LARGE BOWEL OBSTRUCTION
TYPES OF INTESTINAL OBSTRUCTION
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DYNAMIC – where peristalsis is working against a
mechanical obstruction.
ADYNAMIC – where mechanical element is absent.
1. Peristalsis may be absent; eg: paralytic ileus
2. Peristalsis present in a non propulsive form.
CLASSIFICATION (Contd..)
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ACUTE OBSTRUCTION
CHRONIC OBSTRUCTION
ACUTE ON CHRONIC OBSTRUCTION
SUBACUTE OBSTRUCTION
CAUSES OF LARGE BOWEL
OBSTRUCTION
DYNAMIC
INTRALUMINAL
impaction
foreign bodies
bezoar
gall stones
INTRAMURAL
strictures
malignancy
EXTRAMURAL
bands/adhesions
hernia
volvulus
intussusception
ADYNAMIC
paralytic ileus
pseudo obstruction
PATHOPHYSIOLOGY
ABOVE THE LEVEL OF OBSTRUCTION
 Obstruction proximal peristalsis is increased
proportional to the distance of obstruction
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Obstruction not relieved bowel begins to
dilate reduction in peristaltic strength
flaccidity & paralysis
PATHO PHYSIOLOGY
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Distension proximal to obstruction
-GAS (nitrogen & hydrogen sulphide)
-FLUID (digestive juices)
BELOW THE LEVEL OF OBSTRUCTION
 Normal peristalsis & absorption till empty  then
bowel contracts and becomes immobile
STRANGULATION
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Venous return is compromised  increase in capillary
pressure  local mural distension  loss of
intravascular fluid & RBCs occurs
Once the arterial supply is impaired, hemorrhagic
infarction occurs  viability of the bowel wall is
compromised  translocation & systemic exposure to
aerobic & anaerobic organisms with their toxins.
CAUSES OF STRANGULATION
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EXTERNAL hernial orifices adhesions/bands
INTERRUPTED BLOOD SUPPLY volvulus,
intussusception
INCREASED INTRALUMINAL PRESSURE closed
loop obstruction
PRIMARY mesenteric infarction
CLINICAL FEATURES
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1.
2.
3.
The signs & symptoms depend on the site of location of
obstruction
Cancers arising in the left colon & rectum are more likely to
obstruct than the more capacious proximal colon
The symptoms are :
Failure to pass stools or flatus(constipation/opstipation)
Abdominal distention
Cramping abdominal pain
OTHER MANIFESTATIONS
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DEHYDRATION
HYPOKALAEMIA
PYREXIA – may indicate
1. onset of ischemia
2. intestinal perforation
3. associated inflammation
HYPOTHERMIA
ABDOMINAL TENDERNESS
Clinical features of strangulation
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Presence of shock indicates
underlying ischemia
Constant pain
Symptoms usually commence suddenly &
recur regularly
Localised tenderness will always be present
associated with rigidity/rebound tenderness
CLOSED LOOP OBSTRUCTION
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Occurs when the bowel is obstructed
at both the proximal & distal points.
There is no early distension of the
proximal intestine.
When gangrene of the strangulated
segment occurs, retrograde
thrombosis of mesentric veins results in
distension on both sides.
INTERNAL HERNIA
SITES OF INTERNAL HERNIA
 Defect in the mesentery
 Defect in the transverse colon
 Congenital or acquired diaphragmatic hernias,
 Caecal/ appendiceal retroperitoneal fossae
 Inter sigmoid fossa
OBSTRUCTION FROM ENTERIC
STRICTURES
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Occurs secondary to TB or Crohn’s disease
Malignant strictureslymphoma
Presentation is sub a/c or c/c
Standard surgical management
is
resection& anastomosis
Strictureplasty for Crohn’s
BOLUS OBSTRUCTION
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FOOD
GALL STONES
TRICHO BEZOARS
PHYTO BEZOARS
STERCOLITHS
WORMS
TRICHO BEZOAR
STERCOLITH
FABRIC BEZOAR
CHRONIC INTESTINAL OBSTRUCTION
The causes of obstruction may be
ORGANIC
 Intramural - faecal impaction
 Mural - diverticulitis, strictures, anastomotic stenosis
 Extramural -adhesion , metastatic deposits,
endometriosis
FUNCTIONAL - pseudo-obstruction.
