Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3829_Библиотеки_им_академика_М_И_Перельмана
.pdf
e pectoralis major is split between clavicular and ster-
https://t.me/med1917
nal heads. e pectoralis minor tendon is divided and the
axillary and subclavian veins mobilized and surrounded
with vessel loops. Two transverse incisions are made in
the neck to dissect the internal jugular vein. e rst is
2cm above the clavicle, 5 to 6cm long, and directly over
the sternocleidomastoid muscle. e sternal and clavicular heads of this muscle are split, and the internal jugular
vein dissected circumferentially and surrounded with a
Penrose drain. e vein is totally freed as far as possible
both proximally and distally by dividing all bands. Asecond incision, 4 to 5cm long, is made below the mandible.
rough this incision the cephalic portion of jugular vein
is freed proximally to the base of the skull and distally to
meet the freed portion of vein in the tunnel between the
two incisions.
A tunnel is created behind the clavicle between the
subclavian vein and the supraclavicular incision. e subclavius muscle is divided and a kidney pedicle clamp passed
between the two incisions. e tunnel is dilated bluntly
so that the jugular vein can pass easily through it without compression in the tunnel. e jugular vein is marked
with a stitch on its anterior wall for orientation. e vein
is clamped and divided close to the base of the skull. e
cephalic end is suture ligated. e distal end is carefully
passed down the jugular tunnel, brought out through the
lower neck incision, and freed as far as possible below the
clavicle up to the subclavian vein junction. e vein is then
passed though the tunnel beneath the clavicle. e patient
is heparinized and a longitudinal venotomy is performed,
excising a narrow rim of the vein wall. Passing a 12- to
14-French catheter through the vein prior to performing
the anastomosis is a good way to check that the subclavian vein is unobstructed and not kinked in its path to the
innominate vein. An end-to-side anastomosis is performed
with 6-0 Prolene. Some surgeons have elected an end-toend anastomosis; either is e ective.
Because venous repairs are subject to thrombosis due to
11
low ow pressures,
a temporary AVF is created between
the axillary vein and axillary artery, provided there is adequate room on the axillary vein distal to the anastomosis.
We have used ringed or spiral reinforced 6-mm PTFE for
the AVF. is is placed in a loop that comes up into the
subcutaneous tissue to make it easier to nd when the temporary AVF is taken down. We usually remove the AVF in
16
about 3 months.
An alternative AVF can be created in
the arm or antecubital space if creating it between axillary
vessels appears too di cult.
R E F E R E N C E S
1. Sanders RJ . Subclavian vein obstruction. In: Bergan JJ , Yao ST , ed.
Venous Disorders. Philadelphia : WB Saunders ; 1991 : 256 .
2. Dunant JH . Subclavian vein obstruction in thoracic outlet syndrome , Inter Angio . 1984 . 3 : 157–159 .
3 . ompson RW , Schneider PA , Nelken NA , Skioldebrand CG ,
Stoney RJ . Circumferential venolysis and paraclavicular thoracic
outlet decompression for e ort thrombosis of the subclavian vein ,
JVasc Surg . 1992 . 16 : 723–732 .
4 . A z a k i e A , M c El h i nn e y D B , ompson RW , Raven RB , Messina
LM , Stoney RJ . Surgical management of subclavian-vein e ort
thrombosis as a result of thoracic outlet compression , J Vasc Surg .
1998 . 28 : 777–786 .
5. Schneider DB , Dimuzio PJ , Martin ND , etal. Combination treatment of venous thoracic outlet syndrome:Open surgical decompression and intraoperative angioplasty , J Vasc Surg . 2004 . 40 : 599–603 .
6. Melby SJ , Vedantham S , Narra VR , etal. Comprehensive surgical
management of the competitive athlete with e ort thrombosis of
the subclavian vein (Paget-Schroetter syndrome) , J Vasc Surg . 2008 .
47 : 809–820 .
7. Machleder HI . Evaluation of a new treatment strategy for PagetSchroetter syndrome: Spontaneous thrombosis of the axillarysubclavian vein , J Vasc Surg . 1993 . 17 : 305–317 .
