Intestinal infarction: survival, examinations, treatment, aftercare

By Cristiano Antonino On Sep 23, 2022

The medical term ‘intestinal infarction’ refers to the necrosis (death) of a section of intestinal tissue caused by prolonged ‘intestinal ischaemia’, which in turn is caused by insufficient blood perfusion (e.g. by occlusion of a blood vessel)

An intestinal infarction that is not treated in time can result in the death of the patient.

Two main types of intestinal infarction can be distinguished:

Intestinal infarction of the small intestine (mesenteric infarction): the necrosis affects only one segment of the small intestine, or several even discontinuous segments, or the entire small intestine, or part of the intestine and part of the ascending colon. Generally more severe;
intestinal infarction of the large intestine (colic infarction): necrosis affects one or more segments of the colon (transverse, descending, sigma, rectum). Generally less severe.

To fully understand the mechanisms that lead to an intestinal infarction, it is important to understand exactly what intestinal ischaemia is and what causes it

By ‘intestinal ischaemia’, in medicine we identify an alteration of blood circulation in the tissues of the intestine, brought about by various causes, such as the occlusion of an artery that brings oxygenated blood to the intestine, but also the alteration of intestinal venous flow.

A distinction is therefore made between venous or arterial intestinal ischaemia, as well as acute or chronic intestinal ischaemia and also occlusive and non-occlusive intestinal ischaemia. As a result of the altered circulation, the intestinal mucosa has a reduced supply of nutrients and oxygen, with the result that – if the blood flow is not quickly restored – the intestinal mucosa goes into ‘necrosis’ (i.e. dies), resulting in the picture of an intestinal infarction.

Remember that the intestinal mucosa has a high demand for blood flow (it receives almost a quarter of the entire cardiac output), which makes it very sensitive to the effects of decreased perfusion.

Intestinal ischaemia therefore sets in rather quickly and can lead to a series of sequential, even lethal, events:

necrosis of the mucosa
perforation of the mucosa;
release of bacteria, toxins and vasoactive mediators;
myocardial depression;
systemic inflammatory response syndrome (sepsis and septic shock);
multi-organ failure;
patient death.

Necrosis may occur as little as 10 hours after the onset of symptoms.

Mesenteric ischaemia is distinct from ischaemic colitis:

mesenteric ischaemia: blood flow is altered in the small intestine. Less frequent;
ischaemic colitis: blood flow is altered in the colon (large intestine). More frequent.

The underlying causes of an intestinal infarction are the same as for intestinal ischaemia, which is the initial condition that leads to necrosis of the intestine

Intestinal ischaemia can occur due to an obstruction or vascular rupture in the three major vessels that vascularise the abdominal organs:

celiac trunk: irrigates the oesophagus, stomach, proximal duodenum, liver, gallbladder, pancreas and spleen;
superior mesenteric artery: irrigates the distal duodenum, jejunum, ileum and colon up to the splenic flexure;
lower mesenteric artery: irrigates the descending colon, sigma and rectum.

Mesenteric blood flow can be altered at the level of these arteries, but also at the level of the venous vessels that collect the no longer oxygenated blood from the intestine.

Causes of acute and chronic ischaemia, occlusive and non-occlusive

Mesenteric ischaemia may be acute or chronic:

acute mesenteric ischaemia: the interruption of blood supply is sudden and severe (very little blood reaches the tissue). It is generally more severe;
chronic mesenteric ischaemia: blood flow to the intestine decreases gradually and progressively. It is generally less serious than acute ischaemia, although what is not a serious condition in an absolute sense.

Acute mesenteric ischaemia has three main causes occurring in the superior mesenteric artery

occlusion of the artery by a blood clot (embolus) originating in the heart, e.g. in cases of prolonged atrial fibrillation (frequent);
occlusion of the artery by a thrombus caused by the lesion of an atheroma (cholesterol deposit that narrows arterial vessels suffering from atherosclerosis), e.g. in the case of a spike in blood pressure
reduction of flow in the artery by abrupt arterial hypotension, which can be induced by shock, heart failure, internal haemorrhage, renal failure, abuse of certain medications or drugs.

