Carbon monoxide poisoning: what about hyperbaric oxygen?

Abstract

Hyperbaric oxygen (HBO) is used since more than 50 years for carbon monoxide poisoning. However, HBO protocols and indications are still debated. Neurological (coma and delayed neuropsychological sequelae) and cardiac (ischemic changes with normal coronary arteries) clinical scenarios are explained by complex mechanisms. Carboxyhemoglobin formation, cytochrome oxydase inhibition, oxidative stress, as well as ischemia-reperfusion phenomenon are among these mechanisms. Venous and arterial carboxyhemoglobin levels are not correlated with the patient’s final prognosis and thus not mandatory for indicating the treatment. Conversely, troponin IC measurement is strongly recommended if myocardial involvement is suspected. HBO treatment relies on mechanistic bases: earlier detoxification, anti-oxidant properties, and improvement in cerebral physiology (decrease in intracranial pressure and oedema, and ischemic penumbra preservation). Clinical basis is assessed by the results of the randomized clinical trials (RCTs). Four among the 5 RCTs using > 2 ATA OHB protocols were positive. Two RCTs at 2 ATA level were negative. Therefore, international guidelines recommend OHB with at least 2.5 ATA in patients at risk of delayed neuropsychological sequelae, whatever the objective neurological signs are, in pregnant women, and patients with myocardial involvement. If OHB is not required, normobaric oxygen with high flow rates during at least 8-12 hours is mandatory.