2. Joint adaptation 2. Established arthosis 3. Joint deterioration 3. Ankylosis 4. Ankylosis 4. Xray findings nonuniform jt space narrowing; flattening of the met head, osteophytes on 1st met head and base of proximal phalanx (dorsal flag sign), subchondral sclerosis, loose bodies (joint mice), 1st met elevatus Procedure Cheliectomy Kessel&Bonney Regnauld Waterman WatermanGreen Youngwick Van Ness Cotton Labrinudi Procedure Keller Implant arthoplasty Stone Mayo Mckeever Valenti Lapidus Joint preserving surgical procedures for the treatment of Hallux Limitus Description of surgical procedure Removal of osteophytic bone & hypertrophied synovium from the 1st MPJ base, temporary procedure; cleans and remodels jt; stimulates fibrocartilage growth; immediate ambulation & quick recovery; orthotics & PT helps Dorsal DF osteotomy of the base of the proximal phalanx Mexican hat/enclavement procedure; Base of the proximal phalanx is fashioned into a peg and reinserted into the proximal phalanx. Shortens ray DF osteotomy of the 1st met head leaving the plantar articular cartilage intact Similar to bicorrectional Austin; dorsal cut; trapezoidal wedge wider medially; plantar cut-oblique, transverse osteotomy. Angle=45 o , shortens and PF the 1st met head Modified Austin, Rectangular block of bone taken out on dorsal cut. Shortens and PF 1st met. Plantar closing wedge osteotomy at the base of the 1st met Opening base wedge osteotomy of the medial cuneiform PF wedge osteotomy of the 1st met base to correct met primus elevatus Joint Destructive procedures for the treatment of Hallux Limitus/Rigidus Description of surgical procedure Arthroplasty of proximal phalanx with resection of 1/3rd of the proximal phalangeal base; complication cocked up hallux, lack of purchase, shortening & transfer metatarsalgia Total or hemi, primarily a jt spacer, reduce metatarsalgia, increase stability of jt and length of hallux. Indications: crepitation, pain, good bone stock, no infection or allergy to implant, Advan early ROM & ambulation. Prophylactic antibiotics Oblique osteotomy Dorsal to plantar wedge resection of 1/4th of the met head & medial eminence leaving plantar condyle and sesamoid apparatus intact Excision of 5mm of the 1st met head including articular surface, interpose capsule and bursa tissue. 1st MPJ arthrodesis; ideal position of fusion DF 5-10o from ground, slight abduction parallel to 2nd digit or 10-15o in transverse plane, NO frontal valgus or varus rotation Complications IPJ arthriti, delayed/non union onycryptosis, medial callus, impaired gait, subluxation 2nd & 3rd toe V shaped osteotomy; Metatarsal cut: proximal distal to distal plantar leaves plantar 1/3 of the cartilage intact Phalangeal cut-proximal plantar to distal dorsal Fusion of the 1st MC joint

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Hallux Varus

Juvenile HAV

Transverse plane deformity of hallus adductus; Etiology congenital isolated or congenital abnormalities; Acquired _ iatrogenic from HAV surgery d/t over correction of IM & PASA, excessive resection of sagittal grove, excision of fibular sesamoid, post-op bandage & splinting Presents shoe gear problems, pain on medial hallux & 1st MPJ Xrays hallux adducted, staked head of 1st met w/ tibial sesamoid peeping, Negative IM angle and PASA, arthritic changes at jt Tx conservative strapping & splinting; Sx soft tissue medial or lateralcapsulotomy, aBductor hallucis transfer, retransfer aDductor Hallucis laterally; Bone Reverse Austin to correct negative IM & PASA, Keller arthroplasty w/ or w/o implant, McKeeverarthrodesis; Goal is to correct deformity and prevent DJD. HAV < 20 yrs; F>M Etiology family H/O, biomechanics pes planus, limb length discrepancy, STJ pronation, equinus, met primus varus, neuromuscular deformities S & S less severe valgus rotation, NO DJD, few adaptive changes; congruent jts & hypermobile MC jt, Abnormal PASA Tx conservative splinting, toe wedges, bunion shield, wider shoes; Sx No soft tissue; - Lapidus, Akin, Mitchell, Austin, Reverdin, opening wedge of medial cuneioform, closing base wedge osteotomy, cresentic, epiphysiodesis- epiphyseal stapling When to do Sx -< 6 growth plates 40-50% closed; 6-10 60 -80% closed; 10 14 ideal time 90% in boys & 95% in girls

D. Rearfoot Pes Planus o Flat Foot deformity >>> collapse of medial longitudinal arch, RF valgus, FF abduction & supinatus, tight heel cord o Planal dominance refers to the primary plane of the flatfoot deformity (transverse, sagittal or frontal) i.e, what plane is most affected. Although procedures are divided into the primary plane of correction, the other planes are affected to a lesser extent; therefore all procedures provide triplanar correction. o A transverse deformity would clinically show abduction of the FF on the RF, (AP x-rays) an increase in TCA, decrease in TN congruity, and increase in cuboid abduction. o Frontal plane deformities clinically show RF eversion, (lateral & calcaneal axial x-rays) increased superimposition of the lesser tarsus, decreased 1st met declination angle, decreased height of the sustentaculum tali o A sagittal plane deformity would show sagging of the midfoot-navicular-cuneiform breech (lateral x-ray) TDA increase, calcaneal inclination angle decrease, TCA increase, talo-1st met angle increase negative Mearys angle Tests to determine flexibility of flatfoot deformity 1. Hubcheur Manuever-a plantarflexed 1st ray will cause the STJ to supinate and recreate the arch if flexible pes planus deformity 2. Trunk twist-STJ flexibility for supination/pronation 3. Jacks test-pt on heels, heels will invert, checks the PT 4. Supination/inversion stress lateral XR Etiologies of Pes planus Newborn Calcaneovalgus Vertical talus STJ axis Dominant plane Compensation High Transverse plane (higher vertical plane axis) Adduction/abduction Low Frontal plane (higher horizontal plane) Inversion/eversion Correcting pes planus, one must perform a posterior procedure that corrects the equinus (TAL), a medial soft tissue tendon procedure and a lateral calcaneal osteotomy or arthroresis. As a last resort for excessive OA a triple arthrodesis is indicated. Obesity & ligamentous laxity are relative contraindication b/c they >>> poor surgical outcomes. 1. 2. 3. 1. 2. 3. 4. 5. Transverse plane corrections for pes planus Evans-calcaneal osteotomy 1.5cm proximal to the C-C joint with insertion of a bone graft to lengthen the lateral column and put the PL on stretch to increase the supinatory motion at the STJ. Indicated for flexible deformities & corrects FF abductus & heel valgus Kidner-removal of the prominent navicular tuberosity or accessory navicular and transposition of PT plantarly into the navicular; increases the mechanical advantage of PT tendon in elevating the medial arch; increase risk for PT tendon rupture in adulthood C-C joint distraction arthrodesis Sagittal plane correction for flatfoot deformity Lowman-TN fusion, TAL, TA under the navicular into the spring ligament Hoke-Naviculo-cuneiform fusion, indicated with hypermobility of the NC joint & stabilizes the medal column Miller- NC-1st met fusion Lapidus- 1st met base-medial cuneiform fusion Cotton-open plantarflexory wedge osteotomy into the medial cuneiform Teenager Adult Equinus, os tibialis externum, met adductus, peroneal spasm TP dysfunction Tarsal coalition TP dysfunction w/OA

Flexible Rigid

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6. 7.

Young (Keyhole) Tendosuspension of the TA through a keyhole in the navicular, and rerouted (not detached) PT advancement under the navicular to support the medial arch TAL/GR

Frontal plane correction for flatfoot deformity 1. Orthotics 2. Arthroresis: MBA, Sta-peg, to elevate the floor of the sinus tarsi Indications Flexuble flat foot deformity Contraindications No mddle facet coalition, no CN bar, no degernative arthritis Types Vogler Class 1 Self-locking wedge: A device where opposing surfaces of the talus and calcaneus are held apart by an implant inserted between the two segments. Best for adolescents and adults MBA and Valenti Vogler Class 2 Axis altering: Will change the axis of motion of the subtalar joint. Best for pediatric patients The STA-peg Vogler Class 3 Direct impact blocking : Restricts the forward movement of the lateral talar process where motion is limited by contacting only the talus The Sgarlato (Futura) and modified STA-peg l Sgarlato is inserted into the floor of the sinus tarsi w/forward motion of the lateral process of the talus being blocked by the implant which stops the lateral process of the talus from advancing past the posterior facet of the calcaneus 3. Chambers-arthoresis concept with bone graft, to elevate the floor of the sinus tarsi 4. Baker-Hill-osteotomy inferior to the STJ using a bone graft under the sustentaculum tali to elevate the lateral posterior facet 5. Selakovich-opening wedge osteotomy of the sustentaculum tali with bone graft that restricts abnormal STJ motion to medially elevate the sustentaculum tali 6. Calcaneal osteotomies Dwyer: medial closing wedge to produce varus correcting valgus Silver: lateral opening wedge with graft Koutsogiannis-through-through sliding medial displacement transpositional osteotomy Gleich: oblique osteotomy displaced anteriorly Lord-displaces the calcaneus anterirly, inferiorly, and medially Pes Cavus Etiology: usually caused by a present neuromuscular disease CMT, polio, Types anterior metatarsus, FF, lesser tarsus cavus; Posterior muscle weakness or spasticity, pseudoequinus>>inadequate ankle DF Clinical evaluation: Coleman Block test-evaluates flexibility/rigidity of the deformity by removing influence of 1st ray. XR evaluation stress inversion XR to evaluate the position of the lateral process of the talus (w/ pronation, will hit the floor of the sinus tarsi) bullet hole sinus tarsi Signs Normal (degrees) Cavus foot CIA 20-25 >30 Angle of Meary 0 >60 Angle of Hibbs 135-140 >150 Types: Flexible, rigid or digital anterior/global/local flexible with an etiology of extensor substitution Principles of cavus surgery Rearfoot varus in the frontal plane- Dwyer Ankle equinus- TAL or gastrocnemius recession Planterflexed 1st ray - DFWO Rigid anterior cavus - Cole DF wedge osteotomy through the navicular-cuneiform jt and cuboid bone; or Japas displacement V-shaped osteotomy through cuboid, navicular and medial cuneiform Digital claw toes or hammertoes - DIPJ or PIPJ arthrodesis, HIbbs Soft tissue release Subcutaneous fasciotomy Steindler Stripping: Plantar fascia, ABH, FDB, Abductor digiti quinti, long plantar ligament. NWB Cast for 3 wks post-op WB for 2-3wks Soft tissue procedures indicated for flexible cavus: pediatric or adjunctive procedure Tendon Transfers >10-11 years

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Pes Cavus Soft tissue Procedures -EDL detached from insertion (2-5) and distal stumps are sutured to corresponding EDB tendon (4/5 go to 4th EDB (2-4) -Jones, long extensor tendons are transferred to intermediate or lateral cuneiform and a TAL Heyman Transfer of all 5 long extensors to respective met heads w/ anastomsis of distal stumps to brevis Jones Split EHL thru drill hole in 1st met (medial-lateral) & sutured back to itself or EHB with IPJ fusion STATT Transfer of lateral Tibialis Anterior tendon, rerouted down peroneus tertius tendon sheath to its insertion at the base of the 5th met using 3 incisions PL transfer -PL is released at the level of cuboid & transferred through the IM septum down the EDL sheath & inserted into the lesser tarsus. Changes action to DF at ankle limiting strong extensor substitution PT transfer -PT is released from insertion on navicular and transffered through interosseous membrane to dorsal midfoot. Changes action from PL/inversion to DF. Peroneal anastomosis PL to PB at level of lateral ankle or at the styloid process of the 5th met. Hibbs Cole Japas McElvenny-Caldwell DFWO Dwyer Samilson Triple arthodesis Equinus Osseus procedures indicated for rigid deformity/ NMD for foot stabilization, may be used in conjunction w/ s/t release DFWO through navicular-cuneiform joint Maintains STJ and MTJ motion. Shorter wider foot Displacement V osteotomy through cuboid, navicular & medial cuneiform. No bone removed, shifts FF dorsally 1st MC arthrodesis with elevation of the 1st met correcting the anterior cavus Dorsiflexory wedge osteotomy, preserves the function of major joints Lateral closing wedge of the body of the calcaneus. Be careful of the sural nerve DF calcaneal osteotomy STJ, TN and CC joint fusion

Def- less than 10o of DF past 90 degrees is required for normal gait types of equinus - Muscular: (gastrosoleal ve silverskoild, gastrocnemius +ve silerskoild); Spastic Equinus (CP)congenital equinus; acquired or Osseous (talotibial, tibiofibular syndesmosis) and Pseudoequinus anterior cavus foot type Dx - differentiated using Silfverskiold test and charger XR that evaluates anterior osseous structures. Compensation for equinus Genu recurvatum, Hip flexion,Lumbar lordosis, Knee flexion, Digital contractures (Extensor substitution) Gastrocnemius Equinus Gastrocnemius Recessions VulpiusV-shaped lengthening of the gastrocnemius Strayer -transverse cut through the gastrocnemius, suture proximal flap to soleus McGlammary- Tongue and Groove, tongue is distal Baker Inverted McGlammary, tongue is proximal Silfverskiold Release gastrox from origin on the femoral condyles Gastroc soleus Equinus TAL Z-plasty Frontal or sagittal plane Hasuer Section posterior 2/3 proximally and medial 2/3 distally White Section anterior 2/3 distally and medial 2/3 distally Conrad & Frost Section medial at distal end and lateral proximally Hoke Triple hemisection w/ 1st & last medial & 2nd lateral, percutaneus o o o Spastic Equinus Murphy Procedure - transfer advancement of Achilles insertion to dorsum of calcaneus just posterior to the posterior facet of STJ anterior to the FHL (weakens triceps surae at the ankle by 50%, but only weakens toe off by 15%) Osseous Equinus (tibiotalar exostosis) Exostectomy; tibiofibular syndesmosis heel lift accommodations Pseudo-equinus metarsal osteotomies, mid foot osteotomy, triple arthrodesis Heel Spur Syndrome / Plantar Fasciitis

15% of all adult foot complaints caused by heel pain; Conservative Tx 95% successful; PF is mc cause of heel pain. Def Inferior Calcaneal spuring & pain d/t microadhesions that form around the plantar fascia especially at night >> worst pain at 1st step in the morning when adhesions tear Post static dyskenesia. Patho repetitive traction, metabolic dz, increase wt, pronated or Supinated foot; S & S pain on palpation of medial Calcaneal tubercle, tenderness on distal fascia & worsen w/ toe DF, Conservative Tx Stretching exercises, NSAIDS, foot orthosis, heel lifts, night splints, injections, PT ice, heat, E-stim, ultra sound Surgical 20% resolution w/ fasciotomy alone; 42% w/ fasciotomy & exostosis Endoscopic plantar fasciotomy Barrett & Day 1991; percutaneous release of fascia w/o removing spur; Using Endotrac system & release 1/3 of fascia with L-shaped blade. Indications: recalcitrant PF Advantages-decreased post-op pin, faster recovery. Complications: lateral column

