ACUTE MESENTERIC ISCHAEMIA: THE NEED TO BE AWARE

Dr. Meheshinder Singh

SUMMARY
Acute mesenteric ischaemia is a life threatening surgical condition which carries & high mortality. A delay in diagnosis combined with the premorbid condition of the patient is usually responsible for its poor outcome. This review article highlights the importance of awareness of this condition and discusses the aetiopathogenesis, diagnosis and various modalities of surgical and non surgical management.

Key words: Acute mesenteric ischaemia (AMI), superior mesenteric artery (SMA).

INTRODUCTION
Acute mesenteric ischaemia, though a relatively rare condition, poses a particular surgical challenge because failure to diagnose it early results in death. It refers to a threatened or established ischaemic necrosis of the major part of the bowel and tends to occur in patients of either sex predominantly those above 50 years of age. The mortality from acute mesenteric ischaemia has not changed during the past two decades and unless we are aware of its entity and in the absence of an accurate diagnostic test, it is unlikely to do so.

AETIOLOGY
Acute mesenteric ischaemia (AMI) can be a consequence of 4 basic conditions - embolization, thrombosis of pre existing occlusive disease, non-occlusive mesenteric ischaemia, and mesenteric venous thrombosis. Mesenteric arterial emboli account for 30-50% of cases of AMI. They most commonly arise from a mural thrombus in an infarcted left ventricle (Figure 1) or a clot in patients with atrial fibrillation. Emboli may also arise from atheromatous plaques in the aorta (Table 1). The embolus lodges in the Superior Mesenteric Artery (SMA) a few centimeters from its origin and usually spares the middle colic artery and proximal jejunal branches thereby causing an infarction that is less then that seen following SMA thrombosis. Thrombosis of SMA accounts for 20-25% of cases of AMI. It occurs in an artery already diseased by atheroma and commonly follows a sudden decrease in cardiac output such as in congestive cardiac failure or after a myocardial infarction. Less commonly, hypercoagulable states and certain vasculitic conditions (Table 2) may. precipitate thrombosis. The extent of infarction is much more severe in thrombosis as the proximal part of SMA is usually occluded so that the entire small bowel distal to the ligament of Treitz and the proximal two thirds of the transverse colon are affected. Non-occlusive mesenteric ischaemia represents 15-20% of cases of AMI. It results from inadequate arterial blood flow as a consequence of spasm of mesenteric arteries usually with a background of severe systemic illness or cardiac failure and should always be suspected in a critically ill patient.

Figure 1: ECHO showing a mural thrombus within the left ventricle

Mesenteric venous thrombosis is more common than is generally recognized. It accounts for 10-15% cases of AMI. Venous thrombosis does not always progress to bowel infarction. When thrombosis of only the large veins occur, collateral drainage is often adequate to prevent tissue necrosis. It is only when the small veins and venules of the bowel wall are involved that infarction occurs. Predisposing conditions include portal hypertension, trauma, hypercoaguable states due to factor deficiencies, prolonged use of oral contraceptives or malignancy, and less commonly inflammatory conditions such as diverticulitis.

Table 1: Sources of arterial emboli

Cardiac	• Post acute myacardial infarction • Atrial fibrillation -chronic and paroxysmal • Ventricular aneurysm • Endocarditis - infectious • Cardiomyopathy • Prosthetic heart valves • Atrial myxoma
Non-cardiac	• Aortic aneurysm • Aortic atherosclerosis

Table 2: Factors causing acute thrombosis in an already diseased vessel

Acquired	• Low output states   Congestive cardiac failure,   Myocardial infarction • MyeloproIiferative disorders e.g. polycythaemia vera • Vasculitic disorders e.g. polyarteritis nodosa
Inherited	• Antithrombin 3 deficiency • Protein c deficiency • Protein s deficiency • Dysfibrinogenemia • Dysplasminogenemia

