Introduction
• Pyloric stenosis is also known as pylorostenosis or infantile hypertrophic pyloric stenosis. It is the most common cause of intestinal obstruction in infants. It is a form of obstruction in the gastric outlet which means a blockage from stomach to intestine.
• It was First described by Hirschsprung in 1888
• Ramstedt described an operative procedure to alleviate the condition in 1907 – the procedure used to this day to treat pyloric stenosis.
Definition
• Hypertrophic pyloric stenosis is a marked and progressive outgrowth or enlargement of circular muscle fibers of pylorus causing partial or total obstruction of the stomach outlet due to narrowing of lumen.
Anatomy
The stomach sits in the upper abdomen on left side of the body. The top of the stomach connects to a valve called the esophageal sphincter (a muscle at the end of esophagus). The bottom of stomach connects to small intestine.
The stomach is divided into 5 regions:
• The cardia is the top part of the stomach. It contains the cardiac sphincter, which prevents food from traveling back up the esophagus.
• The fundus is a rounded section next to the cardia. It's below the diaphragm (the dome-shaped muscle that helps to breathe).
• The body (corpus) is the largest section of the stomach. In the body, stomach contracts and begins to mix food.
• The antrum lies below the body. It holds food until the stomach is ready to send it to your small intestine.
• The pylorus is the bottom part of the stomach. It includes the pyloric sphincter. This ring of tissue controls when and how stomach contents move to the small intestine.
Incidence
• It is more commonly seen in child with 2-5wks of age.
• 2-9 per 1000 livebirths can be born with this condition.
• Predominant sex: Male > Female (6:1). Males are more prone to get
• Genetic predisposition can be an underlying factor for disease causation.
• Full term babies especially first borne are most commonly affected.
• Death from infantile hypertrophic pyloric stenosis is rare and unexpected; the reported mortality rate is very low and usually results from delays in diagnosis with eventual dehydration and shock.
Etiology
• Idiopathic
• Other factors : *maternal stress especially in third trimester *elevated prostaglandin levels *deficiency of nitric acid *immature pyloric ganglion cells with abnormal muscle innervation.
• In adults, it can occur due to history of peptic ulcer in pylorus region and hypertrophic changes in muscle layer of pylorus.
Risk factors
• Sex. Pyloric stenosis is seen more often in boys — especially firstborn children — than in girls.
• Race. Pyloric stenosis is more common in whites of northern European ancestry, less common in Black people and rare in Asian
4. INTRODUCTION
• Pyloric stenosis is also known as pylorostenosis or
infantile hypertrophic pyloric stenosis.
• Common cause of intestinal obstruction in infants
• First described by Hirschsprung in 1888
• Ramstedt described an operative procedure to
alleviate the condition in 1907 – the procedure
used to this day to treat pyloric stenosis
5. DEFINITION
• Hypertrophic pyloric stenosis is
a marked and progressive
outgrowth or enlargement of
circular muscle fibers of
pylorus causing partial or total
obstruction of the stomach
outlet due to narrowing of
lumen.
9. INCIDENCE
• First 2-5wks
• 2-9 per 1000 livebirths
• Predominant sex: Male > Female (6:1)
• Genetic predisposition
• Full term babies especially first borne
• Deaths are rare-delay in diagnosis----
dehydration----shock
10. ETIOLOGY
• Idiopathic
• Other factors :
maternal stress especially in third trimester
elevated prostaglandin levels
deficiency of nitric acid
immature pyloric ganglion cells with abnormal muscle
innervation.
11. In adults, it can occur due to history
of peptic ulcer in pylorus region and
hypertrophic changes in muscle
layer of pylorus.
12. RISK FACTORS
• Sex
• Race
• Premature birth
• Family history
• Smoking during pregnancy
• Early antibiotic use
• Bottle feeding
13.
14. Persistent vomiting results in loss of stomach
acid (hydrochloric acid).
As a consequence, all ingested food and gastric
secretions can only exit via vomiting, which can
be of a projectile nature.
THE GASTRIC OUTLET OBSTRUCTION DUE TO
THE HYPERTROPHIC PYLORUS IMPAIRS EMPTYING OF GASTRIC
CONTENTS INTO THE DUODENUM.
15. The chloride loss results in a low blood chloride
level which impairs the kidney's ability to excrete
bicarbonate. This is the significant factor that
prevents correction of the alkalosis.
A secondary hyperaldosteronism develops due to
the decreased blood volume.
The vomited material does not contain bile
because the pyloric obstruction prevents entry of
contents (containing bile) into the
duodenal
stomach.
16. THE HIGH ALDOSTERONE LEVELS CAUSES THE
KIDNEYS TO RETAIN NA+ (TO CORRECT THE
INTRAVASCULAR VOLUME DEPLETION), AND EXCRETE
INCREASED AMOUNTS OF K+ INTO THE URINE (RESULTING IN
A LOW BLOOD LEVEL OF POTASSIUM).
The body's compensatory response to the
metabolic alkalosis is hypoventilation resulting in
an elevated arterial pCO2
17.
18. Signs of pyloric stenosis usually
appear within three to five weeks after
birth.
