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					General Medical Officer (GMO) Manual: Clinical Section

Stroke
Department of the Navy
Bureau of Medicine and Surgery
Peer Review Status: Internally Peer Reviewed

(1) Definition

Stroke is a focal disease of the brain caused by the sudden death of brain tissue, either by ischemia or hemorrhage.
It can usually be as well described by the territory of the responsible artery as by the part of the brain involved. As a
focal disease, stroke causes focal deficits. Therefore observation and neurological examination will demonstrate
what part of the brain is affected. Sudden non-focal disturbance of the brain such as stupor or confusion is not
stroke, and metabolic conditions must be considered. Usually it is easy to distinguish from the following two
conditions:
    (a) A seizure is distinguished by positive phenomena such as convulsions or staring spells, and by rapid
        reversal.

    (b) Syncope is brief and immediately reversed. Occasionally, hypoglycemia and hypercalcemia may
        cause focal neurologic deficits, but these will often have other clinical indications usually more notable
        than the focal neurological deficits. Always evaluate the heart. Not only is heart disease (including
        hypertension) the overwhelming greatest risk factor for stroke, but the largest cause of death and
        morbidity in patients with stroke is coronary artery disease.
(2) Warning Signs of Stroke/Transient Ischemic Attacks
    (a) Transient ischemic attacks (TIA) are clinical deficits that resemble cerebral infarction except that they
        clear completely within 24 hours; and in fact usually within an hour. The most common clinical
        presentation is weakness or clumsiness of one side of the body, especially the upper extremity and
        same side of the face. Purely sensory deficits, seizure like movements, or ataxia are seldom transient
        ischemic attacks, and other causes should be considered first. An attack can only be determined to be
        transient after recovery. During the attack, the deficits, while persistent, are ischemic in origin and
        therefore identical to those of a stroke. TIAs are usually caused by disease of the carotid arteries or
        heart, which cause reversible ischemia in the distribution of a major cerebral artery, most often in the
        territory of the middle cerebral artery.

    (b) Another event with similar implications is transient monocular blindness, called amaurosis fugax. The
        patient experiences blurring like a shade or a sheet of wax paper pulled down or up across the vision of
        one eye. The symptoms are attributed to embolization of the retinal artery from carotid artery disease.

    (c) Patients with transient ischemic attacks or amaurosis fugax are at increased risk for complete stroke,
        and require evaluation by a neurologist or vascular specialist. The evaluation of the patient with TIA or
        carotid bruit begins first and foremost with attention to the heart. It is clear that the greatest risk of
        mortality and morbidity to patients with TIA, amaurosis fugax, carotid artery stenosis, and even
        completed stroke, is coronary artery disease. Past cardiac history, valvular disease, congestive failure,
        and arrhythmias are more dangerous for the patient and more likely to cause further neurological injury
        than are the carotid arteries.

    (d) The GMO should obtain an ECG and chest x-ray to assess the heart, in addition to an evaluation by an
        internal medicine specialist or family physician. Cardiac stress tests, echocardiogram, or prolonged
        rhythm monitoring may be indicated.

    (e) Having ruled out coronary or other cardiac disease, there is compelling evidence that aspirin, 325
        mg/day, reduces the incidence of recurrent TIA and myocardial infarction. There is also good but less
        convincing evidence that aspirin can reduce the risk of completed stroke.
   (f) Some transient deficits will turn out to be actual strokes - infarctions - with rapid functional recovery.
       Until the diagnosis is confirmed with thorough evaluation and consultation, the primary doctor must
       treat all patients with cerebral ischemia as though they are infarctions and arrange transport to a
       capable facility.
(3) Acute Stroke
   (a) The cerebral hemispheres are affected most, followed by the cerebellum and the brain stem. The
       severity of deficits however depends more on the region affected than the volume of tissue destroyed.
       Even small infarctions of the brain stem cause profound deficits, and often coma, whereas relatively
       large strokes in the cerebral cortex may cause only minor functional impairment. Infarctions of the
       cerebellum are often not recognized.

