Carbon Monoxide Poisoning

Reviewed and revised 20 May 2016

OVERVIEW

Carbon monoxide (CO) is a colourless, odourless gas produced by incomplete combustion of carbonaceous material. CO poisoning may be acute or chronic

  • Exposure is most commonly from suicide attempts using car exhaust, and accidental exposures from incomplete combustion in charcoal burners, faulty heaters, fires, and industrial accidents
  • Prevalance varies with geography and demographics, and may be high in some groups
  • Chronic CO poisoning may have an insidious presentation (e.g. intermittent headaches), and a high index of suspicion is required in at-risk groups (e.g. fires inside the home)

TOXICODYNAMICS

High-affinity binding to chromophores

  • Carbon monoxide has ~210 times the affinity for haemoglobin than oxygen. Binding therefore renders haemoglobin oxygen carrying capacity and delivery to the tissues. This can result in tissue hypoxia and ischaemic injury.
  • CO also binds to intracellular cytochromes, impairing aerobic metabolism

Other

  • Carbon monoxide also triggers endothelial oxidative injury, lipid peroxidation and an inflammatory cascade
  • These mechanisms are probably responsible for delayed neurological sequelae

Typical clinical symptoms and signs relative to COHb (Normal = 0.5%):

  • <10% (nil, commonly found in smokers)
  • 10 – 20% (nil or vague nondescript symptoms)
  • 30 – 40% (headache, tachycardia, confusion, weakness, nausea, vomiting, collapse)
  • 50 – 60% (coma, convulsions, Cheyne-Stokes breathing, arrhythmias, ECG changes)
  • 70 – 80% (circulatory and ventilatory failure, cardiac arrest, death)

However, the COHb% changes rapidly and variably, but generally to a greater extent in the severely poisoned. Thus on presentation there is little correlation between prior symptoms and signs and the measured COHb%

TOXICOKINETICS

Absorption

  • COHb concentration in blood is a function of the CO concentration in inspired air and the time of exposure
  • Clinical effects occur within 2 hours of exposure at concentrations as low as 0.01% (100 ppm)
  • Uptake (and elimination) of CO is increased by:
    • Decreased barometric pressure
    • increased activity
    • increased rate of ventilation
    • high metabolic rate
    • anaemia
  • Tobacco smokers have higher baseline concentrations of COHb (3 to 10%) and therefore will reach toxic concentrations earlier in any exposure

Distribution

  • Rapidly binds available haemoglobin

Metabolism

  • <1% of the absorbed CO is metabolised endogenously to carbon dioxide

Elimination

  • CO is eliminated unchanged from the lungs in an exponential manner
  • The biological half-life of CO in a sedentary healthy adult is 4–5 hours
  • This half-life decreases with oxygen administration
    • ~ 40–80 minutes with administration of 100% oxygen
    • ~ 23 minutes with  hyperbaric oxygen (2 atmospheres)
  • elimination is affected by the factors as absorption (see above) and is likely faster in many CO poisoned patients due to compensatory measures (e.g. hyperventilation, increased cardiac output)

CLINICAL FEATURES

Acute poisoning

  • CNS: Headahce, nausea, dizziness, confusion, mini mental status examination errors, incorrdination, ataxia, seizures and finally coma.
  • CVS: Dysrhythmias, Ischaemia, hyper or hypotension (exacerbated in patients with anaemia or underlying cardiovascular disease)
  • GI: abdominal pain, N+V, diarrhoea
  • RESP: dyspnea, tachypnea, chest pain, palpitation
  •  Other:
    • Non-cardiogenic pulmonary oedema
    • Lactic acidosis
    • Rhabdomylysis
    • Hyperglycaemia
    • Disseminated intravascular coagulation
    • Bullae
    • Alopecia
    • Sweat gland necrosis

Chronic exposures

  • may have similar effects to acute poisoning, but often with a gradual, insidious onset, and symptoms may fluctuate with varying levels of exposure to CO over time
  • compared with acute exposures, they typically involve a lower dose of carbon monoxide for a long period, which increases the risk of developing neurological complications
  • Symptoms are usually non-specific but can include headache, personality changes, poor concentration, dementia, psychosis, Parkinsonism, ataxia, peripheral neuropathy and hearing loss

Sources of CO exposure

  • fires
  • stoves
  • portable heaters
  • automobile exhaust (e.g. suicide attempt)
  • charcoal grills
  • propane fuelled forklifts
  • gas powered concrete saws
  • inhaling spray paint
  • swimming behind a motor boat
  • solvents and paint removers (metabolised to CO in liver)

INVESTIGATIONS

Bedside

  • ABG
    • HbCO (elevated levels are significant, but low levels do not rule out exposure)
    • lactate (tissue hypoxia)
    • PaO2 should be normal, SpO2 only accurate if measured (not calculated from PaO2)
    • MetHb (exclude)
  • ECG: sinus tachycardia, ischaemia
  • urinalysis (positive for albumin and glucose in chronic intoxification; bHCG for pregnancy)

