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CHAPTER
29
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Superficial thrombophlebitis
Suman Wasan
29.1 INTRODUCTION
Although once considered benign, the morbidity associated with supercial venous thrombophlebitis (SVT) has
recently been evaluated and described. While SVT is considered common, its exact incidence is unknown. Complicating these estimates is the wide variation in presentation
and clinical evaluation and diagnosis.
Recent studies have highlighted its association with
DVT and pulmonary embolism (PE) if left untreated. Studies show that SVT may progress to DVT in 6%–44%,
20%–33% may have asymptomatic PE, and 2%–13%
have symptomatic PE, with SVT located in the saphenous
trunk having the greatest association with VTE (1).
29.2 EPIDEMIOLOGY
SVT is thought to occur in approximately 125,000 people
per year in the United States with estimates of it affecting
3%–11% of the general population (2). The average age at
diagnosis ranges from 54 to 65years; SVT affects females
more than males (3, 4). The most commonly encountered
risk factor is the presence of lower extremity varicose
veins, occurring in 62% of SVT patients. Other associated
risk factors include increasing age, obesity, tobacco use,
previous history of DVT or SVT, hypercoagulable states
as discussed later, immune disorders, pregnancy and the
puerperium, oral contraceptives, hormone replacement
therapy, immobilization, cancer, recent surgery, varicose
vein treatment, and trauma including placement of venous
catheters (5).
29.3 ETIOLOGY AND PATHOGENESIS
The pathophysiology of venous thromboembolic disease
has been attributed to the Virchow triad of endothelial
injury, stasis, and hypercoagulability. As our understanding of this triad has deepened, the importance of inammatory mediators and broadened hypercoaguable states,
like malignancy and obesity, has emerged. The etiology
of SVT remains complex and multifactorial. Basic science
investigation shows that disequilibrium in the expression
of matrix metalloproteinases and the tissue inhibitor of
metalloproteinases occurs due to underlying high hydrostatic pressure and inammation contributing to vein
remodeling and resultant SVT (6).
29.3.1 Associated hypercoagulability
While there are no current guidelines informing which
patients should undergo a hypercoagulable evaluation, in
general, those without an inciting physical event or without
varicosities should be evaluated for these disorders. Martinelli et al.’s case-control study evaluated 63 “low-risk”
patients (dened by the absence of malignancy, autoimmune
disease, and lower extremity varicosities) for factor V Leiden
mutation; prothrombin G20210A mutation; and deciencies in antithrombin III (AT III), protein C, and protein S
(7). An increased risk of SVT was identied in patients with
inherited coagulopathies. The risk of SVT was increased
approximately 6-fold for factor V Leiden mutation, 4-fold
for the prothrombin G20210A mutation, and 13-fold for
the combined factor deciencies. Additionally, patients with
SVT not associated with lower extremity varicosities were
more likely to have an inherited hypercoaguable state.
In a subsequent separate set of data examining patients
with recurrent SVT, anticardiolipin antibodies were
detected in 33% of patients (8). These ndings and others suggest that patients with SVT may have an increased
risk of an underlying hypercoaguable state, although not
all studies have revealed such a strong association (9, 10).
Another emerging risk factor for SVT is immune disorders,
including systemic lupus erythematosus, and vasculitis,
such as Behcet and Buerger diseases (11, 12). Areview of
2319 patients with Behcet disease found that 14.3%, or
332 patients, had vascular involvement; of these, 53.3%
had SVT and 29.8% had DVT (11). Patients with Buerger
disease have been found to have biopsy ndings of acute
supercial thrombophlebitis with inammation of all three
layers of the vessel wall with occlusive thrombosis (12).
Finally, the prevalence of cancer in patients presenting with
SVT has been investigated. In a single-center retrospective
DOI: 10.1201/9781003328971-32
295295
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study of 276 patients with SVT of the legs, the prevalence
of malignancy was 4.2% in those with isolated SVT and
18.8% in those with SVT and concurrent DVT/PE (13).
29.3.2 Disease progression to DVT and PE
While patients may present with pain and swelling as their
primary complaint, the risk of progression to DVT and PE
constitutes the most serious complication of SVT. SVT can
progress to DVT via proximal extension of thrombus into
the deep system, but it also, perhaps counterintuitively, may
arise in association with SVT in noncontiguous vessels (3,4).
