Nuevos Paradigmas en El Tratamiento de Obstruccion Intestinalk

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 procedures 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 difcult 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 Wisemans1 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 oat 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. Bevans review found that 1.9% of all hospital admissions were due to bowel obstruction.3 Menzies and Ellis identied 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 conrmed that 3% of all laparotomies are performed for adhesive obstructions alone.4 In the United States in a
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TABLE 1. History of small bowel obstruction Date 2500 BC 440 BC 1750 AD 1842 AD 1932 AD 1934 AD SBO, small bowel obstruction. Event Ancient Egyptians describe adhesions Pleural adhesions described in Talmud Hunter describes adhesions due to peritonitis Bryant describes fatal bowel obstruction Adhesions cause 7% of SBO in United Kingdom Adhesions cause 27% of SBO in the United States
TABLE 2. Small bowel obstruction in the United States Cause (%) Author Playforth9 Laws10 Stewardson11 Bizer12 Year 1970 1976 1978 1981 Adhesions 54 69 64 74 Hernia 23 8 24 8 Cancer 9 10 7 9 Number 111 465 238 405
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 signicantly 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, nding 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 conrms that in the United States, adhesions constitute the major source of SBO by a large margin9-12 (Table 2). Other causes of SBO include hernia (most common cause of SBO in undeveloped countries), cancer, inammatory bowel
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TABLE 3. Lexicon of small bowel obstruction Less serious Partial Low grade Simple Low Ileus Chronic Intrinsic More serious Complete High grade Closed loop High Mechanical Acute 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.
Classication of SBO
Small bowel obstruction may be classied in a variety of ways, and a lexicon unique to SBO has developed over the years (Table 3). Small bowel obstruction may be classied 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 signicantly distended bowel associated with failure to pass stool or atus 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 atus 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 signicant bowel distention, little to no atus 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 atus and stool, and much less pain and discomfort. It frequently resolves with watchful waiting. A simple bowel obstruction is dened as SBO in which the bowel is occluded at a single point along its length, whereas a closed loop obstruction is dened as an obstruction in which both the afferent and
644 Curr Probl Surg, November 2012
FIG 1. Artists 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 dened 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 obstructions 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 Crohns disease, tumors, radiation injury, hematoma, and intussusception.
Pathophysiology of SBO and Adhesion Formation

Adhesion Formation
Abdominal adhesions are abnormal brous 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, inammation, 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 peritoneum 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 brin deposition and degradation (i.e., brinolysis) seems to be the critical factor in adhesion formation. Fibrin deposition at the surgical site is a requirement for adhesions to form. If brinolysis proceeds unimpeded, formation of postoperative adhesions is greatly reduced; unfortunately, many variables, 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 eld phenomenon 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 eld 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 gure. (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 gure 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 inammation, peritoneal wound healing, and adhesion formation.16,17 Adhesion formation begins with trauma to the peritoneum and the induction of a generalized peritoneal inammatory response (Fig 4). As a component of the response to injury and the coagulation cascade, a brin-rich exudate accumulates on injured peritoneal surfaces.18 This brin-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 brin-rich exudate is resolved by the normally active, peritoneal brinolytic system. However, abdominal surgery often suppresses peritoneal brinolytic 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 inammatory, 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 ScienceBusiness Media from DiZerega GS, ed. Peritoneal Surgery. New York: Springer-Verlag, 2000.)
FIG 4. Generalized peritoneal inammatory response associated with injury. Note the rise and time course for brin and mesothelial cells. (Reprinted with kind permission of Springer ScienceBusiness 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 brinrich exudate through which mesothelial cells can migrate and accomplish 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)
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This brin-rich exudate is a tacky substance and causes adjacent organs or injured serosal surfaces to coalesce.21 Under normal circumstances, the formation of a brin matrix during wound healing is only temporary, and degradation of these lmy brinous adhesions by locally released proteases of the brinolytic 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 surfaces.13,22 If brinolysis does not occur within 5-7 days of peritoneal injury, or if local brinolytic activity is reduced, the brin matrix persists.17 If this occurs, the temporary brin matrix gradually becomes more organized as collagen-secreting broblasts and other reparative cells inltrate the matrix.14,17
Mediators Involved in Adhesion Formation

