High Yield Overview

RHABDOMYOLYSIS

Muscle Breakdown | CK Elevation | Myoglobinuria | Acute Kidney Injury

10,000+CK threshold (U/L)

200ml/hrTarget urine output

pH 6.5Urine alkalinization target

50%AKI if untreated

RHABDOMYOLYSIS SEVERITY

Mild

PatternCK 5,000-10,000, no myoglobinuria

TreatmentIV fluids, monitor

Moderate

PatternCK 10,000-50,000, myoglobinuria

TreatmentAggressive fluids, alkalinize urine

Severe

PatternCK over 50,000, AKI, hyperkalemia

TreatmentICU, dialysis if needed

Critical Must-Knows

CK over 10,000 U/L is diagnostic threshold for rhabdomyolysis
Myoglobinuria (dark tea-colored urine) indicates significant muscle breakdown
Acute kidney injury from myoglobin tubular obstruction - prevent with aggressive fluids
Hyperkalemia from muscle necrosis - cardiac risk, monitor ECG
Urine alkalinization (pH over 6.5) reduces myoglobin precipitation in tubules

Examiner's Pearls

"
Target urine output over 200ml/hr with aggressive IV fluids (4-6L first 24h)
"
Sodium bicarbonate alkalinizes urine - prevents myoglobin precipitation
"
Compartment syndrome is most common orthopaedic cause
"
CK peaks at 24-48 hours, then declines if treated appropriately

Clinical Imaging

Imaging Gallery

Clinical photo demonstrating lithotomy positioning technique in operating room - illustrating risk factor for position-related compartment syndrome and rhabdomyolysis. — Clinical photo demonstrating lithotomy positioning technique in operating room - illustrating risk factor for position-related compartment syndrome anCredit: Stornelli N et al. - Patient Saf Surg via Open-i (NIH) - PMC4960854 (CC-BY 4.0)

2-panel (a-b) urinary sediment microscopy showing pigmented (myoglobin) casts: (a) pigmented granular casts at 400x magnification, (b) additional view with inflammatory cells - classic diagnostic find — 2-panel (a-b) urinary sediment microscopy showing pigmented (myoglobin) casts: (a) pigmented granular casts at 400x magnification, (b) additional viewCredit: Huerta-Alardín AL et al. - Crit Care via Open-i (NIH) - PMC1175909 (CC-BY 4.0)

Critical Rhabdomyolysis Exam Points

Myoglobinuria is Key Sign

Dark tea-colored or cola-colored urine indicates myoglobinuria - this is the clinical sign of significant rhabdomyolysis. Requires immediate aggressive fluid resuscitation to prevent acute kidney injury from myoglobin tubular obstruction.

CK Threshold

CK over 10,000 U/L is diagnostic threshold. Levels can exceed 100,000 in severe cases. CK peaks at 24-48 hours after injury, then declines if treated. Monitor serial levels.

Acute Kidney Injury Prevention

Aggressive IV fluids target urine output over 200ml/hr (4-6L first 24 hours). Alkalinize urine with sodium bicarbonate (target pH over 6.5) to prevent myoglobin precipitation in renal tubules. This is the key to preventing AKI.

Hyperkalemia Risk

Hyperkalemia from massive muscle necrosis can cause cardiac arrhythmias and arrest. Monitor potassium levels and ECG. May require calcium, insulin/glucose, or dialysis. Life-threatening complication.

Rhabdomyolysis Management by Severity - Quick Reference

CK Level	Myoglobinuria	Urine Output	Management
5,000-10,000	Absent	Normal	IV fluids, monitor CK
10,000-50,000	Present	Target 200ml/hr	Aggressive fluids, alkalinize urine
Over 50,000	Severe	Over 200ml/hr	ICU, consider dialysis

Mnemonic

FARMRhabdomyolysis Management

Fluids aggressive

Target urine output over 200ml/hr (4-6L first 24h)

Alkalinize urine

Sodium bicarbonate to pH over 6.5

Renal protection

Prevent myoglobin tubular obstruction

Monitor CK/K/ECG

Serial CK, potassium, ECG for hyperkalemia

Memory Hook:FARM the patient: Fluids Aggressive, Alkalinize urine, Renal protection, Monitor closely!

Mnemonic

CRUSHRhabdomyolysis Causes

Compartment syndrome

Most common orthopaedic cause

Rhabdomyolysis

Muscle breakdown from ischemia

Unconscious (prolonged)

Pressure necrosis from immobility

Seizures

Muscle damage from convulsions

Heat stroke/exertion

Exercise-induced muscle breakdown

Memory Hook:CRUSH causes: Compartment syndrome, Rhabdomyolysis, Unconscious, Seizures, Heat stroke!