The first two situations are called ‘acute occlusive mesenteric ischaemia’, while the third situation is called ‘acute non-occlusive mesenteric ischaemia’.

Chronic mesenteric ischaemia, on the other hand, is almost always caused by an occlusion of the mesenteric artery caused by an atheroma that expands gradually. In this case, atherosclerosis is therefore the cause of chronic ischaemia: chronic mesenteric ischaemia is therefore always of the ‘non-occlusive’ type.

Intestinal ischaemia from venous causes

Intestinal ischaemia can be caused not only by arterial causes, but also by venous ones: when an obstruction prevents venous blood from leaving the intestine properly, it triggers an accumulation and subsequently a reflux, i.e. the blood ‘flows back’.

The basis of venous obstruction is almost always a blood clot (embolus) that blocks the mesenteric vein or its branches.

Such an embolus is generally caused or facilitated by:

acute or chronic pancreatitis
abdominal infection;
abdominal tumour;
ulcerative colitis;
Crohn’s disease;
diverticulitis;
abdominal trauma;
hypercoagulation;
incorrect anticoagulant therapy (inadequate INR);
cardiac arrhythmias;
recent surgery, e.g. after femur fracture.

Intestinal ischaemia from venous causes is also called ‘mesenteric venous thrombosis’

Ischaemia from venous causes is, however, less frequent than arterial ischaemia and, in theory, less severe.

The patients most at risk of mesenteric ischaemia, and therefore of intestinal infarction, are those with the following characteristics and pathologies

men;
age > 50 years;
overweight and obesity;
intestinal obstruction from various causes;
chronic intestinal constipation;
faecaloma;
colon tumours;
large abdominal tumours;
megacolon;
dolichocolon;
sudden severe arterial hypotension (‘very low blood pressure’);
arterial embolism;
coronary artery disease;
heart failure;
heart valve disease;
arterial hypertension;
atrial fibrillation;
intestinal volvulus;
intestinal stricture;
previous surgery;
positive history of previous arterial embolism;
arterial thrombosis (30%);
generalised atherosclerosis;
venous thrombosis (15%);
hypercoagulability;
pancreatitis;
diverticulitis;
chronic inflammation;
cigarette smoking;
high-fat diet;
trauma, especially abdominal trauma (e.g. from road accidents);
heart failure;
renal insufficiency;
portal hypertension;
decompression sickness;
heart failure;
shock;
cardiopulmonary bypass;
splanchnic vasoconstriction;
intestinal adhesions;
cocaine, amphetamine and methamphetamine use;
intestinal artery vasculitis;
systemic lupus erythematosus (SLE);
sickle-cell anaemia;
use of: drugs with vasoconstrictor effect, drugs for treating heart disease, drugs for treating migraine, hormonal drugs (such as oestrogen);
excessive physical exertion, especially prolonged physical exertion.

Early and late symptoms and signs

The first characteristic ‘premonitory’ sign of mesenteric ischaemia is severe pain accompanied by minimal physical findings.

The abdomen remains soft, with little or no tenderness.

Mild tachycardia may be present. Later, when necrosis develops and then actual intestinal infarction, signs of peritonitis appear, with marked abdominal tenderness, defensive reaction, rigidity and absence of bowel sounds.

The faeces may show traces of blood (increasingly likely as the ischaemia progresses), of a different colour depending on the intestinal tract affected: darker brown if the small intestine is affected, gradually becoming brighter red if the lesion affects areas closer to the anus (e.g. descending colon and sigma).

Typical signs of shock develop and are often followed by death.

Symptoms may help the physician in diagnosis: a sudden onset of pain suggests an arterial embolism (but does not permit a diagnosis of certainty), while a more gradual onset is typical of a venous thrombosis. Patients with a history of postprandial abdominal complaints (suggesting intestinal angina) may have arterial thrombosis.

Symptoms and signs can be differentiated according to three main factors

arterial or venous intestinal ischaemia;
ischaemic colitis or mesenteric ischaemia;
acute or chronic ischaemia.