Concomitant DVT may be symptomatic or asymptomatic in patients with SVT and identied only on imaging studies. Most estimates of progression come from
studies of lower extremity SVT. Decousus etal. noted
that 25% of patients presenting with SVT demonstrated
concomitant DVT at presentation, and importantly,
almost half of these DVT cases were not contiguous with
the SVT (4). Of the 586 patients studied with isolated
SVT, 10% went on to develop VTE during the study
period. Across series, the incidence of proximal progression into the deep system ranges between 7% and 44%
(5, 7). The most common route of extension is from
the great saphenous vein (GSV) via the saphenofemoral
junction (SFJ) into the femoral vein (7, 14–16). Progression to VTE may also result from small saphenous vein
SVT into the popliteal vein and into the deep system via
perforating veins (16).
Chengelis et al. identied a group of 263 patients
with isolated SVT without evidence of deep venous
involvement by duplex ultrasound examination. Surveillance duplex ultrasonography performed approximately
1 week following SVT diagnosis without anticoagulation
treatment revealed progression to DVT in 30 patients
(11%), and specically 16% of those with GSV SVT
had extension into the femoral vein—most commonly
via the SFJ (85%) (14). Ameta-analysis found a pooled
DVT and PE event rate of 9.3–16.6 events per 100 person-years after SVT in the absence of pharmacological
treatment (17). The proximity of supercial thrombus to
the SFJ appears to affect the likelihood of progression;
SVT location within 1cm of the SFJ confers a high risk
of DVT progression (18).
29.4 CLINICAL PRESENTATION
Patients will present in most cases with pain and erythema overlying the affected supercial vein, along with
a palpable “cord” and edema of the surrounding soft
tissue. Low-grade fever or malaise may be present. The
supercial veins of the upper or lower extremities, the
breast in the case of Mondor disease, or the dorsal veins
of the penis may all be affected by SVT. The most common locations affected by SVT include the GSV and its
tributaries, followed by the cephalic and basilic veins of
the upper extremity (5). The diagnosis of progression to
DVT is often accompanied by a worsening of symptoms
(18). There are a number of distinct clinical conditions in
which SVT may manifest.
29.4.1 Superficial thrombophlebitis and
lower extremity varicosities
Lower extremity varicose veins and venous insufciency
are the most common risk factors for SVT. Varicose veins
are comorbid with SVT in up to two-thirds of patients
with SVT, and up to 70% of patients may have associated
supercial venous insufciency (19). It has been reported
that only 3%–20% of SVT patients with varicose veins
will develop DVT, compared to 44%–60% of those without varicosities (14, 20, 21). Therefore, it may be that SVT
in patients with varicose veins has a different pathophysiology from those without varicose veins. However, reports
are conicting, and no increased incidence of DVT or PE
was noted when comparing patients with and without varicose veins in the 186 SVT patients identied (3). Nevertheless, targeted approaches to addressing those patients with
SVT involving varicose veins only is essential. This type of
SVT may remain localized to the cluster of tributary varicosities or may extend into the GSV (3). Supercial venous
thrombosis is frequently found in varicose veins surrounding venous stasis ulcers and may present as tender nodules
with localized induration and erythema.
29.4.2 Upper extremity and traumatic SVT
The most common etiologic factor in upper extremity SVT
is trauma associated with an intravenous cannula and intravenous infusions resulting in caustic endothelial damage. It
may be seen in individuals using illicit drugs and especially
in patients receiving chemotherapy through PICC lines.
Typically, the cephalic or basilic veins are involved if the
catheter is inserted near the antecubital fossa. Extension of
upper extremity SVT into upper extremity DVT or PE is a
more rare occurrence when compared with lower extremity SVT (22). Initial treatment of upper extremity SVT is
catheter removal followed by anticoagulation in cases with
severe symptoms or with evidence of progression. The
resultant cord or induration may persist for months notwithstanding treatment.
29.4.3 Septic and suppurative SVT
Suppurative SVT (SSVT) is also associated with the use
of an intravenous cannula; however, SSVT may be lethal
given its association with septicemia. Signs and symptoms
of SSVT include purulence at an intravenous site, fever,
leukocytosis, and local intense pain (23). Treatment consists of catheter removal and broad-spectrum intravenous
antibiotics (tailored to qualitative blood culture results).
