American Journal of Medical Case Reports, 2021, Vol. 9, No. 3, 206-207 Available online at http://pubs.sciepub.com/ajmcr/9/3/18 Published by Science and Education Publishing DOI:10.12691/ajmcr-9-3-18 A Rare Case of Combined Rocuronium Induced Malignant Hyperthermia and Propofol-Induced Lactic Acidosis Mohamedanwar Ghandour 1,* , Heba Osman 2 , Samer Alkassis 3 , Zeenat Y. Bhat 4 , Yahya Osman-Malik 4 1 Department of Internal Medicine, Nephrology division, Wayne State University/Detroit Medical Center, Michigan, USA 2 Department of Internal Medicine/Pediatrics, Wayne State University/Detroit Medical Center, Michigan, USA 3 Department of Internal Medicine, Wayne State University/Detroit Medical Center, Michigan, USA 4 Department of Internal Medicine WSU SOM, Division of Nephrology Wayne State University, Michigan, USA *Corresponding author: Received December 02, 2020; Revised January 05, 2021; Accepted January 14, 2021 Abstract We report an unusual case of A 64-year-old female received rocuronium and propofol and subsequently developed malignant hyperthermia and particularly propofol-related infusion syndrome. Cite This Article: Mohamedanwar Ghandour, Heba Osman, Samer Alkassis, Zeenat Y. Bhat, and Yahya Osman-Malik, “A Rare Case of Combined Rocuronium Induced Malignant Hyperthermia and Propofol-Induced Lactic Acidosis.” American Journal of Medical Case Reports, vol. 9, no. 3 (2021): 206-207. doi: 10.12691/ajmcr-9-3-18. 1. Introduction Malignant hyperthermia (MHS), is a rare inherited, autosomal-dominant disorder of skeletal muscle, which presents clinically as a hypermetabolic crisis. It is precipitated by certain anesthetic gases and neuromuscular blocking agents such as sevoflurane and succinylcholine [1,2]. The pathophysiology is not known at present, however, is believed to result from genetic skeletal muscle receptor defects that allow excessive myoplasmic calcium accumulation in the presence of certain anesthetic triggering agents [3,4]. On the other hand, propofol is commonly used in anesthesia and in the intensive care setting for sedation and refractory status epilepticus due to its rapid sedative effect. However, propofol has been associated with life- threatening adverse effects, particularly propofol-related infusion syndrome (PRIS). PRIS manifests with metabolic acidosis, pulmonary hypertension, myocardial failure, rhabdomyolysis, and death [5,6]. PRIS was initially thought to be more common among children, however, more cases have been reported in adult patients recently [7,8]. Herein, we describe a case of both propofol toxicity and vecuronium- induced malignant hyperthermia simultaneously. 2. Case A 64-year-old female with restrictive lung disease on home oxygen, obstructive sleep apnea on CPAP, and diastolic heart failure was admitted to the medicine floor for pneumonia secondary to COVID-19 then was transferred to the medical intensive care unit (ICU) for acute hypoxic respiratory failure requiring intubation. The patient completed a full course of remdesivir and dexamethasone treatment. She also went into septic shock requiring vasopressors. Of note, she was previously on cisatracurium and midazolam for paralysis and sedation, respectively. Propofol was added on day 24 and cisatracurium was switched to rocuronium on day 26. The patient had normal acid-base status until the 29 th day of her admission when she developed severe acidemia with a pH of 7.08 on ABG which was consistent with predominant metabolic acidosis with concomitant respiratory acidosis. She also had hyperkalemia of 7.1 mMol/L for which the patient received calcium gluconate, sodium bicarbonate, and regular insulin. Repeat potassium was 6.3 mMol/L, which was confirmed with a blood gas sample, and the same medical treatment was given. At the same time, she developed a febrile episode with a temperature of 38.5 C along with a slight worsening of renal function. A brisk increase in lactic acid was noted on her ABG from 1.54 mMol/L to 12.8 mMol/L within 24 hours despite being on norepinephrine and vasopressin drips with broad- spectrum antibiotics. Propofol was highly suspected as the culprit for lactic acidosis as the patient has been on high doses continuously for over 4 days. The decision was made to discontinue propofol, which resulted in a dramatic decrease of lactate level within 24 hours with subsequent normalization in her acid-base status. Also, there was suspicion of rocuronium-induced malignant hyperthermia with the elevated CPK, febrile episode, severe hyperkalemia