Lead poisoning and lead absorption

by Sir Thomas Morison Legge; Kenneth Weldon Goadby

In the record of the experiments by one of us (K. W. G.) on [p. 95] are described the hæmorrhages occurring in the anterior crural nerves of cats poisoned by lead. These animals showed most distinct loss of power in their hind-limbs, as was evidenced by their inability to jump, and other symptoms homologous to wrist-drop in man. In these animals no nerve degeneration or alteration in the spinal cord was found sufficiently gross to account for the paralysis, whereas the amount of pressure produced by the yielding of the vessel walls on the nerve bundles and the associated exudation was evidently sufficient to cause compression, and thereby loss of function in the nerve in question.

Now, the pathological changes described by numerous observers, such as parenchymatous and interstitial changes in the brain, destruction of the anterior grey matter, and, finally, the degenerative changes in the muscle groups, the macroscopical and microscopical atrophy of the muscle bundles with the fibrillation and other changes, are none of them opposed to the view that hæmorrhage and exudation are the earliest and initial change; in fact, in experimental animals minute hæmorrhages could always be traced in the earliest stages of poisoning, frequently before definite symptoms appeared.

Confirmation of this theory is seen in the work of Glibert[40], and the drawings he gives showing fibrous changes in the lungs, hyperplasia, congestion, and emphysema, cirrhotic conditions of the liver, and, as he describes it, blood-stasis caused by elongation and dilatation of the capillaries, are all of them highly confirmatory of the hæmorrhage theory. Further confirmation is also afforded by the observations on the action of lead salts upon the blood itself. From the earliest days lead has been used as a styptic, and its empirical use has been shown by later observation to be due to its power of readily coagulating albumin and peptone. Further, in chronic lead poisoning there is a marked increase in the coagulation time of the blood. Glibert, in the work already referred to, points out the increased ductility of the red blood-cells in lead poisoning. Quite apart from this, there is no doubt that definite alterations in the red blood-cells occur; a species of icterus is common in lead poisoning, the anæmia of lead poisoning is of a destructive type, increased urobilin may occur in the urine, and in some instances hæmatoporphyrin is present in considerable quantities. The bone-marrow in cases of lead poisoning undergoes distinct inflammatory change, and may possibly be the cause of some of the curious aching arthralgias often noted as a clinical symptom. All the pathological evidence that can be adduced points unmistakably to the blood as suffering the initial stress in lead poisoning, and it is therefore by no means surprising that the blood vessels should be the next in order to undergo degenerative changes. It is probably this degenerative change, particularly associated with the increased coagulability, alteration in viscosity, the destruction of the blood-cells themselves, and the permeation of the vessel walls by definite, if exceedingly minute, quantities of lead salts, that determines the yielding of the smaller and generally the weaker bloodvessels. In the histological examination of the experimental animals there was considerable evidence that the venules, rather than the arterioles, are the first to yield.

The following case of chronic lead encephalitis, with the examination of the nervous system described by Mott[41], is a case that has a large bearing on the general pathology of lead poisoning, and has the merit of being so carefully described that we cite it at length, as bringing out some of the special features connected with the pathology of lead poisoning.

The patient was a coach-painter, aged forty-four. Family history of no particular interest. Had been a painter since a boy. No specific history. Treated for enlargement of liver at one time. Married. No children. His wife a widow; four children before married to him.

Before the attack of encephalitis, which ultimately resulted in his death, he suffered from colic and obstinate constipation. The commencement of the final attack of lead infection was associated with an epileptiform fit, from which he recovered and resumed his work, but from this time onwards he suffered from progressive weakness and progressive inability to perform his ordinary work. Constant indulgence in alcohol did not pull him together as before; and although previously he had been able to indulge in large quantities of alcohol, a very little now affected him adversely.

The first epileptiform attack was in July, and in November he commenced to have delusions, was restless, suspicious.

On admission to the asylum he showed marked cachexia. Weight, 8 stone 7 pounds; height, 5 feet 9 inches. There was present well-marked oral sepsis and blue line.

Mental Condition.—Restlessness; disorientation; remitting delirious state; periods of shouting coincident with colic, worse at night; auditory hallucinations.

Physical Condition.—Bilateral wrist-drop; extensor paralysis of the fingers; hand-grip and gait impaired; reaction of degeneration of paralyzed muscles; coarse tremors; fibrillary twitching; staccato articulation.