Bowel obstruction

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hadeel Maksoud M.D.[2]

Bowel obstruction is a mechanical or functional obstruction of the intestines, preventing the normal transit of the products of digestion. It can occur at any level distal to the duodenum of the small intestine and is a medical emergency. Although many cases are not treated surgically, it is a surgical problem. Bowel obstruction has been described as far back as 1550 b.c. in ancient Egypt, however, the earliest record of the first successful treatment of small bowel obstruction was in 350 b.c. by Praxagorus. Bowel obstruction may be classified by 5 different classification methods including; open and closed, incomplete and complete, extrinsic, intrinsic and intraluminal, true and pseudo-obstruction, and finally, small bowel and large bowel. In this chapter, the extrinsic, intrinsic and intraluminal classification method will be used. It is thought that bowel obstruction may occur functionally as a result of abnormal anatomy or impairment of the autonomic nervous system or mechanically, which may occur acutely or chronically. An obstruction that occurs functionally or mechanically can be classified as extrinsic, intrinsic or intraluminal including tumors, strictures and foreign bodies. Excessive bowel distention can lead to ischemia, necrosis and perforation. A functional obstruction may be due to a number of genetic defects including trisomy 21 and the RET proto-oncogene mutation. Associated conditions include post-operative adhesions, complicated hernias, gastrointestinal cancers and endometriosis. Gross pathology may demonstrate adhesions, narrow lumens and volvulus. Microscopic pathology may show evidence of fibrosis, necrosis and ischemia. The incidence of bowel obstruction in the US is 1.47 per 100,000 per year. Colorectal cancer and Crohn’s disease are often complicated by bowel obstruction. The mortality rate is about 4% on average with the mortality rate reaching as high as 60% in the presence of bowel ischemia or when surgery is delayed. Bowel obstruction incidence has a median age of approximately 64 years. The incidence in newborns is about 1 in 2000 live births and 1 in 5000 in children above the age of 2. There is no racial predilection in cases of bowel obstruction. Men and women have an equal incidence of bowel obstruction. The highest incidence of bowel obstruction is found in the continent of Africa. If left untreated, 85% of patients with complete bowel obstruction may progress to develop ischemia, necrosis, and gangrene. Common complications of bowel obstruction include bowel ischemia, bowel perforation, gangrene and sepsis. Prognosis is generally excellent for non-ischemic bowel obstruction, and the mortality rate of patients with bowel obstruction is approximately 4%. In contrast, prognosis for ischemic bowel obstruction is approximately 60%. There is no single diagnostic study of choice for the diagnosis of bowel obstruction, but bowel obstruction can be diagnosed based on plain x-ray and CT scan. An x-ray is performed when obstruction is suspected with clinical findings of nausea, vomiting, abdominal pain, abdominal distension and constipation. The results of plain x-ray that confirm of bowel obstruction include dilated bowel loops with air-fluid level, distal collapsed bowel, gasless abdomen or alternatively, “string of pearls” sign. The results of CT that confirm of bowel obstruction include dilated bowel loops with air-fluid level and distal collapsed bowel. Initially, an x-ray is usually performed before surgical intervention. If urgent intervention is not needed and the diagnosis is equivocal, then a CT may be carried out. The mainstay of treatment for bowel obstruction is surgical. Surgery is specifically indicated for complicated bowel obstruction. Complications include: complete obstruction, closed-loop obstruction, bowel ischemia, necrosis, and perforation.

Bowel obstruction has been described as far back as 1550 b.c. in ancient Egypt, however, the earliest record of the first successful treatment of small bowel obstruction was in 350 b.c. by Praxagorus.

Bowel obstruction may be classified by 5 different classification methods including; open and closed, incomplete and complete, extrinsic, intrinsic and intraluminal, true and pseudo-obstruction, and finally, small bowel and large bowel. In this chapter, the extrinsic, intrinsic and intraluminal classification method will be used.

