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Bowel obstruction
Bowel obstruction
Bowel obstruction
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Bowel obstruction
Other namesIntestinal obstruction, intestinal occlusion
Upright abdominal X-ray demonstrating a small bowel obstruction. Note multiple air fluid levels.
SpecialtyGeneral surgery
SymptomsAbdominal pain, vomiting, bloating, not passing gas[1]
ComplicationsSepsis, bowel ischemia, bowel perforation[1]
CausesAdhesions, hernias, volvulus, endometriosis, inflammatory bowel disease, appendicitis, tumors, diverticulitis, ischemic bowel, tuberculosis, intussusception[2][1]
Diagnostic methodMedical imaging[1]
TreatmentConservative care, surgery[2]
Frequency3.2 million (2015)<!— incidence —>[3]
Deaths238,733 (2019)[4]

Bowel obstruction, also known as intestinal obstruction, is a mechanical or functional obstruction of the intestines that prevents the normal movement of the products of digestion.[2][5] Either the small bowel or large bowel may be affected.[1] Signs and symptoms include abdominal pain, vomiting, bloating and not passing gas.[1] Mechanical obstruction is the cause of about 5 to 15% of cases of severe abdominal pain of sudden onset requiring admission to hospital.[1][2]

Causes of bowel obstruction include adhesions, hernias, volvulus, endometriosis, inflammatory bowel disease, appendicitis, tumors, diverticulitis, ischemic bowel, tuberculosis and intussusception.[1][2] Small bowel obstructions are most often due to adhesions and hernias while large bowel obstructions are most often due to tumors and volvulus.[1][2] The diagnosis may be made on plain X-rays; however, CT scan is more accurate.[1] Ultrasound or MRI may help in the diagnosis of children or pregnant women.[1]

The condition may be treated conservatively or with surgery.[2] Typically intravenous fluids are given, a nasogastric (NG) tube is placed through the nose into the stomach to decompress the intestines, and pain medications are given.[2] Antibiotics are often given.[2] In small bowel obstruction about 25% require surgery.[6] Complications may include sepsis, bowel ischemia and bowel perforation.[1]

About 3.2 million cases of bowel obstruction occurred in 2015, which resulted in 264,000 deaths.[3][7] Both sexes are equally affected and the condition can occur at any age.[6] Bowel obstruction has been documented throughout history, with cases detailed in the Ebers Papyrus of 1550 BC and by Hippocrates.[8]

Signs and symptoms

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Depending on the level of obstruction, bowel obstruction can present with abdominal pain, abdominal distension, and constipation. Bowel obstruction may be complicated by dehydration and electrolyte abnormalities due to vomiting; respiratory compromise from pressure on the diaphragm by a distended abdomen, or aspiration of vomitus; bowel ischemia or perforation from prolonged distension or pressure from a foreign body and subsequently sepsis due to bowel flora.[9]

Tinkly bowel sounds
Tinkly bowel sounds as heard with a stethoscope in someone with a small bowel obstruction.
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In small bowel obstruction, the pain tends to be colicky (cramping and intermittent) in nature, with spasms lasting a few minutes. The pain tends to be central and mid-abdominal. Vomiting may occur before constipation.[9] Common physical exam findings may include signs of dehydration, abdominal distension with tympany, nonspecific abdominal tenderness, and high pitched tinkly bowel sounds.[10]

In large bowel obstruction, the pain is felt lower in the abdomen and the spasms last longer. Common symptoms include abdominal pain, distension, and severe constipation.[11] Constipation occurs earlier and vomiting may be less prominent. Proximal obstruction of the large bowel may present as small bowel obstruction.[9] Patients may notice a history of bloating and narrowing of stools before the onset of more severe symptoms. Symptoms can present quickly in the cases of volvulus and can present over a longer period of time in the setting of cancer. Common physical exam findings may include a palpable hernia, abdominal distension with tympany, nonspecific lower abdominal tenderness, and a rectal mass.[6]

Causes

[edit]

Small bowel obstruction

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Upright abdominal X-ray demonstrating a small bowel obstruction. Note multiple air fluid levels.

Causes of small bowel obstruction include:[2]

After abdominal surgery, the incidence of small bowel obstruction from any cause is 9%. In those where the cause of the obstruction was clear, adhesions are the single most common cause (more than half).[13]

Large bowel obstruction

[edit]
Upright abdominal X-ray of a person with a large bowel obstruction showing multiple air fluid levels and dilated loops of bowel

Causes of large bowel obstruction include:[14]

Outlet obstruction

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Outlet obstruction is a sub-type of large bowel obstruction and refers to conditions affecting the anorectal region that obstruct defecation, specifically conditions of the pelvic floor and anal sphincters. Outlet obstruction can be classified into four groups.[15]

Diagnosis

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Small bowel dilation on CT scan in adults[16]
Diameter Assessment
<2.5 cm Non-dilated
2.5-2.9 cm Mildly dilated
3–4 cm Moderately dilated
>4 cm Severely dilated
A small bowel obstruction as seen on CT
Average inner diameters and ranges of different sections of the large intestine.[17]

The main diagnostic tools are blood tests, X-rays of the abdomen, CT scanning, and ultrasound. If a mass is identified, biopsy may determine the nature of the mass.[citation needed]

Radiological signs of bowel obstruction include bowel distension (small bowel loops dilated >3 cm) and the presence of multiple (more than 2) air-fluid levels on supine and erect abdominal radiographs.[18] Ultrasounds may be as useful as CT scanning to make the diagnosis.[19]

Contrast enema or small bowel series or CT scan can be used to define the level of obstruction, whether the obstruction is partial or complete, and to help define the cause of the obstruction. The appearance of water-soluble contrast in the cecum on an abdominal radiograph within 24 hours of it being given by mouth predicts resolution of an adhesive small bowel obstruction with sensitivity of 97% and specificity of 96%.[20]

Colonoscopy, small bowel investigation with ingested camera or push endoscopy, and laparoscopy are other diagnostic options.

