Small Bowel Obstruction

Etiology

The etiology of SBO encompasses a broad spectrum of mechanical and functional causes, each impacting management strategies and timing of surgical intervention. Mechanical SBO results from a physical barrier to the passage of bowel contents and can be classified based on the location of the obstruction: intraluminal, such as gallstone ileus; intramural, such as malignant lesions; and extrinsic, such as adhesions. In contrast, functional obstruction, termed ileus or paralytic ileus, arises from impaired peristalsis or metabolic disorders rather than a physical barrier.

Adhesions

Postoperative adhesions are the leading cause of SBO in developed countries, accounting for up to 74% of cases, and are the second leading cause in developing nations.[3] They result from fibrotic scar tissue forming after surgeries, which occur in as many as 97% of common surgeries such as appendectomy, colectomy, and gynecological surgery.[4] Adhesions are also seen after laparoscopic surgeries, though less frequently than open procedures. SBO that is secondary to adhesions in an abdomen without prior surgery, ie, a “virgin abdomen,” is very rarely seen but may occur in conditions such as familial Mediterranean fever and recurrent serositis.[5] The rarity of these types of SBO can result in a delay in diagnosis with complications leading to sepsis and death, emphasizing the need for heightened clinical suspicion and timely imaging for diagnosis

Hernias

Abdominal wall hernias, external (eg, inguinal or umbilical) and internal, are the second most common cause of SBO in developed countries (globally the leading cause). These hernias account for approximately 2% to 10% of cases and often require surgical intervention to relieve obstruction and prevent complications such as strangulation or ischemia. Notably, in patients with a “virgin abdomen,” abdominal wall hernias are the most frequent cause of SBO.[3] Internal hernias account for less than 1% of intestinal obstruction cases.[6] They can be congenital or acquired, and SBOs caused by these hernias are managed operatively.[7]

Malignancies and Tumors

Malignancy is the third most common cause of SBO after intraabdominal adhesions and hernias.[8] Malignant bowel obstruction, resulting from primary or metastatic cancers, accounts for approximately 5% to 20% of cases.[9] The most common primary small bowel tumors that cause SBO are adenocarcinomas, carcinoid tumors, and gastrointestinal stromal tumors. Metastases to the small intestine are far more common than primary tumors. The small bowel is a frequent site of metastasis, particularly from tumors of the colon, pancreas, ovary, and melanoma. Other tumors involved in SBO are lymphoma, leiomyomas, and desmoid tumors. 

Gallstone Ileus

A rare cause, gallstone ileus, occurs when a gallstone enters the bowel through a biliary-enteric fistula, causing obstruction, typically at the ileocecal valve. Diagnosis is based on imaging findings, including the Rigler triad: mechanical obstruction, pneumobilia, and an ectopic gallstone within the bowel lumen.[10]

Inflammatory and Infectious Conditions

Crohn disease is a significant cause of SBO, with inflammation due to active disease accounting for 5% of all SBOs.[11] Up to 80% of patients with ileal disease require surgical intervention at some point in their lives.[12] In patients with small bowel Crohn disease, one of the primary surgical indications for small bowel resection is inflammatory SBO, followed by intestinal fistula and abscess. Although many patients develop disease recurrence at the anastomosis, some develop SBO without evidence of inflammation at the transition point.[13]

Endometriosis can also lead to acute SBO through inflammation or adhesions. Acute SBO secondary to intestinal endometriosis underscores the pivotal role of laparoscopic surgery in the evaluation of SBO.[14] Infectious processes, such as radiation enteritis, may cause delayed-onset obstruction due to fibrosis and ischemia. Approximately a third of patients with chronic radiation enteritis may ultimately require surgical intervention for indications such as obstruction.

