INTRODUCTION. 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. AIM. 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?
to 30? 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 ?g/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. DISCUSSION. Although
intravenous atropine is more effective (as shown by Nagita et al [7]), 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
[9, 11, 13], 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. CONCLUSION. 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.
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