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Acute Mesenteric Ischemia Treatment & Management

  • Author: Chat V Dang, MD; Chief Editor: John Geibel, MD, DSc, MSc, MA  more...
 
Updated: Dec 16, 2015
 

Approach Considerations

Recognition of acute mesenteric ischemia (AMI) before permanent tissue damage occurs is the best way of improving patient survival, and only angiography or exploratory surgery makes early diagnosis possible. Computed tomography (CT) angiography (CTA) and magnetic resonance angiography (MRA) have become the cornerstones of modern diagnostic approach, allowing prompt laparotomy in patients with suspected AMI. A second-look procedure is indicated whenever bowel of questionable viability is not resected.

After initial medical or surgical stabilization, patients with AMI typically have a prolonged inpatient recovery time. This is especially true when resection of necrotic bowel is performed. Such patients may need to be kept on nil per os (NPO) status, and they may be maintained on parenteral nutrition for some time. If sepsis is evident, liver abscess should be actively sought. During the inpatient stay, every effort must be made to find and, if possible, treat any predisposing cause(s) of AMI.

Inpatient medications that may be used include the following:

  • Papaverine
  • Heparin/low-molecular-weight heparin (LMWH)
  • Warfarin
  • Broad-spectrum antibiotics and pain medications
  • Thrombolytics

Because timing is essential in preventing bowel necrosis with its attendant severe morbidity and mortality, patients should be transferred only if the primary hospital lacks adequate services for diagnosing and treating the patient. Patients should be optimally resuscitated before transfer. Appropriate services must be available at the receiving hospital.

In 2000, the American Gastroenterological Association released recommended algorithms for the diagnosis and management of mesenteric ischemia (see the images below).[72] However, these recommendations were formulated before the availability of improved data from multidetector CT, as a result of which CT now plays a larger role in the diagnosis of mesenteric ischemia.

Diagnosis and treatment of intestinal ischemia (me Diagnosis and treatment of intestinal ischemia (mesenteric venous thrombosis and major nonembolic arterial occlusion). Solid lines indicate accepted management plan; dashed lines indicate alternate management plan. DVT=deep vein thrombosis; SMA=superior mesenteric artery. Adapted from Gastroenterology. 2000 May;118(5):954-68.
Diagnosis and treatment of intestinal ischemia (mi Diagnosis and treatment of intestinal ischemia (minor arterial occlusion or embolus, major embolus, and splanchnic vasoconstriction without occlusion). Solid lines indicate accepted management plan; dashed lines indicate alternate management plan. DVT=deep vein thrombosis; SMA=superior mesenteric artery. Adapted from Gastroenterology. 2000 May;118(5):954-68.
Management of colon ischemia. Solid lines indicate Management of colon ischemia. Solid lines indicate accepted management plan; dashed lines indicate alternative management plan. BE=barium enema; NPO—nil per os (nothing by mouth); PLC=protein-losing colopathy; IBD=inflammatory bowel disease. Adapted from Gastroenterology. 2000 May;118(5):954-68.

Treatment options depend on the etiology of intestinal ischemia, as well as on the hemodynamic stability of the patient and the experience/expertise of the treating staff. Generally speaking, nonocclusive AMI is treated medically, whereas occlusive AMI is correctable with surgery. Definitive treatment options include the following:

  • Acute mesenteric arterial embolism (AMAE) - Papaverine infusion, surgical embolectomy, and intra-arterial thrombolysis
  • Acute mesenteric arterial thrombosis (AMAT) - Papaverine infusion and arterial reconstruction, either through aortosuperior mesenteric arterial bypass grafting or through reimplantation of the superior mesenteric artery (SMA) into the aorta [81]
  • Nonocclusive mesenteric ischemia (NOMI) - Papaverine infusion [53, 64, 82]
  • Mesenteric venous thrombosis (MVT) - Anticoagulation with heparin or warfarin, either alone or in combination with surgery; immediate heparinization should be started even when surgical intervention is indicated [70, 37, 83, 65, 84, 33]

All cases of mesenteric ischemia with signs of peritonitis or possible bowel infarction,[85] regardless of etiology, generally warrant immediate surgical intervention for the resection of ischemic or necrotic intestines. Hemodynamic instability can also be an indication for surgery. Surgical treatment may be contraindicated if the risks from comorbid conditions preclude survival after general anesthesia. If the ischemia is thought to be caused by vasospasm, surgery is not indicated. Medical management with anticoagulants and intra-arterial vasodilators is appropriate.

