Small Bowel Obstruction CPS 2012

New Paradigms in the Treatment of
Small Bowel Obstruction

Surgery in the 21st century has seen the development of a host of
exciting technological and management innovations such as minimally
invasive surgery, endovascular treatment in vascular disease, endoscopic
proce dures that require no incision, and potent and effective new
medications that have altered the natural history of some surgical
diseases. One disease that has changed very little in its incidence, natural
history, treatment approach, and preventability is small bowel
obstruction (SBO). Small bowel obstruction remains a common and
difficult problem encountered by all surgeons who operate in the
abdomen. Given its common and serious nature, it is surprising that so
little progress has been made in preventing and treating it when it occurs.
Nevertheless, over the past 15 years, some modest progress and
advancements have been made in its treatment, which will be the focus
of this review.
In Wiseman’s1 review of the topic, he noted that Hunter knew about
SBO in the mid 1700s and described a case associated with adhesions,
peritonitis, and infection. In 1842, Bryant reported a fatal case of bowel
obstruction caused by adhesions. Both Muller and Malcolm described
using salt solution to “float the intestines” and prevent adhesions in 1886
and 1889 respectively.1 By 1932, adhesions accounted for 7% of
intestinal obstructions in the United Kingdom, and by 1934, Moss
reported that 27% of intestinal obstructions in the United States were due
to adhesions2 (Table 1).
Scope of the Problem

Small bowel obstruction remains a huge problem in the United States
today. Bevan’s review found that 1.9% of all hospital admissions were
due to bowel obstruction.3 Menzies and Ellis identified 0.9% of 28,297
admissions over 25 years due to intestinal obstruction, 4 and Irvin
revealed that 3.5% of all emergency admissions that lead to laparotomy
were for adhesions.5 Menzies and Ellis confirmed that 3% of all
laparotomies are performed for adhesive obstructions alone. 4 In the
United States in a
Curr Probl Surg 2012;49:642-717.

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TABLE 1. History of small bowel obstruction
Date Event
2500 BC Ancient Egyptians describe adhesions 440 BC Pleural adhesions
described in Talmud 1750 AD Hunter describes adhesions due to peritonitis 1842 AD
Bryant describes fatal bowel obstruction 1932 AD Adhesions cause 7% of SBO in
United Kingdom 1934 AD Adhesions cause 27% of SBO in the United States SBO,
small bowel obstruction.
TABLE 2. Small bowel obstruction in the United States

Cause (%)
Author Year Adhesions Hernia Cancer Number
Playforth9 1970 54 23 9 111 Laws 10 1976 69 8 10 465 Stewardson 11 1978 64 24 7 238
Bizer12 1981 74 8 9 405
recent year, 948,000 hospital days of care were required for treatment of
SBO.6 The same study suggests that Medicare alone is paying $3.2
billion per year for treatment of SBO, and currently there are 117
hospitalizations per 100,000 people for treatment of bowel obstruction. 6
In several countries in Europe, the medical costs for SBO were greater
than the costs for gastric cancer and almost as much as for colon
cancer.7,8 Although initial studies suggested that the increased role of
minimally invasive surgery did not appear to have significantly reduced
the incidence of adhesive SBO, more recent studies suggests that SBO
incidence is lower in patients who undergo a minimally invasive
procedure. Clearly, given the magnitude of this problem, finding a
prevention for or cure of this costly and frustrating complication should
be a priority for American medicine.
Etiology of SBO
Any discussion of SBO mandates a discussion of adhesions and the
role they play in the disease. Although adhesions rarely lead to
obstruction of the large bowel, they account for more than 70% of all
SBOs.2 A review of the literature regarding the etiology of SBO confirms
that in the United States, adhesions constitute the major source of SBO
by a large mar gin9-12 (Table 2). Other causes of SBO include hernia
(most common cause of SBO in undeveloped countries), cancer,
inflammatory bowel
Curr Probl Surg, November 2012 643
TABLE 3. Lexicon of small bowel obstruction
Less serious More serious
Partial Complete
Low grade High grade
Simple Closed loop
Low High
Ileus Mechanical
Chronic Acute
Intrinsic Extrinsic
disease, intussusception, radiation, endometriosis, infection, and foreign

body.
In patients with a “virgin abdomen,” the most common cause of bowel
obstruction is incarceration of small bowel in a hernia. Inguinal, femoral,
ventral, or umbilical hernias can be the source of obstruction and are
usually fairly obvious on physical examination. An elderly patient with a
“virgin abdomen” who presents with SBO should be evaluated for an
obstructing cancer if no hernia is detected.
Classification of SBO
Small bowel obstruction may be classified in a variety of ways, and a
lexicon unique to SBO has developed over the years (Table 3). Small
bowel obstruction may be classified as complete vs. partial, high grade
vs. low grade, simple vs. closed loop, high vs. low, mechanical vs. ileus,
and chronic vs. acute. Complete SBO is characterized by significantly
distended bowel associated with failure to pass stool or flatus and lack of
air in the distal small bowel and colorectum. Partial SBO tends to be
associated with less dramatic small bowel distention, evidence of flatus
and/or stool passage, and radiologic evidence of gas throughout the entire
bowel. Complete SBO virtually always leads to operative intervention,
whereas partial SBO can often be conservatively managed with close
observation via serial examinations and abdominal radiographs.
A high-grade SBO is characterized by significant bowel distention,
little to no flatus passage, abdominal pain, and often an impressively
distended abdomen. A high-grade SBO has little likelihood of resolving
with conservative management. A low-grade bowel obstruction features
much less abdominal distention, some passage of flatus and stool, and
much less pain and discomfort. It frequently resolves with watchful
waiting. A simple bowel obstruction is defined as SBO in which the
bowel is occluded at a single point along its length, whereas a closed
loop obstruction is defined as an obstruction in which both the afferent
and
FIG 1. Artist’s conception of a closed loop obstruction caused by a single adhesive band.
(Reprinted with permission from Lawrence P, Bell R. Essentials of General Surgery (ed 3).
Hagerstown, MD: Lippincott Williams & Wilkins, 2005.)
efferent portions of a single loop of bowel are occluded by a constrictive

lesion (Fig 1). Because the blood supply of a closed loop is often also
entrapped by the constrictive band, loss of blood supply to the loop is
likely with the subsequent development of strangulation and bowel
necrosis. That rarely occurs with simple obstruction. For that reason,
closed loop obstruction is much more dangerous than simple and should
virtually always be treated operatively when diagnosed.
A high SBO is the one that occurs very proximally in the jejunum,
whereas a low SBO is found in the distal ileum. The former is associated
with epigastric distention and high nasogastric (NG) tube outputs that are
bilious, whereas the latter is characterized by global abdominal distention
and more turbid, feculent, NG output.
Mechanical SBO is defined as lumen occlusion by a physical
pathologic lesion. Conversely, ileus is a functional obstruction caused by
a range of disease processes that have the effect of paralyzing the bowel
so that no propulsive motor activity occurs. Paralytic ileus uncommonly
requires operative treatment and usually resolves when the etiologic
disease resolves. Chronic SBO is characterized by multiple low-grade
obstruc tions over a period that cause multiple ER visits and clinic
assessments
but usually do not result in immediate operative intervention. Acute SBO
develops abruptly and usually with no antecedent history and, if no
spontaneous resolution occurs, is more likely to require operation than
chronic SBO.
Finally, SBO may be caused by extrinsic lesions or intrinsic processes.
Extrinsic lesions cause SBO much more frequently than intrinsic ones.
Common extrinsic obstructing lesions include postoperative adhesions,
hernias, endometriosis, metastatic cancer, lymphoma, volvulus, and
abscess. Intrinsic diseases causing obstruction include Crohn’s disease,
tumors, radiation injury, hematoma, and intussusception.
Pathophysiology of SBO and Adhesion

Formation Adhesion Formation
Abdominal adhesions are abnormal fibrous connective tissue bands that
form between intestines, organs, or tissue in the abdominal cavity that are
normally separated.13 The adhesions may be congenital or acquired, the
latter usually because of infection, inflammation, or abdominal surgery.
Most intestinal adhesions are caused by trauma to the peritoneum from
previous operation (60% to 70%), and adhesions are the leading cause of
intestinal obstruction in North America. Typical injuries to the perito
neum at the time of operation that could cause adhesions include
incisions, suturing, abrasion, ischemia, desiccation, and cautery. 14
Adhesions after abdominal surgery are part of the normal healing
process for peritoneal injury. The early balance between fibrin deposition
and degradation (i.e., fibrinolysis) seems to be the critical factor in
adhesion formation. Fibrin deposition at the surgical site is a requirement
for adhesions to form. If fibrinolysis proceeds unimpeded, formation of
postoperative adhesions is greatly reduced; unfortunately, many vari
ables, including operation and anesthesia, impair this important step. 13
The purpose of this section is to review the biochemical and cellular
processes that lead to adhesion formation. A description of current
intraoperative strategies available to the surgeon to prevent postoperative
adhesions is presented in the last section of this monograph.
Biological Pathways That Lead to Adhesion Formation

Adhesions form in response to an injury to the peritoneum in the space
between the parietal and visceral peritoneum. Large and small peritoneal
defects heal at the same rate, suggesting that healing is a field phenom
enon and not centripetal like wounds in the skin (Fig 2). The outer
membrane of the peritoneum is lined by a layer of mesothelium that
FIG 2. Healing of a peritoneal injury or defect is a field phenomenon and does not involve wound
contraction as seen in skin wounds. Therefore, healing of large and small peritoneal wounds
occurs at the same rate, as illustrated in this figure. (Reprinted with permission from DiZerega
GS, Campeau JD. Peritoneal repair and post-surgical adhesion formation. Hum Reprod Update
2001;7:547-55, by permission of Oxford University Press.) (Color version of figure is available
online.)
covers the surface of the peritoneal cavity and the intra-abdominal

organs15 (Fig 3). Mesothelial cells produce and secrete factors that have
an effect on inflammation, peritoneal wound healing, and adhesion
formation.16,17 Adhesion formation begins with trauma to the peritoneum
and the induction of a generalized peritoneal inflammatory response (Fig
4). As a component of the response to injury and the coagulation
cascade, a fibrin-rich exudate accumulates on injured peritoneal
surfaces.18 This fibrin-rich matrix is capable of forming permanent
attachments or “adhesions” between serosal surfaces within the
peritoneal cavity if not resolved.19,20 Normal peritoneal healing and
regeneration occurs if the fibrin-rich exudate is resolved by the normally
active, peritoneal fibrino lytic system. However, abdominal surgery often
suppresses peritoneal fibrinolytic activity primarily by decreasing
peritoneal tissue plasminogen activator (t-PA) levels and increasing
plasminogen activator inhibitor-1 (PA-I) levels18 (Fig 5).
Both adhesion formation and adhesion-free epithelialization are
pathways of peritoneal wound healing. The injury of the peritoneum may
be inflammatory, infectious (as with diverticulitis), or surgical,
FIG 3. Electron micrograph of widely spaced, loosely attached mesothelial cells of the
peritoneum assuming the appearance of cotton balls. (Reprinted with kind permission of Springer
Science Business Media from DiZerega GS, ed. Peritoneal Surgery. New York: Springer-Verlag,
2000.)
FIG 4. Generalized peritoneal inflammatory response associated with injury. Note the rise and
time course for fibrin and mesothelial cells. (Reprinted with kind permission of Springer Science
Business Media from DiZerega GS, ed. Peritoneal Surgery. New York: Springer-Verlag, 2000.)
and the injury may include exposure to intestinal contents. The healing
attempt begins with the formation, through coagulation, of a fibrin rich
exudate through which mesothelial cells can migrate and accom plish
reepithelialization.
FIG 5. Biochemical events associated with peritoneal injury and possible adhesion formation.
tPA, tissue plasminogen activator; PAI, plasminogen activator inhibitor; uPA, urokinase
plasminogen activator. (Reprinted with permission from Attard and MacLean. 13)

This fibrin-rich exudate is a tacky substance and causes adjacent organs
or injured serosal surfaces to coalesce. 21 Under normal circumstances, the
formation of a fibrin matrix during wound healing is only temporary, and
degradation of these filmy fibrinous adhesions by locally released
proteases of the fibrinolytic system occurs within 72 hours of injury. 22
Fibrinolysis allows mesothelial cells to proliferate and the peritoneal
defect to be restored within 4-5 days, preventing the permanent
attachment of adjacent sur faces.13,22 If fibrinolysis does not occur within
5-7 days of peritoneal injury, or if local fibrinolytic activity is reduced,
the fibrin matrix persists. 17 If this occurs, the temporary fibrin matrix
gradually becomes more organized as collagen-secreting fibroblasts and
other reparative cells infiltrate the ma trix. 14,17
Mediators Involved in Adhesion Formation

The newly recruited inflammatory cells release a host of inflammatory
mediators, including cytokines and chemoattractants that may exacerbate
the response at several points of adhesion formation (Fig 5).18 Several
cytokines contribute to the suppression of fibrinolysis and adhesion
formation. Transforming growth factor (TGF-B) has been identified as
having a role in adhesion development by promoting fibrosis and also
mesothelial cell proliferation rather than fibrinolysis. 23 Interleukin-1 has
also been linked to adhesion formation as an inhibitor of fibrinolysis via
stimulation of PA-I.24 Substance P, a tachykinin peptide promotes
adhesion formation by inhibiting fibrinolysis via decreasing the amount
of t-PA in the peritoneum.18 For a comprehensive summary of the media
tors, genes, and factors involved in adhesion formation, we recommend
recent articles by Reed and colleagues18 and Attard and Maclean.13
Strategies for Adhesion Reduction

Adhesion reduction agents can be broadly separated into 2 categories.
The first are the pharmacological therapies given around the time of the
patient’s operation. The second encompasses topical products applied
directly to the operative site.
Attard and Maclean have identified 6 mechanisms by which adhesion
formation can be disrupted (Table 4): (1) decreasing peritoneal damage,
(2) decreasing the early inflammatory response, (3) prevention of fibrin
forma tion, (4) increasing fibrinolysis, (5) preventing collagen
deposition, and (6) providing barriers to adhesion formation. 13 In theory,
each of these processes could be controlled by surgical technique,
pharmacological therapy, and use of topical intra-abdominal products at
the time of operation. Many different pharmacological agents have been
tried to achieve adhesion reduction.25
TABLE 4. Mechanisms by which adhesion formation can be disrupted
Decreasing peritoneal damage
Decreasing the early inflammatory response
Prevention of fibrin formation
Increasing fibrinolysis
Preventing collagen deposition
Providing barriers to adhesion formation
There is sound logic behind the use of such agents, although their
effective ness has been somewhat limited. Reports in the literature
describe the effective use of a large number of pharmacological agents in
experimental animal studies.25 However, few agents progress to clinical
trials.
Several compounds in the laboratory have been noted to decrease adhe
sions by interfering with fibrin deposition: nonsteroidal anti-
inflammatory drugs (NSAIDs), heparin, and corticosteroids. NSAID
action targets prosta glandin synthesis, decreasing the inflammatory
response from the start.26 Heparin acts directly on the coagulation
cascade by inhibiting the internal pathway of the coagulation cascade by
acting on factor Xa and thrombin via antithrombin. Corticosteroids may
also have potential to inhibit adhesion formation via immune modulation,
but studies have not been able to demonstrate this convincingly. 27 Drugs
that alter the inflammatory response following operation have been most
studied. The drugs include steroids and the NSAIDs. The balance
between adhesion reduction and acceptable systemic side effects, such as
bleeding and impaired wound healing has been difficult to overcome for
these agents. Therapeutic anticoagulation to prevent fibrin deposition or
the use of streptokinase to promote fibrinolysis has not had a significant
effect on adhesion reduction in animal studies, and again there is the
concern for the risk of postoperative bleeding. The results from studies
using streptokinase and urokinase have been equivocal or even harmful
in some studies.13
For a thorough review of the status of pharmacological strategies for
adhesion prevention, we recommend recent articles by Attard and
Maclean13; and Lauder and colleagues.,25 Obviously, a pharmacologic
agent that would reduce inflammation and optimize fibrinolysis postop
eratively without causing bleeding or impairing wound healing would be
an ideal candidate for adhesion prevention.18
Laparoscopic vs. Open Surgery and Adhesions
Surgeons who perform laparoscopic surgery appreciate and recognize
that adhesion formation is less after laparoscopic procedures, such as
cholecystectomy and hernia repair, than after the same procedures
performed
as open operations. This is believed to be so because there is less damage
to the peritoneum— both parietal and visceral—and less handling of the
tissue with laparoscopy. Gutt and colleagues, general surgeons, wrote
about this in 2004.28 They reviewed the published literature on this topic
and found 15 reports to evaluate from 1987 to 2001: 3 clinical and 12
experimental. In the 3 clinical studies, adhesions following laparoscopy
were less than after open surgery in comparable groups of patients.
Lundorff and colleagues evaluated adhesions at the operative site after
open and laparoscopic operation for ectopic tubal pregnancy in 73
women.29 The authors found significantly fewer adhesions at the
operative site in the laparoscopic group. Milingos and colleagues found
similar results in patients who had surgical adhesiolysis for infertility. 30
A third study compared adhesion formation between the liver bed, the
omentum, and the duodenum after open or laparoscopic
cholecystectomy.31 After open cholecystectomy, all patients (100%) had
thick extensive adhesions to the operative site vs. 44% of patients after
laparoscopic cholecystectomy, and these adhesions were loose and easy
to separate. In this analysis of the data, the authors concluded that
laparoscopic surgery is associated with a reduction in the formation of
adhesions after abdominal operations in all clinical and most
experimental studies.
An update of the current role of the topical gels and the membrane
barriers for the surgeon to use in the operating room will not be given
here; it is the subject of the last section in this monograph.
Physiology of Small Bowel

