LECTURE 4

Ombilical area abnormalities

Abdominal wall defects
Intussusception
Hypertrofic pyloric stenosis
OMPHALO-MEZENTERIC
(VITELLINE) DUCT
ABNORMALITIES
•The vitelline duct
connects the fetal gut to
the yolk sac
•Involutes during the fifth
to sixth weeks of
gestation

•Failure of regression of
the antimezenteric area -
a true diverticulum
(Meckel’s)

•Persistence may be
present in a number of
anatomic variations.
These anomalies may be
asymptomatic or the
cause of a number of
complications
•Incomplete regression:
•Umbilical sinus
•Vitelline cyst
•Fibrous cord
•Meckel’s diverticulum
•Complete persistence: omphalo-enteric fistula
•Excessive regression: atresia
Urachal
abnormalities
 Meckel’s Diverticulum
 The most common congenital anomaly of the
gastrointestinal tract – 2% in general
population
 Only 4% will be symptomatic :
 Bleeding secondary to heterotopic tissue is the
most common complication
 Lead point for an intussusception, resulting in
a bowel obstruction
 Volvulus
 Acute Inflamation
 Diagnosis

 Clinic
 hemorrhage (40%-60%) - dark, tarry stools or red, gross blood if
bleeding is heavy
 obstruction(25%)
 diverticulitis (10%-20%) – acute appendicitis like symptoms

 Technetium-99m (99mTc) pertechnetate

scintigraphy of the abdomen is commonly
used to help detect ectopic gastric tissue in a
Meckel’s diverticulum
ABDOMINAL WALL DEFECTS
Embriology – abdominal wall

 4th week of gestation from differential growth of the

embryo causing infolding in the craniocaudal and
mediolateral
 The lateral abdominal folds of the embryo meet in
the anterior midline and surround the yolk sac,
eventually constricting the yolk sac into a yolk stalk
that becomes the site of the umbilical cord
 6th week rapid growth of the intestine causes
herniation of the midgut into the umbilical cord


 week 10 - midgut returned to the abdominal cavity

 Omphaloceles
 Occurs if the intestines fail to return to the abdominal cavity

 Varying amounts of bowel may be contained within the

omphalocele sac

 Viscera including liver, bladder, stomach,ovary, and testis can

also be found within the sac

 The sac consists of the covering layers of the umbilical cord,

which include amnion, Wharton’s jelly, and peritoneum.

 The umbilical cord is attached to the sac itself.

Omphalocels diagnosis

 Prenatal

 Associated malformations – multiple

 Cardiac
 Central nervous system
 Genitourinary
 Cromosomial

 Postnatal
 Omphaloceles - treatment

 Intravenous access for fluid resuscitation

 Limit trauma to the sac
 Surgery
 Primary closure – small sac – evaluation of
intrabdominal pressure
 Large defects with the loss of domain in the
peritoneal cavity prevents primary closure
without an undue increase in intra-abdominal
pressure
 Prostetic mesh
 Omphaloceles - treatment

 Surgery
 Staged closure – Schuster – silicone bag

 “Escharotic therapy” which results in gradual

epithelialization of the omphalocele sac
(iodine, polymer membrane, silver sulfadiazine, and
Nystatin powder)
Gastroschisis

 Less clear etiology

 failure of the mesoderm to form in the anterior
abdominal wall

 failure of the lateral folds to fuse in the midline

leaves a defect to the right side of the umbilicus

 thrombosis of the right omphalomesenteric vein

(umbilical vein) causes necrosis of the surrounding
abdominal wall, leading to the right-sided defect
(association with intestinal atresia)
Gastroschisis

 Latero ombilical defect

 No sac
 Eviscerated bowel

 Associated malformations : intestinal atresia

Gastroschisis -diagnosis

 Prenatal
 Sonographically by 20 weeks’ gestation

 Abnormal elevated maternal serum α-fetoprotein

level

 Detection of bowel loops freely floating in the

amniotic fluid and a defect in the abdominal wall
to the right of a normal umbilical cord insertion
are diagnostic of gastroschisis
Gastroschisis – treatment

 Early delivery - to limit exposure of the bowel

to amniotic fluid in an attempt to reduce the
inflammatory peel on the surface of the
bowel

