Obstruccion Intestinal PDF

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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642 Curr Probl Surg, November 2012

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
Laws10 1976 69 8 10 465
Stewardson11 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 H2O 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 ⱕ24 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 ⱖ4 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
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 CO2. 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
Conversion Complication resolved LOS
Author Number (%) Conversion reason (%) (Days) (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 colleagues67 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 Ellis76,77 (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)
Incidence of Re-operation Septic
Study Patient SBO (%) for SBO (%) complications
Author Journal type no. (Con vs. Rx) (Con vs. Rx) (Con vs. Rx)
Fazio102 DCR PRCT 1701 12 vs. 12 3.4 vs. 1.8* 3 vs. 4
Salum104 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 cells121 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 Sheet Peritoneum Animal/human Brittle
carboxymethyl-
cellulose
Preclude Gortex PTFE Sheet Adnexae Animal/human Non-absorb
Repel Synthemed Glycolated Gel Pericardium Animal/human Approved in
polymer the United
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
adhesions130 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/ Allergic reactions:

human withdrawn from
market
Adcon P Gliatech Polyglycan esters Liquid Peritoneum Animal/ FDA problems
human
Flogel Alliance Poloxamer Gel Peritoneum Animal/ —
human
Incert Anika Modified hyal acid Gel Peritoneum Animal Used in spinal
surgery
Hylans Inamed Hyaluronic Liquid Joints Animal Withdrawn from US
modification market
Caprolactone Solvay Cyclic lactone ester Liquid Peritoneum Animal Prevents tendon
adhesions
Hyskon Medisan Dextran Liquid Peritoneum Animal/ Mixed results
human
Carbylan-SX Carbylan Cross-linked Gel Peritoneum Animal More effective than
Biosurgery glycosamino-glycan Seprafilm in
animal studies
LM 609 Scripps Ab against alpha V Liquid Vocal cord, Animal Unique mechanism
Clinic beta 3 integrins Pericardium
Spraygel (spray Covidien Polyethylene glycol Liquid Peritoneum Animal/ Appears to be
shield) human effective in
gynecologic
surgery; used in
Europe
Adhibit Angiotech Fibrin-based Gel Peritoneum Animal/ Effective in
human gynecologic
surgery; used in
Europe
FDA, Food and Drug Administration.
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.
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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

Author Year Adhesions Hernia Cancer Number

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 Formation

Biological Pathways That Lead to Adhesion Formation

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

Curr Probl Surg, November 2012 649

Physiology of Small Bowel Obstruction

Intestinal Blood Flow

Alterations of Intestinal Motility

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 of

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

laparoscopically, direct conversion to limited laparotomy can be performed in

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

Contemporary Progress in Preventing Adhesive SBO

described in the late 1880s. An agent called “fibrinolysin” (thiosinamine and

TABLE 10. Interval from operation to adhesive obstruction

TABLE 12. Other agents used to diminish adhesions

TABLE 13. Strategies for preventing adhesions

Seprafilm was liberally placed at every site serosal or peritoneal injury

Agent Company Composition Form Use Studies Comment

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

Agent Company Composition Form Use Studies Comment

Intergel Lifecore Ferrous hyaluronan Gel Peritoneum Animal/ Allergic reactions:

FDA, Food and Drug Administration.

Other studies suggest that IL-1 contributes to a decrease in fibrinolytic

Curr Probl Surg, November 2012 717

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