Acute evaluation and management of ischemic stroke-1

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Introduction

The subacute and long-term management of patients

who have suffered an ischemic stroke includes physical therapy and testing to determine the precise etiology of the event so as to prevent recurrence. The acute management differs. Immediate goals include minimizing brain injury, treating medical complications,
and moving toward uncovering the pathophysiologic basis of the patient's symptoms.

Initial General Assessment

Sudden loss of focal brain function is the core feature of the onset of ischemic stroke. The goals in this initial phase include

  • Insuring medical stability.
  • Quickly reversing any conditions that are contributing to the patient's problem.

  • Moving toward uncovering the pathophysiologic basis of the patient's neurologic symptoms.

Diagnosing an intracerebral or subarachnoid hemorrhage as soon as possible can be lifesaving. The history may be helpful in this regard. However, it is important to assess and optimize vital physiologic function before sending the patient for an imaging study.

Blood pressure: The mean arterial blood pressure (MAP) is usually elevated in patients with an acute stroke. This may be due to chronic hypertension, which is a major risk factor for ischemic stroke. However, in many cases the acutely elevated blood pressure is necessary to maintain brain perfusion.

  • Patients with an intracranial hemorrhage may have increased intracranial pressure (ICP) due to blood within the cranium. Cerebral perfusion pressure (CPP) equals MAP minus ICP. Thus, increases in MAP may be the only means to maintain CPP above 60 mmHg, the level necessary to maintain perfusion.

  • In patients with ischemic stroke, the perfusion pressure distal to the obstructive vessel is low and the distal vessels are dilated. Blood flow in these dilated vessels is thought to be dependent upon the systemic blood pressure.

The observation that the BP frequently rises spontaneously following cerebral ischemia is consistent with this protective hypothesis, although a stress response to the acute event and to hospitalization may also contribute. The hypertensive effect is transient, as the BP falls by as much as 20/10 mmHg within 10 days.

Numerous reports have documented a clinical decline associated with lowering blood pressure in the patient with an acute ischemic stroke. On the other hand, severe increases in blood pressure can cause hypertensive encephalopathy, a condition that can mimic stroke. In this case, lowering the blood pressure is the indicated treatment.

Elevated blood pressure can also worsen an intracerebral hemorrhage. In patients with subarachnoid hemorrhage (SAH), for example, the mechanical force across the plugged bleeding site is related to the difference between the systemic blood pressure and the cerebrospinal fluid (CSF) pressure. Lowering the blood pressure may decrease the risk of rebleeding, but this benefit is often offset by an increased risk of infarction.

Similar considerations apply to the patient with intracerebral hemorrhage in whom the blood pressure again represents the force for continued bleeding. One difference between the patient with intracerebral and subarachnoid hemorrhage is that the latter is more often normotensive at baseline, suggesting that the elevation in blood pressure is a compensatory response to maintain cerebral perfusion.

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