Sie sind auf Seite 1von 11

Acta chir belg, 2005, 105, 344-354

Acute Mesenteric Ischaemia


N. J. Menon, A. M. Amin, A. Mohammed, G. Hamilton
Academic Department of Surgery, The Royal Free and University College Medical School, London, U.K.

Key words. Mesenteric vascular occlusion ; mesenteric arteries ; mesenteric veins ; thrombosis ; embolism ; surgery ;
angioplasty.
Abstract. Acute Mesenteric Ischaemia (AMI) is an uncommon vascular emergency where the diagnosis is often difficult and overlooked and delay in diagnosis results in a grave outcome. Although extravascular events like intussusception, volvulus, strangulated hernia and adhesive obstruction in neglected cases can result intestinal gangrene, this contribution will be limited to acute mesenteric ischaemia as a primary event. AMI consists of four pathologic processes
(arterial thrombosis, arterial embolism, Non Occlusive Mesenteric Ischaemia (NOMI) and mesenteric venous thrombosis (MVT)) with similar clinical presentation and one potentially fatal pathological endpoint- intestinal gangrene. The
clinical setting and the patients risk profile often give the clue to the etiological process while the presentation is dominated by severe unrelenting abdominal pain out of proportion to the physical findings. The key to the successful management depends on the surgeons ability to suspect the diagnosis, pursue appropriate investigations and institute
aggressive treatment. The mortality remains high due to difficulty and delay in the diagnosis (1).

Introduction
Mesenteric ischaemia was first described by Antonio
Beniviene in the 15th century and later by Virchow in the
19th century (2). The incidence of AMI is increasing parallel to the ageing patient population. The autopsy series
in 1967 of OTTINGER and AUSTEN reported a rate of
8.8 cases of AMI per 10,000 hospital admissions (3).
STONEY and CUNNINGHAM in later years observed an incidence rate of 1 in 1000 hospital admissions (4).
Mortality rates for elderly population over the age of
60 carries a relative risk ratio of 3.0 compared to
younger patients (5). Early intervention is crucial and
the potential for intestinal viability is 100% when symptoms are less than 12 hours, 56% if symptoms are 12 to
24 hours and only 18% if symptoms have been neglected for over 24 hours before diagnosis (6).
Anatomical Considerations
The arterial circulation to the gut is served by three
unpaired anterior branches of aorta namely coeliac,
superior and inferior mesenteric arteries (Fig. 1 & 2).
They can develop extensive collaterals to supply areas of
relative ischaemia in the mesenteric circulation, as often
happens with chronic mesenteric ischaemia. This
explains why vascular occlusion is well tolerated as evidenced by the lack of clinically significant intestinal
ischaemia despite the high prevalence of atherosclerotic
disease of the aorta and visceral arteries quoted in upto

35-70% of unselected patients in autopsy series (7).


Clinical ischaemia results when the Superior Mesenteric
Artery (SMA) is occluded in combination with one of
the other two arteries. However, these collaterals are
insufficient when an acute embolic insult occurs in
mesenteric circulation.Certain collateral patterns are
well recognised. When either the coeliac or superior
mesenteric artery is compromised, the main collateral
circulation is by the gastro duodenal or pancreatico duodenal arteries. The main collateral channels between
the SMA and Inferior Mesenteric Artery (IMA) occur in
the region of the splenic flexure and middle colic arteries through the marginal artery of Drummond and the
arch of Riolan (an ascending branch of the left colic
artery anastomosing with the branches of SMA).In presence of an IMA occlusion, another important collateral
circulation is between internal iliac artery and the left
colic artery via the superior haemorrhoidal arteries.
An embolus lodges preferentially into the SMA due to
its oblique angle of emergence from the aorta. The
occlusion is usually distal to the origin of pancreaticoduodenal and the middle colic branches, which allows
some blood flow to the midgut to be maintained. The
stomach, duodenum and proximal jejunum are spared
with ischaemia extending to the mid transverse colon.
The combination of proximal SMA pulsation and jejunal
sparing are important intraoperative findings of prognostic significance. On the other hand, thrombosis of
SMA occurs at the origin of the artery. In contrast to the
embolic occlusion, the proximal SMA pulse is absent

Acute Mesenteric Ischaemia

345

Fig. 2
Collateral circulation between SMA and IMA territories

Fig. 1
Mesenteric collateral circulation

and the distribution of ischaemia is much more extensive. Only the stomach, duodenum and the distal colon
are spared.
Physiological considerations
About 10 to 20% of the resting cardiac output flows
through the visceral circulation (500 to 1200 ml) and
three fourth of this blood flow preferentially supplies the
mucosa due to its high metabolic activity. The remaining
25% supplies the submucosal and serosal layers of the
gut. When the blood flow becomes critical, mucosal
ischaemia results first and serosal ischaemia occurs
later. Mucosal ischaemia leads to severe unrelenting
periumblical or epigastric visceral pain explaining the
paucity of clinical signs initially i.e. a soft abdomen and
this can be associated with increased bowel irritability
leading to explosive diarrhoea and copious vomiting.
Biochemically, this gives rise to early metabolic acidosis, high anion gap, increased serum lactate and hyperamylasemia. This mucosal ischaemia triggers translocation of bacteria initiating sepsis with fever and marked
leucocytosis, proceeding rapidly to multiorgan failure.
Successful reperfusion releases free radicals causing an
inflammatory response with release of many cytokines,
activated leucocytes and inflammatory mediators. This
results in local mucosal and hepatic inflammation and
systemic effects leading to multiorgan failure (8).

