TRANSIENT ISCHEMIC ATTACK (TIA)

(Warning sign of increased stroke risk/possible stroke)

Pathophys: brief interruption of cerebral blood flow due to vasospasm or systemic arterial HTN

Duration: few minutes to 24 hours

Symptom resolution: 30-60 mins.

Symptoms: blurred vision, diplopia, tunnel vision, blindness in one eye, weakness(arm, hand, leg), gait disturbances(ataxic), numbness(face, arm, hand), vertigo, aphasia, dysarthria(slurred speech)

Treatment

1.)neuro assessment

2.)ECG/EKG

3.)CT Scan

4.)Anticoagulant Therapy (Plavix)

Education

1.)Teach patient about bleeding precautions and signs of stroke

SPECIAL ATTENTION

*Patients older than 65, diabetics, symptoms> 10 mins, and motor/speech difficulties are ADMITTED.

REVERSIBLE ISCHEMIC NEUROLOGICAL DEFICIT (RIND)

*(Warning sign of increased stroke risk/possible stroke)

*Difference between TIA/RIND is duration of symptoms*

Pathophys: brief interruption of cerebral blood flow due to vasospasm or systemic arterial HTN

Duration: longer than 24 hours BUT less than a week.

Symptom resolution: 24 hours to a week

Symptoms: same as TIA

Treatment

1.)Neuro Assessment

2.)ECG/EKG

3.)CT Scan

4.)Anticoagulant Therapy (Plavix)

Education

1.)Teach patient about bleeding precautions

SPECIAL ATTENTION

*Patients older than 65, diabetics, symptoms>10 mins, and motor/speech difficulties are ADMITTED.

STROKE

(BRAIN ATTACK)

*Caused by a change in the normal blood supply to the brain*

*ANY STROKE IS A MEDICAL EMERGENCY AND SHOULD BE TREATED IMMEDIATELY TO PREVENT NEURO DEFICITS/PERMANENT DISABILITY*

*2nd most comon cause of death in the US/World

Pathophys: results from interruption of blood flow to the brain (brain needs constant blood flow due to inability to store glucose/oxygen and the need to remove metabolic waste) causing infarction of brain tissue.  Blood flow post-stroke is affected at site of stroke and contralateral(opposite side) side of brain hemisphere.

ISCHEMIC STROKE (OCCLUSIVE)

*Ischemic Strokes are either THROMBOTIC OR EMBOLIC**

*Stroke caused by a thrombus(clot)- Thrombotic

*Stroke caused by a embolus(dislodged clot)-Embolic

NOTE: MOST STROKES ARE ISCHEMIC!!!!

*Cocaine abuse can cause Ischemic Stroke*

Ischemic: Thrombotic Stroke

*More than half of all strokes AND are due to development of atherosclerotic vessel walls, resulting in clot formation.

Pathophys:  SLOW ONSET (minutes to hours). The process may occur over years because of collateral circulation developed to compensate for occlusion.

Most Common Sites: Bifurcation of common carotid artery and vertebral arteries at basilary artery junction.

Patient Status: Intermittent improvement b/t episodes of worsening; Daytime occurence/Patient is awake

Indicator: TIA

CSF: normal; possible protein

Seizures: NO

Duration: Improvements over weeks to months; permanent deficits possible.

ISCHEMIC: EMBOLIC STROKE

*Caused by an embolus or a group of emboli that break off from one area of the body and travel to the cerebral arteries via the carotid artery of vertebrobasilar system.*

Ischemic: Embolic Stroke

Pathophys:  SUDDEN ONSET.

*As the emboli occlude the vessel, clinical manifestations of stroke are noticed*

Patient Status: Abrupt development of completed stroke; Maximum deficit noted at onset; Possible paralysis and Expressive Aphasia; Daytime occurence/ Patient is awake

CSF: Normal

Seizures:NO

Duration: Rapid Improvements

Most Common Sources:  #1-Heart , Carotid Sinus/Artery

*HIGH RISK PATIENTS: Nonvalvular A-Fib, rheumatic Heart disease, mural thrombi after MI, insertion of prosthetic heart valves.

