Presentation is loading. Please wait.

Presentation is loading. Please wait.

Cerebral Vascular Accident STROKE. RISK FACTORS FOR STROKES ► Nonmodifiable  Age- incidence ↑ with age until age 75.  Race- higher in African Americans.

Similar presentations

Presentation on theme: "Cerebral Vascular Accident STROKE. RISK FACTORS FOR STROKES ► Nonmodifiable  Age- incidence ↑ with age until age 75.  Race- higher in African Americans."— Presentation transcript:

1 Cerebral Vascular Accident STROKE


3 RISK FACTORS FOR STROKES ► Nonmodifiable  Age- incidence ↑ with age until age 75.  Race- higher in African Americans  Gender- higher in men  Heredity- family history increases risk ► Potentially Modifiable  Lifestyle- excessive alcohol, cigarette smoking, obesity, high fat diet, drug abuse.  Pathologic conditions- cardiac disease, DM, HTN, migraine headaches, hypercoagulability states.


5 ETIOLOGY AND PATHO ► Extra-cranial factors- related to the circulatory system.  Systemic blood pressure- 160  cardiac output- when reduced by 30% cerebral blood flow is reduced.  Blood viscosity- anemia increases cerebral blood flow and polycythemia reduces it.

6 INTRACRANIAL FACTORS ► A. Metabolic factors  Increased CO2 and low O2 results in vasodilation to restore blood flow to normal.  CO2 is the most potent regulator of cerebral blood flow.  Increased Hydrogen ion concentration increases cerebral blood flow.

7 Intracranial factors, cont’d ► B. Blood vessels  The condition of the blood vessels supplying the brain is important!!! ► Potential problems- congenital anomalies (tortuosity, coiling, kinking, and AV malformations). ► The malformations interfere with cerebral blood flow and contribute to atherosclerotic disease ► Collateral circulation develops ► Circle of Willis

8 Intracranial factors, cont’d ► C. Intracranial pressure  ICP increases with an assault to brain.  Causes of ICP: stroke, neoplasms, inflammation, trauma, and hydrocephalus.  ICP compresses the brain and reduces cerebral blood flow, which may lead to infarct.  Both extracranial and intracranial factors may lead to stroke

9 Atherosclerosis ► An abnormal accumulation and infiltration of in the intima of the arteries. ► Plaques develop in an area of high turbulence; which may later damage the plaque. ► Platelets and fibrin aggregate or collect on the surface of the plaque. ► Parts of the plaque breaks off and travel to a narrower distal artery ► Cerebral infarct occurs.




13 TYPES OF STROKE ► Ischemic: Most common type of stroke!  Occurs due to decreased blood flow to an area of the brain due to partial or complete occlusion of and artery due to thrombosis.  This lack of blood, oxygen and nutrients to an area of the brain causes necrosis of cerebral tissue.  Two types: thrombotic and embolic  See Lewis, page 1648; table 55-1.

14 Thrombotic stroke ► Most common cause of cerebral infarct! ► Cause: Due to formation of a blood clot or coagulation of blood that results in narrowing of blood vessel or occlusion. ► 2/3 of strokes due to HTN or DM. (accelerate the atherosclerotic process) ► May also be due to oral contraceptives, coagulation disorders, polycythemia, arteritis, chronic hypoxia and dehydration.


16 Thrombotic Stroke ► Thrombotic strokes are usually proceeded by prodromal episodes (warnings) called TIA’s (transient ischemic attacks). ► TIA’s last from 5 to 30 minutes.  Include- paresis or decreased strength and motion of an extremity.  Aphasia or disturbance of language function,  Paralysis, mental confusion, or visual disturbances.

17 Thrombotic stroke ► The extent of the stoke depends on rapidity of onset, size of lesion, and presence collateral circulation. ► There is a pattern to thrombotic stroke!  1. single attack; symptoms occur over several hours  2. intermittent progression toward a stroke over hours or days.  3. partial stroke with permanent neuro deficits  4. series of TIA’s followed by a stroke with permanent neuro deficits.