Symptoms of ischaemic colitis

When ischaemia affects the descending colon (left colon), there are:

sudden abdominal pain in the left lower quadrant;
presence of bright red (if the lower part is affected) or brown (if the upper part is affected) blood in the stool.

When ischaemia affects the ascending colon (right colon) there are:

sudden right lower quadrant abdominal pain;
absence of blood in the stool or minimal presence of brown or black blood in the stool.

Symptoms of acute mesenteric ischaemia from arterial causes

When ischaemia acutely affects the small intestine, there are:

sudden and very intense abdominal pain, especially if the cause is occlusive (e.g. embolus)
general malaise
abdominal distension;
abdominal soreness;
nausea;
vomiting;
abnormal bowel movements;
urgent need to defecate.

Symptoms of chronic mesenteric ischaemia from arterial causes

When ischaemia affects the small intestine chronically, there are:

postprandial abdominal pain (10-30 minutes after meals, peaking after about 2 hours and then gradually decreasing). This pain tends to become more intense over time;
abdominal cramps;
drop in body weight (the patient eats less for fear of feeling pain).

Symptoms of mesenteric ischaemia from venous causes

When ischaemia affects the small intestine from venous causes, there are:

abdominal pain (less intense than in ischaemia from arterial causes);
general malaise;
nausea;
vomiting;
diarrhoea;
blood in the stool (not always).

Diagnosis and differential diagnosis of intestinal infarction

Early diagnosis is particularly important as mortality increases significantly once intestinal infarction has occurred: early diagnosis generally saves the patient’s life.

Mesenteric ischaemia should be considered in any patient > 50 years of age, with known risk factors or predisposing conditions, who presents with sudden and severe abdominal pain.

Patients with clear peritoneal signs should be sent directly to the operating theatre for both diagnosis and treatment.

In others, selective mesenteric angiography or CT angiography is the diagnostic procedure of choice.

Other imaging studies and serum markers may be altered but are not sensitive and specific in the early stages of the disease, when it is most important to make the diagnosis.

Direct X-ray of the abdomen is useful in the differential diagnosis to exclude other causes of pain (perforated bowel), although in advanced stages of the disease the presence of gas bubbles in the portal vein or intestinal pneumatosis may be observed.

These findings are also visible in CT scans, which can also directly visualise the vascular occlusion more accurately on the venous side.

Echodoppler can sometimes identify an arterial occlusion, but the sensitivity is low. MRI is very accurate in proximal vascular occlusion, but less so in distal vascular occlusion.

Haematochemical examinations

Serum markers (creatine phosphokinase and lactate) increase with necrosis, but are non-specific and late findings. Neutrophil leucocytosis and occult blood in the faeces are other important parameters for diagnosis.

Serious intestinal fatty acid binding protein may perhaps prove useful as an early marker in the future.

Introduction to treatment

In intestinal infarction of the small intestine, the diagnosis must be as early as possible.

If determined by a mesenteric vascular occlusion, effective anticoagulant and thrombolytic treatment is possible, whereas if determined by insufficient vascular supply, adequate blood volume and pressure tone must be re-established promptly.

If the diagnosis is later, after 6-8 hours, surgery is required.

At the opening of the peritoneal cavity, the surgeon searches for the affected loops; these, depending on the time elapsed since the vascular insult, have changed colour from the usual pinkish to purplish or blackish (indicating necrosis), and the contiguous free fluid may be serous or haematic.

The surgeon restores patency to the mesenteric vessels and assesses the extent of the affected intestinal tract to be resected.

In intestinal infarction of the large intestine, due to the presence of valid collateral vascular circles, surgical treatment is rarely required.

More frequently, in fact, the acute episode transitions into a subacute and chronic phase, in which a modest thickening of the affected tract remains.

Specific therapies according to cause and type of ischaemia

The specific therapy of an intestinal infarction varies depending on the cause, severity and type of ischaemia.