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destabilization: C-C/MTJ pain, peroneal tenosynovitis, sinus tarsi syndrome, medial column destabilization: central arch pain, intrinsic myositis, hammertoes o Open Plantar Fasciotomy 3-6cm plantar medial incision >> release band of fascia & resect spur. Complications injury to lateral plantar nerve, weakening of calcaneous >> fascia, recurrence, hematoma, scar pain & chronic enthesitis Haglunds Deformity Pump Bump Description: A painful bony prominence and bursitis of the lateral posterior superior aspect of the calcaneus above the insertion of the Achilles tendon; F 20-30yrs Etiology: Compensated RF varus, FF varus, FF valgus, or PF 1st ray. DDx retrocalcaneal exostosis/bursitis XR evaluation: Lateral XR Normal (degrees) Pump bump Fowler and Phillip Angle (FPA) 44-69 >75 Total angle of Vega (CIA +FPA) <90 >90 Parallel pitch lines positive Treatment: Conservative Shoe modification open heel; NSAIDS, Steroid injections, Local PT Surgical Procedures: Keck & Kelly Dorsal wedge osteotomy of calcaneus BK cast for 6-7 wks, then NWB for 3-4 wks Duvries Transverse resection of the bump through lateral incision Fowler & Phillip Transverse skin incision through posterior heel w/ a Mercedes incision through AT resect bump through this incision; weakens TA Dickenson Curvilinear medial incision from superior-medial to inferior-lateral Triple Arthrodesis Def fusion of the STJ, CC & TN Indications: Correct deformities: Cavus foot, pes planus, talipes equinovarus, fixed equinus/dorsiflexion Pain relief: tarsal coalitions, arthritis, ruptured PT, severe calcaneal fx, lateral ankle instability, neuromuscular disorders. Complications neurovascular injury, ankle arthrosis, malunion, nonunion Types: Ryerson simple jt resection Hoke remove talar head, resect cartilage and replace head Haughton-Dunn remove navicular Elmslie indicated for fixed calcaneus foot type Lambrinudi indicated for fixed equinus foot type Grice extraarticularfusion of STJ Tendon Transfers Goal active motor power, eliminate deforming force, produce stability; Indications Muscle imbalance, drop foot, congenital deformities, iatrogenic (HAV); Usually for flexible conditions or as adjunct to osseous procedure Muscle must be at least grade 4 to transfer tendon & it loses 1 grade after transfer; Post-op NWB cast 4wks w/ passive ROM & isometric exercises at 3wks >>> active ambulation 4th wk. Procedure Indications Description Jones Tenosuspension Flexible cavus foot, PF 1st EHL tendon transected & rerouted medial to lateral or dorsal to plantar (Kirk) through head of 1st met & ray sewed back on itself; distal end of EHL sutured to EHB Panmetatarsal Tenosuspension Flexible hammer toes All met heads suspended like Jones procedure Kidner Procedure Flat foot support medial Resection of accessory navicular & hypertrophied navicular tuberosity and transpose the TP to plantar column navicular Hibbs Tenosuspension Equinus, w or Transect EDL at its insertion & transfer to 3rd cuneiform or base of 3rd met; EDB is detached/reattached to w/o claw toes, remaining EDL tendon stumps. Gives EDL mechanical advantage in DF foot & prevent digital contractures Tibialis Anterior Tendon Flexible FF equinus, TA transected at its insertion & transferred to 3rd cuneiform through EDL tendon sheathReduce Transfer clubfoot, drop foot supination & increase DF Split Tibialis Anterior Weak DF; Flexible RF TA split at its insertion proximally to the superior extensor retinaculum; lateral portion passed through P. Tendon Transfer varus, Excesssive tertius tendon sheath & attached to tendon and cuboid. Medial portion remains intact; Increases DF & supination; Equinus balances lateral forces. Young Tenosuspension Flat foot TA passed through keyhole in navicular w/o detaching its insertion Tibialis Posterior Equinus, pes cavus Transected at its insertion, passed through the interosseous membrane (Putti) or around medial Tendon Transfer malleolus (Ober) and transferred to lateral 3rd cuneiform. Peroneus Longus Tendon Flexible equinus, drop foot Released at the level of cuboid & transferred through septum to EDL sheath & inserted into lesser Transfer Pes cavus tarsus or base of 3rd met; PL transected & half anastomosed to TA at its insertion & Peroneus tertius Murphy Procedure Spastic equinus in CP Advancement of Achilles tendon insertion to dorsum of calcaneus just posterior to the posterior facet of STJ anterior to the FHL (weakens triceps surae at the ankle by 50%, but only weakens toe off by 15%) Adductor Tendon Transfer HAV Sx to derotate & Adductor hallucis transected at its attachment to lateral sesamoid & base of proximal phalanx, rerouted realign Sesamoid over met head & attached to medial capsule apparatus Flexor Tendon transfer Digital contractures FDL transected near its insertion on distal phalanx, split longitudinally to base of proximal phalanx & wrapped around proximal phalanx & sutured

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Ankle Arthroscopy Directly viewing joint with Ankle scopes 2.7mm & 4.0mm; Hallux 2.0 2.7mm Indications unexplained ankle pain > 6mths, osteochondral fx, synovitis, DJD, arthritis RA/OA, ligament repair, chondromalacia, Anterior Medial - mc Anterior Lateral Anterior Central Posterior Lateral Med to TA Lat to EDL & P. tertius Lat to EHL & med to EDL Lateral to achilles & med to lat malleoli Saphenous nerve & Intermediate dorsal Anterior Tibial artery, Deep Sural nerve, lesser saphenous vein, vein, TA cutaneous nerve Peroneal peronealtendons **Posterior medial gutter NOT used; medial to ACH & lat to tarsal canal; 2 many vital structures Posterior tibial nerve & artery, Tom Dick, Harry** Ankle arthodesis Indications: most commonly due to a short fibula after an ankle fracture 1mm lateral shift loss of 40% congruency; painful arthritis, Trauma Pilon Fx, Charcot, Drop foot, AVN of talus, osteomyelitis, bone tumor Types of ankle fusions 1. Blair - Tibiocalcaneal arthodesis post AVN talus; post polio or club foot procedure fixated w/ screw, plates, external fixation 2. Fibula inlay bone graft eg Wescott proximal tibia, Hallock bone chips, Campbell- cortico-cancellous iliac graft, What is the position of an ankle/pantalar fusion? Perpendicular to the tibia in the sagittal plane Slight valgus in the frontal plane 12 degrees of abduction in the transverse plane Complications: non-union, infection, misalignment Total ankle replacements Indications joint pain, arthritis, synovitis/capsulitis, loose chondral /osseous fragments in joint Contraindication - Relative: previous deep infection; Absolute: talar necrosis, severe osteoporosis, Charcot, post-polio, vascular insufficiency Types STAR (Scadanavian total ankle replacement) Agility total ankle-must resect 50% of medial and lateral mallelous & 20-30% talar dome. Stability requires solid distal syndesmotic fusion assisted by 2 screws across the syndesmosis only FDA approved. Beuchel-Pappas total ankle- thick talar component, with a long tibial stem, can use with talar AVN, little bone is resected o Doets BP Tibial modification-tibia with 2 short stems, AP is 5mm larger for more tibial coverage Salto, Ramses, AES E. Amputations Def disarticulation/ removal of a part of a limb Epidemiology DM is #1 cause of non traumatic LE amputation 60%; 5-15% of diabetics will require and amputation; 33% of persons w/ unilateral amputation will have contralateral amputation in 3 yrs; 33% 5 year survival post BKA Indications End stage vascular Dz, Life threatening infection, mignancy, Trauma, Congenital deformities, complication of DM, PVD, neuropathy or infection Pre-op Considerations & indications of Healing Potential Level is the most distal point capable of healing & can be shaped into functional stump; Bleeding of skin at the time of surgery is most accurate clinical sign of healing potential. Consider also medical vascular & glycemic control, nutritional, immune status Vascular studies: Doppler ultrasound w/ segmental pressures, Photoplethysmography, ABI > 0.45 - 90% will heal; no blood no healing; Transcutaneous Partial Pressure of Oxygen-most accurate non-invasive predictor of healing, < 26 NO healing; >40 will heal Intra-Op Considerations Eliminate dead space adequate hemostasis & close in layers and Use most non-reactive skin closure that put least amt tension on wound edges staples best b/c high tensile strength & non reactive; Sharply section nerves under tension to prevent stump neuromas, BV cauterized or tied; Tendon balancing & retain muscle function preserve TA & PB to prevent equinus with trans met amputations (equinovarus deformity); PB inserts into 5th met base & everts & PF the foot; TA is still attached to plantar medial cuneioform & 1st met base, functions to DF & invert foot TA Split Tendon transfer to lateral foot prevent this;

Portal Location Structures

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Types Digital Distal Symes Removal of distal phalanx via dorsal plantar, side to side or racquet type incision; Ray Resection Removal of digit & portion or all of the metatarsal; Ind infection in web-space or met. Complication resection of 1st & 2nd ray increased pressures under plantar surfaces more proximal amputations; ensure medial, lat and plantar surfaces are beveled * with 5th met try to preserve insertion of P. brevis if cant transfer it to cuboid or transfer P. longus in an effort to maintain PF/Ever Transmetatarsal Most common proximal foot amputation; metatarsals transected at distal 1/3 in a smooth parabla w/ 2nd longest; mets angled distal Amputation dorsal to proximal plantar; Long distal plantar flap brought up to meet proximal dorsal flap for weight bearing surface; BV, nerves & tendons transected under pressure so they retract into stump; Complication TAL & split TA tendon transfer done to prevent equinus; Post op - AFO & custom molded shoes w/ plastizote insert & transmet filler, rocker bottom shoes Lisfranc Resection at level of lisfranc joint, long plantar flap; TA & PB sacrificed >>equinovarus. TAL necessary; Smooth out uneven Amputation joint and articular surfaces to prevent healing problems; Post op prosthesis & shoe gear necessary Choparts Resection of entire foot except talus and calcaneus with calcaneocuboid + talonavicular jt disarticulation & closed with long platar Amputation flap; TA tendon reattached through drill hole in talar neck to prevent equinus + TAL; Post-op prosthesis Boyd Mid tarsal disarticulation and talectomy; Entire foot except calcaneus which is shifted anteriorly & superiorly & fused to tibia to maintain leg length. Symes Total foot amputated, med & lat malleoli resected above articular cartilage; Transection in line parallel to the ground, preserve calcaneal fat pad beneath the tibia for weight bearing surface. Posterior tibial artery supplies the flap, ACH transferred to distal posterior tibia to prevent drop foot; Skin staples with suture line above anterior margin of distal tibia; drain & compression dressing; High rate of complication distal ulceration; Post op prosthesis needed. Pirogoff Modified proximal symes that preserves calcaneus for limb length, TC arthrodesis Post Op Antibiotics, length of stay, sutures stay in longer, PT & Rehab, Prosthesis Rheumatoid Arthritis Presentation: Pain in the AM with morning stiffness and constitutional s/s. Deformities include swan neck hyperextension of PIPJ & flexion of DIPJ, boutonniere flexion of PIPJ & extension of DIPJ, fibular/ulnar deviation of the digits, RA nodules, and it does not affect DIPJs. Other effects include pericarditis, peripheral neuropathy, peripheral vasculitis, pleuritis ocular, anemia of chronic disease, esophagus contriction and Bakers cyst in the popliteal fossa. Pre-op considerations these pts are usually tx w/ immunosuppressive agents & steroids >> cardiac conditions, fragile non elastic skin, fragile vessels, thin capsules & weak tendons >> poor healing potential; Inaddition d/t deformities in hands & weakness in shoulders may not be able to manage ambulation aids. MUST consult rheumatologist to have them alter or stop meds for Sx. Treatment: Soft Tissue Synovectomy, tenosynovectomy, nerve decompression, excision of rheumatoid nodules, bursectomy, release joint contractures, tendon balancing & transfer, joint manipulation under anesthesia Surgical Treatment: Pan met head resections complications vascular compromise/dry gangrene, recurrent plantar lesions, non purchasing toes & most common successive transmetatarsl amputation; resect enough bone to relieve all soft tissue tension Hoffman 1911 Transverse plantar incision just behind web of toes - Resection of met heads 1-5; ind moderate dz Clayton 1936 Transverse plantar incision, Resection of the base of the proximal phalanges and heads of 1-5 mets; ind severe dz Larmon 1951 3 dorsal longitudinal incisions, only partial met head resections, plantar condylectomies and removal of the proximal phalanges of 2-5, Keller arthroplasty proximal phalanx; ind minimal deformity Hodor 1983 5 dorsal incisions, resection of met heads 1-5 with consideration of the met parabola (2 1 3 4 5 ) Complication of Foot Surgery - General Soft Tissue Infection & Acute: Erythema, edema & pain ; etiology for infection staph; for hematoma strep; Tx po or IV antibiotic for G Hematoma +ve cocci; Prevention meticulous dissection, hemostasis, decrease operating time, deflate tourniquet prior to closing Scar Chronic: contracture and remodeling >> Hypertrohic or keloid scars. Tx Sub-Q steroid injections, silicone sheeting, formation topical Vitamin E, surgical excision; Prevention screen pts; thinnest, least reactive suture and fewest amt of stitches OM Bone infection after Sx. Tx - Dx biopsy & culture, debridement 6 wks antibiotics ; Prevention meticulous dissection, operative time, use peri-operative antibiotics strict sterility of instruments and hardware Poor Delayed union < 6-9mths; Non union - > 6-9mths; healed in undesired position malunion; Tx dx bone scan; electrical bone bone growth stimulator, debridement of necrotic bone; Prevention adequate fixation and NWN; dont cause termal injury to bone in healing sx with saw & avoid soft tissue interposition b/t bone ends. AVN Mc in 1st met head and talar neck post bunion surgery and talar neck fx; Tx NWB, bone stimulator, remove necrotic bone and fuse joint; Prevention meticulous surgical technique, avoid denuding soft tissue from bone & dont create thermal burns with power tools.

Bone

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Complications of Foot Surgery specific Procedure Complication Bunion Joint stiffness, weaken PF & toe purchase, delayed, mal, nonunion, AVN, 2nd met capsulitis, stress fx, under correction and Surgery reccurence, excessive shortening (pick procedure & use axis guide), Hallux varus d/t over correction; Prevention:careful pre-op planning, avoid aggressive resection of medial eminence & IM -0 Eleation 1st Met d/t early ambulation following base procedures; Prevention must be NWB 6 weeks! Keller Lack of toe purchase, weak Flexors; Prevention lengthen EHL tendon to weaken it, tenodese FHL to remaining bone of base 1st MPJ implants Dendritic synovitis, jamming of jt, limited ROM > removal of implant, arthroplasty or arthrodesis Hammer Toe Sx chronic edema, flail toe, recurrence of plantar keratosis, post-op white toe; Prev careful incision planning & dissection Neuroma Sx Chronic numbness & parasthesias in interspace, hematoma, infection, stump neuroma; Prevention meticulous dissection & deflating tourniquette prior to closing Hardware Prominence > soft tissue irritation > removal, hardware failure, backing out, pin tract infection, uncomfortable; Complications Prevention - always countersink for screw Trauma Puncture Wound Nail is common object >>metals, thorns, glass, needles, etc; 57% of pt presenting 1 - 7 days after injury develop cellulitis and infection Goals of Tx convert contaminated wound to clean wound & prevention of tetanus Type I Type II Type IIIA Type IIIB Type IV Resnick & Fallat Superficial penetration of dermis & epidermis; no clinical signs of infection ; Cleanse bid, NWB,weekly f/u Sub-q or articular joint involvement; no clinical signs of infection.; Anesthesia, sterile prep,wound exploration, cultures & pack open Establish s/t infection, retained foreign body;; Anesthesia, sterile prep, wound exploration, cultures, pack open & antibiotics Foreign body penetration to bone; Immediate sx removal of foreign body, s/t and osseous debridement, lavage, open packing IV Ab Secondary osteomyelitis; Immediate sx removal of foreign body, soft tissue and osseous debridement, lavage, open packing IV Ab Complications soft tissue infections, septic arthritis, osteomyelitis, foreign body granuloma, premature epiphyseal closure, joint degeneration,

Osteomyelitis resulting from puncture wounds; Etiology mc staphylococcus aureus; in water aeromonas hydophilia, mycobacterium marinum & vibrio -Tx - Sterile prep, wound cultures, probe wound, copious irrigation & pulse lavage, pack open, TLS drain, moist guaze dressing, F/u 3-5 days, antibiotics 1st gen ceph; for diabetics polymicrobial Unasyn,Augmentin, Timentin or Zosyn + gram negative coverage Tetanus prone if > 6hrs & larger than 1cm deep, Rx TT 0.5mls, Tetanus Immune Globulin 250 500 units IM -Green & Bruno Type I - Rx early I&D &debridement; antibiotics; heal w/o any bone or joint damage Type II - Dx & TX w/i 9 - 14days; Rx debride ment & antibiotics; heal w residual bone & jt destruction Type III - Dx & TX - 3wks or more; chronic infection & bone resection for final cure Bite Wounds Dog Bites Cat Bites Mc 90%; least infection 2nd mc (5%) Infection rate 30 - 50% Mc in males <20yrs on extremities Females on upper extremities Crush injury - 150-450lbs/sq inch Etiology Pasteurella multicida Tx Irrigation w/ NS, immobilization & elevation, pack open, antibiotics Augmentin DOC for animal bites; Tetracycline for PCN allergic or Erythromycin **P. multicida is resistant to PCN & penicillinase resistant PCN, Keflex poor activity Human bites 3rd mc (2-3%) Highest infection rate - 50% Hands Aerobes: S. aureus, Corynebacterium , Eikenella corodens Anerobes: B. fragilis, peptostreptococcu May need IV antibiotics and wound culture; Cefitoxin S. aureus resistant to PCN & E. corrodens is resistant to PCNase resistant PCN

Open Fracture **Gustilo & Anderson** Golden period 3 - 5hrs Stage I Stage II Stage III <1cm clean >1cm clean IIIA sufficient skin to cover defect but periosteal stripping; infection IR - 17%; amputation rate Fx Fx transverse/oblique AR 5% transverse/oblique Rx Cephalosporin & IIIB insufficient skin for coverage & bone exposed IR 26% AR 5-6% Rx Cephalosporin Aminoglycosies IIIC no skin for coverage & require microvascular surgery to save limb. Infection rate 25 Infection rate 0% Infection rate 3% 50%; 25 - 90% > amputation Tx irrigation - 2L Tx irrigation -2L & >5cm dirty, damage to skin, muscular and vascular structures Fx comminuted & 1o closure primary closure Rx Cephalosporin & Aminoglycosies Tx irrigation - 4L & delayed primary closure; maybe skin grafting at this time Closed Fractures Rockwood & Green

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Direct Trauma-closed Fx caused by direct blows of varying velocity o Tapping Fx: low velocity blow w/ no soft tissue damage o Crush Fx: high velocity w/ extensive soft tissue Indirect Trauma - closed Fx resultin from forces acting at distance to Fx site o Traction Fx: transverse avulsion at site of tendon or lig. attach o Angulation Fx: transv. Fx caused by bending forces of long bone Spiral Fx: oblique Fx, 45o to axis of long bones, rotational force Compression Fx: impaction Fx into soft cancellous bone o Angulation & Axial Comp: transv. Fx w/ butterfly fragments o Angulation & Rotation Fx: oblique Fx lines

Charnley's principes of closed reduction: Increase deformity > distract > reverse deformity & realign >Maintain correction w/ immobilization Charnley's Classification of Fractures: Based on intrinsic stability of fx to w/stand forces that tend to telescope the fragments. I Stable II Unstable III - Potentially stable

