I
PYLORIC STENOSIS
v The mo st common surgical cause of vomiting in infancy.v It occurs at a rate of 1 to 4 per 1000 live births in white infants but is seen less in non -white children.
v Male to female ratio is 4:1.
PATHOPHYSIOLOGY
v Hypertrophy without hyperplasia .
v The thickened pyloric muscle protrudes distally into the duodenal lumen, producing a reflection of
duodenal mucosa that is subject to injury at the time of pyloromyotomy .
v The cause of HPS is unknown, but genetic and environmental factors appe ar to play a large role in the
pathophysiology (multifactorial ) .
v Risk factors for HPS include family history, gender, younger maternal age, being a first -born infant and
exposure to erythromycin.
v Abnormalities of local enteric innervations & diminished level of nitric oxide synthase have been
implicated .
v There is hypochloraemi c, hypokalaemi c metabolic alkalosis with paradoxical aciduria in severe cases .
v Jaundice may occure and it is self -limiting once postoperative feeding is initiated and due to transient
impairment of glucoronyl transferase.
CLINICAL FEATURES
v The classic presentation is nonbilious , projectile vomiting in a full -term neonate who is between 2 and 8
weeks old. Initially, the emesis is infrequent and may appear to be reflux. However, over a short period
of time, the emesis occurs with every feeding and becomes forceful (i.e., projectil e). The contents of the
emesis are usually the recent feedings, but signs of gastritis are not uncommon (“coffee -ground”
emesis).
v The vomiting is typically non -bilious and the infant is typically hungry after vomiting, eager to eat, only
to vomit once agai n.
v The presentation is slight later in preterm infants and only 4 % present at an age older than 3 months.
v Failure to thrive.
v Constipation.
v The degree of dehydration depend on the rapidity of diagnosis.
v Visible peristaltic waves may be present in the mid to left upper abdomen .
v Scaphoid abdomen .
v Palpable r ight upper quadrant olive is very important sign 75 -90% .
v Feeding teset: when the infant completely relax (some time do flexion of the hip)and using pacifier with
sugar water palpate the olive mass of the pyloric in the epigastric or Rt hypochondrial .
DIFFERENTIA l DIAGNOSIS
1. Pylorospasm .
2. Gastroesophageal reflux.
3. Gastroenteritis.
4. Increased intracranial pressure.
5. Metabolic disorders.
6. Anatomic causes e.g. an antral web, foregut duplication cyst.
IMAGING
A. U/S:
• Sensitivity 97 %, specificity 100 %.
• The diagnostic criteria for pyloric stenosis is a muscle thickness of greater than or equal to 4 mm
and a length of greater than or equal to 16 mm .
• Distinguish p ylorospasm (periods of relaxation ).
B. upper GI series (an equivocal ultrasound study) :
• String sign .
• Double track sign (shouldering sign) .
• Delayed gastric emptying.
II
PREOPERATIVE PREPARATION
v The mainstay of therapy is typically resuscitation followed by pyloromyotomy.v There are reports of medical treatment with atropine and pyloric dilation, but these treatments require
long periods of time and are often not effective.
v Initially, a 10 -20 -mL/kg bolus of normal saline should be given if the electrolyte values are abnormal.
Then D5/1⁄2NS with 20 to 30 mEq/L of potassium chloride is started at a rate of 1.25 to 2 times the
maintenance rate.
v Electrolytes should be checked every 6 hours until they n ormalize and the alkalosis has resolved. Then
the patient can safely undergo anesthesia and operation.
v It is important to appreciate that HPS is not a surgical emergency and resuscitation is of the utmost
priority.
v NGT is controversial , but may be used for severely distended stomach and to prevent aspiration
following contrast study and in case of perforation postoperatively.
v Preoperative antibiotic is controversial, not with standard incision.
OPERATIVE MANAGENENT (Ramstedt`s , 1912 )
v Evacuation of the stomach in the OR.
v Either open or la paroscopic pyloromyotomy.
v Avoid opening mucosa.
POSTOPERATIVE MANAGEMENT
v NGT is not necessary unless the mucosa has been entered.
v Feeding begin s 4-6 h ou rs after operation with G/W low volume , gradually increasing to full feeds over
the next 12 -24 hr. if vomiting, same volume can be repeated.
v Discharged the day after operation.
POSTOPERATIVE COMPLICATION S
v Unrecognized mucosal perforation.
v Wound infection and dehiscence .
v Postoperative emesis is common, occurring in up to 80% of patients at some point. Prolonged emesis is
less common is usually due to Gastroesophageal reflux or secondary to incomplete myotomy or
due to gastric atony .