Anatomy

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212 N. N. Tun and E. D. Ehrenpreis

Routine use of abdominal CT scanning has resulted in an increasing number of diagnosed cases of MVT and has been responsible for improved survival in acute MVT. The average age at presentation varies between 45 and 60 years with a slight male predominance. The presenting age varies depending on the underlying cause of MVT.

Anatomy

Mesenteric veins parallel their arterial counterparts and drain into the portal venous system. The superior mesenteric vein (SMV) drains blood from the pancreas, small intestine, and the proximal colon. Initially, blood returns through smaller venous structures called the venae rectae. These coalesce to form ileocolic, middle colic and right colic veins which as previously stated combine to form the superior mesenteric vein. The superior mesenteric vein and the splenic vein join together to form the portal vein (Fig. 24.1). The inferior mesenteric vein (IMV) drains blood from distal colon and rectum. The IMV drains the tributaries of sigmoid and left colic veins, as well as the rectal veins and eventually drains into the splenic vein (Fig. 24.2).

Portal vein

Superior

mesenteric vein

Pancreaticoduodenal

veins

Middle colic vein

Right colic vein

Ileocolic vein

Fig. 24.1 Anatomic view of the superior mesenteric vein

Splenic vein

Jejunal veins

Ileal veins

24 Mesenteric Venous Thrombosis 213

Inferior

pancreatico

duodenal

Right colic

Ileocolic

Superior

mesenteric

Por tal

Superior mesenteric

Middle colic

Internal iliac

Middle rectal

Inferior rectal

Inferior vena cava

Splenic

Inferior mesenteric

Left colic

Sigmoid

Superior rectal

Fig. 24.2 Anatomic view of the inferior mesenteric vein

Pathophysiology

Venous thrombosis results from a combination of vascular endothelial injury, hypercoagulability, and stasis of blood ﬂow. These are classically known as Virchow’s triad. As stated previously, MVT almost always involves the superior mesenteric vein distribution whereas the inferior mesenteric vein distribution is rarely involved for reasons which are not clearly understood. Acute MVT may also involve more than one mesenteric vein as well as its branches. The occurrence of a thrombus in a large vein increases venous pressure and vascular resistance within the mesenteric venous bed. A reduction in perfusion pressure follows these processes. Reduced venous ﬂow and translocation of ﬂuid into nearby tissues creates a

214 N. N. Tun and E. D. Ehrenpreis

pathologic state wherein signiﬁcant bowel wall edema, and hemorrhage of the submucosa occurs. Depending on the degree of venous occlusion and the presence or absence of collateral drainage, MVT can cause progressive changes to intestinal tissue, leading in time to intestinal ischemia. In the most severe cases, intestinal infarction may occur. Milder cases of MVT are characterized by intestinal ischemia without infarction.

The presence of chronic MVT often produces dilated venous collaterals as a consequence of elevated venous pressure. These dilated, pressure-ﬁlled veins carry the risk of venous rupture and intestinal bleeding. Patients with chronic MVT may also have concomitant portal vein thrombosis with subsequent portal hypertension.

Patient At Risk for MVT

There are a variety of conditions that predispose to the development of MVT (Table 24.1). Since the initiating event involves the appearance of a clot within the vascular system, any condition that accentuates the risk of coagulation will predispose to MVT. Prothrombotic disorders may be hereditary (such as Factor V Leiden mutation, Protein C deﬁciency, Protein S deﬁciency and antithrombin III deﬁciency) or acquired (as seen in a variety of malignant neoplasms). Hormonal factors including pregnancy and use of oral contraceptive medications are potential risk factors for MVT. Surgery, trauma and inﬂammatory disorders such as acute pancreatitis, inﬂammatory bowel disease, and intra-abdominal infections also have assocaitions with the development of MVT. Stasis within the mesenteric venous system can occur in profound cardiac insufﬁciency, portal hypertension and hyperviscosity (as seen in polycythemia vera and paroxysmal nocturnal hemoglobinuria). A variety of other conditions including nephrotic syndrome and hyperhomocysteinemia may also predispose to MVT. Up to 37% of cases of MVT are classiﬁed as idiopathic with no discoverable predisposing factors. Notably, inﬂammation and other local factors appear to contribute to clot formation in large mesenteric veins, whereas hypercoagulable disorders are more likely to be responsible for clot formation in smaller vessels such as venae rectae and venous arcades.

