The prognosis depends on prompt diagnosis (less than 12–24 hours and before gangrene) and the underlying cause:

- venous thrombosis: 32% mortality

- arterial embolism: 54% mortality

- arterial thrombosis: 77% mortality

- non-occlusive ischemia: 73% mortality.

In the case of prompt diagnosis and therapy, acute mesenteric ischemia can be reversible.

Mesenteric ischemia is a medical condition in which injury of the small intestine occurs due to not enough blood supply. It can come on suddenly, known as acute mesenteric ischemia, or gradually, known as chronic mesenteric ischemia. Acute disease often presents with sudden severe pain. Symptoms may come on more slowly in those with acute on chronic disease. Signs and symptoms of chronic disease include abdominal pain after eating, unintentional weight loss, vomiting, and being afraid of eating.

Risk factors include atrial fibrillation, heart failure, chronic renal failure, being prone to forming blood clots, and previous myocardial infarction. There are four mechanisms by which poor blood flow occurs: a blood clot from elsewhere getting lodged in an artery, a new blood clot forming in an artery, a blood clot forming in the superior mesenteric vein, and insufficient blood flow due to low blood pressure or spasms of arteries. Chronic disease is a risk factor for acute disease. The best method of diagnosis is angiography, with computer tomography (CT) being used when that is not available.

Treatment of acute ischemia may include stenting or medications to break down the clot provided at the site of obstruction by interventional radiology. Open surgery may also be used to remove or bypass the obstruction and may be required to remove any intestines that may have died. If not rapidly treated outcomes are often poor. Among those affected even with treatment the risk of death is 70% to 90%. In those with chronic disease bypass surgery is the treatment of choice. Those who have thrombosis of the vein may be treated with anticoagulation such as heparin and warfarin, with surgery used if they do not improve.

Acute mesenteric ischemia affects about five per hundred thousand people per year in the developed world. Chronic mesenteric ischemia affects about one per hundred thousand people. Most people affected are over 60 years old. Rates are about equal in males and females of the same age. Mesenteric ischemia was first described in 1895.

Mostly the result of a thromboembolism. Commonly the embolism is caused by atrial fibrillation, valvular disease, myocardial infarction, or cardiomyopathy.

In addition, ischemic colitis is a well-recognized complication of abdominal aortic aneurysm repair, when the origin of the inferior mesenteric artery is covered by the aortic graft. In a 1991 review concerning 2137 patients the accidental inferior mesenteric artery ligation was the most common cause (74%) of ischemic colitis. Thus, patients without adequate collateralization are at risk for ischemia of the descending and sigmoid colon. Bloody diarrhea and leukocytosis in the postoperative period are essentially diagnostic of ischemic colitis. The complication can be prevented through careful selection of subjects that may require replanting inferior mesenteric artery (IMA) and completing the pre surgical procedure information with an instrumental evaluation during surgical treatment.

The exact incidence of ischemic colitis is difficult to estimate, as many patients with mild ischemia may not seek medical attention. Ischemic colitis is responsible for about 1 in 2000 hospital admissions, and is seen on about 1 in 100 endoscopies. Men and women are affected equally; ischemic colitis is a disease of the elderly, with more than 90% of cases occurring in people over the age of 60.

Risk factors for thromboembolism, the major cause of arterial embolism, include disturbed blood flow (such as in atrial fibrillation and mitral stenosis), injury or damage to an artery wall, and hypercoagulability (such as increased platelet count). Mitral stenosis poses a high risk of forming emboli which may travel to the brain and cause stroke. Endocarditis increases the risk for thromboembolism, by a mixture of the factors above.

Atherosclerosis in the aorta and other large blood vessels is a common risk factor, both for thromboembolism and cholesterol embolism. The legs and feet are major impact sites for these types. Thus, risk factors for atherosclerosis are risk factors for arterial embolisation as well:

- advanced age

- cigarette smoking

- hypertension (high blood pressure)

- obesity

- hyperlipidemia, e.g. hypercholesterolemia, hypertriglyceridemia, elevated lipoprotein (a) or apolipoprotein B, or decreased levels of HDL cholesterol)

- diabetes mellitus

- Sedentary lifestyle

- stress

Other important risk factors for arterial embolism include:

- recent surgery (both for thromboembolism and air embolism)

- previous stroke or cardiovascular disease

- a history of long-term intravenous therapy (for air embolism)

- Bone fracture (for fat embolism)

A septal defect of the heart makes it possible for paradoxical embolization, which happens when a clot in a vein enters the right side of the heart and passes through a hole into the left side. The clot can then move to an artery and cause arterial embolisation.