The newly recruited inammatory cells release a host of inammatory 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 brinolysis and adhesion formation. Transforming growth factor (TGF-B) has been identied as having a role in adhesion development by promoting brosis and also mesothelial cell proliferation rather than brinolysis.23 Interleukin-1 has also been linked to adhesion formation as an inhibitor of brinolysis via stimulation of PA-I.24 Substance P, a tachykinin peptide promotes adhesion formation by inhibiting brinolysis via decreasing the amount of t-PA in the peritoneum.18 For a comprehensive summary of the mediators, 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 rst are the pharmacological therapies given around the time of the patients operation. The second encompasses topical products applied directly to the operative site. Attard and Maclean have identied 6 mechanisms by which adhesion formation can be disrupted (Table 4): (1) decreasing peritoneal damage, (2) decreasing the early inammatory response, (3) prevention of brin formation, (4) increasing brinolysis, (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 inammatory response Prevention of brin formation Increasing brinolysis Preventing collagen deposition Providing barriers to adhesion formation
There is sound logic behind the use of such agents, although their effectiveness 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 adhesions by interfering with brin deposition: nonsteroidal anti-inammatory drugs (NSAIDs), heparin, and corticosteroids. NSAID action targets prostaglandin synthesis, decreasing the inammatory 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 inammatory 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 difcult to overcome for these agents. Therapeutic anticoagulation to prevent brin deposition or the use of streptokinase to promote brinolysis has not had a signicant 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 inammation and optimize brinolysis postoperatively 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 visceraland 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 signicantly 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 obstruction by focusing on these key components: intraluminal gas, intestinal uid, the microora, the blood ow, and intestinal motility. Small bowel obstruction affects the physiology of the normal intestine and has systemic effects due to changes in uid and electrolyte balance, uid shifts from one space to another, and hemodynamic changes secondary to hypovolemia and dehydration. Simple mechanical obstruction of the small intestine causes the accumulation of gas, uid, 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 sulde 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 atus.33 With mechanical intestinal obstruction, 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 uid 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 uid is reabsorbed by the small intestine, as only approximately 1 L of uid enters the colon from the ileum daily.33 In mechanical obstruction, the intestine proximal to the site of obstruction lls with uid and gas. This uid is not absorbed as in the normal intestine, and the distended bowel over time begins to secrete uid rather than absorb uid and contributes to a state of intravascular dehydration or hypovolemia. Loss of uid 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 reex vomiting leading to the
loss of uid and electrolytes. Second, distention increases intestinal secretion with movement of uid 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 uid into the lumen of the obstructed bowel. This phenomenon compounds the problem of distention and uid movement into the lumen. In addition, uids 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 uid and electrolytes into the intestinal lumen.37 A third route of uid 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 uid from the intravascular space is by transudation of uid through the serosal surface into the peritoneal cavity to produce free intraperitoneal uid.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 uid accumulation.39 In simple open-loop obstruction, distention of the lumen by gas and uid rarely leads to luminal pressures higher than 8-12 cm (H2O).40 Thus, in open-loop obstruction, the contributions of high luminal pressures to uid hypersecretion may not be as important.41 Accumulation of uid in this third space accounts for the dehydration 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 uid loss depend on the site and duration of the obstruction. With a proximal obstruction, dehydration may be accompanied by hypochloremia, hypokalemia, and metabolic alkalosis associated with increased vomiting. Distal obstruction of the small bowel may result in large quantities of intestinal uid into the bowel. Oliguria and hemoconcentration 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 gure is available online.)
Intestinal Blood Flow

Intestinal blood ow is inuenced by luminal pressure, mesenteric ow, and systemic blood pressure. As the intraluminal pressure increases in the bowel, a decrease in mucosal blood ow can occur. With ongoing gas and uid 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 obstruction32 (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 gastrointestinal 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 Microora