It is thought that bowel obstruction may occur functionally as a result of abnormal anatomy or impairment of the autonomic nervous system or mechanically, which may occur acutely or chronically. An obstruction that occurs functionally or mechanically can be classified as extrinsic, intrinsic or intraluminal including tumors, strictures and foreign bodies. Excessive bowel distention can lead to ischemia, necrosis and perforation. A functional obstruction may be due to a number of genetic defects including trisomy 21 and the RET proto-oncogene mutation. Associated conditions include post-operative adhesions, complicated hernias, gastrointestinal cancers and endometriosis. Gross pathology may demonstrate adhesions, narrow lumens and volvulus. Microscopic pathology may show evidence of fibrosis, necrosis and ischemia.

Small bowel obstruction causes include post-adbominal surgery adhesions, foreign bodies and intussusception. Large bowel obstruction causes include neoplasms, hernias and constipation. Miscellaneous causes include, paralytic ileus and Down syndrome. Causes by organ system include, ovarian cancer, bowel strangulation and ascariasis. Mechanical obstruction can be caused by pregnancy, Hirschsprung’s disease and Crohn’s disease. Non-mechanical obstruction may be caused by ovarian torsion, pancreatitis and lead poisoning. Drug induced bowel obstruction can occur by intake of lanthanum carbonate, methscopolamine bromide, and teduglutide.

Bowel obstruction must be differentiated from other diseases that cause abdominal pain, nausea and vomiting, and constipation, such as irritable bowel syndrome, volvulus and acute diverticulitis.

The incidence of bowel obstruction in the US is 1.47 per 100,000 per year. Colorectal cancer and Crohn’s disease are often complicated by bowel obstruction. The mortality rate is about 4% on average with the mortality rate reaching as high as 60% in the presence of bowel ischemia or when surgery is delayed. Bowel obstruction incidence has a median age of approximately 64 years. The incidence in newborns is about 1 in 2000 live births and 1 in 5000 in children above the age of 2. There is no racial predilection in cases of bowel obstruction. Men and women have an equal incidence of bowel obstruction. The highest incidence of bowel obstruction is found in the continent of Africa.

Common risk factors in the development of bowel obstruction include, abdominal surgery, colorectal cancer, and volvulus. Common risk factors in the development of bowel obstruction include congenital gastrointestinal atresias, colorectal carcinoma and surgical resection of the bowel. Less common risk factors in the development of bowel obstruction include pancreatic cancer, ovarian cancer and lymphoma.

There is insufficient evidence to recommend routine screening for bowel obstruction.

If left untreated, 85% of patients with complete bowel obstruction may progress to develop ischemia, necrosis, and gangrene. Common complications of bowel obstruction include bowel ischemia, bowel perforation, gangrene and sepsis. Prognosis is generally excellent for non-ischemic bowel obstruction, and the mortality rate of patients with bowel obstruction is approximately 4%. In contrast, prognosis for ischemic bowel obstruction is approximately 60%.

There is no single diagnostic study of choice for the diagnosis of bowel obstruction, but bowel obstruction can be diagnosed based on plain x-ray and CT scan. An x-ray is performed when obstruction is suspected with clinical findings of nausea, vomiting, abdominal pain, abdominal distension and constipation. The results of plain x-ray that confirm of bowel obstruction include dilated bowel loops with air-fluid level, distal collapsed bowel, gasless abdomen or alternatively, “string of pearls” sign. The results of CT that confirm of bowel obstruction include dilated bowel loops with air-fluid level and distal collapsed bowel. Initially, an x-ray is usually performed before surgical intervention. If urgent intervention is not needed and the diagnosis is equivocal, then a CT may be carried out.

The hallmark of bowel obstruction is abdominal distension with waxing and waning pain and obstipation. A positive history of previous abdominal surgery and abdominal adhesion is suggestive of bowel obstruction. The most common symptoms of bowel symptoms include abdominal pain with nausea and vomiting, abdominal distension, and obstipation. Common symptoms of bowel obstruction include episodic pain, abdominal distension, and constipation. Less common symptoms of bowel obstruction include constant severe pain, sudden severe pain, and postprandial abdominal discomfort.

