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Nov 19, 1992 - Acute intestinal ischaemia. 313. (Fig. 1). A diagnosis of mesenteric embolus was made, but it was too late for embolectomy. The necrotic bowel.
Annals of The Royal College of Surgeons of England (1993) vol. 75, 312-316

Acute intestinal ischaemia: options in surgical management B M Stephenson

MS FRCS Senior Surgical Registrar

A J Thomas

K Shute

I F Lane

MS FRCS Consultant Surgeon

FRCS

Surgical Registrar DM FRCS* Consultant Surgeon

A A Shandall MCh FRCS Consultant Surgeon

Department of Surgery, Royal Gwent Hospital, Newport, Gwent Vascular Unit, University Hospital of Wales, Cardiff

*

Key words: Acute intestinal ischaemia; Massive bowel resection; Exteriorisation

Seven patients (mean age 67 years, range 52-82 years) presented with acute intestinal ischaemia over a 4-year period. Massive bowel resection was performed in ali patients. Exteriorisation and secondary restoration of intestinal continuity was employed in four patients. In two patients a primary anastomosis was performed at the time of resection and one patient underwent a 'second-look' procedure. Massive bowel resection and exteriorisation aliows direct observation of stoma viability, avoids the risk of anastomotic breakdown and should be considered in ali but moribund patients with acute intestinal ischaemia. In elderly patients resection and primary anastomosis may be an alternative option.

Patients with acute intestinal ischaemia are often considered unsalvageable, not only because this catastrophe usually affects an elderly population but also because irreversible systemic changes occur upon revascularisation, resulting in a mortality of over 70% (1-4), although a recent study using an aggressive surgical approach has demonstrated a much lower mortality (5). Indeed, in one series of 274 patients from seven centres the average mortality was 95% (6). In addition, the preoperative diagnosis is often difficult to make as there may be little in the way of abdominal signs. Furthermore, although hypothermia, a persistent metabolic acidosis after resuscitation and a raised leucocyte count is suggestive of the diagnosis, their absence does not rule out the possibility of acute intestinal ischaemia.

Correspondence to: Mr A A Shandall MCh FRCS, Department of Surgery, Royal Gwent Hospital, Newport, Gwent NP9 2UB

The clinical picture of mesenteric arterial embolism in patient in atrial fibrillation is well established but, unfortunately, this recognisable scenario is seen in less than 30% of patients (1-3,7). More commonly, acute intestinal ischaemia is due to arterial and venous thrombosis with 'non-occlusive' ischaemia accounting for 1027% of cases (1,3,4,7). In ischaemia secondary to embolism, superior mesenteric artery (SMA) embolectomy is indicated unless the embolus has lodged distally. However, the surgical management of other causes of ischaemia is both variable and debatable, although it is now recognised that adequate bowel resection and early anticoagulation leads to a better prognosis in cases of venous thrombosis/infarction (8,9). We report our recent experience of patients with acute intestinal ischaemia of variable aetiology managed by a number of surgical techniques. a

Patients The following patients with acute intestinal ischaemia were managed over a 4-year period. Case I

A 56-year-old woman presented with a sudden onset of central abdominal pain and vomiting. Initial abdominal examination was unremarkable and investigations were normal. The following day her pain increased in severity and she became shocked with signs of peritonism. At laparotomy the entire small bowel except the first 25 cm of jejunum and the last 30 cm of the ileum was infarcted

Acute intestinal ischaemia

(Fig. 1). A diagnosis of mesenteric embolus was made, but it was too late for embolectomy. The necrotic bowel was resected and a proximal jejunostomy and distal ileostomy fashioned. Postoperatively she was anticoagulated, treated with broad spectrum antibiotics and given total parenteral nutrition (TPN). She easily became dehydrated as the jejunostomy output was often over 160 ml an hour. This was managed by collecting the output and reinfusing it via the ileostomy. The stomas were closed 2 weeks later and she was discharged 12 days later. An echocardiogram demonstrated a left atrial thrombus and a left ventricular aneurysm and she was warfarinised for life. She quickly regained weight and remains well at 4-year follow-up with her bowels open 2-3 times a day with no signs of malabsorption. Case 2 A 73-year-old man in atrial fibrillation was admitted with a 3-h history of central abdominal pain. Abdominal examination was unremarkable but he had a raised white cell count (17.6). Six hours after admission he deteriorated and at laparotomy the small bowel 50 cm distal to the duodenal-jejunal (D-J) flexure, caecum and lower ascending colon were gangrenous. A weak pulse was felt in the SMA but no pulses were palpable in the small bowel mesentery. A diagnosis of mesenteric embolus was made and the bowel resected with the formation of a jejunostomy and an ascending colon mucous fistula. Other than being digitalised his management was similar to Case 1. Unfortunately, he developed a large sacral pressure sore which progressed to an infected haematoma as he was anticoagulated. He died of septicaemia 20 days after admission.