  • Small bowel obstruction on ultrasound[21]
  • Small bowel obstruction on ultrasound[21]
  • Small bowel obstruction on ultrasound[21]
    Small bowel obstruction on ultrasound[21]

Differential diagnosis

[edit]

Differential diagnoses of bowel obstruction include:

Treatment

[edit]

Treatment of small and large bowel obstructions are initially similar and non-operative management is usually the initial management strategy as the majority of small bowel obstruction resolve spontaneously with non-operative management.[10][23] Patients are monitored by the surgical team for signs of improvement and resolution of the obstruction on imaging; if the obstruction does not clear then surgical management for the treatment of the causative lesion is required.[24] In malignant large bowel obstruction, endoscopically placed self-expanding metal stents may be used to temporarily relieve the obstruction as a bridge to surgery,[25] or as palliation.[26] Diagnosis of the type of bowel obstruction is normally conducted through initial plain radiograph of the abdomen, luminal contrast studies, computed tomography scan, or ultrasonography prior to determining the best type of treatment.[27]

Further research is needed to find out if parenteral nutrition is of benefit to people with an inoperable blockage of the bowel caused by advanced cancer.[28]

Small bowel obstruction

[edit]

In the management of small bowel obstructions, a commonly quoted surgical aphorism is: "never let the sun rise or set on small-bowel obstruction"[29] because about 5.5%[29] of small bowel obstructions are ultimately fatal if treatment is delayed. Improvements in radiological imaging of small bowel obstructions allow for confident distinction between simple obstructions, that can be treated conservatively, and obstructions that are surgical emergencies (volvulus, closed-loop obstructions, ischemic bowel, incarcerated hernias, etc.).[2] Exam findings of bowel compromise requiring immediate surgery include: severe abdominal pain, signs of peritonitis such as rebound tenderness, elevated heart rate, fever, and elevated inflammatory markers on lab work, such as lactic acid.[10][23]

A small flexible tube (nasogastric tube) may be inserted through the nose into the stomach to help decompress the dilated bowel. This tube is uncomfortable but relieves the abdominal cramps, distention, and vomiting. Intravenous therapy is utilized and the urine output may be monitored with a catheter in the bladder.[30][10]

Most people with SBO are initially managed conservatively because in many cases, the bowel will open up. Some adhesions loosen up and the obstruction resolves. The patient is examined several times a day, and X-ray images are made to ensure he or she is not getting clinically worse.[31]

Conservative treatment involves insertion of a nasogastric tube, correction of dehydration and electrolyte abnormalities. Opioid pain relievers may be used for patients with severe pain but alternate pain relievers are preferred as opioids can decrease bowel motility.[10]Antiemetics may be administered if the patient is vomiting. Adhesive obstructions often settle without surgery. If the obstruction is complete surgery is usually required.

Most patients improve with conservative care in 2–5 days. When the obstruction is cancer, surgery is the only treatment. Those with bowel resection or lysis of adhesions usually stay in the hospital a few more days until they can eat and walk.[32]

Small bowel obstruction caused by Crohn's disease, peritoneal carcinomatosis, sclerosing peritonitis, radiation enteritis, and postpartum bowel obstruction are typically treated conservatively, i.e. without surgery.

Prognosis

[edit]

The prognosis for non-ischemic cases of SBO is good with mortality rates of 3–5%, while prognosis for SBO with ischemia is fair with mortality rates as high as 30%.[33]

Cases of SBO related to cancer are more complicated and require additional intervention to address the malignancy, recurrence, and metastasis, and thus are associated with a more poor prognosis.[22] Surgical options in patients with malignant bowel obstruction need to be considered carefully as while it may provide relief of symptoms in the short term, there is a high risk of mortality and re-obstruction.[34]

All cases of abdominal surgical intervention are associated with increased risk of future small-bowel obstructions. Statistics from U.S. healthcare report 18.1% re-admittance rate within 30 days for patients who undergo SBO surgery.[35] More than 90% of patients also form adhesions after major abdominal surgery.[36] Common consequences of these adhesions include small-bowel obstruction, chronic abdominal pain, pelvic pain, and infertility.[36]

See also

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References

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[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Bowel obstruction

