Carbon Monoxide Poisoning- Rob Fenwick
A recent paper by Zorbalar et al (2014) from Turkey found that an astonishing 6.4% (n=483) of patients presenting to their emergency department (ED) with a headache over the winter period were found to have elevated CO levels. Even more worryingly, in 23% of these cases, carbon monoxide poisoning was occult i.e. not even suspected by the attending clinicians. Now whist I completely agree that the findings of this study are unlikely to be generalisable to everyone’s practice, it has led me to revisit this often overlooked topic and share some of information I found.
The scale of the problem
CO poisoning is the commonest cause of death by poisoning in the United Kingdom (UK) (Clarke et al 2005). In the United States (US) there may be up to 2,000 accidental deaths annually, resulting from around 50,000 exposures (Hampson & Weaver 2007).
Sources of exposure
Whilst domestic gas in the UK doesn’t contain CO, the combustion of any fuel gas in the absence of adequate oxygen and ventilation may lead to CO poisoning (Kumar & Clark 2012). Other sources may include the exhaust fumes of petrol engines and from certain appliances that use either propane or butane gases (Kumar & Clark 2012).
An additional and interesting potential source is methylene chloride. This is present in many paint strippers (and is potentially a substance which can be misused through inhalation), is metabolised by the liver into CO and could potentially be an atypical presentation (Kumar & Clark 2012).
During exposure, CO binds to haemoglobin with 210 times the affinity of oxygen. The carboxyhaemoglobin (COHB) subsequently decreases the oxygen-carrying and oxygen-delivery capacity of the blood, leading to hypoxia, resultant end organ damage and occasionally death (Buckley et al 2011).
Can peripheral oxygen saturations help with diagnosis?
The limitations of current peripheral oxygen saturation devices means that they are unreliable in carbon monoxide poisoning and always overestimate the arterial oxygen saturation when COHB exceeds 25% (Hampson 1998).
What are the problems for clinicians?
There are several elements relating to CO poisoning that in my opinion make it really challenging:
- CO is a colourless, odourless and non-irritant gas (Wright 2002) – This means that your patient is unlikely to think of it as a potential cause for their illness (and is less likely to bring it to your attention).
- The symptoms are vague…… really vague. A list of the common symptoms can be seen in table 2, but just think of how many patients you see each and every day who might have one of these symptoms, and the huge list of differentials for each one (Wright 2002). It has been suggested however, that headaches are the most common symptom and could potentially be the best single indicator to prompt screening (Zorbalar et al 2014).
- The diagnosis is made really infrequently – therefore clinicians forget about it (Wright 2002).
- Peripheral oxygen saturations aren’t useful in detecting hypoxia due to CO poisoning – The limitations of current peripheral oxygen saturation devices means that they are unreliable in carbon monoxide poisoning and always overestimate the arterial oxygen saturation when COHB exceeds 25% (Hampson 1998).
- You need a way of measuring COHB. The most common method in-hospital is to use a blood gas analyser – but you need to know which one in your hospital will perform the test for you, and if its working today. Contrary to popular belief, a venous sample is sufficient which means you can save your patient that painful arterial sample (Wright 2002). For those working in pre-hospital care, some monitors have CO monitoring peripherally via SpCO devices (I’ve seen them used on the Lifepak 15), but detection will depend upon whether your service is using these, and whether they are able to provide them on all vehicles.
Table 1 – Common symptoms caused by CO poisoning (Wright 2002)
|Vomiting and Diarrhoea|
|Loss of Conciousness|
So when do we need to worry?
Unfortunately the classical pink appearance of the skin, which has been described in many early texts, is in fact an extremely late sign that is most commonly noted after death, so please don’t wait for this before suspecting CO as a potential cause for the deteriorating patient (Kumar & Clark 2012).
Table 2 demonstrates the progressive relationship between percentage of COHB and development of symptoms. Kumar and Clark (2012) also report that hypotension, bradycardia and bradypnoea are common when levels rise to over 60%.
Another study has also demonstrated a strong correlation between COHB levels of over 45% during an episode of acute CO poisoning and the development of acute myocardial infarction within 56 months of the event (Kaya et al 2016). Despite this relationship the exact mechanisms of this effect remain unclear currently.
