Matthew Baker1, Melissa Thompson Bastin1, Aaron M Cook2, Justin Fraser1, Eugene Hessel1. 1. Matthew Baker, M.D., is Assistant Professor, Anesthesiology, Department of Anesthesiology, University of Kentucky (UK) College of Medicine, Lexington. Melissa Thompson Bastin, Pharm.D., is Critical Care Pharmacist, Pharmacy Services, UK HealthCare, and Department of Pharmacy Practice and Science, UK College of Pharmacy, Lexington. Aaron M. Cook, Pharm.D., is Coordinator, Neuroscience-Pulmonary/Critical Care, Pharmacy Services, UK HealthCare, and Assistant Adjunct Professor, Department of Pharmacy Practice and Science, UK College of Pharmacy. Justin Fraser, M.D., is Assistant Professor, Neurosurgery, Department of Neurosurgery; and Eugene Hessel II, M.D., is Professor, Anesthesiology, Department of Anesthesiology, UK College of Medicine. 2. Matthew Baker, M.D., is Assistant Professor, Anesthesiology, Department of Anesthesiology, University of Kentucky (UK) College of Medicine, Lexington. Melissa Thompson Bastin, Pharm.D., is Critical Care Pharmacist, Pharmacy Services, UK HealthCare, and Department of Pharmacy Practice and Science, UK College of Pharmacy, Lexington. Aaron M. Cook, Pharm.D., is Coordinator, Neuroscience-Pulmonary/Critical Care, Pharmacy Services, UK HealthCare, and Assistant Adjunct Professor, Department of Pharmacy Practice and Science, UK College of Pharmacy. Justin Fraser, M.D., is Assistant Professor, Neurosurgery, Department of Neurosurgery; and Eugene Hessel II, M.D., is Professor, Anesthesiology, Department of Anesthesiology, UK College of Medicine. amcook0@email.uky.edu.
Abstract
PURPOSE: A case of probable nimodipine-induced hypoxemia in a patient undergoing treatment for aneurysmal subarachnoid hemorrhage (SAH) is reported. SUMMARY: A 62-year-old man hospitalized for SAH developed symptoms of respiratory distress on several occasions within days of initiation of nimodipine therapy (60 mg every four hours, with three doses withheld during intubation for intracranial surgery). Several hours after extubation (on hospital day 5), the patient had rapidly worsening tachypnea and declining arterial oxygen saturation (SPO2) despite increased oxygen delivery by mask, necessitating reintubation. When a nurse noted that the declines in SPO2 occurred soon after nimodipine administration, the patient's respiratory and hemodynamic functions were closely monitored after a single dose of nimodipine via nasogastic tube; the monitoring results supported the suspicion that nimodipine's vascular effects were a causal or contributory factor in the hypoxemia episodes. With subsequent fractionated dosing (30 mg every two hours), the patient completed the prescribed 21-day course of nimodipine therapy. Using the rating scale of Naranjo et al., this case was assigned a score of 7, indicating a probable pulmonary adverse reaction to nimodipine. As nimodipine is commonly used in cases of SAH to reduce delayed neurologic deficits due to persistent cerebral vasospasm, clinicians should be mindful of its potential hypoxemic effects in vulnerable patients. CONCLUSION: A patient with aneurysmal SAH developed hypoxemia associated with the administration of nimodipine. Hypoxemia is a known complication of treatment with other vasodilatory agents, particularly in patients who have concomitant pulmonary disease.
PURPOSE: A case of probable nimodipine-induced hypoxemia in a patient undergoing treatment for aneurysmal subarachnoid hemorrhage (SAH) is reported. SUMMARY: A 62-year-old man hospitalized for SAH developed symptoms of respiratory distress on several occasions within days of initiation of nimodipine therapy (60 mg every four hours, with three doses withheld during intubation for intracranial surgery). Several hours after extubation (on hospital day 5), the patient had rapidly worsening tachypnea and declining arterial oxygen saturation (SPO2) despite increased oxygen delivery by mask, necessitating reintubation. When a nurse noted that the declines in SPO2 occurred soon after nimodipine administration, the patient's respiratory and hemodynamic functions were closely monitored after a single dose of nimodipine via nasogastic tube; the monitoring results supported the suspicion that nimodipine's vascular effects were a causal or contributory factor in the hypoxemia episodes. With subsequent fractionated dosing (30 mg every two hours), the patient completed the prescribed 21-day course of nimodipine therapy. Using the rating scale of Naranjo et al., this case was assigned a score of 7, indicating a probable pulmonary adverse reaction to nimodipine. As nimodipine is commonly used in cases of SAH to reduce delayed neurologic deficits due to persistent cerebral vasospasm, clinicians should be mindful of its potential hypoxemic effects in vulnerable patients. CONCLUSION: A patient with aneurysmalSAH developed hypoxemia associated with the administration of nimodipine. Hypoxemia is a known complication of treatment with other vasodilatory agents, particularly in patients who have concomitant pulmonary disease.
Authors: Phillip A Howells; Kerrie A Aldridge; Dhruv Parekh; Daniel Park; Olga Tucker; Rachel C A Dancer; Fang Gao; Gavin D Perkins; David R Thickett Journal: BMJ Open Respir Res Date: 2017-11-02