Mesenteric ischemia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

The factors that regulate the intestinal blood flow play a vital role in the development of mesenteric ischemia. Mucosa of the intestines has a high metabolic activity and accordingly a high blood flow requirement. The majority of blood supply of the intestine comes from the superior mesenteric artery, with a collateral blood supply from superior and inferior pancreaticoduodenal arteries (branches of the celiac artery) as well as the inferior mesenteric artery. The splanchnic circulation (arteries supplying the viscera) receives 15-35% of the cardiac output, making it sensitive to the effects of decreased perfusion. Mesenteric ischemia occurs when intestinal blood supply is compromised by more than 50% of the original blood flow without activation of adaptive responses. This can lead to disruption of mucosal barrier, allowing the release of bacterial toxins (present in the intestinal lumen) and vasoactive mediators which ultimately lead to complete necrosis (cell death) of the intestinal mucosa. This can further progress to depression in myocardial activity, sepsis, multiorgan failure, and without prompt intervention, even death.

In 1843, Tiedemann described mesenteric occlusion and bowel infarction, followed by Virchow who added two more patients to the literature. In 1921, Klein wrote a thesis on embolism and thrombosis, in which he pointed out a relationship between SMA stenosis and episodic abdominal pain. In 1936, Dunphy was the first one to establish an association between mesenteric artery occlusion and bowel infarction. In 1971, the first book written on all aspects of mesenteric ischemia named “Vascular Disorders of the Intestines” was published and edited by Boley, Schwartz, and Williams.

Mesenteric ischemia (MI) is classified into various subdivisions based on the difference in pathogenesis and treatment of each type. MI is primarily classified into acute and chronic, on the basis of severity; occlusive and non occlusive based on their pathophysiology. 

The factors that regulate the intestinal blood flow play a vital role in the development of mesenteric ischemia. Mucosa of the intestines has a high metabolic activity and accordingly a high blood flow requirement. The majority of blood supply of the intestine comes from the superior mesenteric artery, with a collateral blood supply from superior and inferior pancreaticoduodenal arteries (branches of the celiac artery) as well as the inferior mesenteric artery. The splanchnic circulation (arteries supplying the viscera) receives 15-35% of the cardiac output, making it sensitive to the effects of decreased perfusion. Mesenteric ischemia occurs when intestinal blood supply is compromised by more than 50% of the original blood flow without activation of adaptive responses. This can lead to disruption of mucosal barrier, allowing the release of bacterial toxins (present in the intestinal lumen) and vasoactive mediators which ultimately lead to complete necrosis (cell death) of the intestinal mucosa. This can further progress to depression in myocardial activity, sepsis, multiorgan failure, and without prompt intervention, even death.

Narrowing of the arteries that supply blood to the intestine causes mesenteric ischemia. The arteries that supply blood to the intestines travel straight from the aorta. Mesenteric ischemia is often seen in people who have hardening of the arteries in other parts of the body (for example, those with coronary artery disease or peripheral vascular disease). The condition is more common in smokers and in patients with high blood pressure or blood cholesterol. Mesenteric ischemia can also be caused by an embolus that suddenly blocks one of the mesenteric arteries. The emboli usually come from the heart or aorta. These clots are more commonly seen in patients with arrhythmias, such as atrial fibrillation. 

Mesenteric ischemia must be differentiated from other diseases that cause abdominal pain, diarrhea, nausea and vomiting, such as ischemic colitis, inflammatory bowel disease, and irritable bowel syndrome.

The incidence rate of mesenteric ischemia secondary to superior mesenteric artery occlusion is 8.6/100 000/year. 70% of SMA occlusion is caused by embolism and 30% by thrombosis. The annual incidence of mesenteric ischemia is approximately 5.5% per 100,000 individuals. The incidence of mesenteric ischemia increases with age and the median age at diagnosis is 70 years. Mesenteric ischemia affects men and women equally.

Risk factors causing mesenteric ischemia can be divided based on the underlying etiology. Conditions posing a significant risk towards the development of mesenteric ischemia either by interrupting the blood flow through the artery or vein supplying the small intestine (e.g thromboembolism) or by reducing the blood supply (e.g. vasoconstriction). Also, there are certain life-style related risk factors which predominantly cause mesenteric ischemia in the older age group.  

There is insufficient evidence to recommend routine screening for mesenteric ischemia.

If left untreated, 99% of patients with mesenteric ischemia may progress to develop intestinal gangrene, septic shock and subsequently multiorgan failure. The progressive phases of mesenteric ischemia include hyperactive phase, paralytic phase and shock phase. The prognosis mostly depends on prompt diagnosis and timely medical/surgical intervention depending on the underlying etiology. Poor prognostic factors include signs such as tachypnea, tachycardia, hypotension and altered mental status. Common complications of mesenteric ischemia include bowel infarction, perforation, sepsis, peritonitis, septic shock, and multiorgan failure.

