Ogilvie syndrome

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

Ogilvie syndrome is defined as the obstruction of the colon with no mechanical reason and thereby, it is called pseudo-obstruction (not a true obstruction). The colonic pseduo-obstruction pathogenesis is thought to be due to impairement of the autonomic nervous system. The impairment includes the parasympathetic fibers of S2-S4 ending up with atonic colon and obstruction. However, in some cases the autonomic plexus in the colon is intact. The pseudo-obstruction is commonly caused by trauma, major surgeries, and myocardial infarction. Ogilvie syndrome must be differentiated from other causes of abdominal distention as volvulus and diverticulitis.The incidence of Ogilvie’s syndrome is 100 per 100,000 individuals. Ogilvie’s syndrome commonly affects patients more than 60 years and it is more prevelant int he men more than women. Common risk factors of Ogilvie’s syndrome include having neurologic disorders, taking narcotic medications, and trauma. If left untreated, of patients with acute colonic pseudo-obstruction may progress to develop intestinal perforation which is life threatening complication. Common complications of Ogilvie’s syndrome include colonic ischemia and intestinal perforation. Prognosis of Ogilvie syndrome depends on the underlying cause of pseudo-obstruction. Common symptoms of Ogilvie’s syndrome include abdominal pain, abdominal distention, nausea, vomiting, and weight loss.The laboratory findings of colonic pseudo-obstruction may include leukocytosis due to the underlying disease not due to the pseudo-obstruction itself. Many patients with Ogilvie syndrome may have metabolic imbalance which include hypokalemia and hypocalcemia. On abdominal x-ray, Ogilvie syndrome is associtated with dilated bowel with air-filled colon and normal haustral markings. Abdominal CT scan is performed in suspected cases of colonic pseudo-obstruction to detect the site of the obstruction. Management of Ogilvie syndrome depends mainly on the supportive care measures which include include treatment of the underlying cause of the obstruction, terminating the concurrent medications that may cause intestinal dysmotility, and administration of intravenous fluids and saline. Neostigmine can be used for the medical treatment in unresponsive cases to the supportive care. Surgery is usually reserved for patients with either colonic ischemia, intestinal perforation, or sepsis. Surgical techniques include total colectomy, ileostomy, or Hartmann’s procedure.

Acute intestinal pseudo-obstruction was first reported by Dr. William Heneage Ogilvie in 1948 and the syndrome was named on him after that.

Ogilvie’s syndrome can be classified based on the duration of the disease into acute or chronic.

The colonic pseudo-obstruction pathogenesis is believed to be due to impairment of the autonomic nervous system. The autonomic impairment may involve the parasympathetic fibers of S2-S4 which is responsible for innervation of the distal colon and may lead to atonic colon and proximal obstruction. In few cases, Ogilvie’s syndrome (colonic pseudo-obstruction) may show atrophic myopathy with thinned colonic wall and intact myenteric plexus.

Common causes of Ogilvie’s syndrome include trauma, gynecological surgeries, major surgeries as hip replacement, and myocardial infarction. Other causes include causes of non mechanical bowel obstruction as acid base imbalance, acute pancreatitis, apoplexy, and cancers.

Ogilvie syndrome (colonic pseudo-obstruction) must be differentiated from other diseases that cause abdominal distention and abdominal pain such as irritable bowel syndrome, volvulus and acute diverticulitis.

The incidence of Ogilvie’s syndrome is 100 per 100,000 individuals. Ogilvie’s syndrome commonly affects patients more than 60years and it is more prevelant int he men more than women.

Common risk factors of Ogilvie’s syndrome include having neurologic disorders, taking narcotic medications, and trauma. Other risk factors include systemic lupus erythematosus, alcoholism, and multiple myeloma.

There is insufficient evidence to recommend routine screening for Ogilvie’s syndrome.

