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350 Mesenteric vein thrombosis
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will develop intestinal infarction several days to weeks
aer the initial onset. Distinguishing between an acute and
subacute presentation can be quite dicult.
7–9
It is for this
reason that acute and subacute mesenteric venous thromboses are oen discussed together. Patients with chronic
MVT have minimal if any symptoms. e diagnosis is oen
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 correct
inciting etiology. is chapter will focus primarily on the
acute form of MVT.
28.2 ETIOLOGY
Identication and treatment or elimination of the causal
factors for MVT are central to clinical assessment and
therapy. ese factors can be generally categorized as inherited and therefore essentially permanent or acquired (Table
28.1). e acquired conditions may be transient, correct-
able, or permanent. Examples of transient acquired causes
include pregnancy, surgery, and trauma. Predisposing conditions can be broadly divided into systemic or local. In
patients with MVT, local causes such as abdominal or pelvic surgery, organ pathology involving the liver (cancer, cirrhosis, or hepatitis), pancreas (pancreatitis or cancer), and
spleen (splenomegaly of dierent causes or splenectomy) are
particularly relevant.
boembolic events attributed to transient or correctable
acquired risk factors have a suciently low risk of recurrence such that prolonged anticoagulant therapy is neither
Table 28.1 Thrombophilia risk factors for mesenteric
venous thrombosis
Inherited or Primary Thrombophilia
Antithrombin deficiency
Protein C deficiency
Protein S deficiency
Activated protein C resistance and factor V Leiden
mutation
Prothrombin G20210A mutation
Elevated Factor VIII
Hyperhomocysteinemia from genetic defects in
5-methyltetrahydrofolate reductase
Acquired or Secondary 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
3,4,7,12,14,15
In general, provoked throm-
necessary nor advisable.16 For unprovoked thrombotic
events, or for those with acquired and non-correctable risk
factors, the risk of recurrence is deemed suciently high as
to warrant prolonged secondary prevention with anticoagulants, assuming the risk of major bleeding is mild to moderate.16 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 continue to decline.
3,5,6 ,12,14
However, the most recent international registry of splanchnic veins thrombosis including MVT showed that over 27%
of cases were unprovoked.
17
Although there is a general acceptance that inherited
or acquired thrombophilias either cause or contribute to
MVT cases,
3,6 ,18
the precise role of these conditions remains
unclear. Most studies have been retrospective in nature with
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. Lastly, coagulation testing may
be limited by the timing of assay acquisition, thus resulting in over- or under-estimation of coagulation defects.
Test interpretation may be aected 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.19 ese disorders represent a stem cell-derived
clonal myeloproliferation. e most common clinical
manifestation of this malignancy and the cause of death is
venous or arterial thrombosis.20 e JAK2V617F sequence
variation with gain of 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 MVT.
21–23
In fact,
detection of the JAK2 sequence variation has replaced bone
marrow examination as the rst test to screen for myeloproliferative neoplasms.
22,24
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 splanchnic vein thrombosis, 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. ere were
only two MVT patients with antithrombin and one with
protein S deciencies. In this study, although the prevalence
28.3 Clinical presentation 351
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of positive testing for thrombophilia was similar in MVT
compared to leg DVT/pulmonary embolism, the prevalence
of “strong thrombophilia,” dened as deciency of either
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.15
is high prevalence was notably observed for patients with
MVT. While the nding of “strong” thrombophilia usually
mandates long-term secondary anticoagulation prophylaxis, this nding is of practical importance.
28.3 CLINICAL PRESENTATION
e 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 durations of symptoms vary, the majority of
patients will have had symptoms for more than 48 hours
before seeking medical attention.3 In those patients with
ascites, MVT should be high in the dierential diagnosis,
particularly if thrombotic risk factors (e.g., oral contraceptive use or known malignancy) or historical factors such
as a personal and/or family history of venous thromboembolic disease are present. e clinical manifestations
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.
general, the clinical signs and symptoms of intestinal ischemia due to MVT are non-specic. e pathophysiology
includes mesenteric venous outow obstruction that may
lead to profound congestion and capillary malperfusion.
is results in mesenteric ischemia with abdominal pain
that is out of proportion to the physical ndings.
abdominal pain is oen 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,12 but occult blood is detectable in
the stool in nearly 50%.