The definitive diagnosis of mesenteric ischemia relies mainly on the imaging studies of which the most accurate is high resolution computed tomographic angiography. It not only demonstrates the site of occlusion in the vessels but also guides about making the correct choice of treatment. It has a sensitivity of 94% and a specificity of 95%.

The hallmark of mesenteric ischemia symptoms is ‘abdominal pain out of proportion to the examination findings’. A positive history of chronic cardiovascular disorder, old age and abdominal pain is suggestive of mesenteric ischemia. The most common symptoms of mesenteric ischemia include excruciating abdominal pain, bloody diarrhea, and nausea/vomiting. Symptoms of chronic mesenteric ischemia caused by atherosclerosis include abdominal pain after eating and diarrhea, while that of acute mesenteric ischemia due to an embolus include diarrhea, sudden severe abdominal pain, and vomiting.

Physical examination of patients with mesenteric ischemia can be normal in early stages or there may be mild abdominal distension in the absence of peritonitis which presents as rebound tenderness and guarding. As the ischemia progresses to involve all the layers of the intestine (transmural infarction), abdomen becomes distended, peritoneal signs develop and bowel sounds become absent. A feculent odor to the breath may also be noticed. Signs of dehydration and shock may also appear if not treated in time.

No specific biomarker for the diagnosis of mesenteric ischemia has been identified to date. However, certain biomarkers are released into circulation as a result of ischemic injury to the intestine, which can be detected in the blood.

Plain radiographs such as X-ray abdomen can be helpful in ruling out other important causes of acute abdomen such as perforation. The sensitivity of this test is limited because it can show normal findings in as many as 25% of cases of mesenteric ischemia.

Duplex ultrasonograghy is often used for the evaluation of abdominal pain. However, in case of acute mesenteric ischemia its sensitivity is relatively reduced as compared to other radiological tests owing to its diagnostic limitation by the presence of air-filled distended bowel loops. Its primary clinical application is in the diagnosis of high grade arterial stenosis.

Computerised axial tomographic angiography should be performed as soon as possible in order to diagnose mesenteric ischemia becasue of its ability to define the arterial anatomy and demonstrate the site of occlusion.

Magnetic Resonance Angiography(MRA) is another investigation which helps diagnose mesenteric ischemia. However, its clinical application is limted as compared to computed tomography angiography because the latter is readily available and less cost effective.

Although computed tomography angiography remains the diagnostic test of choice for mesenteric ischemia. However, there are newer diagnostic studies which may be helpful in making the diagnosis of mesenteric ischemia and include functional studies such as tonometry, spectroscopic oximetry and MR flow.

Mesenteric ischemia is a medical emergency that requires prompt treatment. The mainstay of treatment is surgery if bowel necrosis or gangrene has occurred , whereas medical therapy is considered initially for hemodynamically stable patients.

Surgery in mesenteric ischemia is done to resect the ischemic bowel in order to prevent the complications. However, in case of acute embolic type of mesenteric ischemia, early laparotomy and surgical resection is the mainstay of treatment.

In order to prevent mesenteric ischemia, the risk factors should be controlled avidly. Healthy life style changes and screening of comorbidities posing a risk to developing mesenteric ischemia are the most important factors.

Effective measures to prevent recurrence of mesenteric ischemia include screening by duplex ultrasonography, nutritional and life style modification, and drug therapy.

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

In 1843, Tiedemann described mesenteric occlusion and bowel infarction, followed by Virchow who added two more patients to the literature. In 1921, Klein wrote a thesis on embolism and thrombosis, in which he pointed out a relationship between SMA stenosis and episodic abdominal pain. In 1936, Dunphy was the first one to establish an association between mesenteric artery occlusion and bowel infarction. In 1971, the first book written on all aspects of mesenteric ischemia named ‘Vascular Disorders of the Intestines’ was published and edited by Boley, Schwartz, and Williams.

