PATHOPHYSIOLOGY

BRAIN TRAUMA
TRAUMA TO THE SKULL RESULTING IN MILD TO
EXTENSIVE DAMAGE TO THE BRAIN

BLUNT OR CLOSED NO EXPOSURE OF BRAIN TO

ENVIRONMENT
CONCUSSIONS
CONTUSIONS
FRACTURES
OPEN OR PENETRATING - EXPOSURE OF CRANIAL
CONTENT
LACERATIONS
FRACTURES IN THE SKULL
INTERRUPTION OF DURA MATTER
BRAIN TRAUMA
PRIMARY INJURY CAUSED BY DIRECT IMPACT
AND INVOLVES THE INITIAL TEAR, NEURAL
INJURY AND HEMORRHAGE

SECONDARY INJURY INTRACRANIAL BRAIN

DAMAGE AND EXTRACRANIAL BRAIN DAMAGE
BRAIN TRAUMA
RESULTS IN:
CONTUSIONS
HEMATOMAS
BRAIN TRAUMA
INTERVENTIONS:
MONITOR FOR VITAL SIGNS INDICATIVE OF ICP
MONITOR RESPIRATORY STATUS
MONITOR NUERO STATUS
ELEVATE HEAD SLIGHTLY
ASSESS NERVE FUNCTION
MONITOR FOR DRAINAGE FROM NOSE OR EARS (SPF)
AVOID COUGHING BECAUSE IT INCREASE ICP

INFORM DOCTOR/SURGEON RIGHT AWAY IF ANY

SIGNS OF ICP!!!
SPINAL CORD INJURY
TRAUMA TO SPINAL CORD WITCH CAUSES
PARTIAL OR COMPLETE DISRUPTION OF THE
NERVE TRACTS AND NUERONS

PATHOPHYSIOLOGY:
MOST COMMONLY OCCUR BECAUSE OF
VERTEBRAL INJURIES
ACCELERATION
DECELERATION

MVA ARE THE MOST COMMON

SPINAL CORD INJURY
INVOLVES CONTUSION, LACERATION OR
COMPRESSION OF THE SPINAL CORD

COMLICATIONS RELATED TO THE INJURY

INCLUDE:
RESPIRATORY FAILURE
AUTONOMIC DYSREFLEXIA
SPINAL SHOCK
DEATH
SPINAL CORD INJURY
INJURY AT C2 C3 IS USUALLY FATAL
C4 IS THE MAJOR INNERVATION TO THE
DIAPHRAGM BY THE PHRENIC NERVE
INVOLVEMENT ABOUT C4 CAUSES RESPIRATORY
DIFFICULTY AND PARALYSIS OF ALL FOUR
EXTREMITIES
INJURIES ABOVE T6 AND IN CERVICAL LESIONS
WILL CAUSE AUTONOMIC DYSREFLEXIA
SPINAL CORD INJURY
NURSING INTERVENTIONS:
RESPIRATORY SYSTEM:
MAINTAIN PATENT AIRWAY
MONITOR ABGS
MONITOR FOR INFECTION
CARDIOVASCULAR:
MONITOR FOR DYSRHYTHMIAS
SIGNS OF SHOCK (HYPOTENSION, TACHY, WEAK
PULSE)
MONITOR FOR ICP
SPINAL CORD INJURY
NUEROMUSCULAR:
ASSCESS NEURO STATUS
ASSESS FOR LEVEL OF INJURY
MONITOR FOR SIGNS OF SPINAL SHOCK AND
AUTONOMIC DYSREFLEXIA
ASSESSS PAIN
SPINAL SHOCK
ALSO KNOWN AS NEUROGENIC SHOCK

CHARACTERIZED BY A COMPLETE LOSS OF

REFLEX FUNCTION IN ALL SEGMENTS BELOW
THE LEVEL OF THE LESION

MAY LAST 7-20 DAYS AFTER ONSET OR MONTHS

SPINAL SHOCK ENDS WHEN THE REFLEXES ARE

REGAINED
AUTONOMIC DYSREFLEXIA
ALSO KNOWN AS AUTONOMIC HYPERREFLEXIA

A SYNDROME OF SUDDEN AND DANGEROUS

INCREASE IN BLOOD PRESSURE THAT GENERALLY
OCCURS AFTER THE PERIOD OF SPINAL SHOCK

MOST COMMON CAUSE IS FROM A DISTENTION IN

THE BLADDER OR IMPACTED RECTUM

IT IS A NEUROLOGICAL EMERGENCY AND MUST BE

TREATED IMMEDIATELY TO PREVENT HYPERTENSIVE
STROKE
STROKE SYNDROMES (CVA)
STROKE SYNDROMES (CVA)
GLOBALLY 4.5- 6 MILLION DIE FORM CVAS PER YEAR