26
Abdominal distention is found in
more than half of patients.25 Peritoneal signs develop in a
third to two-thirds of patients, although the initial physical
ndings may be entirely normal.12 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 septicemia.12 Fluid resuscitation, early diagnosis conrmation, and prompt surgical attention are central
to improving the outcomes of these unstable patients.
3,5–15,25
6,8
In
e
condition is frequently misdiagnosed initially or diagnosed
late, and the outcome is oen unfavorable.11 In patients for
whom the diagnosis of MVT is suspected, sensitive imaging
modalities should be used early in the evaluation.
28.3.2 Computed tomography
Contrast-enhanced computed tomography (CT) is considered by many to be the test of choice for suspected cases
of MVT.
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 (Figure 28.1). Engorgement 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. ese
include thickening of the small bowel wall and peritoneal
uid. If these non-specic signs are seen in the setting of
MVT, bowel infarction should be strongly considered.
(a)
(b)
27–30
e mesenteric vessels are well seen and the
28.3.1 Diagnostic methods
Recent advances in imaging technology have increased the
accurac y and frequency of MVT d iagnosis and improved our
understanding of its underlying causes. Nonetheless, this
Figure 28.1 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 confluence with the splenic vein and
(b)thrombosis of a branch vessel of the SMV (arrow).
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e sensitivity of contrast-enhanced CT imaging for
MVT may be as high as 90%.
3,30
In those patients with early
thrombosis involving small venous branches, the sensitivity is diminished. e new multi-row CT scanners oer the
advantages of signicantly shorter acquisition times, threedimensional reconstruction, and reduced artifacts, thus
improving the overall diagnostic accuracy.
30–32
is technique provides detailed assessment of both intra- and extraluminal abnormalities, mural thrombosis, and mesenteric
edema. Metallic and non-metallic synthetic gra artifacts
are reduced and the organ anatomy is well depicted.
28.3.3 Magnetic resonance imaging
Magnetic resonance imaging (MRI) also has excellent sensitivity and specicity for the diagnosis of MVT
(Figure 28.2).33 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. e bowel and other organ integrity can be assessed
at the same time. Limitations include signal degradation
(a)
due to ow turbulence and motion- and metallic-related
artifacts from vascular stents and vascular clips.
33–36
28.3.4 Ultrasonography
Duplex ultrasound provides a sensitive and specic assessment of mesenteric blood ow in the evaluation of patients
with suspected MVT.
the mesenteric venous system conrms the diagnosis
(Figure 28.3a and 28.3b). e lack of residual mesenteric
venous ow by Doppler assessment is also quite specic for
the diagnosis of MVT (Figure 28.3c and 28.3d). A thickened
bowel wall, free intraperitoneal uid, and biliary disease can
also be demonstrated. Advantages include a noninvasive
and inexpensive assessment that can be obtained urgently
at the patient’s bedside. ere 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. Intravenous
administration of ultrasound-compatible intravascular
contrast agents in conjunction with grayscale harmonic
imaging may increase vessel interrogation.37 Inexperienced
hands, duplex ultrasound is an invaluable technique for this
purpose.
27,33,37
rombus visualization within
(b)
Figure 28.2 Magnetic resonance imaging (MRI) example
of mesenteric vein thrombus. Contrast-enhanced MRI of
the abdomen demonstrates an acute occlusive venous
thrombus (arrows) involving the superior mesenteric vein
(SMV) in both cross-sectional (a) and coronal (b) views.
The SMV is distended with an acute-appearing thrombus.
28.3.5 Venography
Although more invasive than the cross-sectional imaging modalities described, the advantages of conventional
venography include an accurate assessment of mesenteric venous patency and ow direction, venous collaterals, and a comprehensive assessment of thrombus burden
(Figure 28.4). Pressure gradients can be measured directly
and endovascular therapies can be readily accomplished.
Selective mesenteric angiography demonstrates impaired
lling of the accompanying veins, arterial spasm, and prolonged opacication of the arterial arcades, all of which
provide indirect evidence supporting the diagnosis.
27, 38
e
limitations of venography include the requirement of experienced personnel with appropriate imaging hardware. e
evaluation includes transfer of a potentially unstable patient
to a uoroscopy suite for image acquisition, which is invasive and exposes the patient to both nephrotoxic contrast
and ionizing radiation.
28.3.6 Abdominal radiographs
Although abdominal radiographs are abnormal in 50%–
75% of patients, the ndings are not specic for either bowel
ischemia or MVT.
adynamic ileus with dilated, uid-lled loops of bowel.
