Table 5.1 summarises the common causes of AMI. It arises primarily from problems in the SMA circulation or its venous outflow. Arterial disease may be due to occlusion of the SMA either from an embolus (50%) or from thrombosis of a pre-existing atherosclerotic lesion (25%). Arterial vasospasm can severely reduce mesenteric perfusion (20%) and mesenteric venous thrombosis can also cause bowel ischaemia (10%).

AMI does not include ischaemia caused by localised mechanical compression such as strangulated hernia, volvulus or intussusception.

Clinical presentation

The initial presentation of AMI is usually non-specific and diagnosis is therefore often missed initially, resulting in the significantly high mortality. A high clinical index of suspicion is vital in patients with the following presentation:

• Abdominal pain (95%). This is usually sudden and disproportionate to physical findings. Typically, the pain is moderate to severe, diffuse, non-localized and constant. It may be unresponsive to opiates, but peritonitic findings are often absent
  
• Gut emptying. Vomiting and diarrhoea (75%)
  
• Abdominal distension (25%)
  
• As the bowel becomes gangrenous, rectal bleeding and sepsis develops
  
• Clinical presentations that hint at an aetiology include:
  
  
  
  1. Atrial fibrillation or a recent myocardial infarction point to an embolic aetiology.
     
  2. Previous chronic mesenteric ischaemic symptoms (see the following sections) are present in 50% of patients with thrombotic AMI.
     
  3. Arterial vasospasm and mesenteric ischaemia tend to occur in older patients already unwell in the intensive care unit.
     
  4. In patients with mesenteric vein thrombosis, the abdominal pain tends to be less dramatic and can last for some weeks (30% have symptoms >30 days) and most have more than one risk factor for thromboembolic disease.

Investigations

Blood tests are not helpful in diagnosing AMI and tend to reflect developing bowel infarction, such that the white cell count and lactate levels are elevated and metabolic acidosis develops late in the clinical course. Elevated amylase levels are non-specific and phosphate levels are of no help.

If there is suspicion of AMI, radiographic studies should be undertaken without waiting for blood results. CT angiography is recommended as a first-line investigation as it has a greater than 90% sensitivity and specificity for diagnosing AMI. It will confirm the diagnosis and aid in planning treatment (Figure 5.1). Magnetic resonance angiography (MRA) yields findings similar to those of CT scanning in AMI (sensitivity of 100% and a specificity of 91%). It is particularly effective for evaluating mesenteric vein involvement. Therefore, it may be used in preference to CT depending on local radiological expertise. Plain abdominal X-rays and non-contrast CT help exclude other causes of the abdominal pain but identify AMI only when bowel infarction has developed. Duplex ultrasound is not usually performed in AMI as dilated loops of bowel reduce accuracy.

Treatment

Once the diagnosis is made, the treatment should be initiated without delay. The patient should have active resuscitation as per hospital protocol for critically ill patients with a low threshold for involving the intensive care team. Intravenous fluid resuscitation with crystalloids and blood products should be started promptly to restore volume. Haemodynamic monitoring should be instituted with central venous pressure measurements and assessment of urinary output. Optimise cardiac status by treating any arrhythmia or congestive heart failure and providing inotropic support as required, but avoiding use of vasopressors. Ensure adequate tissue oxygenation by maintaining a saturation of over 95%, by endotracheal intubation and ventilation if necessary. The patient should receive adequate analgesia and intravenous broad-spectrum antibiotics should be commenced. Heparin anticoagulation is started as soon as the diagnosis has been made and before an urgent treatment plan has been determined. For venous AMI, this is often the only treatment required.

Revascularisation can be achieved by two methods: endovascular interventions or by open surgery involving a laparotomy.

Endovascular interventions are best undertaken in a hybrid operating theatre (Figure 5.2) in combination with open surgical procedures where potential complications (Table 5.2) can often be better managed. Thrombolytic agent infusion through an angiography catheter is considered when bowel infarction has not yet occurred. Bleeding is the main complication with use of thrombolysis. Angioplasty (after thrombolysis) with stent placement is indicated if the guide wire can cross the stenosis. Owing to the anatomy of the SMA, angioplasty and stenting (Figure 5.3) are technically easier if a brachial approach is used. Suction embolectomy is not used as it often fails.

A laparoscopy may be perfumed to assess the viability of the bowel following a successful endovascular intervention. If there is evidence of irreversible bowel ischaemia, then a laparotomy is required to resect the necrotic bowel. Determination of bowel viability is difficult and the practice of viewing the bowel through a Wood lamp following fluorescein administration has not been universally adopted. Therefore, it is best to resect all areas of obviously necrotic bowel (Figure 5.4) and consider a ‘second-look’ laparotomy at 24–48 hours when the bowel has had sufficient time to recover and resected bowel ends can be anastomosed.

The open surgical approach involves performing an embolectomy to revascularise the ischaemic bowel. The SMA is isolated by palpating lateral to the aorta at the root of the lifted transverse colon mesentery, and because most emboli are near the origin of the middle colic artery, the pulse can be felt. A transverse arteriotomy is made proximal to the point of occlusion, and a balloon-tipped Fogarty catheter (size 3) passed distally. Often, a vein patch is needed to repair the arteriotomy. The small bowel should ‘pink-up’ within 10 minutes and a pulse felt or heard with the intra-operative Doppler machine. A bypass graft may be required if the bowel is not gangrenous and the cause is not embolic. An antegrade aorto-mesenteric bypass is performed using a reversed long saphenous vein (harvested from the upper thigh), as some form of faecal bacterial contamination is likely and insertion of a prosthetic risks infection.

Follow-up

Patients requiring extensive small bowel resection require follow-up by a gastroenterologist. Patients initially have severe diarrhoea but may be able to compensate after a few months with reduced loose bowel motions and begin to put on weight. Some patients have insufficient remnant small bowel and require total parenteral nutrition (TPN). The ileus secondary to intestinal ischaemia can cause adhesions and subsequent bowel obstruction. Patients who have had mesenteric vein thrombosis or are in atrial fibrillation will require warfarin therapy for life. Any cardiovascular risk factor should also be addressed in these patients.

Endovascular surgical interventions are best undertaken in a hybrid theatre (Figure 5.2) under general anaesthetic as the potential complications may require open surgery (Table 5.2).

Vascular surgical intervention options include

• bypass jump grafting, using either a vein or a prosthetic graft (Figure 5.5), and
  
• endarterectomy—surgical removal of the plaque.

It is usual practice to try and revascularise at least two of the three vessels. Treatment approach adopted will depend on the local facilities and expertise, as well as the general health of the patient and their associated co-morbidities. Compared to open surgery, an endovascular approach is considered to be less invasive with lower intra-operative mortality rates (6% versus 12%) and is associated with a shorter hospital stay (3 days versus 12 days), but with a lower long-term durability (30% versus 66% 3-year symptom-free outcome).

Follow-up

Patients who survive surgical revascularisation tend to do well, with excellent long-term prognosis (5-year survival rates approach 80%). Regular follow-up review includes duplex ultrasound and MRI (rather than CTA to reduce radiation exposure) to assess for re-stenosis. However, as the proper management of asymptomatic re-stenosis is unclear, further intervention should only be considered with the recurrence of symptoms, thus achieving an 80% 5-year symptom-free rate.