Pemicu 5B

By : Giovanni Anggasta
405100114
ANATOMY
3
Anatomy of the Large Intestine


RECTUM - ANUS
HISTOLOGY
Histology of colon
No vili in tunica mucosal
A lot of goblet cells among the epithel
+ Cryptus Liberkuhn
Panneth cells and Argentaffin cells
Solitaire lymphonodus spread among
lamina propria



Colon
Histology of Rectum
2 parts of rectum :
1. Upper : colon like structure. Taller
cryptus and walled by goblet cells
2. Lower (anal canal) : Rectal collumn
longitudinal folds in mucosal end about
21/2 inchs from orrificium anal.
The junctional between anal and rectum
called linea pectinata
Histology of Anus
1. Collumnaris zone
2. Intermedia zone
3. Cutanea zone
Anal gland
Squamous to collumnar
In linea pectinata
Thinning squamous epithel
Stratified keratinized squamous epithel
With hair follicle
Motility Secretion Digestion Absorbs
Large
Intesti
ne
Haustral
contractions slowly
shuffle the colonic
contents back and
forth to mix and
facilitate
absorption of most
of the remaining
fluid and
electrolytes.
The alkaline
mucus secretion
of the large
intestine is
primarily
protective in
function.
No secretion of digestive
enzymes or absorption of
nutrients takes place in
the colon. All have been
completed in the small
intestine.
Absorption of some of the
remaining salt and water
converts the colonic
contents into feces.
PHYSIOLOGY
Physiology of Defecation
Peristaltic waves move the feces into the
sigmoid colon and the rectum
Sensory nerves in rectum are stimulated
The very first defecation feeling is when the
pressure in rectum reach 18 mmHg and when
it reach 55 mmHg, both sphincter will limp
and cause an expulsion reflex
Individual becomes aware of need to defecate
Feces move into the anal canal when the
internal and external sphincter relax
Physiology of Defecation
External anal sphincter is relaxed
voluntarily if timing is appropriate
Expulsion of the feces assisted by
contraction of the abdominal muscles and
the diaphragm
Moves the feces through the anal canal
and expelled through anus
Facilitated by thigh flexion and a sitting
position
Physiology of constipation
Delayed of defecation
More water is absorbed
Hard and dry feses
constipation May caused by :
-Ignored the desire of defecation
-Decreased of colon motility (aging,
emotional disorder, Low fibre diet
- obstruction of the feses movement at
the colon (local tumor, colon spasm)
- Defecation reflex disorder (nerve injury)

Biochemical Balance
LOWER GI TRACT DISORDER
Hirschsprung disease
Definition
Absence of ganglion cells in the distal
bowel beginning at the anus and
extending proximally for a variable
distance.
Short segment Hirschsprung- 80-90%
Long segment Hirschsprung- 10%
Total colonic aganglionosis- 5%
Total colonic aganglionosis plus small bowel

Epidemiology
1 in 5000 newborns
4Males:1Female for short segment -> 1:1
7% of cases have a family history of the
disease. In total colonic disease this is
21%.


Pathophysiology
5-12 wk of embryogenesis
Failure of migration, differentiation or
survival of neural crest cells
Absence of myenteric and submucosal
nerve plexus -> affected gut is unable to
relax -> functional bowel obstruction with
dilatation of proximal bowel
Genetics
Inheritance pattern can be autosomal
dominant or recessive.
Mutations increase odds of having
Hirschsprung but is not predictive of the
abnormality.
15% at least have one other congenital
anomaly
12% have chromosomal anomalies
Ex: Down, MEN IIA, Shah-Waardenburg

Clinical presentation
Should be suspected in all infants who
have not passed meconium within 48 hr of
birth and in all infants with signs of bowel
obstruction
Signs: constipation, abdominal
distention, bilious emesis, FTT, CV
collapse, diarrhea
PE:sphincter is N or ; explosive diarrhea;
transition zone (finger in glove); empty
vault
Symptoms in newborn age
Fail to pass meconium (in 24 hours of life)
Abdominal distension, but the abdomen is
palpable
Vomiting
The rectal tube cant be put easily
After irrigation the signs and symptoms
return again in a few days
Symptoms in newborn age
(enterocolitis)
Life-threatening condition
Diarrhea: it can be an early sign
Toxic megacolon
Abdominal distension
Bile-stained vomiting
Fiver and signs of dehydration
Rectal tube:explosive expulsion of gas and
foul-smelling stools




Symptoms in infants
Constipation
Meteorism
Palpable faecaloma
Sometimes putrescent diarrhea
Ulceration, bleeding
Hypoproteinaemia, anaemia
Electrolyt disorders
Symptoms in childhood
Gracile limbs
Dilated drumlike belly
Long history of constipation
Defecation in 7-10 days
Multiple fecal masses
The stimulus of defecation is missing
Rectum is empty and narrow


