Clinical Presentation and Investigations of Crush Syndrome

 MED-NERD



Clinical presentation of crush syndrome:



The release of muscle components including myoglobin and electrolytes affect various organs including the heart, kidney, the metabolic and acid-base balance. Sudden release of compressive forces of a crushed limb is associated with a condition known as reperfusion syndrome which is characterized by metabolic abnormalities, acute hypovolemia, and may lead to fatal cardiac arrhythmias.

According to the organ or the system affected, clinical presentation can be classified as the following:


1-Limbs injury:

Peripheral limb injury ranges from superficial injuries, petechiae, erythema, muscle blisters, swelling, bruising, open fractures, rhabdomyolysis, sensory deficit, paralysis, myalgia and deformities.


2-Chest injury:

Chest compression causes increase in intrathoracic pressure, pulmonary contusions, fracture of ribs, pneumothorax, hemothorax. Pneumonia and fever may also occur.


3-Renal damage:

Muscle injury and rhabdomyolysis lead to release of muscle components including myoglobin, creatinine, potassium, and phosphorous into the blood circulation. If treatments of myoglobinuria is delayed, renal tubular necrosis occur. Moreover, metabolic abnormalities occur due to the release of electrolytes from ischemic muscles. The results of renal damage include oliguria, haematuria or dark urine, and renal failure.


4-Metabolic Abnormalities:

-systemic hypocalcaemia >> due to entry of calcium through the muscle cell membrane

-hyperkalaemia >> due to releasing potassium from ischemic muscle into the circulation

-Imbalance of calcium and potassium may cause cardiac arrhythmias and cardiac arrest

-Metabolic acidosis >> due to releasing lactic acid from ischemic muscle into the circulation. Metabolic acidosis may worsen cardiac arrhythmias.


5-Cardiovascular system impairment:

Cardiovascular damage include tachycardia, cardiac dysrhythmias, haemorrhage, hypovolemia, hypotension, and pallor. Hypotension may worsen renal failure. Third space loss requires fluid therapy during the first 24 hours. More than 12 L of fluid may be trapped in crushed area over 48 hours. Compartment syndrome is a swelling in a closed anatomical space which worsens vascular abnormalities and usually require fasciotomy.


6-Other symptoms:

Delirium, agitation, nausea, and vomiting.




Investigations of crush syndrome:


-Complete Blood Count (CBC)

-Coagulation studies

-Serum creatinine kinase (CKMM) >> normal range of serum creatinine kinase (CKMM) is 25-175 U/l. Greater than 1000 IU/l level of serum creatinine kinase (CKMM) is usually considered an indicator of crush syndrome. CKMM level after a crush injury usually rises after 2-12 hours, reaches maximum within 1 to 3 days, and decreases after 3-5 days.

-Serum myoglobin and myoglobin degradation products >> highly sensitive

-Serum aldolase

-Serum aspartate aminotransferase (AST), alanine transaminase (ALT), lactate dehydrogenase (LDH), Lactic acid >> show steady elevation

-Serum uric acid >> shows moderate elevation

-Serum urea and creatinine >> show steep elevation after prolonged crush injury

-Serum potassium >> early elevation is detected and is a predictor for dialysis

-Serum calcium levels >> show hypocalcaemia

-Blood glucose >> stress related hyperglycaemia may occur

-Arterial Blood Gases (ABGs) >> show acidosis

-Haemogram and Electrocardiogram (ECG)

-Intracompartmental pressure monitoring >> levels greater than 30 mm Hg are indicators for fasciotomy

-Doppler >> to detect limb ischemia

-Emergency CT

-Kidney function tests

-Urine analysis >> show the presence of myoglobin products and creatine kinase

-Measuring body weight




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