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340 Indications, techniques, and results of inferior vena cava filters
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10. Hirsh J. Oral anticoagulant drugs. N Engl J Med
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38. Nicholson W, Nicholson WJ, Tolerico P etal.
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Bard retrievable vena cava filters and clinical implications including cardiac perforation and tamponade.
Arch Intern Med 2010;170(20):1827–31.
39. Lorch H, Welger D, Wagner V etal. Current practice
of temporary vena cava filter insertion: A multicenter
registry. J Vasc Interv Radiol 2000;11(1):83–8.
40. Yamagami T, Kato T, Iida S, Tanaka O, and Nishimura
T. Retrievable vena cava filter placement during
treatment for deep venous thrombosis. Br J Radiol
2003;76(910):712–8.
●
41. Decousus H, Leizorovicz A, Parent F etal. A
clinical trial of vena caval filters in the prevention of pulmonary embolism in patients with
proximal deep-vein thrombosis. N Engl J Med
1998;338(7):409–16.
●
42. Decousus H. Eight-year follow-up of patients with
permanent vena cava filters in the prevention of
pulmonary embolism: The PREPIC (Prévention du
Risque d’Embolie Pulmonaire par Interruption Cave)
randomized study. Circulation 20 0 5;112 (3): 416 – 2 2.
43. Chuu WM, Wang NY, and Perry D. Vena caval filters
for the prevention of pulmonary embolism. N Engl J
Med 1998;339(1):46; author reply 47–8.
44. Murphy TP, Trerotola SO, and Vogelzang RL. Vena
caval filters for the prevention of pulmonary embolism. N Engl J Med 1998;339(1):46–7; author reply
47–8.
★
45. Greenfield LJ and Proctor MC. Vena caval filters for
the prevention of pulmonary embolism. N Engl J
Med 1998;339(1):47; author reply 47–8.
46. Mismetti P, Laporte S, Pellerin O etal. Effect of a
retrievable inferior vena cava filter plus anticoagulation vs anticoagulation alone on risk of recurrent
pulmonary embolism. JAMA 2015;313(16):1627–35.
47. Kim HS, Young MJ, Narayan AK, Hong K, Liddell RP,
and Streiff MB. A comparison of clinical outcomes
with retrievable and permanent inferior vena cava
filters. J Vasc Interv Radiol 2008;19(3):393–9.
48. Andreoli JM, Lewandowski RJ, Vogelzang RL, and
Ryu RK. Comparison of complication rates associated with permanent and retrievable inferior vena
cava filters: A review of the MAUDE database. J Vasc
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Insertion of the Simon Nitinol caval filter: Value of
the antecubital vein approach. AJR Am J Roentgenol
1991;157(3):521–2.
50. Passman MA, Dattilo JB, Guzman RJ, and Naslund
TC. Bedside placement of inferior vena cava filters
by using transabdominal duplex ultrasonography
and intravascular ultrasound imaging. J Vasc Surg
2005;42(5):1027–32.
51. Corriere MA, Passman MA, Guzman RJ, Dattilo
JB, and Naslund TC. Comparison of bedside
transabdominal duplex ultrasound versus contrast
venography for inferior vena cava filter placement:
What is the best imaging modality? Ann Vasc Surg
2005;19(2):229–34.
52. Lucas DJ, Dunne JR, Rodriguez CJ etal. Dedicated
tracking of patients with retrievable inferior vena
cava filters improves retrieval rates. Am Surg
2012;78(8):870–4.
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53. Lynch FC. A method for following patients with
retrievable inferior vena cava filters: Results and
lessons learned from the first 1,100 patients. J Vasc
Interv Radiol 2011; 2 2(11):1507–12.
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filter devices. Clin Chest Med 1995;16(2):295–305.
55. Rousseau H, Perreault P, Otal P etal. The 6-F
Nitinol TrapEase inferior vena cava filter: Results of
a prospective multicenter trial. J Vasc Interv Radiol
20 01;12(3):299–304.
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review. Blood 2000;95(12):3669–77.
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57. Greenfield LJ and Proctor MC. The percutaneous
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58. Vena Caval Filter Consensus Conference.