   (b) The most important consideration for the stroke patient is the heart. Myocardial infarction may be the
       underlying precipitant of a stroke, and can be far more threatening to the patient than his cerebral
       infarction, if not recognized. Rhythm disturbance is particularly important. Atrial fibrillation,
       especially intermittent, may be responsible for embolization. Stroke may also induce a number of
       rhythm disturbances, including heart block and tachyarrhythmias, which can compromise circulation
       and worsen the stroke. With this in mind, when a capable intensive care unit is available, the patient
       should be there within the first 24 to 48 hours if possible.

   (c) Oxygen and airway management are the most important care factors. If there is any question of
       maintaining the airway, as there may be with brain stem or cerebellar lesions, the patient should be
       intubated. Supplemental oxygen should be given, taking care to avoid respiratory suppression in
       patients with chronic lung disease.

   (d) Blood pressure has to be managed carefully. Hypertension may precipitate an infarction or may
       contribute to secondary hemorrhage. As a result, very high pressures should be lowered. However,
       the brain loses autoregulation in the region of an infarction, so if the pressure drops excessively,
       perfusion may suffer, resulting in extension of the ischemic zone. If the pressure is above 180/110
       mmHg, efforts should be made to lower it gradually to this level. Aggressive measures are not
       desirable in an acute infarction.

   (e) The head of the bed should be elevated 30 degrees to facilitate venous return. This will also diminish
       brain edema, which peaks on about the third day following infarction. The doctor should anticipate this
       problem because edema in the area of the infarction may appear to be an extension of the lesion. Fluid
       intake and output must be measured carefully, to assure that intake does not exceed output. Only
       isotonic, non-glucose containing solutions should be used in intravenous fluids. Corticosteroids are not
       helpful for the edema due to an infarction. Usually the local edema subsides within 2 to 3 days. If
       treatment is necessary for local swelling, hyperventilation or osmotic agents may be used.

   (f) Watch out for urinary retention. Intermittent or indwelling urinary catheters may be necessary, but an
       indwelling catheter is most reliable for the patient who will be transported any significant distance.

   (g) Two often overlooked principles are rectal impaction and range of motion. A rectal examination must
       be done every day, and digital disimpaction may be necessary every few days to prevent significant
       difficulty later. For the patient with paresis or paralysis, passive range of motion in all affected
       extremities, twenty to thirty repetitions, are necessary from the very first day, even in an isolated
       setting while awaiting transport. Frequent movements or massage of the calves and ankles may be
       necessary to prevent venous stasis. When possible, a stable patient should be out of bed several times a
       day from the very first day, and if cardiac stability permits, the patient should walk a few steps with
       assistance every day.
(4) Stabilize and Transport
    (a) As in all neurological conditions, the stroke patient should not be transported until hemodynamically
        stable. Do not initiate transport until a receiving physician has reviewed the case and assured that the
        place to which the patient is being transported will be able to provide the required care and testing.
        Ascertain clearly the time that will be required for transport. If this is longer than the patient can
        tolerate, consider delaying transfer until a shorter route can be obtained.

    (b) The patient should travel with supplemental oxygen. An indwelling catheter is almost always
        necessary. IV fluids through two secure indwelling catheters should run at a minimal rate with non-
        glucose containing isotonic solutions. A detailed record that describes the entire situation, detailed
        initial neurological examination, and record of care must accompany the patient. The medical escort
        should be capable of rapid endotracheal intubation. Equipment should include a bag for mechanically
        assisted ventilation, vials of mannitol, and spare IV apparatus. If possible, an ECG monitor,
        percutaneous oximeter, defibrillator and ACLS medications. The medical escort must plan to stay with
        the patient at the receiving site long enough to give a thorough brief.

    Reviewed by CAPT J. F. Morales, MC, USN, Neurology Specialty Leader, Neurology Department,
    National Naval Medical Center, Bethesda, MD (1999).

				
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