A 46‐year‐old right‐handed man with no significant medical history presented to our hospital with a 5‐day history of progressive, painful swelling of his left upper extremity. He was a frequent binge drinker, and 5 days prior to presentation he got drunk and fell asleep in a chair. He fell off the chair and slept on his left arm for 8 hours and woke up with a painful, numb, and swollen left arm that progressively increased in size. He reported no associated fever, chills, nausea, or vomiting, and his symptoms did not resolve with 2 deep massages from a friend. On examination, his whole left upper extremity was swollen from the left supraclavicular area to his fingertips. He had left wrist drop with palpable radial and ulnar pulses, and his capillary refill time was 2 seconds. The admission laboratory panel was significant for hyponatremia (127 mEq/L), hyperkalemia (5.7 mEq/L), hyperuricemia (11.2 mg/dL), hypocalcemia (7.2 mg/dL), and hyperphosphatemia (11.1 mg/dL). His serum creatine kinase was 13,172 U/L, and he had severe acute renal failure (creatinine 12.2 mg/dL) and an anion‐gap metabolic acidosis. Urinalysis was positive for blood and 5 RBCs, and renal ultrasound showed normalsized kidneys. HIV and hepatitis panel were negative. His hemoglobin was 13.3 g/L, white blood cell count 8100/mm3, and C‐reactive protein 2.77. There was concern for compartment syndrome and necrotizing fasciitis (laboratory risk indicator for necrotizing fasciitis score, 8). CT and x‐ray of his left upper extremity showed soft‐tissue swelling with no evidence of fracture or subcutaneous gas. He was urgently evaluated by the orthopedic team, and both conditions were ruled out. His arm swelling was managed conservatively with compression, elevation, and a radial nerve brace. He was aggressively hydrated with normal saline and his serum creatinine level dropped from 12.2 to 9.1 mg/dL; however, his acidemia worsened (pH 7.199, PCO2 26.3, PO2 101.1, HCO3 10, base excess −16.9). He was dialyzed once, and his serum creatinine level dropped further, from 9.1 to 4.6 mg/dL, with resolution of his acidemia. His left arm swelling resolved, and he was discharged home with a left radial nerve brace.
Crush syndrome is a rare and severe complication that can occur following deep sleep on the arm after intoxication with alcohol or recreational drugs. The more common variant of this condition is temporary radial nerve neuropathy, which causes wrist drop, colloquially referred to as “Saturday‐night palsy.” We present a case of alcohol‐induced crush syndrome that resulted in skeletal muscle injury and muscle decay, leading to rhabdomyolysis, pigment nephropathy, and severe acute renal failure.
There are only a handful of cases of alcohol‐induced crush syndrome reported in the literature, and this report adds to the body of evidence of this rare and potentially fatal complication of alcohol intoxication after an episode of binge drinking.
A. T. Abegunde ‐ John H. Stroger Hospital of Cook County, employment; C. H. Onyewenyi ‐ John H. Stroger Hospital of Cook County, employment; B. I. Mba ‐ John Stroger Hospital of Cook County, employment
To cite this abstract:Abegunde A, Onyewenyi C, Mba B. Rhabdomyolysis and Acute Renal Failure Following Alcohol‐Induced Crush Syndrome. Abstract published at Hospital Medicine 2011, May 10-13, Dallas, Texas. Abstract 221. Journal of Hospital Medicine. 2011; 6 (suppl 2). https://www.shmabstracts.com/abstract/rhabdomyolysis-and-acute-renal-failure-following-alcoholinduced-crush-syndrome/. Accessed March 29, 2020.