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Acute Mesenteric Ischaemia 223
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Table 25.2. Repeat blood gas and blood count investigations. Updated
Investigation Finding
Haematology Haemoglobin 10.2 g/dl
Arterial blood gas pH 7.19
White cell count 37,000 × 10
Platelets 235 × 10
pCO
3.1 kPa
2
pO
49.4 kPa
2
–
HCO
11 mmol/l
3
Base excess –15
9
/l
9
/l
intravenous heparin were also given. After 2 h of resuscitation, the patient’s blood
pressure was 130/85 mm Hg, pulse 100 bpm and CVP +8 cm water. She was still in a
lot of pain despite 10 mg of diamorphine, and she was still tachypnoeic. Repeat
blood gas and blood count investigations were as in Table 25.2.
Because the patient was persistently acidotic with an elevated white count and in
severe pain, she was taken to the operating theatre for an emergency laparotomy.
Almost the entire small bowel and most of the large bowel were found to be
ischaemic but viable. There was a pulse in the proximal superior mesenteric artery
(SMA) but nothing was palpable beyond the origin of the middle colic vessel.
Question 4
What operative options are available to achieve restoration of flow to the bowel?
A. Full heparinisation.
B. Catheter thrombectomy.
C. Axillofemoral bypass.
D. Mesenteric bypass with a vein graft.
E. Mesenteric bypass with prosthetic graft.
Clot was removed successfully from the SMA. However, despite the majority of the
bowel receiving a good blood supply, several areas remained dusky in appearance.
Question 5
What features of the bowel’s appearance determine whether it is viable?
A. The presence of peristalsis.
B. Lack of foul odour from the peritoneal cavity.
C. Serosal sheen.
D. Mesenteric pulsation.
E. Active bleeding from the cut surface of the bowel at the time of resection.
224 Vascular Surgery
Question 6
Having determined that an area of the bowel is non-viable, what action should you
take?
A. Revascularise the bowel, then remove that which is non-viable.
B. Remove the non-viable bowel, then revascularise the remaining bowel.
C. Resect all non-viable bowel and primarily anastomose ends; then close the
abdomen.
D. Close the abdomen and start the patient on an intravenous infusion of diamor-
phine.
E. Resect all non-viable bowel and exteriorise viable ends; plan relook laparotomy.
Commentary
The incidence of AMI is approximately 1/100,000 in the UK and USA [1, 2]. AMI is a
life-threatening vascular emergency. It accounts for 0.1 per cent of emergency
admissions [3], and based on several large series it has a mortality of between 60
and 100 per cent [3–7]. Females are affected twice as often as males, and the median
age at presentation is 70 years [6].
The clinical presentation is often not as clear-cut as described in the case above.
However, some if not all of the described features will be present. One must have a
high index of clinical suspicion in anyone aged over 55 years who presents with
abdominal pain out of proportion to the physical signs elicited on abdominal examination [8]. The diagnosis should also be considered in patients with known peripheral arterial disease and abdominal pain. The triad of abdominal pain, a cardiac
source of embolus and gut emptying, as described by Klass [9], make AMI the most
likely diagnosis. In addition to this triad, the finding of a marked leucocytosis,
metabolic acidosis and hyperamylasaemia are also suggestive of AMI. It is also not
unusual for there to have been a history of previous embolic events [8]. Pancreatitis
can be difficult to differentiate from AMI, and laparotomy is indicated if suspicion
of AMI is aroused. [Q1: E]
Defining the aetiology of AMI is important as the different causes have different
treatments. The most common presentation, as described in our case, is of superior
mesenteric embolus; this accounts for about 50 per cent of all cases [3, 5–7]. The
usual source for these clots is the atria in patients in atrial fibrillation or the ventricle if the patient has recently sustained a myocardial infarction. Another potential
source of emboli is atheroma from the aortic wall following radiological procedures
in which catheters and guidewires have been passed up the aorta. The consequence
of such an event can be catastrophic, as the mesenteric circulation has not had time
to develop a collateral circulation.