Most Common Site in Brain:  Middle Cerebral Artery(MCA)

HEMORRHAGIC STROKE

*(Bleeding into the brain tissue or into the spaces surrounding the brain, usually results in an aneurysm)

*Amphetamine/ Cocaine abuse cause Hemorrhagic Stroke*

Pathophys: Results from ruptured aneurysm(localized weakening or distortion of a vessel wall); rupture of an Arteriovenous malformation; or severe HTN (commonly).

Patient Status:  Daytime occurence; SUDDEN ONSET, may be gradual if caused by HTN; patient in deepening stupor or coma; Signs of focal deficits, severe and frequent

CSF: Bloody

Seizures: Usually

Duration: Variable; permanent neuro deficits possible.

Aneurysm rupture causes bleeding into brain.  Larger aneurysms more likely to rupture than small.

*BLOOD FLOW TO DISTAL AREAS  OF BRAIN SUPPLIED BY AREA OF RUPTURE ARE MARKEDLY DIMINISHED, LEADING TO CEREBRAL ISCHEMIA INFARCTION/NEURO DEFICITS.

*Congenital Aneurysm- if a child is born with the defect it may or may not rupture

*Secular Aneurysm-MOST COMMON- weak spot in artery wall, usually vertebrobasilary arteries.

*Dissecting Aneurysm or Pseudoaneurysm- occurs after trauma or from plaque formation.

*Mycotic aneurysm- caused by infectious agent i.e. bacterial infection

*Arteriovenous Malformations- uncommon occurs during embryonic development; abscence of capillary networks/increased arterial pressure leading to rupture.

*Hypertension-elevated blood pressure leads to changes in arterial wall making it more likely to rupture.

STROKE ETIOLOGY/GENETIC RISK

*Cigarette Smoking( doubles risk for stroke)

*Oral Contraceptive Use

*Previous Stroke or TIA

*Genetic or familial tendency

*Heart Surgery, Valve replacement

*Obesity

*Substance Abuse(cocaine)

*Diabetes mellitus

*Atherosclerosis

*Elevated Cholesterol, LDL, Triglyc.

*Migraines

*Sudden discontinuation of anti-HTN drugs

*Older

*Male

*African American, Hispanic, Amer. Indian,

*Sickle Cell Anemia

*Use of PPA, found in antihistamines (in young/middle-aged women)

*Brain trauma

EDUCATION FOR PATIENTS WITH STROKE RISK

*Importance of Complying with treatment

*Teach about other factors increasing their stroke risk.

*Encourage smoking cessation

*Recommend regular exercise

*Diet high in fruits and vegetables and low in saturated fats and trans fat.

*Light to moderate alcohol consumption may decrease risk for stroke BUT heavy may increase it.

STROKE PATIENT: HISTORY

*What were you doing when stroke activity began?

(Hemmorhagic strokes occur DURING activity)

*Ask pt. or family member how symptoms progressed? (gradual vs. sudden)

*Severity of symptoms? (worsening after onset-hemorrhagic or getting better-embolic)

*Do symptoms come and go? (TIA or RIND)

*Headache? (Worst in life.. Aneurysm)

*Changes in LOC??

*Chronic medical conditions(DM, Obesity, Heart Disease)

*OTC or prescription drugs (oral contraceptives or antihistamines)

*Familial history of stroke or aneurysm

SROKE PATIENT: PHYSICAL ASSESSMENT

*(Patient must be evaluated within 10 mins of arrival to ED, or of occurence if in acute care setting)

PRIORITY ASSESSMENT : ABCs!!!!

Then, perform, neuro, motor, sensory, cranial, cardiovascular

1.)neuro assessment-

a.)Cognitive changes-denial of illness, spatial and propioceptive dysfunction, impairment of memory, judgement, or problem-solving, decision making, decreased concentration.