• In 1843, Tiedemann described mesenteric occlusion and bowel infarction, followed by Virchow who added two more patients to the literature.
• In 1887, Welch proposed that ischemic bowel changes occur secondary to 80% stenosis of superior mesenteric artery (SMA).
• In 1904, Jackson, Parker, and Quinby stated that both arterial and venous occlusion of the mesenteric circulation can lead to mesenteric ischemia.
• In 1913, Trotter studied 359 cases of infarcted bowel. He explained a relationship between cardiac diseases and embolus to the SMA. He also elaborated a connection between arteriosclerosis of the aorta and thrombosis of mesenteric vessles.
• In 1921, Klein wrote a thesis on embolism and thrombosis, in which he pointed out a relationship between SMA stenosis and episodic abdominal pain.
• In 1936, Dunphy was the first one to establish an association between mesenteric artery occlusion and bowel infarction.^[1][2]
• In 1971, the first book written on all aspects of mesenteric ischemia named “Vascular Disorders of the Intestines” was published and edited by Boley, Schwartz, and Williams.^[3]

• Until 1967, mesenteric ischemia was a diagnostic dilemma.^{[4][5][5][6][7]}
• Aarhus and Brabrand were the first ones to propose angiography as a diagnostic tool for SMA occlusion.
• In 1967, Britt, Cheek, and Wittenberg included angiography as their management plan in 1967.
• In 1980, endovascular treatment of mesenteric disease was introduced.

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

Mesenteric ischemia (MI) is classified into various subdivisions based on the difference in pathogenesis and treatment of each type. MI is primarily classified into acute and chronic, on the basis of severity; occlusive and non occlusive based on their pathophysiology.

• Based on the severity, mesenteric ischemia is classified as either acute or chronic.^[1][2][3][4]
  • Acute mesenteric ischemia
  • Chronic mesenteric ischemia

• Acute mesenteric ischemia is further classifed into occlusive and non-occlusive subtypes.
• Occlusive MI is further classified into three more subclasses.
• Occlusive mesenteric ischemia: ^[5][6]
  • Mesenteric arterial embolism
  • Mesenteric arterial thrombosis
  • Mesenteric venous thrombosis

• Non-occlusive mesenteric ischemia^[7]

{{familytree

Mesenteric ischemia

Acute mesenteric ischemia

Chronic mesenteric ischemia

Occlusive mesenteric ischemia

Non-occlusive mesenteric ischemia

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

The factors that regulate the intestinal blood flow play a vital role in the development of mesenteric ischemia. Mucosa of the intestines has high metabolic activity and therefore requires high blood flow. The majority of blood supply of the intestine comes from the superior mesenteric artery, with a collateral blood supply from superior and inferior pancreaticoduodenal arteries (branches of the celiac artery) as well as the inferior mesenteric artery. The splanchnic circulation (arteries supplying the viscera) receives 15-35% of the cardiac output, making it sensitive to the effects of decreased perfusion. Mesenteric ischemia occurs when intestinal blood supply is compromised by more than 50% of the original blood flow without activation of adaptive responses. This can lead to disruption of mucosal barrier, allowing the release of bacterial toxins (present in the intestinal lumen) and vasoactive mediators which ultimately lead to complete necrosis (cell death) of the intestinal mucosa. This can further progress to depression in myocardial activity, sepsis, multiorgan failure, and without prompt intervention, death.

• Intestinal mucosal damage occurs in response to ischemic insult.
• In response to providing protection from ischemia, mesenteric vessels undergo intrinsic autoregulation, which is an adaptive response to ischemia.
• In order to compensate for the ischemia, there is vasoconstriction of mesenteric vessels resulting in increased tissue oxygen extraction along with vasodilation of the collateral vessels. Owing to this mechanism, intestine is able to compensate for around 75% reduction in blood flow.^{[1][2][3][4][5][6]}

• Mesenteric blood supply (general circulation)

• Collateral circulation
• Response of mesenteric vasculature to ischemia
• Vasoactive and humoral factors

• The mesenteric circulation receives approximately 25% of the resting and 35% of the postprandial cardiac output.
• Mucosal and submucosal layers of the intestine receive 70% of the mesenteric blood flow, with the rest supplying the muscularis and serosal layers.

• The arterial supply of the intestine originates from three major arteries which include superior mesenteric artery, inferior mesenteric artery, and celiac artery:^[9][10][7]

Arterial supply	Region supplied
Superior mesenteric artery (SMA)	Small intestine, proximal and mid colon up to the splenic flexure.
Inferior mesenteric artery (IMA)	Hindgut starting from the splenic flexure to the rectum.
Celiac artery (CA)	Foregut, hepatobiliary system and spleen.
Venous drainage
The venous system parallels the arterial branches and drains into the portal venous system.

Commonly affected arteries:^[11]

• Embolus can typically lodge into points of normal anatomic narrowing.
• This makes superior mesenteric artery the most vulnerable site because of its relatively larger diameter (more blood flow) and low take off angle (more likely to from the aorta.
• The majority of emboli lodge 3-10 cm distal to the origin of superior mesenteric artery, classically sparing the proximal jejunum and colon.

