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Partial or complete blockage of the bowel that results in the failure of intestinal contacts to pats through.

According to the presence or absence of peristalsis

1- Dynamic (mechanical).
-the onset: Acute Vs chronic.
-the site: high (small bowel) Vs low (larger bowel).
-nature: simple Vs strangulated.
For example: acute high strangulated obstruction.

2-Adynamic "Paralytic/neurogenic ileus": where there is no peristalsis.

According to Etiology: causes could be:

1-Inside the lumen: fecal impaction, food (bezoars in excessive fiber intake), gallstone ileus (duodenal
fistulization and passage of large gallstone), parasites (ascaris lumbricoides), intussusceptions.
2-In the wall: congenital atresia, Crohn’s disease (strictures), tumors, colonic diverticulitis.

3-outside the wall: strangulated hernia, Volvulus, bands and adhesions.

Classification in age-wise manner:

1. Neonatal obstruction: congenital anomalies, Hirschsprung’s disease (congenital absence of

submucosal or myenteric plexuses, leading to obstruction and proximal dilation), and meconium ileus.
2. Infants: intussusception, Hirschsprung’s disaese, strangulated hernia, obstruction due to Meckel’s
3. Young adults:
strangulated hernia, Pseudo-obstruction; Miscellaneous;
5% 5%
adhesions and bands,
Crohn’s. Fecal
impaction; 8%
4. Elderly: strangulated
hernia, CA, diverticulitis, Adhesions;
impacted feces, sigmoid Hernias; 12% 40%
CA; 15%



Loops DISTAL to obstruction will have normal peristalsis and absorption until they are empty, then

Loops PROXIMAL to obstruction go into two phases:

 Increased peristalsis against the obstruction. (colic)

 Dilation, decreased peristalsis, flaccidity and paralysis.

Dehydration is caused by

 Reduced oral intake

 Reduced intestinal absorption
 Vomiting
 Fluid sequestration in bowel lumen

Signs of dehydration: dry skin, sunken eyes, oliguria, poor venous filling.

Cardinal symptoms of mechanical intestinal obstruction:

1. Colicky abdominal pain

2. Distension
3. Vomiting
4. Absolute constipation

According to the site:

High small bowel obstruction:

 Periumbilical pain
 Early profuse vomiting with rapid dehydration
 Minimal distension
 No air fluid levels on AXR.

Low small bowel obstruction:

 Periumbilical pain
 Delayed vomiting
 Central distension
 Multiple central air fluid levels


Large bowel obstruction

 Distension is early and pronounced

 Pain is mild
 Vomiting and dehydration are late
 Distended proximal colon and cecum on AXR.

Late manifestations of obstruction include dehydration, hypovolemic shock, septicemia, peritonism,

respiratory distress, oliguria, pyrexia.

Colicky Pain

 Periumbilical vs suprapubic
 Frequency may indicate the site
Small bowel : 2-20 minutes
Large bowel: 30 minutes or more.


More in chronic large bowel obstruction and volvulus of the sigmoid.

Absolute constipation

 Early in large bowel obstruction

 Late in small bowel obstruction
 Prominent in acute obstruction
 Absolute means complete, relative constipation means passing flatus.
 Constipation not present in: Richter’s hernia, gallstone ileus, mesenteric vascular occlusion.


 Early in small bowel obstruction

 Late in large bowel obstruction
 In late stages it becomes feculent, Why?

Feculent vomiting : smells like feces, because of bacterial metabolism of obstructed food.

Fecal vomiting: means vomiting fecal material, occurs when there’s a gastrocolic fistula (gastric CA,
colon CA)


Physical examination

 Signs of dehydration
 Elevated pulse
 Normal temperature.
 Visible peristalsis (not diagnostic)

Inspection: Always look for hernias and scars

Hernias suggest strangulation

Scarring suggests bands and adhesions

Palpation: Generalized abdominal tenderness.

A mass may be felt in case of intussusception or CA.

Auscultation: Increased ‘tinkling’ bowel sounds

PR may reveal an obstructing mass in the pouch of Douglas, the apex of intussusception or fecal


Bowel strangulation: Twisting of the bowel often around fibrous bands, causing decreased blood supply
and death of bowel tissue. Up to 15% mortality rate. Clinically it’s very difficult to differentiate simple
from strangulated obstruction.

Irreducible hernia; means that the contents of the hernia sac cannot be reduced into the abdomen. Irreducible
hernia can be associated with three other categories of complications – strangulation, obstruction, incarceration.

Incarcerated means that contents are literally imprisoned in the sac of the hernia (usually by adhesions) but are
alive and functioning normally. An incarcerated hernia is not tender.