The next most frequent aetiology is SMA thrombosis, which accounts for between
25 and 50 per cent of cases [3, 5-7]. This results from progression of atheromatous
disease at the origin of the SMA. It is important to note that a long-standing stenosis may have caused symptoms of chronic mesenteric ischaemia in the months
before its ultimate occlusion [10]. Therefore, in a patient with pre-existing symp-
Acute Mesenteric Ischaemia 225
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toms of mesenteric ischaemia, sudden onset of abdominal pain should be regarded
as AMI until proven otherwise.
Non-occlusive mesenteric ischaemia (NOMI), first described by Ende in 1958
[11], is the next most frequently encountered condition, occurring in about 20 per
cent of cases [3, 5, 6]. In this situation, the patient is often critically ill from another
cause and the mesenteric ischaemia is due to vasoconstriction leading to reduced
flow in the splanchnic circulation. This may be due to cardiogenic shock, hypovolaemia or vasoconstricting inotropes. Even after reversal of shock, mesenteric
hypoperfusion may persist for several hours [12, 13].
Mesenteric venous thrombosis (MVT) is the least common cause and accounts
for about 5 per cent of AMI [14–16]. The thrombotic process is thought to start in
the superior mesenteric vein and spreads to the portal vein; the inferior mesenteric vein is usually spared. The onset of symptoms is more insidious and may
have a history of several days. It is caused by the same provoking factors that one
finds in any thrombotic situation: sluggish flow, clotting abnormality and vessel
wall damage (Virchow’s triad). It is associated most commonly with hypercoagulable states, abdominal trauma or intra-abdominal sepsis [17–20]. The diagnosis
is often made at laparotomy and encompasses a spectrum of severity from segmental mesenteric venous thrombosis to the entire portal vein being thrombosed.
[Q2: B, E]
Diagnostic confirmation of AMI poses a dilemma. Should one delay in order to
confirm a suspicion and risk converting a salvageable situation into a non-salvageable one [21]? There is little evidence on which to base sound advice. However, if
the patient is cardiovascularly stable with minimal symptoms, and one has prompt
access to angiography, then this provides accurate diagnosis (Fig. 25.1). Some
authors recommend colour-flow duplex at the bedside during the resuscitation
phase [22, 23]; this procedure is less time-consuming than angiography, but it
requires considerable skill that is not always available. Furthermore, good views are
often hampered by obesity and/or overlying bowel gas.
Transthoracic echocardiography is useful in identifying a cardiac source for
emboli and may help in making the decision regarding postoperative anticoagulation. However, it is not as sensitive as transoesophageal echo in searching for left
atrial emboli and may waste valuable time.
Contrast-enhanced CT may be of use in identifying mesenteric venous thrombosis [24]. This will not prevent laparotomy as bowel resection may well be necessary.
If there is clear evidence of peritonism and a high index of suspicion for AMI, then
the patient should be resuscitated rapidly and this should be followed by urgent
laparotomy. [Q3: B, E]
In order to answer Question 4, one has to be confident of the aetiology of
AMI. In our case, there is embolus in the SMA. The abdomen should be
approached through a long midline incision, which will afford excellent exposure. Having entered the abdomen, a quick survey of the viscera and extent of
ischaemia should give some information on the aetiology of the AMI (see
below). At this point, the main aim of surgery is to restore flow to the ischaemic
viscera if viable. In order to do this, the transverse mesocolon is elevated and
the ligament of Treitz identified and the fourth part of the duodenum mobilised.
The root of the mesentery is palpated to feel for the SMA pulse. If, as in our
case, the AMI is due to an embolic event, then a proximal SMA pulse should be
palpable and the duodenojejunal flexure and proximal few centimetres of
jejunum should be viable. The emboli usually lodge at a variable site 3–8 cm
226 Vascular Surgery
Fig. 25.1.
