Stroke

42 Stroke




Overview/pathophysiology


A stroke (previously known as cerebrovascular accident [CVA]) is the sudden disruption of O2 supply to the brain or rupture in one or more of the blood vessels that supply the brain. Ischemic stroke has three main mechanisms: thrombosis, embolism, and systemic hypoperfusion. Thrombosis or embolism results in a blockage of blood supply to the brain tissue. The resulting ischemia, if prolonged, causes brain tissue necrosis (infarction), cerebral edema, and increased intracranial pressure (IICP). Most thrombotic strokes are caused by blockage of large vessels as a result of atherosclerosis. Thrombi in small penetrating arteries result in “lacunar” strokes. Most embolic strokes are cardiogenic and the result of emboli produced from valve disease or during atrial fibrillation of the heart. Ischemic stroke caused by systemic hypoperfusion usually is the result of decreased cerebral blood flow owing to circulatory failure. Circulatory failure results from too little blood, too low blood pressure (BP), or failure of the heart to pump blood adequately. Hypoxia from any cause also can produce this syndrome.


A transient ischemic attack (TIA), which is a temporary (less than 24 hr) neurologic deficit that resolves completely without permanent damage, occurs when the artery cannot deliver enough blood to meet the O2 requirement of the brain. However, restoration of blood flow is timely enough to make the ischemia (and deficits) transient, thereby avoiding infarction and permanent damage. TIAs usually are associated with thrombosis but may be caused by any of the ischemic mechanisms just mentioned. TIAs may precede a permanent ischemic stroke by hours, days, months, or years. TIAs are a warning sign, and treatment may prevent a stroke. Most TIAs last an average of 5-10 min, although some can last longer than an hour. A reversible ischemic neurologic deficit (RIND) lasts longer than 24 hr but otherwise is similar to a TIA.


Hemorrhagic stroke causes neural tissue destruction because of the infiltration and accumulation of blood. Ischemia and infarction may occur distal to the hemorrhage because of interrupted blood supply. Although a cerebral hemorrhage usually results from hypertension or an aneurysm, trauma also can cause hemorrhagic stroke. Bleeding may spread into the brain tissue itself, causing an intracerebral hemorrhage, or into the subarachnoid space. Usually there is a large rise in intracranial pressure (ICP) with a hemorrhagic stroke because of cerebral edema and the mass effect of blood.


A stroke may be classified as a progressive stroke in evolution, in which deficits continue to worsen over time, or as a completed stroke, in which maximum deficit has been acquired and has persisted for longer than 24 hr. Progressive strokes usually are the result of thrombus formation and often take 1-3 days to become “completed.” Embolic strokes typically have sudden onset with maximal deficits. Stroke syndromes classically have been described according to distribution of the vessels (middle cerebral artery, anterior cerebral artery, posterior cerebral artery, vertebral, basilar) that supply particular regions of the brain and will have typical assessment findings. Stroke is the third most common cause of death and the most common cause of neurologic disability. Half the survivors are left permanently disabled or experience another stroke. Improvement may continue for 1-2 yr, but deficits at 6 mo usually are considered permanent.


A brain attack, also sometimes called a code stroke or stroke alert, is a sudden event and medical emergency with the same urgency as a heart attack. If the stroke is ischemic and the patient qualifies, “time-is-tissue” and the sooner the patient can be treated, the better the outcome. For appropriate patients, treatment with recombinant tissue plasminogen activator (rt-PA) needs to occur within 3 hr of symptom onset. To achieve this, all people should be educated to recognize warning signs of stroke and immediately call 911. Rapid transport to a hospital, preferably a stroke center, should occur, with the emergency medical technician starting the medical history, especially the time of symptom onset, and alerting the hospital before arrival so the stroke team (if available) can be assembled. Upon arrival at the hospital door, the time-to-treatment goal is 60 min and is further broken down into subgoals:


Time from arrival at hospital door to:

Evaluation by physician—10 min

Neurologic expert and “stroke team” (if available) contacted and patient assessed—15-25 min

Head computed tomography (CT) or magnetic resonance imaging (MRI) scan completed; other data (e.g., laboratory values) collected—25 min

Interpretation of CT or MRI scan completed; decision to treat based upon data, contraindications—45 min

Start of treatment (e.g., rtPA) in appropriate patients—60 min

Intraarterial rtPA, available at some research centers, may extend the window of opportunity to 6 hr. Thrombolytic therapy reverses symptoms of stroke by dissolving the clot(s) causing the ischemia before actual cell death. Use of a mechanical blood clot retrieval device (e.g., MERCI) may extend this time window further.