Obstructed means that a loop of bowel is kinked or trapped within the sac of the hernia in such a way that its
lumen but not blood supply is obstructed, the bowel is therefore alive and the patient has the signs and symptoms
of intestinal obstruction but not strangulation, the hernia will not be unduly tender.

Strangulation means that the blood supply to the contents of the sac has been cut off and they are dying. The
patient will usually be obviously unwell and the swelling will be acutely tender. An entrapment that interferes
with the blood supply to the bowel will usually obstruct its lumen, so most strangulated herniae have intestinal


Features of strangulation:

 General: tachycardia, pyrexia, toxic appearance.

 Pain becomes constant rather than colicky
 Signs of peritonitis: abdominal wall rigidity, absent bowel sounds.

A strangulated hernia is tense, tender and has no cough impulse.

Lab: leukocytosis (neutrophils) and raised CRP

Abdominal X-ray (AXR): erect and supine.

 Distended loops
 Air-fluid levels.
 High obstruction: ladder pattern, central and striations.
 Low obstruction: haustrations, peripheral.
 5% show normal AXR!

CT with water-soluble contrast

 Localize the site of obstruction

 Detect the obstructing lesion/ mass
 May diagnose unusual hernias (e.g. obturator)

Contrast enema in emergency large bowel obstruction

>>> Here we don’t give the usual laxative preparation because the bowel is obstructed and this may
exacerbate the picture!

Principles of treatment
-Acute obstruction with the risk of strangulation needs urgent surgical intervention.

-Pre-operative preparation:

 NG tube aspiration (decompression)

 IV fluid replacement
 Plasma expanders in case of shock
 Antibiotics when strangulation is likley (or found in operation)


Dead bowel segment is determined by

 Loss of peristalsis
 Loss of normal sheen "seen during operation"
 Color (greenish/black is non-viable, but purple may recover)
 Loss of arterial pulsation in the mesentery

If still in doubt, plan a second laparotomy 48 hrs later.

o Small bowel segments can be resected with primary anastomosis of proximal and distal segments
because of extensive blood supply.
o Large bowel segments proximal to the splenic flexure: can be resected with primary ileocolic
o Left-sided "distal to splenic flexure": resection with proximal colostomy and distal mucous fistula
If the distal end is short and can’t reach the surface we close it. (Hartmann’s procedure)
o If colo-colonic anastomosis is performed, the proximal bowel is first lavaged.
o “You have to manage: the obstructed segment, the distended proximal bowel and the underlying


It represents 40% of all common causes of obstruction, and 75% of small bowel obstruction cases. Most
commonly caused by previous surgery, that may occur just post-operatively or many years after surgery.

Can be ‘easy’ flimsy or ‘difficult’ dense. Most are


Follow the principles of treatment:

NG decompression and IV fluids.
Urgent laparotomy if suspect strangulation, peritonitis or non-


 Good surgical technique

 Minimizing contact with gauze
 Washing peritoneal cavity with normal saline.
 Covering anastomosis and raw peritoneal surfaces


Conservative treatment is usually curative.

Surgery: divide (release) the adhesion.




A twisting of a portion of bowel around its

mesenteric axis. When complete it forms a
closed loop of obstruction with resultant
ischemia secondary to vascular occlusion at
the base of the involved mesentery.

Common sites:

 Sigmoid colon "common in elderly"

 Caecum
 Small intestine
 Less commonly; the stomach and



-Congenital malrotation of the gut, i.e. abnormally mobile loop of intestine, e.g. congenital failure of
rotation of the small intestine (midgut volvulus), or long sigmoid colon.

-Abnormal mesenteric attachment, i.e. a loop of bowel with a narrow mesenteric attachment.

-Congenital band or adhesion, i.e. a loop fixed at its apex by adhesions around which it rotates.


-Rotation of a piece of bowel around an acquired adhesion or stoma.

-An abnormally loaded loop, as in the pelvic colon of chronic constipation.

Signs & symptoms:

-Regardless of cause, volvulus causes symptoms by two mechanisms:

-One is bowel obstruction, manifested as abdominal distension (due to accumulation of gas and fluid in
the obstructed bowel) and vomiting.

-The other is ischemia (loss of blood flow) to the affected portion of intestine.


Volvulus neonatorum

◦ Congenital malrotation of the bowel.

◦ Narrow mesentery of midgut.

Clinical feature:

◦ Bilious vomiting.

◦ Blood stained stools.

◦ Abdominal distension.

Treatment :

◦ Laparotomy :

▪ untwisting the volvulus

▪ widen the base of small bowel mesentery

▪ divide adhesions (ladd’s bands).

◦ Appendectomy : unusual position of appendix cause a diagnostic difficulty in the future.

Paralytic ileus


-A state in which there is failure of transmission of peristaltic wave (atony or paralysis) due to
neuromuscular failure, the resultant stasis lead to accumulation of gas and fluid in the bowel with
associated distension, constipation, vomiting , absence of bowel sound & Pain.

