Lead poisoning and lead absorption

by Sir Thomas Morison Legge; Kenneth Weldon Goadby

Another cause of colic is suggested by Bokai[9]—namely, hypersensibility of the intestinal nerves—and he cites as evidence the diminution in pain produced by the administration of morphine; and it is not improbable that some hypersensibility of the nervous system of the intestine goes hand in hand with the vaso-constriction that has been shown to exist, while, in addition, many observers have found degenerative and even subacute inflammatory changes in the sympathetic nervous system of the abdomen, mainly in the splanchnic area and the solar ganglion. The action of vaso-dilator drugs on the pain of colic demonstrates the close association of vaso-motor changes with the acute paroxysmal pain.

Riegels[10] investigated the cause of colic in 200 cases. He found that in every instance there was reason to suppose that toxic vaso-constriction of the vessels in the splanchnic area, due to irritation in the vaso-constrictor nerves, was brought about by the action of lead.

Definite gastritis has also been described in some way simulating that caused by arsenic, with thickening in the submucosa of the stomach and intestine. Associated with this enteritis is endarteritis, atrophy of the glands, and Lieberkühn’s follicles. In the colon as well as the ileum was a well-marked enteritis involving the muscular lesions of the gut.

Various other authors describe degenerative processes with cirrhotic changes in the gastro-intestinal tract. Amongst these, Galvini[11] describes, in a case of death from very chronic lead poisoning, extreme cachexia, perihepatitis, perisplenitis, atrophy of the stomach, liver, and spleen, and chronic sclerosing peritonitis (saturnine peritonitis). Associated with general changes in the abdominal cavity, marked inflammation and sclerosis was found in the solar plexus. There is said to be a very considerable correspondence between the condition of the peritoneal cavity and its contents in lead poisoning and barium poisoning. In some of the animals referred to in the description of the experiments, marked inflammatory conditions of the small intestines and colon were found, and in not a few instances definite ulceration and signs of recent hæmorrhages were found scattered along the intestinal tract. No sclerosis was found, however, in the peritoneal cavity, though a common symptom of all the animals, whether poisoned by inhalation, inoculation, or feeding, was the absence of practically all fat from the peritoneal cavity, the omentum being represented by an exceedingly thin membrane without any traces of fat whatever.

Nervous System.

—Perhaps the oldest classical symptom of lead poisoning is the potter’s palsy or wrist-drop due to interference with the nerve-supply of the extensor muscles of the hand, leading to inability to extend the wrist or the fingers on the arm, wasting of the affected extensor muscles, and finally a claw-shaped hand due to contractions produced by the pull of the unopposed flexor groups.

The origin of this extensor paralysis has been the subject of much controversy. One party regards the lesion as of central origin, affecting the upper motor neurons or their connections in the spinal cord; the other takes the view that paralysis is mainly of a peripheral type. Tanquerel[12], whose classical work on lead poisoning still contains one of the best descriptions of the disease from the clinical standpoint, describes an associated affection of the peripheral sensory nerves resulting in definite anæsthesia and hyperæsthesia, and there is no doubt that sensory nerve affection, although not very common in lead poisoning, does occur occasionally, and is due to peripheral affection of the nerves. Occasionally generalized peripheral neuritis is to be met with, but even this is much less common than in alcoholism or other toxic forms of peripheral neuritis.

In the opinion of most of the observers who regard the neuritis as of peripheral origin, the ultimate interference with the motor nerves is due to an ascending neuritis of the peripheral nerves affecting the spinal ganglia, and Pal and Mannaberg[13] have described polyneuritis; whilst Westphal[14], Dejerine[15], Eichhorst[16], Ramond[17], and others, support particularly the primary lesion of the peripheral nerves as the cause of the disease. Marie and Babinski[18] in 1894 evolved the central theory, and supported it by reference to the apparent bilateral occurrence of the paresis and the analogy with many examples of polymyelitis. Vulpian and Steiglitz[19], examining cords of animals poisoned by lead, described vacuolation of the cells in the anterior cornua of the cord.

The original suggestion of the spinal origin of the disease was enunciated by Erb[20], who, without particular reference to either the electrical or histological changes to be found in lead poisoning, based his theory on the similarity of the lesions to polymyelitis. A few cords of persons who have died of lead poisoning do show slight changes in the anterior cornua.

One other theory of the nerve affections in plumbism is that advanced first of all by Hitzig[21], and later by Boerwinkel[22] and Eichhorst[23], who regard the initial disease as one related to the circulation, and not necessarily to the nerve lesions themselves. Potain[24], basing his observations on the anatomical distribution of the blood vessels, points out that the flexor muscles, excluding the supinator longus, are drained by the median cephalic vein, whilst the extensors are drained by the interosseous—a peculiarity of considerable importance, as the supinator longus escapes paralysis in the majority of cases of wrist-drop.