Acute mesenteric ischaemia: imaging and intervention

Clinical Radiology xxx (xxxx) xxx

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Review

Acute mesenteric ischaemia: imaging and intervention B.R. Hawthorn, L.A. Ratnam* Department of Radiology, St George’s Hospital, Blackshaw Road, London SW17 0QT, UK

Acute mesenteric ischaemia (AMI) is an abdominal emergency in which an acute reduction in mesenteric arterial supply threatens bowel viability and may result in bowel infarction, perforation, and death. Despite improvements in diagnosis and treatment over recent decades, mortality rates in AMI remain very high. This article discusses the aetiological classification, pathophysiology, and clinical aspects of AMI. The specific imaging characteristics of each aetiological type of AMI are detailed and the role of different imaging methods in the diagnosis of AMI is discussed. Surgery is the established treatment of choice for AMI, but there is increasing use of endovascular techniques in treating AMI in cases where there are no clinical features of peritonism or radiological evidence of irreversible ischaemia. This article reviews the evidence for different diagnostic and management strategies for patients with AMI and discusses the advantages and disadvantages of surgical and endovascular treatments. Endovascular techniques have been reported to have high technical success rates and favourable outcomes when compared to open surgery; however, patient selection bias and a paucity of data limit the conclusions that can be drawn. Crown Copyright Ó 2019 Published by Elsevier Ltd on behalf of The Royal College of Radiologists. All rights reserved.

Introduction Acute mesenteric ischaemia (AMI) is an abdominal emergency in which an acute reduction in mesenteric arterial supply threatens bowel viability. This may result in bowel infarction, perforation, and death. Despite improvements in diagnosis and treatment over recent decades, mortality rates in AMI remain very high, in the region of 50e69%.1,2 In those amenable to treatment, prognosis can improve significantly with mortality rates dropping to 0e10% with

* Guarantor and correspondent: L. A. Ratnam, Department of Radiology, St George’s Hospital, Blackshaw Road, London SW17 0QT, UK. Tel: þ442087250946. E-mail address: [email protected] (L.A. Ratnam).

immediate treatment. Mortality approaches 100% if treatment is delayed by >24 hours.3 In selected patients, rapid diagnosis and an early, aggressive therapeutic approach can improve survival by restoring mesenteric circulation before irreversible ischaemic damage occurs. Surgery is the established treatment of AMI, but is associated with a high rate of morbidity and mortality. Small case series have demonstrated that endovascular therapies have been successful in the treatment of AMI in selected cases with fewer complications. AMI is distinct from chronic mesenteric ischaemia (CMI), which has a more indolent course and classically presents with intestinal angina, defined as recurrent, post-prandial abdominal pain with associated aversion to food and weight loss. Untreated cases of CMI may progress to AMI, usually as a result of critical stenosis and acute thrombosis.

https://doi.org/10.1016/j.crad.2019.06.001 0009-9260/Crown Copyright Ó 2019 Published by Elsevier Ltd on behalf of The Royal College of Radiologists. All rights reserved.

Please cite this article as: Hawthorn BR, Ratnam LA, Acute mesenteric ischaemia: imaging and intervention, Clinical Radiology, https://doi.org/ 10.1016/j.crad.2019.06.001

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This article discusses the evidence for different diagnostic and management strategies for patients with AMI.

Epidemiology AMI is a rare condition, accounting for approximately 1 in 1,000 acute hospital admissions in European countries and North America.4 The incidence of AMI increases with age, with a mean age at presentation of 70 years.5 Older patients are more likely to have significant comorbidities and poor performance status, and therefore generally have a worse prognosis. One study reported a 30-day survival of 81% for patients with AMI <71 years, but survival fell to 7% for patients the >84 years.2