Mnemonic

BICARBMyoglobinuria Management

Bicarbonate (sodium)

Alkalinize urine to pH over 6.5

IV fluids aggressive

4-6L first 24 hours

CK monitoring

Serial levels every 6-12 hours

Avoid nephrotoxins

No NSAIDs, contrast if possible

Renal function

Monitor creatinine, eGFR

Bicarbonate target pH

Urine pH over 6.5 prevents precipitation

Memory Hook:BICARB: Bicarbonate, IV fluids, CK monitoring, Avoid nephrotoxins, Renal function, Bicarbonate target!

Overview and Epidemiology

Rhabdomyolysis is a syndrome of skeletal muscle breakdown with release of intracellular contents into the circulation, leading to myoglobinuria and potential acute kidney injury. It is a serious complication of compartment syndrome, crush injuries, and other muscle-damaging conditions.

Epidemiology:

Common complication of compartment syndrome (especially if delayed over 6 hours)
Crush injuries (earthquakes, building collapse)
Prolonged immobility (unconscious patients)
Exercise-induced (exertional rhabdomyolysis)
Drug-induced (statins, alcohol)
Heat-related illness

Patient positioning in lithotomy - risk factor for positional rhabdomyolysis — Clinical photograph demonstrating lithotomy positioning in the operating room. The patient's legs are elevated in padded stirrups (yellow boot-type supports). Prolonged lithotomy positioning during surgery is a recognized risk factor for positional compartment syndrome and rhabdomyolysis, particularly in procedures exceeding 4-6 hours. Key preventive measures include proper padding, limiting surgical time, and monitoring for compartment syndrome postoperatively.Credit: Stornelli N et al., Patient Saf Surg - CC BY 4.0

Mechanism of Muscle Breakdown:

Compartment Syndrome Connection

Compartment syndrome is the most common orthopaedic cause of rhabdomyolysis. When compartment syndrome is delayed (over 6 hours), muscle necrosis occurs, releasing myoglobin. This is why post-fasciotomy monitoring for rhabdomyolysis is essential.

Anatomy and Pathophysiology

Muscle Anatomy:

Skeletal muscle contains high concentrations of CK and myoglobin
Myoglobin is an oxygen-binding protein in muscle
Muscle cell membrane disruption releases these into circulation
Renal tubules filter myoglobin, which can precipitate

Renal Anatomy:

Glomeruli filter myoglobin from blood
Renal tubules are where myoglobin precipitates
Acidic urine (pH under 5.6) promotes precipitation
Tubular obstruction leads to decreased GFR and AKI

Pathophysiology: Rhabdomyolysis results from:

Muscle cell membrane disruption
Release of intracellular contents (CK, myoglobin, potassium, phosphate)
Myoglobin filtered by kidneys
Myoglobin precipitates in acidic urine (pH under 5.6)
Tubular obstruction and acute kidney injury

Mechanism of Muscle Breakdown:

Classification Systems

Rhabdomyolysis Severity

Severity Classification by CK Level

Severity	CK Level	Myoglobinuria	Management
Mild	5,000-10,000 U/L	Absent	IV fluids, monitor
Moderate	10,000-50,000 U/L	Present	Aggressive fluids, alkalinize urine
Severe	Over 50,000 U/L	Severe	ICU, dialysis if needed

Mild: Usually resolves with simple hydration. Monitor CK levels.

Moderate: Requires aggressive management to prevent AKI. Most common presentation.

Severe: Life-threatening, requires ICU care. High risk of AKI and hyperkalemia.

Pathophysiology Details

Mechanism of Muscle Breakdown:

Rhabdomyolysis Pathophysiology

Stage	Process	Consequence
Injury	Muscle cell membrane disruption	Release of intracellular contents
Circulation	CK, myoglobin, K+, PO4 enter blood	Elevated serum markers
Kidney	Myoglobin filtered, precipitates in acidic urine	Tubular obstruction
AKI	Tubular necrosis, decreased GFR	Acute kidney injury

Myoglobin Toxicity:

Myoglobin is filtered by glomeruli
In acidic urine (pH under 5.6), myoglobin precipitates
Forms casts that obstruct renal tubules
Direct tubular toxicity
Renal vasoconstriction
Acute kidney injury develops

Hyperkalemia Mechanism:

Massive muscle necrosis releases intracellular potassium
Can cause life-threatening hyperkalemia
Cardiac arrhythmias (peaked T-waves, widened QRS)
May require emergency treatment (calcium, insulin/glucose, dialysis)

Hyperkalemia is Life-Threatening

Hyperkalemia from rhabdomyolysis can cause cardiac arrest. Monitor potassium levels and ECG continuously. Signs: peaked T-waves, widened QRS, bradycardia. Treatment: IV calcium (cardioprotective), insulin/glucose (drives K+ into cells), sodium bicarbonate (alkalinizes, shifts K+), dialysis if severe.

