Acute mesenteric ischemia (AMI) is a medical condition in which bowel injury occurs due to insufficient blood supply.
It can affect the small or large intestine,
be segmental or diffuse,
partial or transmural.
It is a frequent pathology (increases in incidence with age),
potentially fatal,
that compromises intestinal viability.
Rapid diagnosis and initiation of treatment are essential to reduce long-term morbidity and prevent mortality.
The clinical diagnosis is difficult,
the main symptom being severe abdominal pain and disproportionate to clinical findings,
with poor response to analgesics; due to this,
imaging tests play a very important role in making the diagnosis.
In general,
a high degree of clinical suspicion should be based on the combination of history,
examination,
laboratory results and imaging studies to arrive at the diagnosis.
Anatomy: The abdominal aorta has 3 main branches that are directed to the intestines,
which are the celiac artery (CA),
the superior mesenteric artery (SMA) and the inferior mesenteric artery.
CA perfuses the anterior bowel (esophagus distal to the second portion of the duodenum).
Acute mesenteric ischemia of the bowel is very rare,
because AC is a short,
wide artery with good collateral flow.
SMA irrigates the midgut (duodenum to distal transverse colon),
covering almost the entire small intestine and two thirds of the large intestine.
This is the most common embolic site of mesenteric ischemia due to a favorable angle (approximately 45) from the aorta.
The inferior mesenteric artery irrigates the large intestine (transverse colon to the rectum) and is rarely the only vessel involved in mesenteric ischemia.
Collateral circulation from the CA or inferior mesenteric artery generally allows sufficient perfusion in reduced AMS flow,
such as non-occlusive or thrombotic mesenteric ischemia.
Pathophysiology: The layers of the intestine are affected from internal to external (mucosa,
submucosa,
muscle and serous).
The mucosa is the first to become ischemic and is the cause of extreme and visceral pain.
However,
because the external structures (muscular and serosa) have not become ischemic,
there is minimal irritation of the parietal peritoneum.
Therefore,
there is "disproportionate" pain to the examination at the beginning of the disease process,
where there is no focal localization or peritonitis.
Eventually,
the muscular and serous layers become ischemic and infarcted,
leading to peritoneal irritation and stiffness.
The initial ischemic involvement of the mucosa is then worsened by the inflammatory response activated by the different humoral mediators (cytokines,
TNF,
platelet activating factor).
In case of rupture or perforation of the wall,
the invasion of bacteria can lead to bacteremia and sepsis,
situations that contribute to increase the necrosis of the different segments of affected intestine.
The etiology of AMI can be divided into occlusive causes (arterial embolus,
arterial thrombosis and venous thrombosis) and not occlusive.