Small-Bowel Obstruction

Practice Essentials

Small-bowel obstruction (SBO) is caused by a variety of pathologic processes. The most common cause of SBO in developed countries is intra-abdominal adhesions, accounting for approximately 65% to 75% of cases, followed by hernias, Crohn disease, malignancy, and volvulus.^[1]  In contrast, SBO in developing countries is primary caused by hernias (30-40%), adhesions (about 30%), and tuberculosis (about 10%), along with malignancy, Crohn disease, volvulus, and parasitic infections.^[2] The general trend in developing countries is an increased incidence of SBO from adhesions, with a higher incidence of laparotomies. See the image below.

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Small bowel obstruction. Image courtesy of Ademola Adewale, MD.

See Can't-Miss Gastrointestinal Diagnoses, a Critical Images slideshow, to help diagnose the potentially life-threatening conditions that present with gastrointestinal symptoms.

Signs and symptoms

Symptoms of SBO can be characterized as either partial or complete versus simple or strangulated. The classic symptoms of nausea, vomiting, abdominal pain, and constipation are rarely present in all cases of SBO. Abdominal pain associated with SBO is often described as crampy and intermittent. Without treatment, the abdominal pain can increase as a result of bowel perforation and ischemia. Therefore, having a clinical suspicion for the condition is paramount to early identification and intervention. Furthermore, the clinical presentation of the patients varies and no one clinical symptom on its own identifies the majority of patients with SBO. Some studies have suggested that the absence of passage of flatus and/or feces and vomiting are the most common presenting symptoms, with abdominal discomfort/distention the most frequent physical examination findings.^[3] Other studies have shown that abdominal pain is present in the majority of patients found to have SBO. 

Some signs and symptoms associated with SBO include the following:

• Nausea/vomiting (60-80%): The vomitus can often be bilious in nature 
• Constipation/absence of flatus (80-90%): Typically a later finding of SBO
• Abdominal distention (60%)
• Fever and tachycardia: Late findings and may be associated with strangulation

Some risk factors associated with SBO include the following:

• Previous abdominal or pelvic surgery, previous radiation therapy, or both: May be part of the patient's medical history
• History of malignancy: Particularly ovarian and colonic malignancy
• Inflammatory bowel disease 

See Presentation for more detail.

Workup

Laboratory tests

The following are adjunctive laboratory tests used in the evaluation of SBO:

• Serum chemistries: Rarely abnormal early in the disease unless due to vomiting or dehydration 
• BUN/creatinine levels: May be elevated in dehydration due to vomiting 
• CBC count: Elevation can be associated with complications 
• Serum lactate levels: Elevation is suggestive of dehydration or tissue hypoperfusion
• Urinalysis
• Type and crossmatch
• PT, PTT, and INR measurements

Laboratory tests to exclude biliary or hepatic disease are also needed. They include the following:

• Phosphate level
• Creatine kinase level
• Liver panel: AST, ALT, ALP, and bilirubin levels

Imaging tests

Obtain plain radiographs first for patients in whom SBO is suspected. Although not sensitive, upright abdominal films may help substantiate the diagnosis if the presence of air-fluid levels or a paucity of gas is observed. Note that supine films may obscure the detection of air-fluid levels.^[4]

Multislice CT has been show to be a particularly effective imaging tool for evaluating patients suspected of having SBO, with a sensitivity of over 95%.^[5] CT imaging is also capable of detecting complications of SBO not visualized on plain films, including ischemia, perforation, mesenteric edema, and pneumatosis.

Ultrasonography is less costly and invasive than CT scanning and may reliably exclude SBO in as many as 89% of patients; specificity is reportedly 100%. It may be a useful alternative imaging modality in children and pregnant women.

Enteroclysis is another valuable diagnostic test in detecting the presence of obstruction and in differentiating partial from complete blockages. This study is useful when plain radiographic findings are normal in the presence of clinical signs of SBO or when plain radiographic findings are nonspecific. However, CT imaging has superseded enteroclysis due to the increased availability of CT scanners as well as owing to the procedure's increased risk of perforation and aspiration.

See Workup for more detail.

