REVIEW

Mesenteric Venous Thrombosis

Ashwani K. Singal, MD; Patrick S. Kamath, MD; and Ayalew Tefferi, MD

Abstract

The prevalence of mesenteric venous thrombosis has increased over the past 2 decades with the routine
use of contrast-enhanced computed tomography (CT) in patients presenting with abdominal pain and
those with portal hypertension. Concurrent with increasing recognition, routine and frequent use of
anticoagulation has reduced the need for surgical intervention and improved outcome in these patients.
Acute thrombosis often presents with abdominal pain, whereas chronic disease manifests either as an
incidental finding on CT or with features of portal hypertension. Contrast-enhanced CT diagnoses about
90% of cases. The presence of collateral circulation and cavernoma around a chronically thrombosed vein
differentiates chronic from acute disease. The superior mesenteric vein is often involved, whereas
involvement of the inferior mesenteric vein is rare. Associated portal venous thrombosis can be seen if the
disease originates in the major veins instead of the small vena rectae. Thrombophilia and local abdominal
inflammatory conditions are common causes. Management is aimed at preventing bowel infarction and
recurrent thrombosis. Anticoagulation, the mainstay of management, has also been safely used in patients
with cirrhosis and portal hypertension. This review discusses the pathogenesis of thrombosis of mesenteric
veins, the diagnosis and differentiation from arterial ischemia, the emergence of the JAK2 (Janus kinase 2)
sequence variation as a marker of thrombophilia and myelodysplastic neoplasms, and new anticoagulants.
Algorithms for the management of acute and chronic mesenteric venous thrombosis are provided to help
readers understand and remember the approach to the management of acute and chronic mesenteric
venous thrombosis.
ª 2013 Mayo Foundation for Medical Education and Research n Mayo Clin Proc. 2013;88(3):285-294

M
esenteric venous thrombosis (MVT)
may be an incidental finding on
abdominal imaging or a cause of
abdominal pain. Mesenteric venous thrombo-
sis was originally described by Warren and
Eberhard as a distinct entity that is separate
from mesenteric arterial thrombosis.1 Isolated
thrombosis of the portal vein is also a distinct
entity but can occur in association with MVT.
Prothrombotic states or thrombophilia and
local intra-abdominal infections are major
causes of MVT.1 Abdominal pain is the most
common symptom, especially with acute
thrombosis, whereas chronic MVT manifests
as portal hypertension and esophageal varices.
Over the past approximately 2 decades, the
increasing use of computed tomography
(CT) for the investigation of abdominal pain
and anticoagulation as the first approach to
treatment of acute MVT have improved out-
come in these patients. Surgery and bowel
resection may occasionally be needed for pa-
tients with bowel infarction, perforation, and
peritonitis. The management of patients with
chronic MVT is aimed at reducing complica-
tions of portal hypertension.
NORMAL MESENTERIC CIRCULATION
The venous drainage of the intestine follows
the same pattern as the arterial circulation From the Division of
Gastroenterology and
(Figure 1). The superior mesenteric vein (SMV) Hepatology (A.K.S., P.S.K.)
drains the entire bowel from the second por- and Division of Hematol-
tion of the duodenum to approximately the right ogy (A.T.), Mayo Clinic,
two-thirds of the transverse colon. The SMV Rochester, MN. Dr Singal
is now with the Division of
joins the splenic vein posterior to the neck of Gastroenterology and
the pancreas to form the portal vein. The left gas- Hepatology, University of
Alabama at Birmingham.
tric vein draining the lower part of the esophagus
and upper half of the lesser curve of the stomach
enters at the point of formation of the portal vein.
Short gastric veins draining the fundus of the
stomach enter into the splenic vein. The inferior
mesenteric vein (IMV) drains the left colon and
enters into the splenic vein.
ACUTE MVT
Incidence and Prevalence
Mesenteric venous thrombosis is a rare condition
accounting for 1 in 5000 to 15,000 inpatient ad-
missions, 1 in 1000 emergency department ad-
missions, and 6% to 9% of all cases of acute
mesenteric ischemia.2-4 With the widespread
use of abdominal imaging, recognition of MVT