- Paralytic ileus should not be confused with mechanical obstruction, although it is a sequale of the
end-stages of mechanical obstruction.


Clinical feature

 Abdominal distention (tympanitic).

 Absolute constipation.
 Effortless vomiting
 Absence of colicky pain
 Absence of intestinal movement.

On examination:

 Anxious, uncomfortable
 Silent, distended & tender abdomen.

A plain x-ray:

The appearance of generalised adynamic ileus

on plain film is quite characteristic. The large
and small bowel are extensively airfilled but not
dilated, this may be described as the large and
small bowel "looking the same".


 It is a common secondary feature of

peritonitis due to any cause.
 It may occur after any surgical procedure
due to handling of the bowel
 Electrolyte abnormalities as hypokalemia,
hyponatremia, uremia and diabetic
 Secondary to drugs as tricyclic
antidepressants, lithium therapy,
excessive opiate use

-Duration: rarely last more than 3 or 4 days.

-Bowel sounds: absolutely silent abdomen.

-Pain: painless

-Timing: if symptoms start after bowel action or passing flatus; it is mechanical obstruction.



Management is conservative with bowel rest, nasogastric aspiration and fluid and electrolyte support.
Treatment is otherwise focused on the underlying cause.

In prolonged stubborn ileus:

Metoclopramide (motility stimulant)
erythromycin (stimulate the motilin receptor)



Known as adynamic ileus or Ogilvie’s syndrome,

is a form of paralytic ileus, mainly affect the
large bowel, it result from interference with
autonomic supply to the gut.


 fracture of the spine or pelvis

 retroperitoneal hemorrhage
 Retroperitoneal surgery
 Intestinal ischemia
 Ureteric colic
 Parturition
 Malignant infiltration of the celiac plexus

Clinical feature:

 Absolute constipation
 Colicky abdominal pain
 Abdominal distension


 The colon is decompressed by colonoscopy or

 Cholinesterase inhibitor (neostigmine)

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Closed loop obstruction

A condition where one bowel segment is totally obstructed distally with a valve-mechanism proximally
that allows the bowel to fill, but prevents reflux.

-No early distension of proximal segments

-Most commonly in right colonic obstruction with a competent ileocecal valve.

-Complicated by cecal perforation and fecal peritonitis.

-X-ray shows the characteristic cecal dilation.

-Other examples: volvulus, complication of Polya gastrectomy.

Hirschsprung Disease

Hirschsprung disease (HD) is congenital megacolon characterized by the absence of myenteric and
submucosal ganglion cells in the distal alimentary tract; resulting in loss of peristaltic activity distal
to the area that is absent of ganglionc cells that leads to intestinal obstruction.

 Hirschsprung disease results from the absence of parasympathetic ganglion cells in the
myenteric and submucosal plexus of the rectum and/or colon.
 Ganglion cells derived from the neural crest migrate caudally to anorectal area with the
vagal nerve fibers along the intestine.
 Arrest in migration leads to an aganglionic segment.
 These ganglion cells arrive in the proximal colon by 8 weeks of gestational age and in the
rectum by 12 weeks of gestational age.

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 Approximately 1 per 5000 live births.

 Sex: 4 times more common in males than females.
 Age: Nearly all children nowadays with Hirschsprung disease are diagnosed during the first 2
years of life.
One half are diagnosed before they are aged 1 year.
Minority not recognized until later in childhood or adulthood.
 Mortality/Morbidity: The overall mortality of Hirschsprung enterocolitis is 25-30%, which
accounts for almost all of the mortality from Hirschsprung disease.


HD can be classified by the extension of the aganglionosis as follows:

1. Classical HD (75% of cases): Rectosegmoid area and distally to it will be aganglionic and it’s
the most common type.
2. Long segment HD (20% of cases): any part of the colon beyond the recto sigmoid area is
affected. (More than half of the colon -DHMC)
3. Total colonic aganglionosis (3-12% of cases): the terminal ileum will be aganglionic and
distally to it.
4. Rare variants include the following:
 Total intestinal aganglionosis: it’s incompatible with life because the whole GI tract
don’t have ganglion.
 Ultra-short-segment HD: involving the distal rectum below the pelvic floor and the
anus. The aganglionic segment in ultra short is limited to internal sphincter, ganglion
cells present on rectal suction biopsy but rectal motility is abnormal.