View on Grokipedia
from Grokipedia
Bowel obstruction, also known as intestinal obstruction, is a partial or complete blockage of the small or that prevents the normal passage of food, fluids, gas, and stool, resulting in their accumulation proximal to the site of obstruction. This condition can arise from mechanical causes, such as physical barriers within the lumen, wall, or , or from functional causes, including paralytic where intestinal motility is impaired without a physical blockage. As a common , it requires prompt diagnosis and intervention to prevent life-threatening complications like bowel ischemia, , , and . Bowel obstructions are classified by location and , with small bowel obstruction (SBO) being more prevalent than large bowel obstruction (LBO). In SBO, which accounts for the majority of cases, postoperative adhesions represent 55–75% of etiologies, while adhesions, hernias, and neoplasms contribute to approximately 90% of cases. LBO is often linked to (up to 60% of cases in adults), , or , and it carries a higher of hemodynamic instability and due to the colon's larger capacity. Risk factors include prior , inflammatory conditions like , and malignancies. Clinically, patients with bowel obstruction present with colicky , , (often bilious in SBO), progressive distension, and obstipation (inability to pass stool or flatus). relies on history and physical findings, such as a distended, tympanic with hyperactive or absent bowel sounds, supported by : plain abdominal radiographs may reveal dilated loops with air-fluid levels, while computed tomography (CT) provides detailed etiology and obstruction level in over 90% of cases. Initial management involves fluid resuscitation, nasogastric decompression, and bowel rest, with surgical intervention indicated for complete obstructions, ischemia, or failure of conservative within 48–72 hours.

Epidemiology

Incidence and Prevalence

Bowel obstruction remains a significant concern, with intestinal obstruction and paralytic collectively accounting for approximately 15.8 million incident cases worldwide in 2021, translating to an estimated incidence of about 2 cases per 1,000 people annually. Small bowel obstruction (SBO) constitutes the majority of mechanical bowel obstructions, comprising 60% to 80% of cases, and its incidence is notably higher in developed countries, where postoperative adhesions drive up to 75% of occurrences due to increased rates of prior abdominal surgeries. In contrast, large bowel obstruction (LBO) represents 20% to 25% of all intestinal obstructions and shows a stronger age-related increase, with global age-standardized incidence rates for paralytic and intestinal obstruction reaching 643 cases per 100,000 among individuals aged 65 years and older in 2021. Adhesive SBO, the most common subtype, has a postoperative incidence ranging from 4.6% to 9% following abdominal surgery, with cumulative risks up to 25-30% reported after major procedures such as colectomy. Recent analyses from the Global Burden of Disease Study indicate a rising burden in older adults, with incident cases of paralytic ileus and intestinal obstruction among those aged 65 and over increasing by over 50% from 1990 to 2021, and projections suggesting further growth by 2030 due to aging populations and persistent surgical volumes. Geographic variations highlight these patterns: SBO predominates in Western and high-income countries, where adhesions account for 60% to 70% of cases, whereas LBO is more prevalent in developing regions, often linked to higher rates of sigmoid volvulus and infectious etiologies comprising up to 30% of obstructions.

Risk Factors

Prior abdominal or pelvic is the leading risk factor for small bowel obstruction (SBO), primarily due to the formation of postoperative adhesions that account for 65% to 75% of cases. A further elevates this risk by promoting and stricture formation in the bowel wall, with postoperative radiation for rectal cancer associated with a significantly higher incidence of SBO compared to alone. Demographic factors play a notable , including advanced age, where individuals over 65 years experience a higher overall of bowel obstruction, with approximately 10-12% of abdominal presentations in this group attributed to SBO. Male gender increases susceptibility to hernias, particularly inguinal types, which are a common cause of obstruction and occur with a lifetime of 27% in men versus 3% in women. is also implicated, contributing to both SBO and large bowel obstruction (LBO) through mechanisms such as increased intra-abdominal pressure and postoperative complications. Certain medical conditions heighten predisposition, such as , where substantially raises the odds of SBO due to chronic inflammation and stricture development. Malignancies, especially , are a primary driver of LBO, accounting for over 60% of cases. Hernias, including inguinal and incisional varieties, represent another key risk, often leading to mechanical obstruction when bowel loops become incarcerated. Lifestyle factors include , which exacerbates formation following and thereby amplifies the risk of subsequent bowel obstruction. A low-fiber diet contributes to , particularly in cases of outlet obstruction, by promoting hard, dry stool that can block the distal bowel.

Mechanical Obstruction

Mechanical obstruction occurs when a physical barrier impedes the passage of intestinal contents through the bowel lumen or wall, resulting in the accumulation of ingested fluid, electrolytes, and swallowed air proximal to the site of blockage. This leads to progressive dilation of the bowel loops upstream, with increased intraluminal pressure and heightened wall tension as the obstruction persists. Distal to the obstruction, the bowel collapses due to the absence of ongoing content flow, accompanied by systemic from reduced fluid absorption and compromised venous return in the affected segments. In cases of strangulation, where the obstruction compromises the mesenteric blood supply, follows venous obstruction, initiating bowel wall ischemia that can progress to full-thickness and within as little as 6 hours if untreated. A particularly dangerous variant is closed-loop obstruction, in which both the afferent and efferent limbs of a bowel segment are occluded at a single site, forming an isolated loop that traps fluid and gas; this causes rapid intraluminal pressure elevation, exacerbating wall tension and heightening the risk of and . Unlike functional obstructions such as , which stem from failure without structural barriers, mechanical types involve tangible impediments that directly alter luminal dynamics. Physiological differences between small and large bowel obstructions influence symptom onset: small bowel obstruction typically provokes earlier and more frequent due to the shorter distance from the obstruction to the , allowing rapid retrograde accumulation of contents, whereas large bowel obstruction often manifests with greater from the larger luminal capacity and slower pressure buildup proximal to the blockage.