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ARTICLE HIGHLIGHTS
n A high index of suspicion is required for the diagnosis of mes-
enteric venous thrombosis (MVT).
n Computed tomography (CT) diagnoses more than 90% of cases
of MVT.
n The presence of portal cavernoma on CT distinguishes acute
from chronic MVT.
n The JAK2 sequence variation is a new noninvasive marker for
diagnosing underlying thrombophilia and myelodysplastic syn-
drome among patients with MVT.
n The increasing use of anticoagulant medication as initial treat-
ment and the widespread use of abdominal CT have improved
the outcome in patients with MVT.
has increased. The recognition of MVT in Sweden
has increased from 2.0 per 100,000 patient-years
before the year 2000 to 2.7 per 100,000 patient-
years after 2000.5
Pathogenesis
Prothrombotic states, local vessel wall injury,
and venous stasis contribute to MVT (Table 1).
Thrombosis may originate in the vena rectae or
in the major veins. The latter is usually associ-
ated with portal venous thrombosis, whereas
the former manifests as isolated thrombosis of
FIGURE 1. Normal mesenteric circulation.
n n
286 Mayo Clin Proc.
MAYO CLINIC PROCEEDINGS
mesenteric veins.6 The SMV is more commonly
involved, with IMV thrombosis, for unclear rea-
sons, representing only 0% to 11% of cases of
MVT.7-9
When the underlying etiology cannot be
identified, the term primary or idiopathic MVT
is used. The proportion of patients with primary
MVT varies from 0% to 49%, with a decrease
in frequency with more extensive investigation
(Table 1).10,11 In many patients, more than
one factor may account for the thrombosis.12
Prothrombotic states are the most common
cause for patients presenting with isolated
MVT. In contrast, local causes may be more fre-
quently associated with combined mesenteric
and portal venous thrombosis.6 Myeloprolifera-
tive neoplasms and malignancy are the most
commonly diagnosed thrombophilic condi-
tions. Abdominal operations, especially sple-
nectomy, may be a cause of MVT.13-15 The
prevalence of mesenteric and portal venous
thrombosis is higher in cirrhotic patients, prob-
ably due to turbulent venous flow and an
increased tendency for thrombosis,16 and is
reported in approximately 15% of patients
awaiting liver transplant.16
Mesenteric venous thrombosis impairs
venous return from the bowel, resulting in
venous engorgement and ischemia. With rapid
and complete occlusion of mesenteric veins,
there may be insufficient time for development
of a collateral circulation, and transmural bowel
infarction may occur. The transition from nor-
mal to ischemic bowel is gradual, unlike in arte-
rial ischemia in which this transition is abrupt.
Arterial spasm secondary to venous engorge-
ment may occur, with resulting irreversible
bowel ischemia despite treatment of the venous
thrombus. Thrombosis isolated to mesenteric
veins results in earlier and more frequent devel-
opment of infarction as compared to mesenteric
combined with portal venous thrombosis. With
transmural infarction, there is loss of integrity of
the bowel mucosa, allowing bacterial transloca-
tion and potential for occurrence of the fatal
consequences of lactic acidosis, sepsis, multior-
gan failure, and death.
Clinical Presentation
The presentation of MVT is either acute with
sudden onset of symptoms, subacute with pre-
sentation over days to weeks, or chronic.
Acute MVT presents with abdominal pain
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MESENTERIC VENOUS THROMBOSIS