Clinical presentation:
Most of the patients diagnosed at first month so in the:
1. Failure to pass meconium within the first 48 hours of life (meconium is a green blackish first
stool that the child passes and at first 24 to 48 hours), and 95% of HD patients have delay in
passging the stool.
2. Abdominal distension that is relieved by rectal stimulation (then the mother inserts rectal
thermometer to take temp or enema, she notes that the child will pass stool after a while)
3. If the child wasn’t diagnosed early he will complain of serious intestinal obstruction like
vomiting fecal material, severe dehydration and rarely enterocolitis and the mortality rate is
20-30 % without treatment but with, it will reach 100%.
4. failure to thrive (the normal gaining weight is 25 gm/day)

Older children and adults

• Severe constipation
• Abdominal distension
• Bilious vomiting
• Failure to thrive

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Diagnostic workup

Clinically: we take a good history that will reveal abdominal distention, then we do a rectal
examination and we see that there is stool on the finger because when we do PR we make
relaxation of the internal sphincter, and some of the stool or gas will come out.

1. Plain abdominal x-ray: we see distended colon because of the obstruction, later on the
small bowel will be distended also.
2. Contrast enema: barium or gastrografin enema, we see:
 A transitional zone will appear between the normal bowl and the abnormal one.
 Abnormal, irregular contractions of aganglionic segment.
 Delayed evacuation of barium (so even taking image after 24 h will show that
barium is still there).

Contrast enema studies •

demonstrating abnormal recto-
sigmoid ratio of less than 1
with transition zone seen at the

3. Manometry: it’s like a defecation reflex, normally the colon contains the stool and the
rectum is empty, so when we defecate the stool goes to the rectum. The idea is we put a
balloon in the rectum and we inflate it, and we put a manometer in the anal sphincter.
Normally when the balloon is inflated the sphincter relaxes. In HD patients the anal
sphincter remains contracted because absence of ganglionic cells.

4. Biopsy: we take biopsy from the rectum to the histopathology lab to see if there any
ganglionic cells or not. One ganglionic cell is sufficient to exclude HD.
Types of biopsy are rectal suction biopsy (that involves the mucosa and submucosa) and Full
thickness biopsy.

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The treatment is surgical removal or bypass of the aganglionic bowel with preservation of the
sphincter because we don’t want to end with incontinence.


HD associated enteropathy: it’s exactly like the gastroenteritis that happens in children which is
very common. Because of the stagnation of the stool, bacterial overgrowth will occur and starts to
secrets toxins, besides that the mucosa isn’t healthy which finally lead to early sepsis.
So the patient will come firstly with fever, abdominal distention, and even diarrhea (the diarrhea
here because of the overflow that resulted from the inflammatory process and secretions from the
colon), lethargy (drowsiness), rectal bleeding, or shock. So the patient will rapidly deteriorate
because of sepsis and dehydration.
Mortality rate is with treatment is 20%.
Treatment: rehydration, IV antibiotics, colonic washout to treat the primary cause which is stool


 Usually they complain of constipation, because of not extracting all aganglionic cells in
surgery, so we give those suppositories, enemas, lactulose. But in general they live normally.
 Some investigators report a high degree of satisfaction, while others report a significant
incidence of constipation and incontinence.
 Approximately 1% of patients with Hirschsprung disease require a permanent colostomy to
correct incontinence.
 Patients with associated trisomy 21 have poorer clinical outcomes.


Intussusception, the invagination of one portion of the intestine into an adjacent segment, is
uncommon but may be life-threatening. Intussusception typically causes a strangulating bowel
obstruction, which can progress to gangrene and perforation. Intussusception is classified according
to the site of the inner intussusceptum and outer intussuscipiens. In children, more than 80% are
ileocolic, beginning several centimetres proximal to the ileocaecal valve with their apex in the
ascending or transverse colon.

In the majority of affected infants, intussusception is caused by hyperplasia of gut lymphoid tissue,
which may in turn be secondary to viral infection. In 10% of children, intussusception is secondary
to a pathological lead point such as a Meckel’s diverticulum, enteric duplication cyst or even small
bowel lymphoma. Such cases are more likely in children over the age of 2 years and in those with
recurrent intussusception.

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Intussusception can develop at any age and affect
either sex but the peak incidence is between 5 and
10 months of age.

Classically, a previously healthy infant presents with

colicky pain and vomiting (milk then bile). Between
episodes the child initially appears well. Later, they
may pass a ‘redcurrant jelly’ stool.

Clinical signs include dehydration, abdominal

distension and a palpable sausage-shaped mass in
the right upper quadrant.

A plain radiograph commonly shows signs of small

bowel obstruction and crescent sign (see figure).
Diagnosis can be confirmed by an abdominal
ultrasound scan or contrast enema.


After resuscitation with intravenous fluids, broad-spectrum antibiotics and nasogastric drainage,
non-operative reduction of the intussusception can be attempted using an air or barium enema.
This type of reduction (non-operative one) is contraindicated in cases of peritonitis or perforation,
strangulated bowel and pathological lead points are unlikely to reduce.

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