The SMA increases blood flow after eating proportionate to the metabolic activity of mucosa for absorption. This postprandial hyperaemia is not seen in the
coeliac artery. In chronic ischaemia, the bowel becomes
relatively hypoxic after a meal and this is characterised
by recurrent severe postprandial pain (abdominal angina), sitophobia (food fear), and strikingly apparent
weight loss. This history is elicitable in over 65% of the
patients with acute thrombosis (5).
Mesenteric vasoconstriction is a normal physiological response to shock mediated largely by the renin
angiotensin axis (9). In the face of persistent and prolonged hypotension, mesenteric ischaemia can result in
the absence of any mechanical obstruction. This distinct
entity is termed as Non Occlusive Mesenteric Ischaemia
(NOMI).
Aetiology
Mesenteric ischaemia could be thrombotic or nonthrombotic in origin. Non occlusive mesenteric
ischaemia, the dominant cause of non-thrombotic
mesenteric ischaemia, results from low flow states
whereas thrombotic causes include arterial embolism,
arterial thrombosis and mesenteric venous thrombosis.
Most cases are caused by emboli (64%), followed by
arterial thrombosis (27%), venous thrombosis (3.5%)
and NOMI (4.8%) (10). The disease usually presents
after the sixth decade and is three times more common
in women and it is likely that the patient would have atherosclerotic disease in other vascular beds. A summary
of causes is presented in Table 1.
Arterial emboli
The SMA is the most common site of embolic occlusion
although the coeliac artery can also be affected. The

346

N. J. Menon et al.
Table 1
Causes of Acute Mesenteric Ischaemia

1) Emboli (50%)
Cardiac Causes
Atrial Fibrillation
Valvular Diseases
Mural Thrombosis
Aortic Causes
Tumours
Iatrogenic
Cholesterol Embolisation
2) Thrombosis (25%)
Acute occlusion of Chronic Mesenteric Ischaemia
Vasculitis
Fibromuscular Dysplasia
Trauma
Dissection
Cocaine Abuse
3) Non Occlusive Mesenteric Ischaemia (20%)
Cardiac Failure
Cardio Pulmonary Bypass
Systemic Hypotension
Septic Shock
4) Mesenteric Venous Thrombosis (5%)
Primary causes
Protein C Deficiency
Protein S Deficiency
Antithrombin III Deficiency
Factor V Leiden Deficiency
Secondary causes
Paraneoplastic syndrome
Pancreatitis
Portal Hypertension
Previous sclerotherapy for oesophageal varices
Postoperative
Trauma
Oral contraceptives
5) Extravascular Causes
Bands, Strangulated Hernia, Volvulus, Intussusception

commonest source of an embolus is cardiac usually secondary to atrial fibrillation. Less common causes are
mural thrombus following an acute myocardial infarction, paradoxical emboli through septal defects, cardiomyopathies, valvular diseases, endocarditis, and atrial myxoma. A history of previous embolic events is not
uncommon and upto a third of patients with an SMA
embolus have a history of antecedent embolic event
(11). The aorta can be a rare source of embolism from
atheromatous ulcers or more rarely from primary aortic
tumour (12, 13).
Arterial thrombosis
SMA thrombosis may occur as a result of SMA stenosis
that has not been previously diagnosed or treated.
Characteristically, the patient reports postprandial pain
and food fear with severe weight loss. The typical

Fig. 3
Occlusion of SMA at origin (black arrowhead) with reformation of the distal segment via marginal artery of Drummond.

Fig. 4
Patient with renal artery stenosis (white arrow) and complete
occlusion of IMA (black arrowhead). Note the presence of aortoiliac stents (white arrowhead).

patient is a thin female and a heavy smoker with evidence of widespread arterial disease including previous
myocardial infarction or claudication.

Acute Mesenteric Ischaemia


In young patients, fibromuscular dysplasia (14) and
intravenous cocaine abuse (15) should be considered.
The extent of intestinal ischaemia secondary to intravenous cocaine abuse tends to be focal and less severe
than that seen with atherosclerotic thrombosis. The
mechanism of ischaemia appears to be occlusive rather
than due to vasospasm. Mesenteric ischaemia should be
considered in the differential diagnosis when evaluating
a young patient with a history of cocaine abuse presenting with an acute abdomen. Another consideration in
unusual setting is screening for thrombophilia as in
hyperhomocystinemia or 20210 A prothrombin gene
mutation (16, 17).
Other rare causes for mesenteric occlusion include
vasculitis (18), sickle cell disease, isolated SMA dissections (19), vascular toxicity following chemotherapy
with 5-FU, cisplatin and vincristine (20) and occlusion
by Schistosoma mansoni infection (21).
Mesenteric Venous Thrombosis
Mesenteric venous thrombosis (MVT) is rare and
accounts for 5 to 15% of all acute mesenteric ischaemia.
This entity was first described by Elliot in 1895 but characterised by WARREN and EBERHARD in 1935 (22). It is
classified as primary or secondary MVT depending on
the aetiology. Primary thrombosis is most commonly
due to hereditary or acquired hypercoagulation disorders. Deficiency of protein C, protein S, Antithrombin
III, and factor V Leiden could be discovered on screening for thrombophilia ; but these proteins could be falsely low in patients with acute thrombosis. Secondary
MVT may follow hypercoagulable states, portal venous
stasis and hypertension, previous sclerotherapy for
varices, intra abdominal infection, inflammation or
malignancy, use of oral contraceptive pills and splenectomy. Long term anticoagulation is required for the
treatment of MVT because of high recurrence rates.
60% patients give previous history of deep venous
thrombosis (23). The clinical presentation is usually less
acute than that of arterial occlusion. Severe but vague
abdominal pain that tends to be colicky and slowly progressive is usually present. Few abdominal signs are present except tenderness, distension and decreased bowel
sounds. The pain again is out of proportion to the clinical findings. Faecal occult blood is present in the majority of patients. Low grade pyrexia and associated leucocytosis are frequent (24, 25). Frank peritonitis is seen
only when transmural infraction or perforation has
occurred. When thrombosis involves the portal or
splenic veins, the initial presentation may be variceal
bleeding, splenomegaly or ascites (26). Macroscopically
at surgery, there is usually serosanguinous ascitic fluid
and the affected bowel segment is cyanotic and oedematous with rubbery texture. Mesenteric pulsations are pre-