The role of collateral circulation in the development of mesenteric ischemia is as follows:^{[12][13][14][15][16]}

• Intestines receive collateral blood supply at all levels from the superior and inferior pancreaticoduodenal arteries, branches of the celiac artery, which provide protection from ischemia.
• These arteries can compensate for 75% reduction in mesenteric blood flow for up to 12 hours, without substanial injury.
•  An extensive collateral circulation protects the intestines from transient periods of inadequate perfusion. However, prolonged reduction in splanchnic blood flow leads to vasoconstriction in the affected vascular bed, and eventually reduces collateral blood flow.  
• The SMA and IMA communicate via the marginal artery of Drummond and the meandering mesenteric artery.
• Collateralization between the IMA and systemic circulation occurs in the rectum as the superior rectal (hemorrhoidal) vessels merge with the middle rectal vessels from the internal iliac arteries.
• The areas lacking this collateralization are prone to ischemia.

• Mesenteric ischemia occurs when the blood supply to mesentery is reduced leading to disruption of cellular metabolism owing to oxygen and nutrient deficiency.^[17][18]
• In the first 4 hours following ischemia, necrosis of the mucosal villi occurs.
• Persistent ischemia for more than 6 hours results in transmural, mural or mucosal infarction, ultimately leading to bowel perforation.
• Prolonged ischemia leads to progressive vasoconstriction of the mesenetric vessels which raises the pressure in them resulting in lowering the collateral flow.
• This is followed by vasodilation, trying to restore blood flow to the area of ischemic insult.

Ischemic insult

Decreased delivery of oxygen and nutrients

Disruption in cellular metabolism

Tissue injury due to hypoxia and reperfusion

Full thickness necrosis of the bowel

Perforation of the bowel wall

Post ischemic cellular changes:
Time duration since ischemia	Pathological changes in the small intestine
3-4 hours	Necrosis of the mucosal villi
6 hours	Transmural, mural or mucosal infarction
1-4 days	Bowel hemorrhage

Reperfusion injury:

• Restoration of blood flow to the area of ischemic insult results in reperfusion injury.
• This leads to release of oxygen free radicals, toxic byproducts of ischemic injury and neutrophil activation.
• Immune cells remove dead and damaged cells releasing cytokines such as TNF-alpha.
• Blood vessels become more permeable leading to edema of the small intestine.
• As the ischemia progresses from mucosa to all the layers beneath (transmural), it leads to breaks in the epithelial lining.
• This allows bacteria in the intestinal lumen to enter into the peritoneal cavity causing peritonitis.
• If bacteria enter into the blood stream, it results in systemic inflammatory response syndrome, which ultimately results in sepsis and septic shock.

• Vasoactive and humoral factors control the regulation of vascular tone of mesenteric circulation in response to periods of stress such as systemic hypotension or postprandial state.

• Physiologically mesenteric circulation is affected by:^{[19][20][21][22][23][24]}
  • Intrinsic regulatory system that includes metabolic and myogenic factors.
  • Extrinsic regulatory system that includes neural and humoral factors.

Intrinsic regulation:

(a) Metabolic factors:

• Reduction in blood supply to the mesentery causes adaptive changes in the splanchnic circulation.
• A discrepancy between tissue oxyegn demand and supply raises the concentration of local metabolites such as hydrogen, potassium, carbon dioxide, and adenosine, resulting in vasodilation, and hyperemia.

(b) Myogenic factors:

• Myogenic theory suggests that arteriolar wall tension receptors act to regulate vascular resistance in accordance with the transmural pressure.
• An acute decrease in perfusion pressure is compensated for by a reduction in arteriolar wall tension, thereby maintaining splanchnic blood flow.

Extrinsic regulation:

• The extrinsic neural component of splanchnic circulatory regulation comprises the alpha-activated vasoconstrictor fibers.
• Intense activation of vasoconstrictor fibers through alpha-adrenergic stimulation results in vasoconstriction of small vessels and a decrease in mesenteric blood flow.
• After periods of prolonged alpha-adrenergic vasoconstriction, blood flow increases, presumably through β-adrenergic stimulation, which acts as a protective response.
• Although numerous types of neural stimulation (e.g. vagal, cholinergic, histaminergic, and sympathetic) can affect the blood supply of the gut, the adrenergic limb of the autonomic nervous system is the predominant neural influence on splanchnic circulation.

