Carbon monoxide can be common cause of poisoning depending on your location or care of lower socioeconomic groups. It can be quite obvious if a fire has occurred or the patient admits to a suicide attempt. Symptoms can be a little more insidious and subtle if exposure has been chronic and hyper-vigilance is required.
- Carbon monoxide deaths almost exclusively occur pre-hospital.
- A thorough neurological exam and MMSE is required to identify those who have neuropsychological sequelae.
- All patients are at risk of neuropsychological sequelae and should be warned of this on discharge.
- High risk features include
- Significant loss of consciousness
- Persistent neurological dysfunction
- Metabolic acidosis
- Myocardial ischaemia
- Age over 55
- The unborn child (I know we all talk about fetal Hb having an even higher affinity for CO but that might be a little simplistic:Traditionally, it was thought that fetal hemoglobin had a high affinity for CO. Pregnant ewe studies show a delayed but substantive increase in COHb levels in fetuses, exceeding the level and duration of those in the mothers. Thus, it appeared that fetuses are a sink for CO and could be poisoned at levels lower than mothers. However, such data may not apply to humans because it vitro work shows that as opposed to sheep, human fetal hemoglobin actually has less affinity for CO than maternal hemoglobin, at a ratio of 0.8. Under conditions of low oxygenation and high 2,3-BPG, as in serious CO poisoning, the affinity of human fetal hemoglobin starts to approach that of maternal. The more important issue with maternal CO exposure is the precipitous decrease in fetal arterial oxygen content that occurs within minutes at CO concentrations of 3000 ppm. Therefore, the ensuing hypoxia of the fetus, rather than increase in fetal COHb, is of more concern.
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Correlation of COHb levels and clinical features (Adapted from the toxicology handbook) Used to confirm the diagnosis but are a poor indicator for outcome and are altered by any previous oxygen that has been applied or delayed presentation.
- <10% = Background level in a smoker
- 10% = Usually asymptomatic, slight headache
- 20% = Dizziness, nausea, dyspnoea, headache
- 30% = Vertigo, ataxia, visual disturbance
- 40% = Confusion, coma, seizures, syncope
- 50% = Cardiovascular compromise, respiratory failure, seizures, death
The show notes are presented as a ‘show and reveal‘ mini quiz.
- The application of oxygen. Patients who make it to hospital are very unlikely to die and require oxygen to reduce the half life of carbon monoxide. Those in the field or someone that comes in with a reduced GCS may require specific attention to their airway i.e. intubation but the overall objective is the same.
Risk assessment: Can you name the CNS and CVS symptoms associated with carbon monoxide exposure?
- CNS: Headahce, nausea, dizziness, confusion, mini mental status examination errors, incorrdination, ataxia, seizures and finally coma.
- CVS: Dysrhythmias, Ischaemia, hyper or hypotension.
- Non-cardiogenic pulmonary oedema
- Lactic acidosis
- Disseminated intravascular coagulation
- Sweat gland necrosis
- The acute exposure is usually a higher concentration of carbon monoxide for a brief period and is less likely to result in longterm sequelae.
- Chronic exposures have a lower dose of carbon monoxide for a long period and these are high risk for developing complications. These symptoms are usually non-specific but can include personality changes, poor concentration, dementia, psychosis, Parkinsonism, ataxia, peripheral neuropathy and hearing loss.
- Anyone with a neurological deficit will require neuropsychiatric testing in 1-2 months. Complications are present in 30% of survivors at 1 month and 6-10% at 12 months.
- A CT/MRI may demonstrate cerebral oedema, cerebral atrophy, basal ganglia injury or cortical demyelination.
- Foetal monitoring in the form of a CTG +/- an obstetric consultation.
- All pregnant patients
- Significant LOC
- Signs of ischaemia
- Significant neurological deficit
- Metabolic acidosis
- 8 hours of high flow.
- 24 hours of high flow if pregnant.
- This patient could be an index case and you need to inform his work and occupational health as their could be more victims. Similarly if you find someone has been poisoned at home, you need to ask about other members of the household and they should also be investigated.
- Buckley NA, Isbister GK, Stokes B et al. Hyperbaric Oxygen for Carbon Monoxide Poisoning: A Systematic Review and Critical Analysis of the Evidence. Toxicological Reviews 2005: 24(2):75-92.
- Juurlink DN, Buckley NA, Stanbrook MB et al. Hyperbaric oxygen for carbon monoxide poisoning. The Cochrane Database of Systematic Reviews 2005, Issue 1. Art. No.: CD002041.pub2. DOI: 10.1002/14651858.CD002041.pub2
- Scheinkestel CD, Bailey M, Myles PS et al. Hyperbaric or normobaric oxygen for acute carbon
- monoxide posioning: a randomised controlled clinical trial. Medical Journal of Australia 1999; 170:203–210.
- Weaver LK, Hopkins RO, Chan KJ et al. Hyperbaric oxygen for acute carbon monoxide poisoning. New England Journal of Medicine 2002; 347(14):1057–1067.
- Murray L, Little M, Pascu O, Hoggett K. Toxicology Handbook 3rd Edition. Elsevier 2015. ISBN 9780729542241