Note: Right hemisphere- visual/spatial tasks, proprioception, ---> results in time and space disorientation, impulsivity, and judgement

Left hemisphere-dominant in most of the population- language, mathematic skill, and analytic thinking---> results in aphasia, alexia or dyslexia(reading probs), agraphia(dif.writing), and acalculia(dif. with math).

b.) Motor Changes- Right sided motor deficits indicates LEFT brain injury and Left sided motor deficits indicate RIGHT brain injury.

*If brainstem or cerebellum affected pt will have gait disturbance, hemiplegia or quadriplegia.

~Assess for muscle tone-flaccid paralysis/hypotonia

~Assess proprioception, head/trunk control, balance, gait

~CHECK for BLADDER/BOWEL CONTROL -incontinence or retention of urine/stool.

c.)Sensory Changes-

**Neglect Syndrome- common in Right brain injury-patient is unaware of existence of LEFT or paralyzed side (washing or dressing only one side of body for example)

~Assess for ptosis, amaurosis fugax(temporary blindness in one eye, hemianopsia(blindness in one part of visual field)-patient must turn entire head to scan complete range of vision.

d.) Cranial Nerve function-Assess ability to chew (CN. V); Assess swallow (CN. IX/X); Assess facial paralysis (CN. XII)

**At risk for aspiration pneumonia, constipation, and dehydration.**

e.)Cardiovascular assessment-patients with embolic stroke may have murmur, dysrhythmias, or HTN.

After stroke a somewhat higher blood pressure is needed ot maintain cerebral perfusion.

STROKE PATIENT: PSYCHOSOCIAL ASSESS.

*Assess patient's reaction to illness, in relation to body image, self concept, and ability to perform ADLs.

*With family/caregivers identify any probs with coping/personality changes.

*Ask about patient's financial status and occupation due to possible alteration post stroke.

*Assess for EMOTIONAL LABILITY-laughing or cry unexpectedly for no apparent reason. (Explain these UNCONTROLLABLE emotions to the family so they do not feel responsible for them)

STROKE PATIENTS: LAB ASSESSMENT

What lab tests are conducted??

*No tests confirm stroke diagnosis*

*Elevated HCT/HGB-sometimes associated with severe or major strokes as body tries to compensate for lack of O2 to brain.

*Elevated WBC count-infection?

*PT or INR/PTT- to establish baseline in case anticoagulation therapy is started; they may also provide info that hemorrhagic stroke occurred.

STROKE PATIENT: IMAGING

*CT Scan -assists in diagnosis of stroke b/c areas of bleeding in brain can be visualized.

NOTE: For a patient with ischemic or occlusive stroke the CT is usually INITIALLY negative; after the first 24 hours, CT will show progressive changes of ischemia, infarction, and cerebral edema.

*MRI may show changes earlier than CT.

(More notes on Types of MRIs on p. 1036)

STROKE TREATMENT: INEFFECTIVE TISSUE PERFUSION (CEREBRAL)

*Determined by type/extent of stroke.

For patients with ischemic stroke,early intervention is systemic anticoagulatn within 3 hours of onset of stroke.

*Thrombolytic Therapy-rtTPA

*Non-surgical Management- ICP Monitoring

*Drug Therapy-Anticoag./Antiplatelet, anti-seizure, calcium channel blockers

*Monitoring for further complications- pts with aneurysm or AVM for hydrocephalus/vasospasm

*Carotid artery angioplasty w/stent

*(Read other non-surgical techniques p. 1044-1045)

*Surgical Management

1.)Thrombolytic Therapy (Systemic)

*Use of rtTPA  for an ACUTE ischemic stroke dissolves the cerebral artery occlusion and re-establishes blood flow and prevents cerebral infarction.

CRITERIA FOR rtTPA USE IN STROKE PTS:

a.)Within 3 hours of stroke symptom onset.

b.)Therapy is explained to pt/fam; Informed consent is obtained.

c.)Dosage of drug based on patient's ACTUAL wt.

d.)Follow hospital protocol for mixing/administering drug.

Nursing Intervention AFTER administering TPA IV:

Chart 47-5 p. 1037

1.)Infuse 0.9 mg/kg(MAD dose 90 mg) over 60 mins with 10% of dose given as bolus over 1 minute.