Stroke care can be differentiated into these basic types: thrombolytic ischemic stroke care, nonthrombolytic ischemic stroke care (including TIAs), and hemorrhagic stroke care. Care differences center mostly around BP management and use of anticoagulant and antiplatelet agents. Most hospitals, especially stroke centers, have protocols for stroke management.



Health care setting


Critical care unit, step-down unit, acute rehabilitation unit, outpatient rehabilitation program



Assessment


Note: Because of the narrow 3-hr window that may reverse permanent neurologic damage, it is critical to teach patients not to ignore symptoms and to call 911 without delay for the following:


• Sudden numbness or weakness of the face, arm, or leg, especially on one side of the body

• Sudden confusion, trouble speaking or understanding

• Sudden trouble seeing in one or both eyes

• Sudden trouble walking, dizziness, loss of balance or coordination

• Sudden, severe headache with no known cause

A history to determine time of symptom onset is critical inasmuch as this may determine eligibility for treatment. Time of onset is when patient was last known to be “normal,” so if patient woke up after sleeping with symptoms, time of onset would be when the patient went to bed “normal” and not when he or she woke up symptomatic.




General findings:


Classically, symptoms appear on the side of the body opposite the damaged site. For example, a stroke in the left hemisphere of the brain will produce symptoms in the right arm and leg. However, when the stroke affects the cranial nerves, symptoms of cranial nerve deficit will appear on the same side as the site of injury. Similarly, an obstruction of an anterior cerebral artery can produce bilateral symptoms, as will severe bleeding or multiple emboli. Hemiplegia is fairly common. Initially, patient usually has flaccid paralysis. As spinal cord depression resolves, more normal tone is seen and hyperactive reflexes occur.



Signs and symptoms:


Vary with the size and site of injury and may improve in 2-3 days as the cerebral edema decreases. Changes in mentation, including apathy, irritability, disorientation, memory loss, withdrawal, drowsiness, stupor, or coma; bowel and bladder incontinence; numbness or loss of sensation; weakness or paralysis on part or one side of the body; aphasia; headache; neck stiffness and rigidity; vomiting; seizures; dizziness or syncope; ataxia; and fever may occur. A brain stem infarct leaving the patient completely paralyzed with intact cortical function is called locked-in syndrome. With cranial nerve involvement, visual disturbances include diplopia, blindness, and hemianopia. Inequality or fixation of the pupils, nystagmus, tinnitus, and difficulty chewing and swallowing also occur.



Physical assessment:


Papilledema, arteriosclerotic retinal changes, or hemorrhagic retinal areas on ophthalmic examination. Hyperactive deep tendon reflexes (DTRs), decreased superficial reflexes, and positive Babinski’s sign also may be present. To check for Babinski’s response, stroke the lateral aspect of the sole of the foot (from the heel to the ball of the foot) with a hard object. Dorsiflexion of the great toe with fanning of the other toes is a positive sign. Positive Kernig’s or Brudzinski’s sign (see “Bacterial Meningitis,” p. 256) indicates meningeal irritation.



TIA:


Typical symptoms include temporary episodes of slurred speech, weakness, numbness or tingling, blindness in one eye, blurred or double vision, dizziness or ataxia, and confusion.