Some experience with percutaneous endovascular interventions has been accumulated. In select cases, especially in isolated spontaneous dissection of the SMA, stent placement may be the preferred option.[86]

Aside from timely diagnosis and treatment of predisposing conditions, there are no known preventive measures for AMI. In the presence of a clinical syndrome suggesting chronic mesenteric insufficiency, color Doppler evaluation of the mesenteric vessels may help identify at-risk patients for further workup and determine which patients might need angioplasty.

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Initial Resuscitation and Stabilization

Because patients with mesenteric ischemia are usually in a highly toxic state or rapidly progressing toward such a state, resuscitation is often necessary. Every effort should be made to improve patients’ cardiovascular status. Vasopressors should be avoided, because they worsen ischemia. Oxygen should be provided to maintain a saturation between 96-99%, via endotracheal intubation if necessary. Early intubation in unstable patients may improve oxygenation and allow more aggressive fluid resuscitation.

If hypovolemia is considered likely, intravenous (IV) fluid resuscitation is required. This is accomplished with isotonic sodium chloride solution, and blood products are provided as needed. Adequacy of resuscitation can be determined by means of urinary output, central venous pressure, or Swan-Ganz pressure monitoring. A nasogastric tube should be inserted, and any arrhythmia, congestive heart failure (CHF), or myocardial infarction (MI) should be treated.

All patients with possible bowel ischemia should be started on broad-spectrum antibiotics at an early stage to cover the possibility of bowel necrosis with contamination. Adequate pain control should be provided (eg, with parenteral opioid analgesics) while stable blood pressure is maintained.

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Pharmacologic Therapy

Papaverine

Intra-arterial infusion of papaverine through the angiography catheter at the affected vessel is useful for all arterial forms of AMI. Papaverine is an opium derivative that functions as a phosphodiesterase inhibitor, which acts to relax vascular smooth muscle. It is usually infused directly into the superior mesenteric artery (SMA), thus improving intestinal blood flow.

An infusion of 30-60 mg/hr may be started after angiography, with the dosage subsequently adjusted on the basis of the clinical response. This should be continued for at least 24 hours. If the catheter slips into the aorta, significant hypotension can occur. It must be kept in mind that papaverine is incompatible with heparin.

Papaverine relieves reactive vasospasm in occluded arterial vessels and is the only treatment of NOMI other than resection of gangrenous bowel. In some patients with AMAE, intra-arterial papaverine has reversed the ischemia and averted operation. AMAT, however, cannot be cured medically; if vasospasm is observed on arteriography in a patient with AMAT, intra-arterial papaverine may be started to improve flow, but it will not be curative.

Thrombolytics

Thrombolytic agents infused through the angiography catheter can be life-saving for selected patients with AMAE. Bleeding is the main complication. Thrombolytic administration is risky and should only be undertaken if peritonitis or other signs of bowel necrosis are absent.

The infusion must be started within 8 hours of symptom onset. If symptoms do not improve within 4 hours or if peritonitis develops, the infusion should be stopped and surgical treatment instituted.

Thrombolytics have shown no benefit in AMAT. Lytic therapy with urokinase, streptokinase, or tissue plasminogen activator has been found to be beneficial in some cases of MVT.

Heparin

Heparin anticoagulation is the main therapy for MVT. If no signs of bowel necrosis exist, the patient may not even need an operation. Heparin may increase the chance of bleeding complications. A possible avenue for randomized clinical trials is the use of enoxaparin or another low-molecular-weight heparin (LMWH) as a potential substitute for heparin in the treatment of MVT.

Heparin is administered first as a bolus of 80 U/kg, not to exceed 5000 U, and then as an infusion at 18 U/kg/hr until full conversion to oral warfarin. Appropriate monitoring of anticoagulation through measurement of the activated partial thromboplastin time (aPTT) is mandatory.