Obstruction Introduction
In this section, we will describe the pathophysiology of bowel obstruc
tion by focusing on these key components: intraluminal gas, intestinal
fluid, the microflora, the blood flow, and intestinal motility.
Small bowel obstruction affects the physiology of the normal intestine
and has systemic effects due to changes in fluid and electrolyte balance,
fluid shifts from one space to another, and hemodynamic changes
secondary to hypovolemia and dehydration. Simple mechanical obstruc
tion of the small intestine causes the accumulation of gas, fluid, and
electrolytes proximal to the point of obstruction and leads to distention of
the intestine. Intestinal activity increases in an effort to overcome the
obstruction, accounting for the colicky pain and the diarrhea that some
patients experience even in the presence of complete bowel obstruction. 32
The rate at which symptoms and complications develop depends on
luminal volume, bacterial proliferation, and alterations in motility and
perfusion. If the intramural pressure becomes high enough, intestinal
microvascular perfusion is impaired, which leads to intestinal ischemia
and, ultimately, necrosis. This condition is known as strangulated bowel
obstruction.32
Intestinal Gas
Normally, most of the gas in the gut and that seen on plain abdominal
radiographs consists of swallowed air; the remainder can be attributed to
carbon dioxide from the neutralization of bicarbonate in the duodenum,
and organic gases such as methane and hydrogen sulfide from bacterial
metabolism. The intestine rapidly absorbs carbon dioxide, which is then
released from the body through the lungs. Nitrogen and the organic gases
are not absorbed by the intestine and comprise most of the gas normally
expelled from the rectum as flatus. 33 With mechanical intestinal obstruc
tion, gaseous distention of the intestine occurs because the gas has no
route of escape. Because obstructed patients usually continue to swallow
air in varying quantity, they experience progressive accumulation of
intestinal gas consisting mostly of nitrogen. 33-35 This is one reason for
placing an NG tube.
A particularly serious form of bowel obstruction is the closed loop
obstruction in which a segment of bowel is obstructed proximally and
distally as with a twist or volvulus of the bowel around or by an adhesion
that traverses and compresses the bowel in 2 places. In such cases, the
accumulating gas and fluid cannot escape either upstream or downstream
from the blocked segment, and luminal pressure will quickly increase
and lead to decreased bowel wall perfusion and bowel ischemia.
Intestinal Fluid
In addition to ingested food and drink, up to 5 to 10 L of salivary,
gastric, pancreatic, biliary, and intestinal secretions enter the digestive
tract each day. Normally, most of the fluid is reabsorbed by the small
intestine, as only approximately 1 L of fluid enters the colon from the
ileum daily.33
In mechanical obstruction, the intestine proximal to the site of obstruc
tion fills with fluid and gas. This fluid is not absorbed as in the normal
intestine, and the distended bowel over time begins to secrete fluid rather
than absorb fluid and contributes to a state of intravascular dehydration
or hypovolemia. Loss of fluid and electrolytes from the intravascular
space occurs by several routes as the intestine distends; this is a critical
event in bowel obstruction for several reasons.
First, intestinal distention may stimulate reflex vomiting leading to the
loss of fluid and electrolytes. Second, distention increases intestinal

secretion with movement of fluid from the intravascular compartment to
the intestinal lumen. In humans, distention causes increased secretion of
water and electrolytes into the lumen by an incompletely understood
mechanism.36 In the presence of obstruction, the small bowel reverses its
normal function of absorption, and begins to secrete fluid into the lumen
of the obstructed bowel. This phenomenon compounds the problem of
distention and fluid movement into the lumen. In addition, fluids like
bile, gastric juice, and oral liquid intake accumulate in the bowel
proximal to the obstruction and cause further intestinal distention,
resulting in a self-perpetuating cycle. Dehydration can result from the
progressive loss of fluid and electrolytes into the intestinal lumen. 37 A
third route of fluid and electrolyte loss is from intestinal edema, which
gives the intestinal wall the congested, swollen appearance often found at
operation. A fourth route for loss of fluid from the intravascular space is
by transudation of fluid through the serosal surface into the peritoneal
cavity to produce free intraperitoneal fluid. 33
Experimental studies and clinical investigation have demonstrated that
elevation of luminal pressures above 20 cm H 2O inhibits absorption and
stimulates secretion of salt and water into the lumen proximal to an
obstruction.36-38 In closed-loop obstruction, luminal pressures can exceed
50 cm H2O and may account for a substantial proportion of luminal fluid
accumulation.39 In simple open-loop obstruction, distention of the lumen
by gas and fluid rarely leads to luminal pressures higher than 8-12 cm
(H2O).40 Thus, in open-loop obstruction, the contributions of high
luminal pressures to fluid hypersecretion may not be as important. 41
Accumulation of fluid in this third space accounts for the dehydra tion
and hypovolemia observed in cases of SBO. 42 Dehydration can develop
within hours, depending on the degree and location of obstruction and the
amount of vomiting. The metabolic effects of fluid loss depend on the
site and duration of the obstruction. With a proximal obstruction,
dehydration may be accompanied by hypochlo remia, hypokalemia, and
metabolic alkalosis associated with increased vomiting. Distal
obstruction of the small bowel may result in large quantities of intestinal
fluid into the bowel. Oliguria and hemocon centration can accompany the
dehydration as well as hypotension and shock. In severe cases of bowel
obstruction, increased intra-abdominal pressure, decreased venous return,
and elevation of the diaphragm compromising ventilation may occur.
These factors can serve to further potentiate the effects of hypovolemia. 42
FIG 6. Early bowel strangulation associated with small bowel obstruction (SBO). Note the
darkened loop of bowel to the left. (Color version of figure is available online.)
Intestinal Blood Flow

Intestinal blood flow is influenced by luminal pressure, mesenteric
flow, and systemic blood pressure. As the intraluminal pressure increases
in the bowel, a decrease in mucosal blood flow can occur. With ongoing
gas and fluid accumulation, the bowel distends and intraluminal and
intramural pressures increase. These alterations are particularly noted in
patients with a closed-loop obstruction in which greater intraluminal
pressures are attained. A closed-loop obstruction, produced commonly
by a twist of the bowel, can progress to arterial occlusion and ischemia if
left untreated and may potentially lead to bowel perforation and
peritonitis.42 If the intramural pressure becomes high enough, intestinal
vascular perfusion is impaired, which leads to intestinal ischemia and
ultimately necrosis of the wall and perforation. This condition is called
strangulated bowel obstruc tion32 (Fig 6).
Alterations of Intestinal Motility

Abdominal colic is a hallmark of SBO and is related to gut motility.
Small intestinal obstruction alters the normal motility of the gastrointes
tinal tract. Fluid and gas accumulate above the point of obstruction,
causing proximal distention. The bowel responds to distention with
periodic bursts of neuromuscular activity resulting in peristaltic rushes.
These paroxysmal, wavelike movements begin in the proximal bowel
and traverse the entire length of intestine above the point of obstruction.
Periods of activity are followed by quiescent periods of variable
duration. The intestine distal to the obstruction, however, maintains a
reduced level of peristaltic activity. 33 Later in the course of obstruction,
the intestines become fatigued and dilate, and the contractions become
less frequent and less intense.42
Changes in the Microflora

The normal small intestine contains a low concentration of bacteria,
ranging from 102 to 104 viable organisms per milliliter in the proximal
jejunum to 103 to 107 viable organisms per milliliter in the distal ileum.
The composition of the bacterial flora in the proximal jejunum changes
from fungi and predominately gram-positive facultative bacteria, such as
streptococci, staphylococci, and lactobacilli, to predominately aerobic
coliforms and anaerobic species in the distal ileum and colon. 33,43
Small bowel obstruction produces stasis of intestinal contents. A
tremendous overgrowth of aerobic coliforms and anaerobic species
proximal to the site of obstruction alters the normal proximal-to-distal
gradient change in bacterial flora. Bacterial concentrations increase to as
high as 1010 to 1012 viable organisms per mL of intestinal content. 33,44
Studies have shown an increase in the number of indigenous bacteria
translocating to mesenteric lymph nodes and even systemic organs.
However, the importance of this bacterial transloca tion on the clinical
course is not clear.42 If the intestinal wall loses viability, altered intestinal
permeability can allow bacteria and bacte rial products to enter the
circulation or peritoneal cavity, causing toxemia, septicemia, or both. 33
Clinical Presentation
The clinical presentation of patients with SBO may vary widely from
subtle nonspecific pain to florid peritoneal signs related to strangula tion
and bowel perforation. However, classic symptoms of bowel obstruction
include nausea and vomiting, a distended abdomen, colicky abdominal
pain, and alteration in flatus and stool passage. The symptoms vary
widely with the degree of bowel obstruction from a low-grade partial
SBO associated with a scaphoid abdomen and crampy pain with eating to
a complete bowel obstruction characterized by massive abdominal
distension, constant abdominal pain, and obstipation for longer than 24
hours. The clinical features of SBO are a function of the level of
obstruction, degree of lumen obstruction, duration of the obstruction, and
the amount of distension. Physical
examination classically reveals abdominal distension, high-pitched
bowel sounds, and diffuse tenderness to palpation, all of which suggest a
diagnosis of bowel obstruction.
Differential Diagnosis
Obstruction vs. Ileus. Making the distinction between an SBO and an
ileus depends primarily on the patient history, the clinical setting, the
physical examination, the findings on the radiological studies, and a
consideration of the likely causes. Surgeons are usually able to correctly
distinguish patients with SBO from those patients with an ileus. In the
past, even for experienced surgeons, these two diagnoses were often
difficult to separate and identify because standard abdominal radiographs
did not provide the information we are provided on computed
tomography (CT) scans today and because clinical findings and
symptoms overlap: abdominal distention, nausea, vomiting, and
abdominal pain are common to both.
Ileus is a condition of abnormal and inhibited motility of the
gastrointes tinal tract. Gastric content, liquids, and intestinal fluids fail to
move through the intestinal tract because of ineffective intestinal
peristalsis. There is no mechanical obstruction, but effective organized
aboral passage of liquids and gas is absent. Other adjectives that describe
ileus are paralytic, adynamic, and postoperative. It is commonly
observed in a patient who has just had abdominal surgery and the bowels
have not resumed normal function. Ileus is also frequently seen in
intensive care unit (ICU) patients who are critically ill and are receiving
a variety of medications, many of which affect gut motility. In
hospitalized patients, ileus is generally gradual to acute in onset and
resolves once the underlying condition has been corrected. Patients with
a SBO, on the other hand, have normal intestinal motility but, instead,
have a blockage of the gut that prevents normal passage of fluid and gas
through the intestine. There is a physical barrier that obstructs the
intestinal lumen at some point along its path; it could be an adhesion, an
abdominal hernia, or a tumor. Abdominal distention with crampy,
colicky, abdominal pain, nausea and vomiting, and obstipation are the
hallmark symptoms. Early on, bowel sounds are active and high pitched.
The typical patient with an SBO will come to the office or emergency
department complaining of crampy abdominal pain, nausea or vomiting,
and worsening obstipation. The patient will have hyperactive bowel
sounds, tympany to percussion, and likely a history of previous abdom
inal surgery. The most common causes are adhesions and abdominal wall
hernias. Plain radiographs of the abdomen will show gaseous distention
of the small bowel in the supine position and often show an outline of the
valvulae conniventes. The upright radiographs classically will show
FIG 7. Multiple air/fluid levels in inverted U-shaped loops with associated small bowel distention
in adhesive SBO. Arrow points to one of many air/fluid filled levels in this abdominal xray.
(Reprinted with permission from WetPaint, http://wikiradiography.com/page/Small Bowel
Obstruction.)
air-fluid levels in inverted U-shaped loops of small intestine (Fig 7).33

Generally, there is little gas in the colon. Unlike a CT scan, these simple
radiographs do not show points of obstruction in the bowel or transition
points from dilated bowel to normal caliber gut.
The patient with an ileus, on the other hand, is more likely to be in the
hospital receiving treatment for a medical condition or recovering from a
major operation when the postoperative ileus exceeds the expected
period. Plain radiographs of the abdomen show gas in both the small and
large bowel (Fig 8). There are many conditions that can inhibit intestinal
motility and cause an ileus picture. The common conditions are a recent
abdominal operation; acute events in the abdomen such as appendicitis,
pancreatitis, and ureteral colic; multiple trauma with rib fractures or
pelvic fractures; retroperitoneal hematoma; pneumonia or sepsis; or renal
failure, heart failure, multisystem organ failure (MSOF), and just about
any critical illness that places a patient in the ICU. Metabolic derange
FIG 8. Distended small and large bowel with air throughout the entire GI tract, including rectum.
Arrow points to air in the rectum of this patient with paralytic ileus. (Reprinted with permission
from WetPaint, http://wikiradiography.com/page/Small Bowel Obstruction.)
ments, sepsis, organ failure, and drug and medication toxicity each can
contribute to an ileus. Many drugs affect the sympathetic and parasym
pathetic innervation of the gut and thus motility. The opiates, calcium
channel blockers, psychotropic drugs, and pain medicines are common
contributors to ileus. It is important to remember that in the surgical
patient, unrecognized or untreated infection either in the abdomen or the
chest is often a cause of prolonged ileus.45
Distinguishing mechanical SBO from ileus is best assisted by radio
graphic examinations. First, the plain films will demonstrate whether an
obstruction is present. The CT scans of the abdomen and pelvis with oral
contrast show where the obstruction is and what the lesion is. When ileus
is present, there is no focal point of obstruction; gas and liquid are seen
throughout the small bowel and colon. There is no transition zone as one
sees with SBO with dilated bowel upstream and decompressed bowel
distally. An added benefit of the CT scan is that it images the entire
abdomen and its contents and can identify other causes for the ileus and
abdominal distention, such as an abscess, diverticulitis, or pancreatitis,
which is really the patient’s problem.
Fortunately, today we have very good imaging techniques to help us
evaluate the bowel and its neighboring organs. When the gut is not
working, we have total parenteral nutrition (TPN) and good critical care
units to support the patient until the underlying conditions can be treated.
Small Bowel vs. Large Bowel Obstruction. With the assistance of
high-quality body imaging techniques, it is usually possible for the
surgeon to distinguish SBO from a large bowel obstruction (LBO). Yet,
there is some overlap in the signs and symptoms that can make this
distinction a challenge when one first sees the patient in the office or the
emergency department.
The symptoms of SBO are abdominal distention, crampy abdominal
pain, nausea, vomiting, and constipation. Vomiting, bilious or feculent, is
com mon, whereas this is a later event in colonic obstruction. Paroxysms
of abdominal pain occurring at 4-10-minute intervals are typical.
Large bowel obstructions, usually from colon cancer or strictures from
diverticulitis, are seldom acute; there is usually a several-day to several-
week history of constipation and change in bowel habits. Mid abdominal
pain and abdominal distention are the 2 most consistent signs. Blood in
the stool and anemia are strongly suggestive of carcinoma. Per rectal
examination, an empty rectal vault is suggestive of a proximal colon
obstruction, and blood on the examining finger indicates a distal lesion.
Diarrhea may be present as a function of liquid stool passing around the
obstructing lesion. The abdomen is distended and tympanic as with the
SBO. Cascading bowel sounds and borborygmus are often present,
whereas high-pitched bowel sounds are heard only if there is
superimposed SBO. Patients with LBO are likely to be more elderly than
the SBO group of patients.
The progression of symptoms in colonic obstruction depends in part on
the patency of the ileocecal valve. If this valve is incompetent, there is
retrograde decompression of the colon, the onset of symptoms will be
gradual, and there may be some feculent vomiting. Radiologic studies are
the most important diagnostic tools to establish the presence or absence
of colonic obstruction and the location. Plain abdominal radiographs
should be obtained first in the upright (if possible) and supine positions.
These will show mild to marked distention of the colon proximal to the
lesion and may show small bowel distention if the ileocecal valve is
incompetent (Fig 9). The plain radiographs can be diagnostic for cecal
volvulus and sigmoid volvulus (Figs 10, 11A and
FIG 9. Distended large bowel with competent ileocecal valve in a patient with obstructing rectal
carcinoma. (Reprinted with permission from Jon Lund,
http://learncolorectalsurgery.com/#/abdominal x-ray/4549818580.)
B). A CT scan of the abdomen provides valuable information and is part

of the evaluation unless the patient has an acute abdomen and needs
resuscita tion or an exploratory laparotomy first.
The CT scan will demonstrate not only the LBO but also the location
and nature of the lesion plus information about bowel viability, the risk
of perforation, bowel diameter, and involvement of other organs.
In summary, abdominal distention, pain, and anorexia are common to
both SBO and LBO. However, the patients with colonic obstruction are
likely to be older ( 60 years) than the SBO patients; and colon tumors
and strictures are common causes of colon obstruction, whereas SBO is
usually caused by adhesions and abdominal wall hernias.
Evaluation of SBO in the Gastric Bypass Patient
The incidence of SBO following laparoscopic gastric bypass is approx
imately 3.5%, and one half of these are caused by internal hernia, which
FIG 10. Massively dilated colon in a patient with cecal volvulus. (Reprinted with permission from
WetPaint, http://www.wikiradiography.com/page/Large Bowel Obstruction.)
is now generally recognized as a particularly dangerous cause of

abdominal pain in patients after gastric bypass. Clinically, these patients
may present with symptoms of bowel obstruction, and early CT scan is
recommended because of the risk of bowel strangulation. Several CT
findings have been found to be predictive of internal hernia, particularly
the “mesenteric swirl” (Fig 12). Other signs of internal hernia include
mushroom hernia shape, SBO, clustered small bowel, tubular distal
mesenteric fat surrounded by bowel loops, small bowel behind superior
mesenteric artery, and right-sided location of jejunojejunostomy.
Diagnosis
Laboratory Studies in SBO. Patients presenting with SBO usually have
volume deficits caused by vomiting and “third spacing” into the lumen
and wall of the obstructed bowel, and into the peritoneal cavity.
Emergent operation without resuscitation may result in cardiovascular
collapse and
FIG 11. Sigmoid volvulus demonstrating a 14-cm sigmoid colon before (A) and after (B) rectal
tube decompression. (Reprinted with permission from
http://www.learningradiology.com/archives04/ COW%20087-Sigmoid
%20volvulus/sigmoidvolvcorrect.htm. Copyright LearningRadiology.com. All rights reserved.)
death with the induction of general anesthesia. Commonly, the deficit of

isotonic fluid is several liters, and the associated hemoconcentration may
result in a spuriously elevated hematocrit and hemoglobin level. If there
is evidence of recent GI blood loss, this must also be considered when
interpreting the hematocrit in the patient with SBO. Although the white
blood cell (WBC) count may also be elevated somewhat by severe
dehydration, leukocytosis greater than 20,000/mL should prompt concern
for bowel compromise or perforation in the patient with SBO. In patients
with SBO who are being managed nonoperatively, the WBC should be
monitored; although a normal WBC is reassuring and an elevated WBC
is concerning, it must be remembered that when predicting bowel
compromise, the diagnostic accuracy of this test alone is poor. Operation
in SBO should never be delayed or initiated on the basis of WBC alone.
However, in patients with SBO being managed nonoperatively, WBC is
an important part of the clinical picture. In general, compromised bowel
in the setting of SBO is very unlikely if the patient has a WBC less than
16,000/mL, and no fever, and no pain or tenderness, and no tachycardia,
and no ominous radiologic findings.
Electrolyte disorders are common in patients with SBO because of
vomiting and lack of oral intake. The most common acid/base
abnormalities
FIG 12. Dilated small bowel and “mesenteric swirl” associated with internal hernia after gastric
bypass (Peterson’s hernia). Arrow points to pinwheel-like swirl.
are metabolic (contraction) alkalosis (related to maximal renal sodium

reabsorption in exchange for H ) and metabolic acidosis (related to GI
bicarbonate loss and hypovolemic tissue hypoperfusion). The latter is
often associated with a subtle but perceptible increase in minute
ventilation because of respiratory compensation for the metabolic
acidosis. The most common electrolyte abnormality is hypokalemia.
Fluid and electrolyte replacement is with isotonic solution (normal saline
preferably) with additional potassium provided there is evidence of
adequate renal function. The blood urea nitrogen and creatinine are
commonly elevated because of renal hypoperfu sion, as is the blood urea
nitrogen/creatinine ratio.
Serum lactate levels are often routinely followed in patients with SBO,
although their clinical usefulness is questionable. On admission, the
lactate level may be elevated because of volume-related global
hypoperfusion. Although in the resuscitated patient with SBO a sudden
spike in a normalized serum lactate may indicate the onset of small
bowel compromise, this is not necessarily the case. The segmental bowel
infarction or perforation related to bowel obstruction can certainly occur
in the setting of a normal serum lactate. In fact, most patients requiring
bowel resection for ischemia in the setting of SBO probably have normal
serum lactate levels.
Serum amylase levels are useful only to the extent that they rule out
pancreatitis as a cause of the presenting abdominal pain in patients with
SBO; they are not useful in predicting small bowel viability or
perforation.
FIG 13. Massive dilation of small bowel with no air in the colon or rectum. Patient had a complete
bowel obstruction that necessitated laparotomy. (Reprinted with permission from Cameron JL.
Current Surgical Therapy (ed 8). Philadelphia, PA: Mosby, 2004.)
Imaging Studies in SBO. Traditionally, an abdominal series or obstruc