Patients with bowel obstruction usually appear distressed with a distended abdomen with or without fever. Physical examination of patients with bowel obstruction is usually remarkable for tympanic or hyperresonant abdomen, orthostatic hypotension, tachycardia, and dry mucus membranes.

Laboratory findings consistent with the diagnosis of bowel obstruction include hyponatremia and hypokalemia, leukocytosis, metabolic alkalosis and elevated serum lactate.

An x-ray is the initial investigation performed in the diagnosis of bowel obstruction. Findings on an x-ray suggestive of bowel obstruction include dilated bowel loops with air-fluid level, distal collapsed bowel,absence of gas in the abdomen or alternatively, “string of pearls” sign indicating trapped flatus.

Abdominal CT scan may be helpful in the diagnosis of bowel obstruction. Findings on CT scan suggestive of bowel obstruction include dilated bowel loops with air-fluid level, distal collapsed bowel, in addition to, “Target”, “Whirl” and “Venous cut-off” signs.

Other diagnostic studies for bowel obstruction include contrast studies, which demonstrate dilated proximal bowel loops, point of transition, and complete obstruction. Contrast enema is useful in those who have had a previous surgical reconstruction of the bowel. Enteroclysis is a useful study in those with chronic or recurrent bowel obstruction.

The mainstay treatment of bowel obstruction is surgical and non-operative management. The role of medical therapy is supportive and is limited by palliative pain management in cancer patients, fluid and electrolyte replenishment, decreasing abdominal distension, peritumoral edema, intraluminal secretions, peristaltic movements, and control of nausea and vomiting.

The mainstay of treatment for bowel obstruction is surgical. Surgery is specifically indicated for complicated bowel obstruction. Complications include: complete obstruction, closed-loop obstruction, bowel ischemia, necrosis, and perforation.

There are no established measures for the primary prevention of bowel obstruction. However, minimizing the formation of an obstruction is possible. Steroid therapy may be used to minimize the formation of adhesions after bowel surgery, but is controversial. The correction of malrotation early in life, the treatment of Crohn’s disease, and the repair of hernia all contribute to minimizing the risk of bowel obstruction development. Recently, laparoscopic surgery has been preferred over open abdominal surgery because laparoscopy reduced the risk for obstruction post-operatively.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Hadeel Maksoud M.D.[2]

Bowel obstruction has been described as far back as 1550 b.c. in ancient Egypt, however, the earliest record of the first successful treatment of small bowel obstruction was in 350 b.c. by Praxagorus.

• Bowel obstruction was described in the Ebers papyrus in 1550 b.c. in Egypt.^[1]
• Hippocrates was first to diagnose and treat small bowel obstruction.
• The first documented treatment was by Praxagorus in 350 b.c.
• Praxagrous’ treatment involved a fistula created between the skin and bowel that decompressed the obstructed bowel.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Hadeel Maksoud M.D.[2]

Bowel obstruction may be classified by 5 different classification methods including: Open and closed, incomplete and complete, extrinsic, intrinsic and intraluminal, true and pseudo-obstruction, and finally, small bowel and large bowel. In this chapter, the extrinsic, intrinsic and intraluminal classification method will be used.

Bowel obstruction may be classified as follows:^[1][2]

