Page 1137 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

776 PART 6: Neurologic Disorders

Routine management of SAH patients frequently include anticonvul- patient population. Sodium nitroprusside is usually avoided because
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sants and prophylaxis against deep vein thrombosis (DVT) in addition of its tendency to increase ICP and thus reduce the cerebral perfusion
to close neurologic and cardiopulmonary monitoring to detect the early pressure.
complications of hypertension, rebleeding, acute hydrocephalus, pul- Rebleeding Rebleeding is most common in the first 24 hours after the
monary edema, cardiac arrhythmias, and left ventricular dysfunction.
Seizures can be a presenting symptom of SAH; however, the incidence initial hemorrhage. The cumulative risk after 1 week is ~20%, and the
risk remains elevated for several weeks. About one-half of patients
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of recurrent or new events after hospitalization is low. It remains
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unclear as to the effect of seizures on the clinical course of patients with who rebleed will die. Measures employed in the hope of preventing
rebleeding include avoidance of hypertension, cough, the Valsalva
aneurysmal subarachnoid hemorrhage although the use of prophylactic
anticonvulsants has been associated with poor neurological and cogni- maneuver, and excessive stimulation. Treatment may involve the admin-
istration of antitussives, stool softeners, and sedatives when indicated.
tive outcomes. The use of anticonvulsants in the perioperative period
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or until definitive treatment of the aneurysm is supported albeit by Antifibrinolytic medications can reduce the risk of rebleeding, but do
so at the cost of an increased incidence of cerebral ischemia. With the
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retrospective data. 81,82 DVT is common in patients with SAH, therefore
prophylaxis is mandatory. The use of pneumatic compression devices is increasingly wide use of early surgery, the use of antifibrinolytics has
largely been abandoned.
preferred initially because of the risk of intracranial bleeding, however,
The timing of surgical obliteration of the aneurysm has changed
once the aneurysm has been treated, prophylaxis with subcutaneous considerably. Up to the 1970s, surgery was routinely delayed because
heparin or low-molecular weight heparin is generally considered safe.
Routine treatments aimed at reducing the risk of ischemic stroke of reluctance to operate on an edematous brain. Several factors have
secondary to vasospasm include preventing hypovolemia and admin- resulted in a shift to early surgery (days 1-3) for patients who have a
istering nimodipine. Patients should be hydrated with isotonic saline grade of I to III on the Hunt-Hess scale. These include improved surgical
techniques, better results with early surgery in North America, and the
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at 1.5 to 2 mL/kg/h and indicators of volume status should be moni-
tored closely (clinical exam, fluid balance, daily weights, laboratory necessity that the aneurysm be clipped before hypertensive therapy for
vasospasm is administered. The timing of surgery in poor-grade patients
values, and in select cases invasive hemodynamic measurements).
Prophylactic hypervolemia should be avoided as it has not been (Hunt-Hess grades IV or V) remains controversial, but early surgery is
routinely performed in some centers.
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shown to be beneficial and may in fact lead to increased medical
In the past decade, the role of endovascular repair of amenable
complications. 83,84 Several large, prospective, placebo-controlled stud- ruptured and unruptured aneurysms has become widespread and the
ies have demonstrated that nimodipine reduces the incidence and
severity of delayed ischemic deficits and improves outcome in SAH. standard of care at many institutions. Electrolytically detachable coils
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can be placed directly in the aneurysm, where they induce thrombosis.
It remains uncertain whether this drug acts by causing vasodilation or
by exerting direct neuroprotective effects. The recommended dose is In a recent multicenter randomized trial, 20% of all assessed patients
had a ruptured aneurysm that was considered to be amenable to treat-
60 mg every 4 hours for 21 days from the time of hemorrhage. At this
dose, nimodipine can sometimes reduce systemic BP, an effect that is ment with either surgical clipping or endovascular coiling. Among this
