CRUSH INJURY

AND
RHABDOMYLOS
IS
DEFINITION
 Rhabdomyolisis is a syndrome character by muscle necrosis and the
release of muscle constituents into the circulation
ETIOLOGY
 Traumatic muscle injury
 Drugs and toxin
 Infection
 Genetic disorder
 Excessive muscle activity
 Ischemia
 Electrolyte and endocrine
 Immunologic disease
CLASSIFICATION
 Rhabdomyolisis

a. Traumatic/compression
 Multiple trauma

 Crush injury

 Surgery

 Coma

 Immobilization

b. Non traumatic
 Exertional: untrained exertion, marathon running, heat illness, seizures, metabolic myopaths,
malignant, neurodeptic malignant syndrome
 Non exertional: ETOH alcohol, drugs statin, infection, electrolytes hypokalemia, endocrine
hypothyroidsim
 PATHOPHYSIOLOGY
Tolerable-no
permanent
histological Muscle
changes necrosis
Hours of
0 2 4 6 DIE
ischemia
Irreversible
anatomic and
functional
changes
CLINICAL MANIFESTATION
AND DIAGNOSIS
 The classic presentation of rhabdomyolysis includes myalgia, red to brown
urine due to myoglobinuria, and elevated serum muscle enzymes
(including creatine kinase)
 TRIAD: Muscle pain, weakness, dark urine
 Fatigue
 Joint pain
 Seizures
 AKI
 Compartment syndrome
 Disseminated intravascular coagulation
LABORATORY FEATURES
 Urinalysis
 Serum potassium concentration
 Creatine kinase
 Acid-base balance
 Uric acid
 BUN/Cr
 Ca/Ph metabolism
 DIC
 Serum CKMM

Correlates with severity of rhabdomyolysis

Levels peaks within 24 hours >3000 high correlation with renal failure
 Serum myoglobin

T(1/2) 2-3 h
Excreted in bile
 UA-myoglobin

Dipstick will be (+) for hemoglobin, RBCs, and myoglobin

Microscopy: no RBCs, brown casts, uric acid crystals

Electrolyte Abnormalities
Hyperkalemia

Hyperphosphatemia

Hypocalcemia

hyperuricemia
MANAGEMENT
 Plasma volume expansion with intravenous isotonic saline should be given
as soon as possible, even while trying to establish the cause of the
rhabdomyolysis
 Treats the underlying cause of the rhabdomyolysis
 Monitor with the serial measurement of serum potassium, calcium,
phosphate, and creatinine, CPK is recommended
 The metabolic consequences and renal functional impairment due to
rhabdomyolysis should be anticipated, particularly potentially life threating
hyperkalemia
 Hypocalcemia usually self limited and rarely requires therapy
EARLY TREATMENT
FLUIDS
 Begins early, even on the field
 Ideally normal saline with bicarbonate prevents tubular precipitation,
reduces risk of hyperkalemia from damaged mm, corrects academia
LATE TREATMENT
DIALYSIS
 Intermitted preferred to continuous (reduce use of anticoagulants in
trauma)
SUMMARY OF TREATMENT
DO
 Isotonic fluids 1-2L/h UOP 200-300 ml/h

CONSIDER
 Sodium bicarbonate to cause forced alkaline diuresis ph <7,5 HCO3 <30 mEq/L

DON’T
 Loop diuretics
 Mannitol
 Ca supplementations