Rhabdomyolysis for md emergency medicine exams
Reading File
Finding Sources
Searching PubMed
rhabdomyolysis diagnosis management
Searching the Web
rhabdomyolysis emergency medicine MD exam key points 2025
Reading File
Reading File
Reading File
Reading File
Reading File
I now have very rich content from both Tintinalli's and Goldman-Cecil. I have enough material for a comprehensive MD emergency medicine exam review. Let me compile the full answer now.
Rhabdomyolysis - MD Emergency Medicine Exam Review
Definition
Rhabdomyolysis is an acute, potentially fatal clinical syndrome characterized by the destruction of skeletal muscle (striated muscle) with release of intracellular myocyte contents - including myoglobin, creatine kinase (CK), potassium, phosphate, uric acid, aldolase, LDH, and AST - into the systemic circulation. Myoglobinuria is a common sequela and is the key driver of acute kidney injury (AKI).
- Tintinalli's Emergency Medicine, Ch. 89
- Goldman-Cecil Medicine, Ch. 99
Epidemiology
- ~26,000 hospitalized cases/year in the United States
- 13-67% of rhabdomyolysis patients develop AKI
- AKI from rhabdomyolysis accounts for 5-10% of all acute kidney failure in the US
- Most common causes in adults: drugs of abuse and alcohol > medications > muscle diseases > trauma > neuroleptic malignant syndrome > seizures > immobility > infection > strenuous exercise > heat illness
- Most common causes in children: viral myositis > trauma > connective tissue disease > (inherited metabolic disorders if recurrent)
- Multiple causes are present in >50% of patients
Pathophysiology
The final common pathway is disruption of the Na+/K+ ATPase pump and calcium transport, leading to:
- Increased intracellular Ca²⁺ → muscle cell necrosis
- Ca²⁺ activates phospholipase A₂, proteases, and free radical production
- Release of intracellular contents into circulation
How myoglobin causes AKI (three mechanisms):
| Mechanism | Detail |
|---|---|
| Renal vasoconstriction | Volume depletion + myoglobin-mediated endothelin release |
| Direct proximal tubular injury | Oxidant stress from heme iron (Fe²⁺) in myoglobin |
| Intratubular obstruction | Myoglobin precipitates in acidic urine → cast formation |
Key point: Both myoglobin and uric acid have less nephrotoxicity in alkaline urine - the basis for urine alkalinization therapy.
AKI risk is lower when CK < 20,000 U/L, but rhabdomyolysis can cause AKI with CK as low as 5,000 U/L if coexisting sepsis, volume depletion, or acidosis are present.
Causes - The "CAST ME" Mnemonic
| Category | Key Examples |
|---|---|
| Crush / Compression | Crush injury, prolonged immobilization, coma, bariatric surgery |
| Activity / Exertion | Exercise (CrossFit, spinning, eccentric loading), seizures, status epilepticus, delirium tremens |
| Substances / Drugs | Cocaine (20% of overdoses), heroin, alcohol, amphetamines, PCP, MDMA, statins, fibrates, antipsychotics, colchicine, propofol, SSRIs, isoniazid |
| Temperature | Heat stroke, malignant hyperthermia, NMS, hypothermia, burns, lightning |
| Metabolic | Hypokalemia, hypophosphatemia, hyponatremia/hypernatremia, hypothyroidism, DKA, hyperosmolar states |
| Electrical/Infectious | Electrical injury, Influenza A/B, HIV, CMV, EBV, Group A Strep, Legionella, SARS-CoV-2 |
High-yield drug causes for exam:
- Statins: dose-related; higher risk with polypharmacy (cyclosporine, macrolide antibiotics); cerivastatin had highest rates. Can also cause anti-HMG-CoA autoimmune myopathy with profound CK elevation.
