Intestinal Obstruction

INTESTINAL OBSTRUCTION

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Definition:

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

Classification:

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

diverticulum.

3. Young adults:

strangulated hernia,

adhesions and bands,

Crohn’s.

4. Elderly: strangulated

hernia, CA, diverticulitis,

impacted feces, sigmoid

volvulus

Adhesions; 40%

Inflammatory; 15%

CA; 15%

Hernias; 12%

Fecal impaction; 8%

Pseudo-obstruction; 5%

Miscellaneous; 5%


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Pathophysiology

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

collapse

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


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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

SOCRATES

Periumbilical vs suprapubic

Frequency may indicate the site

Small bowel : 2-20 minutes

Large bowel: 30 minutes or more.

Distension

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.

Vomiting

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)


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Physical examination

General:

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

impaction.

Strangulation

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

obstruction.


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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.

Investigations

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)


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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

anastomosis.

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

cause”

Adhesions

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

asymptomatic!

Follow the principles of treatment:

NG decompression and IV fluids.

Urgent laparotomy if suspect strangulation, peritonitis or non-

response

Prevention:

Good surgical technique

Minimizing contact with gauze

Washing peritoneal cavity with normal saline.

Covering anastomosis and raw peritoneal surfaces

Treatment:

Conservative treatment is usually curative.

Surgery: divide (release) the adhesion.


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Volvulus

Definition:

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

gallbladder

Etiology:

Primary:

-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.

Secondary:

-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.


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Volvulus neonatorum

Causes:

◦ 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

Definition:

-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.


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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".

Etiology:

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

ketoacidosis

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.


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Management

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)

Pseudo-obstruction

Definition:

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.

Etiology:

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

Treatment:

The colon is decompressed by colonoscopy or

pharmacologically

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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Epidemiology

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.

Classification: 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: Newborns:

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. Investigations:

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).

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.

• Contrast enema studies

demonstrating abnormal recto-

sigmoid ratio of less than 1

with transition zone seen at the

rectum.


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Treatment 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.

Complications 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 stagnation. Prognosis

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

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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Presentation 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. Management 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.

Intestinal Obstruction

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