347
sent but the veins contain fresh thrombus that extrude
when the veins are cut. Infarction is most common in the
mid bowel. Involvement of the inferior mesenteric vein
and large bowel is unusual. Mortality for MVT with
involvement of the Superior Mesenteric Vein or Portal
vein is about 30% (11).
Nonocclusive mesenteric ischaemia (NOMI)
About 20% of patients with AMI have nonocclusive
ischaemia (11). NOMI typically occurs in the intensive
care setting. These patients have shock either cardiogenic or septic. The mesenteric insult is usually aggravated by the use of inotropic agents such as noradrenalin (alpha agonist causing generalised vasoconstriction).
Long term dialysis patients are another group who are at
high risk for NOMI. The severe and rapid fluid shift
associated with the dialysis is contributory to the
abdominal symptoms (27, 28). Other groups of patients
who are likely to present with NOMI are patients with
myocardial infarction, congestive cardiac failure,
following major abdominal and cardiac surgery and
cardiopulmonary bypass. Digitalis preparations tend to
cause splanchnic arterial and venous contraction and this
is incriminated in the cardiac patients. Watershed areas
of mesenteric circulation in the region of the splenic
flexure tend to be affected with NOMI.
Another group which is vulnerable to NOMI is the
surgical post-operative or polytrauma patient receiving
enteral feeding in the intensive care unit. The reported
incidence of AMI in this group is 0.3 to 8.5% (11). The
increased demand from enteric feeding fails to be met by
the systemic hypoperfusion and the mesenteric vasoconstriction. The diagnosis is difficult to make since the
patients are often unable to alert the attention to the
abdomen. Before this entity was recognised, the mortality was nearly 100% in cardiac patients following use of
vasopressors, but the mortality associated with NOMI
has decreased with increasing awareness and increasing
use of vasodilators and afterload reducing agents.
Iatrogenic intestinal ischaemia
Intra-aortic manipulations related to interventional radiological procedures or intra-aortic balloon pumps following cardiac surgery can lead to visceral malperfusion (29). Embolisation that results is usually global,
involving the kidneys, pelvis and lower limbs as well as
the viscera and hence the high mortality. The ideal treatment is not known but intuitively full intravenous anticoagulation unless specifically contraindicated, appropriate fluid resuscitation and infusion of prostacyclin or
its analogues appear to be justified. Cholesterol emboli
may be suspected by an eosinophilia in the blood film.
This may occur in patients undergoing systemic

348

N. J. Menon et al.

thrombolysis or anticoagulation and with aortic manipulation. Anticoagulation is relatively contraindicated and
the use of statins might be beneficial to stabilize the
plaque.
Left colonic Ischaemia can occur following aortic
reconstruction (Fig. 5-6) (30). It is more common following aneurysm repair after ligation of a patent IMA.
The quoted incidence is 2% (ranging from 0.2% to
10%). Mortality in this condition is 40 to 50% and
approaching 90% if there is full thickness bowel wall
ischaemia (31). To reduce the risk of colonic ischaemia
following aortic surgery, it is imperative that the surgeon
is satisfied with the colour and perfusion of the left
colon prior to closure of the laparotomy. If the IMA had
not been back bleeding on opening the infrarenal aorta,
consideration should be given to reimplanting the IMA
back on to the aortic graft. Diagnosis of ischaemic
colitis can be difficult in the postoperative period and
depends on high index of suspicion. Diarrhoea especially
if bloody should prompt urgent bedside sigmoidoscopy.
A leucocytosis greater than 20000, fever and shock and
severe metabolic acidosis should alert the surgeon to the
possibility of severe colonic ischaemia.
Clinical Presentation
Severe abdominal pain is the cardinal presentation of
AMI. This can be sudden and dramatic in a previously
well and asymptomatic patient (embolism), recurrent
abdominal pain precipitating into unrelenting pain
(thrombosis) or vague colicky abdominal pain which is
progressive over 1 to 2 weeks (MVT). This is often
accompanied by copious vomiting and explosive diarrhoea and intense urge to defaecate. In the unconscious
patient, abdominal distension, gastrointestinal bleeding,
occult sepsis (leucocytosis or fever) and worsening
metabolic acidosis may be the subtle presenting features. Physical examination may reveal a soft abdomen
with non-specific abdominal distension. Peritonism or
blood in the stool or vomitus indicates advanced gastrointestinal ischaemia with likely intestinal gangrene
and is generally a late clinical feature. The paucity of
clinical signs initially to alert the surgeon remains the
main reason for the missed or delayed diagnosis.
Diagnosis
In a patient with a known embolic source, evidence of
widespread atherosclerosis and hypercoagulable state,
the combination of severe abdominal pain out of proportion to the clinical findings should heighten the suspicion of mesenteric ischaemia. Delay in diagnosis contributes directly to ischaemic damage. Biochemical
markers include lactic acidosis, leucocytosis, and raised
CRP (10, 32-34).

Fig. 5
Lateral aortogram of the same patient showing complete occlusion of IMA (arrowhead) and critical stenosis of SMA (arrow).

Elevation of serum inorganic phosphate levels have


been proposed as a marker of mesenteric Ischaemia, but
this only occurs in a third of patients with AMI (32, 34).

Acute Mesenteric Ischaemia

349

Fig. 6
Same patient after renal revacularisation showing ischaemia in the IMA territory.

However, in those patients who did have elevated phosphate levels, it predicted extensive injury and poor prognosis (35). The fibrinolytic marker D-dimer is elevated
in thrombo-embolic occlusion of the SMA, although
levels are also raised in other conditions of acute bowel
ischaemia such as strangulation (36). Normal levels may
serve to exclude the AMI (37).
Animal studies have suggested intestinal fatty acid
binding protein (I-FABP) as a serum marker reflecting
bowel ischaemia. Early human studies show promise, as
patients with ischemic bowel disease demonstrate significantly higher I-FABP levels than either healthy subjects or patients with acute abdominal pain. Patients
with mesenteric infarction had the highest serum IFABP levels (38).
Radiology
Plain abdominal X-ray may reveal distended bowel
loops with thumb printing suggestive of mucosal oedema and gas in the bowel wall or portal vein which is a
late and ominous finding in neglected cases.
Unfortunately plain films are not helpful in most cases.
However they are useful to exclude other causes of acute
abdomen like perforation and obstruction.
Abdominal Computerised Tomogram (CT) is increasingly used due to its universal availability and noninvasive nature. Contrast enhancement allows direct visualisation of the thrombus or embolus with multislice techniques (39). Ancillary evidence of mesenteric ischaemia

