PAIN common types of pain

The pain is usually classified into two categories: Nociceptive pain is caused b
y tissue damage. Usually described as acute pain, continuous or pulsating. May b
e due to a benign or cancerous tumors or cells that are growing and invading par
ts of the body near the area where the cancer. It may also be a cancer that has
spread to bones, muscles or joints, or has caused the blockage of an organ or bl
ood vessels. Neuropathic pain due to nerve damage. Nerves connect the spinal cor
d to the rest of the body and maintain communication between the brain and skin,
muscles and internal organs. Nutritional imbalances, alcoholism, toxins, infect
ions or autoimmune diseases can cause painful neuropathies from diseases such as
kidney failure. Neuropathic pain can be caused by a tumor pressing on a nerve o
r nerve group. Patients often describe this pain as a burning sensation or tight
ness, or numbness along the entire nerve. The cause of neuropathic pain is not d
etermined by one-third of cases. Chronic back pain and leg pain chronic back and
leg pain is described as a sit in the back, legs or both sites may be due to sp
inal disease, such as arachnoiditis, degenerative disease discs, epidural fibros
is post-laminectomy syndrome, herniated discs, osteoporosis and spinal stenosis.
Back pain is often located in the lumbar region, but can spread to other areas
such as thighs, calves and feet. The affected areas may be sensitive or painful
to touch and pain may increase with movement. This type of pain can be acute, su
ch as that caused by a knife, burning, or take the form of dull muscle pain and
continuous. The symptoms range from mildly annoying and completely disabling. Co
mplex Regional Pain Syndrome (CRPS) CRPS usually occurs in the foot or hand afte
r having suffered an injury (a broken bone) or after surgery that caused nerve d
amage. The SDRC is the abbreviation used to describe two pain syndromes also kno
wn as reflex sympathetic dystrophy (RSD) (CRPS type I) and causalgia. (CRPS type
II). The main symptom is extreme pain, often described as burning. Other sympto
ms may include tenderness, skin changes, swelling, weakness and decreased functi
on of the hand or foot. Painful Neuropathies Painful neuropathies are a common g
roup of neurological disorders resulting from injury to the nerves that generate
severe chronic pain. Nerves connect the spinal cord to the rest of the body and
brain get in touch with the skin, muscles and internal organs. Painful neuropat
hies may be due to nutritional imbalances, alcoholism, toxins, infections or aut
oimmunity, or may be caused by diseases such as kidney failure or cancer. In app
roximately one third of cases, the cause of the neuropathy is unknown.
Common symptoms of painful neuropathies are pain, burning sensation, weakness an
d stiffness. These symptoms are most common on hands and feet. Treatment is dire
cted at the underlying disease or condition, if known.
If you suffer from chronic pain, discuss treatment options with your doctor or s
chedule an appointment at a pain unit in your area is exposed PREVENTION Anyone
Anyone can develop chronic pain. Usually presented as older adults or people wit
h illnesses such as diabetes, arthritis or back problems. Persistent pain is not
a normal part of aging and treatment should be introduced. Chronic pain can not
be prevented in all cases. However, early and aggressive treatment of sudden, s
evere pain can reduce the chances that evolve into chronic pain. Certain conditi
ons may increase the risk of chronic pain, such as amputation of a limb (phantom
limb pain), arthritis or anxiety disorders. Lifestyle, unbalanced diets, smokin
g, alcohol or drugs, inactivity, may also predispose to chronic pain. The intens
ity of the pain that each person may experience after apparently identical lesio
ns is highly variable. There are people who have much, while others do not even
need painkillers to relieve minor pain. A particularly troubling situation, but
not uncommon€is suffering from severe and persistent pain after an apparently mi
nor injury, like cutting paper. We do not know why this happens. Some people see
m to have a predisposition to pain, whereas others seem immune to it. These indi
vidual differences may respond in part to the education received or cultural tra
ditions. However, there is increasing evidence that genes may influence the resp
onse to pain. And of course we can not control our genes.
"Pain is a major health problem in Europe. Although acute pain may reasonably be
regarded as a symptom of a disease or injury, chronic and recurrent pain is a s
pecific breakdown of health, a disease in itself" The Chronic pain often determi
nes the appearance of a complex set of physical and psychosocial changes that ar
e an integral part of the problem of chronic pain and significantly increase the
burden of pain for the patient: • • • • • • • • • • Immobility and, therefore,
muscular dystrophy, joint, etc. immune system depression and increased vulnerabi
lity to disease sleep disorders loss of appetite and malnutrition dependence med
ication over-reliance on family and other caregivers excessive and inappropriate
use of health care professionals systems on work performance or incapacity to w
ork , disability and isolation from society and family, introversion, anxiety, f
ear
• bitterness, frustration, depression, suicide DIAGNOSIS Talk to your doctor
Separate myth from reality No one knows how well your pain as you. In fact, you'
re the only person who can tell if your current treatment is effective for pain
control. For this reason it is important to talk with your doctor, nurse, and wi
th his family for pain treatment does not provide satisfactory relief. Be honest
and talk openly about their pain. Keep a diary and record their daily pain expe
rience. Doing so will help you remember important details when talking to your d
octor. To master the pain, you have to talk about it openly and honestly. Many p
eople do not attempt to relieve pain or even tell the doctor to feel. They often
do not say anything because they have a misconception of the nature of chronic
pain or have fears unjustified treatment, "I will become addicted to painkillers
" Medical research has shown that, when taken correctly, analgesics may relieve
pain without creating addiction. "If my current treatment can not control the pa
in, I must learn to endure" This is not always true. Be honest about your pain a
nd how it affects their lives. Ask your doctor for pain treatment known and appr
opriate for you. Often, if a treatment is not effective for pain control, anothe
r can be. Also, many side effects due to pain treatments can be solved or avoide
d. "People think I'm weak because I need help for pain" Some people think that l
iving with pain is a sign of strength, and that seeking help indicates weakness.