Surgery should be reserved for patients with SSVT who fail
conservative management and require source control for
persistent sepsis, including exploration, abscess drainage,
and full venous resection.
29.4.4 Migratory SVT
Migratory thrombophlebitis was rst described by Jadioux
in 1845 as an entity characterized by repeated thrombosis
developing in the supercial veins at varying sites, but most
commonly in the lower extremity (24). This entity may be
29.6 Treatment 297
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associated with carcinoma (Trousseau syndrome) and may
precede the diagnosis of malignancy by several years. Consequently, a workup for occult malignancy may be warranted when the diagnosis of migratory thrombophlebitis
is made. Migratory thrombophlebitis also can occur in the
presence of vasculitis including Behcet disease, Buerger disease, and polyarteritis nodosa (25).
29.4.5 Mondor disease
Mondor disease is dened as thrombophlebitis of the thoracoepigastric vein of the breast and chest wall. It can be
associated with breast carcinoma or hypercoaguable state,
although cases have been reported with no identiable
cause (26). The condition is considered benign, lasting 4–8
weeks and typically managed with NSAIDS and, rarely,
anticoagulation (29). Recently, the term has also been
applied to SVT of the dorsal vein of the penis (28).
29.4.6 Pregnancy and SVT
Pregnancy-associated SVT is frequent, with an estimated
prevalence of 0.1%; however, the risk of VTE doubles in
pregnant women with SVT (29). Risk factors are additive in
pregnant and postpartum women who are known to have
a physiological hypercoagulable state. The Balkan Working
Group for the Prevention and Treatment of VTE has recognized the risk of SVT in pregnancy and provides recommendations for the management of this condition (29).
29.4.7 SVT post–varicose vein treatment
Endovascular ablation, including thermal and nonthermal
techniques, is the standard treatment of patients with varicose veins. The incidence of SVT was found to be 1.5%
in 67 patients undergoing EVLT versus 0% in 66 patients
undergoing RFA of the GSV or SSV (30). However, two
other analyses showed an SVT incidence of 4%–15% in
patients undergoing RFA (31, 32). In a large randomized
prospective study of 500 consecutive patients, the rates of
SVT included 3.2% EVLT, 9.6% RFA, 13.7% foam sclerotherapy, and 4% surgical stripping (33).
29.5 DIAGNOSIS
A presumptive diagnosis of SVT is primarily based on history and physical examination. Patients present with pain
and erythema and a palpable cord with an inammatory
reaction that may last 2–3 weeks. Patients may delay diagnostic testing and present with telltale postinammatory
hyperpigmentation weeks to months later. Duplex ultrasound scanning is the diagnostic modality of choice for the
evaluation of SVT and primarily used to conrm the diagnosis, estimate length and distance from deep veins, and
importantly, evaluate the concomitant presence of DVT.
Duplex imaging of patients with SVT has revealed concomitant DVT in 5%–40% of patients (3, 34–37). Duplex
ultrasound is also noninvasive, inexpensive, and may be
easily repeated for surveillance examinations. Unfortu-
nately, D-dimer has not been validated for exclusion of
SVT and is not useful in evaluating these patients.
29
29.6 TREATMENT
The goals of therapy for SVT are twofold: rst to reduce
the associated pain, erythema, and swelling, and second,
to reduce the extension and progression to DVT and PE.
Historically, treatment involved surgical removal of the
affected vein segment; however, this has evolved to the use
of medication including anticoagulation. While conservative measures such as warm compresses have long been
recommended, there are little data supporting its use or
benet. Further, a trial of 73 patients with SVT comparing the use of compression stockings for 1 week versus no
stockings revealed no difference in quality of life, pain, or
use of analgesics, although thrombus regression by ultrasound was faster with compression (38).
Two recent systematic reviews provide the most comprehensive evaluation of therapeutic approaches to the
management of SVT (1, 17). In interpreting their ndings,
it is important to consider that studies overwhelmingly
include patients with lower extremity SVT of the GSV
that is more than 3cm distal to the SFJ. There is a paucity
of data that informs treatment recommendations for the
other heterogenous presentations of SVT.