If left untreated, of patients with acute colonic pseudo-obstruction may progress to develop intestinal perforation which is life threatening complication. Common complications of Ogilvie’s syndrome include colonic ischemia and intestinal perforation. Prognosis of Ogilvie syndrome depends on the underlying cause of pseudo-obstruction.

Common symptoms of Ogilvie’s syndrome include abdominal pain, abdominal distention, nausea, vomiting, and weight loss.

There are no specific diagnostic laboratory findings associated with Ogilvie’s syndrome. The laboratory findings may include leukocytosis due to the underlying disease not due to the pseudo-obstruction itself. Many patients with Ogilvie syndrome may have metabolic imbalance which include hypokalemia and hypocalcemia. Other laboratory tests that can be performed to exclude other causes include complete blood count, lactate levels, and thyroid hormone levels.

On abdominal x-ray, Ogilvie syndrome is associtated with dilated bowel with air-filled colon and normal haustral markings.

There are no ultrasound findings associated with acute colonic pseudoobstruction (Ogilvie’s syndrome).

Abdominal CT scan is performed in suspected cases of colonic pseudo-obstruction to detect the site of the obstruction. Abdominal CT scan may show the presence of dilation of the large bowel without evidence of mechanical obstruction and the colonic dilation may extend to the rectum.

There are no MRI findings associated with Ogilvie syndrome.

There are no other imgaing findings associated with acute colonic pseudo-obstruction (Ogilvie’s syndrome).

There are no other diagnostic findings associated with acute colonic pseudo-obstruction (Ogilvie’s syndrome).

Supportive care is the first line of management of the colonic pseudo-obstruction. The supportive measures include treatment of the underlying cause of the obstruction, terminating the concurrent medications that may cause intestinal dysmotility, and administration of intravenous fluids and saline. Neostigmine can be used in the cases of pseudo-obstruction resistant to the supportive measures. Non-surgical techniques can be performed to decompress the obstruction and it includes colonoscopic decompression and percutaneous cecostomy.

Surgery is not the first-line treatment option for patients with Ogilvie syndrome. Surgery is usually reserved for patients with either colonic ischemia, intestinal perforation, or sepsis. Surgical techniques include total colectomy, ileostomy, or Hartmann procedure.

Effective measures for the primary prevention of Ogilvie syndrome include supportive care measures as treatment of the underlying cause of the obstruction, terminating the concurrent medications that may cause intestinal dysmotility, and administration of intravenous fluids and saline.

The primary and secondary prevention strategies for Ogilvie syndrome are the same.

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

Acute intestinal pseudo-obstruction was first reported by Dr. William Heneage Ogilvie in 1948 and the syndrome was named on him after that.

• In 1948, Dr. William Heneage Ogilvie was the first to report two cases of intestinal pseudo-obstruction due to a malignancy. After that, the syndrome was named on him as Ogilvie’s syndrome.^[1][2]
• Dr. Ogilvie concluded that both cases are due to interrupted nerve supply due to malignant disease in the region of celiac axis and semilunar ganglia.
• Since 1948 and moving forward, many other cases have been reported about intestinal pseudo-obstruction.

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

The colonic pseudo-obstruction pathogenesis is believed to be due to impairment of the autonomic nervous system. The autonomic impairment may involve the parasympathetic fibers of S2-S4 which is responsible for innervation of the distal colon and may lead to atonic colon and proximal obstruction. In few cases, Ogilvie’s syndrome (colonic pseudo-obstruction) may show atrophic myopathy with thinned colonic wall and intact myenteric plexus.

• 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.^[1][2][3]
• 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:^[4]
    • 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:^[4]
    • 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.^[5]
  • Neurohormonal peptides:^[6][7]
    • Inhibitory neurotransmitters are released and cause the gut motility to slow down.
    • Inhibitory neurotransmitters include, nitric oxide, vasoactive intestinal polypeptide, and substance P.