Do not let these myths keep you from talking to your doctor and other professio
nals to relieve pain. You can get help and relieve the pain, but only if you are
willing to talk about it. Do not have to live with severe chronic pain If the c
urrent treatment of pain does not provide sufficient relief or if bothersome sid
e effects that affect their daily activities or their quality of life, talk to y
our doctor. You can adjust the dose of medication, prescribe another that has fe
wer side effects or offer other options. If this does not solve the problem, you
r doctor may refer you to a pain specialist or a pain unit. In recent years, pai
n clinics have been created specifically to meet the needs of people suffering f
rom chronic pain. In these units work medical professionals with specialized kno
wledge of the problems of people with intractable pain.
Some units offer pain treatment coordinated by a team of healthcare professional
s consists of physiotherapists, nurses, counselors and psychologists, as well as
doctors. This multidisciplinary approach has evolved because it is increasingly
clear that chronic pain has a major negative effect on many aspects of life. In
these circumstances, the combination of treatments is usually the most effectiv
e way to improve welfare. TREATMENT Treatment Overview
The choice of treatment depends on the particular type of pain,€its intensity an
d effectiveness that have had other treatments for relief. You and your doctor m
ay consider using other treatment options if the current treatment does not cont
rol pain or cause unpleasant side effects. There are several possible treatments
: electrical MedicaciónEstimulación / neuroestimulaciónFisioterapiaProgramas tre
atment of pain: nerve block, neuroestimulaciónApoyo psicológicoCirugía: reconstr
uctive surgery, neuroablación alternativosMedicaciónLos analgesic treatments can
 be administered orally, rectal, transdermal and injectable (intravenous, subcut
aneous, intramuscular). These formulations are called systemic administration, b
ecause the painkiller circulates throughout the patient's body. FEVER 1 - INTROD
UCTION - Fever is a rise in temperature above the normal daily variation. - The
control of body temperature in humans occurs in the hypothalamus. This center ma
intains the body temperature of internal organs or body core temperature between
37 and 38 º C, mainly for their ability to balance the heat loss in the periphe
ry with the production of heat in the tissues, especially liver and muscles - Th
e core body temperature follows a circadian rhythm, with an evening peak between
16.00-20.00 hours and a minimum between 2.00 and 4.00 in the morning, with the
amplitude of this variation nictameral of about 0.6 - 1 º C. In women, the half-
degree temperature increases in the second half of the menstrual cycle after ovu
lation. 2 - DEFINITION: FEVER AND HYPERTHERMIA fever and hyperthermia are pathop
hysiologically two different processes. In fever the set point of the internal t
emperature at the hypothalamic level is elevated, preserving the mechanisms of t
emperature control. Thus the cycle is preserved ciradiano it. In hyperthermia me
chanisms fail to control the temperature so that heat production exceeds the los
s of it, with the hypothalamic set point normothermic levels hyperthermia charac
teristically does not respond to antipyretics (drugs that decrease hypothalamic
set point temperature), while there is some decrease in body temperature in febr
ile patients after adequate doses. Other aspects that guide hyperthermia are lac
k of sweating in a patient with high temperature
Absence of circadian variation in temperature hyperthermic syndromes The four la
rgest are: - heat stroke - anesthetic malignant hyperthermia neuroleptic maligna
nt syndrome - drug-induced hyperthermia or central hypothalamic fever. These are
patients where the hypothalamic balance point is raised due to local condition
(trauma, stroke, tumor, encephalitis, etc). This fever is characterized by the a
bsence of circadian variation, anhidrosis (unilateral or bilateral), resistance
to antipyretic with exacerbated response to the external cooling measures decrea
sed level of consciousness. 3 - HEAT BALANCE The body has an internal temperatur
e of 37 º C, while the skin temperature is 33.5 º C. Basically, the body tempera
ture is obtained from the balance between heat produced and eliminated maintenan
ce of body temperature depends on the heat produced by metabolic activity and lo
st body mechanics, as well as environmental conditions and the conductance. Ther
mogenesis or heat production Thermogenesis, or generation of temperature is done
in two ways: Quick (natural thermogenesis) produced largely by the tremor and t
he decrease in peripheral blood flow Slow (chemical thermogenesis) of hormone an
d substrate mobilization from cellular metabolism. Metabolic heat: heat producti
on increases with metabolic activity of the musculoskeletal, as occurs during ex
ercise. At baseline, the total production of heat generated between 1965 to 1980
cal / h, which can be increased to 300-600-900 cal / h during exercise. Moreove
r, when so intense shivering, muscle work increases heat production and increase
s metabolism of muscle cells. It also increases heat production: food intake and
increased basal metabolic rate (by the action of thyroid hormones, adrenaline (
stress), to a lesser degree norepinephrine and sympathetic stimulation) are impo
rtant factors termogenéticos In a body at rest zero heat exchange, metabolic hea
t could increase body temperature about 2 ° per hour thermolysis or heat loss ar
e various mechanisms by which heat is lost: Evaporation is the primary mechanism
.
When body temperature reaches a certain level, you sweat, the sweat evaporates i
t cools the skin and this cooling is transmitted to the tissues. You lose about
1 lime for every 1.7 ml of sweat. Unfortunately, even in cases of maximum effici
ency, the sweat can only remove between 400-500 cal / h. Sweating maintenance re
quires the replacement of lost fluid and Cl and Na ions. Otherwise, it would be
possible to keep the sweat production indefinitely.
