Abstract Introduction Diabetic ketoacidosis (DKA) is a serious metabolic emergency that can cause multiorgan dysfunction. Extreme rhabdomyolysis with concurrent myocardial injury is a rare complication. We present a case of new-onset DKA in a young man complicated by profound rhabdomyolysis, severe acute kidney injury (AKI) requiring renal replacement therapy, and secondary myocardial injury-a rare and life-threatening metabolic triad. Case Discussion A 22-year-old man with no medical history presented with altered mental status, nausea, and retching after a fast-food meal. On arrival, he was obtunded, tachypneic with Kussmaul respirations, hypotensive, tachycardic, and dehydrated. Point-of-care glucose exceeded 500 mg/dL, and venous blood gas revealed pH 7.14 with an anion gap of 36, confirming severe DKA. Creatinine was 6.1 mg/dL, BUN 66 mg/dL, potassium 3.5 mmol/L, and creatine kinase (CK) 98,253 U/L, later reported “100,000 U/L.” Urinalysis showed 3+ blood and protein without red cells, consistent with myoglobinuria. Despite fluids and insulin, he remained oliguric with worsening acidosis and AKI. He was admitted to the ICU for management of severe DKA with rhabdomyolysis and AKI. FeNa was 1.2%, indicating intrinsic renal injury attributed to pigment-induced nephropathy compounded by hypovolemia and acidemia. Renal function declined with persistent hyperkalemia, requiring continuous renal replacement therapy (CRRT). CK remained 100,000 U/L for two days, 50,000 U/L for another two, and declined to 1,000 U/L by day 10. Metabolic derangements improved, and mental status normalized. Cardiac biomarkers were elevated (peak troponin 8,254.8 ng/L; pBNP 975 pg/mL) with QTc prolongation, consistent with secondary myocardial injury. He was started on basal-bolus insulin for new-onset diabetes (HbA1c 12.5%). Infectious and autoimmune workups were negative. He was dialysis-dependent at discharge but achieved renal recovery after several weeks of outpatient dialysis. Discussion This case highlights the interplay between metabolic, renal, and cardiac systems in severe DKA. Profound dehydration, acidemia, and electrolyte shifts precipitated extensive rhabdomyolysis (CK 100,000 U/L) and pigment-induced nephropathy, while metabolic stress caused secondary myocardial injury. Clinicians should remain vigilant for these complications in DKA with severe acidosis or renal dysfunction. Early resuscitation, metabolic correction, and timely renal replacement therapy are essential for recovery. This abstract is funded by: None
Hossain et al. (Fri,) studied this question.