Hirschsprungs disease
Diagnosis
Abdominal plain X-rays
Barium Enema
Rectal Biopsies
Anal manometry
Abdominal X-ray
Barium Enema
Barium Enema
Less sensitive for detecting short lesions,
total colon aganglionosis, and disease of
the newborn
Many newborns do NOT show definitive
transition zone
Delayed evacuation of contrast
Rectal biopsy

Submucosal suction biopsy
Meissners submucosal plexus
Full thickness rectal biopsy
Auerbachs myenteric plexus
Acetylcholinesterase staining
increased staining of neurofibrils
Anorectal manometry

Absent rectoanal inhibitory reflex
Lack of internal anal sphincter
relaxation in response to rectal
stretch
Treatment
Initial tx: Resuscitation, IVF, NGT, rectal
washouts
Colostomy in the neonatal period at the
distal limit of ganglionic bowel
Staged surgical procedures (3-9 mo)
If the patient has enterocolitis, colostomy
is deferred until improvement occurs
Surgical Options

Swenson Procedure (1948)
Duhamel Procedure (1960)
Soave Procedure (1963)
Swenson Procedure

Sharp extrarectal dissection down to 2 cm
above the anal canal
Aganglionic colonic segment resected
End-to-end anastamosis of normal
proximal colon to anal canal
Completely removes defective aganglionic
colon
Swenson Procedure
Duhamel Procedure
Posterior portion of defective colon
segment resected
Side to side anastamosis to left over
portion of rectum
Constipation a major problem d/t
remaining aganglionic tissue
Simpler operation, less dissection
Duhamel Procedure
Soave Procedure
Circumferential cut through muscular coat
of colon at peritoneal reflection
Mucosa separated from the muscular coat
down to the anal canal
Proximal normal colon is pulled through
retained muscular sleeve
Telescoping anastamosis of normal colon
to anal canal

Soave Procedure
Soave Procedure
Advantage: rectal intramural
dissection ensures no damage to
pelvic neural structures
Higher rate enterocolitis, diarrhea
Problems w/ cuff abscesses, often
requires repeated dilations

Overall Mortality

Swenson procedure: 1-5%
Duhamel procedure: 6%
Soave procedure: 4-5%
Operative complications

Leak at anastamosis: 5-7%
Postop Enterocolitis: 19-27%
Constipation
Stricture Formation
Incontinence

One vs Two Stage procedure

Historically, two stage procedure
performed: preliminary colostomy, then
completion pull through
Delicate muscular sphincters of newborn
may be injured
1980s, 1 stage procedures became more
popular
One vs Two Stage procedure
Early complications: No difference in incidence
of anastomotic leak, pelvic infection, prolonged
ileus, wound infection, wound dehiscence
Late complications: No difference in incidence
of anastomonic stricture, late obstruction,
constipation, incontinence, urgency
Postoperative enterocolitis higher in 1
stage (42% vs 22%)
Laparoscopic techniques

Small studies of laparoscopic pull through
procedures
Excised aganglionic tissues removed
through anal canal, no abdominal incision
Better results in terms of pain, return of
bowel function, hospital stay
Similar incidence of leaks, pelvic
abscesses, enterocolitis, postop bowel
function
Complications
60% fecal incontinence
Enterocolitis
Malaise, fevers, abd. pain, constipation or diarrhea
?alteration of bacterial flora, relative gut stasis, impair
mucosal or neuronal immunity
Tx: rectal washouts, antibiotics (Vanco or Flagyl),
probiotics. Sphincterotomy (surgical or chemical).
Urgent colostomy.
6-30% mortality
Anorectal stenosis
Malabsorption, TPN dependence
Dysmotility

Intestinal Obstruction
Intestinal obstruction due to
adhesions
Following trauma or laparotomy
Kinking of bowel or entrapment of bowel
by fibrous bands
Often after open operations, less frequent
after laparoscopic procedures
Risk of obstruction higher pelvic than
upper abdominal procedure
Risk of intestinal obstruction - 10% over
lifetime
Kinds of intestinal obstruction
Simple intestinal
obstruction
One end of the
bowel is obstructed
May be complete
or incomplete
Closed-loop obstruction
Both proximal and distal
ends are obstructed
Herniation of bowel loop
in inguinal hernia or
through mesenteric
defect
Volvulus
Progressive distention of
bowel
Gangrene of bowel loop
Kinds of intestinal obstruction
Strangulating obstruction
Circulation to segment of bowel
is impaired, ischemia
Rapid progression to gangrene
Volvulus
Incarcerated hernia