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 ora 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 ora. 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 translocation on the clinical course is not clear.42 If the intestinal wall loses viability, altered intestinal permeability can allow bacteria and bacterial 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 nonspecic pain to orid peritoneal signs related to strangulation and bowel perforation. However, classic symptoms of bowel obstruction include nausea and vomiting, a distended abdomen, colicky abdominal pain, and alteration in atus 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 ndings 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 difcult 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 ndings 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 gastrointestinal tract. Gastric content, liquids, and intestinal uids 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 uid 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 ofce 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 abdominal 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/uid levels in inverted U-shaped loops with associated small bowel distention in adhesive SBO. Arrow points to one of many air/uid lled levels in this abdominal xray. (Reprinted with permission from WetPaint, http://wikiradiography.com/page/SmallBowelObstruction.)
air-uid 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 derange658 Curr Probl Surg, November 2012
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/SmallBowelObstruction.)
ments, sepsis, organ failure, and drug and medication toxicity each can contribute to an ileus. Many drugs affect the sympathetic and parasympathetic 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 radiographic examinations. First, the plain lms 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 benet 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 patients 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 rst sees the patient in the ofce or the emergency department. The symptoms of SBO are abdominal distention, crampy abdominal pain, nausea, vomiting, and constipation. Vomiting, bilious or feculent, is common, 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 nger 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 rst 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/#/abdominalx-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 resuscitation or an exploratory laparotomy rst. 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 approximately 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/LargeBowelObstruction.)
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 ndings 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 decits 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 decit of isotonic uid 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 ndings. 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 (Petersons 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 hypoperfusion, 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 obstruction 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-uid 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-uid 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-uid 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 nonspecic (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, ndings on plain radiographs may be pathogno666 Curr Probl Surg, November 2012
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/SmallBowelObstruction.)
monic: distal SBO and pneumobilia. Occasionally, the obstructing gallstone is visualized if it contains adequate calcium to render it sufciently radio-opaque. Finally, when there is a preponderance of luminal uid 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 veried by the patient and caregivers that the patient is not completely obstipated, the onus is on the surgeon to document radiologically 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 gastrografn, followed by serial plain abdominal radiographs. If the contrast reaches the cecum in 24 hours, the obstruction is partial and it is very likely
FIG 16. Pneumatosis in the bowel wall (arrows) associated with necrotic bowel secondary to an
SBO. (Reprinted with permission from Kernagis LY, Levine MS, Jacobs JE, et al. Pneumatosis intestinalis in patients with ischemia: correlation of CT ndings with viability of the bowel. Am J Roentgenol 2003;180:733-6.)
FIG 17. Venous air (arrows) associated with pneumatosis.
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FIG 18. Gastrografn 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 gastrografn can lead to the resolution of SBO. Gastrografn 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 pneumoniCurr Probl Surg, November 2012 669
FIG 19. Barium small bowel follow-through revealing a tight stricture (arrow) in the terminal ileum in a patient with partial SBO and known Crohns disease.
tis. Two recent meta-analyses have examined the benet of gastrografn 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% specic 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 benecial effect of gastrografn 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 gastrografn. It can be concluded that the oral administration of gastrografn should be considered in patients with SBO who do not obviously require urgent operation on the basis of clinical and radiologic ndings. Small bowel follow-through using barium is often very helpful in the evaluation of potential SBO due to Crohns disease. In this patient with known Crohns disease, small bowel follow-through identied 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 uid-lled loops with or without peristalsis are readily apparent on ultrasound. Gallstones and
air in the gallbladder suggest gallstone ileus. The absence of abdominal uid 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 specicity 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 specicity 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, Crohns disease (Fig 24) metastatic cancer, primary tumor, or ischemia and signs of bowel compromise such as pneumatosis intestinalis or pneumoperitoneum (Fig 25). Schwenter and colleagues showed on multivariate analysis that the following factors predicted the need for bowel resection in patients with bowel obstruction: the presence of more than 500 mL of ascites on CT (P 0.002); reduction of CT bowel wall enhancement (P 0.011); abdominal pain for 4 days (P 0.007);
FIG 20. CT scan demonstrating SBO with a clear transition zone (arrow) followed by collapsed bowel. (Reprinted with permission from Cameron JL. Current Surgical Therapy (ed 8). Philadelphia, PA: Mosby, 2004.)
FIG 21. Internal hernia after gastric bypass with dilated loops of small bowel and classic mesenteric
swirl (arrow).
672
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.)
673
FIG 24. Patient with a history of subtotal colectomy for Crohns disease and an ileocolostomy presented with a high-grade partial SBO. CT scan reveals recurrent Crohns 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 compromised 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 nding 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 uid 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 patients pain symptoms on physical examination. While the uid 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 SBOhigh grade Partial SBOlow grade Bowel obstruction in virgin abdomen Recurrent SBO SBO immediately after surgery SBO in patient with known malignancy SBO in patient with Crohns 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-lled 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 efcacy 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 controversial. 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 SBOlow 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 Crohns 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 difcult 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 signicantly 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 signicantly distended bowel and crampy abdominal 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 atus (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 occasionally a CT scan will conrm the point of obstruction and edema of the bowel proximal to the obstruction. The category of patients who have a low-grade partial SBO characteristically 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 improvement 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 benet 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 resolution of air-uid levels, the patient may be cautiously placed back on clear liquids and advanced to a low-ber 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/SmallBowelObstruction.)
include a tumor, intussusception, and previously undiagnosed Crohns 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 exploration, the area of intussusception almost always requires resection so the leading point of the intussusception can be surgically removed. Finding obstructing Crohns 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 laparotomies, a number of which were for lysis of adhesions. Often, the most recent operation is described as a very difcult 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 population requires a good deal of thought. The surgeon should schedule no other major cases on a day in which 1 of these difcult 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 authors 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 Stammtype gastrotomy and with the balloon inated 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 deated 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 Crohns 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 inating the balloon in the cecum to prevent retrograde retraction. The tube can be removed 3 weeks postoperatively. (Color version of gure is available online.) (Courtesy of Teleex 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 difculty 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 nal area of concern is the patient who presents with bowel obstruction with known intra-abdominal malignancy or in whom recurrent 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 Crohns disease. The CT scan demonstrates dramatic luminal narrowing caused by active inammation.
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 difcult 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 inuences 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 sucCurr Probl Surg, November 2012 681
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 dened, 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 lmy 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 identied. 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 eld 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 uorescein 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 identied, 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 lmiest and the bowel most easily identied, and work to the more difcult 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 denitive 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, lmy 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 ow to the bowel and make abdominal closure easier. The simplest way to manage decompression is to place the bowel between the second and third ngers, and while gently squeezing, milk the uid 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 accomplished 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 inatable 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 materials, 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 laparoscopically, 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 eld was able to be visualized only by the operative surgeon, who held the laparoscope in 1 hand and operated with the other. The rst reports of laparoscopic surgery for adhesiolysis were in the gynecologic literature, mostly for infertility due to mbrial 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 eld. After the computer chip digital camera was coupled to the laparoscope in the 1980s, the entire operative team was able to visualize the operative eld, 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 laparoscopic surgeon improved, and as the equipment became better, more difcult 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 rst 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 (especially 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 gure is available online.)
