Intestinal Obstruction
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Transcript of 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.