What is the most likely cause and immediate management for a 69‑year‑old woman with severe non‑verbal progressive dementia, non‑ambulatory with limb contractures, recent falls, tachycardia, low‑grade fever, right‑upper‑quadrant abdominal and leg tenderness, elevated liver transaminases, elevated C‑reactive protein, normal procalcitonin, normal PT/INR, raised creatine kinase, normal D‑dimer, and a negative CT pulmonary angiogram?

Most Likely Diagnosis and Immediate Management

The most likely diagnosis is rhabdomyolysis secondary to immobility and recent falls, with immediate management focused on aggressive IV hydration, discontinuation of any statin medications, and systematic investigation for occult infection as a precipitating factor. 1

Clinical Reasoning for Rhabdomyolysis

The constellation of elevated creatine kinase, right upper quadrant tenderness (potentially reflecting hepatic involvement from myoglobin), leg tenderness (muscle breakdown), low-grade fever, tachycardia, and elevated CRP in a non-ambulatory patient with limb contractures and recent falls strongly suggests rhabdomyolysis. 1

• Elevated CRP with normal procalcitonin indicates an inflammatory process rather than bacterial infection, consistent with muscle injury and necrosis 2
• Elevated liver enzymes may reflect either direct hepatic involvement from myoglobin toxicity or release of muscle-derived transaminases (AST particularly) 2
• Normal D-dimer and negative CTA effectively rule out pulmonary embolism as the cause of tachycardia 1
• Immobility with contractures creates sustained pressure on muscle groups, predisposing to pressure-induced rhabdomyolysis 3

Immediate Management Protocol

Step 1: Confirm Diagnosis and Assess Severity

• Check serum creatine kinase level immediately – values >1,000 U/L confirm rhabdomyolysis, >5,000 U/L indicate severe disease requiring ICU-level monitoring 1
• Obtain urinalysis to check for myoglobinuria (tea-colored urine, positive blood on dipstick without RBCs on microscopy) 1
• Measure serum potassium, calcium, phosphate, and uric acid – hyperkalemia is life-threatening and requires immediate treatment 1
• Monitor renal function closely (BUN, creatinine) as acute kidney injury is the primary life-threatening complication 1

Step 2: Initiate Aggressive Fluid Resuscitation

• Begin IV normal saline at 200-300 mL/hour (adjust based on cardiac status and urine output) to maintain urine output >200-300 mL/hour 1
• Target urine output of 3 mL/kg/hour to prevent myoglobin precipitation in renal tubules 1
• Monitor fluid balance meticulously – elderly patients with dementia may have unrecognized heart failure 1

Step 3: Discontinue Nephrotoxic and Myotoxic Medications

• Review all medications immediately and stop any statins, fibrates, or other drugs that lower seizure threshold or cause muscle toxicity 4
• Identify and discontinue anticholinergic medications (diphenhydramine, oxybutynin, cyclobenzaprine) that worsen confusion and may contribute to immobility 1, 4

Step 4: Systematic Investigation for Precipitating Causes

Despite normal procalcitonin, occult infection remains a critical consideration in non-verbal dementia patients who cannot communicate discomfort:

• Obtain urinalysis and urine culture – urinary tract infections are major contributors to acute deterioration in dementia patients 1, 5
• Obtain chest X-ray – aspiration pneumonia is common in advanced dementia with contractures 1, 5
• Check for pressure ulcers – infected decubitus ulcers may not elevate procalcitonin but drive systemic inflammation 1
• Assess for constipation and urinary retention – both significantly contribute to agitation and systemic stress 1, 5
• Perform systematic pain assessment – untreated pain is a major contributor to behavioral disturbances and immobility in non-verbal patients 1, 5

Step 5: Address Underlying Immobility and Contractures

• Consult physical therapy to develop gentler transfer techniques and positioning strategies to prevent further muscle compression 1
• Implement pressure relief protocol with repositioning every 2 hours and use of pressure-reducing surfaces 1
• Ensure adequate nutrition and hydration – malnutrition exacerbates muscle breakdown 5

Monitoring and Reassessment

• Check CK, potassium, calcium, and renal function every 6-12 hours until CK is declining and renal function is stable 1
• Monitor urine output hourly – decreasing output despite adequate fluids suggests evolving acute kidney injury 1
• Watch for compartment syndrome in affected limbs (increased pain, tense swelling, diminished pulses) – this is a surgical emergency 1
• Evaluate for cardiac arrhythmias secondary to hyperkalemia or hypocalcemia with continuous telemetry 1

Critical Pitfalls to Avoid

• Do not attribute elevated CK solely to falls without investigating for ongoing muscle compression from immobility 3
• Do not delay fluid resuscitation while awaiting confirmatory tests – early aggressive hydration is the cornerstone of preventing renal failure 1
• Do not overlook occult infection despite normal procalcitonin – infections in dementia patients may present atypically 1, 5
• Do not restart potentially myotoxic medications (statins, fibrates) until CK has normalized and the patient's mobility status has improved 4

Alternative Diagnoses to Consider

If rhabdomyolysis is ruled out or CK elevation is mild:

• Acalculous cholecystitis – right upper quadrant tenderness with fever and elevated inflammatory markers in an immobile patient 1
• Occult intra-abdominal infection – diverticulitis, appendicitis, or bowel perforation may present atypically in dementia 1, 5
• Drug-induced hepatotoxicity – review all medications for hepatotoxic agents 4
• Rapidly progressive dementia with systemic inflammation – consider autoimmune encephalitis or prion disease if neurological decline is accelerating 6, 7