The ability to sweat may also be delayed if ingested glucose Environmental humid
ity is also a major factor. Through evaporation, sweat it cools the skin and blo
od, can lose up to 585 calories per liter of sweat. If the humidity is above 60%
and the temperature above 32 º, the sweat does not evaporate, does not dissipat
e the heat. Other forms of heat gain or loss are: Leadership: The transfer of he
at by direct contact of body surfaces with the outside Convention involves the t
ransfer of heat from one place to another by means of a gas, in this case air or
water. When the air circulates around the body sweeps heat that has been heated
by contact through the skin, the greater the movement or the colder, for exampl
e in water, the greater the rate of heat removal. Although the conduction and co
nvention constantly removed the heat when the outside temperature is lower than
the body, makes only a minor loss of between 10 and 20%. However a body immersed
in water can lose up to twenty-six times more heat than a similar temperature o
f the air. Radiation at rest is the primary method of losing excess body heat. A
pproximately 60% of the heat expelled corresponds to radiation. It is released b
y means of infrared rays, which are a form of electromagnetic waves. If the outs
ide temperature exceeds the body is received by the same method radiated heat. T
he radiation is emitted in inverse proportion, the hot and cold to hot to cold.
The sun is radiating tremendous heat. Conductance The condutancia respect of tra
nsport or communication between the internal structures of the body (muscles, ti
ssues, control centers) and body surface area.
The increase of the conductance required when you need to remove heat from insid
e the body, which is caused by increased blood flow and loosening of the surface
vessels. The objective of bringing to the surface as much body heat inside in o
rder to be eliminated. On the other hand when the body he wants to preserve the
heat, it creates a cutaneous vasoconstriction. 4 - ADJUSTMENT hypothalamus to ke
ep the temperature constant, there are multiple mechanisms that are controlled b
y the hypothalamus, which centralizes the temperature regulation. The hypothalam
us is responsible for regulating the properties of the internal and works simila
rly to thermostat. When the temperature is lower than that to which we have adju
sted the thermostat, this sets up certain mechanisms until the temperature is eq
ual to the desired. If the temperature detected is higher than the set point, ap
propriate responses to temperature decreases. The hypothalamus may act on body t
emperature through multiple mechanisms. The cutaneous circulation: When the temp
erature is low, the hypothalamus activates the nerve fibers
are sympathetic to the skin, so less blood reaches the skin. However, when the t
emperature is high cutaneous arteries dilate, the blood reaches the skin surface
and there is cooled in contact with air (so hot when the skin becomes red). Swe
at. When the temperature is high sweat glands produce sweat, it evaporates on th
e surface of the body and that removes heat. Muscle contraction. The cold causes
involuntary muscle contractions, which increase the basal muscle tone or contra
ction with the muscles, and produces more intense if a perceptible tremor. These
contractions power which is transformed into heat. Pilorección. Skin hair rises
due to contraction of tiny muscles at the base of each hair. This produces the
"goose bumps." In humans, this reflex has little significance, but in species wi
th thick hair, means that a layer of trapped air under the hair that insulates a
nd reduces heat loss. Increased metabolism. The hypothalamus increases the produ
ction of the hormone TRH, this stimulates the pituitary production of TSH, which
in turn increases the secretion of hormones in the thyroid gland€and finally th
ese stimulate the production of heat in all body cells. This response is not wel
l developed in humans but it is important in other animal species. May - PATHOGE
NESIS OF FEVER Many proteins, products of metabolism of proteins and other chemi
cals, especially polysaccharide type toxins released from the cell walls of bact
eria, which can raise the set point of the hypothalamic thermostat. Substances t
hat produce this effect are called pyrogens. Exogenous pyrogens: Are agents (ani
mate and inanimate) that induce the synthesis of an intermediary substance, the
endogenous pyrogen, which determines changes in the CNS and leads to the product
ion of fever. Includes: - infectious agents (viruses, fungi, bacteria and parasi
tes) - bacterial products (LPS and exotoxins) - fungal products (lipopolysacchar
ides, proteins) - steroids (etiocolanona) - pharmacological agents (bleomycin co
chicina) - non-microbial antigens (penicillin G, bovine gamma globulin) - synthe
tic adjuvants, etc. Because of their size or complexity, is possible that these
agents exert their action directly on hypothalamic centers, or that have specifi
c receptors that level. It has been shown to act on cells producing endogenous p
yrogen, inducing their formation and release. Among the most potent exogenous py
rogens is the lipopolysaccharide from gram negative bacteria, known as endotoxin
, which is capable of producing fever. Endogenous pyrogen: We show that the endo
genous pyrogen is synthesized from amino acids when macrophages are activated by
exogenous pyrogens. The non-activated leukocytes has repressed the genome for e
ndogenous pyrogen. When activated, the genome is derepressed mentioned, which
transcribed into new messenger RNA, protein synthesis determined for the formati
on of endogenous pyrogen. Besides the mentioned cells, there are also other endo
genous pyrogen production, they are the monocytes and eosinophils, tissue macrop
hages and Kupffer cells, keratinocytes, endothelial cells, B cells, mesangial, a
nd some glial tumor cells. When bacteria or degradation products of bacteria are
present in tissues or blood, are engulfed by white blood cells, tissue macropha
ges and killer T cells. All these cells, in turn, digest the bacterial products
and then released to body fluids interleukin I substance called endogenous pyrog
en. Currently endogenous pyrogen speaking we refer to: IL I - tumor necrosis fac
tor - Interferon - Family of receptor activating substances gp 130 (IL 6, IL 11,
leukemia inhibitory factor, ciliary neurotrophic factor and oncostatin M) Mecha
nisms Temperature control: After the occurrence of the endogenous pyrogen is rel
eased into the circulation, where it reacts with receptors of the anterior hypot
halamus thermoregulatory center, by direct action of endogenous pyrogen, or loca
l production of prostaglandins, the hypothalamus transmits information anteriorl
y through the posterior hypothalamus which causes the stimulation of sympathetic
nerves, skin vasoconstriction, decreased heat loss and fever. Since the formati
on of endogenous pyrogen trigger mechanisms that culminate in the heat rise. The
first step is to modify the set point of the hypothalamic thermoregulatory cent
ers that conform to a higher temperature than normal. As a result, the anterior
hypothalamus preoptic area acts as if the blood supply was at a temperature belo
w normal and sends signals to the posterior hypothalamus, from where the stimulu
s to the hypothalamic areas that regulate heat production and conservation heat.
