INTESTINAL OBSTRUCTION DUE

TO ADHESION

By

DR ADEKO OLUSEUN
dept of family medicine
olabisi onabanjo university
teaching
hospital, sagamu, nigeria.
 OUTLINE
• STATISTICS AND CASE PRESENTATION

• INTRODUCTION

• EPIDEMIOLOGY

• CLINICAL SIGNIFICANCE

• PATHOGENESIS

• CLINICAL PRESENTATION

• MANAGEMENT

• PROGNOSIS

• CONCLUSION
 ADHESIVE INTESTINAL
OBSTRUCTION
• This refers to the blockage of the
intestines, usually following surgery
due to formation of adhesion as part
of normal process of healing
preventing the normal transit of
products of digestion, intestinal
secretions and gas.

• It can occur at any level of GIT, but

commonly in the small intestine.
• Adhesions are abnormal deposits of
fibrous tissue which form within the
peritoneal cavity.

• Adhesion formation after abdominal

and pelvic operations remains
extremely common and is a source of
considerable morbidity.
• In clinical and autopsy studies of
patients who had prior laparotomies,
the incidence of intra-abdominal
adhesions was 70-90%
 CLASSIFICATION OF ADHESIONS

• Congenital adhesions: these are

present as embryological anomaly in
the development of the peritoneal
cavity. (vitello-intestinal bands,
adhesions seen across the lesser sac).

• Acquired adhesions: these may

inflammatory and post-surgical.
• Inflammatory adhesions: arise after intra-
abdominal inflammatory processes e.g.
appendicitis, acute cholecystitis, PID, TB
abdomen.

• Post-surgical adhesions: account for vast

majority of adhesions. It occurs when
injured tissue surface, following incision,
cauterization or suturing fuse together to
form scar tissue.
• Post-surgical adhesions form between
the wound and omentum in over 80%
of the pts.

• The intestines are involved in 50% of

the pts.
 FACTORS ASSOCIATED WITH THE
FORMATION OF POST-SURGICAL ADHESIONS

• These include: trauma, thermal

injury, infection, ischaemia and
foreign body.

• Others are: tight suturing, abrasions,

intestinal contents, blood, overheating
by lamps and irrigation fluid.
 CLINICAL SIGNIFICANCE
• Intestinal obstruction: occurs commonly in
the small bowel and results from kinking,
angulation or creation of bands of tissue
that compress the bowel.

• Adhesions create a lifetime risk of IO. An

operation 4 obstruction due to adhesions
carries a higher likelihood of recurrence
than a laparotomy 4 other indications

• When obstruction recurs, the possibility of

a cause other than adhesions is lower.

• The no of prior episodes a pt has

experienced is the strongest predictor of
recurrence.
• Most of the pts with AIO have been
found to have had surgery in the
infracolic part of the abdomen, where
loops of small intestine adhere and
become obstructed.

• Operations that frequently lead to AIO

include: colon & rectal surgery, non-
elective appendectomy, gynecological
procedures, gastrectomy, abdominal
vascular op, e.t.c.
• It should be noted that congenital and
inflammatory adhesions rarely give
rise to IO.

• The problem of post-surgical

adhesions +ses with the pt’s age, no
of laparotomies and complexity of
surgical procedures .
• Pts with a relatively low risk of
adhesion formation are those who
have undergone an elective
appendectomy thru a small incision or
a caesarian section thru a pfannestiel
incision.

• Prior lap thru a midline vertical

incision has significantly increased the
frequency of ant abd wall adhesion.
• Propensity to form adhesion appears
to be patient specific.

• Various individual factors e.g.

nutritional status, disease like DM
and the presence of concurrent
infectious process, which alter
leucocytes and fibroblast function
affect adhesion formation.
• Other clinical conditions that may arise
due to adhesions are:
difficult re-operative surgery

chronic abdominal pain

chronic pelvic pain

female infertility.
 EPIDEMOLOGY OF AIO
• AIO are responsible for a large
proportion of general surgical
admission.

• Approx 1% of all surgical admission

and 3% of laps are the results of
AIO.

• Over 20% of AIO occur within 1

month of surgery, and up to 40%
occur within 1 year.
• Study done at ife revealed that out
of 99 cases of IO seen btw 1985-
1994, 44% were due to adhesion.
(Lawal 2005).
• Similar study done at ilesha revealed
that out of 142 cases of IO seen
during the same period, 41.5% were
due to adhesion. (Adesunkanmi 1996).
• Findings at OOUTH showed that 111
cases of IO were seen from 1997 till
date, out of which 44 cases were
reviewed. 15% were due to adhesion.
• Study done in Ghana btw 1998-2003
revealed 652 cases of IO and AIO
was the 2nd commonest cause 27.2%
with the M:F of 1.7:1 (Ohene-Yeboah
2006).

• Findings at a UK hospital over a

period of 12 months revealed 228
cases of IO, and AIO was the cause
in 32%. (McEntee 1987).
 PATHOGENESIS OF ADHESION
• Peritoneal healing differs from that
of the skin. Skin re-epithelialization
takes place thru proliferation of
epithelial cells from the periphery
toward the centre of the skin wound.