Management

Nonoperative treatment

Nonoperative treatment for several types of SBO are as follows:

• Malignant tumor - Obstruction by tumor is usually caused by metastasis; initial treatment should be nonoperative (surgical resection is recommended when feasible)
• Inflammatory bowel disease - To reduce the inflammatory process, treatment generally is nonoperative in combination with high-dose steroids; consider parenteral treatment for prolonged periods of bowel rest, and undertake surgical treatment, bowel resection, and/or stricturoplasty if nonoperative treatment fails.
• Intra-abdominal abscess - CT scan ̶ guided drainage is usually sufficient to relieve obstruction
• Radiation enteritis - If obstruction follows radiation therapy acutely, nonoperative treatment accompanied by steroids is usually sufficient; if the obstruction is a chronic sequela of radiation therapy, surgical treatment is indicated
• Incarcerated hernia - Initially use manual reduction and observation; advise elective hernia repair as soon as possible after reduction
• Acute postoperative obstruction - This is difficult to diagnose because symptoms are often attributed to incisional pain and postoperative ileus; treatment should be nonoperative
• Adhesions - Decreasing intraoperative trauma to the peritoneal surfaces can prevent adhesion formation

Surgical care

A strangulated obstruction is a surgical emergency. In patients with a complete small-bowel obstruction (SBO), the risk of strangulation is high and early surgical intervention is warranted. Laparoscopy has been shown to be safe and effective in selected cases of SBO.^{[6, 7]}

See Treatment and Medication for more detail.

• References

Background

In the United States, 15 of every 100 admissions for abominal pain are due to small-bowel obstruction (SBO), with 300,000 admissions annually.^[8]  An SBO is caused by a variety of pathologic processes. The leading cause of SBO in industrialized countries is postoperative adhesions (65-75%), followed by malignancy, Crohn disease, and hernias, although some studies have reported Crohn disease as a greater etiologic factor than neoplasia. Surgeries most closely associated with SBO are appendectomy, colorectal surgery, and gynecologic and upper gastrointestinal (GI) procedures (see the image below). (See Etiology.)

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Small bowel obstruction. Image courtesy of Ademola Adewale, MD.

One study from Canada reported a higher frequency of SBO after colorectal surgery, followed by gynecologic surgery, hernia repair, and appendectomy. Lower abdominal and pelvic surgeries lead to obstruction more often than upper GI surgeries. (See Etiology.)

SBOs can be partial or complete, simple (ie, nonstrangulated) or strangulated. Strangulated obstructions are surgical emergencies. If not diagnosed and properly treated, vascular compromise leads to bowel ischemia and further morbidity and mortality. Differentiating the characteristics and etiologies of obstruction is critical to proper patient treatment because as many as 40% of patients have strangulated obstructions. SBO accounts for 20% of all acute surgical admissions. (See Presentation, Workup, and Treatment.)

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Pathophysiology

Small-bowel obstruction (SBO) leads to proximal dilatation of the intestine due to accumulation of gastrointestinal (GI) secretions and swallowed air. Bowel dilatation stimulates cell secretory activity, resulting in more fluid accumulation. This, in turn, leads to increased peristalsis above and below the obstruction, with frequent loose stools and flatus early in its course.

Vomiting occurs if the level of obstruction is proximal. Increasing small-bowel distention leads to increased intraluminal pressures. This can cause compression of mucosal lymphatics, leading to bowel wall lymphedema. With even higher intraluminal hydrostatic pressures, increased hydrostatic pressure in the capillary beds results in massive third spacing of fluid, electrolytes, and proteins into the intestinal lumen. The fluid loss and dehydration that ensue may be severe and contribute to increased morbidity and mortality.

Strangulated SBOs are most commonly associated with adhesions and occur when a loop of distended bowel twists on its mesenteric pedicle. The arterial occlusion leads to bowel ischemia and necrosis. If left untreated, this progresses to perforation, peritonitis, and death.

Bacteria in the gut proliferate proximal to the obstruction. Microvascular changes in the bowel wall allow translocation to the mesenteric lymph nodes. This is associated with an increase in the incidence of bacteremia due to Escherichia coli, but the clinical significance is unclear.

• References

Etiology

The most common cause of small-bowel obstruction (SBO) in developed countries is intra-abdominal adhesions, accounting for approximately 65% to 75% of cases.^[1] Postoperative adhesions can be the cause of acute obstruction within 4 weeks of surgery or of chronic obstruction decades later. The incidence of SBO parallels the increasing number of laparotomies performed in developing countries.

