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Infantile hypertrophic pyloric stenosis

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In 95% of infants with pyloric stenosis the age at ... postprandial, non-bilious, often projectile VOMITING and demands to be re-fed soon afterwards ... – PowerPoint PPT presentation

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Title: Infantile hypertrophic pyloric stenosis


1
Infantile hypertrophic pyloric stenosis
  • Dr Rajesh
  • 22/08/07

2
CHPS
  • 25 days old infant with repeated projectile
    vomiting
  • Dehydrated
  • ? Tumor felt in right hypochondrium

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5
CHPS

6
Historical Perspective
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8
Normal pylorus
9
IHPS
10
Mucosal thickness
11
Pathology
  • Thickened and elongated Pyloric channel
  • Hypertrophied and redundant pyloric mucosa
  • Gastritis
  • Decreased nerve cells, NO syntetase activity in
    the muscle

12
Age of presentation
  • In 95 of infants with pyloric stenosis the age
    at presentation is between 3 and 12 weeks of
    life, typically between 3 and 8 weeks.
  • Pyloric stenosis has been reported in neonates
    within the first day of life.

13
etiology
  • 3 in 1,000 live births
  • more commonly in males
  • 30 percent of cases occur in firstborn
  • genetic predisposition
  • Sibling has 5 times more incidence
  • environmental factors
  • Neonatal hypergastrinemia and gastric
    hyperacidity may have a role

14
Etiology
  • Multifactorial
  • Environmental Adequate folic acid and
    multivitamin supplementation,during pregnancy
    have resulted in a reduced occurrence of pyloric
    stenosis in the infants
  • Intrauterine exposure to Bendectin
    (doxylamine/dicyclomine/pyridoxine), which until
    1983 was widely used to treat nausea and vomiting
    in pregnancy, is considered a risk factor for the
    development of pyloric stenosis in infants.
  • Pyloric stenosis has been seen following
    ingestion of erythromycin given as pertussis
    prophylaxis or through breastmilk. Pyloric
    stenosis has also been suspected to follow
    transpyloric feedings of infants.
  • Geneticpyloric stenosis in chromosomal anomalies
    and in inherited disorders such as X-linked
    ichthyosis. Family trees of patients with pyloric
    stenosis have been described, The incidence in
    siblings of affected infants is as high as
    85/1000, and pyloric stenosis in twins and
    triplets has been reported
  • Three major malformations occurred more
    frequently in children with pyloric stenosis
    intestinal malrotation, defects of the urinary
    tract, and esophageal atresia.

15
Patophysiology
  • Failure of pylorus relaxation,Absence, reduction,
    or delayed maturation of Interstitial cells of
    cajal ( Intestinal pacemaker)
  • Increased gastric acid secretion and an increased
    parietal cell mass with enhanced release of
    secretin and cholecystokinin have been described
  • Prostaglandin E2 was increased in the gastric
    juice
  • Increased amounts of insulin-like growth factor,
    transforming growth factor, platelet derived
    growth factor, epidermal growth factor, as well
    as growth factor receptors in hypertrophied
    circular and longitudinal smooth muscle of
    patients with pyloric stenosis.
  • Abnormal innervation of smooth muscle cells of
    the pylorus in pyloric stenosis. Recently,
    interest has been directed at the role of nitric
    oxide in pyloric stenosis, It mediates relaxation
    of smooth muscle,

16
Metabolic Changes
  • Repeated vomiting loss of water, sodium,
    potassium, chloride, and hydrogen ions develops
    hypochloremic metabolic alkalosis with
    hyponatremia and hypokalemia
  • Sodium Consevation The urine is initially
    alkalotic from excreted bicarbonate, Sodium is
    mostly reabsorbed in an attempt to maintain
    extracellular volume, but there is some
    obligatory sodium loss accompanying bicarbonate
    in the urine, In spite of low serum potassium,
    additional potassium excretion may occur in
    exchange for sodium reabsorption under the
    influence of aldosterone, adding to the potassium
    loss. Similarly, excretion of hydrogen ions in
    the kidney in exchange for reabsorbed sodium may
    result in paradoxical aciduria in the presence of
    a systemic metabolic alkalosis
  • Metabolic alkalosis from pyloric stenosis can
    cause hypoventilation with a resultant
    hypercapnia.
  • As dehydration progresses, metabolic acidosis,
    starvation ketosis, and possibly hyperkalemia
    from prerenal failure may be seen

17
CLINICAL MANIFESTATIONS
  • The classic presentation of IHPS is the three- to
    six-week-old baby who develops immediate
    postprandial, non-bilious, often projectile
    VOMITING and demands to be re-fed soon afterwards
  • (a "hungry vomiter").

18
CLINICAL MANIFESTATIONS
  • In a major study infants diagnosed between 1957
    to 1969, the mean age in which the infants
    beganvomiting was 22 days

19
Palpable mass
  • The mass is most easily felt immediately after
    emesis because it may otherwise be obscured by a
    distended antrum and/or tensed abdominal muscles

20
VGP
  • Peristaltic waves may be seen progressing across
    the child's upper abdomen from left to right just
    before emesis.