Causes and classification There are four main causes of AMI, each with different pathophysiological mechanisms and their own diagnostic and therapeutic considerations. These are (in order of incidence): (1) mesenteric arterial embolism (MAE), (2) mesenteric arterial thrombosis (MAT), (3) non-occlusive mesenteric ischaemia (NOMI), and (4) mesenteric venous thrombosis (MVT). MAE is the most common cause of AMI, accounting for 40e50% of cases.6 Emboli usually have a cardiac origin and underlying causes such as atrial fibrillation, ventricular aneurysm, or myocardial infarction should be investigated and excluded. The superior mesenteric artery (SMA) is the most vulnerable to emboli due to its narrow angle of origin from the aorta. Emboli typically lodge 6e8 cm beyond the SMA origin, near or within the origin of the middle colic artery resulting in a sudden cessation in mesenteric circulation. Therefore, the presentation is typically with sudden, severe pain. As the emboli lodge distally, the proximal SMA branches are usually unaffected and this allows for continued partial perfusion of the proximal intestine. MAT accounts for approximately 25% of cases and typically occurs in elderly patients with atherosclerotic risk factors and a background of atherosclerotic disease at other sites. Atherosclerotic plaque usually develops at the vessel origins and acute ischaemia develops when a pre-existing atherosclerotic stenosis reaches a critical diameter and acutely thromboses. Therefore, clinical presentation can be with an acute exacerbation of symptoms on a background of longstanding abdominal angina. As all the mesenteric arteries communicate with each other through a network of collateral connections, ischaemia usually only develops when two of the three major mesenteric arteries (usually the coeliac axis and SMA) suffer severe stenosis or occlusion. Ischaemia can also occur with severe stenosis without complete occlusion, in the context of generalised hypotension or low cardiac output. In cases of MAT, occlusion occurs at the vessel origin, proximal to the arterial branches, so a larger proportion of the bowel is vulnerable to ischaemia. Consequently, the prognosis is usually worse in cases of MAT compared to MAE. NOMI accounts for 20% of cases and arises as a result of prolonged, severe mesenteric arterial spasm without major

vascular occlusion. This poorly understood entity can occur in the setting of severe systemic illness, such as shock, heart failure, cardiac arrhythmia, myocardial infarction, renal or hepatic disease, or postoperative stress, and complicates 0.5e1% of all cardiac operations.7 Mesenteric vasospasm often persists even after correction of the precipitating event. NOMI is difficult to detect as it often occurs in sedated, artificially ventilated patients, in whom the clinical signs and symptoms are masked. It should be suspected when an unexpected deterioration occurs in a critically ill patient. MVT is an uncommon cause of AMI, accounting for 5e10% cases. Of all the causes of AMI, this condition has the youngest peak age of onset. Although it can occur spontaneously, in 50e75% of cases an underlying secondary cause of venous thrombosis is identified.8 Secondary causes include portal hypertension, hypercoagulability states, abdominal trauma, malignancy, intra-abdominal infections, or inflammatory conditions such as pancreatitis. Approximately, 50% of patients have a history of previous deep vein thrombosis or pulmonary embolism.9 Oral contraceptive pill and pregnancy are also risk factors in young women.10 The superior mesenteric vein (SMV) is most commonly affected. Obstructed venous return causes bowel wall oedema and luminal distension, which in turn decreases arterial inflow and subsequently leads to ischaemia. The clinical presentation is typically subacute, with abdominal pain over a period of up to 2 weeks. If untreated, MVT may have long-term sequelae such as portal hypertension. Other rare causes of AMI include arterial dissection, trauma, retroperitoneal fibrosis, fibromuscular dysplasia, and vasculitis.11 Bowel strangulation is a common cause of intestinal ischaemia, but should be considered a secondary rather than a primary cause of AMI as the pathophysiological mechanism is different.

