Failure of Induced Hypertension for Symptomatic Vasospasm in the Setting of Clozapine Therapy
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PRACTICAL PEARL
Failure of Induced Hypertension for Symptomatic Vasospasm in the Setting of Clozapine Therapy Jonathan G. Leung1 • Sarah Nelson1 • Sara Hocker2
Ó Springer Science+Business Media New York 2015
Abstract Background Hemodynamic augmentation is utilized as a treatment in the setting of symptomatic cerebral vasospasm. This approach includes the use of vasopressors to induce hypertension with the aim of improved cerebral blood flow. Agents with potent alpha-1 antagonism properties, including clozapine, can inhibit or blunt the response of several vasopressor agents. Methods Case report. Results A 54-year-old schizophrenic male with an aneurysmal subarachnoid hemorrhage required hemodynamic augmentation in which several vasopressor trials resulted in no or poor response. The addition of epinephrine resulted in a decrease of mean arterial pressure. Vasopressin initiation demonstrated an immediate vasopressor effect. Conclusions Vasopressors are an important treatment modality in symptomatic cerebral vasospasm. This case highlights the potential for clozapine to blunt the effects of vasopressors; or in the case of epinephrine, it causes a reversal effect. Vasopressin may be considered an agent of choice in patients who have recently taken clozapine and require hemodynamic augmentation. Keywords Cerebral vasospasm Clozapine Dobutamine Epinephrine Hemodynamic augmentation Norepinephrine Vasopressin & Jonathan G. Leung [email protected] 1
Department of Pharmacy, Mayo Clinic, 1216 2nd Street SW, Rochester, MN 55902, USA
2
Department of Neurology, Mayo Clinic, Rochester, MN, USA
Introduction Cerebral vasospasm is a complication associated with aneurysmal subarachnoid hemorrhage (aSAH) that commonly occurs 7–10 days after aneurysmal rupture [1]. Approximately, 50 % of those that suffer from angiographic cerebral vasospasm will develop delayed cerebral ischemia (DCI), although the presence and severity of vasospasm cannot always predict DCI [1]. Ongoing cerebral ischemia has been associated with increased morbidity and healthcare resource utilization and decreased quality of life following aSAH [2, 3]. Guidelines for the treatment of aSAH recommend induction of hypertension for patients with DCI unless blood pressure is elevated at baseline or cardiac status precludes it [1]. When patients with symptomatic cerebral vasospasm are not rapidly responding to induced hypertension, cerebral angiography and/or selective intraarterial vasodilator therapy is considered reasonable. Clozapine is an atypical antipsychotic indicated in the treatment of schizophrenia. Along with clozapine’s main mechanism of action, antagonizing dopamine (D2) and serotonin (5HT2A) receptors, this antipsychotic exerts potent antagonism at the alpha-1 adrenoreceptor producing peripheral vasodilation [4]. The Food and Drug Administration has placed a boxed warning on clozapine alerting clinicians to the possibility of profound hypotension which can be accompanied by respiratory and/or cardiac arrest [5]. Epinephrine is a vas
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