Introduction: KetoACIDOSIS is commonly occurred in uncontrolled diabetes mellitus patients. However, severe metabolic ACIDOSIS due to starvation is rarely reported in literature. We describe a case of ketoACIDOSIS in a 27-year old pregnant female at week 30 of gestation, with normal former pregnancy.She was admitted to hospital with a 24-hour history of vomiting (more than 30 times in a day). There was no additional pain or symptoms.Case Report: On admission, she was normotensive.Blood glucose was 111 mg/dL, serum creatinine0.6 mg/dL, and urine dipstick showed acetone (3+) without Proteinuria. Urine pH was 6. Blood gas analysis showed severe metabolic ACIDOSIS with a PH of 7.24 (HCO3- 7.9 meq/L, BE -14, PCO2 15.2 mmHg, PO2 72 mmHg). Then, we checked serum electrolytes. Serum chloride was 102 mg/ dL, Na=135 meq/L, K=5 meq/L. Based on these data, there was high anion gap metabolic ACIDOSIS in patient. After 3 days hydration with dextrose in saline, gradually blood gas improved as on discharge it showed pH 7.44, PCO2=44 mmHg, HCO3-=28 meq/L, and her vomiting had been disappeared.Conclusions: We conclude that in this case ACIDOSIS was due to starvation and inhibition of insulin secretion that led to ketone production. After correction of dehydration by glucose replacement, she was improved and discharged.

Forty two small ruminants, 26 (61.90%) sheep and 16 (38.10%) goats were treated for rumen ACIDOSIS. 19 (45.24%), 12 (28.57%), 6 (14.29%) and 5 (11.90%) animals had eaten apple, cooked rice (wazwan left over) turnip and chapatti respectively and manifested clinical form of ruminal ACIDOSIS with, 2.86%; (n=18) as mild (Rumen fluid pH=6.32 ±0.09316), 38.09%; (n=16) moderate (Rumen fluid pH=5.71 ±0.074) and 19.05%; (n=8) (Rumen fluid pH=4.54 ±0.159) as severe ruminal ACIDOSIS and accordingly they were classified as group I, II and III, respectively. In group I rumen motility was reduced (1.67±0.162) and subsequently it was almost absent in group III (0.13±0.125). Rectal temperature recorded to be 102.58±0.166, 101.26±0.188 and 100.83±1.061 in group I, II and III respectively. There was a significant increase heart and respiratory tares before treatment in all the groups. A significant increase in blood glucose and Hb, PCV and TEC was also observed in mild, moderate and severe acidotic animals. Therapeutic measures consisted of neutralization of acidity by oral and / or parenteral use of isotonic (1.3%) and hypertonic (5%) sodium bicarbonate with adequate fluid therapy. Oral and parenteral use of isotonic (1.3%) sodium bicarbonate was given to moderate rumen ACIDOSIS. Administration of oral sodium bicarbonate, bolus Rumentas was given to groups I and II and a course of antihistaminic drug was also given to all the groups of animals. Moreover, animals of group II and III were also offered intravenous injection of high dose vitamin B1 along with fluids. Gastric lavage and cud transplantation following rumenotomy was done in animals of group III. All animals except two (one each from group II and III) were recovered uneventfully.

A case of renal tubular ACIDOSIS (RTA) who had gradual onset of paralysis of lower extremities and persisted for a long time is presented. His primary workups were mistaken for muscular dystrophy. Eventually, an abdominal ultrasonography revealed small stones in both of the kidneys and his workup for the stones were in favour of distal renal tubular ACIDOSIS and advanced rickets with hypokalemia. He had a dramatic response to alkaline therapy. There are many reports of periodic paralysis in RTA but no report of prolonged paralysis is found in the literature.