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Abstract: PUB134

An Unusual Cause of Rhabdomyolysis

Session Information

Category: Trainee Case Report

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Sula Karreci, Esilida, BIDMC, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States
  • Kruger gomes, Larissa, BIDMC, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States
  • Schulman, Ruth, BIDMC, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States
  • Agarwal, Krishna A., BIDMC, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States
  • Pandit, Amar, BIDMC, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States
  • Denker, Bradley M., BIDMC, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States

Group or Team Name

  • Beth Israel Deaconess
Introduction

Rhabdomyolysis results from muscle cell injury and often leads to AKI. Common causes include trauma, medications, electrolyte abnormalities, and metabolic myopathies. The clinical presentation includes muscle pain, dark urine, and possibly oliguria. Here, we present an unusual etiology of rhabdomyolysis resulting from sustained hyperosmolarity due to severe hyperglycemia and hypernatremia.

Case Description

23-year-old male with no significant medical history presented with fatigue, poor appetite for 10 days. He denied fever, nausea, vomiting, abdominal pain, diarrhea,. Despite drinking large amounts of fluids, he felt thirsty, with frequent urination. Family history: diabetes. Social history; no alcohol, smoking or drug use. No prescription/OTC medicines, or herbal supplements. Vital signs were notable for a heart rate of 110-120 beats/min. He appeared lethargic. Physical exam showed dry mucous membranes and tachycardia, otherwise unremarkable. Initial laboratory values showed blood glucose of 1132 mg/dL, Cr 3.5 mg/dl, Na 147 mEq/L (see table). Urine showed glucosuria and ketones, sediment was bland. He was started on an insulin drip. Corrected Na was 172 with a free water deficit 10L. Initially given 3L NS bolus followed by1/2NS to correct hypernatremia, with goal correction of 10-12 mEq in the first day. On day 3, he complained of weakness and difficulty getting up but no muscle soreness. He developed a temperature of 101oF and his exam was unremarkable. Creatinine and Na improved (see table), however, ALT/AST continued to rise. Right upper quadrant US showed hepatic steatosis. Repeat UA showed large blood, but no red blood cells on sediment. CPK returned at 111850 IU/L, and peaked at 195380 IU/L on day 5. He was given isotonic fluids at 500cc/h. He remained tachycardic with low grade fevers and on day 9, CTA showed bilateral pulmonary emboli.

Discussion

This case highlights an unusual cause of rhabdomyolysis caused by hyperosmolarity in HHS. Although, the literature suggests that rhabdomyolysis may be present in up to 50% of HHS cases, this is an extreme case and highlights the importance of looking for rhabdomyolysis in HHS. It is unclear why our patient showed such a severe phenotype.

Laboratory findings
 HgbHctPltGlBUNCrNaKGapCaPALTASTCPK
Day 117522961131963.51475.641109103128 
Day 3113658238221.315341382.6254870111850