crush syndrome comprises of compartment syndrome and crush injury. its effects , pathophysiology and management is discussed. it will be helpful for post graduate orthopaedic theory exam

1. CRUSH INJURY
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.
The diagnostic criteria for crush syndrome are:
• Crushing injury to a large mass of skeletal muscle.
• The sensory and motor disturbances in the compressed limbs, which subsequently
become tense and swollen.
• Myoglobinuria and/or hematuria.
• Peak creatine kinase (CK) > 1000 U/L.
Patients with nephrological problems are defined as crush injury and one of the following
characteristic:
- oliguria (urine output <400 ml/24 h),
- elevated levels of blood urea nitrogen (BUN) (>40 mg/dl),
- serum creatinine (2 mg/dl),
- uric acid (8 mg/dl),
- potassium (>6 mg/dl),
- phosphorus (> 8 mg/dl),
- decreased serum calcium (< 8 mg/dl)12
.
PATHOGENESIS AND CLINICAL FEATURES
The mechanism behind the crush syndrome is the leakiness of the sarcolemmal
membrane caused by pressure or stretching. A crush insult opens stretch-activated
channels in the muscle cell membrane and disrupts the Na/K transporter, allowing
calcium to move freely into the cell. As the sarcolemmal membrane is stretched, sodium,
calcium and water leak into the sarcoplasm, trapping extracellular fluid inside the
muscle cells (Table 1). In addition to the influx of these elements into the cell, the cell
releases potassium and other toxic substances such as myoglobin, phosphate and
urate into the circulation. The post-ischemic tissues have high concentrations of
neutrophil chemoattractants, leading to activation of neutrophils with release of
proteolytic enzymes and generation of free radical superoxide anions once perfusion is
restored.

2. The result
- hypovolemic shock,
- hyperkalaemia,
- metabolic acidosis,
- compartment syndrome, and
- acute renal failure.
Following systems are compromised
1.CVS: due to hyperkalemia. Hypocalcemia and hypovolemic shock
2.Respiratory: ARDS from inflammatory mediators and pulmonary edema which occurs
during treatment of ARF with excessive crystalloids
3.Hematolical: DIC due to systemic inflammation
4.Infection: due to fasciotomies
5.Renal: The ARF is caused by
- hypovolemia with subsequent renal vasoconstriction,
- metabolic acidosis
- nephrotoxic substances such as myoglobin, urate and phosphate.
6.Compartment syndrome
Compartment syndrome occurs after crush because of the uptake of fluid into muscle
cells contained within a tight compartment. Once compartment pressure exceeds capillary
perfusion pressure at about 30 mmHg, the tissue inside the compartment becomes
ischemic, and compartment syndrome develops.

3. Table 1: Flow of solutes and water across the sarcolemma in
rhabdomyolysis.
Consequences
Influx from extracellular compartment into muscle cells
Water, sodium
chloride, and
calcium
Hypovolemia and hemodynamic shock, prerenal
and acute renal failure; hypocalcemia, aggravated
hyperkalemic cardiotoxicity; increased cytosolic
calcium, activation of cytotoxic proteases
Efflux from damaged muscle cell
Potassium
Hyperkaliemia and cardiotoxicity aggravated by
hypocalcemia and hypotension
Purines from
disintegrating cell
nuclei
Hyperuricemia, nephrotoxicity
Phosphate
Hyperphsphatemia, aggravation of hypercalcemia,
and metastatic calcification, including the kidney
Lactic acid and
other organic acids
Metabolic acidosis and aciduria
Myoglobin
Nephrotoxicity, particularly with coexisting
oliguria, aciduria, and uricosuria
Thromboplastin Disseminated intravascular coagulation
Creatine kinase Extreme elevation of serum creatine kinase level
Creatinine Increased serum creatinine
APPROACH TO TREATMENT
• The treatment of crushed casualties should begin as soon as they are discovered.
Administer 2 amps of Sodium Bicarb just prior to extrication
• After airway, breathing, and circulation are assessed, if possible, the oxygen and
any obvious hemorrhage should be controlled.

4. • Intravenous access should be obtained, and the patient should receive fluid. The
most critical therapy in crush syndrome is early and aggressive fluid resuscitation
with 0.9% saline to restore circulating blood volume.
• Patient should be urine catheterized.
• Once in hospital, ECG, electrolytes, arterial blood gases, and muscle enzymes
should be measured.
• Administer 1 amp of Calcium Chloride if dysrhythmias continue
Fluid-resuscitation :
In the adult, a saline infusion of 1000-1500 ml/h should be initiated during extrication.
When a urine flow has been established, a forced mannitol-alkaline diuresis up to 8 L/d
should be maintained (urine pH greater than 6.5). Mannitol for three purposes, as an
osmotic diuretic, as a free-radical scavenger, and as an osmotic agent, to reduce the
swelling of the affected limb and decrease the risk of compartment syndrome.
Once the patient reaches hospital, 5% dextrose should be alternated with normal saline to
reduce the potential sodium load.
Alkalinization increases the urine solubility of acid hematin and aids in its excretion. This
may protect against renal failure and should be continued until myoglobin is no longer
detectable in the urine. In addition to its protective effect as an osmotic diuretic, mannitol
also is an effective scavenger of oxygen free radicals and may help reduce the reperfusion
component of this injury by this mechanism
The treatment of compartment syndrome is still the subject of debate, although evidence
would point to a trial of conservative management before fasciotomy.