foreign bodies). All the aforementioned can initially be approached via laparoscopy. The most obvious advantages of performing laparoscopy rather than open surgery for SBO include avoiding laparotomy, and therefore the postlaparotomy recovery, as well as minimizing the postoperative risks of laparotomy-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 magnied 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 signicantly 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 appendectomies 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 directly 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%), adenocarcinoma of the colon (13.1%), Crohns disease of the small bowel (5.1%), colonic diverticulitis (5.1%), internal hernias (3.4%), ischemic or radiation-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 laparoscopically without conversion to laparotomy. The conversion rate was 7.8%. Inability to visualize and control the operative eld 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%), signicant intestinal ischemia with necrosis (8%), and an iatrogenic 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 inadvertent 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 specied). 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 instrumentation. 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 complications 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 difcult than open surgery include reduced operative space and difculty with anterograde or retrograde voiding of the intestinal contents (ie, milking out the intestinal contents). They also recommend that laparoscopic 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 consecutive patients who underwent laparoscopic exploration for SBO between 1998 and 2003.60 Diagnosis was made by gastrografn upper gastrointestinal (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 openreferred 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 difculties. Three patients in each group had an iatrogenic bowel injury, which did not reach statistical signicance. 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 algorithm 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 review of all patients undergoing laparoscopic adhesiolysis between 1997 and 2006.61 All 33 laparoscopic operations were performed by experienced laparoscopic surgeons. They reported that contraindications to a laparoscopic approach were massive distension, a rm scarred abdomen, or peritonitis. They noted that 66.6% of the patients treated laparoscopically had signicant 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 insufcient 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 postoperative complications (21.2%), including urinary tract infection (2), wound infection (2), renal insufciency (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 identied several clinical predictors for the successful laparoscopic management of adhesive SBO, including SBOs that temporarily 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 treatment 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 insufate more than 1 L of CO2. Success was also more likely if the obstructed segment was not xed 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 signicant 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 laparoscopically.62 Of the 11 patients converted to open surgery, the causes were dense adhesions (4/11), inability to nd 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 specied 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 signicance 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 signicantly decreased OR time, less blood loss, and shorter length of stay. The authors stated that the overall number of complications contributing to morbidity were signicantly lower in those who underwent laparoscopic 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 identied 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 necessitating 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 retrospective 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) Conversion (%) 8% 41% 33% 12% 32% 19% 33% Complication (%) 22% 10% 24% 39% 4% 15% Ileus resolved (Days) 2 2 3.2 3.2 LOS (Days) 5 4 3.9 6 4.6
Author Franklin58 Levard59 Lujan60 Zerey61 Chopra62 Tierris63 Ghosheh65
Number 167 308 61 33 285 32 1061
Conversion reason Massive dilation Intestinal necrosis Massive adhesions Massive dilation Dense adhesions Dense adhesions Dense adhesions
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 signicance. 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%), unidentied etiology (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 (dened 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 operation in patients presenting for laparoscopic colorectal surgery. The authors were interested specically 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 signicant 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 signicant 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 uid in the bowel, and decrease bowel distension. The heavy uid-lled bowel is difcult to handle as compared with air-lled 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 laparoscopic procedure. The arms should be tucked at the patients 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 performed. 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 ow CO2 insufator will allow for maintenance of pneumoperitoneum. On initial assessment of the peritoneal cavity, if adhesions are extensive, 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 benets 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 exemplies 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 minimizing 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 avoiding 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 laparoscopically, conversion to the open operation is part of the spectrum of a surgeons 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 hydrootation of the bowels was
TABLE 8. Location of postoperative adhesions Adhesion site Omentum to incision site Operative site alone Omentum to operative site Small bowel to incision site Small bowel to operative site Small bowel to small bowel Other Number of patients 170 57 47 42 33 17 31
Reprinted with permission from Menzies and Ellis,4 The Royal College of Surgeons of England.
described in the late 1880s. An agent called brinolysin (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-beaters skin, shark peritoneum, lanolin, chyme, amniotic membrane, and sh bladder. The sheer number of agents studied conrms their lack of efcacy 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 procedures most likely to result in clinically signicant 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 rst 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 Appendectomy Rectal surgery Gynecological surgery Left colon Total colon Right colon Cholecystectomy Duodenal ulcer Unknown Other Number 12 12 11 8 7 4 4 4 8 10
TABLE 10. Interval from operation to adhesive obstruction Interval from operation 1 mo 1 mo-1 y 1-5 y 5-10 y 10 y Unknown Percent 21 17 21 6 21 12
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 generally 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 lled 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 1886 1892 1902 1905 1920 1940 1957 1994 Rubbing oil used to prevent adhesions Saline hydrooatation described Fibrinolysin (sodium salicylate and thiosinamine) marketed Gum Arabic used as visceral lubricant Cargile (bovine cecal peritoneum) introduced Intra-abdominal proteases described Heparin rst studied Amfetin (amniotic uid) marketed Sepralm studied in prospective randomized trial
TABLE 12. Other agents used to diminish adhesions Oral phosphorus Collodion Physostigmine Liquid petroleum Omental grafts Metal foils Shark skin Lanolin Chyme Fish bladder Peritoneum Gold-beaters skin
TABLE 13. Strategies for preventing adhesions Irrigants Anticoagulants Anti-inammatories Fibrinolytics Cellular modication 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 difculty in solving this clinical conundrum.
Irrigants
As previously mentioned, both normal saline and lactated Ringers solution have been used to ll the peritoneal cavity at the end of a case.
The presumption has been that oating 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 conducted evaluating hydrootation as a method to reduce adhesions postoperatively. In the meta-analysis of the aforementioned studies, Wiseman and colleagues reported that no signicant difference was seen between control and experimental groups.78
Anticoagulants
A large number of studies have been conducted to assess the efcacy of anticoagulants in preventing adhesive SBO. A number of investigations have evaluated dextran 70 as a possible antiadhesion irrigant. The benecial effects of dextran were observed in several animal studies. Indeed, 2 prospective clinical studies in humans demonstrated some efcacy of dextran in preventing pelvic adhesions, which cause infertility.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-Inammatory Agents
Nonsteroidal anti-inammatory 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 postoperative 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 developed 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 investigators 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 brinolytic 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 Sepralm (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 efcacy 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 assessment 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 signicantly 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 eld for incidence, severity, and complications of adhesions. The investigation reported a signicant decrease in severity but not incidence of adhesions (OR, 0.34; 95% condence 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 Sepralm 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 signicant 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 signicantly 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 Sepralm revealed that use of the membrane signicantly reduced the extent and incidence of adhesions.101 Although the early studies of Sepralm were conducted to ascertain the membranes efcacy 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. Efcacy of Sepralm in reducing small bowel obstruction (SBO) Study type PRCT Retro Retro Retro Patient no. 1701 438 368 51 Incidence of SBO (%) (Con vs. Rx) 12 vs. 12 6.1 vs. 4.5 14.2 vs. 6.5* 20 vs. 0* Re-operation for SBO (%) (Con vs. Rx) 3.4 vs. 1.8* 3.9 vs. 1.5 4.4 vs. 1.6 Septic complications (Con vs. Rx) 3 vs. 4 1.1 vs. 3.4 13 vs. 15
Author Fazio102 Salum104 Mottri105 Kudo103
Journal DCR DCR Am Surg Surg Today
*p 0.05.
Sepralm 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 signicantly 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 Sepralm group and 20% in the no-membrane group (P 0.05).103 Thus, the debate regarding use of Sepralm to prevent SBO continues (Table 14). What can be said is that Sepralm 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 rst 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 uid. The gelatinous material persists during adhesion formation and is nally 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 Similarly, 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 signicant reduction in the incidence and severity of adhesions on the membrane-wrapped side.107 A host of smaller studies and 2 meta-analyses108,109 conrm that Interceed reduces the incidence 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 signicant clinical benet in preventing SBO, Interceed is rarely used by general surgeons today.
Expanded Polytetrauoroethylene
Polytetrauoroethylene is widely used in vascular surgery and has been used to prevent pelvic adhesions in women with adhesion-related infertility. It is an extremely inert nonabsorbable membrane that generates minimal inammatory reaction after placement. The membrane is occasionally 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 efcacy 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 abdominal 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, Deereld, 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 signicantly.114,115 In a large multicenter, prospective, randomized, double-blind study by Brown and colleagues, Adept was compared with lactated Ringers solution in women undergoing laparoscopic gynecologic surgery for adhesiolysis. At a second laparoscopy 4 to 8 weeks later, the icodextrin solution was signicantly 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 (Conuent 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 statistical signicance 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 experimental trial involving patients undergoing myomectomy surgery.120
Fibrin Glues
Some anecdotal observations in operative elds in which brin glues were utilized demonstrated a paucity of adhesions during reoperative surgery. These preparations consist of brinogen and thrombin and, when mixed, produce tenaciously adherent gelatinous brin. Studies reveal that brin increases t-PA and PA-I by peritoneal cells121 and may impact adhesion formation. However, experimental studies are conicting and few
TABLE 15. Preventing adhesions