includes intramural or portal venous gas, segmental


bowel thickening with lack of bowel wall enhancement
and liver or splenic infarcts. Conspicuous prominence of
peripheral mesenteric vessels arranged in a palisade or
comb fashion is seen in mesenteric ischaemia due to
vasculitis. This may be associated with genito-urinary
and splenic involvement which would be evident in CT.
Perivascular oedema and inflammatory cell infiltration
associated with vascular stasis or pooling results in the
comb-sign described in vasculitis (18). The main disadvantage of CT angiography is its need for a large contrast load in patients who may have associated renovascular disease.
MVT can be diagnosed on contrast enhanced CT
scanning by demonstration of thrombus within the superior mesenteric vein and is superior to angiography in
this respect (40). Superior Mesenteric Vein may be visualised as enlarged vein with central lucency and contrast
enhanced surrounding vessel wall- the so called halo
sign in MVT (12). Mesenteric angiography is traditionally considered to be the gold standard for the diagnosis
of arterial occlusion but at the cost of delay in treatment.
If there are convincing abdominal signs of peritonitis
urgent laparotomy is the best course of action. In the
remainder of patients where AMI is suspected biplanar
angiography is indicated. A lateral flush aortogram will
help in assessing the origins of the mesenteric vessels
and the antero-posterior views will demonstrate the distal arcades. Selective angiograms are performed when
intervention is considered appropriate.In acute SMA

350

N. J. Menon et al.

Fig. 7
Algorithm for the management of acute mesenteric ischaemia.

thrombosis, there is usually non- visualization of this


artery because of the ostial nature of the disease (Fig. 3),
although delayed views may show slow filling of the
distal vessel. In SMA emboli, the proximal artery to just
beyond the origin of the middle colic artery can be
demonstrated angiographically.Delayed arterial filling
and lack of venous phase on angiograms suggest MVT.
Selective angiography of mesenteric arteries in NOMI
will show vasospasm and is useful to exclude a significant arterial lesion (41). Narrowing of the origin of SMA
with alternating dilatation and narrowing of the enteric
branches gives rise to the radiological appearance of
string of sausage sign in NOMI. Once the diagnosis is
made on selective angiogram, the angiocatheter should
not be removed until all therapeutic possibilities are discussed with the surgeon.
Magnetic resonance angiography (MRA) with three
dimensional gadolinium enhanced reconstruction does
not require ionising radiation and is particularly useful
in chronic mesenteric ischaemia since it is noninvasive.
However its role in acute setting remains controversial.
The distal mesenteric vessels cannot be well visualised
on MRA (42) and it is unhelpful in cases of NOMI.

Duplex scanning is limited by the increased intestinal


gas that is frequently present in association ; it is again
non-invasive and in good hands gives comparable
results (43).
Treatment
Expedient revascularisation to prevent intestinal gangrene is the main aim of treatment. In all cases, the
patient should be aggressively resuscitated, broad-spectrum intravenous antibiotics instituted and fully
heparinised once the diagnosis is confirmed. As yet, the
twin goals of mesenteric revascularization and resection
of nonviable bowel can only be achieved by surgical
means. Treatment pathways is summarised in Figure 7.
Surgical
Surgery is indicated in all patients with peritonitis after
rapid resuscitation. At laparotomy the surgeon should
establish the diagnosis, consider appropriate revascularisation and resect the already damaged bowel. The decision for relook laparotomy should be made at the initial

Acute Mesenteric Ischaemia


surgery itself and is independent of the clinical status of
the patient between the two procedures (5).
The first step is to identify the underlying pathology.
The presence of proximal artery pulsation and jejunal
sparing are intraoperative clues for an embolus.
Conversely, absence of proximal mesenteric pulsation
and jejunal involvement indicate thrombosis.
The crucial and most taxing step is to assess the
degree and extent of bowel viability. Ischaemic bowel
has a characteristic appearance with loss of its normal
sheen. It is dull, grey in colour and flabby in tone without any peristalsis. Infarcted bowel is purplish black in
colour, often friable and perforated. Free, foul smelling
peritoneal fluid is a sign of advanced necrosis even if
perforation has not occurred. In many cases the bowel
ischaemia will be so extensive and advanced that it
would be prudent to offer palliation alone.Where there is
hope of sufficient bowel viability, revascularization
should be first performed before any bowel resection is
considered. After successful revascularization, previously precarious segments of intestine may recover and
resection of clearly ischaemic bowel can then take place.
SMA embolectomy
The proximal portion of the SMA is dissected free from
the paraaortic fat and lymphatic tissue just as it emerges
from the pancreatic neck into the base of the mesentery.
The artery is medial to the vein and approximately 3 to
4 centimetres of artery is cleared, with care taken not to
cause any collateral damage. Heparin 80 iu/kg is given
intravenously and the vessel is controlled between
slings. A transverse arteriotomy is made in the SMA
proximal to the middle colic artery take off unless reconstruction is anticipated and a 3F or 4F embolectomy
catheter is passed proximally and distally to clear the
embolus and re-establish vigorous pulsatile flow. If
proximal flow cannot be established, SMA thrombosis
is likely and reconstructive surgery will be required. The
use of intraoperative thrombolysis after embolectomy is
likely to help in removing the thrombus from distal
branches which cannot be cleared completely by
catheter trawl alone (44). Anticoagulation is continued
in the postoperative period with heparin at 18 iu/kg to
maintain APTT ratio of over twice normal.
SMA reconstruction
Revascularization can be performed either by re-implantation of the healthy portion of the SMA after thromboendarterectomy into the aorta or using bypass grafting
from the aorta to the patent SMA. The clear advantage
of autologus saphenous vein over prosthetic graft
observed in other vascular beds is not so evident in the
visceral circulation (45). In presence of a potentially or