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Surgical Intervention

Before operative management of AMI, patients should be stabilized as described above (see Initial Resuscitation and Stabilization). If possible, they should undergo bowel preparation the night before surgery and take nothing by mouth after midnight the evening before surgery.

If the surgeon thinks a patient may require extensive resection and that lifelong hyperalimentation is likely to be the only option, this possibility should be thoughtfully discussed with the patient and the family to help guide the surgeon during the exploration. Such issues are best decided preoperatively, with educated input from the patient, rather than intraoperatively by the surgeon.

It is essential to determine the locations of viable and nonviable bowel during surgery. In patients with AMAT, laparotomy reveals that the entire small bowel and proximal colon are affected, reflecting a proximal obstruction. In patients with AMAE, however, the proximal jejunum is spared, reflecting a more distal obstruction. When extensive bowel involvement is noted, every effort must be made to retain every centimeter of viable bowel. If determining bowel viability is difficult, a second look may be required 24-48 hours later.

Evaluation of viability begins with direct visualization of the bowel. If the first part of the jejunum is not involved, an embolus may be present, and immediate embolectomy may be indicated. Peristalsis should be sought, and the color of the bowel should be observed (pink and healthy vs red and edematous; see the image below). After reconstitution of arterial flow, the viability of the bowel is reassessed. This reassessment is based on clinical findings, including the color of the bowel and the presence or absence of palpable pulses.

Gross specimen showing hemorrhagic dead bowel afte Gross specimen showing hemorrhagic dead bowel after resection from patient with acute mesenteric ischemia.

Intraoperative Doppler scans of the bowel can provide valuable information on the patency of the vessels. Differentiation of nonviable from viable bowel can be enhanced by intraoperative fluorescein administration. During laparotomy, 1 g of fluorescein is infused. Viable bowel fluoresces brightly under a Wood lamp, thus allowing the surgeon to better identify the segments that must be resected.

Because of fat absorption, fluorescein can be used only once. Most patients can benefit from a 24- to 48-hour second-look operation to assess the viability of the remaining bowel. Intraoperative fluorescein administration may be performed either at the primary operation or during the second-look operation.

A second-look laparotomy is the most reliable method of determining bowel viability. The decision to perform a second-look procedure is made during the initial exploration. If a second look is deemed necessary, the surgeon should not change his or her mind, regardless of the patient’s clinical progress.

Acute mesenteric arterial embolism

For AMAE (ie, embolic AMI), unless the involved bowel is clearly gangrenous, reperfusion should be attempted. The SMA is exposed and isolated below the mesocolon distal to the middle colic artery, and the location of the blockage is determined by palpation of pulses. Because most emboli are near the origin of the middle colic artery, the proximal SMA pulse should be noted in AMAE.

A transverse (or, according to some surgeons’ preference, longitudinal) arteriotomy is made proximal to the point of occlusion, and a balloon-tipped Fogarty catheter (size 3 or 4) is passed distally. The balloon is then inflated and the clot extracted. The arteriotomy can be closed primarily or vein-patched to prevent lumen compromise. If primary closure or patching is difficult, the patient may require an endarterectomy. A bypass may be required if embolectomy is unsuccessful.

After restoration of flow, the intestines are observed for 10-15 minutes to allow assessment of bowel viability. As noted (see above), this assessment can be enhanced by intraoperative duplex ultrasonography, fluorescein use, and palpation of pulses distal to the occlusion.

Other methods of reperfusion involve prosthetic bypass grafting or autogenous vein grafting.

Acute mesenteric arterial thrombosis

Surgical treatment of AMAT (ie, thrombotic AMI) involves exploratory laparotomy, followed by identification of the involved artery and bowel. Anticoagulation therapy with IV heparin, if not already started, should be initiated.

Emergency surgical revascularization is indicated. Simple thrombectomy is of little or no benefit, because most patients have clinically significant atherosclerosis at the time of the acute decompensation. Unlike patients with AMAE, patients with AMAT have a lesion at the origin of the SMA, and no SMA pulsation is detected at the origin.

