Oliguria

OLIGURIA (from Greek oligos-small and ouron-urine), decreased amount of urine excreted by the kidneys. Clinically, O. is observed relatively frequently, and it can be caused by various factors, both within the kidneys themselves and outside them. However, a strict division of O. into renal and extrarenal forms is hardly possible, since in the very act of urination renal and extrarenal factors are always inextricably intertwined. Predominantly renal forms of O. generally have a single pathogenesis, which reduces to impaired blood circulation in the renal glomeruli, resp. a drop in filtration pressure in them. It is universally recognized that water excretion is carried out exclusively or mainly by the glomerular system; O. is therefore an expression of profound, resp. acute impairment of their function. This group includes O. in nephritis, nephrosclerosis, and cardiac congestion. O. in the initial stage of acute glomerulonephritis serves as a typical symptom and occurs due to ischemia of the glomeruli, or the formation of inflammatory exudate in them. O. is no less characteristic in cardiac congestion, when the kidneys are in a state of severe anoxia, and blood pressure in the arterial limb of the capillary network falls. It should be noted that in these cases other kidney functions (salt and nitrogen excretion) may be preserved. Finally, with the destruction of the vascular system of the kidneys in the final stage of their shrinkage-regardless of the cause-O. sometimes replaces the preceding 'compensatory' polyuria (see). O. is also observed in a number of diseases in which renal function is little or not at all involved in the pathological process. These are the so-called physiological O., observed after profuse sweating or insensible perspiration (from prolonged walking, mountain climbing), as well as O. in febrile patients. In such cases, O. is caused by a sharply negative water balance due to increased water loss extrarenally (through the skin and with exhaled air). Persistent O. is also observed in the retention of unusual amounts of salt in the blood and tissues (e.g., in myxedema, lobar pneumonia, in the stage of increasing edema, etc.). O. is also observed after abundant fluid loss due to vomiting, diarrhea, or in the retention of large amounts of fluid in the body (pylorostenosis, formation of pleural exudates). Tissue retention of water in the liver also leads to oliguria with the excretion of small amounts of urine (opsiuria), which is observed in diffuse liver lesions (cirrhosis without ascites, acute yellow atrophy), as well as in splenomegalies. Many are inclined to see the cause of opsiuria in liver patients in the disruption of the liver's regular role in water metabolism. Piqu and his students have even described special mechanical clamps in the hepatic veins, which in their opinion act as locks (Venensperre) in the release or retention of water by the liver. This view is not generally accepted (see Metabolism, water), although the presence of O. in liver patients is clinically indisputable.-Relatively rare cases of persistent 'primary' O. stand apart, which are extremely difficult to explain by any pathological-anatomical changes in the organs. Zondek associates them with lesions of the autonomic centers of water-salt metabolism, usually located in the diencephalon. Sometimes such O. is combined with a number of other neuro-endocrine disorders (obesity, disorders of thermoregulation), forming characteristic syndromes.-O. is usually a symptom of a disease, therefore the determination of its origin depends on the overall clinical symptomatology of the case. In general, it should be noted that the presence of pathological components in the urine (protein and especially erythrocytes) in O. indicates its renal origin. A normal qualitative composition of urine rather characterizes O. of extrarenal origin.-Treatment of O. consists in eliminating the underlying disease causing it (e.g., nephritis, cardiac decompensation, etc.).-O. should be strictly distinguished from various disorders of urination, accompanied by the retention of urine excretion from the kidneys and bladder due to mechanical or neuro-reflex causes, as occurs in hypertrophy of the prostate, bends of the ureter, etc. Lit.