Narrowed atherosclerotic aorta with no coeliac or superior mesenteric filling.
from the origin of the SMA, usually at the point where the middle colic artery
arises [6, 8, 21] (Fig. 25.2a, b).
In order to expose the SMA, the inferior leaflet of the mesocolon is entered along
the course of the vessel and a 5-cm section of artery is dissected out and slung with
Silastic sloops. At this point, if the patient has not been heparinised previously, then
they should be given an intravenous dose of 5000 units of unfractionated heparin. A
longitudinal arteriotomy is made in the cleared SMA (on the left margin of the
vessel, to permit easier graft placement, should a bypass be necessary) [21], and a
size 3 or 4 Fogarty embolectomy catheter is passed up and down the vessel to
retrieve the embolus. Once adequate backward and forward flow has been achieved,
the vessel should be flushed with heparinised saline; the arteriotomy can then be
closed primarily or with a patch (depending on size), using a 6/0 or 7/0 Prolene
suture.
At this point, the anaesthetist should be warned that you are about to reperfuse
the viscera. Metabolites that have accumulated in the ischaemic viscera will pass
rapidly from the mesenteric venous circulation into the systemic circulation, which
can precipitate circulatory collapse and, over several hours, result in the development of systemic inflammatory response syndrome (SIRS). There is no point in
revascularising dead bowel; indeed, this is dangerous. Irrefutably dead bowel
should be removed before revascularisation. It is important to note that if, on
Acute Mesenteric Ischaemia 227
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a
b
Fig. 25.2. a, b
Patchy mid-gut infarction due to atherosclerotic occlusion of superior mesenteric artery.
opening the abdomen, the entire small bowel is black and irreversibly ischaemic,
then the most appropriate thing to do is close the abdomen and keep the patient
comfortable with morphine: death will usually follow within a matter of hours.
In the event that there is no pulse palpable at the SMA origin, then the revascular-
isation strategies are similar to those for chronic visceral ischaemia (see Chapter
24). In this case, attempts at thrombectomy will fail as the catheter will not cross the
occlusion. The options available are retrograde bypass from the infrarenal aorta to
the SMA, antegrade bypass from the supracoeliac aorta (with concomitant revascularisation of the coeliac trunk if it is occluded), aortomesenteric endarterectomy, or
side-to-side anastomosis between the SMA and aorta. Prosthetic material should be
avoided since transmural migration of bacteria is likely to contaminate the graft.
Also, if the lower aorta and iliac systems are heavily calcified, then it may be better
228 Vascular Surgery
to select the supracoeliac aorta for the inflow site of the bypass. The use of a temporary shunt for immediate reperfusion while the bypass is being constructed seems
sensible [21].
At this point in the procedure, the viscera need to be inspected again and any
dubiously viable bowel resected. If the patient is otherwise young and fit, then it
may be better to resect all the necrotic bowel, exteriorise the remaining ends, and
consider long-term total parenteral nutrition or small-bowel transplantation. If
there is no evidence of arterial compromise and a pulse is palpable in the SMA, then
one should suspect either NOMI or MVT.
NOMI usually results in widespread patchy ischaemia. Treatment entails resection of obviously non-viable bowel, attempting to be as conservative as possible.
The remaining bowel must be inspected at a second-look laparotomy 24–48 h later.
During surgery, several strategies have been described to improve mesenteric flow:
a combination of systemic dopamine and an opiate epidural [25], papaverine infusion (30–60 mg/h) into the SMA either via direct puncture fine bore or angiographically placed catheter [13, 26, 27]. At relook laparotomy, the extent of the ischaemia
should be reassessed; treatment may need to be abandoned if the gangrene is progressing. Mortality of this condition is depressingly high at 70–80% despite the therapeutic measures outlined above [13].