Motility Disorders

SBO can also result from intestinal dysmotility (ie, impaired bowel movement without a physical blockage) that can be caused by functional gastrointestinal disorders like chronic intestinal pseudoobstruction, where the intestines lack normal peristaltic activity, or by drug-induced motility issues, such as those caused by opioids or anticholinergics.[15] Additionally, enteric myopathies, either primary or secondary to conditions like muscular dystrophy, affect the smooth muscle of the small bowel, leading to motility dysfunction. Enteric neuropathy, caused by neurological or metabolic conditions (eg, diabetes or Parkinson disease), can also disrupt normal motility, presenting with symptoms similar to mechanical SBO. Proper diagnosis requires imaging and sometimes specialized tests to differentiate functional obstructions from mechanical causes, and treatment focuses on managing the underlying condition and supporting motility.

Rare Causes

Small bowel encapsulation is a rare cause of SBO. In this condition, the small intestine is encased by a fibrous membrane within the peritoneum, limiting its movement and potentially causing obstruction. This condition can present as acute or chronic SBO, often requiring imaging such as CT scans for diagnosis.[16] Encapsulation can result from congenital conditions or be secondary to inflammatory or infectious processes.

Small bowel volvulus is another uncommon cause, where the bowel twists around its mesentery, obstructing blood flow and causing ischemia. Volvulus can occur anywhere in the small bowel but is more common in the midgut; this leads to bowel distention, pain, and potentially ischemia or necrosis if not treated promptly. Volvulus may be associated with abnormal intestinal mobility or congenital malformations, like malrotation. Diagnosis is typically confirmed through radiographic imaging (ie, CT or contrast studies), and surgical intervention is often required to untwist the bowel and prevent ischemia.

Pediatric 

Congenital or acquired adhesions are the most common causes of SBO. The second most common cause is intussusception. Other causes include congenital atresia, volvulus, ingestion of foreign bodies, and Meckel diverticulum.[17]

Epidemiology

SBO is a common surgical emergency, contributing to 15% to 20% of hospital admissions for acute abdominal pain and accounting for approximately 80% of all bowel obstructions. Each year, over 300,000 laparotomies are performed in the United States for SBO. The incidence of SBO is closely associated with the prevalence of abdominal surgeries, as postoperative adhesions are the leading cause, responsible for more than 75% of cases.[18] The risk of SBO increases with the number of prior intraabdominal procedures, emphasizing the importance of surgical history in assessing patient risk.

SBO is observed across all age groups but is more common in older adults due to higher rates of abdominal surgeries, malignancies, and hernias. Sex differences in etiology are evident, with women more prone to adhesion-related SBO due to gynecological procedures, while men are more likely to experience hernia-related obstruction. In low-resource settings, hernias are a predominant cause due to limited access to elective hernia repair surgeries. SBO is less common in children and typically results from congenital abnormalities such as malrotation or intussusception.

Over the past 4 decades, advancements in imaging, diagnostic laparoscopy, and laparoscopic techniques have significantly altered the management of SBO. Before 1981, surgery was the definitive treatment. Since then, adopting nonoperative protocols has improved patient selection for timely surgical intervention, such as laparoscopic lysis of adhesions. Despite these advancements, recurrent SBO remains a concern, with a recurrence rate of 12% to 32% after initial surgical management.

Delayed diagnosis and intervention can lead to complications such as strangulation, bowel ischemia, and sepsis—conditions associated with a mortality rate exceeding 25%. While improved diagnostic modalities have enhanced outcomes in developed nations, delays in care and limited access to advanced surgical techniques remain significant challenges in resource-constrained settings. Understanding the epidemiology of SBO is critical for developing preventive measures, optimizing treatment protocols, and reducing the global burden of this condition.

Pathophysiology

SBO results from an interruption in the normal flow of intestinal contents due to a mechanical blockage or functional impairment. This disruption triggers a series of pathological processes affecting the bowel wall, vascular supply, and systemic physiology. These processes can escalate rapidly, especially in cases of strangulation or ischemia, underscoring the critical need for timely diagnosis and intervention.