Pathophysiology of AMI The gastrointestinal tract is supplied by three major arteries. The coeliac axis supplies the stomach and duodenum. The SMA supplies the jejunum, ileum, and colon from the caecum to the splenic flexure. The inferior mesenteric artery (IMA) supplies the colon from the splenic flexure to the rectum. Each artery and its branches are part of a rich network of collaterals, which protects the bowel against ischaemia. When there is arterial occlusion, the severity of ischaemic injury depends on the number of mesenteric vessels involved, the quality of the arterial collateral network and the duration of reduced blood flow. Interruption to the arterial supply results in microscopic ischaemic injury within the bowel wall within minutes; however, the bowel can survive a 75% reduction in arterial supply for up to 12 hours without significant injury.12 Irreversible ischaemia develops when arterial supply drops below this minimum threshold. Ischaemia can be classified as reversible, referring to infarction of the mucosa or submucosa, or irreversible, in which there is transmural infarction. Irreversible ischaemia

Please cite this article as: Hawthorn BR, Ratnam LA, Acute mesenteric ischaemia: imaging and intervention, Clinical Radiology, https://doi.org/ 10.1016/j.crad.2019.06.001

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occurs within 6 hours in cases of complete vascular occlusion.13 Muscular and neurological infarction leads to adynamic ileus and bowel dilatation. Ultimately, transmural infarction will result in perforation, peritonitis, and death; however, septic shock or multi-organ failure can cause death before perforation occurs.

Clinical aspects of AMI Early detection of AMI is difficult as the symptoms and signs are often non-specific and the clinical presentation can mimic other causes of acute abdomen in 20e25% cases.14 Abdominal pain is the most prominent symptom and is usually severe, constant, and diffuse. Nausea, vomiting, and diarrhoea are less common features. Classically, in the early stages of ischaemia, there is a discrepancy between the severity of the abdominal pain and a lack of significant findings on clinical examination. Clinical indicators of advanced ischaemia include abdominal rigidity, marked abdominal distension with reduced bowel sounds, and features of hypovolaemic or septic shock. Clinical assessment does not reliably distinguish the underlying causes of AMI; however, a thorough history and careful consideration of the patient’s comorbidities may give clues as to the underlying cause. For example, a patient with atrial fibrillation and sudden onset of pain is more likely to have MAE, whereas an older patient with a history of peripheral vascular disease and acute on chronic symptoms is more likely to have MAT. There is no reliable laboratory test that can be used for the early detection of AMI. Serum lactate level is not sensitive or specific and a normal measurement does not exclude ischaemia. Lactic acidosis generally develops late in the clinical course of AMI when mortality is already very high. D-dimer is often positive in AMI, but lacks specificity.15

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end-organ enhancement. Coronal and sagittal reconstructions are useful for assessing the origins of the mesenteric arteries.

Non-specific CT findings Bowel wall thickening is the most common, but nonspecific, finding in AMI and represents mural oedema, haemorrhage, or infection.18 It is important to note that bowel wall thickness is not increased in all causes of AMI, and can in fact be thinned in complete arterial occlusion.19 Mural thickening is more prominent in cases of venous occlusion. In MAE and MAT, mural thickening is usually only seen after reperfusion. Mesenteric oedema and ascites are also non-specific signs, which can be seen as a result of venous congestion or following arterial reperfusion. Bowel wall enhancement patterns vary. High attenuation of the bowel wall seen on unenhanced imaging represents intramural haemorrhage. Hyperenhancing bowel wall after contrast enhancement indicates congestion or reperfusion. A target or halo appearance is described, which is the result of differential enhancement of the bowel wall layers, with enhancing mucosa and non-enhancing submucosal layers. This feature can be seen after arterial reperfusion.

CT features of advanced ischaemia Features that are suggestive of advanced or irreversible ischaemia include adynamic ileus and a paper-thin bowel wall, which indicate loss of muscle volume and tone related to muscular and neurological infarction. Absent bowel wall enhancement, especially when present 6e12 hours after onset of symptoms, is another feature of advanced ischaemia. Intramural gas and portal venous gas indicate transmural infarction and are ominous signs of advanced ischaemia (Fig 1), whereas free intraperitoneal gas signifies perforation.

