Acute SMA Thrombolic Mesenteric Ischamia

Acute SMA Thrombolic Mesenteric Ischamia

• SMA takes off at less obtuse angle than the celiac axis. Hence thromboembolism most commonly involves the
• SMIschaemia affects the mucosa first—most sensitive to hypoxia. Subepithelial oedema occurs within 30 min, loss of epithelial cells along the villus in 1 hour and total loss of villi with sloughing of mucosa in 2 hours.
• Within 4 hours gangrenous changes start. Thus the condition is rapidly fatal.

Acute Mesenteric Ischamia Etiopathogenesis

• It is common in elderly patients who are hypertensive and usually obese.
• It is due to atherosclerosis causing thrombosis of the superior mesenteric artery or due to emboli which originate from atheromatous plaques or from the infarcted heart.
• Smokers are more often affected by this condition.
• Superior mesenteric vein can also get thrombosed due to injury during pancreatectomy or thrombosis as a result of oral contraceptive pills.

SMA Thrombolic Mesenteric Ischamia Effects

• The pathological effects of arterial occlusion and venous occlusion are the same.
• Superior mesenteric arterysupplies the entire midgut starting from the duodenojejunal flexure to right one-third of the transverse colon. mall bowel and portion of the large bowel becomes gangrenous (if there is a thrombus at the origin of superior mesenteric artery).

It is an end-artery. As a result of thrombosis, the entire

Splanchnic Circulation

• It is better to have some idea about the splanchnic circulation to understand the effects of ischaemia to the gut.
• The splanchnic circulation receives approximately 25% of the resting and 35% of the postprandial cardiac output.
• 70% of the mesenteric blood flow is directed to the mucosal and submucosal layers of the bowel. Hence early cases present with bleeding due to mucosal ulcerations.
• 30% supplies the muscularis and serosal layers. Blood flow is regulated by intrinsic (metabolic and nmyogenic) and the extrinsic (neural and humoral) factors.
• Reactive hyperaemia and hypoxic vasodilation are considered intrinsic controls and are responsible for instantaneous fluctuations in splanchnic blood flow.
• An imbalance between tissue oxygen supply and demand will raise the concentration of local metabolites (example, . hydrogen, potassium, carbon dioxide, and adenosine), resulting in vasodilation and hyperaemia

Acute Mesenteric Ischaemia Causes 

1. Arterial emboli: Arterial emboli are the most frequent cause of AMI and are responsible for approximately 40 to 50% of cases. Most mesenteric emboli originate from a cardiac source. They lodge in the superior mesenteric artery (SMA) because it emerges from the aorta at an oblique angle. A few emboli lodge in the origin of middle colic artery.

Embolic: Majority of emboli originate in the heart

• Valvular heart disease
• Dilated left atrium
• Recent myocardial infarction
• Atrial arrhythmias
• Ventricular dilatation with mural thrombus
• Atheroemboli
• Aneurysm

2. Acute mesenteric thrombosis:

• Accounts for 25 to 30% of all ischaemic cases. Atherosclerotic disease is the cause of thrombosis.
• It typically occurs at the origin of the superior mesenteric artery.
• Gangrene is more extensive in cases of thrombosis than embolism.

3. Nonocclusive mesenteric ischaemia (NOMI):

• Typically happens in cases of hypotensive patients. Low cardiac output,
• ICU patients on vasoconstrictors and inotropes precipitate the problem.
• Splanchnic vasoconstriction occurs in response to hypovolemia.
• Vasoactive drugs, particularly digoxin, have been implicated in the pathogenesis of NOMI.