Focal thickening of the mucosa (“thumb-printing”) or
mesentery and intramural or venous gas suggest advanced
39
e most common ndings include
28.3 Clinical presentation 353
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(a)
(b)
Figure 28.3 Duplex ultrasound example of mesenteric vein thrombosis. This duplex ultrasound example depicts an acute-
appearing, non-occlusive thrombus (arrows) involving the superior mesenteric vein in cross-sectional
(b) views. Both color (c) and Doppler interrogation (d) of the venous segment reveal that the thrombus is incompletely
obstructing mesenteric venous outflow.
(c)
(d)
(a) and longitudinal
IVC
Figure 28.4 Venogram example of the transjugular
intrahepatic portosystemic shunt (TIPS) procedure
showing partially occlusive mesenteric venous thrombus (large white arrow). The stented communication
(thin black arrows) with the inferior vena cava is readily
apparent.
intestinal ischemia.40 Barium contrast studies should be
avoided in these patients.
In summary, there are a number of imaging studies to
choose from in the evaluation of patients with suspected
MVT. e choice involves a careful clinical assessment of
the patient to determine the likelihood of MVT versus other
diagnoses (assessing the pre-test probability of disease). For
the stable patient with reasonable creatinine clearance, contrast-enhanced CT imaging will provide considerable clinical
information. Contrast-enhanced MRI provides an excellent
alternative for stable patients. For patients who are less stable,
bedside duplex ultrasound will provide an assessment of mesenteric vascular patency. e ultimate choice of imaging will
depend on the radiology expertise and machinery available at
the institution that is caring for the patient. Discussion of the
patient-specic variables with the attending radiologist prior
to decision making is a very valuable and fruitful place to start.
28.3.7 Blood tests
Blood tests may be very helpful but are not very specic in
the evaluation of patients with suspected MVT. e complete
blood count with dierentials is important for assessing both
the hemoglobin and hematocrit in order to ensure that occult
bleeding is not overlooked. Polycythemia rubra vera, essential thrombocythemia, leukemia, and other hematologic disorders which may predispose to venous thrombosis can also
be screened for with this test. e white blood count will alert
the physician to infections related to bowel infarction or perforation. Elevated serum lactate levels and metabolic acidosis
354 Mesenteric vein thrombosis
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will help to identify those patients with a severely ischemic
or infarcted bowel.41 If levels are higher than 1000 U/L, acute
pancreatitis should be considered. Transaminase elevation implies additional involvement of the portal or hepatic
venous system. is is particularly relevant to the initiation
of treatment with vitamin K antagonists. Fibrin D-dimer
elevation may also be helpful in determining the timing of
thrombosis. An acute thrombus is anticipated to be accompanied by signicant D-dimer elevations. In the subacute
or chronic setting, thrombosis evolution may no longer be
associated with D-dimer abnormalities.
e timing of thrombophilia laboratory assessment may
be a dicult decision to make. Ideally, one would obtain
these types of tests once the thrombus has been appropriately treated and the patient is no longer taking warfarin or
heparin. Typically, this type of testing (Table 28.1) would be
performed more than 2 weeks aer warfarin has been discontinued in order to maximize the test sensitivity and specicity.
28.4 TREATMENT
28.4.1 Medical management
e appropriate treatment of patients with MVT involves
multidisciplinary input from both medical and surgical
services. Clinical observations suggest that immediate anticoagulation with heparin early in the course of the disease,
even intraoperatively, improves survival, reduces thrombus propagation, and reduces the risk of recurrence.
16 ,17,4 0
Gastrointestinal bleeding is not necessarily a contraindication to anticoagulant therapy, whereas the risk of bleeding
must be weighed against the risk of bowel infarction. is
decision requires careful and thorough patient evaluation,
including measures of bowel ischemia, thrombus burden
and acuity, collateral circulation, and an assessment of
bleeding risk. Although improved survival rates have been
shown among patients receiving anticoagulant therapy
(63% vs. 44%), the need for chronic anticoagulant therapy
in these patients is less clear.
14,42
Observational studies suggest that chronic anticoagulant use reduces the incidence of
recurrent venous thrombosis by a third.
3,7,11,17
e ecacy
and optimal duration of anticoagulant therapy, however, has
not been dened by randomized trials. In general, anticoagulation should be continued until provoking factors have
been eliminated if possible. In those patients whose MVT
can be attributed to temporary risk factors, 3–6 months
of anticoagulants is likely reasonable.