Risk factors:


TIAs; hypertension; atherosclerosis; high serum cholesterol or triglycerides; high homocysteine levels; diabetes mellitus; gout; smoking; obesity; cardiac valve diseases, such as those that may result from rheumatic fever, valve prosthesis, and atrial fibrillation; cardiac surgery; blood dyscrasias; anticoagulant therapy; neck vessel trauma; oral contraceptive use; cocaine or methamphetamine use; family predisposition for arteriovenous malformation (AVM); aneurysm; advanced age; or previous stroke.



Assessment scales (e.g., GCS and NIHSS):


The Glasgow Coma Scale (GCS) is helpful for quickly assessing level of consciousness (LOC). The National Institutes of Health Stroke Scale (NIHSS) not only assesses LOC but also assesses deficits and provides a standardized approach to neurologic examinations. An NIHSS total score of 0-1 is normal; 1-4 is a minor stroke; 5-15 is a moderate stroke; 15-20 is a moderately severe stroke; and more than 20 is a severe stroke. The NIHSS score also strongly predicts likelihood of recovery, with higher scores resulting in more disability and poorer outcomes. Use of thrombolytics (e.g., rtPA) is considered appropriate for ischemic stroke if the total score is more than 4-6 and there is sustained, nonimproving deficit. NIHSS is used for assessing effects of thrombolytic therapy and should, at minimum, be done initially as a baseline, 2 hr post treatment, 24 hr post onset of symptoms, and 7-10 days after symptom onset. The complete scale with instructions can be obtained from www.strokecenter.org



Diagnostic tests


Selection, sequence, and urgency of the following tests will be determined by the patient’s history and symptoms. For example, a patient whose symptoms have resolved from a TIA will have a different set or sequence of tests compared to the patient who is in coma. Since usage of rtPA is time limited, speed is essential in determining type of stroke (ischemic vs. hemorrhagic) and other contraindications to rtPA. Obtaining CT scan to determine type of stroke is a top priority along with laboratory tests to assess for contraindications.




CT scan:


To reveal site of infarction, hematoma, and shift of brain structures. CT scan is of particular value in identifying blood released early during hemorrhagic strokes. CT scan is the test of choice for unstable patients. Generally, identifying ischemic areas is difficult until they start to necrose at around 48-72 hr. Xenon-enhanced CT may be done to study cerebral blood flow; CT angiography may be performed to evaluate blood vessels.



MRI scan:


To reveal site of infarction, hematoma, shift of brain structure, and cerebral edema. MRI diffusion and perfusion weighted studies are of particular value in identifying ischemic strokes early and in differentiating between acute and chronic lesions. Other magnetic resonance (MR) techniques include MR angiography to evaluate vessels and MR spectrography.



Laboratory tests:


Certain tests (e.g., serum electrolytes, complete blood count including differential and platelet count, prothrombin time with international normalized ratio, and partial thromboplastin time) should be done immediately to assess for contraindications such as hypoglycemia or clotting abnormalities if patient is a candidate for thrombolytic therapy. Other tests will be done depending on patient (e.g., toxicology screen, pregnancy test, blood culture and erythrocyte sedimentation rate for endocarditis or vasculitis process, hemoglobin AIC for diabetics). Lipid panel, C-reactive protein, and homocysteine levels also may be obtained.



Electrocardiogram:


To evaluate for atrial fibrillation and myocardial ischemia.



Phonoangiography/doppler ultrasonography:


To identify presence of bruits if the carotid blood vessels are partially occluded. B-mode imaging and duplex scanning also may be done to evaluate the carotids to detect occlusive disease. Dimensional ultrasound improves three-dimensional visualization and includes the potential for quantitative monitoring of plaque volume changes in all three directions—circumferential, length, and thickness.



Transcranial doppler ultrasound:


To provide information (noninvasively) about pressure and flow in the intracranial arteries.



Swallowing examination/videofluoroscopy:


All patients should be screened for dysphagia. Videofluoroscopy identifies problem or pathology, determines most appropriate treatment, and enables teaching of proper swallowing technique. This test is not performed for individuals known to aspirate saliva because it involves swallowing a barium-containing liquid, semisolid, and/or solid.



