Adhesive intestinal obstruction

ADHESIVE INTESTINAL OBSTRUCTION, adhesiolysis, nobles intestinal plication, child-phillips mesenteric plication, gilroy bevan triad, intestinal obstruction, expectant management

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ADHESIVE INTESTINAL OBSTRUCTION. WHAT A RESIDENT SHOULD KNOW.
DR BASHIR BIN YUNUS
OUTLINE
 INTRODUCTION
 PATHOPHYSIOLOGY
 CLINICAL FEATURES
 MANAGEMENT
 PREVENTION OF ADHESIONS
 PERITONEAL ADHESION INDEX
 CONCLUSION
INTRODUCTION
Intra-abdominal adhesions are the most common cause of small bowel obstruction (SBO) in
industrialised countries, accounting for approximately 65-75% of cases. Estimated risk of SBO;
Appendectomy 1-10%, cholecytectomy 6.4%, intestinal surgery 10-25%, restorative proctocolectomy
17-25%. There is a changing trend in causes of intestinal obstruction in semi-urban Nigerian
hospitals; adhesive obstruction is the commonest cause. Obstructed hernia becoming increasingly less
common.
Causes;
1. Post operative in most cases
2. Post inflammatory with or without operation; peritonitis, appendicitis, acute pelvic infection.
3. Foreign body; materials used during surgery- sutures, gauze, talc powder from gloves
4. Bowel ischemia
5. Radiation induced enteritis
6. Inflammatory bowel disease
7. Specific conditions like tuberculosis, malignancy
Types;
1. Type 1; fibrinous adhesion occur during 5-10
th
post surgical period. It usually get resolve
completely. It is avascular and flimsy.
2. Type 2; fibrous adhesion. Becomes collagenised and vascularised
PATHOPHYSIOLOGY
The peritoneal fluid contains inflammatory cells including leucocytes and macrophages. These cells,
along with the mesothelium secrete various cellular mediators that have roles in peritoneal healing.
Following peritoneal injury, there is bleeding and increase vascular permeability with leakage of
protein rich fluid (esp. fibrinogen) from injured surface.
The inflammatory cells release pro-inflammatory cytokines and activation of the complement and
coagulation cascade. Activation of the coagulation cascade results in formation of thrombin, which is
necessary for the conversion of fibrinogen to fibrin. Fibrin functions to restore injured tissue and once
generated, is deposited along peritoneal surfaces. It causes adjacent organs or injured serosal surfaces
to coalesce.

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Under normal circumstance, degradation of this filmy fibrous adhesion by locally released proteases
of the fibrinolytic system occurs with 72hours of injury. The fibrinolysis allows mesothelial cells to
proliferate and the peritoneal defects to be restored within 4 to 5 days, preventing the permanent
attachment of adjacent surfaces.
If fibrinolysis does not occur within 5-7 days, or if local fibrinolytic activity is reduced, the fibrin
matrix persists. The matrix gradually becomes organized as collagen-secreting fibroblast infiltrate the
matrix. Over time, it becomes cellular structure that contains arterioles, venules, capillaries and nerve
fibres.
In the body systems, there is maintenance of balance between the Activators and inhibitors of
fibrinolysis.
Activators;
 Tissue plasminogen activator( tPA)- most important
 Urokinase- like plasminogen activator uPA
They activate plasminogen to plasmin which in turn degrades extracellular matrix including fibrin.
Inhibitors;
 Plasminogen activator inhibitors ( PAI). PAI-1 (dominant) and PAI-2
PAI prevents the formation of plasmin bydirectly binding to and inhibiting tPA and uPA.
Under normal conditions, fibrinolytic capacity exceeds coagulation in the peritoneum. However,
conditions causing peritoneal injury depress the fibrinolytic capacity. Cytokines especially TGF-B
release contributes to a decrease in peritoneal fibrinolytic capacity and may have role in preventing
the early dissolution of fibrous adhesions.

CLINICAL FEATURES
1. Abdominal pain: colicky type, recurrent and episodic (commonest symptom)
2. Distension , vomiting
3. Constipation
4. Previous surgical scars commonly observed.
NB:
 Gilroy Bevan triad of adhesive pain;
o Pain gets aggravated or relieved on change of posture
o Pain in the region of old abdominal scar
o Tenderness is elicited by pressure over the scar
 Presents with features of obstruction initially and later features of strangulation-toxicity,
fever, tachycardia, guarding, rigidity and rebound tenderness may occur.
 Adhesions may be asymptomatic for many years but later become symptomatic.

