Severe Atraumatic Rhabdomyolysis Complicated by Bilateral Lower-Extremity Compartment Syndrome: A Case Report

Rhabdomyolysis involves breakdown of skeletal muscle with release of intracellular contents into circulation.Although classically linked to trauma, nontraumatic and nonexertional etiologies now account for most hospitalized cases.Compartment syndrome is a well-documented complication in which massive myocyte injury and edema raise intracompartmental pressure and propagate a cycle of ischemia and necrosis.The co-occurrence of severe atraumatic rhabdomyolysis and compartment syndrome without an identifiable precipitant is rare.A 48-year-old Chuj-speaking male with no known past medical history presented with severe bilateral lower extremity pain, swelling, and paresthesias beginning on awakening with associated periumbilical abdominal pain, nausea, and emesis.He reported only moderate social alcohol intake the prior evening and denied trauma, prolonged immobility, exertion, heat exposure, illicit drug use, medications, or recent illness.He was tachycardic, tachypneic, and hypoxemic with tense lower extremity compartments and a right-sided pulse deficit identified only by Doppler.Creatine kinase (CK) was profoundly elevated at 255,720 U/L; CK-MB 1,897 ng/mL, with leukocytosis, polycythemia (hemoglobin 20.1 g/dL) reflecting hemoconcentration, acute kidney injury (AKI), aspartate aminotransferase (AST)-predominant transaminitis, hyperphosphatemia, and severe high anion-gap metabolic acidosis (lactate 8.9 mmol/L).Serum ethanol was 76 mg/dL.EKG decreased the likelihood of acute coronary syndrome.Imaging excluded fracture and deep vein thrombosis (DVT).CT angiography showed proximal right anterior tibial and peroneal artery occlusion with preserved distal perfusion and bilateral muscle edema consistent with rhabdomyolysis and secondary bilateral compartment syndrome.The arterial and hematologic abnormalities likely represented downstream consequences.The patient underwent emergent right thigh and bilateral four-compartment lower leg fasciotomies.His 26day hospitalization was complicated by dialysis-dependent AKI requiring continuous renal replacement therapy (CRRT), transition to intermittent hemodialysis, staged fasciotomy closures, and new-onset cardiac dysfunction.He demonstrated renal recovery with a final hemodialysis session approximately one month after presentation and creatinine declining to 1.4 mg/dL.No acquired etiology was definitively identified, but the presentation may be consistent with unwitnessed positional rhabdomyolysis in the setting of ethanol exposure.This is supported by onset on awakening, dependent right-sided predominance, and alcohol myotoxicity with sustained compression.Limited interpretation in the patient's preferred language may have impacted history-taking.Equitable care requires professional interpretation in the patient's preferred language.This case underscores the need for a high index of suspicion for compartment syndrome in any patient with severe rhabdomyolysis regardless of mechanism, as early recognition and aggressive management are critical to preventing AKI, limb loss, and death.When no acquired cause is found, systematic evaluation for inherited myopathy is warranted.An inherited myopathy cannot be excluded in this case.