2.)Admit patient to critical care or stroke unit.

3.)Perform neuro assess. w/vitals q15min during infusion and q30min after that for 6 hours, then hourly for the next 24 hours after treatment.

4.)If systolic BP is >180 or diastolic> 105, give anti-HTN drugs

5.)Do not place NG tubes or foleys until patient is stable to prevent bleeding.

6.)DISCONTINUE INFUSION if pt c/o severe headache or has severe HTN, nausea/or vomiting; CALL THE DR.

7.)Obtain follow up CT after 24 hours of treatment /before starting anti-coag/anti-platelet drugs.

Non-Surgical Management- ICP Monitoring

**PATIENT IS MOST AT RISK FOR ICP INCREASE FROM EDEMA THE "FIRST 72 HOURS AFTER STROKE ONSET"**

Monitor for

Symptoms of increased ICP:

**FIRST SIGN: Decreased LOC(lethargy-coma), behavior changes(restlessness, irritability,confusion),headache, N/V, aphasia, dysarthria, pupillary changes, cranial nerve dysfunction, ataxia, seizures(within 24 hours of stroke), Cushing's triad-(late sign of Increased ICP) severe hypertension, widened pulse pressure, bradycardia, abnormal postures(decerebrate-extensor OR decorticate-flexion), and change in sensorimotor status.

ICP > 15-20 mmHg

Management of Increased ICP:

*Monitor Vital Signs and Neuro Status, and Cerebral Perfusion Pressure- Fever increases ICP/CBF. LOC changes correspond to increases to ICP.

*Monitor the patient's ICP and neurologic response to care activities- ICP may elevate in response to stimulation from activities. (Elevated ICP decreases CPP)

*Monitor respiratory status(rate,rhythm, depth)

*Administer colloid, blood products, and crystalloid- to maintain proper blood volume ranges.

*Maintain blood glucose level within normal range-brain does not store glucose and needs constant cellular energy.

*Consult with physician to determine HOB placement (0, 15, 30 degrees), and monitor patient's response.

*Avoid head flexion or extreme hip and knee flexion-abscence of neck or hip flexion enhances venous drainage/prevents increased ICP.

*Administer osmotic and loop diuretics to treat cerbral edema.

*Administer pain meds as appropriate.

Specifics,

1.Manage fever. Normal manifestation due to hypothalamic damage-high and last several weeks, but must be treated with cooling by hypothermia blanket and sponge bath (not antipyretics)

2.)Prophylactic hyperventilation is AVOIDED the first 20 hours post injury (can be used to decrease ICP in acute neuro deterioration)

3.)In Mechanical Vent patients monitor blood gases (should be PA CO2 of 35-38). Increased CO2 causes increased ICP.

4.)Pulmonary secretions should be monitored due to decreased LOC, chest phys. may be performed; monitor ICP for increase during this activity.

5.)Ventilate intubated patient w/100% oxygen b/4 suctioning. and give Lidocaine IV or via ET to suppress cough reflex-cough increases ICP as well.

6.)Provide quiet environment in case of headache; and keep lights low-photophobia

Management of Stroke Patients:

Drug Therapy-Anticoag./Antiplatelet, anti-seizure, calcium channel blockers

*The purposes of drug therapy are to prevent further thrombotic episodes and to protect the neurons from hypoxia*

ANTI-COAGULANTS AND ANTI-PLATELETS

*These are NOT the drugs of choice for BEST practice by the American Stroke Assoc. b/c they cause bleeding and intracerebral hemorrhage-heparin and warafin are also not recommended*

DO GIVE:  Initial dose of 325mg of aspirin.

NOTE: Aspirin should NOT be given within 24 hours of TPA administration.

(Teach patient to report any unusual bruising or bleeding to healthcare provider-Side effect of antiplatelet drugs)

NOTE: Do not give Plavix or Ticlid with aspirin POST Stroke.  These drugs have not been studied  for their use in this manner.