Prevention of SBO may be essentially limited to decreasing the risk of adhesion formation by decreasing the number of intra-abdominal procedures (ie, laparotomies) and resultant scar formation. In a study by Van Der Wal et al, the incidence of chronic abdominal symptoms was significantly reduced after the use of a hyaluronic acid ̶ carboxymethylcellulose membrane (Seprafilm). However, Seprafilm placement did not provide protection against SBO.^[9]

Following adhesions, the most common causes of SBO in developed regions are hernias (incarcerated groin hernias) (10-20%), malignancy (10-20%), inflammatory bowel disease (5%), volvulus (3%), and miscellaneous causes (2%).^[1]  The causes of SBO in pediatric patients include congenital atresia, pyloric stenosis, and intussusception.

In contrast, SBO in developing countries is primarily caused by hernias (30-40%), adhesions (about 30%), and tuberculosis (about 10%), along with malignancy, Crohn disease, volvulus, and parasitic infections.^[2]

• References

Prognosis

With proper diagnosis and treatment of the obstruction, prognosis in small-bowel obstruction (SBO) is good. Complete obstructions treated successfully nonoperatively have a higher incidence of recurrence than do those treated surgically.

Morbidity/mortality

Morbidity and mortality are dependent on the early recognition and correct diagnosis of obstruction. If untreated, strangulated obstructions cause death in 100% of patients. If surgery is performed within 36 hours, the mortality rate decreases to 8%. The mortality rate is 25% if the surgery is postponed beyond 36 hours in these patients.

Some factors associated with death and postoperative complications include age, comorbidity, and treatment delay. According to one Norwegian group, morbidity and mortality from SBO decreased from 1961 to 1995; the mortality was reported to be about 5%.^[10]  

Complications

Complications of SBO also depend on the severity of the condition, the patient's age, the presence of comorbities and, often, the duration of symptoms/signs, and include the following:

• Sepsis: Due to translocation of intestinal bacteria from tissue breakdown
• Intra-abdominal abscess
• Wound dehiscence
• Aspiration
• Short-bowel syndrome (as a result of multiple surgeries)
• Disability and death (secondary to delayed treatment)

Cardiac and pulmonary complications may result from procedures and hospitalization, neurologic complications, thrombosis/embolism, major hemorrhage, incision infection or rupture, and abdominal abscess or fistula formation. They include the following^{[3, 10]} :

• Pneumonia: Including aspiration, ventilator associated, and/or hospital acquired
• Bowel ischemia/perforation
• Peritonitis
• Acute kidney injury/acute renal failure
• Surgical complications

• References

History

Obstruction can be characterized as either partial or complete versus simple or strangulated. No single accurate clinical picture exists to detect early strangulation of obstruction, although signs of peritonitis, elevated lactate levels, leukocytosis, and the presence of free air and pneumatosis coli are known complications.

Abdominal pain associated with SBO is often described as crampy and intermittent. Without treatment, the abdominal pain can increase as a result of bowel perforation and ischemia; therefore, having a clinical suspicion for the condition is paramount to early identification and intervention. Furthermore, the clinical presentation of the patients varies and no one clinical symptom on its own identifies the majority of patients with SBO. Some studies have suggested that the absence of passage of flatus and/or feces and vomiting are the most common presenting symptoms, with abdominal discomfort/distention the most frequent physical examination findings.^[3] Other studies have shown that abdominal pain is present in the majority of patients found to have SBO.

Changes in the character of the pain may indicate the development of a more serious complication (ie, constant pain of a strangulated or ischemic bowel).

Patients presenting with SBO often report the following:

• Previous abdominal or pelvic surgery, previous radiation therapy, or both
• History of malignancy: Particularly ovarian and colonic malignancy
• Inflammatory bowel disease 
• Nausea/vomiting (60-80%): The vomitus can often be bilious in nature 
• Constipation/absence of flatus (80-90%): Typically a later finding of SBO
• Abdominal distention (60%)
• Fever and tachycardia: Late findings; may be associated with strangulation

• References

Physical Examination

Abdominal distention is present in about 60% of patients with small-bowel obstruction (SBO).^[3] The duodenal or proximal small bowel has less distention when obstructed than the distal bowel has when obstructed. Hyperactive bowel sounds occur early as gastrointestinal (GI) contents attempt to overcome the obstruction; hypoactive bowel sounds occur later in the disease process.

