Lead poisoning and lead absorption

by Sir Thomas Morison Legge; Kenneth Weldon Goadby

An accident of this description may conceivably occur; the treatment of such a case should be energetic, as the poisoning is chiefly due to lead swallowed. An emetic should be given, followed by sublimed sulphur, or, better still, the stomach washed out with dilute hydrogen sulphide water slightly acidulated with sulphuric acid, so as to change any lead present in the stomach into the least soluble form. A brisk purge should be given, and the patient encouraged to drink considerable quantities of lemonade containing sodium or potassium citrate. Alcohol, even during collapse, should be avoided; a hypodermic injection of strychnine is preferable. It must be borne in mind that lead is absorbed in the upper part of the intestine, and only in a minute degree, if at all, from the stomach; it is re-excreted mainly by the large bowel and by the urine; to some extent also by the sweat and saliva. Treatment is therefore directed towards (a) forming an insoluble compound as far as possible; (b) promoting the elimination of the poison; (c) placing as little work as possible upon the tissues most affected. Only milk should be given as food for two to three days.

The diagnosis of lead poisoning is not in itself of any great difficulty where any one of the classical symptoms of lead poisoning is present, such as lead colic, paresis, or the characteristic lead anæmia or cachexia. On the other hand, the premonitory symptoms of poisoning, as seen by a club doctor, particularly in persons engaged in industrial processes, are more difficult to determine; but for the appointed surgeon, who has an opportunity of watching them from week to week, the gradual development of anæmia, extensor weakness, and other early symptoms, should give no difficulty. The clinical diagnosis requires to be made earlier by the appointed surgeon than by the general practitioner; for the appointed surgeon’s duty in a white lead works is not only to treat lead poisoning when it is once established, but, by carefully noting premonitory signs, to avoid the development of actual symptoms in susceptible persons. It is convenient, therefore, to divide the diagnosis of lead poisoning, from the clinical standpoint, into two divisions—incipient and pronounced. Such incipient changes are for the most part noticed amongst lead-workers, and in many cases are more strictly signs of lead absorption than signs of lead poisoning.

The earliest symptoms of poisoning are found in the vascular system, and the curious pallor of the face in persons who have worked in lead for a considerable period is often pronounced, although the conjunctiva may not show such a diminution in colour as might be expected from the facial change, while the actual determination of hæmoglobin may be almost normal. In addition to this, a person of fresh colour working in lead, if susceptible, very quickly loses his florid appearance, often heightened by the colour of the face only remaining on the cheek-bones as a hectic flush. Such a person will also show diminution in the colour of the conjunctival vessels, and invariably a distinct yellowish appearance of his sclerotics, due to the pigmentation of that tissue by broken-down blood-pigment. The yellow colour of the eyes is definite evidence that blood-destruction is in progress.

Following on the anæmia, or, more strictly speaking, the pallor of the face, a well-marked wasting of the subcutaneous fat takes place. In animals poisoned with lead in small or large doses—particularly in small doses given over a considerable period—this wasting of all subcutaneous and other fat is a very marked feature, so much so that practically no kidney, mesenteric or abdominal fat is to be found. The fat is lost in a greater proportion than other body tissues. In man the infra-orbital fat, together with the fat about the buccinator muscle, suffers early, and a curious facial contour is produced, two well-marked folds being seen—one the ordinary naso-labial fold, and the other situated at the anterior margin of the masseter. This, together with the loss of the orbital fat, gives the face a curious pinched appearance. Such a pinched appearance is also to be found in animals (cats) poisoned by lead. The wasting frequently precedes any other symptoms, and it is no uncommon thing to find that a man who has been working in a lead process exposing him to inhalation of dust for a year is losing weight. In one case a man of 10 stone 7 pounds was reduced in weight to 9 stone 2 pounds in fourteen months, during the whole of which time he showed no signs at all of lead poisoning, and only towards the latter end of the time did he exhibit any blue line on his gums; there were no symptoms referable to lead poisoning. Such a case is typically one of lead absorption, which, if continued, would ultimately result in pronounced anæmia with either colic or paralysis, probably the former. The man in question was not engaged in any lead process, but was an electrician attending to the electric light and motors in a smelting works. His occupation necessitated work above the general ground-level, and therefore he inhaled the fumes and finer dust particles detached especially from the arc lamps which required adjustment.