For Seizures post stroke: Lorazepam(Ativan) drug of choice (short term)

For long term Seizure activity, AEDs such as Dilantin, Topamax, Neurontin.

Give Calcium Channel Blockers- may be given to prevent cerebral vasospasm (occurs 4-14 days after stroke worses ischemia) after subarachnoid hemmorhage.

Stool softeners!!! Prevent vasalva maneuver during defacation which increases ICP!!

*Monitor for other complications such as hydrocephalus (increased CSF within the subarachnoid/ventricular spaces) which can cause ICP-->same symptoms as increased ICP.

*Monitor for vasospasm-symptoms are: decreased LOC, motor/reflex changes, increased neuro deficits. Symptoms may flucuate b/t episodes of vasospasm.

*Management of Stroke Patients: 

CAROTID ARTERY ANGIOPLASTY W/STENT(CAS)

*To assist in increasing blood flow to cerebrum*

*performed under local anesthesia or moderate sedation by cardiologist or radiologist*

*A distal/embolic protection device (DSP) placed through a catheter beyond the stenosis via catheter into the femoral artery at the groin- breaks up clot debreas that break off during CAS.

Post procedure care after CAS is same as for  the Carotid endarectomy.

Management of Stroke Patients: Surgical Management

*Surgical treatment depends on the cause of the stroke*

Carotid Endarectomy- used in treating progressing stroke in patients with recurrent TIAs or carotid stenosis by removing atherosclerotic plaaque from the inner lining of the artery.

Procedure details:

*Patient is inpatient for 2 nights unless complications occur.

*Monitor Vital Signs, neuro status, and peripheral pulses. 

*Check incision site for bleeding.

*Monitor for signs of stroke

*Monitor for cerebral hyperperfusion as a result of the increased vascular pressure from the open artery and lead to intracranial

hemorrhage-->Stroke.

Educate patients to be aware of/report to DR:

Severe headache

Change in brain function(drowsiness, decreased cognition)

Muscle weakness

Severe neck pain

Neck swelling

Hoarseness or difficulty swalling(nerve damage)

Extracranial-intracranial bypass-surgeon performs a craniotomy and bypasses the blocked artery by making a graft or bypass from the first artery to the second artery

*Two most common techniques are: superficial middle temporal to middle cerebral artery (STA-MCA) and occiptal to posterior inferior cerebellar artery (PICA)

* This procedure, if done immediately, increases risk of intracranial hemorrhage.

Removal of AVMs-when possible AVMs are removed via craniotomy and the surgeon ligates the affected vessels.

Cerebral aneurysms-may be repaired via a craniotomy as soon as patient's condition is stabilized.

MIDDLE CEREBRAL ARTERY STROKES

Manifestations of Middle Cerebral Artery Strokes:

*Contralateral hemiparesis. arm>leg

*Contralateral sensory deficit

*Homonymous hemianopsia

*Unilateral neglect or inattention

*Aphasia, anomia, alexia, agraphia, and acalculia

*Impaired vertical sensation

*Spatial Deficit

*Perceptual Deficit

*Visual field Deficit

*Altered LOC: drowsy to comatose

POSTERIOR CEREBRAL ARTERY STROKE

Manifestations of Posterior Cerebral Artery Stroke:

*Perseveration (word or action repetition)

*Aphasia, amnesia, alexia, agraphia, visual agnosia, and ataxia

*Loss of deep sensation

*Decreased touch sensation

*Stupor, coma

Manifestations of Internal Carotid Artery Stroke:

*Contralateral hemiparesis

*Sensory deficit

*Hemianopsia, blurred vision, blindness

*Aphasia (dominant side)

*Headache

*Bruits

ANTERIOR CEREBRAL ARTERY STROKE

Manifestations of Anterior Cerebral Artery Stroke:

*Contralateral hemiparesis. Leg>arm

*Bladder incontinence

*Personality/Behavior changes

* Aphasia and amnesia

*Positive grasp and sucking reflex

*Perseveration(repetition of words)

*Sensory deficit(lower extremity)