Physical examination can help exclude incarcerated umbilical, inguinal, femoral triangle, and obturator foramina hernias. Proper abdominal, genitourinary, and pelvic examinations are essential in identifying possible causes of incarceration as well as helping to exclude causes from the differential diagnosis. Look for the following features during rectal examination:

• Gross or occult blood, which suggests late strangulation or malignancy
• Masses, which suggest obturator hernia

Check for signs commonly believed to be more diagnostic of intestinal ischemia, including the following:

• Fever (temperature >100°F)
• Tachycardia (>100 beats/min)
• Peritoneal signs (guarding, rigid abdomen, rebound tenderness, pain out of proportion to the examination)

No reliable physical examination method exists to differentiate simple from early strangulated obstruction. Serial abdominal examinations are important and may detect changes early.

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Laboratory Studies

If the diagnosis is unclear, admission and observation are warranted to detect early obstructions. Essential laboratory tests are needed, including the following:

• Serum chemistries: Results are usually normal or mildly elevated; abnomal results early in the disease are generally due to vomiting or dehydration
• Blood urea nitrogen (BUN)/creatinine levels: May be increased due to a decreased volume state (eg, dehydration)
• Complete blood cell (CBC) count: The white blood cell (WBC) count may be elevated with a left shift in simple or strangulated obstructions; increased hematocrit is an indicator of volume state (ie, dehydration)
• Serum lactate levels: Increased levels are suggestive of dehydration or tissue underperfusion
• Lactate dehydrogenase studies
• Urinalysis
• Type and crossmatch as well as prothrombin time (PT), international normalized ratio (INR), and partial thromboplastin time (PTT): These are adjunctive laboratory tests used in the evaluation of SBO; the patient may require surgical intervention

Laboratory studies to exclude biliary or hepatic disease are also needed and include the following:

• Phosphate level
• Creatine kinase level
• Liver panel: aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and bilirubin levels

• References

Plain Radiography

Obtain plain radiographs first for patients in whom small-bowel obstruction (SBO) is suspected. At least 2 views, supine or flat and upright, are required. Plain radiographs are diagnostically more accurate in cases of simple obstruction. However, diagnostic failure rates of as much as 30% have been reported.^[4]

In a study of 103 patients with suspected SBO, the sensitivity of plain radiography was reported to be 75%, with a specificity of 53%, whereas computed tomography (CT) scanning had a 92% sensitivity and 71% specificity.^[11]

The experience of a radiologist also appears to play a role in the evaluation of SBO. Among 6 reviewers in one study, the sensitivity of SBO was between 59% and 93%, with senior staff members having significantly higher sensitivity.^[4] The radiographic signs that were most significant included, two or more air-fluid levels, air-fluid levels wider than 2.5 cm, or air fluid levels differing more than 5 mm in same bowel loop.^[4]

X-ray imaging is further limited by the decreased ability to visualize the transition point or grade the degree of bowel obstruction.

Plain radiography is of little assistance in differentiating strangulation from simple obstruction. Some have used abdominal radiography to distinguish between complete obstruction and partial or no SBO.

A study by Lappas et al proposed that 2 findings were more predictive of a higher grade or complete SBO: (1) the presence of an air-fluid differential height in the same small-bowel loop and (2) the presence of a mean level width greater than 25 mm.^[12]  When the 2 findings were present, the obstruction was most likely high grade or complete. When both were absent, the authors proposed, a low-grade (partial) SBO was likely or nonexistent.

Dilated small-bowel loops with air-fluid levels indicate SBO, as does absent or minimal colonic gas. SBO is demonstrated in the radiographs below.

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Small bowel obstruction. Image courtesy of Ademola Adewale, MD.

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Small bowel obstruction. Image courtesy of Ademola Adewale, MD.

View Image

Small bowel obstruction. Image courtesy of Ademola Adewale, MD.

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Enteroclysis and CT Enterography

Enteroclysis

Enteroclysis is the use of a contrast agent normally administered through a nasogastric tube. Enteroclysis is valuable in detecting the presence of obstruction and in differentiating partial from complete blockages. This study is useful when plain radiographic findings are normal in the presence of clinical signs of small-bowel obstruction (SBO) or when plain radiographic findings are nonspecific. Enteroclysis is often less desirable when compared to computed tomography (CT) scanning due to the risk of perforation or aspiration with the administration of contrast medium. 