Clinical Presentation

MVT can be acute, subacute or chronic and its signs and symptoms are often nonspeciﬁc, making the initial diagnosis highly challenging. Yet early diagnosis is crucial to increase survival in patients with MVT. The clinical features of MVT depend on the location and acuity of clot formation within the mesenteric vasculature.

24 Mesenteric Venous Thrombosis 215

Table 24.1 Conditions predisposing to MVT

A. Thrombophlia B. Inﬂammation C. Stasis D.

Heritable Intraabdominal Cirrhosis

Deﬁciency of protein C or S or antithrombin II

Factor V Leiden mutation Prothrombin gene mutation

Sickle cell disease Trauma Congestive

Acquired Surgery (most

Hematologic conditions: Infection

Polycythemia

Myeloﬁbrosis

Myeloproliferative disease

Monoclonal gammopathy

JAK2 mutation

Anti-phosphoidal antibodies

Paroxysmal nocturnal hemoglobinuria

Disseminated intravascular coagulation

Heparin-induced thrombocyopenia and thrombosis

Pancreatitis Congenital

Inﬂammatory bowel disease

commonly splenectomy)

venous anomaly

Heat failure

splenomegaly

Idiopathic

The most common symptom in acute MVT is abdominal pain. The symptom of abdominal pain is reported in 91–100% of MVT cases. Like other causes of acute mesenteric ischemia, acute MVT often presents with severe abdominal pain that is out of proportion to the ﬁndings on physical examination of the abdomen. Approximately 50% of patients have nausea and vomiting. Gastrointestinal bleeding occurs in about 15% of patients and is characterized by the presence of hematemesis, hematochezia, or melena. Occult blood in the feces is detectable in up to 50% of the cases. About 75% of patients report having symptoms for more than 48 h before seeking medical attention. Some authors suggested that the arbitrary duration of symptoms of acute MVT is less than 4-weeks. Although ﬁndings on abdominal examination can be variable, the presence of peritoneal signs indicate that the disease has progressed to bowel necrosis and infarction. In one study, 6– 29% of pati ents with acute MVT also manifest hemodynamic instability on presentation.

216 N. N. Tun and E. D. Ehrenpreis

MVT can also present more insidiously with a subacute or chronic pattern. Those patients can be asymptomatic or may present with only intermittent, nonspeciﬁc abdominal pain, likely as a result of the development of collateral circulation to compensate for diminished ﬂow in the affected large vessel.

Chronic MVT may also present with complications related to portal hypertension such as ascites or variceal bleeding.

Diagnosis

As no clinical features are speciﬁc for MVT, it is essential to have a high index of suspicion to arrive at a timely, and potentially life-saving diagnosis. Given a suggestive clinical presentation, thorough history taking can uncover further clinical clues that increase the likelihood that MVT is present. This process, in turn, results in further, appropriate diagnostic testing.

Imaging

Imaging studies play a major role to establish the diagnosis of MVT by revealing the presence of thromboses within the mesenteric venous system.

Contrast-enhanced computerized tomography (CT) is the initial diagnostic modality of choice for MVT. When present, MVT is characterized on contrast-enhanced CT by the presence of a ﬁlling defect within a mesenteric vein (Figs. 24.3, 24.4 and 24.5). Other ﬁndings on the CT scan include bowel wall thickening, indistinct bowel margins, gas within bowel wall (pneumatosis intestinalis) and the presence of a thickened mesentery (see Figs. 24.3, 24.4, 24.5 and

24.6). The sensitivity and speciﬁcity of contrast-enhanced CT scan for the diagnosis

of MVT are reported to be 93% and 100% respectively with positive and negative predictive values of between 94 and 100%.

