HYPERAMMONEMIA IN UNCONTROLLED DIABETES MELLITUS

Abstract

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