The increase in thermogenesis is effective mainly by stimulating the dorsomedia
l area of the posterior hypothalamus, where neurons that transmit impulses throu
gh the brain stem to the lateral columns of the spinal cord and from there to th
e anterior horn motor neurons. These stimuli increase the tone of skeletal muscl
es to reach a certain critical level of occurrence Chills. Moreover, by the exci
tation of sympathetic nuclei of the hypothalamus after peripheral vasoconstricti
on occurs which leads to prevent heat loss. Added to this is the sensation of co
ld experienced by the person wearing it seeks to raise its temperature by all av
ailable means (shelter, heating, etc.)..€The gradual increase of temperature con
tinues until the temperature of blood supplying the hypothalamus is equal to the
new level set point. From that moment away the chills and feel cold, reducing s
omewhat the vasoconstriction. The removal and heat gain sway pear again at a lev
el higher than normal. This situation persists until the cause is this that keep
s the stimulus for the production of endogenous pyrogen. By eliminating the noxa
, endogenous pyrogen disappears from circulation, the heat set point returns to
normal and the body is at stake you need to lower the temperature. This means pr
ofuse sweating, cutaneous vasodilation and
inhibition of thermogenesis until body temperature reaches the normal range. 6 -
Rating: The etiology of foot types
Fever is the most common manifestation of infection, however, can also be caused
by many disorders - vascular disorders (pulmonary embolism and myocardial infar
ction) - immune disorders (drug fever and connective tissue disorders) - maligna
ncies ( particularly lymphomas and solid tumors) metabolic diseases (thyroid cri
sis, acute attack of gout) - trauma. Fever of unknown origin According to evolut
ion:
Continuous: daily variations of less than 1 º C, with little fluctuation. Is sho
wn in typhoid fever, pneumococcal pneumonia, in typhus, but not intravascular in
fections. Intermittent or "needles": large daily swings. The temperature fluctua
tes from fever to normal throughout each day. Usually caused by pyogenic bacteri
a septic processes, but may also miliary tuberculosis, lymphomas and drogas.13 T
his type is characteristic of malaria fever (malaria), transmitted by female Ano
pheles mosquito, the agent is the sporozoon plasmodium, fulfilling a life cycle
that repeats every 48 to 72 hours. Lisando erythrocytes, which causes this type
of fever. Sender: the temperature returns to normal every day, but not reach. It
occurs in many febrile diseases, oozing and sinusitis. Relapsed, recurrent, per
iodic or rolling: alternating periods of continuous fever with other normal ther
mal (apyrexia). The temperature becomes normal one or more days between continuo
us fever episode. Appears in malaria, relapsing fever and louse or tick fever Pe
l - Ebstein Hodgkin's disease, also in brucellosis. But the best example of this
type of fever is a relapsing or "relapsing fever." This disease is of sudden on
set with a febrile period of 3-4 days followed by an afebrile for more than a we
ek (with a range of 3-36 days) only to be followed by a febrile period of the sa
me length as the first , but with less severity. Thus there are successive perio
ds febrile and afebrile periods gradually decreased in severity febrile until th
e disease is over, usually after 3 months if not treated according to the intens
ity: sub-fever or feverishness: less than 37.5 ° C fever light: 38 ° C menso mil
d fever: 38-39 º C high temperature: 40 º C hyperpyrexia: 41 º C according to th
e length: Short-term: from hours or days, less than two weeks
Examples: upper respiratory tract infection, streptococcal pharyngo-amigadlitis
acute otitis media, urinary infections, atypical pneumonia, hypersensitivity to
drugs, etc.
persistent: of weeks or months. Examples are three common infectious causes: dis
seminated tuberculosis, pyrogen hidden intra-abdominal abscesses, and rarely, in
fective endocarditis. Lasting and significant levels of fever often come from th
e so-called collagen vascular diseases and some cancers, particularly lymphomas.
7 - FEVER CLINIC We can distinguish three phases: prodromal or preparation:
It is the beginning phase in which they appear arthralgia, myalgia, headaches, d
epression, pallor, and malaise, the individual does not have a fever but it feel
s wrong. There is a gradual temperature rise. This period lasts several hours an
d although the temperature is in the normal range and begin to operate the syste
ms producing endogenous pyrogen and they are in circulation. Increase the heat p
roduction and conservation, endogenous heat accumulating as a result of the pred
ominance of the phenomena on the thermolysis thermogenesis, hence the pale, and
cold skin, and piloerection (responsible for the "chicken skin" as well as the m
uscle contraction (shivering). The fever may be accompanied by several symptoms,
€but can also be asymptomatic and go unnoticed. It is most evident clinically wh
en the form of introduction is abrupt. Stationary or state:
The temperature rises to the new set point regulatory centers and reaches this p
lateau. Level is reached fever with a new thermal equilibrium where the changes
are numerous and are the febrile syndrome. At this stage increases cardiac outpu
t and heart rate increases in parallel with the increase of temperature. Decreas
es vasoconstriction. Hyperventilation this at this stage, probably due to temper
ature rise at the respiratory center and also to the accumulation of CO2 in the
respiratory center as a result of decreased cerebral blood flow during the chill
s. This phase can last for hours, days, weeks, months, depending on the process
causing the syndrome
febrile, treatment instituted, the host, etc.. Metabolism is increased about 12.
