Congenital Hypertrophic Pyloric Stenosis with Jaundice.

338 DR. BARNETT: I think few of us would consider that we know enough new about pyloric stenosis to justify presenting an infant with it to a group of this type. However, the patient to be presented had what appears to be a cornplication of p loric stenosis, which we had not encountered previously and one which is of both practical and theoretic interest. The patient will be described and the discussion opened by Dr. Fraad. DR. LEWIS FRAAD: Infants with congenital h pertrophic stenosis with or without eomplications continue to fascinate pediatricians, even though the first American cases were reported in 1788. The patient is a boy, the first-born infant of a 21-year-old mother. The pregnancy and delivery were uneventful. The birth weight was 2.5 kg. Upon discharge from the newborn nursery at 6 days of age, occasional regurgitation of feeding was noted. By the age of 3 weeks the infant had gained only 90 gm. Five days prior to admission to the hospital, vomiting became profuse and projectile. One day before admission the infant’s skin appeared yellow to the mother. Upon admission to the hospital at the age of 4 weeks, the infant’s weight had decreased to 2,360 gm. He appeared dehydrated and markedly jaundiced. The liver was palpated at the eostal margin. An olive-shaped mass measuring approximately 2.5 by 1.5 cm was easily palpated in the midepigastric region. The pertinent laboratory findings in the blood at the time of admission were as follows: Hemoglobin, 19.5 gm/100 ml; CO2 content, 37.2 meq/l; chlorides, 79 meq/l; sodium, 142 meq/l; potassium, 3.0 meq/l; bilirubin, 18 mg,/100 ml of which 13.1 mg was reported to be of the indirect-reacting variety. Oral feedings were discontinued. With hydration by intravenous fluids, the electrohte concentrations in the serum returned to normal values but the high value for bilirubin and the jaundice persisted. Identification of the type of bilirubin by paper chromatography revealed that it was all of the indirect variety. Ramstedt pylorotomy and liver biopsy were performed on the third hospital day. The infant had an ulleventful postoperative course. The gross and microscopic appearance of liver tissue obtained by biopsy s ’as considered normal. The jaundice faded rapidly after operation. On the fifth postoperative day the bilirubin level in the serum reached 0.44 mg/ 100 ml. At the time of discharge on the fourteenth hospital day the bab ’s weight was 2,600 gm. The patient, now 4 months of age, has continued to thrive without signs of jaundice or of vomiting. Although pediatricians, surgeons and pathologists have been interested in pyloric stenosis for many ears, the etiology of this condition is still unknown. The following list of theories regarding the cause of pylonic stenosis shows at a glance the confusion reigning in the sphere of etiology: 1) Muscle hypertrophv is the primar lesion; 2) muscle hvpertrophy is secondary to (a) pvlonic (b) gastrointestinal allergy; (c) vitamin deficiency in the pregnant mother, (d) h ’pertonia of the vagi, (e) mventeric ganglion disorder of the stomach analogous to congenital aganglionic megacolon, (f) adrenal cortical disease, (g) pituitary changes, (h) maternal emotional disturbance. This is a partial list. Obvioush with so mans competing theories none is acceptable. The genetic factors in p lonic stenosis are worthy of mention. The disease seems to involve a far higher percentage of monozygous twins than it does fraternal twin pairs.’ The