• Ogilvie’s syndrome (acute colonic psuedo-obstruction) may be associated with the following conditions:^[1]
  • Major surgeries as hip replacement surgery
  • Acute cardiac diseases as myocardial infarction
  • Systemic infections

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

Common causes of Ogilvie’s syndrome include trauma, gynecological surgeries, major surgeries as hip replacement, and myocardial infarction. Other causes include causes of non mechanical bowel obstruction as acid base imbalance, acute pancreatitis, apoplexy, and cancers.

• Common causes of Ogilvie’s syndrome include the following: ^[1][2]
  • Trauma
  • Obstetrical and gynecological surgeries
  • Surgeries as cardiothoracic, abdominal and pelvic
  • Pneumonia
  • Myocardial infarction
  • Drug induced as the phenothiazines, narcotics, and calcium channel blockers

• 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

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

Ogilvie syndrome (colonic pseudo-obstruction) must be differentiated from other diseases that cause abdominal distention and abdominal pain such as irritable bowel syndrome, volvulus and acute diverticulitis.

Ogilvie syndrome (colonic pseudo-obstruction) must be differentiated from other diseases that cause abdominal distention and abdominal pain 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

Disease Clinical manifestations Diagnosis Comments Symptoms Signs Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo- tension Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Acute suppurative cholangitis RUQ + + + + − − − − + + + N Abnormal LFT WBC >10,000 Ultrasound shows biliary dilatation/stents/tumor Septic shock occurs with features of SIRS Acute cholecystitis RUQ + − + + − − − − − − − Hypoactive Hyperbilirubinemia Leukocytosis Ultrasound shows: Gallstone Inflammation Murphy’s sign Acute pancreatitis Epigastric + − + ± − − − − ± − − N Increased amylase / lipase Ultrasound shows evidence of inflammation CT scan shows severity of pancreatitis Pain radiation to back Chronic pancreatitis Epigastric − − ± ± − + + − − − − N Increased amylase / lipase Increased stool fat content Pancreatic function test CT scan Calcification Pseudocyst Dilation of main pancreatic duct Predisposes to pancreatic cancer Pancreatic carcinoma Epigastric − − + + − + + − − − − N ↑ Alkaline phosphatase ↑ serum bilirubin ↑ gamma-glutamyl transpeptidase ↑ CA 19-9  MDCT with  PET/CT MRI Skin manifestations may include: Bullous pemphigoid Cicatricial pemphigoid Migratory superficial thrombophlebitis (classic Trousseau’s syndrome) Pancreatic panniculitis Disease Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo- tension Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Comments Cholelithiasis RUQ/Epigastric ± − ± ± − − − − − − − Normal to hyperactive for dislodged stone Leukocytosis Ultrasound shows gallstone Fatty food intolerance Peptic ulcer disease Diffuse ± − + − − − + Gastric ulcer- melena and hematemesis Duodenal ulcer- melena and hematochezia Positive if perforated Positive if perforated Positive if perforated N Ascitic fluid LDH > serum LDH Glucose < 50mg/dl Total protein > 1g/dl Air under diaphragm in upright CXR Upper GI endoscopy for diagnosis Gastritis Epigastric ± − + − − − Positive in chronic gastritis + − − − N H.pylori infection diagnostic tests Endoscopy H.pylori gastritis guideline recommendation Gastroesophageal reflux disease Epigastric − − ± − − − − − − − − N N Gastric emptying studies Esophageal manometry Endoscopy for alarm signs Gastric outlet obstruction Epigastric − − ± − − − + − − − − Hyperactive Complete blood count Basic metabolic panel Abdominal x-ray– air fluid level Barium upper GI studies- narrowed pylorus Succussion splash Gastroparesis Epigastric − − + − − − + − ± − − Hyperactive/hypoactive Hemoglobin Fasting plasma glucose Serum total protein, albumin, thyrotropin (TSH), and an antinuclear antibody (ANA) titer HbA1c Scintigraphic gastric emptying Succussion splash Single photon emission computed tomography (SPECT) Full thickness