A 30-year-old man comes to the emergency department with sudden onset of severe headache and confusion. He has a history of autosomal dominant polycystic kidney disease. Neurological examination shows no meningeal signs or focal neurological deficits. CT scan of the head reveals blood in the subarachnoid space. The patient is admitted to the critical care unit for further management. On the fifth day after admission, he experiences new-onset weakness in the right arm and leg. Which of the following medications could have most likely prevented the neurological complications this patient developed in the hospital?

Question

A 30-year-old man comes to the emergency department with sudden onset of severe headache and confusion.  He has a history of autosomal dominant polycystic kidney disease.  Neurological examination shows no meningeal signs or focal neurological deficits.  CT scan of the head reveals blood in the subarachnoid space.  The patient is admitted to the critical care unit for further management.  On the fifth day after admission, he experiences new-onset weakness in the right arm and leg.  Which of the following medications could have most likely prevented the neurological complications this patient developed in the hospital?

Quizplus · Accepted Answer

This patient with subarachnoid hemorrhage (SAH) developed new-onset focal neurological deficits 5 days after his initial symptoms; a presentation characteristic of delayed cerebral ischemia due to cerebral vasospasm. SAH is most often caused by the rupture of a saccular (berry) aneurysm, which occurs frequently in patients with autosomal dominant polycystic disease. Cerebral vasospasm with subsequent ischemia is the most common complication of SAH and typically manifests 3-12 days after the initial incident with a change in mental status and/or new focal neurological deficits. Nimodipine, a selective calcium channel blocker, improves outcomes in patients with SAH by preventing or reducing the extent of ischemic neurological deficits caused by cerebral vasospasm. This neuroprotective effect is likely due to a combination of increased cerebral vasodilation and decreased calcium-dependent excitotoxicity. (Choices A and B) Enalapril (an ACE inhibitor) and labetalol (a beta-adrenergic blocker with some alpha-antagonist activity) can be used to control hypertension (lowering the chance of rebleeding) in patients after SAH. However, rebleeding usually occurs in the first 24 hours after SAH, and acute onset of new neurological deficits 5 days after SAH is more indicative of delayed ischemia due to cerebral vasospasm. (Choice D) Central sympatholytics (eg, methyldopa, clonidine) stimulate alpha-2A receptors centrally, resulting in a decrease in generalized sympathetic outflow and reduced blood pressure. They do not have a role in prevention of ischemic deficits due to cerebral vasospasm following SAH. (Choice E) Nitrates (eg, nitroglycerin, isosorbide mononitrate) are used as vasodilators primarily for the treatment of angina pectoris. In patients with a recent SAH, nitrates should be avoided because they can increase cerebral blood flow and intracranial pressure, which can worsen bleeding. (Choice F) Osmotic diuretics (eg, mannitol) are part of the treatment for increased intracranial pressure (ICP). Although hydrocephalus can be a complication of SAH and result in elevated ICP, it typically presents with a gradual change in level of consciousness accompanied by ocular changes (eg, downward eye deviation, miosis) rather than focal extremity deficits. Ventricular dilation on neuroimaging is diagnostic. (Choice G) Thiazide diuretics are a first-line therapy for essential hypertension in the outpatient setting. They are not indicated for use in preventing complications due to cerebral vasospasm following SAH. Educational objective: Delayed cerebral ischemia due to cerebral vasospasm usually presents 3-12 days after the initial subarachnoid hemorrhage (SAH) with an acute change in mental status and/or new focal neurological deficits. Nimodipine, a selective calcium channel blocker, improves outcomes in patients with cerebral vasospasm by inducing cerebral vasodilation and decreasing calcium-dependent excitotoxicity. __________ References: Nimodipine and its use in cerebrovascular disease: evidence from recent preclinical and controlled clinical studies. (http://www.ncbi.nlm.nih.gov/pubmed/19021025) Calcium antagonists for aneurysmal subarachnoid haemorrhage. (http://www.ncbi.nlm.nih.gov/pubmed/17636626)

A 30-Year-Old Man Comes to the Emergency Department with Sudden