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the physical findings. MVT causes anorexia in 49%, nausea or vomiting in 36–70%,
diarrhoea in 15–42% and melena in 22%. Up to 21% developed upper GI bleeding in acute
MVT and in 50% the fecal occult blood test is positive (68,7). The initial pain is usually
central and colicky in nature. The presentation depends on whether primarily the large or the
small veins are involved and to what degree the bowel wall is ischemia. If the ischemia is
limited to the mucosa abdominal pain and diarrhoea are common and the patient rarely
develops transmural infarction. If the ischemia has caused transmural infarction and
necrosis MVT will present as peritonitis. This is then followed by signs of a progressing
systemic sepsis. A systemic pressure of !90 mmHg is a sign of a poor prognosis (68).
At presentation 33–43% patients have clinical signs of peritonitis and most patients have
symptoms lasting longer than 48 hours (7,4) with an average of 5–7 days (4).
Differential Diagnosis of Mesenteric Venous Thrombosis
Arterial mesenteric ischemia is the main differential diagnosis of MVT. However, a more
insidious onset and longer duration of symptoms may suggest MVT. Occlusive and non
occlusive arterial mesenteric ischemia accounts for 75–95% of cases of mesenteric
ischemia (7) but a strangulated internal hernia or bowel ischemia due to adhesions can also
present with similar symptoms. 15–44% of patients give a history of a previous DVT or PE
or known coagulopathy whichshould alert the clinician toward suspecting MVT ina patient
with somewhat unspecific abdominal signs and symptoms (69,70) whilst underlying atrial
fibrillation or known PVD or atherosclerosis points more at an arterial mesenteric event.
Archibald described a case of a 32-year-old male who presented with abdominal pain and
rectal bleeding due to ischemic colitis caused by a SMV thrombosis (71). Roman
highlighted a case of pseudo-obstruction with a grossly dilated colon caused by MVT (72).
Investigations
Blood Tests
The WBC can be raised. Rhee found 50.9% of patients of acute MVT had a leucocytosis
and similarly 44.4% with chronic MVT exhibited a leucocytosis (7). Lactate levels are a
sensitive but nonspecific marker of bowel ischemia. The rise in lactate levels is temporary
and returns to normal within hours after the onset of ischemia (73–78). Rhee (7) found in
his review of MVT a raised lactate in 28.3% of patients with acute cases, but in chronic
MVT in only 5.3%.
Plain X-Ray
Plain X-ray studies are usually unhelpful. Possible findings are ground glass appearance
with ascitis and thickening of the bowel wall, air in the bowel wall and portal vein and free
gas may be seen if perforation has occurred (79,80).
Duplex Ultrasound
Duplex ultrasound is useful for the assessment of the portal and mesenteric vein flow but
is often limited by bowel gas, has a low sensitivity to detect slow flow and is highly
operator dependant. Despite these limitations it has a good sensitivity for PVT 84% (81).
In a recent review the diagnosis of port-MVT was made with duplex sonography in 57%
of 23 cases (43).
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Computer Tomography and Magnetic Resonance Angiography
Spiral abdominal computer tomography (CT) and magnetic resonance (MR) angiography
are becoming the investigation of choice for the diagnosis of MVT. Recent fast
acquisition, high resolution breath holding imaging can compete with venous phase DSA
angiography except for the distal mesenteric branches. Sensitivity reaches 100% in several
series (70). These techniques also are readily available, non-invasive, and also provide
morphological and functional information (82). Kreft found no statistical difference in
comparing MR angiography with intra-arterial DSA of the portal venous system in 36
patients with portal hypertension. The overall sensitivity, specificity, and accuracy for the
detection of thrombosis were 100%, 98%, and 99% for MR angiography and 91%, 100%,
and 96% for DSA (83).
Management of Mesenteric Venous Thrombosis
If the diagnosis is made preoperatively the patient should be started on intravenous
heparin. Laparotomy is required only if the patient displays signs of peritonitis and or there
is radiological evidence of perforation. Laparoscopy may be useful to identify patients
who need resection (84). At laparotomy resection should be performed only of clearly non
viable bowel since bowel may potentially recover once venous drainage is restored (85).
