Volume 43 No.3, July 2001
POSTOPERATIVE ADHESIVE INTESTINAL OBSTRUCTION
Ketan R Vagholkar
Practising Surgeon; Dr. Vagholkar’s Fracture
and Accident Hospital, Thane - 400602
_________________________________________________________________________________
Adhesions have now become the leading cause
of intestinal obstruction. The diagnosis though being straight forward,
management poses a lot of problems due to the high incidence of recurrence.
The advent of laparoscopic surgery may alter the incidence of adhesions.
Despite the promise of laparoscopic surgery adhesions still continue to
be a major source of concern for surgeons not only because of technical
difficulties but also because of the volume of work they generate.
In the absence of any clinically proven means
of preventing adhesions from forming, the onus lies with the surgeon to
try and reduce their occurrence by improved and meticulous surgical techniques.
_________________________________________________________________________________
INTRODUCTION
The clinical presentation of intestinal obstruction
is well known to all surgeons when the patient presents with a previous
history of abdominal surgery, the most likely diagnosis is adhesions.[10]
The incidence of postoperative adhesive intestinal obstruction has been
gradually increasing over the last few decades.
Vick in 1932 reported
that adhesions accounted for 7% of all cases of intestinal obstruction.[35]
During the last few decades the leading cause of intestinal obstruction
was strangulated external hernia.
The overall incidence of adhesive intestinal obstruction
in 30% as shown in the studies conducted by Nemir, Perry, Bevan and Mc
Entee.[2],[23],[26]
Subsequent studies have revealed a steady rise in the incidence of intestinal
obstruction to the present day incidence of about 40%.[2]
INCIDENCE
Various studies have been carried out to assess
the severity of problems posed by adhesions. Weibel and Majno carried out
a study in a post mortem series to find out the incidence of adhesions.[21,22]
In cadavers with no preceding abdominal surgery, adhesions were found
in 28% and in those that had minor
abdominal surgery 67% had adhesions[21,22]
With other abdominal surgery the reported
incidence was 50%. If major surgery had been performed adhesions were present
in 76% and in cases of multiple abdominal surgery 93% had adhesions.[18]
The incidence of adhesions has also been studied
in living subjects. Inflammatory adhesions in patients who has not undergone
any preceding abdominal surgery were found to be present in 10%. In patients
who had previous abdominal surgery postoperative adhesions were found in
93% and inflammatory adhesions in 20%.[18]
In a review over the last 25 years it has been
shown that adhesions accounted for 1% of all surgical admissions and 3%
of all laparotomies in a particular surgical unit.[18]
It is likely that although the incidence of adhesive obstruction is increasing,
it is doing so because more and more patients are being submitted to laparotomies
each year.[27]
AETIOPATHOGENESIS OF ADHESIONS
Adhesions can be classified as either congenital
or acquired. The acquired type is further classified into inflammatory
and post surgical. Of all the types described majority of cases are postsurgical.
Many studies have been performed to study the time interval from surgery
to obstruction. As yet results are not conclusive. The incidence though
difficult to be determined is put forward to be 3% of all laparotomies
for adhesive obstruction.[18]
All operations which involve handling of the viscera
in the infracolic compartment are more likely to produce adhesive intestinal
obstruction[32]
The possible explanation put forward for them is trauma to the small bowel
at the time of surgery.[7]
The anatomical distribution of all adhesions
have been studied in various studies.[33]
The most common site for adhesions were to the undersurface of the abdominal
wound which occurred in 84% or to the site of previous surgery in 58%.[14,15,16]
The omentum was commonly involved in adhesions to the scar (72%) and to
the site of previous surgery (22%). Adhesions from the small bowel to the
wound occurred in only 18% of wounds and from the small bowel to the site
of surgery in 16%.[14,15,16]
Adhesions which involved the small bowel alone
occurred in only 8% of cases. Overall the omentum was involved in 57% of
sites for adhesions and the small bowel was involved in 27% of sites. Adhesions
between the small bowel and the site of previous surgery caused obstruction
in 52%. Adhesions which involved the small bowel alone caused obstruction
in 24%.[14,15,16]
If the distribution of these obstructing adhesions is compared with that
of any adhesions that develops after abdominal surgery, it is clear that
although omental adhesions are the most common adhesions to be found they
are at low risk of producing intestinal obstruction. Adhesions between
small bowel and other viscera or other loops of small intestine occur less
frequently but are far more likely to cause adhesive obstruction.
The omentum plays a protective role in adhesion formation. Adhesive obstruction
after total colectomy is well known. This is because the operation involves,
omentectomy and this will remove the organ that forms safe adhesions. As
a result it would leave adhesiogenic areas exposed to the small bowel and
will result in higher incidence of small bowel adhesions.
Another significant factor is a frequent practice
to divide any adhesions that are encountered. The division of adhesions
which involves the small bowel are at a high risk of later obstruction.