*Memory impairment

*Apraxic Gait

VERTEBROBASILAR ARTERY STROKES

Manifestations of Vertebrobasilar Artery Strokes:

*Headache and Vertigo

*Coma

*Memory loss and confusion

*Flaccid paralysis

*Areflexia, ataxia, and vertigo

*Cranial nerve dysfunction

*Disconjugate gaze

*Visual deficits(uniorbital) and homonymous hemianopsia

*Sensory loss: numbness

Stroke Patients: Impaired Swallowing

Interventions

*Test for swallow reflex before giving foods

*Observe for facial drooping, drooling, impaired voluntary cough, hoarseness, incomplete mouth closure, or cranial nerve palsies.

*Check gag and cough reflex.

*Check w/speech therapy for bedside swallow test or Barium Swallow test.

**Patient must remain NPO until determined that they can tolerate liquids/food and will not aspirate.

*Watch for fatigue or impulsivity or easy distractibilty -which can also put patient at risk for aspiration.

Care of Stroke Patients: Impaired Physical Mobility/Self-Care Deficit

*The patient is expected to be able to independently, with or without an assistive device; the patient is also expected to perform basic personal care activities.

Nursing Interventions for Impaired Physical Mobility/Self-Care Deficit:

*Patients with flaccid paralysis/spastic arm must begin rehab ASAP to prevent complications of immobility, such as pneumonia, atelectasis, and pressure ulcers.

*DVT prevention-increased risk of DVT in elderly in severe stroke. Apply SCDs or compression boots; change patient's position and ambulate frequently if possible.

*Rehab therapists work with patient on abiliity to complete ADLs and function at home.

Care of the Stroke Patient:  Impaired Verbal Communication

*Language or speech problems are usually the result involving the dominant hemisphere (LEFT) and may be the result of aphasia or dysarthria.

Nursing Interventions: Impaired Verbal Communication

*Aphasia- caused by cerebral hemisphere damage

*Dysarthria(slurred speech)- due to a loss of motor function to the tongue or to the muscles of speech.

(Patients should practice their exercises for dysarthria to strengthen their facial and oral muscles.)

Aphasia Classifications:

a.)Expressive(Broca's or motor) Aphasia- the result of damage in Broca's area in the frontal lobe.; difficulty speaking/writing

*Patient can understand what is said but cannot communicate verbally*

b.)Receptive (Wernicke's, or sensory) Aphasia- due to injury at Wernicke's area in the temporoparietal area.

*Patient cannot understand the spoken and often written word; although able to talk speech is often meaningless; uses neologisms-made up words*

c.)Mixed aphasia-Patient has some degree of dysfunction in areas of expression and reception.

Nursing Interventions for Aphasia:

*Present ONE idea per sentence.

*Use simple one step commands instead of multiple steps.

*Speak slowly but not loudly; use cues/gestures

*Avoid yes/no questions with patients with Expressive Aphasia(may give automatic responses which are incorrect)

*Use alternative forms of communication if needed such as computer, communication board, or flash cards w/pictures.

Care of the Stroke Patient: Total Urinary/Bowel Incontinence

*Goal is for pt. to recognize urge to void, maintain predictable pattern of voiding, respond to urges in a timely manner, get to toilet on time, empty bladder and bowel completely*

Nursing Interventions for Bowel/Urinary Incontinence

*Establish cause of bowel/urinary incontinence (altered LOC, impaired innervation, or inability to communicate the need to relieve themselves)

*Bladder retraining program-place pt on bedpan q2hours, encourage fluid intake of 2000mL daily unless contraindicated b/c of renal or cardiac issues, check for retained urine in bladder with US-can cause UTI.

*Bowel retraining program-determine patient's normal time for bowel elimination and any routine that promotes stool, follow same routine as is followed at home; Provide apple juice, diet high in fiber/bulk; and Colace may be prescribed to aid in bowel elimination.

*Foley should be removed ASAP to prevent infection; confused elderly pts should be eval. for UTI.

