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Download MBBS Pediatric Surgery Presentations 12 Hirschsprungdisease Lecture Notes

Download MBBS (Bachelor of Medicine, Bachelor of Surgery) 1st Year, 2nd Year, 3rd Year and Final year Pediatric Surgery 12 Hirschsprungdisease PPT-Powerpoint Presentations and lecture notes

This post was last modified on 08 April 2022

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HIRSCHSPRUNG'S

DISEASE

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Introduction
Incidence and spectrum of disease
Etiology and genetic basis of disease
Clinical Presentation and diagnosis

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Pre-operative preparation
Surgical management
Post-operative management
Long term outcomes

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Also known as congenital megacolon.

Characterised by absence of ganglion

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Introduction

cells in the myenteric (Auerbach) and

submucosal (Meissner)plexus of the

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intestine.
In 1887, Harald Hirschsprung, a

paediatrician from Copenhagen,

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described two cases of the condition

that ultimately bore his name.

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Occurs in approx. 1 in 5000 live

births.

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Most commonly extent of

Incidence and

involvement is rectosigmoid- 80%

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spectrum of

disease

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Proximal colon involvement- 10%

Total colon involvement with part

of distal ileal involvement- 5-10%

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Male to female ratio=

4:1

For total colonic

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aganglionosis, male to

female ratio= 1:1

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Ganglion cells are derived from the

neural crest.

Etiology and

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By 13 weeks post-conception, the

genetic basis

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neural crest cells have migrated from

proximal to distal through the

of disease

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gastrointestinal tract
Differentiation into mature ganglion

cells.

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Two theories

Early maturation of neural

Inhospitable micro-

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crest cells before reaching

environment for neural

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distal part of colon and

crest cells in the distal

rectum.

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bowel leading failure of

survival of neural crest cells.

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? Most common gene involved is RET proto-

oncogene. (Probably early cell death)

? Other genes are:

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Genetics

? SOX-10 genes (probably early maturation)

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? S1P1

? Phox 2B

? Hedgehog notch complex.

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Trisomy 21

Associated

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Opitz syndrome

syndromes

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Congenital central hypoventilation

and

syndrome

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conditions

Neurofibromatosis

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Neuroblastoma

Prenatal diagnosis is rare.

Most affected patients present in the

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CLINICAL

neonatal period

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PRESENTATION

? Abdominal distension

AND

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? Bilious vomiting

? Feeding intolerance

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DIAGNOSIS

? Delayed passage of meconium beyond the first

24hours (90%)

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? Prolonged passage of meconium

Occasional caecal or appendiceal

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perforation.


Radiology

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? Plain abdominal X-rays- Dilated loops of bowel

and absence of air in the pelvic region.

? Contrast enema or Barium enema-

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? Presence of transition zone between normal

and aganglionic bowel

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? Retention of the contrast beyond 24hours




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Rectal biopsy using suction

technique and histopathology

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showing absence of the

ganglion cel s is pathognomic.

Most patients wil also have

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evidence of hypertrophied

nerve trunks

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Chronic constipation with presence of meconium

history

Usual y on and off constipation is present til the

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child is on breast feeds but, it becomes profound

Presentation

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once weaning is started.

in late infancy

Failure to thrive

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Dependence on laxatives and enemas for

constipation

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Distended bowel loops

X-rays

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abdomen

Reversal of rectosigmoid

ratio and retention of

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contrast on a 24hours post

evacuation film.

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Anorectal manometry

The recto-anal inhibitory reflex (RAIR) is defined as reflex

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relaxation of the internal anal sphincter in response to

rectal distension and is present in normal children but

absent in children with Hirschsprung disease.

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The RAIR can be documented using anorectal manometry

by inflating a bal oon in the rectum while simultaneously

measuring the internal sphincter pressure.

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A- Normal child

B- Hirschsprung's disease
Older children

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In older children, the suction

rectal biopsy may be less

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reliable because of a higher

risk of sampling error.

Full-thickness biopsies,

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usually under general

anesthesia, may be

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necessary in these patients.


Approximately 10% of neonates present with fever,

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abdominal distention, and diarrhea due to Hirschsprung

-associated enterocolitis (HAEC)- can be life-threatening.

Hirschsprung-

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Since HD characteristically causes constipation rather

than diarrhea, this presentation may be confusing and

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associated

the diagnosis may not be considered.

enterocolitis

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A careful history, including a history of delayed passage

of meconium and intermittent stooling, should lead to

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(HAEC)

an investigation for HD.

Aggressive treatment with IV fluids and IV antibiotics is

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done.

Rectal irrigations do not help.