Functional Obstruction

Functional obstruction, also termed paralytic or pseudo-obstruction, arises from neuromuscular dysfunction that impairs bowel , resulting in aperistalsis and failure of propulsive peristaltic waves despite a patent intestinal lumen. This condition halts the normal forward movement of intestinal contents without any physical barrier, often due to disruption in the or smooth muscle activity. Inflammation within the intestinal muscularis, triggered by various insults, plays a key role in inhibiting coordinated contractions across the bowel. Common triggers include electrolyte imbalances, such as , which disrupt ion channels essential for depolarization and contraction, leading to widespread motility failure. Medications like opioids, which bind to mu-receptors in the gut to reduce , and anticholinergics, which block parasympathetic signaling, frequently precipitate this state, causing diffuse bowel dilation without a distinct transition point on radiographic imaging. These factors result in accumulation of gas and fluid throughout the intestine, mimicking obstruction symptoms but lacking anatomical blockage. A notable variant is Ogilvie's syndrome, or acute colonic pseudo-obstruction, involving pronounced dilation of the colon, particularly the , due to autonomic dysregulation favoring sympathetic over parasympathetic activity. Cecal diameters exceeding 10 cm heighten the risk of ischemia and , necessitating urgent intervention to avert complications. Postoperative represents another frequent manifestation, typically enduring 2 to 5 days post-surgery as inflammatory mediators and surgical manipulation suppress ; it resolves spontaneously in most cases with supportive care. Differentiation from mechanical obstruction relies on , which reveals uniform dilation without evidence of , masses, or a transition point, confirming the functional nature of the blockage. While presenting with similar , distension, and , functional obstruction stems purely from deficits rather than structural impediments.

Causes

Small Bowel Obstruction

Small bowel obstruction (SBO) arises from various mechanical etiologies that impede the passage of intestinal contents through the or , with adhesions, hernias, , neoplasms, and other rare conditions being the primary culprits. Adhesions from prior represent the most common cause, accounting for 60-80% of SBO cases; these form as fibrous bands between peritoneal surfaces, often kinking or compressing the bowel loops and leading to partial or complete blockage. Hernias, either external (such as inguinal or femoral) or internal (such as paraduodenal), contribute to 10-15% of SBO incidents, where a segment of small bowel herniates through a defect in the or , potentially resulting in incarceration. Incarceration occurs when the herniated bowel becomes trapped, and in approximately 10% of these cases, it progresses to strangulation, compromising blood supply and risking ischemia or . Inflammatory conditions also play a role, particularly in patients with underlying gastrointestinal disorders. leads to strictures in the small bowel due to chronic transmural inflammation and , accounting for about 5% of SBO cases; these narrow segments progressively obstruct luminal flow. Patients with Crohn's disease-related strictures should avoid self-treatment for constipation using laxatives, enemas, or fiber supplements during suspected obstruction, as these can exacerbate the blockage and lead to harm. Similarly, radiation enteritis, often a of pelvic or abdominal radiotherapy, induces and scarring in the small bowel wall, causing delayed-onset strictures and obstruction. Neoplastic causes are less frequent, with primary small bowel tumors—such as adenocarcinomas, tumors, or gastrointestinal stromal tumors—responsible for fewer than 5% of SBO episodes, given their rarity in the . Metastases from distant primaries, including or , more commonly cause extrinsic compression or intraluminal growth leading to blockage. Other etiologies include intussusception, which in adults often stems from a lead point like a tumor and accounts for about 1% of SBO cases, where one bowel segment telescopes into another, causing obstruction. , resulting from the ectopic migration of a large through a cholecystoenteric into the small bowel (typically lodging at the ), represents 1-4% of mechanical obstructions and is more prevalent in elderly females.

Large Bowel Obstruction

Large bowel obstruction (LBO) arises from various etiologies that impede the passage of contents through the colon or , with being the predominant cause. accounts for approximately 50-60% of LBO cases, frequently involving left-sided tumors that produce circumferential narrowing known as apple-core lesions, which constrict the lumen and lead to progressive blockage. These tumors often manifest in the sigmoid or , contributing to the higher incidence of obstructive presentations in advanced disease. Volvulus represents another significant etiology, comprising 10-15% of LBOs, where the colon twists upon itself, creating a closed-loop configuration that risks ischemia due to compromised blood supply. Sigmoid volvulus is the most common variant in Western populations, while cecal volvulus occurs less frequently but can lead to rapid deterioration; both are more prevalent among elderly individuals or those in institutional settings, often linked to chronic constipation or redundant colonic loops. Diverticulitis contributes to about 20% of LBO cases, typically through the formation of strictures or pericolic abscesses that narrow the colonic lumen following repeated episodes of . These complications arise from inflamed diverticula, particularly in the , leading to and obstruction over time. Outlet obstruction, a subtype of LBO affecting the distal and , often results from , , or , predominantly in debilitated or elderly patients with impaired mobility or neurological conditions. Fecal impaction involves hardened stool accumulation that mechanically blocks evacuation, while rectal prolapse entails protrusion of the rectal wall, and anal stenosis features scarring that narrows the , all exacerbating and . Benign causes also play a role, including post-radiation strictures from prior pelvic radiotherapy, which induce fibrotic narrowing in the rectosigmoid region, and flares of such as or that provoke colonic inflammation and subsequent stricture formation. These non-malignant etiologies underscore the diverse mechanisms leading to LBO, often with a slower symptom onset compared to small bowel obstruction.

