Mesenteric ischemia

Mesenteric ischemia
In the earlier days the surgical treatment of mesenteric ischemia was removal of infracted bowel before the patient was moribund. Klass, in 1951 was the first surgeon to focus on restoration of arterial supply to salvage the gut and performed the first SMA embolectomy. In the next two decades, many more reports of mesenteric revascularization came in but mortality remained high, to the tune of 70 – 90%.
Presently with improved surgical and endovascular techniques and improvement in anesthesia and critical care, morbidity and mortality still remains high. Delay in diagnosis remains the greatest obstacle to the reduction of morbidity and mortality surrounding this disease.

Anatomy
Three major branches from the abdominal aorta supply the GI tract. Celiac artery arises at level T12-L1 and divides into common hepatic, left gastric and splenic arteries. The superior mesenteric artery arises at level of L1 and branches into inferior pancreaticoduodenal, middle colic and jejunal and ilieal branches. The inferior mesenteric artery arises at level of L3 and divides into left colic and sigmoidal branches. The splanchnic circulation is characterized by a wide network of collateral blood pathways that impart redundancy and resultant protection from ischemia or infarction. The celiac axis and SMA are connected by the superior and inferior pancreatico-duodenal arteries and the SMA and IMA by the marginal artery of Drummond.

Pathophysiology
Splanchnic blood flow can range from 10 to 35% of cardiac output. The increase occurs in response to food intake. Two of the three mesenteric arteries must be significantly diseased to cause symptoms of chronic mesenteric ischemia (CMI) and SMA must be one of them. Sudden occlusion of SMA alone can cause acute ischemia.

Acute mesenteric ischemia
It can be due to emboli to SMA or thrombosis of SMA. Most emboli are cardiac in origin and sometimes are from proximal aorta. Sudden onset of abdominal pain in a patient with cardiac disease must alert the clinician to the possibility of mesenteric embolism. Thrombosis usually occurs on pre-existing chronic disease.
For diagnosis, a clinical suspicion is mandatory. Patient with cardiac disease, sudden onset of severe, continuous abdominal pain, often accompanied by diarrhea or vomiting must alert the clinician. There is accompanying leucocytosis. Other lab parameters and x-ray findings are seen only later in the course of the disease once bowel is infarcted. Elevated levels of intestinal fatty acid binding protein may offer some promise as a diagnostic tool.
Duplex scan requires the presence of a trained vascular radiologist, a fasting patient and bowel bereft of gas: a combination nearly impossible to achieve in an emergency setting. Multi-slice CT scan can demonstrate occluded vessels (upto second generation branches), bowel wall edema, stranding in the mesentery. In addition, other pathologies could also be easily detected.
A high index of suspicion followed up by multi-slice CT on emergency basis is likely to provide the best chance of diagnosis and an opportunity for revascularization.
On angiography, SMA is found occluded at or near origin in case of thrombosis and affects the entire bowel from ligament of Treitz to mid transverse colon. In contrast, an embolus lodges at a branch point and the proximal jejunal branches are often spared.

Treatment
Initial management includes correction of fluid and electrolyte imbalances, baseline cardiac assessment, broad spectrum parenteral antibiotics and anticoagulation.
Endovascular therapy with fibrinolysis should not be attempted since there is a very high risk of ongoing bowel damage during the period of lysis.
Surgery is the mainstay of treatment and begins with a complete exploratory laparotomy and assessment of bowel viability. Lower limbs must be included in draping for vein harvesting. In case there is extensive bowel infarction incompatible with life, it is appropriate to close with no further intervention. Revascularization is done either by SMA embolectomy or superior mesenteric artery bypass, usually from the infra-renal aorta. Bowel viability must be re-assessed after restoring blood supply and appropriate resection done. When there is doubt about bowel viability, re-look laparotomy is done after 12-36 hours.


