568 ABNORMALITIES IN METABOLISM 



diet is also accompanied bj^ a marked acetonuria,^ no matter how much fat 

 is supplied, and may reach a point where several grams of oxybutyric acid are being 

 excreted per day without symptoms of serious intoxication. A relativel}- small 

 amount of carbohydrate (80 grams) is sufficient to prevent this acidosis. If the 

 meat-fat diet is continued for some time, however, there seems to be some sort of 

 adaptation so that the acetonuria diminishes until practically normal figures maj^ 

 be reached. 



Pregnancy. — During pregnancy the urine usually contains acetone bodies in 

 slight excess, and occasionally in large excess in women who are suffering from 

 the toxemias of pregnancy. Here there is a rise in ammonia far bej'ond the propor- 

 tion of acetone bodies, partlj^ because of the large amounts of lactic acid which are 

 excreted, and partly from abnormal protein metabolism and tissue destruction, but 

 the proportion of the urinary nitrogen which is constituted bj' ammonia is too 

 inconstant to serve as a prognostic and operative guide. Ewing has obsen'ed a 

 case of pernicious vomiting with 75 per cent, of the total nitrogen as ammonia, and 

 no urea, — while there maj^ occur fatal cases without large excess of ammonia. 

 Higher ammonia figures are usually reached in pernicious vomiting of pregnancy 

 than in eclampsia; in neither is the acidosis present sufficient to account for the 

 intoxication. (See discussion of "Eclampsia.") Even normal pregnant women 

 seem to show a reduced abilitv to tolerate a deficiency in the carbohydrates of the 

 diet. 3 



Cyclic Vomiting. — Here the urine usually shows acetone bodies, lactic acid, 

 indican in excess, and a rise in the proportion of neutral to oxidized sulphur (How- 

 land and Richards). As these findings may persist in spite of absorption of 

 carbohydrates, they are not entirely due to starvation, and there are severe fatty 

 changes in the liver and kidneys, indicating a toxemic origin associated with defec- 

 tive oxidation. Mellanby^ found a considerable creatine elimination in a tj-pical 

 case. There is, however, usually no acidosis, although it maj' develop. 



Inanition and Cachexia. — Under this heading may be grouped the acetonuria 

 observed in intestinal disturbances in children,* hysterical vomiting, psychoses, 

 and cancer. In each of these conditions coma of the type of diabetic coma has 

 sometimes been observed, and in all of them acetonuria is common, the reasons 

 being obvious after the above discussion. A relative acidosis may also result 

 from deficiency of bases in the diet of gro^\ing infants. In many cases of acidosis of 

 infants there is not sufficient increase in the acetone bodies of the blood to account 

 for the acidosis;'' on the other hand, most of the children excreting acetone bodies 

 in the urine do not have acidosis. 



Retention of placenta or fetus, acetonuria being considered of diagnostic value 

 in determining the death of the^fetus in utero,' but not in extrauterine pregnancy 

 (Wechsberg).* 



In uremia, as previously mentioned, organic acids may appear in the urine, 

 but apparently as a result, and not as the cause, of the uremia (Orlowski). There 

 is usually some acidosis in advanced nephritis, but marked only in uremia as dis- 

 cussed above. 



Other Conditions. — Acetonuria is observed inconstantly in fever, especially in 

 children;^" also after poisoning by many driigs, including, besides the heavy metals, 

 morphine, atropine, antipyrine, and phlorhizin. Pneumonia is accompanied by 

 acidosis,^ often of serious degree, subsiding rapidly after the crisis. Acidosis seems 

 to be an important feature in gas gangrene. i° At high altitudes there is always an 

 acidosis, which stimulates the respiratory center to increased activity. In asphy.x- 



2 See Higgins, Peabody and Fitz. Jour. Med. Pes., 1916 (34), 263. 



3 Porges and Novak, Berl. klin. Woch., 1911 (48), 1757. 

 ^Lancet, July 1, 1911. 



6 See Howland and Marriott, Amcr. Jour. Dis. Child., 1916 (11), 309; (12), 

 459. 



« Moore, Amer. Jour. Dis. Child., 1916 ri2). 244. 



^ See Frommer, Berl. klin. Woch., 1905 (42), 1008. 



8 Wien. klin. Wocli., 190{) (19), 953. 



8" See Garland, Arch. Pediat., 1919 (36), 468; Veoder and Johnston, Amor. Jour. 

 Dis. Chil., 1920 (19), 141. 



» Lewis and Barcroft, (Juart. Jour. Med., 1915 (8), 108. 

 »» Wright and Fleming, Lancet, Feb. 9, 1918. 