Magnetic resonance venography (MRV) is an excellent diagnostic tool for the diagnosis of acute or chronic MVT with reports of 100 percent sensitivity and speciﬁcity in some studies. It can also be used in patients with allergy to iodinated contrast. However, contrast-enhanced CT scan is preferred over MRV because of its widespread availability and shorter testing time unless contrast allergy precludes its use.

In patients with an uncertain diagnosis of MVT with a non-diagnostic CT or MRI where the suspicion remains high, catheter-based mesenteric angiography is an appropriate study. Angiography also offers access for interventional measures such as thrombolysis. Although Doppler ultrasound can be rapidly performed at the bedside and is widely available, it is not as sensitive as CT and MRI and not able to detect blood clots in smaller mesenteric vessels.

24 Mesenteric Venous Thrombosis 217

Fig. 24.3 Coronal CT image in a patient with history of ulcerative colitis demonstrates a ﬁlling defect within the superior mesenteric vein (arrow) extending distally to the portosplenic con ﬂuence and proximally into the jejunal and ileocolic tributaries. Perivascular hazy fat-stranding (arrowheads), one appearance of “misty mesentery”, represents mesenteric edema from venous congestion. With permission from Dr. Abraham Dachman and Dr. Justin Ramirez

Laboratory Findings

Although laboratory tests are neither sensitive nor speciﬁc for MVT, patients often have abnormal laboratory ﬁndings such as leukocytosis, elevated lactic acid level and metabolic acidosis with an increased anion gap. Increased mortality occurs in patients with high serum lactic acid level, and metabolic acidosis, however normal serum lactate and pH do not rule out MVT. D-dimer testing is not helpful as it can also be increased in other infectious or inﬂammatory pathologic processes.

After conﬁrmation of MVT, testing for hypercoagulab ility is recommended in patients without known provoking conditions. Those tests will help predict associated complications of the underlying hypercoagulable state and determine the duration of anticoagulant therapy.

Treatment

The treatment of MVT involves nonoperative management alone or in combination with interventional radiological options and surgery.

218 N. N. Tun and E. D. Ehrenpreis

Fig. 24.4 Axial CT image from the same patient shows additional thrombus within the main portal vein extending into the right portal vein (arrowheads). Inﬂammatory bowel disease confers an in increased risk of venous thrombosis. With permission from Dr. Abraham Dachman and Dr. Justin Ramirez

Fig. 24.5 Coronal CT image in a different patient again demonstrates a thrombus ﬁlling defect within the SMV (arrow) and ill-deﬁned peri-visceral fat stranding (arrowheads). With permission from Dr. Abraham Dachman and Dr. Justin Ramirez

24 Mesenteric Venous Thrombosis 219

Fig. 24.6 Axial CT image from the same patient demonstrates bowel-wall edema with associated fat-stranding (arrowheads) suspicious for bowel ischemia. With permission from Dr. Abraham Dachman and Dr. Justin Ramirez

Nonoperative Management

In patients with MVT (acute or subacute) but no evidence of bowel infarction, the mainstay of treatment is systemic anticoagulation combined with supportive treatment. Supportive measures include bowel rest, nasogastric tube insertion for bowel decompression, intravenous ﬂuid administration and pain control. The beneﬁt of routine prophylactic antibiotics usage is not clear though they are required if the suspicion is high for bowel ischemia, infarction, and peritonitis.

Anticoagulant therapy is administered without delay and is the cornerstone of treatment. Anticoagulation limits thrombus progression, allows for venous recanalization, promotes bowel perfusion and improves survival. Anticoagulation therapy is initiated with either intravenous infusion of unfractionated heparin or subcutaneous injection with low molecular weight heparin (LMWH). The latter should not be used in patients who may undergo operative interventions or in those with renal dysfunction. After stabilization of patient’s condition, anticoagulation is transitioned to oral agents (vitamin K antagonist such as warfarin or non-vitamin K oral anticoagulant, such as rivaroxaban). Anticoagulation for at least 3–6 months is recommended for cases with provoked and reversible causes. Idiopathic cases and those with hypercoagulable state usually requi re extended-duration anticoagulation.