PATHOGENESIS
The consequences of mesenteric vascular occlusion depend upon the vessel involved, the level of occlusion, status of other visceral vessels, the development of collaterals, presence of contributing diseases like cardiac failure and the establishment of reperfusion. Tissue injury results from event; related to ischaemia or by the return of blood flow, either spontaneous or as a result of treatment (reperfusion injury). Complete interruption of oxygen supply to the intestine produces necrosis first at the tips of the villi. Mucosal slough begins within 3 hours after onset of ischaemia and ulceration and bleeding soon become extensive. Full thickness infarction of bowel wall occurs as early as 6 hours. Haemorrhage into the lumen, accumulation of bloody abdominal fluids, perforation, bacterial translocation and death from sepsis and multi organ system failure are the end result. There is increasing recognition of the importance of reperfusion injury. Reperfusion of the affected segment of bowel either from spontaneous events, lysis of clot by medical therapy or arterial reconstruction converts the enzyme xanthinedehydrogenase to xanthine oxidase. This results in the release of oxygen free-radicals (OFR) which destabilize cell membranes, disrupt the mucosal barrier and flood the systemic circulation with mediators of damage to other organs leading to multi system organ failure.

CLINICAL FEATURES
Acute abdominal pain is the initial symptom in 85% of patients with AMI. Pain is severe, poorly localised and the diagnosis should be considered if the pain is unresponsive to narcotic analgesia. The rate of progression is variable but usually is accompanied by abdominal distension, vomiting and passage of mucus and bloody stools. Physical findings in early stages are minimal, resulting in the dictum that AMI is characterised by "pain that is out of proportion to physical findings". Later in the course, pyrexia, abdominal distension, tenderness and guarding occurs. Generalized peritonitis and eventually shock develops if treatment is further delayed. The minority of cases of AMI caused by venous obstruction or non-occlusive mesenteric ischaemia will follow a similar course but at a slower and more variable rate.

DISCUSSION
Acute mesenteric ischaemia is an abdominal catastrophe that carries high morbidity and mortality rates. Current diagnostic methods lack sensitivity and specificity and do not provide adequate information regarding viability of the afffected bowel. Leucocytosis and elevatad serum lactate levels are common^1,2. The other laboratory investigations are of little value. Elevated serum amylase is non-specific. Metabolic acidosis occurs only after advanced ischaemia. Plain abdominal X-rays are also non-specific. An ileus pattern, diffuse distension with air-fluid levels, evidence of bowel wall oedema, or even gas in the bowel wall or within mesenteric or portal veins are some of the findings that may allow a presumptive diagnosis of mesenteric ischaemia. CT scan is not a specific diagnostic study of choice but it is often used to rule out other pathology. However, it exhibits sensitivity and specificity that is found to be higher than conventional radiography. Duplex ultrasonography³ in experienced hands can be accurate in assessing flow in proximal visceral arteries as well as superior mesenteric and portal veins. Gaseous abdominal distension can cause some amount of technical difficulty. Other forms of non-invasive detection include SQUID⁴ (superconducting quantum interference devices) which detects basic electrical rhythm (BER) by measuring the magnetic fields generated by the electrical activity of the smooth muscle of the small bowel. SQUID has been shown to have a high degree of sensitivity and specificity in detecting bowel ischaemia in animal models. The most important diagnostic modality is angiography⁵ It confirms the clinical diagnosis and aids in planning specific therapy. However, some argue that it is time consuming, delays treatment and does not provide information that cannot be determined at laparotomy. Due to the short ischaemic tolerance time of the intestine, diagnostic and therapeutic decisions have to be made under extreme time pressure. The principles of treatment are adequate rehydration, broad-spectrum antibiotics and early surgical intervention. Various studies have shown an improved survival following early diagnosis and aggressive management. Surgical techniques involve revascularisation techniques and/or bowel resection. At laparatomy, the appearance of the bowel wall may vary from pallor to haemorrhagic infarction. Established infarcted bowel should be resected and a second look procedure planed 24-48 hours later. Revascularisation techniques include isolated embolectomy, thromboendarterectomy, bypass techniques and intraarterial thrombolysis^6-10. The main difficulty at operation is to predict intestinal recovery and to accurately assess amount of bowel that needs to be resected. Clinical assessment relies on color, contractility and capillary bleeding, all of which are insensitive¹¹. Several methods have been described which can help judge viability. Doppler ultrasonic flowmeter may be helpful but results with the laser Doppler system proves to be promising¹¹. Another technique known as fluorescein dye technique¹¹ is still under study.