5 to 15% for each degree of temperature above 37 º C, with a predominance of cat
abolic pathways that include muscle proteolysis level. Proteolysis would be caus
ed by endogenous pyrogen through the formation of PE2 locally, this is reflected
by aminoaciduria and proteinuria. It also increases the urinary elimination of
calcium comes from bone decalcification. It decreases the intestinal absorption
of iron, and increases their uptake by the mononuclear phagocytic system resulti
ng in a decline in circulation, could play a role in the anemia seen in prolonge
d febrile processes. 3,4,11 defervescence or decline:
after the statement period, body temperature is still high but the hypothalamus
is trying to regulate the temperature at 37 ° C.2 When skin temperature approach
es 34 º C starts the sweat marks the defervescence of fever response, and will r
each the normothermia, pyrogen disappearing from circulation. There is a new set
ting with more heat loss, thermolysis exceeds thermogenesis, and remove the accu
mulated heat. (SP), therefore there is sweating, warm skin by vasodilation wides
pread, not concentrated polyuria when suddenly in form of crisis to be less obvi
ous if it occurs slowly, or in the form of analysis. The hemodynamic and respira
tory recede quickly, while the metabolic imbalances require several days to reco
ver. Before the antibiotic era, the crisis was always expected, because once tha
t occurred, the doctor knew immediately that the patient's temperature would fal
l soon. SIGNS AND SYMPTOMS TO THE FEVER: Pyrexia: temperature rise Cardiovascula
r: tachycardia, 10-15 beats above normal for every degree of temperature elevati
on, which leads to increased cardiac output necessary to meet the largest tissue
energy needs; in elderly patients circulatory overload can be a meaningful fact
or negativo.4 This increase in cardiac output corresponds to the increased consu
mption of oxígeno.1 relationship was found, increased circulatory rate, pulse po
unding, irregular , initial arteriolar vasoconstriction and vasodilation in defe
rvescence. Respiratory: increased respiratory rate (tachypnea) and depth (batisp
nea). The increase in respiratory activity serves to eliminate some of the heat
and is stimulated by increased temperature of the blood that supplies the center
respiratorio.1 respiratory alkalosis due to hyperventilation. Neurological: hea
dache mainly. The fever is usually throbbing headache at the beginning of the th
ermal reaction, then it becomes a dull pain of varying intensity. It is usually
generalized and seen predominantly in the frontotemporal areas, occipital or sub
occipital. Is aggravated by body movements. Several mechanisms may be involved i
n the pathogenesis of headache that occurs during fever infection dependent. 1
insomnia, stupor, excitement, delirium and convulsions from neuronal dysfunction
, if the fever is very high, especially in children.4 In alcoholics, the elderly
and is responsible arterioesclerosos fever, sometimes, delirium and drowsiness.
13 Loss of consciousness is almost constant from 42 ° C and exceptional surviva
l from 43 º C. 13 Musculoskeletal: arthralgia and myalgia. Digestive: anorexia,
dyspepsia, intestinal motility disorders, thirst, dry mouth, coated tongue. Rena
l: oliguria, and hyper-concentration, urine scanty and concentrated, highly colo
red due to the aqueous phase predominantly by the sudor.4. Dehydration and sodiu
m depletion by sweating. Also Azouri and albuminuria.€Metabolic: metabolic incre
ase: 10-15% for each degree of temperature, higher energy consumption and increa
sed hepatic gluconeogenesis and muscle. Protein destruction: gluconeogenesis and
loss of muscle mass. Lipolysis: gluconeogenesis, ketosis (tendency to acidosis)
and weight loss. hydrosaline: initial fluid retention and ultimate loss. minera
l: intestinal iron malabsorption. Hematologic: anemia, increased erythrocyte sed
imentation rate, leukocytosis (usually granulocytosis) and increased immunoglobu
lins. Endocrine: overproduction of corticosteroids, tyrosine, antidiuretic, pitu
itary dystrophin. The high fever causes damage to the central nervous system whe
n it takes longer wasting (weight loss and muscle loss) infections in more than
half of the cases we can say that fever is a consequence of some event infectiou
s. Again the assessment of the patient should be careful. The complexity of crit
ical patients makes possible the existence of multiple infectious outbreaks simu
ltaneously, catheter-related infection, respiratory infection, etc. The fever ma
y represent a complication of infection that we are trying (as collections compl
ications, treatments failed ATB) or a new infectious event. There is no typical
infection in critically ill patients and can affect any system. Pneumonia associ
ated with mechanical ventilation and catheter-related infection are the most imp
ortant and
common in critically ill patients.