FDA-approved barrier agents Agent Interceed Sepralm Company J&J Genzyme Composition Oxidized cellulose Hyaluronate carboxymethylcellulose PTFE Glycolated polymer Icodextrin Form Sheet Sheet Use Adnexae Peritoneum Studies Animal/human Animal/human Comment Ineffective in blood Brittle
Preclude Repel
Gortex Synthemed
Sheet Gel
Adnexae Pericardium
Animal/human Animal/human
Adept
Baxter
Liquid
Peritoneum
Animal/human
Non-absorb Approved in the United States Mixed results
FDA, Food and Drug Administration; PTFE, polytetrauoroethylene.
well-designed studies have been conducted to assess its efcacy.122-124 Another disadvantage of brin glue is an exorbitant expense, as well as an awkward application process. In summary, barrier products come the closest to an effective antiadhesion 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 demonstrated its ability to reduce adhesions without weakening the anastomosis 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 nd any role in preventing intra-abdominal adhesions.
Inammatory Mediators
Extensive research has been done looking at the role of inammatory 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 brinolysis.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 brinolytic activity, and thus, may worsen adhesion formation.128,129 In one animal study, an antibody neutralizing TGF- resulted in signicant reduction in adhesions130 possibly through regulation of PAI-1.131
TABLE 16. Preventing adhesions