Case 3 A 52-year-old woman with a long history of postprandial epigastric pain was admitted with an exacerbation of 24 h duration. She was thin with tenderness localised to the epigastrium. A diagnosis of mild pancreatitis was made (serum amylase 540) and she was treated conservatively. The following day she passed bloody stools and deteriorated. At laparotomy the entire small bowel except the proximal 50 cm of jejunum and the terminal 15 cm of ileum was gangrenous. The small bowel was resected and a jejunostomy and ileostomy formed. Two days later the jejunostomy looked ischaemic and a duplex colour flow scan (Fig. 2) showed a > 90% stenosis of the SMA. This was confirmed by an aortogram which also demonstrated an occluded coeliac axis (CA) and collaterals via the inferior mesenteric and internal iliac arteries (Fig. 3). Three days later an aorto-CA and aorto-SMA bypass graft, using autogenous saphenous vein, was performed to augment the blood supply of the remaining fore- and midgut (Fig. 4). The jejunum (now infarcted) was also excised and intestinal continuity restored. She was maintained on TPN and made a good recovery but suffered a fatal myocardial infarction 3 weeks later. Case 4 A 68-year-old man presented with a 4-h history of epigastric pain. He was distressed but had only slight

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tenderness over an easily palpable 4 cm abdominal aortic aneurysm. He was confused and complained of further pain 8 h later. At laparotomy for a suspected leaking aneurysm, the small bowel was ischaemic 30 cm distal to the D-J flexure and extending to the ascending colon. This had been caused by a thrombosis of the SMA 3 cm from its origin. The artery was exposed and thrombectomy performed with subsequent improvement in distal mesenteric pulsation. As the bowel improved in colour and appeared to have been saved, a decision was taken to undertake a second-look laparotomy the following day. At operation the proximal jejunum (approximately 70 cm) appeared normal but the remaining jejunum, ileum and caecum were gangrenous. The bowel was resected and bowel continuity restored. TPN was given for 3 weeks and he was discharged 42 days after admission and remained well for the 2 years he was followed up.

Case 5 A frail 65-year-old woman with a previous myocardial infarction was admitted with a 48-h history of central abdominal pain. She was in uncontrolled atrial fibrillation, hypothermic (35°C) and had signs of peritonitis. After resuscitation a laparotomy revealed gangrenous small bowel except 20 cm at either end. The bowel was resected and the ends exteriorised. Although digitalised, her low cardiac output needed inotropic support in intensive care for 1 week. Management included TPN and passing the jejunal effluent through the ileostomy. Bowel continuity was restored 4 weeks later and she was discharged 46 days after admission. At 1 year later she remains well, on warfarin, with her bowels open 2-4 times a day. Case 6 A 76-year-old man presented with a 12-h history of poorly localised abdominal pain, distension and vomiting. He was dehydrated, pyrexial and had a raised leucocyte count (26). At laparotomy there was a clearly demarcated area of gangrene which extended from 20 cm distal to the D-J flexure to the mid-transverse colon. As pulses were palpable in the mesentery of the viable bowel massive resection and primary anastomosis was performed. He was discharged 17 days later. Histology showed extensive venous infarction with viable resection margins. At 1 year later he had not lost weight and had his bowels open 5 or 6 times a day. Case 7 An 82-year-old woman presented with a 10-h history of generalised abdominal pain after 2 days of vomiting. She was hypotensive, dehydrated and had a marked leucocytosis (WBC 46). After resuscitation a laparotomy revealed infarcted small bowel extending from 50 cm of the D-J flexure to the mid-transverse colon. As the area was clearly demarcated a decision was made to proceed to resection and anastomosis. Her recovery was uncomplicated and she was discharged after 26 days. Histology

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Figure 3. Arteriogram showing an occluded CA, stenosis of the SMA and a collateral circulation via the inferior mesenteric and internal iliac arteries.

Discussion

Figure 1. Operative appearance of massive intestinal ischaemia.

showed infarction but there was no evidence of intrinsic vascular disease in the vessels of the mesenteric pedicle. She remains well 1 year later, although is troubled with occasional symptomatic diarrhoea.

Figure 2. Duplex colour flow scan showing SMA stenosis

(>90%).

