Carbon Monoxide Headquarters




Carbon Monoxide Poisoning - Historical Perspective (cont.)


NEUROLOGY, 1940

by Samuel A. Kinnier Wilson, M.A., M.D., D.Sc., FRCP, edited by A. Ninian Bruce, FRCP, D.Sc., M.D., FRS, Lt. Col. RAMC
A William Wood Book, The Willliams & Wilkins Company, Baltimore

Chapter XXXVII - Carbon Monoxide Poisoning (cont.)

1. Cortex. - A peculiar involvement of the third and fourth cortical layers has been observed; they are the seat of continuous and unbroken softening throughout both hemispheres, the zone being packed with fatty debris, among which are neuronic structures in every stage of decay, though a few put up resistance. Limited with some sharpness on both outer and inner side, it contrasts with the relative integrity of the remaining cortex, where, however, satellite microglia is grouped round ganglio-cells. Overgrowth of macroglia and of blood vessels is also a feature of the necrotic band......
2. Basal Ganglia. - A predeliction for the inner part of the globus pallidus, or for that nucleus as a whole, has long been remarked; 12 examples were collated by Poelchen in 1888 and the lesions have often been observed since. Their degree and extent depend on the severity and duration of the poisoning and on the subject's age; slight perivascular dissolution may be found, and all grades to complete tissue necrosis, with glial reaction around, and numerous macrophages. The putamen too is at times concerned, more rarely optic thalamus, hypothalamus, substantia nigra and internal capsule. Apart from softening, moderate or intense fatty degeneration may involve striatal parenchyma, with productive glial reaction but also with some glial involution, while analagous processes affect the smaller blood vessels of the region. Lesions of the same kind are seen now and again in subcortical white matter, in mid-brain, pons, medulla oblongata, cerebellum, and cord; spinal and cranial nerve-roots may likewise be damaged. Zipf describes paraplegia at upper lumbar segments.....

Pathogenesis - A number of theories have been advanced to account for the lesions, none of which by itself, perhaps, can be considered adequate.

(a) Ischemic necrosis is believed to follow destruction of vascular endothelium due to omnipresent anoxaemia, with occlusion as a result.
(b) Functional vasomotor paralysis and stasis are induced by the action of the gas, neural lesions being the consequence.
(c) Carbon monoxide has a specific effect on parenchyma, producing a form of encephalitis.
(d) Cerebral oedema and hydrocephalus are factors; papilloedema has been seen to develop in the experimental variety, while clinically pronounced rise of intracranial pressure accompanies the asphyxia; intravenous injection of hypertonic saline relieves headache and stupor at once......

Little if any obsurity veils diagnosis when the tinting of the skin and the circumstances of the case compel attention. The spectroscope can be used, and Kinkel's colour test. Prognosis must ever be guarded; much hangs on length of exposure and on the patient's age and general health. The gas is said to vanish from the blood in a few days, but possible tardy development of serious symptoms after initial recovery should not be forgotten, mysterious as it is. Some allege that vascular lesions advance though carboxyhaemoglobin disappears; others suppose the sequelae a result of disturbed nutrition and faulty elimination.

At the acute period treatment consists in removing the subject from the contaminated atmosphere at once and in the use of oxygen as an antidote; to it carbon dioxide (7 per cent) can be added with a view to quickening lung ventilation. Artificial breathing may be required. Injections of coramine (5 c. cm. intravenously or intramuscularly) have been employed with success. At a subsequent period, if damage has been done to nerve tissues, only symptomatic measures apply. Allusion has already been made to the value of intravenous hypertonic saline in the relief of chronic headache.


...... last changed 12/18/00


Previous Page

Back to CO HQ Main Index