70% of patients with carotid arterial dissection are between the ages of 35 and 50, with a mean age of 47 years.

Several factors may increase the tendency for clot formation, such as specific infections (such as infectious mononucleosis, cytomegalovirus infection, malaria, or babesiosis), inherited clotting disorders (thrombophilia, such as Factor V Leiden, antiphospholipid syndrome), malignancy (such as pancreatic cancer) or metastasis, or a combination of these factors.

In some conditions, blood clots form in one part of the circulatory system and then dislodge and travel to another part of the body, which could include the spleen. These emboligenic disorders include atrial fibrillation, patent foramen ovale, endocarditis or cholesterol embolism.

Splenic infarction is also more common in hematological disorders with associated splenomegaly, such as the myeloproliferative disorders. Other causes of splenomegaly (for example, Gaucher disease or hemoglobinopathies) can also predispose to infarction. Splenic infarction can also result from a sickle cell crisis in patients with sickle cell anemia. Both splenomegaly and a tendency towards clot formation feature in this condition. In sickle cell disease, repeated splenic infarctions lead to a non-functional spleen (autosplenectomy).

Any factor that directly compromises the splenic artery can cause infarction. Examples include abdominal traumas, aortic dissection, torsion of the splenic artery (for example, in wandering spleen) or external compression on the artery by a tumor. It can also be a complication of vascular procedures.

Splenic infarction can be due to vasculitis or disseminated intravascular coagulation. Various other conditions have been associated with splenic infarction in case reporters, for example granulomatosis with polyangiitis or treatment with medications that predispose to vasospasm or blood clot formation, such as vasoconstrictors used to treat esophageal varices, sumatriptan or bevacizumab.

Splenic infarction can be induced for the treatment of such conditions as portal hypertension or splenic injury. It can also be used prior to splenectomy for the prevention of blood loss.

Major risk factors for cerebral infarction are generally the same as for atherosclerosis: high blood pressure, Diabetes mellitus, tobacco smoking, obesity, and dyslipidemia. The American Heart Association/American Stroke Association (AHA/ASA) recommends controlling these risk factors in order to prevent stroke. The AHA/ASA guidelines also provide information on how to prevent stroke if someone has more specific concerns, such as Sickle-cell disease or pregnancy. It is also possible to calculate the risk of stroke in the next decade based on information gathered through the Framingham Heart Study.

Once considered uncommon, spontaneous carotid artery dissection is an increasingly recognised cause of stroke that preferentially affects the middle-aged.

The incidence of spontaneous carotid artery dissection is low, and incidence rates for internal carotid artery dissection have been reported to be 2.6 to 2.9 per 100,000.

Observational studies and case reports published since the early 1980s show that patients with spontaneous internal carotid artery dissection may also have a history of stroke in their family and/or hereditary connective tissue disorders, such as Marfan syndrome, Ehlers-Danlos syndrome, autosomal dominant polycystic kidney disease, pseudoxanthoma elasticum, fibromuscular dysplasia, and osteogenesis imperfecta type I. IgG4-related disease involving the carotid artery has also been observed as a cause.

However, although an association with connective tissue disorders does exist, most people with spontaneous arterial dissections do not have associated connective tissue disorders. Also, the reports on the prevalence of hereditary connective tissue diseases in people with spontaneous dissections are highly variable, ranging from 0% to 0.6% in one study to 5% to 18% in another study.

Internal carotid artery dissection can also be associated with an elongated styloid process (known as Eagle syndrome when the elongated styloid process causes symptoms).

Bowel infarction results from restricted blood supply to the bowel, most often due to bowel obstruction or occlusion of one of the mesenteric arteries.

Bowel obstruction is most often caused by intestinal adhesions, which frequently form after abdominal surgeries, or by chronic infections such as diverticulitis, hepatitis, and inflammatory bowel disease. The condition is difficult to diagnose properly, as the symptoms may resemble those of other bowel disorders.

Patients who have undergone extensive resection of the small bowel may develop malabsorption, indicating the need for dietary supplements.