351
de facto infected field, prosthetic grafts should be avoided. Reversed saphenous vein aortomesenteric grafting or
direct SMA re-implantation is the procedure of choice in
this situation. Bypass with vein or prosthesis is prone to
kinking due to its configuration, and great care must be
taken to align the grafts to avoid this complication.
Antegrade bypass grafting from relatively disease free
supracoeliac aorta resists kinking better than retrograde
bypass grafts (45). Single vessel revascularization is
usually adequate in emergency (46) and probably also in
the non emergency situation, but opinion is varied as to
whether SMA or celiac axis should be revascularised in
preference (5, 47).
After successful revascularization, previously precarious segments of intestine may recover and resection of
clearly ischaemic bowel can then take place. However,
determination of viability by eyeballing could be deceptive. The decision about how much to resect can be crucial to the long-term outcome. Clinical assessment by
detecting pulsation in the arcades, colour of the bowel,
peristalsis and bleeding from cut edges are most commonly used. This is often complemented by the use of
the intraoperative Doppler probe to detect flow in the
intestinal wall in addition to flow in the arcade vessels.
Other techniques include the use of fluorescein and
inspection under Woods lamp, pulse oximetry and laser
Doppler flowmetry. Since most of the ischaemic damage
is at the mucosal level, the gross appearance of the
serosal aspect is often misleading. For the same reason,
it may be advisable to avoid anastomosis after resection.
Some even advocate stapling off both ends of the
remaining gut so that the surgeon would be forced to
undertake relook laparotomy prior to establishing
intestinal continuity (48).
In cases of MVT, resection of infarcted bowel with
liberal margins should be performed with a primary
anastomosis considered only if perfusion is adequate.
Venous thrombectomy has poor results with a high
recurrence rate and is rarely indicated. Laparoscopy in
suspected MVT is appealing and can be useful in the
management algorithm to reduce the surgical stress (49).
Post aortic aneurysm repair colon ischaemia requiring surgery usually necessitates a Hartmanns procedure, a primary anastomosis being contraindicated. Consideration must be made to protect the aortic graft and its
limbs from contamination by using antiseptic soaked
swabs.
Abdominal compartment syndrome is more commonly recognised now and in cases of massive fluid shifts
associated with infarcted gut, closure of the abdomen
with Bogota bag or its variation may be appropriate (50,
51).
Second look laparotomy to assess marginally viable
bowel left behind at the original surgery should take
place as a planned procedure (48). Laparoscopy under

352
local anaesthesia is also in vogue now to reduce the trauma of repeated laparotomies in these sick patients (49,
52). The concept of bedside laparoscopy in a critically ill
patient to avoid the trauma of a relook laparotomy, with
laparoscopic trocar inserted and secured at the initial
surgery appears very appealing (53).
Continued intensive care is required in the postoperative period with optimization of cardiac and respiratory
status. There is an associated deterioration in hepatic
function with transaminases rising 90- to 100-fold (8).
The hepatic impairment and associated coagulopathy is
usually transient, returning to normal within seven to ten
days. Total parenteral nutrition may be started early in
the postoperative period, and may need to be continued
for months in cases with short gut syndromes.
In cases of MVT, long-term anticoagulation is required because of the high recurrence rates. Complications such as ascites and portal hypertension may
require specific treatment (25).
Nonsurgical/conservative treatment
Non surgical treatment is contemplated only in absence
of clinical evidence of peritonitis. In NOMI, treatment is
nonoperative and depends on treating the underlying
conditions such as sepsis and optimizing cardiac output
with judicious use of inotropes and after load reducing
agents. Noradrenalin is best avoided. If the diagnosis of
AMI is made without angiography, intravenous
glucagon infused at 1g/kg per minute and titrated upto
10 g/kg/minute as tolerated may help to reduce the
associated vasospasm. If the diagnosis is made on
angiography, the catheter is left in-situ and intra arterial
infusion of papaverine at a dose of 30 to 60 mg/ h may
be attempted (11). Papaverine, a phosphodiesterase
inhibitor increases the mesenteric flow to improve bowel
salvage. Up to 65% of patients who underwent cardiac
surgery have had symptomatic improvement within
hours when AMI was diagnosed early (54).
If MVT is diagnosed at angiography, intra-arterial
thrombolytic therapy can be given successfully (55, 56).
However, thrombolysis is contraindicated when bowel infarction is suspected (11). Nonoperative management by
full anticoagulation for acute MVT is feasible when the
initial diagnosis is certain and when the bowel infarction
has not led to transmural necrosis and bowel perforation.
The morbidity, mortality, and survival rates are similar in
cases of surgical and nonoperative management (56).
Other reported endovascular procedures for acute
intestinal ischaemia include fenestration and stent placement in aortic dissection (57, 58), angioplasty and stenting in acute occlusion in patients with chronic mesenteric
insufficiency (59, 60) and angioplasty alone (61). This
contrasts with an increasing use of angioplasty for chronic mesenteric ischaemia (62).The role of thrombolysis in