Table 2 – Significance of carboxyhaemoglobin levels (Harty et al 2008 & Blumenthal 2001)
|5-10%||Normal in Smokers|
|>10%||Potentially pathological and patients generally become symptomatic.|
|>40%||Generally associated with coma and death|
Thankfully the treatment options are slightly more straightforward than the recognition.
- Remove the patient from the site of exposure.
- Administer high flow oxygen. The elimination half-life of COHB is around 300 minutes (5 hours) in room air but this is shortened to just 1 hour by the administration of 100% oxygen.
- Support ABCD. Remember that as COHB progressively rises there will be a multitude of systemic effects that may require intensive and invasive support during treatment.
- Consider hyperbaric oxygen (HBO) treatment. A Cochrane systematic review found that some patients with “severe” poisoning may derive benefit from treatment (Buckley et al 2011). The absence of definitive evidence for when to initiate this treatment makes recommendations difficult to determine and perhaps the best approach might be to discuss all symptomatic cases with your local hyperbaric medicine centre.
- CO poisoning is difficult to identify because of a number of factors.
- When assessing patients with vague symptoms, it may be worthwhile taking that blood gas you were getting anyway, to the device that will also tell you their COHB..…. It might just surprise you.
- A venous COHB is just fine – save your patient that arterial sample.
- The treatment is pretty simple – support ABC’s, give high flow oxygen and consider contacting a HBO centre.
- Finally………..Refresh your knowledge on CO poisoning every once in a while, just to keep it in your list of differentials.
Blumenthal, I. (2001) Carbon monoxide poisoning. Journal of the Royal Society of Medicine. Volume 94, pp270-72.
Buckley, N. A., Juurlink, D. N., Isbister, G., Bennett, M. H & Lavonas, E. J. (2011) Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database of Systematic Reviews. Issue 4. Article number: CD002041.
Clarke, S. J. F., Crosby, A & Kumar, D. (2005) Early carbon monoxide intoxication: happy to be poisoned? Emergency Medicine Journal. Volume 22, pp754-755.
Harty, E., Haskins, K & Robinson, K. (2008) Carbon monoxide poisoning measurement. Emergency Medicine Journal. Volume 25, pp862.
Hampson, N. P. (1998) Pulse oximetry in severe carbon monoxide poisoning. Chest. Volume 114, pp1036-41.
Hampson, N. B & Weaver, L. K. (2007) Carbon monoxide poisoning: a new incidence for an old disease. Undersea & Hyperbaric Medicine: Journal of the Undersea and Hyperbaric Medical Society. Volume 34, number 3, pp163-8.
Kaya, H., Coskun, A., Beton, O., Zorlu, A., Kurt, R., Yucel, H., Gunes, H & Yilmaz, M. B. (2016) Carboxyhaemoglobin levels predict the long-term development of acute myocardial infarction in carbon monoxide poisoning. American Journal of Emergency Medicine. Epub ahead of print. Available from: http://dx.doi.org/10.1016/j.ajem.2016.01.036 (last accessed 24/3/16).
Kumar, P & Clark, M. (2012) Clinical Medicine (8th Edition). Saunders. London.
Wright, J. (2002) Chronic and occult carbon monoxide poisoning: we don’t know what we’re missing. Emergency Medicine Journal. Volume 19, pp386-90.
Zorbalar, N., Yesilaras, M & Aksay, E. (2014) Carbon monoxide poisoning in patients presenting to the emergency department with a headache in winter months. Emergency Medicine Journal. Volume 31, e66-70.
Rob qualified from the University of Nottingham in 2004 and has worked in a variety of emergency and critical care settings. He spent 8 years as a charge nurse in the emergency department prior to becoming a trainee Advanced Clinical Practitioner (tACP) last year.
He has also worked extensively in prehospital care since 2006 with both the West Midlands CARE team and West Midlands Ambulance Service MERIT team (until 2014), gaining his Diploma in Immediate Medical Care (DIMC) from the Royal College of Surgeons of Edinburgh last year.
He has a keen interest in both education and research, teaching regularly on a number of popular courses and is one of the lead authors of the work produced by the EXtrication In Trauma (EXIT) project.