Imaging of AMI

Identifying the underlying causes of AMI

Clinical assessment and laboratory tests are often not helpful so imaging plays an important role in the diagnosis of AMI. Plain radiography is often normal until late in the disease process and when abnormal, the findings are nonspecific.16 Features that may be identified on plain radiographs include bowel dilatation, bowel wall thickening (thumb printing), intramural gas, portal venous gas, or pneumoperitoneum. Computed tomography (CT), often combined with CT angiography (CTA), is the most sensitive and specific imaging test available and should be the first-line technique in cases of suspected AMI. Not only will CT demonstrate more specific features of AMI, it will also exclude other causes of abdominal pain. The sensitivity of CTA for AMI is reported as 93.3%, whilst specificity is 95.9%.17 A triphasic scan offers the most complete assessment, comprising unenhanced CT for detection of vascular calcification, high-attenuation intravascular thrombus, or high-attenuation intramural haemorrhage, as well as arterial and portal venous phase imaging for assessment of intravascular filling defects and

CT is also useful in determining the underlying cause of AMI. In cases of MAE, emboli may be visualised as highattenuation material within the arterial lumen on precontrast imaging. On arterial phase imaging, emboli may appear as a central intraluminal filling defect or an abrupt transition to non-opacified artery. The SMA is the most commonly affected vessel, with embolic material usually lodged distally within the vessel, close to the origin of the middle colic artery (Fig 2b). CT may also reveal emboli in other parts of the body (Fig 2a) and, or infarcts affecting other abdominal organs, such as the liver, kidneys, or spleen (Fig 3b,c), which is strong supporting evidence of MAE. Calcification at the origins of the mesenteric arteries is typical in atherosclerotic disease and is more suggestive of MAT as the underlying cause. Corresponding arterial stenosis or occlusion are well visualised on CTA, and are often best appreciated on coronal or sagittal reformats (Fig 4a). Acute and chronic thrombotic occlusive disease have identical appearances and can only be reliably distinguished if there are bowel or mesenteric abnormalities suggestive of

Please cite this article as: Hawthorn BR, Ratnam LA, Acute mesenteric ischaemia: imaging and intervention, Clinical Radiology, https://doi.org/ 10.1016/j.crad.2019.06.001

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Figure 1 A 73-year-old woman presenting with worsening abdominal pain and rising serum lactate. (a,b) Axial and coronal portal venous phase CT images showing extensive intramural gas affecting multiple jejunal loops indicating transmural infarction (thick white arrows). Note a small locule of portal venous gas on the coronal image (thin white arrow). (c) Twelve hours later, there is extensive portal venous gas (thin white arrows), which is an ominous sign of advanced ischaemia.

acute ischaemia and a corresponding clinical presentation. CTA may demonstrate developed collateral pathways, which imply a degree of chronicity. Evidence of atherosclerotic disease affecting other sites is also supportive evidence for MAT. CTA is suboptimal in the assessment of the terminal mesenteric vasculature and traditionally, catheter angiography has been relied upon to diagnose NOMI. Findings at catheter angiography include diffuse constriction of mesenteric arterial branches with alternate dilatation and narrowing referred to as the “string of sausages” sign and reduced enhancement of bowel wall (Fig 5); however, improvements in the diagnostic quality of modern CT technology and new methods of quantitative analysis of vessel diameter mean that non-invasive assessment of arterial spasm is becoming more reliable.20 NOMI should be suspected on CTA if the distribution of bowel ischaemia is

segmental and discontinuous, and there is no gross occlusion evident, especially if arterial diameters are small. Improved CT diagnostic performance may bring the benefit of earlier detection of NOMI, and may expedite confirmatory catheter angiography and treatment. In >90% of cases of MVT, a venous filling defect is evident on portal venous phase CT (Fig 6).21 Typically, the venous thrombus is surrounded by mural rim enhancement (Fig 6b). Mesenteric engorgement and ascites are the most common associated findings (Fig 7).22 Prominent bowel wall thickening is less commonly seen and reflects severe mural oedema. A target pattern of mural enhancement may be visualised and implies reduced arterial perfusion, whilst absent enhancement is a feature of advanced ischaemia. Contrast-enhanced magnetic resonance angiography (MRA) can also be used to demonstrate arterial occlusion or mesenteric venous thrombosis; however, rapid diagnosis