Clinical Assessment

History:

Compartment syndrome (most common orthopaedic cause)
Crush injury (prolonged compression)
Prolonged immobility (unconscious patient)
Exercise-induced (exertional)
Drug history (statins, alcohol)
Heat exposure

Physical Examination:

Muscle Findings

Swollen, tender muscles
Weakness
Myalgia
Compartment syndrome signs (if present)

Systemic Signs

Dark tea-colored urine (myoglobinuria)
Decreased urine output
Signs of hyperkalemia (ECG changes)
Signs of AKI (oliguria, fluid overload)

Urine Assessment:

Color: Dark tea-colored or cola-colored = myoglobinuria
Dipstick: Positive for blood (but no RBCs on microscopy) = myoglobin
Output: Decreased output indicates AKI developing

Myoglobinuria Recognition

Dark tea-colored or cola-colored urine is the clinical hallmark of myoglobinuria. Dipstick will be positive for blood, but microscopy shows no red blood cells (myoglobin, not hemoglobin). This requires immediate aggressive management.

Investigations

Laboratory Tests:

Essential Laboratory Tests

Test	Finding	Significance
CK (creatine kinase)	Over 10,000 U/L (diagnostic)	Peaks 24-48h, then declines
Myoglobin (serum)	Elevated	Confirms muscle breakdown
Myoglobin (urine)	Positive	Dark urine, tubular obstruction risk
Potassium	Hyperkalemia	Cardiac risk - monitor ECG
Creatinine	Rising	AKI developing
Phosphate	Elevated	Muscle breakdown
Calcium	Hypocalcemia early	Precipitates in necrotic muscle

Monitoring Protocol:

Laboratory Monitoring

On diagnosisInitial

CK, myoglobin (serum and urine)
UEC (potassium, creatinine, urea)
FBC, coagulation
ECG (hyperkalemia assessment)

Every 6-12 hoursSerial

CK levels (peak at 24-48h)
Potassium (hyperkalemia risk)
Creatinine (AKI progression)
Urine output monitoring

Daily until normalizingResolution

CK declining
Renal function improving
Potassium normalized

CK Kinetics

CK peaks at 24-48 hours after injury, then declines with half-life of 1.5 days if treated appropriately. If CK continues rising after 48 hours, ongoing muscle damage is occurring (incomplete fasciotomy, recurrent compartment syndrome, or other cause).

Urinary Sediment Findings

Urinary sediment showing pigmented myoglobin casts in rhabdomyolysis — Two-panel microscopy of urinary sediment in rhabdomyolysis. Panel (a): Brown/pigmented granular casts at 400x magnification - these are myoglobin casts, the hallmark diagnostic finding of myoglobinuria. The characteristic dark pigmentation is due to myoglobin deposition within the tubular casts. Panel (b): Additional view showing pigmented casts with inflammatory cellular elements. These findings confirm active myoglobin excretion and risk of tubular obstruction - aggressive fluid resuscitation and urine alkalinization are essential to prevent acute kidney injury.Credit: Huerta-Alardín AL et al., Crit Care - CC BY 4.0

Management Algorithm

CK 5,000-10,000, No Myoglobinuria

Management:

IV fluids: 1-2L over 24 hours
Monitor CK levels
Monitor urine output
Usually resolves without complications

Prognosis: Excellent with simple hydration.

Surgical Technique

Note: Rhabdomyolysis itself is a medical condition, not a surgical procedure. However, if compartment syndrome is the underlying cause, fasciotomy is required. This section addresses fasciotomy technique when rhabdomyolysis is present or suspected.

