Rhabdomyolysis presenting as abdominal pain: importance of early creatine kinase testing

Introduction

Rhabdomyolysis is a clinical syndrome caused by the disruption of skeletal muscle, with the release of muscle tissue content into the circulation, which can lead to life-threatening systemic complications like acute kidney injury (AKI), compartment syndrome, and disseminated intravascular coagulopathy[1]. Although the common causes of rhabdomyolysis include trauma or prolonged immobilization, exertional rhabdomyolysis occurs after strenuous physical activity and has been increasingly diagnosed worldwide due to the growing popularity of physical activity and exercise[2].

Rhabdomyolysis typically presents with myalgia and muscle weakness with dark urine; however, atypical presentation may delay diagnosis[3]. Elevated creatine kinase (CK) levels and myoglobinuria are critical diagnostic markers. An initial diagnosis is typically made if CK levels are elevated five times the upper limit of normal, along with recent strenuous physical activity[4].

We present a case of exertional rhabdomyolysis presenting primarily with abdominal pain, preserved urine output, normal electrolytes, and markedly elevated transaminases, mimicking gastrointestinal and hepatic pathology. This case adds to the existing literature by reinforcing important diagnostic pitfalls and underscores the need for a high index of suspicion for rhabdomyolysis in patients with atypical symptoms following intense physical activity to enable early diagnosis and prevent complications.

Case presentation

A 32-year-old dyslipidemic man presented to the emergency department of our hospital with a 1-day history of abdominal pain associated with one episode of vomiting. There was no history of fever, chills, diarrhea, altered mental status, or prolonged immobilization. He denied any history of anabolic steroid use, drug abuse, nutritional supplement intake, insect or snake envenomation, or carbon monoxide exposure. However, he had been taking rosuvastatin 5 mg for the past 5 months.

HIGHLIGHTS

• Atypical presentation: Rhabdomyolysis may present as abdominal pain without classical muscle symptoms, with normal electrolyte levels.

• Exertional trigger: Strenuous physical activity can precipitate rhabdomyolysis even in otherwise healthy individuals. Individuals with comorbid dyslipidemia on a low-dose statin may have increased susceptibility.

• Diagnostic challenge: Elevation of liver transaminases with preserved urine output and normal. Electrolytes may mimic gastrointestinal or hepatobiliary pathology. Such presentations may delay recognition, highlighting the need for high clinical suspicion.

• Importance of early testing: Prompt measurement of creatine kinase aids timely diagnosis and prevents complications, such as acute kidney injury.

His symptoms started 1 day after rejoining the gym, following a break of around 3 weeks. The workout consisted predominantly of a leg-focused routine involving eccentric muscle-strengthening exercises. Though he used to exercise earlier as well, he developed these symptoms for the first time.

On presentation to the emergency department, he was alert and oriented but appeared to be in pain. His vitals were as follows: temperature 97°F, blood pressure 130/80 mmHg, heart rate 90 bpm and regular, and oxygen saturation was 95% on room air, with no signs of dehydration. Chest, cardiovascular, and abdominal examinations were unremarkable.

Given the nonspecific abdominal pain and lack of overt musculoskeletal findings at presentation, the working diagnosis initially focused on gastrointestinal and hepatic causes.

Laboratory findings of the patient on the day of admission are summarized in Table 1.

Table 1.

Blood and urine test results on the day of admission.

Test	Normal range	Results
Sodium (mEq/l)	135.0–148.0	138.0
Potassium (mEq/l)	3.5–5.3	4.2
Creatinine (mg/dl)	0.6–1.3	2.3
Urea (mg/dl)	10–45	62
Alkaline phosphatase (U/l)	<115	70
Total protein (g/dl)	6.5–8.2	6.9
Serum albumin (g/dl)	3.5–5	4.2
AST (SGOT) (IU/l)	5–40	2999.0
ALT (SGPT) (IU/l)	5–40	304.0
Bilirubin, total (mg/dl)	0.3–1.4	1.8
Bilirubin, direct(mg/dl)	<0.5	0.8
Lipase (U/l)	23–300	84.0
Amylase (U/l)	30–110	54,0
HbsAg		Negative
NS1		Negative
Dengue IgM		Negative

Bold values indicate parameters that are elevated beyond normal reference ranges and are clinically significant to our patient’s diagnosis.