• Numerous endogenous and exogenous humoral factors affect the splanchnic circulation.
• Norepinephrine and high doses of epinephrine produce intense vasoconstriction by stimulating the adrenergic receptors.
• Other pharmacologic compounds that decrease splanchnic blood flow include:
  • Vasopressin
  • Phenylephrine
  • Digoxin
• Low-dose dopamine causes splanchnic vasodilation, whereas higher doses lead to vasoconstriction by stimulating alpha adrenergic receptors.
• Exogenous agents that increase mesenteric blood flow include:
  • Papaverine
  • Adenosine
  • Dobutamine
  • Fenoldopam
  • Sodium nitroprusside
• In addition, numerous natural neurotransmitters can serve as splanchnic vasodilators, such as:
  • Acetylcholine
  • Histamine
  • Nitric oxide
  • Leukotrienes
  • Thromboxane analogues
  • Glucagon

Factors regulating mesenteric blood flow
Extrinsic reguatory system
Humoral (endogenous and exogenous)		Neural component
Decrease blood flow	Increase blood flow	Decrease blood flow	Increase blood flow
Epinephrine (high dose) Norepinephrine (moderate to high dose) Dopamine (high dose) Phenylephrine Vasopressin Angiotensin Digoxin	Epinephrine (low dose) Norepinephrine (low dose) Dopamine (low dose) Dobutamine Sodium nitroprusside Papaverine Nitric oxide Acetylcholine Histamine	Alpha-adrenergic receptors Dopaminergic receptors	Beta adrenergic receptors
Intrinsic regulatory component
Decrease blood flow (Myogenic factors)		Increase blood flow (Metabolic factors)
Arteriolar tension receptors		Hydrogen Potassium Carbon dioxide Adenosine

Areas prone to ischemia	Blood supply
Splenic flexure	End arteries of superior mesenteric artery
Rectosigmoid junction	End arteries of inferior mesenteric artery
Middle segment of jejunum

• Splenic flexure
  • Supplied by the end arteries of SMA with no collateral circulation.
• Rectosigmoid junction
  • Supplied by the end arteries of IMA with no collateral circulation.

• Middle segment of jejunum^[25]
  • This area is the farthest from collateral circulation and hence prone to ischemia as compared to other segments of jejunum.

Vascular occlusion

Blood flow<metabolic demand

Mucosal barrier disruption and bacterial translocation into the circulation

Anaerobic glycolysis in mucosa and lactate production

Activation of vascular and humoral factors leading to vasoconstriction

Systemic activation of inflammatory response

Lactic acidosis

Intestinal necrosis

Multiorgan failure

Hypovolemia

Cardiac failure

Endogenous vasoconstriction

Splanchnic vasoconstriction

Gut mucosal hypoperfusion

Restoration of blood by vasodilation of collaterals

Gut mucosal barrier disruption

Ischemia-reperfusion injury

Increased mucosal perfusion to bacterial toxins

Activation of inflammatory response

Gross pathology shows following changes:

• Early stage of ischemia
  • Intestinal wall in congested.
• Late stage of ischemia
  • Edematous, friable and hemorrhagic bowel wall.

Mesenteric ischemia is classified histopathologically into five grades:^[26]

• Grade 1. Normal. Vascular congestion is absent, and both the villous architecture and muscular layer are preserved. 

• Grade 2. Villous architecture is preserved, with some mucosal congestion and dilated capillaries. 

• Grade 3. There is congestion of mucosa with loss of superficial glandular architecture, but deep villous architecture is preserved.

• Grade 4. Muscular layer is preserved, but the mucosa is completely involved, with loss of all superficial and deep glandular architecture. 

• Grade 5. There is total loss of glandular architecture, and the muscularis propria shows degeneration, fragmentation, and myocyte death, all of which indicate transmural infarction.

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

Narrowing of the arteries that supply blood to the intestine causes mesenteric ischemia. The arteries that supply blood to the intestines travel straight from the aorta. Mesenteric ischemia is often seen in people who have hardening of the arteries in other parts of the body (for example, those with coronary artery disease or peripheral vascular disease). The condition is more common in smokers and in patients with high blood pressure or high blood cholesterol. Mesenteric ischemia can also be caused by an embolus that suddenly blocks one of the mesenteric arteries. The emboli usually come from the heart or aorta. These clots are more commonly seen in patients with arrhythmias, such as atrial fibrillation.