PREVENTION
As yet there are no definite methods of completely
preventing adhesions. The two commonly used solutions that have anti-adhesive
effects in animals povidone iodine and 30% dextran 70.[13]
Povidone iodine is used by surgeons more for its antimicrobial action rather
than that of its anti adhesive effect.[11]
Dextran is a popularly used solution in gynaecologic practice to prevent
adhesions in infertility surgery.
The most important way of preventing adhesions
is by meticulous technique.
The following are a few operative steps which
could be undertaken to reduce the
incidence of post operative adhesions.
Careful handling of the bowel to reduce serosal
trauma.
Avoid rough unnecessary dissection.
Avoid contact of foreign material from the
peritoneum e.g. use of absorbable material as far as possible, avoid excess
use of guaze swabs, or wearing starch free gloves.
Adequate excision of ischaemic or infected
debris within the peritoneum.
Preserve the omentum as far as possible. Placement
of omentum around the site of surgery and run the omentum under the wound
to encourage low risk adhesions to form.
Avoid dividing adhesions which do not involve
the small intestines.
SURGICAL MANAGEMENT
Adhesions producing intestinal obstruction usually
require surgical intervention in 30 to 60% of cases.[1,2,3]
Simple adhesiolysis is usually employed in those
patients who require surgery for adhesive obstruction. Recurrence rate
after adhesiolysis is 11% to 21%.[5]
In patients with recurrent obstruction adhesiolysis is combined with a
plication procedure or with an insertion of a long intestinal tube.[6]
The plication procedures of Noble or Childs and Philips depend upon sutures
to hold the small bowel in a specific position so that further adhesive
obstruction cannot occur.[9]
The long intestinal tube is designed to hold the small bowel in a series
of open loops until subsequent adhesions form to maintain the bowel in
position and then the tube can be removed.[4]
The noble plication has a high incidence of complication hence it is abandoned.[24,26]
Although
good results have been reported for the long intestinal tubes its use should
be confined to patients after division of extensive intraabdominal adhesions.[6]
If used after division of only a few adhesions when the adhesions reform
they may not be extensive enough to hold all the small bowel in an open
looped position and therefore will permit movement and twisting of the
bowel and allow subsequent adhesive intestinal obstruction to develop.[2],[19]
RECENT ADVANCES
Though there is a better understanding of the
mechanisms which lead to adhesion formation, yet
there is no pharmacological means of preventing the formation of adhesions.
Peritoneal trauma and ischaemia are potent stimuli for adhesion formation.
Von Benzer has demonstrated fibrinolytic properties
in peritoneum.[20]
The fibrinolytic activity is thought to be contained within the mesothelial
cell layer.[28,29]
The fibrinolytic activity has been identified as plasminogen activation.[30,34]
A reduction in this activity is linked to adhesion formation. Changes in
plasminogen activator activity levels were shown to be due to stimuli well
known to cause adhesions and were particularly marked in the presence of
ischaemia. This reduction was not only due to removal of plasminogen activity
but also due to the release of plasminogen activator inhibitors present
during inflammation and ischaemia.[7,8,12]
This mechanism for adhesion formation supports
the use of fibrinolytic agents as anti-adhesion agents.[7]
The commercial production of tissue plasminogen
activator rt-PA by recombinant DNA techniques has permitted the study of
the use of this agent in adhesion formation.[21,22]It
has been used to replace the reduced plasminogen activity of traumatised
peritoneum. The effectiveness of rt-PA as an anti adhesive has been confirmed
in animal models. Its effectivity in humans has still to be tried out.
But it appears to be the most promising agent. Laparoscopic surgery may
prove to be the solution to the problem. A study conducted by Luciano demonstrated
that when a stimulus is applied at open laparotomy in an animal it produces
more adhesions than when the same stimulus is applied through the laparoscope.[17]
CONCLUSION
The advent of laparoscopic surgery will undoubtedly
alter the incidence of adhesions developing after surgery. The reduced
bowel trauma from handling, the absence of large abdominal wounds and the
exclusion of foreign material such as starch and guaze from the abdominal
cavity will reduce adhesion formation after laparoscopic surgery.
It is possible that in the future these problems
may be reduced by some form of rt-PA peritoneal lavage after surgery that
will prevent adhesion formation or reformation.
REFERENCES
Adhesion study group. Reduction of post operative
pelvic adhesions with intraperitoneal 32%
dextran 70 : a prospective randomised clinical
trial. Fertil steril 1983; 40 : 612-19.
Bevan PG. Adhesive Obstruction. An R Coll surg
Engl 1984; 66 : 164-9.
Bizer LS, Liebling RW, Delaney HM, Gliedman HL.
Small bowel obstruction. The role of non operative treatment in simple
intestinal obstruction and predictive criteria for strangulation obstruction
surgery 1980; 407-13.
Brightwell NL, Mcfee AS, Aust JB. Bowel obstruction
and the long tube stent. Arch Surg 1977; 112 : 505-11.