tion series was the most common and useful radiologic test in the patient
with SBO, but it has now been supplanted in many settings by the CT
scan. This set of plain radiographs consisted of an upright chest and
upright abdominal radiograph, and a supine abdominal radiograph. If
upright radiographs are not possible, a decubitus cross table lateral
radiograph of the abdomen may be substituted to look for free air.
Patients with an SBO may have a radiographic pattern ranging from
massively distended small bowel with no air in the colon or rectum (Fig
13), to a radiograph that reveals multiple air-fluid levels with less
abdominal distension and some air in the colon and rectum (Fig 14). The
radiologist reading the former case will usually assign a diagnosis of
complete bowel obstruction. The latter circumstance would be labeled a
partial SBO. Studies demonstrate that in those patients diagnosed as
having
FIG 14. Partial SBO associated with air-fluid levels, abdominal distention, and air in the colon
and rectum. Arrows point to colorectal air. (Reprinted with permission from Cameron JL. Current
Surgical Therapy (ed 8). Philadelphia, PA: Mosby, 2004.)
a “complete” bowel obstruction by the radiologist, more than 80% will

require an operation compared with 10% to 15% of those labeled as
having a “partial” bowel obstruction. Occasionally, the abdominal series
with 1 or 2 air-fluid levels will reveal a single loop of bowel that is
somewhat distended.
If the SBO is quite proximal, the stomach, duodenum, and short
segment of jejunum proximal to the obstruction may be adequately
decompressed by repeated vomiting or NG suction, and the plain
abdominal radiographs may be interpreted as normal or nonspecific (Fig
15). Pneumatosis in the bowel wall and/or portal venous gas may be seen
on plain radiograph, and in the setting of abdominal pain and small
bowel distention, this is an ominous sign that warrants urgent operation
(Figs 16 and 17). In patients with obturation of the small bowel, usually
the terminal ileum, with a gallstone, findings on plain radiographs may
be pathogno
FIG 15. Arrow points to a single dilated segment of small bowel in a high jejunal obstruction.
Note the paucity of dilated loops and distention. (Reprinted with permission from WetPaint, http://
wikiradiography.com/page/Small Bowel Obstruction.)
monic: distal SBO and pneumobilia. Occasionally, the obstructing gall

stone is visualized if it contains adequate calcium to render it sufficiently
radio-opaque. Finally, when there is a preponderance of luminal fluid
and a paucity of luminal air, the diagnosis of SBO may be missed by
plain radiographic studies.
If the SBO is deemed to be partial on clinical grounds and the patient is
stable, nonoperative management is appropriate. However, unless it can
be reliably verified by the patient and caregivers that the patient is not
completely obstipated, the onus is on the surgeon to document radiolog
ically that the SBO is incomplete if nonoperative management is
continued for more than 24 hours. This may be accomplished by the oral
administration of a small amount (100 mL) of barium or gastrograffin,
followed by serial plain abdominal radiographs. If the contrast reaches
the cecum in 24 hours, the obstruction is partial and it is very likely
FIG 16. Pneumatosis in the bowel wall (arrows) associated with necrotic bowel secondary to an
SBO. (Reprinted with permission from Kernagis LY, Levine MS, Jacobs JE, et al. Pneumatosis
intestinalis in patients with ischemia: correlation of CT findings with viability of the bowel. Am J
Roentgenol 2003;180:733-6.)
FIG 17. Venous air (arrows) associated with pneumatosis.

FIG 18. Gastrograffin small bowel follow-through in a patient with “partial” SBO that failed to
resolve. Failure of the contrast to reach the colon is an indication for surgery. (Reprinted with
permission from Small Bowel Obstruction. The original article was published at
www.surgwiki.com) (Blackwell Publishing Asia Pty Ltd and such article can be found at the
following URL: http://www.surgwiki.com/ wiki/Small_bowel_obstruction.)
( 95%) that there will be clinical resolution without the need for
operation; otherwise the SBO must be considered complete and
operation should be planned if there are no clinical signs of resolution
(Fig 18).
It has been suggested that the oral administration of a small quantity
(eg, 100 mL) of gastrograffin can lead to the resolution of SBO.
Gastrograffin is a hyperosmolar liquid that draws water into the bowel
lumen, perhaps improving bowel edema and enhancing contractility. It
should be used cautiously in patients at risk for pulmonary aspiration, as
introduction of the material into the bronchial tree can cause life-
threatening pneumoni
FIG 19. Barium small bowel follow-through revealing a tight stricture (arrow) in the terminal ileum
in a patient with partial SBO and known Crohn’s disease.
tis. Two recent meta-analyses have examined the benefit of gastrograffin

in patients with SBO. Branco and colleagues evaluated 14 prospective
studies and found that the appearance of oral contrast in the colon within
24 hours of administration was 96% sensitive and 98% specific in
identifying those patients with SBO who would have clinical resolution
of SBO without the need for operation. 46 These authors also found that
the oral administration of water-soluble contrast reduced the need for
operation by approximately 35% (P 0.05) and shortened hospital stay
by almost 2 days (P 0.05). In another meta-analysis, Abbas and
colleagues found a similar beneficial effect of gastrograffin on hospital
stay in patients with SBO ( 1.83 days, P 0.05), but not on the need for
operation (OR 0.81, P 0.3).47 Neither study discussed any adverse
effects of gastrograffin. It can be concluded that the oral administration
of gastrograffin should be considered in patients with SBO who do not
obviously require urgent operation on the basis of clinical and radiologic
findings.
Small bowel follow-through using barium is often very helpful in the
evaluation of potential SBO due to Crohn’s disease. In this patient with
known Crohn’s disease, small bowel follow-through identified a very
tight stricture in the terminal ileum (Fig 19). The study provides a useful
road map for surgery.
Ultrasound is a noninvasive study that may yield useful information
regarding the patient with SBO. Dilated fluid-filled loops with or without
peristalsis are readily apparent on ultrasound. Gallstones and
air in the gallbladder suggest gallstone ileus. The absence of abdom inal
fluid can be reassuring in the stable patient being managed
nonoperatively, as new ascites can be an ominous sign in patients with
bowel obstruction.
Double contrast CT scan has become the imaging procedure of choice
for most patients with the clinical diagnosis of SBO. Mallo and
colleagues reviewed 15 studies evaluating the diagnostic usefulness of
CT scan in identifying patients with SBO who had bowel ischemia or
complete obstruction.48 Eleven of the studies reviewed evaluated the CT
diagnosis of ischemia in SBO. The aggregated statistics from these 11
studies were as follows: positive predictive value (PPV) 79% (167 of
212; range, 69% to 100%), negative predictive value (NPV) of 93% (496
of 531; range, 33.3% to 100%), sensitivity of 83% (167 of 202; range,
63% to 100%), and specificity of 92% (496 of 541; range 61% to 100%).
Seven of the studies reviewed by Mallo and colleagues evaluated CT in
the diagnosis of complete or high-grade obstruction (vs. partial
obstruction) in patients with SBO. The aggregated PPV of CT for
complete obstruction was 92% (168 of 182; range, 84% to 100%), NPV
was 93% (211 of 226; range, 76% to 100%), sensitivity was 92% (168 of
183; range, 81% to 100%), and specificity was 94% (211 of 225; range,
68% to 100%). This study underscores the diagnostic usefulness of
abdominal CT scan in patients with the clinical diagnosis of SBO.
Typically, the initial CT scan in the patient with SBO shows proximal
dilated small bowel with luminal contrast, and distal collapsed small
bowel and colon void of luminal contrast (Fig 20). If there is no oral
contrast in the bowel distal to the transition point and if nonoperative
management is planned, follow-up scan or plain radiograph is done in 12
to 24 hours to document movement of the contrast into the lumen of the
distal small bowel and colon. If this is not demonstrated, the SBO should
be considered complete and operation planned. The presence of a
transition point per se predicts neither the need for operation nor the
failure of nonoperative treatment in SBO. 49 CT scan can be helpful in
identifying the etiology of the SBO, such as internal hernia (Fig 21),
abdominal wall hernia (Fig 22), intussusception (Fig 23), tumor or mass,
Crohn’s disease (Fig 24) metastatic cancer, primary tumor, or ischemia
and signs of bowel compromise such as pneumatosis intestinalis or
pneumoperitoneum (Fig 25). Schwenter and colleagues showed on
multivariate analysis that the following factors predicted the need for
bowel resection in patients with bowel obstruction: the presence of more
than 500 mL of ascites on CT (P 0.002); reduction of CT bowel wall
enhancement (P 0.011); abdominal pain for 4 days (P 0.007);
FIG 20. CT scan demonstrating SBO with a clear transition zone (arrow) followed by collapsed
bowel. (Reprinted with permission from Cameron JL. Current Surgical Therapy (ed 8).
Philadelphia, PA: Mosby, 2004.)
FIG 21. Internal hernia after gastric bypass with dilated loops of small bowel and classic
mesenteric swirl (arrow).

FIG 22. CT scan demonstrating incarcerated right inguinal hernia (arrow) in a patient with SBO.
(Reprinted with permission from Furukawa A, Yamasaki M, Furuichi K, et al. Helical CT in the
diagnosis of small bowel obstruction. Radiographics 2001;21:341-55, © The Radiological Society
of North America.)
FIG 23. Typical “bulls eye” (arrow) or “target sign” associated with small bowel intussusception
causing SBO. (Reprinted with permission from James Heilman, MD,
http://commons.wikimedia.org/ wiki/File:VolvulusCT.PNG.)

FIG 24. Patient with a history of subtotal colectomy for Crohn’s disease and an ileocolostomy
presented with a high-grade partial SBO. CT scan reveals recurrent Crohn’s disease with a tight
stricture at the previous anastomosis (arrow).
abdominal tenderness with guarding (P 0.009); WBC 10,000/mL (P

0.085); and C-reactive protein 75 mg/L (P 0.007).50 All patients with 4
or more of these variables required resection, whereas only 1 patient who
had no positive variables required resection. Fever and transition point on
CT scan were not independent predictors of compro mised bowel in this
study. Zielinski did a similar type of analysis and found on multivariate
analysis that the independent predictors of the need for operation in SBO
were vomiting (OR 4.67; P 0.007); ascites on CT (OR 3.80; P
0.006); mesenteric edema on CT (OR 3.59; P 0.011); and the lack of
the small bowel feces sign (OR 0.19; P 0.011).51 Again, fever and
transition point on CT were not independent predictors of operation;
neither were leukocytosis and serum lactate level. In a subsequent
prospective validation, Zielinski and colleagues distilled the predictive
model down to 3 independent variables: obstipation, mesenteric edema
on CT scan, and lack of small bowel feces sign on CT scan. 52
The “whirl sign” is a “swirl of mesenteric soft tissue and fat attenuation
with adjacent loops of bowel surrounding rotated intestinal vessels” (Fig
12). In a retrospective study, Duda and colleagues reviewed 194 CT
scans showing SBO and found that 40 scans contained the “whirl sign.”
Eighty percent of patients with the “whirl sign” required operation (PPV
80%), but only 14% of patients without the sign required operation (NPV
86%).53 The “small bowel feces sign” is the presence of particulate
material in dilated small bowel. This sign is present on CT
FIG 25. Bowel strangulation with necrotic bowel seen on CT scan. Arrows point to nonviable
segment of bowel. (Reprinted with permission from Cameron JL. Current Surgical Therapy (ed 8).
Philadelphia, PA: Mosby, 2004.)
scan in approximately 50% of patients with SBO and may be more

common in patients with more high-grade obstruction. However, by itself
it is not a particularly useful finding in patients with SBO.
Management
Before any diagnostic maneuvers are initiated, the patient with an SBO
should undergo immediate resuscitation with intravenous isotonic
volume replacement. Most patients with a prolonged course of nausea
and vomiting will develop a hypochloremic hypokalemic metabolic
alkalosis. Accordingly, the replacement fluid of choice is normal saline
with potassium supplementation. Fluids should be administered rapidly,
with a Foley catheter placed to monitor urine output as an index of
euvolemia. The use of narcotic pain medications is somewhat
controversial, but patients in whom a decision to operate has already
been made should be given adequate pain medication to give them some
relief. In patients in whom the diagnosis is uncertain, the use of opiate
medications is less clear. Many surgeons prefer that the patient not be
receiving narcotics while they monitor the patient’s pain symptoms on
physical examination.
While the fluid and electrolyte resuscitation is being conducted,
placement of a standard length NG tube is indicated to decompress the
stomach and prevent accumulation of any other gas behind the point of
TABLE 5. Clinical spectrum of small bowel obstruction (SBO)
Complete SBO
Partial SBO—high grade
Partial SBO—low grade
Bowel obstruction in virgin abdomen
Recurrent SBO
SBO immediately after surgery
SBO in patient with known malignancy
SBO in patient with Crohn’s disease
SBO in patient s/p gastric bypass
obstruction. This virtually always brings relief to the patient and also
protects against aspiration. Although long tubes with mercury-filled bags
at the end were used in past surgical periods, virtually nobody uses long
tubes today because of the complexity of their management and little
evidence that their efficacy is any greater than standard length NG
tubes.54 In fact, multiple prospective studies show no advantage to using
the longer tubes.
The use of antibiotics in patients with SBO is also somewhat contro
versial. Although no one argues with the need for preoperative
antibiotics in the patient with bowel obstruction who is going to surgery,
there appears to be little evidence that antibiotic use in the patient with
SBO is indicated, and few practitioners administer antibiotics while
patients are being observed.
The clinical spectrum of SBO varies widely, but the 9 most common
clinical scenarios include (l) complete bowel obstruction, (2) partial SBO
— high grade, (3) partial SBO—low grade, (4) bowel obstruction in a
virgin abdomen, (5) recurrent SBO, (6) bowel obstruction immediately
after operation, (7) bowel obstruction in a patient with known
malignancy or recurrent malignancy, (8) bowel obstruction with a known
history of Crohn’s disease and (9) SBO after gastric bypass (Table 5). A
brief consideration of each of these clinical scenarios is helpful in
deciding the best management course. The actual decision-making
process for patients with SBO is often the most difficult and challenging
of any area in gastrointestinal surgery. The clinician must be very alert
and aware as he or she manages the patient after admission to look for
any signs of improvement or deterioration. Multiple follow-up abdominal
radiographs must be obtained associated with frequent clinical
reexaminations to monitor the progress of the patient.
Patients with complete bowel obstruction merit the closest and most
critical attention. Because of the dangers of incarceration leading to
strangulation as well as closed loop obstructions, patients with complete
bowel obstruction demand immediate attention. If a patient presents with
significantly distended bowel, a history of obstipation for the past 12
hours, and no recent improvement, consideration should be given to
going to the operating room immediately. This is particularly true if the
patient has unrelenting pain and the classic tetrad associated with
strangulated bowel, including leukocytosis, fever, tachycardia, and
severe abdominal pain. The dictum that “the sun should never set on a
complete bowel obstruction” is as true today as it was 50 years ago.
Patients presenting with significantly distended bowel and crampy
abdom inal pain, but who have evidence of gas in the colon and rectum
on the abdominal radiographs as well as a recent history of having passed
flatus (high-grade partial SBO), may be admitted for initial observation.
These patients also require very close vigilance. They should be
reexamined on a regular basis, and repeat abdominal radiographs should
be obtained every 8 to 12 hours to see whether the distended bowel is
worsening or improving. Patients with partial high-grade SBO should
begin to improve within 24 to 48 hours. It is clear that most cases of
adhesive SBO that are likely to resolve will do so within 48 hours.
Patients with high-grade obstruction who do not improve within 24 hours
of admission should be taken to the operating room for exploration. Few
other diagnostic studies are indicated, although occa sionally a CT scan
will confirm the point of obstruction and edema of the bowel proximal to
the obstruction.
The category of patients who have a low-grade partial SBO
characteristi cally have less abdominal distension and have passed some
gas or stool recently but continue to have crampy abdominal pain and
appear to partially resolve but become symptomatic on liquid or oral
intake. With less distension, less abdominal pain, and radiographs that
reveal some improve ment in the bowel gas patterns, these patients can
be safely watched up to 5-7 days as long as improvement is seen. This
group of patients often benefit from an enteroclysis study to demonstrate
the site of obstruction and degree of luminal narrowing. A contrast study
that shows substantial dilation proximal to the obstruction site and slow
passage of contrast through the obstructed site after 5 days indicates the
patient should probably be taken to the operating room for adhesiolysis.
On the other hand, if the patient continues to improve, distension
diminishes, and radiographs reveal resolu tion of air-fluid levels, the
patient may be cautiously placed back on clear liquids and advanced to a
low-fiber diet as tolerated.
Patients with bowel obstruction and a virgin abdomen virtually always
merit an exploratory laparotomy for either diagnostic purposes or
surgical treatment of the offending etiology. Most commonly, the cause
is incarceration in an abdominal wall hernia (Fig 26), but other causes
FIG 26. Cross table lateral radiograph revealing incarcerated umbilical hernia (arrow) in a patient
with a virgin abdomen. (Reprinted with permission from WetPaint, http://wikiradiography.com/
page/Small Bowel Obstruction.)
include a tumor, intussusception, and previously undiagnosed Crohn’s