21
Metabolic changes
  • Bicarbonate gt 29 mEq/l and serum chloride lt 98
    mEq/l are considered indicative of hypochloremic
    metabolic alkalosis in pyloric stenosis.
  • The severity of dehydration and metabolic
    alkalosis
  • Mild serum bicarbonate lt 32 mEq/l, serum
    chloride gt 100 mEq/l,
  • Moderate serum bicarbonate 32-42 mEq/l, serum
    chloride 90-100 mEq/1,
  • Severe serum bicarbonate gt 42 mEq/l, serum
    chloride lt 90 mEq/l,

22
D/D
  • GER
  • Hiatal hernia
  • Pylorospasm
  • Preampulary duodenal obstruction

23
DIAGNOSIS
  • mass is palpable
  • ultrasound or upper gastrointestinal (UGI)
    contrast study
  • pyloric muscle length (PML), and pyloric diameter
    (PD). Published criteria have ranged from 3 to 4
    mm for PMT, 15 to 19 mm for PML, and 10 to 14 mm
    for PD

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Barium studies

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Double track sign
29
Non-surgical management
  • Balloon catheter dilatation of the stenotic
    pylorus,
  • Injection of botulinum toxin,
  • Antispasmodics to relieve pylorospasm,
  • Transpyloric nasoduodenal feeding
  • AtropineOral or intravenous atropine has been
    used successfully in patients with pyloric
    stenosis. Atropine temporarily suppresses spastic
    contractions of pyloric muscle in pyloric
    stenosis, and it resulted in cessation of
    vomiting and eventual regression of pyloric
    hypertrophy.

30
Successful Management of Infantile Hypertrophic
Pyloric Stenosis with Atropine Sulfate IP
2001Utpal Kant Singh, Ranjeet Kumar and Shivani
Suman
  • Atropine was initially administered intravenously
    in a dose of 0.06 mg/kg/day in eight divided
    doses, increased by 0.15 mg/kg/day till vomiting
    ceased and remained so for a period of 24 hours
    at a stretch, then substituted by oral atropine
    at double the effective IV dose for 3 weeks.
  • Results Medical treatment of IHPS with atropine
    was successful in 50/52 (96.2) cases. Vomiting
    ceased in 1-3 days in all patients with mild
    hypertrophy and in 4-7 days in all the cases with
    moderate hypertrophy. In all except 2 patients
    with severe hypertrophy, vomiting ceased in 8-12
    days. These two cases continued to vomit at least
    once daily even after 2 weeks of IV treatment and
    ultimately opted out for pyloromyotomy. All the
    50 medically treated children made uneventful
    recovery during oral therapy except 3 cases (6)
    in whom vomiting recurred during the follow-up.
    These 3 children later responded by increasing
    the dose of oral atropine. All of them began to
    gain weight by the time oral therapy was
    commenced and ultrasonographic evidence of
    normalization of pylorus was observed in all
    these children 3-15 months after completion of
    oral therapy.
  • Conclusion Atropine sulfate proved to be an
    effective and safe treatment option for IHPS.

31
Intravenous atropine treatment in infantile
hypertrophic pyloric stenosis ADC 2002 H
Kawahara, K Imura, M Nishikawa, M Yagi and A
Kubota
  • Of the 19 infants, 17 (89) ceased projectile
    vomiting after treatment with intravenous (median
    seven days) and subsequent oral (median 44 days)
    atropine administration. The remaining two
    infants required surgery. No significant
    complications were encountered. Ultrasonography
    showed a significant (p lt 0.05) decrease in
    pyloric muscle thickness, but no significant
    shortening of the pyloric canal after completion
    of the atropine treatment. The patients exhibited
    failure to thrive at presentation, but were
    thriving at 6 months of age (p lt 0.01).

32
Medical Vs Surgical
  • Medical management may be successful in less
    severe cases, but treatment takes longer and the
    complication rate from medical management was
    higher.
  • Surgical therapy is considered superior to
    conservative management, since complications are
    seldom, long-term results are equal, and patients
    get better sooner.

33
TREATMENT
  • The timing of surgery depends upon the clinical
    status of the infant. If the diagnosis is made
    early and the child is well-hydrated with normal
    electrolytes, surgery may take place on the day
    of diagnosis. Surgery should be delayed in the
    setting of dehydration and/or electrolyte
    derangements

34
High Anaesthetic risk
  • Small infant
  • Metabolic derangements
  • Full stomach

35
Pre-op management
  • Rehydration
  • May require initial saline bolus
  • 45 DNS twice the maintanance
  • Add potassium 20 meq/L after infant passes urine
  • Correction of alkalosis is important serum
    chloride of 100 mEq/l and higher generally
    reflects satisfactory rehydration,

36
Ramstedt extramucosal pyloromyotomy
  • Highly effective simple, elegant, and inexpensive
    operation
  • Described as 'one of the most easy and gratifying
    procedures performed by pediatric surgeons
  • 'the most consistently successful operation ever
    described

37
Complications of surgery
  • Most frequent complications as GER (11 percent),
    duodenal perforation (8 percent), and wound
    infection (5 percent). The incidence of wound
    dehiscence and bleeding is very low .

38
Post-op management
  • Watch for apnea
  • Intravenous administration of 5 dextrose in 0.25
    to 0.45 NaCl solution at a maintenance rate
  • Blood sugar levels may be checked intermittently
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