Plumbum



38b. Alterations consecutive to neighbouring organic lesions – engorged papilla (Grafe) or false neuritis (Landott). – This consists in an oedema of the papillae, due to pressure on the optic nerve by liquid collected in the intervaginal space. A worker in lead has had an attack of encephalopathy, and rapidly his sight diminishes. Examination by the ophthalmoscope shows typical engorged papillae (i.e evening very swollen), veins dilated, opacity extending scarcely beyond the papillae to the retina. The sight is restored in a few weeks; no albuminuria present at any period.

38c. Albuminuric retinitis, and anaemic amaurosis. – These are met with in cases of chronic lead – poisoning suffering from albuminuria. The prognosis is more unfavourable in the first and second group, especially when there is pronounced atrophy of papillae, and much more favourable in the third.

38d. Gower mentions a transient amblyopia, without ophthalmoscopic changes, which is usually sudden in onset, and may be complete. It has been observed in some cases of acute saturnism after but short exposure to the exciting cause. It commonly soon passes away, and is probably due to a direct effect of the lead on the nerve centres, analogous to the temporary amaurosis of uraemia and diabetes. In one case recorded by Fano there was, for some months, a periodical transient failure of sight at the same hours every day (Medical Ophthalmoscopy, Lond., 1879, p. 206). (Ibid.)

39a. The elimination of lead takes place principally through the kidneys; this has been proved experimentally on animals, and by observations on patients. The appearance of albuminuria in chronic lead – poisoning had been casually noticed, from time to time, by various physicians, but Ollivier was the first to show its dependence on lead. His experiments on animals demonstrated the presence of lead in the kidney and in the urine, and to its elimination he attributed the morbid lesions of albuminuric nephritis. In his examination of 37 lead cases in La Charite he found in 13 of them that albuminuria was present in various degrees. In 8 the albuminuria was temporary, not lasting more than 10 days; in 1 it was intermittent, in 4 it was persistent. In one case which died, the kidneys showed the lesions of Bright’s disease in the stage of atrophy of the cortical substance. The anatomical appearances in this case, and in the animals poisoned by lead, presented the same differences which exist between the first and last stages of albuminous nephritis.

39b. Dickinson in this country has fully confirmed the observations of Ollivier. Out of 42 deaths occurring in St. George’s Hospital, among workmen suffering from lead, 26 had distinct granular degeneration of the kidneys; in most of these cases this renal lesion led to their death. Granular degeneration is (with few exceptions, which take the form of tubal nephritis) the only form of renal disease which lead appears to induce. Granular degeneration, in consequence of lead – poisoning, frequently is present when there are no external signs of gout. The constancy with which permanent albuminuria and granular degeneration are produced by saturnine occupations is one of the most definite points in pathology. Dickinson thinks that lead may also set up a temporary tubal nephritis. The stage of the lead impregnation has to be considered in estimating the condition of the urine. According to Bouchard, in the early stages the urea, uric acid, phosphoric acid, and chlorides are diminished; the colouring matter is increased. When the impregnation is confirmed the same changes continue, together with a diminution in the quantity and sp. gr. of the urine. He at the same time examined the blood, and found the urea, uric acid and phosphoric and increased in quantity. On these grounds Bouchard suppose that the changes in the confirmed cases are due more to loss of the eliminating power of the kidneys than to disturbances in disassimilation. Garrod had previously shown that, in chronic saturnine impregnation, the blood contains uric acid in excess, and that the administration of lead diminishes the excretion of uric acid by the kidneys.

39c. Renaut, under the clinique of Gubler, at the Beaujon, Paris, has carefully noted the urinary conditions in 49 cases, with additional observations from other sources. Without following his divisions it may be stated that if the lead influence has not caused much cachexia, the urine may be normal in colour, density, and quantity. Sometimes, but rarely, the acidity is diminished and the urine is alkaline. As the cachexia advances the urine takes a colour like old Rhine wine, no change in quantity, clear, and containing no excess of uric acid. As the cachexia is confirmed, so the urine changes to the type which Gubler calls “haemapheic”. This haemapheic urine is generally accompanied by more or less yellow tinge of the skin. These two symptoms appear and disappear together. Whenever saturnine icterus is present the urine is always haemapheic. Gubler attributes this appearance of the urine to the destruction of blood – corpuscles, hence an excess of haemoglobin which the liver ought to convert into bile. Haemaphein is an intermediate step between haemoglobin and the colouring matter of the bile. It indicates either excess of corpuscle destruction or hepatic insufficiency; probably both causes operate. The haemapheic urine resembles in appearances that in hepatic jaundice, it has no greenish reflection, nitric acid gives it a mahogany colour; signs of biliary acids absent; the quantity of urine is diminished; it stains the linen a rose salmon colour. If acute symptoms now come on, such as colic or encephalopathy, there are considerable changes in the urine. The characteristic appearances are a brick – coloured sediment and albumen. The latter may, however, appear, in advanced cachexia, without the occurrence of an acute attack. This albuminuria may be either temporary or permanent, and be attended with more or fewer microscopic appearances of renal disease.

