Poppers Not Only Make You High: A Rare Case of Amyl Nitrate-Induced Hypoxia

Abstract

SESSION TITLE: Fellow Case Report Poster - Pulmonary Physiology SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 25, 2016 at 01:30 PM - 02:30 PM INTRODUCTION: “Poppers” are inorganic nitrites that have become an increasingly popular recreational inhalant. They cause vasodilation, smooth muscle relaxation, and aphrodesia. Amyl nitrites act as oxidizing agents which can cause methemoglobinemia. As a result, tissue hypoxia occurs from decreased oxygen binding capacity of methemoglobin. CASE PRESENTATION: A 55 year old male with occasional cocaine use and no significant medical history presented with slurred speech for one day. Initial vital signs showed BP 122/73, HR 64, RR 18, Tm 97.2, SaO2 84% on room air. Physical examination was notable for lethargy and slurred speech. There was no facial asymmetry or focal deficits noted. Blood work was remarkable for Na 147 and Hgb 11. Urinalysis was positive for cocaine. CT head and brain MRI were negative. Patient was given IVF with resolution of symptoms. He was noted to be persistently hypoxic without symptomatology. CT angiogram of the chest was negative for pulmonary embolism. ABG showed pO2 142 and O2 sat of 92% on 2L NC, and co-oximetry disclosed a methemoglobin level of 0.5%. Transthoracic echocardiogram with bubble study ruled out an intra-atrial shunt, and no other etiology for persistent hypoxia could be determined. On directed questioning, the patient admitted to using a combination of cocaine, tylenol PM and “poppers” the night before onset of symptoms. Patient was educated about complications from drug use. His oxygen saturation normalized spontaneously and patient was discharged with pulmonary follow up. DISCUSSION: A low oxygen saturation by pulse oximetry measured in patients with normal arterial blood gases can be an indication of methemoglobinemia. Intravenous (IV) methylene blue is the first-line antidotal agent. Additional adverse effects from poppers include retinal toxicity, esophageal burns, memory impairment, neuropathy, and coma. CONCLUSIONS: This case serves to demonstrate how methemoglobinemia may not always be detected on routine co-oximetry. A fixed abnormal pulse oximetry without an alternate etiology for hypoxia in the setting of methemoglobinemia should prompt a more thorough history. Polysubstance abuse in which cocaine and amyl nitrite is combined may predispose individuals to develop methemoglobinemia with greater severity. In the absence of measured methemoglobinemia, clinicians managing patients with unexplained cyanosis or hypoxia must consider the possibility of acute nitrite toxicity, particularly in patients with a recent or remote history of substance abuse. Reference #1: Edwards R.J., Usma, J. et al. Extreme methaemoglobinaemia secondary to recreational use of amyl nitrite. J of Accident and Emerg Med 1995 12,138-142 Reference #2: Faley B, Chase H. A Case of Severe Amyl Nitrite Induced Methemoglobinemia Managed with Methylene Blue. J Clin Toxicology 2012, 2:4 Reference #3: Hunter L, Gordge L, et al. Methaemoglobinaemia associated with the use of cocaine and volatile nitrites as recreational drugs: a review. Br J Clin Pharmacol 2011 72: 18-26 DISCLOSURE: The following authors have nothing to disclose: Coral Olazagasti, Janvi Paralkar, Michael Vishnevetsky, Aloke Chakravarti, Roxana Sulica, Kristine Favila No Product/Research Disclosure Information