Fasciotomy Technique (When Rhabdomyolysis Present)

Pre-operative Considerations:

Rhabdomyolysis may already be present if delayed over 6 hours
Monitor for myoglobinuria post-operatively
Plan for aggressive fluid resuscitation
Consider ICU admission if severe

Technique:

Standard fasciotomy approach (leg: 2-incision, 4-compartment)
Release all compartments completely
Assess muscle viability (pink, contractile = viable; dark, non-contractile = necrotic)
Debride obviously necrotic muscle
Leave wounds open

Post-operative:

Immediate aggressive fluid resuscitation
Monitor for rhabdomyolysis
Serial CK levels
Urine output monitoring

Fasciotomy prevents further muscle necrosis and may limit rhabdomyolysis progression.

Treatment Details

Aggressive IV Fluid Therapy

Goal: Maintain urine output over 200ml/hr (or over 1ml/kg/hr)

Protocol:

Initial: 1-2L bolus if dehydrated
Maintenance: 4-6L over first 24 hours
Type: Normal saline or lactated Ringer's
Monitoring: Hourly urine output, daily weights, clinical assessment

Rationale:

High urine flow prevents myoglobin precipitation
Maintains renal perfusion
Prevents tubular obstruction

Fluid Target

Target urine output over 200ml/hr (or over 1ml/kg/hr) is essential to prevent myoglobin tubular obstruction. This requires aggressive IV fluid administration - 4-6L in first 24 hours is common.

Complications

Rhabdomyolysis Complications

Complication	Incidence	Management
Acute kidney injury	30-50% if untreated	Prevent with aggressive fluids, alkalinization
Hyperkalemia	Common in severe cases	Monitor ECG, treat with calcium/insulin/bicarb
Hypocalcemia (early)	Common	Usually resolves, avoid overcorrection
Hypercalcemia (late)	During recovery	Calcium released from necrotic muscle
Compartment syndrome	If underlying cause	Fasciotomy if present
DIC	Rare	Supportive care

Acute Kidney Injury:

Most serious complication
Develops in 30-50% if untreated
Prevention is key: aggressive fluids, urine alkalinization
Most recover renal function with treatment
May require temporary dialysis

Hyperkalemia:

Life-threatening complication
Can cause cardiac arrest
Requires immediate treatment
Monitor ECG continuously

AKI Recovery

Most patients with rhabdomyolysis-induced AKI recover renal function with appropriate treatment. Dialysis is often temporary. Long-term renal impairment is uncommon if treated early and aggressively.

Postoperative Care

After Fasciotomy (if compartment syndrome cause):

Post-Fasciotomy Rhabdomyolysis Management

0-6 hoursImmediate

Aggressive IV fluids (target 200ml/hr urine output)
Alkalinize urine (sodium bicarbonate)
Monitor CK, potassium, creatinine
ECG monitoring

6-24 hoursFirst 24 Hours

Continue aggressive fluids
Serial CK every 6-12 hours
Monitor urine output hourly
Assess for hyperkalemia
Consider ICU if severe

24-72 hoursDays 2-3

CK should peak then decline
Continue monitoring
Assess renal function
Wean fluids as CK normalizes

Days 3-7Recovery

CK declining
Renal function improving
Can reduce monitoring frequency
Continue until CK under 5,000

Key Monitoring:

Urine output (target over 200ml/hr)
Urine color (should lighten as myoglobinuria resolves)
CK levels (should decline after 24-48h peak)
Potassium (hyperkalemia risk)
Creatinine (AKI progression)

Outcomes and Prognosis

Recovery:

CK normalization: 3-5 days with treatment
Renal function: Most recover completely
Mortality: Low if treated appropriately (under 5%)
Long-term: Usually no sequelae if treated early

Prognostic Factors:

Early treatment: Better outcomes
CK level: Higher CK = worse prognosis
Time to treatment: Delayed treatment = higher AKI risk
Underlying cause: Treatable causes (compartment syndrome) have better outcomes

Evidence Base

Rhabdomyolysis and Acute Kidney Injury

Bosch X, Poch E, Grau JM • N Engl J Med (2009)

Key Findings:

CK over 10,000 U/L diagnostic threshold
Myoglobinuria causes tubular obstruction
Aggressive fluid resuscitation prevents AKI
Urine alkalinization reduces myoglobin precipitation

Clinical Implication: Early aggressive fluid resuscitation and urine alkalinization are essential to prevent acute kidney injury in rhabdomyolysis. Target urine output over 200ml/hr and urine pH over 6.5.