• Peritoneum becomes mesothelialized

simultaneously, and regardless of the
injury, with new mesothelium
developing from Islands of cells.
• The key site in adhesion formation is the
surface lining of the peritoneum.

• The delicacy of the peritoneal surface

and its subsequent susceptibility to
damage as well as the rapid rate of re-
mesothelialization within 5-8 days are
important factors in adhesion formation.

• A wide variety of inflammatory stimuli

(op, trauma, bacteria infection,
irradiation, chemical) result in peritoneal
injury.
• Peritoneal injury/inflammation triggers
coagulative cascade which results in the
formation of inflammatory exudate
containing fibrin.

• The fibrinous exudate is organized and

fibroblast invasion is followed by the
deposition of collagen and the formation of
permanent fibrous tissue.

• This process is not inevitable as the

peritoneum possesses fibrinolytic activity
which if not impaired, will lysed the fibrin
within the exudate be4 organisation of the
exudate can take place.
• This biological balance is illustrated below:

Peritoneal injury

Fibrinous adhesion

Lysed Organised

Resolution Adhesion
formation
• Studies have shown that injury to the
peritoneum reduces its fibrinolytic
capacity and the same injury also
produces intra-abd adhesions.

• Organisation of peritoneal exudate

and collagen deposition commences
within 5 days of peritoneal injury,
suggesting that prolonged depression
of mesothelial fibrinolysis may allow
permanent fibrous adhesion formation
• Peritoneal injury results in a high conc
peritoneal pro-inflammatory cytokines
response esp TNFα, IL-1 and IL-6.

• These cytokines inhibit fibrinolysis.

• In conclusion, fibrous adhesion are

formed within the peritoneal cavity
when the normal fibrinolytic activity
of the peritoneum is lost.
 CLINICAL FEATURES
• The symptoms and Simpl Stran
signs in AIO depend e gulate
on nature of Pain Colick d
contin
obstruction- simple, y, uous
strangulation.
inter
Tende mitten
absen prese
rness tt nt
Bowel Hyper Absen
sound t
• Pain- earliest symptom

• Vomiting- severity depends on

whether high or low

• Constipation – high/low

• Distension- high/low

• History of previous
surgery/inflammatory conditions
• GPE- painful distress, dehydration,
signs of shock

• Vital signs- tachycardia, tachypnoea,

hypotension, fever.

• ABD- previous op scar, distension,

tenderness, guarding and
rebound tenderness in strangulation
bowel sounds- hyper or absent
DPR- empty rectum.
 MANAGEMENT
• Investigations

• Treatment

• Prevention

• Prognosis

• conclusion
 INVESTIGATIONS

• Laboratory- FBC, E, U& Cr,

Urinalysis, ABG

• Imaging studies- plain abd x- ray,

CT-scan,
Abd USS.
 Imaging studies
:Plain radiography -
Order plain radiographs first for patients in whom SBO•
.is suspected

Plain radiographs are diagnostically more accurate in•

.cases of simple obstruction

Plain radiography is of little assistance in•

.differentiating strangulation from simple obstruction
•
.Dilated small bowel loops indicate SBO•
.Absent or minimal colonic gas indicate SBO *
Radiograph for adhesive
intestinal obstruction
:CT scanning -
CT is useful in making an early diagnosis of*
strangulated obstruction and in delineating the myriad
.other causes of a cute abdominal pain
It also has proved useful in distinguishing the etiology
of SBO (If it was extrinsic causes such as adhesions
and hernia from intrinsic causes such as neoplasm or
.Crohn's
CT scanning is about 90% sensitive and specific in *
.diagnosing CBO
CT scanning enables the clinician to distinguish *
between ileus and mechanical small bowel in
.postoperative patients
.Bowel wall thickening indicates early strangulation *

.Portal venous gas indicates early strangulation *

CT scanning is useful in identifying abscess, hernias and *

.tumors

Strangulated obstruction
:Ultrasonography -

Ultrasonography is less costly and less invasive than CT *

. scanning

It may reliably exclude SBO in as many as 89% of *

.patients
 Treatment

• General principles
• Conservative
• Surgical
 General principles
• Stabilize pt

• Replace ivf-diligent ivf resuscitation

• NGtube –early bowel decompression

• Urethral catheterization

• Administer broad spectrum

antibiotics-necrosis suspected
 Conservative mgt
• History- Abd pain, Distention,
Vomiting, Fever

• Monitor vital signs

• Monitor NGTube effluent- Color, Volume

• Monitor Abdomen- Abd girth, Tenderness,

Guarding, Bowel sounds

• Oral gastrograffin- Test

 Surgical Mgt
• Adhesiolysis

• Bowel resection & anastomosis

• Close follow up-non operative

mgt
 PREVENTION
• There are no of possible measures of
preventing post-surgical adhesion
formation. These are:

