Intestinal Angina: A Complete Overview


Intestinal Angina, more commonly known as mesenteric ischemia, is an atypical reason for an acute abdomen. It is distinguished by reduced blood flow to the intestine. Clinically, mesenteric ischemia occurs due to hypoperfusion (reduced blood flow) to the gut mucosa. The aetiology (cause) of the disease is multifactorial. The mortality rate associated with the disease is still around 30% to 70%, even though progress has been made to surgically improve the blood circulation (revascularisation) of the gut over the past 20 years.1

Anatomy of Intestinal Circulation

The mesenteric arterial circulation consists of three main branches of the abdominal aorta, specifically, the celiac axis (CA), superior mesenteric artery (SMA), and inferior mesenteric artery (IMA). The stomach, liver, spleen, and some parts of the duodenum (first part of the small intestine) and pancreas receive blood from the CA. The rest of the duodenum, jejunum (middle part of the small intestine), ileum (last part of the small intestine), ascending colon, and some of the transverse colons get blood from SMA. The IMA delivers blood to the distal colon, descending colon, sigmoid colon, and rectum.2 The mesenteric blood flow is usually around 15–20% of the cardiac output while fasting, and in the postprandial state (during/ after consuming a meal), it is around 35%. After the intake of food, blood flow increases in around 10–20 minutes, and its level generally depends on the type and amount of the meal. Apart from collaterals, mesenteric circulation is also able to auto-regulate the blood supply through various complex mechanisms. As a result, the small intestine can endure up to a 75% decrease in overall blood flow for about 12 hours.3 However, with overall obstruction, permanent ischemia can occur within about 6 hours.4

Mesenteric ischemia is categorized into acute and chronic forms depending on the severity of associated symptoms.

Acute Mesenteric ischemia (AMI)

AMI mainly refers to the sudden occurrence of small intestinal hypoperfusion due to various factors like mesenteric arterial thrombosis (15–25%), mesenteric arterial embolism (50%), or mesenteric venous thrombosis (5–15%).5 AMI only happens in around 1% of all patients with an “acute abdomen,” but its incidence is considerably more in patients over 70 years old.6 The most common risk factors for AMI are atrial fibrillation, heart failure, coronary heart disease, peripheral vascular disease, and arterial hypertension.7 The diagnosis of AMI is quite critical because it is a time-based life-threatening emergency, causing irreversible hypoperfusion of the mesenteric organs within hours, leading to a  high mortality rate. Acute mesenteric ischemia is further characterized as occlusive or nonocclusive. Occlusive forms are more common and usually account for 70–80% of the cases, and it results from the obstruction of mesenteric arteries or veins.

Occlusive AMI


AMI due to arterial occlusion is a vigorous event. If the acute ischemia is persistent i.e. it lasts for about 6 to 12 hours after the beginning of the ischemic event without restoration of arterial supply, it causes irreversible injury to the complete thickness of the intestinal wall. This is known as transmural necrosis with peritonitis, and it is generally associated with a high mortality rate.


Mesenteric vein thrombosis (MVT) is depicted by sub-acute abdominal pain that may occur for over 2–4 weeks, with common symptoms of nausea and vomiting.8 MVT occurs due to underlying diseases like portal hypertension, right-sided heart failure, hypercoagulable states (protein C deficiencies, factor V Leiden mutation or polycythemia), abdominal trauma, acute pancreatitis, abdominal infection, nephrotic syndrome, malignancies, and cirrhosis is more common. It accounts for 50–75% of all MVT diagnosed cases.9 Pregnancy, use of oral contraceptives, and puerperium are common risk factors in young women for MVT.

Acute Nonocclusive Mesenteric Ischemia (NOMI)

This is defined as intestinal hypoperfusion when vascular occlusion is absent. It accounts for around 5–15% of all cases of AMI, with a mortality rate of around 50%.10 This condition is usually observed in patients with cardiac disorders, shock, pancreatitis, post-operative stress, burn, and dehydration.11 The diagnosis is quite challenging in these patients, as they are often unable to communicate verbally since they are ventilated or sedated.12

Chronic Mesenteric Ischemia (CMI)

This is characterized by patients having ischemic symptoms for around three months, which are caused by the inadequate blood supply to the gastrointestinal tract.13 CMI is much more commonly seen in women (70%). The pain in CMI is generally confined to the mid-abdomen or epigastrium, and it typically begins 20 to 30 minutes after a meal and it may last for 1–2 hours. With time, patients learn to relieve their pains by eating small amounts of food and avoiding fatty foods. This slowly leads to fear of food and hence weight loss.14 Atypical symptoms include abdominal discomfort, vomiting, nausea, diarrhoea or constipation.15 However, this “classic CMI triad” of postprandial abdominal pain, abdominal bruit and weight loss, is only observed in about 16–22% of patients with CMI.14



There is no defined set of serologies (the examination of blood serum) that can help in the detection of early AMI. The most common laboratory abnormalities include hemoconcentration, neutrophilic leukocytosis, elevated lactic acid levels, elevated serum levels of amylase, aspartate aminotransferase and lactate dehydrogenase (LDH), and anion gap metabolic acidosis.16 Studying lactic acid levels in AMI diagnosis is gaining interest but still has been observed to be neither sensitive nor specific enough. This may be due to the increase in lactic acid levels, which can also be a result of renal injury or intravascular volume depletion. 

