Carbon Monoxide Toxicity
(Redirected from Carbon monoxide toxicity)
Other Names
- Carbon Monoxide Poisoning
- CO toxicity
Background
- This page refers to carbon monoxide (CO) toxicity, which can be seen in scuba diving
History
Epidemiology
- Epidemiology is not well described, limited to case reports
- In a review of 451 diving fatalities occurring from 1993- 1997 in the Divers Alert Network database, only two that were felt to have been caused by carbon monoxide poisoning[1]
Pathophysiology

- General
- Colorless, odorless gas which occurs due to incomplete combustion of hydrocarbons
- Often called the "great mimmicker" because of the varied, nonspecific presentations
- Uncommon in diving but thought to be under-reported as symptoms mimic decompression sickness and respond to oxygen therapy
Etiology

- Diving
- Can occur as a result of a faulty air compressor
- From air contamination by the exhaust of nearby petrol engines.
- Seen in sport divers and inshore/ inland divers
- Unlikely to occur in deep offshore divers where air is supplied by decanting mixtures of oxygen and inert gases
- Symptoms get worse at depth as partial pressure of CO increases
- Symptoms can be mild or asymptomatic at atmosphere/ surface
- During descent, symptoms may be rapid and severe
- Non-diving
- Most toxic component of smoke inhalation
- Can be seen in the following:
- Automotive exhaust
- Propane-fueled heaters
- Wood or coal-burning heaters
- Structure fires
- Gasoline-powered motors
- Natural gas-powered heaters
- Waterpipe/Hookah[3]
- Methylene chloride (a degreasing solvent found in most paint strippers) fume inhalation
Mechanism
- Hypoxia
- Binding affinity of hemoglobin for CO (carboxyhemoglobin) is 200x that of O2
- Half-Life
- Room air: ~5hrs
- 100% O2: ~1hr
- HBO 2.5atm: 24min
- Lactic Acidosis
- CO inhibits oxidative phosphorylation
- Hypotension
- CO induces NO2 and guanylate cyclase release → vasodilation release
- CO binds to myoglobin and alters its function
- CO Damage at cellular level
- Due to reactive oxygen species, lipid peroxidation, and cellular apoptosis
- Occurs in CNS and leads to neurological sequela
Risk Factors
- Tobacco Use Disorder
- Smokers have a baseline CO between 5-10%
Differential Diagnosis
Differential Diagnosis Dive Medicine
- Barotrauma of descent
- Otic Barotrauma: "ear squeeze"
- Sinus Barotrauma: "sinus squeeze"
- Mask Squeeze: air in the mask decreases in volume during a dive, creating negative pressure
- Barodentalgia: trapped dental air causing squeeze
- At depth injuries
- Oxygen Toxicity: harmful effects of breathing oxygen at higher partial pressures than normal
- Nitrogen Narcosis: toxic effects of breathing nitrogen-containing gases while at depth
- Hypothermia: decrease core temperature with prolonged exposure to cold water
- Carbon Monoxide Toxicity: CO toxicity typically results from a faulty air compressor
- Caustic Cocktail: Inhalation of absorbent material used to scrub CO2 mixes with water
- Barotrauma of ascent
- Pulmonary Barotrauma: occurs when diver breathing compressed air ascends too rapidly
- Decompression Sickness: Dissolved nitrogen comes out of solution, forms bubbles in blood and tissue ("the bends")
- Arterial Gas Embolism
- Alternobaric vertigo
- Facial baroparesis (Bells Palsy)
- Other
- Immersion Pulmonary Edema: also termed swimming induced pulmonary edema
- Salt water aspiration
- Submersion Injury: includes drowning, near drowning
Clinical Features
| Symptom[4] | % |
|---|---|
| Headache | 85 |
| Dizzy | 69 |
| Fatigue | 67 |
| Nausea or Vomiting | 52 |
| Confusion | 37 |
| LOC | 35 |
| Dyspnea | 7 |
- History
- Wide spectrum of clinical features from flu-like illness to coma
- CNS: headache, visual disturbances, confusion, ataxia, seizure, syncope, focal deficit, coma
- Ophtho: retinal hemorrhage
- GI: Vomiting
- Pulm: Dypsnea, tachypnea
- Cardio: Chest pain, dysrhythmias
- Derm: bullous skin lesions, cherry red oral mucosa
- Physical Exam
- Very important to perform a thorough neurological examination
- Special Tests
Evaluation
- Diagnosis
- Requires high level of clinical suspicion
- Carboxyhemoglobin level
- Interpretation must take into account time since exposure and O2 treatment
- Normal value in non-smokers is ~1%, normal value in smokers may be up to 10%
- Symptoms and COhemoglobin levels do not always correlate well
- Pulse oximetry is unreliable