According to the reports, he presented with high creatinine and deranged liver enzymes. Electrolytes, including sodium and potassium, were within normal limits. Baseline renal function prior to this illness had been normal, as per previous outpatient records.

His initial electrocardiography and chest X-ray were normal. Viral and bacterial infectious workups were negative.

Immediately, IV fluid resuscitation using normal saline and analgesics was started. Despite adequate rehydration, renal function continued to deteriorate in the initial days of admission, as evidenced by worsening creatinine levels (Fig. 1). He developed tea-colored urine and generalized swelling, which started from the upper limbs on the second day of hospital admission. These new findings prompted further evaluation for a possible muscle injury syndrome.

Figure 1.

The trend of creatinine during admission.

Due to the atypical presentation, including abdominal pain as the chief complaint and preserved urine output initially, serum CK was not measured upon admission. It was only tested later in the course, after progressive renal dysfunction developed. The markedly elevated CK levels (Fig. 2) confirmed the diagnosis of exertional rhabdomyolysis.

Figure 2.

The trend of creatine kinase during admission.

Urinalysis did not show hematuria, excluding other possible causes of AKI, including glomerulonephritis or urological obstruction, supporting pigment-related renal injury. There was no clinical or laboratory evidence of obstructive uropathy or acute glomerulonephritis.

In light of the high CK and suspicion of possible inflammatory myopathy overlap, a 3-day pulse of intravenous methylprednisolone was administered, in addition to continued fluid resuscitation. The patient gradually improved, with stabilization of renal function and resolution of edema over the following days.

The patient’s kidney function and CK level gradually improved. He was discharged as soon as his kidney function returned to normal.

On follow-up, there was no recurrence of symptoms, and the patient was counseled regarding gradual return to physical activity, avoidance of sudden high-intensity or eccentric exercise after periods of deconditioning, maintenance of adequate hydration during workouts, and prompt medical evaluation if muscle pain, weakness, or dark-colored urine occur.

Discussion

This case describes an atypical presentation of exertional rhabdomyolysis with AKI in a previously healthy 32-year-old man with dyslipidemia, who was on low-dose rosuvastatin (5 mg daily). Although exertional rhabdomyolysis is a well-recognized cause of AKI, this case diverges from the classical profile in several key aspects, highlighting the variable manifestations of the condition and the importance of early recognition to prevent diagnostic delays and related complications.

Exertional rhabdomyolysis refers to the breakdown of skeletal muscle following a period of strenuous activity. Strenuous exercise precipitates both membrane dysfunction and intracellular ATP depletion, which propagate a cascade of muscle fiber damage[5]. The patient will often present with pain, weakness, and swelling in the muscles affected[6]. However, this patient presented with abdominal pain and vomiting as chief complaints, not with the more expected symptoms of rhabdomyolysis. Moreover, the pain was localized to the peri-umbilical region, which could mislead clinicians toward gastrointestinal or intra-abdominal causes, potentially delaying the diagnosis of rhabdomyolysis. Such pain is uncommon in rhabdomyolysis and may result from involvement of abdominal wall muscles or systemic effects of muscle breakdown. This highlights the need to consider rhabdomyolysis in patients with an exertional history, even when presenting with atypical symptoms.

Although the patient developed AKI, he maintained normal urine output, which contrasts with the typical oliguric or anuric AKI often seen in rhabdomyolysis. Additionally, serum sodium and potassium levels remained within normal limits, despite extensive muscle breakdown. Hyperkalemia is often considered a hallmark complication of ER due to intracellular potassium release, and its absence here may have delayed suspicion for rhabdomyolysis[7]. These findings highlight a rare case of non-oliguric and normokalemic rhabdomyolysis.