Mechanical Obstruction

In mechanical SBO, a physical barrier obstructs the bowel lumen, creating a transition point where proximal bowel distention and distal bowel decompression occur. The obstructing lesion prevents the passage of intestinal contents, leading to increased intraluminal pressure proximal to the obstruction. This pressure gradient causes:

• Proximal bowel distention
  • This may induce vomiting as the bowel attempts to relieve pressure.
• Distal bowel decompression
  • This occurs along with inhibition of peristalsis distal to the obstruction, while proximal peristalsis temporarily increases to overcome the blockage.

Common causes of mechanical obstruction include adhesions, hernias, tumors, strictures, and volvulus.

Physiological Consequences

• Impaired venous flow and bowel wall edema
  • As the proximal bowel distends, venous outflow from the bowel wall is compromised, resulting in bowel wall edema and inflammation. These changes can exacerbate luminal narrowing and impair the oxygenation of the bowel tissue.
• Third spacing and fluid loss
  • Increased bowel wall permeability leads to fluid and electrolyte sequestration into the bowel lumen and third spacing into the peritoneal cavity as ascitic fluid. This fluid loss, coupled with vomiting and decreased oral intake, contributes to dehydration, hypovolemia, and metabolic disturbances.
• Bacterial translocation
  • The thickened, inflamed, and ischemic bowel wall becomes more permeable, allowing bacteria, predominantly Escherichia coli, to translocate into the bloodstream or peritoneal cavity. This can result in peritonitis, bacteremia, and systemic infection.
• Ischemia and infarction
  • Prolonged obstruction increases intraluminal pressure to a point where arterial blood flow is compromised. This results in ischemia, necrosis, and, if untreated, perforation. Perforation leads to peritonitis, which can progress to sepsis and death.[19]
• Systemic effects
  • The combination of fluid loss, bacterial translocation, and ischemia activates a systemic inflammatory response syndrome, increasing the risk of septic shock and multiorgan failure.

Distinction Based on Obstruction Location

• Proximal SBO
  • Characterized by significant vomiting, minimal abdominal distension, and rapid onset of dehydration and electrolyte imbalances
• Distal SBO
  • Associated with more pronounced abdominal distension, delayed vomiting, and slower progression of systemic complications

Functional Obstruction

In functional SBO, peristalsis fails due to metabolic disturbances, neural inhibition, or inflammation (paralytic ileus). While there is no mechanical barrier, the resulting pathophysiology is similar, with stasis leading to fluid sequestration, bowel distention, and bacterial overgrowth.

Histopathology

The histopathological changes in SBO evolve in response to the obstruction's severity, duration, and underlying cause. The diagnosis can be confirmed with histology in a unit with expertise in this pathology area.[15] Early stages are marked by mucosal edema, hyperemia, and increased intraluminal pressure, impairing venous return and causing fluid accumulation in the mucosa and submucosa. This fluid results in villous edema and mild inflammatory cell infiltration, primarily by neutrophils and lymphocytes. Capillary dilation and vascular engorgement in the lamina propria lead to hyperemia and increased permeability. As the obstruction progresses, ischemia exacerbates tissue damage, causing mucosal ulceration and sloughing of the epithelial layer, compromising the mucosal barrier. Bowel wall inflammation intensifies with polymorphonuclear neutrophil infiltration, and bacterial translocation, particularly by E coli, increases the risk of peritonitis or bacteremia.

Prolonged ischemia leads to necrosis, initially affecting the mucosa and extending to the muscularis propria and serosa. The bowel wall thickens with fibrin deposition and inflammation, and in severe cases, full-thickness necrosis appears as coagulative necrosis, where cellular details are lost and tissues exhibit hypereosinophilic staining. In cases of strangulated obstruction caused by herniation, volvulus, or adhesions, hemorrhagic necrosis and venous congestion are common—with the bowel wall darkened and thickened due to blood accumulation. Gangrenous changes, marked by liquefactive necrosis and mixed inflammatory infiltrates, may develop; the serosal surface may show fibrinopurulent exudates, indicating secondary peritonitis. Prolonged ischemia can also cause vascular thrombosis in mesenteric veins, worsening ischemia and infarction. Reperfusion after ischemia leads to oxidative stress and neutrophilic infiltration, contributing to cellular injury and inflammation.