18 Thrombotic stroke ► Symptoms at 72 hours are usually due to resulting edema to tissues; symptoms improve after edema subsides (@ 2 weeks). ► This type of stroke occurs during or after stroke.



21 EMBOLIC STROKE ► Cerebral embolism results from occlusion of cerebral artery by an embolus. ► Necrosis and cerebral edema results. ► Embolus is the second most common cause of stroke. ► Most emboli originate in the endocardium with plaques or tissue breaking off and entering circulation.


23 Embolic Stroke ► Emboli are associated with heart conditions such as;  A fib  MI  Infective endocarditis  Rheumatic heart disease  Valvular prostheses  ASD

24 Embolic stroke ► Less common causes of emboli:  Air  Fat from long bone fracture  Amniotic fluid postpartum  tumors

25 Embolic stroke ► Prodromal warning less likely; single events ► sudden onset ► Most commonly related to head trauma ► High rate of re-occurrence if cause is not treated.

26 Hemorrhagic stroke ► Intracerebral hemorrhage is bleeding within the brain caused by rupture of a blood vessel that lasts from minutes to days. ► Most commonly caused by HTN ► May be caused by brain tumors, trauma, thrombolytic drugs, and ruptured aneurysms.

27 Hemorrhagic stroke ► Blood within the closed area of the brain imposes pressure on the brain tissue and displaces brain tissue and decreases blood flow to brain. ► Clinical manifestations depends on the site and amount of hemorrhage and resultant damage. ► Poor prognosis; 70% die


29 Subarachnoid stroke ► Caused by aneurysms, AV malformations, trauma, and HTN. ► May have prodromal symptoms if ballooning or dilation applies pressure to brain tissue. ► May suddenly rupture, causing neuro changes ► Majority of aneurysms are in the Circle of Willis

30 Subarachnoid hemorrhage, cont’d ► If aneurysm leaks, pt may have a headache! ► Rupture of aneurysm causes pressure in subarachnoid space due to bleeding. Clinical manifestations:  Headache, lethargy, confusion, nausea, vomiting, fever, neck pain, and backaches, paralysis, coma and death. Massive hemorrhage is defines as 30 to 50 ml of blood. Watch for re-bleeding when clot starts to dissolve. (usually within first 2 weeks post rupture). Reduce activity and prevent straining.

31 Temporal Development of CVA ► Transient Ischemic Attacks (TIA’s)-  Brief episodes of neuro manifestations (less than 24 hours).  Leaves no residual effects  Three categories: ► 1/3 never have another TIA ► 1/3 will have more than one TIA ► 1/3 will have a stroke WARNING SIGNS OF PROGRESSING CVA!

32 TIA’s ► s/s vary depending on the part of brain affected. ► Treatment:  Medications such as aspirin, Persantine (dipyridamole), Ticlid, and anticoagulant medication.  Long term therapy post TIA  Surgical treatment- carotid endartarectomy, extra-cranial- intracranial bypass (EC-IC bypass), and transiluminal angioplasty.

33 Reversible ischemic Neurologic Deficit ► A neuro deficit which remains 24 hours after onset; but leaves no residual signs or symptoms. ► Considered a completed stroke with minimal to no residual deficits ►

34 Stroke –In- Evolution ► A progressive stroke which develops over hours or days. ► Characteristic of an enlarging intra-arterial thrombus. ► A stepwise or intermittent progression of deterioration of neurological symptoms. ► Manifestations do not resolve and leave residual damage.

35 Completed Stroke ► Neuro defects unchanged over 2 to 3 days. ► Usually embolic in nature ► Also called “stable stroke”. ► Signals readiness for aggressive rehab therapy. (unless an aneurysm is involved).

36 Clinical Manifestations ► All deficits are directly related to area of brain that is involved. ► See Lewis, page 1650, Table 55-2.