- Cocaine: nearly 20% of cocaine overdoses complicated by rhabdomyolysis
- "Bath salts" (MDPV) and synthetic cannabinoids ("spice") - important newer causes
Inherited causes (recurrent rhabdomyolysis): McArdle disease (myophosphorylase deficiency), carnitine palmitoyltransferase II deficiency, G6PD deficiency, myoadenylate deaminase deficiency
Clinical Features
The classic triad: myalgias + weakness + dark (cola-colored) urine
BUT: muscle symptoms are present in only ~50% of cases - rhabdomyolysis can be completely asymptomatic with a normal exam.
| Feature | Details |
|---|---|
| Myalgias, weakness | Localized or diffuse; postural muscles of thighs, calves, lower back commonly involved |
| Dark/brown urine | Due to myoglobinuria |
| Malaise, low-grade fever | Common |
| Nausea, vomiting, abdominal pain | In severe disease |
| Tachycardia | Due to volume depletion |
| Mental status changes | Uremic encephalopathy |
| Muscle swelling | May only appear AFTER IV fluid resuscitation |
| Oliguria/anuria | Indicates AKI |
Life-threatening complications:
- AKI (most important)
- Hyperkalemia → cardiac arrhythmias (K⁺ release from necrotic muscle)
- Hypocalcemia (Ca²⁺ deposits in necrotic muscle) → tetany, arrhythmias
- DIC (release of thromboplastin from muscle)
- Compartment syndrome (muscle swelling)
- Liver failure (direct toxic effect)
Diagnosis
Lab Workup
| Test | Finding / Significance |
|---|---|
| Serum CK | Most sensitive and reliable marker. CK > 5× ULN (or typically >1,000 U/L) suggests rhabdomyolysis. Peaks at 24-72h, falls ~50%/day. CK >20,000 = significant AKI risk. |
| Urinalysis | Dipstick positive for blood but no RBCs on microscopy (myoglobin cross-reacts with heme). Pigmented granular (muddy brown) casts. |
| Urine myoglobin | Confirms diagnosis. Clears rapidly (t½ 1-3h); may be negative by the time of testing. |
| BMP | BUN/Cr (AKI), K⁺ (hyperkalemia), Ca²⁺ (hypocalcemia early, hypercalcemia in recovery), phosphate (elevated), uric acid (elevated) |
| LFTs | AST and ALT elevated (released from muscle, not necessarily liver injury) |
| CBC | Hemoconcentration if volume depleted |
| Coagulation | PT/PTT - screen for DIC |
Key diagnostic pearl: Dipstick positive for "blood" + absent RBCs on urine microscopy in appropriate clinical setting = myoglobinuria until proven otherwise. The pigmented granular cast is pathognomonic.
AST and CK: Both are released from skeletal muscle, so elevated AST does not always mean liver disease in this context - always check CK and clinical context.
McMahon Risk Score
The McMahon score predicts AKI risk. Score ≥5 indicates high risk requiring inpatient management.
Variables include: age, female sex, initial creatinine, CK, bicarbonate, phosphate, and whether cause was exertional (lower-risk) or non-exertional (higher-risk).
Management
1. Aggressive IV Fluid Resuscitation - The Cornerstone
- Goal: Maintain urine output 200-300 mL/hour (or ≥3 mL/kg/hour in some protocols)
- Fluid: Normal saline (0.9%) is the standard first-line fluid
- Initial rate: typically 1-1.5 L/hour in adults, then titrated to urine output
- Continue until CK is trending down and urine clears
- Monitor for fluid overload - particularly in elderly or those with cardiac/renal disease
2. Urine Alkalinization (Controversial)
- Sodium bicarbonate (150 mEq/L in D5W) added to IVF
- Aim for urine pH >6.5 to prevent myoglobin precipitation in renal tubules
- Also helps with hyperkalemia
- Caution: Can worsen symptomatic hypocalcemia; avoid if serum bicarbonate is already elevated or if urine pH cannot be raised above 6.5 (not beneficial in those cases)
- Evidence base is observational - not proven in RCTs to improve outcomes vs NS alone; many centers still use it in severe cases
3. Electrolyte Management
| Electrolyte | Treatment |
|---|---|
| Hyperkalemia | Aggressive IVF, bicarbonate, insulin/dextrose, kayexalate; dialysis if severe |
| Hypocalcemia | Treat ONLY if symptomatic (tetany, arrhythmia) - do NOT treat asymptomatic hypocalcemia (calcium deposits in muscle and can worsen rebound hypercalcemia during recovery) |
| Hyperphosphatemia | Correct with dietary restriction; contributes to secondary hypocalcemia |
4. Mannitol (Controversial)
- Has been used as an osmotic diuretic to "flush" myoglobin
- Also theoretical free radical scavenging benefit
- Not well-supported by evidence; not routinely recommended
- Risk: can worsen AKI if patient is volume depleted
5. Loop Diuretics
- Not routinely recommended and may actually worsen outcome by acidifying the urine (counterproductive to alkalinization goal)
6. Renal Replacement Therapy (Dialysis)
Indicated for:
- Persistent oliguria/anuria despite IVF
- Refractory hyperkalemia
- Severe metabolic acidosis
- Fluid overload
- BUN/Cr rising despite treatment
7. Treat the Underlying Cause
- Stop offending drug/agent
- Decompress compartment syndrome (fasciotomy)
- Treat infection, seizures, NMS, etc.