RADIOLOGY 15%
Exposure: Rad = rem = Roentgen o Occupational exposure (annual maximum): 5 rem o Public exposure (annual maximum): .5 rem o Fetal exposure (total dose) 0.5 or monthly (0.05 rem) o Maximum Permissable Dose (MPD) 5 (N-18) where N= age in yrs, and the answer equals the total cumulative whole body absorbed dose permitted during the course of 10 yrs. o ALARA concept: As Low As Reasonably Achievable: use of technical factors which will produce ther lowest dose of radiation yet to achieve a diagnostic study Physics radiation is energy in motion; xrays are produced when one form of energy is converted to another; in the xray tube heating tungsten filament >>fast moving electrons >>strike target and 1% is converted to xrays; the filament is the cathode & target is the anode. Number of electrons passing from cathode to anode in 1 sec is milliamperes (mA); the potential difference is kilovolts (kV). Maximum peak potential difference is kVp quality/penetrating power of xrays produced; mA quantity of xrays. Photons generated are heterogeneous some are high energy & pass through pt to contribute to diagnostic image and others are low energy photons that do not contribute to diagnostic image b/c they do not reach the film but are absorbed by pt. Other beams scatter in the room >> occupational exposure. The Higher the mA>> increases the QUANTITY of x-ray photons; increases radiographic density>> increasing darkness of the film; A higher kVp will have a greater penetrating power, and will produce less contrast - less soft tissue detail and increased radiographic density; Lower kVp will have less grays, better soft tissue visualization, higher contrast, and decreased radiographic density Effects of Radiation Short term large doses >> Acute radiation syndrome - death in 72 hrs; Lethal Dose LD50/30 kill 50% people in 30 days = 200-300 rems Long Termexposure to small amt of radiation over time >> decrease life span d/t carcinogenesis, embryological defects, genetic mutations Radiosensitivity Increase with high rate of division and immature cells; Rapidly growing cell most susceptible epithelial cell - hair, skin, gonadal, lymphocytes, immature RBCs and fetal cells Operator & patient protection least amt of time in x-ray beam, distance further away from beam > 6ft and use of shields reduce exposure; Shielding -Lead apron must be > 0.5mm thick; use barriers b/t operator/unit 1.5 mm thickness, 7ft high and permanently affixed to floor -High kVp / low mAs technique reduces patient exposure by 70% Positioning Weight-bearing or non-weight bearing films; Standard view: Foot AP, MO, LAT; Ankle AP, Mortise, LAT; Tib/Fib AP & LAT; Sesamoids axial; Calcaneus axial, LAT View Positioning Structures viewed AP /DP 15o from vertical, aim central ray at 2nd metatarsal base Forefoot and rearfoot talo-navicular, Calcaneo-cuboid jts LAT 90o from vertical, central ray aimed at 4th metatarsal base Forefoot and rearfoot talo-navicular, Calcaneo-cuboid jts LO Angulation 0 o; foot obliqued 45 o laterally; central ray aimed at first metatarsal cuneiform joint Best visualization of medial column MO Angulation 0 o; foot rotated medially 45 o; central ray is aimed at the 4th metatarsal cuboid articulation Broden MO; post calcaneous on cassette front & rotate leg 45o medially invert & DF foot. Angles Posterior facet, talar 10 o 20 o 30 o 40 o; central ray aimed 2cm inferior & 2cm anterior to lateral malleolus sustentaculum tali articulation Harris Pt faces away from tube, plantar aspect on cassette, slight flexion in knees; angle varies 35Medial & posterior sustentaculum Beath 45o; central ray 5cm superiorly from posterior Calcaneal prominence tali Sesamoidal Cassette vertical, angulation 90o; Digits extend against the plate and heel elevated; central Sesamoids, crista of 1st met head axial ray aimed at plantar surface of metatarsals Calcaneal axial Horizontal cassette, tube is angled 45o central ray aimed at posterior heel Post/medial/lateral margins of calcaneus AP Ankle Cassette vertical angulation 90o ray at anterior ankle Ankle joint, talar dome, malleoli Ankle Mortise Cassette vertical, angulation 90o foot internally rotated 15 -20o Better visualization of lateral malleolus & talar dome

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Radiographic Pathology AP projection l Normal forefoot will have mild MT convergence at the bases l FF varus will have increased MT convergence l FF valgus will have decreased MT convergence Lateral projection l Normal FF with MT superimposition (but 5th in plantar position). l FF varus with ladder configuration of MT and 5th in plantar position l FF valgus with MT superimposition (1st MT in plantar position) Osteoarthritis (DJD) Osteophyte formation, eburation, subchondral cysts (intraarticular osseous fragment) jt collapse, deformity/malalignment Psoriatic arthritis Acro-osteolysis (distal tuff resorption), periostitis, ivory phalanx (distal phalanx of hallux) IPJ involvement of hallux, abnormal widening of joint spaces, normal mineraliation (in contrast to RA), pencil-in cup deformity of MPJs Reiters Disease Exuberant infra-calcaneal spur formation , similar to psoriatic arthritis Ankylosing spondylitis Bilat sacroiliitis with S-1 jt fusion = bamboo spine Rheumatoid Arthritis Periarticular s/t edema jt space widening, juxta-articular osteopenia initially, erosive changes, uniform jt space narrowing, Sero-positive Calcaneal erosions, retro Calcaneal bursa, ankylosis, swan-neck and boutonniere deformities of the hand Gouty arthritis Extra-articular involvement a hallmark, joint effusion and edema, tophi formation: Na urate deposits, C shapd erosions with overhanging ridge of bone (Martels Sign) , calcification of tophi ankylosis Pseudogout Calcification of articular cartilage and peri-articular tissue Charcot Joint Hypertrophic -Jt distention, increased density of bone and s/t, osseous debris, dislocation, disorganization, destruction; decrease s/t swelling fragments begin to unite & resorption of fine particulate debris. Fusion of osseous components, loss of normal osseous configuration & alignment Atrophic whiskering of articular endresembling licked candy stick CVD - scleroderma Diffuse osteoporosis, soft tissue atrophy, tuftal resorption, soft tissue calcification in subcutaneous tissue CVD - SLE Joint space narrowing , deforming non-erosive arthropathy of hands and feet, soft tissue calcification, osteonecrosis Osteoporosis Ostepenic bone, w/decrease tensile/compressive trabecular pattern in calcaneal/femoral head, decrease cortical thickness CRPS Spotty osteoporosis stage 2 = sudecks atrophy, general osteoporosis, joint abnormalities Diabetes Mockenbergs medial calcinosis, loss of normal osseous architecture w tapering of long bones (licked candy stick) Special Imaging Modalities CT Scan (Computed Axial Tomograghy) Physics: Cross sectional radiography utilizes thinly collimated x-ray beams that circumferentially rotate around the body part; x-ray penetration converted to electrical signal and collected by computer and displayed. Slices - 2-5mm. Tissue density measured in Hounsfield units: 2000 to +2000. Air -1000 -black; Water = 0; Bone +1000 - white Window width bone wide 2000; soft tissue narrow 600; o Indications Best for pathology of cortical bone; trauma, coalitions, tumors of bone & soft tissue, bone & soft tissue infections, AVN, osteochondrosis dissecans, arthritis o Contrast material: iodinated contrast may be given IV, will accumulate in the tissues based on vascularity. It may also be given intraarticularly for CT arthrograms o Contraindications: ist trimester of pregnancy, claustrophobia, allergy to contrast agent, weight limit for gantry MRI Best imaging modality for soft tissue evaluation; Physics: No ionizing radiation is used. based on H+ atom (proton) which has highest gyromagnetic ration; Mobile hydrogen ions in the body are first aligned by a stationary magnetic field and then excited by radiofrequency pulses. As the protons relax from the pulses, they emit radiofrequency signals. The signal from a body tissue depends on the number of mobile protons, and the interactions between the protons in that tissue. Spatial encoding of the signal allows cross-sectional images to be obtained in any plane. There are no known biological effects, but MRI is avoided in the first trimester b/c of lack of data. Body parts with lots of water show better because of the high Hydrogen content; low signal from substances with few hydrogen atoms such as air, cortical bone, tendon, fibro-cartilage and ligaments. Pulse sequences Proton Density balanced T1 T2 (fat suppression) TE <50 TR > 1000 TE <50 TR <1000 TE >50 TR >1000 Fat & Fluid Bright 90 Fat and bone marrow is bright Fluid and blood are bright STIR fat suppression technique, good for evaluating edema in high lipid regions bone marrow; GE takes shorter time, good for joint imaging. Heavily T2 weighted o o o Contrast material: gadolinium used IV and intra-articular; Good with fat suppression techniques Indications tumor, infection, trauma, congenital anomalies, AVN, osteochondrosis, cartilage abnormalities, arthritis, unexplained pain Contraindications Pacemakers, pregnancy (1st trimester), Metallaic implants will create artifact and cause pt harm: iron or sheet metal workers w/ ocular foreign bodies, aneurtsm clips, post-op clips, cardiac valve prosthesis, claustrophobia

Nuclear Medicine Physics: Based on the injection of radioactive isotope into the body and the analysis of its distribution and accumulation. The isotope emits gamma radiation for a brief period of time which are recorded by a gamma camera or scanner Hot increased uptake of isotopes eg fx, infection; cold spots Indications no isotope uptake d/t absence of blood flow eg AVN

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o o o

Indications osteomyelitis, trauma, inflammatory arthritis, stress or occult fx, tumors, non-specific pain, neuropathic osteoarthropathy, RSD, Contraindications poor vascular supply,, immunocompromised pt, renal dysfunction Isotopes: Tc99 most useful measures osteoblastic activity; nonspecific and dependent upon intact vascular supply TC-MD99 bone scan is a triple phase scan; (non-specific) life 6hrs 1st phase-blood pool (1-3s) 2nd phase-blood flow (3-5 min) represents relative vascularity to a particular area or lesion prior to skeletal uptake 3rd phase-delayed- (2-4 hrs) represents relative osteoblastic activity, not active if pt has porr renal clearance in which case phase 4 is also performed can differentiate OM from cellulitis; seen in stressed Fx, bone tumors, OA, & osteomyelitis 4th pase-scanned 24hrs post injection to allow for adequate tissue clearance in pts who have poor renal activity Gallium-67 citrate - binds to WBC plasma proteins (and lactoferrin) measuring their activity in the soft tissue and is used in conjunction with the TC-99 bone scan to differentiate OM vs cellulitis. Best for subacute and chronic infection life-> 79hrs; more reliable in differentiating b/t benign vs malignant tumors GC+ TCmd99 + OM GC+ TCmd99- cellulitis GCTCmd99+ osteoarthropathy, stress fx, chronic OM Indium-111 - WBC binding - measuring their activity, checks for cellulitis, best for acute infections and more conclusive than GC Ceretec HMPAO scan-WBC labeled scan Differentiate OM from Charcot using bone scans? On X-ray and clinically, stage 1 Charcot & OM is indistinguishable, so a ceretec bone scan will be hot in the 4th phase with OM and stay cold in charcot Contrast Studies injection of contrast medium to visualize an area not normally seen on plain radiographs, CT, MRI Agents Iodine contrast Xrays & CT; Air nontoxic medium; Gadolinium used with MRI Indications Tenogram, sonogram, arthrogram (CT & MRI) Contraindications allergy to contrast agent (iodine) unless premedication is given; cellulitis

Orthopedics, biomechanics and sports medicine

A. Funciton and structure (normal and abnormal) 1. Osseous system Bone ossification dates Primary ossification Secondary ossification Maturance/fusion 9th week IU 3-4 yrs (head) 17-20 yrs 10th week 3-4 yrs (head) 17-20 yrs 10th week 3yrs (base) 17-20 yrs 9-12 week 2-8 yrs (base) 18th year 11-15 week 2-8 yrs (base) 18th year >15 week 2-8 yrs (base) 18th year 3 mo IU 8-12 yrs 6 mo IU If present 8-9 yrs Cuboid 9 mo-at birth Lateral cuneiform 1st yr Medial cuneiform 2nd yr Intermediate cuneiform 3rd yr Navicular 4th yr Sesmoids 8-14 yrs 2. Muscular system The muscle groups of the lower extremity are composed of 5 regions: iliac, gluteal, femoral, and muscles of the leg and foot. The Illiac region is composed of the iliac, psoas major and minor muscles. Superficial gluteal region Muscle Origin Insertion Blood supply Nerve Action Gluteus medius Illium: between the anterior Lateral surface of the Superior gluteal Superior Abducts thigh and posterior gluteal lines greater trochanter gluteal Medially rotates thigh Gluteus Illium: between the anterior Anterior border of the Superior gluteal Superior Abducts thigh minimus and inferior gluteal lines greater trochanter gluteal Medially rotates thigh Tensor fascia Outer lip of the iliac crest Iliotibial band Superior gluteal Superior Flexes thigh lata ASIS Lateral circumflex gluteal Medially rotates thigh Glueteus Behind posterior gluteal line Gluteal tuberosity, Superior gluteal Inferior Extends thigh maximus iliotibial band, linea Inferior gluteal gluteal Flexes the hip aspera and medially to 1st perforating branch of L5-S1-S2 Abducts the thigh the STJ profunda femoris Laterally rotates thigh Ossicle 2nd-4th met 5th met 1st met Distal phalanx Proximal phalanx Middle phalanx Calcaneus Talus

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Muscle Piriformis Superior Gameullus Obdurator internus Inferior Gamellus

Deep muscles of the gluteal region Origin Sacrum SV-4 Sacrotuberous ligament Ilium, below the PIIS Ischial spine Greater sciatic notch, obdurator foramen, EXITS the Lesser sciatic foramen Ischial tuberosity Lateral margin of the ischial tuberosity Along the margin of the obdurator foramen

Insertion Upper border of the greater trochanter medial surface of the greater trochanter medial surface of the greater trochanter medial surface of the greater trochanter Intertrochanteric crest, quadrate tubercle Trochanteric fossa passes across hip jt

Nerve Ventral rami of S1, S2 N. to the obdurator internus L5, S1, S2 N. to the obdurator internus L5, S1, S2 N. to quadratus femoris L4, L5, S1 N. to quadratus femoris Posterior branch of the obdurator (L2, L3, L4)

Blood supply Superior & inferior gluteal, internal pudendal Inferior gluteal Superior & inferior gluteal, internal pudendal Inferior gluteal Inferior gluteal, medial femoral circumflex Obdurator a Medial femoral circumflex

Action Laterally rotates thigh Abducts thigh Latterally rotates thigh Laterally rotates thigh Abducts thigh Latterally rotates thigh Laterally rotates thigh ADDucts thigh Laterally rotates thigh ADDucts thigh

Quadratus femoris Obdurator externus

The femoral region is divided into anterior, posterior and medial compartments. The anterior medial septum separates the anterior from the medial compartment, the posterior medial septum separates the medial from the posterior compartment and the lateral septum separates the posterior from the anterior compartment. Anterior femoral region Quads Origin Insertion ASIS-has its own Medial surface of the tibia anterior fascial (covers tendons of pes compartment anserinus) Rectus femoris AIIS Upper border of the patella by ligamentum patellae into tibial tuberosity Vastus lateralis Greater trochanter Lateral border of the patella into Linea aspera the ligamentum patella Vastus medialus Spiral line Medial border of the patella into Linea aspera the ligamentum patella Muscle Sartorius Vastus intermedius Artucularis genus Linea aspera Front and lower pt of femur Tendon of rectus femoris Medial border of the patella into the ligamentum patella Capsule of the knee, suprapatellar bursa Insertion Pectineal line of the femur Medial surface of the tibia, just below thetuberosity linea aspera on the femur Pectineal line of the femur, linea aspera Gluteal tuberosity linea aspera linea aspera, adductor tubercle Nerve Anterior Femoral Posterior femoral Posterior femoral Posterior femoral Posterior femoral Anterior femoral Blood supply Femoral a Lateral femoral circumflex Lateral femoral circumflex Femoral a, profunda femoris, genicular branches of the popliteal Lateral femoral circumflex Superior genicular branches of popliteal Blood supply Obdurator, medial femoral circumflex Obdurator, medial femoral circumflex M. branches of profunda femoris Obdurator, medial femoral circumflex Obdurator, medial femoral circumflex Obdurator, medial femoral circumflex M. branches of profunda femoris Action Flexes leg Flexes thigh Laterally rotates thigh Flexes thigh Extends leg Extends the leg Draws patella laterally Extends the leg Draws patella medially Extends the leg Tightens the capsule of the knee jt Action Flexes thigh ADDucts thigh Medially rotates thigh Flexes leg ADDucts thigh Medially rotates thigh Flexes thigh ADDucts thigh Flexes thigh ADDucts thigh Flexes leg ADDucts thigh Extends the leg

Muscle Pectinues Gracillus

Medial femoral region Origin Pectineal line of the pubis Inferior pubic ramus and pubic symphysis Between pubic crest and pubic symphysis, floor of femoral triangle Inferior pubic rami Ischiopubic ramus Ischial tuberosity

Nerve Femoral Accessory obdurator Anterior obdurator

Adductor longus Adductor brevis Adductor pt of the adductor magnus Extensor pt of Adductor magnus

Anterior obdurator Anterior obdurator Posterior obdurator Tibial nerve

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Posterior femoral region hamstrings Origin Insertion Linea aspera Combined tendon forms the lateral boundary of the popliteal fossa-can form pt of the fibular collateral ligament at the Ischial tuberosity fibular head Sacrotuberous ligament Semimembranosus Ischial tuberososity Oblique politeal ligament of the knee Ischial ramus and fascia of the popliteal muscle, medial border of the soleal line, groove on the medial condyle of the tibia Semitendonosis Ischial tuberostiy in Medial surface of the tibia, deep to the common w/ long head Sartorius, and distal to the gracilus of the biceps femoris Muscle Short head of biceps femoris Long head of the biceps femoris