Figure 2 A 71-year-old woman initially presents with a painful and cold left upper limb. (a) Maximum intensity projection (MIP) CT angiogram in coronal reformat shows non-occlusive embolus within the axillary artery (black arrow) and occlusion of the brachial artery (white arrow). The next day, the patient begins to deteriorate with abdominal distension and rising serum lactate. (b) MIP CTA in sagittal reformat shows an occlusive filling defect within the SMA (white arrows). The location of the filling defect is typical for MAE. The other CT findings of MAE are demonstrated in Fig 3. Please cite this article as: Hawthorn BR, Ratnam LA, Acute mesenteric ischaemia: imaging and intervention, Clinical Radiology, https://doi.org/ 10.1016/j.crad.2019.06.001

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Figure 3 Other CT findings in MAE. (a) Coronal reformat portal venous phase CT shows multiple loops of small bowel in the SMA vascular territory, which demonstrate absent mural enhancement (white arrow). Compare this to the duodenum which demonstrates normal enhancement (black arrow). (b,c) Hepatic infarcts (black arrows) and splenic infarct (white arrow).

and treatment are necessary in order to improve survival in AMI, and limited access to MRI along with long acquisition times may result in unacceptable delays. Percutaneous catheter angiography has been largely replaced by CTA in the initial evaluation of AMI as it is invasive and time-consuming. In cases of MAE, angiograms typically

show a filling defect, which completely or partially occludes the artery. The “tram-track” sign refers to the appearance of two thin parallel stripes of contrast between the embolus and the vessel wall. The main advantage of catheter angiography is that it can be coupled with catheter-directed intervention in the same sitting. Catheter angiography is now reserved for

Figure 4 An 80-year-old man presents with acute on chronic abdominal pain and hypovolaemia. (a) CT angiogram in sagittal reformat shows calcification at the origins of the coeliac axis and SMA (black arrow). There is an occlusive filling defect extending distally from the SMA origin (white arrow). The proximal location of the filling defect and the associated vascular calcification are typical of MAT. (b) Digital subtraction angiogram performed in lateral projection via catheter in the abdominal aorta. The coeliac axis opacifies normally but only a short stump of the SMA is visible (black arrow). A wire is advanced into the thrombus and a catheter is positioned within the proximal SMA and thrombolytic therapy is initiated. (c) Following successful thrombolysis, angiography demonstrates patent distal branches of the SMA. (d) An underlying atherosclerotic stenosis in the proximal SMA is treated with a balloon expandable metal stent (black arrows). Please cite this article as: Hawthorn BR, Ratnam LA, Acute mesenteric ischaemia: imaging and intervention, Clinical Radiology, https://doi.org/ 10.1016/j.crad.2019.06.001

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Figure 5 A 61-year-old woman, who has been in intensive care for 3 days after coronary artery bypass graft surgery, deteriorates unexpectedly and develops abdominal ridigity and high serum lactate. (a) Axial image from a CT angiogram shows that the SMA is patent with no obvious occlusive disease, but is extremely diminutive in calibre (thin white arrow). There are multiple dilated and poorly enhancing loops of bowel (thick white arrows). A diagnosis of non-occlusive mesenteric ischaemia was suspected and catheter angiogram was arranged to confirm. (b,c) Anteroposterior projection digital subtraction angiograms, taken a few seconds apart, performed via a catheter in the proximal SMA; (b) demonstrates diffuse constriction of mesenteric arterial branches (black arrowheads) with alternate dilatation (thick black arrows) and narrowing (thin black arrows) referred to as the “string of sausages” sign. (c) The image obtained a few seconds later shows enhancement of the duodenum and proximal jejunum, but the rest of the bowel in the SMA territory does not enhance.