Histological features vary depending on the etiology of SBO. For example, adhesions and bands typically show fibrosis and mesothelial hyperplasia at adhesion sites, while strangulated hernias display congestion, necrosis, and inflammation. Tumor-related obstructions reveal malignancy-specific features, such as glandular structures in adenocarcinoma or spindle cells in stromal tumors. Crohn disease presents with transmural inflammation, noncaseating granulomas, and fibrosis, whereas radiation enteritis shows vascular sclerosis, submucosal fibrosis, and ulceration.

Increased intraluminal pressure also leads to endothelial tissue remodeling, which alters the epithelial cell type to withstand the mechanical forces exerted by extraluminal factors such as tumors and adhesions.[20] Fibrous tissue thickening and adhesions can also replace simple columnar epithelial cells, obstructing gastrointestinal absorption and interfering with normal small intestine functions. Consequently, patients with SBO often present with severe abdominal pain, vomiting, obstipation, constipation, and abdominal distention.[21]

History and Physical

History

A patient's history and physical examination are essential for diagnosing SBO and determining its severity. Patients typically present with acute abdominal pain, which is often crampy and colicky, correlating with peristalsis as the bowel attempts to overcome the obstruction. The pain may become constant and severe if the obstruction worsens. Vomiting is another hallmark symptom, especially with proximal obstructions, and may start with gastric contents before becoming bilious as the obstruction becomes more distal. Persistent vomiting can lead to dehydration, electrolyte imbalances, and metabolic alkalosis.

Abdominal distension, due to the accumulation of gas and fluids above the obstruction, is common and may be particularly noticeable in high or complete obstructions. Changes in bowel movements, including obstipation or decreased stool and gas passage, are also typical, though partial obstructions may still allow for some output early on.[22] A key component of the history is identifying prior abdominal surgeries, particularly those that could lead to adhesions, as postoperative adhesions are the most common cause of SBO. A history of abdominal hernias or malignancies should also be explored, as these conditions are significant risk factors for SBO. Additionally, the patient’s medical history may reveal conditions like Crohn disease, radiation therapy, or neurological disorders, which can predispose them to impaired motility and SBO.

Physical

On physical examination, the patient may appear uncomfortable or anxious due to pain, with signs of dehydration such as dry mucous membranes and tachycardia, especially in the case of persistent vomiting. Abdominal inspection may reveal visible peristalsis and distension, particularly in thin patients. Palpation often demonstrates tenderness, especially over the obstruction site, and may reveal palpable dilated bowel loops in more severe cases. Percussion typically reveals a tympanic abdomen due to gas-filled loops, though dullness can occur in cases of fluid accumulation or bowel perforation.

Early in the obstruction, bowel sounds may be hyperactive or high-pitched as the body attempts to overcome the blockage. However, in more severe cases, bowel sounds may become absent, mainly if strangulation or ischemia is present.[23] A rectal examination may be helpful to check for fecal impaction, which could contribute to the obstruction. In some cases, the absence of stool could suggest a more proximal obstruction. Finally, if peritonitis or bowel perforation is suspected, the patient may develop signs of peritonitis, such as rigidity, rebound tenderness, and guarding, indicating a surgical emergency. This history and physical exam are critical in establishing the diagnosis, determining whether the obstruction is partial or complete, and guiding further imaging studies and treatment decisions.

Evaluation

The evaluation of SBO involves a combination of laboratory tests, radiographic imaging, and occasionally more specialized studies. These tests are crucial for confirming the diagnosis, determining the severity and cause of the obstruction, and guiding appropriate management.