Nerve Common peroneal Tibial nerve Tibial nerve

Blood supply Perforating branches of the profunda femoris, muscular branches of the popliteal artery Perforating branches of the profunda femoris, muscular rbranches of the popliteal artery Perforating branches of the profunda femoris, muscular branches of the popliteal

Action Flexes the leg Flexes the leg Extends the thigh Laterally rotates the leg Flexes the leg Extends the thigh Medially rotates the leg Flexes the leg Extends the thigh Laterally rotates the leg

Tibial nerve

The leg is dicided into 4 compartents contained within the crural fascia of the leg which is continuous with the fascia lata: anterior, superficial and deep posterior and lateral compartments. Anterior crural muscles Extensors of the leg Origin Insertion Tibia Medial plantar surface of the medial cuneiform and medial aspect of the base of the 1st metatarsal w/PL Extensor Hallucis Fibula Superior aspect of the base of the distal phalanx of the big toe Extensor digitorum Tibia and Divides into 4 tendons in front of the AJ, forms an longus fibula expansion over the dorsum of the MPJ where it fuses with the capsule near the PIPJ. That expansion divides into 3 slips: at the base of the middle phalanx, and 2 collateral slips to the bast of the distal phalanx Peroneus tertius Fibula Base of the 4th and 5th metatarsal Muscle Tibialis anterior Muscle Gastrocnemius Superficial posterior crural muscles Plantarflexors of the leg Origin Insertion Lateral head from the lateral (2/3rd) Posterior surface of the calcaneus frmoral condyle Fabella via the tendoachilles tendon in conjunction Medial head from medial with the soleal muscle. The direction of turn femoral condyle of the fibers of the Achilles tendon from superior to inferior AMPL LAMP (antFibula, tibia, soleal line med to post-lat and v/v) Lateral to the supracolndyle of Medial side of the posterior part of the the femur calcaneus and Achilles tendon Nerve Deep peroneal Deep peroneal Deep peroneal Blood supply Anterior tibial Aterior tibia Aterior tibia Action Dorsiflexion Inversion of the foot DF/inversion of the foot Extends hallux Extends the 4 toes at the MPJ Everts the foot Deep Peroneal Nerve Tibial nerve Aterior tibia Blood supply DF and everts the foot Action Plantarflexes the foot

Soleus Plantaris

Tibial nerve Tibial nerve

Plantarflexes the foot Plantarflexing the foot

Deep posterior crural muscles separated from the superficial by the deep transverse septum and from the anterior compartment by the interosseus membrane between the tibia and fibula Muscle Origin Insertion Nerve Blood supply Action Popliteus Lateral condyle of the femur, Triangular area above the Tibial nerve Genicular branches Flexes the leg, medially arcuate popliteal ligament, back of soleal line- antagonist to of popliteal rotates the leg, in CKC, the lateral meniscus vastus medialis laterally rotates leg Tibialis posterior Tibia, FibulaTendon descends behind the medial malleolus, bound by Tibial Peroneal a Plantaflexes and inverts sesmoid bone that the lacinate ligament below the FDl under the ABH below nerve Posterior tibial the foot inserts into the the spring ligament inserting into the navicular tuberosity, Principal invertor of the navicular continues onto the plantar surface to insert into all the tarsal foot bones except the talus and base of 2-4 metatarsals FDL Tibia, below the Tendon descends behind the medial malleoli, below the Tibial Posterior tibial Flexes the lateral 4 toes soleal line sustentaculum tali, to insert in the base of the distal phalanx nerve Planatarflexion of the in the lateral 4 toes below the FHL foot FHL Fibula Deep to the lacinate ligament along a groove on the Tibial Muscular Plantarflexes the foot posterior surface of the talus and sustentaculum tali, nerve branches of the Flexes the big toe running obliquely across the sole of the foot above the FDL popliteal between the sesmoids and the belly of FHB (campers chiasm) into the base of the distal phalanx

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Master knot of Henry is where FDl/FHL crosses right above the navicular and marks the distal limit of the tarsal tunnel Lateral crural muscle of the leg Muscle Origin Insertion Nerve Blood Action Peroneal longus Tibia and Behind the lateral malleolus in common with the peroneus Superficial Anterior Plantarflexes the foot Fibula brevis through a notch on the lateral side of the cuboid peroneal tibial Everts the foot where a sesmoid bone maybe present, crosses the sole Plantarflex the 1st met enabling the oblique to inset in the lateral aspect of the medial cuneiform Common foot to remain plantigrade and base of the 1st met peroneal Peroneal brevis Fibula Winds around the back of the lateral malleolus and inserts Superficial Peroneal Plantarflexion and eversion of the into the tuberosity of the 5th met peroneal foot. Major pronator of the foot Dorsal foot muscle: Extensor Digitorum brevis/ extensor hallucis brevis Origin Upper/lateral surface of the calcaneus, lateral talocalcaneal lig, cruciate crural lig, extensor retinaculum over the sinus tarsi Insertion EHB most medial tendon-inserts in the proximal phalanx of the hallux; EDB-4 tendons (2-4) into the lateral side of the EDL. Blood/nerve supply Dorsalis pedis and lateral tarsal a, deep peroneal nerve Action Extends the medial 4 toes a t the MPJs and IPJs and abducts There are 4 plantar intrinsic muscle layers of the foot from plantar to dorsal 1ST layer-most plantar layer: FDB, ADH, Abductor digiti quinti Muscle Origin Insertion Flexor digitorum medial process of 4 pt tendon for the lateral 4 toes, each pt divides brevis the calcaneus into 2 pts and inserts in the middle phalanx. FDL is located between the split on the way to the distal phalanx of the lateral 4 toes Abductor hallucis Medial process of Medial sesmoid at the base of the proximal brevis the tuber calcanei phalanx of the big toe in common with the medial head of the FHB Abductor digiti Lateral/medial Lateral side of the proximal phalanx of the lillte minimi process of the toe-some fibers are inserted in the 5th metatarsal calcaneus Muscle Quadratus plantae 1st lumbrical 2nd lumbrical 3rd lumbrical 4th lumbrical 2nd layer-quadratus plantae, lumbricales Origin Medial head-Medial surface of the calcaneus Lateral head-lateral surface of the calcaneus and long plantar ligament Medial side of the FDL of the 2nd toe Unipennate Medial side oFDL of the 2nd/ 3rd toe Bipennate Medial side of the FDL of the 3rd/4th toe Bipennate Medial side of the FDL of the 4th/5th toe Bipennate Insertion Deep surface of the tendon of the FDL Below the deep transverse intermetatarsal ligament Medial side of the base of the proximal phalanx of the respective 2-5th toes and into the extensor hood apparatus Nerve Medial plantar nerve Medial plantar nerve Lateral plantar nerve Baxters nerve Nerve Lateral plantar nerve Medial plantar n Lateral plantar nerve Blood supply Medial plantar a Medial plantar a Lateral plantar artery Action Flexes the proximal and middle phalanges at the PIPJ Flexes and ADDucts the hallux Flexes and Abducts the little toe

Blood supply Lateral plantar a Plantar metatarsal a

Action Flexes the terminal phalanages of the lateral 4 toes Increases the slack of the FDL, aids the interossei in the flexion at the MPJ and extension at the IPJ Wave bye-bye

3rd layer-FHB, transverse and oblique head of the adductor hallucis, flexor digiti minimi Muscle Origin Insertion Nerve Flexor hallucis brevis Medial head-Medial pt of the Medial sesmoid, base of proximal Medial plantar plantar surface of the cuboid, phalanx of the hallux w/ABH nerve Lateral head-lateral cuneiform, Lateral sesmoid in common with and tibialis posterior the oblique head of the ADH Adductor hallucis Oblique head-base of the 2-4 Lateral sesmoid, proximal phalanx Lateral plantar mets and sheath of PL of the hallux with the lateral head nerve of FHB Transverse head-capsule of Fibrous sheath of the FHL the 2-5 MPJ, deep transverse intermetatarsal ligament Flexor digiti minimi Base of the 5th met Lateral side of base of the proximal Lateral plantar phalanx of the 5th toe

Blood supply 1st plantar metatarsal artery 1st plantar metatarsal artery

Action Flexes hallux

ABDucts an dlfexes hallux

Lateral plantar

Flexes little toe

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4th layer-4 dorsal interossei, (DAB) 3 plantar interossei (PAD) Muscle 1st dorsal interossei 2nd dorsal interossei 3rd dorsal interossei 4TH dorsal interossei 1st plantar interossei 2nd plantar ineterossei 3rd plantar interssei Origin Adjacent sides of the 1st/2nd mets (bipennate) 2nd/3rd (bipennate) 3rd/4th (bipennate) 4th/5th (bipennate) Medial side of the 3rd met (unipennate) Medial side of the 4th met (unipennate) Medial side of the 5rd met (unipennate) Insertion Above the deep transverse intermetarsal ligament, medial side or the proximal phalanx of the 2nd toe Lateral side of the proximal phalanx of the 2nd toe Lateral side of the proximal phalanx of the 3rd toe Lateral side of the proximal phalanx of the 4nd toe Medial side of the bases of the proximal phalanx of the 3rd toe Medial side of the bases of the proximal phalanx of the 4th toe Medial side of the bases of the proximal phalanx of the 5th toe Nerve Lateral plantar nerve Deep peroneal Lateral plantar nerve Blood supply Dorsal metatarsal a Action Dorsiflexion and Abduction, aisst the lumbricals with flexion antagonist to the long extensors

Lateral plantar nerve

Plantar metatarsal arteries

Dorsiflexion and ADDuction of the 3rd5th toes, assist in flexing the PIPJ sans extending the DIPJs

3. Neurological system 4. Congenital and developmental Normal development Embryology in biomechanics 4 wks post ovulation Limb buds begin the plantar surface of the foot is initially cephalid and undergoes internal rotation where it faces the midsagital plane at 6 weeks 7 weeks-primitive shape of the LE is present (1st ossification center in the femur and tibia) 3rd month the foot is in 90 degree equinus with marked adduction and supination, by the mid month the foot deigns to DF and supinate with the 1st met adducted, by the end of the 3rd month, the foot begins to pronate to midsupination, slight met varus persists therefore a normal MA value at birth is 22-25 degrees. Reaches and recognizes Crawls Rolls, plays Creeping Walking Developmental history and pertinent milestones 4 months 3-5 months 6 months 7-9 months 9-16 months

Femur development: frontal and transverse planes Frontal plane: angle of femoral inclination Infants 135-155 Abnormality Slipped femoral epiphysis Adult (18 months) 120-135 Coxa valga >130 at adulthood bow legs with compensatory genu varum Coxa varum <120 at adulthood knock knees with compensatory genu valgum Common during childbirth, M>F (10-16yrs) where the femoral epiphysis slips inferior and posterior. TX: surgical

Transverse plane (bony) angle of femoral declination antetorsion Infants Adult 30 degrees internal (8-10) degrees internal via external rotation Antetorsion Failure to externally rotate, the femur is still internally rotated leading to squinting patellainternal knees and intoed gait Retrotorsion Externally rotates beyond the normal frog-eyed patella Reduction pattern Rapid : Adult value in 18 months Gradual : Adult value in 14 yrs Spurt: correlates in growth spurts Transverse plane (soft tissue) version Infants Adult (18 months) 60 degrees external 12 degrees external via internal rotation Anteversion Too much internal rotation external knee position Retroversion Overly internally rotated internally rotated knee and intoed gait

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Hip Development: Frontal plant Frontal plane Infants 2-3:1 external to internal ratio Total hip joint ROM 155 Adult (6 yrs) 1:1 ratio 90 Geriatric (>45 yrs) 2:1 along with an increase in the patients base of gait >90 degrees

Total hip joint ROM is measured with the knee flexed or in full extension. An increase in internal hip joint range of motion or internal knee position is generally significant clinically. Total ROM is 80-120 Internal rotation> external rotation is NEVER normal femoral anteversion is most common cause Knee Development: Transverse, frontal and sagittal planes Transverse Plane Alignment Internal Genicular Position Infant >15. Internal genicular position (pseudoloack of malleolar torsion) Age 3 Age 6 (adult) 0 via internal rotation 5 Present when an excess of 20 to 25 transverse plane excursion is present and the internal:external range of motion ratio is 2:1internally rotated and intoed gait

Frontal Plane Alignment of the knee Genu Varum and Genu Valgum Birth-2 2 yrs 4 -6yrs 6-8 yrs Girls (12-14)

Genu varum Straight Valgum Straight Secondary valgum

From the ages of 4 to 6, secondary to an increased rate of growth of the medial epiphysis of the tibia, a valgus alignment is normal. At age 6 to 8, alignment should again be straight.

Sagittal Plane Alignment of the knee Genu Recurvatum It is important to evaluate the etiology of genu recurvatum it may be secondary to functional adaption or ligamentous laxity extension of the knee joint beyond 180 and behind the frontal cardinal plane of the body is significant. TibiA: frontal and transverse planes Frontal Plane Tibial Varum and Valgum Infants-3 yrs 3yrs + Varum 15 degrees varus <3 degrees of varus Valgum Malunion of the tibial epiphysis, trauma occurs almost never Tibial varum/valgum assesses the relationship between the lower one third of the leg and the ground. Tibial varum/valgum plus subtalar joint neutral position primarily determine the presentation of the foot to the ground. Measurement is taken with the patient in his/her angle and base of gait. The patient should be placed in neutral calcaneal stance position to eliminate the influence of subtalar joint position. Transverse Plane Alignment Malleolar Position/ External Tibial Torsion childs age x 3 >6 yrs Infant-1 yrs 2-3 yrs Age 7 (adult) 0 11 degrees 17-23 degrees 13-18 degrees via external rotation Failure to externally rotate intoed gait with the femur in the frontal plane This reflects transverse plane alignment of the lower leg. Abnormal values can result in deviations from the normal angle (approximately 15) and base of gait (approximately 2 inches when measured between the medial malleoli.) The measure of malleolar position is the clinical method utilized to assess tibial torsion. Actual tibial torsion is accepted to be malleolar position plus 5. A closer look at rotational developmental abnormalities Patellar postion Management

Description

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Femoral antetorsion Femoral retroversion Pseudolack of malleolar torsion Malleolar position

Not enough normal external rotation of Internally rotated Outgrown. By 14 yrs. Modify the sitting position of the the femur Causes intoed gait where child, functional orthoses, bars, gait plates and twister interal >external hip ROM cables are necessary if fx problem Too much external rotation of the femur Externally rotated Outgrown, Functional orthoses Causes outoed gait where ext>internal hip ROM Not enough external rotation of the tibia, 2o to tight Midline Manipulation via external rotation, serial gastrox and hamstrings intoed gait casting, and functional orthoses High out toe gait, Low intoe gait, 2o to persistent Midline Not outgrown, bars and splints, casting, fx medial development of talar head/neck orthoses, gait plates and twister cables Ankle Joint Range of Motion

Infant >50 Axis Motion

The anatomy of the triceps surae enables this muscle to influence motion at the level of both knee and ankle joints. AJ ROMdifferentiates between a gastroc equinus, soleus equinus, gastrosoleus equinus and osseous equinus Age 10 Age 15 (adult) 15 10 average axis position of the ankle is 83 from the frontal plane, it is angulated 20-30 from the transverse axis of the knee provides the majority of its motion primarily in the sagittal plane A simple guideline to remember is that AJ dorsiflexion should be 15 by the age of 10 and 10 by the age of 15. <10 equinus, evaluated w/ positive silfverskiold test which elicits more DF with the knee flexed indicating gastrosoleal equinus Subtalar Joint axis and Range of Motion