The use of fluorescein may be useful to identify bowel that is still viable (86). A second
look laparotomy should be performed at 24–48 hours. Surgical thrombectomy may be
attempted but has a high recurrence rate. Transjugular intrahepatic portosystemic shunt
(TIPS) and thrombolysis combined with or without laparotomy/scopy appears to be
a attractive technique (87–92). Long-term anti-coagulation is usually required.
Outcome of Mesenteric Venous Thrombosis
The mortality of venous mesenteric thrombosis is significantly lower than for arterial
mesenteric ischemia. Wang (93) reported a 7/16 (43%) mortality in patients with MVT,
Morasch (70) reported a 7/31 (22.1%) 30 day mortality and Rhee (7) a 27% 30 day
mortality. Survival at 3 years was 36% for acute MVT and 83% for chronic MVT (7).
Conclusions
The mortality of MVT is significant, but lower than the mortality of arterial mesenteric
ischemia. History and clinical examination are unreliable and often inconclusive. A high
index of suspicion is required to make the diagnosis early. A conservative approach with
anticoagulation, as long there is no evidence of infarction is indicated and may reduce the
mortality of a MVT compared with a primary surgical approach. Reports of thrombolysis
and thrombectomy have been promising but the rarity of the condition has so far prevented
the evaluation of these techniques in larger series or a randomised trial.
PORTAL VEIN THROMBOSIS
Etiology and Incidence of Portal Vein Thrombosis
Thrombosis of the portal vein can occur either outside of the liver (extrahepatic) or within
the liver (intrahepatic). The etiology of PVT is heterogeneous and its occurrence can be
influenced by both local and systemic etiological factors.
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Local factors comprise disorders leading to decreased portal flow. This is commonly
seen in adult patients with cirrhosis—(25%). The annual incidence in patients with
cirrhosis is less than 1%, although this risk increases with more advanced liver disease.
In the presence of the mutation 20210 of the prothrombin gene the incidence increases
fivefold (62).
Other commonly associated conditions include hepatobiliary malignancies such as
HCC (62) and cholangio-carcinoma (94) usually as a result of direct tumour invasion.
Bland thrombosis of the extrahepatic PV may also result from occlusion by enlargement of
hilar lymph nodes, inflammation of the portal vein due to ascending pylephlebitis
secondary to infection in the appendix or colon, ascending cholangitis, intra-abdominal
sepsis, and ulcerative colitis. Portal and splenic vein thrombosis is a common complication
secondary to complicated pancreatitis (95–102).
Systemic risk factors for PVT consist mainly of acquired and inherited abnormalities
leading to hypercoagulability. This may be general prothrombotic states like
hyperhomocysteinemia, myeloproliferative syndromes—especially polycythemia rubra
vera, APS, antithrombin deficiency, protein C or S deficiencies, or factor II, factor V gene
mutations. Collagen vascular diseases, such as lupus have been implicated as well as
pregnancy and women on the OC Pill. The disorder usually results from the association of
causal factors, which should all be investigated. In addition profound dehydration may
worsen a hypercoagulable state.
Table 2 Causes of Portal Vein Thrombosis
1. Inherited prothrombotic states
Antithrombin III deficiency (103)
Factor V Leiden mutation (104)
Prothrombin gene mutation (104)
Protein C deficiency (104)
Protein S deficiency (105)
Antithrombin deficiency (106,107)
Factor II (PTHR A
20210
mutation) (108)
2. Acquired prothrombotic states
Liver cirrhosis (109)
Hepatocellular carcinoma (62)
Antiphospholipid syndrome (110)
Cholangiocarcinoma (94)
Pancreatic carcinoma (111) and gastric carcinoma (112)
Splenectomy (113)
Intra abdominal sepsis (101,113)
Myeloproliferative disorders
Oral contraceptives (114)
Pregnancy (115)
Trauma (116)
Acute pancreatitis (95)
Appendicitis (54)
Inflammatory bowel disease (117)
Diverticulitis (102)
Ascending cholangitis (118)
Cholecystitis (119)
Following liver transplantation (120)
3. Idiopathic
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Less commonly it is seen following liver transplantation (1–3% in adult whole
grafts and up to 6% in split/pediatric grafts), or secondary to abdominal surgery such as
splenectomy and shunt surgery (Table 2) (113,121–124).