• Open or closed bowel
  • Open type of bowel obstruction refers to an obstruction at a single location where the rest of the bowel is patent. A closed bowel obstruction refers to an obstruction occurring at two locations, so that there is no proximal or distal outlet.
• Complete or incomplete obstruction
  • Obstructions can either completely occlude the lumen of the bowel, or can partially (incompletely) occlude the bowel.
• Extrinsic, intrinsic/intramural or intraluminal obstruction
  • An obstruction may be due to an external cause, for example, a tumor that pushes on the bowel from the outside.
  • An obstruction may be caused by an intrinsic (intramural) wall abnormality, for example, a tumor or stricture or hematoma.
  • An intraluminal obstruction describes the process by which a luminal defect prevents the normal passage of bowel contents, for example, a foreign body, gallstone or an intussusception.
• Small or large bowel obstruction
  • Small bowel obstruction include obstructions that occur along the duodenum up to the ileocecal junction, obstructions beyond this junction are classified as large bowel obstructions. A subset of large bowel obstruction includes outlet obstructions.
• True or pseudo-obstruction
  • Ogilvie’s syndrome and adynamic (paralytic) ileus represent pseudo-obstructions, and are not true mechanical obstructions as the bowel is dilated and patent but intestinal contents are not able to pass.

Bowel obstruction classification algorithm:

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Hadeel Maksoud M.D.[2]

It is thought that bowel obstruction may occur functionally as a result of abnormal anatomy or impairment of the autonomic nervous system or mechanically, which may occur acutely or chronically. An obstruction that occurs functionally or mechanically can be classified as extrinsic, intrinsic or intraluminal including tumors, strictures and foreign bodies. Excessive bowel distention can lead to ischemia, necrosis and perforation. A functional obstruction may be due to a number of genetic defects including trisomy 21 and the RET proto-oncogene mutation. Associated conditions include post-operative adhesions, complicated hernias, gastrointestinal cancers and endometriosis. Gross pathology may demonstrate adhesions, narrow lumens and volvulus. Microscopic pathology may show evidence of fibrosis, necrosis and ischemia.

• Normally, the small intestine functions to pass gastrointestinal contents for absorption. The large surface area provided by the villi, plicae circularis and valvulae conniventes (Kerckring folds) allow for this exchange to happens.^[1][2][3]
• In addition, the small bowel is free of microbes, in comparison to the large bowel that houses commensal flora that facilitate digestion and vitamin synthesis, namely vitamin K.
• Continuous transit throughout the bowel is important to prevent bowel dilatation, ischemia and necrosis.
• Obstruction of the bowel can occur functionally (due to abnormal anatomy) or mechanically, which can be acute or chronic.
• Obstructions that occur functionally or mechanically, can be classified as extrinsic, intrinsic or intraluminal obstruction:
  • Extrinsic obstructions can happen as the result of a tumor, post-operative adhesions or hernias.
  • Intrinsic obstructions can happen as a result of a tumor, stenosis or hematoma.
  • Intraluminal obstructions are sometimes referred to intramural obstructions and include, foreign bodies, intussusception and gallstones.
• However an obstruction occurs, proximal to the blockage there will be a dilated segment, whilst distal to the obstruction the segment of bowel will collapse as the contents cannot pass.
• Bowel distention occurs as air that is swallowed and gases produced by the commensal flora begins to accumulate.
• Eventually, the bowel wall becomes edematous and fluid gathers inside the lumen of the bowel. This disrupts the absorptive properties of the gut.
• Some fluid may be lost to the peritoneal cavity, moreover, the proximal obstruction can cause severe emesis which will lead to further loss of fluid that contains vital electrolytes. This process may result in metabolic alkalosis and hypovolemia.
• The obstruction also causes the normally sterile proximal bowel to become overgrown with bacteria and vomitus may contain feces.
• When a massive dilation of the bowel occurs, the vessels that perfuse the walls of the bowel become compressed and will not be able to supply the bowel loop adequately, which leads to ischemia.
• If ischemia is not reversed within a timely manner, then necrosis, volvulus and perforation may ensue.

• The association of spinal anaesthesias, drugs and nervous trauma has lead to the understanding that Ogilvie syndrome (colonic dilatation without true obstruction) may be caused by impairment of the autonomic nervous system.^[4][5][6]
• Damage to the parasympathetic fibers of S2 – S4 causes the distal colon to become atonic and become obstructed proximally.
• However, the exact mechanism is unknown, especially in patients who present with this syndrome without an obvious injury to the parasympathetic nerves.
• Acute colonic pseudo-obstruction occurs when the colon’s diameter rises quickly, which increases the tension in the colonic wall, leading to colonic ischemia and possibly, perforation with a diameter exceeding 10 – 12cm.
• A rare case of Ogilvie syndrome showed atrophic myopathy with a thinned out colonic wall, despite a perfectly intact myenteric plexus and unaffected ganglion cells, with no evidence of fibrosis or inflammation.