-see lit. to art. Diuresis and Kidneys. M. Vovoy. TIN, Stannum (Sn), belongs to the group of heavy metals; atomic weight 118.7. It is mined from tin stone (oxide of Sn-SnO₂), found in East India, Australia, South Africa, Peru. Tin is a shiny, silvery-white metal with a bluish tint; it is soft, flexible, and malleable. It has a crystalline structure, which is particularly clearly manifested under the action of hydrochloric acid. Sp. gr. 7.29; melting point 231.7°. It can be easily rolled into thin sheets (foil, staniol). In the air, tin retains its metallic luster; in the molten state, it oxidizes on the surface in contact with air to form tin dioxide. It dissolves in HCl and slowly in warm dilute sulfuric acid with the formation of H. In concentrated sulfuric acid, tin dissolves upon heating, turning into tin sulfate, SnSO₄, with the formation of sulfur dioxide. In excess of aqua regia, tin turns into tin tetrachloride, SnCl₄, in cold dilute nitric acid-into tin nitrate, Sn(HO₃)₂ without the formation of H, in hot concentrated nitric acid-into insoluble hydrate of metatinic acid, H₂SnO₃, in concentrated potassium hydroxide-into potassium metatinate, K₂SnO₃, with the evolution of H. In its compounds, tin can be divalent and tetravalent. Tin was used against epilepsy. In ancient times, tin in powder form was used as an anthelmintic. In recent years, it has been recommended as an internal antiseptic in the treatment of furunculosis. According to Chome and Pronin (1919), tin perchlorate in 0.3-0.5% solutions has a specific effect on staphylococci; therefore it is used in abscesses, lymphangitis, etc. In furunculosis and other dermatitis, 1-2 g (several times a day) of metallic tin or tin oxide powder is given orally. When tin is administered per os, it can be considered that it also acts directly on the digestive tract, irritating its walls and stimulating the intestinal muscles to enhanced peristalsis. Cases of tin poisoning are rare, since this metal does not easily pass into a soluble form, and apparently does not have a cumulative effect. Data on cases of acute poisoning in humans are almost nonexistent. After the administration of soluble tin compounds into the blood, phenomena from the central nervous system (excitation followed by paralysis) and cardiac arrest are observed. In chronic poisoning, gastroenteritis, ataxia, and motor paralysis are observed, which resembles chronic lead poisoning (Sollman). Salzer in 1918 described a case of chronic poisoning due to the presence of a Watt's metal plate in the mouth. In this case, phenomena from the central nervous system and anemia were observed. In frogs, tin salts paralyze the central nervous system, and later the heart. In mammals, diarrhea, colic, vomiting, general weakness, as well as paralysis of some parts of the central nervous system and excitation of others were observed, resulting in ataxia, stiffness of movement, and sometimes convulsions, which in dogs are often preceded by twitching of individual muscle groups. The paralyzing effect on the central nervous system apparently extends mainly to the spinal cord. The amount of urine in animal experiments was found to be decreased, and the urine contained protein and epithelium of the urinary bladder. A possible source of tin poisoning are canned goods packed in tin cans. Tin dissolves differently in various organic acids: poorly in acetic, better in malic, and even better in tartaric. In canned fish, amines formed there promote the dissolution of tin. The tin content in various types of canned goods can reach several hundred mg per 1 kg of weight. It is possible that in some cases of consumption of old, mainly fruit canned goods, symptoms of acute but mild poisoning may indeed be observed. Usually, however, tin is contained in canned goods in such insignificant quantities that it is hardly possible to consider it a possible source of poisoning. In any acute symptoms after consuming canned goods, it is more likely to assume poor quality of the canned goods themselves. Of course, one should strive for such packaging of canned goods that it would not be necessary to introduce even the smallest amounts of tin into the body. Of tin preparations, the following can be mentioned: 1) Stannum foliatum (tin foil, staniol)-tin rolled into thin sheets. Used for packaging various products, e.g., chocolate, cheese, tobacco. Often contains more than 1% lead. For packaging pharmaceutical products, e.g., suppositories, only the purest grades of Stannum foliatum should be used, containing at most only traces of lead. 2) Stannum praecipitatum-a gray, loose powder.

Dissolves in hydrochloric acid with the release of hydrogen. Used externally for corneal opacities. 3) Stanni compo-s i t i (Cort. Granati radic. plv. 10.0, Cort. Cinnamomi plv., Stanni pulverati a"a 5.0, Sirupi simplicis q. s. f. Boli 10). A remedy for tapeworms; 1 pill after 1-2 hours. 4) Stannosa n-tablets containing metallic O. Used for furunculosis and pyodermias. 5) Stannum chloratum (chloride of O.) crystallisatum, SnCl₂ + 2H₂O, colorless crystals that usually appear moist, characterized by an acidic reaction. In water acidified with hydrochloric acid, as well as in alcohol, chloride of O. dissolves to almost complete transparency of the solution; in a large amount of water it decomposes, with basic tin chloride, Sn(OH)Cl, precipitating. Chloride of O. absorbs oxygen from the air and converts into insoluble basic dichloride of tin, SnOCl₂. In the past, chloride of O. was administered in the form of pills or solution in doses of 0.005-0.01-0.03 several times a day for epilepsy and some neuroses and for tapeworms. Externally, it is used in a 0.1-0.2% solution against eczema.