Figure 6 A 45-year-old woman presents with vague abdominal pain. Portal venous phase CT demonstrates superior mesenteric vein thrombosis. (aed) Magnified coronal reformats: (a) white arrow shows that the portal vein is patent. (b) Black arrow shows non-occlusive filling defect at the portosplenic confluence with a peripheral rim of contrast enhancement. (c,d) There is occlusive thrombus within the SMV (black arrows) but the splenic vein is patent. (white arrow). The other associated findings of SMV thrombosis are shown in Fig 7. Please cite this article as: Hawthorn BR, Ratnam LA, Acute mesenteric ischaemia: imaging and intervention, Clinical Radiology, https://doi.org/ 10.1016/j.crad.2019.06.001

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Figure 7 A 45-year-old woman presents with vague abdominal pain. Portal venous phase CT demonstrates superior mesenteric vein thrombosis. Axial (a) and coronal (b) images showing thick-walled, hyperenhancing small bowel loops indicating severe mural oedema and vascular congestion (thick white arrow). There is a small volume of ascites (black arrow) and prominent mesenteric stranding and engorgement of the mesenteric vasculature (thin white arrows).

cases of suspected NOMI, cases where there is diagnostic uncertainty and a delay in treatment is acceptable; and cases when endovascular therapeutic options are being considered.

surgical revascularisation challenging.24 Furthermore, anticoagulant therapy is hazardous alongside open surgery due to the risk of uncontrollable bleeding.

Management of AMI secondary to MAE and MAT

Catheter-directed thrombolysis

Once the diagnosis of AMI has been established, rapid and aggressive management is required in order to prevent progression to irreversible ischaemia. Numerous studies have shown that mortality is lowest if intervention is performed within 12 hours of the onset of symptoms.23 Definitive treatment includes restoration of mesenteric arterial flow and resection of necrotic bowel. Initial supportive therapies should include fluid resuscitation, broadspectrum antibiotic cover, nasogastric tube decompression, and if possible, anticoagulation. Vasopressor drugs should be avoided whenever possible.15

Surgical management For any cause of AMI, if there are signs of peritonism and the clinical status of the patient makes curative treatment possible, urgent laparotomy is indicated. Patients with severe septic shock should undergo lifesaving damage-control surgery, comprising resection of ischaemic bowel, surgical thromboembolectomy, and transfer to intensive care unit for ongoing resuscitation. In such cases, second-look laparotomy procedures usually occur within 48 hours of damage-control surgery, to assess for viability of bowel after reperfusion. The main disadvantage of open surgery is its high associated morbidity and mortality. In addition, surgical techniques may not always be best suited to certain scenarios. For example, emboli within peripheral, segmental branches of the SMA may not be amenable to surgical embolectomy and severely calcified atherosclerotic disease may make

Although surgical embolectomy and bypass are the established treatments of choice for revascularisation, there is increasing use of endovascular techniques in treating AMI in cases where there are no clinical features of peritonism or radiological evidence of irreversible ischaemia. The main advantage of endovascular treatment is that it is less invasive, with lower rates of procedural complications24,25; however, unlike open surgery, the bowel is not directly visualised and so definitive assessment of bowel viability is not possible. Careful patient selection is therefore essential to avoid delayed detection and management of irreversible ischaemia. When used appropriately, endovascular techniques have been shown to be safe and effective and may reduce the need for open surgery.26 Direct intra-arterial thrombolytic therapy is probably the simplest endovascular technique and is an attractive option for frail, elderly patients who present in the early stages of AMI. This technique involves percutaneous transarterial access, usually via the common femoral artery. Anteroposterior and lateral aortography combined with selective catheterisation and angiography of mesenteric arteries are performed in order to determine the site and degree of obstruction and to assess collateral circulation (Fig 4b and c). After a guidewire is threaded across the occlusion, a catheter is advanced over the wire into the thrombus/ embolus. An initial bolus injection of thrombolytic agent directly into the occlusion is performed. Usually, the catheter is then withdrawn so that the tip is just proximal to the target and a continuous infusion of thrombolytic agent is administered under close surveillance. There is no consensus on duration of thrombolytic therapy. Arterial

