pyloric stenosis Flashcards
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Diagnosis is most commonly made by ultrasound
[plyroic muscle diameter >3-4mm + pyloric channel >18mm in length is diagnostic]
Bloods- u&es: hypochloremic, hypokalemic alkalsis 2ry to vomiting [low Cl-, low K+, high bicarb, high urea, + base excess
ddx
GORD - small effortless vomiting, not projectile like PS
overfeeding - these infants have no difficulty gaining weight
malroation- billous emesis [unlike in PS where there is non billous emesis]
acute infectious diorrhoea - diarrhoea usually follows vomiting
duodenal atresia - seen in neonates, billous emesis
jejunoileal atresia- billous atresia
plyroic atresia- non billous emesis in neonates upon feeding, confirmed by GI contrast study showing gastric outlet
Epidemiology
incidence of 4 per 1,000 live births
4 times more common in males
10-15% of infants have a positive family history
first-borns are more commonly affected
Features
🌹’projectile’ vomiting, typically 30 minutes after a feed
🌹hunger after vomiting until dehydration leads to decrease interest in feeding
🌹constipation and dehydration may also be present
🌹a palpable mass [olive sized]may be present in the upper abdomen
🌹hypochloraemic, hypokalaemic alkalosis due to persistent vomiting
🌹 visible peristalsis from L to RUQ during feed
distended abdo w/ air: must be emptied w/ NG tube before palpation
weight loss if presentation delay/failure to thrive
define
typically presents in the second to fourth weeks of life with vomiting,
although rarely may present later at up to four months. It is caused by hypertrophy and hyperplasia of the circular muscles of the pylorus= causing gastric outflow obstruction
complications
recurrence = uncommon
intraop: gastric/duodenal perforation can occur, <1% morbidity
prog
excellent post surgery
initial pre op vomiting is common but settles after 24-48 hrs
Management
is with Ramstedt pyloromyotomy
pre op–> do fluid resus, correct electrolye imbalance [fluid to correct dehydration w/ K+ correction]