4. Mesenteric venous thrombosis (MVT): 

• Is the least common cause of mesenteric ischaemia, representing up to 10% of all patients with mesenteric ischaemia related to primary clotting disorders.
• Thrombi usually originate in the venous arcades and propagate

Aetiology of Mesenteric Venous Thrombosis:

• Hypercoagulable states (e.g. polycythaemia vera, protein C and S deficiencies)
• Visceral infection
• Portal hypertension
• Blunt abdominal trauma
• Pancreatic malignancy
• Pancreatitis
• Women taking oral contraceptives
• Post-splenectomy
• Smokers

Acute Mesenteric Ischaemia Clinical Features

Acute Mesenteric Ischaemia  Symptoms:

1. Abdominal pain: Severe, poorly localised, unresponsive to narcotics, out of proportion to the physical findings.
2. Onset may be abrupt (embolism) or insidious (thrombosis).
3. Gastrointestinal emptying: Vomiting, diarrhoea, with occult or frank bleeding once infarction sets in.
4. Condition presents as severe abdominal pain which is sudden onset, constant and more in the periumbilical region. It is often preceded by palpitations, arrhythmia, catheterization or myocardial infarction.
5. There is urge to defecate. Loose stools develop within 2–3 hours of the onset of symptoms. Attack of melaena indicates gangrene. Patients often present in an agitated or anxious state.

Acute Mesenteric Ischaemia Signs

• Abdomen is flat or scaphoid with a little to no pain on palpation. Abdomen is often soft and “Pain out of proportion to the signs” is often typical of AMI.
• Peripheral pulses may be feeble as it is common to have multiple emboli.
• Peritoneal signs with guarding and rigidity is a
  late sign and implies bowel gangrene and perforation.
• Very soon septic shock develops with dehydration, cold clammy extremities, hypotension, desaturation, acidosis, and oliguria.

Acute Mesenteric Ischaemia Investigations

1. Total counts are raised, in about 75% of cases >15,000 cells/mm3.
2. Plain X-ray abdomen (erect) reveals absence of gas within the bowel loops and intramural gas. Blunt plicae are seen. This is called thumb printing
3. Metabolic acidosis in > 50% of cases.
4. Serum phosphate levels are raised within 3–4 hours following ischaemia as smooth muscle layer of smallbowel is rich in phosphates.
5.  D-dimer is elevated in all cases.
6. CT angiogram is the investigation of choice. It can detect intramural air pockets in the bowel wall, air within biliary radicle, perforation, etc.
7. Emergency angiography is the test of choice and can be done within 6 hours of ischaemia. (It can also be therapeutic.)
8.  Hypercoagulability disorders—protein C and protein S antithrombin III, factor V, anticardiolipin antibody (MVT).

Acute Mesenteric Ischaemia Treatment

Patient is admitted in intensive care unit.

• Resuscitation is done. Nasogastric tube is inserted.
• Antibiotics started, heparinisation heparin given.

Once CT confirms the diagnosis, exploratory laparotomy is done.

1. Majority of the patients present late with massive gangrene.

• Massive resection of the gangrenous bowel followed by end-to-end anastomosis is done.
• These patients suffer from short bowel syndrome (vide infra), if they survive.

2. If patients come within 4–6 hours of ischaemia

• Emergency angiography followed by papaverine infusion (30 to 60 mg/h) into the superior mesenteric artery can be tried.
• Otherwise, emergency laparotomy is done and the superior mesenteric artery is explored.
• A Fogarty catheter is introduced and embolectomy is done.
• These patients may require a second look operation within 24–48 hours to rule out gangrene developing later due to thrombosis of the artery. BEfore resection check for bowel viability.

Assessing bowel viability:

• Doppler (84%)
• Absent arterial flow on antimesenteric border of the bowel.
• Absent mesenteric arterial flow
• Fluorescein test (100%)
• Sodium fluorescein 1 g was administered IV over 30 to 60 seconds and the bowel examined using a hand-held long wave UV Wood’s lamp (yellow).

3. Other vasodilator agents used are: Tolazoline, glucagon, nitroglycerine, nitroprusside, prostaglandin E, phenoxybenzamine, isoproterenol.

4. Sympathetic epidural block

Recent advances: In cases of mesenteric ischaemia

1. Catheter-directed thrombolysis
2. Percutaneous transluminal angioplasty
3. Endovascular fenestration of aortic dissection:
   • Techniques to assess bowel viability
   •  Pulse oximetry
   • Infrared photoplethysmography
   •  Bowel surface oximetry
   • Quantitative fluorescence using perfusion fluorometer.

Acute Mesenteric Ischaemia Prognosis

Majority of the cases present with massive gangrene. Even after massive resection, they succumb to the sepsis and multiorgan failure