MON-634 Rhabdomyolysis - A Rare Cause of Mortality from Hyperosmolar Hyperglycemic State

Abstract Disclosure: F.O. Asemota: None. L. Sangurima: None. A. Sajan: None. Introduction: Rhabdomyolysis is a rare sequelae of hyperosmolar hyperglycemic state (HHS). We present a case of HHS complicated by rhabdomyolysis resulting in mortality. Case: A 73-year-old Hispanic male with hypertension and diabetes mellitus presented with lethargy after being found unconscious at home. On admission, he had tachycardia (106 beats per minute) and tachypnea (25 breaths per minute). He was unresponsive to pain or verbal commands and had dry mucous membranes. Initial investigations revealed an elevated anion gap metabolic acidosis (pH 6.938 [7.300-7.400], bicarbonate level 7.1 mEq/L [24 - 30], serum glucose 1647 mg/dL [70-99], and anion gap 37 mEq/L [7-16]. Further evaluation showed serum lactate 16 mmol/L [0.5 - 2.2], a small amount of urine ketones, and serum osmolality 422 mOsm/kg [290 - 300], establishing the diagnosis of severe diabetic ketoacidosis with hyperosmolar hyperglycemic state. Initial potassium level was normal. The patient was started on intravenous fluids and insulin drip. The electrolytes were replaced as needed. Additionally, initial blood culture showed growth of Streptococcus and Klebsiella pneumoniae for which empiric antibiotics were initiated. An electrocardiogram showed ST elevation in anterior leads, which was deemed related to demand ischemia by the cardiology team and was treated empirically with heparin. The patient had a cardiac arrest the next day and passed. A careful review of labs drawn a few hours before the arrest revealed creatine kinase of 15,432 IU/L [38 - 174], potassium 6.3 mEq/L [3.5-5.3], and phosphorus of 5.0 mg/dL [2.7 - 4.5] consistent with rhabdomyolysis which was missed. Discussion: Rhabdomyolysis is a known, rare, and usually subclinical complication of HHS precipitated by hyperosmolarity and electrolyte abnormalities. Low insulin or insulin resistance leads to decreased glucose inside the muscle cells and attenuates Na+/K+ ATPase activity. This causes accumulation of intracellular sodium and calcium due to the reduced exchange of calcium and sodium. The intracellular calcium accumulation results in the dissolution of muscle fibers causing myoglobin to be released into the bloodstream. The myoglobin in turn blocks the tubules within the nephrons, leading to severe kidney damage. In addition, insulin infusion causes a rapid shift of electrolytes into the cell, leading to hypokalemia and hypophosphatemia, which can also contribute to the development of rhabdomyolysis. Conclusion: Although most cases of rhabdomyolysis are subclinical in HHS, it has the potential to be fatal in unrecognized cases as in our patient. The early recognition of rhabdomyolysis is needed for electrolyte monitoring and careful fluid resuscitation to prevent morbidity and mortality. Presentation: Monday, July 14, 2025