There have been many studies to identify other serum markers for diagnosis of early AMI, but with no success in clinical practice.17,18 The gold standard for diagnosis of AMI is computed tomography angiogram (CTA). It is also known as biphasic multidetector computed tomography (MDCT). It has a sensitivity of 85–98% and specificity of 91–100% for the diagnosis of AMI.12 It not only substantiates the diagnosis but also evaluates the severity and complications associated with AMI. Moreover, it is also helpful in ruling out other causes that may be causing abdominal pain. If there is clinical suspicion of the presence of AMI, CTA should be definitely considered, even if there is renal injury or there is a concern for contrast-induced nephropathy.12,19


As is the case with AMI, the role of serum markers in the diagnosis of CMI is very restricted.20 Postprandial increase in L-lactate and D-dimer has been linked with this diagnosis, but this is very non-specific. CRP, I-FABP, LDH levels, and leukocyte counts are also not very valuable in diagnosis. Duplex ultrasonography (US) is quite a useful screening tool for suspected mesenteric stenosis. It is not associated with any radiation exposure and has no adverse effects. CTA has the potential to reconstruct images, and it imparts maximum details about the mesenteric vasculature and other intra-abdominal organs. As it is 100% sensitive and 95% specific, it has surpassed digital subtraction angiography as the choice of imaging in the mesenteric artery stenosis (MAS) diagnosis.21 Magnetic resonance angiography (MRA) is also very helpful for the diagnosis of mesenteric stenosis. It is associated with no radiation exposure, and it allows more precise estimation of flow velocity and volumes than CTA.



The management for patients with AMI can be concise with “3R”s – Resuscitation, Rapid diagnosis, and Revascularization.22 Assertive supportive care and volume restoration have to be initiated as early as possible. The main goal is to improve perfusion and oxygen delivery. The use of vasopressors should be avoided in suspected or proven AMI patients unless completely necessary, as they cause a further decrease in mesenteric perfusion. Systemic anticoagulation should be started in all patients with AMI unless there is a contra-indication.23 Unfractionated heparin (anti-coagulant) is generally given as it has a short half-life and the capability to monitor and titrate anticoagulation. Broad-spectrum antimicrobials are also started after the diagnosis.5,22 There are various endovascular techniques for treating embolic AMI, like endovascular thrombolysis, percutaneous aspiration, and percutaneous transluminal angioplasty (PTA) with stenting. Local thrombolysis is also treated by recombinant tissue plasminogen activator (rtPA). The initial management for NOMI involves treatment of the underlying medical condition and terminating any pharmacological agents that contribute to the low flow state. Damage control surgery (DCS) is usually performed in critically ill patients.24

Risk Factors for Acute Mesenteric Ischemia

In AMI patients, older age, delayed diagnosis, increased lactic acid levels at diagnosis and 24 hours after diagnosis, and NOMI, are all connected with a high risk of 30-day colectomy and mortality.25 Aggravated results are generally associated with the kind of vessel involved and their distribution. AMI, because of arterial occlusion, has a considerably higher mortality rate than MVT. Arterial occlusion and the lack of thickening and improvement mark the initial stages of AMI and are generally associated with a better prognosis. Portal venous gas, pneumatosis linearis, loop dilatation and pneumoperitoneum mainly happen in the late stage of the disease and are associated with increased mortality.26


Due to its impact on the quality of life of patients, the initial management of CMI is by modification of lifestyle. Postprandial pain can be improved by decreasing meal size and increasing meal frequency. Furthermore, treatment of primary medical comorbidities which lead to atherosclerotic disease is quite essential and must be managed by a multidisciplinary care team.

The initial concern for the treatment involves the presence of typical symptoms, whether single or multi-vessel stenosis and the patient's overall health status. The multi-vessel disease is characterized by stenosis (>70%) of both SMA and CA.

In CMI patients, endovascular revascularisation is being used more often as it is less invasive.27,28 However, in situations when this treatment does not work out, especially in younger patients, open surgical revascularisation is opted for as the initial choice of treatment as their overall health status is in good shape.14 Open revascularisation (bypass) can be retrograde (iliac artery to SMA), antegrade (supraceliac aorta to SMA), or hybrid (open SMA access and retrograde stenting). Even though surgical revascularisation is associated with higher long-term patency rates,29 endovascular approaches are still used whenever possible because they are associated with lower morbidity and mortality, decreased costs, and shorter lengths of stay.30,31 Following revascularisation, generally antiplatelet therapy is started for 3–12 months, particularly after stent placement.15 Surgical interventions are taken into consideration for patients with severe symptoms. There are laparoscopic and open methods to section the ligament and release the compression of the CA.32


Mesenteric ischemia is a rare condition which is associated with high mortality and morbidity in its acute form. A high degree of clinical suspicion linked with imaging outcomes is quite relevant for early diagnosis to improve clinical results. Treatment should be channelled by clinical stability and extent of ischemia with a multidisciplinary attitude, including physicians, gastroenterologists, interventional radiologists, and surgeons. Though treatment methods have improved with advances in scientific research on percutaneous interventions, pharmacotherapy, and critical care, diagnosing AMI before bowel necrosis initiates or spreads still remains important to improve the outcomes.


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This content is purely informational and isn’t medical guidance. It shouldn’t replace professional medical counsel. Always consult your physician regarding treatment risks and benefits. See our editorial standards for more details.

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Dr. Aastha Malik Dahra

Doctor of Philosophy - PhD, Life Sciences (Diabetes and Gene Polymorphisms), Post Graduate Institute of Medical Education and Research, Chandigarh

"I was chosen for the PhD program through a Senior Research Fellowship awarded by the Indian Council of Medical Research, New Delhi, India.

My thesis work focused on the association of genetic polymorphisms in Angiotensin converting enzyme (ACE), Serotonin transporter (SERT), Adrenergic receptor beta 2 and Adrenergic receptor beta 3 with gastrointestinal dysmotility in Type 2 Diabetes Mellitus patients. "

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