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Letters to the Editor

Indian Pediatrics 2004; 41:291-292

A Case of Carbon Monoxide Poisoning

A 12-year-old boy was brought un-conscious to our casualty nearly 12 hours after he fell asleep in a covered tractor, close to a working generator. He was normotensive, had decerebrate rigidity, equal and reacting pupils, normal optic fundi and no focal deficits. Pulse oximetry showed 95% saturation. ECG revealed sinus tachycardia. Liver and kidney functions were normal. Blood spectro-photometry showed a band of carboxy-hemoglobin (COHb). CT scan revealed bilateral symmetrical white matter hypo-density and bilateral round hypodensities in the globus pallidus extending to the internal capsule. He was treated with cerebral decongestive measures and oxygen (10 L/min) delivered by facemask. He expired on the third day of admission. Autopsy disclosed softening of the globus pallidus and other evidence of generalized hypoxic damage.

Carbon monoxide poisoning is the leading cause of death by poisoning in industrialized countries(1). There is a dearth of Indian literature on this subject; a PUBMED search yielded only two references(2,3). Under-diagnosis is probably the reason for this. Nonlethal exposure often goes undetected; the estimate is that 30% of cases are undiagnosed even in the best of centers(4). Exposure to vehicle exhaust fumes, generator fumes, fires in closed spaces, "bukhari" burning and vapours of paint removers containing methylene chloride can all lead to CO poisoning(2).

CO alters the dissociation properties of Hb and reduces oxygen delivery to tissues, leading to central hyperventilation and respiratory alkalosis, which further shifts the oxygen- hemoglobin dissociation curve to the left. The half-life of COHb is 320 minutes, which is drastically reduced to 80 minutes by 100% oxygen at 1 atmosphere and to 23 minutes by 100% oxygen at 3 atmospheres(5). This is the basis for the use of hyperbaric oxygen in the treatment of poisoning.

Diagnosis can be made by spectro-photometry and estimation of COHb If facilities are not available, Kunkel’s test may be done. A few drops of 3% tannic acid are added to patient’s blood diluted 1:10 with distilled water; the appearance of a crimson red coagulum indicates the presence of COHb(2). Early initiation of oxygen therapy is essential. 100% oxygen should be provided with a non-rebreathing mask to the conscious patient and via endotracheal tube if comatose.

Janaki Menon,
Lulu Mathews,

Department of Pediatrics,
Medical College, Trissur,
Kerala 680 004, India.
E-mail: janakimenon@hotmail.com


1. Raub JA, Mathieu-Nolf M, Hampson NB, Thom SR. Carbon monoxide poisoining–a public health perspective. Toxicology 2000; 145: 1-14.

2. Mehta SR, Niyogi M, Kasthuri AS, Dubal U, Bindra S, Prasad D, et al. Carbon monoxide poisoning. J Assoc Phys India 2001; 49: 622-625.

3. Krishnan S, Kuppuswamy G, Mani S, Majid MA. Carbon monoxide poisoning. J Assoc Phys India 1971; 19: 409-411.

4. Thom SR, Taber RI. Delayed neuro-psychologic sequelae after carbon monoxide poisoning: Prevention by treatment with hyperbaric oxygen. Ann Emerg Med 1995; 25: 474-480.

5. Olson KR, McGuigan MA. Toxicology and accidents. In: Rudolph’s Pediatrics 20th ed. Rudolph AM. Prentice Hall International Inc. London. 1996; p 822-823.


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