Laboratory Tests

Laboratory testing in SBO primarily assesses the patient's overall health, identifies complications, and helps to monitor for signs of dehydration, electrolyte imbalance, or infection:

• Complete blood count (CBC)
  • A CBC may show leukocytosis, indicating infection or inflammation, which can be seen in strangulated obstruction or peritonitis cases. Anemia may be present in cases of chronic obstruction due to subclinical blood loss or nutritional deficiencies.
• Electrolytes and renal function
  • A basic or comprehensive metabolic panel can assess hydration status, electrolyte imbalances (such as hyponatremia, hypokalemia, and metabolic alkalosis), and kidney function. Vomiting, fluid sequestration in the intestines, and third-spacing of fluids can lead to dehydration, which, if severe, may result in prerenal acute kidney injury.
• Arterial blood gas (ABG)
  • An ABG panel
  • may reveal metabolic alkalosis in prolonged vomiting or bowel ischemia, while lactic acidosis may indicate bowel ischemia or infarction.
• Lactate levels
  • Elevated lactate levels can suggest tissue hypoxia, indicating ischemia or necrosis of the bowel, particularly in the context of strangulated obstruction.
• Amylase/lipase
  • Although these tests are typically used to evaluate pancreatitis, they may be elevated in cases of SBO if there is associated pancreatic involvement or strangulation of a segment of the small intestine.
• Blood cultures
  • If there is suspicion of peritonitis or sepsis due to bowel perforation or bacterial translocation, blood cultures may be warranted to guide antibiotic therapy.

Radiographic Imaging

Radiologic evaluation is central to confirming the diagnosis of SBO and assessing its location, severity, and complications.

Abdominal X-Rays

The initial imaging study of choice is usually a plain abdominal radiograph (x-ray). This study can reveal characteristic findings such as:

• Dilated loops of small bowel
  • Air-fluid levels are visible on upright images, indicating proximal bowel distention.
• Absence of gas in the colon
  • This finding suggests a complete obstruction, especially if the obstruction is distal to the small intestine.
• Step ladder pattern
  • This pattern of air-fluid levels in the small intestine can indicate obstruction.
• Signs of perforation
  • Free air under the diaphragm on an upright chest x-ray suggests perforation.

Plain radiography has poor sensitivity, with rates ranging from 50% to 80%. While radiography can serve as an initial screening test for detecting air-fluid levels or free air in the abdomen, it does not provide sufficient imaging to identify the cause, extent, or complications of SBO. A small bowel diameter greater than 6 cm is concerning and indicates a severe obstruction that may pose a high risk for compromised viability.

CT Scan

A CT scan of the abdomen is considered the gold standard for diagnosing SBO. CT scans are more sensitive than x-rays for detecting SBO, particularly in assessing the underlying cause. This study can help differentiate between simple and complicated (strangulated or ischemic) SBO. This imaging can be enhanced using intravenous contrast, provided the patient has normal kidney function and no contraindications. Key findings include:

• Bowel distention
  • This appears similar to that on x-rays but is more detailed and can help quantify the extent.
• Transition point
  • This is the location of the obstruction, which is critical in planning surgical or conservative management.
• Bowel wall thickening
  • This finding is suggestive of ischemia, inflammation, or infection.
• Mesenteric stranding
  • In cases of bowel ischemia or perforation, this can be seen. 
• Signs of perforation
  • Free air or fluid in the abdomen can indicate perforation.
• Absence of contrast in bowel
  • In cases of a complete obstruction, contrast may not reach beyond the obstruction site.

Ultrasound

Although not typically the first choice for diagnosing SBO, abdominal ultrasound can be useful, particularly in children and pregnant women, due to its noninvasive nature. Additionally, ultrasound does not result in radiation exposure and has the benefit of rapid and serial examinations.[24][25] This study can detect bowel distention, peristalsis, and the presence of fluid or air in the bowel, and is often used in cases of suspected bowel perforation or other intraabdominal pathology. The following are pathological findings that can be seen on ultrasound:

• A dilated small bowel loop measuring more than 3 cm in diameter suggests an obstruction or ileus.
• An edematous bowel wall measuring more than 3 mm indicates an obstruction or other intestinal inflammatory cause.
• The noncompressibility of the bowel and the appearance of free fluid suggest obstruction.
• Anterograde-retrograde peristalsis is specific for obstruction.
• The visualization of a transition point is specific for obstruction. A transition point on ultrasound is demonstrated by a thick-walled, noncompressible bowel loop adjacent to a loop of decompressed small bowel.[26]

Ultrasound does not replace a CT scan and should not delay surgical consultation. This study is useful in cases where it can facilitate diagnostic evaluation and rule out other causes.[27]

Contrast Studies

If the diagnosis remains unclear, a contrast-enhanced study may be performed:

• Upper gastrointestinal series with small bowel follow-through 
  • This is useful if there is a suspicion of a partial obstruction or when evaluating the motility of the bowel.
• Barium enema
  • This is rarely used in acute SBO but can help visualize obstruction in the colon or ileocecal valve.

Other Diagnostic Tests

• Endoscopy
  • In some cases, especially if there is a concern for a nonmechanical cause such as a malignancy, endoscopic evaluation (eg, upper endoscopy or colonoscopy) may be performed. This is particularly useful for evaluating patients suspected of tumors or foreign bodies causing the obstruction.
• Diagnostic laparoscopy
  • In cases where the etiology of the SBO is unclear or there is a suspicion of strangulation, peritonitis, or ischemia, diagnostic laparoscopy may be employed. This minimally invasive operation allows direct visualization of the abdominal cavity, aiding in the diagnosis of the cause and in planning surgical intervention.
• Magnetic resonance imaging (MRI)
  • MRI is occasionally used, particularly in special circumstances such as with patients who are pregnant or when CT is contraindicated. This study provides detailed soft tissue imaging and can be useful for detecting complications like ischemia or tumors.

Treatment / Management

The treatment and management of SBO require a multidisciplinary approach that prioritizes early recognition and intervention to optimize patient outcomes. 

Initial Resuscitation

The initial management of SBO begins with fluid resuscitation to address hypovolemia caused by third-spacing of fluids, vomiting, and reduced oral intake. Isotonic intravenous fluids, such as lactated Ringer or normal saline, are administered to restore intravascular volume and correct electrolyte imbalances, particularly hypokalemia and metabolic alkalosis. Nasogastric tube decompression is employed to alleviate gastric distension and vomiting, reduce the risk of aspiration, and provide symptomatic relief.

In prolonged cases or when surgery is delayed, nutritional support via enteral or parenteral routes may be necessary to prevent malnutrition. Broad-spectrum antibiotics targeting gut flora, including gram-negative and anaerobic bacteria, should be administered, particularly when strangulation or perforation is suspected.[28][29][30] Surgical consultation should be obtained promptly, as many cases of SBO, especially those involving complete obstruction or signs of ischemia, require operative management.[31](B3)

Nonoperative Management

Nonoperative or conservative management is suitable for simple SBO without signs of ischemia, peritonitis, or clinical deterioration. This approach involves bowel rest with the patient kept nil per os to minimize bowel distension. Serial monitoring of vital signs, abdominal exams, and laboratory tests is essential to detect any worsening condition. Water-soluble contrast studies using agents like gastrograffin can help resolve adhesional obstructions and offer prognostic value by indicating whether the obstruction may resolve without surgery.

Indications for Surgery

Surgical intervention is indicated for patients with evidence of strangulation, such as fever, tachycardia, localized tenderness, leukocytosis, or acidosis. Surgical intervention is imperative when SBO fails to resolve with conservative measures or when there are signs of peritonitis or bowel ischemia, ensuring timely and effective treatment.[32](B3)

Surgical Management

Surgical options depend on the underlying cause of SBO. Adhesiolysis is the most common procedure, performed laparoscopically or via open surgery, to release fibrous bands causing the obstruction. For strangulated obstruction, resection of the necrotic bowel may be required, followed by either primary anastomosis or stoma formation, depending on the extent of damage and patient stability. In cases of questionable bowel viability or extensive ischemia, second-look laparotomy or temporary abdominal closure techniques, such as vacuum-assisted closure, may be required.[33][34] 

Hernia-related obstructions are managed with hernia reduction and repair, while tumor-related obstructions often necessitate bowel resection, sometimes with palliative intent in advanced malignancy cases. Palliative options like octreotide can be employed for malignant obstructions.[35] Preventative strategies, such as laparoscopic techniques and barrier agents like a chemically modified membrane made of sodium hyaluronate and carboxymethylcellulose that's applied to the surface of tissues, help reduce adhesion formation.

