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PENYAKIT SEREBROVASKULER 1. Definisi 2. Etiologi 3. Jenis-jenis penyakitnya 4. Patogenesis STROKE 1. Definisi 2. Epidemiologi · Prevalence in the US: 550/100,000 · Predominant age: Risk increases >45, and is highest in the 7th and 8th decades. · Predominant sex: Male > Female (3:1), but equalizes after menopause Hypertension is the most important risk factor for ischemic and hemorrhagic stroke. The incidence of stroke increases directly in relation to the degree of elevation of systolic and diastolic arterial blood pressure above threshold values . More important, there has been conclusive evidence for more than 30 years that control of hypertension prevents strokes. Meta-analyses of randomized controlled trials confirm an approximate 30 to 40% reduction in stroke risk with lowering of blood pressure. Approximately 7 to 10% of men and 5 to 7% of women older than 65 years have asymptomatic carotid stenosis of greater than 50%. Epidemiologic studies suggest that the rate of unheralded stroke ipsilateral to a stenosis is about 1 to 2% annually. Nonvalvar atrial fibrillation carries a 3 to 5% annual risk for stroke, with the risk becoming even higher in the presence of advanced age, previous TIA or stroke, hypertension, impaired left ventricular function, and diabetes mellitus. In epidemiologic studies, the risk for stroke in smokers is almost double that in nonsmokers, but the risk becomes essentially identical to that of nonsmokers by 2 to 5 years after quitting. The relative risk for stroke is two to six times greater for patients with insulin-dependent diabetes . Patients with sickle cell disease have a markedly increased risk for stroke. Hyperlipidemia also increases the risk for stroke, and reduction of low-density lipoprotein cholesterol levels with statins reduces this risk. Some evidence suggests that abdominal obesity in men and obesity and weight gain in women are independent risk factors for stroke. Weight reduction in overweight people is recommended, but weight loss has not been proved to reduce the risk for stroke. Epidemiologic studies have found that consumption of fruits and vegetables is associated with a lower risk for stroke, but no randomized trials have proved the value of changing dietary

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PENYAKIT SEREBROVASKULER

1. Definisi2. Etiologi3. Jenis-jenis penyakitnya4. Patogenesis

STROKE

1. Definisi2. Epidemiologi

· Prevalence in the US: 550/100,000· Predominant age: Risk increases >45, and is highest in the 7th and 8th decades.· Predominant sex: Male > Female (3:1), but equalizes after menopause

Hypertension is the most important risk factor for ischemic and hemorrhagic stroke. The incidence of stroke increases directly in relation to the degree of elevation of systolic and diastolic arterial blood pressure above threshold values . More important, there has been conclusive evidence for more than 30 years that control of hypertension prevents strokes. Meta-analyses of randomized controlled trials confirm an approximate 30 to 40% reduction in stroke risk with lowering of blood pressure.

Approximately 7 to 10% of men and 5 to 7% of women older than 65 years have asymptomatic carotid stenosis of greater than 50%. Epidemiologic studies suggest that the rate of unheralded stroke ipsilateral to a stenosis is about 1 to 2% annually.

Nonvalvar atrial fibrillation carries a 3 to 5% annual risk for stroke, with the risk becoming even higher in the presence of advanced age, previous TIA or stroke, hypertension, impaired left ventricular function, and diabetes mellitus.

In epidemiologic studies, the risk for stroke in smokers is almost double that in nonsmokers, but the risk becomes essentially identical to that of nonsmokers by 2 to 5 years after quitting. The relative risk for stroke is two to six times greater for patients with insulin-dependent diabetes. Patients with sickle cell disease have a markedly increased risk for stroke. Hyperlipidemia also increases the risk for stroke, and reduction of low-density lipoprotein cholesterol levels with statins reduces this risk. Some evidence suggests that abdominal obesity in men and obesity and weight gain in women are independent risk factors for stroke. Weight reduction in overweight people is recommended, but weight loss has not been proved to reduce the risk for stroke.

Epidemiologic studies have found that consumption of fruits and vegetables is associated with a lower risk for stroke, but no randomized trials have proved the value of changing dietary habits. Heavy alcohol consumption may be a risk factor for ischemic and hemorrhagic stroke.

