Part 73

Tests for Sugar in the Urine. For one who can go through it the touching of the tip of the tongue with a drop of the suspected urine will give a prompt and reliable test.

Fehling’s cupric test is the next best for simplicity and availability. Dissolve 34.639 grammes (1⅕ oz.) pure cupric sulphate in 200 cubic centimeters of distilled water: 173 grammes (6 ozs.) of pure neutral sodio-potassic tartrate and 80 grammes of potassium hydrate in 500 cubic centimetres of distilled water. Add the copper solution slowly to the potassium one and dilute the clear mixture to one litre. One cubic centimeter of this fluid will be discolorized by 0.005 gramme of sugar; or 200 grains will be discolorized by 1 grain of sugar.

Trommer’s test is even simpler for a mere qualitative test. Pour the suspected urine, freed from albumen, into a test tube and add a solution of caustic potassa or soda until distinctly alkaline. Should this throw down earthy phosphates or carbonates filter these out. Then add drop by drop a solution of pure cupric sulphate in distilled water (3.5:100) so long as it throws down a yellowish red precipitate of oxide of copper. When the supernatent liquid remains clear and assumes a distinctly bluish tint, the sugar has all been precipitated. The amount of precipitate is a criterion of the quantity of sugar, which may be otherwise estimated by the amount of copper salt used.

The fermentation test is made by adding a teaspoonful of liquid yeast to four ounces of the suspected urine, stopping the flask lightly and placing it in a temperature of 60° to 80° F. for 12 to 24 hours when the sugar will have been converted into alcohol and dioxide of carbon. The loss of weight will indicate the amount of sugar, as also will the lowering of the specific gravity. If before testing the urine was 1060, and after 1035, it contained 15 grains of sugar to the fluid ounce.

Prognosis. This is always rendered more grave in the horse than in man, because of the impossibility of putting him on a purely albuminous diet. The great tendency is to a rapidly fatal issue, especially in cases of irremediable structural lesions in the brain and liver. Where the disorder is largely functional, as in connection with hæmoglobinuria or as the result of poisons ingested the prospect of recovery is often good.

Treatment. In cases due to poisoning the use of antidotes and eliminating agents will be effectual, and in transient and curable diseases like pulmonary disorder, hæmoglobinuria and paralysis the appropriate treatment will restore. In the more inveterate or constitutional cases all treatment is liable to prove ineffectual. At the outset some apparent amelioration may be obtained from salicylic acid, salicylate of soda, bicarbonate, acetate, citrate, sulphate or chloride of soda, nitro-muriatic acid and other cholagogues. Blisters to the perichondrium may also be employed. Later, when degeneration of the liver has reached an extreme point, these will be of no avail. Cadeac recommends acetanilid, antipyrine, and benzo-naphthol largely on their antiseptic merits, and Jong claims a recovery in a horse under daily doses of 12 grains of codeine. Opium has long been employed in man with partially good results, and croton chloral, strychnia, phosphoric acid, iodoform and ergot are recommended in different cases.

One of the most beneficial agents is skim milk or buttermilk as an exclusive diet, and this may be to a large extent adopted for the horse. Under its use the sugar may entirely disappear, and though rheumatoid pains in the joints may be brought on, these usually subside on withdrawing the source of lactic acid. They may further be met by the use of salicylates. The greatest care should be taken of the general health, an open air life, with protection against colds and storms, and a healthy condition of bowels, kidneys and skin being particularly important.

The impaired digestion and assimilation usually demand carminatives, stomachics, bitters, and mineral acids, particularly the nitro-muriatic. With the same intent a fair amount of exercise short of absolute fatigue should be secured. But each case will require a special study and treatment consonant to its special attendant lesions, its causative functional disorders, and its stage. One case may demand attention to bacteridian poisoning, one to a better regimen and diet, one to liver disease, and one to disease of the brain, etc. After this treatment specially directed to the abnormal function or structure, would come the more specific treatment for mellituria which would be more or less applicable to the general glycolytic disorder.

GLYCOSURIA IN CATTLE.

Accompaniment of parturition fever and apoplexy. Essential glycosuria. Dense saccharine urine, passed often, congested mucosæ, emaciation. Lesions uncertain. In parturition fever and apoplexy the congested medulla is the reasonable starting point. Toxic glycosuria. Treatment: addressed to the primary disease or poison; otherwise treat as in the horse.

In cattle this has been observed as a symptomatic affection in connection with parturition fever or apoplexy (Nocard, St. Cyr, Violet). One case of essential mellituria has been recorded by Darbas.

Symptoms. In the last mentioned case in a work ox, the animal, when at work, would stop every five or ten minutes to urinate, passing a small quantity of amber colored urine of a high density and containing a large amount of glucose. The conjunctiva was pink, the animal considerably emaciated, and rest and generous feeding brought about no improvement, so that the subject was finally sent to the butcher to anticipate a natural death.

The lesions in this case are altogether hypothetical. The red eyes might imply congestion of the encephalon (medulla), but the redness might be caused by active disease in the liver, pancreas or kidney. The failure to notice jaundice does not indicate a healthy liver, as some of the most fatal diseases of that organ are unattended by icterus. The frequent emission of urine in small amounts would imply irritation in kidneys or bladder, from which the glycogenic stimulus may have started. In the absence of any more definite evidence of disease in other organs it is, however, more probable that the fundamental disorder resided in the liver, the great glycogenic factor of the body.