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inferior vena cava filter placement for the prevention
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Greenfield filter. Surg Technol Int 1993;2:289–91.
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Greenfield vena caval filter experience: Late results
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and Greenfield L. Use of the Greenfield filter for
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68. Athanasoulis CA, Kaufman JA, Halpern EF, Waltman
AC, Geller SC, and Fan CM. Inferior vena caval
filters: Review of a 26-year single-center clinical
experience. Radiology 2000;216(1):54–66.
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and Lanuti S. Pulmonary embolus after vena cava
filter placement. Am Surg 1999;65(4):341–6.
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Superficial thrombophlebitis
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BENJAMIN JACOBS AND DAWN M. COLEMAN
27
27.1 Introduction 343
27.2 Epidemiology 343
27.3 Clinical presentation 343
27.4 Etiology 343
27.1 INTRODUCTION
Supercial venous thrombophlebitis (SVT) is common,
although its incidence is likely underestimated, as many
cases are subclinical and go unreported. ere are a number of misconceptions about this diagnosis amongst physicians, the most pernicious of which is that it is entirely
benign, oering no life- or limb-threatening complications. While this is true of some cases, SVT carries a risk
of association and progression to deep vein thrombosis
(DVT) and pulmonary embolism (PE). Consequently, a
thorough understanding of the pathophysiology, diagnosis, and management of SVT is of great importance to the
venous health physician.
27.2 EPIDEMIOLOGY
e incidence of SVT approximates 1:1000, although this is
generally believed to reect an underestimate. SVT aects
almost 125,000 patients in the United States annually.1 e
average age at diagnosis ranges from 54 to 65 years; SVT
aects females more than males.
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, pregnancy
and the puerperium, oral contraceptives, hormonereplacement therapy, immobilization, recent surgery, and
trauma.
4
2,3
e most commonly
27.3 CLINICAL PRESENTATION
Patients will present in most cases with pain and erythema overlying the aected supercial vein, along with a
27.5 Diagnosis 345
27.6 Treatment 345
27.7 Conclusion 346
References 347
palpable “cord” and edema of the surrounding so tissue.
Low-grade fever or malaise may be present. e supercial
veins of the upper or lower extremities, the breast in the
case of Mondor’s disease, or the dorsal veins of the penis
may all be aected by SVT. e most common locations
aected by SVT include the great saphenous vein (GSV)
and its tributaries, followed by the cephalic and basilic
veins of the upper extremity.4 e diagnosis of progression to DVT is oen accompanied by a worsening of
symptoms.
5
27.4 ETIOLOGY
Traditionally, the pathophysiology of venous thromboembolic disease has been attributed to Virchow’s 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. e etiology of SVT is complex and oen multifactorial; it remains
an area of active discovery.
27.4.1 Superficial thrombophlebitis and
lower extremity varicosities
Lower extremity varicosities and lower extremity venous
insuciency 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 insuciency.
reported that only 3%–20% of SVT patients with varicose
veins will develop DVT, compared to 44%–60% of those
without varicosities.
patients with varicose veins has a dierent pathophysiology
7–9
erefore, it may be that SVT in
6
It has been
343

344 Superficial thrombophlebitis
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from those without varicose veins. However, in a more
recent study, no increased incidence of DVT or PE was
noted when comparing patients with and without varicose
veins in the 186 SVT patients identied.2 Consequently,
the question of whether SVT patients with or without
associated varicose veins should be thought of as separate
classications remains ambiguous.10 Conversely, addressing those patients with SVT involving varicose veins only
is essential. is type of SVT may remain localized to the
cluster of tributary varicosities or may, from time to time,
extend into the GSV.2 Supercial venous thrombosis is frequently found in varicose veins surrounding venous stasis
ulcers.
27.4.2 Disease progression to DVT and PE
In as much as the primary threat to the patient with SVT is
due to the potential for venous thromboembolism (VTE), it
is important to clarify the connection between these entities. It has been shown that SVT can progress to DVT via
proximal extension of thrombus into the deep system, but it
also, perhaps counterintuitively, has been shown to arise in
association with SVT in non-contiguous vessels.