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INVESTIGATIONS
1. Plain Xray abdomen shows dilated bowel loops (investigation of choice)
2. Contrast enhanced CT scan; features of strangulation;
a. Intramesenteric fluid
b. Mesenteric oedema, congestion
c. Bowel wall thickening more than 2mm
d. Reduce mural enhancement in strangulated bowel compared to adjacent
bowel.
e. Whirl sign. Small bowel volvulus
3. E/U,Cr, FBC, Blood grouping.
MANAGEMENT
Expectant management
1) IV fluid
2) N-G tube
3) IV antibiotics
4) Urethral catheter
5) An enema saponis or use of flatus tube insertion may be considered
6) Observation
a) Half-hourly pulse and blood pressure
b) Four-hourly measurement of abdominal girth
c) N-G tube drainage- amount and colour
d) Passage or otherwise of flatus
e) Persistence or otherwise of pain
f) Presence or otherwise of abdominal tenderness or rebound tenderness
Reasons to abandon expectant management for laparotomy;
I. A rising pulse rate and or falling BP. Indicative of worsening of general condition
II. Increasing girth suggestive of increasing distension of gut
III. Persistence of abdominal pain indicative of continuing obstruction
IV. Increasing amount of N-G tube aspiration or change in colour from clear or bilous to brown.
Suggestive of worsening of obstruction
V. Tenderness, rebound tenderness and or guarding or rigidity or palpable tender mass denoting
onset of strangulation.
Duration for non-operative management;
Some surgeons advocate operative intervention in any patient who fails to show improvement within
48 hours. Others advocate a more liberal use of nonoperative therapy, citing a mean time to
successful resolution of up to 4.6 days.
However, prompt operative intervention is mandatory in patient who develop signs and symptoms
suggestive of strangulation obstruction. These parameters include fever, tachycardia, leukocytosis,
localized tenderness, continuous abdominal pain and peritonitis.
The presence of any three of these signs has 82% predictive value for strangulation, presence of four
has near 100% predictive value for strangulation.

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Operative management
ADHESIOLYSIS;
 Open
 Laparoscopic: is becoming popular, safer, ideal with less recurrent adhesion rate and gives
good results
NB; laparotomy can predispose to more subsequent adhesions.
Approach; At laparotomy, safe entrance may be best achieved by approaching this from the extreme
of the previous incision at virgin area rather than going through the mid portion of the incision.
Once in the peritoneal cavity, first is to identify site and cause of obstruction. Release fibrous
adhesions with sharp dissection. Inspect bowel for viability non-viable bowel should be resected.
Explore all four quadrants look for bowel injury or nonviable segments.
NOBLE’S PLICATION OF INTESTINE;
In noble placation of the intestine, adjacent coils of small intestine, arranged parallel are sutured at the
antimesenteric ends to prevent in-going for further recurrent adhesion. The bowel is initially freed
from the DJ junction to the ileocecal junction. Placation starts from above. Done for recurrent
adhesions.
CHILDS-PHILLIPS MESENTERIC PLICATION;
Similarly, after freeing the bowel from adhesions from DJ junction to the ileocecal junction, the
mesentry is plicated 2-3cm from the bowel. It prevents crumpling of bowel and adhesion formation.

PREVENTION OF ADHESIONS
1. Gentle handling of bowel
2. Use gloves free of talc
3. Prevention of spillage of content of viscous
4. Ensure meticulous hemostasis
5. Copious lavage of abdomen with saline, get rid of cloths before closure.
6. Careful placement of drain
7. Pulling omentum over bowel before closure to prevent adhesion of bowel to laparotomy scare
8. Instillation of drugs;
a. Hyaluronidase
b. Dextran 70
c. Amniotic membrane
d. Streptokinase
e. recombinant tPA
f. steroids
9. laparoscopic procedure
To this day, there is no means of completely preventing post-operative adhesion formation.

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PERITONEAL ADHESION INDEX
This is a classification system for adhesion to standardize their definition. It is based on the
macroscopic appearance of adhesions and their extent to the different region of the abdomen. The
surgeon can assign the index ranging from 1-30, there by giving the precise description of the intra
abdominal condition.
Regions of the abdomen;
 Right upper
 Epigastrium
 Left upper
 Left flank
 Left lower
 Pelvis
 Right flank
 Central
 Bowel to bowel
Adhesion grade score;
0 – no adhesion
1 – filmy adhesion, blunt dissection
2 – strong adhesions, sharp dissection
3 – very strong vascularised adhesion, sharp dissection, damage hardly preventable.
PAI is then estimated by computing the adhesion grade score for each of the regions. It ranges
from 1-30
A standardized classification and quantification of adhesion allows more integration of results from
several studies and comprehensive approach to the management.

COMPLICATIONS OF ADHESIONS
 Intestinal obstruction
 Secondary female infertility
 Ectopic gestation
 Chronic abominal and pelvic pain

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REFERENCES
1. Attad JP, MacLean AR. Adhesive small bowel obstruction: epidemiology, biology and
prevention. Can J Surg 2007, 50:4 p 291-300
2. Coccolilni et al. Peritoneal adhesion index(PAI): proposal of a score for the ignored
iceberg of medicine and surgery. World journal of emergency surgery 2013,8:6 p3-5.
3. McGregor AL. Treatment of chronic adhesive obstruction by noble procedure. S A Med
J 1956, 30:9 p937-941
4. Guido M S et al. Small bowel obstruction. In: Maingot’s Abdominal operation. 12
th
ed.,
McGrawHill; 2013. 600-607
5. SRB manual of surgery. 5
th
ed.,Jaypee Brothers; 2016.p934-936.
6. Naaeder SB, Tandoh JFK. Acute intestinal obstruction.In: BAJA’s principles and
practice of surgery including pathology in the tropics. 5
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ed., Repro India Ltd; 2015.
601p