disease. A CT scan preoperatively is often obtained but there is no reason
to delay operating on a patient with this history because surgical
treatment is virtually always indicated. Any hernia encountered in the
course of treating this disease should be repaired at the time of operation.
The only exception to this might be in a patient who has strangulated
bowel, in whom a permanent mesh would be required. In that case, an
absorbable mesh may be indicated until the patient heals, followed by an
elective hernia repair with permanent mesh at a later date. Patients with a
primary malignancy should undergo resection of the obstructing tumor
with lymphadenectomy as indicated. If intussusception is found on
explora tion, the area of intussusception almost always requires resection
so the leading point of the intussusception can be surgically removed.
Finding obstructing Crohn’s disease in a patient with a virgin abdomen
virtually always mandates removing the involved area of small bowel.
The decision to create a stoma vs. a primary anastomosis is a function of
bowel distension and general condition of the intestine.
Patients who develop a bowel obstruction immediately after operation
require a different operative plan. The obstruction resolves in most of
these patients within 10 to 14 days after operation, and the risk of
strangulation seems to be quite small. The management plan of choice
usually involves resting the gut, initiating NG suction, and starting
hydration. Occasionally, short-term TPN may be required while the
obstruction is resolving. Most of these patients will probably not require
reoperation. Those who do present a clinical scenario of no improvement
for a prolonged period and often show some worsening of symptoms.
The patient with recurrent SBO represents another unique clinical
scenario. These patients often present with a history of multiple laparot
omies, a number of which were for lysis of adhesions. Often, the most
recent operation is described as a very difficult laparotomy with multiple
serosal injuries and enterotomies. All attempts should be made to avoid
another laparotomy in these patients. Particularly in those patients with a
history of resolution with conservative management, NG decompression,
hydration, and gut rest are indicated. TPN may be required while the
obstruction is resolving and one should be patient enough to wait 10 to
14 days in these patients. However, in those patients who remain
obstructed with little progress or show some evidence of deterioration
manifested by increasing distension and failure to resolve the obstipation,
operation may have to be considered. Preparation for laparotomy in this
patient popu lation requires a good deal of thought. The surgeon should
schedule no other major cases on a day in which 1 of these difficult
patients is treated surgically. The operation usually involves a generous
midline incision and a plan to take adhesions down from the ligament of
Treitz all the way to the ileocecal valve. Although there is some literature
regarding plication of the small bowel after this procedure, it does not
appear to be very effective and there is little evidence that it prevents
further obstructions. More successful in the author’s hand has been the
Baker tube, which is a long intestinal tube with a balloon at the end of it
(Fig 27). This can be brought through the abdominal wall and through a
Stamm type gastrotomy and with the balloon inflated can slowly be
milked all the way to the ileocecal valve. This long tube has the effect of
preventing the small bowel from kinking in any given location. This long
tube should be left in place for 2.5-3 weeks, although most patients can
be given a liquid diet around the tube. At the end of 3 weeks, the balloon
should be deflated and the tube very slowly withdrawn during a 5- to 10-
minute period. Even patients who have undergone bowel resection and
have an anastomosis can usually have use of this tube with no problems
with perforation. The other option in this patient population is placement
of an absorbable barrier, which can be wrapped around the bowel from
the ligament of Treitz to the ileocecal valve. This material is a
combination of hyaluronic acid and carboxymethylcellulose (see later in
the text). Although the evidence in support of its use is not clear, in these
desperate patients, any attempt to decrease adhesions seems warranted.
Patients with a known history of Crohn’s disease and obstruction Curr
Probl Surg, November 2012 679
FIG 27. Lengthy Baker intestinal tube for use in stenting the small bowel of a multiply recurrent
SBO patient. Tube is passed through the entire small bowel inflating the balloon in the cecum to
prevent retrograde retraction. The tube can be removed 3 weeks postoperatively. (Color version
of figure is available online.) (Courtesy of Teleflex Medical Incorporated, Research Triangle Park,
NC.)
represent another challenging clinical scenario. These patients have a

history of 1 or 2 previous resections, and now they are having difficulty
eating solid foods and even occasionally vomit up liquid. Most of the
time, they do not have complete bowel obstruction, and enteroclysis
study or CT scan will reveal the site of obstruction and whether a string
sign is present (Fig 28). If the area of obstruction is fairly new and the
patient has had symptoms only recently, an attempt at conservative
management with gut rest, TPN, and steroids is warranted to see if this
area will open up and the patient can be advanced on diet. However, if
after a 7- to 10-day period, the patient does not resolve, consideration
should be given to reoperation and resecting the strictured area.
The final area of concern is the patient who presents with bowel
obstruction with known intra-abdominal malignancy or in whom recur
rent malignancy is a possibility. Although there tends to be a nihilistic
attitude regarding these patients, studies reveal that 30% of patients who
present with this history will have an adhesion that can be lysed with
resolution of the problem, 30% have a malignancy obstructing the bowel
that can be resected, and 30% have carcinomatosis for which no
operation is possible. Patients with this critical scenario deserve a
laparotomy, particularly if it is unknown whether they have
carcinomatosis.
To summarize, the principles that guide the clinical management of
patients with suspected SBO are shown in Table 6. Thus, the diagnostic
evaluation and management of patients with SBO are largely focused on
FIG 28. Long “string sign” (arrow) in terminal ileum of a patient with diagnosed Crohn’s disease.
The CT scan demonstrates dramatic luminal narrowing caused by active inflammation.
TABLE 6. Principles of clinical management of small bowel obstruction (SBO)

1. Bowel infarction and/or perforation rarely complicate partial SBO but not infrequently
complicate complete SBO.
2. Complete SBO, except perhaps in the postoperative period, rarely resolves without an
operation; partial SBO frequently resolves without operation.
3. It can be difficult on the basis of history, physical examination, bloodwork, and plain
radiography:
a. To correctly identify all patients with threatened small bowel in the setting of bowel
obstruction.
b. To accurately differentiate between partial and complete small bowel obstruction. 4.
Some patients with partial SBO suffer serious morbidity and mortality from unnecessary
operation.
5. The etiology of the small bowel obstruction influences the clinical outcome.
the issues of etiology, the degree of obstruction (partial or complete), and

small bowel viability (ischemia or perforation). Not surprisingly then,
modern abdominal imaging techniques, particularly CT scanning, have
become important in addition to the diagnostic armamentarium in the
care of patients with SBO.
Operative Management and Technical Considerations
When operative therapy becomes mandatory in patients with SBO,
timing of the procedure is often important. For example, in early
postoperative bowel obstruction, often conservative management is suc
cessful. However, if operation is required, it is preferable to proceed
before the 14- to 16-day period when adhesions appear to be the most
tenacious, poorly defined, and vascular. For patients with a low-grade
partial obstruction, it is preferable to wait for a 3-week period to do a
complete lysis of adhesions when the adhesions have softened and are
filmy and less vascular. The incision should be a generous midline
incision made over the previous incision but extended down to virgin
abdomen if there is an area that has been previously unoperated. In
general, the abdomen should be entered through the easiest part of the
abdominal wall, which is usually the unoperated area. The incision
should be extended slowly through the previous scar tissue using a
scalpel. Use of a Bovie electrocautery in this setting is treacherous and
risks thermal injury to bowel and an enterotomy. As the incision is
carried down to the scar tissue, entering the abdomen in the unoperated
area will allow the surgeon to place his or her hand inside of the
abdomen and palpate the undersurface of the abdominal wall to check for
any bowel loops that are adherent and at risk during the opening.
Visually inspecting the undersurface of the abdominal wall is often a
good idea if the abdomen is open enough. As the abdominal cavity is
entered, dissecting the midline contents away from the scar must be done
in a meticulous fashion using Metzenbaum scissors or a scalpel. Blunt
dissection with dense scar tissue is unwise, and tearing the bowel is a
likely result. After the abdomen is entered and midline adhesions taken
down, the massively distended small bowel should be eviscerated so that
the site of obstruction may be identified. The offending adhesive band
should then be divided, as well as any other bands that appear to be
contributing to the obstruction.
This part of the operation is the point at which viability of the bowel is
assessed. If the bowel is pink, edematous, and somewhat thickened, it
obviously is at low risk for ischemia. However, if the bowel is deeply
cyanotic, thickened, or is a concern, time must be taken to assess the
viability (Fig 6). Initially, placing a warm laparotomy pad over the bowel
for 5 to 10 minutes is indicated. If the bowel remains cyanotic and
questionable, a Doppler ultrasound brought onto the operating field can
usually assess whether arterial pulses are present. If arterial signals are
present, and there is no evidence of venous thrombosis, merely observing
the bowel for another 10 to 15 minutes is indicated before making a
decision. If the assessment is still uncertain, administration of fluorescein
dye intravenously with use of a Woods lamp is helpful in assessing
whether the injured section of bowel has blood supply. Obviously, the
aforementioned maneuvers are conducted if a large area of the bowel is
involved. If a much shorter segment of small bowel is involved, merely
resecting that segment may be prudent. If the adhesions are diffuse, and a
single transition point is not identified, it is likely the surgeon will have
to do a complete lysis of adhesions from ligament of Treitz to the
ileocecal valve. In this setting, a few simple rules are helpful. First, the
adhesiolysis should proceed from the easiest portion of the dissection
where the adhesions are filmiest and the bowel most easily identified,
and work to the more difficult areas. If serosal rents occur, they should
be sutured with absorbable suture. Any enterotomies that occur during
the course of an extensive adhesiolysis should be immediately oversewn
with plans to do a definitive closure at another time. This should
minimize the amount of contamination. During this portion of the
dissection, the bowel should be kept warm and moist to minimize
desiccation injury. In general, filmy adhesions can be separated largely
by blunt dissection, but dense thick adhesions should always be taken
down sharply.
A question often arises regarding dissecting obstructed bowel stuck
down into a scarred pelvis. In most cases, it is wise to take the time and
effort to dissect the bowel out of the pelvis even though it may require
resecting part of the bowel so freed. Bypassing large segments of small
bowel has generally been associated in the past with clinical problems.
After the small bowel has been freed up throughout its entire length, it
is wise to decompress the bowel before closure to both improve blood
flow to the bowel and make abdominal closure easier. The simplest way
to manage decompression is to place the bowel between the second and
third fingers, and while gently squeezing, milk the fluid back up into the
duodenum where the NG tube has been passed. In this fashion, the entire
length of the bowel can be slowly decompressed. One must be careful
during this decompression process not to treat the bowel in a rough
fashion because it is likely to result in serosal splitting and hematoma
formation. Occasionally, a small bowel resection is required during this
process, and decompression can be accom plished during the course of
constructing the anastomosis by use of a suction tip placed through the
enterotomy used for the anastomosis.
If the patient has had only 1 or 2 previous laparotomies for lysis of
adhesions, at this point closure is indicated. In those patients who have
had a multitude of SBOs with multiple laparotomies, placement of a
Baker tube (long intestinal tube with inflatable balloon at the end) is
indicated. Before closure, placement of the omentum between the freed
small bowel and abdominal wall is indicated. With the advent of
antiadhesion barrier materi als, a prudent thing to do at this point is lay
down a couple of sheets of the antiadhesion material so that reentry into
the abdomen will be facilitated
should a subsequent laparotomy be required. Before closure in which
extensive adhesiolysis is required, it is wise to carefully run the small
intestine from ligament of Treitz to ileocecal valve to look for any
evidence of missed enterotomies or deep serosal rents. They can be
repaired at this time. Fascial closure is then performed in the standard
fashion with closure of the skin usually possible.
Laparoscopic Treatment of SBO

Introduction
When a surgeon is asked what procedures he or she performs laparo
scopically, many operations may be included, but until recently, few
would place exploration for bowel obstruction on the list. Indeed, the
“gold standard” approach to bowel obstruction is still considered by
many to be open surgery. Slowly this trend is changing as more
experience is gained with advanced laparoscopic surgical procedures.
Various forms of laparoscopic surgery have been performed for years.
Before the advent of the computer chip digital camera, the operative field
was able to be visualized only by the operative surgeon, who held the
laparoscope in 1 hand and operated with the other. The first reports of
laparoscopic surgery for adhesiolysis were in the gynecologic literature,
mostly for infertility due to fimbrial or fallopian tube adhesions. These
were usually localized pelvic adhesions. Early laparoscopy was limited
by the fact that the surgeon was required to hold the laparoscope to the
eye, and could work with only 1 hand. The assistant could blindly hold
an instrument for retraction, but could not view the operative field.
After the computer chip digital camera was coupled to the laparoscope
in the 1980s, the entire operative team was able to visualize the operative
field, and the modern era of laparoscopic surgery was born. In the early
days of laparoscopic surgery, it was believed that adhesions were a
contraindication to performing the procedure laparoscopically. As the
skills of the laparo scopic surgeon improved, and as the equipment
became better, more difficult procedures could be performed. Surgeons
became accustomed to lysing adhesions during other surgical procedures,
and adhesions became a “relative contraindication” to laparoscopic
surgery. In 1991, Bastug and colleagues first reported laparoscopic
adhesiolysis for SBO secondary to abdominal adhesions. 55
Bowel obstruction occurs for a variety of reasons, including adhesions,
incarcerated hernia (incisional, umbilical, or groin), internal hernia (espe
cially in the era of laparoscopic gastric bypass surgery [Fig 29]),
obstruction from cancer, diverticulitis, or foreign body (bezoar, gallstone
ileus, or ingested
FIG 29. Laparoscopic view of internal hernia in a patient after gastric bypass. Retractor is
holding up the Roux Y limb under which the internal hernia occurred. (Color version of figure is
available online.)
foreign bodies). All the aforementioned can initially be approached via

laparos copy.
The most obvious advantages of performing laparoscopy rather than
open surgery for SBO include avoiding laparotomy, and therefore the
postlapa rotomy recovery, as well as minimizing the postoperative risks
of laparoto my-related adhesions and ventral hernia. Even if it becomes
prudent to convert to an open operation (cancer-related adhesions or
inability to technically complete the operation laparoscopically), the
eventual laparotomy incision may be limited based on the
laparoscopically diagnosed location of the problem.
An initial laparoscopic approach can allow for access away from the
midline incision to minimize enterotomy of bowel adherent to a previous
midline laparotomy. Even if a later conversion to open surgery is
required, the adhesions might be able to be laparoscopically cleared from
a portion of the midline incision, allowing for safer open access. With the
creation of pneumoperitoneum, the bowel tends to hang from the
abdominal wall, creating natural traction on the adhesive bands. The
tented abdominal wall acts to create countertraction. This effect can be
enhanced for adhesions off the midline by tilting and rotating the table to
maximize this effect. In small condensed spaces, the laparoscope can be
brought in close to the tissues to be lysed, and the magnified view may
facilitate better visualization (Fig 30). If localized dense adhesions are
encountered that cannot be lysed
FIG 30. Excellent view of adhesions seen through the laparoscope. Lysis with “cold” scissors can
be safely done in this setting.
laparoscopically, direct conversion to limited laparotomy can be