If the gut is not gangrenous, revascularization may proceed. An antegrade aortomesenteric bypass is preferred. Bypass may also be done with a prosthetic graft. If bowel perforation is discovered on laparotomy, an autogenous saphenous vein graft should be used because of the decreased risk of infection. Transaortic endarterectomy is an alternative when no vein is suitable for harvesting or when a prosthetic graft is contraindicated (eg, with massive fecal contamination).[87, 88] After revascularization, the viability of the bowel is reassessed.

Endovascular therapies have been described, and some authors have tried thromboaspiration.[89] The criterion standard remains operative exploration to allow assessment of bowel viability.

Mesenteric venous thrombosis

For patients with severe MVT, exploratory laparotomy with assessment of bowel viability is indicated (see above). Anticoagulation therapy with IV heparin should be initiated immediately and continued intraoperatively. Definitive surgical treatment is required for patients with signs of bowel infarction or peritonitis.[90, 33] Treatment involves resecting the dead bowel segment(s) and reanastomosing the remaining bowel ends.

Direct venous surgery to remove the clot is usually unsuccessful and is best reserved for patients with portal vein or superior mesenteric vein (SMV) involvement. Thrombectomy has little use in MVT, because it can only be performed if the thrombus is fresh (ie, no more than 1-3 days old) and because the thrombosis is usually so widespread that all the thrombi cannot be removed completely. Mechanical transhepatic thrombectomy has been described in one patient.[91]

To minimize the amount of bowel loss, a second-look laparotomy should be seriously considered, especially in patients with significant bowel involvement. However, unlike patients with mesenteric arterial ischemia, patients with MVT generally do not require a second-look laparotomy unless progression of the disease is observed or suspected (typically ~40% of cases).

Reports of diagnostic laparoscopy in patients with venous thrombosis suggest that this modality may be of some utility in preventing fruitless laparotomies in MVT patients; however, the decreased mesenteric blood flow that occurs with laparoscopy may worsen bowel ischemia.

Patients with severe intestinal loss due to MVT may be considered for intestinal transplantation in specialized centers.

Angioplasty and stenting

Some experience with percutaneous endovascular interventions has been accumulated. A few patients who have atherosclerotic plaques at the origin of the SMA after thrombolysis are eligible for angioplasty. Angioplasty is technically difficult because of the anatomy of the SMA. Restenosis rates are 20-50%. Limited study findings indicate a definite role for angioplasty in the treatment of AMI. A case of successful transcutaneous catheter aspiration of an embolic clot from SMA has been reported.[92]

In select cases, especially in isolated spontaneous dissection of the SMA diagnosed before the onset of intestinal infarction, stent placement has been successful and may constitute the best therapeutic option.[19, 20, 21, 22, 86]

Postoperative care

Postoperative care should include close monitoring of blood pressure and hemoglobin level to evaluate for sepsis or hemorrhage. Heparin anticoagulation should be continued postoperatively to reduce thrombotic events.[93] Antibiotics should be continued postoperatively to prevent any septic events. Papaverine may be administered to reduce vasospasm.

A 12-lead electrocardiogram (ECG) should be obtained to evaluate for myocardial dysfunction. Echocardiography should be considered to identify any for valvular vegetations. A workup for a hypercoagulable state is required postoperatively if it was not done preoperatively. Postoperative ileus due to bowel reperfusion should be expected and appropriately managed.

Complications of surgery

Because patients with MVT are typically in a hypercoagulable state, the incidence of deep vein thrombosis (DVT) is increased. Proper anticoagulation and liberal use of sequential compression stockings can help prevent this postoperative complication.

Because of the high incidence of atherosclerosis in patients with AMI, it is not surprising that one of the most common postoperative complications is myocardial infarction (MI). Prevention of postoperative MI involves preoperatively identifying correctable coronary artery disease. A Swan-Ganz catheter may be used during the perioperative period to monitor fluid status and cardiac function. During the cross-clamping of the supraceliac aorta, the anesthesiologist can ensure myocardial protection and afterload reduction to maximize cardiac output.

Because patients become acutely hypovolemic, acute renal failure may occur in the immediate postoperative period. This complication can be prevented by keeping the patient well hydrated and administering mannitol before the aorta is cross-clamped.

Other possible complications include bleeding, infection, bowel infarction, prolonged ileus, and graft infection.