The 2018 Cochrane review included 33 studies involving 7296 patients with SVT of the legs and evaluated treatment with fondaparinux, rivaroxaban, LMWH, UFH,
NSAIDs, compression stockings, and topical, intramuscular, or intravenous treatment as well as surgical thrombectomy or ligation (1). Aminority of studies compared
treatment to placebo, and most studies were small and of
poor quality. Their recommendations are primarily based
on one large placebo-controlled RCT of 3002 participants
with SVT above the knee who received fondaparinux with
a signicant reduction in symptomatic VTE, SVT extension, and SVT recurrence compared to placebo (4). Major
bleeding was infrequent in both groups. Asecond systematic review and meta-analysis published in 2019 included
17 articles and 6862 patients with SVT and conrmed that
fondaparinux achieved the lowest rate of progression to
DVT and PE without conclusions about other treatments
due to low-quality evidence (17). The Surprise study in
people with SVT and one or more risk factors for VTE
randomized to 45 days of fondaparinux or rivaroxaban
10 mg found that that rivaroxaban was as effective as
fondaparinux; however, the study was not powered to
prove noninferiority (39). In addition, there was a nonstatistically signicant increase of the primary composite
outcome and clinically relevant nonmajor bleeding in the
rivaroxaban group, prompting the call for further studies.
Low-quality evidence in one study found that prophylactic-dose LMWH signicantly reduced extension of SVT,
but did not reduce symptomatic VTE, while therapeutic-dose LMWH evaluated in one study reduced both SVT
extension and VTE progression, but improvement was less
signicant at 3-month follow-up due to a catch-up phenomenon (1). NSAIDs were also found in one study to signicantly reduce SVT extension without differences in the
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incidence of VTE or in the resolution of local symptoms
and signs (40). While no major bleeding episodes were
recorded in any of the NSAID or placebo groups, indomethacin increased the rate of adverse effects and NSAIDs
increased the risk of gastric pain threefold compared with
placebo (40, 41). The majority of studies evaluating surgery and topical treatments did not report SVT progression, VTE, or adverse events (1).
The treatment of patients with SVT within 3cm of the
SFJ has not been well studied. Most commonly, patients are
treated with full anticoagulation for a duration similar to
proximal DVT. Arecent analysis from the RIETE registry
of patients with thrombosis involving the most proximal
tract of the GSV, with the thrombus head being within 3cm
from the SFJ, evaluated patients who received full-dose
fondaparinux and LMWH followed by VKA (229 patients)
compared to those (147 patients) who received preventative
doses of fondaparinux or intermediate-dose LMWH (42).
There was no statistical difference in VTE or recurrent SVT
between the groups and no statistical difference in the safety
outcomes of major bleeding or clinically nonmajor bleeding
complications at 3-month follow-up. The authors concluded
that these ndings are hypothesis-generating to support a
trial to evaluate that the efcacy of preventative-dose anticoagulation may not be lower than therapeutic anticoagulation for treatment of SVT approaching the SFJ. Asmall
study showed that the dose of dalteparin did not impact the
degree of thrombus regression in SVT (43).
There is a paucity of studies evaluating the management of SVT in varicose veins. In a prospective observational study of 195 limbs with SVT and varicose veins
treated with surgery or anticoagulation with follow-up to 6
months, there was no difference in the primary composite
outcome of SVT extension/recurrence, DVT, or symptomatic PE (44). The authors concluded that urgent surgery is
not associated with reduction in VTE compared to anticoagulation alone, but could safely be performed in selected
patients with isolated thrombosis of varicose tributaries
or limited involvement of the saphenous trunk. Patients
treated for SVT involving truncal varicose veins often
develop reux in the affected vein and benet from thermal or nonthermal ablation or phlebectomy to eliminate
the source of recurrent thrombosis (45).
Finally, the updated CHEST 2021 guidelines for treatment of SVT provide a weak recommendation for prophylactic anticoagulation if SVT involves the GSV (a large area)
close to the SFJ or in patients with active cancer, severe
symptoms, history of DVT or SVT, or using fondaparinux
2.5 mg daily or rivaroxaban 10 mg daily for 45 days (46).
