Alan Sobey

University of Alberta, Edmonton, Alberta, Canada

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Publications (2)4.64 Total impact

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    ABSTRACT: In a carcinoid crisis, numerous vasoactive agents, such as bradykinin precursors, serotonin, and histamine, are secreted by tumour cells. Bradykinin has been shown to increase pulmonary vascular permeability and hypotension in animal models; however, little is known about its in vivo effects or targeted pharmacotherapy in a carcinoid crisis. We describe a case of acute respiratory distress syndrome (ARDS) in a carcinoid crisis refractory to conventional antiserotonin and antihistamine therapies. A 56-yr-old male with known liver metastases and previous resection of a small intestinal carcinoid tumour in 1991 underwent successful tricuspid and pulmonary valve replacements. On postoperative day 10, he developed hypotension, a fever, leukocytosis, and flushing. His hypotension was treated with a 200 μg octreotide iv bolus followed by a 150 μg·hr(-1) infusion, vasopressin, norepinephrine, and hydrocortisone. He also required tracheal intubation for ARDS (Pa02:FI02 ratio 96). After 72 hr of broad spectrum antibiotics and no clinical improvement, antiserotonin and antihistamine therapies were augmented with cyproheptadine, ranitidine, and serial octreotide boluses with an infusion of 1,500 μg·hr(-1). These interventions improved his oxygenation (Pa02:F i 02 ratio 162) and reduced his norepinephrine requirements. Following a methylene blue bolus (1 mg·kg(-1)) and 12-hr infusion (0.5 mg·kg(-1)·hr(-1)), all vasopressors were discontinued and his oxygenation improved (Pa02:F i 02 ratio 297). In a patient with a carcinoid crisis and ARDS refractory to conventional therapies, substantial hemodynamic and oxygenation improvements were observed following methylene blue administration. This case highlights the potential pathophysiologic role of bradykinin and methylene blue as an adjunct therapeutic option in carcinoid crises.
    Canadian Anaesthetists? Society Journal 09/2013; 60(11). DOI:10.1007/s12630-013-0026-4 · 2.53 Impact Factor
  • Leah Johnson-Coyle · Louise Jensen · Alan Sobey ·
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    ABSTRACT: Peripartum cardiomyopathy, a type of dilated cardiomyopathy of unknown origin, occurs in previously healthy women in the final month of pregnancy and up to 5 months after delivery. Although the incidence is low-less than 0.1% of pregnancies -morbidity and mortality rates are high at 5% to 32%. The outcome of peripartum cardiomyopathy is also highly variable. For some women, the clinical and echocardiographic status improves and sometimes returns to normal, whereas for others, the disease progresses to severe cardiac failure and even sudden cardiac death. In acute care, treatment may involve the use of intravenous vasodilators, inotropic medications, an intra-aortic balloon pump, ventricular-assist devices, and/or extracorporeal membrane oxygenation. Survivors of peripartum cardiomyopathy often recover from left ventricular dysfunction; however, they may be at risk for recurrence of heart failure and death in subsequent pregnancies. Women with chronic left ventricular dysfunction should be managed according to guidelines of the American College of Cardiology Foundation and the American Heart Association.
    American Journal of Critical Care 03/2012; 21(2):89-98. DOI:10.4037/ajcc2012163 · 2.12 Impact Factor