Volvulus is a rare but life-threatening cause of bowel infarction which requires immediate medical attention. Central abdominal pain which is resistant to narcotic analgesia may be an indication of bowel infarction.

There is evidence to suggest that a major cause of spontaneous coronary artery dissection (SCAD) is related to female hormone levels, as most cases appear to arise in pre-menopausal women, although there is evidence that the condition can have various triggers. Other underlying conditions such as hypertension, recent delivery of a baby, fibromuscular dysplasia and connective-tissue disorders (e.g., Marfan syndrome and Ehlers-Danlos syndrome) may occasionally result in SCAD. There is also a possibility that vigorous exercise can be a trigger. However, many cases have no obvious cause.

Causes include:

- Thrombosis (approximately 40% of cases)

- Arterial embolism (approximately 40%)

- arteriosclerosis obliterans

Another cause of limb infarction is "skeletal muscle infarction" as a rare complication of long standing, poorly controlled diabetes mellitus.

The differential diagnoses of acute abdomen include but are not limited to:

1. Acute appendicitis

2. Acute peptic ulcer and its complications

3. Acute cholecystitis

4. Acute pancreatitis

5. Acute intestinal ischemia (see section below)

6. Acute diverticulitis

7. Ectopic pregnancy with tubal rupture

8. Ovarian torsion

9. Acute peritonitis (including hollow viscus perforation)

10. Acute ureteric colic

11. Bowel volvulus

12. Bowel obstruction

13. Acute pyelonephritis

14. Adrenal crisis

15. Biliary colic

16. Abdominal aortic aneurysm

17. Familial Mediterranean fever

18. Hemoperitoneum

19. Ruptured spleen

20. Kidney stone

21. Sickle cell anaemia

A very large range of medical conditions can cause circulatory collapse. These include, but are not limited to:

- Surgery, particularly on patients who have lost blood.

- Blood clots, including the use of some platelet-activating factor drugs in some animals and humans

- Dengue Fever

- Severe dehydration

- Shock (including, among other types, many cases of cardiogenic shock- e.g., after a myocardial infarction or during heart failure; distributive shock, hypovolemic shock, resulting from large blood loss; and severe cases of septic shock)

- Heart Disease (myocardial infarction- heart attack; acute or chronic congestive or other heart failure, ruptured or dissecting aneurysms; large, especially hemorrhagic, stroke; some untreated congenital heart defects; failed heart transplant)

- Superior mesenteric artery syndrome

- Drugs that affect blood pressure

- Drinking seawater

- As a complication of dialysis

- Intoxicative inhalants

An arterial embolism is caused by one or more emboli getting stuck in an artery and blocking blood flow, causing ischemia, possibly resulting in infarction with tissue death (necrosis). Individuals with arterial thrombosis or embolism often develop collateral circulation to compensate for the loss of arterial flow. However, it takes time for sufficient collateral circulation to develop, making affected areas more vulnerable for sudden occlusion by embolisation than for e.g. gradual occlusion as in atherosclerosis.

The major tissues affected are nerves and muscles, where irreversible damage starts to occur after 4–6 hours of cessation of blood supply.Skeletal muscle, the major tissue affected, is still relatively resistant to infarction compared to the heart and brain because its ability to rely on anaerobic metabolism by glycogen stored in the cells may supply the muscle tissue long enough for any clot to dissolve, either by intervention or the body's own system for thrombus breakdown. In contrast, brain tissue (in cerebral infarction) does not store glycogen, and the heart (in myocardial infarction) is so specialized on aerobic metabolism that not enough energy can be liberated by lactate production to sustain its needs.

Bone is more susceptible to ischemia, with hematopoietic cells usually dying within 2 hours, and other bone cells (osteocytes, osteoclasts, osteoblasts etc.) within 12–20 hours. On the other hand, it has better regenerative capacity once blood supply is reestablished, as the remaining dead inorganic osseous tissue forms a framework upon which immigrating cells can reestablish functional bone tissue in optimal conditions.

