Congenital hypertrophic pyloric stenosis; case report.
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The epidemiology of Infantile Hypertrophic Pyloric stenosis (IHPS) was studied in a geographically well-delineated and demographically representative Danish region (The County of Funen), covering the period 1 January 1950 to 31 December 1984. Based upon 679 cases, the cumulative incidence from birth of IHPS was found to be virtually unchanged during the study period at a level of 4.8 per 1000 liveborn boys and 1.3 per 1000 liveborn girls. In an analysis of clinical and demographic variables, the development of IHPS was found to be associated with low parity status (regardless of maternal age). The preterm cases had a longer interval from birth to onset of symptoms, compared with those born at term. No statistically significant associations were found between IHPS and seasonal variations at onset of symptoms, ABO and Rhesus blood groups, and maternal age.
Congenital hypertrophic pyloric stenosis (CHPS) is primarily a surgical process of the neonate and infant. Diagnosis and treatment of CHPS in a 26-month-old male prompted an inquiry of the military health service database for age of onset, sex, and birth position data. Data were analyzed on 604 cases found in a 71-month time period. The incidence for first-born males was .43 percent, for other than first-born males .34 percent, and for females .091 percent, the peak age being 3 weeks and 1 month old. Children diagnosed at age 6 months and older, as well as adults, were identified. Utilization of the Federal Health Care System data base allowed the study of a large number of patients with a broad spectrum of social, racial, and geographic backgrounds. We feel the study of this data provides a unique understanding of the epidemiology of this entity (CHPS).
Thirty infants presenting with vomiting were examined sonographically. In 18 of these patients, a hypoechoic mass medial to the gallbladder and anterior to the right kidney was demonstrated. The mass measured more than 1 cm in diameter in all cases, with an average of 1.7 cm, and was interpreted as representing the hypertrophied muscle mass in pyloric stenosis. Sixteen of these infants had subsequent confirmation of this diagnosis by upper gastrointestinal tract examination and surgery. In two infants, both of whom had a small-diameter mass, the upper gastrointestinal tract study showed an atypical appearing pyloric canal; these two infants were thought to have atypical hypertrophic pyloric stenosis. Of importance technically is operator experience and patience and the use of different patient positions and even real-time imaging for completeness. Potential pitfalls include the fluid-filled duodenal bulb and gastric antrum, which cause a false positive diagnosis, and obscuration of a lesion by overlying bowel gas, which leads to a false negative diagnosis.
BACKGROUND: Gastric outlet obstruction secondary to chronic duodenal ulceration is an indication for surgery as conservative management with balloon dilatation frequently fails. The standard operation is truncal vagotomy and a drainage procedure. However, development of minimally invasive surgery has revolutionized the surgical approach to this clinical problem. METHODS: Twelve male patients with pyloric stenosis secondary to duodenal ulceration underwent laparoscopic truncal vagotomy and gastrojejunostomy. The perioperative and long term outcome of this group of patients were analyzed. RESULTS: The median operating time was 210 (range 180 to 240) minutes. Median postoperative stay was 6 (range 4 to 41) days. Conversion to laparotomy was necessary in one patient. Delayed gastric emptying occurred in two patients but resolved on conservative measures. At a median postoperative followup of 6 (range 1 to 12) months all patients had a good symptomatic outcome (Visick grades I or II). CONCLUSIONS: Laparoscopic truncal vagotomy and gastrojejunostomy is a feasible technique. Intermediate followup shows good symptomatic results when used for pyloric stenosis.
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The patient was a 80-year-old male with advanced gastric cancer (Type 3) accompanied by multiple liver and lymph node metastases. Histological findings in the stomach showed poorly differentiated adenocarcinoma. He had nausea, vomiting and anorexia due to pyloric stenosis, and was treated with 600 mg of UFT E granules/day orally for 5 consecutive days followed by 2 drug-free days (weekly-5 method), and 2 mg of lentinan intravenously twice a week. After 4 weeks of treatment, the primary tumor and metastatic lesions of the liver and lymph nodes were markedly reduced. His symptoms had completely disappeared along with lessening of the pyloric stenosis after 6 weeks of treatment. The patient survived for 7 months in a state of CR and PR. The adverse effects were very mild and negligible. A weekly-5 method of UFT, in comparison with conventional daily administration, may induce maximal antitumor effects with minimal adverse effects.