N. J. Menon et al.
AMI is not well defined and remains anecdotal. The body
of experience with endovascular therapy is emerging (7,
60, 63) but it is likely that it would be favoured only in
those with unacceptable surgical risk. There may be a role
for endovascular treatment followed by laparoscopy to
assess bowel viability but currently the evidence is not
sufficient to support this strategy (64).
The use of allopurinol, angiotensin converting
enzyme inhibitors and other free oxygen scavengers
may help to reduce the reperfusion syndrome (11).
Prognosis
Most studies tend to report dismal outcome in acute
mesenteric ischaemia in comparison to chronic
ischaemia. Perioperative mortality for arterial thrombosis remains high, in part because of delayed diagnosis,
the extensive nature of the bowel ischaemia and the need
for complex surgical revascularisation (11).
A retrospective multicenter study by the French associations of surgical research comparing the periods from
1980 to 1985 and 1990 to 1995, appear to hold promise
(65). Mortality rates decreased from 83% to 63% in
thrombotic acute mesenteric ischaemia and from 51% to
19% in MVT. There were no significant increases in frequencies of angiography, vascular or second look procedures to account for the change. Patients with NOMI
have fewer treatment options since the offending stimulus often results from treatment for another disorder.
Unless the original insult is reversed, the outcome is
grave.
Conclusion
Earlier in the last century, it was felt that in AMI the
diagnosis is impossible, the prognosis hopeless and the
treatment useless (66). The same pessimistic attitude is
shared by many and is reflected in Taylors words mortality rate for patients with AMI will probably always
remain high (67). With high index of suspicion for the
diagnosis, aggressive approach to early restoration of
perfusion, second-look laparotomy and supportive care,
patient outcome has improved over the years. Though
the results of surgical treatment remain unsatisfactory,
improved imaging and thrombolytic therapies hold
much promise (68). The contemporary management of
AMI with revascularisation with open surgical techniques, resection of non-viable bowel and liberal use of
second look laparotomy results in the early survival of
two thirds of patients with embolism and thrombosis(5).
References
1. DEEHAN D. J., HEYS S. D., BRITTENDEN J., EREMIN O. Mesenteric
ischaemia : prognostic factors and influence of delay upon outcome. J R Coll Surg Edinb, 1995, 40 (2) : 112-115.

Acute Mesenteric Ischaemia


2. BOLEY S. J., BRANDT L. J., SAMMARTANO R. J. History of mesenteric
ischemia. The evolution of a diagnosis and management. Surg
Clin North Am, 1997, 77 (2) : 275-288.
3. OTTINGER L. W., AUSTEN W. G. A study of 136 patients with mesenteric infarction. Surg Gynecol Obstet, 1967, 124 (2) : 251-261.
4. STONEY R. J., CUNNINGHAM C. G. Acute mesenteric ischemia.
Surgery, 1993, 114 (3) : 489-490.
5. PARK W. M., GLOVICZKI P., CHERRY K. J., Jr., HALLETT J. W., Jr.,
BOWER T. C., PANNETON J. M. et al. Contemporary management of
acute mesenteric ischemia : Factors associated with survival.
J Vasc Surg, 2002, 35 (3) : 445-452.
6. WADMAN M., SYK I., ELMSTAHL S. Survival after operations
for ischaemic bowel disease. Eur J Surg, 2000, 166 (11) : 872877.
7. SHEERAN S. R., MURPHY T. P., KHWAJA A., SUSSMAN S. K.,
HALLISEY M. J. Stent placement for treatment of mesenteric artery
stenoses or occlusions. J Vasc Interv Radiol, 1999, 10 (7) : 861867.
8. HARWARD T. R., BROOKS D. L., FLYNN T. C., SEEGER J. M. Multiple
organ dysfunction after mesenteric artery revascularization. J Vasc
Surg, 1993, 18 (3) : 459-467.
9. BAILEY R. W., BULKLEY G. B., HAMILTON S. R., MORRIS J. B.,
HAGLUND U. H. Protection of the small intestine from nonocclusive mesenteric ischemic injury due to cardiogenic shock. Am J
Surg, 1987, 153 (1) : 108-116.
10. CZERNY M., TRUBEL W., CLAEYS L., SCHEUBA C., HUK I., PRAGER M.
et al. [Acute mesenteric ischemia]. Zentralbl Chir, 1997, 122 (7) :
538-544.
11. OLDENBURG W. A., LAU L. L., RODENBERG T. J., EDMONDS H. J.,
BURGER C. D. Acute mesenteric ischemia : a clinical review. Arch
Intern Med, 2004, 164 (10) : 1054-1062.
12. VICENTE D. C., KAZMERS A. Acute mesenteric ischemia. Curr Opin
Cardiol, 1999, 14 (5) : 453-458.
13. HIGGINS R., POSNER M. C., MOOSA H. H., STALEY C., PATAKI K. I.,
MENDELOW H. Mesenteric infarction secondary to tumor emboli
from primary aortic sarcoma. Guidelines for diagnosis and management. Cancer, 1991, 68 (7) : 1622-1627.
14. HAMED R. M., GHANDOUR K. Abdominal angina and intestinal
gangrene a catastrophic presentation of arterial fibromuscular
dysplasia : case report and review of the literature. J Pediatr Surg,
1997, 32 (9) : 1379-1380.
15. HOANG M. P., LEE E. L., ANAND A. Histologic spectrum of arterial
and arteriolar lesions in acute and chronic cocaine-induced
mesenteric ischemia : report of three cases and literature review.
Am J Surg Pathol, 1998, 22 (11) : 1404-1410.
16. GRADMAN W. S., DANIEL J., MILLER B., HAJI-AGHAII M.
Homocysteine-associated acute mesenteric artery occlusion treated with thrombectomy and bowel resection. Ann Vasc Surg, 2001,
15 (2) : 247-250.
17. SEEBURGER J. L., STEPAK M., FUKUCHI S. G., SIEGEL J. E.,
ROLANDELLI R. H. Multiple arterial thromboembolisms in a patient
with the 20210 A prothrombin gene mutation. Arch Surg, 2000,
135 (6) : 721-722.
18. KIM J. K., HA H. K., BYUN J. Y., YANG S. K., JUNG H. Y., MIN Y. I.
et al. CT differentiation of mesenteric ischemia due to vasculitis
and thromboembolic disease. J Comput Assist Tomogr, 2001,
25 (4) : 604-611.
19. VIGNATI P. V., WELCH J. P., ELLISON L., COHEN J. L. Acute mesenteric ischemia caused by isolated superior mesenteric artery dissection. J Vasc Surg, 1992, 16 (1) : 109-112.
20. ALLERTON R. Acute mesenteric ischaemia associated with 5-FU,
cisplatin and vincristine chemotherapy. Clin Oncol (R Coll
Radiol), 1996, 8 (2) : 116-117.
21. ANAYI S., AL NASIRI N. Acute mesenteric ischaemia caused by
Schistosoma mansoni infection. Br Med J (Clin Res Ed), 1987,
294 (6581) : 1197.
22. CHOUDHARY A. M., GRAYER D., NELSON A., ROBERTS I. Mesenteric
venous thrombosis : a diagnosis not to be missed ! J Clin Gastroenterol, 2000, 31 (2) : 179-182.
23. BOLEY S. J., KALEYA R. N., BRANDT L. J. Mesenteric venous thrombosis. Surg Clin North Am, 1992, 72 (1) : 183-201.
24. KUMAR S., SARR M. G., KAMATH P. S. Mesenteric venous thrombosis. N Engl J Med, 2001, 345 (23) : 1683-1688.