A decision to perform a second look operation is made at the time of initial laparatomy. Since there are no certain predictive criteria for the progression of ischaemia, and not all patients are reoperated for a second look, some patients will undergo unnecessary surgical and anaestheological procedure (negative second look). For this reason a laparoscopic second look is done routinely in some centres^11-13 as a substitute to the standard laparotomy.

CONCLUSION
Acute mesenteric ischaemia is a life threatening vascular emergency which has high mortality rates. The population is usually elderly with coexistent medical illnesses and the diagnosis often delayed. Multisystem organ failure is a common postoperative sequlae. Results can be optimised by prompt diagnosis, adequate resuscitation, effective revascularisation and meticulous postoperative care.

REFERENCES
1. Lange H et al. Usefulness of plasma lactate concentration In diagnosis of acute
abdominal disease Eur J. Surg 1994, Jun; 160 (6-7), 381-4
2. Murray MJ, Gonze MD, Nowak LR, Cobb CF. Serum D(-) lactate levels as an aid to diagnosing acute intestinal ischaemia. Am J Surg 1994, Jun; 167(6);575-8
3. Danse EM, Van Beers BE, Goffette P, Dardenne AN, Laterre PF. Pringot J. Acute
intestinal ischaemia due to occIusion of superior mesenteric arrary: detection with Doppler sonography. J Ultrasound Med 1996 Apr; 15(4); 323-6
4. Seidil SA. Bradshaw LA, Ladipo JK, Wikso JP Jr, Richards WO. Non invasive detection of ischaemic bowel. J Vasc Surg 1999 Aug; 30(2); 309-319.
5. Lock C, Schiolnierkh J. Non occlusive mesenteric ischaemia. Hepatogastroenterology 1995 Jul; 42(3); 234-9.
6. Christensen MC, Lorentzen JE, Schroeder TV. Revascularisation of
atherosclerotic mesenteric arteries. Eur J Vasc Surg 1994 May; 8(3); 297-302
7. McBride KD, Caines PA. Thrombolysis of a partially occluding superior mesenteric artery thromboembolus by infusion of streptokinase. Cardiovasc Intervent Radiol 1994 May 17(3); 164-6.
8. Gentile AT, Moneta GL, Taylor LM Jr, Park TC, McConnell DB, Porter JM. Isolated bypass to the superior mesenteric artery for intestinal ischaemia. Arch Surg 1994 Sept;129(9); 926-31.
9. Bradbury AW, Brittenden J, McBride K, Ruckley CV. Mesenteric ischaemia: rnultidisciplinary approach. Br J Surg 1995 Nov; 82(11):1446-59.
10. An aggressive approach to acute superior mesenteric arterial ischaemia. PA Grace, M Da Costa, A. Qureshi, S Sheehan. P Burke, D Bouchier-Hayes Eur J Vasc Surg 1993; 7:731-732.
11. Ballard JL, Stone WM, Hallett JW, Pairolero PC, Cherry KJ. A critical analysis of adjuvant techniques used to assess bowel viability in acute mesenteric ischaemia. Am Surg. 1993; 59(5):309-11.
12. Sackier JM. Second look laproscopy in management of acute mesenteric ischaemia. Br J Surg 1994; 81(10);154-6.
13. Nassar A. Second look laproscopy in management of acute mesenteric ischaemia. Br J Surg 1994; 81(7); 108-13.

return to main page