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33
Mesenteric and Portal Vein Thrombosis
Klaus Overbeck
Northern Vascular Centre, Freeman Hospital, Newcastle upon Tyne, U.K.
Derek Manas
Hepatic Surgery Unit, Freeman Hospital, Newcastle upon Tyne, U.K.
Gerard Stansby
University of Newcastle upon Tyne, Newcastle upon Tyne, U.K.
INTRODUCTION
Mesenteric venous thrombosis (MVT), although rare, can be associated with a high rate of
morbidity and mortality. Portal vein thrombosis (PVT) has better prognosis but, it is like
MVT, difficult to diagnose and can be found in combination with MVT.
MVT was first described as early as 1876 by Fagge (1) at Guy’s Hospital in a patient
with a previous deep venous thrombosis and subsequently by Elliot (2) in 1895 who
reported the first successful resection for MVT. PVT was first describes 8 years earlier by
Balford and Steward (3) in a case of an enlarged spleen and ascitis.
Because of their rarity many aspects of their diagnosis and management still remain
controversial or unclear. In this chapter we aim to summarise current knowledge and
recent advances relating to MVT and PVT.
MESENTERIC VENOUS THROMBOSIS
Etiology and Classification
Anatomy
Venous blood from the left colon and rectum drains into the inferior mesenteric vein
(IMV), which in turn joins the splenic vein. The superior mesenteric vein (SMV) drains
blood via the ileal and jejunal veins from the small intestine as well as from the caecum,
the ascending and the transverse colon. The SMV then joins with the splenic vein behind
the neck of the pancreas to form the portal vein.
The SMV or IMV alone may be thrombosed (isolated MVT) or it may be associated
with PVT (4,5). Patients with isolated MVT are more likely to have an underlying
thrombophilia and are more likely to require surgery (4).
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Thrombosis of the mesenteric veins are usually segmental and as the vasa recta and
venous arcades act as collaterals, infarction is more common if these vessels are also
involved (6). Rhee et al. (7) found in a series of cases of MVT that the ileum and jejunum
were infarcted in 81.1% and 83.3% of cases respectively. In contrast colonic infarction
was found in only 13% of cases. This may be due to the colon possessing additional
drainage via the middle and inferior rectal veins into the iliac veins.
Incidence of Mesenteric Venous Thrombosis
In his literature review of 273 cases of MVT (1911–1984), Abdu (8) found that the
condition was most common in the sixth and seventh decades of life. By contrast a more
recent series of 170 cases (1993–2000) by Endean found the average age to be 43 years
(range 20–63) (9) although MVT can affect even young children (10,11). Of the 170
patients described by Endean (9) found with thrombotic acute intestinal ischemia, MVT
accounted for 26% (15/58). In addition Clavien (12) reported a 13.2% incidence in 89
cases (13/98). Other reports identify MVT as the cause of intestinal ischemia in 5–25% of
cases (7,13). Although the true overall incidence of MVT is not clear, one autopsy study
found 0.5–1.5% of the mesenteric veins thrombosed (14).
Etiology and Classification of Mesenteric Venous Thrombosis
MVT are conventionally described as “primary” or “secondary.” However, the proportion
of true primary MVT cases in more recent series is in decline due to the increasing
recognition of specific inherited or acquired thrombotic and hypercoagulopathic disorders.
In current series “primary” MTV accounts only for 10–21% of all cases (15,7,16). Because
of this it is probably more sensible to classify MVT into “spontaneous” and “secondary.”
“Spontaneous” then includes cases where thrombosis is secondary to a coagulation
disorder or where no specific cause is found.