Barrier agents being studied (NOT FDA-Approved) Agent Intergel Company Lifecore Composition Ferrous hyaluronan Form Gel Use Peritoneum Studies Animal/ human Animal/ human Animal/ human Animal Animal Animal Animal/ human Animal Comment Allergic reactions: withdrawn from market FDA problems Used in spinal surgery Withdrawn from US market Prevents tendon adhesions Mixed results More effective than Sepralm in animal studies Unique mechanism Appears to be effective in gynecologic surgery; used in Europe Effective in gynecologic surgery; used in Europe
Adcon P Flogel Incert Hylans Caprolactone Hyskon Carbylan-SX
Gliatech Alliance Anika Inamed Solvay Medisan
Polyglycan esters Poloxamer Modied hyal acid Hyaluronic modication Cyclic lactone ester Dextran
Liquid Gel Gel Liquid Liquid Liquid Gel
Peritoneum Peritoneum Peritoneum Joints Peritoneum Peritoneum Peritoneum
Carbylan Cross-linked Biosurgery glycosamino-glycan Ab against alpha V beta 3 integrins Polyethylene glycol
LM 609 Scripps Clinic Spraygel (spray shield)
Liquid Liquid
Covidien
Vocal cord, Pericardium Peritoneum
Animal Animal/ human
Adhibit
Angiotech
Fibrin-based
Gel
Peritoneum
Animal/ human
FDA, Food and Drug Administration.
Other studies suggest that IL-1 contributes to a decrease in brinolytic 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 signicantly fewer adhesions than in controls.132 A well-known neuropeptide substance P (SP) has recently been recognized as having some actions that might impact adhesion formation. SP has been detected in neurons found in adhesions and is a well-known inammatory 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 therapeutically, further study is justied 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-carboxymethylchitosan (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 evaluations. 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 signicant 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 phosphodiesterase-5 results in breakdown of cGMP, which leads to decreased collagen production and broblast apoptosis.144,145 An inhibitor of phosphodiesterase-5, sildenal, 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 anastomotic 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 signicantly reduced adhesions.148 In the same study, investigators gave the NK-1R antagonist and found that it lead to a signicant 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-inammatory 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 angiogenesis inhibitors,152 some antibiotics,153 and chemotherapeutic agents, such as 5-uorouracil, 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 function.
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Nuevos Paradigmas en El Tratamiento de Obstruccion Intestinalk