LEADING CAUSE OF DISABILITY IN THE US

5-14% HAVE ANOTHER STROKE WITHIN 1 YEAR

50% OF CVAS OCCUR IN PERSONS OVER 70

BLACKS ARE THE MOST AT RISK NEARLY TWICE

THAT OF A WHITE PERSON
STROKE RISK FACTORS:
ATHEROSCLEROSIS
ATRIAL FIBRILLATION
HYPERTENSION
ANTICOAGULATION THERAPY
DIABETES MELLITUS
STRESS
OBESITY
ORAL CONTRACEPTIVES
TYPES OF STROKES:
THROMBOTIC STROKE

HEMORRHAGIC STROKE

EMBOLIC STROKE
THROMBOTIC STROKE
ARISE FROM ARTERIAL OCCULUSIONS CAUSED BY
THROMBI IN THE ARTERIES SUPPLYING THE
BRAIN OR INTRACRANIAL VESSELS

USSUALLY ARISE WHEN A CLOT BREAKS LOOSE

AND TRAVELS UP THE VESSELS

TRANSIENT ISCHEMIC ATTACK (TIA) BRIEF

EPISODE OF NEUROLOGIC DYSFUNTION. LESS
THAN 1 HOUR
CAUSED BY THROMBOTIC PARTICLES OR SPASMS
EMBOLIC STROKE
ACCOUNT FOR 30% OF ALL STROKES
INVOLVES FRAGMENTS THAT BREAK FROM A
THROMBUS FORMED OUTSIDE THE BRAIN OR IN
THE HEART, AORTA, COMMON CAROTID, OR
THORAX
AT RISK:
AFIB
RECENT MI
ENDOCARDITIS
LEFT VENTRICULAR ANEURYSM OR THROMBU
HEMORRHAGIC STROKE
3RD MOST COMMON CAUSE OF CVA -
HYPERTENSION
MASS OF BLOOD IS FORMED AND ITS VOLUME
INCREASES. BRAIN TISSUE IS DISPLACED AND
COMPRESSED AND RUPTURE MAY OCCUR
DESCRIBED AS:
MASSIVE
SMALL
SLIT
PETECHIAL
PATHOPHYSIOLOGY OF STROKE
CEREBRAL INFARCTION:
GLOBAL PROCESS THAT AFFECTS NEURONS, CELLS,
AND ARTERIES OF THE BRAIN
FOCAL PROCESS WITH A CENTRAL ZONE OF CELL
LOSS SURROUNDED BY INJURED CELLS

ISCHEMIC MOST COMMON STROKE

HEMORRHAGIC HIGH BLOOD PRESSURE
SIGNS OF A STROKE
SUDDEN WEAKNESS OR NUMBNESS
HEADACHE
LOSS OF CONCIOUSNESS

WHAT TO DO:
CALL 911 OR GET TO HOSPITAL
CT OR MRI TO DETERMINE STROKE
ASSESSING FOR STOKE
CHANGE IN LEVEL OF CONSCIOUSNESS
SIGNS OF INCREASING ICP NUERO SIGNS!!
ASSESSEMENT OF CRANIAL NERVES V, VII,IX,X
AND XIII
NERVE V DIFFICULTY CHEWING
NERVE VII FACIAL PARALYSIS OR PARESIS
NERVE IX AND X DYSPHAGIA
NERVE IX ABSENT GAG REFLEX
NERVE XII IMPAIRED TONGUE MOVEMENT
ASSESSING FOR STROKE
YOU MAY FIND:
AGNOSIA INABILITY TO RECOGNIZE OBJECTS OR
PEOPLE
APRAXIA LOSS OF ABILITY TO CARRY OUT
MOVEMENTS
HEMIANOPSIA BLIDNESS IN VISUAL FIELD
NEGLECT UNAWARE OF EXISTANCE ON
PARALYZED SIDE
DYSARTHRIA INABILITY TO SPEAK CLEARLY OR
SPEAK AT ALL
DYSPHAGIA DIFFICULTY SWALLOWING
TREATMENT
IT IS CRITICAL TO ID MANIFESTATIONS AND
ESTABLISH A PROPER ONSET OF THE
MANIFESTATIONS

