Compartment syndrome resulting from carbon monoxide poisoning: a case report

Carbon monoxide (CO) poisoning is known to cause complications of the neurological, respiratory and cardiac systems. Rhabdomyolysis, acute kidney injury (AKI) and compartment syndrome (CS) are rarer complications. We herein present a patient who had CO poisoning and developed all these complications.

Case report

A 45-year-old male, immigrant beekeeper slept with coal fire on during a cold night. The next afternoon, his friends found him confused, with reduced level of consciousness. On admission to hospital, he was complaining of nausea, leg, chest and back pain.

He had no past medical history. On initial assessment, he was found to be conscious, oriented with oxygen saturation of 82% at room air. His heart and lung examinations were unremarkable. Abdomen examination revealed bilateral flank tenderness but no organomegaly.

Initial management of high-flow oxygen and intravenous fluids were given. A day after admission, it was noted that his left calf had swollen along the anterior and lateral compartment. Bedside point-of-care ultrasound revealed multicompartmental oedema suspicious of CS. Urgent fasciotomy was performed and a vacuum-assisted closure dressing was placed. In addition to CS, he developed rhabdomyolysis (Table 1, Figure 1), anuric AKI needing dialysis and type 2 myocardial injury. He needed kidney replacement therapy for a week, after which his AKI resolved. Echocardiogram was normal and troponins down-trended as well. He is now fully recovered.

View Table 1, Figure 1.

Discussion

CO is the most common poison that leads to death and injuries world-wide.¹ CO is a colourless, odourless, tasteless gas that results from incomplete combustion. CO poisoning rates spike during the colder season, when there is an increased use of indoor heating, gas heaters and chimneys. CO in lesser levels results in vague symptoms such as headache, nausea, vomiting, confusion, dizziness, visual disturbance and palpitations.² However, in higher or toxic amounts, CO can lead to hospitalisation and eventually death.³

The first ever case of CS associated CO poisoning was in the United States in 1977.⁴ Since then, there have only been a handful reported; this would be the first ever case reported in New Zealand.

The pathophysiology of CS-associated CO poisoning is still under speculation. There are at least three postulated mechanisms. The first is hypoxia and ischemia because of CO and its higher affinity for binding haemoglobin than that of oxygen.⁵ The displacement of oxygen from haemoglobin causes a shift of the oxygen–haemoglobin dissociation curve to the left, which results in inhibition of cytochromes/mitochondrial respiration and possible direct, toxic effects.⁶ The second is the direct toxicity of CO.⁷ A rise in oxygen-derived free radicals causes lipid peroxidation, leading to increased capillary permeability and thus CS.⁷ While the first two hypothesis are responsible for atraumatic causes of CS, the third hypothesis is more trauma related. It is a result of carboxyhaemoglobin buildup at the local muscle, thus raising pressure, resulting in swelling and CS.⁸

Our patient developed left leg CS. We suspect that CS was a result of combination of both ischemia and direct CO toxicity. Peripheral neuropathy and CS from CO poisoning has also been reported.⁹ However, our case had CS in absence of peripheral neuropathy.

This patient also developed rhabdomyolysis. AKI is a result of increased myoglobin and myoglobinuria causing direct damage to the renal tubules.¹⁰ Timely fasciotomy and resolution of CS resulted in apt renal recovery.

Conclusion

Our case is the first report of CO poisoning, CS and rhabdomyolysis with AKI in New Zealand. Prompt management with oxygen support, timely fasciotomy and dialysis helped in his speedy recovery. Emergency physicians and internists should be aware of these potential complications of CO poisoning.