39d. Ollivier, Dickinson and Bouchard consider the albuminuria to be essentially renal. On the contrary, Gubler attributes it to changes in the blood, and ranks the kidney lesion as secondary. There is not, as yet, sufficient evidence to determine this point, but probably further experience may show that, as in Bright’s disease, so in lead – poisoning, Gubler’s theory may in many cases, but not all, be correct.

39e. When lead excites colic, especially in the renal form, the cramplike pain sometimes causes more or less retention and even some amount of suppression of urine. Adams (Trans. Am. Medorrhinum Ass., 1852, p. 163) reports a rare circumstance in the case of a man, aet. 38. temperate and previously healthy, who from drinking water conveyed in lead pipes suffered from lead – poisoning. He had colic, arthralgia, and slight paralysis; then he suffered from paralysis of the sphincter of the bladder which allowed the urine to pass guttatim. Soon after this he had epileptic attacks. The recovery was tedious; the paralysis of the bladder was the first symptom which disappeared. [“After the administration of lead, as of that of iron and other metals, an increased quantity of the metal is detectable in the urine; an increased amount of mucus too, simultaneously with signs of irritation of the lining membrane of the bladder, even to the extent of inducing a catarrhal condition”. (RINGER, op, cit.)] (Ibid.)

40a. The circumstance that lead is a predisposing cause of gout has been noticed by various early writers – Musgrave, Huxham, Falconer; and Dr. Parry in 1807 wrote a paper headed “Gout from Lead” (publ. Lond., 1825). In later times various writers, especially Todd, Charcot, and Garrod, have established the prevalence of gout among workers in lead. The last writer suggests the question, Can lead impregnation induce gout without the co – operative aid of other predisposing causes? To ascertain the manner in which lead acts, he made several observations and experiments, consisting first in ascertaining in several instances the condition of the blood and urine of patients under the influence of this metal, and secondly in determining the effect which lead has upon the secretion of uric acid when administered medicinally. From a table of 12 cases it will be observed that uric acid is almost invariably present in the blood in cases of lead – poisoning, not only in those who have previously suffered from gout, but even where no symptoms of that disease had ever shown themselves. Nine never had gout, in one of them no uric acid was found in the blood, but in the others it was noticed – in some moderate, in the others abundant. He had two opportunities of testing the action of lead upon the secretion of uric acid by the kidneys. In both patients a well – marked diminution occurred; in the first it was most marked, being more than one half. A peculiar phenomenon was observed, namely, that after the drug had been given for a day or so a sudden arrest of the excretion of uric acid ensued, and the function of the kidneys then became more or less intermittent. “It would appear, therefore, that in individuals impregnated with lead the blood becomes loaded with uric acid, not from its increased formation, but from its imperfect excretion; and this is of much interest in connection with the fact that the subjects of lead – poisoning are, coeteris paribus, more liable to be affected by gout, and that those who inherit the gouty diathesis are more likely to become poisoned by the imbibition of lead.” He has seen several cases where the medical administration of lead salts has caused severe attacks of gout in patients who had previously suffered from the disease. plus [RINGER reports a similar experience EDS]

Richard Hughes
Dr. Richard Hughes (1836-1902) was born in London, England. He received the title of M.R.C.S. (Eng.), in 1857 and L.R.C.P. (Edin.) in 1860. The title of M.D. was conferred upon him by the American College a few years later.

Hughes was a great writer and a scholar. He actively cooperated with Dr. T.F. Allen to compile his 'Encyclopedia' and rendered immeasurable aid to Dr. Dudgeon in translating Hahnemann's 'Materia Medica Pura' into English. In 1889 he was appointed an Editor of the 'British Homoeopathic Journal' and continued in that capacity until his demise. In 1876, Dr. Hughes was appointed as the Permanent Secretary of the Organization of the International Congress of Homoeopathy Physicians in Philadelphia. He also presided over the International Congress in London.