Arterial Emboli in Mesenteric Arteries - Causes, Symptoms, Diagnosis, and Treatment

Introduction

Arterial emboli in mesenteric arteries (AEMA) fall under the category of occlusive mesenteric arterial ischemia (OMAI) which is further a subdivision of acute mesenteric ischemia (AMI). The condition poses extreme challenges to the physician with a difficult diagnosis and hopeless prognosis. Due to current advances in diagnostic imaging like MRI and sonography, the diagnosis has become easier and an approximate 4-hour window has been proposed, beyond which if no improvement is observed, the patient must undergo surgical exploration.

What Is the Anatomy of the Mesenteric Arteries?

The superior mesenteric artery (SMA) and the inferior mesenteric artery (IMA) supply the midgut and hindgut respectively.

The SMA arises from the ventral aorta and gives rise to inferior pancreaticoduodenal arteries, middle colic, right colic, jejunal and ileal branches. The pancreaticoduodenal arteries give rise to their corresponding anteroinferior and posteroinferior branches, which anastomoses with each other and help maintain bowel perfusion during any mesenteric artery pathology.

The ileocolic artery gives the blood supply to the ileum, cecum, and ascending colon. The middle colic artery supplies blood to the transverse colon and forms anastomoses with the IMA. The right and missile colic arteries branch at the same level and act as an important supply to the marginal artery of Drummond, giving rise to the terminal vasa recta which forms the blood supply to the colon.

IMA, the smallest mesenteric vessel, arises from the anterior aorta and supplies the distal transverse, descending, sigmoid colon, and rectum. The IMA forms anastomoses with the SMA while the rectal branch communicates with the visceral and common blood supply.

Who Is Susceptible to Arterial Emboli in Mesenteric Arteries?

The prevalence of acute mesenteric ischemia is about 0.1 percent of all hospital admissions out of which about 17.5 percent of the cases report mesenteric artery stenosis. AEMA is 66 percent more susceptible in women and with a typical age of onset over 60 years. The condition has shown a predilection for the African-American population over the whites.

Risk factors of AEMA include atherosclerosis, arrhythmias, hypovolemia, congestive heart failure, recent MI, valvular disease, advanced age, intra-abdominal malignancy, younger people who have atrial fibrillation, or risk factors for MVT, oral contraceptive or hypercoagulable states. Emboli of the superior mesenteric artery is the most important and common reason for mesenteric ischemia, accounting for over 40 to 50 percent of the cases.

What Causes Arterial Emboli in Mesenteric Arteries?

Arterial emboli are mostly seen in the SMA than in the IMA. The origin of the emboli or thrombus is often of cardiac origin. Due to the larger diameter of the SMA, the emboli can easily flow into the artery with the blood circulation and get lodged leading to various cascades of events of mesenteric ischemia.

The origin of the emboli from valvular heart disease, coronary heart disease, bacterial endocarditis, prior myocardial infarction, atrial fibrillation, detached atherosclerotic plaque, mural thrombus in the aneurysm, venous thrombosis, Q-fever endocarditis of the aortic valve.

What Is the Pathophysiology of Arterial Emboli in Mesenteric Arteries?

Due to the diameter and parallelism to the abdominal aorta, the emboli can easily pass into the SMA and partially or completely interrupt the distal blood supply about the region of lodgement in the various branches and bifurcations of the SMA, leading to intestinal ischemia, edema, necrosis, and perforation.

Due to the normally high metabolic demand of the mucous, they are the first to be affected followed by the serosa. Initially, the walls of the hypoperfused intestine undergo congestion and become edematous, friable, and hemorrhagic. The condition is reversible at this stage, immediate treatment may result in a better prognosis. Following a cascade of mechanisms, lead to the preservation of splanchnic tissue perfusion, direct arteriolar smooth muscle relaxation, and a metabolic reaction of adenosine and other metabolites of mucosal ischemia. The intestinal mucosa tries to extract increased amounts of oxygen to preserve the integrity of the mucosa. Persistent ischemia leads to disruption of the mucosal barrier through reactive oxygen metabolites and polymorphonuclear neutrophilic activity. Lack of treatment for over 72 hours, results in mucosal barrier collapse and enteric bacterial infiltration which leads to gangrene, ultimately causing intestinal perforation, severe sepsis, and multiple organ failure.

What Are the Signs and Symptoms of Arterial Emboli in Mesenteric Arteries?

The signs and symptoms of AEMA are:

• Constant, diffuse, non-localized, or periumbilical, cramp-like abdominal pain.

• The pain does not get resolved by antispasmodic medications.

• Vomiting.

• Diarrhea.

• Nausea.

• Abdominal distension.

• Fever.

• Rectal bleeding.

• Intestinal edema

• weakened peristalsis

• Hyperactive bowel sounds.

• Peritoneal irritation sign.

How To Diagnose Arterial Emboli in Mesenteric Arteries?

Due to the vague manifestation of AEMA and non-specific laboratory studies, the condition is often misdiagnosed and ultimately proves fatal. The diagnosis begins by recognizing and differentiating the non-specific abdominal pain and ordering further investigatory tests.

Laboratory Studies Reveal:

• Leukocytosis.

• Metabolic acidosis.

• Elevated D-dimer.