STJ ROM assesses the relationship of the RF to the lower 1/3 of the leg measurement in terms of how the foot is presented to the ground and how the foot will be able to accommodate for any osseous or functional abnormalities. triplanar axis average axis position to the sagittal plane 16 (supinatory/pronatory) average axis position to the transverse plane 42 Motion Frontal:Transverse plane 1:1 (High) Transverse plane ROM increases if STJ has a more vertical axis (more compensation of ad/duuction) (Low) Frontal plane ROM increases if STJ has a more horizontal axis (more compensation of inv/eversion) Total ROM Child: 30-45 Adults: 30 in frontal plane, inversion: eversion 2:1 The normal range of subtalar joint motion in the adult is approximately 30 and ROM > 10 may suggest a coalition of the tarsal or midtarsal bones. Forefoot to Rearfoot Relationship Midtarsal Joint axes and ROM oblique midtarsal joint longitudinal midtarsal this joint is comprised of the C-C joint and affects the lateral this is a functional joint is comprised of the TN articulation affecting the column of the foot medial column of the foot although it is triplanar, the majority of its motion occurs in the the majority of motion in the LMTJ occurs in the frontal plane, transverse and sagittal planes compensating in the same accommodating GRF by pronating and supinating opposite to that of direction of the STJ the STJ total ROM 4-6 57 from the sagittal plane 9 from the sagittal plane 52 from the transverse plane 15 from the transverse plane when the subtalar joint is in a pronated position, the axes of the midtarsal joint become more parallel to each other the more parallel the axes, the greater the available range of motion, particularly of the oblique midtarsal joint First Ray Range of Motion 45o from the frontal and transverse plane Dorsiflexion with inversion; Plantarflexion with eversion 65-70 degrees of dorsiflexion with 45 degrees of plantarflexion at the MPJ 1 cm total ROM 5 mm of DF and 5 mm of PF Deviation from a 1:1 dorsiflectory to plantarflectory ratio suggests either osseous deformity (metatarsus primus elevatus or plantarflexed first ray) or soft tissue adaptation (forefoot supinatus). 5 ray ROM 35 degrees from sagital; 20 degrees from the transverse plane Dorsiflexion with eversion with promation and plantarflexion with inversion supination CKC, DF with abduction PF with adduction of the 5th ray
th

triplanar axis (supinatory/pronatory) Motion 1:1 frontal:transverse Total ROM

triplanar axis (supinatory/pronatory) Motion sagital < frontal plane

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Calculated Subtalar Joint Neutral Position Subtalar joint neutral position is historically calculated on the belief that the subtalar joint possesses twice as much inversion as it does eversion. That is two-third inversion to one-third eversion. Formula Subtalar joint neutral position = Eversion (Inversion + Eversion / 3) Calculated Neutral Calcaneal Stance Position Neutral calcaneal stance position reflects the actual degree of neutral inverted or everted presentation of the lower leg to the ground. Formula STJN + Tibial position Measurement of Resting Calcaneal Stance Position Resting calcaneal stance position is the summation of leg presentation to the ground and the compensation of forefoot to rearfoot relationships (be it compensation at the subtalar or midtarsal joint.) It is measured by evaluating the relationship of the calcaneal bisection to the ground when the patient is standing in their angle and base of gait. From 0-5 yrs, the foot is flat and everted, so to calculate RCSP in children 7 - age Formula in adults Availabe eversion + STJN Measured Limb Length from ASIS to Medial Malleolus Limb length discrepancies can influence foot function and compensatory mechanisms. Limb length is measured from the anterior supierior iliac spine to the tip of the medial malleolus. It is generally accepted that a limb length of less than inch is not treated. Normal angular development Infants (degrees) Adults (degrees Metatarsus 30 (20 at ambulation) 5-15 by age 7 Used to asses adduction of the FF to theh MF, assists in assessment of HAV adductus angle Calcaneal 10-15 arch increases 15-25 by age 6 Angle formed by comparing the proximal and distal aspects of the calcaneal inclination angle inferior surface with WB surface. Increases with supination and decreases with pronation and ples planus Talar declination 15-25 decreases 10-15 Compares bisection of talar neck to the WB surface. Increases with pronation, decreases with supination, angle may approach 90 with VT deformity Talocalcaneal 30-50 decreases 20-40 by age 4 Bisection of talar neck to calcaneal bisection, increases with pronation and (kites) decreases with supination. Is negative in clubfoot deformity Congenital disorders Def & Symptoms Etiology Xrays DDx Tx CalcaneoValgus Identified at birth, marked DF (calcaneus) at the ankle and eversion of the foot. Dorsum of foot in contact with anterolateral leg; Foot completely relaxed with loose skin folds below lateral maleolus & medial skin stretched. Relaxed TA NO EQUINUS! Intrauterine position; 1:1,000 F>M; more common in young mothers 1st baby tight uterus, CIA normal, Calcaneus DF Vertical Talus, Neuromuscular Dz, None necessary; Reassure parents, Casting Club foot (Talipes Equinovarus) 1/1000 live births w/2:1 M:F and 50% b/l. Autosominal dominant trait w/ 40% penetrance; 33% in identical twins It is a triplanar deformity where the ankle is in equinus, the hindfoot is in varus, and forefoot is adducted. Unlike VT, the TN joint is dislocated in a supinatory position and the navicular is plantarly dislocated on the talus EQUINUS + RIGID SUPINATION Causes are idiopathic from intrauterine position or intrinsic (mc) and extrinsic: acquired via neurogenic spina bifida, CP, MD, meningitis, post-polio or post-traumatic. Theory retracing fibrosis during 10th -12th IU week. Bone deformity 1o - talar neck & head ; 2o metatarsus adductus Joint deformity 1o Talonavicular; 2o STJ, ankle, midfoot & MPJ

Pathologic Anatomy Talus Smaller head & neck angulated medial plantar; anterior lateral deviation in the ankle mortise;

Calcaneus Normal shaped, under developed sustentaculum tali, anterior & medial facets fused and

Navicular Normal shape Hypertrophic tuberosity Plantar medial subluxation May articulate w/ medial

Soft Tissue All on MEDIAL side contracted: deltoid ligament, spring ligament, laterally-posteriorly: PTF, ATF, CF, interosseus and bifurcate ligaments must be released comprehensively

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TDA decreased 115 135o Talar neck obliquity 50-60o

angulated plantar medial beneath talus

malleolus

and circumferentially (posterior, medial, lateral and plantar); Peroneals elongated lateral side

Radiographic evaluation: Normal Clubfoot Kites angle (TCA) 20-40 0-15 (decreased or parallel) CIA 20-25 ~17 Talar head/neck relative Adduction 10-20 80-90 Transverse plane to the body Plantarflextion 25-30 45-65 Sagittal plane Simons rule of 15 Predicts the presence of TN subluxation using AP x-ray TCA <15 Talo-1st met angle >15 Symptoms club like foot, small drawn up heel, adducted foot, calf atrophy, decreased foot size, medial skin creases & furrows, prominent; navicular, FF adducted; lateral skin thin & stretched, talus prominent & fibular posterior. Treatment Conservative Ponsetti method -Manipulation 10 15 minutes, abduct FF, evert & distract heel >> Serial casting for FF adductus 1st, varus 2nd, equinus 3rd (AVE) & AK cast q 1-2wks >> night splints, orthotics, PT, stretching Complications - Rocker bottom, flat top talus or talar AVN, Met adductus, pes valgus-overcorrection, wedge shaped naviular Surgical Comprehensive circumferential release posterior >medial> lateral> plantar via cincinatti incision; Ideal age 3 -12mths & b4 3yrs; Turco procedure posteromedial plantar soft tissue release with internal fixation via hockey stick incision posterior >medial>plantar Lengthen TP, Spring ligament, FDL, FHL, Deltoids, Interosseous ligament, Calcaneofibular lig, ACH, Plantar fascia, TN joint & Posterior ankle joint capsulotomy, bifurcate lig, Osseous Indication rigid deformity in children & adults only; Fixated w K-wire to STJ & TNJ 4-6wks, BK cast changed wkly 6mths Lateral Column Ogston 1902 cuboid closing wedge Shortening Evans 1961 Calceneocuboid joint closing wedge & arthrodesis Lichtblau Anterior calcaneus closing wedge Medial column Fowler 1959 medial cuneiform opening wedge osteotomy with interposition of bone graft lengthening Ganley closing abductory cuboid osteotomy Salvage Triple arthrodesis > 12yrs; Talectomy 4-8yrs old Complications Wound dehiscencs, residual deformity, navicular wedging and subluxation, flat top talus, Rocker-bottom foot, overcorrection; 25-50% have repeat Sx for residual deformity Soft Tissue Metatarsus Adductus Description: Transverse plane deformity (C-shaped adduction) in which the mets medially deviates w/ the apex of the deformity at the LisFranc articulation. Commonly associated with tibial or femoral torsion, congenital hip dysplasia, club foot and a windswept deformity (met adductus on 1 foot and calcaneovalgus on the other) Incidence: 1/1000 F>M 4:3 or 3rd child, 10:1 met adductus to club foot Cause: IUP, tight ABH, absent or hypoplastc medial cuneiform, abnormal insertion of AT, sitting/sleeping position Classification: Flexible-deformity is reducible w/manual manipulation <6mo, Rigid-not manually reducible, casting only sometimes effective>2yrs, Dynamic-only present upon WB d/t tight ABH Clinical features: adducted ff, convex lateral border and concave medially, Cigar sign wide 1st interspace, prominent styloid process, tight or spastic ABH, RF varus Clinical diagnoses: Lichtblaus test The ABH is palpated just proximal to the met head; tightness or spasticity can be detected Combined deformities: tibial torsion, spina bifida, arthrogryphosis multiplex congentia XR evaluation: Normal degrees Met Adductus MA Birth (15-35) 1 (20) 4 yrs (15) >21 is considered pathologic Engles angle 24 >24o Simons angle Talus-1st met bisector 0-20 negative TCA 20-25 increases Cuboid sign Normal cuboid position Medially displaced cuboid Treatment Conservative passive stretching, manipulation, serial casting before the age of 2 Casting order: midfoot, forefoot, rearfoot, equinus and maintained with a Ganley splint, Wheaton Brace; modify sleeping position, orthotics, shoes, splints Surgical procedures are age dependent: 3-8yrs-soft tissue, >8yrs-osseous Soft tissue procedure (3-8 yrs)

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Heyman Herndon and Strong 1958 Thompson 1960 Lichtblau 1975 Johnson Lange #1 LaPorta & Sokoloff Peabody & Muro1933 McCormick & Blount 1949 Steytler & Van Der Walt 1966 Berman & Gartland 1971 mc Lepird 1982 Fowler Lange #2 Brink & Levtsky

3 dorsal incisions capsulotomies and ligament releases of all met joints at the Lis Franc joint, leave plantar structures intact to prevent dorsal dislocation Resection of ABH, tenotomy and medial capsulotomy. Cast for 4-6 weeks Modified Thompson, tenotomy or partial resection of ABH. Closing base wedge osteotomy of 1st met base + Resection of cartilages chondrotomies at met bases 2-5 Capsulotomy of the 1st MC joint, division of the ABH tendon, correction by casting Tibialis Posterior lengthening + TN capsulotomy Osseous procedures (>8yrs) Excision of the bases of the 3 central mets (2-4) with closing wedge osteotomy of the 5th Mobilization and luxation of the 1st MC jt with correction of abnormal TA insertion Arthrodesis of the 1st MC joint, with Osteotomies of 2-4 and wedge resection of the cuboid Base wedge V-shaped oblique osteotomies of all the mets, apex angled at RF Dome-shaped osteotomies through 1-5 met bases, 1st & 5 mets fixated w/ steinmen pins. Oblique wedges removed from 1-5 mets where the osteotomies are performed at proximal 1/3 of 2-4 mets in an oblique fashion (distal dorsal to proximal plantar) parallel to WB surface. Release of ABH tendon with opening wedge osteotomy of the MC with bone graft Osteotmies of 2-4 mets Cuneioform and cuboid wedge osteotomies w/ K-wire fixation

1st met base at least 6mm from physis Untreated Met adductus Hammertoes, HAV, Pes planus Skew foot: Adducted FF results in severe STJ pronation. Midfoot abducts and RF everts Z-shaped foot Skew Foot Aka Z foot, Serpitine, compensated met adductus; Metatarsus adductus FF, normal midfoot w/ pathological RF valgus; Etiology improper manipulation and serial casting for met adductus >> RF pronated; untreated met adductus compensated w/ excessive STJ pronantion; congenital met adductus w/ calcaneovalgus. S & S mets angled medially, prominent base of 5th met, large space b/t hallux & 2nd toe, digits abducted in stance, talar bulging (ptosis) on wt bearing w/ low medial archabducted midfoot w/ internal rotationof malleoli, RF equinus Xrays Increased MA angle > 21o Increased Cuboid abduction (calcaneocuboid) angle > 5o Indications for Sx failed conservative tx or too old, deformity increasing despite conservative Tx, secondary deformities emerging, painful compensatory symptoms, increased difficulty with standard shoe gear. Sx Tx Multiple corrections; Equinus Gastroc recession or TAL; Pes planovalgus Evans opening calcaneal osteotomy & medial arch tenosuspension. Evans lengthens the lateral column and realigns the midtarsal joint; Met adductus modified Berman-Gartland or Lepird; STJ instability STJ arthrodesis Club Foot FF ADDucted Navicular subluxed medially RF varus Equinus Simons angle - positive Kites angle decreased Talonavicular relationship navicular medial

Met Adductus vs Club Foot (TEV) Metatarsus Adductus FF aDDucted Lateral navicular subluxation RF neutral or valgus NO equinus Radiographic Simons angle - positive Kites angle normal or increased Talonavicular relationship normal or navicular lateral Clinical

Tarsal Coalition Description: Bridge that causes restriction or absence of motion between 2 or more tarsal bones, can produce dramatic symptom complex ultimately resulting in rigid peroneal spastic flatfoot. Incidence: M>F 4:1, 50% b/l Etiology: Acquired Trauma, arthritis, infection Ca;or congenital accessory ossicles or genetic Associated abnormalities: synphalangism, metatarsal, vertebral, sacroiliac fusions Classification: Tachdjians-descriptive classification that suggests the importance of assessing other areas of the foot and the remainder of the body. Types: synostosis, synchondrosis, syndesmosis. In order of most common- TC, CN, TN, CC, cuboidnavicular, navicularcuneiform TN 3-5 ossification CN bar 6-12 ossification reset bar with interposition of EDB TC bridge 12-16 years ossification fuse a bridge * mc 90%* Bar coalition b/t 2bones that dont normally articulate extraarticular (CN); Bridge coalition b/t 2 bones that normally share articular surface intraarticular (TC, TN, CC)

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Clincal Findings-insidious onset of pain developing after trauma or unusual activity, pain aggravated by activity, relieved with rest, limitation of ROM with spasm, recurrent ankle sprain, sinus tarsi syndrome. Most common cause of Peroneal spastic flat foot d/t P. brevis attempting to restrict painful STJ motion TC CN bar X-ray Evaluation Lateral XR : Halo sign-absence or diminished visualization of the middle facet with enhancement of the sustenculum tali; Ball and socket ankle adaptive changes; TN beaking Calcaneal axial XR: fused middle facet/nonparallel relationship of middle/posterior facets lose their normal parallel relationship MO XR: Comma sign-protrusion of calcaneus toward navicualar, anteater nose sign:anterior facet toward navicular on Lat XR Mc osseous coalition in foot = 5th middle & proximal phalanx; Treatment Restriction of STJ & MTJ motion shoe modifications, orthoses, padding, casting; PT, NSAIDS, local steroid injections prn Bridge intra-articular fusion/arthrodesis. If small or incomplete - arthroplasty TC Middle facet arthroplasty resect 4-7 mm of bone. With significant arthritis >>>isolated TC or triple arthrodesis. CN Bar excise bar (1-1.5 mm) & interpose EDB is Juvenile CN Tx of choice = CN resection arthroplasty (Badgely Procedure); Post op BK cast 4wks; Complication recurrent bone growth d/t inadequate resection TN asymptomatic resection then fusion Calcaneocuboid fusion ; cubonavicular resection

Conservative Surgical

Vertical Talus AKA Congenital Convex pes plano valgus, Reverse Clubfoot, Persian Slipper, Rockerbottom Flatfoot Vertical Talus Description: Primary button-hole dislocation of the navicular dorsally on talar neck locking the talus in a vertical position 1o joint deformity is the TN jt in a pronatory position & 2o jt deformity at STJ, CC and AJ EQUINUS AND RIGID PRONATION w/ a contracted Achilles & elongated spring ligament Remember club foot = equinus & rigid supination Epi 50% B/L R>L, M=F 50% w/ isolated deformity; 4 clinical patterns: Assoc w/arthrogryphosis, spina bifida, neurofibromatosis & an isolated defect (50%) Pathological Anatomy Osseous Wedge shaped navicular w/ hypoplastic plantar segment PF ankle, Tibia articulates w/ talus only in posterior 1/3 Calcaneus close to distal tip of fibular & is everted & PF Hypoplastic sustentaculum tali, , NO anterior talar facet, Soft tissue P. longus is major deforming force; Talonavicular lig thick & blend w/ deltoids; superior peroneal retinaculum attenuated >> subluxation; TP tendon attenuated under talar head >> subluxed anteriorlly. Contractures to TA, EHL, EDL, PB, Triceps surae, Peroneus Tertius Dislocated TP, PL, PB

Clinical presentation: HPK beneath prominent talar head, deep dorsolateral creases, sulcus anterior to the fibula, peg-leg gait, and the entire foot remains rigid in relationship to the leg. FF abducted & pronated, tight ACH, hallow anterior to lateral malleolus, gait abnormalities and pain X-ray evaluation: Stress lateral XR to check TN dislocation will see on AP XR Kohler-like changes of the navicular, CC diastasis, elevated 1st met, flexion contracture of the 1st MPJ, and hour-glass talus. Dorsal dislocation of navicular. Remember navicular ossifies at 3-4yrs so will not see on xray, Norm Vertical talus Club foot Kites angle (TCA) 20-40 >40 (increased) 0-15 (decreased or parallel) CIA 20-25 Negative angle ~17 Surgical procedures staged FF correction then RF Soft tissue lengthen contracted & dislocated tendons capsulotomy of TN, ankle & CC joints TAL, Transfer TA into talar neck ,Transfer PT into navicular Osseous Resect head and neck of the talus Partial resection of the navicular Fibular arthroeresis

Total talectomy Total naviculectomy

Description

Brachymetatarsia Short, hypoplastic metatarsal d/t premature closure of epiphyseal plate; Epidemiology uni or bilateral, 25:1 F:M, 4th met most common, evident b/t 4-16; Etiology congenital, developmental, iatrogenic, traumatic, Infectious

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Associated Conditions Classification S&S Treatment