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flow is thought to be re-established within the first few hours of therapy, but longer treatment times may give more complete clot dissolution. An arbitrary limit of 48 hours is usually applied, as the risk of bleeding complications increases after this point. Commonly, an adjunctive heparin infusion is administered via the side arm of the arterial sheath for the duration of thrombolytic therapy.27 Systemic heparin may be beneficial in the treatment of small residual thrombi or distal embolic fragments within the peripheral intestinal branches. Fortunately, because marginal arteries provide collaterals to maintain sufficient perfusion to the bowel, it is not essential to achieve complete restoration of blood flow in all distal branches. One of the main disadvantages of pharmacological thrombolysis is the long period of continuous infusion required for thrombus dissolution to occur. In one case series, the median duration of thrombolytic therapy was 22 hours.28 The main concern is that reversible ischaemia may progress to irreversible ischaemia even after therapy has been initiated and thus close monitoring for signs of peritonism is required during treatment. Pharmacological thrombolysis is therefore frequently combined with mechanical thrombus fragmentation, using a guidewire or angioplasty balloon, or thrombo-aspiration using a vacuum aspiration device, in order to reduce the embolic mass more rapidly and achieve arterial reperfusion sooner. Decreasing treatment time also has the added benefit of reducing the dose of thrombolytic agent required, which may lower the risk of associated bleeding complications. Pharmacological thrombolysis, mechanical thrombus fragmentation, or thrombo-aspiration are techniques that can be used effectively alone or when combined.24,29 Technical success with endovascular therapy has been reported to be as high as 89% in patients treated for acute SMA occlusion. The likelihood of technical success is dependent on the age of the thrombus/embolus, with the best results obtained when treatment occurs within 72 hours of occlusion.27 Successful endovascular therapy has been shown to be associated with reduced rates of laparotomy, significantly less bowel resection, and improved mortality rates when compared to traditional surgical therapy.26 One systematic review reported survival of 89% for patients treated with endovascular therapy with or without additional surgery, which is in great contrast to the overall reported mortality rates for AMI.27

Risks and complications of thrombolysis Contraindications to thrombolytic therapy are well established and can be divided into absolute (e.g., central nervous system tumours, recent haemorrhagic stroke) or relative (e.g., pregnancy, recent major surgery). The bleeding risk from direct intra-arterial thrombolysis is low with most bleeding complications occurring at the percutaneous access site. Bjornsson and colleagues reported six minor, self-limiting bleeding complications in 34 patients treated with thrombolysis for acute SMA occlusion. None of the bleeding complications required discontinuation of thrombolysis, blood transfusion, or surgery.28

Haemorrhagic transformation of ischaemic bowel and consequent life-threatening gastrointestinal haemorrhage is a theoretical risk, which may be exaggerated. Major haemorrhage has not be reported during acute SMA occlusion treatment, but it occurs in 9% of patients being treated with thrombolysis for lower limb arterial occlusion.27,30 Given the mortality associated with AMI, fear of bleeding complications should not deter clinicians from thrombolytic therapy. If necessary, laparotomy can still be performed after reversal of heparin and discontinuation of thrombolysis, as it has a short duration of effect.