- COhemoglobin registers the same as O2hemoglobin so will have artificially high SpO2
- O2 saturation gap reflects discordance of SpO2 by pulse oximeter vs by VBG
Laboratory
- VBG
- Check co-oxemtry
- ABG not necessary
- Consider
- Lactate
- Metabolic panel
- Troponin
- Total CK
- Pregnancy test
Monitor
- Co-oximetry
- Special coixemeter can accurately determine CO level
Electrocardiogram
- Findings
- Range from normal to STEMI
- Most commonly ST-T wave changes and prolonged QTc
CT
- Head CT
- Demonstrates findings within 12 hours of exposure
- Bilateral hypodense lesions in the basal ganglia: globus pallidus, putamen, and caudate nuclei[5]
Classification
- No explicit classification system
Management
- ABCs
- In critically ill patient, ABCs must by prioritized
- Oxygen therapy
- Provide O2 until COhemoglobin value <10%
- Positive pressure: Early PEEP prevents progressive atelectasis and improves O2 diffusion
- In general, COhemoglobin levels fall rapidly to < 10% within 30 min of 100% O2
- Maintain 100% O2 for additional 2-3 hrs after < 10%, since anaerobic Cometabolism is occuring due to cytochrome oxidase poisoning[6]
- Anaerobic metabolism universally seen with COhemoglobin > 40%
- Monitor for return of aerobic metabolism with normal serum bicarbonate levels
- Disposition
- Minimal or no symptoms
- Discharge
- Mildly symptomatic
- Symptoms: headache, vomiting, elevated carboxyhemoglobin
- Monitor for at least 4 hours in ED
- Severe symptoms
- Symptoms: ataxia, syncope, chest pain, focal deficit, dypsnea, ECG changes, pregnant
- Admit, possibly ICU
- Discuss with hyperbaric specialist
- Minimal or no symptoms
Hyperbaric Oxygen Therapy (HBOT)
- General
- Decision to initiate should be made in consultation with specialist
- Generally accepted indications[7]
- Syncope
- Confusion/altered mental status
- Seizure
- Coma
- Focal neuro deficit
- Pregnancy with Cohemoglobin level >15%
- Fetal Hb has a higher affinity for CO
- Blood level >25%
- Acute myocardial ischemia
- Prolonged CO exposure with minor clinical findings
- Controversy regarding benefit
Prevention
- See: Dive Medicine Prevention
- Preventing carbon monoxide toxicity
- Test the gas in scuba tanks for CO prior to each dive
- Fill tank at a reputable dive shop that tests for CO
Rehab and Return to Play
Rehabilitation
- No clear rehabilitation guidelines
Return to Play/ Work
- Needs to be updated
Complications and Prognosis
Prognosis
- Long term sequalae
- Can occur days to weeks after apparent resolution in up to 46% of patients (need citation)
- Cognitive sequalae lasting one month or more appear ot occur in 25-50% of patients with loss of consciousness or CO level > 25%
Complications
- Cognitive
- Cognitive effects
- Motor disturbances
- Ataxia
- Neuropathies
- Psychosis
- Dementia
See Also
- Internal
- External
References
- ↑ Caruso, J. L., et al. "CARBON MONOXIDE POISONING IN RECREATIONAL DIVING: AN UNCOMMON BUT POTENTIALLY FATAL PROBLEM." (1998).
- ↑ 2.0 2.1 Image courtesy of dan.org, "Carbon Monoxide Safety"
- ↑ Eichhorn, L., Michaelis, D., Kemmerer, M., Jüttner, B., & Tetzlaff, K. (2018). Carbon monoxide poisoning from waterpipe smoking: a retrospective cohort study. Clinical Toxicology , 56(4), 264–272
- ↑ Lavonas EJ. Carbon monoxide poisoning. In: Shannon M, Borron S, Burns M, eds. Haddad and Winchester’s Clinical Management of Poisoning and Drug Overdose. Philadelphia, Pa: Elsevier; 2007:1297-1307.
- ↑ Lee, DC: Hydrocarbons, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 7. St. Louis, Mosby, Inc., 2010, (Ch) 156:p 2035-2038
- ↑ MetroHealth Medical Center Burn ICU Handbook (Not a policy manual), Cleveland, OH
- ↑ Practice Recommendations in the Diagnosis, Management and Prevention of Carbon Monoxide Poisoning. Hampson NB et al. Am J Respir Crit Care Med 2012 Oct 18
- ↑ Weaver, L. et al. Hyperbaric Oxygen For Acute Carbon Monoxide Poisoning. NEJM. 2002:347(14):1057 http://emed.wustl.edu/Portals/2/Answer%20Key%20PDF/2012/January2012/SecondYear.pdf
- ↑ Scheinkestel C. et al. Med J Aust 1999; 170 (5): 203-210. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomized controlled clinical trial http://www.mja.com.au/journal/1999/170/5/hyperbaric-or-normobaric-oxygen-acute-carbon-monoxide-poisoning-randomised
Created by:
John Kiel on 11 July 2022 14:02:42
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Last edited:
11 July 2022 15:05:13
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