Downs Syndrome, Turners, Sickle cell Anemia, Dystrophic dwarfism, Albrights , pseudohypothyroidism, pseudohypoparathyroidism, poliomyelitis, myositis ossificans I shortening of 1st met only; Type II shortening of 1-2 lesser mets, Type III shortening of 1st & 1 or more of lesser mets, Type IV shortening of all mets short contracted floating toe, short met, metatarsalgia on adjacent metatarsals, plantar calluses under adjacent met heads, deep sulcus underneath short metatarsal; Xrays: Short underdeveloped metatarsal, osteoporosis of the metatarsal head Conservative orthotics or accomadative devices, padding Surgical soft tissue: V-Y skin plasty- relieve tension of contracted skin. Z-plasty lengthening of long extensor tendon, tenotomy of short extensor tendon, MPJ capsulotomy (dorsal,med/lat release) sectioning of deep transverse intermetatarsal ligament Tx Surgical Osseous osteotomy lengthening frontal plane Z osteotomy; insertion of cortico-cancellous bone graft >>>NWB cast; Callus distraction 1mm/day, delay 5-7days Complications lengthening too aggressive >> neurovascular compromise, Lesser MPJ limitus, delayed union / nonunion, resorption/collapse of bone graft, painful pseudoarthrosis, painful limitation of joint motion

Other congenital deformities Description/Treatment Classification Macrodactyly Digital gigantism localized NF, fibrolipomatosis of all tissues 1. Macrodactly simplex congenita except blood vessels and tendons. Usually unilateral. Tx: 2. Macrodystrophia lipomatosis progressive epiphysiodesis to arrest growth and de-bulking procedures Syndactyly Congenital webbing of the toes does not interfere with function 1. Davis and German a. Incomplete b Complete c. and is not objectional cosmetically. No tx is needed Simple d. Complicated Polydacyly Supernumary digits. 1. Temtamy and McKusick (post-axial [lateral digits] or pre-axial [hallux]) Autosomal dominant 2. Venn and Watson preaxial polydactyl (wide or short 1st met) Post-axial polydactyly blacks>whites and F>M. Tx: a. Wide metatarsal b. T-shaped met c. Y-shaped met excision, optimum age for d. Partial polydactyly e. complete duplication surgery between 9-12 mo 3. Central Fibular hemomelia Congenital longitudinal deficiency 1. Achterman and Kalamanchi of the fibula interference w/limb 2. Stanitski and Stanistski bud development. Associated a. Fibular morphology (I nearly normal, II small, III absent) b. Tibiotalar joint amd w/tarsal coalitions and absent foot distal tibial epiphyseal morphology (H horizontal, V valgus, S spherical) c. rays Presence of tarsal coalition ( c) d. Number of foot rays, medial to lateral (1-5) Ectrodactyly Autosomal dominant. Assoc w/syndactyly, cleft palate, polydactyly and deafness. Tx: reconstructive surgery is required Congential digital Skin is shortened dorsally; the digit is contracted on the long axis w/nail pointing laterally b/c hard w/callus. Assoc w/ minimus varus flexor stabilization. Tx: PIPJ arthroplasty and derotational skin arthroplasty incision is proximal lateral to distal medial Clinodactyly Congenital curly toe-may be d/t to differential epiphyseal growth or overcrowding from adjacent digits. Tx: splints, taping, sx as w/overlapping 5th toe Ainhum Dactylosis spontanea, fibrous bands begins on medial side of the toe (5th esp) encircles and autoamputates Milroys dz Hereditary edema of the legs, inherited Achondroplasia Autosomal dominant-defective enchondral bone formation. Associated with ligamentous laxity and trident hand deformity Osyeogenesis imperfecta Inherited disorder of defective collagen maturation fx in various stages of healing Osteochondroses True AVN Blount a lateral slippage of the proximal Tibial epiphysis Freiberg Met heads Renandiers dz Tibial sesmoid Trevers dz Fibular sesmoid Diaz or Mouchet Talar body Legg-Calve-perthes Femoral head Kohler Navicular Not true AVN Islen 5th met base Bushke Cuneiforms Theiman Phalanges Lance Cuboid Sever Calcaneal apophysis Osgood-Schlatter Tibial tuberosity Assmans head of 1st metatarsal 5. Kinesiology and gait analysis

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B. Trauma 1. Sprains, strains and soft tissue injuries Lateral Ankle Sprains Definition: stretching injury which may involve partial or complete tearing of the lateral ankle ligaments Anatomy 3; Intracapsular anterior & posterior talofibular ATF/PTF ligaments; extracapular calcaneofibular CF ligament Shape of the talar dome: wider anterioly than posteriorly which results in decreased frontal plane stability of the ankle when plantarflexed and increased w/dorsiflexion. (CAM puts ankle in DF) Recall that the ankle is almost parallel to the frontal plane so the STJ provides the inversion that leads to this injury. ATF and CFL make an angle of 70-140 degrees. Mechanism of injury repetitive inversion injury to ankle Associated injuries: Ankle fractures syndesmotic high ankle injury if suspected tx with NWB cast for 4-6 weeks Shephards fx of os trigonum Tx: NWB 6-8wks talar dome fx evaluate with a talar dome compression test and a AP ankle in max PF calcaneal anterior process fx via avulsion of bifurcate ligament Tx: NWB 6-8 weeks 5th met base avulsion fx via avulsion of lateral slip of plantar fascia and to a lesser extent the PB, TX: NWB 6-8wks sinus tarsi syndrome Damage to the lateral malleolar artery, CPN drop foot and acute compartment syndrome Risk factors: Biomechanical: ankle equinus, gastrox or soleal weakness, FF/RF deformity and transverse plane abnormality History of previous ankle injury is the #1 risk factor Incidence: 40% of all sports injuries (most common injury in all of sports) Physical examination: 1. evaluate anterior-inferior syndesmosis A. Squeeze test B. Tibio-talar shuck test C. External rotation test 2. Anterior and drawer test (Push-pull test) - evaluates ATF, >2mm anterior displacement as compared to the contralateral side indicates rupture. A positive test dimple sign The ATF is on stretch when the ankle is PF 1st to be ruptured 3. Posterior drawer test - evaluates PTF clinically. 4. Anterior and posterior ankle palpation 5. Muscle testing especially peroneals and flexors possible rupture or tear of these tendons 6. DF and PF of MTPJ shepherds fracture or flexor tendon injury X-ray examination: Ottawa ankle rules-who gets an x-ray someone who canot bear wt or w pain over syndesmosis or posterior malleolus (AP/MP/Lat ankle and MO foot) 1. Stress inversion to evaluate the CFL A. Radiographic grading: 1. Grade 1: + push-pull test and +/- inversion stress not possible to have a +inversion stress and a push-pull test because the ATF will rupture b/f the CFL 2. Grade 2: +push-pull and + inversion stress (10 degrees) 3. Grade 3: +push-pull and + inversion stress (15 degrees) 4. Grade 4: +push-pull and + inversion stress (>15 degrees) 2. Talar tilt >5 degrees as compared to contralateral ankle: >5 ATF rupture, >15-30 ATF and CF rupture and >30 ATF, CF and PTF rupture 3. + Anterior drawer (push-pull) >10mm of anterior displacement or >4mm compared with the contralateral side 4. MO foot checks for C-C crush, fx of anterior process of calcaneus, and fx of 5th met base Classifications 1. Leech: Anatomical Classification Grade 1: ATFL sprain, Grade 2: ATFL and CFL sprain, Grade 3: ATFL, CFL and PTFL sprain 2. ODonoghue Classification Grade 1: Partial tear of the ATF, Grade 2: Complete tear of the ATF, and partial tear of the CF, Grade 3: Complete tear of ATF and CF Grade 4: PTF injury 3. Dias - Grade I - partial rupture of CF, Grade II - ATF rupture, Grade III - ATF, PTF and CF rupture Management: Casting vs functionalCAM (1: allows for early WB 2: ankle DF to reapproximate ATF), begin rehabilitation ASAP vs surgical Jones compression for 0-5 days, consider bone scan, MRI and CT to r/o other possible injuries Syndesmotic injury: wb immobilization 4-6weeks limit pd of NWB Treatment: Acute sprain Protection, Rest, Ice, Compression, Elevation and NSAIDS (PRICEN) Rehabilitation (4-8 weeks) Phase I: Acute phase contrast bathing, interferential stimulation, Jobst compression, CPM Phase II: Rehabilitation phaseactive ROM, peroneal muscle strengthening, stretching, massage, jt ROM, u/s

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Phase III: Functional phase (Proprioceptive excercises) BAPS, plyometrics, toe raises- balancing exercises Phase IV: Return to activity phase sport specific mvmt, preventive strategies, and equipment modifications When should a pt return to activity? Minimal to no edema, no limp, be able to perform 1 legged toe raise, ability to descend stairs, 1 legged lateral hop test, ankle dorsiflexion test Ankle braces >>tape: both reduce the incidence of ankle inversion sprains by increasing peroneal reactivity and strength through direct contact with the skin (proprioception). Atheletes should be braced for up to 6 months following an injury. Tapes last 10min (40% reduction) Contraindicated in pts with high tibial varum, may increase lateral instability Chronic lateral ankle instability Definition: #1 complication of inversion ankle sprains Functional vs mechanical (anatomic lateral ankle instability) Functional cannot be adequately evaluated via radiography or manipulation Disabling loss of reliable static/ dynamic support of a jt, deficit in peripheral reflexes, proprioceptive de-afferentiation, proprioceptive nerve ending located primarily in the skin, and pain results increasing stability b/c of the anesthetic blockade of the STJ and AJ. Loss of: mobility, strength, position sense, stability in single leg stance, detection of passive mvmt, functional ability and reflex speed 60% of functionally unstable ankles do not show pathologic talar tilt Treatment: Conservative: more rehab, a better brace, MRI/CT/Bone scans to r/o additional injury or prioltherapy (thermal shrinking of the lateral ligs with a wand and prolotherapy (injectable sugar solution to enhance proprioception Surgical Procedures do a stress x-ray as a prelude to surgery Delayed primary Brostrum -repair of lateral ligaments/ retinaculum by overlapping (imbrication) & suturing via 00-2-0 ethibond sutures ligamentous repair Gould modification: use of the anterior inferior extensor retinaculum, reinforce over fibula, repair of CFL is unecessary Post-op: NWB 2wks, WB 2wks in CAM and PT for 1 month. Yields better results than stabilization procedures Lateral stabilization procedures Disruptive to normal anatomy, technically difficult, results in overtightening of AJ-Use in pts w/ligamentous laxity or with collagen vascular diseases Repair ATF by passing tendons through Watson-Jones P. brevis sutured to P. longus fibula, talus & calcaneus following Lee P. brevis to PL anatomic orientation of the ATF Suppan P brevis Repair ATF & CF Elmslie fascia Lata Split PB ankle stabilization procedure Peroneus brevis Christmas and Snook split P. brevis Repair ATF, CF & PTF Hambly,k Sammarco & DiraimondoRepair without following specific anatomic Nilsonne P. brevis orientation Keilikian Evans P. brevis Other ankle conditions 1. Talar dome fractures Description Mechanism of injury Compression fracture of the talar dome via the tibial plafond, most commonly misdiagnosed following an inversion ankle sprain DIAL-A-PIMP AnteroLateral lesions occur with dorsiflexion/inversion injuries - wafer shaped 44%, mortise view; PosteroMedial lesions occur with plantarflexion-inversion injuries - deep cup shaped 56% AP view

Classification: Berndt-Hardy ''Osteochondritis dissecans'' is a chronic condition that leads to loose bodies d/t spontaneous necrosis w/o dz, trauma or tumor. Stage I - subchondral bone compression fx; not seen on radiographs; painless lesion Stage II - partially avulsed, detached osteochondral fragment; rupture of the lateral collateral ligaments of the ankle Tx RICE, 4 wks NWB BK cast immobilization or 2-4 wks WB cast Stage III - completely detached, nondisplaced transchondral fragment Stages III - surgical excision of small fragment, curettage & drill-hole fenestration to subchondral bone to aid revascularization & stimulate fibrocartilage production; 4wks NWB w/CPM machine and then 4wks WB cast Stage IV - completely detached and displaced transchondral fragment from the talus; Larger fragments - If >2cm fragment ORIF via malleolar osteotomy or arthroscopy fragment excision, saucerize the crater, drill-hole (1.5mm) fenestration of the subchondral bone to enhance fibrocartilage production with early NWB ROM & resumption of WB 2-3 weeks postop. Posterior medial lesions may require malleolar osteotomies for visualization. Stage V-subchondral cycst is present OATs MosiacPlasty chondroplasty can be used with large defects from the trochlear talar surface or non-articaular surface of the knee. The size of the graft is usually 5-9mm. This procedure is ideal for focal defects and for young patients.

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Autologous Chondrocyte Implantation (ACI) Cultured chondrocytes originally harvested from the pt are re-implanted after 3-4weeks of culturing. Prognosis post traumatic OA 2. Talar lateral process fracture Snowboarders ankle Tx: non-displaced: 6-8wks NWB, displaced: ORIF 3. Eversion ankle sprina/medial ankle pain (5-10% of all ankle injuries) Medial malleolar contusion/fracture WB for 4-6wks Medial malleolar stress fracture (insidious) Posterior tibialis tendonitis Spring ligament injury navicular tuberosity avulsion fx, os tibialis externum Tarsal tunnel syndrome Flexor tendonitis Deltoid ligament injury 4. Peroneal syndromes: tendonitis, tenosynovitis, rupture, dislocation/subluxation Tendonitis Consider with a history of lateral ankle sprains, on PE pt has weak/painful eversion and pain w/forced inversion or a LLD Tx: RICE, NWB for 4-6 weeks and PT, injectable phosphate corticosteroid into sheath, sx debridement if necessary Tenosynovitis Often d/t impingement, hx of chronic tendonitis. Tx is similar to tendonitis however sx debridement is required Dislocation Secondary to rapid ankle DF, m.c. in skiing, not common in inversion ankle injury. Tx requires surgery. Subluxation only significant if painful. Tx requires surgical intervention Peroneal Tendon Dislocation Eckert & Davis Classification Grade Description Treatment Grade I superior peroneal retinaculum is damaged only Primary repair of retinaculum 6 wks short leg cast Fibular rotational osteotomy; CFL with bone block Grade II Fibrocartilagenous ridge and retinacular damage Groove deepening procedures Grade III Retinacular damage and Eckert fracture Sx correction is required for all 4 grades d/t ineffectiveness of closed tx. Post-op immobilization in short leg NWB cast 3wks > walking cast. 5. Anterior ankle impingent exostosis footballers ankle Descriprion Insidious onset anterior ankle pain with deep anterior ankle palpation and forced DF. Diagnosis Equinus, radiographic spurring do a stress lateral X-ray or a MRI for soft tissue impingment Management Heel lift, injectable ccs, massage, u/s, arthroscopic debridement 6. Posterior ankle pain Causes Posterior impingment, painful Os trigonum, shepards fx (medially), retrocalcaneal bursitis, pre-achilles bursitis, FHL injury dancers tendonitis PE Pain with releve; ankle PF or with forced PF Management Injectable ccs, jt mobilization, dexamethasone iontophoresis, surgical debridement 7. Medial Ankle Instability Rare; Anatomy 5; extracapsular tibionavicular, tibiocalcaneal, superficial tibotalar; intracapsular deep anterior and posterior tibiotalar ligaments Mechanism of injury - forceful eversion; Dx stress eversion mortise Xray - Talar Tilt >10o d/t rupture of TC & superficial TT ligaments Surgical procedures: Duvries - repair of the lax deltoid ligament Wittberger and Mallory - split PT (leave insertion intact) passed through drill hole in medial malleolus & sutured down on itself; acts as tendon graft Schoolfield detached damaged deltoid, invert foot & re-suture into periosteum superior to detachment site; advances the deltoids 2. Fractures and dislocations Nail Trauma Subungual Hematoma runners toe Acute tx: PRICEN, and a digital aperture may be necessary for athelete to resume activity If involves >25% or more of nail plate >> remove nail plate and inspect nail bed. Laceration to nail bed examine, repair and suture under LA use absorbable sutures - 5, 6, 7-0 If the nail bed is lacerated, the fracture is considered an open fracture The basic tx for an open distal phalangeal fx is local wound care, tetanus prophylaxis and antibiotic therapy Classifications: Rosenthal - goal - try to preserve or restore tip of toe; general treatment of cleaning, debridement and packing Zone I distal to bony phalanx; Tx close by 2o intension using STSG, FTSG, Reverse dermal graft Zone II distal to lunula; Tx Local pedicle graft , V to Y Advancement Zone III proximal to lunula Tx not amenable to reconstruction

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Digital Injury /Fractures Can be displaced, non-displaced, avulsion, oblique, spiral, transverse fractures and require splinting to the adjacent digits with coban or with a silicon appliance. Most hallux fractures require a rigid surgical shoe for 4-6 weeks. Mechanism of Injury crush, stub, laceration puncture, direct trauma, hyperextension, abduction-adduction Presentation- pain edema, eccymosis, subungual hematoma 1st MPJ Injury/Dislocation Anatomy Tib & Fib sesamoids, MPJ collateral lig, FHB tendon, FHL, inter-sesamoidal lig, Adductor & abductor hallucis Classification Jahss Turf toe Mechanism - 1st mpj hyperextension (mva, falls from height, sports injuries) S&S hallux dorsally subluxed @ MPJ w/ met head prominent plantarly; POP & ROM; extensor apparatus relaxed & flexor apparatus tightened; hallux flexed @ IPJ. Treatment: RIICE, strapping, NSAIDS