Care of Stroke Patient: Disturbed Sensory Perception

*Patients should adapt to the deficits and be free from injury*

Nursing Interventions for Stroke Pt w/Disturbed Sensory Perception:

*Pts w/ Rt Hemisphere brain damage usually have problems with visual-perceptual/spatial perceptual tasks.

*Families and caregivers should assist with ADLs; and give verbal and tactile cues and break down tasks into smaller steps.

*Approach patient from unaffected side, which should FACE THE DOOR.

*Place objects within patient's field of vision, use a mirror.

*Place patch on eye of patient with diplopia

*Make sure room is safe and w/o clutter

~Patient w/ Left side Lesion may have memory deficits---> re-orient patient to month, year,day of week, and circumstances surrounding admission.; may exhibit inability to perform previously learned skills (apraxia) and be hesitant/cautious in movement

Care of Stroke Patients: Unilateral Neglect

*Patient should adjust and use techniques to compensate for one-sided neglect)

*Unilateral NEGLECT SYNDROME- Occurs in patients with RIGHT CERERAL STROKE!!!!!

Educate Pt:

~To touch and use both sides of the body

i.e. wash both sides of the body/ dress affected side first.

~If hemianopsia is a problem, tell pt to turn head from side to side to increase visual field.

CARE OF STROKE PTS: HOME MANAGEMENT

Home Management

PT or OT works with the patient or significant others to obtain all needed assistive devices.

*Pts with hemiparesis should have homes free of scatter, rugs, and other obstacles in walking pathways.

*POST STROKE DEPRESSION-patients unable to exhibit normal signs of depression due to cognitive, physical , and emotional impairments.

*Strong predictors of PSD- hx of depression, severe stroke, and post stroke cognitive/physical impairment.

(Associated with increased morbidity and mortality, especially in older men)

TRAUMATIC BRAIN INJURY

*used to describe brain injuries that occur when a mechanical force is applied either directly or indirectly to the brain*

Direct injury- force produced by a blow to the head

Indirect injury-force applied to other part of the body w/rebound effect to the brain.

Primary vs. Secondary

Definition of Primary/Secondary Brain Injury:

Primary Brain Injury-occurs at time of injury and results from the physical stress(force) within the tissue caused by open or closed trauma.

*open head injury-occurs when the skull is fractured or when it is pierced by a penetrating object; integrity of brain and dura is broken/there is exposure to outside or environmental contaminants.

*closed head injury(MORE SERIOUS THAN OPEN)-the result of blunt trauma; the integrity of skull is not broken

Secondary Brain Injury-includes any process that occur after the initial injury and worsen or negatively influence outcome.

CLASSIFICATION OF TRAUMATIC BRAIN INJURY(TBI)

*Use Glasgow Coma Scale*

Classification of TBI using GCS

Mild TBI(MTBI)-GCS of 13-15- loss of consciousness for up to 15 minutes

Moderate TBI-GCS of 9-12-loss of consciousness for up to 6 hours/other systemic injury

Severe Head Injury-loss of consciousness for more than 6 hours-GCS of 3-8-more serious of hemodynamic stability/ ICP.

SYMPTOMS OF TRAUMATIC BRAIN INJURY

*Amnesia

*Seizure

*Loss of consciousness/sleepiness/drowsiness

*Restlessness or irritability

*Disorientation or confusion

*Scalp bruising and tenderness

*Personality Changes

*Diplopia

*Gait changes

*SEVERE HEAD INJURIES:

~pupil changes

~bradycardia

~hypertension(widened pulse pressure)

~pappilledema

~hypotension/tachycardia(hypovolemic shock)

~Nuchal Rigidity(CSF leak)

*NOTE: Symptoms of minor head injury should resolve within 72 hours (in some cases symptoms last days, weeks, or months)

PRIMARY BRAIN INJURY: Open Head Injury

Types (4)

Types of Open Head Injury

1.)Linear fracture-simple, clean break in which the impacted area of bone bends inward and the area around it bends outward. (most common type)

2.)Depressed fracture-the bone is pressed inward into the brain tissue to at least the thickness of the skull.

