Carbon Monoxide Poisoning

Context

Carbon monoxide (CO) is a colourless, odourless, tasteless, non irritating gas that is produced by incomplete combustion of organic material due to insufficient oxygen.

Important causes of carbon monoxide poisoning include inhalation of:

• Smoke in burning buildings
• Petrol or diesel engine exhaust gases retained in closed spaces
• Burnt gases from faulty gas or solid fuel appliances used for domestic heating or cooking
• Burnt gases from gas or solid fuel appliances intended for outdoor use only such as charcoal BBQ or camping stoves

In 2013, there were 40 fatalities and 200 hospital admissions from carbon monoxide exposure [8]. The true incidence is likely to be higher because low level CO toxicity is insidious and may easily be misdiagnosed as flu-like illness, food poisoning or depression.

Learning bite

While the exposure to CO from car fumes may have been reduced due to the introduction of catalytic converters, exposure to car fumes and especially diesel fumes may still have serious acute and chronic health effects.

When to suspect CO poisoning

Always consider CO poisoning as a cause of symptoms, particularly if more than one member of a household (including pets) are affected. CO poisoning presentations depend on the severity of the exposure based on concentration and exposure time.

At low levels, it can easily be mistaken for a flu-like illness, food poisoning, or depression.

Suspect CO poisoning when:

• Clinical features of poisoning are present, and
• Exposure to a potential source of carbon monoxide has occurred, particularly if
  • Symptoms correlate with exposure
  • There are unexplained symptoms that resolve on leaving a building
  • There is an unconscious patient, especially if more than one and indoors

The mechanism of CO poisoning is not completely understood. CO binds to haemoglobin (Hb) with an affinity of approximately 220 times that of oxygen. CO shifts the oxygen dissociation curve to the left. It also binds to myoglobin and mitochondrial cytochrome oxidase, impairing adenosine triphosphate production.

CO poisoning causes platelet and neutrophil activation, free radical formation and lipid peroxidation in brain and other tissues through an immunological mechanism. The importance of these non-hemoglobin-mediated effects has been best documented in the heart, where mitochondrial dysfunction due to CO can produce myocardial stunning despite adequate oxygen delivery [7].

CO binds to fetal haemoglobin and shifts the already left-shifted fetal oxyhaemoglobin dissociation curve further to the left. The half-life of CO in the fetus is longer than that in the mother and is of particular concern when considering treatment options.

CO is produced continuously in the body as a by-product of haem breakdown. This leads to a normal baseline COHb concentration of about 0.5%. In pregnancy and especially in haemolytic anaemias this can rise towards 5%. Cigarette smoking leads to COHb concentrations of up to about 12% in heavy smokers [2].

Administration of oxygen speeds the elimination of CO from the body. Without therapy, the elimination half life of CO is 4-6 hours. Administration of high flow oxygen by a tightfitting mask at normal atmospheric pressure reduces half life to approximately 76 mins. In hyperbaric oxygen chamber at 2.5 atmosphere absolute pressure, the elimination half life is further decreased to 20 mins.

With lower-level or chronic CO poisoning, the person has no abnormal physical signs and has mild symptoms, including [1]:

• Headache (90%)
• Nausea and vomiting (50%)
• Vertigo (50%)
• Alteration of consciousness (30%)
• Subjective weakness (20%)

Higher-level CO poisoning

There are 4 key questions to help diagnose domestic carbon monoxide poisoning. They follow the COMA acronym [8]:

C – Co-habitees and co-occupants: Is anyone else (including pets) in the house affected?

O – Outdoors : Do your symptoms improve outside of the house?

M – Maintenance: Are boilers and cooking appliances properly maintained?

A – Alarm: Do you have a functioning CO alarm

With higher-level CO poisoning, the above symptoms are more severe and are associated with the following symptoms and signs:

• The appearance of intoxication or a personality change
• Impaired mini mental-state examination
• Vertigo and ataxia
• Breathlessness and tachycardia
• Chest pain (due to angina or myocardial infarction)
• Loss of consciousness (with very high levels of carbon monoxide, this may be followed by death within a few minutes)
• Seizure or multiple seizures
• Abnormal neurological signs including blindness, deafness, and extrapyramidal effects. The onset of neurological deterioration may be delayed by several days. Memory impairment and changes in personality may persist long term
• High risk features include chest pain, history of unconsciousness, any continuing neurological symptoms or signs (especially cerebellar features) and pregnancy due to the effects on the foetus

Learning bite

The classic description of cherry pink or red complexion is very rare and associated with the most severe and fatal cases.

In addition to clinical assessment, some specific and non-specific investigations should be considered in symptomatic patients:

• Measure COHb – arterial or venous (caution should be taken in interpreting the results after the administration of therapeutic oxygen)
• Blood glucose to exclude hypoglycaemia
• FBC, U&E, CK, Trop and ABGs
• Lactate (also in the context of combustion, a high lactate (>10 mmol/L) may suggest concurrent cyanide exposure)
• 12 lead ECG

For low level and chronic exposures, it is unlikely that a confirmatory level of COHb will be found.

Some responders may have access to exhaled breath CO monitoring, although this assessment has not been validated.

