A premonitory indication of chronic lead poisoning is a blue line on the gum, indicated by a slate gray or bluish black edging to the teeth, the appearance of which is usually accompanied by an unpleasant sweetish taste in the mouth. The cause of this blue line was for some time disputed. It is obviously due to the formation and deposit of sulphide of lead through the action of sulphuretted hydrogen arising from decomposition in the mouth cavity. At the same time a general feeling of malaise and weakness often comes on, occasionally accompanied by tremor of the muscles and disinclination for food, at which stage the sufferer consults the doctor. Frequently he complains also of pains in the stomach, not difficult to distinguish from the lead colic to be described later. Usually the patient already exhibits at this stage general emaciation and marked pallor.
The blue line was formerly considered a characteristic early indication of lead poisoning; but it has now been proved that occasionally it is absent even in severe attacks. But although the blue line may fail as an ‘initial symptom,’ it will nevertheless be a valuable aid to the practitioner in the recognition of lead poisoning. It is worth while to mention the fact that other metallic poisons produce a very similar ‘line,’ especially mercury, also iron and silver (as in the case of argyria); it has been stated that the blue line can be simulated by particles of charcoal on the gum. The pallor of the patient at the commencement of lead poisoning drew attention to the condition of the blood. The diminution in the amount of hæmoglobin often met with, which under certain circumstances is accompanied by diminution of the red blood cells, offers nothing characteristic. On the other hand, structural changes in the red blood cells—presence of basophil granules in them—are asserted by a number of writers to be characteristic of the first stages of lead poisoning. The basophil granules are believed to be due to regenerative changes in the nucleus. But these changes are also found in pernicious anæmia, cancer, leucæmia, anæmia, tuberculosis, &c.; also in a number of poisonings such as phenylhydrazine, dinitrobenzene, corrosive sublimate, and others; they are therefore the less characteristic of chronic lead poisoning, as occasionally they cannot be found in actual lead poisoning, a point upon which I have convinced myself in the case both of men and animals. Still, the appearance of much basophilia in the red blood cells is a valuable aid to diagnosis, especially as the method of staining to demonstrate them is simple.
Other anomalies of the blood observed in lead poisoning may here be mentioned. Glibert found a striking diminution in the elasticity of the red blood corpuscles, and experiments I have made point to the fact that the power of resistance of the red blood corpuscles to chemically acting hæmolytic agents, such as decinormal soda solution, is considerably reduced.
The pulse is generally hard and of high tension, especially during the attacks of colic. Further, cramp of the bloodvessels (also in the retinal arteries) has been observed. To these functional disturbances in the circulation are added sometimes definite changes in the vessel wall. Later, obliterative arteritis comes on (in the brain arteries), and arteriosclerosis.
The most important symptom of fully developed lead poisoning is colic, which is usually preceded by the initial symptoms described (especially the gastric symptoms), but not always so, as occasionally colic sets in without any warning. The colic pains often set in with marked vehemence. They radiate from the navel on all sides, even through the whole body; the abdomen is contracted and as hard as a board. Pressure on the lower part diminishes the pain somewhat, so that the sufferer often involuntarily lies flat on his stomach. During the attack the pulse is often remarkably slow. Constipation occurs, and often does not yield to purgatives. The attacks last sometimes for hours, occasionally for days, or the pains can (with remissions) even distress the patient for weeks. The frequency of attacks is also very variable. Occasionally one attack follows another, often there are intervals of weeks, even years, according to the severity of the poisoning and duration of exposure. If the patient is removed from the injurious action of lead, as a rule recovery soon ensues.
Fig. 34.—Paralysis of the Ulnar Nerve in Lead Poisoning
Fig. 34a.—Different Types of Paralysis of the Radial Nerve in Hungarian Potters poisoned by Lead (after Chyzer)
Often with the colic, or at any rate shortly after it, appear lead tremor and arthralgia, paroxysmal pain mostly affecting the joints, but occasionally also the muscles and bones. They are often the precursor of severe nervous symptoms which affect the peripheral and central nervous system. In a lead poisoning case running a typical course the predominant feature is the peripheral motor paralysis of the extensors of the forearms. Next the muscles supplied by the radial and ulnar nerves are affected. Often the progress of the paralysis is typical; it begins with paralysis of the extensor digitorum communis, passes on to the remaining extensors, then to the abductor muscles of the hand; the supinator longus and triceps escape. Sometimes the shoulder muscles are attacked; also paralysis in the region supplied by the facial nerve and of the lower extremities is observed. It appears plausible that overstrain of single groups of muscles plays a decisive part; this seems proved by the fact that paralysis first affects, among right-handed people, the right hand (especially of painters), but in the case of left-handed, the left hand; and among children the lower extremities are often attacked first. Disturbance of sight increasing to amaurosis is often an indication of severe brain symptoms. The view of some writers that the cause of the sight disturbance lies in vasomotor influences (cramp of the bloodvessels) is very probable, and supports the view that the brain symptoms are entirely due to diseases of the arteries (arteritis). These symptoms are distinguished by the collective name of saturnine encephalopathy; they include apoplexy, hemiplegia, epilepsy, delirium, and mania. The brain symptoms may cause death.