SURGICALNEONATAL INTESTINAL OBSTRUCTION

Khaled H.K BahaaeldinProfessor of Pediatric Surgery

Cairo, University

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NEONATAL INTESTINAL OBSTRUCTION(NIO)

Definition:

An intestinal obstruction occurring during the first month of life.

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CAUSES OF NIO

Esophageal:Atresia (TOF)

Gastric Duodenal:

AtresiaStenosisDiaphragmMalrotation with bands or volvulusAnnular pancreas

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CAUSES OF NIO Jeujunal & ileal obstruction:

Obstructed inguinal hernia Intussusception Atresia Stenosis Meconium ileus Peritoneal bands or herniae Duplication cysts

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CAUSES OF NIO

Large bowl obstruction: Hirschsprung’s disease Anorectal anomalies Meconium plug syndrome Atresia (rarest)

Necrotizing enterocolitis Complicated Inguinal Hernias

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GENERAL PRINCIPLES

Any baby presenting with persistent, bile stained vomiting should be considered to be surgical emergency until proven otherwise.

Clinical picture:

The cardinal signs are 2C, 2V, 2D

Colics, Constipation

Vomiting, Visible peristalsis

Distension, Dehydration

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MANAGEMENTFirst aid: Gastric decompression (naso-gastric tube) IV line (for fluid replacement)

Deficit therapyMaintenance

Urinary catheter (to monitor urine output) Fluids:

Lactated Ringer’s solution 10-20ml/kg over an hour, to be repeated according to response

Drugs: To cover anaerobes as well as Gram stained bacteria

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CONGENITAL HYPERTROPHIC PYLORIC STENOSIS (CHPS)

Any neonate presenting with projectile, non bilious vomiting, associated with hunger and constipation should be considered CHPS

Incidence: 8:1000 M/F ratio=4:1 More in first born babies More in infants born to a mother who had suffered

from CHPS More during spring and autumn!

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Etiology: Unknown, but appears to be polygenic

(environmental, and genetic)

Pathology:Progressive hypertrophy of circular pyloric

musclesPersistent vomiting leads to development of

hypochloremic hyponatremic alkalosis and dehydration

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Clinical picture:Symptoms:

projectile, progressive, non bilious vomiting after which the baby is hungry and ready to suckle again. Classically the symptoms start 2-3 weeks after birth

Signs: Signs of dehydration which may be severe and life

threatening. Visible peristalsis in the upper abdomen can usually

be seen after the baby is given a test feed followed by projectile vomiting.

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Differential diagnosis: Gastroenteritis Gastro-esophageal reflux Other obstructive lesion of the gut Increased Intracranial tension

Investigations: Imaging: sonography and contrast X ray Laboratory: to detect and correct electrolyte and

metabolic disturbances Treatment:

First aid treatment to correct dehydration and metabolic disturbances

Definitive surgery, the Ramstedt’s pyloromyotomy

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DUODENAL OBSTRUCTION Atresia

Types: Type I: mucosal diaphragmatic (web) membrane Type II: short fibrous cord connects two atretic ends Type III: complete separation of two atretic ends

Commomly associated with Down’s syndrome 30% Vomiting is bilious in around 85% of cases Shows characteristic double bubble sign in X ray Treatment is by duodeno-duodenostomy with high

success rate Annular pancreas

Incidence is around 1:7000 Failure of normal fusion of the two pancreatic buds which may obstruct the duodenum from without

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ERRORS OF MIDGUT DEVELOPMENT AND ROTATION

Stage I:Exomphalos major (umbilical defect

>5cm)Exomphalos minor (umbilical

defect<5cm)Gastroschisis, refers to extrusion of

intestines through a defect to the right of a normally formed umbilicus

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ERRORS OF MIDGUT DEVELOPMENT AND ROTATION

Stage II: Non-rotation: leaving the major part of the colon

on the left side and the small intestine to the right of the midline

Incomplete rotation: the coecum is situated in the sub-hepatic region

Reversed rotation: the final 180o rotation occurs in a clockwise manner so that the colon is lying posterior to the duodenum and the superior mesenteric artery

Hyper-rotation: the rotation continues to 360o or 450o so that the coecum rests in the region of the splenic flexure.