constipation, anorexia, and fever. Fever at the

TABLE 1. Causes of Mesenteric Venous Thrombosis
onset of symptoms suggests pylephlebitis or an
Thrombophilia infected portal venous thrombosis seen with in-
Inherited
testinal infections, usually acute diverticulitis or
Protein C or S deficiency
appendicitis.
Factor V Leiden deficiency
Antithrombin deficiency
About 75% of patients are symptomatic for
Prothrombin gene sequence variation (G20210A) more than 48 hours before presentation, with
Methylene tetrahydrofolate reductase gene the mean duration of symptoms reported to
sequence variation vary from 6 to 14 days.3,6,10,13,17 Abdominal
Acquired signs such as abdominal tenderness,3,6 abdomi-
Hematologic conditions nal distention,2,3,13 and ascites2,9,18 may occur
Polycythemia veraa with increasing ischemia. Patients may be dehy-
Myelofibrosisa drated from volume loss or third-space com-
Thrombocythemiaa partmentalization of fluid. In severe cases,
JAK2 gene sequence variation
peritoneal signs such as rebound tenderness,
Antiphospholipid antibodies
guarding, and/or rigidity may be noted because
Paroxysmal nocturnal hemoglobinuria
Nonhematologic conditions
of transmural infarction and bowel gangrene.
Malignancyb About 6% to 29% of patients, especially those
Oral contraceptive pills with severe disease, may be hemodynamically
Pregnancy unstable.2,3,18 Peritoneal signs, hemodynamic
Nephrotic syndrome instability, and fever suggest severe disease with
Hyperhomocysteinemia bowel infarction and poor outcome.
Local factors causing vessel wall injury
Inflammatory conditions Diagnosis
Pancreatitis
Inflammatory bowel disease
Differentiation between ischemia due to MVT
Diverticulitis and that due to mesenteric arterial thrombosis
Peritonitis is usually possible. The former usually occurs
Appendicits in the setting of thrombophilia, whereas cardiac
Intra-abdominal surgeryc causes and atrial fibrillation are commonly
Abdominal trauma
Stasis
associated with arterial ischemia. Other causes
Congestive splenomegaly of acute abdomen such as acute pancreatitis, in-
Cirrhosis testinal obstruction, viscous perforation, acute
Congestive heart failure cholecystitis, and acute appendicitis can be
Idiopathic ruled out by clinical presentation and compat-
a
Either one of these is included in the diagnosis of myelo-
ible abdominal imaging. A personal or family
proliferative neoplasms. Sequence variation analysis for the history of deep venous thrombosis, present in
Janus kinase gene (JAK2V617F) is a diagnostic criterion and about 17% to 44% of cases, heightens suspi-
b
identifies latent cases of myeloproliferative neoplasms. cion for a diagnosis of MVT.2,19 Similarly,
Intra-abdominal cancers in most patients, with pancreatic
development of ascites in a patient with acute
cancer being the most common.
c
The most common surgery is splenectomy.
abdominal pain heightens suspicion for MVT.
Routine laboratory evaluation is usually not
helpful for the diagnosis of MVT. Patients with
and chronic MVT with complications of portal severe disease and dehydration may show evi-
hypertension such as variceal hemorrhage. dence of hemoconcentration. Nonspecific leuko-
Acute disease is more likely to result in bowel cytosis may be present. Patients with small-vessel
infarction compared with subacute MVT. disease and isolated MVT may have higher plate-
The mean age at presentation is 40 to 60 let counts compared to patients with combined
years, and the disease is most common in males. portal and mesenteric vein involvement.6 This
Abdominal pain is the dominant symptom and may be due to associated thrombophilic condi-
is usually severe, located in the mid abdomen, tions in those with small-vessel disease and iso-
and out of proportion to physical signs. Nausea, lated MVT. Amylase levels may be elevated
vomiting, diarrhea, or gastrointestinal bleeding with bowel ischemia, but levels higher than
may also occur. Other reported symptoms are 1000 U/L suggest acute pancreatitis. Liver