2,3
Concomitant DVT can be present but asymptomatic at presentation for SVT, and identied only on deep
vein ultrasound studies. Decousus et al. 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.3 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%.
4,11
e most common route
of extension is from the GSV via the saphenofemoral junction (SFJ) into the femoral vein.
9,12
Progression to VTE may
also result from short saphenous vein SVT progression into
the popliteal vein, and into the deep system via perforating
4
veins.
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 revealed progression to deep venous
involvement in 30 patients (11%) and specically 16% of
those with GSV SVT had extension into the femoral vein—
most commonly via the SFJ (85%).
9
Proximity of supercial
thrombus to the SFJ inuences the likelihood of progression; SVT location within 1 cm of the SFJ confers a high risk
of DVT progression.
5
27.4.3 Associated hypercoagulability
Which patients, if any, presenting with SVT merit workup
for hypercoaguable states remains an area of controversy and active research. ere are no current guidelines
that support concise recommendations. Martinelli et al.’s
case–control study tested 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.11 An
increased risk of SVT was identied in patients with inherited coagulopathies. Risk of SVT was increased approximately six-fold for factor V Leiden mutation, four-fold
for the prothrombin G20210A mutation, and 13-fold for
the combined factor deciencies. Similarly, de Moerloose
et al. demonstrated that the presence of factor V Leiden
mutation increased risk of SVT, although this was no longer statistically signicant aer controlling for obesity.13
Additionally, patients with SVT not associated with lower
extremity varicosities were more likely to have an inherited
hypercoaguable state.
Another study of 29 patients with SVT investigated this
relationship.14 All patients underwent duplex ultrasonography of the supercial and deep venous systems. Patients
with isolated SVT were treated with non-steroidal antiinammatory drugs (NSAIDs) and those with DVT were
treated with heparin and warfarin. ese patients had a
similar coagulation prole performed that included protein C antigen and activity, activated protein C resistance,
protein S antigen and activity, AT III, and the lupus anticoagulant. Twelve patients (41%) were found to have abnormal
results consistent with a hypercoaguable state. Five of the
patients (38%) with combined SVT and DVT and seven of
the patients (44%) with SVT alone were found to be hypercoaguable. Four patients had decreased levels of AT III only
and four patients were identied with activated protein
C (APC) resistance. One patient had decreased protein C
and protein S, and three patients had deciencies of AT III,
protein C, and protein S. e most prevalent anticoagulant
deciency was AT III. Furthermore, in a subsequent separate set of data examining patients with recurrent SVT, anticardiolipin antibodies were detected in 33% of patients.
15
ese 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.
4,16,17
Consequently, whether routine testing of
these patients is necessary remains unclear. It is reasonable
to conclude that those patients presenting with SVT in the
absence of any clear risk factor, especially if recurrent, merit
such investigation.
27.4.4 Upper extremity SVT
e most common etiologic factor in upper extremity SVT
is trauma associated with an intravenous cannula and intravenous infusions resulting in caustic endothelial damage.
Treatment consists of cannula removal and warm compresses. e resultant lump may persist for months notwithstanding this treatment. Extension of upper extremity SVT
into upper extremity DVT or PE is a very rare occurrence
when compared with lower extremity SVT.
18

27.6 Treatment 345
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27.4.5 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. e associated signs
and symptoms of SSVT include purulence at an intravenous site, fever, leukocytosis, and local intense pain.19
Treatment consists of catheter removal, warm compresses,
NSAIDs 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 to the extent that brisk back-bleeding is
encountered.
27.4.6 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.20 is entity may
be associated with carcinoma and may precede diagnosis
of the carcinoma by several years. Consequently, a workup
for occult malignancy may, in fact, be warranted when the
diagnosis of migratory thrombophlebitis is made.
27.4.7 Mondor’s disease
Mondor’s 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.21 Recently, the term has also been applied to SVT of
the dorsal vein of the penis.