29.7 CONCLUSION
In conclusion, SVT is common, heterogenous in presentation, and carries a risk of association with and progression to DVT and PE, especially in the setting of underlying
thrombophilia. Current evidence supports the use of preventative-dose LMWH or DOAC for a minimum of 45
days with consideration of surgical removal and/or endovenous treatment of associated varicose veins in selected
cases. Further research is required for risk stratication
and specic population management recommendations.
Guidelines and Statements 29.0 of the American Venous Forum on supercial thrombophlebitis
No. Guideline Grade of
29.1 For patients with SVT of the main saphenous trunks and tributaries above the knee >3cm from
the SFJ and >5cm in length, whether associated with varicose veins or not, we recommend
fondaparinux 2.5 mg subcutaneously daily for 45 days. Alternatively, rivaroxaban 10 mg daily for
45 days may be appropriate for patients unwilling or unable to perform subcutaneous injections.
Consensus Statement
29.2 For patients with SVT of the main saphenous trunks ≤3cm from the SFJ, treatment with full anticoagulation for a minimum of 6
weeks should be continued.
No. Guidelines Grade of
29.3 For patients with SVT of the main saphenous trunks, we recommend against using prophylactic or
therapeutic-dose LMWH and NSAIDs. While both have been found to reduce SVT pain and extension, they have failed to prevent VTE.
If NSAIDs are used for treatment of short-segment distal SVT, surveillance with DUS for VTE extension is recommended due to the high prevalence of concomitant DVT.
29.4 For selected patients with isolated thrombosis of varicose tributaries or limited involvement of the
GSV, we suggest phlebectomy as a safe alternative.
Consensus Statement
29.5. In patients with saphenous thrombophlebitis, ablation should be performed once the inammation has resolved if there is evidence of pathologic reux on DUS.
Source: Based on the recommendations of References 1, 40–42, 44, and 46.
recommendation
1
(strong)
recommendation
1
(strong)
2
(weak)
Quality of
evidence
A
(high)
Quality of
evidence
A
(high)
B
(moderate)
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patients with supercial vein thrombosis
involving the sapheno-femoral junction.
Vascular Medicine. 2022;29(3):
290–292.
43. Spirkoska A., Kaja Jezovnik M., Poredos
P. Time course and the recanalization
29
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rate of supercial vein thrombosis
treated with low-molecular-weight-heparin. Angiology. 2015;66(4):1–6.
44. Casian D., Bzovii F., Culiuc V., Guta E.
Urgent surgery versus anticoagulation
for treatment of supercial vein thrombosis in patients with varicose veins.
Vasa. 2022;51(3):174–181.
♦45. Gloviczki P., Lawrence P.F., Wasan S.M.
etal. The 2023 Society for Vascular
Surgery, American Venous Forum, and
American Vein and Lymphatic Society
clinical practice guidelines for the
management of varicose veins of the
lower extremities. Part II: Endorsed by
the society of interventional radiology
and the society for vascular medicine. J
Vasc Surg Venous Lymphat Disord. 2024
Jan;12(1):101670.
♦46. Stevens S., Woller S., Baumann Kreuziger
L., etal. Antithrombotic therapy for VTE
disease: Second update of the CHEST
guideline and expert panel report. Chest.
2021 Dec;160(6):e545–e608.
CHAPTER
30
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Mesenteric vein thrombosis
Elizabeth A. Andraska and Mohammadreza Zarisfi
30.1 INTRODUCTION
Mesenteric vein thrombosis (MVT) was rst described by
Elliot in 1895.
MVT remains a serious thrombotic disorder that is difcult
to both diagnose and treat. MVT is a rare disease entity, with
an incidence of 2.7 per 100,000 person-years and accounts
for 6%–9% of patients with mesenteric ischemia.
autopsy study evaluating patients over a 12-year period
of time, the cause-specic mortality incidence of MVT
was 1.8 per 100,000 persons.
increased in recent decades, with the incidence increasing
with age, and up to 11.3 per 100,000 persons in patients
aged 70–79.
etiology; for example, MVT associated with an oncologic
process presents later, on average, than an MVT associated with oral contraceptive use. While some studies suggest a slight male predominance, overall, both genders are
equally represented.
diagnosed with MVT have been previously diagnosed with
a deep vein thrombosis. Despite its rare presentation, the
mesentery is the most common site for venous thrombosis,
behind the lungs and the limbs.