16,4 3
Expert opinion
would suggest that antibiotic therapy should be provided
for patients with signs or symptoms of bowelcompromise.
28.4.2 Endovascular intervention
Endovascular therapies may be pursued for selected patients
with acute MVT that is diagnosed early in the course of the
disease before bowel infarction or peritonitis develop.
Candidates for this approach include those patients with
acute and extensive mesenteric venous thrombosis with
44–47
portal vein involvement for whom surgical thrombectomy
or balloon embolectomy are not feasible options.44 Catheterdirected thrombolysis requires gaining access either by
cannulation of the portal venous system via a percutaneous transhepatic or transjugular approach, intraoperative
catheterization, or through direct cannulation of the superior mesenteric artery. Indirect thrombolytic therapy via
the mesenteric artery is particularly ecient for resolving
thrombosis within capillaries and venules.
44–48
Mechanical
thrombectomy could be combined with lytic therapy. Newer
mechanical thrombectomy devices such as the AngioJet
reholytic mechanical thrombectomy system (Possis
Medical) have demonstrated promising ecacy in MVT
treatment.48 Although this represents an attractive alternative to surgical intervention which appears safe and eective, prospective studies with adequate patient numbers are
necessary for a reliable assessment of this treatment method.
28.4.3 Surgical treatment
e need for surgical intervention in patients with MVT is not
universal and may be necessary for only a minority.
mesenteric ischemia accompanied by evidence of peritonitis or
bowel infarct ion is an accepted indicat ion for surgica l intervention and resection of the involved bowel. e key to successful
surgery is to resect sucient bowel to ensure proper anastomic healing and halt thrombus propagation while preserving
as much viable intestine as possible. e decision-making process may be complex and may require the technical skill and
expertise of a surgeon who has familiarity with operations of
this type. Management is dictated by the intraoperative ndings, which range from segmental bowel ischemia to widespread mesenteric necrosis. Bowel perforation may or may
not be present. Oen, the surgical procedure is staged with
a repeat (“second-look”) laparotomy performed 1 day later.49
Post-operatively, anticoagulants should be initiated as soon
as hemostasis is adequately achieved. Under these circumstances, disease progression is uncommon. rombectomy
remains a potential treatment option for selected patients, yet
must be pursued quickly, as thrombus maturation (beyond
3days) reduces the success of this operation.
50
28.5 OUTCOMES
Reported mortality rates vary considerably and range
from 2% to 50% within the follow-up range of 1 month
to 5 years.
istries or retrospective analyses and are heterogeneous
in nature, with varying proportions of acute and chronic,
surgical, and non-surgical cases. Warren and Eberhard2
compiled published reports of 75 cases of MVT, to which
they added two of their own. In this historic description,
the overall mortality rate was 58.8%. Of the 55 patients
who underwent surgical resection, the mortality rate was
45.4%. Of the remaining 20 who were treated medically,
only one patient survived to hospital discharge. More recent
reports have yielded more favorable results with declining
3,6,12–14,17
ese studies, however, are either reg-
3,6 ,14
Acute
References 355
https://t.me/med1917
mortality rates. Delay of diagnosis and intervention, postsurgical complications, and underlying malignancy carry
worse prognoses.11 e recurrence rate of venous thrombosis in these patients is not completely clear. Although the
rates are said to be increased, Kumar and Kamath8 reported
only two recurrences among 30 patients with MVT limited to the superior mesenteric vein over a median followup of 18months. Recurrent thrombosis was noted in ve
out of 39patients with combined porto-mesenteric-splenic
thrombosis during a median follow-up period of 27 months.
ese data suggest recurrence rates of 5%–6% per year.
Morasch et al.11 reported that all 22 long-term survivors
of MVT (19 treated with warfarin) were thrombosis free at
the last follow-up visit (mean 57.7-month period). Recently
published results from the European International Registry
of Splanchnic Vein rombosis (44% with MVT) reported
rates of 3.8 per 100 patient-years for major bleeding, 7.3 per
100 patient-years for thrombotic events, and 10.3 per 100
patient-years for all-cause mortality. Anticoagulant treatment was associated with an essentially unchanged rate
of major bleeding at 3.9 per 100 patient-years, but a lower
rate of thrombotic events at 5.6 per 100 patient-years. When
anticoagulation was discontinued, rates were 1.0 per 100
patient-years for bleeding and 10.5 per 100 patient-years for
thrombosis recurrence. e highest rates of major bleeding and thrombotic events during the whole study period
were observed in patients with cirrhosis (10.0 and 11.3 per
100 patient-years, respectively), while the lowest rates were
observed in patients with thrombosis secondary to transient
risk factors (0.5 and 3.2 per 100 patient-years, respectively).
