HYPERAMMONEMIA IN UNCONTROLLED DIABETES MELLITUS

TOPIC: Critical Care TYPE: Fellow Case Reports INTRODUCTION: Hyperammonemia is a known cause of encephalopathy due to neurotoxic effect. While predominantly attributed hepatic cirrhosis, other non-cirrhotic causes hyperammonemia such as malignancy, infection with urea-producing bacteria, and metabolic disorders have also been described. 1 Uncontrolled diabetes mellitus (DM) lesser understood sudden or substantial increase in ammonia level. 2 We present case patient ketoacidosis (DKA) the setting hyperammonemia. CASE PRESENTATION: The 57-year-old female past medical history hypertension, type DM, liver cirrhosis presenting lethargy two days nausea vomiting insulin noncompliance. She was noted be significantly volume depleted depressed level consciousness. received intravenous crystalloid resuscitation, vasopressor support, broad-spectrum antimicrobials. developed progressive obtundation, necessitating endotracheal intubation. Laboratory workup consistent DKA, glucose 979, anion gap >24, HCO3 <10, BHB >2, pH 6.74. Her ALT, AST, alkaline phosphatase, bilirubin were all within normal limits. Additional for demonstrated an 1181. CT head showed no evidence cerebral edema intracranial pathology. abdomen surface nodularity. In elevated ammonia, treatment infusion electrolyte repletion DKA started. On repeat 3 hours later, decreased 594 normalized on day 2. Neurological including EEG, MRI unremarkable. remained encephalitic precluding extubating until 9 discharged home shortly thereafter. DISCUSSION: Serum result protein degradation primarily produced GI system removed mostly by extent musculature. can caused variety urea cycle disorders, medications, infections, bleed, renal failure. Undiagnosed either acute chronic setting, irreversible neurological damage. Insulin increases synthesis, deficiency resistance it happens I II respectively, catabolism production.2–5 mainstay aggressive resuscitation DKA. 6–8 CONCLUSIONS: uncontrolled under-recognized should considered patients REFERENCE #1: Cichoz-Lach H, Michalak A. Current pathogenetic aspects noncirrhotic hyperammonemic encephalopathy. World J Gastroenterol. 2013;19(1):26-34. doi:10.3748/wjg.v19.i1.26 #2: K G, Dasan.S S, Sheriff D. Type2 Diabetes Mellitus. IOSR Journal Dental Medical Sciences. 2016;15:14-19. doi:10.9790/0853-1510031419 #3: Nair KS, Garrow JS, Ford C, Mahler RF, Halliday Effect poor diabetic control obesity whole body metabolism man. Diabetologia. 1983;25(5):400-403. doi:10.1007/BF00282518 DISCLOSURES: No relevant relationships Michael Bonk, source=Web Response Seyed Kamran Hejazi Kenari, Arman Hemmat,