1
Now, 120years after the rst description,
2
In an
3
The incidence of MVT has
2,4
The age at presentation varies depending on
2,5
Between 20% and 40% of patients
6
30.2 ETIOLOGY
MVT is an insidious disease process, which makes identication and timely management difcult. However, identication and treatment of the causal factors related to MVT
are critical to clinical assessment and therapy. These factors
can be generally categorized as inherited and/or acquired
(Table 30.1). Inherited factors include genetic abnormalities, which are summarized in Table 30.1. The acquired
conditions include pregnancy, surgery, and trauma. In
patients with MVT, local causes such as abdominal or
pelvic surgery or infection, organ pathology involving the
liver (cancer, cirrhosis, or hepatitis), pancreas (pancreatitis
or cancer), and spleen (splenomegaly of different causes or
splenectomy) are particularly relevant.
causes include acquired thrombophilias such as disseminated intravascular coagulation or heparin-induced thrombocytopenia. Medication-induced hypercoagulability (i.e.,
oral contraceptive use) is also an important etiology of
MVT. In general, acquired thromboembolic events have
5,7,8
Other acquired
TABLE 30.1 Thrombophilia risk factors for mesenteric
venous thrombosis
Inherited thrombophilia
Antithrombin deciency
Protein C deciency
Protein S deciency
Activated protein C resistance
Factor V Leiden mutation
Prothrombin G20210A mutation
Elevated factor VIII
Hyperbrinogenemia
Sickle cell disease
Hyperhomocysteinemia from genetic defects in 5-methyltetrahydrofolate reductase
Acquired thrombophilia
Heparin-induced thrombocytopenia
Disseminated intravascular coagulation (DIC)
Lupus anticoagulant and antiphospholipid antibody syndrome
Paroxysmal nocturnal hemoglobinuria
JAK2 (V617F) mutation
Hyperhomocysteinemia from acquired conditions, mainly
vitamin deficiencies
Oral contraceptive use
Nephrotic syndrome
Malignancy
Intra-abdominal states
Cirrhosis
Inammatory bowel disease
Intra-abdominal infection
Pancreatitis
Postoperative
Trauma
a sufciently low risk of recurrence such that prolonged
anticoagulant therapy is neither necessary nor advis-
9,10
able.
Patients with MVT who have identiable transient,
acquired risk factors can be surveilled on anticoagulation
for 3–6 months safely. For unprovoked thrombotic events
or for those with acquired and noncorrectable risk factors,
DOI: 10.1201/9781003328971-33
301301
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the risk of recurrence is deemed sufciently high to warrant prolonged secondary prevention with anticoagulants,
assuming the risk of major bleeding is mild to moderate. As
our understanding and recognition of the factors involved
in the genesis of venous thrombosis improves and as imaging modalities advance, the number of patients with unprovoked MVT should decline.
Although there is a general acceptance that inherited
or acquired thrombophilias either cause or contribute to
MVT cases, the precise role of these conditions remains
unclear. While the majority of cases are associated with at
least one of the aforementioned risk factors, idiopathic cases
have been reported to range from 21% to 49% of all MVT
5
Most studies have been retrospective in nature with
cases.
incomplete coagulation assessment and limited by referral
bias. Furthermore, in those patients in whom an underlying local etiology has been identied, coagulation testing is
infrequently performed or not completely comprehensive.
Lastly, coagulation testing may be limited by the timing of
assay acquisition or concomitant anticoagulation use, thus
resulting in overestimation or underestimation of coagulation defects. Test interpretation may be affected by the
thrombus itself, hepatic ischemia secondary to the thrombus, or treatment with heparinoids or vitamin K antagonists.
Myeloproliferative neoplasms, including polycythemia vera, essential thrombocythemia, and primary
myelobrosis, are found in about a third of MVT cases
and therefore are important considerations in the search
for an underlying mechanism.