353
25. DIVINO C. M., PARK I. S., ANGEL L. P., ELLOZY S., SPIEGEL R.,
KIM U. A retrospective study of diagnosis and management of
mesenteric vein thrombosis. Am J Surg, 2001, 181 (1) : 20-23.
26. SREENARASIMHAIAH J. Diagnosis and management of intestinal
ischaemic disorders. BMJ, 2003, 326 (7403) : 1372-1376.
27. DAHLBERG P. J., KISKEN W. A., NEWCOMER K. L., YUTUC W. R.
Mesenteric ischemia in chronic dialysis patients. Am J Nephrol,
1985, 5 (5) : 327-332.
28. GUSMAO L., SANTANA A., RIOCARVALHO I., MARTINHO A.,
MESSIAS H., PONCE P. [Mesenteric ischemia in hemodialysis]. Acta
Med Port, 1992, 5 (4) : 169-171.
29. OGINO H., MIKI S., UEDA Y., TAHATA T. A case of bowel necrosis
due to acute mesenteric ischemia following pulsatile cardiopulmonary bypass. Ann Thorac Cardiovasc Surg, 1998, 4 (1) : 34-36.
30. BJORCK M., BERGQVIST D., TROENG T. Incidence and clinical
presentation of bowel ischaemia after aortoiliac surgery
2930 operations from a population-based registry in Sweden. Eur
J Vasc Endovasc Surg, 1996, 12 (2) : 139-144.
31. FARKAS J. C., CALVO-VERJAT N., LAURIAN C., MARZELLE J.,
FICHELLE J. M., GIGOU F. et al. Acute colorectal ischemia after aortic surgery : pathophysiology and prognostic criteria. Ann Vasc
Surg, 1992, 6 (2) : 111-118.
32. GOREY T. F., OSULLIVAN M. Prognostic factors in extensive mesenteric ischaemia. Ann R Coll Surg Engl, 1988, 70 (4) : 191-194.
33. MEYER T., KLEIN P., SCHWEIGER H., LANG W. [How can the prognosis of acute mesenteric artery ischemia be improved ? Results of
a retrospective analysis]. Zentralbl Chir, 1998, 123 (3) : 230-234.
34. TSAI C. J., KUO Y. C., CHEN P. C., WU C. S. The spectrum of acute
intestinal vascular failure : a collective review of 43 cases in
Taiwan. Br J Clin Pract, 1990, 44 (12) : 603-608.
35. MAY L. D., BERENSON M. M. Value of serum inorganic phosphate
in the diagnosis of ischemic bowel disease. Am J Surg, 1983,
146 (2) : 266-268.
36. ACOSTA S., NILSSON T. K., BJORCK M. Preliminary study of Ddimer as a possible marker of acute bowel ischaemia. Br J Surg,
2001, 88 (3) : 385-388.
37. ACOSTA S., OGREN M., STERNBY N. H., BERGQVIST D., BJORCK M.
Incidence of acute thrombo-embolic occlusion of the superior
mesenteric artery a population-based study. Eur J Vasc
Endovasc Surg, 2004, 27 (2) : 145-150.
38. KANDA T., FUJII H., TANI T., MURAKAMI H., SUDA T., SAKAI Y. et al.
Intestinal fatty acid-binding protein is a useful diagnostic marker
for mesenteric infarction in humans. Gastroenterology, 1996,
110 (2) : 339-343.
39. HORTON K. M., FISHMAN E. K. Multi-detector row CT of mesenteric ischemia : can it be done ? Radiographics, 2001, 21 (6) :
1463-1473.
40. MORASCH M. D., EBAUGH J. L., CHIOU A. C., MATSUMURA J. S.,
PEARCE W. H., YAO J. S. Mesenteric venous thrombosis : a changing clinical entity. J Vasc Surg, 2001, 34 (4) : 680-684.
41. TROMPETER M., BRAZDA T., REMY C. T., VESTRING T., REIMER P.
Non-occlusive mesenteric ischemia : etiology, diagnosis, and
interventional therapy. Eur Radiol, 2002, 12 (5) : 1179-1187.
42. BADEN J. G., RACY D. J., GRIST T. M. Contrast-enhanced threedimensional magnetic resonance angiography of the mesenteric
vasculature. J Magn Reson Imaging, 1999, 10 (3) : 369-375.
43. DANSE E. M., LATERRE P. F., VAN BEERS B. E., GOFFETTE P.,
DARDENNE A. N., PRINGOT J. Early diagnosis of acute intestinal
ischaemia : contribution of colour Doppler sonography. Acta Chir
Belg, 1997, 97 (4) : 173-176.
44. BINGOL H., ZEYBEK N., CINGOZ F., YILMAZ A. T., TATAR H., SEN D.
Surgical therapy for acute superior mesenteric artery embolism.
Am J Surg, 2004, 188 (1) : 68-70.
45. CHO J. S., CARR J. A., JACOBSEN G., SHEPARD A. D., NYPAVER T. J.,
REDDY D. J. Long-term outcome after mesenteric artery reconstruction : a 37-year experience. J Vasc Surg, 2002, 35 (3) : 453-460.
46. FOLEY M. I., MONETA G. L., ABOU-ZAMZAM A. M., Jr.,
EDWARDS J. M., TAYLOR L. M., Jr., YEAGER R. A. et al.
Revascularization of the superior mesenteric artery alone for treatment of intestinal ischemia. J Vasc Surg, 2000, 32 (1) : 37-47.
47. BJORCK M., ACOSTA S., LINDBERG F., TROENG T., BERGQVIST D.
Revascularization of the superior mesenteric artery after acute
thromboembolic occlusion. Br J Surg, 2002, 89 (7) : 923-927.