General Management on Scene

If on scene, personal safety is paramount and should include:

• Shutting down all potential sources of CO poisoning and ventilating the area, if it is possible to do so safely
• Removing the person (and all others) from the suspected source of poisoning
• Liaising with other emergency and environmental health responders to assess risk of CO exposure including faulty gas appliances or ventilation, and any confirmatory recording of high CO levels. However, a negative CO reading after ventilation does not exclude CO as a cause

Clinical management

• Assessing and managing the airway, breathing and circulation
• Administration of oxygen in the highest available concentration, preferably via a tightfitting face mask with a reservoir
• Arranging an ambulance for immediate transport to hospital, consider triaging to a hospital that may have a hyperbaric unit (if locally available)
• Arranging follow up and investigation of the potential sources of CO poisoning. The local Health Protection Unit will coordinate Environmental Health and Local Authority services to protect all vulnerable persons. View website for local contact details
• Where a death may have occurred, the scene is likely to be treated as a scene of crime

Learning Bite

Decontamination is not required for CO poisoning in isolation.

 

Management of Mild Cases of CO Poisoning

If features of lower level poisoning are present, management includes:

• Removing the person (and all others) from suspected sources of poisoning until all potential sources of CO are shut down and the area has been ventilated
• Arranging immediate hospital assessment for pregnant women
• Arranging an assessment of the potential sources of CO poisoning (see previous page).
• Arranging the measurement of carboxyhaemoglobin levels

If in doubt, a specialist should be contacted. Advice is available 24 hours a day from the UK National Poisons Information Service (NPIS).

 

Management of Severe Cases in the ED

Severe cases of CO poisoning should be managed as follows in the ED:

• Maintain clear airway and ensure adequate ventilation
• Administer 100% oxygen as soon as possible
• Measure COHb – venous or arterial
• In the symptomatic patient – check FBC, U&E, CK, Trop and ABG
• 12 lead ECG and measure QRS duration and QT interval. There are specific treatments for QRS prolongation (such as sodium bicarbonate) and QT prolongation (such as magnesium sulphate)
• Hypotension – correct by raising the foot of the bed and by adequate fluid resuscitation with crystalloid
• Metabolic acidosis – if severe metabolic acidosis persists despite correction of hypoxia and adequate fluid resuscitation, consider correction with intravenous sodium bicarbonate

Indications for hyperbaric oxygen therapy (HBOT)

There is debate about the added value provided by hyperbaric oxygen [4,5]. The National Poisons Information Service does not currently recommend hyperbaric oxygen therapy. Contact your local NPIS advice line if you are considering it. A COHb concentration of >25% should be an indication to consider hyperbaric oxygen [9] although the decision should be taken with other indicators listed below:

• Loss of consciousness at any stage
• Neurological signs other than headache
• Myocardial ischaemia/arrhythmia diagnosed by ECG
• The patient is pregnant

HBOT is also thought to be of use for chronic exposure to CO and neurological damage is suspected. Its use should be on a case-by-case basis.

Other indications (other than diving emergencies) for HBOT include:

• Air or gas embolism
• Clostridial myositis and myonecrosis (gas gangrene)
• Crush injury, compartment syndrome and other acute traumatic ischemias
• Arterial insufficiencies:
  • Central retinal artery occlusion
  • Enhancement of healing in selected problem wounds
• Severe anaemia
• Intracranial abscess
• Necrotizing soft tissue infections
• Osteomyelitis (refractory)
• Delayed radiation injury (soft tissue and bony necrosis)
• Compromised grafts and flaps
• Acute thermal burn injury
• Idiopathic sudden sensorineural hearing loss

CO remains a difficult diagnosis to make due to its insidious and non-specific symptoms.

Investigations may also be misleading unless the case is severe and co-oximetry taken early.

Due to the continuing high incidence, CO awareness campaigns often target the autumn in order to prevent cases occurring by highlighting the importance of gas appliance safety as well as informing health professionals on the symptoms and signs to look out for.

1. Carbon monoxide poisoning: needless deaths, unnecessary injury. CMO guidance letter, 2010.
2. Toxbase. Carbon monoxide.
3. Wolf SJ, Lavonas EJ, Sloan EP, Jagoda AS; American College of Emergency Physicians. Clinical policy: Critical issues in the management of adult patients presenting to the emergency department with acute carbon monoxide poisoning. Ann Emerg Med. 2008 Feb;51(2):138-52.
4. Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med 2002;347:1057-1067.
5. Buckley NA, Juurlink DN, Isbister G, Bennett MH, Lavonas EJ. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database of Systematic Reviews 2011, Issue 4. Art. No.: CD002041.
6. HPA Diagnosing poisoning: Carbon monoxide. Gov.uk 2009.
7. ritapepe L, Macchiarelli G, Rocco M, et al. Functional and ultrastructural evidence of myocardial stunning after acute carbon monoxide poisoning. Crit Care Med. 1998 Apr;26(4):797-801.
8. Carbon Monoxide poisoning: Recognise the symptoms and tackle the cause. CMO guidance letter. NHS England, 2013.
9. Manaker S. Carbon monoxide poisoning. UpToDate, 2023.