Another distinguishing feature is the disproportionately elevated liver transaminases, particularly AST. Although often misattributed to liver pathology, AST and ALT are also present in skeletal muscle, and their elevation in rhabdomyolysis is well documented to reflect muscle injury rather than hepatocellular damage[8]. Misinterpretation of this biochemical overlap can delay the diagnosis of rhabdomyolysis; therefore, CK should be routinely tested in patients with unexplained AKI and transaminitis to enable timely recognition and prevention of complications.

A broad differential diagnosis was systematically considered. Genetic and inherited myopathies, including McArdle disease, mitochondrial myopathies, and dystrophinopathies, were unlikely given the absence of childhood-onset exercise intolerance, lack of prior similar episodes, no family history of neuromuscular disease, and complete clinical and biochemical recovery without recurrence.

Autoimmune and inflammatory myopathies, such as polymyositis, dermatomyositis, and immune-mediated necrotizing myopathy, were ruled out as there was an absence of proximal muscle weakness, characteristic skin manifestations, or systemic autoimmune features. Similarly, malignant syndromes, including neuroleptic malignant syndrome and malignant hyperthermia, were excluded due to the absence of exposure to neuroleptic medication or peri-anesthetic triggers, as well as the lack of hyperthermia, altered mental status, autonomic instability, or generalized muscle rigidity.

Myopathy attributed to rosuvastatin occurs in ≤ 0.03% of patients receiving 10–40 mg of rosuvastatin, and rhabdomyolysis is even rarer with rosuvastatin, particularly at low doses[9]. In our case, the patient was on a low dose of 5 mg, further underscoring the unusual nature of this adverse event. Statin use may have lowered the threshold for muscle injury when combined with sudden, intense eccentric exercise after deconditioning[10].

In our patient, corticosteroid therapy was initiated empirically as a precaution due to initial concern for statin-induced immune-mediated myopathy. Although statin-induced necrotizing autoimmune myopathy has been reported to respond to corticosteroids[11], the mainstay of prevention and treatment of rhabdomyolysis-associated AKI remains early and aggressive hydration because patients with rhabdomyolysis are usually fluid depleted as water sequestrates in the injured muscle[12].

Treatment for rhabdomyolysis, at least initially, is mainly supportive, centering on the management of the ABCs (airway, breathing, and circulation) and measures to preserve renal function, including vigorous rehydration.

Conclusion

Exertional rhabdomyolysis can present atypically with abdominal pain and preserved urine output, leading to delayed diagnosis; therefore, clinicians should maintain a high index of suspicion in patients with recent strenuous exercise and unexplained AKI. Early measurement of creatine kinase in such presentations may prevent diagnostic delay and reduce the risk of renal complications.

Ethical approval

Ethical approval was not required for this study, as it is a single case report and does not involve experimental intervention.

Consent

Written informed consent was obtained from the patient for the publication of this case report and any accompanying images. A copy of the written consent is available for review by the editor-in-chief of this journal upon request.

Sources of funding

This research did not receive any specific grant from funding agencies in the public, commercial, or non-profit sectors.

Author contributions

P.K.K.: Writing original draft, writing - review and editing, and visualization. D.S.: Supervision and validation. K.G.: Resources.

Conflicts of interest disclosure

The authors declare that they have no conflicts of interest.

Research registration unique identifying number (UIN)

This case report has not been registered because it describes a single clinical case and does not constitute a clinical trial.

Guarantor

Dr Deepak Sharma.

Provenance and peer review

Not commissioned, externally peer reviewed.

Data availability statement

The data supporting the findings of this study are contained within the manuscript. Further details are not publicly available due to patient confidentiality.

Assistance with the study

The authors would like to thank the patient for providing consent to publish this case report. We also extend our gratitude to the Department of Nephrology and Internal Medicine for their assistance during the clinical management and follow-up of the patient.

Presentation

None.