STOKE REHABILITATION
ASPIRIN
SYSTEMIC ANTICOAGULANTS
HEPARIN
LOVENOX
COUMADIN
TREATMENT
THROMBOLYSIS TPA (TISSUE PLAMINOGEN
ACTIVATOR) DISSOVES CLOT CLOT BUSTER
GIVE WITHIN 3 HOURS OF ONSET OF SYMPTOMS
NO LONGER GIVE STREPTOKINASE

ACUTE BLOOD PRESSURE LOWERING

SUPER IMPORTANT DURING FIRST 24 HOURS
REDUCES ISCHEMIA
NURSING INTERVENTIONS:
FIRST 24 HOURS:
MAINTAIN PATENT AIRWAY
MONITOR VITAL SIGNS
MAINTAIN PRESSURE OF 150/100 FOR ADEQUATE
PROFUSION
MONITOR SECRETIOS AND SUCTION PRN
MONITOR FOR ICP
MONITOR LEVEL OF CONCIOUSNESS, PUPIL
RESPONSE, MOTOR & SENSORY RESPONSE, NERVE
AND REFLEXES
NURSING INTERVENTIONS:
PLACE OBJECTS IN VISUAL FIELD
MOUTH CARE (SIT UP WITH HEAD TILTED
FORWARD TO PREVENT ASPIRATION)
EYE CARE
PHYSICAL THERAPY
ENCOURAGE EXPRESSING FEELINGS
STOOL SOFTNERS
ENCOURAGE INDEPENDENCE IN ADLS
MENINGITIS
INFECTION OF THE MENINGES CAUSED BY
BACTERIA, VIRUSES, FUNGI, PARASITES, OR
OTHER TOXINS
25% DEATH RATE
TRANSMITTED VIA DIRECT CONTACT OR
DROPLET
DORMS, PRISIONS, HIGH POPULATED AREAS, ETC.
MENINGITIS
BACTERIAL INFECTION OF BRAIN AND CSF
CAUSED BY BACTERIA IN ANOTHER PART OF
BODY

ASEPTIC CAUSED BY VIRUSES (MUMPS, HERPES,

WEST NILE, ENCEPHALITIS, INFLUE A&B,
EPSTEIN-BARR

TUBERCULAR MOST COMMON AND SEROUS.

CAUSED BY bacterium, mycobacterium tuberculosis.
USUALLY STARTS IN LUNGS
MENINGITIS
ASSESS FOR:
LETHARGY
PHOTOPHOBIA
MENINGEAL IRRITAION
NUCHAL RIGIDITY INABILITY TO FLEX NECK FORWARD
POSITIVE KERNIGS SIGN STIFFNESS OF THE
HAMSTRINGS
POSITIVE BRUDZINSKI SIGN SEVERE NECK STIFFNESS
THAT CAUSES KNEES TO FLEX
TREATMENT
MAINTAIN ISOLATION
MONITOR FOR ICP
ANTIBIOTICS
ANALGESICS
AMYOTROPHIC LATERAL SCLEROSIS
1 IN 3 CASES PER 100,000

2 DEATHS PER 100,000

5000 NEWLY DIAGNOSED CASES PER YEAR IN US

DIFFERS FROM OTHER MOTOR NUERON

DISORDERS IN THAT THE UPPER AND LOWER
MOTOR NUERONS ARE INVOLVED
AMYOTROPHIC LATERAL SCLEROSIS
LOU GEHRIGS DISEASE

PROGRESSIVE DEGENERATIVE DISEASE

INVOLVING THE MOTOR SYSTEM

RESULTS IN PROGRESSIVE MUSCLE WEAKNESS

LEADING TO RESPIRATORY FAILURE AND DEATH

USSUALLY 2-5 YEARS FROM SYMPTOM ONSET

ALS
Gehrig is chiefly known for playing in 2,130
consecutive games for the Yankees, a magnificent
streak long thought to have been unbreakable, until
Cal Ripken, Jr. came along.
Gehrigs consecutive games streak came to an end on
May 2, 1939, when he removed himself from the lineup
after a dismal start caused by his mysterious
neuromuscular disease, amyotrophic lateral sclerosis,
or ALS, later known as Lou Gehrigs Disease.
ALS
In 1939, after getting off to a horrid start to the baseball
season, Gehrig checked himself into the Mayo Clinic,
where after a series of tests, doctors informed him that
he was suffering from amyotrophic lateral sclerosis
(ALS)