Symptoms of intestinal obstruction
Pain
Vomiting
Abdominal distention
Physical examination
Vital signs pulse, respiratory rate, blood
pressure are normal initially. Tachycardia,
hypotension, fever.
Dehydratation
Abdominal scar
Abdominal mass abscess, bowel loops,
infarcted bowel
Peritoneal signs
PR empty rectum
Auscultation high pitch peristalsis
Laboratory studies
Hemoconcentration
Leucocytosis
Metabolic alkalosis proximal obstruction
Metabolic acidosis distal obstruction

Radiologic studies


Plain radiographs
Supine and upright
Distended bowel
loops with air/fluid
levels
Treatment of intestinal obstruction
Volume replacement
Nasogastric decompression
Conservative treatment up to 4 days
20-30% of patients develop criteria for
laparotomy
Surgical treatment
Intravenous antibiotics preoperatively
Incision beyond the area of original
incision
Division of adhesions
Careful handling of bowel
Milking of intestinal contents
Prevention of adhesions
Gentle bowel handling
Avoiding of glove powder, no absorbable
sutures, bits of sponges
Removal of necrotic tissue
About 15 % of operated patients develop
recurrent small bowel obstruction. Of
these, two-thirds respond to conservative
treatment and one-third require another
operation.
Functional Constipation
Intestinal
Atresia and
Stenosis


Clinical findings
1vomiting
onset: from first time of feeding
to a few days after birth
vomitus: bilious or feculent

2abdominal distention
high: confined to epigastrium
low: full abdomen distention

3failure to pass meconium:
normally meconium was passed within the first 24hrs
of life and cleared in 2-3 days.

4General condition

Diagnosis

1prenatal ultrasound

2Clinical findings:
bilious vomiting 24-48hrs after
birth
abdominal distention
failure to pass meconium

3X-ray
duodenal atresiaDouble bubble sign
jejunal atresiatriple bubble sign
low intestinal atresiamultiple air-
fluid level

Treatment

The only option is surgery

intestinal septum excision

Intestine resection and
anastomosis

Congenital
Malrotation of
Intestine

Definition
Malrotation is the term used to define the group of
congenital anomalies resulting from aberrant intestinal
rotation and fixation

Embryology
Week 6~8: Herniation of midgut into the umbilical
cord with a 180 degree of counterclockwise rotation
along the axis of superior mesenteric artery
Week 10: Return to the abdominal cavity with a
final 90 degree of rotation to complete the 270-degree
counterclockwise rotation

Pathology
Nonrotation and Incomplete rotation: abnormal positioning
of the proximal small bowel and the cecum

Duodenum compressed by abnormal peritoneal
band(Ladds band): high incomplete extrinsic obstruction

Midgut volvulus: torsion of the narrow mesenteric pedicle
produces an acute closed-loop intestinal obstruction and
vascular insufficiency.

Proximal jejunum fused to the ascending colon by
anomalous peritoneal attachments

Malrotation
Pathology
Compression of duodenum
Kinked and foreshortened proximal jejunum by peritoneal band
Midgut volvulus

Clinical manifestations

Emesisbilious, intermittentoccur at 3-5 days after birth
or asymptomatic

Abdominal distention: confined in epigastrium, diffuse to
the full abdomen in bowel necrosis

Stool: normal meconium, bloody stool suggests volvulus
and necrosis

Newborn: normal meconiumintermittent vomiting after
3-5 days of birthno abdominal distention, hard stool

Children and infantasymptomatic since birth,
intermittent onset or sudden onset of volvulus

Clinical manifestations
Symptoms of volvulus: bloody vomitus
and stool, abdominal tenderness


X-ray film

1Plain X-ray film: double-
bubble sign

2barium enema: cecum
in the upper or left
abdomen

3GI incomplete
duodenal obstruction;
ligament of Treitz not to
the left of the midline;
abnormal position of the
proximal jejunal loops to
the right of the midline

Treatment
Principles
Asymptomatic malrotation
most recommend surgical treatment
some believe operation only necessary in young children
High intestinal obstruction
operated on promptly, but not necessarily emergently
Volulus with sign of bowel necrosis immediate operation




Treatment
Ladds operation
All volvulus is clockwise so the small bowel must be
rotated in a counterclockwise fashion
Expose duodenum by division of the Ladds bands
Dissection additional peritoneal bands to convert the
mesenteric pedicle to a wide plane
Alignment of small bowel to the right and colon to
the left of the abdominal cavity
Bibliography
Walker, et al. Pediatric Gastrointestinal Disease.
2004, pages 1031-1040
Stewart D, Von Allmen D, Piccoli D.
Gastroenterology Clinics of North America: The
genetics of Hirschsprung Disease. Vol 32 (3).
Pages 819-839
Neville, H. Hirschsprung Disease.
www.emedicine.com
Warner B. Whats new in pediatric surgery.
Journal of the American College of Surgeons
Vol 1999 (2)