Mesenteric ischemia is classified into four categories. Each category has their own cause:^{[1][2][3][4][5][6][7][8][9][10][11][12][13]}

• Arterial thrombosis
• Arterial embolism
• Venous thrombosis
• Non-occlusive ischemia

Classification based on etiology
Etiology	Cause	Incidence	Examples	Mechanism
Occlusive causes	Arterial embolism	50-70%	Superior mesenteric artery obstruction (most common cause) Arrhythmia Myocardial infarction Infective endocarditis Valvular heart diseases Ventricular aneurysms History of embolic events Recent angiography	Acute mesenteric arterial embolism: Attributes to 50% cases of mesenteric ischemia. Mesenteric embolus can originate from the left atrium, associated with cardiac arrythmias such as atrial fibrillation. Recent myocardial infarction resulting in segmental wall motion abnormality leading to poor ejection fraction and embolus formation. Infective endocarditis: vegetations on the cardiac valves resulting in turbulence in blood flow predisposing to formation of emboli into the blood stream.
	Arterial thrombosis	15-25%	Atherosclerosis Advanced age Prolonged hypotension Hypercoagulabilty states Peripheral arterial disease Traumatic injury	Acute mesenteric arterial thrombosis: 25% cases of mesenteric ischemia result from mesenteric arterial thrombosis. Most likely due to underlying atherosclerosis(plaque formation) leading to stenosis. An underlying plaque(fatty streak) in the superior mesenteric artery leads to critical stenosis over the years forming collaterals.
	Venous thrombosis	5%	Right-sided heart failure Previous deep venous thrombosis (20-40% risk) Primary clotting disorder Pancreatitis Polycythemia Sickle cell anemia Recent abdominal surgery or infection Visceral infections Perforated viscus Inherited thrombophilia– Factor V Leidin mutation Prothrombin G20210A mutation Protein S deficiency Antithrombin III deficiency Activated protein C resistance Anti-phospholipid syndrome Myeloproliferative disorders(JAK2 V617F) mutation.	Mesenteric venous thrombosis: Thrombosis is attributed to the combination of virchow’s triad: Stasis Vascular inflammation Hypercoagulability
Non-Occlusive causes	Non-occlusive ischemia	20-30%	Low cardiac output states(most common cause) Hypovolemia Vasoconstrictive drugs (Digoxin, alpha-adrenergic agonists) Septic shock Aortic insufficiency Cocaine abuse or ergot poisoning Inflammatory bowel disease	Occurs mainly because of superior mesenteric artery vasoconstriction leading to low splanchnic blood flow.
Rare causes	Splanchnic artery stenosis Superior mesenteric artery syndrome

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

Mesenteric ischemia must be differentiated from other diseases that cause abdominal pain, diarrhea, nausea and vomiting, such as ischemic colitis, inflammatory bowel disease, and irritable bowel syndrome.

It is important to differentiate ischemic colitis, which often resolves on its own, from the more immediately life-threatening condition of acute mesenteric ischemia of the small bowel.

Other diseases to include in the differential diagnosis are as follows:

• Acute pancreatitis
• Chronic pancreatitis
• Pancreatic carcinoma
• Acute appendicitis
• Acute diverticulitis
• Inflammatory bowel disease
• Irritable bowel syndrome
• Whipple disease
• Celiac disease
• Toxic megacolon
• Tropical sprue
• Infective colitis
• Spontaneous bacterial peritonitis

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

Differentiating Mesenteric Ischemia from Other Diseases with Abdominal pain and Diarrhea

Mesenteric ischemia must be differentiated on the basis of abdominal pain and diarrhea from the following diseases:

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 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 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 Inflammatory bowel disease Diffuse ± − − ± − + + + − − − Normal or hyperactive Anti-neutrophil cytoplasmic antibody (P-ANCA) in Ulcerative colitis Anti saccharomyces cerevisiae antibodies (ASCA) in Crohn’s disease String sign on abdominal x-ray in Crohn’s disease Extra intestinal findings: Uveitis Arthritis Irritable bowel syndrome Diffuse − − − − ± ± + − − − − N Normal Normal Symptomatic treatment High dietary fiber Osmotic laxatives Antispasmodic drugs Whipple’s disease Diffuse ± − − ± − + + − ± − − N Thrombocytopenia Hypoalbuminemia Small intestinal biopsy for Tropheryma whipplei Endoscopy is used to confirm diagnosis. Images used to find complications Chest and joint x-ray CT MRI Echocardiography Extra intestinal findings: Uveitis Endocarditis Encephalitis Dementia Hepatosplenomegaly Arthritis Ascites 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 Toxic megacolon Diffuse + − − − − + − − + ± + Hypoactive Anemia Leukocytosis especially in patients with Clostridium difficile infection Hypoalbuminemia Metabolic alkalosis associated with a poor prognosis Metabolic acidosis secondary to ischemic colitis CT and Ultrasound shows: Loss of colonic haustration Hypoechoic and thickened bowel walls with irregular internal margins in the sigmoid and descending colon Prominent dilation of the transverse colon (>6 cm) Insignificant dilation of ileal bowel loops (diameter >18 mm) with increased intraluminal gas and fluid Tropical sprue Diffuse + − − − − + + − − − − N Fat soluble vitamin deficiency Hypoalbuminemia Fecal stool test Barium studies: Dilation and edema of mucosal folds Steatorrhea– 10-40 g/day (Normal=5 g/day) Celiac disease Diffuse − − − − − + + − − − − Hyperactive IgA endomysial antibody IgA tissue transglutaminase antibody Anti-gliadin antibody Small bowel biopsy US: Bull’s eye or target pattern Pseudokidney sign Gluten allergy Infective colitis Diffuse + − ± − − + − + Positive in fulminant colitis ± ± Hyperactive Stool culture and studies Shiga toxin in bloody diarrhea PCR CT scan Bowel wall thickening Edema 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 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 Spontaneous bacterial peritonitis Diffuse + − − Positive in cirrhotic patients − + − − ± + + Hypoactive Ascitic fluid PMN>250 cells/mm³ Culture: Positive for single organism Ultrasound for evaluation of liver cirrhosis 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