The classic laparotomy findings in MVT are ascites and swollen omentum with
bowel infarction. Like NOMI, MVT is managed by resection of non-viable bowel,
which is most frequently sharply demarcated and found in the mid-small bowel.
Again, second-look laparotomy is mandatory. Anticoagulation with heparin and
then warfarin is mandatory in view of the high incidence of recurrent MVT.
Investigation of any underlying prothrombotic disorder along with long-term anticoagulation improves survival [28, 29].
Thrombolysis has been used successfully in MVT in two studies where the diagnosis had been established by non-invasive means and peritoneal signs had not
developed [30, 31]. Venous thrombectomy has also been reported to be successful
in a handful of cases [19, 32–34]. This procedure is likely to be difficult, as the peritoneum is usually oedematous. [Q4: B, D]
The classic features of ischaemia are oedema, loss of peristalsis, loss of surface
sheen, staining of the serosa, absent mesenteric pulsation, or frank gangrene with or
without perforation (Fig. 25.3). The decision at surgery is, after revascularisation
(providing it was appropriate or feasible), how much small bowel to resect. Once
there is good flow to the viscera, then reversibly ischaemic segments should declare
themselves viable and the rest will need to be resected. Other adjuncts to inspection
and palpation are continuous-wave Doppler, pulse oximetry and fluorescein dye
[35]. The next question is whether to exteriorise or anastomose the open ends of the
bowel. The arguments against exteriorising are that many stomata may be necessary
and they do not guarantee that the intervening segments may not subsequently
become ischaemic; however, this is extremely safe and avoids the complication of a
necrotic anastomosis. Performing primary anastomoses and leaving the abdomen
open and covering it with a see-through bag (a cut-open bag of saline) [36] allows
direct visualisation of the viscera at all times; second-look laparotomy can then be
planned on the appearance of the gut [36]. If all looks well by 72 h and the patient’s
condition is stabilising, then they can be returned to theatre for planned abdominal
closure. [Q5: A, C, E], [Q6: B, E]
The short-term management of these cases is demanding on staff and time, but if
best results are to be achieved, then no short cuts can be taken.
Acute Mesenteric Ischaemia 229
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Fig. 25.3.
Gut showing features of fixed staining.
AMI is a treatable vascular emergency. It requires a high index of clinical suspicion, rapid aggressive resuscitation and diagnostic manoeuvres to determine the
specific underlying cause. This will allow a prompt, directed revascularisation procedure after optimisation of cardiac performance, or correction of a hypercoagulable state. This effort is directed at maximising the amount of salvageable bowel.
These strategies are the cornerstones for a successful outcome in this life-threatening vascular catastrophe.
References
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2. Stemmer EA, Connolly JE. Mesenteric vascular insufficiency. Identification and management. Calif
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3. Stoney RJ, Cunningham CG. Acute mesenteric ischemia. Surgery 1993;114:489–90.
4. Klempnauer J, Grothues F, Bektas H, Pichlmayr R. Long-term results after surgery for acute mesenteric ischemia. Surgery 1997;121:239–43.
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6. McKinsey JF, Gewertz BL. Acute mesenteric ischemia. Surg Clin North Am 1997;77:307–18.
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8. Bergan JJ. Diagnosis of acute intestinal ischaemia. Semin Vasc Surg 1990;3:143–8.
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10. Dunphy JE. Abdominal pain of vascular origin. Am J Med Sci 1936;192:109–12.
11. Ende N. Infarction of the bowel in cardiac failure. N Engl J Med 1958;258:879–81.
12. Fry RE, Huber PJ, Ramsey KL, Fry WJ. Infrarenal aortic occlusion, colonic blood flow, and the effect
of nitroglycerin afterload reduction. Surgery 1984;95:479–86.
13. Boley SJ, Sprayregan S, Siegelman SS, Veith FJ. Initial results from an aggressive roentgenological
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14. Rhee RY, Gloviczki P. Mesenteric venous thrombosis. Surg Clin North Am 1997;77:327–38.