Type IIA Type IIB dorsal dislocation of the proximal dorsal dislocation of the proximal phalanx; phalanx & the sesamoids; ISL rupture & sesamoids displaced medial & lateral to met head; sesamoids subluxed to each side of met transverse avulsion fx of one sesamoids ISL intact head; sesamoids not fractured sesamoid is fractured Tx - cannot be closed reduced; must be can be closed reduced; slipper or bk cast can be closed reduced; slipper or BK cast 6wks open reduced 3 - 4 wks; surgical shoe 3wks NWB; surgical shoe 3wks Complication immediate compromised circulation AVN; recurrent dislocation and up to 50% of turf toe injuries result in long term mobility Pre-dislocation syndrome 2nd digit at MPJ - pain, swelling, capsulitis, tendonitis, metatarsalgia; Acute dislocation of lesser mets - rare; chronic dislocation seen in RA, cavus foot type, Tx PRICE, Immobilization - buddy splinting, closed reduction & external fixation, ORIF, soft tissue release, bone resection, flexor tendon transfer, PIPJ arthrodesis, arthroplasty, implant or capital osteotomy w/ K-wire fixation Sesmoiditis Anatomy: 2 sesmoid bones are present, plantar to the 1st met head in 85% of population. They are invested in the tendons of the FHB, FHL, ADH, ABH muscles. They function as a fulcrum for motion at the MPJ. Etiology: Crush injury in which the sesamoids are crushed in the sagittal plane between the 1st met and the ground, jumping or improper shoe gear Biomechamical abnormalities that predispose: Pes Cavus, peroneus longus spasm, metatarsus primus elevatus Clinical presentation: pain and swelling is sually unsidious, is in the appropriate location Treatment; casting, padding, orthoses, icing, NSAIDS, and relative rest. When chronic: iontophoresis, ccs injection. If fx of sesmoid is present poor prognosis and high non-union rate owing to poor vascularity, must be excised Ilfelds disease- agenesis of one or both of the sesmoids 5th Metatarsal Fractures Anatomy Peroneous brevis inserts at styloid process, lateral band of plantar facia and peroneus tertius at the met base Vassal Principle intact soft tissue structures assist in the reduction of fractures Complications of met Fx compartment syndrome, neurovascular injury, AVN, Neuropraxia

Type I dorsal dislocation of the proximal phalanx & the sesamoids on met head; ISL remains intact; sesamoid not fx

Types of 5th metatarsal fractures: 1. Styloid fracture- common in lateral inversion ankle sprains Tx: 4-6 wks WB immobilization 2. Metatarsal shft fracture dancers fracture Tx: 4-6 wks WB immobilization 3. Jones fractures: 1-1.5cm proximal from styloid process at metaphyseal-diaphseal junction Poor blood supply and the tendency to to go onto delayed or non-unions True stress fracture Tx is aggressive due to high reccurence of injury with 6-8 wks NWB immobilization and bone stimulation or until no evidence of fracture is seen on X-ray. ORIF may be indicated in severe diastasis or non-union Classifications 1. Stewart - E-I-E-I-Epiphysis

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Type I - Classic extra-articular jones fx Type II intra-articular fx of 5th met base o This injury is the result of shearing force caused by the internal twisting of the forefoot while the peroneus brevis is contracted Type III extra-articular avulsion fx of styloid process o Fracture line is usually perpendicular to the long axis of the met base Type IV intra-articular comminuted fx o The mechanism of injury is similar to Type II, but in this case the 5th met base gets crushed between the cuboid and the ground/shoe causing the fragmentation Type V - extraarticular avulsion fx of epipysis w longitudinal fragment; in peds o Can be classified as a Salter Harris I Type III Chronic fx w non-union & complete obliteration of the medullary canal by sclerotic bone; Hx of repetitive trauma & recurrent symptoms; periosteal new bone formation Tx - bone graft produres

2. Torg - Fx of distal base of 5th metatarsal classification system for Jones fracture Type I Acute Type II Subacute fx w/ absence of intramedullary sclerosis; fx w delayed union & intramedullary narrow sharp fx margins; minimal sclerosis; widened fx margins involving both cortical hypertrophy of periosteal cortices; hx of previous injury or fx; increased reaction to chronic stress evidence of periosteal new bone formation Tx Unna boot w NWB BK cast immobilization or ORIF w/medullary curettage + autogenous inlay bone graft 3. Chapman

Type IA - accute non-displaced fracture at metaphyseal -diaphyseal junction (Jones fx) Type IB - Jones fx, displaced or comminuted Type II - clinical/radiographic evidence of prior injury non-union type IA or IB Type IIIA - non-articular styloid process fx Type IIIB - intraarticular styloid process fx LISFRANC'S [Tarsometatarsal jt] FRACTURES/DISLOCATIONS

Anatomy - Lisfranc ligament is the strongest interosseous lig attaches med cuneiform to 2nd met base; avulsion fx of medial 2nd met base & lateral base of 1st met > diastasis = fleck sign in 90%; No ligament b/t 1st & 2nd met base This ligament is key to the stability of the Mortisse Mechanism - direct crush injuries to jt or indirect forced abduction of forefoot or loading of plantarflexed foot; twisting or equestrian injury occuring as foot is caught in stirrups; industrial injuries or MVA; Dx - xrays - always do contralateral films; AP diastasis 2-5mm bt base of 1st & 2nd met base; LAT flattening of medial column; dorsal displacement of mets; MO - disruption of normal continuity bt medial 4 met & cuboid, bt lat 3rd met & lateral cuneiform; CT is best study for Liscfranc injury

Classification Hardcastle (Queno & Kuss) Type A (total or homolateral) mc - disruption of entire TMJ/Lisfranc's jt. in a sagittal or tranverse plane, displacement of all mets usually lateral; Type B (partial or isolateral incongruity) dislocation of a portion of TMJ in a sagittal or tranverse plane B1 medial displacement of 1st met. alone or with met's 2 -4, but not 5 B2 lateral displacement of one or more of lesser mets; 1st met not affected Type C (divergent) C1 partial divergence with 1st met medially and some of lesser mets. 2 & 3 laterally C2 total divergence with 1st met medially and all lesser mets. laterally Tx - ORIF 83% success; 6wks immobilization; k-wires vs screws; open vs percutaneous sx & fixation, consider compartment syndrome Complication frequently missed injury >> post-traumatic arthritis Trauma to the cuboid Cuboid (Nutcracker) Fractures 5% of all tarsal fractures; mc on lateral aspect at calcaneocuboid jt & base of 5th met base; avulsion fx d/t tension on inferior calcaneocuboid ligament Mechanism of injury axial & rotatory forces while foot contacts ground in PF assoc w/ 5th met base & calcaneus fx; direct trauma, crush fx; avulsion fx must be differentiated from os cuboideum secondarium, os perineum or os vasalianum DDx - P. longus tendonitis, calcaneocuboid arthritis, dropped cuboid, capsule ligamentous strain in cavus foot; Tx simple short leg walking cast 6-8wks; crush arthrodesis

Cuboid syndrome subluxed cuboid

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An uncommon cause of overuse syndrome or traumatic midfoot pain. The ability to walk on heels or toes but not heel-toe is pathognomonic. Reduction is accomplished with the black snake heel whip maneuver and maintained with a strapping and a cuboid pad. Cuneiform Fractures

4.2% of midfoot; avulsion fx, body fx & stress fx; assoc w/ lisfranc dislocation; Mechanism of injury direct trauma or rotational forces; Dx bone scan Tx compression dressing & elevation , short leg walking cast Complication chronic pain and arthritis Trauma to the navicular Os tibialum externum fracture Commonly a disruption of the existing synchondrosis or synfibrosis of the os and the navicular Tx: Immobilization, PT tendon strengthening, icing and orthosis. High rate of recurrence is indicative of early excision Navicular Fracture Anatomy o The blood supply is precariousanastomsing of the DP & medial plantar artery-where the central portion of the navicular is relatively avascular owing to the large amount of cartilage covering the surface increasing the risk of AVN and pseudoarthrosis o PT tendon attached at navicular tuberosity Mechanism of injury-compression forces that impact the medial column against the head of the talus Classification Watson & Jones Type I - tuberosity fracture (24%) mechanism: forceful eversion >> avulsion fx by PT tendon; must r/o os tibiale externum & MTJ subluxation; Tx short leg cast NWB immobilization x 4-6wks Type II - dorsal avulsion lip fracture (most common navicular fx - 40%) o mechanism: plantarflexion & forced inversion causes avulsion fx via dorsal talonavicular ligament; plantarflexion -eversion causes avulsion via dorsal tibionavicular ligament; Tx short leg cast NWB immobilization 6-8 wks; Orthotics & shoe modification Type III - transverse fx of the body (29%) w dorsal fragment dislocation vertical or horizontal o mechanism: Fall from height /longitudinal force along the ray when ankle PFed; horizontal plane fx - lg dorsal fragment & small plantar fragment; Tx - closed reduction; skeletal transfixation; if crif/orif fails >>> loss of keystone of the medial longitudinal arch >>> flatfoot deformity; tx w TN & NC arthrodesis. Short leg cast -12 wks (6NWB & 6 WB Type IV (as described by Eftekhar) - stress fx of middle 1/3 in young athletes; differentiate from overuse syndrome, Dx CT, bone scan; Tx NWB short leg cast 4-6wks & resume activity in 3-6 mths Fractures of Talus Anatomy no muscular or tendinous insertion or origin; 60% covered in articular cartilage, widest anteriorly & more secure in mortise in DF; 2nd most common tarsal fx; 3-5% of foot fx Blood supply to talus: Head - Anterior tibial dorsalis pedis Body - Posterior tibial deltoid artery & artery to tarsal canal; Peroneal art A to sinus tarsi Posterior Tubercle - Posterior tibial > medial calcaneal artery Classifications 1. Hawkins Classification - Talar Neck Fx (50%) describes injury + predicts prevalence of AVN; Mechanism of injury - hyperextension & forced dorsiflexion of foot causing the neck of the talus to impact and fracture against the anterior lip of the distal tibia; mva, motorcycle & plane accidents aviators astragalus Type I (20%) - nondisplaced vertical fx of the neck of the talus; 1 of the 3 main blood supplies to the talar neck is disrupted - artery of the sinus tarsi; avascular necrosis - 0-15% Type II (42%) - displaced vertical fx of the talar neck w/ dislocation of the STJ; 2 of 3 main blood supplies to the talar body is disrupted - artery of the sinus tarsi & artery of the tarsal canal; AVN - 42% (15 - 50%) Type III - displaced vertical fx of talar neck with STJ & Ankle joint dislocation; All 3 main blood supplies to the talar body is disrupted - artery of the sinus tarsi; artery of the tarsal canal; deltoid artery; AVN - 91% Type IV - displaced vertical fx of the talar neck with dislocation of STJ, AJ & TNJ; All of the 3 main blood supply to talar body is disrupted - artery of the sinus tarsi, artery of the tarsal canal & deltoid artery AVN - 100% Treatment Type I - BK, NWB cast for 6-8 weeks Type II -IV closed reduction; ORIF via anteromedial approach w screw fixation through head & neck of talus perpendicular to fx line; if not work longer immobilization 3-4 mths, STJ, pantalar or triple arthrodesis, bone graft or amputation, talectomy, Blair fusion, bone stimulation, external fix Healing Hawkin's sign subchondral radiolucency at fx site 6-8wks after injury; indicates revascularization & r/o AVN.

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Complications- degenerative OA of the STJ, AJ, non or mal-union, infection, intra-articular fx, AVN 2. Sneppen - Talar Body Fx Group I - transchondral or compression fx to talar dome including osteochondritis dessicans Group II - coronal, sagittal or horizontal shearing fx of entire talar body; Etiology - severe dorsiflexion w/ compressive forces when talus is sandwiched b/t tibia & calcaneus o Type I - coronal or sagittal fx IA - non-displaced IB - displacement of trochlear articular surfaces IC - displacement of trochlear articular surfaces w STJ dislocation ID - total dislocation of talar body w displacement of STJ & AJ o Type II - horizontal fx IIA non-displaced fx dividing talar body into superior & inferior halves Tx - BK NWB cast 6-8 wks IIB - displaced fx, superior portion shifts on inferior portion Tx - closed reduction or ORIF, BK NWB cast x 6-8wks, then 6-8 wks BK WB cast if no sign of AVN or delayed or nonunion. Group III -fx in the posterior tubercle (most common fx of talar body; d/t severe plantarflexory force); DDx - Steida's process or sheperd's fx, os trigonum syndrome; seen in athletes esp ballet dancers o Sym - pain in posterior ankle causing limited ROM reproduced on FHL movement; o Tx - injection therapy of LA/steroid q3wks, BK WB cast x 6wks or surgical excision of lateral tubercle Group IV - fx of the lateral process of talus; 2nd most common talar body fx AKA Snowboarders Fx eversion injury w/ lateral process caught b/t fibula and calcaneus, Group V - crush fx (comminuted) of talar body o Dx xrays AP, LAT, CT Subtalar Joint Dislocationbasketball foot Atraumatic inversion force to the STJ may result in medial dislocation of the clacaneus, navicular and distal bones with the talus undisturbed. When complete dislocation occurs the talocalcaneal and cervical ligaments are injured (cruciate ligaments of the foot). Buckingham classification Type A - Medial STJ dislocation, AKA "basket-ball" or acquired clubfoot; calcaneus medial to talus Type B - Lateral STJ dislocation, calcaneus lateral to talus Type C Anterior & posterior STJ dislocation Tx RICE, manipulation with knee flexed to 30o ankle at 90o and foot everted and immobilization in short leg cast after 7 days for 6-8 wks; complication - AVN Calcaneal Fractures 60% of all tarsal fx, 75% intrarticular M:F 5:1 Mechanism of injury - axial load drives lateral process of talus into calcaneus; associated w falling from a height > 6ft; males >45yrs; 20% associated w spinal fx b/t T12 & L2, L1 mc; Symp - Mondor's sign (ecchymosis from lat malleolus to sole of foot) & inability to bear wt Dx - LAT xray Bohler's angle n 20-40 Decreased; Gissane's angle n 120-140; Increase; Classification 1. Rowe - Extraarticular fx of calcaneus Type I o IA) Fx of the medial tuberosity o IB) Fx of the sustentaculum tali o IC) Fx of the anterior process mc (avulsion fx of bificate ligament) Type II o IIA) Beak Fx no ACH involvemt o IIB) Avulsion Fx of Tendo Achilles Type III - extraarticular oblique Fx of calcaneal body not involving STJ Type IV - Fx involving STJ w/o jt depression or comminution Type V - comminuted fx of STJ w/ central or severe depression Tx surgery pull calcaneus tuberosity distally, elevate posterior facet, fill calcaneal defect with bone chips, screw fixation from lateral into sustentaculum tali 2. Essex-Lopresti - Intra-articular calcaneal fxs BIG ON BOARDS Type I - tongue type fx d/t vertical fall, 1 line exists plantarly; 2 fx line exists posteriorly Type II - joint depression fx d/t posterior fall; mc; 1 fx line exists plantarly; 2 fx line exists posterosuperiorly (dorsally)

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3. Sanders (CT) CT classification of intraarticular calcaneal fxs; use CT to determine location & fx lines through posterior facet & # of articular fragments; guide for surgical repair & prognosis Talus divided into 3 equal columns by 2 fx lines (A & B) & 3 pieces of posterior facet; C is 3rd fx line separting posterior facet from sustentaculum & creating a 4th fragment; Type I - nondisplaced articular Fx of posterior facet; Tx - NWB cast x 6wks Type II - articular Fx of posterior facet; 1 fx line, 2 fragments; A- lateral; B - central; C - lateral Type III - articular Fx of posterior facet; 2 fx line, 3 fragments w depression of central fragment Type IV - articular Fx of posterior facet; 3 fx lines, 4 fragments w commminution Tx - II-IV - obj to restore architecture of calcaneus by reestablishing height & width of the heel & relocating the posterior facet to its anatomical position. ORIF via lateral hockey stick (palmer) incision to maintain peroneal tendons & sural nerve in flap Ankle Fractures Anatomy Bones - fibula, tibia, talus; Ligaments lateral colateral ligaments (ATF. PTF and CFL) syndesmotic interval (AITF, PITF interosseous talotibial, interosseous talofibular ligament and interosseous membrane), deltoids, syndesmosis Blood supply anterior tibial artery, posterior tibial artery, peroneal artery Nerve supply- Sural saphenous, posterior tibial, superficial peroneal Muscles/tendons anterior AT, EHL, EDL & PT; posterior PT, FHL, FDL; Lateral PL, PB Ginglymus (hinge) joint DF & PF and gliding Dx Xrays AP, MO, LAT, Mortise ankle, Stress views, Arthrography, CT, MRI, Bone scanning 1.