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enzymes may be elevated to a modest degree,
especially in patients with portal vein involve-
ment.3 Hypoxemia and lactic acidosis are late
findings and predict poor outcome. Blood cul-
tures should be obtained in patients with high fe-
ver, peritoneal signs, hemodynamic instability,
and perforation. Paracentesis and cultures may
be helpful because hemorrhagic ascites may
develop in some patients.
Abdominal Imaging. With routine use of
abdominal imaging, the diagnosis of MVT is
usually made noninvasively.3,7,13,14,20 Plain
abdominal radiography shows abnormalities in
50% to 75% of cases, with mostly nonspecific
findings such as dilated bowel loops, ileus, and
thumbprinting from mucosal edema. Specific
findings of bowel ischemia are seen in fewer
than 5% of cases.1 The presence of gas within
the portal vein or intestinal wall and free air
within the abdomen suggest bowel gangrene
and bowel perforation, respectively. Computed
tomography with contrast medium is the diag-
nostic modality of choice. The diagnostic find-
ing for MVT is the presence of thrombus within
the vein seen as focal translucency (Figure 2).
Other findings are expansion of the vein with
a sharply defined wall. The accuracy of CT is
about 90% for the diagnosis of MVT.2,14,21
Findings of intestinal ischemia such as bowel
wall thickening of greater than 3 mm, thickened
mesentery, indistinct bowel margins, and asci-
tes may also be noted. Homogeneous bowel
enhancement along with bowel wall thickening
of 10 mm or more has about 90% accuracy for
identification of transmural infarction.22
Abdominal Doppler ultrasonography can
detect thrombosis of larger veins but is limited
by its inability to visualize small vena rectae.
Magnetic resonance angiography is an excellent
technique, but experience with its use is limited.
Further, motion artifacts may affect its accuracy.
Nuclear scintiangiography is relatively easily
performed, but the technique is limited by
a lower accuracy of 75% and the lack of wide
availability.4,19 Mesenteric angiography is sel-
dom required for the diagnosis of MVT.6
Identifying the Cause of Mesenteric Throm-
bosis. Local causes such as an abdominal
malignant neoplasm, surgery, or inflammatory
conditions are usually obvious on history,
physical examination, and abdominal imaging.
n n
288 Mayo Clin Proc. March 2013;88(3):285-294
MAYO CLINIC PROCEEDINGS
FIGURE 2. Computed tomographic image from
a patient with acute mesenteric and portal vein
thrombosis (arrow). The 53-year-old previously
healthy man presented with a 2-week history of
epigastric abdominal pain. Acute thrombus is
visible as a central lucency within the expanded
vein with a surrounding white rim but no col-
lateral vessels.
Before starting anticoagulants, blood should be
withdrawn for a thrombophilia screen, looking
especially for a myeloproliferative neoplasm
(MPN)dnamely, polycythemia vera, essential
thrombocythemia (ET), and myelofibrosis. The
diagnosis of MPN may be difficult in the pres-
ence of portal hypertension and splenomegaly
because hemodilution and hypersplenism may
result in lower blood counts.
The JAK2V617F sequence variation with
gain of function resulting in growth factore
independent proliferation of blood cell lines has
been reported in 5% to 46% of cases without overt
MPN.12,23-28 Further, the presence of the JAK2
sequence variation can differentiate reactive
thrombocytosis from ET and primary from sec-
ondary polycythemia with reported positivity of
the JAK2 sequence variation in nearly all cases of
polycythemia vera and in 50% of cases of ET
and myelofibrosis.29,30 Hence, detection of the
JAK2 sequence variation has replaced bone mar-
row examination as the first test to screen for
MPNs (Table 2).27,28,31,32
Treatment
The goals of treatment of MVT are to prevent
extension of the thrombus and intestinal
infarction in the short term and to prevent
recurrence of thrombosis in the long term.
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MESENTERIC VENOUS THROMBOSIS
Medical Management. Medical management
includes general measures and anticoagulation.
