Abstract

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Risperidone is a second-generation atypical antipsychotic medication (APD) commonly used to treat schizophrenia and bipolar disorder. An infrequent dangerous side effect of APDs is hypothermia, defined as a core body temperature < 35 Celsius (C) [1]. CASE PRESENTATION: A 61-year-old male with hypertension, epilepsy, and schizophrenia was transferred to the emergency department for bilateral lower extremity weakness and slow speech for two days. Medications included carbamazepine and risperidone. He denied being outside in the cold and stated he has a heater at home. A week prior, at a follow-up with his primary physician, his oral temperature was 35.5C. A clinical exam revealed dysphasia and right lower leg weakness. Core rectal temperature was 29.1C, indicating moderate hypothermia. Computed tomography of the head and neck with contrast displayed no acute intracranial abnormality. Blood work revealed a normal thyroid-stimulating hormone, cardiac enzymes, and lactic acid. Urinalysis was negative for infection. Chest x-ray showed no acute abnormalities. Carbamazepine level was in the therapeutic range. In the intensive care unit, he was given warmed intravenous fluids and placed on an external warmer with constant temperature monitoring. Due to central hypothermia concerns, risperidone was held, and external warming was applied. Gradually, core temperature increased to 36.5C over the next 14 hours. He had no signs of infection or metabolic derangements to increase his hypothermia risk. He improved quickly and was downgraded to the medical floor. DISCUSSION: Experimental animal model studies reveal a dose-dependent decline in temperature with risperidone [2]. The exact incidence is higher than reported medical literature based on reports submitted to Food and Drug Administration. Mild hypothermia was common and moderate hypothermia was rare after few years of therapy [3]. Mild hypothermia symptoms are inconspicuous and odd, like apathy, confusion, shivering, or hunger, and are often missed [1]. Clinical thermometers fail to register a temperature < than 34.4C. The risk is more in men and patients with schizophrenia and bipolar disorder. Risk factors such as age > 70 years, other APDs, and organic diseases amplify it [3]. APDs are highly antagonistic at serotonin receptors (5-HT2a) than dopamine (D2) and a2 adrenergic receptors. 5-HT2a and a2 receptors act to increase core temperature while D2 acts to decrease it [3]. APD use leads to an imbalance promoting lower core temperature. Monitoring temperature is essential at APDs initiation and dosage changes. Consideration of other medical comorbidities is a must. CONCLUSIONS: APDs induced moderate central hypothermia is a rare, reversible cause. Failure to recognize it by critical care providers can be fatal. REFERENCE #1: Polderman KH. Mechanisms of action, physiological effects, and complications of hypothermia. Crit Care Med. 2009;37(7 Suppl):S186-202 REFERENCE #2: Oerther S, Ahlenius S. Atypical antipsychotics and dopamine D(1) receptor agonism: an in vivo experimental study using core temperature measurements in the rat. J Pharmacol Exp Ther. 2000;292(2):731-736. REFERENCE #3: : Szota AM, Araszkiewicz AS. The risk factors, frequency and diagnosis of atypical antipsychotic drug-induced hypothermia: practical advice for doctors. Int Clin Psychopharmacol. 2019;34(1):1-8. DISCLOSURES: No relevant relationships by Dennis Chairman, source=Web Response No relevant relationships by Sahithi Katragadda, source=Web Response No relevant relationships by Parth Patel, source=Web Response No relevant relationships by Tarang Patel, source=Web Response No relevant relationships by SACHIN PATIL, source=Web Response

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