Postoperative Care

Postoperative care involves close monitoring for complications such as infection, anastomotic leaks, or recurrent obstruction. Early ambulation is encouraged to reduce the risk of venous thromboembolism and expedite recovery. Nutritional support with gradual reintroduction of oral intake is guided by the resolution of bowel function, evidenced by decreased NG tube output, bowel sounds, and passage of gas or stool.

Management of Functional Obstruction

Functional obstructions, such as paralytic ileus, are treated with supportive measures, including bowel rest, correction of metabolic abnormalities, reduction in narcotic use, and the potential use of prokinetic agents like metoclopramide.

Recurrent Obstructions

For patients with recurrent SBO, often due to adhesions, preventive strategies may include minimally invasive surgical techniques and adhesion barriers during surgery to reduce the formation of future adhesions.

Interdisciplinary Approach

Optimal management of SBO relies on collaboration among surgeons, radiologists, gastroenterologists, critical care specialists, pharmacists, and nursing teams. This interdisciplinary approach enhances patient-centered care, reduces complications, and improves outcomes while minimizing the risk of recurrence.

Differential Diagnosis

The differential diagnosis of SBO encompasses a range of conditions that can mimic or contribute to its clinical presentation. Differentiating among these conditions is critical for accurate diagnosis and appropriate management. The primary categories of differential diagnoses include:

• Mechanical 
  • Adhesions
  • Hernias
  • Neoplasms
  • Gallstone ileus
  • Volvulus
  • Intussusception
  • Foreign bodies
  • Crohn disease
• Functional 
  • Postoperative ileus
  • Ogilvie syndrome
  • Neuromuscular disorders
  • Medications
• Gynecological 
  • Endometriosis
  • Ovarian torsion or masses
• Vascular 
  • Mesenteric ischemia
  • Strangulated obstruction
• Metabolic and systemic 
  • Electrolyte imbalances
  • Diabetes mellitus
• Infectious
  • Tuberculosis
  • Intraabdominal abscesses
• Pediatric-specific 
  • Malrotation with volvulus
  • Meckel diverticulum
  • Congenital atresia or stenosis

Surgical Oncology

Neoplasms involving the peritoneal cavity, whether primary or metastatic and benign or malignant, represent a significant cause of SBO. The surgical and oncological management of such cases is tailored based on the type of tumor, its grade, stage, and the extent of peritoneal involvement. Treatment strategies may range from nonoperative medical management to a multimodality approach incorporating chemotherapy, radiation, and surgical intervention.

Palliative management plays a critical role for patients with advanced disease or those unsuitable for curative treatment. Approaches to palliate bowel obstruction include medications to reduce symptoms, nasogastric or intestinal decompression tubes, stoma formation, tube enterostomy, or the placement of intestinal stents.[36] These measures aim to relieve symptoms, improve quality of life, and manage complications associated with obstructive neoplastic conditions.

Prognosis

The prognosis of SBO depends on several factors, including the underlying etiology, the patient's overall health status, the timeliness and appropriateness of treatment, and whether the obstruction is simple or complicated (eg, involving strangulation or perforation). Early diagnosis and prompt management significantly improve outcomes, while delays in treatment are associated with higher morbidity and mortality rates.

Simple SBO

Patients with simple SBO, where there is no evidence of ischemia or perforation, generally have a favorable prognosis. Nonoperative management resolves most cases of partial or adhesional obstructions without surgery. Recovery is typically rapid if managed appropriately, with mortality rates in these cases being low (1%–5%). However, recurrent SBO remains a challenge, particularly in patients with prior surgeries and adhesions.

