CARBON MONOXIDE POISONING


Runciman, WB and Gorman, DF
AIC (1991);19,4: 506

CO - colourless, odourless, tasteless and non irritant gas produced by incomplete organic combustion.
Motor vehicles (petrol and LPG) involved in most cases; suicide attempts in many cases.

TOXIC MECHANISMS AND PATHOPHYSIOLOGY OF CO
Toxicity related to (a) HbCO formation and effects on O2 carriage;
(b) inhibition of other haemoproteins;
(c) lipid peroxidation;
(d) competition for enzyme adsorption sites with possible inhibition of reaction rates.
CNS toxicity - necrosis of globus pallidus, cortex, hippocampus, substantia nigra, cerebellum (on CT and MRI).
Differ in pattern to "simple" anoxic brain injury.
Concomitant cynanide (Cn-) poisoning common in industrial and domestic fires - synergistic toxicity.

CLINICAL PRESENTATION AND COURSE
CNS dysfunction particularly, decreased LOC dominate presentation.
CVS manifestations are common - asymptomatic ST changes,
- arrhythmias, hypotension, pulm. oedema & cardiac arrest uncommon.
"Cherry-red lips" rare and late sign - less common than cyanosis,
- reflection of HbCO absorption peak in red part of spectrum.
Unless patient dies recovery occurs as CO is removed from the circulation, accelerated by breathing O2.
Late deteriorations up to 1 day - 6 weeks occur - ? due to post-ischaemic encephalopathy, or lipid peroxidation.

ASSESSMENT OF SEVERITY
HbCO levels - poor outcome correlation, reflecting the other mechanisms of injury.
t1/2 HbCO = 320 - 480 minutes at FiO2 = 0.21 at sea level;
= 60 -80 mins at SL and FiO2 = 1.0;
= 8 - 23 mins under hyperbaric conditions.
\ prolonged morbidity often due to other possible mechanism of injury.
ABGs and clinical assessment on admission also correlate poorly with outcome.
Without reliable marker of severe CO poisoning, all patients with convincing history of exposure and intoxication should be treated.

TREATMENT

1. ABC

2. DEFINITIVE TREATMENT.

(a) Increasing FiO2 - increases the dissolved O2 content;
- decreases lipid peroxidation;
- optimal duration is unknown.
(b) Concurrent Cn- poisoning - does not interfere with O2 delivery;
- O2 has a role in reducing the toxicity of conventional Cn antidotes, amyl and sodium nitrates.
(c) Hyperbaric O2 - requires repeated treatments for any measurable efficacy, eg. on admission plus daily or PRN.
Documented and tested decrease in mortality and morbidity.
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