Congenital hypertrophic pyloric stenosis

Pyloric stenosis (PS) has been reported in multiple births. We report the presentation of PS in identical twins, whose symptoms led to simultaneous referral for surgical care. The theories of inheritance of PS are reviewed. Correspondence to: J. S. Young     

Congenital hypertrophic pyloric stenosis

Congenital hypertrophic pyloric stenosis, an important cause of intractable vomiting in infants is diagnosed clinically and confirmed ultrasonographically. Other useful interventions are plain radiography and berium study. Differential diagnosis includes pylorospasm and gastroesophageal reflux. Management protocol includes correction of dehydration and electrolyte imbalance and either Fredet Ramstedt pyloromyotomy or medical treatment with atropine sulphate. Atropine is initially given intravenously till vomiting is controlled and then orally at double the effective I.V. done for another 3 weeks. Atropine sulphate is generally well tolerated and side effects are few like tachycardia, raised SGPT and hyperthermia. Atropine sulphate is very effective, cheap, safe and perhaps more acceptable treatment option for CHPS.     

Diagnostic imaging in hypertrophic pyloric stenosis

This report discusses hypertrophic pyloric stenosis (HPS) and the current approach to diagnostic imaging in the vomiting infant. Signs and symptoms include dehydration and vigorous gastric peristalsis with vomitus. Palpation of an olive-shaped firm muscular tumor is pathognomonic of this condition. The radiographic signs of HPS are well known. Previously published criteria for the sonographic diagnosis of HPS are discussed, these include: measurements of pyloric length, diameter and muscle thickness. The thickened muscle is the most discriminated and accurate one. It was concluded that real-time ultrasound is a simple, and reliable method for the diagnosis of HPS and should be the initial imaging procedure.     

Antenatal prediction of hypertrophic pyloric stenosis

This is the first reported case where the diagnosis of hypertrophic pyloric stenosis (HPS) was entertained in the antenatal period and the neonate was followed up in the postnatal period on a prospective basis until the HPS became manifest. Accepted: 16 August 2000     

Current management of hypertrophic pyloric stenosis

Hypertrophic pyloric stenosis (HPS) is a common condition affecting infants that presents with progressive projectile nonbilious vomiting. The pyloric portion of the stomach becomes abnormally thickened and manifests as gastric outlet obstruction. The cause is unknown. Pyloromyotomy remains the standard of treatment and outcome is excellent. This article reviews the diagnostic work up and imaging, preoperative resuscitation, the various surgical approaches used, and the effect of subspecialty training on outcomes after pyloromyotomy. Postoperative care and the variety of postoperative feeding regimens applied after pyloromyotomy are reviewed, as well as intra- and postoperative complications. Finally, medical management, in lieu of surgery, is discussed.     

Ultrasound diagnosis of hypertrophic pyloric stenosis

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.