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A 57-year-old man with history of hypertension and gastric ulcer presents after a sudden onset of severe headache followed by nausea and vomiting. The patient arrived in the emergency department (ED) after becoming stuporous in the ambulance. On arrival to the ED, he is hemodynamically unstable,with blood pressure (BP) 80/40 mm Hg and is promptly intubated. He is given fluid resuscitation with the infusion of 2 L of crystalloids, and blood pressure recovers to 140/80 mm Hg. Computed tomography (CT) of the head reveals acute subarachnoid hemorrhage (SAH) filling the basal cistern and bilateral sylvian fissures with thick hemorrhages (modified Fisher grade 3) and early evidence of hydrocephalus (Figure 17-1). The patient is transferred to the neurologic intensive care unit (NeuroICU) where an external ventricular drainage (EVD) is urgently placed and urgent angiography planned. After EVD placement the patient was comatose, with intact brainstem reflexes, and pupils were symmetric and reactive to light bilaterally. Vital signs were as follows: BP, 150/70 mm Hg; heart rate, 120/minute; respiration rate, 22/minute (mechanical ventilation at assist-control pressure-controlled mode), and temperature, 37°C.

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Figure 17-1.

Poor-grade subarachnoid hemorrhage (modified Fisher 3) caused by a right internal carotid artery aneurysm rupture.

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Patients in the acute phase after aneurysmal SAH are at increased risk for rebleeding. The highest rates of rebleeding occur in the first 3 days after SAH, and surgical clipping or endovascular coiling of the ruptured aneurysm should be pursued as soon as possible after admission. Although the aneurysm is unsecure, systemic hypertension should be avoided; however, hemodynamic stability is crucial to avoid cerebral hypoperfusion, acute ictal infarcts, and cerebral circulatory arrest.1–4

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Liberal fluid resuscitation with crystalloids is commonly necessary in patients with poor-grade SAH before securing the aneurysm. Although frequently hypertensive, patients are admitted with relative intravascular volume depletion—due to natriuresis and the systemic inflammatory response associated with severe brain injury—and 2 L of normal saline is acutely administered to maintain organ perfusion. On arrival to the ICU, the patient should receive a central venous access and an invasive arterial line. If a mean arterial pressure (MAP) goal of 70 mm Hg is not achieved, norepinephrine should be initiated. If, instead, the MAP is > 110 mm Hg or systolic blood pressure is > 160 mm Hg, continuous infusion of nicardipine should be started to avoid unsafe BP levels. At this point, urine output, central venous pressure, arterial lactate levels, and central venous oxygen saturation (Scvo2) are assessed to refine the evaluation of hemodynamic stability. Urine output < 0.5 mL/kg/h, lactate levels > 2 mmol/L and Scvo2 < 65% generally represent systemic hypoperfusion and further fluid resuscitation should target CVP > 8 mm Hg, Scvo2 > 70%, and the reduction of arterial lactate.1,4–8

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The patient is submitted to cerebral angiography that reveals an aneurysm in the intracranial part of the right internal carotid artery. Endovascular coiling is undertaken with successful occlusion of the ...

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