 Poor motility of the bowel is thought to be

related to exposure to the amniotic fluid and
altered bowel wall cellular and extracellular
matrix composition
Gastroschisis – treatment
 Significant evaporative water losses from the open abdominal
cavity and exposed bowel
 Intravenous access and fluid resuscitation
 Nasogastric decompression

 The child should be positioned on the right side to prevent

kinking of the mesentery and resultant bowel ischemia
 The herniated bowel should be wrapped in warm saline-soaked
gauze
 The bowel should be wrapped with plastic wrap or the infant
placed with the bowel and legs in a plastic bag to reduce
evaporative losses and improve temperature homeostasis
Gastroschisis – surgical
treatment
 Primary closure
 incorporate the umbilicus as an allograft or
nonabsorbable mesh
 reduce the bowel and place a piece of Silastic
sheeting under the abdominal wall to prevent
evisceration
 !!!!!! Intraabdominal pressure > 10-15 mmHg -
ischemia
Gastroschisis – surgical
treatment
 Staged closure

 Introducing the bowel in a preformed silo bag

 The bowel is gentle reduced twice a day

 Definitive closure 1-14 days

INTUSSUSCEPTION
Intussusception

 One of the most frequent causes of bowel

obstruction in infants and toddlers
 Acquired invagination of one portion of the
intestine into the adjacent bowel
 the proximal, inner segment of intestine
(intussusceptum)
 the outer distal, receiving portion of intestine
(intussuscipiens) last

 80- 95 % of pediatric intussusceptions are

ileocolic
Intusssuception

 Primary (idiopathic)

 do not have a pathologic lead point

 hypertrophied Payer’s patches within the ileal wall
(upper respiratory tract infection or an episode of
Gastroenteritis)
 Adeno/rotaviruses
 6 to 36 months
 Secondary
Intusssuception
 Secondary
 Identifiable lesion that serves as a lead point, drawing
the proximal bowel into the distal bowel by peristaltic
activity

 Tend to increase in proportion to age, especially after

2 years of age
 Meckel’s diverticulum
 polyps and duplications
 appendix,
 hemangiomas,
 carcinoid tumors,
 foreign bodies,
 ectopic pancreas or gastric mucosa, hamartomas from Peutz-
Jeghers syndrome
 lipomas
 Diagnosis - clinic
 a young healthy child
 intermittent, crampy abdominal pain
 pain is sudden in onset in a child who was previously
comfortable
 between attacks, the child may appear
comfortable or may fall asleep.
 followed by vomiting

 with “currant jelly” stools

 a palpable mass on physical examination
 prolapse of the intussusceptum through the anus
Diagnosis - radiology

 Plain abdominal xray – fluid air levels ,

abdominal mass

 Ultrasound – intussusception “tumor”

 alternating rings of low and high echogenicity
representing the bowel wall and mesenteric fat
within the intussusceptum. This characteristic
finding has been referred to as a “target” or
“doughnut” lesion
 Treatment - nonoperative
 hydrostatic reduction -85%
 Barium under xray controll
 Hydrosoluble contrast study under x ray controll
 Pneumatic
 Ultrasound
Treatment - surgery

 Failure of hydrostatic reduction

 Signs of perforations
 Symptoms lasting more than 48 h

 Open/laparoscopic procedures
HYPERTROPHIC PYLORIC
STENOSIS (HPS)
 HPS

 Aquired lesion – progressively hypertrophy of

the muscular pyloric fibres
 HPS

 1 to 4 per 1000 live births in white infants

 4:1 male-to-female ratio
 Risk factors
 family history
 gender
 younger maternal age
 being a first-born infant
 Diagnosis

 Typical vomiting

 Palpation of the pyloric olive (Benson

maneuver) – relaxed infant (pacifier); fingers
under hepatic edges will “trap” the “ olive”
 Diagnosis

 Nonbilious, projectile, forceful vomiting

 2-8 weeks old child
 Initially, the emesis is infrequent, over a short
period of time, occurs with every feeding
 30min after meal
 Recent and digested milk
 Dehydration
 Visible peristaltic waves
 Diagnosis

 Contrast meal

 Ultrasound – standard technique

 muscle thickness > 4 mm and a length > 16 mm
 Diagnosis

 Lab tests:
 Hipocloremia

 Hipokalemia

 Metabolic acidosis
 Treatment

 Fluid resuscitation

 Surgical treatment : Extramucousal

piloromiotomy Fredet Ramstedt Weber
 Open
 Laparoscopic