8. Kreienberg PB , Chang BB , Darling C II I, etal. Long - term results
in patients treated with thrombolysis, thoracic inlet decompression,
and subclavian vein stenting for Paget-Schroetter syndrome , J Vasc
Surg . 2001 . 33 : S100–S105 .
9. Molina JE . Need for emergency treatment in subclavian vein e ort
thrombosis , J Am Coll Surgeons . 1995 . 181 : 414–420 .
10. Molina JE . A new surgical approach to the innominate and subclavian vein , J Vasc Surg . 1998 . 27 : 576–581 .
11. Johnson V , Eiseman B . Evaluation of arteriovenous shunt to maintain patency of venous autogra , Am J Surg . 1969 . 118 : 915–920 .
12. Gloviczki P , Kazmier FJ , Hollier LH . Axillary subclavian venous
occlusion: e morbidity of a nonlethal disease , J Vasc Surg . 1986 .
4 : 333–337 .
13. Doty DB , Baker W . Bypass of superior vena cava with spiral vein
gra , Ann orac Surg . 1976 . 22 : 490–493 .
14. Hashmonai M , Schramek A , Farbstein J . Cephalic vein cross-over
bypass for subclavian vein thrombosis:Acase report , Surgery . 1976 .
80 : 563–564 .
15. Sanders RJ , Cooper MA . Surgical management of subclavian vein
obstruction, including six cases of subclavian vein bypass , Surgery .
1995 . 118 : 856–863 .
16. Sanders RJ , Rosales C , Pearce WH . Creation and closure of temporary arteriovenous stulas for venous reconstruction or thrombectomy:Description of technique , J Vasc Surg . 1987 . 6 : 504–505 .
17. Sanders RJ . Subclavian vein obstruction. In: Bergan JJ , Kistner RL ,
eds. Atlas of venous surgery . Philadelphia : WB Saunders . 1991 .
18. Sanders RJ , Haug CE . oracic outlet syndrome:Acommon sequela of
neck injuries. Philadelphia : JB Lippincott . 1991 .
418 • VENOUS THROMBOEMBOLISM
50.
https://t.me/med1917
SUPERFICIAL THROMBOPHLEBITIS
RECOMMENDATIONS FOR DIAGNOSIS AND MANAGEMENT
J o a n n M . L o h r
uper cial thrombophlebitis is a relatively common
in ammatory process that a ects the super cial veins.
S
is may include the upper extremity, lower extremity, trunk, chest wall or penis, and has been described in
various locations. e symptoms include pain, reddening
of the skin, and swelling of the surrounding tissue.
e predisposing risk factors for super cial vein
thrombophlebitis (SVTP) and super cial venous thromboembolism (SVT) are similar and include immobilization, varicose veins, postoperative time period, trauma,
pregnancy, postpartum, active malignancy, use of oral
contraceptives and hormone replacement therapy, obesity, chemotherapy, and prolonged immobilization.
Treatment is aimed at reducing the local symptoms, especially pain, and preventing the development of more serious complications, especially thrombus propagation or
embolization.
e incidence of SVT increases with age, in the third
decade it is 0.05 per 1,000 per year in males and 0.31 per
1,000 per year in females. In the eighth decade it is 1.8
per 1,000 per year in males and 2.2 per 1,000 per year in
females. It has a female proportion of 55–70% with a mean
age of 60years.
Virchow’s Triad is well established. It includes changes
in blood ow, changes in vessel walls, and changes in the
characteristics of the blood ow, all of which come into play
with the development ofSVT.
Local in ammatory mediators are altered with
development of SVT. is includes the prostaglandins,
leukotrienes, metabolites of arachidonic acid, nitric
oxide,swelling of the endothelial cells, and polymorphonuclear leukocyte in ltration of the tunica media resulting
in vessel wall injury and potentiation of the thrombotic
process.