Enteroclysis distinguishes adhesions from metastases, tumor recurrence, and radiation damage. It offers a high negative predictive value and can be performed with 2 types of contrast agents. Barium is the classic contrast agent used in this study; it is safe and useful when diagnosing obstructions, provided that no evidence of bowel ischemia or perforation exists. Barium has been associated with peritonitis and should be avoided if perforation is suspected.

CT enterography/CT enteroclysis

This modality is replacing enteroclysis in clinical practice.^{[13, 14, 15]}  In addition, it is the examination of choice for intermittent SBO and in patients with a complicated surgical history (eg, prior surgery, tumors).^{[16, 17, 18]}

CT enterography displays the entire thickness of the bowel wall and allows evaluation of surrounding mesentery and perinephric fat.^[13]  It uses CT-scanning technology to scan thin slices of bowel while simultaneously using large-volume enteric contrast material for imagery.^[13]

CT enterography is more accurate than conventional CT scanning at finding the cause of SBO (89% vs 50%, respectively), as well as at locating the site of the obstruction (100% vs 94%, respectively).^[19]  It is useful in patients being managed conservatively (ie, nonoperatively).^[19]

• References

CT Scanning and MRI

Computed tomography (CT) scanning

CT scanning is the study of choice if the patient has fever, tachycardia, localized abdominal pain, and/or leukocytosis.

CT scanning is useful in making an early diagnosis of strangulated obstruction and in delineating the myriad other causes of acute abdominal pain, particularly when clinical and radiographic findings are inconclusive. It also has proved useful in distinguishing the etiologies of small-bowel obstruction (SBO), that is, in distinguishing extrinsic causes (such as adhesions and hernia) from intrinsic causes (such as neoplasms and Crohn disease). In addition, CT scanning differentiates the above from intraluminal causes, such as bezoars. The modality may be less useful in the evaluation of small bowel ischemia associated with obstruction.

CT scanning is capable of revealing abscess, inflammatory process, extraluminal pathology resulting in obstruction, and mesenteric ischemia and enables the clinician to distinguish between ileus and mechanical small bowel obstruction in postoperative patients.^[20]

The modality does not require oral contrast for the diagnosis of SBO, because the retained intraluminal fluid serves as a natural contrast agent.

Obstruction is present if the small-bowel loop is greater than 2.5 cm in diameter dilated proximal to a distinct transition zone of collapsed bowel less than 1 cm in diameter. A smooth beak indicates simple obstruction without vascular compromise; a serrated beak may indicate strangulation. Bowel wall thickening, portal venous gas, or pneumatosis indicates early strangulation.

One series of 32 patients reported a sensitivity of 93%, a specificity of 100%, and an accuracy of 94% for CT scanning in the detection of obstructions.^[21] Another series reported a sensitivity of 92% and specificity of 71% in the correct identification of partial or complete SBO.^[11] Additional studies have shown sensitivities above 95% for CT scanning in identifying obstructions and its complications.^[5]

Magnetic resonance imaging (MRI)

The accuracy of MRI almost approaches that of CT scanning for the detection of obstructions.^[13] MRI is also effective in defining the location and etiology of obstruction.^[22] MRI has several limitations, however, including lack of availability (transporting sicker patients is difficult) and poor visualization of masses and inflammation.^{[23, 24]}

In a retrospective study (2005-2015) of 12 prenatally diagnosed cases of SBO evaluated by both ultrasonography and MRI, Rubio et al noted that MRI was useful in providing the following information^[25] :

• The distribution of meconium in the small bowel, clarifying the level of obstruction
• Abnormally diminished meconium in the rectum, suggestive of cystic fibrosis or combined SBO and colonic obstruction (which may be useful in family counseling and postnal care preparation)
• The evaluation of colon and rectal contents, serving as a fetal enema

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Ultrasonography

Ultrasonography is less costly and invasive than CT scanning and may reliably exclude SBO in as many as 89% of patients; specificity is reportedly 100%.

