(P81) Malignant Hyperthermia Due to Glufosinate Poisoning

Chief Complaint : A 59-year-old male presented to the Emergency Department (ED) after a suicidal consumption of glufosinate.

History of Present Illness : A patient with a history of HTN and DM, after fighting with others, ingested glufosinate ammonium 50cc for suicide and visited the emergency department in a state of stuporous mentality.
Initial vital signs were stable and there was no fever, but after intubation with stupor mentality, the patient was hospitalized for ICU care.
No recovery of consciousness on the first day of hospitalization, but no signs of meningeal irritation, observed with empirical antibiotics.
From the second day of hospitalization, a fever of 39 degrees or higher persisted, and the body temperature was lowered using a cooling device, and medications including acetaminophen (AAP) and NSAID were administered, but the fever persisted. The patient's temperature is rapidly rising, rhabdomyolysis and hyperkalemia occurred with a high fever of 40 degrees or more. The patient expired as metabolic acidosis worsened and hyperkalemia worsened despite continued use of antipyuritic drugs and electrolyte imbalance correction.

Pertinent Physical Exam: During the general physical examination in the ED, the patient mentality was stupor. His vitals were stable with a blood pressure 110/70 mm Hg, respiratory rate 20 breaths/minute, body temperature 36 degrees and an oxygen saturation of 96% in room air. A nontender abdomen were revealed during his gastrointestinal examination.
Initially, there were no signs of muscle rigidity and meningeal irritation. The fever continued, but there was nothing that could be the fever focus, and nothing was identified in the culture results. On the second day of hospitalization, the fever continued and the muscle rigidity increased.

Pertinent Laboratory Data: The patient's consciousness was consistently stuporous, but the ammonia level was 19 uMol/L at the time of visit to the emergency department and 21uMol/L on the first day of hospitalization, showing no significant difference. Leukocytosis was not present during admission. There was no elevation of inflammation markers such as CRP. On the second day of hospitalization, fever persisted, rhabdomyolysis occurred, and hyperkalemia and metabolic acidosis occurred.

Case Discussion: Glufosinate is a common herbicied drug and is widely used worldwide, and reports of accidental and suicidal poisoning are not uncommon.
Malignant hyperthermia is a rare but potentially life-threatening condition that is typically triggered by certain types of anesthesia during surgery or genetic disorders.
Malignant hyperthermia due to glufosinate is rare and has not yet been reported. In this case, the patient experienced an malignant hyperthermia crisis, likely triggered by glufosinate. Malignant hyperthermia results in uncontrolled release of calcium from muscle cells, leading to muscle rigidity, hypermetabolism, and a potentially fatal increase in body temperature. Treatment with dantrolene, intravenous fluids, and cooling measures can be life-saving in the event of an MH crisis. However, the possibility of malignant hyperthermia was not recognized and only IV hydration, NSAID, acetaminophen and cooling methods were used without the use of drugs such as dantrolene. Since no case of malignant hyperthermia caused by glufosinate has been reported yet, it was not quickly recognized in this case.
Our case raises the possibility that glufosinate may also be associated with malignant hyperthermia, aggressive treatment may be required in the presence of uncontrolled fever.

References and Acknowledgements (Optional): References
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2. Rosenberg H, Pollock N, Schiemann A, Bulger T, Stowell K. Malignant hyperthermia: a review. Orphanet J Rare Dis. 2015;10:93. doi: 10.1186/s13023-015-0310-1

3. Kobayashi S, Yano M, Suetomi T, Ono M, Tateishi H, Mochizuki M, Xu X, Uchinoumi H, Okuda S, Yamamoto T, et al. Dantrolene, a therapeutic agent for malignant hyperthermia, markedly improves the function of failing cardiomyocytes by stabilizing interdomain interactions within the ryanodine receptor. J Am Coll Cardiol. 2009;53:1993-2005. doi: 10.1016/j.jacc.2009.01.065