1
PATHOPHYSIOLOGY
2,3
Predisposing factors include varicose veins; inherited
thrombophilias including Factor V Leiden, prothrombin
(2102A) gene mutations, de ciencies of antithrombin,
heparin cofactor, protein C or S de ciencies, lupus anticoagulant antibodies, and anticardiolipin antibodies; and
abnormal brinolytic activity.
Characteristic patient populations and triggering risk
factors include female proportion 55–70% with a mean
age of 60 years, obesity 20%, pregnancy, oral contraceptives, hormonal replacement, history of deep vein thrombosis (DVT), long-haul ights, prolonged immobilization,
recent surgery, trauma, or sclerotherapy.
A red, hot, tender, palpable cord along a super cial vein
is the most common physical examination nding. When
looking at risk factors, clinical ndings, venous duplex ultrasound ndings and treatment in all of the patients, Gorty
and colleagues found the most common risk factor was the
presence of varicose veins followed by a history of SVT, previous DVT, recent surgery, leg trauma, cancer, hormone use,
(either oral contraceptive or replacement), or hypercoagulable state. Pain was by far the most common symptom.
Super cial vein thrombophlebitis appears in two distinct forms. One is varicose vein thrombophlebitis, representing the vast majority of cases. It is characterized by a
large thrombus in a varicose vein and a modest in ammatory process localized in the surrounding vessel but not
in its wall. e other rarer form of SVTP a ects a nonvaricosed vein. Abundant intima proliferation and media
brosis with nonimportant thrombosis are the hallmarks
of this form, which may be associated with a systemic disease. Although SVTP is perceived as trivial and benign, the
coexistence of mostly distal DVT with propagation to the
popliteal or femoral and even pulmonary emboli (PE) have
been reported. e prevalence of these complications varies
widely from 6–53% for coexistence of DVT to 2.6–15% for
propagation, and 0–33% for asymptomatic PE. Risk factors
for these complications are those known to be associated
withDVT.
6
4
5
419
N A T U R A L H I S T O R Y
https://t.me/med1917
Patients with a SVTP of the leg have a ten-fold increased
risk of developing DVT during the subsequent 6months
when compared with an age- and sex-matched group without SVTP. e absolute risk of DVT, however is just 2.7%.
7
Swelling of a leg within 6 months a er a SVTP should
7
prompt diagnostic testing forDVT.
Treatment with low molecular weight heparin (LMWH)
or nonsteroidal anti-in ammatory drugs (NSAIDs) during
the 10 d following SVTP decreases the risk of the develop-
7
ing DVT by about 15% and 9% respectively.
Independent predictive factors for complications were
SVT of recent onset (odds ratio [OR], 3.01; 95% con dence interval [CI], 1.44–6.27), severe chronic venous
insu ciency (OR, 2.75; CI, 1.10–6.89), male gender (OR,
2.17; CI, 1.28–36.8), and a history of venous thromboembolism (VTE) (OR, 2.07; CI, 1.06–4.04). Only severe
chronic venous insu ciency was an independent risk factor and predictor of the development of DVT or PE (OR,
8
4.50; CI, 1.30–15.61).
Knowledge of the predictive factors
may be useful in determining the appropriate treatment in
8
patients withSVTP.
Vascular surgeons have given little attention to super cial thrombophlebitis involving the lesser saphenous vein.
Dr.Ascher and e NewYork Group in 2003 reported that
lesser saphenous vein thrombosis more o en is associated
with DVT (65.6%) than previously believed. While most
lesser saphenous vein thrombophlebitis will improve in
18months, that associated with DVT will resolve sooner.