performed in cases in which there is adhesion-free bowel proximal and
distal to the point of obstruction.
Advantages of laparoscopic surgery are well known, including faster
return of bowel function (shorter postoperative ileus), less postoperative
pain, shorter length of hospital stay, lower wound infection rate, and a
reduced risk of wound dehiscence or postoperative incisional ventral
hernia. It is well documented that laparotomy is an independent risk
factor for formation of postoperative adhesions, and the laparoscopic
approach may limit recurrence of SBO. Schnuriger and colleagues found
that in most abdominal procedures, the laparoscopic approach is
associated with a significantly lower incidence of adhesive SBO or
adhesion-related admission than in the open approach. 56 They performed
a collective review of recent literature and found that the incidence of
adhesion-related readmissions was 7.1% in open vs. 0.2% in laparoscopic
cholecystectomies, 9.5% in open vs. 4.3% in laparoscopic colectomy,
15.6% vs. 0% in laparoscopic total abdominal hysterectomy, and 23.9%
in open vs. 0% in laparoscopic adnexal surgery. Only in appendec tomies
was there no difference between the 2 techniques. They believed that
techniques that avoided unnecessary peritoneal dissection, and spillage of
intestinal contents, led to reduced adhesions. Weibel and Manjo noted
that patients undergoing laparotomy for various reasons have a 90% risk
of
developing intraperitoneal adhesions.57 The incidence of readmissions di
rectly related to those adhesions varies from 5% to 20%.
Comparison of Open and Laparoscopic
Treatment of SBO
One of the earliest large series of laparoscopy for SBO was conducted
by Franklin and colleagues.58 The authors reported a single-institution
10-year retrospective review of patients who underwent laparoscopic
operation for SBO from 1991 to 2001. A total of 167 patients underwent
laparoscopy for diagnosis and/or treatment of intestinal obstruction. The
investigators used laparoscopy to successfully diagnose the site of
obstruction in all patients. The procedures were performed by pioneers in
laparoscopy. They reported that all cases (of SBO) were approached
laparoscopically regardless of etiology, excluding patients with a prior
known abdominal cavity that would make the laparoscopic approach
unfeasible, such as concrete abdomen or known massive adhesions. The
sites of obstruction were found to be stomach in 7 (4.2%), small bowel in
116 (69.5%), and colon in 44 (26.3%) cases. The causes of obstruction
included adhesions (30.7%), abdominal wall hernias (26.7%), adenocar
cinoma of the colon (13.1%), Crohn’s disease of the small bowel (5.1%),
colonic diverticulitis (5.1%), internal hernias (3.4%), ischemic or radia
tion-induced colitis (3.4%), colonic volvulus (2.3%), benign colonic
tumors (1.1%), gallstone ileus (0.6%), and ileocecal intussusception
(0.6%).
Approximately 154 patients (92.2%) were successfully treated laparo
scopically without conversion to laparotomy. The conversion rate was
7.8%. Inability to visualize and control the operative field because of a
massively dilated bowel was the most common cause of conversion
(46%), followed by extensive involvement of surrounding structures by
tumor (23%), dense adhesions that could not be managed
laparoscopically (15%), significant intestinal ischemia with necrosis
(8%), and an iatro genic bowel injury in 1 patient that could not safely be
repaired laparoscopically (8%). Operative time varied from 20 minutes to
3 hours. The intraoperative complication rate was 3.5% and consisted of
inadver tent enterotomies in 6 patients, 5 of which were repaired
laparoscopically. The average return of bowel function was at 2 days
(range 1-8), and average postoperative stay was 5 days (range 2-42). The
postoperative complication rate was 18.6%. Complications included
prolonged ileus (4.8%), wound infection (4.2%), and septic
complications (2.9%). The overall recurrent obstruction rate was 4.2%,
consisting of one case in the immediate postoperative period, and 6
delayed cases. Of the 6 delayed
cases, recurrent adhesions occurred in 3, recurrence of cancer in 2, and
radiation-induced stricture in 1. The perioperative death rate was 2.3%
(cause of death was not specified). The authors summarized that all
suspected cases of intestinal obstruction can be approached initially by
laparoscopy, and the vast majority can be treated without conversion.
They stressed the importance of advanced laparoscopic skills and instru
mentation.
In a large multicenter retrospective study, Levard and colleagues
retrospectively reviewed records from 308 patients with SBO treated
laparoscopically in 35 centers from 1986 to 1998. Approximately 40
patients (13%) had not had previous abdominal surgery, 159 patients
(59.3%) had undergone 1 previous abdominal operation, and 79 patients
(29.4%) had undergone 2 operations. 59 The initial onset of symptoms
began 48 hours before hospitalization, and the patients underwent
surgery on average 1 day after admission (range: 2 hours to 12 days).
They reported a 54.6% success with laparoscopic surgery, a 40.9%
failure requiring immediate conversion, and a 4.5% short-term failure
rate requiring a return to OR an average of 4 days after the initial
procedure (range: 1-12 days). Success was noted to be higher in patients
who only had a previous appendectomy with obstruction due to localized
adhesions and in those with no antecedent surgery. Success was lower in
patients with multiple dense adhesions. The 2 most common causes for
conversion were intestinal necrosis in 22.8% of failures (10.3% overall)
and intestinal injury in 18% of failures (8.4% overall). The reason for
delayed conversions was mainly due to persistent obstruction or
peritonitis secondary to leak of repaired intestinal injury or intestinal
necrosis. Early death rate was 1.1% in the patients who completed
laparoscopically, and 3.6% in the converted patients. The postoperative
ileus rate was 2 days in the laparoscopic group, and 4 days in the open
group. Wound complica tions in the laparoscopically completed group
occurred in 2 patients (1.2%) and in 15 patients (10.7%) in the converted
group. Hospital length of stay was 4 days in the laparoscopic group and
10 days in the open group. The average follow-up was 1.6 months
(range: 1-78 months). Recurrent obstruction was noted in 5% of each
group.
The authors suggest that factors making laparoscopic surgery more
difficult than open surgery include reduced operative space and difficulty
with anterograde or retrograde voiding of the intestinal contents (ie,
milking out the intestinal contents). They also recommend that laparo
scopic treatment should probably be limited to patients who have
undergone fewer than 3 previous abdominal operations. They favor the
laparoscopic approach in patients with previous appendectomy or
patients
suspected to have adhesive bands rather than dense adhesions. The
authors suggest that conversion may be related to the learning curve, as
only 11 of 43 centers had performed more than 10 laparoscopic lysis of
adhesion cases. The follow-up in this study was short, and therefore
intermediate and long-term recurrence rates cannot be determined based
on this report.
Lujan and colleagues performed a retrospective review of 61 consecu
tive patients who underwent laparoscopic exploration for SBO between
1998 and 2003.60 Diagnosis was made by gastrograffin upper gastroin
testinal (UGI) study or CT scan, or both. All patients had a tight partial
SBO or a complete SBO. Patients were excluded if they had free air or
evidence of malignant causes of obstruction. Approximately 15% of the
patients had no previous history of abdominal surgery, whereas 85% had
a previous abdominal operation. Two thirds of the cases were able to be
completed laparoscopically. Of the 33% patients reportedly converted to
open operation, 7 of 20 were converted to “mini open”—referred to by
other authors as a “laparoscopic assisted operation.” Only 13 of the 61
patients (21%) required a full laparotomy while the most common cause
of obstruction was a single band. The single band cases were short
ranging from 12 to 60 minutes (comprising 41% of the cases). The stated
reasons for conversion included massive or dense adhesions, ischemic
bowel, iatrogenic enterotomy, and technical difficulties. Three patients in
each group had an iatrogenic bowel injury, which did not reach statistical
significance. The mean length of stay was 3.9 days in the laparoscopic
group vs. 8.5 days for the mini-open and 11 days for laparotomy.
The authors believed that less emphasis should be placed on the fear of
conversion and that laparoscopy should be incorporated into the algo
rithm for these patients. They contend that conversion does not equal
failure, but simply the necessary sequence of events in the optimal
management of these patients. They conclude that any surgeon with
advanced laparoscopic skills who has performed a standard midline
incision to release a single adhesive band, regrets that the operation was
performed in an open fashion when it could have been performed
laparoscopically, often with only 3 5-mm ports.
Zerey and colleagues performed a retrospective single-institution re
view of all patients undergoing laparoscopic adhesiolysis between 1997
and 2006.61 All 33 laparoscopic operations were performed by experi
enced laparoscopic surgeons. They reported that contraindications to a
laparoscopic approach were massive distension, a firm scarred abdomen,
or peritonitis. They noted that 66.6% of the patients treated laparoscopi
cally had significant distension. The authors were able to diagnose the
site
of obstruction laparoscopically in all patients. Approximately 88% were
treated laparoscopically, and 12% required conversion to open operation
because of either dense adhesions or insufficient working space. Of
interest, all 4 conversions occurred in patients with only 1 previous
abdominal operation, and the authors found no statistical difference in
success based on number of operations. The mean procedural time was
100 minutes (range: 19-198), and there was no difference in blood loss
between the 2 groups. There was 1 intraoperative complication (3%), an
enterotomy, which was repaired laparoscopically. There were 7 postop
erative complications (21.2%), including urinary tract infection (2),
wound infection (2), renal insufficiency (1), congestive heart failure (1),
and pseudomembraneous colitis (1). The average return to bowel
function was 3.2 days (range: 1-6), and the average hospital length of
stay was 6 days (range: 1-19) in both the laparoscopic and converted
groups.
The authors identified several clinical predictors for the successful
laparoscopic management of adhesive SBO, including SBOs that tempo
rarily resolve after placement of a NG tube, but recur when the patient is
fed, patients in whom the abdomen is not very tightly distended, patients
with proximal bowel obstruction, patients with previous operative treat
ment in a limited area of the abdomen, and patients whose last operation
was more than 1 year before the SBO. They also stated that success was
predicated on the ability to gain safe access to the peritoneal cavity, and
ability to initially insufflate more than 1 L of CO 2. Success was also
more likely if the obstructed segment was not fixed to the
retroperitoneum.
In this study, the authors described a possible selection bias for
laparoscopic surgery primarily in patients who had previous surgery in a
limited area of the abdomen. They noted that there were no significant
differences in the proportion of patients who had a single band as the
etiology of the obstruction compared with multiple adhesions in the
patients who underwent laparoscopic surgery.
In another single-institution study of 285 cases of SBO, Chopra and
colleagues noted that 75 were due to adhesions, 34 of these 75 cases
were attempted laparoscopically, and 23 (68%) could be completed
laparo scopically.62 Of the 11 patients converted to open surgery, the
causes were dense adhesions (4/11), inability to find the point of
obstruction (4/11), inability to achieve pneumoperitoneum (2/11), and
ischemic bowel (1/11). There was 1 intraoperative bowel injury in the
laparoscopic group, and 10 in the open group (4.6% in the laparoscopy
group, 19% in the open group). However, the converted patients were
crossed over to the open group, and it was not specified whether any of
these bowel injuries were in the converted group, or, if so, when the
injury occurred. The
enterotomy rate did not reach statistical significance in either group.
Bowel resection rates were 4.3% in the laparoscopic group, 9% in the
converted group, and 22.6% in the open group. The operative times were
2.3 hours in the laparoscopic group, 3.4 hours in the open group, and 3.9
hours in the converted group. Morbidity was 39% for the laparoscopic
group, 74.5% in the open group, and 63% in the converted group. These
included prolonged ileus in 8.7% of laparoscopic group and 40.4% in the
open group, pneumonia in 9.6% of the open group, but none in
laparoscopic group. One patient in the laparoscopic group required open
reoperation for unresolved SBO. The laparoscopic group had
significantly decreased OR time, less blood loss, and shorter length of
stay.
The authors stated that the overall number of complications
contributing to morbidity were significantly lower in those who
underwent laparo scopic adhesiolysis, and morbidity was unchanged in
the converted group when compared with the open group. They
concluded that it is important to maintain a low threshold for conversion
to laparotomy to prevent iatrogenic injury to friable or distended bowel.
In a retrospective study of the authors’ experience with laparoscopic
treatment of SBO during a 6-year period, Tierris and colleagues reported
on 32 patients with SBO who underwent elective laparoscopic treatment
after a failure of conservative measures. 63 Laparoscopic surgery was
performed after 3 to 4 days of nonoperative management in patients
without peritoneal signs, or rising white blood counts. Adhesions were
identified in 62.5% of patients. The conversion rate was 18.7%: 2
patients for excessively dense adhesions, 2 for iatrogenic intestinal
perforation, and 2 for inability to relieve the obstruction laparoscopically.
The mean OR time was 78 minutes, and only 1 postoperative
complication occurred (3.25%), which was due to unrecognized
iatrogenic bowel injury neces sitating a laparotomy. The average time to
return of bowel function was 3.2 days, and length of stay averaged 4.6
days. The authors believed that CT scan proved to be helpful in the
diagnosis and localization of the obstruction.
In the pediatric literature, Aguayo and colleagues performed a retro
spective review of 34 laparoscopic procedures for SBO between 2001
and 2008.64 The mean age was 8.1 years (range: 2.3-14). The most
common cause was postoperative adhesions, in 73.5%. Approximately
32% of patients required conversion to laparotomy because of poor
working space, intestinal volvulus, or inability to identify source of
obstruction, or enterotomy. There was a 9% enterotomy rate.
Recurrent bowel obstruction occurred in 14.7% of patients in the
adhesiolysis group, with a mean time to recurrence of 2.6 months.
TABLE 7. Series of laparoscopic exploration for small bowel obstruction (SBO) Ileus
Author Number (%) Conversion Complication (%) LOS (Days)

Conversion reason resolved (Days)
Franklin58 167 8% Massive dilation 22% 2 5 Levard59 308 41% Intestinal necrosis 10% 2 4
Lujan60 61 33% Massive adhesions — — 3.9 Zerey61 33 12% Massive dilation 24% 3.2 6
Chopra62 285 32% Dense adhesions 39% — — Tierris63 32 19% Dense adhesions 4% 3.2 4.6
Ghosheh65 1061 33% Dense adhesions 15% — —
Interestingly, the recurrences were in the laparoscopic group, and no

recurrence occurred in the open group. Follow-up was only a mean of 7.3
months, and this recurrence rate did not reach statistical significance. The
authors stated that in patients who required conversion, the laparoscopic
evaluation did aid in identifying the etiology of the obstruction, and
allowed a directed surgical approach when appropriate.
Ghosheh and Salameh65 reviewed the literature for laparoscopy and
bowel obstruction evaluating 19 studies from 1994 through 2005 (Table
7). Laparoscopy for acute SBO was performed in 1061 patients. The
causes of SBO were reportedly adhesions (83.2%), abdominal wall
hernia (3.1%), malignancy (2.9%), internal hernia (1.9%), and bezoars
(0.8%). The overall success rate was 66.5%. A total of 705 cases were
completed either laparoscopically or in a laparoscopic-assisted fashion,
as they included patients requiring a small targeted incision for limited
bowel resection or repair of enterotomy. Conversion to laparotomy was
required in 33.5%. The reasons for conversion in these 365 patients
included dense adhesions (27.7%), need for bowel resection (21.3%),
unidentified etiol ogy (13.0%), iatrogenic injury (10.2%), inadequate
visualization (4.2%), hernia (3.2%), and other causes (11.1%).
The total number of patients with enterotomies was 45 (6.5%), but less
than one half required conversion. There were, however, 9 missed
perforations, including 1 trocar injury. Early recurrence of SBO (defined
as within 30 days) was 2.1%. Only 7 of the 19 studies reported long-term
outcomes ranging from 24.4 to 61.7 months, and therefore long-term
recurrence rates cannot be determined. Of those studies, 162 of 223
patients’ operations (72.6%) were completed laparoscopically; 17
patients (7.6%) had SBO in the longer follow-up period.
Morbidity and mortality rates were 15.5% and 1.5%, respectively. The
authors stated that this rate compares favorably with open series listing
morbidity rates as high as 32% and mortality as high as 3.8%. However,
they also added that selection bias in these nonrandomized trials may
well account for this difference. They also summarized that in contrast to
open management, which traditionally involves extensive adhesiolysis,
no attempt is generally made during laparoscopic management to take
down the entire abdominal wall and intraloop adhesions. Instead, only
the adhesions impeding exposure, and those causing the obstruction are
treated.
In a survey of 87 surgeons in Connecticut regarding opinions on
operative management of adhesive SBO (laparoscopy vs. laparotomy),
84% believed that laparoscopy had a role in the management of adhesive
SBO, 71% believed it was safe, and 60% of the surgeons answering the
survey do perform laparoscopic lysis of adhesions in their practice. 66
However, only 68% of this group use this technique for more than 15%
of their adhesive SBO cases (ie, 40.8% of the total group use it for more
than 15% of adhesive SBO). The survey found that surgeons more
recently trained or with membership to minimally invasive surgery
associations were more likely to use laparoscopic lysis of adhesions.
In the colorectal literature, Franko and colleagues 67 performed a
retrospective study to ascertain the impact of previous abdominal opera
tion in patients presenting for laparoscopic colorectal surgery. The
authors were interested specifically in the impact on conversion and
complication rates. Charts from 1000 consecutive laparoscopic colorectal
cases were reviewed. The past surgical history was available on 820
patients, and a previous abdominal operation was present in 347 patients
(42.3%). Overall, there was a higher conversion rate to open operation in
the patients who had previous abdominal surgery (19.6% vs. 11.4%;
overall 14.8% conversion rate). An increased risk of conversion was
noted in patients with a history of previous pelvic surgery (26% vs.
13.7%). Previous appendectomy or cholecystectomy had no statistically
significant effect on conversion rates.
The authors noted that in the patients with previous abdominal surgery,
there was a higher inadvertent enterotomy rate at 1.4% vs. 0.2%, higher
postoperative ileus rate 6.6% vs. 3.0%, and a higher reoperation rate, at
2.3% vs. 0.2%. There was no statistical difference in operating time or
blood loss between the 2 groups. There was no statistical difference in
postoperative bowel obstruction, readmission, leak, abscess, wound
infection, intraoperative bladder or ureter injury, intraoperative
significant bleeding, or death. In this series, there was no difference if the
patient had only 1 previous abdominal operation or several.
Techniques for Laparoscopic Surgery for SBO
Positioning and Access. There are several techniques that may be used
to facilitate the laparoscopic approach. For the patient with a bowel
obstruction, NG decompression before and during operation will help
minimize volume of air and fluid in the bowel, and decrease bowel
distension. The heavy fluid-filled bowel is difficult to handle as
compared with air-filled bowel. Similarly, bladder decompression with a
Foley catheter may improve space in the peritoneal cavity, and minimize
the risk of bladder injury.
Patient positioning can greatly affect the feasibility of the laparo scopic
procedure. The arms should be tucked at the patient’s sides bilaterally to
allow for the assistant holding the laparoscope to stand on the same side
as the surgeon, preventing a “backward view” for the assistant. An
electric table able to tilt in all directions can maximize the effect of
gravity pulling the bowel away from the distended abdominal wall.
Access to the peritoneal cavity should be obtained at a site removed
from previous surgery. Most surgeons will access either the subcostal left
upper quadrant or the subcostal right upper quadrant based on which is
more likely to be free of preexisting adhesions. Other choices could
include the umbilicus if previous midline incision has not been per
formed. Initial access with Veress needle or optical trocar is the most
common approach at the current time. A muscle splitting incision for
open port placement can be performed in the lateral abdomen in any
quadrant. A high flow CO2 insufflator will allow for maintenance of
pneumoperitoneum.
On initial assessment of the peritoneal cavity, if adhesions are exten
sive, and preclude placement of a second port, gentle blunt dissection
with the telescope many times will clear enough space for placement of
the next port. Conversely, a port could be placed in another abdominal
quadrant using the techniques described earlier in the text. The goal is to
have at least 3 laparoscopic ports dispersed in a pattern to allow
triangulation. Additional ports should be placed as needed.
Use of an angled telescope is highly recommended to facilitate the best
view in a tight space. A 5-mm angled scope allows placement in any
port, and is also recommended. Allowing gravity to help mobile bowel
fall away and to pull down adherent bowel to place stretch on the
adhesions is helpful. Tilting the patient as needed to maximize this effect
is also recommended.
Techniques for Adhesiolysis
To manipulate tissue, atraumatic bowel graspers should be used to
grasp mesentery, omentum, or pericolic fat when possible. When the
bowel must be grasped, the tissue should be grasped as broadly as
possible to spread the pressure, and minimize injury to the bowel from
the instrument. Many adhesions are avascular and may be divided with
cold scissors. Once the leading edge of an adhesion is incised, a gentle
prodding with a blunt instrument may be able to develop the plane, and
residual adhesions may then be lysed with the scissors. Energy
application should be used as sparingly as possible. When using
monopolar electrocautery, care must be taken to prevent direct injury to
the bowel. Use of harmonic instruments may generate a dissection plane
with the steam vapor created when the energy is applied to the tissues,
but the blade does become hot, and can injure the bowel.
After a free peritoneal space is created, it is often easiest to work from
terminal ileum in a retrograde fashion, or if this is not feasible, work
from collapsed bowel and run in each direction. This minimizes the
amount of manipulation of dilated bowel. After the obstructive band or
adhesions are lysed, many times the dilated bowel is able to decompress
by expelling its contents into the distal collapsed bowel. Complete lysis
is controversial. If the obstruction appears to be clearly found and lysed,
the risk of bowel injury may override the benefits potentially gained by
lysing all remaining adhesions. It may be disadvantageous to divide
nonobstructing adhesions only to have them reform in a more obstructive
pattern. The patient can return to surgery if needed for further lysis of
adhesions.
If an enterotomy is encountered, it may be repaired with suture if the
injury is small. If open repair or limited resection is required, a mini
laparotomy either in the midline or as a muscle splitting incision can be
performed, precluding the need to convert to full laparotomy.
If a transition zone is not clearly determined, it might be prudent to
convert to open laparotomy. If adhesions are too dense to safely lyse
laparoscopically, conversion to open surgery is recommended. If at any
time the surgeon feels uncomfortable proceeding laparoscopically, it
would be prudent to convert to open operation. Conversion should not be
considered a failure of laparoscopic surgery, but rather the natural
progression of an operation performed in the least invasive fashion that is
safe and reasonable. In other words, conversion usually exemplifies
sound surgical judgment.
Conclusions
Laparoscopy as an initial approach to patients with SBO is slowly
being accepted. It appears to be a safe initial approach, which, if
completed successfully, may result in shorter length of hospital stay,
quicker recovery, and less postoperative morbidity. Selection of
appropriate patients is important, but there are ever-widening indications
to begin a procedure laparoscopically.
Initial port placement at a site remote to expected adhesions, using a
variety of techniques, may limit the risk of access injuries. A methodical
approach to patient preparation and positioning is important in minimiz
ing the need to convert to open operation. Surgical technique should
include cold scissors and blunt dissection when possible, and application
of energy should be used carefully and judiciously. One of the most
dreaded complications in laparoscopic management of SBO is the risk of
enterotomy, which occurs 6.5% of the time. The real concern, however,
is that this bowel injury may be missed at the time of operation, a
complication that can have devastating consequences. Although a missed
enterotomy can occur in association with laparotomy, the incidence is
higher with laparoscopic surgery. The risk of bowel injury can be
diminished by following good surgical technique, which includes avoid
ing the use of electrocautery, minimization of grasping dilated bowel,
manipulation of the bowel using atraumatic graspers, and by handling the
mesentery whenever possible.67
Although not all of these operations can be completed laparoscopically,
the ones that can may limit operative times. It is important to recognize
when it is not reasonable to continue a procedure laparoscopically, and to
convert to open surgery. It should not be considered a surgical failure to
convert to open operation, as laparoscopic instruments and techniques
are only a portion of the tools available to a surgeon. The goal of any
surgical procedure is for the patient to have a successful operative result
with the least invasion and risk. When it is not possible to achieve this
laparo scopically, conversion to the open operation is part of the
spectrum of a surgeon’s operative scope.
Contemporary Progress in Preventing Adhesive SBO