Chronic mesenteric ischemia
It is a life-threatening problem that can result in death due to inanition or bowel infarction. The underlying pathophysiology is the failure to achieve post-prandial hyperemic blood flow. While atherosclerosis is the leading cause for CMI, other etiologies include Takayasu’s disease, aortic dissection, fibromuscular disease, SLE, Rheumatoid arthritis and drugs like cocaine and ergot.
A typical patient is cachectic, middle-aged, with history of smoking who presents with post-prandial abdominal pain and weight loss. The pain is usually epigastric and causes patients to avoid certain foods or eating altogether (food fear). Most patients often undergo extensive GI checkup before someone suspects CMI. Gastric ulceration or gastroduodenitis are often seen due to ischemia.
A Duplex ultrasound is a good screening modality. Angiography is diagnostic and helps in planning revascularization strategies.

Treatment
All patients with CMI should be taken up for revascularization even if co-morbid factors increase risk of surgery. While long term total parenteral nutrition has been considered an option in high risk patients, it is practically inconvenient, carries risk of catheter related infections and does not alleviate the risk of bowel infarction.
Revascularization options include angioplasty and stenting and mesenteric artery bypass. There is no clear cut agreement in literature as to which is the better option and as to how many vessels should be revascularized. Synthetic grafts or femoral veins are best conduits for mesenteric bypass. Inflow may be taken from supraceliac aorta, infra-renal aorta or an aortic graft. All patients are maintained on anti-platelet agents and statins.

Median arcuate ligament syndrome
The median arcuate ligament of the diaphragm compresses the origin of celiac axis which is augmented by full expiration in a large number of individuals. Its contribution to CMI is uncertain and it is unlikely to be able to produce CMI on its own. It is a diagnosis of exclusion. Surgical therapy may offer relief in patients who are females, have postprandial pain, weight loss more than 8 kgs, absence of drug abuse or psychiatric history and angiographic confirmation of celiac axis compression with post-stenotic dilatation. Effective treatment includes relief of compression and mesenteric bypass. Another option could be laparoscopic division of the ligament followed by angioplasty of celiac axis.

Non-Occlusive Mesenteric Ischemia (NOMI)
NOMI is caused by primary splanchnic vasoconstriction and has high mortality. It is associated with shock state, cardiopulmonary bypass and use of vasoactive drugs like digoxin, vasopression and α-adrenergic agents.
Management
Early arteriographic diagnosis and subsequent intervention offer the best chance for better outcome and survival. Pain out of proportion to physical findings and normal radiographic findings are suggestive of early ischemia and should prompt consideration of immediate diagnostic arteriography. Other biochemical and radiological findings as seen in acute ischemia, are indicative of bowel infarction. Arteriographic criteria for diagnosis of NOMI include narrowing origins of multiple branches of SMA, string of sausage sign, spasm of mesenteric arcades and impaired filling of intramural branches.
Treatment includes immediate management of precipitating factors like shock and cardiac events and use of vasodilators that diminish cardiac preload and afterload. Definitive treatment is selective intra-arterial infusion of papaverine into the SMA. It is best to start with 30 mg/hr. Arteriography is repeated once pain resolves and infusion is continued for 24 hours. One needs to be vigilant for signs of bowel infarction and intervene appropriately.

Mesenteric venous thrombosis
It is a rare disorder with a wide range of clinical presentations. It usually involves the superior mesenteric and splenic veins and may involve inferior mesenteric and portal veins.
One should suspect this diagnosis in patients with acute abdomen with history of previous thrombotic episodes or known thrombophilia. Others may present pain and loss of appetite, often of a few days duration, diarrhea, occult GI bleed and occasionally bowel infarction and peritonitis. There may be mild leucocytosis and slightly elevated LDH. Diagnosis can be confirmed by venous phase of CT scan or with contrast enhanced MR venography. Color Doppler can often show presence of thrombi in the veins.
Treatment is usually conservative with life-long anticoagulation. Aggressive management with surgery or thrombolysis can be done in selected patients. Any associated hypercoagulable state must be appropriately treated.