• The majority of paralytic (adynamic) ileus cases occur after major abdominal surgery, such as hysterectomy.
• Paralytic ileus is thought to occur with manipulation and trauma of the intestinal tract.
• Post operative dysmotility is associated with inflammation, impaired neural reflexes and the release of neural hormone peptides.
  • Inflammation:^[7]
    • Intestinal manipulation leads to intestinal ischemia, and shifting of endogenous cellular danger molecules and cytokines away from the site of trauma.
    • Leukocytic infiltration, macrophage and mast cell stimulation commences and causes muscular dysfunction, and therefore inflammation in the manipulated segment.
  • Neural reflexes:^[7]
    • Inhibitory sympathetic neural reflexes increase due to noxious spinal afferent signals, therefore, the use of epidural local anesthetics or topical capsaicin is encouraged to prevent paralytic ileus.^[8]
  • Neurohormonal peptides:^[9][10]
    • Inhibitory neurotransmitters are released and cause the gut motility to slow down.
    • Inhibitory neurotransmitters include, nitric oxide, vasoactive intestinal polypeptide, and substance P.

The development of congenital bowel obstruction is the result of multiple genetic mutations:^{[11][12][13][14]}

• Chromosome 21 trisomy can lead to imperforate anus and duodenal atresias in 50% of babies with down syndrome.
• Chromosome 7 mutation locus leads to cystic fibrosis that predisposes to a thickened meconium which may lead to an intraluminal obstruction of the terminal ileum and microcolon.
• Hirschsprung’s disease is associated with several gene mutations:
  • The RET proto-oncogene located on chromosome 10q11.21 that interacts with the EDNRB protein located on chromosome 13.
  • Mutations in the RET and 3p21, 9q31, and 19q12 genes leads to failure of migration of the enteric neural crest cells.
  • Hirschsprung syndrome is associated with PHOX2B homeobox gene mutations.
  • The following protein mutations may also lead to Hirschsprung’s disease:
    • Chromosome 5 – GDNF protein
    • Chromosome 20 – EDN3 protein
    • Chromosome 22 – SOX10 protein
    • Chromosom 1 – ECE1 protein
    • Chromosome 19 – NTN protein
    • Chromosome 2 – SIP1 protein

• Conditions associated with extrinsic bowel obstruction include:^{[15][16][17][18]}
  • Adhesions
  • Hernia
  • Volvulus
  • Endometriosis
• Conditions associated with intrinsic bowel obstruction include:^{[15][16][17][18]}
  • Large and small bowel cancers
  • Cystic fibrosis
  • Hirschsprung’s disease
  • Down syndrome
  • Strictures:
    • Anatomical
    • Inflammatory
    • Ischemic
    • Radiation
• Conditions associated with intraluminal bowel obstruction include:^{[15][16][17][18]}
  • Gastrointestinal foreign body
  • Intussusception
  • Gallstones
  • Constipation
  • Bezoar
  • Volvulus
  • Hematoma

• On gross pathology, adhesions, volvulus, narrow lumen with proximal dilatations and exudate are characteristic findings of bowel obstruction.^[18]

• On microscopic histopathological analysis, fibrosis, necrosis, and ischemia are characteristic findings of bowel obstruction.^[18]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Hadeel Maksoud M.D.[2]

Small bowel obstruction causes include post-adbominal surgery adhesions, foreign bodies and intussusception. Large bowel obstruction causes include neoplasms, hernias and constipation. Miscellaneous causes include, paralytic ileus and Down syndrome. Causes by organ system include, ovarian cancer, bowel strangulation and ascariasis. Mechanical obstruction can be caused by pregnancy, Hirschsprung’s disease and Crohn’s disease. Non-mechanical obstruction may be caused by ovarian torsion, pancreatitis and lead poisoning. Drug induced bowel obstruction can occur by intake of lanthanum carbonate, methscopolamine bromide, and teduglutide.

