title: [Conservative treatment of hypertrophic pyloric stenosis in children].
abstract: BACKGROUND
  Hypertrophy of the pylorus causing obstruction of the gastric outlet, or infantile hypertrophic pyloric stenosis (IHPS), is the most common indication for abdominal surgery in infancy. The incidence of the condition is 3-4 per 1000 live births, and male infants are affected more often than females, in 4:1 ratio. Vomiting, as the first symptom, most often occurs between the third and fourth week after birth, rarely after second month, but there have been few reports of vomiting as late as 5 months. Etiology of IHPS is still controversial. Two theories have been quoted most: absence of non-adrenergic and non-cholinergic nerve fibers which are mediators of smooth muscle contraction, and absence of nitric oxide inhibitory innervation of pyloric smooth-muscle resulting in unopposed contraction of the sphincter in response to muscarinic stimulation. Atropine sulfate is known to inhibit acetylcholine competitively in neuroreceptors, acting peripherally as a competitive inhibitor of the muscarinic effects of acetylcholine, leading to decreased gastrointestinal peristalsis. This action is believed to be important in IHPS cases.
  
  
  OBJECTIVE
  The aim of this paper is to provide further information on potential role of atropine in the management of patients with IHPS.
  
  
  METHODS
  From April 2000 to October 2002, 22 patients (16 boys and 6 girls), aged 21 days to 3 months, with IHPS were treated by oral administration of atropine sulfate in our institution. Diagnosis of IHPS was based on US examination in all cases. A nasogastric tube was inserted and left in situ. Medical treatment involved initial correction of fluid and electrolyte imbalance combined with oral administration of atropine sulfate. Atropin was given in the form of aqueous solution in initial dose of 0.05 mg/kg/d. The total daily dose was divided into 8 equal doses. Each dose was formulated to be given in a volume of 1 ml. Before the administration of each dose of atropine, stomach was decompressed by suction via nasogastric tube. The infant was placed on the right side with the head on the cot elevated 20 degrees to 30 degrees for 15 to 30 minutes after each atropine dose. Oral feeding with 10 ml of 10% glucose was then attempted. If feeding was tolerated, the same dose of atropine was administered 3 hours later, followed by a trial of 20 ml of 10% glucose. If tolerated, 10 ml of conventional formula was then tried after atropine administration 3 hours later. The volume of formula was then increased 10 ml per feed until full feeding (120 ml/kg/d) was tolerated. Dribbling (2-3 times per day) was ignored. If vomiting occurred, the same dose of atropine, volume and type of feed, were tried again 3 hours later, and if still not tolerated, atropine was increased by 1 microg/kg/dose without increasing the volume of feed. This approach was repeated until oral feeding was tolerated at least twice, and only then the volume of oral feed was increased. During night shift (between 11 p.m. and 5 a.m.), atropine concentration and amount of oral feed were not increased. If vomiting recurred, the volume of oral feed was decreased to the last tolerated volume and maintained until the following day. Oral atropine was increased until predetermined maximum oral dose (0.1 mg/kg/d) was reached. If oral administration of atropine was ineffective, a decision to perform pyloromyotomy was made no later than 7 days after commencement of oral atropine.
  
  
  RESULTS
  Atropine had effect (vomiting frequency less than twice per day) on average 3.29 days (range 1-7 days) from commencement. Oral atropine was tolerated very well, and was effective in 18 cases. Four cases were referred to pyloromyotomy, on day 4 (2 patients), day 5 (1 patient) and on day 6 (1 patient) of atropine treatment. Therapy was continued until US showed normalization of pyloric muscle thickness, passage of food through wide pyloric channel and until patients started gaining weight. Average duration of therapy was 24.05 days (11-39 days). Neither of patients from our group was treated with intravenous atropine sulfate.
  
  
  CONCLUSIONS
  Although intravenous atropine is more effective (as shown by Nagita et al), there is an increased incidence of side effects such as flushing and tachycardia. Oral atropine has been used successfully by other teams without side effects, and there were no side effects or complications related to the use of atropine in this study. Prospective, randomized study comparing outcomes of medical versus surgical management of IHPS in our hospital has been currently in progress and will provide further information on potential role of atropine in the management of patients with IHPS.
  
  
  CONCLUSIONS
  We believe it is unlikely that oral or intravenous atropine will ever replace surgery for IHPS, but it may be a good alternative to pyloromyotomy, particularly in children with major concurrent primary disease, or when parents are not enthusiastic about surgery in so young children.
authors.forename: Aleksandar
authors.initials: A
authors.lastname: Sretenović
authors.forename: Zeljko
authors.initials: Z
authors.lastname: Smoljanić
authors.forename: Gradimir
authors.initials: G
authors.lastname: Korać
authors.forename: Sanja
authors.initials: S
authors.lastname: Sindjeć
authors.forename: Marija
authors.initials: M
authors.lastname: Lukac
authors.forename: Zoran
authors.initials: Z
authors.lastname: Krstić
mesh_terms: D000284:Administration, Oral; D001285:Atropine / Q000008:administration & dosage*; D005260:Female; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D018727:Muscarinic Antagonists / Q000008:administration & dosage*; D046248:Pyloric Stenosis, Hypertrophic / Q000188:drug therapy*
chemical_list: D018727:Muscarinic Antagonists; D001285:Atropine