Bizer LS, Delaney HM, Genut Z. Observations on
recurrent intestinal obstruction and modern non operative management. Diag
Surg 1986; 3 : 229-31.
Baker JW. A long jejunostomy tube for decompression
in intestinal obstruction. Surg Gynaecol obstet 1959; 109 : 518-20.
Buckman RF, Woods M, Sargent L, Gervin AS. A
unifying pathogenetic mechanism in the etiology of intraperitoneal adhesions.
J surg Res 1976; 20 : 1-5.
Buckman RF, Buckman PD, Hufnagel HV, Gervin AS.
A physiologic basis for adhesion free healing of deperitionealized surfaces.
J surg Res 1976; 21 : 67-76.
Childs WA, Philips RB. Experience with intestinal
plication and a proposed modification. Ann surg 1960; 152 : 258-65.
Fuzun M, Kayona KE, Harmanciouglu O, Astarciglu
K. Principal causes of mechanical bowel obstruction in surgically treated
adults in Western Turkey. Br J Surg 1991; 78 : 202-3.
Gilmore OJA, Reid C. Prevention of peritoneal
adhesions by a new povidone iodine /PVP solution. J surg Res 1978; 25 :
477-81.
Germin AS, Puckett CL, Silver D. Serosal hypofibrinolysis.
A cause for postoperative adhesions. Am J Surg 1973; 125 : 80-8.
Holtz G, Baker ER. Inhibition of peritoneal adhesion
formation after lysis with 32% dextran 70 fertil steril 1980; 34 : 294-5.
Hofstetter SR. Acute Adhesive obstruction of
the small intestine. Surg Gynaecol obst 1981; 152 : 141-4.
Hall RI. Adhesive obstruction of the small intestine;
a retrospective review. Br J clin Pract 1984; 38 : 89-92.
Laws HL, Aldrete JS. Small bowel obstruction;
a review of 465 cases. South med J 1976; 69 : 733-4.
Luciano AA. Laparotomy versus laparoscopy. prog
clin Biol Res 1990; 358 : 35-44.
Menzies D, Ellis H. Intestinal obstruction from
adhesions-how big is the problem? Ann R coll Surg Engl 1990; 72 : 60-3.
Maetani S, Tobe T, Kashiwara S. The neglected
role of torsion and constriction in pathogenesis of simple adhesive bowel
obstruction. Br J surg 1984; 71 : 127-30.
Mryhe Jenson O, Lassen SB, Astrup T. Fibrinolytic
activity in seasonal and synovial membranes. Arch Path 1969; 88 : 623-30.
Menzies D, Ellis H. Intra abdominal adhesions
and their prevention by topical tissue plasminogen activator. J R Soc Med
1989; 82 : 534-5.
Menzis D, Ellis H. The Role of plasminogen activator
in adhesion prevention. Surg Gynaecol obstet 1990; 172 : 362-6.
Nemir P. Intestinal obstruction: ten year surgery
at the hospital of the University of pennsylvania. Ann Surg 1952; 135 :
367-75.
Noble TB. Plication of small intestine as prophylaxis
against adhesions. Am J surg 1937; 35 : 41-4.
Nikitin Yu P, Shunkova EI, Sysoev AN, Severmy
VY, Ledeneva OA. Fibrinolytic properties of human serous membranes. Arkh
patol 1968; 30 : 66-9.
Perry JF, Smith GA, Yonehiro EG. Intestinal obstruction
caused by adhesions: a review of 388 cases. Ann surg 1955; 142 : 810-16.
Plyforth RH, Holloway JB, Griffin WO. Mechanical
small bowel obstruction: a plea for surgical intervention. Ann surg 1970;
171 : 183-8.
Porter JM, MC Gregor FH, Mullen DC, Silver D.
Fibrinolytic activity of mesothelial surfaces. surg forum 1969; 20 : 80-4.
Raftery AT. Method of measuring fibrinolytic
activity in a single layer of cells. J clini pathol 1981; 34 : 625-9.
Raftery AT. Effect of peritoneal trauma on peritoneal
fibrinolytic activity and intraperitoneal adhesion formation. An experimental
study in the rat. Eur Surg Res 1981; 13 : 397-401
Stewardson RH, Bombeck CT, Nyus LM. Critical
operative management of strangulation obstruction. Ann surg 1978; 187 :
189-93.
Stewart RM, Page CP, Brendar J, Sch wesinger
W, Eisinhut D. The incidence and risk of early postoperative small bowel
obstruction: a cohort study. Am J surg 1987; 154 : 643-7.
Turner DM, Croom RD. Acute Adhesive obstruction
of the small intestine. Am Surg 1983; 49 : 126-30.
Vipond MN, Whavell SA, Thomson JN, Dudley HAF.
Peritoneal fibrinolytic activity and intra abdominal adhesions. Lancet
1990; 335 : 1120-2.
Vick RM. Statistics of acute intestinal obstruction.
Br Med J 1932; 2 : 546-8.
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