Whether a cerebral infarction is thrombotic or embolic based, its pathophysiology, or the observed conditions and underlying mechanisms of the disease. In thrombotic ischemic stroke, a thrombus forms and blocks blood flow. A thrombus forms when the endothelium is activated by a variety of signals to result in platelet aggregation in the artery. This clump of platelets interacts with fibrin to form a platelet plug. This platelet plug grows into a thrombus, resulting in a stenotic artery. Thrombotic ischemia can occur in large or small blood vessels. In large vessels, the most common causes of thrombi are atherosclerosis and vasoconstriction. In small vessels, the most common cause is lipohyalinosis. Lipohyalinosis is when high blood pressure and aging causes a build-up of fatty hyaline matter in blood vessels. Atheroma formation can also cause small vessel thrombotic ischemic stroke.

An embolic stroke refers to the blockage of an artery by an embolus, a traveling particle or debris in the arterial bloodstream originating elsewhere. An embolus is most frequently a thrombus, but it can also be a number of other substances including fat (e.g. from bone marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious endocarditis). The embolus may be of cardiac origin due to Atrial fibrillation, Patent foramen ovale or from atherosclerotic plaque of another (or the same) large artery. Cerebral artery gas embolism (e.g. during ascent from a SCUBA dive) is also a possible cause of infarction (Levvett & Millar, 2008)

An acute abdomen refers to a sudden, severe abdominal pain. It is in many cases a medical emergency, requiring urgent and specific diagnosis. Several causes need surgical treatment.

Coronary artery dissection results from a tear in the inner layer of the artery, the tunica intima. This allows blood to penetrate and cause an intramural hematoma in the central layer, the tunica media, and a restriction in the size of the lumen, resulting in reduced blood flow which in turn causes myocardial infarction and can later cause sudden cardiac death.

One of the most important features differentiating ischemic cardiomyopathy from the other forms of cardiomyopathy is the shortened, or worsened all-cause mortality in patients with ischemic cardiomyopathy. According to several studies, coronary artery bypass graft surgery has a survival advantage over medical therapy (for ischemic cardiomyopathy) across varied follow-ups.

After return of heart function, there has been a moderately higher risk of death in the hospital when compared to MI patients without PVF. Whether this still holds true with the recent changes in treatment strategies of earlier hospital admission and immediate angioplasty with thrombus removal is unknown. PVF does not affect the long-term prognosis.

The incidence of myocardial rupture has decreased in the era of urgent revascularization and aggressive pharmacological therapy for the treatment of an acute myocardial infarction. However, the decrease in the incidence of myocardial rupture is not uniform; there is a slight increase in the incidence of rupture if thrombolytic agents are used to abort a myocardial infarction. On the other hand, if primary percutaneous coronary intervention is performed to abort the infarction, the incidence of rupture is significantly lowered. The incidence of myocardial rupture if PCI is performed in the setting of an acute myocardial infarction is about 1 percent.

A "general failure" is one that occurs across a wide range of locations in the body, such as systemic shock after the loss of a large amount of blood collapsing all the circulatory systems in the legs. A "specific failure" can be traced to a particular point, such as a clot.

Cardiac circulatory collapse affects the vessels of the heart such as the aorta and is almost always fatal. It is sometimes referred to as "acute" circulatory failure.

Peripheral circulatory collapse involves outlying arteries and veins in the body and can result in gangrene, organ failure or other serious complications. This form is sometimes called "peripheral vascular failure", "shock" or "peripheral vascular shutdown".

A milder or preliminary form of circulatory collapse is circulatory insufficiency.

Coronary thrombosis is the formation of a blood clot inside a blood vessel of the heart. This blood clot restricts blood flow within the heart. It is associated with narrowing of blood vessels subsequent to clotting. The condition is considered as a type of ischaemic heart disease, also known as a heart attack or myocardial infarction.

Thrombosis in the heart can lead to a myocardial infarction. Coronary thrombosis and myocardial infarction are sometimes used as synonyms, although this is technically inaccurate as the thrombosis refers to the blocking of blood vessels, while the infarction refers to the tissue death due to the consequent loss of blood flow to the heart tissue. The heart contains many connecting blood vessels, and depending upon the location of the thrombosis, the infarction may cause no symptoms. Coronary thrombosis is caused by atherosclerosis.This is when there is build up of cholesterol and fats in the artery walls. So the blood will clot because there isn't enough room for it to flow. The main causes of coronary thrombosis are stress, smoking, high blood pressure, and lack of exercise. Symptoms are sharp pains around the chest area, breathing difficulties, dizziness, and fainting. This is treated by taking Aspirin, Nitrates, or Beta Blockers.

Coronary thrombosis can be a complication associated with drug-eluting stents.