Whether anticoagulation accounted for this di erence
9
remains to be demonstrated.
e risk of development of subsequent DVT following
SVT is really not fully appreciated. e mechanisms, time
relations, and risks factors for DVT arising on earlier SVT
are still unclear. Most patients will have complete resolution
of symptoms at 3 weeks. At that time, thrombus disappeared
completely in 26% of cases. rombus regression was similar to venous blood ow out ow direction—proximal to
femoral area. rombus propagation has been observed fol-
10
lowing regression of local symptoms ofSVT.
e William Beaumont Group in 1996 identi ed 263
patients with isolated SVT. Eleven percent of these patients
had documented progression to deep involvement. e
most common site of deep vein involvement was progression of the disease from the great saphenous in the thigh to
the common femoral vein with the majority of these being
nonocclusive and up to two-thirds having a free- oating
component. Other sites of extension were the above-knee
saphenous vein through thigh perforators to occlude
the femoral vein in the thigh, as well as extension of the
below-knee saphenous vein into the popliteal vein or extension of the below-knee thrombi into the tibioperoneal veins
with calf perforators. is group recommended proximal
vein thrombosis be treated with anticoagulation or at least
followed with sequential duplex scanning so that de nitive
therapy may be initiated if progression was noted. Most distal SVT should be followed carefully clinically and repeat
duplex scan performed if progression is noted or patient
11
symptoms worsen.
DIAGNOSIS
e diagnosis of SVT is made in a clinical setting, but ultrasonography is useful to eliminate the diagnostic or concomitant DVT. For SVT of the lower limb varicose veins
represent the principal cause, but underlying conditions
(i.e., autoimmune diseases, malignancy, or thrombophilia)
must be sought in cases of idiopathic, migrant, or recurrent
DVT and in the absence of varicose veins. Concomitant
DVT and PE can occur in approximately 15% and 5%
respectively. A1-month prophylactic dose of low-molecular
weight heparin plus elastic stockings could be an appropri-
12
ate strategy in most cases.
In all cases of clinical SVT a duplex examination of both
the super cial and deep venous symptoms is necessary in
order to provide a complete diagnosis. e treatment of
SVT depends on the situation and the size of the thrombi.
In case of associated DVT, the most important treatment
is of the DVT. e use of heparin or LMWH (therapeutic doses) is proved for patients with coexisting DVT, and
is thought to be appropriate for ascending SVT as well.
Super cial vein thrombosis must be considered a risk factor
for the development of DVT, and patients should be treated
from this point of view. Biologic analysis and complete
check-up are mandatory in cases of varicose thrombosis in
13
young patients and in cases of recurrence.
Duplex ultrasound is somewhat controversial but it can
be used to con rm the diagnosis of thrombus and identify
the popliteal and saphenofemoral functions. It can also rule
out contiguous and noncontiguous DVT. Super cial vein
thrombosis and concomitant DVT have been reported in a
14
wide spectrum from 2.6 to 65.6%.
e di erential diagnosis includes the clinical setting, cellulitis, panniculitis, erythema nodosum, insect bites, and lymphangitis. In at least one case, a ruptured infected super cial
femoral artery aneurysm has been misdiagnosed as anSVT.
e main histopathologic di erential diagnosis of super cial and venous thrombophlebitis is cutaneous polyarteritis nodosa. Biopsy and complementary techniques as well as
clinical signs and symptoms will usually allow the diagnosis
to be made. Super cial vein thrombosis is usually characterized by an autoresolving vasculitis of medium-sized veins
of the upper subcutaneous tissue or the deep dermis that
clinically manifests as a tender or painful palpable cordlike structure. Super cial vein thrombosis for the most part
involves the lower extremity, but special locations including the anterior chest wall or the penis, characterize speci c
16
clinical forms including Mondor’s disease.
15
420 • VENOUS THROMBOEMBOLISM
rombophlebitis migrans is a footprint for Buerger’s
https://t.me/med1917
disease and has been discussed in a descriptive study from
17
northeast Iran.
Congenital malformations and venous
abnormalities may also present as migratory SVT or unusual
18
presentations ofDVT.
Mondor’s disease was originally described in 1939 as a
super cial venous thrombophlebitis of the thoracoepigastric veins in women. is term has also been applied to the
super cial dorsal vein of the penis. is may actually be
underreported as patients may be reluctant to seek medical
care, especially if they associate their condition with deviant behavior. Injection of illegal substances in subcutaneous
veins may also cause thrombosis. Extrinsic venous compression may also result in occlusion and this may occur with
infection, sexual devices, and neoplastic diseases as well as
a tool belt worn around the waist causing venous pooling
and vessel trauma. Acareful history is critically important
19
in evaluating the patients.