Pain control, bowel rest, and replacement of
fluids and electrolytes should be initiated for
patients with an acute presentation. Red blood
cell transfusion may be needed for gastrointesti-
nal bleeding and nasogastric aspiration for
patients with abdominal distention, ileus, and
severe intractable nausea or vomiting. Broad-
spectrum antibiotics are used for patients with
pylephlebitis or septic thrombophlebitis of the
mesenteric vein and in patients with super-
imposed sepsis due to bacterial translocation
from bowel infarction.7,33
Anticoagulation is the initial approach to
management, and heparin should be admin-
istered as soon as the diagnosis is made
(Figure 3).2,3,7,13,17 The degree of gastrointes-
tinal bleeding rarely is a contraindication to
initiation of anticoagulation. Unfractionated
heparin requires monitoring with activated
partial thromboplastin time; monitoring is
not required with low-molecular-weight hepa-
rin. The advantages of using unfractionated
heparin are safety in the presence of renal fail-
ure and when invasive procedures are planned.
In contrast, low-molecular-weight heparin is
cleared through the kidneys with a half-life of
6 to 12 hours and cannot be used in the pres-
ence of renal failure. Once improvement is
noted and invasive procedures are no longer
likely, warfarin therapy is initiated. When the
international normalized ratio reaches the tar-
get range of 2 to 3, heparin is discontinued and
warfarin alone is continued. The duration of
anticoagulation is about 6 months for patients
with known reversible conditions but lifelong
in patients with prothrombotic states and with-
out any identifiable etiology.
Warfarin has the disadvantages of required
regular monitoring of the international normal-
ized ratio, drug-drug interactions, and interac-
tion with food due to its metabolism via the
cytochrome P450 enzyme pathway. In this
respect, newer oral anticoagulants such as direct
thrombin inhibitors (ximelagatran, dabigatran,
and AZD0837) and direct inhibitors of factor
Xa (rivaroxaban, apixaban, edoxaban, otamixa-
ban, LY517717, TAK-442, and fondaparinux)
have fewer problems. However, because the
dose is fixed on the basis of the patient’s body
weight, lower doses of these newer agents may
be required in the presence of extensive liver
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TABLE 2. Recommended Testing After Diagnosis of MVT
Acute MVT
Detailed history and physical examination
Abdominal computed tomography to confirm the diagnosis of MVT and the extent
of thrombosis, to differentiate acute from chronic MVT, and to identify local
causes of thrombosis and complications such as bowel gangrene or perforation
Surgical consultation for infarction or perforation of bowel
Coagulation profile
Complete blood cell counts, basic panel, and hepatic function panel
Thrombophilia screen
JAK2 sequence variation screen
Bone marrow examination
Chronic MVT
All tests for acute MVT plus
Upper gastrointestinal endoscopy for detection of varices
Cholangiography for evaluation of portal hypertensive cholangiopathy
MVT ¼ mesenteric venous thrombosis.
and renal disease. Further, in case of overdos-
ing, the action cannot be reversed because of
the unavailability of an antidote.34
Anticoagulation helps recanalize the throm-
bosed vein.35 Among patients awaiting liver
transplant, recanalization of the portal vein oc-
curs in 50% of those receiving anticoagulation
but in none who are not given anticoagulants.
Associated splenic vein occlusion, ascites, and
the extent of thrombus predict failure to recan-
alize the vein.36 In a retrospective study, 13 pa-
tients seen before 1995 who did not receive
Abdominal pain out of proportion to abdominal signs;
compatible imaging findings
Mesenteric venous thrombosis
Evidence of perforation, peritonitis, or bowel infarction
Yes No
Surgery
Viable bowel Nonviable bowel
SMV occluded SMV patent Resection
Vasodilator with and
Thrombectomy
without thrombolytics
Screening for thrombophilia; anticoagulation therapy
FIGURE 3. Algorithm for management of acute mesenteric venous
thrombosis. SMV ¼ superior mesenteric vein.
289