Positron emission tomography:


To provide information on cerebral metabolism and blood flow characteristics. This test is useful in identifying ischemic stroke by showing areas of reduced glucose metabolism.



Single photon emission CT:


To identify cerebral blood flow.



Electroencephalograph:


To show abnormal nerve impulse transmission and indicate amount of brain wave activity present.



Lumbar puncture and cerebrospinal fluid (CSF) analysis:


Not done routinely, especially in the presence of IICP, but may reveal increase in CSF pressure; clear to bloody CSF, depending on stroke type; and presence of infection or other nonvascular cause for bleeding. CSF glutamic oxaloacetic transaminase (GOT) will be increased for 10 days after injury. Blood in the CSF signals that a subarachnoid hemorrhage has occurred.



Cerebral and carotid angiography:


If surgery is contemplated, this procedure is done to pinpoint site of rupture or occlusion and identify collateral blood circulation, aneurysms, or AVM.



Digital subtraction angiography:


To visualize cerebral blood flow and detect vascular abnormalities, such as stenosis, aneurysm, and hematomas.



Echocardiography (e.g., transthoracic and transesophageal):


To evaluate valvular heart structures for thrombus and myocardial walls for mural thrombi that may provide a source of emboli.



Evoked response test:


Provides measurement of the brain’s ability to process and react to different sensory stimuli. Responses from these sensory stimuli can indicate abnormal areas in the brain.



Electronystagmography:


Evaluates patients who have dizziness, vertigo, or balance dysfunction and provides objective assessment of oculomotor and vestibular systems.





Nursing diagnosis:


Impaired physical mobility

related to neuromuscular impairment with limited use of upper and/or lower limbs


Desired Outcome: By at least 24 hr before hospital discharge, patient and significant other demonstrate techniques that promote ambulating and transferring.




































ASSESSMENT/INTERVENTIONS RATIONALES
Assess for subluxation of the shoulder (e.g., shoulder pain and tenderness, swelling, decreased range of motion [ROM], altered appearance of bony prominences). Shoulder subluxation occurs when weight of the affected arm is unable to be supported by the weakened shoulder muscles causing separation of the shoulder joint.
Never pull on the affected arm. Guide upper extremity movement from the scapula and not from the arm; use a lift sheet to reposition in bed. Ensure that the arm has a firm support surface when patient is sitting. These measures help prevent subluxation. When in bed the shoulder should be positioned slightly forward to counteract shoulder rotation. The affected arm should be placed in external rotation when the patient is supine or lying on affected side.
Teach methods for turning and moving, using stronger extremity to move weaker extremity. For example, to move affected leg in bed or when changing from a lying to a sitting position, slide unaffected foot under affected ankle to lift, support, and bring affected leg along in the desired movement.
Encourage patient to make a conscious attempt to look at extremities and check position before moving. These are safety measures to prevent falling. For example, remind patient to make a conscious effort to lift and then extend foot when ambulating.
Instruct patient with impaired sense of balance to compensate by leaning toward stronger side. The tendency is to lean toward weaker or paralyzed side. For example, patient may need to be reminded to keep body weight forward over feet when standing.
Recommend wearing well-fitting shoes. Slippers, for example, tend to slide.
Prevent shoulder-hand syndrome with regular, gentle joint ROM exercises and proper arm positioning. Never place arm under the body. When patient is in bed, place arm on abdomen or pillow for support. Encourage repeated shoulder movement, elevation of the arm above cardiac level, and regular fist clenching and reclenching. Shoulder-hand syndrome is a neurovascular condition characterized by pain, edema, and skin and muscle atrophy caused by impairment of the circulatory pumping action of the upper extremity.
Protect impaired arm with a sling. The sling will support the arm and shoulder when patient is out of bed.
Position patient in correct alignment, and provide a pillow or lapboard for support. Encourage active/passive ROM to improve muscle tone. These measures will help maintain anatomic position.
Teach and implement the following:
– Encourage weight bearing on patient’s stronger side.
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Jul 18, 2016 | Posted by in NURSING | Comments Off on Stroke

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