Common to all therapies are three objectives

to restore normal blood flow to the intestine;
to reduce the patient’s painful symptoms;
surgically remove the intestinal tract that is no longer viable (necrotic).

Specific therapies for ischaemic colitis

If the cause is atherosclerosis, therapy involves pharmacological treatment:

anticoagulant;
vasodilator.

In more severe cases, it may be necessary

stent angioplasty surgery (the occlusion is removed with a kind of balloon)
a bypass surgery, to create an ‘alternative route’ that allows blood to still reach the ischaemic tract.

In other cases (not an embolus), the specific cause is intervened on if possible: intestinal volvulus, colon cancer, heart failure, vasculitis, drug abuse… these are all situations that are intervened on to interrupt the ischaemia.

If the damage to the intestine is irreversible, surgery is performed to remove the necrotic intestinal tract.

Specific therapies for acute mesenteric ischaemia from arterial causes

If the cause is an embolus, therapy includes:

anticoagulant therapy;
vasodilator therapy;
embolectomy (if the embolus is not removed with pharmacological remedies).

If the cause is a thrombus, therapy involves angioplasty with a stent.

In other cases (not an embolus, nor a thrombus), the specific cause is addressed if possible: heart failure, renal failure, occluding tumour, drug abuse… these are all situations in which we intervene to interrupt the ischaemia.

If the damage to the intestine is irreversible, surgery is performed to remove the necrotic intestinal tract.

Specific therapies for chronic mesenteric ischaemia from arterial causes

Therapy includes:

stent angioplasty surgery (the occlusion is removed with a sort of balloon)
bypass surgery, to create an ‘alternative route’ that allows blood to still reach the ischaemic tract.

It is important to reduce the atherosclerotic risk (e.g. with diet and statins).

Specific therapies for mesenteric ischaemia from venous causes

Therapy involves taking anticoagulants for 3-6 months (in some cases therapy is for life).

In the presence of irreversible damage to the intestine, in addition to anticoagulant therapy, surgery is performed to remove the necrotic intestinal tract.

Postoperative course

The postoperative course basically depends on the patient’s condition, the type of therapy applied and the portion of the intestine that has gone into necrosis.

In the case of removal of large parts of the intestine, the hospital stay may be prolonged.

Patients generally return to normal activities within 3-4 weeks, during which they should avoid exertion and follow the diet recommended by their doctor.

An intestinal infarction, whether it affects the colon or the intestine, whether from occlusive or non-occlusive causes, is a potentially fatal event, especially if acute and especially if diagnosis and treatment are not rapid

In the absence of prompt treatment or if it is very severe, ischaemia can lead to various complications

necrosis of the intestinal tract involved (intestinal infarction)
perforation of the intestinal tract involved
intestinal haemorrhage;
leakage of intestinal contents (digested food or faeces depending on the perforated tract);
peritonitis (infection of the peritoneum);
scarring in the affected intestinal tract, with narrowing of the lumen of the intestinal tract that favours future intestinal occlusions;
myocardial depression;
systemic inflammatory response syndrome (sepsis and septic shock);
multi-organ failure;
patient death from haemorrhage and/or shock and/or sepsis and/or other related causes.

Survival

Survival to acute mesenteric ischaemia is highly variable and strongly influenced by the timeliness of intervention: if diagnosis and treatment take place before the ischaemia leads to intestinal infarction, the prognosis is much better, with a low mortality.

If diagnosis and treatment take place after the intestinal infarction, mortality is generally very high, reaching 70-90%, with variability due to many factors, such as the patient’s age and any other pathologies such as diabetes or coagulopathies: elderly patients with such pathologies have a higher average risk.

Early diagnosis and early treatment, as and more than in other diseases, make the real difference between life and death in this case.

It is possible to reduce the risk of ischaemia and intestinal infarction and recurrence by making a few simple lifestyle changes that help prevent atherosclerosis and other risk factors.

A diet rich in fruit, vegetables and whole grains and reducing the amount of added sugar, carbohydrates, cholesterol and fat is essential.

Fibre should be neither too much nor too little.

It is also recommended to: