Management of Mesenteric Vascular Occlusion.

 Mesenteric vascular disease encompasses a family of diseases in which the end result is ischemic injury to the small or large bowel.  Early recognition and appropriate management offers the best outcome, but this is not easily achieved because in the early stages the presentations are vague and non-specific.

 The classic presentation for mesenteric ischemia will be in a patient :  Older than 50 years of age.  sudden onset of abdominal pain.  Nausea.  Vomiting.  Diarrhea.

 The abdominal pain will initially be severe and diffuse without any localization.  One of the distinctive findings in mesenteric ischemia is that of abdominal pain that is out of proportion to examination.

 The patient may be screaming in pain, but their abdomen is soft with no guarding or rebound. As the disease progresses and the bowel becomes infarcted, the patient will develop abdominal distension with guarding, rebound, and absence of bowel sounds.  Heme-positive stools are also a late finding.

 Mesenteric Artery Embolus  Mesenteric Artery Thrombosis  Mesenteric Vein Thrombosis (MVT)  Non-occlusive Ischemia

 This is the most common cause of mesenteric ischemia accounting for 40 to 50% of cases.  The prognosis is poor with a 70% mortality rate.  Onset of symptoms is sudden due to the acute nature of an embolus lodging in the artery with little time for collaterals to form.  Patients with mesenteric artery embolus will present with the classic abdominal pain out of proportion to exam.

 Risk factors:  Arrhythmias (atrial fibrillation being the most common).  Post-myocardial infarction with mural thrombi.  Valvular heart disease.  Structural heart defects (such as right to left shunts).

 The most common location of an embolus is in the superior mesenteric artery (SMA) due to the oblique angle of the SMA from the aorta.  The embolus usually lodges distal to the origin of the middle colic artery, sparing the duodenum and proximal jejunum as compared to a mesenteric artery thrombosis which causes a more proximal blockage leading to extensive bowel ischemia.

 It accounts for 25 to 30% of mesenteric ischemia cases and possibly carries the worst prognosis with a mortality of 90%. This high mortality is due to the thrombus usually being near the origin of the SMA causing an enormous amount of bowel necrosis.  Most patients with a mesenteric artery thrombosis have a history of chronic mesenteric ischemia with vague and insidious symptoms such as weight loss, abdominal angina (abdominal pain after meals), diarrhea, and fear of food.

 Risk factors:  systemic atherosclerosis and older age.

 MVT is the least common cause of mesenteric ischemia involving 10% of cases with a mortality of 20 to 50%. It occurs in a relatively younger patient population.  Symptoms can occur acutely or occur over time depending on the pace at which the thrombus progresses. Accordingly, the abdominal pain onset and location can be variable as well, however, there is no postprandial abdominal pain or food fear as seen in mesenteric artery thrombosis.  Patients may also have other accompanying symptoms such as vomiting and diarrhea

 Risk factors :  Hypercoagulable states (Factor V Ledien, protein C deficiency, etc.)  Recent surgery.  Malignancy.  Cirrhosis.  In addition, up to 50% of patients will have a history of deep vein thrombosis.

 Non-occlusive ischemia accounts for 20 to 30% of cases with mortality rates ranging from 50 to 90%.  This type of mesenteric ischemia occurs in low flow states in absence of an arterial or venous occlusion.  Any condition associated with decreased cardiac output can cause non-occlusive ischemia including cardiogenic shock, congestive heart failure, and arrhythmias.

 Sepsis, hypotensive states, and drugs inducing mesenteric vasoconstriction (Digoxin, Cocaine, Alpha-agonists, Beta- blockers) can also be causes.  This disease process often develops during hospitalization in sick patients suffering from other illnesses so a high index of suspicion is required to diagnose it. Treatment involves targeting the underlying cause and correcting it.

 Labs:  Generally, labs by themselves are not helpful in making the diagnosis of mesenteric ischemia from other abdominal pathologies.  The white blood cell count is commonly elevated, but is a non-specific finding and a normal white count does not rule out the disease.  Hemoconcentration, elevated amylase levels, and a metabolic acidosis may also be found in mesenteric ischemia, but again are non-specific findings.  An elevated lactate level is sensitive for mesenteric ischemia. However, the lactate is only elevated late in the disease course after bowel has infarcted and its specificity is low.