• Elevated serum lactate.

• An elevated level of C-reactive protein (CRP).

• Elevated creatine kinase.

• Hemoconcentration.

• High anion gap.

• High amylase.

• High aspartate aminotransferase.

• High dehydrogenase.

• Elevations in some AMI serum makers like L-lactate.

Imaging Studies:

• Plain Radiographs are often not diagnostic of AEMA but are useful in excluding other abdominal conditions like perforated viscus with free intraperitoneal air.

• Angiography has been a standard for diagnosis and preoperative planning for AEMA. The aortogram demonstrates the filling of the proximal SMA vessels with a sharp cutoff without any visualization of the distal vessels or collateral circulation which is of diagnostic importance.

• Abdominal CT (computed tomography) and CT with contrast help assess both larger and smaller vessels of the abdominal cavity. CTs may reveal bowel-wall edema, thrombus in the SMV, enlargement of the SMV, sharply defined vein wall with a rim of increased density, and low density within the vein (diagnostic of thromboembolism).

• MRI (magnetic resonance imaging) and MRA (magnetic resonance angiography) findings are similar to CT but are not preferable due to their cost.

• Ultrasonography may show a thrombus or absent flow in the involved arteries or veins. This is mostly considered a second line of study in the US for AEMA cases while echocardiography may locate the source of embolization or show evidence of valvular pathology.

Other Tests:

• ECG (electrocardiogram) report might indicate myocardial infarction or atrial fibrillation.

• Decompression of the nasogastric tube may be diagnostic and also relieve distention.

• Foley catheterization allows monitoring of urinary output, a lower output may be indicative of minimal fluid resuscitation.

How To Treat Arterial Emboli in Mesenteric Arteries?

The treatment of AEMA can be summarized using the 4Rs:

1. Resuscitation.

2. Rapid diagnosis.

3. Revascularization.

4. Reassessment of the bowel.

Resuscitation with 96 to 99 percent oxygen via mask or even endotracheal intubation, and intravenous administration of isotonic sodium chloride solution, and blood products, if necessary. All patients must be started on broad-spectrum antibiotics and have adequate pain management with blood pressure monitoring.

Pharmacotherapy includes an intra-arterial infusion of Papaverine, thrombolytics, lytic therapy with Urokinase, Streptokinase, or tissue plasminogen activator, and anticoagulation therapy by Enoxaparin or Heparin.

Traditional surgical treatment options include embolectomy, endarterectomy, and bypass grafting. Old-age patients often present with pre-existing conditions where traditional open surgeries might be detrimental and laparoscopic surgery options are indicated. Percutaneous aspiration embolectomy, thrombolysis, balloon thrombectomy, percutaneous transluminal angioplasty, and primary SMA stenting surgeries may be indicated and often followed by explorative laparotomy for resection of the infarcted bowel.

What Is the Differential Diagnosis of Arterial Emboli in Mesenteric Arteries?

• Ovarian torsion.

• Volvulus of the midgut.

• Splenic vein thrombosis.

• Crohn’s disease colitis.

• Ulcerative colitis.

• Perforated viscus.

• Hepatic disease.

• Differential diagnoses.

• Abdominal abscess.

• Abdominal angina.

• Abdominal aortic aneurysm.

• Acute abdomen.

• Acute cholecystitis.

• Biliary colic.

• Acute intermittent porphyria.

• Acute pancreatitis.

• Acute pyelonephritis.

• Aortic dissection.

• Appendicitis.

• Bacterial pneumonia.

• Bacterial sepsis.

• Biliary disease.

• Biliary obstruction.

• Boerhaave syndrome.

• Cholangitis.

• Acute cholecystitis.

• Diverticulitis.

• Ectopic pregnancy.

• Esophageal rupture.

• Gallstones (Cholelithiasis).

• Gastric volvulus.

• Helicobacter pylori infection.

• Hypovolemic shock.

• Postoperative ileus.

• Intestinal perforation.

• Lactic acidosis.

• Large-bowel obstruction.

• Multiple organ dysfunction syndrome in sepsis.

• Myocardial infarction.

• Nephrolithiasis.

• Pneumothorax.

• Septic shock.

• Small-bowel obstruction.

• Testicular torsion imaging.

What Are the Complications of Arterial Emboli in Mesenteric Arteries?

deep vein thrombosis

• Atherosclerosis

• Acute renal failure.

• Bleeding.

• Infection.

• Bowel infarction.

• Prolonged postoperative ileus.

• Graft infection.

• Bowel necrosis.

• Sepsis and septic shock.

• Multiple organ dysfunction syndrome (MODS).

• Death.

What Is the Prognosis of Arterial Emboli in Mesenteric Arteries?

Even after leaps in advancements in patient care with AEMA, the condition remains one with a grave prognosis. Early diagnosis and aggressive treatment greatly reduce mortality. Despite hospitalization, the mortality stands at 70 percentage, so it is crucial to act immediately on primary symptoms rather than waiting on confirmatory reports.

Conclusion

AEME is a surgical emergency with high mortality. The non-specific abdominal pain that does not subdue with antispasmodic mediation requires urgent intervention. Early hospitalization and surgical intervention can greatly decrease mortality. The patients require extensive postoperative care and have a long road to rehabilitation.