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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The use of sucrose in oral rehydration therapy solutions in place of glucose was tested in 18 patients, 17 males and 1 female, admitted for treatment of severe dehydration due to diarrhea and vomiting. 13 of these patients were positive for cholera (1 with untyped vibrio), whereas 4 others cultured no recognizable pathogen. Patients received an average 1100 ml of intravenous fluids to keep the intravenous drip open during the oral therapy period, and the intravenous therapy was stopped or slowed during oral (or nasogastric) therapy. Average patient age was 32 years. Oral solutions contained either 48 or 38 gm of sucrose per liter plus (in all solutions) sodium chloride (4.2 gm/liter), sodium bicarbonate (2 gm/liter), and potassium citrate (2.7 gm/liter). Of the 18 patients, 15 could be maintained using this solution, but 3 developed massive increases in net fluid losses with increases in plasma specific gravity, which necessitated terminating the therapy. In these failure cases, plasma specific gravity increased over 1.031. Stool samples of 12 patients tested were found to contain reducing sugar: prehydrolysis 436 mg/100 ml, posthydrolysis 957 mg/100 ml. The breakdown of sucrose by intestinal enzymes or by bacteria accounts for the presence of reducing sugar in the stool. These data contrast with the rarity of treatment failures of oral glucose therapy; therefore, glucose is the preferable component in oral rehydration electrolyte solution therapy.
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PMID:Sucrose in oral therapy for cholera and related diarrhoeas. 4 61

A boy with pseudohypoaldosteronism was followed from birth to the age of 7 years. Failure to thrive, vomiting, dehydration, hyponatraemia and urinary sodium loss were prominent findings. Urinary excretion of corticosteroid metabolites was normal. Before treatment, excessively high plasma renin concentration was found, associated with a marked activation of aldosterone secretion. A renal biopsy showed pronounced hypertrophy of the juxtaglomerular apparatus. Persisting metabolic acidosis and an insufficient urinary acidifying capacity suggested the presence of distal renal tubular acidosis. Treatment with sodium bicarbonate and sodium chloride from 19 to 31 months of age resulted in normal growth and normal physical and mental development. The plasma electrolytes were normalized but a pronounced activation of the renin-aldosterone system persisted after therapy, and on sodium restriction this system responded with a considerable further activation.
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PMID:Pseudohypoaldosteronism. Clinical, biochemical and morphological studies in a long-term follow-up. 62 83

A newborn boy (birth weight 2550 g) presented from the first days of life with poor drinking, moderate vomiting and persistent weight loss. On hospital admission at age 4 weeks, there were severe dehydration, dystrophy and electrolyte disturbances (Na 107, Cl 80, K 5,4 mval/l). The usual causes of salt wasting were excluded, but plasma renin activity, plasma aldosterone and urinary aldosterone-18-glucuronide were markedly increased. DOCA had no salt-retaining effect, but a sodium chloride supplement of 3 g per day improved the clinical condition dramatically and normalized the electrolyte values. With this treatment, plasma renin activity and aldosterone were normal or almost normal beyond the age of 6.5 months, but urinary aldosterone-18-glucuronide remained slightly increased. Considerable augmentation of the plasma renin activity and of urinary aldosterone-18-glucuronide, but no clear salt loss were induced by spironolactone. With salt restriction, there was evidence for marked salt loss. Its progress could be inhibited by administration of indomethacin. Since indomethacin inhibits the synthesis of prostaglandins with saluretic activity, it is probable that the prostaglandins participate in the pathogenesis of the salt wasting in pseudohypoaldosteronism.
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PMID:Congenital pseudohypoaldosteronism: case report and review. Effect of indomethacin during sodium chloride depletion. 65 59

The results of 102 cases treated with an oral electrolyte-glucose solution for rehydration caused by mild cases of small bowel diarrhea without using an antimicrobial agent in conjunction are presented. Clinical features, such as frequency of loose bowel movement, age distributions, and other relevant symptomatology are provided tabularly. The solution used consisted of: sodium chloride, .85 gm; potassium bicarbonate, 1 gm.; glucose, 17.5 gm.; boiled and cooled water, 500 ml. 97 of 102 were treated only with the oral electrolyte-glucose solution, and the remainder received intravenous fluid before initiation of oral rehydration. Due to follow-up problems, 13 cases were omitted from the statistical analysis; of the remaining 89, 84 were controlled within 72 hours (as judged by cessation of loose bowel movements). During therapy, breastfeeding or cow's milk was expressly forbidden, but 4 of the 5 failures were later discovered to have recieved breastfeedings, and 1 was marasmic. The treatment of small diarrhea, not having persistent vomiting or shock, with some suitable oral electrolyte-glucose solution only is highly successful, safe, and inexpensive. Success rate was 94.38%.
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PMID:Treatment of small bowel diarrhea with electrolyte glucose drink. 101 Jun 48

Salt is generally contraindicated as an emetic in toxicological emergency situations. It can only be recommended when its rapid disappearance from the stomach can be guaranteed in the case of lack of vomiting. Less than 1 g salt per kg body weight may be lethal. The danger of sodium chloride becomes apparent from two severe cases of intoxication in children one of which was fatal. One of the two children was given salt as an emetic.
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PMID:[Intoxication after use of salt as an emetic (author's transl)]. 124 20