 Good surgical technique

 pharmacological adjuvant therapy

 Adjuvant barrier therapy

 SURGICAL TECHNIQUES
• Tissue injury- steps to avoid injury to
tissue

• Peritoneal suturing- sutures are

foreign body, so may +se the risk of
adhesion formation. Cover areas at
higher risk of adhesion formation with
omentum, peritoneal flap, falciform
ligament, broad ligament.
• Foreign materials- glove powder (talc,
starch), fluff from surgical packs,
materials extruded from GIT all
provoke inflammatory rxn which
potentiate adhesion formation

• Sponges- strong association btw

adhesion formation and use of
sponges. When bowel need to be
packed use atraumatic bag to reduce
injury to the serosa.
• Intra-peritoneal blood deposit-
haemostasis is essential. Blood should
be aspirated in irrigation solution

• Minimally invasive surgery- use of

MIS and laparoscopy technique
 PHARMACOLOGICAL ADJUVANT THERAPY
• Involve use of agent against various
causes & component of inflammatory
process (infection, endotoxin,
exudation) and/or of adhesion
formation (coagulation, fibrin
deposition, fibroblastic activity and
proliferation)

• Obstacle to overcome are:

Ischaemic site are cut off from
systemic drug delivery
Peritoneal membrane has an extremely
rapid absorption mechanism

Agent to be used should not affect

normal wound healing process. The
process of adhesion formation uses
the same pathway as normal wound
healing.

• Some of the agent used are:

• NSAID- inhibits PG& TXA2 formation
thereby modulate a no of aspect of
inflammation.
been found to reduce peritoneal
adhesion in some animal models.

• Glucocorticoid & Antihistamines- these

agents attenuate inflammatory
response
mixed results from sutdies so far.
side-effect of steroid:
immunosuppression & delayed wound
healing.
• Progesterone/Estrogen- In animal
models progesterone was found to
reduce adhesion formation while
estrogen +ses adhesion. No
confirmatory study in human yet.

• Anticoagulant- crystalloid isotonic

irrigation containing heparin reduces
adhesion formation by inhibiting fibrin
coagulation. Note that heparin may be
associated with bleeding & delayed
wound healing.
• Fibrinolytic- use of rtPA locally to
enhance fibrinolysis has recorded
limited success. There is risk of
bleeding.

• Antibiotic- broad spectrum antibiotic

are used commonly 4 prophylaxis
against post-op infections & adhesion
formation.
Antibiotic in intra-abdominal irrigation
fluid actually causes adhesion
formation.
 ADJUVANT BARRIER THERAPY
• Anti-adhesion barriers fall into 2 groups

 Macromolecular solution barrier

 Mechanical devices

• Barrier solutions- These are:

 Crystalloids- Intra-peritoneal instillation of

normal saline or ringer’s lactate is thought
to dilute the fibrin & also separate raw
areas of peritoneum thereby preventing
adhesion.
 32% DEXTRAN 70- by hydroflotation of
intra-abd structures with dextran solution,
a physiological separation occurs btw
peritoneal surfaces. Thru dilution, dextran
reduces local fibrin conc & preserve local
plasminogen activators. Results in
preventing adhesion has been inconsistent.

 Hyaluronic acid (HA)- naturally occurring,

biocompatible & non-immunogenic. It coats
serosal surfaces & provides a certain
degree of protection from desiccation and
other types of injury.
HA Combined with phosphate-
buffered solution (seprarcoat)- this is
applied intra-op prior to dissection to
protect peritoneal surfaces from
indirect surgical trauma (abrasion,
desiccation).

Carboxymethylcellulose- a derivative
of cellulose. It works by separating
raw surfaces and allows independent
healing of traumatized peritoneal
surfaces.
• Solid barriers are:

 Autologous peritoneal transplant- covering

lesions of parietal peritoneum with micro-
surgically applied autologous transplant can
completely prevent severe adhesion
formation

 PTFE (Gore-tex)- a non-reactive,

antithrombogenic, non-toxic synthetic
fabric with small pores that inhibit cellular
transmigration & tissue adherence. It is
strictly reserved 4 non- contamination ops.
It prevents adhesion regardless of the type
of injury or whether hemostasis is
achieved.
Oxidized regenerated cellulose
(Interceed):
The only adjuvant approved 4 specific
purpose of post-surgical adhesion
prevention. It works by forming a barrier
and physically separate raw peritoneal
surfaces. It works well only when
hemostasis is perfect as blood interferes
with its fxn.

HA-CMC-(Seprafilm)- non toxic, non

immunogenic and biocompatible material.
 PROGNOSIS

• Difficult operation results in increased

morbidity, e.g. enterocutaneous
fistula may occur.

• Risk of recurrence- previous hx of

AIO is a strong predictor of
recurrence. Operation 4 recurrence
may further generate adhesion.
 CONCLUSION
Adhesion formation is a complex process
involving biochemical and biomechanical
factors. The cascade leading to adhesion is
the result of body response to an injury.
Current knowledge about these steps have
been discussed.
A multifactorial approach including minimizing
tissue injury with meticulous surgical
technique, appropriate antibiotic use and
biochemical agents and barriers will reduce
amount and severity of adhesion.
However, it is unlikely that the problem of
adhesion with the resultant morbidity and
economic cost will be resolved in the near