354
48. ENDEAN E. D., BARNES S. L., KWOLEK C. J., MINION D. J.,
SCHWARCZ T. H., MENTZER R. M., Jr. Surgical management of
thrombotic acute intestinal ischemia. Ann Surg, 2001, 233 (6) :
801-808.
49. CHO Y. P., JUNG S. M., HAN M. S., JANG H. J., KIM J. S., KIM Y. H.
et al. Role of diagnostic laparoscopy in managing acute mesenteric venous thrombosis. Surg Laparosc Endosc Percutan Tech,
2003, 13 (3) : 215-217.
50. SULLIVAN K. M., BATTEY P. M., MILLER J. S., MCKINNON W. M.,
SKARDASIS G. M. Abdominal compartment syndrome after mesenteric revascularization. J Vasc Surg, 2001, 34 (3) : 559-561.
51. TIWARI A., HAQ A. I., MYINT F., HAMILTON G. Acute compartment
syndromes. Br J Surg, 2002, 89 (4) : 397-412.
52. SESHADRI P. A., POULIN E. C., MAMAZZA J., SCHLACHTA C. M.
Simplified laparoscopic approach to second-look laparotomy : a
review. Surg Laparosc Endosc Percutan Tech, 1999, 9 (4) : 286-289.
53. ANADOL A. Z., ERSOY E., TANERI F., TEKIN E. H. Laparoscopic
second-look in the management of mesenteric ischemia. Surg
Laparosc Endosc Percutan Tech, 2004, 14 (4) : 191-193.
54. KLOTZ S., VESTRING T., ROTKER J., SCHMIDT C., SCHELD H. H.,
SCHMID C. Diagnosis and treatment of nonocclusive mesenteric
ischemia after open heart surgery. Ann Thorac Surg, 2001, 72 (5) :
1583-1586.
55. TRAIN J. S., ROSS H., WEISS J. D., FEINGOLD M. L., KHOURYYACOUB A., KHOURY P. T. Mesenteric venous thrombosis : successful treatment by intraarterial lytic therapy. J Vasc Interv
Radiol, 1998, 9 (3) : 461-464.
56. BRUNAUD L., ANTUNES L., COLLINET-ADLER S., MARCHAL F.,
AYAV A., BRESLER L. et al. Acute mesenteric venous thrombosis :
case for nonoperative management. J Vasc Surg, 2001, 34 (4) :
673-679.
57. LEUNG D. A., SCHNEIDER E., KUBIK-HUCH R., MARINCEK B.,
PFAMMATTER T. Acute mesenteric ischemia caused by spontaneous
isolated dissection of the superior mesenteric artery : treatment by
percutaneous stent placement. Eur Radiol, 2000, 10 (12) : 19161919.
58. SLONIM S. M., MILLER D. C., MITCHELL R. S., SEMBA C. P.,
RAZAVI M. K., DAKE M. D. Percutaneous balloon fenestration and
stenting for life-threatening ischemic complications in patients
with acute aortic dissection. J Thorac Cardiovasc Surg, 1999,
117 (6) : 1118-1126.
59. LOOMER D. C., JOHNSON S. P., DIFFIN D. C., DEMAIORIBUS C. A.
Superior mesenteric artery stent placement in a patient with acute
mesenteric ischemia. J Vasc Interv Radiol, 1999, 10 (1) : 29-32.

N. J. Menon et al.
60. BROUNTZOS E. N., CRITSELIS A., MAGOULAS D., KAGIANNI E.,
KELEKIS D. A. Emergency endovascular treatment of a superior
mesenteric artery occlusion. Cardiovasc Intervent Radiol, 2001,
24 (1) : 57-60.
61. RUNDBACK J. H., ROZENBLAT G. N., POPLAUSKY M., CREA G.,
MADDINENI S., OLSON C. et al. Re : jejunal artery angioplasty and
coronary stent placement for acute mesenteric ischemia. Cardiovasc Intervent Radiol, 2000, 23 (5) : 410-412.
62. HALLISEY M. J., DESCHAINE J., ILLESCAS F. F., SUSSMAN S. K.,
VINE H. S., OHKI S. K. et al. Angioplasty for the treatment of
visceral ischemia. J Vasc Interv Radiol, 1995, 6 (5) : 785-791.
63. SIMO G., ECHENAGUSIA A. J., CAMUNEZ F., TUREGANO F.,
CABRERA A., URBANO J. Superior mesenteric arterial embolism :
local fibrinolytic treatment with urokinase. Radiology, 1997,
204 (3) : 775-779.
64. MUNNEKKE G. J., LOOSEMORE T. M., ANNA-MARIA BELLI.
Mesenteric Vascularistion. In : WYATT M. G., WATKINSON A. F.,
(eds.). Endovascular Interventions- Current Controversies.
Shrewsbury UK : TFM PUBLISHING, 2004 : 227-236.
65. DURON J. J., PEYRARD P., BOUKHTOUCHE S., FARAH A., SUC B. [Acute
mesenteric ischemia : changes in 1985-1995. Surgical Research
Associations]. Chirurgie, 1998, 123 (4) : 335-342.
66. COKKINS A. J. Mesenteric Vascular Occlusion. London UK :
Bailliere, Tindall & Cox, 1926.
67. TAYLOR L. M., MONETA G. C., PORTER J. M. Treatment of acute
mesenteric ischeamia caused by arterial occlusion. In :
RUTHERFORD R.B. (ed.). Philadelphia : W.B. Saunders & Co, 2005,
1512-1519.
68. SCHOOTS I. G., KOFFEMAN G. I., LEGEMATE D. A., LEVI M., VAN
GULIK T. M. Systematic review of survival after acute mesenteric
ischaemia according to disease aetiology. Br J Surg, 2004, 91 (1) :
17-27.

Prof. G. Hamilton
The Royal Free and University College Medical School
Pond Street
Hampstead
London
NW3 2QG
Tel.
: 020 7830 2163
Fax
: 020 7472 6278
E-mail : g.hamilton@rfc.ucl.ac.uk