11
These disorders represent
a stem cell–derived clonal myeloproliferation. The most
common clinical manifestation of this malignancy and
the cause of death is venous or arterial thrombosis. The
JAK2V617F sequence variation with gain in function that
leads to independent proliferation is found in 90% of cases
of polycythemia vera and up to 50% of cases of essential
thrombocythemia. Screening for this mutation is therefore
appropriate in the initial evaluation of patients who are
suspected of having these disorders, including patients with
12–14
MVT.
In fact, detection of the JAK2 sequence variation
has replaced bone marrow examination as the rst test to
screen for myeloproliferative neoplasms.
A good illustration of the role of thrombophilia in
MVT patients is the analysis of 341 cases of splanchnic
vein thrombosis, including 67 with MVT and 3621 control
patients with leg deep vein thrombosis (DVT).
15
Factor V
Leiden mutation was the most common thrombophilia in
MVT, particularly those with splenic vein thrombosis and
MVT; one in every two cases with a homozygous mutation was a patient with MVT. Antiphospholipid antibody
syndrome was the second most prevalent thrombophilia in
these series; nearly 10% of those with MVT were diagnosed with this acquired thrombophilia. Over 7% of MVT
patients were heterozygous carriers of the prothrombin
G20210A mutation. There were only two MVT patients
with antithrombin and one with protein S deciencies. In
this study, although the prevalence of positive testing for
thrombophilia was similar in MVT compared to leg DVT/
pulmonary embolism, the prevalence of “strong thrombophilia”—dened as a deciency of antithrombin, protein
C, or protein S; antiphospholipid antibody syndrome;
homozygous factor V Leiden or prothrombin G20210A
mutations; or compound heterozygous mutations of factor
V Leiden and prothrombin G20210A—was greater in
patients with splanchnic vein thrombosis. This high prevalence was notably observed for patients with MVT.
15
30.3 CLINICAL PRESENTATION
The clinical course and symptomatology in MVT are determined by both the aggression of the thrombotic process
and the extent of venous segments involved, determining
the possibility of collateral circulation development. The
superior mesenteric vein is much more frequently involved
relative to the inferior mesenteric vein. The onset of progressive abdominal pain in the patient with disproportionally few physical ndings should prompt the clinician to
think about MVT as a possible diagnosis. Although the
duration of symptoms varies, the majority of patients will
have had symptoms for more than 48hours before seeking medical attention. There should be a high suspicion
of MVT in patients with vague abdominal pain if there
are associated thrombotic risk factors such as oral contraceptive use or cancer. Apersonal or family history of VTE
should prompt the clinician to evaluate for MVT.
The clinical manifestations of MVT depend largely on
the extent of the thrombus, the size and number of vessels
involved, the acuity of venous obstruction, and the extent
of venous collateral development.
signs and symptoms of intestinal ischemia due to MVT
are nonspecic. The pathophysiology includes mesenteric
venous outow obstruction that may lead to profound
congestion and capillary malperfusion. This results in mesenteric ischemia with abdominal pain that is out of proportion to the physical ndings.
is often localized to the mid-abdomen and is described as
“colicky,” suggesting a compromised small bowel. Nausea, anorexia, vomiting, and diarrhea are also common.
Hematemesis, hematochezia, or melena occur in about
15% of patients. Abdominal distention is found in more
than half of patients. Peritoneal signs develop in one-third
to two-thirds of patients, although the initial physical ndings may be entirely normal. When fever, guarding, and
rebound tenderness are found, intestinal infarction must be
anticipated. Hemodynamic instability is a grave prognostic nding and may result from hypovolemia due to uid
collection within the bowel lumen or the development of
ascites or sepsis. Fluid resuscitation, early diagnosis conrmation, and prompt surgical attention are central to
improving the outcomes of these unstable patients.
There is a subset of patients who develop subacute or
chronic MVT. This is often due to subacute thrombus or
recurrent thrombus. These patients may present differently
from those with acute MVT. Patients with subacute onset
present primarily with abdominal pain that has developed
over days to weeks.
16,17
In these patients, neither bowel infarction nor chronic complications of portal hypertension are
likely. Occasionally, however, patients with prominent and
persistent abdominal pain will develop intestinal infarction
several days to weeks after the initial onset. Distinguishing
between an acute and subacute presentation can be quite difcult. It is for this reason that acute and subacute mesenteric
venous thromboses are often discussed together. Patients with
chronic MVT have minimal, if any, symptoms. The diagnosis
18
In general, the clinical
19,20
The abdominal pain
30.4 Diagnostic methods 303
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is often made as an incidental nding on cross-sectional
imaging studies when extensive venous collaterals are noted.