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Diet and Activity

To prepare for surgery and to reduce oxygen demand on the ischemic bowel, patients must be on NPO status. No other specific dietary measures are mandatory.

Patients’ activities are dictated by their conditions. Bed rest to allow for monitoring and to reduce demand on cardiac output is balanced against ambulation to prevent DVT.

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Consultations

The following consultations should be considered in the setting of AMI:

  • Vascular surgeon - To evaluate the patient and to perform a revascularization procedure if required; this consultation should be obtained as soon as the diagnosis is considered
  • Interventional radiologist - To perform any needed angiographic drug infusions or angioplasty
  • Critical care specialist - To evaluate the patient for possible insertion of a Swan-Ganz catheter or admission to a critical care unit; patients with AMI are often hemodynamically unstable or highly likely to progress to instability
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Long-Term Monitoring

Because of the high likelihood of concomitant vascular disease in the rest of the arterial tree, patients must be closely monitored. Cardiac and renal status should be determined at follow-up. Carotid duplex studies may be necessary if diffuse atherosclerotic disease is a strong possibility.

Outpatient medications include antiarrhythmics for patients with atrial fibrillation (AF) and warfarin for long-term treatment of patients with MVT or AF. Patients who have had MVT need warfarin therapy for at least 6 months or for life if a hypercoagulable state was discovered during treatment. Patients with AF should also be discharged on warfarin. Patients with other treatable predisposing conditions should be continued on appropriate therapy.

Periodic evaluation of coagulation status is required as well. To ensure proper anticoagulation, patients should have frequent visits for monitoring of the international normalized ratio (INR).

Patients who have had extensive small bowel resection have severe diarrhea for a few weeks, but many appear to be able to compensate for the reduced bowel length after a few months. Thereafter, they may have one to three liquid bowel movements a day and may maintain or gain weight with oral intake. On the other hand, patients who have undergone total resection of the small intestine need lifelong IV hyperalimentation (ie, total parenteral nutrition).

A number of patients who recover from ileus secondary to intestinal ischemia may develop fibrosis of a segment of small bowel with intermittent partial obstruction.

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Contributor Information and Disclosures
Author

Chat V Dang, MD Clinical Professor of Emergency Medicine, Charles Drew University of Medicine and Science; Clinical Professor, Department of Medicine, University of California, Los Angeles, David Geffen School of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Mark Su, MD, MPH, FACEP, FACMT Consulting Staff and Director of Fellowship in Medical Toxicology, Department of Emergency Medicine, North Shore University Hospital

Mark Su, MD, MPH, FACEP, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Daniel K Nishijima, MD, MAS Assistant Professor of Emergency Medicine, Associate Research Director, Department of Emergency Medicine, University of California, Davis, School of Medicine

Daniel K Nishijima, MD, MAS is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, DSc, MSc, MA Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, Surgical Research, Department of Surgery, Yale-New Haven Hospital; American Gastroenterological Association Fellow

John Geibel, MD, DSc, MSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, Society for Surgery of the Alimentary Tract

Disclosure: Received royalty from AMGEN for consulting; Received ownership interest from Ardelyx for consulting.

Acknowledgements

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: lippincott Royalty textbook royalty; wiley Royalty textbook royalty

Burt Cagir, MD, FACS Assistant Professor of Surgery, State University of New York Upstate Medical University; Consulting Staff, Director of Surgical Research, Robert Packer Hospital; Associate Program Director, Department of Surgery, Guthrie Clinic

Burt Cagir, MD, FACS is a member of the following medical societies: American College of Surgeons, American Medical Association, Association of Program Directors in Surgery, and Society for Surgery of the Alimentary Tract

Disclosure: Nothing to disclose.

Brian James Daley, MD, MBA, FACS, FCCP, CNSC Professor and Program Director, Department of Surgery, Chief, Division of Trauma and Critical Care, University of Tennessee Health Science Center College of Medicine

Brian James Daley, MD, MBA, FACS, FCCP, CNSC is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Chest Physicians, American College of Surgeons, American Medical Association, Association for Academic Surgery, Association for Surgical Education, Eastern Association for the Surgery of Trauma, Shock Society, Society of Critical Care Medicine, Southeastern Surgical Congress, Southern Surgical Association, andTennessee Medical Association

Disclosure: Nothing to disclose.