Knowledge of adhesions extends back to ancient Egyptians who
described severe pelvic adhesions in a patient; no treatment was
suggested.68 In a recent review, as mentioned previously, Hunter knew
about adhesions (mid 1700s), Bryant reported a fatal case of adhesive
bowel strangulation in the mid 1800s, 1 and use of salt solutions for
hydroflotation of the bowels was
TABLE 8. Location of postoperative adhesions
Adhesion site Number of patients
Omentum to incision site 170
Operative site alone 57
Omentum to operative site 47
Small bowel to incision site 42
Small bowel to operative site 33
Small bowel to small bowel 17
Other 31
Reprinted with permission from Menzies and Ellis,4 © The Royal College of Surgeons of
England.
described in the late 1880s. An agent called “fibrinolysin” (thiosinamine
and sodium salicylate) was introduced in 1892 but was found not to be
effective and soon fell into disfavor.1 Gum Arabic was recommended as a
“lubricant between the viscera” in 1902, and Johnson and Johnson
marketed a preparation of bovine cecal peritoneum that was
commercially available well into the 20th century. Since then a wide
variety of exotic substances have been used in an attempt to diminish
postoperative adhesions, including omental grafts, metal foils, gold-
beater’s skin, shark peritoneum, lanolin, chyme, amniotic membrane, and
fish bladder. The sheer number of agents studied confirms their lack of
efficacy in eliminating this troublesome postoperative complication.
In the study by Menzies and Ellis, the most common site of
postsurgical adhesions occurred between the omentum and the
undersurface of the abdominal wall incision site. 4 The second most
common was small bowel to small bowel. However, the most common
site of an obstructing adhesion almost always involved small bowel
(85%) as opposed to omentum (3%)4 (Table 8). Operative procedures in
the hypogastrium are also more likely to result in adhesive obstruction
than those in the epigastrium (Table 9). In the previously referenced
study, appendectomy, rectal surgery, colon surgery, and gynecological
procedures were the proce dures most likely to result in clinically
significant adhesive obstructions.
There are few data available regarding the timing of onset of
obstructive adhesions. Stewart and others prospectively followed all
laparotomy patients and found that at 1 month after operation, 0.5% had
obstruction from adhesions; at 1 year after operation, 1% of patients had
obstructing adhesions.69 Most studies suggest that 15% to 20% of
adhesive SBO occur within 1 month postoperatively, another 20% to
30% within the first year, and another 20% in the next 1 to 5 years (Table
10). However, adhesive SBO can develop even at times remote from the
original procedure, commonly exceeding 10 years. Studies vary, but
between 36%
TABLE 9. Previous operative sites producing adhesions
Operations performed Number
Appendectomy 12
Rectal surgery 12
Gynecological surgery 11
Left colon 8
Total colon 7
Right colon 4
Cholecystectomy 4
Duodenal ulcer 4
Unknown 8
Other 10
England.
TABLE 10. Interval from operation to adhesive obstruction

Interval from operation Percent
1 mo 21
1 mo-1 y 17
1-5 y 21
5-10 y 6
10 y 21
Unknown 12
England.
and 60% of all patients who present with an SBO require operation, 70,71
and after an operation for lysis of adhesions, the incidence of recurrent
adhesive SBO leading to an operation ranges from 11% to 21%. 72,73
Operative procedures to prevent recurrent SBO have been generally
disappointing and only occasionally successful. Suture plication has
gener ally had poor results and is used by few surgeons today. Somewhat
more successful has been an operatively placed Baker long intestinal
tube, which is passed through the stomach like a Stamm gastrostomy,
traverses the entire length of the small intestine, and reaches the cecum
where a 30 mL balloon is filled with saline to prevent the tube from
retracting back into the small bowel. Obstructive recurrence occurs in
3.3% to 8.0% of patients.74,75
Adhesion Prevention
A voluminous literature on adhesion prevention has been written,
including reviews by Connolly and Ellis 76,77 (Table 11, Table 12). In his
review, Ellis suggested that the best way to prevent adhesions was to
minimize trauma during surgery: (1) avoid introduction of foreign
TABLE 11. History of attempts to prevent adhesion
1885 Rubbing oil used to prevent adhesions
1886 Saline hydrofloatation described
1892 “Fibrinolysin” (sodium salicylate and thiosinamine) marketed 1902 Gum
Arabic used as visceral lubricant
1905 “Cargile” (bovine cecal peritoneum) introduced
1920 Intra-abdominal proteases described
1940 Heparin first studied
1957 “Amfetin” (amniotic fluid) marketed
1994 “Seprafilm” studied in prospective randomized trial
TABLE 12. Other agents used to diminish adhesions
Oral phosphorus Shark skin
Collodion Lanolin
Physostigmine Chyme
Liquid petroleum Fish bladder
Omental grafts Peritoneum
Metal foils Gold-beater’s skin
TABLE 13. Strategies for preventing adhesions

Irrigants
Anticoagulants
Anti-inflammatories
Fibrinolytics
Cellular modification
Barrier agents
material (talc, etc), (2) leave raw serosal areas open, (3) cover injured
areas with viable tissue, such as omentum, and (4) place omentum
behind the abdominal wall incision. Additional suggestions should
include preventing serosal desiccation with moist lap pads, use of wound
protectors, gentle handling of peritonealized structures, and meticulous
dissection in as small an area as possible.
Strategies for preventing adhesions have generally fallen into the
categories listed in Table 13. A review of the experimental work done in
each of these areas is appropriate and helpful to understand the difficulty
in solving this clinical conundrum.
Irrigants
As previously mentioned, both normal saline and lactated Ringer’s
solution have been used to fill the peritoneal cavity at the end of a case.
The presumption has been that “floating the bowels” would prevent the
injured serosal surfaces from coming in contact with each other, thus
preventing adhesion formation. More than 20 studies have been con
ducted evaluating “hydroflotation” as a method to reduce adhesions
postoperatively. In the meta-analysis of the aforementioned studies,
Wiseman and colleagues reported that no significant difference was seen
between control and experimental groups.78
Anticoagulants
A large number of studies have been conducted to assess the efficacy of
anticoagulants in preventing adhesive SBO. A number of investigations
have evaluated dextran 70 as a possible antiadhesion irrigant. The
beneficial effects of dextran were observed in several animal studies.
Indeed, 2 prospective clinical studies in humans demonstrated some
efficacy of dextran in preventing pelvic adhesions, which cause infertil
ity.79,80 However, an equal number of studies have demonstrated no
improvement with dextran,81,82 and because of possible serious side
effects, dextran is not commonly used in adhesion prevention today.
Similarly, intraperitoneal heparin has been extensively studied to
evaluate its potential antiadhesion effect. Initial studies in animals
suggested that intraperitoneal heparin might be effective, but human
studies with heparin were disappointing and were complicated by
bleeding complications.82,83
Anti-Inflammatory Agents
Nonsteroidal anti-inflammatory agents were shown to reduce
peritoneal adhesions in a variety of animal models. However, Nishimura
and colleagues and Holtz demonstrated that ibuprofen had no impact
when given to humans postoperatively. 84,85 Generally, NSAIDs have
been unpredictable and erratically effective.
Corticosteroids were shown in animal and humans to reduce postoper
ative adhesions.86-88 However, intraperitoneal steroids in human studies
have had mixed and unpredictable results in work done by Glucksman
and colleagues and Seitz and colleagues. 87,89 In addition, use of steroids
in a postoperative situation is limited by immunosuppression and delayed
wound healing.
Fibrinolytics
Fibrinolytic preparations would intuitively seem like the ideal agents to
prevent postoperative adhesions. Both streptokinase and urokinase have
been shown to have some impact on adhesion formation,90,91 but further
studies have been disappointing,92,93 and the surgeon worries about the
impact of such preparations on anastomotic and fascial wound healing.
Recombinant t-PA has been shown to diminish adhesions in animal
models without having a detrimental effect on wound or anastomotic
healing.94,95 However, other studies revealed that adhesions still devel
oped at the site of colonic anastomoses and ischemic small intestine. 96
Clearly, this agent must be studied more thoroughly in humans and holds
some promise as a future antiadhesion agent. Currently, most investiga
tors agree that the balance between t-PA and t-PA inhibitors (PA-I) holds
the key to successful treatment of obstructive adhesions in the future.
Fear of bleeding, anastomotic disruption, and wound dehiscence have
further limited the use of fibrinolytic agents.
Barriers
The area in which the greatest strides have been made in adhesion
prevention in the past 15 years is that of barriers that separate the various
injured serosal surfaces while they are healing. The concept is simple but
quite effective: placement of a mechanical barrier between the injured
healing serosal surfaces, which persists until all serosal healing has taken
place, will prevent adhesive bowel obstruction. An added advantage of
this approach is that it should have little impact on the normal healing
mechanisms, and if the agent is inert, nonreactive, and absorbable, there
should be little associated morbidity. Several products in membrane form
have been used clinically to obviate adhesions after lower abdominal or
pelvic operations. There are also a few liquid or gel preparations that
have been tested.
Hyaluronate/Carboxymethylcellulose
By far, the membrane tested most extensively in adhesion prevention is
a hyaluronic acid/carboxymethylcellulose preparation marketed as Sepra
film (Genzyme, Cambridge, MA). This somewhat brittle membrane is
absorbed within 7 to 10 days after placement in the abdomen, and
excreted within a month. It has been extensively studied for safety and
efficacy in a number of clinical studies and appears to have very few, if
any, side effects except some questions of a slightly increased risk for
anastomotic leak if wrapped entirely around a fresh anastomosis. A host
of retrospective and prospective randomized studies have been conducted
to ascertain whether it decreases adhesions. The earliest study by Becker
and colleagues was prospective and randomized with adhesion assess
ment by blinded observers.88 Approximately 175 patients who underwent
ileal-pouch anal anastomosis (IPAA) and protective loop ileostomy were
randomized to receive the membrane or not, and adhesion evaluation was
conducted at the second-look laparotomy to close the ileostomy 8 weeks
later. The authors reported significantly fewer and less severe adhesions
in the membrane group.
In a group of patients undergoing rectal surgery who needed an
ileostomy, Tang and colleagues randomized patients who would seek
stoma closure into membrane vs. no membrane groups. At the second
operation, the authors encountered fewer and less severe adhesions in the
membrane group and fewer stoma complications (mean adhesion score
5.81 0.5 vs. 7.82 0.6, P 0.05). The authors of both this and the
previous study observed that the dissection was much easier in the
membrane group.97 Similarly Vrijland and colleagues prospectively
randomized a group of 71 patients undergoing a colorectal resection with
Hartmanns into membrane and no-membrane groups. At operation to
close the stoma, a blinded evaluator assessed the field for incidence,
severity, and complications of adhesions. The investigation reported a
significant decrease in severity but not incidence of adhesions (OR, 0.34;
95% confidence interval, 0.06-1.98).98
A Canadian group led by Cohen in a prospective multicenter trial used
the model of the original group to randomize IPAA patients into
membrane and control groups. The membrane used in this study was
Seprafilm with glycerol added to make the membrane softer, pliable, and
less brittle. Using laparoscopy at the time of ileostomy closure, adhesions
were graded according to incidence and severity. The investigators
reported a significant decrease in incidence and severity in the membrane
group.99 A similar prospective randomized study by Kusunoki and
colleagues was conducted in patients who needed a protective ileostomy
after low anterior resection. During stoma closure, the severity of
adhesions was assessed and found to be significantly reduced in both the
peristomal area and posterior midline. Once again the authors comment
on shorter surgical time and less blood loss. 100 Finally, a Cochrane review
conducted by Kumar and colleagues evaluating 6 randomized trials using
Seprafilm revealed that use of the membrane significantly reduced the
extent and incidence of adhesions.101
Although the early studies of Seprafilm were conducted to ascertain the
membrane’s efficacy in reducing adhesions, they were not designed to
assess impact of the membrane on actual SBO. The most important study
in the literature, which truly assessed the impact of the hyaluronate/
carboxymethylcellulose membrane on actual bowel obstruction, was
published in 2006. In a prospective, randomized, multicenter trial
involving 1791 patients, Fazio and colleagues designed the study so that
TABLE 14. Efficacy of Seprafilm in reducing small bowel obstruction (SBO)
Author Journal Study type Patient no. (Con vs. Rx) (Con vs. Rx) complications
Incidence of Re-operation Septic (Con vs. Rx)
SBO (%) for SBO (%)
Fazio102 DCR PRCT 1701 12 vs. 12 3.4 vs. 1.8* 3 vs. 4 Salum 104 DCR Retro 438 6.1 vs. 4.5
3.9 vs. 1.5 1.1 vs. 3.4 Mottri105 Am Surg Retro 368 14.2 vs. 6.5* 4.4 vs. 1.6 13 vs. 15
Kudo103 Surg Today Retro 51 20 vs. 0* — —
*p 0.05.
Seprafilm was liberally placed at every site serosal or peritoneal injury

occurred (instead of merely placing it between the abdominal wall and
omentum as in the early studies). The authors followed their patients for
3.5 years and found that although the overall incidence of SBO was not
diminished in the membrane group, the incidence of SBO requiring
surgical treatment was significantly lower (1.8% vs. 3.4%; P 0.05).102 In
a second nonrandomized study by Kudo and colleagues in patients
undergoing AAA repair, the incidence of SBO was 0% in the Seprafilm
group and 20% in the no-membrane group (P 0.05).103
Thus, the debate regarding use of Seprafilm to prevent SBO continues
(Table 14). What can be said is that Seprafilm reduces the incidence and
severity of postoperative adhesions and clearly makes abdominal reentry
at a second procedure much easier. Considerations should be given to
placing it in the abdomen of any patient for whom the surgeon plans on
reoperation for any reason.
Oxidized Regenerated Cellulose
A preparation consisting of oxidized regenerated cellulose was the first
antiadhesion barrier to be FDA approved. Marketed under the name
Interceed, this agent changes to form a gel-like material when coming in
contact with peritoneal fluid. The gelatinous material persists during
adhesion formation and is finally excreted 14 days after placement.
In a prospective randomized study, Azziz performed laparotomy on
134 patients for lysis of adhesions and placed Interceed on one pelvic
sidewall and nothing on the other side. At a second-look laparoscopy 10
to 98 days later, the incidence and severity was found to be much
diminished in the experimental group with the membrane. 106 Simi larly,
Larsson and colleagues studied Interceed in a prospective, randomized,
multicenter trial in which 66 women had lysis of adhesions around both
ovaries, wrapped one set of adenexae with the
cellulose preparation, and used nothing on the opposite side. At 4 to 10
weeks after laparotomy, a second-look laparoscopy was performed,
which revealed a significant reduction in the incidence and severity of
adhesions on the membrane-wrapped side. 107 A host of smaller studies
and 2 meta-analyses108,109 confirm that Interceed reduces the inci dence
and severity of adhesions in women undergoing pelvic surgery.
Unfortunately, experimental trials have shown poor results of Interceed
in the presence of blood and/or infection, 110 and most studies with this
product have been conducted in women with infertility problems.
Because there does not appear to be significant clinical benefit in
preventing SBO, Interceed is rarely used by general surgeons today.
Expanded Polytetrafluoroethylene
Polytetrafluoroethylene is widely used in vascular surgery and has been
used to prevent pelvic adhesions in women with adhesion-related infer
tility. It is an extremely inert nonabsorbable membrane that generates
minimal inflammatory reaction after placement. The membrane is occa
sionally used in the repair of pericardium or peritoneum and has been
experimentally shown to reduce adhesions. 111 Marketed as Preclude, one
(W.L. Gore & Associates, Inc, Newark, DE) clinical study showed a
reduction in postsurgical adhesions with its use, 112 and its ability to
reduce abdominal adhesions as part of a composite mesh material (Dual-
Mesh) in ventral hernia repair has been reported. 113
However, like Interceed, most studies evaluating the efficacy of
Preclude in adhesion prevention have been in women with pelvic
adhesion-related infertility. A major disadvantage of this product is that
it must be removed eventually and cannot stay in place on a permanent
basis.
Icodextrin
A 4% solution of icodextrin, a glucose polymer, has been used with
some success in preventing adhesions. The solution is a less concentrated
form of the liquid used in peritoneal dialysis, 7.5% icodextrin. It is the
most thoroughly studied and the only FDA-approved liquid antiadhesive
agent commercially available. At the conclusion of an operative abdom
inal procedure, 1000 mL of 4% icodextrin is left in the peritoneal cavity
to separate loops of bowel while their injured serosal surfaces heal. The
solution remains in the peritoneal cavity for a few days and prevents the
damaged serosal surfaces from coming in contact with each other. The
solution is marketed as Adept (Baxter Healthcare, Deerfield, IL) and has
been fairly thoroughly studied in both animals and humans.
In both rabbits and rats, placing Adept in the peritoneal cavity in both
peritonitis and wound healing models, postoperative adhesions were
reduced significantly.114,115 In a large multicenter, prospective, random
ized, double-blind study by Brown and colleagues, Adept was compared
with lactated Ringer’s solution in women undergoing laparoscopic
gynecologic surgery for adhesiolysis. At a second laparoscopy 4 to 8
weeks later, the icodextrin solution was significantly more likely to
reduce adhesions116 but was also associated with labial swelling in the
experimental group. In another randomized clinical study by DiZerega
and colleagues, the incidence of adhesions was decreased from 52% to
32% at a second laparoscopy.117 However, a meta-analysis of prospective
randomized studies evaluating Adept was equivocal and could not
recommend it for intra-abdominal adhesion prevention. It currently has
little use in general surgery circles. 118 Adept was recently approved by
the FDA primarily for use in reducing pelvic adhesions, which cause
infertility.
Polyethylene Glycol
A commercially available preparation comprised of an old standard
used in bowel preps, polyethylene glycol, has been developed, which
involves spraying 2 precursors on the injured serosal or peritoneal
surfaces. The combined agents form a viscous gelatinous material, which
adheres to peritoneal surfaces and prevents serosal surfaces from coming
into contact. This preparation carries the name Spraygel (Confluent
Surgical, Waltham, MA) and is available in Germany and Australia.
Animal studies have shown positive outcomes in reducing intraperitoneal
adhesions, and a few randomized studies have shown a reduction in
pelvic adhesions from patients receiving Spraygel on closing the
abdomen.119 However, once again, a Cochrane meta-analysis failed to
achieve statis tical significance when Spraygel was used compared with
the control.118 A single component gel marketed as Adhibit (Angiotech
Pharmaceuticals, Vancouver, BC) has shown encouraging results in a
randomized experi mental trial involving patients undergoing
myomectomy surgery.120
Fibrin Glues
Some anecdotal observations in operative fields in which fibrin glues
were utilized demonstrated a paucity of adhesions during reoperative
surgery. These preparations consist of fibrinogen and thrombin and,
when mixed, produce tenaciously adherent gelatinous fibrin. Studies
reveal that fibrin increases t-PA and PA-I by peritoneal cells 121 and may
impact adhesion formation. However, experimental studies are
conflicting and few
TABLE 15. Preventing adhesions
FDA-approved barrier agents
Agent Company Composition Form Use Studies Comment

Interceed J&J Oxidized cellulose Sheet Adnexae Animal/human Ineffective in blood
Seprafilm Genzyme Hyaluronate carboxymethyl cellulose
Sheet Peritoneum Animal/human Brittle
Preclude Gortex PTFE Sheet Adnexae Animal/human Non-absorb

Repel Synthemed Glycolated polymer United
Gel Pericardium Animal/human Approved in the States
Adept Baxter Icodextrin Liquid Peritoneum Animal/human Mixed results FDA, Food and Drug
Administration; PTFE, polytetrafluoroethylene.
well-designed studies have been conducted to assess its efficacy. 122-124

Another disadvantage of fibrin glue is an exorbitant expense, as well as
an awkward application process.
In summary, barrier products come the closest to an effective antiad
hesion agent of any studied. Tables 15 and 16 summarize the current
state of barrier agents in the United States.
Bioactive Polypeptides
Work done by a Scandinavian group has produced a unique bioactive
peptide whose positively charged peptide (poly- L-lysine) adheres to the
injured peritoneum or serosa and then forms a matrix with negatively
charged poly-L-glutamate. Three experimental animal studies have dem
onstrated its ability to reduce adhesions without weakening the anasto
mosis or affecting bleeding. The polycation has not been tested in
humans, and a more recent publication demonstrated a very narrow
therapeutic window without toxicity. 125 It is unlikely it will find any role
in preventing intra-abdominal adhesions.
Inflammatory Mediators
Extensive research has been done looking at the role of inflammatory
mediators in adhesion formation. Results suggest that several cytokines
and growth factors play a role in regulating the genes that play a part in
initiating adhesion formation probably by inhibiting fibrinolysis. 126,127
Gene products, such as TGF- , ICAM-1, VCAM-1, and NK-1 are
potential candidates. Studies on TGF- suggest that it contributes to
reduced fibrino lytic activity, and thus, may worsen adhesion
formation.128,129 In one animal study, an antibody neutralizing TGF-
resulted in significant reduction in adhesions 130 possibly through
regulation of PAI-1.131
TABLE 16. Preventing adhesions
Barrier agents being studied (NOT FDA-Approved)
Agent Company Composition Form Use Studies Comment