gastric and small intestinal biopsy Dumping syndrome Lower and then diffuse − − + − − + + − + − − Hyperactive Glucose challenge test Hydrogen breath test Upper GI series Gastric emptying study Postgastrectomy Disease Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo- tension Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Comments Acute appendicitis Starts in epigastrium, migrates to RLQ + Positive in pyogenic appendicitis + − − ± − − Positive in perforated appendicitis + + Hypoactive Leukocytosis Ct scan Ultrasound Positive Rovsing sign Positive Obturator sign Positive Iliopsoas sign Acute diverticulitis LLQ + ± + − + ± − + Positive in perforated diverticulitis + + Hypoactive Leukocytosis CT scan Ultrasound History of constipation Infective colitis Diffuse + − ± − − + − + Positive in fulminant colitis ± ± Hyperactive Stool culture and studies Shiga toxin in bloody diarrhea PCR CT scan Bowel wall thickening Edema Viral hepatitis RUQ + − + + − Positive in Hep A and E + − Positive in fulminant hepatitis Positive in acute + N Abnormal LFTs Viral serology US Hep A and E have fecal-oral route of transmission Hep B and C transmits via blood transfusion and sexual contact. Liver abscess RUQ + + + + − ± + − + + ± Normal or hypoactive CBC Blood cultures Abnormal liver function tests US CT Disease Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo- tension Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Comments Pyelonephritis Unilateral + ± + − − − − − + − − Hypoactive Urinalysis Urine culture Blood culture CT MRI CVA tenderness Renal colic Flank pain − − + − − − − − − − − N Hematuria Ultrasound CT scan Colicky abdominal pain Dysuria Small bowel obstruction Diffuse + − + − + − + − + + ± Hyperactive then absent Leukocytosis with left shift indicates complications Abdominal X ray Dilated loops of bowel with air fluid levels Gasless abdomen “Target sign”– , indicative of intussusception Venous cut-off sign” – suggests thrombosis Volvulus Diffuse – − + − + − − − Positive in perforated cases + + Hyperactive then absent Leukocytosis CT scan and abdominal X ray U shaped sigmoid colon “Whirl sign” Biliary colic RUQ − − + + − − − − − − − N ↑ bilirubin and alkaline phosphatase Ultrasound Disease Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo- tension Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Comments Mesenteric ischemia Periumbilical Positive if bowel becomes gangrenous − + − − + + + Positive if bowel becomes gangrenous Positive if bowel becomes gangrenous − Hyperactive to absent Leukocytosis and lactic acidosis Amylase levels D-dimer CT angiography SMA or SMV thrombosis Also known as abdominal angina that worsens with eating Acute ischemic colitis Diffuse + ± + − − + + + + + + Hyperactive then absent Leukocytosis Abdominal x-ray Distension and pneumatosis CT scan Double halo appearance, thumbprinting Thickening of bowel May lead to shock Ruptured abdominal aortic aneurysm Diffuse ± − + − − − + + + − − N Fibrinogen D-dimer Focused Assessment with Sonography in Trauma (FAST)  Unstable hemodynamics Intra-abdominal or retroperitoneal hemorrhage Diffuse ± − ± − − − − + + − − N ↓ Hb ↓ Hct CT scan History of trauma Disease Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo- tension Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Comments Torsion of the cyst RLQ / LLQ − − + − − − − − − ± ± N ↑ ESR ↑ CRP Ultrasound Sudden onset & severe pain Cyst rupture RLQ / LLQ − − + − − − − − + ± ± N ↑ ESR ↑ CRP Ultrasound Ruptured ectopic pregnancy RLQ / LLQ − − + − − − − − + + + N Positive pregnancy test Ultrasound History of Missed period Vaginal bleeding Pneumonia RUQ/LUQ + + + − − ± − − + − − Normal or hypoactive ABGs Leukocytosis Pancytopenia CXR CT chest Bronchoscopy Shortness of breath Cough Myocardial Infarction Epigastric ± − + − − − − − Positive in cardiogenic shock − − N Cardiac enzymes ECG Echocardiogram Wall motion abnormality Wall rupture Septal rupture Chest pain, tightness, diaphoresis Complications: Arrythmias Mitral regurgitation Ventricular wall rupture Septal rupture