Causes of small bowel obstruction include:^[1]

• Adhesions
  • From previous abdominal surgery
• Carcinoid tumor
  • Rare, preferred location is the ileum
• Crohn’s disease
  • Causes adhesions or inflammatory strictures
• Foreign bodies
  • Including gallstones in gallstone ileus and swallowed objects
• Hernia
  • Especially hernias containing bowel
• Intestinal atresia
• Intussusception
  • Specifically in children
• Ischaemic strictures
• Neoplasms
  • Including both benign and malignant neoplasms
• Volvulus

Causes of large bowel obstruction include:^[1]

• Neoplasms
• Hernias
• Inflammatory bowel disease
• Volvulus
  • Specifically sigmoid, caecal, and colonic volvulus
• Faecal impaction
• Colon atresia
• Benign strictures
  • Such as those that occur with diverticular disease

• Functional outlet obstruction
  • Internal anal sphincter spasm
  • Short-segment Hirschsprung’s disease
  • Chagas disease
  • Hereditary internal sphincter myopathy
• Spasm of the striated pelvic floor muscles
  • Anismus
  • Multiple sclerosis
  • Spinal cord lesions
• Mechanical outlet obstruction
  • Intussusception
  • Enterocele
  • Rectocele
  • Rectal prolapse
• Impaired rectal sensitivity
  • Megarectum
  • Rectal hyposensitivity

• Miscellaneous syndromes^[2][3]
  • Paralytic ileus
  • Pseudo-obstruction (Ogilvie’s syndrome)
• Chromosomal abnormalities
  • Down syndrome
• Autosomal dominant conditions
  • Neurofibromatosis type 1
• Malignant neoplastic conditions
  • Carcinoid tumours
  • Carcinoid syndrome
  • Colorectal cancer
  • Ovarian cancer
  • Pseudomyxoma peritonei
  • Small bowel lymphoma
  • Stomach cancer
• Trauma, mechanical and physical conditions:
  • Bowel strangulation
  • Femoral hernia
  • Ileus
  • Inguinal hernia
  • Intestinal stricture
  • Intestinal volvulus
  • Intussusception
  • Large bowel obstruction
  • Obturator hernia
  • Peritoneal adhesions
  • Small bowel obstruction
• Infectious disorders
  • Ascariasis
  • Intra-abdominal sepsis
  • Pneumonia
• Drug Induced
  • Panitumumab
  • Pergolide

• Adenomatous polyps^[4][5]
• Adhesions
• Adhesive bands
• Annular pancreas
• Ascariasis
• Atresia
• Biliary calculus
• Bowel duplication
• Carcinomatosis
• Colon Cancer
• Congenital megacolon
• Crohn’s Disease
• Cysts
• Diverticular stricture
• Diverticulitis
• Endometriosis
• Foreign body
• Gallstone ileus
• Hematoma of the bowel wall
• Hernia
• Hirschprung’s disease
• Iatrogenic
• Imperforate anus
• Incarcerated hernia
• Intrabdominal abscess
• Intussusception
• Ischemia
• Malrotation
• Meckel’s Diverticulum
• Megacolon
• Multiple polyposis syndromes
• Neoplasm
• Ovarian Cancer
• Pneumatosis intestinalis
• Iatrogenic
• Pregnancy
• Radiation induced stenosis
• Sarcoma
• Scleroderma
• Surgical anastomosis
• Therapy with dietary fiber
• Trauma
• Tuberculosis
• Ulcerative colitis
• Volvulus