Intergel Lifecore Ferrous hyaluronan Gel Peritoneum Animal/ human
human Flogel Alliance Poloxamer Gel Peritoneum Animal/ human
Allergic reactions: withdrawn from market
Adcon P Gliatech Polyglycan esters Liquid Peritoneum Animal/ FDA problems —
Incert Anika Modified hyal acid Gel Peritoneum Animal Used in spinal surgery
Hylans Inamed Hyaluronic modification Liquid Joints Animal Withdrawn from US market
Caprolactone Solvay Cyclic lactone ester Liquid Peritoneum Animal Prevents tendon adhesions
Hyskon Medisan Dextran Liquid Peritoneum Animal/ human Mixed results
Carbylan-SX Carbylan Biosurgery glycosamino-glycan than Seprafilm in

Cross-linked Gel Peritoneum Animal More effective animal studies
LM 609 Scripps Clinic integrins Animal Unique mechanism
Ab against alpha V beta 3 Liquid Vocal cord, Pericardium
Spraygel (spray shield) Appears to be gynecologic

Covidien Polyethylene glycol Liquid effective in surgery; used in Europe
Peritoneum Animal/ human
Adhibit Angiotech Fibrin-based Gel Peritoneum Animal/ human FDA, Food and Drug Administration.
Effective in
gynecologic
surgery; used in Europe
Other studies suggest that IL-1 contributes to a decrease in fibrinolytic
activity possibly by releasing PAI-1. 24 In a study conducted with rats,
administration of an anti-IL-1 agent resulted in the development of
significantly fewer adhesions than in controls. 132
A well-known neuropeptide substance P (SP) has recently been recog
nized as having some actions that might impact adhesion formation. SP
has been detected in neurons found in adhesions and is a well-known
inflammatory mediator that works by altering the expression of ICAM-1,
VCAM-1, and TGF- —all of which impact adhesion formation.133 Neural
endopeptidase is an enzyme that breaks down SP, and knock out mice
lacking this enzyme develop adhesions much more easily than
controls.134 Although it is unlikely that SP would ever be used therapeu
tically, further study is justified in an attempt to understand more fully
the mechanisms of adhesion formation.
Another intriguing agent that seems to inhibit adhesion formation is a
substance derived from the exoskeleton of crustaceans. NO-carboxym
ethylchitosan (NOCC) has been demonstrated to reduce adhesions in
both
rat and rabbit studies.135,136 In a prospective randomized study involving
multiple centers, NOCC reduced both the extent and severity of pelvic
adhesions.137
Estrogen levels are also thought to have some impact on adhesion
formation. Administration of gonadotropin releasing hormone (GnRH) or
an estrogen antagonist, mifepristone, reduces postoperative adhesions in
rats and monkeys.138,139 Levels of t-PA and PA-I were measured in both
experimental and control groups and were found to be diminished in
short-term follow-up, whereas PA-I was increased in long-term evalua
tions. However, studies in humans have revealed mixed results. In a
randomized study evaluating patients after myomectomy, patients who
received GnRH were found to have no significant reduction in
adhesions.140 However, recent studies evaluating the impact of aromatase
inhibitors and tamoxifen on postoperative adhesions in rats were
encouraging.141,142
Having excess levels of free radicals such as nitric oxide (NO) have
been implicated as a mechanism of increased adhesion formation in a
postoperative setting.143 NO simulated the production of cGMP and
resulted in activation of protein kinase G. Reduction of phosphodiester
ase-5 results in breakdown of cGMP, which leads to decreased collagen
production and fibroblast apoptosis. 144,145 An inhibitor of phosphodies
terase-5, sildenafil, has shown the capacity to reduce adhesions in animal
studies.146 Similarly, an inhibitor of NO synthase, methylene blue,
decreases postoperative adhesions in animals. Unfortunately, it also
impairs anasto motic healing.147
Reed and colleagues demonstrated elevated levels of mRNA for NK-1
receptor (NK-1R) and SP in early postoperative adhesions. 133 Follow-up
work showed that an antagonist to NK-1R after surgery significantly
reduced adhesions.148 In the same study, investigators gave the NK-1R
antagonist and found that it lead to a significant increase in mRNA for t-
PA.
Recently, a study was conducted using a mini-osmotic pump in
evaluating new agents for experimental pelvic adhesion reduction.
Agents included dipyridamole, lazaroids, trans-retinoic acid, and anti-
inflamma tory peptide-2.149 A potent thrombin inhibitor RecHirudin has
also been demonstrated to reduce peritoneal adhesions in 2 animal
models.149
Other agents that have been studied and demonstrated varying levels of
adhesion inhibition include pentoxifylline, 150 ACE inhibitors,151 angio
genesis inhibitors,152 some antibiotics,153 and chemotherapeutic agents,
such as 5-fluorouracil, and mitomycin C.154,155
Although much has been learned about adhesion inhibitors from the
multitude of studies referenced previously in the text, there appears to be
a need for thorough ongoing studies to further evaluate the mechanisms
of adhesion formation because no agent has yet been discovered that
inhibits adhesion formation without interfering with other healing func
tion.
REFERENCES
1. Wiseman DM. Adhesion prevention: past the future. Perit Surg 1998;VII. 39:1-38.
2. Moss W, McFetridge EM. Acute intestinal obstruction: a comparative study of 511
cases, with special reference to the lowered mortality achieved by modern methods of
therapy. Ann Surg 1934;100:158-66.
3. Bevan PG. Adhesive obstruction. Ann R Coll Surg Engl 1984;66:164-9. 4. Menzies
D, Ellis H. Intestinal obstruction from adhesions: how big is the problem? Ann R Coll
Surg Engl 1990;72:60-3.
5. Irvin TT. Abdominal pain: a surgical audit of 1190 emergency admissions. Br J Surg
1989;76:1121-5.
6. Ray NF, Larsen JW, Stillman RJ, et al. Economic impact of hospitalizations for
lower abdominal adhesiolysis in the United States in 1988. Surg Gynecol Obstet
1993;176:271-6.
7. Tingstedt B, Johansson J, Nehez L, et al. Late abdominal complaints after
appendectomy—readmissions during long-term follow-up. Dig Surg 2004;21:23-7. 8.
Kössi J, Salminen P, Rantala A, et al. Population-based study of the surgical workload
and economic impact of bowel obstruction caused by postoperative adhesions. Br J
Surg 2003;90:1441-4.
9. Playforth RH, Holloway JB, Griffen WO. Mechanical small bowel obstruction: a
plea for earlier surgical intervention. Ann Surg 1970;171:783-7.
10. Laws HL, Aldrete JS. Small-bowel obstruction: a review of 465 cases. South Med J
1976;69(6):733-4.
11. Stewardson RH, Bombeck CT, Nyhus LM. Critical operative management of small
bowel obstruction. Ann Surg 1978;187:189-93.
12. Bizer LS, Liebling RW, Delany HM, et al. Small bowel obstruction. Surgery
1981;89:407-13.
13. Attard JP, MacLean AR. Adhesive small bowel obstruction: epidemiology, biology
and prevention. Can J Surg 2007;50(4):291-300.
14. Dijkstra FR, Nieuwenhuijzen M, Reijnen MM, et al. Recent clinical developments
in pathophysiology, epidemiology, diagnosis and treatment of intra-abdominal
adhesions. Scand J Gastroenterol Suppl 2000;(232):52-9.
15. 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.
16. Cheong YC, Laird SM, Li TC, et al. Peritoneal healing and adhesion formation/
reformation. Hum Reprod Update 2001;7:556-66.
17. Holmdahl L, Ivarsson ML. The role of cytokines, coagulation, and fibrinolysis in
peritoneal tissue repair. Eur J Surg 1999;165:1012-9.
18. Reed KL, Stucchi AF, Leeman SE, et al. Inhibitory effects of a neurokinin-1
receptor antagonist on postoperative peritoneal adhesion formation. Ann N Y Acad
Sci 2008;1144:116-26.
19. Thompson J. Pathogenesis and prevention of adhesion formation. Dig Surg
1998;15:153-7.
20. Liakakos T, Thomakos N, Fine PM, et al. Peritoneal adhesions: etiology, patho
physiology, and clinical significance. Recent advances in prevention and manage
ment. Dig Surg 2001;18:260-73.
21. Holmdahl L. Making and covering of surgical footprints. Lancet 1999;353:1456-7.
22. Sulaiman H, Dawson L, Laurent GJ, et al. Role of plasminogen activators in
peritoneal adhesion formation. Biochem Soc Trans 2002;30:126-31. 23. Falk K,
Björquist P, Strömqvist M, et al. Reduction of experimental adhesion formation by
inhibition of plasminogen activator inhibitor type 1. Br J Surg 2001;88:286-9.
24. Whawell SA, Thompson JN. Cytokine-induced release of plasminogen activator
inhibitor-1 by human mesothelial cells. Eur J Surg 1995;161:315-8. 25. Lauder CIW,
Garcea G, Strickland A, et al. Abdominal adhesion prevention: still a sticky subject. Dig
Surg 2010;27:347-58.
26. Montz FJ, Monk BJ, Lacy SM, et al. Ketorolac tromethamine, a nonsteroidal anti-
inflammatory drug: ability to inhibit post-radical pelvic surgery adhesions in a
porcine model. Gynecol Oncol 1993;48:76-9.
27. Risberg B. Adhesions: preventive strategies. Eur J Surg Suppl 1997;577:32-9. 28.
Gutt CN, Oniu T, Schemmer P, et al. Fewer adhesions induced by laparoscopic surgery?
Surg Endosc 2004;18:898-906.
29. Lundorff P, Hahlin M, Källfelt B, et al. Adhesion formation after laparoscopic
surgery in tubal pregnancy: a randomized trial versus laparotomy. Fertil Steril
1991;55:911-5.
30. Milingos S, Kallipolitis G, Loutradis D, et al. Adhesions: laparoscopic surgery
versus laparotomy. Ann N Y Acad Sci 2000;900:272-85.
31. Polymeneas G, Theodosopoulos T, Stamatiadis A, et al. A comparative study of
postoperative adhesion formation after laparoscopic vs open cholecystectomy.
Surg Endosc 2001;15:41-3.
32. Whang EE, Ashley SW, Zinner MJ. Small intestine. In: Brunicardi FC, Andersen
DK, Billiar TR, et al, eds. Schwartz’s Principles of Surgery. New York: McGraw-
Hill, 8th edn, 2005:1017-54. (Note section: Small-Bowel Obstruction 1027-1031.).
33. Ishitani MB, Jones RS. Intestinal obstruction in adults. In: Scott HW, Sawyers JL,
eds. Surgery of the Stomach, Duodenum, and Small Intestine. Cambridge:
Blackwell Scientific Publications, 2nd edn, 1992:770-88.
34. Wangensteen OH, Rea CE. The distention factor in simple intestinal obstruction.
Surgery 1939;5(3):327-39.
35. Wangensteen OH. Historical aspects of the management of acute intestinal
obstruction. Surgery 1969;65:363-83.
36. Wright HK, O’Brien JJ, Tilson MD. Water absorption in experimental closed
segment obstruction of the ileum in man. Am J Surg 1971;121:96-9. 37. Shields R. The
absorption and secretion of fluid and electrolytes by the obstructed bowel. Br J Surg
1965;52:774-9.
38. Sung DT, Williams LF. Intestinal secretion after intravenous fluid infusion in small
bowel obstruction. Am J Surg 1971;121:91-5.
39. Ruf W, Suehiro GT, Suehiro A, et al. Intestinal blood flow at various intraluminal
pressures in the piglet with closed abdomen. Ann Surg 1980;191:157-63. 40. Ohman U.
Studies on small intestinal obstruction. I. Intraluminal pressure in experimental low
obstruction in the cat. Acta Chir Scand 1975;141:413-6.
41. Soybel DI. Ileus and bowel obstruction. In: Greenfield LJ, ed. Surgery Scientific
Principles and Practice. Philadelphia: Lippincott Williams & Wilkins, 3rd edn,
2001:798-9.
42. Evers BM. Small intestine. In: Townsend CM, Beauchamp RD, Evers BM, Mattox
KL, eds. Sabiston Textbook of Surgery. Philadelphia: Elsevier Saunders, 17th edn,
2004:1323-77.
43. Gorbach SL. Intestinal microflora. Gastroenterology 1971;60:1110-29. 44. Sykes
PA, Boulter KH, Schofield PF. The microflora of the obstructed bowel. Br J Surg
1976;634:721-5.
45. Bar-Natan M, Larson GM, Stephens G, et al. Delayed gastric emptying after gastric
surgery. Am J Surg 1996;172:24-8.
46. Branco BC, Barmparas G, Schnüriger B, et al. Systematic review and meta-analysis
of the diagnostic and therapeutic role of water-soluble contrast agent in adhesive
small bowel obstruction. Br J Surg 2010;97:470-8.
47. Abbas S, Bissett IP, Parry BR. Oral water soluble contrast for the management of
adhesive small bowel obstruction. Cochrane Database Syst Rev 2007;(3):
CD004651.
48. Mallo RD, Salem L, Lalani T, et al. Computed tomography diagnosis of ischemia
and complete obstruction in small bowel obstruction: a systematic review. J
Gastrointest Surg 2005;9(5):690-4.
49. Colon MJ, Telem DA, Wong D, et al. The relevance of transition zones on
computed tomography in the management of small bowel obstruction. Surgery
2010;147:373-7.
50. Schwenter F, Polleti PA, Platon A, et al. Clinicoradiological score for predicting the
risk of strangulated small bowel obstruction. Br J Surg 2010;97:1119-25. 51. Zielinski
MD, Eiken PW, Bannon MP, et al. Small bowel obstruction—who needs an operation?
A multivariate prediction model. World J Surg 2010;34(5):910-9.
52. Zielinski MD, Eiken PW, Lohse HSF, et al. Prospective, observational validation of
a multivariate small-bowel obstruction model to predict the need for operative
intervention. J Am Coll Surg 2011;212(6):1068-76.
53. Duda JB, Bhatt S, Dogra VS. Utility of CT whirl sign in guiding management of
small-bowel obstruction. Am J Roentgenol 2008;191(3):743-7.
54. Fleshner PR, Siegman MG, Brolin RE, et al. A prospective randomized trial ofshort
vs. long tubes in adhesive small bowel obstruction. Am J Surg 1995;170:366-70. 55.
Bastug DF, Trammell SW, Boland JP, et al. Laparoscopic adhesiolysis for small bowel
obstruction. Surg Laparosc Endosc Percutan Tech 1991;1:259-62. 56. Schnüriger B,
Barmparas G, Branco BC, et al. Prevention of postoperative peritoneal adhesions: a
review of the literature. Am J Surg 2011;201:111-21. 57. Weibel MA, Majno G.
Peritoneal adhesions and their relation to abdominal surgery. A postmortem study. Am J
Surg 1973;126:345-53.
58. Franklin ME, Gonzalez JJ, Miter DB, et al. Laparoscopic diagnosis and treatment of
intestinal obstruction. Surg Endosc 2004;18:26-30.
59. Levard H, Boudet M-J, Msika S, et al. Laparoscopic treatment of acute small bowel
obstruction: a multicentre retrospective study. ANZ J Surg 2001;71:641-6. 60. Lujan
HL, Oren A, Plasencia G, et al. Laparoscopic management as the initial treatment of
acute small bowel obstruction. JSLS 2006;10:466-72.
61. Zerey M, Sechrist CW, Kercher KW, et al. Laparoscopic management of adhesive
small bowel obstruction. Am Surg 2007;73(8):773-8.
62. Chopra R, McVay C, Phillips E, et al. Laparoscopic lysis of adhesions. Am Surg.
2003;69(11):966-8.
63. Tierris I, Mavrantonis C, Stratoulias C, et al. Laparoscopy for acute small bowel
obstruction: indication or contraindication? Surg Endosc 2011;25:531-5. 64. Aguayo P,
Fraser JD, Ilyas S, et al. Laparoscopic management of small bowel obstruction in
children. J Laparoendosc Adv Surg Tech A 2011;21(1):85-8. 65. Ghosheh B, Salameh
JR. Laparoscopic approach to acute small bowel obstruction: review of 1061 cases. Surg
Endosc 2007;21:1945-9.
66. Oyasiji T, Helton SW. Survey of opinions on operative management of adhesive
small bowel obstruction: laparoscopy versus laparotomy in the state of
Connecticut. Surg Endosc 2011;25:2516-21.
67. Franko J, O’Connell BG, Mehall JR, et al. The influence of prior abdominal
operations on conversion and complication rates in laparoscopic colorectal
surgery. JSLS 2006;10:169-75.
68. Carson HW. The evolution of the modern treatment of septic peritonitis. Lancet
1923;i:1035-7.
69. Stewart RM, Page CP, Brender J, et al. The incidence and risk of early postoperative
small bowel obstruction. A cohort study. Am J Surg 1987;154:643-7. 70. Wolfson PH,
Bauer JJ, Gelernt IM, et al. Use of the long tube in the management of patients with
small-intestinal obstruction due to adhesions. Arch Surg 1985;120:1001-6.
71. Hofstetter SR. Acute adhesive obstruction of the small intestine. Surg Gynecol
Obstet 1981;152:141-4.
72. Close MB, Christensen NM. Transmesenteric small bowel plication or intraluminal
tube stenting. Indications and contraindications. Am J Surg 1979;138:89-96. 73. Bizer
LS, Delaney HM, Gerut Z. Observations on recurrent intestinal obstruction and modem
non-operative management. Dig Surg 1986;3:229.
74. Jones PF, Thomson SR. The surgical treatment of adhesive obstructions, with
critical appraisal of intra-operative small bowel intubation. In: Ellis H, Lennox M,
eds. Adhesions: the Problems. London: Westminster Hospital Medical School
1983;37-44.
75. Weigelt JA, Snyder WH, Norman JL. Complications and results of 160 Baker tube
plications. Am J Surg 1980;140:810-5.
76. Connolly JE, Smith JW. Intestinal adhesions - present status of prevention and
treatment. Calif Med 1960;92(6):397-9.
77. Ellis H. The cause and prevention of postoperative intraperitoneal adhesions. Surg
Gynecol Obstet 1971;133:497-511.
78. Wiseman DM, Trout JR, Diamond MP. The rates of adhesion development and the
effects of crystalloid solutions on adhesion development in pelvic surgery. Fertil
Steril 1998;70:702-11.
79. Adhesion Study Group. Reduction of postoperative pelvic adhesions with intra
peritoneal 32% dextran 70: a prospective, randomized clinical trial. Fertil Steril
1983;40:612-9.
80. Rosenberg SM, Board JA. High-molecular weight dextran in human infertility
surgery. Am J Obstet Gynecol 1984;148:380-5.
81. Larsson B, Lalos O, Marsk L, et al. Effect of intraperitoneal instillation of 32% 712
Curr Probl Surg, November 2012
dextran 70 on postoperative adhesion formation after tubal surgery. Acta Obstet