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ERRORS OF MIDGUT DEVELOPMENT AND ROTATION Stage III:

Non fixation may predispose to volvulus of the gut or caecum

Interference with the blood supply of a segment of gut during rotation may result in an atresia of a segment or segments of intestine

The Yolk sac which was attached to the midgut by the vitello-intestinal duct normally disappears completely. The common remnant of this system is the Meckel’s diverticulum

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MECONIUM ILEUS

Obstruction of Ilieum due to thick inspissated meconium

Occurs in 10% of patients with cystic fibrosis Gives the characteristic “Ground glass”

appearance in plain X ray Gastrografin enema is both diagnostic and

has potential therapeutic effect Operative intervention may be needed in non

responsive cases

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HIRSCHSPRUNG’S DISEASE(AGANGLIONIC MEGA COLON)

It is the commonest cause of intestinal obstruction in infancy

Epidemiology: Affects 1:1000 live births Male/Female ratio = 4:1 Most cases are sporadic Long segment and total colonic aganlionosis

have strong familial association (15% &25%)

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Pathology: Failure of caudal migration of neuroblasts derived

form the neural crest There is absence of ganglions in the submucous

and the myenteric plexuses There is failure of propulsive peristalsis manifesting

by obstruction Grossly there is a spastic distal segment with a

funnel connecting it to a dialated segment In about 75% of cases the affected region is the

recto sigmoid junction

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Clinical picture: History of delayed passage of meconium and

persistent constipation On examination there is abdominal distention Rectal examination reveals a tight spastic rectum

Investigations: Imaging: Ba enema (Without preparation!!) Anal manometry Rectal biopsy is the gold standard

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Treatment: Temporary measures include laxatives and

enemas. Colostomy may be a life saving procedure in some

cases Definitive treatment is surgical excision of the

spastic segment an re-anastomosis to the anal canal. Various procedures can be done e.g Swenson’s, Duhamel’s and Soave’s procedures

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Definition: The main pathology is atresia of the esophagus! Tracheoesophageal fistula is secondary to that. Incidence:

•1-2500 to 1-10000•males slightly more affected than females•the second sibling of an affected child has 0.2-0.5% chance of being also affectedAssociations:

Other congenital anomalies occur in 50-70% of infants affected with esophageal atresia. These are most common with esophageal atresia and distal fistula. Anomalies include cardiovascular (the majority), genitourinary, gastrointestinal and skeletal.

VACTERL association consists of Vertebral, Anorectal, Cradiac, Tracheo-Esophageal, and radial Limb deformities. It is not correlated with a known genetic abnormality or syndrome.

 

TRACHEOSOPHAGEAL FISTULA3/23/2014

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Types:

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D.Diagnosis 

Antenatal:

Maternal ultrasound

Postnatal:

Tracheoesophageal fistula present within the first few hours of life by:

 excessive salivation

 respiratory distress

 cyanosis

 inability to pass a nasogastric tube.

 Attempts at feeding cause choking, coughing, cyanosis, regurgitation.  

 Radiography:

•Plain X-ray

•Contrast study(pouchogram)

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Plain X-rayWith Ryle’s tube

Note:•Coiling loop denotes approximate length of upper pouch of esophagus.•Presence of air in the abdomen denotes a distal fistula.

MANAGEMENT

The treatment is ultimately surgical but management strategy include also preoperative, operative and postoperative measures

 

Surgical treatment:

Division and closure of the fisula and primary anastomosis of the two esophageal segments.

If the “Gap” between the two segments is too long, the infant is managed temporarily with an esophagostomy and gastrostomy. Later in life an procedure to replace the esophagus is considered e.g. colon interposition bypass.

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IMPERFORATE ANUS

Definition:Strictly the term should be agenesis or atresia but the term is

widely used. Incidence:

Affects 1:4500 live births Classification:

Can be broadly classified into

Low anomalies: High anomalies

-Covered anus -Anorectal agenesis

-Ectopic anus -Rectal atresia

-Stenosed anus -Cloaca

-Membranous stenosis

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Above LeftCovered Anus (Bucket handle anomaly)Note stool particles (arrows)

Above Right: Anal stenosis

LeftLow Imperforate AnusNote translucent membrane& ano-cutaneous fistula showingMeconium (arrows)

HIGH ANOMALIES (MALE & FEMALE)3/23/2014

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LeftVesibular AnusNote meconium comingOut of vaginal vestibule

RightNote meconium coming outOf the urethra (arrow), Indicating recto-urinary fistula

Management

As there are frequent association with other anomalies these should be also looked for, diagnosed or excluded

•Clinical examination:Usually the clinical diagnosis is made a birth either by inspection or by failing to pass a thermometer easily into the anus

•Radiography:Invertogram, done after six hours of birthContrast studies (distal loopogram): in a colostomized child to diagnose the site of any fistulous connection to the genito-urinary system

•Treatment:-Colostomy: early in the neonatal period for high anomalies-Local procedure: for low anomalies-Full correction of high anomalies is done later in life starting from the 6th month after which the colostomy maybe closed

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Invertogram

Low Anomaly High Anomaly

COMPLICATED INGUINAL HERNIA

Inguinal Hernias affect around 1-2% of newborns (high numerical probability).

Complications may be the first presentation of the inguinal hernia (Parents maybe unaware their child has a hernia).

Early diagnosis and Taxis allow for a smoother management.

It’s a strangulating obstruction (ischemic countdown).

Remember to examine the groin in a case of NIO!

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