Compartment Syndrome and Rhabdomyolysis

McQueen MM, Court-Brown CM • J Bone Joint Surg Br (1996)

Key Findings:

Compartment syndrome is most common orthopaedic cause
Delayed fasciotomy (over 6 hours) increases rhabdomyolysis risk
Post-fasciotomy monitoring essential
Early fasciotomy prevents muscle necrosis

Clinical Implication: Compartment syndrome must be recognized and treated early (under 6 hours) to prevent rhabdomyolysis. Post-fasciotomy, monitor for rhabdomyolysis with serial CK and urine assessment.

Hyperkalemia in Rhabdomyolysis

Better OS, Stein JH • Kidney Int (1990)

Key Findings:

Hyperkalemia from massive muscle necrosis
Can cause life-threatening cardiac arrhythmias
Requires immediate treatment
Dialysis may be needed if refractory

Clinical Implication: Hyperkalemia is a life-threatening complication requiring immediate treatment. Monitor ECG continuously and treat with calcium, insulin/glucose, and bicarbonate. Dialysis if severe.

Crush Injury and Rhabdomyolysis

Better OS, Abassi ZA • Nephrol Dial Transplant (2001)

Key Findings:

Crush injuries cause severe rhabdomyolysis
Early fluid resuscitation before extrication improves outcomes
Hyperkalemia is immediate life threat
Most require ICU care initially

Clinical Implication: Crush injuries require immediate aggressive management even before extrication if possible. Hyperkalemia is the immediate life threat requiring urgent treatment. Most patients require ICU care.

Urine Alkalinization in Rhabdomyolysis

Zager RA • Kidney Int (1989)

Key Findings:

Myoglobin precipitates in acidic urine (pH under 5.6)
Alkaline urine (pH over 6.5) prevents precipitation
Reduces tubular obstruction and AKI risk
Sodium bicarbonate is effective alkalinizing agent

Clinical Implication: Urine alkalinization to pH over 6.5 is essential to prevent myoglobin precipitation and acute kidney injury. Sodium bicarbonate added to IV fluids achieves this goal.

Exam Viva Scenarios

Practice these scenarios to excel in your viva examination

VIVA SCENARIOStandard

Scenario 1: Post-Fasciotomy Rhabdomyolysis

EXAMINER

"A 35-year-old man underwent fasciotomy for compartment syndrome 12 hours after injury. Post-operatively, his urine is dark tea-colored, CK is 25,000 U/L, and creatinine is rising. How do you manage this?"

EXCEPTIONAL ANSWER

This patient has developed rhabdomyolysis following delayed fasciotomy for compartment syndrome. The dark tea-colored urine indicates myoglobinuria, and the elevated CK (25,000 U/L) confirms significant muscle breakdown. I would manage this aggressively: First, aggressive IV fluid resuscitation - I would aim for urine output over 200ml/hr, which typically requires 4-6L of fluid in the first 24 hours. I would use normal saline or lactated Ringer's. Second, urine alkalinization - I would add sodium bicarbonate to the IV fluids to maintain urine pH over 6.5. This prevents myoglobin precipitation in the renal tubules, which is the mechanism of acute kidney injury. Third, close monitoring - I would check CK, potassium, and creatinine every 6-12 hours. I would monitor ECG continuously for hyperkalemia signs (peaked T-waves, widened QRS). Fourth, avoid nephrotoxins - no NSAIDs, avoid contrast if possible. Fifth, consider ICU admission if severe or if hyperkalemia develops. The key is preventing acute kidney injury through aggressive fluid resuscitation and urine alkalinization. Most patients recover renal function if treated early and appropriately.

KEY POINTS TO SCORE

Recognize myoglobinuria (dark tea-colored urine)

Aggressive IV fluids (target 200ml/hr urine output)

Alkalinize urine (sodium bicarbonate, pH over 6.5)

Monitor CK, potassium, creatinine, ECG

Prevent AKI through early aggressive treatment

COMMON TRAPS

✗Not recognizing myoglobinuria as sign of rhabdomyolysis

✗Inadequate fluid resuscitation - must target 200ml/hr

✗Not alkalinizing urine - key to preventing AKI

✗Missing hyperkalemia - life-threatening complication

LIKELY FOLLOW-UPS

"What if the patient develops hyperkalemia?"

"When would you consider dialysis?"

"How long do you continue aggressive management?"

VIVA SCENARIOChallenging

Scenario 2: Crush Injury Rhabdomyolysis

EXAMINER

"A 45-year-old construction worker is extracted from a building collapse after 8 hours. He has a crushed leg, is hypotensive, and his urine is dark. CK is 75,000 U/L, potassium is 6.8mmol/L, and ECG shows peaked T-waves. Describe your immediate management."

EXCEPTIONAL ANSWER

This is a severe case of rhabdomyolysis from crush injury with life-threatening hyperkalemia. I would manage this as an emergency: First, immediate hyperkalemia treatment - IV calcium gluconate 10ml 10% (cardioprotective, stabilizes cardiac membrane), then insulin 10 units with 50ml 50% dextrose (drives potassium into cells), and sodium bicarbonate (alkalinizes, shifts potassium). This is urgent as hyperkalemia can cause cardiac arrest. Second, aggressive fluid resuscitation - large-bore IV access, bolus 1-2L normal saline, then maintain urine output over 200ml/hr. This requires 4-6L in first 24 hours. Third, urine alkalinization - add sodium bicarbonate to IV fluids to maintain urine pH over 6.5. Fourth, immediate ICU admission for continuous monitoring - ECG, potassium levels, renal function. Fifth, assess the crushed leg - may need fasciotomy if compartment syndrome present, or may need amputation if limb non-viable. Sixth, consider early dialysis if hyperkalemia refractory or if severe AKI developing. The hyperkalemia is the immediate life threat - must treat before addressing other issues. Most patients with crush injury rhabdomyolysis require ICU care initially.

KEY POINTS TO SCORE

Hyperkalemia is life-threatening - treat immediately

IV calcium (cardioprotective), insulin/glucose, bicarbonate

Aggressive fluids and urine alkalinization

ICU admission for monitoring

Consider dialysis if refractory

COMMON TRAPS

✗Not treating hyperkalemia immediately - can cause cardiac arrest

✗Inadequate fluid resuscitation

✗Not recognizing severity - needs ICU

✗Delaying dialysis if needed

LIKELY FOLLOW-UPS

"What are the ECG changes of hyperkalemia?"

"When would you dialyze this patient?"

"How do you manage the crushed limb?"

VIVA SCENARIOCritical

Scenario 3: Delayed Recognition

EXAMINER

"A 28-year-old athlete presents 48 hours after a marathon with severe muscle pain, weakness, and dark urine. CK is 45,000 U/L, creatinine is 250 micromol/L, and urine output is 30ml/hr. How do you manage this?"

EXCEPTIONAL ANSWER

This is exertional rhabdomyolysis with established acute kidney injury. The delayed presentation (48 hours) and low urine output indicate AKI is already developing. I would manage aggressively: First, immediate aggressive fluid resuscitation - large-bore IV access, bolus 1-2L normal saline, then maintain high urine output target (over 200ml/hr if possible, though may be difficult with established AKI). Second, urine alkalinization - add sodium bicarbonate to IV fluids to maintain urine pH over 6.5. Third, nephrology consultation - established AKI may require dialysis. Fourth, monitor closely - serial CK, potassium, creatinine, ECG. Fifth, avoid nephrotoxins - no NSAIDs, no contrast. Sixth, consider ICU admission for close monitoring and potential dialysis. The key challenge is that AKI is already established - aggressive management may still help, but dialysis may be needed. Most patients recover renal function even with established AKI if treated appropriately, though recovery takes longer.

KEY POINTS TO SCORE

Established AKI from delayed presentation

Aggressive fluids still indicated

Urine alkalinization essential

Nephrology consultation for potential dialysis

Most recover renal function with treatment

COMMON TRAPS

✗Not being aggressive enough - still need fluids and alkalinization

✗Not consulting nephrology - may need dialysis

✗Giving up - most recover even with established AKI

✗Using nephrotoxins - will worsen AKI

LIKELY FOLLOW-UPS

"What are the indications for dialysis in rhabdomyolysis?"

"How long does renal recovery take?"

"What is the prognosis for established AKI?"

MCQ Practice Points

CK Threshold Question

Q: What is the diagnostic threshold for rhabdomyolysis? A: CK over 10,000 U/L - this is the widely accepted diagnostic threshold. Levels can exceed 100,000 in severe cases. CK peaks at 24-48 hours after injury, then declines if treated appropriately.

Myoglobinuria Question

Q: What is the clinical sign of myoglobinuria? A: Dark tea-colored or cola-colored urine - this indicates significant myoglobin release from muscle breakdown. Dipstick will be positive for blood, but microscopy shows no red blood cells (myoglobin, not hemoglobin).

Urine Output Target Question

Q: What is the target urine output for rhabdomyolysis management? A: Over 200ml/hr (or over 1ml/kg/hr) - this high urine flow prevents myoglobin precipitation in renal tubules and maintains renal perfusion. Requires aggressive IV fluid administration (4-6L first 24 hours).

Urine Alkalinization Question

Q: Why is urine alkalinization important in rhabdomyolysis? A: Myoglobin precipitates in acidic urine (pH under 5.6), causing tubular obstruction and AKI. Alkaline urine (pH over 6.5) prevents precipitation. Sodium bicarbonate is added to IV fluids to maintain urine pH over 6.5.

Hyperkalemia Question

Q: Why does rhabdomyolysis cause hyperkalemia? A: Massive muscle necrosis releases intracellular potassium into circulation. This can cause life-threatening hyperkalemia with cardiac arrhythmias. Requires immediate treatment (calcium, insulin/glucose, bicarbonate) and may need dialysis.

Australian Context and Medicolegal Considerations

Healthcare System:

Rhabdomyolysis management available in all major hospitals
ICU capacity for severe cases
Dialysis services available
Trauma centers equipped for crush injuries

Medicolegal Considerations:

Documentation: Time of injury, time to fasciotomy (if compartment syndrome), CK levels, urine output, treatment provided
Recognition: Early recognition and treatment prevent complications
Monitoring: Serial CK, potassium, creatinine monitoring documented
Communication: ICU consultation if severe, nephrology if AKI

Common Issues:

Delayed recognition of rhabdomyolysis post-fasciotomy
Inadequate fluid resuscitation
Failure to alkalinize urine
Missing hyperkalemia

Medicolegal Risk

Failure to recognize and treat rhabdomyolysis can lead to preventable acute kidney injury and death. Always monitor for rhabdomyolysis after compartment syndrome, especially if fasciotomy was delayed. Document all monitoring and treatment.

RHABDOMYOLYSIS

High-Yield Exam Summary

Key Facts

•CK over 10,000 U/L is diagnostic threshold
•Dark tea-colored urine = myoglobinuria
•Compartment syndrome is most common orthopaedic cause
•CK peaks at 24-48 hours, then declines

Management (FARM)

•Fluids Aggressive: Target 200ml/hr urine output (4-6L first 24h)
•Alkalinize urine: Sodium bicarbonate to pH over 6.5
•Renal protection: Prevent myoglobin tubular obstruction
•Monitor: CK, potassium, creatinine, ECG

Hyperkalemia Treatment

•IV Calcium (cardioprotective, stabilizes membrane)
•Insulin/Glucose (drives K+ into cells)
•Sodium Bicarbonate (alkalinizes, shifts K+)
•Dialysis if refractory or severe

Complications

•Acute kidney injury: 30-50% if untreated
•Hyperkalemia: Life-threatening, cardiac risk
•Hypocalcemia early, hypercalcemia late
•Most recover with appropriate treatment

CK Level

Myoglobinuria

Urine Output

Management

5,000-10,000

Absent

Normal

IV fluids, monitor CK

10,000-50,000

Present

Target 200ml/hr

Aggressive fluids, alkalinize urine

Over 50,000

Severe

Over 200ml/hr

ICU, consider dialysis

Severity

CK Level

Myoglobinuria

Management

Mild

5,000-10,000 U/L

Absent

IV fluids, monitor

Moderate

10,000-50,000 U/L

Present

Aggressive fluids, alkalinize urine

Severe

Over 50,000 U/L

Severe

ICU, dialysis if needed

Stage

Process

Consequence

Injury

Muscle cell membrane disruption

Release of intracellular contents

Circulation

CK, myoglobin, K+, PO4 enter blood

Elevated serum markers

Kidney

Myoglobin filtered, precipitates in acidic urine

Tubular obstruction

AKI

Tubular necrosis, decreased GFR

Acute kidney injury

Test

Finding

Significance

CK (creatine kinase)

Over 10,000 U/L (diagnostic)

Peaks 24-48h, then declines

Myoglobin (serum)

Elevated

Confirms muscle breakdown

Myoglobin (urine)

Positive

Dark urine, tubular obstruction risk

Potassium

Hyperkalemia

Cardiac risk - monitor ECG

Creatinine

Rising

AKI developing

Phosphate

Elevated

Muscle breakdown

Calcium

Hypocalcemia early

Precipitates in necrotic muscle

Aggressive IV Fluid Therapy

Goal: Maintain urine output over 200ml/hr (or over 1ml/kg/hr)

Protocol:

Initial: 1-2L bolus if dehydrated
Maintenance: 4-6L over first 24 hours
Type: Normal saline or lactated Ringer's
Monitoring: Hourly urine output, daily weights, clinical assessment

Rationale:

High urine flow prevents myoglobin precipitation
Maintains renal perfusion
Prevents tubular obstruction

Fluid Target

Target urine output over 200ml/hr (or over 1ml/kg/hr) is essential to prevent myoglobin tubular obstruction. This requires aggressive IV fluid administration - 4-6L in first 24 hours is common.

Complication

Incidence

Management

Acute kidney injury

30-50% if untreated

Prevent with aggressive fluids, alkalinization

Hyperkalemia

Common in severe cases

Monitor ECG, treat with calcium/insulin/bicarb

Hypocalcemia (early)

Common

Usually resolves, avoid overcorrection

Hypercalcemia (late)

During recovery

Calcium released from necrotic muscle

Compartment syndrome

If underlying cause

Fasciotomy if present

DIC

Rare

Supportive care

Category	Examples	Mechanism
Traumatic	Compartment syndrome, crush injury	Muscle ischemia/necrosis
Exertional	Exercise, heat stroke	Metabolic exhaustion
Drug-induced	Statins, alcohol	Direct muscle toxicity
Metabolic	Hypophosphatemia, hypokalemia	Electrolyte imbalance
Infectious	Viral myositis	Direct muscle infection

Category	Examples	Mechanism
Traumatic	Compartment syndrome, crush injury	Muscle ischemia/necrosis
Exertional	Exercise, heat stroke	Metabolic exhaustion
Drug-induced	Statins, alcohol	Direct muscle toxicity
Metabolic	Hypophosphatemia, hypokalemia	Electrolyte imbalance
Infectious	Viral myositis	Direct muscle infection

Rhabdomyolysis

Rhabdomyolysis

RHABDOMYOLYSIS

RHABDOMYOLYSIS SEVERITY

Critical Must-Knows

Examiner's Pearls

Clinical Imaging

Imaging Gallery

Critical Rhabdomyolysis Exam Points

Myoglobinuria is Key Sign

CK Threshold

Acute Kidney Injury Prevention

Hyperkalemia Risk

Rhabdomyolysis Management by Severity - Quick Reference

FARMRhabdomyolysis Management

CRUSHRhabdomyolysis Causes

BICARBMyoglobinuria Management

Overview and Epidemiology

Anatomy and Pathophysiology

Classification Systems

Rhabdomyolysis Severity

Severity Classification by CK Level

Causes of Rhabdomyolysis

Etiology Classification

Pathophysiology Details

Rhabdomyolysis Pathophysiology

Hyperkalemia is Life-Threatening

Clinical Assessment

Muscle Findings

Systemic Signs

Investigations

Essential Laboratory Tests

Laboratory Monitoring

Urinary Sediment Findings

Management Algorithm

CK 5,000-10,000, No Myoglobinuria

CK 10,000-50,000, Myoglobinuria Present

CK Over 50,000, AKI, Hyperkalemia

Surgical Technique

Fasciotomy Technique (When Rhabdomyolysis Present)

Crush Injury Surgical Considerations

Treatment Details

Aggressive IV Fluid Therapy

Sodium Bicarbonate Therapy

Alkalinization Caution

Hyperkalemia Treatment

When Dialysis is Needed

Complications

Rhabdomyolysis Complications

Postoperative Care

Post-Fasciotomy Rhabdomyolysis Management

Outcomes and Prognosis

Evidence Base

Rhabdomyolysis and Acute Kidney Injury

Compartment Syndrome and Rhabdomyolysis

Hyperkalemia in Rhabdomyolysis

Crush Injury and Rhabdomyolysis

Urine Alkalinization in Rhabdomyolysis

Exam Viva Scenarios

Scenario 1: Post-Fasciotomy Rhabdomyolysis

Scenario 2: Crush Injury Rhabdomyolysis

Scenario 3: Delayed Recognition

MCQ Practice Points

Australian Context and Medicolegal Considerations

Medicolegal Risk

RHABDOMYOLYSIS

Key Facts

Management (FARM)

Hyperkalemia Treatment

Complications

Rhabdomyolysis

Rhabdomyolysis

RHABDOMYOLYSIS

RHABDOMYOLYSIS SEVERITY

Critical Must-Knows

Examiner's Pearls

Clinical Imaging

Imaging Gallery

Critical Rhabdomyolysis Exam Points

Myoglobinuria is Key Sign