On June 2, 1941, he passed away in his sleep at his

home in New York City.
ALS MANIFESTATIONS
RESPIRATORY DIFFICULTY

FATIGUE

MUSCLE WEAKNESS & ATROPHY

WEAKNESS OF HANDS & ARMS

DYSARTHRIA
NURSING INTERVENTIONS
TREATMENT OF SYMPTOMS

MONITOR RESPIRATORY STATUS

RESPIRATORY SUPPORT

ADVANCE DIRECTIVES

CLIENT AND FAMILY SUPPORT

TREATMENT
SYMPTOM RELEIF

PREVENT COMPLICATIONS

MAINTENANCE OF MAXIMAL FUNCTION

MAINTENANCE OF OPTIMAL QUALITY OF LIFE

MYASTHENIA GRAVIS
CHRONIC AUTOIMMUNE DISEASE MEDIATED BY
ACETYLCHOLINE RECEPTOR ANTIBODIES THAT
ACT AT THE NEUROMUSCULAR JUNCTION

CHARACTERIZED BY:
EXERTIONAL FATIGUE AND WEAKNESS THAT
WORSENS WITH EXERTION
IMPROVES WITH REST
RECURS WITH RESUMPTION OF ACTIVITY
MYASTHENIA GRAVIS
PATHO:
RESULTS FROM A DEFECT IN NERVE IMPULSE
TRANSMISSION AT THE NUEROMUSCULAR
JUNCTION

IN ADVANCE STAGES, ALL MUSCLES ARE WEAK

THE PT WITH MG IS AT RISK FOR RESPIRATORY

FAILURE!!
TREATMENT
ANTICHOLINESTERASE DRUGS
MESTINON (PYRIDOSTIGMINE)

STEROIDS

IMMUNOSUPPRESSANT DRUGS

CYCLOSPORINE
TENSILON TEST
USED TO DIFFERENTIATE CRISIS:
MYASTENIC CRISIS TENSILON IS ADMINISTERED
AND STRENGTH IMPROVES, THE CLIENT NEEDS
MORE MEDICATION

CHOLINERGIC CRISIS TENSILON IS

ADMINISTERED AND WEAKNESS IS MORE SEVERE,
CLIENT IS OVERMEDICATED, ADMINISTER
ATROPINE
MYASTENIA GRAVIS
MYASTHENIC CRISIS OCCURS 3-4 HOURS AFTER
THE PERSON TAKES MEDICATION

EXTREME MUSCLE WEAKNESS CAUSES EXTREME

QUADRIPARESIS OR QUADRIPLEGIA,
RESPIRATORY INSUFFICIENCY

S&S = INCRESED PULSE, RESP, BLOOD PRESSURE,

ABSENT COUGH AND GAG, DIFFICULTY
SWALLOWING
MYASTENIA GRAVIS
CHOLINERGIC CRISIS ARISE SECONDARY FROM
DRUG OVERDOSE (ANTICHOLINESTERASE DRUG
TOXICITY)
RESEMBLES MYASTENIC CRISIS BUT WEAKNESS
OCCURS 30-60 MIN AFTER TAKING MEDICATION
AT RISK FOR RESPIRATORY ARREST

S&S= CRAMPS, N, V, D, BLURRED VISION,

HYPOTENSION, PALLOR
MYASTENIA GRAVIS
INTERVENTION FOR CRISIS

HOLD ANTICHOLINESTERASE MEDICATIONS

PREPARE TO ADMINISTER ANTIDOTE

ATROPINE SULFATE
MESTINON
ACTIONS
Mestinon inhibits the destruction of acetylcholine by
cholinesterase and thereby permits freer transmission of
nerve impulses across the neuromuscular junction.
Contraindications
Mestinon is contraindicated in mechanical intestinal or
urinary obstruction, and particular caution should be
used in its administration to patients with bronchial
asthma.
GUILLAIN-BARRE SYNDROME
ACUTE INFECTIOUS NEURONITIS OF THE CRANIAL
AND PERIPHERAL NERVES
IMMUNE SYSTEM OVERRACTS TO THE INFECTION
AND DESTROYS THE MYELIN SHEATH
SYMPTOMS:
PARESTHESIAS
PAIN
WEAKNESS
REGRESSION TO RESPIRATORY FAILURE
CSF THAT SHOWS POSITIVE PROTEIN
THE MAJOR CONCERN IN GB SYNDROME IS
DIFFICULTY BREATHING
TRIGEMINAL NEURALGIA
SENSORY DISORDER OF THE TRIGEMINAL (5TH)
NERVE
RESULTS IN SEVERE, SHARP, FACIAL PAIN

WHAT SHOULD YOU ASSESS:

CLIENT HAS SEVERE PAIN ON THE LIPS, GUMS, OR
NOSE AND ACROSS CHEEKS
SITUATIONS THAT STIMULATE PAIN
COLD, WASHING OF FACE, CHEWING, AND FOOD OR
FLUIDS OF EXTREME TEMP