37 Neuromotor Function ► Destruction of motor neurons in the pyramidal pathway causes:  Mobility  Respiratory function  Swallowing and speech  Gag reflex  Self-care abilities

38 Motor deficits ► Loss of skilled voluntary movement (akinesia). ► Impairment of integration of movements ► Alterations in muscle tones ► Alteration in reflexes ► Initial hypo-reflexia which progresses to hyper-reflexia for most patients.

39 Patterns of deficits ► Contralateral deficits  A lesion on one side of the brain affects the motor function on the other side of the brain.  The arms and legs on the affected side may be weak or paralyzed to different degrees depending the degree of cerebral circulation compromised.  See Lewis, Page 1651; Table 55-5

40 ► The affected shoulder tends to rotate internally; the hip rotates externally. ► The affected foot is plantar flexed and inverted. ► An initial period of flaccidity may lasts for several days to weeks. ► Spasticity of muscles follows the flaccid stage and is related to interruption of upper neuron influence.

41 Communication ► Aphasia- total loss of comprehension and use of language due to damage to the dominant hemisphere (left hemisphere). ► Dysphasia-dysfunction related to comprehension or use of language due to partial disruption or loss.  Non-fluent (minimal speech activity with slow speech that requires obvious effort)  Fluent- (speech is present, but contains little meaningful communication).

42 Communication ► Conductive aphasia- mixture of both expressive and receptive aphasia ► Global aphasia- results from a massive lesion and there is virtual loss of all language ability.

43 Communication, cont’d ► Wernicke’s area damage  Receptive aphasia where neither the sound or speech or its meaning can be understood.  Impaired comprehension of both spoken and written language. Boca’s area damage Expressive aphasia (difficulty speaking and writing) Dysarthria- disturbance in muscular control of speech. (pronunciation, articulation, phonation) DOES NOT EFFECT COMPREHENSION OF LANGUAGE.


45 Affect ► May be unable to control emotions ► May be depressed RT body image and loss of function ► May be frustrated RT immobility and communication issues

46 Intellectual Function ► Memory and judgment may be impaired ► Left-sided stroke patients are more cautious in judgment and movement. ► Right-sided stroke patients more impulsive and move quicker.

47 Spatial-Perceptual Alterations ► Right sided stroke patient has more spatial- perceptual orientation issues:  Erroneous perception of self and illness (may deny illness or body parts).  Erroneous perception of self in space (may ignore affected side; can’t judge distances)  Agnosia or inability to recognize an object by sight, touch or hearing.  Apraxia or the inability to carry out learned sequential movements on command.

48 Elimination ► Most occur initially and are transient. ► Frequent constipation DT immobility, weak abdominal muscles, dehydration, and diminished defecation reflexes. ► Urinary and bowel elimination may be DT functional inabilities to express needs and manage clothing.

49 Diagnostic Studies ► CT Scan- indicate size and location of lesion, differentiates between infarct and hemorrhage, effectiveness of treatment, and evaluate the course of healing. ► MRI- considered best method to differentiate between hemorrhage and infarct.

50 Diagnostics ► PET shows chemical activity and depicts extent if tissue damage. ► DSA- IV or arterial injection of contrast material to visualize blood vessels. ► TDA- transcranial doppler measures velocity of cerebral blood flow in the arteries, also detects micro-emboli. ► LP may be done to detect blood or WBC’s (not done if increased ICP is suspected)


52 Collaborative care ► PREVENTION  Healthy diet  Weight control  Regular exercise  No SMOKING  Limiting alcohol  Routine health assessment

53 DRUG THERAPY ► Prophylactic low dose aspirin, daily. ► Persantine 50 mg 3 X day decreases platelet aggregation which helps to decrease risk of thrombus and embolus formation. ► TICLID or PLAVIX- platelet aggregation inhibitors

54 Surgical Therapy ► Carotid endarterectomy (CEA)- the atheromatous lesion is removed from the carotid artery to improve blood flow  Decreases stroke and death in patient with TIA’s.  Done on patient with 70-99% occlusion

55 Transluminal Angioplasty ► Insertion of balloon to open stenosed artery to permit blood flow.  Patient with symptomatic stenosis of vertebrobasilar or carotid arteries  Risk of dislodging emboli

56 EC-IC BYPASS ► Extracranial-intracranial bypass  Used when obstruction cannot be removed directly  A branch of extracranial artery is anastomosed to a branch of intracranial artery just beyond the area of obstruction.  Patients at high risk for stroke and require close-long term assessment and management.