The true incidence of mortality from acute intestinal vascular insufficiency is difficult to quantify. However, this condition is certainly not uncommon, with at least 2000 to 2500 deaths per annum over the last decade (1980-1990) in England and Wales (10,11). Much of our knowledge of the epidemiology, aetiology and pathophysiology of acute intestinal ischaemia is as a consequence of the pioneering work of Marston, including an Arris and Gale lecture nearly 30 years ago (12,13). Despite this earlier work, intestinal infarction is still generally considered to have a poor outcome with most series reporting a mortality of 70-90% (1-4,6), although a mortality of 21% has been reported when revascularisation procedures were used (5). Nevertheless, this policy

Figure 4. Duplex colour flow scan demonstrating a functio saphenous vein aorto-CA and aorto-SMA bypass graft.

i

Acute intestinal ischaemia

of 'vascularise at all costs' has rightly been questioned as the vast majority of general surgeons faced with a patient with ischaemic gut can resect rather than revascularise and thus avoid reperfusion injury (14). However, there are few series describing the use of massive bowel resection (MBR) in the management of acute intestinal ischaemia (1,2,4,5,7). Kairaluoma et al. (1) and Hildebrand and Zierler (7) have both achieved a 41% survival after resection, and Sitges-Serra et al. (4) a 54% survival after MBR. Despite these studies being retrospective, these figures are superior to the mortality commonly associated with this condition. After our initial success with this procedure and the improved mortality reported, we continued this approach with these seven cases managed over a 4-year period. Despite the different aetiologies of ischaemia in our cases, MBR was ultimately the only viable surgical option. The mortality in this series was 29% with no deaths attributable to the resection. It is unclear whether exteriorisation was performed in the previous series using MBR (1,2,4,7). However, it is of interest to note that in the Finnish study (1) there was clinical evidence of an anastomotic leak in two of nine patients surviving MBR and primary anastomosis. Similarly, in the Spanish study, 20% of patients undergoing MBR developed enterocutaneous fistulas and over 50% of deaths after MBR were due to 'intractable intra-abdominal infection' (4). No doubt these complications were as a result of ischaemia at the resection margins, and such a complication would certainly have developed had a primary anastomosis been performed in at least our third case. With this in mind it is important to remember that the extent of the true ischaemia is difficult to determine at operation as has been noted when post-mortem examinations were carried out (1). In this respect the measurement of surface tissue oxygen tension may prove to be of value in assessing tissue viability, adequacy of resection and siting of anastomoses (15,16). The early postoperative management of patients undergoing MBR, with or without exteriorisation, is of particular importance. Fluid losses need to be carefully monitored and measures taken to avoid potassium depletion which commonly occurs in the early phase of recovery after MBR. This is especially so if both ileum and colon are resected. Although the nursing staff disliked collecting the proximal stomal effluent, we believe that this was essential in the management of the patient's fluid balance allowing ileal absorption of bile salts, fatty acids and otherwise unabsorbed carbohydrates. Indeed, although we did not observe a significant decrease in the proximal effluent as a result of this policy of fluid replacement, it has been reported to have an inhibitory effect on gastrointestinal secretions (17). However, it is essential that the viability of the distal stoma be ascertained so as to avoid infusion down potentially ischaemic distal bowel. In addition, all except the last two of our patients were started on TPN in the early postoperative period. It is important to realise that the amount of bowel resected is irrelevant, but what matters is the length of viable bowel that remains. It is

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interesting to note that none of our survivors had evidence of malnutrition, and that although diarrhoea was a frequent symptom, at least two patients had regained their original weight. This emphasises the remarkable potential for recovery after MBR and the ability of the remaining bowel to adapt (18). Indeed, in one series there were no metabolic or nutritional problems in the majority of patients surviving MBR (4). Our experiences and review of the literature support the use of MBR in many cases of intestinal ischaemia. In addition, we would recommend exteriorisation, which allows direct observation of stoma viability and thus avoids the risks associated with anastomotic dehiscence. However, if revascularisation is possible extensive resection may be avoided with a 'second-look' operation to confirm bowel viability as recommended by the results of the recent Israeli review (5). This allowed the preservation of approximately 40 cm of jejunum in one of our patients. However, it must be remembered that obviously infarcted bowel needs to be removed at the first operation. Despite recommending MBR and exteriorisation in the management of acute intestinal ischaemia, we chose to perform resection and primary anastomosis in our two oldest patients. This decision was taken because we felt our earlier experiences of problems with fluid balance and the need for a second operation were best avoided in these elderly patients. However, if there had not been clearly demarcated areas of ischaemia this would not have been undertaken. Furthermore, in addition to choosing the most appropriate and beneficial type of surgery in patients with acute intestinal ischaemia, the clinician must be aware of the effects of restoring blood to the ischaemic splanchnic tissue. Combating this reperfusion injury, which leads to the release of oxygenderived free radicals and other depressant factors, with substances such as free-radical scavengers or xanthine oxidase inhibitors may find a role in future clinical practice with further improvement in the mortality figures commonly associated with this condition (14,19). Finally, as 10% of patients with acute intestinal ischaemia give a history of postprandial pain (mesenteric angina) (2,7) and 60-80% have evidence of myocardial disease (1-4,7) and 40% peripheral atheroma (1,4), a simple non-invasive investigation may be of use in identifying those individuals at risk of acute ischaemia/ infarction. In this respect duplex scanning, as used in our third case, may also prove to be of value. Recent studies (20,21) using colour duplex scanners with low-frequency scanheads (2.5 or 3.5 MHz) have suggested that patients in whom the SMA or CA is well-visualised need no further investigation, with arteriography reserved for those in whom scanning demonstrates significant stenosis or occlusion in one or both arteries. Patients with stenosis or occlusions can then be revascularised electively before acute ischaemia ensues. In summary, the outlook of patients with acute ischaemia, from whatever cause, seems to have improved within the last decade. We believe an aggressive approach, rather than the more traditional pessimistic one is necessary to optimise the patient's chance of