anticoagulants were compared with 28 patients
seen after 1995 who were given anticoagulants.
The patients in the later group had a shorter
mean duration of hospital stay (13 vs 26 days),
reduced hospital mortality (11% vs 39%), less
need for surgery (33% vs 85%), and lower
risk of short bowel syndrome.13
Surgical Management. Patients with im-
pending transmural infarction and peritoneal
signs are treated with surgery (Figure 3).
Bowel viability at surgery is determined by
visual inspection, Doppler ultrasonography, or
fluorescein infusion, with fluorescein infusion
being the most accurate means for detecting
bowel viability.19 Resection and anastomosis is
the standard procedure, with the goal of con-
serving as much bowel as possible. Among
various series, the average length of bowel
resected is 50 to 60 cm.5,15 Surgery and/or
resection is often needed in patients with dis-
ease of small veins and thrombosis limited to
the mesenteric vein as compared with com-
bined portal and mesenteric veins.6 After initial
resection, second-look operations may be per-
formed within 24 to 48 hours to determine the
need for additional resection.2
Interventional Radiologic Options. Interven-
tional radiologic options are considered for pa-
tients at risk for bowel infarction but without
peritonitis. These are typically patients who have
worsening abdominal pain despite 48 to 72 hours
of anticoagulation therapy. If the mesenteric vein
is patent, vasodilator therapy with papaverine
infusion with or without thrombolytics (tissue
plasminogen activator or streptokinase) may be
considered (Figure 3). The mesenteric vein can
be approached by the transhepatic or transjugular
route, the latter preferred for patients with asci-
tes.37 These procedures are not a substitute for
anticoagulation, which should continue after a
successful procedure. Data on the use of throm-
bolytic therapy are limited to case reports, and
small case series have suggested a high rate of
bleeding with thrombolysis. In the largest retro-
spective study to date that included 20 patients
with MVT treated with thrombolysis, 75% had
partial or complete clot resolution, 85% had res-
olution of symptoms, and 60% experienced
a major complication; bleeding was the most
common complication, and death from bleeding
occurred in one patient.37
n n
290 Mayo Clin Proc.
MAYO CLINIC PROCEEDINGS
A transjugular intrahepatic portosystemic
shunt (TIPS) may be used in patients with acute
MVT with or without portal venous thrombosis
in whom anticoagulation is unsuccessful and
whose clinical condition worsens. A TIPS is
placed with the goal of recanalizing the oc-
cluded portal vein segment and maintaining
blood flow across the occluded segment. To
achieve this, the shunt may need to be extended
into the main portal vein. Contraindications to
TIPS placement and complications after the
procedure are similar to those that occur in
other patients with cirrhosis.38 In one study,
the use of TIPS resulted in successful recanaliza-
tion with immediate symptomatic improve-
ment in 20 of 24 patients (83%).39
Outcome
With the widespread availability of imaging
techniques such as CT and the change to early
use of anticoagulation, mortality rates in patients
with MVT have decreased to 0% to 23% among
various series.5,14,17,40 The most common cause
of death is sepsis with multiorgan failure. Other
causes include recurrent thrombosis, short
bowel syndrome, and pulmonary embolism.
The most important factor predicting the
short-term (within 30 days) outcome is the pres-
ence of bowel infarction. Other factors that have
been reported in various series are age, the lack
of use of anticoagulation, treatment on a nonsur-
gical ward, and the presence of colonic ische-
mia.5,9-11,17 The long-term outcome of patients
depends on the following factors.
Underlying Prothrombotic State. Patients with
MPNs have the potential for clonal evolution to
acute leukemia and myelodysplasia. This risk can
be reduced considerably with the use of cytore-
ductive therapy and hydroxyurea.41 These pa-
tients also have poor quality of life including
fatigue, bone pain, pruritus, and weight loss.42
Bleeding, usually mild, can occur because of
thrombocytopenia or platelet dysfunction.
Short Bowel Syndrome. Short bowel syn-
drome occurs in patients with extensive resec-
tion and should be avoided by preserving as
much of the bowel as possible at laparotomy.
Recurrent Thrombosis. Recurrent thrombo-
sis at any site has been reported in 3% to
40% of patients and within the mesenteric
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MESENTERIC VENOUS THROMBOSIS