22
27.5 DIAGNOSIS
Duplex ultrasound scanning is the diagnostic modality of
choice for the evaluation of DVT and SVT. e availability
of reliable duplex ultrasonography of the deep and supercial venous systems has made routine determination of the
location and extent of venous thrombosis accurate and practical. Furthermore, the extent of involvement of the deep
and supercial systems can be more accurately assessed utilizing this modality; routine clinical examination may not
precisely evaluate the proximal extent of the involvement of
the deep or supercial systems. Duplex imaging of patients
with SVT has revealed concomitant DVT in 5%–40% of
patients.
of these patients’ DVTs may not be contiguous with the
SVT, or may even be in the contralateral lower extremity.
Consequently, bilateral imaging is necessary. Duplex ultrasound is also noninvasive, inexpensive, and may be easily
repeated for surveillance examinations. Venography, alternatively, has fallen out of favor, with little indication.
2,23–26
It is important to note again that up to 25%
2
27.6 TREATMENT
e extent of thrombus burden, thrombus location, the
presence of concomitant DVT, and associated local infection should direct SVT treatment. Ambulation, warm compresses, elastic compression, intermittent elevation, and
NSAIDs remain appropriate for cases of mild SVT in order
to alleviate the inammatory reaction.27 While NSAIDs
have been shown to signicantly reduce the risk of SVT
extension and/or recurrence by 67% compared to placebo,
this therapy oers no protection against VTE, nor resolution of local signs and/or symptoms.
erapeutic anticoagulation and venous ligation or ablation have become increasingly popular for decreasing the
risk of DVT in patients with SVT that demonstrate thrombus extension toward the level of the SFJ or carry additional
risk factors for DVT extension. Historically, thrombus
within 3 cm of the SFJ was felt to warrant surgical ligation
of the SFJ with or without simultaneous GSV stripping/
ligation, while more recent data support anticoagulation
and compression over surgical measures.
A 1999 prospective trial comparing various anticoagulant treatment groups (prophylactic unfractionated heparin,
prophylactic low-molecular-weight heparin [LMWH], and
therapeutic warfarin) to elastic compression alone or saphenous ligation identied lower rates of SVT extension in the
anticoagulant treatment groups by surveillance imaging,
without major bleeding complication.31 Several contemporary trials have followed, further supporting the benets of
anticoagulation for SVT. e 2003 SVT Enoxaparin Study
Group published their double-blind randomized trial comparing 8 days of treatment for SVT with prophylactic enoxaparin (40 mg) daily, therapeutic enoxaparin (1.5 mg/kg)
daily, oral tenoxicam, and placebo for 8–12 days.32 e incidence of deep and supercial venous thromboembolism was
signicantly decreased in all treatment groups (from 30.6%
in the placebo group to 8.3% in the prophylactic enoxaparin
group, 6.9% in the therapeutic enoxaparin group, and 14.9%
in the tenoxicam group) without any hemorrhagic morbidity or heparin-induced thrombocytopenia. e randomized
controlled Vesalio trial compared 1 month of prophylactic
versus therapeutic doses of nadroparin for SVT.33 ese
authors failed to demonstrate a dierence in thrombus progression or VTE in either group, and moreover, they failed
to meet recruitment goals, resulting in premature study
termination.
A contemporary multicenter, randomized, double-blind,
placebo-controlled trial reported on the safety and ecacy
of fondaparinux for SVT.34 Approximately 3000 patients
with acute, symptomatic lower limb SVT involving a segment of at least 5 cm in length located at least 3 cm distal to the SFJ were assigned to 45 days of treatment with
fondaparinux (2.5 mg subcutaneously daily) or placebo.
e fondaparinux group demonstrated an 85% lower rate of
PE or DVT than the placebo group aer 77 days, along with
a signicantly reduced rate of symptomatic SVT recurrence
27, 28
29,30

346 Superficial thrombophlebitis
Algorithm
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or extension to the SFJ without major hemorrhage or alternative morbidity.