15. Bassiouney HS. Non-occlusive mesenteric ischaemia. Surg Clin North Am 1997;77:319–26.
16. Krupski WC, Selzman CH, Whitehill TA. Unusual causes of mesenteric ischaemia. Surg Clin North
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17. Clavien PA, Durig M, Harder F. Venous mesenteric infarction: a particular entity. Br J Surg
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230 Vascular Surgery
18. Grewal HP, Barrie WW. Congenital antithrombin III deficiency causing mesenteric venous infarction: a lesson to remember – a case history. Angiology 1992;43:618–20.
19. Vates P, Cumber PM, Sanderson S, Harrison BJ. Mesenteric venous thrombosis due to protein C
deficiency. Clin Lab Haematol 1991;13:137–9.
20. Tossou H, Iglicki F, Casadevall N, Delamarre J, Dupas JL, Capron JP. Superior mesenteric vein
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21. Whitehill TA, Rutherford RB. Acute intestinal ischaemia caused by arterial occlusions: optimal management to improve survival. Semin Vasc Surg 1990;3:149–56.
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26. Renovascular Hypertension
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David Bergqvist and Martin Björck
A 58-year-old male smoker had had essential hypertension for about 15 years. It
was well balanced with diuretics. He came for regular checks over the years. At
such a check 3 months ago, his blood pressure was 195/110 mm Hg. With the
addition of a beta-blocker and an angiotensin-converting enzyme (ACE)
inhibitor, it was possible to keep the pressure at around 180/100 mm Hg; thus it
was not an optimal treatment result. Creatinine had increased over the last 3
months from 90 to 180–200 µmol/l. The patient lived an active life and felt well.
Question 1
Which of the following statements support your suspicion that the patient has renovascular hypertension?
A. The patient has had essential hypertension for more than 10 years.
B. There is difficulty in controlling the blood pressure with three different drugs.
C. There was an increase in serum creatinine when starting ACE inhibitor
treatment.
D. There is an absence of an epigastric bruit.
Question 2
What is the best investigation to carry out to decide whether the hypertension has a
renovascular origin?
A. Renin in serum.
B. Renography with captopril provocation.
C. Magnetic resonance angiography (MRA).
231
232 Vascular Surgery
D. Duplex scanning.
E. Angiography with pressure gradient.
In this patient, an isotope renogram showed a prolonged uptake on the left side
after captopril provocation. Duplex investigation showed a peak systolic velocity in
the left renal artery of 2.7 m/s with normal findings on the right side. Both kidneys
measured about 9 cm in length, the left being perhaps 0.5 cm shorter. MR angiography showed a left-sided ostial stenosis with a suspect post-stenotic dilatation. It
was decided to perform an angiography with the aim to establish whether there was
a left-sided stenosis, and if there was to give a basis for deciding the optimal treatment. The suspicion of a left-sided stenosis was verified. It was localised near the
aortic wall. The narrowest part of the renal artery was about 1.5 mm, with a distinct
post-stenotic dilation. A pressure gradient of 40 mm Hg was measured. Corkscrew
collaterals were seen along the ureter.
Question 3
What is the first treatment option to normalise the renal artery stenosis?
A. Aortorenal bypass.
B. Thromboendarterectomy.
C. Percutaneous transluminal angioplasty (PTA) with stent.
D. PTA.
E. Nephrectomy.
Question 4
What is the main complication that may occur directly after renal artery PTA?
A. Arterial rupture.
B. Occlusion.
C. Microembolisation.
The patient underwent dilation with a stent without complications and was
sent home the day after treatment in good condition. During the next 3 weeks,
he was able to stop taking the beta-blocker and ACE inhibitor, and his blood
pressure was maintained at around 160/90 mm Hg. Creatinine was around
100 µmol/l.
Question 5
How should the patient be followed up?
A. Serum creatinine.
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