circulation in 0% to 25%. Most recurrences

occur within the first 30 days after presenta-
tion. Recurrence rates may be as low as 0% to
3% in patients who continue to receive antico-
agulation treatment.11,40 Underlying throm-
bophilia and oral contraceptive therapy predict
recurrent disease.9,11

Bleeding From Anticoagulation. Bleeding

rates among patients treated with anticoagula-
tion is low at less than 10%, with gastrointesti-
nal bleeding being the most common.6,9,11,35
Varices predict bleeding and if present should
be managed as in patients with cirrhosis.9 Such
management includes the use of pharmaco-
logical therapy with b-blockers or endoscopic
ligation of varices. Pharmacological therapy is
preferred because variceal ligation may be
associated with ligation ulcers and risk of
bleeding in patients who are receiving antico-
agulants. Unless associated with intracranial
bleeding, hemorrhage is rarely the cause of
death in patients treated with anticoagulation.

CHRONIC MVT FIGURE 5. Magnetic resonance cholangiopancreatographic image from

Chronic MVT accounts for about 20% to 40% of
all cases of MVT, may be detected incidentally on
abdominal imaging, and is differentiated from
a patient with portal hypertensive cholangiopathy secondary to chronic
mesenteric and portal venous thrombosis showing scalloping of the
extrahepatic common bile duct with filling defects as a result of extensive
peribiliary varices (arrow). A ¼ anterior; I ¼ inferior; P ¼ posterior; S ¼
superior.

acute MVT by the presence of an extensive collat-

FIGURE 4. Computed tomographic image from
a patient with chronic mesenteric and portal
venous thrombosis. The 36-year-old man known
to have cirrhosis presented with variceal bleeding.
Chronic thrombus within the portal and mes-
enteric vein is visible as a central lucency within
extensive collateral vessels around portal vein
(arrow).
eral circulation.6,11 The diagnosis of chronic MVT
is usually made on CT (Figure 4). Patients with
portal venous thrombosis present with features
of portal hypertension such as splenomegaly, var-
iceal hemorrhage, and thrombocytopenia. If the
thrombosis is distal to the junction of the left gas-
tric vein and portal vein, both esophageal and gas-
tric varices occur. However, if the thrombosis is
proximal to this junction, gastric varices are pre-
dominant. Extensive thrombosis involving the
portal vein, SMV, splenic vein, and IMV results
in extensive bowel edema, with sequelae being
persistent abdominal pain, small-bowel stric-
tures, and inability to meet nutritional needs via
the gastrointestinal tract. Some patients may
require long-term home parenteral nutrition.
Chronic MVT may also be associated with edema
and extensive collateral vessels around the bile
ducts, giving rise to portal hypertensive cholangi-
opathy mimicking primary sclerosing cholangitis