Two college students developed symptoms of poisoning following ingestion of a salt solution during a college physiology laboratory exercise. Symptoms included nausea, vomiting, diarrhea, and altered consciousness. The ingested solution was identified as isotonic buffered saline containing sodium azide in a concentration of 1.0 g/L. The solution was commercially prepared for instrumentation use only and was used inadvertently for the exercise instead of freshly preparing sodium chloride in water. One student drank three sips of the solution and survived. The other student drank 700 to 800 mL and over several days became progressively ill, suffering myocardial damage and cardiac dysrhythmias, and, finally, died. Toxicologic studies confirmed the presence of azide in an antemortem urine sample from the deceased. Sodium azide is an uncommon but potent poison which can cause serious illness and death.
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PMID:Death following accidental sodium azide ingestion. 231 59

Hypernatremia is a potentially life-threatening electrolyte abnormality. This problem develops most often because of loss of water from the animal, but in rare cases hypernatremia results from gain of sodium chloride. Important conditions predisposing to hypernatremia include diarrhea, vomiting, heat stroke, fever, limited access to water, excessive diuretic use, renal diseases, and pituitary diabetes insipidus. This condition rarely develops if animals have adequate access to water. Clinical signs relate to central nervous system derangements and can progress to seizures and coma. Diagnosis is based on the serum sodium concentration; treatment should be instituted if it is greater than 170 mEq per L. Treatment is based on knowledge of the volume status of the patient and the probable cause for the hypernatremia. In general, 5 per cent dextrose in water or other hypotonic fluids are given slowly intravenously. The rate of administration should be adjusted so the water deficit is replaced over 48 to 72 h. Too rapid correction of hypernatremia can lead to cerebral edema and worsening of the animal. In cases of salt intoxication, diuretics must be given in addition to slow water replacement to avoid the development of pulmonary edema.
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PMID:Hypernatremia. 264 64

The etiology, pathophysiology, clinical features, diagnosis, and medical treatment of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) are reviewed. SIADH is a common cause of hyponatremia in hospitalized patients. Increased concentrations of antidiuretic hormone (ADH) result in retention of free water, increased excretion of sodium, and hyponatremia. Symptoms generally occur only when hyponatremia is severe (less than or equal to 125 meq/L) and may include anorexia, vomiting, and confusion, followed by seizures, coma, and death. SIADH may result from a variety of diseases, as well as from the use of drugs such as chlorpropamide, carbamazepine, diuretics, and some antineoplastic agents. Diagnosis of SIADH is confirmed by demonstration of a high urine osmolality with a low plasma osmolality, in the absence of diuretic use. Immediate treatment of the symptomatic patient with SIADH includes intravenous furosemide and 3% sodium chloride injection to produce a negative free-water balance. If the underlying cause of SIADH cannot be corrected, the treatment of choice for chronic SIADH is fluid restriction. If this is not tolerated by the patient, demeclocycline can be used to induce a negative free-water balance. Urea, lithium, phenytoin, and loop diuretics have been reported to be effective, but there are few data to support their use. Future research into the treatment of SIADH must be directed at developing effective antagonists of ADH. Treatment of SIADH consists of elimination of underlying causes and restriction of fluid intake; if these measures are unsuccessful or poorly tolerated, long-term drug therapy may be indicated.
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PMID:Management of the syndrome of inappropriate secretion of antidiuretic hormone. 312 Dec 40

Two adolescents with serum theophylline concentrations in excess of 100 mg/L were treated with continuous nasogastric infusion of activated charcoal after an intentional overdose. In both cases, nasogastric boluses of 20 to 50 gm of charcoal resulted in prompt emesis of stomach contents despite the presence of a functional nasogastric tube. For nasogastric infusion, activated charcoal was diluted in 0.9% sodium chloride and infused at a rate of 0.25 to 0.5 gm/kg/hr up to a maximal rate of 50 gm/hr. Despite the high initial serum concentrations, the theophylline elimination half-lives during the first 20 hours after the start of charcoal were 7.7 and 13.5 hours. Subsequently, this decreased to 2.6 and 3.2 hours. No serious neurologic, cardiovascular, or metabolic derangements were observed. Continuous nasogastric infusions of activated charcoal may be safe and effective alternatives to charcoal hemoperfusion in patients with theophylline overdose.
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PMID:Continuous nasogastric administration of activated charcoal for the treatment of theophylline intoxication. 373 69

The medical records of 330 patients treated with terbutaline infusion for the inhibition of preterm labor were reviewed over a five-year period. In patients with intact membranes the results were uniformly good, particularly when treatment was instituted before the 30th week. Half these patients had a prolonged labor of six weeks or more; in most cases of treatment failure complications already existed on admission. In only nine patients (2.7%) terbutaline treatment was stopped due to side effects: predominantly maternal tachycardia or vomiting. Two patients had chest symptoms, but in no case was pulmonary edema diagnosed. The results suggested that a low incidence of severe side effects can be obtained if the following precautions are taken: glucose is used as the infusion medium, instead of sodium chloride; concentrated solutions are given to avoid fluid overload; the patients are carefully controlled; and the infusion is immediately reduced or stopped if signs of severe side effects appear.
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PMID:A five-year experience with terbutaline for preterm labor: low rate of severe side effects. 402 80


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