In a small study by Jang et al in which the use of bedside ultrasonography by emergency physicians was compared with radiography for the detection of small-bowel obstruction (SBO), emergency physician ̶ performed ultrasonography compared favorably with radiography. Dilated bowel on ultrasonography had a sensitivity of 91% and a specificity of 84% for SBO, while radiography had a sensitivity of 46% and a specificity of 66%.^[26]

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Approach Considerations

In 2013, the World Society of Emergency Surgery published updated guidelines for the diagnosis and management of adhesive SBO (ASBO). The recommendations include the following^[27] :

• In the absence of signs of strangulation and a history of persistent vomiting or combined computed tomography (CT) scan signs, patients with partial ASBO can be safely managed with nonoperative management; tube decompression should be attempted
• Water-soluble oral contrast medium (WSCM) is recommended for both diagnostic and therapeutic purposes in patients undergoing nonoperative management
• Nonoperative management can be prolonged for up to 72 hours in the absence of signs of strangulation or peritonitis; surgery is recommended after 72 hours of nonoperative management without resolution
• Open surgery is frequently used for patients with strangulating ASBO and after failed conservative management; in appropriate patients, a laparoscopic approach using an open access technique is recommended
• Hyaluronic acid: Carboxycellulose membrane and icodextrin decrease the incidence of adhesions, and icodextrin may reduce the risk of reobstruction

Emergency Department Care

Initial emergency department (ED) treatment of small-bowel obstruction (SBO) consists of aggressive fluid resuscitation, bowel decompression, administration of analgesia and antiemetic as indicated clinically, early surgical consultation, and administration of antibiotics. (Antibiotics are used to cover against gram-negative and anaerobic organisms.)

Initial decompression can be performed by placement of a nasogastric (NG) tube for suctioning GI contents and preventing aspiration. Monitor airway, breathing, and circulation (ABCs).

Blood pressure monitoring, as well as cardiac monitoring in selected patients (especially elderly patients or those with comorbid conditions), is important.

Nonoperative inpatient care

Continued NG suction provides symptomatic relief, decreases the need for intraoperative decompression, and benefits all patients. No clinical advantage to using a long tube (nasointestinal) instead of a short tube (NG) has been observed.

A nonoperative trial of as many as 3 days is warranted for partial or simple obstruction. Provide adequate fluid resuscitation and NG suctioning. Resolution of obstruction occurs in virtually all patients with these lesions within 72 hours. Good data regarding nonoperative management suggest it to be successful in 65-81% of partial SBO cases without peritonitis.^{[10, 13]} Nonoperative treatment for several types of SBO are as follows:

• Malignant tumor: Obstruction by tumor is usually caused by metastasis; initial treatment should be nonoperative (surgical resection is recommended when feasible)
• Inflammatory bowel disease: To reduce the inflammatory process, treatment generally is nonoperative in combination with high-dose steroids; consider parenteral treatment for prolonged periods of bowel rest, and undertake surgical treatment, bowel resection, and/or stricturoplasty if nonoperative treatment fails.
• Intra-abdominal abscess: CT scan ̶ guided drainage is usually sufficient to relieve obstruction
• Radiation enteritis: If obstruction follows radiation therapy acutely, nonoperative treatment accompanied by steroids is usually sufficient; if the obstruction is a chronic sequela of radiation therapy, surgical treatment is indicated
• Incarcerated hernia: Initially use manual reduction and observation; advise elective hernia repair as soon as possible after reduction
• Acute postoperative obstruction: This is difficult to diagnose, because symptoms often are attributed to incisional pain and postoperative ileus; treatment should be nonoperative
• Adhesions: Decreasing intraoperative trauma to the peritoneal surfaces can prevent adhesion formation

Water-soluble oral contrast medium

Studies have evaluated the use of WSCM as a tool in the management of SBO and as a predictive tool for nonoperative resolution of adhesive SBO. Although it does not cause resolution of the SBO, WSCM may reduce the hospital stay in patients not requiring surgery.

However, a more recent systematic review that analyzed retrospective data (2006-2009) from 242 patients in 10 studies with uncomplicated acute adhesive SBO indicated no benefit of administering gastrografin compared with saline solution in reducing the need for surgical intervention (24% vs 20%, respectively) or bowel resection (8% and 4%). Results were similar for both groups with respect to the time interval between the initial CT scan and surgery, as well as the time interval between oral refeeding and discharge.^[28] The sole potential risk factor for failure of nonoperative management was age.