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Constipation appears first. It is initially relative and
then absolute
Associated with distension and pain
Vomiting is a late feature
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Plain abdominal radiography may be useful.
Contrast water-soluble enema study to rule out
functional disease.
Organic disease requires a laparotomy
Functional disease requires colonoscopic
decompression and conservative management
ADYNAMIC
OBSTRUCTION
PARALYTIC ILEUS
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It is a state in which there is failure of peristaltic
waves secondary to neuromuscular failure
Stasis  accumulation of fluid and gas within the
bowel with associated distension, vomiting, absence
of bowel sounds and absolute constipation
TYPES OF PARALYTIC ILEUS
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Postoperative — self-limiting with a duration of
24—72 hours.
Infection — intra-abdominal sepsis
Reflex ileus — fractures of the spine or ribs,
retroperitoneal haemorrhage or application of a
plaster jacket.
Metabolic — uraemia and hypokalaemia .
CLINICAL FEATURES
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Occurs 72 hours after laparotomy
No bowel sounds on auscultation
No passage of flatus.
Abdominal distension becomes more marked and
tympanitic.
Pain is not a feature.
Radiologically, the abdomen shows gas-filled loops
of intestine with multiple fluid levels
MANAGEMENT
Prevention by
 Nasogastric suction
 Restriction of oral intake
 Electrolyte balance must be
maintained
General principles of specific treatment are
 The primary cause must be removed
 GI distension must be relieved by decompression
 Close attention to fluid and electrolyte balance
 Catchpole regime with neostigmine may be used in
resistant cases
 If prolonged and threatens life laparotomy
TREATMENT OF LARGE BOWEL
OBSTRUCTION
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HISTORY
PHYSICAL EXAMINATION
ABDOMEN SHOULD BE PALPATED FOR MASSES
GROIN PALPATED FOR HERNIAS
DIGITAL RECTAL EXAMINATION TO EXCLUDE
RECTAL CANCERS
PRINCIPLES OF TREATMENT OF ACUTE
INTESTINAL OBSTRUCTION
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GASTROINTESTINAL DRAINAGE
FLUID & ELECTROLYTE
REPLACEMENT
RELIEF OF OBSTRUCTION
SUPPORTIVE MANAGEMENT
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NASOGASTRIC DECOMPRESSION
4th hourly aspiration by Ryle’s or Salem tube.
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REPLACEMENT OF SODIUM
AND WATER LOSS
with Hartmann’s solution or
normal saline.The volume required
is determined by clinical,
haematological & biochemical
criteria.
ANTIBIOTICS
SURGERY
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1.
2.
3.
Surgical options in case of sigmoid colon cancer
include:
Hartmann’s Operation – simoidectomy with
descending colostomy & closure of rectal stump
Sigmoidectomy with primary colorectal
anastamosis
Abdominal colectomy with ileorectal anastamosis
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Right sided colonic obstruction whether caused by
cancer or volvulus is generally treated by resection
& primary anastamosis
PSEUDO OBSTRUCTION
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Pseudo-obstruction of the colon (also called Ogilvie's
syndrome, after its description by Sir Heneage Ogilvie
in 1948) describes the condition of distention of the
colon, with signs and symptoms of colonic obstruction, in
the absence of an actual physical cause of the
obstruction.
Ogilvie described two patients with clinical features of
colonic obstruction despite a normal barium enema.
Both patients underwent laparotomy for the condition;
neither had mechanical obstruction, but both had
unsuspected malignant disease involving the area of the
celiac axis and semilunar ganglion.
Contd…..
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The cause of the dilation was attributed to the
malignant infiltration of the sympathetic ganglia.
Subsequently there have been numerous descriptions of
cases of colonic distention in the absence of mechanical
obstruction and without malignant involvement of the
visceral autonomic nerves.
Very few cases of pseudo-obstruction have malignant
infiltration of the autonomic nerves as the cause; in fact,
the exact pathogenesis of the syndrome remains
unknown, and it has been associated with a
heterogeneous group of conditions.