Infectious causes of fever in the hospitalized patient respiratory ventilator as
sociated pneumonia (VAP) ventilator-associated tracheobronchitis (TAVM) Sinusiti
s Infection Endovascular catheter-related suppurative thrombophlebitis Endocardi
tis Nosocomial diarrhea associated with Clostridium Digestive difícille abdomina
l sepsis. Deep surgical wound infection surgical wound postsurgical mediastiniti
s SNC Complicated UTI Urinary Surgical Wound Drainage internal / external Mening
itis Ventriculitos Respiratory ventilator-associated pneumonia (VAP) and tracheo
bronchitis associated with mechanical ventilation (TAVM) is most often the cause
of new fever in critically ill patients. The presence of purulent airway secret
ions, impaired gas exchange, permanent changes in chest radiology and microorgan
ism isolation of potential are the main topics in the diagnosis of VAP. It is im
portant to always obtain samples of tracheal secretions for quantitative microbi
ological culture. The TAVM has the same layout except that it has no radiologica
l changes. Many authors accept this as a primary stage of VAP and treated as suc
h because they say most of them end up in VAP in time. Sinusitis is a condition
misdiagnosed and more common than thought. It is clearly a cause of fever in cri
tically ill patients novo. Nasotracheal intubation, nasogastric intubation, and
severe facial injuries are important risk factors when considering why nosocomia
l sinusitis. Plain radiography provides few details given the difficulty of imag
ing studies performed at the foot of the bed. A CT scan and MRI, breast diagnosi
s facial shapes us. Both antimicrobials as the removal of nasal tubes are import
ant in treatment. Otolaryngologist should be valued by the possibility of surgic
al drainage of breast occupied. Endovascular invasive vascular catheterization i
s used in more than 90% in critically ill patients both for monitoring as to inf
use drugs or nutrition. This leads to secondary infection with a high rate of mo
rbidity and mortality. After respiratory infection is the most common cause of f
ever of infection in the critic. There is a broad diagnostic algorithm. The exte
rnal appearance where the catheter is inserted, with clear inflammatory elements
(edema, erythema, oozing) guides us significantly to catheter-related infection
. Definitive diagnosis currently assumes the culture of the catheter tip, this r
equires removing the catheter. There are other alternatives that would prevent v
enous catheter removal. Differential Blood cultures, blood cultures lysis-centri
fugation are the two methods used today. The imaging tests can we rule out auxil
iary locoregional complications such as suppurative thrombophlebitis or other em
bolic phenomena. Nosocomial endocarditis should always be considered especially
on patients with a postoperative valve replacement. It is imperative intraesopha
geal echocardiogram and blood cultures.€Digestive Diarrhea is by far the most co
mmon digestive effects in critically ill patients. Enteral nutrition and drugs a
re the most common. However, in an up to 25% of patients the diarrhea episode is
related to Clostridium difficile. Previous use of antibiotics (ATB) broad-spect
rum beta-lactam antibiotics is closely especially diarrhea C. whose highest expr
ession is difficile pseudomembranous colitis. The search for the toxin in stool
by ELISA method we are rapidly approaching diagnosis. The crop is only used in o
utbreaks because it can not distinguish the states of the infected carriers with
out determining l as toxins. Besides crops take longer than 72 hours making it d
ifficult for treatment. Investigations
are the imaging studies such as plain abdominal radiography where you can see co
lonic distention, computed tomography and endoscopy although this is controversi
al because of the high risk of colonic perforation during the procedure. Viewing
pseudomembrane is sufficient for diagnosis. The treatment of choice is metronid
azole. Vancomycin as immunoglobulins are reserved for special cases, mainly of r
ecurrence. Finally do not forget that other organisms can cause diarrhea as Sigh
ella, Salmonella, etc. The suspicion is key epidemiological and on these occasio
ns will be requested from feces. Urinary tract instrumentation of the urinary tr
act is frequent in patients hospitaliazado with a high rate of infection of abou
t 30% -50%. The bladder catheter is synonymous with colonization / infection. Ov
er 30% of patients with bladder catheter have significant counts in the urine. U
rine culture remains the diagnostic tool for urinary tract infection (UTI). Howe
ver, the finding of bacteruria significant (> 104 cfu) does not always correlate
with UI. The value depends, among other things how the sample is obtained, must
be the connection between the drainage and catheter, collection bag ever. It al
so imports transport to the laboratory as well as its cooling when it is process
ed quickly. Perhaps the most effective measure is to ensure adequate asepsis whe
n placing the catheter, using closed drainage equipment and optimize the indicat
ions of use. In each case, must assess the situation and possibly additional stu
dies (imaging) to rule the same complications as abscesses, obstructions, etc. I
nfection of Central Nervous System: Although the neurological manifestations are
very common in critically ill patients, most of the time do not represent an in
fectious cause. A separate chapter starring the patients enrolled in a post-oper
ative neurosurgery (surgical drainage as a potential source and external monitor
ing of both intracranial pressure and ventricular bypass.) Clinical follow-up in
search of neurological deficit, seizures, or meningeal irritation coupled with
fever are the elements for suspected CNS infection. Always be complemented with
imaging (CT and MRI) and cerebrospinal fluid collection for microbiological cult
ure both reservoir and lumbar puncture. The latter
will always be conditioned by focal clinical signs present and must eventually b
e evaluated by brain imaging study of previously. Candida Infection Candida spp
infection. is from last years one of the most important problem being up to 7% -
10% of all nosocomial infections. Endovascular infection is undoubtedly the most
common. In the critically ill patient is frequently found multiple sites of Can
dida colonization without a pathological role of certainty as in candiduria labo
ratory findings or in isolated tracheal aspirates. Each situation must be evalua
ted to determine the pathological value of these findings because although there
is a tendency to judge candidates as usual settlement agent can be an agent of
disseminated infections with high mortality. Neutropenic patients, those plans h
ave received multiple broad spectrum ATB, which are under parenteral nutrition o
r undergoing abdominal surgery population are at increased risk of Candida infec
tion. It is assumed that multiple sites f or candida colonization is risk of inf
ection it is recommended as treatment. When the discovery is in blood cultures,
regardless of other findings, it is always and should always be changed central
venous catheter if available.€Importance of Nosocomial fever is important to kno
w that the origin is not always infectious and remember that, although originati
ng in the hospital after 48 hours of stay can be community-acquired infections t
hat were incubating, we take into account in our environment tuberculosis, Q fev
er and brucellosis. The diagnostic aggressiveness will be conditioned by the sev
erity of the clinical situation and the degree of suspicion of threatening etiol
ogies (endocarditis, meningitis, sepsis, etc.).. The empirical administration of
antibiotics should be avoided except in situations that threaten the patient's
life. Initially confirm the existence of fever, and prevent where possible the u
se of antipyretics, except in cases of extreme fever, at the extreme ages of lif
e or when serious underlying pathology. Spiking fever with chills, bacteremia us
ually home, but not always. The non-infectious origin (myocardial infarction, pu
lmonary embolism, DVT, acute pancreatitis or drugs), usually present with temper
ature below 38.9 º C. Temperatures of 41 º C or more, with an almost flat plot a
nd poor response to antipyretics oriented fever of central origin.