Postmenopausal hormone replacement therapy has been shown to increase the risk for stroke. The absolute risk for stroke remains low, however, in otherwise healthy, low-risk patients. Meta-analysis suggests an increase in the relative risk for stroke in women taking oral contraceptives, but the absolute risk for stroke is small. Women who smoke, are hypertensive or diabetic, have migraine headaches, or have previously suffered thromboembolic events may be at increased risk for stroke when taking oral contraceptives.

GOLDMAN - CECIL MEDICINE. 23RD EDITION. LEE GOLDMAN. SAUNDERS. 2007

3. Etiologi

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NEUROLOGY.MARK MUMENTHALERS. THIEME. 2004

4. Klasifikasi

Table 64–1. Classification and Etiology of Cerebrovascular Accidents (CVA; Stroke).

Ischemic   Cerebral infarction    Nonocclusive    Cerebral arterial thrombosis    Cerebral embolism  Transient ischemic attack  Hypertensive encephalopathy with vasospasm  Venous occlusion in hypercoagulable states, infection  Arteritis: polyarteritis nodosa, giant cell arteritis  Dissecting aneurysm of the aorta  Carotid injuryHemorrhagic   Intracerebral hemorrhage: hypertensive  Subarachnoid hemorrhage: berry aneurysms  Associated with vascular malformations and neoplasms  Associated with bleeding diatheses such as coagulation disorders, thrombocytopenia;

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anticoagulant therapy  Mycotic aneurysm

CONCISE_PATHOLOGY. CLIVE R. TAYLOR. MCGRAW-HILL. 2006

5. Factor resiko6. Patofisiologi

Vascular lesions causing ischaemia. A Thrombosis: initiated by either abnormal flow (e.g. stasis, turbulence), damage to vessel wall (e.g. denudation of endothelial lining) or abnormal blood constituents. B Embolism. C Spasm: due to contraction of smooth muscle in media of vessel, for example due to lack of nitric oxide from endothelium. D Atheroma: occurs only in arteries and may in turn be complicated by thrombosis and embolism. E Compression: veins are more susceptible because of their thinner walls and lower intraluminal pressure. F Vasculitis: inflammation of vessel wall narrows lumen and may be complicated by superimposed thrombosis. G Vascular steal: for example, an artery may be narrowed by atheroma but flow is

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still sufficient to maintain viability of perfused territory; however, flow may be compromised by increased demands of a neighbouring territory. H Hyperviscosity: increased viscosity, in for example hypergammaglobulinaemia resulting from myeloma, causes impaired flow and predisposes to thrombosis.

CONCISE_PATHOLOGY. CLIVE R. TAYLOR. MCGRAW-HILL. 2006

Mmmmmm

MECHANISM OF DISEASE. AN INTRODUCTION TO CINICAL SCIENCE. 2 ND EDITION. STEPHEN TOMLINSON. CAMBRIDGE UNIVERSITY PRESS. 2008

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Table 26-4. Comparison of the major causes of stroke

Cause %Clinical presentation

30-day mortality (%) Pathogenesis Predisposing factors

Cerebral infarction

85Slowly evolving signs and symptoms

15-45 Cerebral hypoperfusion Embolism Thrombosis

Heart disease (e.g. infective endocarditis, endocardial thrombus) HypertensionAtheroma Diabetes mellitus

Intracerebral haemorrhage

10Sudden onset of stroke with raised intracranial pressure

80 Rupture of micro-aneurysm or arteriole

Hypertension Vascular malformation

Subarachnoid haemorrhage

5Sudden headache with meningism

45 Rupture of saccular aneurysm on circle of Willis

Hypertension Polycystic renal disease Coarctation of the aorta

7. Manifestasi klinis

Effect of ischemia on the brain. Diagram of the effect of sudden total deprivation of blood supply to the brain on tissue metabolism, consciousness, the EEG, neuronal morphology, and tissue glucoseconcentration.

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NEUROLOGY.MARK MUMENTHALERS. THIEME. 2004

COLOR ATLAS OF PATHOPHYSIOLOGY. STEFAN SILBERNAGL. THIEME. 20008. Diagnosis banding

Table 142-2 Differential Diagnosis of Acute Stroke

HypoglycemiaPostictal paralysis (Todd paralysis)Bell's palsy

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Hypertensive encephalopathyEpidural or subdural hematomaBrain tumor or abscessComplicated migraineEncephalitisDiabetic ketoacidosisHyperosmotic comaMeningoencephalitisWernicke encephalopathyMultiple sclerosisMeniere diseaseDrug toxicity (lithium, phenytoin, carbamazepine)

EMERGENCY MEDICINE MANUAL. 6 TH EDITION. O. JOHN. MA. THE MCGRAW-HILL COMPANIES. 2007

9. Penegakan diagnosis

History

• Attempt to identify, as accurately as possible, the onset, course, and type of symptoms, as well as the patient’s activity at onset.• Determine the patient’s stroke risk factors, other potential causes for the patient’s symptoms, and any contraindications to thrombolytics or other agents.• Neurologic deficits that occur abruptly, and are maximal at onset, suggest an embolic stroke. Stepwise, incremental deficits are more indicative of thrombosis.• Hemorrhagic strokes often have a rapid onset. Maximum deficit may be present immediately but worsening may occur. Consciousness may be impaired.• Subarachnoid hemorrhage (SAH) is characterized by symptoms of variable onset and progression; severe headache and neck stiffness; and often impaired consciousness.

Vital Signs• Hypotension may be the underlying cause of a stroke; markedly elevated blood pressure is suggestive but not diagnostic of a hemorrhagic stroke.• An irregular cardiac rhythm may indicate chronic or new-onset atrial fibrillation and an embolic source.• Increased ICP may be accompanied by bradycardia. • Focus on searching for an underlying systemic cause, especially a treatable one.• HEENT• Note any signs of trauma. Palpate the temporal arteries.

• Fundoscopic exam may reveal evidence of embolization. Papilledema indicates increased

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Physical Examination

ICP. Retinal hemorrhages may be noted in SAH.

• Determine patency of the airway and ensure the airway is protected.

• Neck: evaluate the carotid pulses and check for carotid bruits, Neck stiffness may or may not be present in SAH.• Cardiac exam: note any arrhythmias or evidence of valvular disease (i.e., murmurs).• Neurologic exam• The initial neurologic exam should be a brief search for signs of increased ICP or impending transtentorial herniation (e.g., dilated pupil, depressed consciousness, or posturing).

• Neurologic deficits that do not conform to the distribution of any single cerebral artery suggest a hemorrhagic or mass lesion.

• Assess the level of consciousness and mental status. Determine whether the patient has aphasia (expressive or receptive?) or dysarthria.

• Evaluate cranial nerve function, with special attention paid to pupils, extraocular

movements, visual fields, facial symmetry, gag reflex and corneal reflex.

• The presence of a gaze palsy may help localize the lesion. A patient with a cerebral

hemispheric stroke will typically gaze toward the side of the insult; a brainstem

infarct will cause the patient to gaze away from the side of the lesion.

• Motor exam: the most sensitive indicator of upper extremity weakness is the

presence of a pronator drift. Whenever possible, lower extremity strength should

be assessed by observing the patient’s gait.

• Sensory exam: peripheral sensation (light touch, pinprick, and vibration/position

sense). Double simultaneous stimulation: assess sensation on both sides of

the body simultaneously; patients with cortical infarcts will only notice the unaffected

side.• Cerebellar exam: look for nystagmus, ataxia, or poor coordination.

• Reflexes: recent stroke is

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accompanied by hyporeflexia (and flaccidity). Search for pathologic reflexes (e.g., presence of a Babinski reflex indicates an upper motor neuron disorder).

Evaluation

• Pulse Oximetry• Rapid determination of oxygen saturation

may reveal impending respiratory failure and the need for mechanical ventilation. Supplemental oxygen may suffice.

• Laboratory• Bedside glucose testing is crucial to exclude

hypoglycemia as a cause of focal neurologic deficits.

• A complete blood count may reveal an underlying hematologic disorder presenting as a stroke.

• Prothrombin time (PT) and partial thromboplastin time (PTT) are helpful in excluding

coagulopathy.• Baseline serum electrolytes are

recommended.• An elevated ESR may suggest giant cell

arteritis or other vasculitis.• Blood for type and cross match (patients

with SAH)• Consider a toxicology screen in patients

suspected of drug abuse (although the results seldom change the patient’s acute management).

• Pregnancy test in females of child-bearing age.

• Lumbar puncture (LP) is indicated when CNS infection or SAH is suspected. In the case of SAH, LP is performed after a negative CT scan. LP may also suggest a venous or sinus thrombosis (CSF pressure is typically increased and pleocytosis may occur), or granulomatous angiitis (CSF pleocytosis occurs).

• EKG• May detect cardiac ischemia, or cardiac

arrhythmias which predispose to stroke (e.g., atrial fibrillation). In addition, multiple abnormalities are described in patients with subarachnoid hemorrhage, including peaked or symmetric, deeply inverted T waves; shortened PR intervals; and tall U waves.

• Chest radiograph• In selected patients, chest X-ray (CXR) may

reveal an infectious process, malignancy, or evidence of heart failure. In intubated patients, CXR is used to confirm placement of the endotracheal tube.

• Imaging• Noncontrast CT scan is the emergency

radiologic study of choice when evaluating patients with suspected stroke, TIA, or SAH. CT is able to distinguish between ischemic and hemorrhagic strokes, and will detect blood in more than 90% of cases of

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aneurysmal rupture. In addition, early signs of cerebral edema are identified with noncontrast CT scanning.

• When available, MRI is useful for early ischemic infarcts. MRI may also be more sensitive for ischemic strokes in the brainstem or cerebellum, as well as in detecting thrombotic occlusion of venous sinuses.

• Electroencephalogram (EEG) is rarely useful in the acute evaluation of stroke. It may, however, help to differentiate between seizure disorder and TIA, or between lacunar and cortical infarcts.

EMERGENCY MEDICINE. SEAN. O. HANDERSON. LANDES BIOSCIENCE. 200610. Penatalaksanaan

• General Management Issues • As with all emergent conditions, evaluation of the patient with a neurologic deficit begins with airway, breathing, and circulation. Patients with severely depressed mental status and patients with an unprotected airway may require intubation and mechanical ventilation.• All patients should be placed on continuous pulse oximetry and cardiac monitoring, and have peripheral intravenous access established. • Patients noted to have signs of increased ICP should be aggressively managed.

• Oxygen • Supplemental oxygen may be required to maintain oxygen saturation >95%. However, in the absence of hypoxia, supplemental oxygen has not been shown to affect outcome.

• Blood Pressure Control • In the first few hours following acute stroke, mild to moderate hypertension is commonly observed. Over the next few hours to days, the blood pressure generally declines spontaneously. The ischemic penumbra may be dependent upon a moderately increased blood pressure for adequate perfusion; thus, use of antihypertensive agents may exacerbate the patient’s condition.• Cautious blood pressure control—with easily titratable, short-acting parenteral medications—is recommended in the following situations: (1) hypertensive encephalopathy; (2) cardiac ischemia or aortic dissection; (3) intracerebral hemorrhage; (4) when thrombolytic therapy is considered (see exclusion criteria below); and (5) the mean arterial pressure (MAP) is >130, or the SBP is >220.

Anticoagulants • Heparin has been shown to benefit patients at risk for cardioembolic stroke (especially patients with ischemic or rheumatic heart disease). In addition, patients with venous sinus occlusion benefit from heparin use.

Antiplatelet Agents • Aspirin has been shown to reduce the rate of nonfatal recurrent stroke and death after acute stroke (versus placebo). Aspirin is recommended in patients who are not candidates for thrombolytics or other anticoagulants.• Ticlopidine inhibits the ADP pathway of platelet aggregation; it also reduces blood fibrinogen levels. In patients with TIA or minor stroke, ticlopidine results in

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significant risk reduction in stroke recurrence or death versus aspirin. However, the hematologic side effects (TTP, thrombocytopenia, and neutropenia) have limited its recommended use to patients who have a contraindication to aspirin and who can be closely monitored in this setting; clopidogrel is preferred by many practitioners.• Clopidogrel is similar in action and effect to ticlopidine. It is recommended for aspirin-intolerant patients and has a significantly lower rate of TTP than ticlopidine.

EMERGENCY MEDICINE. SEAN. O. HANDERSON. LANDES BIOSCIENCE. 2006

11. Rehabilitasi 12. Pencegahan13. Prognosis14. Komplikasi