Eponyms: Potts fracture: transverse fracture of the fibula 5.0-7.5cm above the distal end and associated with a tear of the delotoid ligament and lateral subluxation of the talus secondary to valgus injury 2. Cotton fracture: Trimalleolar fracture 3. Bosworth fracture: Bimalleolar fracture; posterior displacement of the fibula and Volkmans fracture 4. Dupuytren fracture: a fracture of the fibula about 6.0cm (2 1/2in) proximal to its tip accompanied by a rupture of the syndesmosis and either fracture of the medial malleolus or a tear of the deltoid ligament (PER III) 5. Maissoneuve fracture: Spiral fracture of the fibula that occurs at the anatomical neck 6. Cowtail fracture: an anterioposterior tibiofibular PER frcture involving rupture of th einterosseus membrane with an associated high fibular fracture 7. Tillaux fracture: Avulsion fracture of the tubercle of Chaput of the tibia 8. Wagstaffe-Lefort fracture: avulsion fracture of the fibula 9. Frost fracture: pediatric triplane fracture with the combinationof a SH2 lateral view and SH3 (Tillaux fracture on AP view) of the distal tibia Classification 1. Lauge Hanson Ankle Fx Named after a Denmark physician; first term describes position of foot at time of injury; second term is direction/motion of pathologic force on the talus; talus move relative to the leg & tibia moves relative to talus; staged relative to sequential pattern of injury; fx occur in clockwise pattern for rotational injuries & direct blows pattern across the ankle for abduction & adduction injuries. SER most common; PER most destructive Supination/ADD Rupture of the lateral collateral ligaments Transverse fibular fracture DWA Oblique fracture of the medial malleolus Lauge Hansen Classification of Ankle fractures Pronation/Abduction Supination/External rotation Rupture of the deltoid ligament Rupture of the AITF/PITF or TC Transverse fracture of the medial or WF fx malleolus Rupture of the AITF/PITF or TC or WF fx Oblique fracture of the fibula DWB Butterfly fragment Spiral fracture of the fibula DWB Posterior spike on lat X-ray Volkmans fracture or PITF rupture Rupture of the deltoid ligament Transverse fracture of the medial malleolus ORIF Pronation/External rotation Rupture of the deltoid ligament Transverse fracture of the medial malleolus Rupture of the AITF/PITF or TC or WF fx Spiral fracture of the fibula DWC Massoineuve Volkmans fracture or PITF rupture <30% of the articular surface is not fixated ORIF

II III IV TX

closed reduction, short leg walking cast

closed reduction & short leg cast; ORIF

2. Danis-Weber - Fibular Fx in Ankle Injuries Type A - fibular fx line below the tibiofibular syndesmosis Most likely a stable fx and does not need ORIF; = SAD 1

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 Type B - fibular fracture at the level of the tibiofibular syndesmosis Usually a spiral (SER 2) or oblique fx ( PAB 3) of the fibula; unstable and needs ORIF; Type C - fibular fracture line begins above the tibiofibular syndesmosis; may or may not be stable so clinical judgement is indicated; = PER 3 Tx - Re-establishing the length & position of the lateral malleolus is the most critical element of management. If superiorly & posteriorly displaced ORIF; Tension band wiring used for compression or lag screw technique with 4.0mm cancellous screws; Fibula fixated with 3.5mm cortical screws and Tubular plate w two screws both above & below the fx; 2 syndesmotic screws are used to correct diastasis & should engage a minimum of 3 cortices; screw placed 3-5cm proximal to ankle joint Pilon Fractures Mechanism of injury direct impact of talar trochlear against the distal tibial articular surface; Soft cancellous metaphysis of distal tibia is compacted >> large void when length is resotred. Classification Reudi Algower Type I Type II Type III Distal tibial Fx without displacement Distal tibial fx with significant Distal tibial fx with significant displacement and displacement comminution Tx combination of internal & external fixation; 4 steps 1- reconstruct the fibular 2- reconstruction of tibial articular surface 3- bone graft the metaphyseal deficit 4 buttress plate the tibia medially; if fracture unfixable - ex fix 5-8 wks then ankle fusion Epiphyseal Fractures Physis is radiolucent cartilaginous growth plate. Injury d/t disturbance of physeal blood supply based on fx type - good if physis separates from metaphysis; poor when fx cross the physis; worse when fx crosses physis completely covered by articular cartilage. Physeal injuries comprise 10% of all pediatric fx (4.4% tibia\fibula; 5.9% foot) are more common during the first year average age 10-12 & puberty, and more frequent in boys. Mechanism of injury - shear, avulsion, bending, axial compression. Indirect trauma is the mc mechanism of ankle injury in children. Type I & II - shear force - younger kids; Types III & IV -bending/ compression force - older children. If blood supply is not disturbed heals in 3 wks. Tx Type I & II closed reduced; Type III, IV, V ORIF restoration of jt congruency using smooth k-wires may cross physis; Classification Salter-Harris - physeal injury I I III IV V V VI VII VIII Epiphyseal Plate fractures: Salter Harris Same Along the growth plate Above Above the growth plate-exhibits a Thurston Holland Sign (triangular spicule of bone) Werinskoild sign Lower Below the growth plate Through Through the growth plate Really Bad Compaction of the growth plate Zone of Ranvier fracture Epiphyseal fracture, does not involve physis Metaphyseal fracture, does not involve physis Periosteal avulsion

POSTERIOR TIBIAL TENDON RUPTURE Anatomy PT originates from fibular and tibia inserts into navicular + medial & intermediate cuneioform, base of 2nd, 3rd & 4th met; PF, inverts & Adducts foot; Nerve posterior tibial, Blood sural, peroneal & posterior tibial arteries Mechanism of injury direct laceration rare eg medial malleolus fx (PER IV); chronic or acute stress on degenerated tendon CVD, pes valgus, chronic tenosynovitis, corticosteroid injection, RA; Watershed area behind medial malleolus; Jacks test lose heel inversion with heel lift; Rupture >> PF adducts & subluxes TN joint; longitudinal arch collapses, spring ligament stretched, choparts jt abducts, calcaneus everts Classification 1. Funk's Classification surgically Based, 1986 Group 1 - Avulsion of PT tendon at the insertion; Tx reattach tendon at navicular Group 2 - Midsubstance tear at the level of the medial malleolus; Tx FDL side to side anastomosis Group 3 - Longitudnial splits without complete rupture;Tx debridement & synovectomy and sheath decompression Group 4 - Tenosynovitits without visible disruption Treatment conservative: - Not Tx of choice, BK, NWB cast 6wks, Foot FF adduction & inversion then neutral BK WB 2-4 wks; Surgical Tx of choice 2. Johnson & Strom Stage I Stage II Stage III Tendon length normal, peritendonitis & or Tendon elongated, hindfoot mobile >> increasing pain Tendon elongated, hindfoot

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tendon degeneration >> normal foot focal pain proximal to medial malleolus 3-6mths of rest, NSAIDS, orthoses, deep heel cup 4-6mm Kirby skive Synovectomy, tendon debridement, rest BK cast 3 wks

along tendon, RF valgus, FF abduction, weakness on deformed & stiff >> fixed flat foot, heel raise pain on medial side d/t DJD FDL transfer under tension, undersurface of navicular via drill Realignment with STJ hole, BK cast 6wk + PT proximal attachment of TP muscle to arthrodesis , Evans, FDL; Kidner, Young, STJ arthroereisis, Evans, Dwyer, Dwyer, Koutsougianis, Koutsougianis, isolated arthrodesis isolated arthrodesis

Stage IV added by Myerson rigid hindfoot & valgus angulation of talus; early ankle joint degeneration; tendon length TENDOACHILLES RUPTURE Is anastomosis of tendons of gastrocnemius and soleus and inserts into calcaneus; Watershed area 2-6cm above insertion, area of poor vascularity Mechanism of injury direct injury laceration, crush, puncture; indirect, spontaneous post traumatic, degenerative, corticosteroid injection, fluoroquinolones Dx Tenography, u/s CTand MRI is best; Magic angle tendon oriented 55o from main magnetic field will create illusion of a tear in a normal tendon Type II Complete rupture, defect < 3cm Typically end to end anastomosis Type III Complete rupture, defect 3-6cm Repair end to end anastomosis with autogenous tendon graft flap, possible augmentation w/ synthetic graft Type IV Complete rupture, defect >6cm Gastrocnemius recession followed by end to end anastomosis with a free or synthetic tendon graft

Classification: Kuwada Type I Partial tendon tear 8 wks cast immunization if tear constitutes less than 50% of tendon

Compartment Syndrome Excessisve pressure in the muscular compartments of leg or foot ischemia and death of muscle tissue. 80% occur in LE. Resting compartment pressure - 5mmHg; During exercise pressure increases to 50mmHg and then returns to normal in 5-10minutes. Anterior and deep posterior compartments are most often involved. Anatomy Review Compartments in Leg ** Remember No Medial compartment** Anterior Compartment Lateral Compartment TA, EHL, EDL, Peroneus Tertius Peroneus Longus Peroneus Brevis

Posterior Compartment Superficial: Grastocnemius , Soleus, Plantaris Deep: FHL, FDL, TP, Popliteus

Compartment in Foot 1st Layer 2nd Layer 3rd Layer 1 4th Layer FDB, ABH, ABDM Quadratus Plantae, Lumbricals FHB, FDMQ, ADH 4DAB interossei and 3PAD interossei Etiology Trauma, surgery, burns, exercise, tight cast, crush injuries, fractures (Calcaneal), Symptoms 6- Ps Pain out of proportion, Paresthesia, Pulses present or pulselessness, Paralysis, Pink, Pressure Diagnosis Wick catheter (eg. Stryker) inserted into muscular compartment and measures pressure. Intramuscular pressure > 30mmHg for > 8 hours is diagnostic Formula MAP (mean arterial pressure) Pulse = ^P (Delta P) if GREATER than 30mmHg normal NO COMPARTMENT SYNDROME Treatment Podiatric Emergency Supportive: Remove all dressings & casts; Do not elevate limb >> ^ ischemia; Hydration IV fluids helps protect kidneys and prevent renal failure from excess myoglobin; Surgical - take to OR & perform open fasciotomy ASAP to prevent tissue necrosis & contractures; Long incisions made to depressurize the compartment, wound packed open & delayed primary closure in 5- 7 days; NO TOURNIQUET! Protect from infection. Incisions: Foot - 2 dorsal and / or 1 medial; Dorsal over 2nd & 4th mets; Medial ?? Leg - single incision over peroneal compartment & all compartments can be decompressed; or double incisions through anterolateral compartment for anterior & lateral compartments and posteromedial compartment to decompress both superficial and deep posterior compartments Complications Volkmans contracture of muscle , muscle ischemia, muscle necrosis, muscle contracture, Renal failure secondary to myoglobinuria

C. Physical Medicine and rehabilitation 1. Evaluation and assessment

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Description: Treatment of pain and disease by physical means. It is the health profession concernes with of health, with prevention of physical disabilities and with restoration of function to patients disabled with disease, injury or pain. Advantages-Modality is applied directly to that body part, immediate results can be gained, it is non-habit forming when need to treat chronic infections Disadvantages-Time consuming, costly, chronic treatment, compliance and consistensy of the patient is an issue 2. Diagnosis Complete H&P working differential diagnosis 3. Treatment (physical medicine modalities) Modality Cold therapy Description Icing vasoconstriction, decreases metabolic activity, slows nerve conduction, lessens muscle tone, reduces muscle spasms and spasticity and produces superficial anesthesia reflex vasodiltion: Hunters response Vasodilation, increase in tissue metabolism, increase in the extensibility of collagen tissue, decrease in jt stiffness and edema, reduction in muscle spasm, pain relief, asisstance in the resolution of inflammatory infiltrates Indications Acute inflammation Mechanical trauma, pain, muscle spasms and spasticity, adjunct in muscle re-education, Subactue or chronic inflammation Chronic stages of arthritis, tendonitis, myositis, bursitis, tenosynovitis, sprains, strains, dislocations, contractures and pain Contraindications Vasospastic dz, fibrocytic stiffness, arthritis, HBP, preganancy and pts with peripheral neuropathy Loss of sensations, infections, open wounds, malignancy, hemorrhagic dz, metal implants, open epiphyseal sites, pregnancy, PVD, pacemakers

Therapeutic heat
Hot packs, paraffin baths, infrared, UV

Superficial heating modalities Monochromatic Infrared Radiation Anodyne stimulates the RBCs and cells of the endothelial lining of the microvasculature to release NO into the blood stream reducing tissue inflammation and promoting wound healing. Hydrotherapy Mechanical effects: reduce weight bearing (buoyancy), reduce edema by deep immersion using the hydrostatic pressure effect, and ulcer debridement is performed using the mechanical effects of the moving water. Fluidotherapy Deep heating modalities Ultrasound High frequency electrical current causes vibration of crystals in the U/S head producing a sound wave. Can be contraindicated in pulsed (greater mechanical or non-thermal effects that are to stimulate healing.) or continuous. peds with Peizoelectric effect: electrical to mechanical energy conversion. The sound is transmitted into the tissue, apophysitis, gradually absorbed and converted to heat with the greatest build up of heat in the: peripheral nerves- hematomas, bone muscle fat blood, with possible nerve damage if over irradiated. thrombophlebitis, Average time of treatment is 6-8 minutes which is dependent upon depth and area affected. over heart, eye, or Phonophoresis use of U/S to drive molecules into the skin for anti-inflam or anesthetic properties (Lidocaine, testicles hydrocortisone, ASA, dexamethasone-not creams-are air filled emulsions and poor transmitters) 1.0 MHZ is absorbed into deeper tissues, penetrates 3-5cm. 3.0 MHZ is absorbed in superficial tissues, penetrates 1-2 cm. Short Wave Application of high frequency currents (radiowaves) for therapeutic use. Acute inflammation, bleeding, fluid collection in Diathermy Conversion of electrical to magnetic to heat energy w/greatest build-up of heat tissues, ischemia, joint effusion, excessive in fat musclebone peripheral nerves. It heats tissue with a combo of induced sweating, moist dressings, exposure to gonads, or electrical currents and the vibration it imposes on the molecules of a tissue. boney prominence, menstruation Electrotherapy Description

Physiologic response

Clinical use Ambulatory aids

Stimulation os muscle tissue using direct or alternating currents. Direct (Galvanic) current: monophasic currents that provide a constant electron flow from the (-) electrode to the (+) with no oscillation or alterations major chemical and thermal rx in the tissue leading to muscle stimulation Alternating current: Biphasic or polyphasic current that provides alternating current from the (-) to (+) and v/v. There is no concomitant thermal or chemical rx, only stimulation of muscle. Iontophoresis use of low voltage DC current to move ions through tissues Excitation of nerve cells, changes in membrance permeability, protein synthesis, and fibroblastic and osteoblastic stimulation, changes in microcirculation, smooth and skeletal muscle contraction, tissue healing, increase joint mobility, enhance muscle fiber recruitment, muscle pumping action to improve lymphatic and venous flow. Analgesic effects (Peripheral and central) Gate theory of pain control Mucle contraction, pain control, enhance tissue and bone healing

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Crutches Canes Walkers Footgear Metatarsal bar Rocker bottom bar or sole

Measurement: 1) from the acillary area to the bottom of the heel and add 1 or 2 more inches 2) Measure fomr the anterior fold of the axilla to 6in anterolaterally from the foot. Instruction for walking crutches should be placed 6-12 in in front and outside both feet. Move both crutches forward simultaneously, then advance the weak extremity, and next advance the strong extremity Use on the opposite side of the injury, can and involved limb move together Walker height is set so that the elbows are flexed 20o A rubber, leather or synthetic piece of rounded material applied externally to the sole or internally to the innersole with its apex just behind the met heads An angulated sole with its apex just behind the met heads which promotes a rocking action and eliminates the toe break at push off, reducing WB pressure on bony prominences

Orthoses-A device used to mechanically assist, restrict or control function of the muscusculoskeletal system UCBL Used for the treatment of flexible flat foot, fabricated around a WB impression of the foot and utilizes a deep heel cup with long high medial and lateral flanges to restrict pronation. Frequently used with CP or other neurological conditions Blake inversion Originally developed to counteract marked pronatory forces encountered in running. Utilizes a significantly inverted standard off WB cast to produce a heel cup inverted 15o to as much as 75 o. Kirby medial heel skive Gait plates Rigid devices with extended medial (induces in toe) or lateral (induces out toe) anterior margins used to alter a childs gait to achieve a more cosmetic appearance 1st ray cut-out Developed to address the need for independent 1st ray motion and propulsion. Commonly used with hallux limitus, and HAV pts AFO CROW Bracing and biomaterials Leather Earliest orthotic material, can be used for functional or accomodative orthoses Steel Used for brace components and shoe shanks Aluminum Used for brace components and shoe shanks-lighter weight Rubber Neoprene or Spenco

a closed cell expanded rubber material , it is good for absorbing vertical forces
Polyurethane foams Thermosetting, not heat moldable, commonly used of rrunning or walking shoe insoles. Poron-PPT

It is an open cell material made of polyurethane foam It has excelled abilities to reduce direct pressure as well as shear It generally is smooth on one side and abraded on the other making it somewhat uncomfortable when applied directly against the foot Its advantages include the fact that it does not bottom out with use, it is grindable and it is washabale
Polyolefins Polyethylenes-accomodative, will deform over time and can be used to produce a temporary function device Plastizote #1 soft #2 firm # 3 rigid

this is a closed cell, cross-linked polyethylene foam it is a high quality, lightweight, closed cell polyethylene foam that is non-allergenic. It is heat moldable, grindable and washable. It will quickly mold to foot contours during weight bearing, enhancing total contact. It is used extensively in the treatment of the diabetic and arthritic foot. It is not very effective as a shock absorber
Polyethylene thermoplastics Ortholen-High density Sub-ortholen- ultra high density Polopropylenes-high density thermoplastic, excellent memory-will not deform if thickness is appropriate for the pts wt. Usually posted with EVA or ethylene vinyl acetate acrylnitrile designed to replace Rohadur which is rigid, unbreakable and heat moldable TL-2100-tough, resilient, heat moldable

Polydur Graphite

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