Signs and Symptoms

General Presentation

Bowel obstruction typically presents with a constellation of symptoms arising from the mechanical or functional blockage of intestinal contents, leading to accumulation of gas and fluid proximal to the site of obstruction. Patients commonly experience crampy that waxes and wanes, often starting in the periumbilical region and potentially localizing over time as the condition progresses. This pain results from increased attempting to overcome the obstruction and distension of the bowel wall. Vomiting is a frequent early symptom, initially bilious in proximal obstructions and becoming feculent in distal or prolonged cases, which contributes to significant fluid loss and . The , combined with third-spacing of fluids into the bowel lumen and , can lead to , manifesting as and . Abdominal distension develops progressively as gas and fluid accumulate, often resulting in a visibly bloated . Constipation or obstipation follows, with patients unable to pass stool or flatus; this is absolute in complete obstructions and relative in partial ones. Systemic signs may include due to and fever if bowel ischemia develops, alongside signs of such as reduced urine output from third-spacing. These manifestations can vary slightly by the segment of bowel affected, but the core presentation remains consistent across cases. Red flag symptoms requiring immediate medical attention include severe abdominal pain or cramping; persistent vomiting or nausea; inability to pass gas or stool at all; significant bloating or swollen abdomen; blood in stool or vomiting blood; fever, dizziness, or feeling very unwell.

Differences Between Small and Large Bowel

Bowel obstructions in the (SBO) and (LBO) share some overlapping features such as and , but they exhibit distinct symptom profiles due to differences in anatomy and the progression of luminal blockage. In SBO, typically occurs early, often within hours of onset, as the blockage is proximal and leads to rapid accumulation of gastrointestinal contents. This contrasts with LBO, where is delayed, usually appearing after several days, because the obstruction is more distal and allows initial decompression through vomiting less readily. Abdominal distension also varies significantly between the two. SBO often presents with minimal initial distension, as the small bowel has limited capacity for expansion, though it may become more noticeable later. In LBO, marked distension develops prominently and early, with visible loops of bowel in the abdomen due to the larger diameter and greater gas/fluid retention in the colon. Bowel sounds further differentiate the presentations: SBO is associated with high-pitched, tinkling hyperactive sounds proximal to the obstruction, reflecting increased peristalsis attempting to overcome the blockage. Conversely, LBO typically features absent or hypoactive bowel sounds, indicating more advanced ileus and reduced motility. The nature of the obstruction influences additional symptoms. Partial SBO may manifest as intermittent colicky pain with passage of some stool or , allowing partial decompression, whereas complete SBO leads to rapid from persistent and fluid sequestration. In LBO, particularly outlet obstructions near the , patients often experience tenesmus—a sensation of incomplete evacuation— along with or paradoxical , and if the cause is malignant such as . Pediatric presentations, especially intussusception as a cause of bowel obstruction, highlight age-specific differences. In children, intussusception commonly produces a "currant jelly" stool—mucoid and bloody—due to mucosal ischemia and sloughing, accompanied by episodic pain and vomiting. This feature is absent in adults, where intussusception tends to present with more chronic, intermittent abdominal pain without the characteristic bloody stool.

Diagnosis

Clinical Evaluation

The clinical evaluation of suspected bowel obstruction begins with a detailed to identify key features suggestive of the condition. Patients typically report an acute onset of crampy, colicky that may become constant if complications arise, often localized to the periumbilical region in small bowel involvement. is a prominent symptom, usually bilious and occurring early and frequently in proximal small bowel obstructions, with increasing volume and feculent character in distal cases. A of obstipation or absence of bowel movements and flatus for at least 24-48 hours is highly indicative, distinguishing obstruction from other abdominal disorders. Inquiry into prior abdominal surgery is essential, as adhesions account for 60-75% of small bowel obstructions and have 85% sensitivity and 78% specificity for adhesive etiology. Additional elements include recent radiation therapy or malignancy , which may suggest extrinsic or functional causes. Physical examination focuses on assessing for signs of obstruction and its severity. Abdominal distention is evident in approximately 60% of cases, more pronounced in distal obstructions, with tympany on percussion and high-pitched, hyperactive bowel sounds early in the process, potentially progressing to hypoactive or absent sounds. Tenderness is common, with voluntary guarding indicating localized inflammation and involuntary guarding or rebound tenderness signaling peritonitis from perforation. Palpation should evaluate for masses, such as tumors or fecal impaction, and inspection of hernia sites for incarcerated or strangulated defects, which require urgent attention. A digital rectal examination is performed to detect fecal impaction, blood, or rectal masses contributing to outlet obstruction. Vital signs assessment is critical to identify systemic involvement. and suggest from third-space fluid losses or , while fever may indicate or ischemia. Signs of , including dry mucous membranes, sunken eyes, and reduced skin turgor, are frequently observed due to and sequestration of fluids in the bowel. Red flags during prompt immediate intervention. Sudden worsening of to a constant, severe quality raises concern for strangulation, and rebound tenderness or peritonism indicates , both necessitating emergent surgical consultation.