17
28.6 CONCLUSIONS
●
MVT, although less common than arterial thrombosis,
remains an important cause of mesenteric ischemia
(5%–15%).
●
MVT has lower morbidity and mortality than arterial
mesenteric ischemia.
●
e incidence of underlying thrombophilia in MVT is
similar to leg thrombosis, but the higher incidence of
“severe” thrombophilia observed in MVT impacts on
recommendations for long-term anticoagulation.
●
Both CT angiography and magnetic resonance angiography are recommended tests for MVT diagnosis.
●
ere is still a considerable delay in diagnosis because
of a low degree of clinical suspicion and the non-specic
clinical presentation.
●
Immediate use of anticoagulation can improve outcomes,
and if liver cirrhosis and esophageal/gastric varicosities are not present, an excessive bleeding rate is not
observed.
●
Surgery should be limited to patients with peritonitis or
perforation, with the objective of conserving as much
bowel as possible, yet ensuring viable margins.
●
In patients with high-risk inherited thrombotic diathesis or another permanent risk for thrombosis, lifelong anticoagulation is a reasonable option; when the
predisposing cause is temporary or can be eliminated, at
least 3 months of anticoagulation is recommended.
●
e long-term prognosis of patients without cancer or
other life-threatening conditions is generally good.
Guidelines 3.12.0 of the American Venous Forum on mesenteric vein thrombosis
Grade of
recommendation
No. Guideline
3.12.1 We recommend computed tomography angiography and
magnetic resonance angiography for the diagnosis of
mesenteric venous thrombosis (MVT).
3.12.2 We recommend immediate anticoagulation for the
treatment of MVT to improve outcomes.
3.12.3 We recommend surgery for patients with MVT if they
have evidence of peritonitis or perforation.
3.12.4 In patients with high-risk inherited thrombotic disorders
or other permanent risk for thrombosis, we recommend
long-term anticoagulation.
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PART 4
https://t.me/med1917
Management of Chronic Venous
Disorders
29 Clinical presentation and assessment of patients with venous disease 361
Sarah Onida, Tristan R. A. Lane, and Alun H. Davies
30 Diagnostic algorithm for telangiectasia, varicose veins, and venous ulcers: Currentguidelines 371
Robert B. McLafferty
31 Compression therapy for venous ulceration 379
Louise Corle, Hugo Partsch, and Gregory L. Moneta
32 Drug treatment of varicose veins, venousedema, and ulcers 391
Philip D. Coleridge Smith
33 Liquid sclerotherapy for telangiectasia andvaricose veins 399
Edward G. Mackay
34 Percutaneous laser therapy of telangiectasia and varicose veins 409
Thomas M. Proebstle
35 Foam sclerotherapy for ablation of the saphenous veins, varicose tributaries, andperforating veins 421
Huw Davies, Katy Darvall, and Andrew W. Bradbury
36 Techniques and results of the modern surgical treatment of the incompetent saphenous vein 429
Anjan Talukdar and Michael C. Dalsing
37 Radiofrequency treatment of the incompetent saphenous vein 443
Alan M. Dietzek and Stuart Blackwood
38 Laser treatment of the incompetent saphenousvein 455
Nick Morrison
39 Emerging endovenous technology for chronic venous disease: Mechanical occlusion chemically assisted
ablation (MOCA), cyanoacrylate embolization (CAE), and V block-assisted sclerotherapy (VBAS) 465
Steve Elias
40 Phlebectomy 475
Lowell S. Kabnick and Omar L. Esponda
41 Recurrent varicose veins: Etiology andmanagement 485
Pamela S. Kim, Angela A. Kokkosis, and Antonios P. Gasparis
42 Treatment of varicose veins: Current guidelines 493
Jose I. Almeida
43 Surgical repair of primary deep vein valve incompetence 499
Ramesh K. Tripathi
44 Surgical treatment of post-thrombotic valvular incompetence 513
Oscar Maleti and Marzia Lugli
45 Endovascular reconstruction for primary iliac vein obstruction 523
Peter Neglén
46 Endovascular treatment of post-thrombotic iliofemoral venous obstruction 533
Erin H. Murphy and Seshadri Raju
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