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

In distal (type 1) RTA, renal acid excretion is impaired by the inability to establish adequate pH gradients between plasma and distal tubular fluid at any level of acidosis. Main clinical signs in infancy are anorexia, vomiting and failure to thrive. Despite low serum bicarbonate levels the renal threshold of bicarbonate is normal, while urinary pH levels are high even with values below the threshold. Under conditions of bicarbonate-induced systemic alkalosis urinary the pCO2 exceeds blood pCO2 in normal subjects. by contrast, the urinary pCO2 tension is not significantly greater in distal RTA, indicating a failure of the cells of the distal nephron to secrete hydrogen ions even without a gradient. Red cell carbonic anhydrase is within the normal range, whilst the inhibition of carbonic anhydrase activity has no effect on distal tubular function. Until now no histological or enzymatic defect could be detected to explain the ineffective acidification. Bicarbonate loading is followed by a lowering of calcium excretion to within the normal range and a decrease in the uncharacteristic renal hyperaminoaciduria.
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PMID:[Investigations on the pathogenesis of distal renal tubular acidosis (author's transl)]. 3 16

In Britain more mothers want to breastfeed their infants. For medical staff who have been trained in a traditional of bottle feeding the problem of failure to thrive because of inadequate breastfeeding may be less well recognized than formerly. There appears to be 2 main types of clinical presentation: fretful underfed infants and "contented" underfed infants. With the fretful underfed infants there is often a history of constant crying and irritability associated with frequent but short feeds. Colic and vomiting are common and the infants look undernourished and show poor weight gain. The "contented" underfed infants give the impression of being satisfied after feedings, but they look undernourished and do not show adequate weight gain. The extent to which inadequate breastfeeding contributes to the problem of failure to thrive in Britain is unknown. Among a group of 21 infants under the age of 6 months who were admitted to the hospital during the January 1 to December 31, 1978 period, failure of breastfeeding was diagnosed in 9 babies. In antenatal classes the practical aspects of breastfeeding should be discussed, particularly with primigravidas. There needs to be emphasis on the management of breastfeeding. The importance of frequent feeding in establishing lactation should be stressed. Hospitals have an important role in getting breastfeeding off to a good start, and community health workers need to become aware that breastfeeding does not exempt babies from being underfed. Underfeeding at the breast must be recognized as a likely diagnosis in breast-fed infants who are failing to thrive. For the contented underfed baby it is sometimes worthwhile trying to increase the frequency of breastfeeding. For the fretful underfed infant possible reasons for poor milk production must be considered.
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PMID:Is inadequate breast-feeding an important cause of failure to thrive? 8 17

In a screening program in Cincinnati urine specimens from over 20,000 infants and children were tested for inherited metabolic disorders involving amino acids, carbohydrates, phenolic acids, organic acids, keto acids, mucopolysaccharides, and imidazoles. The subjects were selected on the basis of symptoms such as vomiting, diarrhea, acidosis, seizures, failure to thrive, delayed development, mental retardation, and others. The tests were based primarily on paper chromatographic techniques. Patients with 21 different metabolic disorders were found. The patterns of abnormal excretion of amino acids and other metabolites are often useful in making a diagnosis.
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PMID:Screening for metabolic disorders among high risk infants and children. 14 35

Gastro-oesophageal reflux can lead to peptic oesophagitis and stricture formation. This is particularly true in infants in whom the condition should be suspected if the patient presents with vomiting, anaemia and failure to thrive. The anatomy of the oesophago-gastric junction is described. The inferior oesophageal sphincter is the main barrier to reflux, and marks the functional junction between oesophagus and stomach. It is under nervous and hormonal control. It is weak in the neonate who therefore frequently refluxes. An hiatus hernia can cause problems due to its bulk but the main problem of peptic oesophagitis is due to gastro-oesophageal reflux. The radiological examination should be carried out carefully with the patient swallowing in a prone position. The patient should be put in the Trendenlenberg position and compression applied to the abdomen. Reflux is intermittent and a negative examination should be repeated if the clinical findings suggest a diagnosis of peptic oesophagitis. Associated pyloric stenosis should always be excluded. Radiological examination of the gastro-oesophageal junction remains the quickest, simplest, and most convenient and safe technique as long as its limitations are appreciated.
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PMID:Gastro-oesophageal reflux, hiatus hernia and the radiologist, with special reference to children. 32 Oct 66