Other unusual cases of super cial thrombophlebitis have been reported in association with sickle cell
20
episodes.
rombophilias may also present as recurrent SVTs or
21
SVTs of unusual locations.
Laparoscopy and laparoscopic procedures may have an
increased risk for the development of thrombosis due to
increased abdominal pressure and negative Trendelenburg
positioning. In patients with varicose veins and a history of
thromboembolism, laparoscopy-associated risk factors for
the development of thromboembolic complications may be
aggravated. ese patients with varicose veins and a history
of venous thromboembolism need to be considered carefully for prolonged laparoscopic and robotic procedures.
22
Primary care practitioners may be confronted with this
complication more o en because, due to legislative regulations, patients are discharged earlier from the hospital a er
22
laparoscopic interventions.
Several studies have shown an increased incidence of
inherited thrombophilias, in particular the presence of
Factor V Leiden and/or hyperhomocysteinemia in patients
a ected by SVT. Acquired molecular prothrombotic conditions associated with SVT are mainly represented by the
antiphospholipid syndrome or acquired activated protein
C resistance. Few studies have focused on the association
of molecular prothrombotic conditions in oncological
23
patients a ected bySVT.
From a pathologic point of view, it is important to distinguish SVT localized at the lower or upper extremity or
also unusual sites of thrombosis. Moreover, it is also important to di erentiate SVT of large venous vessels from SVT
of small venous vessels because of the possibility of embolization. Another relevant problem is related to the possibility of detection of small thrombus because of the presence
of a short peripheral venous catheter placed for the administration of drugs, uids, antibiotics, parenteral nutrition,
chemotherapy, and blood derivatives. Nursing surveillance
and catheter maintenance at the site of IV access is critical
23
to decrease the risk of infectiousSVT.
Trousseau described spontaneous, recurrent super cial
migratory thrombophlebitis associated with occult cancers,
and this was later correlated with disseminated microangiopathy (platelet-rich clots in small blood vessels). is is o en
associated with mucinous adenocarcinomas, which secrete
abnormally glycosylated mucins and mucin fragments into
the bloodstream. Since carcinoma mucins can have binding sites for selectins, the hypothesis is that selectin-mucin
interactions might trigger this syndrome. When highly
puri ed, tissue-factor-free carcinoma mucin preparations were intravenously injected into mice, platelet-rich
microthrombi were rapidly generated. is pathology was
markedly diminished in P- or L-selectin-de cient mice.
Heparin (an antithrombin-potentiating agent that can
also block P- and L-selectin recognition of ligands) ameliorated this platelet aggregation, but had no additional
e ects on P- or L-selectin-de cient mice. Inhibition of
endogenous thrombin by recombinant hirudin also did
not block platelet aggregation. Mucins generated plate
aggregation in vitro in hirudinized whole blood, but not in
platelet-rich leukocyte-free plasma nor in whole blood from
L-selectin-de cient mice. us, Trousseau syndrome is likely
triggered by the interactions of circulating carcinoma mucins
with leukocytes L-selectin and platelet P-selectin without
requiring accompanying thrombin generation. Wahrenbrock
and colleagues’ data may also explain why heparin ameliorates Trousseau syndrome, while vitamin K antagonists that
24
merely depress thrombin production donot.
One of the problems with migratory thrombophlebitis
is that patients may have advanced disease prior to presentation. e exact workup of patients with SVT for occult
malignancy is unsettled at thistime.
Super cial vein thrombosis is commonly encountered
in pregnancy. It is critical the obstetrician recognize the
potential for complications and embolic events and that
Doppler ultrasound be utilized to rule out potential deep
venous extension in these patents. While thromboembolism remains a leading cause of maternal death, the potential dangers of symptomatic thrombophlebitis should not
25
be overlooked.
