INFANTILE HYPERTROPHIC PYLORIC STENOSIS

(IHPS)

 Previously called Congenital Hypertrophic Pyloric Stenosis (CHPS)

But changed as the baby is born completely normal (usually full-

term) not congenitally abnormal

 Isolated congenital anomaly

Incidence:

1- 2 - 3.5 / 1000 live born infants

2- Males: Females ratio 4:1 up to 6:1

3- 30 - 40% of the affected babies are usually the first-born

child
 4- It affects pre-mature infants slightly higher than the full-

term neonates

Etiological Factors:

1- Family history:

 high in certain families.

 20% of boys and 10% of girls born to a mother who had an

operation for IHPS will suffer from the condition.

2- Smoking mothers will have 1.5 double the incidence to have an

infant with IHPS

3- Certain antibiotics (the macrolides group ex: Erythromycin and

Azithromycin) used by the mother during last weeks (8th or 9th

month) of pregnancy or given to the neonate during the first 2

weeks of life

4- Bottle feeding increases the risk of developing IHPS by 4 folds

regardless the formula used.

5- Genetic predisposition and Environmental factors

6- Hypergastrinemia and hyperacidity but with a little evidence of

connection

7- An autonomic nervous system imbalance and humoral factors may

cause hypertrophy of the pyloric circular muscle fibers

Symptoms and signs:

 Timing: Usually starts between the end of the 2nd and 5th

week. Rarely after the 12th post-natal week (if after 12th week

look for other causes of vomiting)

 Vomiting (4Ps): Progressive, Persistent, Projectile and Non-bilious

(as it’s before the bile duct insertion)

o Progression:

At the end of the 2nd week (day 10 or 11 usually) the

vomiting is a couple of minutes after the meal 

immediately after the feeding  in the middle of the

feeding
  Characters of the vomiting?

1- Starts as week projectile vomiting  increase in the

power (ejected for a longer distances)

2- At first form the mouth  then both mouth and nose

3- Starts intermittent  then become persistent (after

every meal)

4- Progressive (increase in power also frequency)

 At the end the infant becomes

 At the end of the first year it will decline

to 2-3 times/day
Physical Examination:

o If early: the baby is still in good condition

o If Late: signs and symptoms of dehydration, loss of weight and

malnutrition (face muscle are wasted, skin wrinkled, sunken eyes,

depressed fontanels)

1- Inspection:

 Dehydration signs

 Epigastric fullness (dilated stomach unless post vomiting)

 Peristaltic movement common from Lt to Rt (visible but not

palpable) if seen during the examination take a step back as

it precedes the vomiting!

Mass

 not easily palpable

 At the pylorus to the rt side of the epigastrium, below the

edge of the Rt lobe of the liver

 Found immediately after vomiting

Metabolic Derangement:

1- when the baby vomits, he loses hydrochloric acid and sodium in

the vomitus and becomes alkalotic and hyponatremic

2- Kidney compensation:

secretion of Hydrogen ions and Potassium ions in exchange for

Sodium ions to correct the already present hyponatremia 

paradoxical aciduria

3- The end result will be:

 Hypochloremia

 Hypokalemia

 Alkalosis

Investigation:

1- Labs:
  CBC: check for Hb

 Electrolyte panel

 ABG

 Kidney function

 Prothrombin time and concentration

2- Imaging:

 U/S shows:

 dimension of the pyloric tumor/mass causing the

obstruction

 Length and width of the pyloric canal

 X-Ray:

Thin barium meal and follow through:

 dilated stomach

 delayed gastric empty

 narrowed elongated pyloric canal

Management:

Preoperative preparation:

1- Nasogastric tube or gastric lavage with normal saline or Ringer

lactate to AVOID chemical or bacterial gastroenteritis

general condition to OVERCOME dehydration and hypoglycemia

3- Na/K adjustment to reach normal levels

4- 6 hrs Preoperative give Vit. K (konakion) and Ca to decrease the

incidence of bleeding

Operative management
Question: WHAT about endoscopic dilatation?

Ramstedt's operation Or Balloon dilatation trials have been done but

Pyloromyotomy 1- You may need to repeat

2- Over inflation may cause complication

So, it’s not successful and not traditionally used

1- Laparoscopically / open around the umbilicus or through right

small transverse subcostal incision above the pyloric tumor

2- The incision in the pyloric tumor is done in its antero-superior

aspect (the least vascular area)

3- Serosa and partial (very thin layer) thickness of the circular

muscle fibers of the pyloric tumor are incised by scalpel 11

 Cutting is done:

 Perpendicular to muscle fibers

 For the whole pyloric tumor

 Starting from the prepyloric vein to the near the

duodenum
 4- Muscle fibers are separated by an artery forceps till the pyloric

mucosa plugs

5- Avoid perforation the mucosa specially at the duodenal forensics.

6- If bleeding  diathermy or cautery

7- Do not close the incision

8- Use tube or rubber drain

9- No need for truncal vagotomy

Keep in Mind:

 HOW to check for serosal perforation?

1- By your finger: distal to the duodenum and try to squeeze the stomach with

closing near to it

2- Injection of saline or Air in the stomach using Ryle tube

 If perforated, HOW to deal with?

1- Close the opening by vicryl 5-0 with inverting sutures

2- Omental patch attached to the edges of the incision

Postoperative management:

1- In non-complicated cases,

 start oral feeding by glucose 5% small feeds for 24 hrs

 Breast feeding can be re-started 48 hours later.

least 48 hours post-operatively

3- Inform the parents that the vomiting will decrease gradually as

there might be gastric congestion and edema of the gastric wall

or the pyloric canal

4- Females don’t do well after the pyloromyotomy

 Vomiting continue for a while after the operation

 Duodenal ileus

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Best wishes,

Rawan Sayed