Vomiting and failure to thrive were the presenting complaints of a patient with gastric duplication. The case is presented and features of gastric duplication are summarized with other cases reported in the literature.
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PMID:Gastric duplication. 42 71

Eighty-three infants and children underwent surgical correction of gastroesophageal reflux (GER) from 1973 to 1978. Fifty-four patients had coexistent brain damage (most commonly due to cerebral palsy), eight were previously treated for esophageal atresia, and four had gastroschisis or omphalocele repair. Clinical presentation included failure to thrive in 64 patients, vomiting in 59, and recurrent bouts of aspiration pneumonitis in 43. Barium roentgenography showed GER in 61 patients, whereas additional tests (particularly pH monitoring) were required for detection of GER in 22 patients. After failure of medical management, transabdominal Nissen fundoplication was performed in 80 cases and a Hill repair in three cases. The surgical mortality was zero, but there were five late deaths. Results were considered excellent in 54 patients, good in 22 patients, and poor in seven. Ten of 12 patients with preoperative stricture responded to dilation after fundoplication. Nissen fundoplication was a safe and effective antireflux procedure in 76 of the 83 cases.
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PMID:Gastroesophageal reflux in infants and children. Diagnosis and management. 43 65

A retrospective analysis of the case histories of 176 infants and children with documented coeliac disease born between 1953 and 1975 revealed the following data: Gluten was introduced into the diet of 49% of these patients at an age of 3 to 4 months. The interval between the introduction of gluten and the appearance of first symptoms was very variable and independent of age, occurring within 4 weeks in 32% and within 2 weeks in 20% of cases. In 13% this interval was 6 to 13 months. 91% of cases presented during the first year of life. Signs were also variable, the most frequent combination being failure to thrive, abnormal stools, anorexia vomiting and abdominal distension. In young infants symptoms tended to be more severe, whilst in children older than 2 years stunting of growth was the most frequent single clinical finding.
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PMID:[Coeliac disease: an analysis of the clinical data in 176 patients (author's transl)]. 51 43

Nineteen infants suspected of having cow's milk protein-sensitive enteropathy were studied. They all showed failure to thrive, diarrhoea and/or vomiting when fed a diet of cow's milk, and improved when their diet was changed to casein hydrolysate. Jejunal biopsy was done before and 18--23 hours after a milk challenge. Of the 19 infants, 12 presented histological evidence of cow's milk protein intolerance. Eight suffered from vomiting and diarrhoea within 9 days of the milk challenge, but in 4 cases the histological abnormalities were not accompanied by clinical symptoms. In one case a chicken meat intolerance was documented. The histological appearance of the intestinal mucosa after chicken challenge was identical to that observed after milk challenge. In our opinion, repeated intestinal biopsies before and after an acute challenge is the best method to establish the diagnosis not only of cow's milk protein intolerance but also of intolerance to other alimentary proteins.
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PMID:Cow's milk protein-sensitive enteropathy. Clinical and histological results of the cow's milk provocation test. 52 Dec 97

A 10-year-old boy with severe familial lactose intolerance in infancy (vomiting, failure to thrive, lactosuria (5.25 g/l), sucrosuria (12 g/l), and aminoaciduria. Intestinal disaccharidases (including lactase and sucrase) normal at age 6 and 20 weeks. Oral lactose tolerance test at this age resulted in lactosuria (4.6 g/l); sucrose tolerance test, in sucrosuria (18.5 g/l). In contrast, intraduodenal lactose tolerance test gave only low lactose excretion in urine (0.28 g/l). He improved rapidly and had no lactosuria on intraduodenal feeding with citric acid milk. The lactosuria diminished as age increased, but was still higher at age 6 years than that of controls. He tolerated normal disaccharide containing food after 1.5 years of age. At 5.5 to 6 years, he had symptoms of lactose malabsorption, and an isolated lactase deficiency was proved. At 10 years, he still tolerates only limited amounts of milk. The defect in severe familial infantile lactose intolerance seems to be localized in the gastric mucosa. Acquired lactase deficiency can appear later in childhood in this syndrome.
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PMID:A boy with severe infantile gastrogen lactose intolerance and acquired lactase deficiency. 52 43

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


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