• Acid-base imbalance
• Acute pancreatitis
• Apoplexy
• Brain tumor
• Cancer
• Cholecystolithiasis
• Connective tissue disease
• Diabetic coma
• Empyema
• Hyperparathyroidism
• Hypokalemia
• Lead poisoning
• Lymphoma
• Mechanical ventilation
• Mesenteric infarction
• Meropenem
• Osteomyelitis of the spine
• Ovarian torsion
• Pancreatitis
• Penetrating wounds
• Perinephric abscess
• Peritoneal carcinomatosis
• Peritonitis
• Pneumonia
• Porphyria
• Iatrogenic
• Psoas abscess
• Pyelonephritis
• Renal colic
• Retroperitoneal hematoma
• Spinal cord inflammation
• Spinal cord injury
• Spinal cord trauma
• Systemic infection
• Testicular torsion
• Ulcer perforation
• Uremia
• Urosepsis
• Vitamin deficiency

• Aerophagia
• Functional bowel disease

• Lanthanum carbonate
• Methscopolamine bromide
• Teduglutide
• Morphine
• Narcotics
• Anticholinergics
• Antihistamines
• Catecholamines

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Hadeel Maksoud M.D.[2]

Bowel obstruction must be differentiated from other diseases that cause abdominal pain, nausea and vomiting, and constipation, such as irritable bowel syndrome, volvulus and acute diverticulitis.

Bowel obstruction must be differentiated from other diseases that cause abdominal pain, nausea and vomiting, and constipation, such as irritable bowel syndrome, volvulus and acute diverticulitis.

The following tables discusses differential diagnoses based on abdominal pain with nausea and vomiting:

Abbreviations: RUQ= Right upper quadrant of the abdomen, LUQ= Left upper quadrant, LLQ= Left lower quadrant, RLQ= Right lower quadrant, LFT= Liver function test, SIRS= Systemic inflammatory response syndrome, ERCP= Endoscopic retrograde cholangiopancreatography, IV= Intravenous, N= Normal, AMA= Anti mitochondrial antibodies, LDH= Lactate dehydrogenase, GI= Gastrointestinal, CXR= Chest X ray, IgA= Immunoglobulin A, IgG= Immunoglobulin G, IgM= Immunoglobulin M, CT= Computed tomography, PMN= Polymorphonuclear cells, ESR= Erythrocyte sedimentation rate, CRP= C-reactive protein, TS= Transferrin saturation, SF= Serum Ferritin, SMA= Superior mesenteric artery, SMV= Superior mesenteric vein, ECG= Electrocardiogram

Abbreviations: RUQ= Right upper quadrant of the abdomen, LUQ= Left upper quadrant, LLQ= Left lower quadrant, RLQ= Right lower quadrant, LFT= Liver function test, SIRS= Systemic inflammatory response syndrome, ERCP= Endoscopic retrograde cholangiopancreatography, IV= Intravenous, N= Normal, AMA= Anti mitochondrial antibodies, LDH= Lactate dehydrogenase, GI= Gastrointestinal, CXR= Chest X ray, IgA= Immunoglobulin A, IgG= Immunoglobulin G, IgM= Immunoglobulin M, CT= Computed tomography, PMN= Polymorphonuclear cells, ESR= Erythrocyte sedimentation rate, CRP= C-reactive protein, TS= Transferrin saturation, SF= Serum Ferritin, SMA= Superior mesenteric artery, SMV= Superior mesenteric vein, ECG= Electrocardiogram

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Hadeel Maksoud M.D.[2]

The incidence of bowel obstruction in the US is 1.47 per 100,000 per year. Colorectal cancer and Crohn’s disease are often complicated by bowel obstruction. The mortality rate is about 4 per 100,000 on average with the mortality rate reaching as high as 60 per 100,000 in the presence of bowel ischemia or when surgery is delayed. Bowel obstruction incidence has a median age of approximately 64 years. The incidence in newborns is about 1 in 2000 live births and 1 in 5000 in children above the age of 2. There is no racial predilection in cases of bowel obstruction. Men and women have an equal incidence of bowel obstruction. The highest incidence of bowel obstruction is found in the continent of Africa.

