Carbon Monoxide Poisoning

Original article by Joseph Machta | Last updated on 28/6/2014
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Introduction

Carbon Monoxide (CO) poisoning, also known as the “silent killer” is a life-threatening situation. CO is an scentless, colourless gas (hence silent). Common clinical scenarios where CO poisoning alarm bells should start ringing include all patients involved in fire-related injuries, due to the risk of inhalation, as well as the typical story of the “family who are all feeling unwell, apart from Mum who has just gone to spend the weekend away with her parents”.
 

Aetiology

Intentional: CO poisoning may occur as a result of intentional suicidal poisoning, e.g. exposure to car exhaust fumes in a garage
Accidental: patients involved in fires, patients with unknown gas leaks at home

Signs and Symptoms

Symptoms: Headache, nausea and vomiting, malaise, lethargy, arrhythmia
Signs: very often, patients with CO poisoning will have no overt clinical signs but may be hypotensive. Oxygen saturations will be deceptively high. [The notion of “cherry red lips” common amongst medical students is an erroneous one – it is a rare and very late stage sign, so is of very little use clinically!]
 

Pathology

CO has a high affinity for haem proteins and so CO binds to haemoglobin with great ease – around 200x more effectively than oxygen – preventing oxygen from binding to the Hb, shifting the oxyhaemoglobin dissociation curve to the left and reducing the amount of oxygen accessible to cells and tissues.
 

Investigations

ABG: COHb - >30% is considered serious; bear in mind that levels of up to 15% may be detected in heavy smokers. Patients may have a metabolic acidosis on ABG too.
ECG should be performed to exclude any arrhythmias/cardiac ischaemia

Management

Patients should be started on 15L/min O2 (humidified) by tight fitting mask and reservoir for >24 hours – regardless of O2 saturations!
Hyperbaric O2 should be considered in patients with neurological impairment
 

Complications

Cerebral oedema, pulmonary oedema, MI, arrhythmia, barotrauma secondary to hyperbaric O2 therapy [creation of a pressure gradient across tympanic membrane, followed by haemorrhage/serious effusion]