Imaging and Laboratory Tests

plays a central role in confirming the of bowel obstruction, identifying its location, and assessing for complications such as ischemia or . abdominal serves as the initial modality due to its and low cost. and upright views can reveal dilated bowel loops and air-fluid levels, which are characteristic findings. Small bowel loops greater than 3 cm in diameter or colonic loops exceeding 6 cm suggest obstruction, though these thresholds may vary slightly based on factors. The sensitivity of plain X-rays for detecting bowel obstruction is approximately 70%, making it a useful first-line tool but often requiring further for definitive . Computed tomography (CT) scanning with intravenous contrast is considered the gold standard for diagnosing bowel obstruction, offering high sensitivity exceeding 90% and superior anatomic detail. It accurately identifies the transition point between dilated proximal bowel and collapsed distal segments, detects free intraperitoneal air indicating , and reveals signs of ischemia such as bowel wall thickening greater than 3 mm, target sign, or mesenteric stranding. Multidetector CT further enhances detection of underlying causes like adhesions or tumors. In cases of suspected strangulation, CT can guide urgent surgical intervention by highlighting vascular compromise. Ultrasound is particularly valuable in pediatric patients and pregnant individuals to avoid , with sensitivity approaching 90% for small bowel obstruction in children. It can detect dilated fluid-filled loops, free intraperitoneal fluid, or intussusception as a cause of obstruction. In pregnancy, transabdominal helps confirm obstruction while minimizing fetal risk, though its use is limited by operator dependence and patient body habitus. Contrast studies, such as water-soluble contrast enema, are employed primarily for suspected large bowel obstruction to evaluate completeness and potential therapeutic decompression. Administered under low pressure, it delineates the site of obstruction and rules out , with high accuracy in confirming or strictures. This modality is contraindicated if is suspected. Laboratory tests complement imaging by assessing for complications and guiding management. A often shows with left shift, indicating infection or inflammation. Elevated serum lactate levels suggest bowel ischemia or , prompting urgent evaluation. panels may reveal imbalances such as or due to and . Serum is measured to differentiate obstruction from , as mild elevations can occur in either condition.

Differential Diagnosis

Bowel obstruction presents with symptoms such as , distension, , and , which overlap with several other acute abdominal conditions, necessitating a careful to guide appropriate management. Common mimics include inflammatory processes in the , motility disorders, vascular emergencies, and gynecologic pathologies, each distinguished by specific clinical features, laboratory findings, and characteristics. In the category of acute abdomen causes, typically manifests as right lower quadrant (RLQ) pain with localized tenderness, often accompanied by anorexia and low-grade fever, but without significant or bilious vomiting seen in small bowel obstruction. , more common in the large bowel context, presents with left lower quadrant (LLQ) pain, fever, and , along with possible localized , differing from the diffuse distension and obstipation of colonic obstruction. Motility disorders must also be considered, as they can produce similar obstructive symptoms without mechanical blockage. Gastroparesis leads to upper gastrointestinal symptoms like early satiety and nausea after meals, with delayed gastric emptying confirmed by scintigraphy, contrasting the mid-abdominal cramping and bilious emesis of small bowel obstruction. Simple constipation or narcotic bowel syndrome may cause abdominal discomfort and reduced bowel movements but lacks the acute vomiting and progressive distension of true obstruction, often resolving with conservative measures. Paralytic ileus, a functional adynamic state, features diffuse bowel dilation without a transition point on imaging, typically following surgery or electrolyte imbalances, unlike the proximal dilation and distal collapse in mechanical obstruction. Vascular conditions like acute mesenteric ischemia pose a critical differential, characterized by severe, diffuse out of proportion to physical findings, often with bloody stools indicating mucosal sloughing, and elevated lactate levels, setting it apart from the colicky and absence of early bloody diarrhea in uncomplicated bowel obstruction. This entity requires urgent vascular imaging to identify or , as delayed leads to high mortality. Gynecologic emergencies, particularly in reproductive-age females, include and , which present with acute pelvic or lower , vaginal spotting, and adnexal tenderness, but typically without prominent vomiting or bowel distension. is confirmed by positive and transvaginal showing extrauterine gestation, while involves sudden unilateral pain with possible nausea, differentiated by Doppler revealing absent ovarian blood flow. A pivotal differentiator across these conditions is imaging, particularly computed tomography (CT), which identifies a discrete transition point—the site of mechanical blockage with proximal dilation and distal decompression—in true bowel obstruction, versus uniform, diffuse dilation without such a point in ileus or pseudo-obstruction. Absence of a transition point, combined with clinical context like recent surgery or medications, shifts suspicion toward functional ileus, while focal findings like fat stranding or free fluid may point to inflammatory mimics such as appendicitis or diverticulitis.