Angioplasty and stenting Angioplasty and stent placement are performed when there is underlying vascular stenosis, and are therefore frequently employed in the management of MAT. When bowel viability has not been compromised, endovascular treatment should be performed as the first-line therapy for cases of MAT.15,31 Pre-dilatation using an angioplasty balloon is usually performed, followed by deployment of a balloon-expandable stent across the stenotic lesion (Fig 4d). These mechanical procedures can be complicated by distal embolisation of thrombus fragments and are therefore frequently combined with thrombo-aspiration or thrombolysis. Other potential complications include arterial dissection, occlusion, or stent migration. Severely calcified stenosis can be difficult to recanalise. If attempts at antegrade stent insertion fail, surgical recanalisation should be considered and retrograde open mesenteric stenting (ROMS) is one method that can be employed at the time of laparotomy. This hybrid technique combines the advantages of open surgical and endovascular approaches and has been shown to be successful with a relatively low mortality and morbidity rate.32 If endovascular techniques fail, conventional bypass surgery is another option, using vein or synthetic grafts to redirect flow to the bowel from the supracoeliac aorta, renal artery, or common iliac artery.33

Management of AMI secondary to NOMI and MVT Early recognition and initiation of treatment is essential in cases of NOMI. Initially, efforts should be made to identify and correct the clinical and pharmacological factors causing mesenteric vasoconstriction. Frequently, however, vasoconstriction persists even after the underlying cause is corrected. In advanced cases, surgery is indicated in order to resect infarcted bowel, but there is no surgical option for restoring bowel perfusion in NOMI. If there is no evidence of bowel necrosis, direct intra-arterial vasodilator therapy can be initiated at the same time as diagnostic angiography. A catheter is inserted into the affected vessel, usually the SMA, and an initial bolus injection of vasodilator agent is followed by a slow infusion for 24 hours. A variety of vasodilator agents have been used successfully, including prostaglandin E1 (alprostadil) and papaverine, which has been shown to reduce the mortality rate for NOMI from 70% to 50e55%.6

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MVT is usually managed without surgery or endovascular therapy. Systemic anticoagulation therapy with heparin is considered the first-line treatment in cases of MVT and patients will likely require long-term anticoagulation.15 Patients who deteriorate during conservative anticoagulant therapy can be offered more aggressive endovascular treatment in order to restore venous blood flow more rapidly. Some case series recommend early direct intervention as a means of preventing long-term sequelae such as portal hypertension.34 Various endovascular techniques have been described. Direct approaches to the mesenteric veins include access via a transjugular intrahepatic portosystemic shunt (TIPS), percutaneous transhepatic access to a portal vein branch or access via a surgically placed SMV catheter. Once access is obtained, mechanical thrombo-aspiration can be combined with thrombolysis in order to restore flow. Any residual venous stenosis can be treated with balloon venoplasty with or without stent placement. Several case reports and small case series have described the feasibility of these techniques.35e37 One case series showed successful restoration of venous flow and resolution of symptoms in 10 of 11 patients treated with percutaneous transhepatic thrombectomy and direct thrombolysis for SMV thrombosis.38 Thrombolytic therapy can also be administered indirectly via a catheter placed in the SMA.39 This indirect method may be less effective as thrombolytic agent may be diverted through patent branches and collaterals, whilst bypassing the thrombosed venous branches, requiring longer treatment times and higher doses of thrombolytic agent.

Conclusion There are no randomised controlled trials to guide the treatment of AMI and original data are from small case series only. Advances in imaging now enable more accurate diagnosis of AMI with good anatomical information. Traditionally surgery has been the established treatment for AMI, but carries a high morbidity and mortality rate. Endovascular techniques have been reported to have high technical success rates and favourable outcomes when compared to open surgery; however, patient selection bias and a paucity of data limit the conclusions that can be drawn. The use of endovascular options should be reserved for patients without clinical signs of peritonism or radiological signs of irreversible ischaemia. Although more evidence is needed in this area, outcomes may be improved with rapid diagnosis, clinical optimisation, and rapid revascularisation by the best means available. In cases where immediate surgical intervention is not required, the decision to perform endovascular or open surgery should be determined by local expertise and available resources.

Conflict of interest The authors declare no conflict of interest.

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Please cite this article as: Hawthorn BR, Ratnam LA, Acute mesenteric ischaemia: imaging and intervention, Clinical Radiology, https://doi.org/ 10.1016/j.crad.2019.06.001