- Remove patient from heat environment
Indications for Admission (High-Risk Features)
- Dark urine or confirmed myoglobinuria
- CK > 20,000 U/L (some say >5,000-10,000)
- Potential compartment syndrome
- Hypotension or tachycardia
- Body temperature > 40°C
- Hyperkalemia, metabolic acidosis, hypocalcemia, hyperphosphatemia
- McMahon score ≥5
- Sickle cell trait carrier
- Limited outpatient follow-up capability
Complications Summary
| Complication | Mechanism | Timing |
|---|---|---|
| AKI | Myoglobin tubular toxicity + renal vasoconstriction | Early (hours-days) |
| Hyperkalemia | Direct K⁺ release from necrotic muscle | Early |
| Hypocalcemia | Ca²⁺ sequestered in necrotic muscle | Early |
| Hypercalcemia | Ca²⁺ mobilized from muscle during repair | Recovery phase |
| DIC | Release of thromboplastin | Early |
| Compartment syndrome | Muscle swelling | Early |
| Liver failure | Direct toxicity | Severe cases |
| Cardiac arrhythmia | Hyperkalemia + hypocalcemia | Early |
High-Yield Exam Points
- CK is the most sensitive marker - serum myoglobin clears too quickly and is unreliable
- Dipstick (+) blood + no RBCs on microscopy = myoglobinuria - don't miss this!
- Treat asymptomatic hypocalcemia with observation, not calcium - giving calcium can cause metastatic calcification and rebound hypercalcemia during recovery
- Most common adult causes: drugs of abuse/alcohol, then medications (statins)
- Most common pediatric cause: viral myositis
- Recurrent rhabdomyolysis = think inherited metabolic disorder (McArdle disease, CPT-II deficiency)
- Cocaine overdose has 20% rhabdomyolysis rate - always check CK in cocaine intox
- Exertional rhabdomyolysis is less likely to cause AKI than non-exertional causes
- Sickle cell trait is a risk factor for exertional rhabdomyolysis
- Urine output target during treatment: 200-300 mL/hour
- Polypharmacy with statins + cyclosporine or macrolides dramatically increases rhabdomyolysis risk
- NMS vs malignant hyperthermia: both cause rhabdomyolysis - NMS from antipsychotics, MH from volatile anesthetics/succinylcholine
- "Propofol infusion syndrome" = rare but fatal: metabolic acidosis + rhabdomyolysis + cardiac failure in patients on high-dose propofol infusions
- AST elevation in rhabdomyolysis does not mean liver injury - it comes from muscle
- CK peaks 24-72h post-injury, then falls ~50%/day if no ongoing muscle injury
Key Differences: Hemolysis vs Myoglobinuria on UA
| Feature | Hemoglobinuria | Myoglobinuria |
|---|---|---|
| Dipstick (heme) | Positive | Positive |
| Urine color | Red/pink | Cola/brown |
| Microscopy RBCs | Present | Absent |
| Serum color | Pink (red) | Normal/clear |
| CK | Normal | Markedly elevated |
This distinction on the exam is critical - hemoglobin turns serum pink; myoglobin is rapidly cleared and serum appears normal.
Sources: Tintinalli's Emergency Medicine: A Comprehensive Study Guide, Ch. 89 | Goldman-Cecil Medicine, Ch. 99 | Comprehensive Clinical Nephrology, 7th Ed., Ch. 72 | Recent pediatric rhabdomyolysis meta-analysis (PMID: 41146051) confirms viral myositis as top pediatric cause.
This is a shared conversation. Sign in to Orris to start your own chat.