References

[[Category:Up-To-Date]

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

The incidence rate of mesenteric ischemia secondary to superior mesenteric artery occlusion is 8.6/100 000/year. 70% of SMA occlusion is caused by embolism and 30% by thrombosis. The annual incidence of mesenteric ischemia is approximately 5.5% per 100,000 individuals. The incidence of mesenteric ischemia increases with age and the median age at diagnosis is 70 years. Mesenteric ischemia affects men and women equally.

• The incidence rate of mesenteric ischemia secondary to superior mesenteric artery occlusion is 8.6/100 000/year.
• 70% of SMA occlusion is caused by embolism and 30% by thrombosis.^{[1][2][3][4][5][6][7][8]}
• The annual incidence of mesenteric ischemia is approximately 5.5% per 100,000 individuals.
• The incidence due to non-occlusive mesenteric ischemia is 2/100,000 persons and 1.8/100,000 per person due to mesenteric venous thrombosis.
• In the United States, between 1995-2010 incidence of mesenteric ischemia declined from 8.4 to 6.7% per 100,000 individuals.
• Between the year 1970 and 1982, in the population of Sweden, the incidence of mesenteric ischemia was estimated to be 12.9 cases per 100,000 individuals.

• The prevalence of mesenteric ischemia:^[9]
  • Occlusive mesenteric ischemia due to mesenteric venous thrombosis is approximately per 100,000 individuals worldwide.
  • Non-occlusive mesenteric ischemia is approximately 6000 per 100,000 individuals worldwide.

• In 2017, the incidence of mesenteric ischemia is approximately 90-200 per 100,000 of all the surgical admissions with a mortality rate of 50%.^[10]

• The incidence of mesenteric ischemia increases with age and the median age at diagnosis is 70 years.^[11]
• Mesenteric ischemia commonly affects individuals older than 60 years of age, a few cases are reported in their 20s. Younger age group having risk factors such as atrial fibrillation or other hypercoagulable states such as protein C and protein S deficiency are also predisposed to the risk.

• There is no racial predilection to mesenteric ischemia.
• Mesenteric ischemia usually affects individuals of the African american race because of their higher predilection towards developing atherosclerosis.

• Mesenteric ischemia is more prevalent in women as compared to males.^[12]

• The majority of mesenteric ischemia cases are reported in Sweden.

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

Risk factors causing mesenteric ischemia can be divided based on the underlying etiology. Conditions that pose a significant risk to the development of mesenteric ischemia include the interruption of blood flow through the artery or vein supplying the small intestine (e.g thromboembolism) or reduction of blood supply (e.g. vasoconstriction). Also, there are certain life-style related risk factors which predominantly cause mesenteric ischemia in the older age group.

• The following conditions pose a significant risk towards the development of mesenteric ischemia either by interrupting the blood flow through the artery or vein supplying the small intestine (e.g.thromboemboli) or by reducing the blood supply (e.g. vasoconstriction). Also, there are certain life-style related risk factors which predominantly cause mesenteric ischemia in the older age group.^[1][2][3]

• Venous thrombosis is more frequently seen in women and arterial thrombosis is more commonly seen in men.^[4][5]

• Mesenteric ischemia is more prevalent in women as compared to males.^[6]

