Sudden onset of postprandial non-biliary vomiting and increase of indirect bilirubin. Insidious respiratory and infectious evolution. Management starts with fasting, oxygen therapy, ampicillin and amikacin for seven days due to premature membrane rupture. Baby born vaginally with Apgar 8-9, Capurro “B” 35 weeks, gestation, weight 2550 g, height 48 cm. Discharge of clear transvaginal fluid for 30 h. 8–11 Case reportĪ male newborn (NB), from the second pregnancy of a 27-year-old mother. The symptoms do not usually appear before the second or third week of life, and earlier onset is exceptional. Some patients present jaundice derived from elevated indirect bilirubin, from a not completely understood mechanism that reduces glucuronyl transferase and increases enterohepatic bilirubin circulation this is corrected when the patient undergoes surgery. The lack of actual ingestion leads to malnutrition and greater sensitivity to metabolic, haemodynamic and infectious complications.
Repeated vomiting favours oedema of the pyloric mucous membrane, which exacerbates the symptoms, leading to loss of fluids, hydrogen ions and chlorine, all of which leads to hypochloraemic alkalosis. The origin is unknown, but the most accepted hypotheses suggest the use of concentrated baby formulas, lack or reduction of pyloric muscle innervation, elevation of gastrin and gastric somatostatin and even allergy. Prompt diagnosis prevents complications, reduces the morbidity rate and enables surgical treatment with an excellent prognosis.
Hypertrophic pyloric stenosis (HPS) is a disease which occurs in the second week of life, of unknown origin, which consists of the narrowing of the pylorus due to concentric muscular hypertrophy, causing gastric outlet obstruction with progressive vomiting that leads to malnutrition, dehydration and serious metabolic disorders.