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Long segment

Needs a diverting colostomy or

involvement

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ileostomy to relieve obstruction.

Barium enema shows- Question

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Mark sign.




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Question

mark sign

Hematoxylin and eosin

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Stains for Acetylcholinesterase

Immunological staining with calretinin

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Histopathology

The gold standard for the diagnosis is the absence of

ganglion cel s in the submucosal and myenteric

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plexuses on histological examination.
Most patients wil also have evidence of

hypertrophied nerve trunks.

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PREOPERATIVE PREPARATION

? Once the diagnosis of HD is made, the child should be

? appropriately resuscitated with intravenous fluids

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? treated with broad-spectrum antibiotics

? Nasogastric drainage

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? rectal decompression using rectal stimulation and/or irrigation.



Once the infant or child has been resuscitated and

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stabilized, the operation can be done semi-

electively.

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While waiting, many infants can be discharged

home on breast milk or an elemental formula, in

combination with rectal stimulations or irrigations.

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In the older child with an extremely dilated colon, pull-through

should be delayed until the diameter of the colon has decreased

sufficiently to perform a safe procedure.

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Weeks or months of irrigations may occasionally be needed.

Some of these children may need an initial colostomy to adequately

decompress the dilated colon.

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Goals:

? Remove the aganglionic bowel

? Reconstruct the intestinal tract by bringing the

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normal y innervated bowel down to the anus

? Preserve normal sphincter function.

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SURGICAL

MANAGEMENT

Name of surgery: Pul through procedure

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Stages:

? Single stage

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? Three stages: Level ing colostomy+ Pul through

procedure + Colostomy closure

Swenson

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? The goal of the Swenson pull-through is to

remove the entire aganglionic colon, with an

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Procedure

end-to-end anastomosis above the anal

sphincter.

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? Designed to avoid the risk of injury to

Soave

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important pelvic structures by performing a

Procedure

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submucosal endorectal dissection and

positioning the pull-through bowel within an

aganglionic muscular `cuff'

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? Involves bringing the normal colon down

Duhamel

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through the bloodless plane between the

rectum and sacrum, and joining the two

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Procedure

walls with a linear stapler to create a new

lumen which is aganglionic anteriorly and

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normally innervated posteriorly.


Other

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? Transanal pull through

approaches

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? Laparoscopic pull through
Complications

? Anastomotic leaks are the most common early complication of the Duhamel and

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Swenson techniques, at a rate of up to 11 per cent for the Swenson technique.

? The management of a leak is usually to form an enterostomy and then allow

the anastomosis to heal.

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? Depending on the degree of anastomotic disruption, and subsequent

stricturing, redo pull-through ultimately may be required.

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? Cuff abscess or retraction of the proximal bowel may occur with the Soave

technique and increase the chance of long-term stricturing.

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? Voiding dysfunction may occur postoperatively with any of these operations.

? Bladder innervation may be disrupted partly at the time of surgery, rather

than it being a congenital problem.

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? This is more common in older children and with the extensive pelvic

dissection of the Swenson technique
? Long-term complications include

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Long term

? anastomotic stricture

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complications

? recurrent enterocolitis

? constipation

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? faecal incontinence

? Anal dilatation may be required in Soave's

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procedure and Swenson's procedure post-

operatively for avoiding anastomotic stricture

Anastomotic

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? Stricture is very rare after the Duhamel

operation, where, alternatively, a rectal spur or

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stricture

diverticulum may be left or may develop with

time.

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? Presents as recurrent enterocolitis,

constipation.

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? Division of the spur is required- Usually

done endoanal approach.
Enterocolitis may occur at any time.

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Infectious agents such as Clostridium dificile or

rotavirus have been postulated as being causative.

Enterocolitis

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The incidence does decrease with age.

Maturation of the gut mucosal immune defences

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may account for this decrease.

Needs aggressive treatment.

? Constipations occurs most commonly because of

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? disordered motility in the residual colon or smal

bowel- Use of laxatives and prokinetic agents

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Constipation

? internal sphincter achalasia- Internal

sphincterotomy, local application of botulinum

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toxin or nitroglycerine application

? functional megacolon caused by stool-holding

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behaviour- Bowel management by behaviour

modification
? Abnormal sphincter function may be due to

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sphincter injury during the pull-through.

? There are two forms of abnormal sensation.

Faecal soiling/

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? The first is lack of sensation of a full rectum.

incontinence

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? Inability to detect the difference between

gas and stool

? Biofeedback training, dietary modifications are

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used for preventing faecal soiling.

? Overall survival has improved.
? Late deaths are due to:

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? Recurrent enterocolitis

? Associated comorbidities

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