subgroup of patients (predominantly of good clinical grade with small
undesirable in patients with vasospasm (see below). This effect can
be ameliorated by increasing fluid administration and by altering the ruptured aneurysms of the anterior circulation), the risk of death or
dependency at 1 year was significantly lower with endovascular coiling.
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dose to 30 mg every 2 hours; however, pharmacologic blood pressure
support is necessary in some patients. Follow-up data for an average of 9 years have demonstrated the con-
tinued efficacy in this patient population. There was a small increased
Early Complications rerupture rate among the patients treated with coiling; however, the risk
Hypertension Elevated BP often initially accompanies acute SAH. Several of death remained significantly lower at 5 years. 92
factors may contribute to an increase in BP, including headache, elevated Acute Hydrocephalus Acute hydrocephalus can develop very quickly after
ICP in patients with hydrocephalus, increased sympathetic nervous SAH. It is most common in patients with a poor neurological grade on
system activity, and preexisting hypertension. The rationale for treating admission and higher Fisher Scale scores. The hallmark of symptom-
hypertension is to reduce the risk of aneurysmal rebleeding. There are atic hydrocephalus is a diminished level of consciousness, sometimes
few compelling reasons not to treat the elevated BP before the onset of accompanied by downward deviation of the eyes and poorly reactive
vasospasm. As definitive data on optimal BP are lacking, it seems pru- pupils. The diagnostic evaluation can be complicated if the patient
dent to take the patient’s usual BP as a target. When the patient’s usual has received sedative drugs; it is important that analgesics be adminis-
BP is not known, it is probably better to overtreat than to undertreat. tered in doses that provide adequate relief from pain, but not excessive
There is one important exception—comatose patients in whom CT sedation. If sedatives are required for agitated patients, judicious admin-
shows marked hydrocephalus. In such cases BP should be treated very istration of short-acting agents is prudent.
cautiously until the ICP is known, to avoid causing a critical reduction Hydrocephalus can be diagnosed reliably with CT and treated
in cerebral perfusion pressure. In patients who present several days after effectively with external ventricular drainage. Since less than half of
hemorrhage and are at risk for vasospasm, the appropriate management patients with CT evidence of hydrocephalus will deteriorate clinically,
of hypertension is less clear. The benefit of preventing rebleeding must ventriculostomy is typically reserved for patients with a diminished level
be weighed against the risk of worsening neurologic symptoms by low- of consciousness.
ering BP in the presence of vasospasm.
The first step in treating elevated BP is to administer a short-acting Cardiac Complications Cardiac arrhythmias and electrocardiographic abnor-
analgesic such as fentanyl as pain can be the sole cause of BP elevation. malities are common in the first 24 to 48 hours after SAH. Most arrhyth-
Patients are routinely given nimodipine to prevent vasospasm, and it mias are benign and include atrial fibrillation and atrial flutter. More
alone may be adequate to control BP. Otherwise, short-acting agents serious arrhythmias include supraventricular and rarely ventricular
are preferred, since BP may be labile. Labetalol administered as inter- tachycardia and are associated with electrolyte abnormalities such as
mittent intravenous boluses is frequently used, since it appears to have hypokalemia. Mild elevations in cardiac enzymes also commonly occur
little effect on ICP and is easily titrated. Other useful agents include however the significance of these elevations is not clear.
intravenous hydralazine and enalapril. If frequent intravenous boluses A significant number of patients will have some degree of ventricular
are required, one should consider starting a continuous intravenous dysfunction; however, those at highest risk for neurogenic stunned myo-
infusion of an antihypertensive agent. Nicardipine is ideal as it is short cardium are of a high clinical grade. Neurogenic stunned myocardium
acting, can be titrated every 5 to 15 minutes, does not require inva- is characterized by diffuse T-wave inversions, moderate elevations in
sive hemodynamic monitoring, and has been shown to be safe in this troponin-I, pulmonary edema, cardiogenic shock, and reversible left

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