Finally, it may simply be idiopathic. Up to 30% of patients with PVT do not have
a clear etiology, although approximately 70% of patients will have an identifiable
hypercoagulable condition. Importantly, PV involvement may be complete or partial and
may involve any portion of the portal venous system.
Pathophysiology of Portal Vein Thrombosis
The portal vein forms from the junction of the SMV and the splenic vein and divides into
two main intrahepatic branches followed by a further segmental division to each lobe. The
portal vein provides approximately two thirds of the total hepatic blood flow and about
50% of its oxygen delivery under normal circumstances.
Acute PVT may not produce acute manifestations. Immediately there is
vasodilatation of the hepatic arterial supply (125). Thrombosis due to intrahepatic causes
originates distally and extends into the extrahepatic portal vein as found in cirrhosis and
hepatic malignancies. In most of the other causes the thrombus forms proximally and
propagates distally. Portal venous obstruction due to cirrhosis can be complicated by
thrombosis due to the low flow state. Tumor invasion of the portal vein is found in
hepatocellular carcinomas leading to thrombosis.
Recent thrombosis of the portal vein is characterized by a thrombus, which may not
give rise to any symptoms or may be associated with a systemic inflammatory syndrome or
with intestinal ischemia syndrome. Old thrombosis of the portal vein is usually only
recognizable by its anatomic consequences—the cavernoma. The cavernoma is made up
of multiple collateral veins linking the venous bed upstream from the obstacle to the
venous bed downstream. The cavernoma still represent an obstruction to portal blood flow,
causing portal hypertension (Fig. 1).
The main complication of chronic PVT is gastrointestinal bleeding and is due to the
rupture of the varices or portal hypertensive gastropathy. The intrahepatic venous pressure
is normal, but hepatic blood flow is usually reduced in comparison to both normal subjects
and patients with cirrhosis.
Figure 1 Cavernous transformation of the portal vein. Source: Freeman hospital archive.
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Symptoms
Up to 40% of patients will be asymptomatic and may be overshadowed by those of the
underlying cause. Symptoms often develop from complications of portal hypertension
such as variceal bleeding. The location of the gastroesophageal varices often correlates
with the segment of the portal vasculature that is occluded.
Splenic vein thrombosis for example, often results in gastric varices in the fundus.
PVT is renowned for causing ectopic varices outside of the gastroesophageal region.
Splenomegaly often develops as a result of long standing presinusoidal portal
hypertension. Occasionally, abdominal pain and/or intestinal infarction may result from
concomitant mesenteric vein involvement. Other symptoms include nausea, vomiting,
anorexia, weight loss, diarrhoea (126). Liver function testes are usually normal.
Ascites is not a prominent feature of presinusoidal hypertension because of the
greater compliance of the gastric and intestinal interstitium compared with the liver, which
permits more fluid to be accommodated in the interstitium before it spills in to the
peritoneal cavity. The large capacity of intestinal lymphatics accommodates the increases
in intestinal lymph production due to filtration of fluid in the intestinal capillaries. The
ultra structure of the layers of the intestine allows preferential passage of fluid filtered into
the submucosal capillary network and then to the mucosal surface and then the lumen
rather than to the serosal surface and the peritoneal cavity.
Imaging and Investigations in Portal Vein Thrombosis
Since the advent of modern cross sectional imaging invasive diagnostic methods like
portal venography and selective mesenteric arteriography have been replaced.
Color Duplex ultrasound will reveal flow direction and echogenic structure within
the portal vein, enlargement of the thrombosed portion of the portal vein. Cavernous
transformation of the portal vein produces characteristic patterns on color duplex (127).
However, a recently formed thrombus in the portal vein can show an anechoic or
hypoechoic structure. CT is an excellent method for demonstrating thrombosis of the
Figure 2 Computer tomography image of an acute portal vein thrombosis. Source: Freeman
hospital archive.
