ACUTE UR-EMIA includes all the varie ties in which the symptoms develop sud denly. Acute urwmia occurs not only with the different forms of nephritis, but also with angina pectoris, pulmonary em physema, and chronic endarteritis. Three forms are commonly recognized: the comatose, the convulsive, and the mixed; less frequently met with are the delirious, dyspnceic, ocular, and articular.
In the acute comatose form coma rap idly develops, after the appearance of headache, giddiness, more or less disturb ance of vision, vomiting, or delirious ex citement; or it may be unattended by premonitory symptoms. The face is usu ally pale; the pupils react slowly to light and are dilated or unaltered; in other cases we may observe a red spot on the cheek, injected conjunctiva:, and con tracted pupils. There is a peculiar, ster torous breathing—not the deep snoring observed in hanuorrhagic apoplexy, but a sharper, more hissing sound, produced by the rush of expired air on the hard palate or teeth ('P. Grainger Stewart). Death may occur in a few hours from a rapid deepening of the coma; or the patient may recover and continue per manently free from the symptoms; or uralnia may recur, sooner or later, in one of its many forms and death follow. Acute uraemic coma may occur in any of the various forms of Bright's disease, but is most frequent in the cirrhotic and in flammatory varieties.
The acute convulsive form may be marked by symptoms almost exactly simulating those of epilepsy; or may not be attended by loss of consciousness; or may be confined to certain groups of mus cles, and thus simulate tetanus. The at tack is sudden, with or without warning. It may be a single attack, or a rapid suc cession of attacks may occur: five or six, or even more, in the course of twelve horns. These attacks may prove rapidly fatal, either during the paroxysm, or in the coma which succeeds it; or they may be recovered from. Convulsive attacks may occur in any of the various forms of Bright's disease, but most frequently in the cirrhotic and inflammatory varieties; they may, indeed, be the first warning of the existence of cirrhosis of the kidney.
Case of a woman who had several at tacks of convulsions followed by coma, with conjugate deviation of both eyes to the left, with unilateral twitchings, while the right side seemed paralyzed. At the autopsy the kidneys were found to be nephritic, the brain slightly oedematous and congested, but no gross lesions were found. F. Krauss (Phila. Med. Jour., Apr. 14, 1900).
Air-hunger, first described by Kuss maul, was for a long time considered characteristic of intoxication by oxy butyric acid, as it occurs only in diabetic coma. Later investigations, however, showed that a similar symptom-complex may occur in a number of other condi tions, such as severe anmmia, carcinoma, cachexia, gastro - enteric disturbances, and salicylic acid poisoning. The possi bility of the dyspncea being urmmic had already occurred to Kussmaul, but the absence of headache, slowing of the pulse, diminished diuresis, and catarrh of the finer bronchi in diabetic coma led him to consider it something different. F.
Dineles (Wiener klin. Lund., April 20, 1902) has observed a case of pure urmmia in which acetone and diacetic acid could be detected in the urine and in which a distinct diabetic air-hunger was present, while in several similar ones no excre tion of acetone or allied bodies occurred. No disturbances of heart or respiration were present to explain the symptom; probably an irritation of the respiratory centre existed. The character of the renal change played no part, since in his patients the various, different lesions of chronic nephritis were found; a point of importance, however, was the fact that epileptic attacks did not occur. (Medical News, July 19, 1902.) The other forms mentioned (mixed, delirious, dyspnceic, etc.) need no detailed description.