PRIMARY PSEUDO OBSTRUCTION
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Primary pseudo-obstruction is a motility disorder
that is either a familial visceral myopathy (hollow
visceral myopathy syndrome) or
a diffuse motility disorder involving the autonomic
innervation of the intestinal wall.
The latter may be modified by a disturbance of
intestinal hormones or may be principally due to
disordered autonomic innervation.
SECONDARY PSEUDO-OBSTRUCTION
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Secondary pseudo-obstruction is more common and has been
associated with neuroleptic medications, opiates, severe
metabolic illness, myxedema, diabetes mellitus, uremia,
hyperparathyroidism, lupus, scleroderma, Parkinson's disease,
and traumatic retroperitoneal hematomas.
One mechanism thought to play a role in the pathogenesis is
sympathetic overactivity overriding the parasympathetic
system.
Indirect support for this theory has been derived from the
success in treating the syndrome with neostigmine, a
parasympathomimetic agent.
Further support comes from reports of immediate resolution of
the syndrome after administration of an epidural anesthetic
that provides sympathetic blockade.
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Pseudo-obstruction may present in acute or chronic
forms.
The acute variety most commonly affects patients
with chronic renal, respiratory, cerebral, or
cardiovascular disease. It usually involves only the
colon, whereas the chronic form affects other parts
of the gastrointestinal tract, usually presents as
bouts of subacute and partial intestinal obstruction,
and tends to recur periodically.
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Acute colonic pseudo-obstruction should be
suspected when a medically ill patient suddenly
develops abdominal distention.
The abdomen is tympanitic, usually nontender, and
bowel sounds are usually present. Plain abdominal
radiographs reveal a distended colon, with the right
and transverse segments tending to be most
dramatically affected.
The radiologic appearance is one of large bowel
obstruction.
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The most useful investigation is a water-soluble
contrast enema, which should be performed in all
patients in whom the diagnosis is suspected,
provided their condition is stable enough to warrant
the procedure.
The contrast enema can reliably differentiate
between mechanical obstruction and pseudoobstruction, a differentiation that is essential to
guide appropriate therapy.
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Colonoscopy is the alternative diagnostic
investigation for pseudo-obstruction and has the
attractive advantage that it can be used for
treatment. However, at the present time, the watersoluble contrast enema is generally the preferred
initial test.
TREATMENT
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When the diagnosis of acute pseudo-obstruction is
suspected, treatment should accompany the diagnostic
evaluation.
Initial treatment includes nasogastric decompression,
replacement of extracellular fluid deficits, and correction
of electrolyte abnormalities.
All medications that inhibit bowel motility, such as
opiates, should be discontinued.
Patient response is monitored by serial abdominal
examinations and radiographs. Most patients improve
with this regimen.
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Until the mid-1990s, the treatment usually used
when the colonic distention failed to resolve with
supportive measures was colonoscopic
decompression. Although this approach was
generally successful, it required skilled personnel
and equipment and carried the risk for colonic
perforation from both instrument trauma and
insufflation. In addition, the procedure often had to
be repeated because of recurrence of the colonic
distention.
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At the present time, the trend has been to treat this
condition with neostigmine, a parasympathomimetic
agent.
It is obviously imperative that mechanical
obstruction be excluded (either by water-soluble
contrast enema or colonoscopy) before the
administration of neostigmine because the
subsequent high pressures generated in the colon
against a distal obstruction could cause colonic
perforation.
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Neostigmine enhances parasympathetic activity by
competing with acetylcholine for acetylcholinesterase
binding sites. In the treatment of colonic pseudo-obstruction,
2.5 mg of neostigmine is given intravenously over 3 minutes.
The resolution of the condition is indicated within less than
10 minutes of administration of the drug, by the passage of
stool and flatus by the patient.
The recurrence rates following the administration of
neostigmine appear to be far lower than those associated
with colonoscopic decompression, with satisfactory
decompression being achieved in about 90% of patients
after a single administration of the medication.
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A significant side effect of neostigmine is
bradycardia, and all patients must be monitored by
telemetry during administration of the drug.
Atropine must be immediately available, and
patients with significant cardiac disease are not
candidates for this treatment.