Laboratory

  • FBC (mild leukocytosis)
  • BSL (hyperglycaemia)
  • UEC (hypokalaemia, acute renal failure from myoglobinuria)
  • CK (rhabdomyolysis)
  • LFT derangement (ischaemia)
  • ethanol level (polypharmacy OD)
  • cyanide level (industrial fire, cyanide exposure)

Imaging

  • CT/MRI brain: may demonstrate cerebral oedema, cerebral atrophy, basal ganglia injury or cortical demyelination
  • CXR: pulmonary symptoms

MANAGEMENT

Resuscitation

  • FiO2 1.0 (continue until patient asymptomatic or CO level < 10%)
  • cardiac monitoring
  • intubate the comatose patient

Specific Treatment

  • High flow O2 via non-rebreather mask until asymptomatic
    • or for 24 hours while fetal well-being is assessed if pregnant
  • Hyperbaric oxygen (HBO)
    • role is uncertain
    • 3 atmospheres will decrease the half life of carboxyHb from 6 hours to ~ 24 minutes
    • often considered for therapy if:
      • All pregnant patients
      • Significant LOC
      • Signs of ischaemia
      • Significant neurological deficit
      • Metabolic acidosis
    • contra-indications
      • chest trauma
      • other major comorbidity or acute instability (e.g. serious drug overdose, severe burns)
      • uncooperative patient
    • complications
      • decompression sickness
      • rupture of tympanic membranes
      • damaged sinuses
      • oxygen toxicity
      • problems due to lack of monitoring

Supportive care and monitoring

Seek and treat cause and complications

  • address suicidality if present
  • treat coexistent cyanide toxicity if suspected (e.g. house fire)
  • seek and treat ischaemic complications and neurological sequelae

Disposition

  • depending on severity:
    • home, ward environment, ICU and/or hyperbaric chamber
  • consider transfer to hyperbaric facility if severe intoxication or persistent symptoms after 4h
  • suicidality requires a psychiatric referral/ admission
  • work or home environment assessment
  • check if other household members are affected
  • Follow up
    • 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

PREGNANCY

  • Significant CO poisoning in the mother often results in foetal death or neurological damage
  • The foetus is thought to be especially susceptible to CO poisoning due to:
    • low oxygen pressures
    • high affinity of foetal haemoglobin for CO
    • much longer half-life of CO in the foetal circulation
  • There may be an added benefit from HBO in this setting
    • HBO shortens the half-life of CO
    • allows delivery of oxygen to the tissues independent of haemoglobin
    • HBO appears to be safe in pregnancy

References and Links

LITFL

Journal articles

  • Annane D, Chadda K, Gajdos P, Jars-Guincestre MC, Chevret S, Raphael JC. Hyperbaric oxygen therapy for acute domestic carbon monoxide poisoning: two randomized controlled trials. Intensive Care Med. 2011 Mar;37(3):486-92. PMID: 21125215.
  • Buckley NA, Juurlink DN, Isbister G, Bennett MH, Lavonas EJ. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev. 2011 Apr 13;(4):CD002041. PMID: 21491385.
  • Elkharrat D, Raphael JC, Korach JM. Acute carbon monoxide intoxication and hyperbaric oxygen in pregnancy. Intensive care medicine. 17(5):289-92. 1991. [pubmed]
  • Fisher JA, Rucker J, Sommer LZ. Isocapnic hyperpnea accelerates carbon monoxide elimination. American journal of respiratory and critical care medicine. 159(4 Pt 1):1289-92. 1999. [pubmed]
  • Henry CR, Satran D, Lindgren B, Adkinson C, Nicholson CI, Henry TD. Myocardial injury and long-term mortality following moderate to severe carbon monoxide poisoning. JAMA. 295(4):398-402. 2006. [pubmed]
  • Koren G, Sharav T, Pastuszak A. A multicenter, prospective study of fetal outcome following accidental carbon monoxide poisoning in pregnancy. Reproductive toxicology (Elmsford, N.Y.). 5(5):397-403. 1991. [pubmed]
  • Pang L, Bian M, Zang XX. Neuroprotective effects of erythropoietin in patients with carbon monoxide poisoning. Journal of biochemical and molecular toxicology. 27(5):266-71. 2013. [pubmed]
  • Park E, Ahn J, Min YG. The usefulness of the serum s100b protein for predicting delayed neurological sequelae in acute carbon monoxide poisoning. Clinical toxicology (Philadelphia, Pa.). 50(3):183-8. 2012. [pubmed]
  • Pepe G, Castelli M, Nazerian P. Delayed neuropsychological sequelae after carbon monoxide poisoning: predictive risk factors in the Emergency Department. A retrospective study. Scandinavian journal of trauma, resuscitation and emergency medicine. 19:16. 2011. [pubmed]
  • Scheinkestel CD, Bailey M, Myles PS, Jones K, Cooper DJ, Millar IL, Tuxen DV. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial. Med J Aust. 1999 Mar 1;170(5):203-10. Review. PubMed PMID: 10092916.
  • Weaver LK, Hopkins RO, Chan KJ, Churchill S, Elliott CG, Clemmer TP, Orme JF Jr, Thomas FO, Morris AH. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. 2002 Oct 3;347(14):1057-67. PubMed PMID: 12362006.

FOAM and web resources


CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

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