Mondor’s disease or “wire-like” changes most commonly presents in middle-aged women and is idiopathic. It
may be related to strenuous exercise or trauma and it has
been associated with breast cancer. It may also be seen however in pregnant women and it may also be mistaken for
26
scleroderma.
rombophilias may play a minor role in the etiology of
27
SVT associated with pregnancy.
Acareful obstetrical and
gynecological history is important and is critical to maintain a high index of suspicion.
Primary hypercoagulable states are those conditions
associated with an increased risk of thrombosis caused by
a speci c measurable defect in the proteins of coagulation
SUPERFICIAL THROMBOPHLEBITIS • 421
and/or brinolytic systems. ese disorders are frequently
https://t.me/med1917
inherited and include de ciencies with antithrombin III,
heparin cofactor 2, protein C, protein S, abnormal brinolytic activity, dys brinogenemia, and Hageman trait.
Patients with lupus anticoagulant and anticardiolipin antibody syndrome with thrombotic episodes are also consid-
28
ered to have a primary hypercoagulable state.
A high suspicion of underlying thrombophilia needs
to be considered in patients who have SVT in unusual
sites or in patients who have SVT with no varicose vein
29–31
involvement.
High Factor VIII concentration is an independent risk
31
factor forSVT.
e lower threshold for testing for hypercoagulable
disorders should be maintaining patients with recurrent
32
33,34
2
)
recalcitrant or unusual patterns of SVT thrombosis.
In addition, elevated body mass index (BMI ≥28kg/m
has also been associated with increased risk of SVT.
Association of eosinophilia with SVT is a rare situation that can reveal neoplasia, malignancy blood disorders,
or vasculitis, but SVT has recently been described with the
35
hypereosinophilic syndrome.
rombophlebitis may be a complication of the incompetent greater saphenous vein and usually has a benign
outcome when this occurs (see Figure 50.1). However,
a free- oating thrombus tip in the femoral vein is a challenge to treat, and surgical ligation may be needed to prevent the risk of embolization when ascending SVT extends
to the femoral vein with a free- oating thrombus tip (see
Figure50.2). Use of color duplex sonography is important
36,37
in di erentiating this and establishing the diagnosis.
Dr.Lowell S.Kabnick and colleagues presented endovenous heat induced thrombus (EHIT ) following endovenous
vein obliteration at the American Venous Forum in 2006.
ey tried to categorize this process as producing a nonnormal SVT as the thrombus a er endovenous procedures
is hyperechoic whereas a de novo thrombus is hypoechoic.
Figure50.1 rombus in greater saphenousvein.
Figure50.2 SVT extending through the sapheno-femoral junction into
the common femoralvein.
ey classi ed their patients’ thrombi into four categories.
AClassIvenous thrombus is super cial and extends just to
the deep junction. It is located at the saphenofemoral junction or saphenopopliteal junction and does not extend into
the deep system. For this class, no treatment was needed.
AClassII nonocclusive venous thrombus with a less than
50% extension into the deep system and a cross-sectional
diameter of less than 50% was thought to need follow-up
and possible antiplatelet agents. AClassIII venous thrombus has a cross-sectional extension into the deep system,
is nonocclusive but greater than 50%. Finally, a ClassIV
venous thrombus completely occludes the common femoral
38
vein and should be treated asDVT.
Upper extremity SVT is most frequently associated with
iatrogenic conditions using intravenous catheters, drugs,
chemotherapy, and heroin. Suppurative thrombophlebitis
is an infection of the vein wall. It is usually associated with
intravenous catheter placement and accounts for approximately 10% of all nosocomial infections. It is more common
in patients with burns or cancer or those receiving steroids.
e skin ora, especially Staphylococcus aureus , are the most
common pathogens. Suppurative thrombophlebitis should
be suspected when the patient is having phlebitis or presents
with a fever greater than 102°F. e diagnosis of suppurative
thrombophlebitis is usually straightforward. It can be made
by the demonstration of pus coming from the wound of the
removed intravenous device or aspiration of pus percutaneously from the involved vein. Treatment of super cial suppurative thrombophlebitis consists mainly of venotomy of
39,40
the a ected vessel and systemic antimicrobial therapy.