Pyloric stenosis is rare in babies older
than age 3 months. Signs and
symptoms include:
19. Vomiting after feeding. The baby may vomit
forcefully, ejecting breast milk or formula up
to several feet away (projectile vomiting).
Vomiting might be mild at first and gradually
become more severe as the pylorus opening
narrows. The vomit may sometimes contain
blood.
21. Stomach contractions. Notice wave-
like contractions (peristalsis) that ripple
across baby's upper abdomen soon
after feeding, but before vomiting. This
is caused by stomach muscles trying
to force food through the narrowed
pylorus.
22. Dehydration. Baby might cry without
tears or become lethargic. You might
find yourself changing fewer wet
diapers or diapers that aren't as wet as
you expect.
23. Changes in bowel movements.
Since pyloric stenosis prevents food
from reaching the intestines, babies
with this condition might be
constipated.
27. DIAGNOSTIC EVALUATION
• CLINICAL SIGN : OLIVE like mass
• LABORATORY:
• · Early - evidence hypochloremic alkalosis, with low
serum chloride and high bicarbonate
• · Later - may have acidosis with low bicarbonate and
low potassium
• · Elevated unconjugated bilirubin level
28. CONTD….
IMAGING:
• Upright plain film of
abdomen may reveal dilated
stomach (filled with fluid
and/or air).
• Ultrasound (first choice if
available) shows thickened
and elongated pyloric
muscle·
29. • Barium swallow (performed only when
diagnosis is not clinically clear) reveals strong
gastric contractions and elongated, narrow
pyloric canal (string sign); now rarely
performed if ultrasound available
31. THERAPEUTIC MANAGEMENT
• In infants who present with dehydration, fluid resuscitation
begins before diagnostic procedures are initiated.
• Correction of alkalosis and hypokalemia is essential before
surgical treatment, which is non emergent and performed
only after the baby is stabilized.
32. • Initial treatment
Insert 8fr NG tube
2hrly aspiration
• Fluid Regimen and Electrolyte Correction
a) Correct hypovolemia-rehydrate with 0.9%NACL in boluses of 10ml/kg
and monitor central & peripheral capillary return(<2s)
b) Maintenance fluids-
• If sr. bicarb >25mmol/l –use 0.9%NaCl+5% Dextrose+10mmol KCl
per 500ml @ 150mlml/kg/day
• If sr. bicarb >/25mmol/l –use 0.9%NaCl+5% Dextrose+10mmol KCl
per 500ml @ 100mlml/kg/day
c) Replace NG losses-every 1ml of gastric losses must be replaced with
1ml of either
* 0.9%NaCl+13.5mmol KCl per 500ml
* 0.9%NaCl+10mmol KCl per 500ml
33. • Medications
• IV Atropine : Various studies-0.04-0.225mg/kg for 1-10days
• Oral Atropine : after iv therapy deemed successful
0.08-0.45mg/kg/day for 3wks to 4mons
34. Surgical Management
Ramstedt pyloromyotomy
• A longitudinal incision divides the serosal muscle on the
anterior surface of the pylorus down to the submucosa.
• Minimally invasive through laparoscope.
36. Consider thermoregulation at all
times,
Before transport to theatre, transfer
thermal environment
infant to incubator set at neutral
(NTE)
temperature.
Ensure incubator be plugged in and
pre-warmed for the infant to be
transferred.
After return ensure
temperature
to the ward,
is stable prior to
transferring to open cot.
37. Post operative management
Monitor temperature hourly until stable.
Routine post anaesthetic observations.
Monitor wound and report abnormalities
to surgeon.
Observe for bleeding, redness, swelling,
ooze from incision site.
Maintain adequate fluid balance chart.
Monitor IV site.
Ensure adequate pain relief; use pain
assessment tool.
38. NURSING ASSESSMENT
h/o vomiting-when, character of vomitus.
Elimination-constipation, scanty urine.
P/E- s/o dehydration, wt. skin turgor, ant.
fontanelle, temperature, apical pulse, irritability,
lethargy, lips & mucous membranes of mouth,
eyes, visible gastric peristalsis while feeding.
39. NURSING DIAGNOSIS
Imbalanced nutrition less than body
requirements related to inability to retain food
Deficient fluid volume related to frequent
vomiting.
Impaired oral mucous membrane related to
NPO status
Risk for impaired skin integrity related to fluid
and nutritional deficit.
Compromised family coping related to
seriousness of illness and impending surgery
40. NURSING INTERVENTIONS
Maintain adequate nutrition & fluid intake
Mouth care and use of pacifier
Promote skin integrity-positioning, diaper change,
linolin oinment for dry areas.
Promote family coping.
41. Practice Quiz: Pyloric Stenosis
1. Nurse Nancy is assessing a child with pyloric
stenosis; she is likely to note which of the
following?
A. “Currant jelly” stools.
B. Regurgitation.
C. Steatorrhea.
D. Projectile vomiting.
42. 2. An infant diagnosed with pyloric stenosis
is admitted with history of vomiting for
several days. Which nursing diagnosis would
be the priority?
A. Deficient fluid volume related to
prolonged vomiting.
B. Ineffective airway clearance related
to impaired swallowing.
C. Imbalanced nutrition: less than body
requirements related to prolonged
vomiting.
D. Anxiety related to loss of body control.