Michael A Grosso, MD Consulting Staff, Department of Cardiothoracic Surgery, St Francis Hospital

Michael A Grosso, MD is a member of the following medical societies: American College of Surgeons, Society of Thoracic Surgeons, and Society of University Surgeons

Disclosure: Nothing to disclose.

Chandler Long, MD Resident Physician, Department of Surgery, University of Tennessee Medical Center-Knoxville

Disclosure: Nothing to disclose.

Ashis Mandal, MD Professor, Department of Surgery, Drew University of Medicine and Science and UCLA College of Medicine

Disclosure: Nothing to disclose.

Robert M McNamara, MD, FAAEM Chair and Professor, Department of Emergency Medicine, Temple University School of Medicine

Robert M McNamara, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Association, Pennsylvania Medical Society, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David L Morris, MD, PhD, FRACS Professor, Department of Surgery, St George Hospital, University of New South Wales, Australia

David L Morris, MD, PhD, FRACS is a member of the following medical societies: British Society of Gastroenterology

Disclosure: RFA Medical None Director; MRC Biotec None Director

Yale D Podnos, MD, MPH Consulting Surgeon, Department of Surgery, City of Hope National Medical Center

Disclosure: Nothing to disclose.

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Deron J Tessier, MD Staff Surgeon, Kaiser Permanente Medical Center, Fontana, CA

Deron J Tessier, MD is a member of the following medical societies: American College of Surgeons and American Medical Association

Disclosure: Nothing to disclose.

Jeff Wade, MD Resident Physician, Department of Emergency Medicine, Long Beach Community Hospital, Greater El Monte Medical Center

Disclosure: Nothing to disclose.

Russell A Williams, MBBS Program Director, Professor, Department of Surgery, University of California Medical Center at Irvine

Disclosure: Nothing to disclose.

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Pneumatosis intestinalis (black stripes of air) in advanced acute mesenteric ischemia (AMI) with gangrenous bowel.
CT scan (with contrast) of nonocclusive mesenteric ischemia with resulting bowel wall edema (arrows).
Aortogram showing narrowing of superior mesenteric artery.
Radiograph showing bowel spasm (early sign of ischemia).
Gas in colon wall (typical of advanced ischemia).
Ischemia stricture.
Thumbprinting of bowel, characteristic of mesenteric artery ischemia.
Pathologic findings 2 hours after bowel ischemia starts.
Microscopic findings 24 hours after ischemia starts.
Gross specimen showing hemorrhagic dead bowel after resection from patient with acute mesenteric ischemia.
Pneumatosis intestinalis, one of few radiographic findings in patients with mesenteric ischemia.
Diagnosis and treatment of intestinal ischemia (mesenteric venous thrombosis and major nonembolic arterial occlusion). Solid lines indicate accepted management plan; dashed lines indicate alternate management plan. DVT=deep vein thrombosis; SMA=superior mesenteric artery. Adapted from Gastroenterology. 2000 May;118(5):954-68.
Diagnosis and treatment of intestinal ischemia (minor arterial occlusion or embolus, major embolus, and splanchnic vasoconstriction without occlusion). Solid lines indicate accepted management plan; dashed lines indicate alternate management plan. DVT=deep vein thrombosis; SMA=superior mesenteric artery. Adapted from Gastroenterology. 2000 May;118(5):954-68.
Management of colon ischemia. Solid lines indicate accepted management plan; dashed lines indicate alternative management plan. BE=barium enema; NPO—nil per os (nothing by mouth); PLC=protein-losing colopathy; IBD=inflammatory bowel disease. Adapted from Gastroenterology. 2000 May;118(5):954-68.
Complete aortic occlusion (Leriche syndrome) with acute embolism of superior mesenteric artery.
Gross specimen of dead bowel.
Meandering artery (radiographic sign of preexisting bowel ischemia).
CT scan demonstrating thrombosis of superior mesenteric vein.
CT scan demonstrating thrombosis of portal vein.
CT scan demonstrating cavernous change of superior mesenteric vein as consequence of venous thrombosis.
 
 
 
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