Hypocalcaemia is the Expected Early Abnormality in Crush Injury
The correct answer is (b) hypocalcaemia, which occurs universally in crush injury patients from the earliest stages and persists throughout hospitalization.
Pathophysiology of Early Hypocalcaemia
Hypocalcaemia develops immediately in crush injury through multiple mechanisms:
- Calcium sequestration into damaged muscle tissue occurs as injured myocytes take up calcium from the extracellular space, creating a massive calcium sink in the crushed compartments 1, 2
- Precipitation with released phosphate from muscle breakdown creates calcium-phosphate complexes that further deplete ionized calcium 1
- Hypovolemia and acidosis from third-spacing and tissue ischemia compound the problem by affecting calcium homeostasis 3, 2
Clinical Evidence Supporting Hypocalcaemia
The evidence overwhelmingly demonstrates hypocalcaemia as the hallmark early abnormality:
- 100% of crush syndrome patients were hypocalcemic on admission in a comprehensive study of earthquake victims, with 92.3% remaining hypocalcemic after 10 days of treatment 1
- European trauma guidelines specifically recommend monitoring ionized calcium levels during massive transfusion in trauma patients, emphasizing that early hypocalcaemia following traumatic injury shows significant correlation with injury severity 3
- Hypocalcaemia causes life-threatening arrhythmias and must be treated urgently in crush injury patients 2
Why the Other Options Are Incorrect
Hyperkalaemia (not hypokalaemia) is the actual electrolyte abnormality seen:
- Life-threatening hyperkalemia occurs even before extrication from entrapment as potassium is released from damaged muscle cells 4, 2
- Potassium-containing fluids like Lactated Ringer's must be avoided in crush injury management 5
Hyperphosphataemia (not hypophosphataemia) is characteristic:
- 90.5% of crush syndrome patients had hyperphosphatemia on admission, with 66.7% still affected after 10 days 1
- Phosphate release from muscle breakdown contributes to calcium precipitation 1
Metabolic acidosis (not alkalosis) develops:
- Crush injury causes metabolic acidosis from tissue ischemia, lactic acid accumulation, and release of acidic metabolites from damaged muscle 3, 2, 6
- Dialysis is initiated for life-threatening acidosis in severe cases 3, 7
Hyperuricemia (not hypouricemia) occurs:
- Uric acid is released from damaged tissue and accumulates, particularly when renal function is compromised 6
Clinical Implications
The universal presence of hypocalcaemia has critical management implications:
- Calcium supplementation should be considered a primary intervention in severe crush injury, as hypocalcaemia potentiates coagulopathy and cardiovascular instability 8
- Avoid bicarbonate administration in large doses during initial resuscitation, as alkalinization decreases free ionized calcium and worsens the existing hypocalcemia 3
- Monitor ionized calcium levels closely as total calcium measurements may be misleading due to protein binding alterations 3
Common Pitfall
A critical error is administering aggressive bicarbonate therapy for acidosis without recognizing that this will precipitate severe symptomatic hypocalcaemia by further decreasing the ionized calcium fraction 3. The guideline evidence shows that current data does not support active alkalinization over aggressive fluid resuscitation alone 7.