Treatment

Conservative Management

Conservative management, also known as non-operative treatment, is the initial approach for many cases of bowel obstruction, particularly partial small bowel obstruction (SBO) without signs of strangulation or ischemia. This strategy aims to resolve the obstruction through supportive measures that alleviate symptoms, restore fluid and electrolyte balance, and promote bowel recovery, avoiding the risks associated with . It is typically employed after confirming the via clinical evaluation and , with close monitoring to assess response. A key component is nasogastric (NG) tube decompression, which involves inserting a tube through the into the to out accumulated gastrointestinal contents, thereby reducing , , and the risk of aspiration. Initial often yields 1-2 L per day, helping to decompress the proximal bowel and prevent further distension. This intervention is standard in uncomplicated SBO and has been shown to contribute to symptom relief in the majority of suitable cases. In cases of adhesive partial SBO, administration of water-soluble (e.g., Gastrografin, 100-150 mL orally or via NG tube) is recommended as both a diagnostic and therapeutic measure. If the contrast reaches the colon within 4-24 hours, it predicts successful non-operative resolution (sensitivity ~96%); the hyperosmolar agent also exerts a effect to facilitate obstruction relief. This approach shortens hospital stay and reduces need for in select patients. Intravenous (IV) fluid resuscitation is essential to correct and resulting from , third-space fluid losses, and reduced oral intake. Crystalloid solutions, such as normal saline or lactated Ringer's, are administered to maintain hemodynamic stability, with a target output greater than 0.5 mL/kg/hour to guide adequacy. A may be used for precise monitoring of intake and output. Concurrently, imbalances must be addressed, as bowel obstruction commonly leads to and hypomagnesemia due to gastrointestinal losses and translocation. Potassium and magnesium supplementation facilitates resolution and prevents complications like arrhythmias. Patients with suspected bowel obstruction, particularly those with underlying conditions such as Crohn's disease, should avoid self-administering laxatives, enemas, or home remedies like fiber supplements for constipation relief, as these interventions can worsen the obstruction and cause harm. Conservative management is indicated primarily for partial SBO without evidence of strangulation, , or closed-loop obstruction, where success rates range from 65% to 81%. Patients are monitored for 48-72 hours with serial abdominal exams, , and repeat if needed to evaluate for resolution, defined by passage of flatus or stool and reduced distension. Pharmacologic support may include prokinetic agents like metoclopramide to enhance gastrointestinal in functional or partial mechanical obstructions, but these are avoided in complete mechanical blockages to prevent worsening distension. If no improvement occurs within the monitoring period, transition to surgical intervention is warranted.

Surgical Management

Surgical management is indicated for bowel obstruction when conservative approaches fail or when there is of complications necessitating urgent intervention. Specifically, is warranted for complete obstructions unresponsive to nonoperative after 72 hours, signs of strangulation such as peritoneal or systemic , or closed-loop obstructions at risk of ischemia. These indications prioritize preventing bowel , which can rapidly progress to if untreated. For small bowel obstruction (SBO), the mainstay procedure is adhesiolysis to release bands causing the blockage, often performed via laparotomy or laparoscopy. In cases of ischemia or necrosis, which occur in approximately 10-20% of operative SBO patients, segmental resection with primary anastomosis is required to remove nonviable bowel. Enterotomy may be used for retrieval of foreign bodies or bezoars contributing to the obstruction. The laparoscopic approach is preferred for adhesive SBO in stable patients without peritonitis, offering shorter hospital stays and reduced morbidity compared to open surgery, though conversion to laparotomy occurs in 20-30% of cases due to dense adhesions or unclear anatomy. In large bowel obstruction (LBO), management options depend on the underlying etiology. For malignant causes, such as tumors, endoscopic placement of self-expanding metallic stents (SEMS) is often used as a bridge to or for palliation, with technical success rates of 80-90% and lower short-term complications compared to . Surgical options include oncologic with , often with primary if feasible or a temporary if precludes safe reconnection. is managed by detorsion and decompression, followed by resection if viability is compromised or recurrence risk is high. In settings with distal obstruction or , Hartmann's procedure— involving sigmoid resection, rectal stump closure, and end creation—is commonly employed to rapidly divert the fecal stream and avoid in unprepared bowel. Strangulated obstructions demand immediate surgical exploration via to assess and restore bowel viability, as delays can lead to mortality rates of 10-40% due to or multiorgan failure. may follow for partial obstructions after optimization, allowing for laparoscopic techniques to minimize adhesions and recovery time. Overall, timely operative intervention improves outcomes, with laparoscopic methods reducing postoperative and hospital length of stay in suitable candidates.

Complications

Acute Complications

Bowel obstruction can lead to bowel ischemia and , particularly in cases of strangulation where compromised blood flow results in tissue death and . This complication occurs in approximately 10-15% of small bowel obstructions (SBO), often due to adhesions, hernias, or volvuli that impair venous and arterial supply, leading to hemorrhagic if not addressed promptly. In cases of gut stenosis causing mechanical obstruction, strangulation risks dead tissue and life-threatening infection. Perforation is another critical acute issue, manifesting as free intraperitoneal air and subsequent , which is more prevalent in closed-loop obstructions where both proximal and distal segments are blocked. In large bowel obstructions with a competent ileocecal valve, cecal distension increases wall tension, with risk rising significantly when the cecal diameter exceeds 10 cm, potentially causing a cecal blowout. High pressure in gut stenosis can cause wall tear (perforation), spilling contents and leading to peritonitis or sepsis. Sepsis and septic shock may develop from bacterial translocation across the ischemic bowel wall, progressing to multi-organ failure in delayed presentations, affecting 5-10% of untreated cases with mortality rates up to 25-40%. This systemic response is exacerbated by translocation of enteric pathogens into the bloodstream, leading to hemodynamic instability and . and (AKI) arise from persistent vomiting, reduced oral intake, and third-space fluid losses into the distended bowel, resulting in and prerenal . AKI occurs in about 20-25% of SBO patients at admission, often with serum creatinine elevations exceeding 2 mg/dL in moderate to severe cases, necessitating fluid resuscitation to prevent further renal compromise. Aspiration pneumonia is a notable risk, especially among elderly patients, due to repeated and impaired gag reflex, allowing gastric contents to enter the lungs and cause followed by bacterial infection. This complication contributes to morbidity in geriatric SBO cohorts, with reported cases leading to and increased mortality.