In the history taken into account the unity of origin, recent history of surgery
or invasive procedures. Consider roads, drilling, NPT and an impairment of cons
ciousness or swallowing disorders (aspirations). Observe previous diseases (DM,
connective, hyperthyroidism, etc.).. Assess all medications. If IDU find out if
there has been recent use. On examination, phlebitis rating, especially if centr
al line at the neck Discard DVT and PE, to assess surgical wounds, abscesses due
to infection and possible infected pressure ulcers. Search the presence of rash
(drug fever) or the presence of large hematomas by surgery. Rate arthritic phen
omena rule out pneumonia and, if in doubt, endocarditis. Hypotension can be of s
eptic origin and also by adrenal insufficiency. 13. POST-SURGICAL FOOT AND A wel
l-known causes of FUO are added postoperative pyrexia. Statistics show that 20%
are infectious aetiology and the remaining 80% are not infectious, since a signi
ficant number of cases is not possible to determine the cause of the fever. It i
s quite common in the immediate postoperative period (up to 48 hours) appears fe
ver without infectious explain some event. The absorption of hematoma, phlebitis
, deep vein thrombosis may be the most common cause of fever in the postoperativ
e period. It is important to the clinical management of surgical wounds. Do not
lose sight of the reason for surgery. If it is an infectious disease such as per
itonitis, the clinical and paraclinical monitoring of the patient may alert us o
f early complications related to the initial infection. Continuous clinical obse
rvation and assessment through analytical and imaging tests is essential at this
stage to determine.
FOD postoperative catheter Phlebitis Phlebitis Chemistry not dependent on deep v
ein thrombosis abscess puncture sites Operation urinary tract infections, respir
atory, etc. Postanesthesia hepatitis drug fever Operation Dependent Infection of
surgical wound infections serous visceral and systemic
Independent Operation
of
the coexisting diseases unrelated to the surgery that led to (collagen vascular,
lymphoid, etc.).
14. FEVER Fever in immunocompromised patients in neutropenic patients fever was
defined as> or = 38.3 ˚ C, repeated several times in a patient with less than 50
0 neutrophils per cubic millimeter (or at risk of decline below this level withi
n a to 2 days). The diagnosis of neutropenic FUO is justified when it is not cle
ar the cause of fever after three days of study, including two days at least for
the incubation of the cultures. Fever in HIV + patients with fever is a common
symptom in patients infected with HIV. Arguably, the infection often opened, acc
ompanying the patient in different periods of its evolution, and finally often p
oint or accompany the terminal event. 15. IMPORTED FEVERS infectious disease sho
uld be suspected when it appears exotic unknown fever in a patient, who has trav
eled a month earlier or more. If the epidemiological history is appropriate, be
included in the differential diagnosis of malaria, amebiasis, trypanosomiasis, r
elapsing fever, brucellosis, and leishmaniasis. When the onset of fever occurs a
fter one month of return, the most extensive list bucho.€The differential diagno
sis of febrile illnesses with this shorter incubation period (less than one mont
h) includes the following: certain viral diseases (dengue, yellow fever, Chikung
unya, Rift Valley fever), hemorrhagic fevers (eg., Lassa fever, Marburg virus di
sease), bacterial diseases (leptospirosis, typhoid fever, meningococcal septicem
ia, staphylococcal, streptococcal or Pasteurella pestis), and rickettsial infect
ions (louse-borne typhus, tick typhus, scrub typhus, Q fever). Malaria The usual
presenting symptoms of malaria are chills and fever. Often lack the classical f
ebrile paroxysms that recur at regular intervals, especially during the initial
cycles. Other common symptoms include: headache, nausea, vomiting, diarrhea and
myalgia, often motivate a misdiagnosis of the flu. Hepatomegaly and splenomegaly
occur only in approximately half the patients. CNS involvement, renal failure o
r pulmonary edema suggest P. falciparum. The WBC count is usually normal. There
may be anemia and thrombocytopenia, but no eosinophilia. As we consider the diag
nosis of malaria, make a Giemsa stain of a preparation of thin blood and careful
ly considered. You may need to repeat smears
blood for the diagnosis, since the parasite may be intermittent. Preparations of
blood should be collected at different times of day, especially after a chill.
