By Karla R. Hauersperger, MD
Clinical Case
A 10 year-old male with medical history significant for sickle cell trait presented to urgent care with his father for leg pain and body aches. Father reported that patient developed fever two days ago that broke the night before this visit. He awoke on day of presentation with legs and arms hurting. He had no other symptoms. Father had given over the counter generic pain medication which helped but pain worsened the evening of presentation and patient was reporting that it hurt to walk.
Initial exam vital signs: BP (!) 124/87 | Pulse (!) 103 | Temp 98.7 °F (37.1 °C) | Resp 24 | Wt 38.3 kg (84 lb 7 oz) | SpO2 99%
He was described as alert in no acute distress, appearing to not feel well but nontoxic with age appropriate interaction. His mucous membranes were moist, and he had good skin turgor. Nasal mucosa normal. Oral Pharynx with no local lesions, erythema or tonsillar enlargement/exudate. Neck was nontender with full range of motion. Chest was clear to auscultation with no respiratory distress. Cardiovascular exam revealed regular rate and rhythm without murmur/gallop/rub and he had brisk capillary refill. Skin had no rash. Extremities exam showed tenderness to both thighs and upper arms without swelling. Gait was antalgic. Neurological exam had no sensory or motor deficit.
Rapid Influenza testing was positive for Type A.
A urine was obtained and described as amber in color with large protein, small bilirubin and large occult blood with specific gravity of 1.025
He was transferred to the Emergency Department by family car for further evaluation and management. An IV was placed and 20 mL/kg normal saline bolus was initiated and upon completion he was placed on twice maintenance IV hyperhydration. Initial blood work revealed Chemistries significant for Creatinine of 0.92 mg/dL (Ref: 0.30.6 mg/dL) and Creatinine Kinase 239,359 U/L (Ref: < 430 U/L). Urinalysis in ED was described as brown and turbid with a pH of 6 with >300 mg/dL protein and other items unable to be determined due to urine color; microscopy positive for 6 WBC, transitional epithelial cells and granular casts. He was admitted to General Pediatrics. Oral Oseltamivir was initiated and he completed a 5day course. His pain was treated with acetaminophen, initially scheduled then transitioned to as needed, and oxycodone intermittently early in his stay.
During his hospital stay, CK peaked at 281,752 U/L. He had intake/output closely monitored and daily weights obtained. Nephrology services were consulted for AKI Stage 2, persistent CK elevation and intermittent hypertension. He never required antihypertensive medication as his intermittent hypertension never exceeded 130/90. He was transitioned off IV hydration and tolerated oral hydration with resolution of his muscle pain/tenderness without recurrence. By Day 3 of hospitalization, he was pain free and able to ambulate without difficulty. He had a normal renal ultrasound with Doppler study. At time of discharge on Day 5 of hospitalization, his CK was 77, 053 U/L and Cr of 0.55 mg/dL and his urine had cleared of all protein and blood.
Discussion
This case highlights a well recognized pattern in pediatric acute care: viral illness, most commonly influenza, triggering substantial skeletal muscle injury and subsequent rhabdomyolysis. Although influenza associated myositis is often self limited, a subset of children experience profound muscle breakdown severe enough to cause myoglobinuria, marked elevations in creatine kinase, and acute kidney injury (AKI). The patient’s clinical trajectory mirrors what is described across large pediatric series: rapid onset of severe myalgias following resolution of fever, difficulty walking due to thigh and calf pain, and darkening of urine as muscle injury progresses.
Rhabdomyolysis in children has distinct epidemiologic features. Viral infections are the leading cause in the pediatric population and are particularly prevalent in schoolaged children. Influenza A and B viruses have been repeatedly identified as major triggers, with influenza related myositis often presenting after several days of fever when children suddenly refuse to walk. This pattern is thought to involve a combination of direct viral invasion of muscle cells, circulating viral toxins, and immune mediated inflammatory responses. Children with underlying conditions such as sickle cell trait, metabolic myopathies, or dehydration may be more susceptible to extensive muscle injury.