To evaluate the usefulness of ultrasound in hypertrophic pyloric stenosis (HPS) and to analyse the correlation between the dimensions of the pyloric muscle and the age and the weight of the child, 34 children with suspected HPS and 34 controls were examined. An overlap between the dimensions of the pyloric muscle in the HPS group and in the controls stresses the need to assess the muscle length, the muscle diameter, and the muscle wall thickness in establishing the sonographic diagnosis of HPS. We found the following criteria useful: muscle length greater than or equal to 19 mm, muscle diameter greater than or equal to 10 mm, and muscle wall thickness greater than or equal to 4 mm. The results did not confirm previous reports of increasing dimensions of the pyloric muscle with age and weight.
In a two-year study on 24 newborn infants, diagnosis of hypertrophic pyloric stenosis (HPS) was intraoperatively confirmed, following preoperative ultrasonography. By means of real time sonography three parameters of the pyloric muscle were measured; the mean length was 19.6 mm, diameter 13.4 mm and the muscle thickness was 5.1 mm.
Twenty-four patients with infantile hypertrophic pyloric stenosis were admitted to the University Department of Paediatrics, Singapore General Hospital, from 1974 to 1980 were reviewed. The male to female ratio was 2.4:1. The age of onset of vomiting ranged from birth to 7-week. All except 2 had palpable pyloric tumour. Barium meal studies were required in these two patients to confirm the diagnosis preoperatively. Significant abnormal laboratory findings on admission were: metabolic alkalosis (71%), hypochloraemia (63%), hyponatraemia (54%), hypokalaemia (21%), haemoconcentration (39%) and pre-renal azotaemia (17%). Two-thirds of the patients were operated within 24 to 48 hours after intravenous correction of fluid deficit and electrolyte imbalance. Common complications after Ramstedt's pyloromyotomy were vomiting and fever which were, however, mild and subsided in two to three days. Serious complications were uncommon and there was no mortality in this series. Majority of the patients were discharged well after one to two weeks of hospitalization.
AIMS: To assess the efficacy of a new regimen of intravenous atropine treatment for infantile hypertrophic pyloric stenosis (IHPS) with special reference to regression of pyloric hypertrophy. METHODS: Atropine was given intravenously at a dose of 0.01 mg/kg six times a day before feeding in 19 patients with IHPS diagnosed from radiographic and ultrasonographic findings. When vomiting ceased and the infants were able to ingest 150 ml/kg/day formula after stepwise increases in feeding volume, they were given 0.02 mg/kg atropine six times a day orally and the dose was decreased stepwise. RESULTS: Of the 19 infants, 17 (89%) ceased projectile vomiting after treatment with intravenous (median seven days) and subsequent oral (median 44 days) atropine administration. The remaining two infants required surgery. No significant complications were encountered. Ultrasonography showed a significant (p < 0.05) decrease in pyloric muscle thickness, but no significant shortening of the pyloric canal after completion of the atropine treatment. The patients exhibited failure to thrive at presentation, but were thriving at 6 months of age (p < 0.01). CONCLUSIONS: This atropine therapy resulted in satisfactory clinical recovery. Pyloric muscle thickness was significantly reduced.
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The maternal use of Bendectin (Debendox) in the first trimester of pregnancy was examined in a case-control (n = 1,427 and 3,001, respectively) study of malformed infants whose mothers were interviewed between 1974 and 1976. Mothers of infants with congenital malformation showed an increased likelihood (odds ratio = 1.40) of having used Bendectin, with a stronger association of Bendectin with birth defects for mothers who also smoked (odds ratio = 2.91). A significant association was observed between the occurrence of pyloric stenosis in the infant and exposure to Bendectin in utero (odds ratio = 4.33). When maternal sociodemographic factors, including smoking, and smoking alone, were controlled, the association between Bendectin and pyloric stenosis was further increased (odds ratio = 4.63 and 5.24, respectively). Except for a possible association of Bendectin with heart valve anomalies (odds ratio = 2.99), we were unable to document other significantly increased risks for congenital malformations.
Rhabdomyolysis and acute tubular necrosis (ATN) are described in a patient with pyloric stenosis in whom severe hypokalemia developed due to repetitive vomiting. Furthermore, the importance of hypokalemia in the development of acute renal failure is emphasized.