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Surgical Care

A strangulated obstruction is a surgical emergency. In patients with a complete small-bowel obstruction (SBO), the risk of strangulation is high and early surgical intervention is warranted. Patients with simple complete obstructions in whom nonoperative trials fail also need surgical treatment but experience no apparent disadvantage to delayed surgery.

Laparoscopy has been shown to be safe and effective in selected cases of SBO.^{[6, 7]} A review of retrospective clinical trials showed that laparoscopy showed better results in terms of hospital stay and mortality reduction versus open surgery, but prospective, randomized, controlled trials to assess all outcomes are still needed.^[29]

Surgical outcomes for SBO, particularly malignant bowel obstruction, have relatively high risk for mobidity and mortality.^[30] In a retrospective study (2012-2015) of 2233 patients who underwent surgery for bowel obstruction, those with malignant bowel obstruction had a 14.5% adjusted mortality rate and a 32.2% adjusted complication rate. Independent prognostic factors for mortality included bowel resection, disseminated disease, advanced age, higher American Society of Anesthesiologists score (IV/V), as well as the presence of sepsis, albumin level below 3.5 g/dL, hematocrit below 30%, cirrhosis, ascites, and urinary tract infection.^[30]

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Medication Summary

Fluid replacement with aggressive intravenous (IV) resuscitation using isotonic saline or lactated Ringer solution is indicated. Oxygen and appropriate monitoring are also required. Antibiotics are used to cover gram-negative and anaerobic organisms. In addition, analgesia and antiemetic are administered as indicated clinically. As previously mentioned, a nonoperative trial of as many as 3 days is warranted for partial or simple obstruction. Resolution of obstruction occurs in virtually all patients with these lesions within 72 hours.

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Cefazolin

• Dosing, Interactions, etc.

Clinical Context:  Cefazolin is a first-generation semisynthetic cephalosporin that arrests bacterial cell wall synthesis, inhibiting bacterial growth.

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Cefoxitin (Mefoxin)

• Dosing, Interactions, etc.

Clinical Context:  Cefoxitin is a second-generation cephalosporin indicated for gram-positive cocci and gram-negative rod infections. Infections caused by cephalosporin- or penicillin-resistant gram-negative bacteria may respond to cefoxitin.

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Cefotetan

• Dosing, Interactions, etc.

Clinical Context:  Cefotetan is a second-generation cephalosporin indicated for infections caused by susceptible gram-positive cocci and gram-negative rods. Dosage and route of administration depend on the condition of patient, the severity of infection, and the susceptibility of the causative organism.

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Cefuroxime (Ceftin, Zinacef)

• Dosing, Interactions, etc.

Clinical Context:  Cefuroxime is a second-generation cephalosporin that maintains the gram-positive activity of first-generation cephalosporins; it adds activity against Proteus mirabilis, Haemophilus influenzae, E coli, Klebsiella pneumoniae, and Moraxella catarrhalis. The condition of the patient, the severity of the infection, and the susceptibility of the microorganism determine the proper dose and route of administration.

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Meropenem (Merrem)

• Dosing, Interactions, etc.

Clinical Context:  Meropenem is a bactericidal, broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis. It is effective against most gram-positive and gram-negative bacteria.

• References

Class Summary

These agents are for prophylaxis in surgical intervention, if needed.

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Promethazine (Phenergan, Phenadoz, Promethegan)

• Dosing, Interactions, etc.

Clinical Context:  Promethazine is for the symptomatic treatment of nausea and vomiting. It is an antidopaminergic agent that is effective in treating emesis. Promethazine blocks postsynaptic mesolimbic dopaminergic receptors in the brain and reduces stimuli to the brainstem reticular system.

• References

Ondansetron (Zofran, Zuplenz)

• Dosing, Interactions, etc.

Clinical Context:  Ondansetron is a selective 5-HT3-receptor antagonist that blocks serotonin peripherally and centrally; it is used in the prevention of nausea and vomiting. Ondansetron is metabolized in the liver through the P-450 pathway.

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Class Summary

These agents should be administered for symptomatic relief, usually in conjunction with GI decompression via placement of an NG tube for suction.

• References

Morphine sulfate (Astramorph, MS Contin, Kadian, Duramorph)

• Dosing, Interactions, etc.

Clinical Context:  This is the drug of choice for analgesia due to its reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Various IV doses are used; morphine sulfate is commonly titrated until the desired effect is obtained.

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Class Summary

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who experience pain.

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