Risk factors
Occlusive	Embolic	Atrial fibrillation
		Cardiac arrhythmia
		Valvular heart disease
		Infective endocarditis
		Recent myocardial infarction
		Ventricular aneurysm
		Aortic atherosclerosis
	Thrombotic	Advanced age
		Low cardiac output states
		Peripheral arterial disease
		Traumatic injury
		Inherited thrombophilia– Factor V Leidin mutation Prothrombin G20210A mutation Protein S deficiency Antithrombin III deficiency Activated protein C resistance Antiphospholipid syndrome Myeloproliferative disorders(JAK2 V617F) mutation.
		Acquired thrombophilia– malignancy, oral contraceptives intake.
Non-occlusive		Heart failure
		Aortic insufficiency
		Septic shock
		Vasoconstrictive drugs: Digoxin Alpha-adrenergic agonists
		Cocaine abuse or ergot poisoning
		Hemodialysis
Other factors		Lifestyle related risk factors:[7] High cholesterol levels History of smoking Immobility Hypertension Hyperlipidemia Diabetes Less common risk factors: Fibromuscular dysplasia Beta receptor blocking agents Hepatitis

Common risk factors in the development of mesenteric ischemia include:

(a) Embolic causes:^[1]

• Atrial fibrillation
• Cardiac arrhythmias
• Valvular heart diseases
• Infective endocarditis
• Recent myocardial infarction
• Ventricular aneurysm
• Aortic atherosclerosis
• Aortic aneurysm

(b) Thrombotic causes:^[2]

• Advanced age
• Low cardiac output states
• Traumatic injury
• Peripheral artery disease

• Heart failure
• Aortic insufficiency
• Septic shock
• Vasoconstrictive drugs (e.g. Digoxin, alpha-adrenergic agonists)
• Cocaine abuse or ergot poisoning
• Hemodialysis

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

If left untreated, 99% of patients with mesenteric ischemia may progress to develop intestinal gangrene, septic shock and subsequent multiorgan failure. The progressive phases of mesenteric ischemia include a hyperactive phase, paralytic phase and a shock phase. The prognosis largely depends on prompt diagnosis and timely medical/surgical intervention depending on the underlying etiology. Poor prognostic factors include signs such as: tachypnea, tachycardia, hypotension and altered mental status. Common complications of mesenteric ischemia include: bowel infarction, perforation, sepsis, peritonitis, septic shock, and multiorgan failure.

• If left untreated, 99% of patients with mesenteric ischemia progress to develop intestinal gangrene, septic shock and subsequent multiorgan failure.
• It can be divided into three phases:^[1][2]
  • Hyperactive phase
  • Paralytic phase
  • Shock

• Hyperactive phase is the phase of mesenteric ischemia in which the most common symptoms are excruciating abdominal pain and the passage of bloody stools.
• Many patients get better and do not progress beyond this phase if treated in time.

• Paralytic phase follows if ischemia continues.
• In this phase, the abdominal pain becomes more widespread, the abdomen becomes tender to touch, and bowel motility decreases, resulting in abdominal bloating, no further bloody stools, and absent bowel sounds on exam.

• Shock phase can develop as fluids start to leak through the damaged colon lining.
• This can result in shock and metabolic acidosis with dehydration, low blood pressure, rapid heart rate, and confusion.
• Patients who progress to this phase are often critically ill and require intensive care.

• Mesenteric ischemia is difficult to diagnose.^[3]
• The prognosis mostly depends on prompt diagnosis and timely medical/surgical intervention depending on the underlying etiology.^[4]
• Generally, the prognosis is poor when there is delay in the treatment, ranging from 0% to 40%.^[5]
• In case of occlusive type of acute mesenteric ischemia, mortality can be up to 90% without surgical intervention.^[6][7]

• In embolic type of mesenteric arterial occlusion, there is improved outcome after surgical intervention, which is not the case in thrombotic and non-occlusive type of mesenteric ischemia.

Type of mesenteric ischemia	Survival rate	Mortality rate
Arterial embolism	41%	54%
Arterial thrombosis	38%	77%
Venous thrombosis	87%	32%

• Venous thrombosis – 32% mortality
• Arterial embolism – 54% mortality
• Arterial thrombosis – 77% mortality
• Non-occlusive ischemia – 70-90% mortality^[8]

Poor prognostic factors
Signs and symptoms	Signs of shock and dehydration: Tachypnea Tachycardia Fever Hypotension Foul smelling breath (from bowel necrosis) Altered mental status Signs of atherosclerosis: Xanthelasmas Peripheral artery disease Coronary artery disease
Laboratory findings	Metabolic acidosis Bandemia Elevated AST (aspartate transferase) Elevated blood urea nitrogen

Prognostic indicators of mesenteric ischemia:^[9]

• Mannheim Peritonitis Index (MPI)
• Platelet to lymphocyte ratio

• Common complications of mesenteric ischemia include:
  • Bowel infarction
  • Perforation
  • Sepsis
  • Peritonitis
  • Septic shock
  • Multiorgan failure