• The incidence of bowel obstruction is 1.47 per 100,000 per year in the United States.^[1][2][3]
• The incidence of large bowel obstruction is approximately 0.15 – 0.29 per 100,000 in patients with colorectal cancer.
• It should be noted that 770 per 100,000 of surgical emergencies with colorectal carcinoma are attributed to bowel obstruction.
• The incidence of bowel obstruction in cases of Crohn’s disease may be as high as 250 per 100,000.

• The prevalence of small bowel obstruction is approximately 100 – 500 per 100,000 – 5% in patients who have not undergone previous abdominal surgery.
• The prevalence of small bowel obstruction is approximately 600 per 100,000 in patients who have undergone previous abdominal surgery.

The mortality rate of small bowel obstruction is approximately 4 per 100,000 and may reach 600 per 100,000 if bowel ischemia is present or if surgery is delayed.^[4]

• The incidence of bowel obstruction increases with age; the median age at diagnosis is 64 years.^[5]
• The incidence of bowel obstruction in newborns is 1 in 2000 live births.^[6][7]
• The incidence of bowel obstruction in children after the first 2 years of life is 1 in 5000.

There is no racial predilection to bowel obstruction.

Bowel obstruction affects men and women equally.^[5]

• The majority of bowel obstruction cases are reported in Africa with an incidence of 12 per 100,000 per year.^[8][9]
• The incidence in the US and the UK is more rare with incidences of 1.47 per 100,000 per year and 1.7 per 100,000 per year respectively.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Hadeel Maksoud M.D.[2]

Common risk factors in the development of bowel obstruction include, abdominal surgery, colorectal cancer, and volvulus. Common risk factors in the development of bowel obstruction include congenital gastrointestinal atresias, colorectal carcinoma and surgical resection of the bowel. Less common risk factors in the development of bowel obstruction include pancreatic cancer, ovarian cancer and lymphoma.

Common risk factors in the development of bowel obstruction include, abdominal surgery, colorectal cancer, and volvulus.

• Common risk factors in the development of bowel obstruction include:^[1][2]
  • Congenital gastrointestinal atresias
  • Colorectal carcinoma
  • Adhesive bowel disease
  • Colorectal resection
  • Diverticulitis
  • Hernias
  • Volvulus
  • Diverticulitis

• Less common risk factors in the development of bowel obstruction include:^[3][4][5]
  • Pancreatic cancer
  • Ovarian cancer
  • Lymphoma
  • Tuberculosis
  • Radiotherapy
  • Endometriosis
  • Lymphogranuloma venereum

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Hadeel Maksoud M.D.[2]

If left untreated, 85% of patients with complete bowel obstruction may progress to develop ischemia, necrosis, and gangrene. Common complications of bowel obstruction include bowel ischemia, bowel perforation, gangrene and sepsis. Prognosis is generally excellent for non-ischemic bowel obstruction, and the mortality rate of patients with bowel obstruction is approximately 4 per 100,000. In contrast, prognosis for ischemic bowel obstruction is approximately 600 per 100,000.

• The symptoms of bowel obstruction include nausea, vomiting, constipation and abdominal pain and commonly manifests acutely or can be chronic.^[1]
• If left untreated, 85% of patients with may progress to develop bowel ischemia, bowel necrosis, and sepsis.

• Common complications of bowel obstruction include:^[2]
  • Bowel ischemia
  • Bowel perforation
  • Gangrene
  • Sepsis
    • Mostly, with gram negative organisms such as E.coli
  • Dehydration
  • Electrolyte imbalance
    • Mostly hypokalemia and alkalosis
  • Kidney failure
  • Intra-abdominal abscess
  • Short bowel syndrome
    • A malabsorption disorder

• Prognosis is generally excellent for non-ischemic bowel obstruction, and the mortality rate of patients with bowel obstruction is approximately 4 per 100,000.^[2]
• In contrast, prognosis for ischemic bowel obstruction is approximately 60 per 100,000.

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