Complications of portal vein or splenic vein thrombosis such
as portal hypertension or esophageal variceal hemorrhage
may also lead the clinician to MVT as the etiology.
8
30.4 DIAGNOSTIC METHODS
Due to the clinical ambiguity described earlier, MVT is frequently misdiagnosed initially or diagnosed late, and the
outcome is often unfavorable. In patients for whom the
diagnosis of MVT is suspected, sensitive imaging modalities should be used early in the evaluation.
30.4.1 Computed tomography
Contrast-enhanced computed tomography (CT) is the test
of choice for suspected cases of MVT. The mesenteric vessels are well seen, and the extent of bowel involvement can
be simultaneously evaluated. Furthermore, other causes
of abdominal pain can be excluded at the same time. An
acute venous thrombus is identied as a central lling
defect within the mesenteric vein (Figure30.1). Engorge-
ment of the superior mesenteric vein with varying degrees
of wall enhancement may also be observed. Other CT ndings are less specic and represent manifestations of the
accompanying bowel ischemia. These include thickening of
the small bowel wall and peritoneal uid. If these nonspecic signs are seen in the setting of MVT, bowel infarction
should be strongly considered. Acute-on-chronic MVT can
also occur, in which case there may be integration of the
thrombus with the vein wall and more enhancement of the
vein wall. Collaterals in the mesentery also suggest acuteon-chronic etiology. Thrombus can extend proximally or
distally but often extends into the portomesenteric conuence and into the portal vein. About one-third of MVT
cases will have extension into the portal vein, with half of
those involving the splenic vein as well.
The sensitivity of contrast-enhanced CT imaging for
MVT is as high as 93% and specicity as high as 100%.
In those patients with early thrombosis involving small
venous branches, the sensitivity is diminished. Multirow
CT scanners offer the advantages of signicantly shorter
acquisition times, three-dimensional reconstruction, and
reduced artifacts, thus improving the overall diagnostic
accuracy. This technique provides detailed assessment of
both intraluminal and extraluminal abnormalities, mural
thrombosis, and mesenteric edema. Metallic and nonmetallic synthetic graft artifacts are reduced, and the organ
anatomy is well depicted.
21
30
22
30.1 Computed tomography with intravenous contrast shows
(a) nonocclusive thrombus projecting into the lumen of the
superior mesenteric vein (SMV) up to the level of the conuence
with the splenic vein and (b) thrombosis of a branch vessel of
the SMV (arrow).
30.4.2 Magnetic resonance imaging
Magnetic resonance imaging (MRI) also has excellent
sensitivity and specicity for the diagnosis of MVT (Figure30.2). Advantages of this technique include no exposure to ionizing radiation and the ability to tailor the image
acquisition to correspond to the desired vascular territory.
The bowel and other organ integrity can be assessed at the
same time. Limitations include signal degradation due to
ow turbulence and motion- and metallic-related artifacts
from vascular stents and vascular clips.
30.4.3 Ultrasonography
Duplex ultrasound provides an alternative noninvasive
assessment of mesenteric blood ow in the evaluation of
patients with suspected MVT without the use of contrast.
Thrombus visualization within the mesenteric venous
system conrms the diagnosis. The lack of residual mesenteric venous ow by Doppler assessment is also quite
specic for the diagnosis of MVT. Athickened bowel wall,
free intraperitoneal uid, and biliary disease can also be
demonstrated. There is neither nephrotoxic contrast nor
ionizing radiation exposure during image acquisition. Limitations of this modality include operator skill and expertise, appropriate equipment capable of assessing slow-ow
states, and patient-specic variables, including unsuitable
acoustic windows and overlying bowel gas. In addition,
large periportal collateral vessels in portal venous thrombosis may be mistaken for a patent portal vein, and bowel
gas or dilatation can also obstruct the operator’s view.
In experienced hands, however, duplex ultrasound is an
invaluable technique for this purpose.
23
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