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Altered mental status as a presentation of rhabdomyolysis in a patient with sickle cell anemia

To the Editor: Prior to the introduction of sickle cell-modifying therapies, 5%–10% of patients presented with acute stroke by 14 years old.1 National guidelines provide recommendations surrounding central nervous system (CNS) complications, emphasizing rapid assessment of neurologic deficits and early initiation of transfusion therapy if acute stroke is suspected.2,3 Nevertheless, altered mental status (AMS) is a symptom of other CNS events.4 Here, we present an unusual case of rhabdomyolysis presenting as AMS in a patient with sickle cell anemia (SCA). A 15-year-old male with hemoglobin SS presented to the emergency department with fever, emesis, diarrhea, and disorientation, unable to answer questions. The AMS resolved quickly, but he appeared unwell with diffuse tenderness of all extremities. Laboratory evaluation revealed baseline anemia (hemoglobin 9 g/dl) with an elevated creatinine (1.39 mg/dl) and indirect hyperbilirubinemia (10.8 mg/dl). Emergent computed tomography of the head was unremarkable. Due to concern for sepsis, antibiotics were initiated, along with fluid resuscitation (several isotonic boluses). Given his acute kidney injury (AKI) and diffusemyalgia, creatine kinase (CK) was obtained and was elevated (2454 U/L), prompting admission. Six hours later, his CK increased (6067 U/L) and he developed transaminitis (alanine transaminase [ALT] 22.5 U/L; aspartate transaminase [AST] 101 U/L). His urinalysis (2+ blood and <1 + urine RBCs) was felt to be consistent with myoglobinuria. His social and medical histories were unremarkable for potential causes of rhabdomyolysis including drug use or infections; he reported no recent athletics or strenuous activities. Drug toxicology screenwasnegative.Aside fromnonadherencewithhydroxyurea, his sickle cell history was noncontributory. In the setting of AKI and rhabdomyolysis, the patient was started on isotonic fluids at 1.5-times maintenance. Despite aggressive rehydration, hisCK,ALT, andAST remainedpersistently elevated (Figure 1).On hospital day 3, he developed mild hyperkalemia, hypophosphatemia, proteinuria, and decreased urine output concerning for oliguric renal failure. Furosemide was initiated, and sodium bicarbonate was added to his intravenous fluids. Magnetic resonance imaging of the brain and lower extremities were performed due to persistent lower extremityweakness. His brain was unremarkable, while soft tissue and muscle enhancements in his lower extremities were concerning for myositis. He remained persistently febrile despite broad-spectrum antibiotics and an extensive infectious workup (Table S1). To reduce his hemoglobin S (HbS) level, the patient received three simple blood transfusions, resulting in an HbS level of 50.4%per institutional guidelines for a non-CNSevent. His myalgias, weakness, fevers, and laboratory abnormalities all resolved by hospital day 17, thus he was discharged. Rhabdomyolysis is defined by a CK level five-times the upper limit of normal or>1000U/L.5 Inciting events for rhabdomyolysis are broad but include infection, muscle overexertion or trauma, medication side effects, metabolic conditions, and myopathies. Initial studies should include a serum CK level, metabolic panel with liver function, urinalysis, and a complete blood cell count. Of note, serum CK levels often rise 12 hours after the initial insult, peak at 2–5 days, and return to normal within 6–10 days.5 It is vital to monitor for signs of AKI and provide appropriate fluid management to decrease serum CK, as myoglobin byproducts are toxic to renal parenchyma.6 Rhabdomyolysis is important to consider in that its symptoms overlap with those in other sickle cell complications. Rhabdomyolysisrelated pain can mimic an acute vaso-occlusive pain event. Blood on a urine dip without RBCs on urinalysis may occur with myoglobinuria in rhabdomyolysis or with brisk intravascular hemolysis in SCA patients with baseline hemolysis. Lastly, AMS in SCA is often due to CNS events including stroke, migraines, and cerebral sinus venous thrombosis. While rhabdomyolysis is rare in patients with SCA, there is military literature identifying rhabdomyolysis in patients with sickle cell trait (SCT).7–9 Metabolic changes during exercise may promote HbS polymerization and red cell sickling; the resulting microvascular obstruction leads to muscle ischemia, and rhabdomyolysis.9 Therefore, patients with SCA may have a higher incidence of rhabdomyolysis at a similar level of exertion. The lack of rhabdomyolysis reported in SCA may represent either a true higher prevalence in SCT or a lower awareness of rhabdomyolysis in patients with SCA due to overlapping disease-related symptoms and complications. The primary management goal in rhabdomyolysis is to prevent and treat AKI by administering intravenous isotonic fluids with a fluid rate that maintains a urine output of at least 200–400 ml/h until plasma CK levels fall below 1000 U/L.5 Some studies suggest a benefit of administering bicarbonate and mannitol if CK >30,000 U/L.10 Diuretics should be considered in the event of volume overload. Lastly, clinicians should monitor for disseminated intravascular coagulation as a rare complication.11 Specific to patients with SCA, close monitoring for kidney injury is warranted due to the increased propensity of patients with SCA to developing acute and chronic kidney disease.12–14 Second, respiratory status shouldbemonitored closely during aggressivehydration for