The malaria parasites can be mistaken for platelets. A preparation with thick fi
lm is more sensitive to the diagnosis, but more difficult to interpret. If still
suspected malaria despite repeated negative smears, should be sent to the Paras
itic sera Branch of the Center for Disease Control to determine the indirect flu
orescent antibody. The titles of 1:16 or more indicates a recent infection. Once
the diagnosis is confirmed, the choice of treatment depends on the infecting sp
ecies and whether the organisms P. resistant falciparum malaria is endemic or no
t the location of the probable infection. Amebiasis Amebiasis is another reason
to study in travelers who have unexplained gastrointestinal disease, hepatic dis
ease or fever. Symptoms range from mild diarrhea to fulminant hemorrhagic dysent
ery. The intestinal amebiasis may be diagnosed as an inflammatory bowel disease
(eg., Ulcerative colitis). Metastatic infection may be diffuse, but the liver in
volvement is common. Patients usually present with a solitary abscess, most ofte
n in the right lobe of the liver. The diagnosis of intestinal disease depends on
the demonstration of cysts or trophozoites in the stool. The identification of
E. histolytica in the stool is hard, since fecal leukocytes may be confused with
the agencies. Many substances hinder the examination of the stool (tetracycline
, sulfonamides, castor oil, magnesium hydroxide, barium sulfate enemas solutions
antidiarrheal preparations) and may be delayed 10 to 14 days the discovery of t
he amoeba. Sigmoidoscopy and rectal biopsy can provide the diagnosis. An indirec
t hemagglutination test was positive in 80 to 90% of patients. The serological t
est is useful in amoebic liver abscess (98% being positive), since the feces ten
d to be negative for amoebae in extraintestinal disease. African Trypanosomiasis
(Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense) While under t
he risk of acquiring African trypanosomiasis, the clinician must recognize this
possibility in travelers from Eastern, Central and West. The infection is usuall
y acquired in the course of a safari, and is unlikely after visiting an African
city. The incubation period is about 8-10 days but varies from a few days to 3 w
eeks. The presenting symptoms are malaise, fever, personality changes, anorexia
and headache. On examination, a cutaneous nodule can be seen, the injury to ente
r the site
tsetse fly bite, lymphadenopathy (especially posterior cervical lymph nodes) and
a skin rash. The diagnosis is confirmed by the finding of trypanosomes in an un
stained preparation or Giemsa stain of a blood sample, the product of a lymph no
de aspiration or CSF spin. Lyme disease (Borrelia burgdorferi) relapsing fever l
ouse-bite caused by Borrelia species can be acquired in traveling to Ethiopia€Ce
ntral or South America and the Far East. Infection occurs after an incubation pe
riod of one week and is characterized by high fever, chills and headache, which
extend from 3 to 6 days and is followed by an afebrile period of 6-10 days. Febr
ile access reappear later, and each relapse is shorter and mild. The WBC count i
s normal and the diagnosis is confirmed by Wright staining of peripheral blood p
reparation in febrile periods. Brucellosis (Brucella melitensis) Brucellosis occ
urs most frequently in the workers in the canneries and meat, but infections hav
e been reported in tourists who have traveled to Mexico and countries of the Med
iterranean. The intake of dairy products, especially milk and cheese unboiled co
ntaminated with Brucella melitensis is the usual source of infection. The incuba
tion period ranges from a few days to several months. The onset is usually gradu
al, with fever, chills, headache, fatigue and myalgia reported frequently. Physi
cal examination is negative, in general, but may encontrars lymphadenopathy and
hepatosplenomegaly. The WBC count is normal and the diagnosis is made by the fin
ding of a Brucella agglutination titer of 1:160 or higher, or a rising titer at
least four times in the course of the disease. False positive reactions may occu
r in patients with tularemia infections, Salmonella, Y. enterocolitica., Campito
-Bacter fetus or anger (or immunizations). Blood cultures may be positive after
3-4 weeks, and granulomas can be detected by liver biopsy. Visceral Leishmaniasi
s
Visceral leishmaniasis (kala-azar) is a febrile illness that can have an insidio
us onset months after the return of the patient who has visited an endemic area.
This disease is part of the differential diagnosis of cases of patients who hav
e traveled to certain countries (Mediterranean, China, East Africa, Indonesia an
d South America) and who have splenomegaly, hyper, pancytopenia, or unexplained
fever. Other conditions include: weight loss, fatigue and dizziness. The diagnos
is is made by the finding of Leishman-Donovan bodies (amastigotes) in a Giemsa s
tain product of bone marrow aspirations, which was confirmed by culture. A story
of a journey to a foreign country should alert the clinician to l exotic diseas
es research, not to mention the most common in febrile patients. 16. ETIOLOGY OF
FOOT OF LOW AND HIGH IMPACT ON OUR ENVIRONMENT While common infections are the
most common causes of elevated body temperature, fevers have a long list of othe
r causes, including toxins, cancers and autoimmune diseases. In Spain the most c
ommon causes of fever are viral diseases and bacterial infections or colds flu-l
ike sore throat and strep throat ear pain Viral gastroenteritis or bacterial gas
troenteritis Acute bronchitis Infectious mononucleosis Urinary tract infections
Infections of the upper airway, such as tonsillitis , pharyngitis or laryngitis
Medications such as antibiotics, antihistamines, barbiturates, and drugs for hig
h blood pressure Occasionally, more serious problems like pneumonia, appendiciti
s, tuberculosis and meningitis may have fever babies are overdressed in hot weat
her or hot environments collagen vascular disease , rheumatoid diseases and auto
immune disorders
Erythematosus, juvenile rheumatoid 0Artritis 1Lupus
2Periarteritis 3SIDA nodosa and HIV infection inflammatory bowel 4Enfermedad reg
ional 5Enteritis 6Colitis ulcerative
8Leucemia 7Cáncer
10Enfermedad 9Neuroblastoma 11Linfoma non-Hodgkin's lymphoma