Gynecol Scand 1985;64:437-41.
82. Jansen RPS. Failure of intraperitoneal adjuncts to improve the outcome of pelvic
operation in young women. Am J Obstet Gynecol 1985;153:363-71. 83. Diamond MP,
Linsky CB, Cunningham T, et al. Synergistic effects of INTER CEED(TC7) and
heparin in reducing adhesion formation in the rabbit uterine horn model. Fertil Steril
1991;55:389-94.
84. Nishimura K, Shimanuki T, DiZerega GS. Ibuprofen in the prevention of experi
mentally induced postoperative adhesions. Am J Med 1984;77:102-6. 85. Holtz G.
Failure of a nonsteroidal anti-inflammatory agent (ibuprofen) to inhibit peritoneal
adhesion reformation after lysis. Fertil Steril 1982;37:582-3. 86. Eskand G. Prevention
of experimental adhesions in the rat by intraperitoneally administered corticosteroids.
Acta Chir Scand 1963;125:91.
87. Glucksman DL, Warren WD. The effect of topically applied corticosteroids in the
prevention of peritoneal adhesions: an experimental approach with a review of the
literature. Surg 1966;60:352.
88. Becker JM, Dayton MT, Fazio VW, et al. Prevention of postoperative abdominal
adhesions by a sodium hyaluronate-based bioresorbable membrane: a prospective,
randomized, double-blind multicenter study. J Am Coll Surg 1996;183:297-306.
89. Seitz HM, Schenker JG, Epstein S, et al. Postoperative intraperitoneal adhesions: a
double-blind assessment of their prevention in the monkey. Fertil Steril
1973;24:935-40.
90. Gervin AS, Puckett CL, Silver D. Serosal hypofibrinolysis: a cause of postoperative
adhesions. Am J Surg 1973;125:80-8.
91. James DCO, Ellis H, Hugh TB. The effect of streptokinase on experimental
intraperitoneal adhesion formation. J Pathol Bacteriol 1965;90:279-87. 92. Whitting
HW, Young BA. The effect of varidase in carboxymethyl cellulose jelly on peritoneal
adhesion formation. Virchows Arch Pathol Anat Physiol Klin Med 1966;341:155-63.
93. Rivkind AI, Lieberman N, Durst AL. Urokinase does not prevent abdominal
adhesion formation in rats. Eur Surg Res 1985;17:254-8.
94. Menzies D, Ellis H. Intra-abdominal adhesions and their prevention by topical tissue
plasminogen activator. J R Soc Med 1989;82:534-5.
95. Doody KJ, Dunn RC, Buttram VC. Recombinant tissue plasminogen activator
reduces adhesion formation in a rabbit uterine horn model. Fertil Steril 1989;51:509-12.
96. Menzies D, Ellis H. Adhesion prevention: the role of plasminogen activation. Surg
Gynecol Obstet 1991;172:362-6.
97. Tang CL, Seow-Choen F, Fook-Chong S, et al. Bioresorbable adhesion barrier
facilitates early closure of the defunctioning ileostomy after rectal excision: a
prospective, randomized trial. Dis Colon Rectum 2003;46:1200-7.
98. Vrijland WW, Tseng LN, Eijkman HJ, et al. Fewer intraperitoneal adhesions with
use of hyaluronic acid-carboxymethylcellulose membrane: a randomized clinical
trial. Ann Surg 2002;235:193-9.
99. Cohen Z, Senagore AJ, Dayton MT, et al. Prevention of postoperative abdominal
adhesions by a novel, glycerol/sodium hyaluronate/carboxymethylcellulose-based
bioresorbable membrane: a prospective, randomized, evaluator-blinded multicenter
study. Dis Colon Rectum 2005;48:1130-9.
100. Kusunoki M, Ikeuchi H, Yanagi H, et al. Bioresorbable hyaluronate-carboxymeth
ylcellulose membrane (Seprafilm) in surgery for rectal carcinoma: a prospective
randomized clinical trial. Surg Today 2005;35:940-5.
101. Kumar S, Wong PF, Leaper DJ. Intra-peritoneal prophylactic agents for preventing
adhesions and adhesive intestinal obstruction after non-gynaecological abdominal
surgery. Cochrane Database Syst Rev 2009;1:CD005080.
102. Fazio VW, Cohen Z, Fleshman JW, et al. Reduction in adhesive small-bowel
obstruction by Seprafilm adhesion barrier after intestinal resection. Dis Colon
Rectum 2006;49:1-11.
103. Kudo FA, Nishibe T, Miyazaki K, et al. Use of bioresorbable membrane to prevent
postoperative small bowel obstruction in transabdominal aortic aneurysm surgery.
Surg Today 2004;34:648-51.
104. Salum MR, Lam DT, Wexner SD, et al. Does limited placement of bioresorbable
membrane of modified sodium hyaluronate and carboxylmethcellulose (Seprafilm
(R)) have possible short-term beneficial impact? Dis Colon Rectum 2001;44(5):
706-12.
105. Mohri Y, Uchida K, Araki T, et al. Hyaluronic acid-carboxycellulose membrane
(Seprafilm) reduces early postoperative small bowel obstruction in gastrointestinal
surgery. Am Surg 2005;71(10):861-3.
106. Azziz R. Microsurgery alone or with INTERCEED absorbable adhesion barrier for
pelvic sidewall adhesion re-formation (The INTERCEED (TC7) Adhesion Barrier
Study Group. II). Surg Gynecol Obstet 1993;177:135-9.
107. The efficacy of Interceed(TC7)* for prevention of reformation of postoperative
adhesions on ovaries, fallopian tubes, and fimbriae in microsurgical operations for
fertility: a multicenter study (Nordic Adhesion Prevention Study Group). Fertil
Steril 1995;63:709-14.
108. Wiseman DM, Trout JR, Franklin RR, et al. Metaanalysis of the safety and efficacy
of an adhesion barrier (Interceed TC7) in laparotomy. J Reprod Med 1999; 44:325-
31.
109. Ahmad G, Duffy JM, Farquhar C, et al. Barrier agents for adhesion prevention after
gynaecological surgery. Cochrane Database Syst Rev 2008;16:CD000475. 110. Wiseman
DM, Gottlick-Iarkowski L, Kamp L. Effect of different barriers of oxidized regenerated
cellulose on cecal and sidewall adhesions in the presence and absence of bleeding. J
Invest Surg 1999;12:141-6.
111. Hellebrekers BW, Trimbos-Kemper GC, van Blitterswijk CA, et al. Effects of five
different barrier materials on postsurgical adhesion formation in the rat. Hum
Reprod 2000;15:1358-63.
112. Haney AF, Hesla J, Hurst BS, et al. Expanded polytetrafluoroethylene (Gore-Tex
surgical membrane) is superior to oxidized regenerated cellulose (Interceed® TC7
) in preventing adhesions. Fertil Steril 1995;63:1021-6.
113. Koehler RH, Begos D, Berger D, et al. Minimal adhesions to ePTFE mesh after
laparoscopic ventral incisional hernia repair: reoperative findings in 65 cases.
JSLS 2003;7:335-40.
114. Müller SA, Treutner KH, Haase G, et al. Effect of intraperitoneal antiadhesive fluids
in a rat peritonitis model. Arch Surg 2003;138:286-90.
115. Rodgers KE, Verco SJ, diZerega GS. Effects of intraperitoneal 4% icodextrin
solution on the healing of bowel anastomoses and laparotomy incisions in rabbits.
Colorectal Dis 2003;5:324-30.
116. Brown CB, Luciano AA, Martin D, et al. Adept (icodextrin 4% solution) reduces
adhesions after laparoscopic surgery for adhesiolysis: a double-blind, randomized,
controlled study. Fertil Steril 2007;88:1413-26.
117. DiZerega GS, Verco SJ, Young P, et al. A randomized, controlled pilot study of the
safety and efficacy of 4% icodextrin solution in the reduction of adhesions
following laparoscopic gynaecological surgery. Hum Reprod 2002;17:1031-8.
118. Metwally M, Watson A, Lilford R, et al. Fluid and pharmacological agents for
adhesion prevention after gynaecological surgery. Cochrane Database Syst Rev
2006;19:CD001298.
119. Mettler L, Audebert A, Lehmann-Willenbrock E, et al. A randomized, prospective,
controlled, multicenter clinical trial of a sprayable, site-specific adhesion barrier
system in patients undergoing myomectomy. Fertil Steril 2004;82:398-404.
120. Mettler L. Adhibit® adhesion prevention gel myomectomy study. In: 19th Annual
European Congress of Obstetrics and Gynecology, Turin, 2006.
121. Diamond MP, Kruger M, Saed GM. Effect of Tisseel on expression of tissue
plasminogen activator and plasminogen activator inhibitor-1. Fertil Steril
2004;81:1657-64.
122. De Virgilio C, Elbassir M, Hidalgo A, et al. Fibrin glue reduces the severity of intra-
abdominal adhesions in a rat model. Am J Surg 1999;178:577-80. 123. Peacock KE,
Hurst BS, Marshburn PB, et al. Effects of fibrin sealant on single-layer uterine incisions
closure in the New Zealand white rabbit. Fertil Steril 2006;85:1261-4.
124. Nur I, Lyahovetsky Y, Bar L, et al. Commercial fibrin sealants are not equivalent in
a rabbit liver-resection model which quantitatively evaluates hemostasis and
formation of adhesions. Eur Surg Res 2005;37:159-65.
125. Isaksson K, Akerberg D, Andersson R, et al. Toxicity and dose response of intra-
abdominally administered poly-L-alpha-lysine and poly-L-glutamate for post
operative adhesion protection. Eur Surg Res 2010;44(1):17-22.
126. Cheong YC, Laird SM, Li TC, et al. Peritoneal healing and adhesion formation/
reformation. Hum Reprod Update 2001;7:556-66.
127. Ray NF, Denton WG, Thamer M, et al. Abdominal adhesiolysis: inpatient care and
expenditures in the United States in 1994. J Am Coll Surg 1998;186:1-9. 128. Tietze L,
Elbrecht A, Schauerte C, et al. Modulation of pro- and antifibrinolytic properties of
human peritoneal mesothelial cells by transforming growth factor beta1 (TGF-beta1),
tumor necrosis factor alpha (TNF-alpha) and interleukin 1beta (IL-1beta). Thromb
Haemost 1998;79:362-70.
129. Williams RS, Rossi AM, Chegini N, et al. Effect of transforming growth factor beta
on postoperative adhesion formation and intact peritoneum. J Surg Res
1992;52:65-70.
130. Lucas PA, Warejcka DJ, Young HE, et al. Formation of abdominal adhesions is
inhibited by antibodies to transforming growth factor-beta1. J Surg Res
1996;65:135-8.
131. Holmdahl L, Kotseos K, Bergström M, et al. Overproduction of transforming
growth factor-beta1 (TGF-beta1) is associated with adhesion formation and
peritoneal fibrinolytic impairment. Surgery 2001;129:626-32.
132. Kaidi AA, Gurchumelidze T, Nazzal M, et al. Tumor necrosis factor-alpha: a
marker for peritoneal adhesion formation. J Surg Res 1995;58:516-8. 133. Reed KL,
Fruin AB, Bishop-Bartolomei KK, et al. Neurokinin-1 receptor and
substance P messenger RNA levels increase during intraabdominal adhesion
formation. J Surg Res 2002;108:165-72.
134. Sturiale S, Barbara G, Qiu B, et al. Neutral endopeptidase (EC 3.4.24.11) terminates
colitis by degrading substance P. Proc Natl Acad SciUSA 1999; 96:11653-8.
135. Zhou J, Elson C, Lee TD. Reduction in postoperative adhesion formation and re-
formation after an abdominal operation with the use of N, O-carboxymethyl
chitosan. Surgery 2004;135:307-12.
136. Costain DJ, Kennedy R, Ciona C, et al. Prevention of postsurgical adhesions with
N,O-carboxymethyl chitosan: examination of the most efficacious preparation and
the effect of N,O-carboxymethyl chitosan on postsurgical healing. Surgery
1997;121:314-9.
137. Diamond MP, Luciano A, Johns DA, et al. Reduction of postoperative adhesions by
N,O-carboxymethyl chitosan: a pilot study. Fertil Steril 2003;80:631-6. 138. Grow DR,
Coddington CC, Hsiu JG, et al. Role of hypoestrogenism or sex steroid antagonism in
adhesion formation after myometrial surgery in primates. Fertil Steril 1996;66:140-7.
139. Wright JA, Sharpe-Timms KL. Gonadotropin-releasing hormone agonist ther apy
reduces postoperative adhesion formation and reformation after adhesioly sis in rat
models for adhesion formation and endometriosis. Fertil Steril 1995;63:1094-100.
140. Coddington CCGD, Ahmed MS, Brown SE, et al. Role of gonadotropin-releasing
hormone agonist in post-operative adhesion formation after myomectomy. Fertil
Steril 2005;84(Suppl 1):S465-6.
141. Kaya U, Oktem M, Zeyneloglu HB. Impact of aromatase inhibitors on adhesion
formation in a rat model. Fertil Steril 2007;87:934-9.
142. Chau D, Mancoll JS, Lee S, et al. Tamoxifen downregulates TGF-beta production in
keloid fibroblasts. Ann Plast Surg 1998;40:490-3.
143. Alpay Z, Saed GM, Diamond MP. Female infertility and free radicals: potential role
in adhesions and endometriosis. J Soc Gynecol Investig 2006;13:390-8. 144. Sirotkin
AV, Makarevich AV, Pivko J, et al. Effect of cGMP analogues and protein kinase G
blocker on secretory activity, apoptosis and the cAMP/protein kinase A system in
porcine ovarian granulosa cells in vitro. J Steroid Biochem Mol Biol 2000;74:1-9.
145. Chiche JD, Schlutsmeyer SM, Bloch DB, et al. Adenovirus-mediated gene transfer
of cGMP-dependent protein kinase increases the sensitivity of cultured vascular
smooth muscle cells to the antiproliferative and pro-apoptotic effects of nitric
oxide/cGMP. J Biol Chem 1998;273:34263-71.
146. Batukan C, Ozgun MT, Basbug M, et al. Sildenafil reduces postoperative adhesion
formation in a rat uterine horn model. Eur J Obstet Gynecol Reprod Biol
2007;135:183-7.
147. Dinc S, Ozaslan C, Kuru B, et al. Methylene blue prevents surgery-induced
peritoneal adhesions but impairs the early phase of anastomotic wound healing.
Can J Surg 2006;49:321-8.
148. Reed KL, Fruin AB, Gower AC, et al. A neurokinin 1 receptor antagonist decreases
postoperative peritoneal adhesion formation and increases peritoneal fibrinolytic
activity. Proc Natl Acad SciUSA 2004;101:9115-20.
149. Rodgers KE, DiZerega GS. Developing pharmacologic agents for adhesion 716 Curr
Probl Surg, November 2012
prevention. In: DiZerega GS, ed. Peritoneal Surgery. New York: Springer-Verlag,
2000:441-57.
150. Chalkiadakis GE, Kostakis A, Karayannacos PE, et al. Pentoxifylline in the
treatment of experimental peritonitis in rats. Arch Surg 1985;120:1141-4. 151. Bulbuller
N, Ilhan US, Kirkil C, et al. Can angiotensin converting enzyme inhibitors prevent
postoperative adhesions? J Surg Res 2005;125:94-7. 152. Epstein JC, Wilson MS,
Wilkosz S, et al. Human peritoneal adhesions show evidence of tissue remodeling and
markers of angiogenesis. Dis Colon Rectum 2006;49:1885-92.
153. Bothin C, Midtvedt T, Perbeck L. Orally delivered antibiotics which lower bacterial
numbers decrease experimental intra-abdominal adhesions. Langenbecks Arch
Surg 2003;388:112-5.
154. Pestieau SR, Marchettini P, Stuart OA, et al. Prevention of intraperitoneal adhesions
by intraperitoneal lavage and intraperitoneal 5-fluorouracil: experimental studies.
Int Surg 2002;87:195-200.
155. Cubukçu A, Alponat A, Gönüllü NN. Mitomycin-C prevents reformation of intra-
abdominal adhesions after adhesiolysis. Surgery 2002;131:81-4.

Small Bowel Obstruction CPS 2012

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Small Bowel Obstruction CPS 2012

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New Paradigms in the Treatment of

Small Bowel Obstruction

Scope of the Problem

Curr Probl Surg 2012;49:642-717.

642 Curr Probl Surg, November 2012

TABLE 2. Small bowel obstruction in the United States

disease, intussusception, radiation, endometriosis, infection, and foreign

efferent portions of a single loop of bowel are occluded by a constrictive

Pathophysiology of SBO and Adhesion

Biological Pathways That Lead to Adhesion Formation

covers the surface of the peritoneal cavity and the intra-abdominal

Curr Probl Surg, November 2012 649

Mediators Involved in Adhesion Formation

Strategies for Adhesion Reduction

Physiology of Small Bowel

loss of fluid and electrolytes. Second, distention increases intestinal

Intestinal Blood Flow

Alterations of Intestinal Motility

Changes in the Microflora

air-fluid levels in inverted U-shaped loops of small intestine (Fig 7).33

B). A CT scan of the abdomen provides valuable information and is part

is now generally recognized as a particularly dangerous cause of

death with the induction of general anesthesia. Commonly, the deficit of

are metabolic (contraction) alkalosis (related to maximal renal sodium

Imaging Studies in SBO. Traditionally, an abdominal series or obstruc

a “complete” bowel obstruction by the radiologist, more than 80% will

monic: distal SBO and pneumobilia. Occasionally, the obstructing gall

FIG 17. Venous air (arrows) associated with pneumatosis.

668 Curr Probl Surg, November 2012

tis. Two recent meta-analyses have examined the benefit of gastrograffin

672 Curr Probl Surg, November 2012

Curr Probl Surg, November 2012 673

abdominal tenderness with guarding (P 0.009); WBC 10,000/mL (P

scan in approximately 50% of patients with SBO and may be more

include a tumor, intussusception, and previously undiagnosed Crohn’s

represent another challenging clinical scenario. These patients have a

TABLE 6. Principles of clinical management of small bowel obstruction (SBO)

the issues of etiology, the degree of obstruction (partial or complete), and

Laparoscopic Treatment of SBO

foreign bodies). All the aforementioned can initially be approached via

laparoscopically, direct conversion to limited laparotomy can be

Author Number (%) Conversion Complication (%) LOS (Days)

Interestingly, the recurrences were in the laparoscopic group, and no

Contemporary Progress in Preventing Adhesive SBO

TABLE 10. Interval from operation to adhesive obstruction

TABLE 13. Strategies for preventing adhesions

Seprafilm was liberally placed at every site serosal or peritoneal injury

Agent Company Composition Form Use Studies Comment

Preclude Gortex PTFE Sheet Adnexae Animal/human Non-absorb

well-designed studies have been conducted to assess its efficacy. 122-124

Agent Company Composition Form Use Studies Comment

Carbylan-SX Carbylan Biosurgery glycosamino-glycan than Seprafilm in

Spraygel (spray shield) Appears to be gynecologic

dextran 70 on postoperative adhesion formation after tubal surgery. Acta Obstet

Curr Probl Surg, November 2012 717

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