3.)Open fracture-the scalp is lacerated, creating a direct opening to the brain tissue.

4.)Comminuted fracture- involves fragmented bone with depression into the brain tissue.

5.)Basilar skull fracture- occurs at the base of the skull usuallly extending to the anterior, middle, or posterior fossa and results in CSF leakage from the nose or ears, w/potential for hemorrhage and cranial damage of nerves (I, II, VII, VIII) and infection

**Open head injury is at risk from infection from piercing object and env't.

Primary Brain Injury: Closed Head Injury

Types(3)

Types of Closed Head Injury

1.)Contusion- bruising of the brain tissue and is most commonly found at the site of impact (coup injury) or in a line opposite the site of impact (countecoup injury) Base of frontal/temporal lobes involved.

2.)Concussion-a shaky movement of the brain and may be mild or more severe; possibly lose consciousness for a short time.

*Diffuse Axonal Injury(DAI)-usually related to high-speed acceleration/deceleration as with automobile crashes causing damage to axons and white matter.

(possible immediate coma; most survivors require long term care)

3.)Lacerations- cause actual tearin of the cortical surface vessels, which may lead to secondary hemorrhage and significant cerebral edema/inflammation. (more dangerous than contusion)

TYPES OF FORCE

*Acceleration injury-caused by an external force contacting the head, suddenly placing the head in motion.

*Deceleration injury-occurs when the moving head is suddenly stopped or hits a stationary object.

May result in shearing, straining, and distortion of the brain tissue; mostly affected basilar nuclei and hypothalamus

SECONDARY BRAIN INJURY result in Increased ICP

*Increased ICP is the leading cause of death from head trauma who reach the hospital alive*

(increase in ICP-->decreased cerebral perfusion-->increased tissue hypoxia-->decrease in serum pH level-->increase in level of CO2)

Secondary Brain Injury: Increased ICP

Two types of edema

1.Vasogenic edema- seen most often and involves an increase in the volume of brain tissue due to abnormal permeability of walls of cerebral vessels, allowing fluid to collect in white matter.

2.)Cytotoxic,cellular edema-occur as a result of hypoxic insult which causes a disturbance in the cell metabolism, sodium pump, and active ion transport.  Brain depleted of O2, glucose, and glycogen--->converts to anaerobic metabolism.

*leading to vasogenic edema and increased ICP.

3.)Interstitial edema- occurs with acute brain swelling and is associated with elevated BP or increased CSF pressure.

*can be controlled by controlling BP, decrease CSF pressure or increase CPP- normal above 70mmHg

SECONDARY INJURY: HEMORRHAGE

*All hematomas are potentially life threatening b/c they act as space occupying lesions and are surrounded by edema.

Types(3)

Types of Secondary Injury: Hemorrhage

1.)Epidural Hematoma-results from arterial bleeding into space b/t the dura and the inner skull(often caused by fx of temporal bone,housing meningeal artery)

--->Patients with Epid. Hemat. have "lucid intervals" that last for minutes where patient is awake and talking; followed by momentary unconsciousness w/in moments of injury; followed by rapid increase in ICP and deterioration of condition/unstable.  NEUROSURGICAL EMERGENCY!!!!!

2.)Subdural Hematoma-results from venous bleeding into the space beneath the dura and above the arachnoid.

(due to laceration of brain tissue or bridging veins w/in cerebral hemispheres)

--->Bleeding from this injury occurs SLOWER than epidural  hematoma.

~Acute SDH-w/in 48h after impact

~Subacute SDH- b/t 48h and 2 weeks after impact

~Chronic SDH-2 weeks to several months after impact

*SDH have the HIGHEST mortality rate!!

Intracerebral Hemorrhage(ICH)-accumulation of blood within the brain tissue caused by the tearing of small arteries and veins in the sub cortical white matter.

~Subarachnoid Hemorrhage-most common ICH-may act as a space occupying lesion and maybe potentially devastating depending on location; can increase ICP levels.

*Brainstem hemorrhage-occurs as a result of direct trauma, fractures, or torsion injuries to the brainstem.