In many persons who have worked in lead for long periods, wasting does not progress beyond a certain point, and these persons may be regarded as having established a certain degree of immunity. Men are met with who have worked in white lead factories and in smelting works for periods of from twenty to, in one case, forty-three years, a considerable portion of such period being antecedent to the time at which the regulations in force for dust removal and general protection of the workers were established, and they must have been exposed to much lead dust. Nevertheless they were less emaciated than many who have only worked a year or two years in a factory under modern hygienic conditions and special regulations. Such persons are either immune from the commencement, or they have established a certain degree of tolerance towards the metal; the latter supposition is the more probable, as there is reason to think several of them suffered from a mild degree of poisoning during the earlier years of their employment.

The rate of development of pallor and wasting are the important facts in incipient poisoning. Anæmia, together with the presence of basophile granules in the red cells, in a previously healthy person, and diminution in the hæmoglobin to 75 per cent., is definite evidence that absorption is leading on to poisoning—that is, blood-destruction—and coincidently insidious damage to the finer bloodvessels and their nerve-supply (see [Chapter V.]). Such a person may at any moment develop a sudden attack of colic or paresis.

Associated with the wasting and pallor comes wasting of the muscles themselves, quite apart from any nerve lesions, and with it a certain degree of mental lethargy, slowness in comprehension, and loss of power over individual muscles or groups of muscles, more usually the latter. The mental lethargy shows itself in many ways—amongst others, heaviness and drowsiness—and careful examination should be made of any man who, previously a good time-keeper, commences somewhat suddenly to be late in the morning. The muscles of the hands and the arms, may show no definite wasting as compared one with another; but early loss of power, particularly of the extensors of the wrist or fingers, may be present for six months to a year before definite wrist-drop makes its appearance. In two cases under our own observation, loss of power of the extensor muscles of the wrist was present—in the one case for eight, and in the other case eleven, months before definite paresis occurred. In the one case the first symptom of paralysis was inability to extend the little fingers of both hands; the case was at once suspended from work, and was given treatment. Within forty-eight hours both wrists were so far affected that they could not be extended. In the second case the first symptom of paresis other than the loss of extensor power was the inability to oppose the thumb to the first index-finger of the left hand; within seven days complete wrist-drop of the left hand, partial drop of the right hand, including the middle and ring fingers, occurred. Both cases made a complete recovery.

By no means all wrists which show weakness of the extensor muscles ultimately develop paralysis; for, on looking through the records of the examination of three factories, only 4 per cent. of persons whose wrists were noted as showing loss of extensor power ultimately developed definite paralysis. In the extended position of the hands, when the surgeon is examining for extensor weakness, note should be made of any tremor, as fine tremor is frequently an early symptom of ensuing paralysis. The tremor is generally fine, increased on attempting to perform concerted acts (intention tremor); some loss of co-ordination may be found.

Where the nerve supplying the muscle has suffered alteration in its conductivity, as by the occurrence of a small hæmorrhage in its sheath, gradual diminution in the nutrition of the muscle takes place; but whether or not this is sufficient explanation for the chronic wasting which is seen in the hands is not yet definitely proved.

In examining the hands outstretched for tremor and loss of muscular power, wasting of the interossei may be seen before any definite evidence of paralysis supervenes. On the palm of the hand both the thenar and the hypothenar eminences may show flattening, and attention should always be paid to this portion of the hand, as an early flattening of the hypothenar eminence particularly is one of the earlier symptoms of wrist paralysis.