Congenital hypertrophic pyloric stenosis (CHPS): Integrated approach

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Introduction:

  • “Congenital” is a misnomer as it is never present at birth
  • It presents 4-6 weeks after birth with non-bilious vomiting
  • Common in first male child
  • Associated with “Erythromycin” use in early life.

Examination:

  • On examination, an “olive shaped” mass is felt on epigastrium, which is hypertrophied pylorus
  • Direction of gastric peristalsis is: Left to right.

Investigation:

  • IOC is USG; characteristic finding is length of pylorus ≥16 mm & thickness ≥4 mm

 

  • Signs on USG:
  1. Target sign
  2. Antral nipple sign
  3. Cervix sign.

  • Signs of barium meal (proximal to distal):
  1. Caterpillar sign, Shoulder sign, Beak sign, Teat sign
  2. String sign, Double/ Triple track sign, Diamond sign
  3. Mushroom sign.

  • X-ray sign: “Single bubble” sign.

Electrolyte imbalance in CHPS:

  • Electrolyte imbalance is the MC cause of death in CHPS
  • MC electrolyte imbalance: Hypochloremic hypokalemic metabolic alkalosis with paradoxical aciduria
  • Urine is initially alkaline, but gets acidic later due to aldosterone activity; so, paradoxical aciduria is a late feature
  • All ions are depleted (H/ Cl/ Na/ K)
  • Most important ion to be corrected: ??−
  • Concentration of NS used in CHPS: 0.45%

 

Surgery:

  • TOC is Ramstedt’s pyloromyotomy (Transverse incision → Splitting of pyloric muscle)

  • If surgery is done without correcting electrolyte imbalance, it may lead to postoperative apnea due to loss of respiratory drive as ?+ ions are depleted.
  • Medical management (not good): Atropine injection/ Balloon dilatation.

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