Most recently, a 14-day treatment course of dalteparin (200 U/kg at presentation followed by 10,000 U daily)
for SVT was identied as superior to ibuprofen (800 mg
three times daily) for both major upper and lower SVT.35
Interestingly, this benet was lost by the 3-month followup, and thrombus extension, including VTE, occurred
in the time period following cessation of dalteparin and
ibuprofen dosing, suggesting the treatment duration (2
weeks) may have been too brief. Finally, both therapies
signicantly reduced symptoms of pain during the treatment periodand appeared safewithout episodes of major or
minor hemorrhage.
A 2013 Cochrane review including 30 randomized
controlled trials and 6507 patients with SVT summarized that: both LMWH and NSAIDs reduce SVT extension and recurrence without any eect on symptomatic
VTE; topical treatments relieve local symptoms; surgical
treatment and elastic stockings oer a lower rate of VTE
and SVT progression over elastic stockings alone; and
fondaparinux appears to be an adequate treatment option
as it oers a signicant reduction in symptomatic VTE and
SVT extension/recurrence.36 e 2012 American College
of Chest Physicians CHEST guidelines advocate medical
treatment with a prophylactic dose of fondaparinux or
LMWH for 45 days over no anticoagulation (grade 2B)
for patients with SVT of the lower limb that measures at
least 5 cm in length, with grade 2C evidence favoring a
daily dose of fondaparinux (2.5 mg) over a prophylactic
dose of LMWH for patients with SVT being treated with
anticoagulation.
37
Finally, GSV disconnection and ligation at the SFJ
remains appropriate for patients with SVTwhocannot tolerate anticoagulation and demonstrate moderatethrombus burden (i.e., ≥5 cm in length or within 3 cm of the
SFJ). Surgical treatment with GSV ablation and phlebectomies of the involved branch varicosities should be
considered as the optimal treatments for patients with
symptomatic SVT and evidence of venous insuciency by
duplex ultrasound in order to prevent recurrent phlebitis
aer the phlebitis has resolved, which is typically staged
by 3–6 months.
27.7 CONCLUSION
In conclusion, SVT is common and carries a risk of association and progression to DVT and PE. e vein health
physician must consider an individualized treatment plan.
While patients with milder forms of SVT may be successfully managed with NSAIDs, compression, and warm
compresses, those with moderate disease, dened as SVT
located 3 cm distal to the SFJ and 5 cm in length, should
be managed more aggressively, with either prophylactic
LMWH or fondaparinux. erapeutic anticoagulation
should be considered for any patient that develops DVT or
PE. For patients who cannot tolerate anticoagulation, GSV
disconnection and ligation at the SFJ are appropriate when
thrombus burden is moderate. Surgical treatment with
GSV ablation and phlebectomies of the involved branch
varicosities should be considered as the optimal treatments for patients with symptomatic SVT and evidence
of venous insuciency conrmed by duplex ultrasound,
which is usually performed aer the phlebitis has resolved.
SVT
- <5 cm of thrombus length
Mild
Moderate
- At least 3 cm distal to SFJ
At least 5 cm of thrombus length
Associated venous insufficiency
Associated VTE
- or -
Thrombus <3 cm from (or involving) the
SFJ
NSAIDs
Compression
Warm compresses
Fondaparinux 2.5 mg daily
- or -
LMWH 40 mg daily
Medical management (as above) and
interval GSV ablation and phlebectomy
Therapeutic anticoagulation

Guidelines 3.11.0 of the American Venous Forum on superficial thrombophlebitis
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References 347
No. Guideline
3.11.1 For saphenous vein thrombophlebitis within 3 cm of the
saphenofemoral or saphenopopliteal junction, we
recommend therapeutic anticoagulation.
3.11.2 For moderate thrombophlebitis with at least 5 cm thrombus
length and at least 3 cm distal to the saphenofemoral
junction, we recommend fondaparinux 2.5 mg daily or
low-molecular-weight heparin 40 mg daily for 45 days.
3.11.3 For thrombophlebitis localized in the distal segment or in
tributaries of the great saphenous vein with thrombus
length <5 cm, we suggest ambulation, warm soaks, and
non-steroidal anti-inflammatory agents.
3.11.4 For moderate thrombophlebitis as described above, or
thrombophlebitis within 3 cm of the saphenofemoral
junction, if anticoagulation is contraindicated, high ligation
and division of the great saphenous vein is suggested.
