ACIDOSIS 91 



patient, with uncompensated acidosis, regained and held a normal acid- 

 base balance after bicarbonate dosage, and is still alive some months later. 



Diarrhea of Infants. Type and Cause of Acidosis. The clinical con- 

 dition which is frequently accompanied by alkali deficit is described by 

 H. Schwarz (personal communication) as follows: "Half the cases oc- 

 curred in children up to 6 months of age, the other half from the 6th to 

 the 12th months. Temperature varies from subnormal to high. Heart 

 rate is often rapid. Urine is diminished in quantity. The toxic symptoms 

 consist of marked irritability, gradually subsiding into apathy, semi- 

 coma, and coma. Some of the children present rapid shallow breathing, 

 others the deep and labored breathing typical of diabetic coma." 



Some of these cases described by Schwarz show high blood urea, others 

 show lowered plasma bicarbonate, and a third group show both changes. 

 Of 23 cases of toxic diarrhea, Schwarz found 7 with acidosis and urea re- 

 tention, 4 with acidosis alone, 6 with urea retention alone, and 6 with 

 blood figures normal for both bicarbonate and urea. The prognosis was 

 bad for all. 



Lowered plasma bicarbonate in such cases appears, as a rule at least, 

 indicative of a genuine alkali deficit (Area 6, Fig. II), although perhaps 

 in some cases (see observations of Schloss below) it may be secondary 

 effect of hyperpnea due to an unknown respiratory stimulant (Area 2, 

 3, Fig. II). 



Howland and Marriott (a) (1916) found associated with hyperpnea and 

 low alveolar CO 2 abnormally large bicarbonate retention and decreased 

 alkalinity of the blood by Sellard's test (color of concentrated alcoholic 

 filtrate with phenolphthalein). These effects combined are explicable only 

 by a genuine loss of buffer alkali from the body. Schloss and Harrington 

 (1919) found lowered plasma bicarbonate and urine of high acidity (pH 

 below 5.3) in similar cases. Rapid breathing and consequently lowered 

 alveolar CO 2 sometimes occurred without bicarbonate deficit in the blood. 

 Such cases were characterized by a urine of pH greater than 5.3. Schloss 

 has more recently observed a small proportion of marasmic infants with 

 low plasma bicarbonate and high urinary pH (personal communication). 

 The condition in such cases is perhaps that indicated by Area 3, Fig. II, 

 the fall in plasma BHCO 3 being a secondary effect of H 2 CO 3 deficit 

 caused primarily by prolonged hyperpnea. 



Concerning the nature of the acids which cause the alkali deficit in 

 these cases we have no knowledge. The acetone bodies appear to be ex- 

 cluded, since they appear irregularly, and in amounts too slight to ac- 

 count for marked changes in the acid-base balance. 



Diagnosis. The present data indicate that in the cases of the type 

 described a diagnosis of acidosis may be made in most cases by a determina- 

 tion of the plasma bicarbonate, although it is possible that an erroneous 

 positive diagnosis may occasionally be made unless the pH of the blood 