The pathophysiology of rhabdomyolysis involves disruption of muscle cell membranes or ATP dependent ion channels, leading to uncontrolled influx of calcium into myocytes. This cascade triggers sustained contraction, enzyme activation, mitochondrial dysfunction, and ultimately, muscle fiber necrosis. As muscle contents enter the bloodstream, large quantities of myoglobin, electrolytes, and intracellular enzymes circulate and may overwhelm the kidneys. Myoglobin can obstruct renal tubules, promote oxidative damage, and combine with acidic urine to form casts that further reduce filtration. This multifactorial stress explains why AKI is one of the most important complications of rhabdomyolysis in children.
The patient’s lab profile, extremely elevated CK levels, dark, proteinrich urine, and elevated creatinine, signaled imminent risk for renal injury. Early aggressive hydration remains the single most effective intervention to prevent AKI. The approach used here, including an initial fluid bolus followed by highrate intravenous hydration targeted toward high urine output, aligns with widely recommended pediatric management strategies. Maintaining adequate perfusion, diluting nephrotoxic myoglobin, and promoting brisk diuresis help minimize tubular injury. Monitoring electrolytes is essential because disturbances such as hyperkalemia, hypocalcemia, and metabolic acidosis commonly accompany significant muscle breakdown.
This child’s hospital course demonstrates the expected CK trajectory: levels rising for the first 48–72 hours before gradually falling once muscle injury abates. Careful clinical and laboratory monitoring allowed safe transition from hyperhydration to oral hydration as symptoms resolved. The absence of hypertension requiring therapy, rapid improvement in kidney function, and clearance of hematuria and proteinuria all suggest a favorable recovery—consistent with what is typically observed in viral associated cases.
Pediatric outcomes in rhabdomyolysis vary widely by etiology. Infection related rhabdomyolysis, especially due to influenza, generally carries a lower risk of longterm renal impairment compared with trauma, toxin, or metabolic related cases. While AKI is not uncommon, it is usually reversible when promptly treated. Only a very small proportion of children progress to chronic kidney disease, and recurrence is rare unless an underlying metabolic or myopathic condition exists. The patient’s dramatic CK elevation alone does not predict longterm outcomes; rather, the speed of hydration, severity of accompanying metabolic derangements, and presence of complications like sepsis or multi-organ involvement are more predictive of prognosis.
This case underscores the importance of recognizing early warning signs of rhabdomyolysis during viral seasons. Bilateral leg pain severe enough to impair ambulation, refusal to walk after a febrile illness, or unusually dark urine should prompt evaluation for muscle injury. Simple screening tests, urinalysis and serum CK, are often sufficient to identify children who require urgent management. This patient’s timely evaluation and transfer facilitated rapid initiation of treatment, likely preventing more severe AKI or prolonged hospitalization.
In summary, influenza associated rhabdomyolysis is a critical yet manageable condition when promptly recognized. This case exemplifies the typical presentation, expected laboratory course, and favorable recovery seen in children with viral triggered muscle injury. Ongoing education for frontline pediatric providers—especially during influenza season—remains essential for ensuring early detection and optimal outcomes.
References
- Szugye, H. S. (2020). Pediatric rhabdomyolysis. Pediatrics in Review, 41 (6), 265–275. https://doi.org/10.1542/pir.20180300
- Zaki, H. A., Elmelliti, H., Malik, W. A., et al (2025). Pediatric rhabdomyolysis: A systematic review and metaanalysis of etiologies, management, and outcomes. BMC Pediatrics, 25, 866. https://doi.org/10.1186/s1288702506081x
- Kuok, M. C. I., & Chan, W. K. Y. (2025). Rhabdomyolysis in children: A stateoftheart review. Children (Basel, Switzerland), 12(4), 492. https://doi.org/10.3390/children12040492
