Rice water is not rice cereal oral rehydration solution.
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Biomedical subjects
Publications and source records attributed to A M Molla.
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Somatostatin has been shown to inhibit intestinal secretion induced by a variety of secretagogues. The ability of somatostatin to reduce stool output in patients with cholera was therefore investigated in a double-blind randomized controlled trial. Twenty-two patients with severe purging due to infection with Vibrio cholerae (less than or equal to 12.5 ml/kg X h) received either somatostatin at a dose of 250 micrograms/h in saline (n = 12) or placebo (n = 10). The study drug was given for 12 h followed by a control period of the same duration. No difference in stool output was apparent between somatostatin- and placebo-treated groups. No side effects of somatostatin were observed. It is concluded that somatostatin is ineffective as an antidiarrheal agent in Asiatic cholera in humans.
The intake of breast milk during acute and early convalescent stages of diarrhoea (over a 7-day period) and a fortnight after discharge from hospital (late convalescent stage) was monitored in 33 breastfed children aged 8-24 months. 16 were exclusively breastfed and 17 were partially weaned at the time of admission. On admission, weaning food was introduced to the exclusively breastfed children, whose intake of breast milk in the acute stage made up slightly more than half the total calorie intake of 70 +/- 4 kcal/kg/day. Their total calorie intake increased to 91 +/- 5 and 103 +/- 5 kcal/kg/day in the early and late convalescent stages, respectively, but the proportion made up by breast milk dropped to about a quarter. The breast milk intake of the partially weaned children made up nearly half their total calorie intake of 72 +/- 5 kcal/kg/day, and about a fifth of their total calorie intake of 94 +/- 5 kcal/kg/day and 104 +/- 5 kcal/kg/day, respectively, during the early and late convalescent stage, respectively.
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Whole gut transit time (TT) was measured in 68 children aged up to 5 years (29 cholera, 17 rotavirus, 13 enterotoxigenic Escherichia coli, and 9 Shigella) during acute stages of diarrhoea and 2 weeks after recovery. Absorption of calories, fat, protein, and carbohydrates contained in a normal Bangladeshi diet was studied for 72 h after the first appearance of a charcoal marker in the stool, both during acute diarrhoea and 2 weeks after recovery. Mean TT varied from 5.5 to 7.3 h during the acute stage and from 14.1 to 15.5 h during the recovery period of diarrhoea of all aetiologies; the increase in the TT was significant as expected (P less than 0.001). Correlation coefficients were calculated between TT and the coefficients for absorption of fat, nitrogen, calories, and carbohydrates in the acute and recovery stages of cholera, rotavirus, E. coli, and Shigella. No significant relation was found between TT and absorption of nutrients in any stage of diarrhoea of any aetiology. The results of this study suggest that the mechanism for absorption of nutrients is independent of the whole-gut transit time. Further studies are necessary to identify the role of transit of a meal and its absorption along the whole gut.
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124 patients with acute diarrhoea due to Vibrio cholerae or Escherichia coli were treated with either the standard sucrose-electrolyte solution or a cereal-based electrolyte solution, containing 30 g rice powder per litre and electrolytes as recommended by the World Health Organisation. The treatments were compared by measuring the rate of purging, change in body weight, serum specific gravity, urine output, and post-hydrolysis sugar content in the stool. The proportions of successfully treated patients in the rice-powder group were 80% for cholera patients and 88% for E. coli patients--no different from those in patients receiving the sucrose-electrolyte solution. Failure was due to rates of purging that exceeded the patient's ability to drink enough replacement solution. This study suggests that a rice-powder electrolyte solution is efficient and safe to use as a rehydrating oral fluid in acute diarrhoea.
We studied a group of patients with rotavirus diarrhea to determine the association of carbohydrate malabsorption during diarrhea with the degree of acidosis and severity of purging. Unlike enterotoxigenic diarrhea in which the metabolic acidosis is due to loss of bicarbonate in an alkaline stool, patients with rotavirus develop a metabolic acidosis while passing an acid stool with little detectable bicarbonate. Also unlike enterotoxigenic diarrhea, rotavirus stool contains large quantities of reducing substances suggesting significant carbohydrate malabsorption. Our findings are consistent with the hypothesis that carbohydrate malabsorption is an important secondary pathophysiological mechanism in the rotavirus diarrhea syndrome. This model for rotavirus diarrhea helps to explain the electrolyte and acid-base pattern of the rotavirus stool and stresses the importance of further nutrition balance studies to determine the optimal dietary management of patients with rotavirus diarrhea.
One hundred twenty children below 5 years of age with diarrhea caused by Vibrio cholerae, enterotoxigenic Escherichia coli, or rotavirus were studied for stool electrolyte composition and purging rates. The mean purging rate in cholera was 60.1 ml, in ETEC 39.2 ml, and in rotavirus infection 31.4 ml/kg/8 hour. The mean stool sodium concentration in cholera was 88.9 mMol/L, in ETEC 53.7 mMol/L, and in rotavirus infection 37.2 mMol/L. Stool potassium concentration did not show much variation, Mean CO2 concentration in rotavirus infection was 6 mMol/L, significantly lower than in cholera and in ETEC diarrhea. In cholera, stool sodium concentration increased significantly with increase in purging rates; the same was not true in rotavirus and ETEC diarrhea. These differences are considered important factors in formulating replacement therapy in diarrhea.
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