Coagulation abnormalities covering the whole spectrum of inherited and acquired
forms of thrombophilia have been described as causes of MVT. They include hereditary
disorders like antithrombin III deficiency (17–19), Protein C deficiency (20–22), Protein S
deficiency (23,24), Factor V Leiden (25–27) and 20210A mutation in the prothrombin
gene (28,29). Acquired prothrombitic forms of thrombophilia are also described, including
Anticardiolipin antibodies (30,31), Antiphospholipid syndrome (APS) (32), Hyperhomo-
cysteinemia (33,29) and Plasminogen activator deficiency. Oral contraceptives are
responsible for up to 18% of MVT cases in some series (8,34–36). Nephrotic syndrome
(37–40), myeloproliferative disorders (41), polycythemia vera (42), Essential thrombo-
cythemia (43), Paroxysmal nocturnal hemoglobinuria (44,45) and pregnancy (46) have all
also been found to be associated with MVT.
Secondary MVT describes the other group of conditions known to cause MVT.
Malignancy (4) leads to paraneoplastic syndrome (47) and external compression of the
portal vein or SMV. Inflammatory disorders like pancreatitis (48–50) and Crohn’s disease
(51) are also well known to lead to MVT. Postoperative splenectomy MVT is well
described (52,53), Appendicitis is associated with MVT in cases of portal pyemia (54,55)
and laparoscopic surgery has been reported to trigger MVT (56,57). In a retrospective
review Fichera (58) found that 4.8% 4/83 of patients after a total colectomy for
inflammatory bowel disease had developed a symptomatic MVT. Sclerotherapy related
propagation of thrombus leading to MVT is well described (59,60). Portal hypertension
and cirrhosis are also part of the long list of causes (Table 1) (66).
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Kumar et al. (4) have suggested a further possible classification. They noted that
“the location of the thrombus may be determined on the basis of the underlying cause.”
With intra-abdominal causes the thrombosis tends to start in the large vessels at the site of
compression and then progresses peripherally to involve the smaller venous arcades and
arcuate channels. In prothrombotic states the thrombosis begins in the smaller vessels and
progresses to involve the larger veins. Subsequently the same authors have published
a retrospective review of 69 cases of acute MVT in which two groups were identified (4).
In the isolated group onlythe small vessels and SMV were involved and in the second group
or combined group the SMV and the portal or splenic vein were thrombosed. In the subgroup
analysis in the isolatedgroup signs of peritonitis were more likely to be seen (pZ0.009)and
surgical interventionwas required in 70% versus 26% of cases(pZ0.0002). Thrombophilia
was five times more common in the isolated group.
Clinical Features of Mesenteric Venous Thrombosis
The clinical picture can vary greatly. MVT can present acute with sudden onset of
symptoms, subacute with symptoms lasting for days or weeks and chronic where the patient
presents with complications of MVT such as oesophageal variceal bleeding (67). The most
common clinical presentation iswith abdominalpain (83–91%) often out of proportion with
Table 1 Causes of Mesenteric Venous Thrombosis
“Spontaneous” MVT
Hereditary Thrombophilia
Antithrombin III deficiency (17–19)
Protein C deficiency (20–22,61), Protein S deficiency (23–27,62) and 20210A mutation in the
prothrombin gene (28,29)
Acquired Thrombophilia
Anticardiolipin antibodies (30,31,63)
Antiphospholipid syndrome (32)
Hyperhomocysteinemia (29,33) and
Plasminogen activator deficiency
Oral contraceptives (8,34–36)
Nephrotic syndrome (37–40,61)
Myeloproliferative disorders (41)
Polycythemia vera (42)
Essential thrombocythemia (64)
Paroxysmal nocturnal hemoglobinuria (44,45)
Pregnancy (46)
Secondary MVT
Malignancy (4)
Paraneoplastic syndrome (65)
Inflammatory disorders
Pancreatitis (48–50)
Crohn’s disease (51)
Post-Splenectomy (52,53)
Appendicitis (54,55)
Laparoscopic surgery (56,57)
Colectomy for inflammatory bowel disease (58)
Sclerotherapy (59,60)
Portal hypertension and cirrhosis (66)
Abbreviation: MVT, mesenteric venous thrombosis.
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