Chronic Complications

Chronic complications of bowel obstruction arise in the months to years following resolution of acute episodes, particularly after surgical interventions, and can significantly impair . One of the most common long-term issues is recurrent obstruction, with readmission rates ranging from 10% to 30% within 5 years, especially in patients who have undergone adhesiolysis for small bowel obstruction (ASBO). For mild stenosis, blockages often partial/intermittent with lower risks like pain/bloating, but repeated episodes can worsen fibrosis. This recurrence is driven by the underlying , such as adhesions from prior , and is lower (around 12%) after operative management compared to conservative approaches (up to 27%). Adhesions frequently reform despite surgical adhesiolysis, occurring in 20% to 97% of cases, which elevates the risk of future small bowel obstruction by approximately 20%. This reformation contributes to the cycle of recurrent episodes, necessitating repeated interventions and increasing cumulative morbidity. In cases requiring extensive small bowel resection to relieve obstruction, may develop, characterized by due to reduced intestinal length (typically less than 200 cm remaining). Patients often experience chronic diarrhea, weight loss, and dependence on (TPN) for nutrient delivery, with lifelong management needed to mitigate and electrolyte imbalances. Large bowel obstruction (LBO) resections, such as those involving the , can lead to specific nutritional deficiencies, including due to loss of the terminal 's absorption sites, affecting up to 31% of patients post-ileostomy. is also prevalent, occurring in about 17% of cases, often requiring supplementation to prevent and other hematologic complications. These deficiencies arise from altered gastrointestinal and reduced absorptive surface, underscoring the need for ongoing monitoring and dietary adjustments. Recurrent bowel obstruction episodes can exert a profound psychological toll, manifesting as , anxiety, and depression, which negatively impact and daily functioning. The persistent threat of readmission and associated pain often heightens emotional distress, with studies showing elevated scores on anxiety (SAS) and depression (SDS) scales in affected patients, responsive to targeted psychological interventions.

Prognosis

Survival Rates

Survival rates for bowel obstruction vary significantly depending on the location, , and timeliness of intervention. For small bowel obstruction (SBO), recent studies report a 30-day of 5-10%, with one multicenter analysis documenting 7.3% overall mortality at 30 days among 315 patients managed surgically or conservatively. Large bowel obstruction (LBO) carries a higher risk, with 30-day mortality ranging from 10-20%, as evidenced by evidence-based reviews highlighting this range for emergency interventions in colonic obstructions. Strangulated bowel obstruction, characterized by compromised blood supply, exhibits elevated mortality of 10-40%, reflecting the rapid progression to ischemia and if untreated. However, prompt surgical intervention within 24-36 hours can substantially mitigate this risk, lowering mortality to under 5% through prevention of irreversible tissue damage. In cases of malignant LBO, often due to colorectal or ovarian cancers, surgical palliation extends median survival to 2-8 months (approximately 60-240 days) post-procedure, compared to 28-69 days (1-2.3 months) with conservative approaches like stenting or medical management alone. This difference underscores the role of decompression in improving and longevity, though overall remains guarded due to underlying disease progression. Age profoundly influences outcomes, with patients over 80 years experiencing roughly double the of younger cohorts, reaching 15-30% within 30 days, primarily from comorbidities and delayed recovery. Globally, mortality from bowel obstruction has declined over decades, attributed to advancements in diagnostic and multidisciplinary care.

Influencing Factors

The timeliness of intervention plays a pivotal role in determining outcomes for patients with bowel obstruction. Delays in treatment exceeding 24 hours are associated with a more than twofold increase in mortality risk, largely attributable to the progression of bowel ischemia and potential strangulation. Further prolongation, such as beyond 72 hours, can elevate mortality by threefold compared to prompt surgical management. Patient comorbidities significantly influence , with conditions like and heart disease increasing the risk of adverse outcomes approximately fourfold, including higher postoperative mortality. The nature of the obstruction—partial versus complete—markedly affects recovery potential. Partial obstructions resolve conservatively in approximately 85% to 90% of cases, avoiding the need for invasive procedures. In contrast, complete obstructions necessitate surgical intervention in about 70% of instances due to higher risks of progression to strangulation. Etiology further modulates , with benign causes like adhesions generally conferring a favorable outlook through effective resolution and low recurrence if managed appropriately. Malignant obstructions, however, carry a dismal , with median survival often less than one year owing to underlying disease progression and treatment limitations. Surgical approach also impacts recovery, as laparoscopic techniques reduce postoperative complications by roughly 50% relative to open , facilitating shorter stays and faster return to function.

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