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portal vein. On the precontrast scan the portal vein is enlarged and an increased attenuation
of the portal vein contents may indicate recent thrombus (Fig. 2).
Postcontrast CT images reveal rim enhancement of the wall of the portal vein but
lack of enhancement of its contents if the occlusion is due to thrombus. If, however,
a tumour thrombus is present inhomogeneous or streaky enhancement within the portal
vein may be observed. With chronic PVT numerous small enhancing structures,
representing venous collaterals, surround the portal vein.
Moreover, CT may show perfusion changes as either decreased parenchyma
enhancement during the portal venous phase or transiently increased segmental or lobar
enhancement seen during the late arterial and early portal venous phases. This localized
increased enhancement is explained by compensatory hepatic arterial flow or arterioportal
shunting towards the segment or the lobe supplied by the portal vein branch, which
is thrombosed.
MRI is at least as good as CT in showing PVT by demonstrating absence of flow.
Transient segmental or lobar enhancement, similar to that seen on contrast-enhanced CT
can be visualized with gadolinium-enhanced T1-weighted images (128–130).
Treatment
Since most cases are identified incidentally and the natural history is unclear, treatment
usually focuses on the underlying condition. Treatment is more important in recent PVT.
In the absence of severe liver disease or major contraindication to anticoagulation,
antithrombotic therapy should be initiated on presentation and continued for
approximately six months. After initial intravenous heparin infusion anticoagulant
therapy is commenced, which generally allows recanalization of the thrombosed veins in
recently constituted thrombosis (106,131).
Permanent anticoagulant treatment is recommended when a permanent prothrom-
botic state exists, even in patients with a history of gastrointestinal bleeding. Prognosis
is good.
In rare cases of acute portal vein thrombus with total occlusion, thrombolysis with
TIPS placement has been shown to be feasible and efficacious (132–134).
It is still a matter of debate if anticoagulation is of benefit in patients with chronic
PVT (104,135). The patient with PVT is at risk of bleeding as well as thrombosis.
Condat (136) found in 136 adults with non-malignant, non-cirrhotic PVT the incidence
of bleeding at 1.25% per year and the risk of thrombosis 0.55% per year. 85 of his
patients received anticoagulation therapy without increasing the bleeding incidence. In
patients with intraabdominal sepsis spontaneous resolution of the PVT has been observed.
Transjugular or transhepatic thrombolysis and thrombectomy have been used successfully
(137–142). That said, the data come from small case series some of which involve liver
transplant patients.
Bleeding can be treated in most cases by beta-adrenergic blockade, endoscopic
ligation, or endoscopic sclerosis of varices.
If PVT is complicated by recurrent variceal bleeding and hypersplenism
reconstituting the portal vein by stent insertion across the occluded segment of the portal
vein with or without a transjugular portosystemic shunt (TPIS) may be beneficial
(143,144). Shunt surgery especially splenorenal (Warren) shunts may still be a successful
treatment in exceptional cases where endoscopic management and TIPS have failed to
control variceal bleeding (145,146).
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Outcome of Portal Vein Thrombosis
The overall outcome of extrahepatic PVT is good with an overall mortality of 13% or less.
Janssen (147) found in a review of 172 cases of extrahepatic PVT that in absence of cancer,
cirrhosis, and mesenteric vein thrombosis the 1 year survival can be as high as 95%.
PVT due to pylephlebitis has a high mortality without prompt antibiotic therapy.
Bacteraemia (often polymicrobial) is present in up to88% ofthe patients.The mostcommon
blood isolate were bacteroides species (148).
Variceal bleeding is associated with a significant better prognosis if the portal
hypertension is due to PVT rather than liver cirrhosis. Poor outcome of PVT is related
rather to the underlying disease than the PVT itself (136,149).
KEY POINTS
† PVT is often a asymptomatic condition.
† PVT in itself is a benign condition, but can be associated with a high mortality
due to the underlying conditions.
† Cross sectional imaging techniques are available, sensitive, and diagnostic in
most cases.
† Bleeding due to PVT has a more benign character than that caused by portal
hypertension due to liver cirrhosis.
† Treatment is primarily anticoagulation and sufficient in most of the cases.
† Addressing the underlying condition is essential.
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