Abstract
Acute aortic occlusion is a rare but catastrophic disease with a high mortality rate. Severe perioperative complications could result from revascularization of infarcted muscles. Muscle cell ischaemia and massive volume cell death lead to the release of myoglobin, potassium, and lactic acid, which could be fatal if not recognised or treated early. We highlight the life-threatening adverse effects resulting from bulk tissue infarction from non-traumatic causes such as aortic occlusion followed by the metabolic sequelae of reperfusion. This is similar to the pathophysiology of traumatic crush injuries and rhabdomyolysis. The case highlights the vigorous pre-emptive treatment of acidosis and hyperkalaemia required during surgical revascularisation to potentially avert adverse surgical outcomes in acute aortic obstruction.
Highlights
We describe the de novo hyperacute development of totally occlusive extensive infrarenal aortic thrombus that progressed to bilateral limb-threatening ischaemia that on surgical reperfusion led to a metabolic surge (acidaemia, hyperkalaemia) that eventuated in irreversible cardiac arrest
Acute aortic occlusion is a rarely encountered but frequently fatal emergency, resulting from de novo thrombus formation subjacent to atherosclerotic aortic mucosal lining or the peripheral embolisation of dislodged centrally located thrombus to obstruct a previously healthy aorta
We describe the de novo hyperacute development of totally occlusive extensive infrarenal aortic thrombus that progressed to bilateral limb-threatening ischaemia that on surgical reperfusion led to a metabolic surge that eventuated in irreversible cardiac arrest
Summary
We describe the de novo hyperacute development of totally occlusive extensive infrarenal aortic thrombus that progressed to bilateral limb-threatening ischaemia that on surgical reperfusion led to a metabolic surge (acidaemia, hyperkalaemia) that eventuated in irreversible cardiac arrest. The case highlights the need to anticipate early, and pre-emptively treat, life-threatening toxic metabolic surge from acute compartment release and reperfusion of non-traumatic bulk tissue infarction, a risk well recognised in rhabdomyolysis from traumatic crush injury. The lower limb muscle compartments were not firm or tender, and active extension of the knee and ankle did not exacerbate pain.
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