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Chronic mesenteric venous thrombosis
Screen for thrombophilia
Esophageal or gastric varices
Endoscopic management with or
without β-blockers
Controlled Failure
Anticoagulation
TIPS
therapy
FIGURE 6. Algorithm for management of chronic mesenteric venous thrombosis. TIPS ¼ transjugular
intrahepatic portosystemic shunt.
on cholangiography (Figure 5). This entity pre-
sents with biochemical cholestasis, biliary stric-
tures, biliary stones, and cholangitis.
Diagnosis
As stated previously, chronic MVT is usually
diagnosed on CT. However, magnetic resonance
cholangiopancreatography is preferred when-
ever this diagnosis is suspected (Figure 5).43,44
Endoscopic retrograde cholangiopancreatogra-
phy may also be used but may be complicated
by hemorrhage from puncture of the biliary vari-
ces by the biliary catheter used to inject radio-
logic contrast medium for delineation of the
bile ducts.
Management
Esophageal and/or Gastric Varices. Esoph-
ageal and/or gastric varices are managed as in
patients with cirrhosis. Management includes
prevention of a first variceal bleed for patients
with varices but no history of bleeding, control
of variceal hemorrhage, and prevention of
recurrent bleeding (Figure 6). If feasible, TIPS
may be recommended for patients who con-
tinue to experience bleeding despite combined
endoscopic and pharmacological therapy.43
Patients without cirrhosis, especially in the pe-
diatric age group, are managed by creation of
n n
292 Mayo Clin Proc.
MAYO CLINIC PROCEEDINGS
Portal biliopathy
with stones or strictures
Endoscopic treatment feasible
Yes No
Combine with
Hepaticojejunostomy
shunt surgery
a surgical shunt between the left portal vein and
SMV (Rex bypass).43 Patients with isolated
gastric varices due to splenic venous thrombosis
are amenable to cure by splenectomy.45
Portal Hypertensive Cholangiopathy. Portal
hypertensive cholangiopathy requires treatment
if patients are symptomatic from cholangitis or
biliary obstruction. Stones within the common
duct are removed at endoscopic retrograde cho-
langiopancreatography. Caution is required dur-
ing the procedure because the presence of portal
hypertension makes bleeding more likely. Stric-
tures in the bile ducts are treated with endo-
scopic stenting and in selected patients by
portosystemic shunt surgery. Rarely, hepaticoje-
junostomy may be required.43
Anticoagulation. Anticoagulation should be
considered for patients with chronic portal
venous thrombosis, especially those with pro-
thrombotic states. However, data are limited
on the use of anticoagulants in patients with
chronic MVT. In one retrospective study, 18 of
60 patients with chronic portal venous throm-
bosis underwent long-term anticoagulation.
Five patients who had bleeding before anti-
coagulation had eradication of varices before
starting anticoagulation. Of the other patients, 4
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MESENTERIC VENOUS THROMBOSIS
had bleeding on follow-up; good control of
bleeding was achieved in 3, and the fourth
patient died.46 These data suggest that varices
should be adequately treated and obliterated
before initiating anticoagulation.
For patients with chronic MVT, 5-year sur-
vival rates are 78% to 83%, with outcome usu-
ally related to the severity and nature of the
underlying disorder.2,46
CONCLUSION
Acute MVT is a rare but important cause of intes-
tinal ischemia. Early diagnosis requires a high in-
dex of suspicion. Anticoagulation should be
started as soon as the diagnosis is confirmed
and is associated with improved outcome. Pa-
tients with underlying thrombophilia should
undergo lifelong anticoagulation. Surgery is
reserved for patients who have bowel infarction
with peritonitis or perforation. The goal of sur-
gery should be to preserve as much bowel as
possible in order to avoid short bowel syn-
drome. Patients with chronic MVT may be
asymptomatic or present with complications of
portal hypertension. In selected patients, antico-
agulation is safe and effective provided therapy
is initiated to prevent variceal bleeding. The
long-term outcome of patients depends both
on the underlying cause of the thrombosis and
the efficacy of long-term anticoagulation.
Abbreviations and Acronyms: CT = computed tomogra-
phy; ET = essential thrombocythemia; IMV = inferior mes-
enteric vein; MPN = myeloproliferative neoplasm; MVT =
mesenteric venous thrombosis; SMV = superior mesenteric
vein; TIPS = transjugular intrahepatic portosystemic shunt
Correspondence: Address to Patrick S. Kamath, MD, Division
of Gastroenterology and Hepatology, Mayo Clinic, 200 First St
SW, Rochester, MN 55905 (kamath.patrick@mayo.edu).
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