Carbon monoxide poisoning
Signs
The "cherry red" colouration often referred to in textbooks is exceedingly rare.
Disturbances of gait, balance, short term memory and intellect are common. Simple psychometric testing such as serial 7's, digit span and trail making tests allow rapid screening to be undertaken without delaying treatment.
The ECG may show non-specific ischaemic changes, particularly of ST segments, as well as arrhythmias. A history of loss of consciousness at any time and presentation with coma are indicative of serious poisoning.
A biphasic effect on arterial blood gases has been suggested with a respiratory alkalosis in milder cases, progressing to a metabolic acidosis in more severe poisoning, Hypokalaemia of unknown origin may coexist with acidosis.
CO poisoning may also generate Delayed Neurological Sequelae (DNS), usually with onset some days after exposure. Such sequelae may prove permanent.
Symptoms
Symptoms of CO poisoning are non specific. In a recent study from Utah (Weaver et al 1998) the commonest were found to be:
- Headache 74%
- Nausea 51%
- Dizziness 46%
- Weakness 24%
- Confusion 24%
- Lethargy 30%
- Vomiting 20%
- Abdominal Pain 6%
Symptoms can easily be attributed to viral illness, but suspicion should be raised when several members of a family are complaining of concurrent, possibly progressive symptoms in the absence of fever. Children present with a higher incidence of "gastrointestinal" symptoms than adults.
Diagnosis
- Estimation of Carboxyhaemoglobin (COHb) from a venous blood sample will usually serve to confirm the diagnosis.
- Levels of COHb of up to 10% may be found in smokers.
- It is important to remember however that COHb levels do not correlate with the severity of the poisoning.
- There is no way to measure tissue uptake and levels of CO, this being arguably the more important parameter.
- The most important factors determining severity of poisoning are the inspired levels of CO and the duration of exposure. In dealing with suicide attempts it is important to consider the possibility of concomitant overdoses.
Pathophysiology
CO competes with O2 for binding to Haemoglobin and causes a left shift of the O2 Dissociation Curve.
Although CO has an affinity for Haemoglobin 200 times greater than that of oxygen, hypoxia from this mechanism alone does not account for all the clinical and biochemical manifestations of CO poisoning.
A biphasic pattern to CO poisoning has been shown in experimental animals (Langston: Toxicology 1996). Initially, cerebral oxygen supply and utilisation is held constant due to an increase in cerebral blood flow.
A secondary hypoxic phase is then caused by haemodynamic collapse. This seems to be due to CO binding to myocardial myoglobin. Cardiac myoglobin binds three times as much CO as skeletal muscle.
At the same time, CO also binds to intracellular haemoproteins such as the cytochrome systems in mitochondria, leading to inhibition of oxidative phosphorylation.
Together with intracellular hypoxia, this in turn causes formation of toxic free radical species and consequent endothelial damage.
CO also causes a several hundred fold increase in the release of nitric oxide from platelets. Nitric oxide derived oxidants such as peroxynitrite (ONOO-) can inactivate mitochondrial enzymes and further generate free radical species.
As a final pathway, leucocyte adherence to the cerebral microvasculature subsequently leads to lipid peroxidation of cell membranes. Areas such as the globus pallidus, the hippocampus and the sub-cortical white matter show particular vulnerability.
Pregnancy and CO
The foetus is particularly vulnerable to carbon monoxide poisoning.
Foetal haemoglobin has a high affinity for carbon monoxide. Consequently the foetus may be more susceptible to toxic effects than the mother.
This may explain why pregnant patients with only moderate symptoms and no syncope have had devastating fetal outcomes.
Carbon monoxide is also an abortifacient and a teratogen and is associated with physical deformities and psychomotor disabilities.
The primary concern in pregnant patients is that COHb clearance may take 4 to 5 times longer in the foetus than in the mother.
To date, there are no controlled studies showing that the indications for hyperbaric oxygen therapy are different in pregnant patients than in others. However, pregnant patients with carbon monoxide poisoning do need aggressive treatment, and hyperbaric oxygen therapy should be offered if neurologic symptoms or signs of foetal distress are present.
Several studies of animals and successful clinical outcomes confirm the safety of hyperbaric oxygen therapy during pregnancy. Therefore, many centers use hyperbaric oxygen in any pregnant patient with a COHb level of at least 15%, regardless of symptoms.
Treatment
Patients should receive 100% O2 via a tightly fitting mask with reservoir or CPAP mask as initial therapy.
As agreed with the National Poisons Centre, the following patient groups should receive Hyperbaric Oxygen Therapy (HBO), preferably within six hours of exposure.
- All patients who present with coma.
- History of loss of consciousness
- Neurological Deficit (Frank or on psychometric testing)
- ECG abnormalities (ST changes or Arrhythmias)