57 ACUTE CARE ► Table 55-5; Lewis page 1654. ► Initially  Ensure patent airway DT altered level of consciousness. ► Remove dentures Administer oxygen via nasal cannula or non- rebreather mask DT respiratory distress

58 Acute Care ► Establish IV access with normal saline to maintain BP ► Remove clothing ► Obtain immediate CT Scan ► Monitor VS, LOC, O2 sats, cardiac rhythms, Glasgow Coma Scale, pupil size and reactivity.

59 Acute Care ► Maintain patient warmth ► Reassure patient and family

60 Ischemic Cascade ► Series of events in response to thrombotic and embolic strokes.  Ischemic area becomes discolored and soft, initially. However, around the border there is an area of perfusion called the ischemic penumbra that maintains perfusion for 3 to 6 hours post stroke.  If adequate blood flow is reinitiated during this period, less neuro damage results

61 Treatment ► Control fluid and electrolyte balance  Adequate hydration promotes perfusion to the brain; however over hydration may increase cerebral edema!  Total intake (oral, tube feedings, IV etc., 1500- 2000 per day)  Monitor urine output ( if ADH released urine output will decrease)

62 Treatment ► IV solutions with glucose and water are avoided. (hypertonic solutions may increase cerebral edema) ► Increased ICP from cerebral edema peaks in 72 hours and may cause brain herniation.

63 How to manage ICP ► Enhance venous drainage by:  Elevating HOB  Maintain head and neck in alignment  Avoidance of hip flexion Limit cerebral tissue metabolism and vasodilation by: avoiding hyperthermia, avoiding hypervolemia, manage constipation

64 Medications ► Diuretics (decrease cerebral edema)  Mannitol (Osmitrol)  Lasix, (Furosemide)  Dexamethasone for patients with vasogenic edema

65 Drug Therapy ► Thrombolytic therapy  Recombinant tissue plasminogen activator (t- PA)- to re-establish blood flow and prevent cell death for patients with ischemic strokes.  Patients who receive t-PA within 3 hours after a stroke more likely to have 32% less injury three months after stroke.  T-PA works by lysis thrombus/clot by binding and digesting the fibrin and fibrinogen.

66 t-PA Clot specific ► Less likely to cause hemorrhage as compared to streptokinase or urokinase. ► Single most important factor is timing!!!

67 t-PA ► Patients are screened for coagulation disorders, GI bleeding, and hemorrhagic stroke before initiation of treatment. ► Major side effect is cerebral hemorrhage. ► Monitor VS during treatment/ control BP ► O anticoagulants or antiplatelet drug for 25 hours post treatment.

68 Platelet inhibition/anticoagulant therapy ► Heparin, coumadin, aspirin, ticlipidine (Ticlid), clopidrogel (Plavix), dipyridamole (Persantine). ► Contraindicated for patients with hemorrhagic strokes ► Monitor PT/ PTT ► Monitor patient for bleeding

69 Drug therapy ► Calcium channel blockers are given for patients with hemorrhagic strokes. ► Excess intracellular calcium may be harmful to brain tissue. ► Nimodipine (Nimotop) decreases effects of vasospasm and minimizes tissue damage. ► Aspirin decreases platelet aggregation at site of plaque.

70 Drug therapy ► Tylenol treats hyperthermia ► Dilantin may be given for seizures

Download ppt "Cerebral Vascular Accident STROKE. RISK FACTORS FOR STROKES ► Nonmodifiable  Age- incidence ↑ with age until age 75.  Race- higher in African Americans."

Similar presentations

Ads by Google