3.11.5 In patients with saphenous thrombophlebitis, we suggest
ablation once the inflammation resolved if there is evidence
of venous insufficiency confirmed by duplex ultrasound
scanning.
Grade of
recommendation
(1: strong; 2:
weak)
1 B
1 B
2 B
2 B
2 B
Grade of evidence
(A:high quality;
B:moderate quality;
C:low or very low quality)
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vein thrombophlebitis (SVT): A deceptively benign
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17. Karthanos C, Sfyroeras G, Drakou A etal. Superficial
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Mesenteric vein thrombosis
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WALDEMAR E. WYSOKINSKI AND ROBERT D. McBANE
28
28.1 Introduction 349
28.2 Etiology 350
28.3 Clinical presentation 351
28.4 Treatment 354
28.1 INTRODUCTION
Mesenteric vein thrombosis (MVT) was rst described by
Elliot in 1895.1 Four decades later, Warren and Eberhard2
recognized this as a distinct clinical entity and an important cause of bowel infarction. Now, 120 years aer the rst
description, MVT remains a serious thrombotic disorder
that is dicult to both diagnose and treat.3 It is important
to recognize very unique features of the mesenteric venous
circulation that impact on the thrombotic process:
●
ere is a noticeable variation in mesenteric blood ow
and viscosity associated with the time of day, nutrition
intake, physical activity, emotional stress, diarrheal
and/or vomiting related uid loss, and dehydration
from poor uid intake.
●
Mesenteric venous blood is rich in nutrients and intestinal elements such as microbial ora and both senescent
and damaged cells.
●
is circulation is subject to a number of blood-borne
gastrointestinal peptides such as glucagon, vasoactive
intestinal polypeptide (VIP), and cholecystokinin,
which may further impact hemostasis and blood ow,
particularly as mesenteric circulation is richly innervated by the sympathetic nervous system.
●
e mesenteric veins do not contain venous valves, at
least not in the larger channels.4 is is important, as
venous thrombi, occurring in the deep veins of the leg
are thought to originate in the valve pockets; therefore,
spatial and structural dierences between leg vein and
mesenteric vein thrombi might exist.
●
Finally, the interrelationship of the mesenteric venous
circulation with splenic and portal vein ow is such that
a local pro-thrombotic milieu related to splenic or liver
pathology (malignancy, inammation, or infection)
28.5 Outcomes 354
28.6 Conclusions 355
References 355
increases the propensity for thrombus propagation
into the mesenteric venous segment. rombosis of
one venous segment alters blood ow within the entire
system; in particular, occlusion of the portal system will
have a huge impact on venous blood stagnation within
the mesenteric vein.
For these combined reasons, the mesenteric venous
circulation is entirely unique and thrombosis occurring
within this system should be considered as a distinct entity
requiring special consideration and evaluation.
e incidence of MVT in the general population is poorly
dened, but seems to be rather uncommon. Kazmers noted
that MVT may be found in as few as one in 1000 laparoto-
5
e incidence of MVT has increased in Sweden from
mies.
2.0 per 100,000 patient-years between 1970 and 1982 to 2.7
per 100,000 patient-years between 2000 and 2006.6 e age
at presentation varies from 45 to 80 years and both genders are equally represented.
be limited to the mesenteric veins or may propagate to or
from other regional vessels.
of patients with intestinal ischemia.
and symptomatology is determined by both the aggression
of the thrombotic process and the extent of venous segments
involved, determining the possibility of collateral circulation
development. e superior mesenteric vein is much more
frequently involved relative to the inferior mesenteric vein.
Patients with acute MVT may note a sudden onset of
abdominal pain, which may quickly progress within hours
to include signs of peritonitis with bowel infarction. Patients
with subacute onset present primarily with abdominal pain
that has developed over days to weeks.
neither bowel infarction nor chronic complications
( variceal hemorrhage) are likely. Occasionally, however,
patients with prominent and persistent abdominal pain
3,5–14
Venous thrombosis may
6– 8,14
MVT accounts for 5%–15%
9–12
e clinical course
8–11
In these patients,
10
349
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