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New Paradigms in the Treatment of Small Bowel Obstruction

Scope of the Problem

Curr Probl Surg, November 2012

Pathophysiology of SBO and Adhesion Formation

Biological Pathways That Lead to Adhesion Formation

Curr Probl Surg, November 2012

Mediators Involved in Adhesion Formation

Strategies for Adhesion Reduction

Laparoscopic vs. Open Surgery and Adhesions

Physiology of Small Bowel Obstruction

Intestinal Blood Flow

Alterations of Intestinal Motility

Changes in the Microora

Evaluation of SBO in the Gastric Bypass Patient

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

Curr Probl Surg, November 2012

Curr Probl Surg, November 2012

Curr Probl Surg, November 2012

Operative Management and Technical Considerations

Laparoscopic Treatment of SBO

Comparison of Open and Laparoscopic Treatment of SBO

Author Franklin58 Levard59 Lujan60 Zerey61 Chopra62 Tierris63 Ghosheh65

Number 167 308 61 33 285 32 1061

Techniques for Laparoscopic Surgery for SBO

Techniques for Adhesiolysis

Contemporary Progress in Preventing Adhesive SBO

Author Fazio102 Salum104 Mottri105 Kudo103

Journal DCR DCR Am Surg Surg Today

Oxidized Regenerated Cellulose

TABLE 15. Preventing adhesions

Non-absorb Approved in the United States Mixed results

FDA, Food and Drug Administration; PTFE, polytetrauoroethylene.

TABLE 16. Preventing adhesions

Adcon P Flogel Incert Hylans Caprolactone Hyskon Carbylan-SX

Gliatech Alliance Anika Inamed Solvay Medisan

Liquid Gel Gel Liquid Liquid Liquid Gel

Peritoneum Peritoneum Peritoneum Joints Peritoneum Peritoneum Peritoneum

LM 609 Scripps Clinic Spraygel (spray shield)

Vocal cord, Pericardium Peritoneum

Animal Animal/ human

FDA, Food and Drug Administration.

84. 85. 86. 87.

90. 91. 92.

93. 94. 95. 96. 97.

Curr Probl Surg, November 2012

141. 142. 143. 144.

150. 151. 152.

Curr Probl Surg, November 2012

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