In parturition fever, the presumption is in favor of considering the congested medulla as the starting point of the disease, yet in view of the manifest paralysis of stomach and bowels, it is not improbable that the vascular congestion and paralysis of the chylopoietic viscera constituted the initial step in the morbid process, while the glycogenesis was the result of a reflex operation on the liver.

Toxic mellituria would occur in cattle under the same conditions as in the horse.

Treatment is only hopeful in the sympathetic and toxic forms. These must be treated according to the nature of the primary disease or the poison. To these the general principles of treatment as recommended for the horse should be superadded. For essential diabetes an exclusively milk diet and any one of the agents that have given good results in man or horse can be tried, but with an animal in fair condition it will be better as a rule to turn him over to the butcher.

GLYCOSURIA IN THE DOG.

More common than in horses and cattle. Causes: pampered in diet, sweets, liver, disease of pituitary body, or mostly of the liver. Removal of pancreas. Brain and nervous lesions and reflex action. Symptoms: pampered asthmatic subject, with dysuria and lameness, dense, saccharine urine, bulimia, loss of weight, corneal ulcers, cataracts, palsy, coma. Duration: 4 to 8 months, sugar may disappear with complete liver degeneration. Diagnosis: by pampered condition, asthma, thirst, diuresis, later by loss of weight, troubles of vision, saccharine urine. Lesions: usually hypertrophied, fatty or caseated liver, thickened capsule, disease of thyroid, heart and eye. Treatment: skim or butter milk as sole diet, restricted diet of lean meat clear of fat, warmth, dryness, pure air, sunshine, gentle exercise only, cholagogues, sodium sulphate, or chloride, or carbonate, or salicylate, salol, nitro-muriatic acid, antithermics, ergot, codeine, bitters, mineral acids, derivatives.

Among domestic animals the dog has furnished the greatest number of cases, yet even in this animal the disease appears to be far from common.

Causes. The relative frequency of diabetes in the dog is probably dependent on his life in human dwellings and on gourmandizing on dishes prepared for man. Friedberger and Fröhner have produced the disease artificially by feeding a great quantity of sugar and W. Williams has met the disease in dogs fed exclusively and generously on liver. Thiernesse records one case complicated by atrophy and steatosis of the pituitary body, but in all other instances the appreciable lesions were confined to the liver. In one case, reported by St. Cyr, the liver was hypertrophied, yellow, mottled, marked by irregular elevations of congested and hypertrophied hepatic tissue, and showing extensive degeneration—mucous, caseous and fatty. Thiernesse found the liver of a yellowish white color, and the seat of fatty degeneration implicating the hepatic cells. Franzenberg in one case found fatty degeneration of the liver, and Fröhner and Schindelki, in four cases, met with extensive hepatic disease. The macroscopic lesions of the disease in dogs as in horses appear to be mainly hepatic.

On the other hand the complete removal of the pancreas in the dog by Mering, Minkowski, Thiroloix, Lancereaux and others was invariably followed by mellituria, so that even in the absence of clinical examples, we must recognize pancreatic lesions and functional disorders as possible primary causative factors in glycosuria. In the light of experimental medicine we must similarly recognize brain and nervous lesions and reflex actions as possible causes, even if as yet unsupported by clinical facts observed in the dog.

Symptoms. The disease usually appears in an old, fat, pampered dog, affected with dyspnœa or asthma, with dysuria and lameness. The urine is high colored, viscid, and of a high density (1055 to 1060, the normal canine urine being about 1020), and charged with glucose. The subject may have an enormous appetite but fails to gain in weight, and after a time loses flesh and becomes badly emaciated. The pulse is small and frequent, and the temperature which at the outset may reach 102°, falls to the normal as the end approaches. Watering eyes, corneal ulcers, and cataracts as well as hemiplegia and diabetic coma may precede death. The amount of sugar has been found to vary in different cases from 3.2 to 12 per cent. of the urine.

Course. Duration. The dog may live from four to eight months and, as in the horse, sugar may finally entirely disappear from the urine, in connection with the progressive degeneration of the liver. If the patient is unable to take exercise, the case reaches a more speedily fatal issue.

Diagnosis is deduced from the bulimia, pampered condition, breathlessness, thirst, and diuresis, the subsequent loss of condition, ocular troubles, and dropsy or coma, the whole being confirmed by the dense, high colored, viscous, saccharine urine.

Lesions. As already noticed the most constant lesion is hypertrophy of the liver, which is swollen unevenly, has thickened borders, is yellow or red, very friable and often fatty, or caseated. The capsule of Glisson is thickened and fibrous. Hypertrophy and fatty degeneration of the thyroid have been found in different cases and in one instance insufficiency of the mitral valve with systemic venous congestion. Ocular troubles are constant.

Treatment. Put the patient on an exclusive diet of skim or butter milk or if this is impossible it may be conjoined with lean meat—raw or cooked—keep warm and dry, but give plenty of open air and sunshine. Avoid fatigue and over exertion. Restricted diet is of great importance. During the siege of Paris the short rations led to the disappearance of glycosuria from many human patients.

Among medicinal agents, cholagogues come first, sulphate of soda with chloride of sodium, bicarbonate of soda, salicylate of soda, salol, nitro-muriatic acid, may be named. For the febrile condition, antipyrine, acetanilid, or phenacetin may be employed, and iodoform, ergot or codeine may be tried when other measures fail. Bitter tonics and mineral acids may be beneficial, and lastly blisters to the region of the liver may prove of service.

OBESITY AND EMACIATION.