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survival. MBR and exteriorisation is an option that should be considered in all but moribund patients in whom acute intestinal ischaemia is discovered at laparotomy (Fig. 1). We would like to thank Mr G H Griffith and Mr J M Price-Thomas for their help.

References 1 Kairaluoma MI, Karkola, P, Heikkinen E, Huttunen R, Mokka REM, Larmi TKI. Mesenteric infarction. Am J Surg 1973; 133: 188-93. 2 Krause MM, Manny J. Acute superior mesenteric arterial occlusion: a plea for early diagnosis. Surgery 1978; 83: 482-5. 3 Wilson C, Gupta R, Gilmour DG, Imrie CW. Acute superior mesenteric ischaemia. Br J Surg 1987; 74: 279-81. 4 Sitges-Serra A, Mas X, Roqueta F, Figueras J, Sanz F. Mesenteric infarction: an analysis of 83 patients with prognostic studies in 44 cases undergoing a massive smallbowel resection. BrJ Surg 1988; 75: 544-8. 5 Levy PJ, Krausz MM, Manny J. Acute mesenteric ischaemia: improved results-a retrospective analysis of ninetytwo patients. Surgery 1990; 107: 372-80. 6 Bergan JJ, Dean RH, Conn JJ, Yas JST. Revascularisation in the treatment of mesenteric infarction. Ann Surg 1975; 182: 430-7. 7 Hildebrand HD, Zierler RE. Mesenteric vascular disease. Am J Surg 1980; 139: 188-92. 8 Abdu RA, Zakhour BJ, Dallis DJ. Mesenteric venous thrombosis-1911 to 1984. Surgery 1987; 101: 383-8. 9 Clavien P-A, Durig M, Harder F. Venous mesenteric infarction: a particular entity. BrJ Surg 1988; 75: 252-5.

10 Office of Population Censuses and Surveys. Mortality Statistics: Causes. 1980 (DH 2). 7: 36. London: HMSO, 1982. 11 Office of Population Censuses and Surveys. Mortality Statistics: Causes. 1990 (DH 2). 17: 46. London: HMSO, 1991. 12 Marston A. Patterns of intestinal ischaemia. Ann R Coll Surg Engl 1964; 35: 151-81. 13 Marston A. Diagnosis and management of intestinal ischaemia. Ann R Coll Surg Engl 1972; 50: 29-44. 14 Marston A. Acute intestinal ischaemia. Resection rather than revascularisation. Br Med J 1990; 301: 1174-5. 15 Shandall A, Lowndes R, Young HL. Colonic anastomotic healing and oxygen tension. BrJ' Surg 1985; 72: 606-9. 16 Sheridan WG, Lowndes RH, Young HL. Tissue oxygen tension as a predictor of colonic anastomotic healing. Dis Colon Rectum 1987; 30: 867-71. 17 Levy E, Palmer DL, Frileux P, Parc R, Huguet C, Loygue J. Inhibition of upper gastrointestinal secretions by reinfusion of succus entericus into the distal bowel. A clinical study of 30 patients with peritonitis and temporary enterostomy. Ann Surg 1983; 198: 596-600. 18 Williamson RCN. Intestinal adaptation. N Engl J Med 1978; 298: 1393-1402 and 1444-50. 19 Clavien P-A. Diagnosis and management of mesenteric infarction. Br7 Surg 1990; 77: 601-3. 20 Moneta GL, Yeager RA, Dalman R, Antonovic R, Hall LD, Porter JM. Duplex ultrasound criteria for diagnosis of splanchnic artery stenosis or occlusion. 7 Vasc Surg 1991; 14: 511-20. 21 Bowersox JC, Zwolak RM, Walsh DB et al. Duplex ultrasonography in the diagnosis of celiac and mesenteric artery occlusive disease. J Vasc Surg 1991; 14: 780-8.

Received 19 November 1992