Patients with chronic MVT may also beneﬁt from anticoagulation assuming that the beneﬁt of long- term anticoagulation outweighs its risk. In cases of chronic MVT presenting with gastrointestinal bleeding, anticoagulation is often withheld until control of bleeding is achieved.

220 N. N. Tun and E. D. Ehrenpreis

Interventional Radiology Procedures

In patients with inadequate response to anticoagulation but without evidence of bowel infarction, inte rventional radiology is indicated. These procedures are generally performed in specia lized centers with available technical expertise. However, these procedures are not a substitute for anticoagulation. According to some literature, catheter-directed ﬁbrinolysis results in improvement of symptoms as well as reduces the rate of bowel resection. However, bleeding is a serious complication of catheter-directed ﬁbrinolysis, and its reported rate is as high as 60%. Therefore, candidacy for ﬁbrinolysis needs to be carefully determined depending on potential beneﬁts and risks.

Catheter-assisted thrombectomy is considered as an option in cases of sizeable venous thromboses for patients in whom use of thrombolytic agents is contraindicated. Thrombectomy is most effective in the setting of an acute thrombus.

Surgery

Surgery should be performed without delay when there is evidence of bowel infarction or perforation. Surgical resection of necrotic bowel and anastomosis is the standard procedure with open laparotomy preferred over a laparoscopic procedure. Determining the extent of bowel resection can be challenging as the differentiation between viable and ischemic bowel is often difﬁcult in the acute stage of MVT. Some surgeons advocate the use of intraoperative Doppler ultrasound or ﬂuorescein infusion to assess bowel viability. Some authors recommend a conservative strategy to limit the extent of initial resection when there are areas of bowel with questionable viability, followed by second-look surgery within 24–48 h to reassess bowel viability as well as to determine the need of additional resection. The intention of a conservative strategy is to minimize unnecessary bowel resection, short bowel syndrome and its long-term consequences.

Prognosis

Compared to other forms of acute mesenteric ischemia, acute mesenteric venous thrombosis has a better prognosis. According to an extensive systematic review of acute mesenteric ischemia cases, the overall mortality rate of MVT was 44%, compared with 66–89% for arterial occlusive or nonocclusive ischemia. Early recognition and treatment have led to improved survival in MVT cases. In rapidly diagnosed and treated cases, some recent studies report mortality rates between 10 and 20% for acute MVT. Patients with intestinal infarction have a higher mortality rate that is greater than 75%. Important prognostic factors for survival from MVT also include age, the comorbidities predisposing to MVT and timing of diagnosis and treatment.

24 Mesenteric Venous Thrombosis 221

Table 24.2 Prognosis and mortality of MVT

∙ Prognostic factors

- Age

- Co-morbidities (e.g. malignancy, cirrhosis, portal hypertension, gastrointestinal bleeding)

- Time to diagnosis and treatment

- Complications (e.g. intestinal infarction or perforation)

∙ The overall mortality rate of acute MVT = 44% ∙ Cases of early diagnosis and treatment = 10 and 20%

mortality

∙ Cases complicated with intestinal infarction >75% ∙ Prognosis of chronic MVT is variable depending on nature

and severity of underlying etiology. 5-year survival rates are 78 to 82%

The prognosis of chronic MVT is related to the nature and severity of underlying illness. 5-year survival rates have been reported as high as 78 to 82% (Table 24.2).

Anatomy

Pathophysiology

Patient At Risk for MVT

Clinical Presentation

Diagnosis

Imaging

Laboratory Findings

Treatment

Nonoperative Management

Interventional Radiology Procedures

Surgery

Prognosis

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