Ischemic Stroke - Hennepin County Medical Center

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Case Reports She is continent of bowel and bladder. A left field cut is easily demonstrated and she has obvious left hemi-neglect on sensory testing. The patient is articulate and can express herself quite clearly but often interrupts others and appears to be somewhat disinhibited in social situations. The patient is scheduled for longterm physical and rehabilitation therapy to regain as complete functioning as possible. Discussion This patient, whose outcome was decidedly better than may have been estimated initially, presented several difficult management challenges. The patient presented with a history and physical examination very suggestive of stroke, a luxury not always available to the clinician. While clinical exam findings are unquestionably useful, the diagnosis is usually confirmed with imaging. A cranial CT scan without contrast is critical to differentiating ischemic from hemorrhagic stroke. An ischemic stroke can begin to show changes such as a hyperdense artery sign, sulcal effacement, loss of graywhite interface, mass effect, and acute hypodensity as soon as three hours after the event, but more often between 6-12 hours. Presence of early ischemic changes does not change the management with intravenous fibrinolytic therapy within the three-hour time window. An electrocardiogram helps diagnose atrial fibrillation (which account for 60% of cardio-embolic strokes) and myocardial infarction. Out-of-hospital providers and emergency physicians need to document as best as they are able the exact time of stroke onset and presence of any neurologic deficits, since these findings may rapidly progress or resolve by the time the patient arrives at the hospital. Such information is critical for the decision in administration of fibrinolytics. Management of blood pressure should use pre-established guidelines and will vary depending on whether the patient is a candidate for fibrinolytic therapy. The sBP shoud be less than 185 mmHg and the dBP less than 110 mmHg before giving fibrinolytics because of concern for increased intracranial hemorrhage risk with higher blood pressures. If fibrinolytics are given, strict blood pressure control is indicated, with the goal of having sBP 120 mmHg, according to the most recent American Heart Association guidelines. Aspirin given within 48 hours of the stroke onset has been shown to have mild efficacy in preventing early recurrent stroke but does not improve outcomes from the current stroke. Aspirin should be held for 24 hours after fibrinolytic therapy in case there is an intracranial hemorrhage. Improved outcome has not been shown for treatment with heparin for ischemic stroke in several clinical trials. Recent studies show no benefit from heparin, or a small potential benefit of heparin, that is counterbalanced by an increased risk of hemorrhage. In addition to the focal neurologic injury from the ischemic stroke itself, cerebral edema that develops following the insult can lead to intracranial hypertension and further devastating neurologic effects. The clinical manifestations of increased ICP include: Depressed level of consciousness Headache Vomiting Cushing's triad (bradycardia, respiratory depression, and hypertension) Additional focal deficits can be caused by ischemic injury or herniation. These manifestations are caused either by direct mass effects of the increased intracranial volume (e.g. herniation, Cushing's triad) or the decrease in cerebral blood flow caused by the ICP. 4 | Approaches in Critical Care | December 2008
Case Reports In normal adults, ICP is 20mmHg. Cerebral perfusion pressure (CPP) is a clinical marker for the adequacy of cerebral blood flow. (CPP = MAP - ICP). Cerebral blood flow is normally maintained at a relatively constant level by vascular autoregulation over a wide range of CPP (50-100 mmHg). When intracranial hypertension develops, cerebral blood flow decreases, leading to hypoperfusion and ischemic injury. Therefore in the presence of ICP, CPP should be maintained between 60-75 mmHg. Management of the cerebral edema and associated ICP is critical to minimize worsening the ischemic deficit. An important early goal in this management of ICP is placement of a monitoring device that improves insight into the patient's condition and can guide the therapies needed to maintain adequate CPP and oxygenation. Patients should be kept euvolemic and slightly hyperosmolar (295-305 mOsm/L). Hypertonic saline acutely lowers ICP but is unproven in longterm outcomes. Cerebral metabolic demand, and consequently cerebral oxygen consumption, can be reduced by sedating patients. Blood pressure, especially when hypertensive, needs to be carefully managed. The optimal blood pressure in these patients is still a matter of debate. Some argue that lowering the sBP will help decrease the ICP and improve outcomes. However, others argue that inducing systemic hypertension may increase cerebral perfusion and is more important. Osmotic diuretics such as mannitol can be used to draw free water from the cerebral tissues back into the vascular space where it can be managed by the kidneys. Despite occasional use, glucocorticoids have not been shown to improve outcomes and may increase the risk of infections, so generally should be avoided. While hypocapnia (PaCO2 between 26-30 mmHg), induced through hyperventilation, leads to vasoconstriction and a decrease in intracranial blood volume in the early management of an acute stroke, it is often counter to the need to maintain cerebral perfusion and is probably best avoided. Prophylactic therapy for seizures in the setting of large hemispheric stroke is unproven, but sometimes still administered. Removal of CSF can be immensely useful in lowering ICP, and is generally easily done through a ventriculostomy draining to gravity. The drainage should be done slowly at a rate of 1-2 mL/minute in cycles of 2-3 minutes draining with a similar period of being clamped. This can be repeated until ICP is
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Ischemic Stroke - Hennepin County Medical Center

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