Rescue of Nimodipine-Induced Refractory Vasoplegia With Hydroxocobalamin in Subarachnoid Hemorrhage: A Case Report.

BACKGROUND: We report a case of refractory vasoplegia after nimodipine administration that was unresponsive to triple vasopressor therapy and was rescued by IV hydroxocobalamin. CASE SUMMARY: An 84-year-old male presented comatose from a subarachnoid hemorrhage and developed severe hypotension unresponsive to three vasopressors following a single dose of enteral nimodipine. Multisystem point-of-care ultrasonography ruled out alternate etiologies of shock, indicating that this was likely a vasoplegic state caused by nimodipine. We administered 5 grams of IV hydroxocobalamin over 15 minutes due to the possibility of impaired nitric oxide metabolism as the driver of vasoplegia. This led to immediate improvement in hemodynamics and rapid discontinuation of vasopressors. The patient experienced chromaturia but no other adverse effects due to hydroxocobalamin. CONCLUSIONS: Nimodipine administration is a standard practice for patients with aneurysmal subarachnoid hemorrhage to reduce unfavorable outcomes from cerebral vasospasm. Although mild hypotension is a common side effect of nimodipine, in rare cases, it may become profound, leading to refractory vasoplegia. There is no evidence-base for reversal agents for nimodipine-induced vasoplegia, and this case is the first to demonstrate successful use of hydroxocobalamin as a potential rescue therapy. We also propose an algorithm for treatment of vasoplegia with consideration of medications that act on nitric oxide-mediated vasodilation and their side-effect profiles.

A Rare Case of Plastic Bronchitis in an Adult Patient After Cardiopulmonary Bypass.

Plastic bronchitis is a rare life-threatening complication observed after cardiopulmonary bypass (CPB). We describe a case of a 54-year-old man in whom a fulminant case of plastic bronchitis developed after coronary artery bypass grafting (CABG) and mitral valve repair. A brief review of the literature is also presented.

Q fever as a biological weapon.

Q fever is a bacterial zoonosis caused by Coxiella burnetii, a unique intracellular coccobacillus, adapted to live within the phagolysosomes of macrophages and monocytes. It is highly infectious, with as little as one organism needed to cause clinical infection, making it an attractive organism for use in biowarfare. Despite its high infectivity, it has low virulence, and most patients undergo only asymptomatic seroconversion. Acute clinical manifestations are a nonspecific febrile illness, pneumonia, hepatitis, and neurologic abnormalities ranging from headache to meningoencephalitis. Chronic Q fever can result in endocarditis, hepatitis, or a chronic fatigue syndrome. Diagnosis usually is made by serology because culture of the highly contagious organism is potentially hazardous. Tetracyclines are the antibiotics of choice. When individualized therapy is possible, a 14- to 21-day course of doxycycline usually is used. In a mass casualty situation, a 5- to 7-day course of doxycycline is recommended, both for therapy and prophylaxis. For chronic infections such as endocarditis, 18 months of doxycycline supplemented with hydroxychloroquine is currently the best therapy.