The following table discusses differential diagnoses of abdominal pain with constipation:

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

Disease Clinical manifestations Diagnosis Comments Symptoms Signs Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo- tension Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Acute diverticulitis LLQ + ± + − + ± − + Positive in perforated diverticulitis + + Hypoactive Leukocytosis CT scan Ultrasound History of constipation Irritable bowel syndrome Diffuse − − − − ± ± + − − − − N Normal Normal Symptomatic treatment High dietary fiber Osmotic laxatives Antispasmodic drugs Colon carcinoma Diffuse/localized − − − − ± ± + + ± − − Normal or hyperactive if obstruction present CBC Carcinoembryonic antigen (CEA) Colonoscopy Flexible sigmoidoscopy Barium enema CT colonography  PILLCAM 2: A colon capsule for CRC screening may be used in patients with an incomplete colonoscopy who lacks obstruction Small bowel obstruction Diffuse + − + − + − + − + + ± Hyperactive then absent Leukocytosis with left shift indicates complications Abdominal X ray Dilated loops of bowel with air fluid levels Gasless abdomen “Target sign”– , indicative of intussusception Venous cut-off sign” – suggests thrombosis Volvulus Diffuse – − + − + − − − Positive in perforated cases + + Hyperactive then absent Leukocytosis CT scan and abdominal X ray U shaped sigmoid colon “Whirl sign”

References

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

The incidence of Ogilvie’s syndrome is 100 per 100,000 individuals. Ogilvie’s syndrome commonly affects patients more than 60years and it is more prevelant int he men more than women.

• Worldwide, the incidence of Ogilvie’s syndrome is 100 per 100,000 inidividuals.^[1]

• Ogilvie’s syndrome commonly affects patients more than 60 years old.^[2]

• Ogilvie’s syndrome is more prevalent in the men more than women.^[2]

• There is no racial predilection for Ogilvie’s syndrome.

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

Common risk factors of Ogilvie’s syndrome include having neurologic disorders, taking narcotic medications, and trauma. Other risk factors include systemic lupus erythematosus, alcoholism, and multiple myeloma.

Common risk factors for Ogilvie’s syndrome include the following:^[1][2]

• Having cerebral palsy or other nervous system (neurologic) disorders
• Taking narcotic medications
• Trauma
• Cardiac diseases as myocardial infarction

Less common risk factors for Ogilvie’s syndrome include the following:^[3]

• Systemic lupus erythematosus
• Alcoholism
• Multiple myeloma
• Systemic sclerosis

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

There is insufficient evidence to recommend routine screening for Ogilvie’s syndrome.

There is insufficient evidence to recommend routine screening for Ogilvie’s syndrome.

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

If left untreated, of patients with acute colonic pseudo-obstruction may progress to develop intestinal perforation which is life threatening complication. Common complications of Ogilvie’s syndrome include colonic ischemia and intestinal perforation. Prognosis of Ogilvie syndrome depends on the underlying cause of pseudo-obstruction.

• If left untreated, of patients with acute colonic pseudo-obstruction may progress to develop intestinal perforation which is life threatening complication.

• Common complications of Ogilvie’s syndrome include:
  • Colonic ischemia
  • Intestinal perforation

• Prognosis of Ogilvie syndrome depends on the underlying cause of the pseudoobstruction and the developed complications.^[1]
• Prognosis is generally poor with mortatlity rate is estimated to be 15% with early treatment.
• The mortality rate is 36-44% in case the colonic ischemia or intestinal perforation develop.

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