Complicated SBO

Complicated SBO, involving bowel strangulation, ischemia, or perforation, carries a significantly worse prognosis due to the risk of sepsis, peritonitis, and multiorgan failure. Mortality rates in these cases range from 10% to 40%, depending on the extent of bowel compromise and the speed of surgical intervention. Strangulated obstructions, which may progress to gangrene or perforation, demand urgent surgical treatment to minimize life-threatening complications.

Prognostic Factors

Several factors influence prognosis:

• Etiology
  • Adhesional SBO generally has a better prognosis than obstruction caused by malignancy or inflammatory bowel disease. Malignant bowel obstruction often indicates advanced disease, with limited curative options and a focus on palliative care.
• Age and comorbidities
  • Elderly patients and those with significant comorbid conditions, such as cardiovascular or respiratory disease, have higher risks of complications and mortality.
• Timeliness of treatment
  • Delays in diagnosis or intervention can worsen outcomes due to prolonged ischemia, necrosis, or systemic infection.
• Extent of bowel damage
  • The need for extensive bowel resection may lead to short bowel syndrome, nutritional deficiencies, and long-term morbidity.

Long-Term Outcomes

SBOs, particularly those caused by adhesions, can recur in about 20% of patients.[37] Preventive strategies, including minimally invasive surgery and adhesion barriers, can help reduce recurrence. Functional recovery after SBO varies; most patients resume normal bowel function, while some may experience prolonged ileus or other complications requiring further intervention.

Survival Rates

Long-term survival is excellent for simple SBO, especially when the obstruction is resolved nonoperatively or via uncomplicated surgery. In cases of malignant obstruction, survival is dictated by the stage and progression of the underlying malignancy, often requiring a palliative approach.

Complications

SBO can lead to a range of complications, many of which are life-threatening if not promptly recognized and managed. These complications arise from the mechanical disruption of intestinal flow, vascular compromise, or secondary systemic effects.

Mechanical and Local Complications

• Bowel ischemia and strangulation
  • Increased intraluminal pressure compromises venous return, leading to bowel wall edema and, eventually, arterial ischemia. Strangulation occurs in approximately 25% of cases, particularly in closed-loop obstructions or hernias, and may result in necrosis, perforation, and gangrene.[38]
• Perforation and peritonitis
  • Persistent ischemia or bowel necrosis can lead to perforation, spilling luminal contents into the peritoneal cavity and causing bacterial peritonitis. This is a surgical emergency with a high mortality risk.
• Adhesion formation
  • Surgical or inflammatory causes of SBO may result in further adhesion formation, increasing the risk of recurrent obstructions.
• Fistula formation
  • Chronic obstructions or associated diseases, such as Crohn disease, can lead to abnormal connections between bowel loops or other organs, complicating management.

Systemic Complications

• Sepsis and multiorgan failure
  • Bacterial translocation across ischemic or necrotic bowel walls can lead to bacteremia, septic shock, and multiorgan dysfunction.
• Electrolyte imbalance and dehydration
  • Fluid sequestration within the bowel and vomiting lead to significant fluid and electrolyte losses, causing hypovolemia, metabolic alkalosis (from vomiting), or acidosis (with bowel ischemia or necrosis).
• Malnutrition
  • Prolonged obstruction, especially in chronic or partial cases, can result in malabsorption, weight loss, and nutritional deficiencies.

Postsurgical Complications

• Anastomotic leak
  • In cases requiring bowel resection, anastomotic leaks may occur, leading to peritonitis or abscess formation.
• Wound infection and dehiscence
  • Postoperative infections and delayed wound healing are common complications following surgical intervention for SBO.

Palliative Complications

In patients managed palliatively for malignancy-related SBO, complications may include recurrent obstruction, inadequate symptom relief, and device-related issues such as stoma malfunction or infection.