 Plain Radiography  An upright film should be a part of the abdominal x-ray series to help rule out free air. As the ischemia progresses, subtle signs such as thickening of bowel wall and distended loops of bowel can be seen, but like the labs are non- specific signs.  Pneumatosis of the intestinal wall can occasionally be seen on plain film, but is a late finding when bowel has become necrotic.

 Angiography:  Is the gold standard for mesenteric ischemia allowing for diagnosis and therapy. Lateral views allow for examination of the origins of the major vessels while AP views allow for visualization of distal mesenteric vessels. The site and type of occlusion can be identified via angiography.  Non-occlusive ischemia can also be identified via this modality. Medications such as papaverine and thrombolytics can also be infused during angiography (more details in the Treatment section).  The downsides of angiography are that it is an invasive and lengthy procedure and may not be readily available at all hospitals or all times of day.

 CT angiography (CTA)  Is rapidly becoming an alternative to angiography. CTA is fast, less invasive than angiography, and readily available in most hospitals. In addition to the vascular findings of thrombus and emboli, CTA can also demonstrate more subtle signs of mesenteric ischemia such as circumferential thinking of the bowel wall, bowel dilatation, bowel wall attenuation, and mesenteric edema.

 Intravenous rehydration Vigorous replacement of water and electrolytes is initiated with balanced saline or colloid solution. Adequacy of replacement is monitored by serial measurements of the urine output, vital signs and central venous or wedged pulmonary arterial pressure.  Intravenous antibiotics Blood culture is taken and broad-spectrum antibiotics covering Gram-negative organisms and anaerobes are commenced. This will usually be a second- or third- generation cephalosporin together with metronidazole. .

 Correction of metabolic acidosis Metabolic acidosis is due to a combination of low tissue perfusion, absorption of products of tissue necrosis, and impaired respiratory exchange. Restoration of circulating blood volume will help to correct acid-base equilibrium. Occasionally, bicarbonate therapy may be necessary.  Heparin Continuous infusion with heparin is given for thromboembolic disease to prevent clot extension and to counteract disseminated intravascular coagulation. This therapy is interrupted during surgery

 Mesenteric Artery Embolus  Thrombolytics can be directly infused into the artery containing the embolus during angiography. This is a good technique to use in non-operative candidates. The drawback is that bowel viability generally assessed during laporatomy cannot be done. In addition, contraindications to thrombolytics include recent surgery or GI bleed, recent stroke, and peritoneal signs indicating bowel infarction.  If operative management is decided, revascularization is done first so that any ischemic-looking bowel can recover with the return of blood flow. Once blood flow is reestablished, any bowel that remains infarcted and necrotic is then resected. Surgeons will do "second look" procedures hours later if the viability of a section of bowel was in question during the first surgery.

 Mesenteric Artery Thrombosis  In this etiology, heparin should be started as soon as the diagnosis is made and prior to surgery. The corrective operative measures for mesenteric artery thrombus are the same as for mesenteric artery embolus.  For non-operative candidates, percutaneous transluminal angioplasty is done. In patients with chronic mesenteric ischemia and mesenteric artery thrombosis, there has been complete resolution of symptoms after intervention.

 Mesenteric Vein Thrombosis  If there are signs of infarction, then operative care is required. Otherwise anticoagulants, thrombolytic therapy, or a combination of both is incorporated. These patients will generally require life-long anti-coagulation.

 Non-occlusive Mesenteric Ischemia  The treatment is to correct the underlying cause of the low flow state to the bowel whether it be sepsis or decreased cardiac output. Papaverine can help treat the vasoconstriction of the vessels to the mesentery which will maximize blood flow. Patients who develop peritoneal signs must go to the OR.

 Mesenteric ischemia must be considered early in a patient's course with aggressive management including the early use of CTA or angiography  It is very important to know the risk factors and treatment modalities of the four different types of mesenteric ischemia: mesenteric artery embolus, mesenteric artery thrombosis, mesenteric vein thrombosis, and non-occlusive ischemia  The signs and symptoms for mesenteric ischemia are vague with "pain out of proportion to exam" being the classic presentation  Currently, there are no highly sensitive and specific lab tests for mesenteric ischemia  Despite the new advances in medicine, the mortality for mesenteric ischemia remains very high

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