Crush syndrome is caused by prolonged pressure on muscle tissue, leading to rhabdomyolysis. This releases myoglobin and other intracellular contents into the bloodstream, which can cause kidney damage, metabolic abnormalities, and complications affecting other organs. Treatment involves aggressive fluid resuscitation, dialysis if needed to manage kidney dysfunction, and surgery such as fasciotomy to release pressure in compartments. Early medical management is important to prevent further complications from crush syndrome.

1. CRUSH
SYNDROME
SARVARSH SINGH SAINI
57-

2. DEFINITION
• Crush syndrome is the systemic manifestation
of RHABDOMYOLYSIS caused by prolonged continuous
pressure on muscle tissue.
• Crush syndrome includes crush injury and compartment
syndrome.

3. CAUSES OF CRUSH SYNDROME
Immobility against firm surface for > 1 hour
• Drug or alcohol intoxication.
• Carbon monoxide poisoning.
• Cerebrovascular accident.
• Head trauma with coma.
• Elderly with hip fracture.
• Improper positioning of
surgical patient.
• Assault with beating.
• Pneumatic antishock
garment(PASG OR MAST)

4. PATHOPHYSIOLOGY
Stretch of muscle sarcolemma
Sarcolemma permeability increases
Influx of sodium, water and extracellular
calcium into the sarcoplasm

5. Results in cellular swelling , ↑sed intracellular
calcium , disrupted cellular function &
respiration
↓sed ATP production
Subsequent myocytic death

7. CLINICAL FEATURES
• Petechiae , blisters and muscle bruising.
• Myalgia, muscle paralysis and sensory deficit are common.
• Fever, cardiac arrhythmia, pneumonia, (tea or cola) coloured
urine, oliguria and renal failure.
• Nausea, vomiting, agitation and delirium are seen in delayed
rescue patients

9. CONTENTS RELEASED DURING
RHABDOMYOLYSIS & THEIR EFFECTS
• Hyperkalemia & cardiotoxicity
• Provoked by hypocalcemia & hypovolemia.
Potassium
• Hyperphosphatemia.
• Metastatic calcification.
Phosphate
• Myoglobinuria.
• Nephrotoxicity.
Myoglobin

10. •Elevation of serum ck level
Creatine kinase
•Disseminated intravascular
coagulation
Thromboplastin
•Metabolic acidosis & aciduria
Organic acids

11. INVESTIGATIONS
• Complete haemogram.
• ECG
• Arterial blood gas analysis, myoglobin.
• Serum creatinine kinase (CKMM) > 1000IU/I with clinical feature is taken as
an indicator of crush syndrome. Peaks in 1 to 3 days.
• Normal range 25-175U/I.
• Serum aldolase, myoglobin degradation.

12. • Serum lactic acid, AST, ALT and LDH show steady rise.
• Serum urea and creatinine – steep rise after
prolonged crush.
• Serum potassium show early rise and is predictor for
dialysis.
• Intracompartmental pressure monitoring if > 30mm
Hg fasciotomy may be required.

13. TREATMENT
Medical
management
1.Fluid replacement
2.Ventilatory support
3.Correction of
metabolic acidosis
4. Dialysis if required
Surgical
management
1. Emergency
fasciotomy
2.Debridement of
nacrotic tissue
3. Delayed VAC and
skin grafting

14. FLUID RESUSCITATION
• It is the mainstay of treatment 0.9% normal saline is
preferred.
• Early most preferably within first 6 hours is essential.
• To counter metabolic acidosis bicarbonate and lactate or
even oral citrate is essential.
• 50 mmol of bicarbonate for every lit of isotonic saline is
used.

16. Diuresis-
• This is to maintain effective kidney function.
• Mannitol diuresis is indicated in setting of
compartment syndrome.
Dialysis-
• Important predictive factors:-
1. Anuria
2. Fluid overload
3. ↑sed creatinine level
4. ↑sed BUN and bicarbonate level

17. • Potassium > 7meq/l is independent and
important predictive factor for dialysis.
• It may be required for 15 days.
Hyperbaric oxygen-
It ↓ses outflow from vascular compartment
Reduces tissue edema promotes wound healing
by fibroblast proliferation
Reduces anaerobic bacterial growth

18. • Multiple broad spectrum non nephrotoxic antibiotic
may be needed.
Surgery-
• Laparotomy and thoracotomy with debridement of
necrosed muscles.
• Fasciotomy if compartmental pressure rises can be
done as early as possible.
• Fractures need fixation and conservative amputations
may have to be performed.