Septic thrombophlebitis in the super cial veins is a
potentially devastating complication. Local in ammatory
changes are present in less than half of the patients with sepsis and may not manifest until several days a er the catheter
has been removed. Ahigh index of suspicion is necessary
to reach a timely diagnosis and proceed with de nitive surgical therapy. In the setting of persistent sepsis without an
identi able source, the diagnosis of septic thrombophlebitis
422 • VENOUS THROMBOEMBOLISM
should be considered and the evidence of its presence
https://t.me/med1917
40
actively sought.
Fungi are increasingly recognized as microorganisms
causing super cial suppurative thrombophlebitis and are
again managed by aggressive surgical therapy and antifun-
41
gal agents.
Clinically silent DVT is much more common in patients
without varicose veins. Aclinical marker for complications
of SVT is the occurrence of SVT in a patient who does not
have varicose veins. is should prompt a search for under-
42
lying associated diseases.
A substantial number of patients with SVT exhibit
venous thromboembolism at presentation; however, some
do not develop this complication until the subsequent
3 months. Risk factors for complications at 3 months
were male sex, history of DVT or PE, previous cancer, and
absence of varicose veins. ese ndings should prompt
consideration of alternative therapy and prolonged treat-
43
ment for patients in these high risk groups.
Gorty, Milio, and colleagues reported that SVT in a
normal vein with extension occurred in 20.8 to 23.7% of
44,45
their patient populations with thrombus propagation.
Super cial venous thrombosis occurs in 125,000 new
cases per year in the United States. A “healthy vein” is
involved in 25% of these cases with propagation reported
to occur in 2.6 to 15% of cases and 5% to have PE. e
mortality rate for SVT is 0–1% and the mortality rate for
4
DVTis5%.
e course of SVT is usually benign with septic complications occurring more commonly with upper extremity
thrombi and more commonly iatrogenic. e DVT that
occurs has been associated in 5.6 to 36% of cases. is may
be contiguous in 50–70% or noncontiguous. With a noncontiguous pattern, a hypercoagulable state should be considered. Patients with concomitant DVT have symptomatic
PEs reported in 0.5 to 4%. Physicians who systematically
perform lung scans on patients should know that PEs may
4
be present in up to 33% of patients.
e lower extremities account for 60–80% of SVTs for
the most part involving the great saphenous vein; 10–20%
involved the short saphenous vein. Other veins are involved
10–20% of the time and 5–10% of cases are bilateral. Upper
extremity and neck SVTs are more commonly iatrogenic.
e anterior thoracic or thoracoabdominal wall veins or
4
veins of the penis or groin may also be involved.
patients without complications and is found in 7.9% of
patients with spreading SVT. e methylenetetrahydrofolate reductase (MTHFR), a C677T mutation, is found
in 6.7% of patients with nonspreading SVT and 21.4% of
45
patients with spreading complications.
If you compare this same study looking at patients with
SVT involving normal veins, Factor V Leiden is found in
26.3% of patients with nonspreading situation and 60% in
patients with spreading. Prothrombin mutation is found
in 7.9% of nonspreading and 20% of those with ascending
complication. e MTHFR C677T mutation is found in
40% of those with spreading or present in only 23.7% of
45
patients with nonspreading.
Knowledge and correct identi cation of all veins routinely imaged in the upper extremities and lower extremities is critical to the proper management of SVT and DVT.
Unfortunately, in Ziehler and colleagues’ survey only 12%
of physicians were able to correctly identify all of the veins
routinely imaged in either upper extremity or lower extrem-
46
ity duplex venous scans.
At the Good Samaritan Hospital John J. Cranley
Vascular Laboratory, thrombus location is reported as super cial or deep, and also according to the location by zones to
allow sequential comparison and comparison between technologists. (See Figures50.3 and50.4.)
Ascending phlebitis closer than 5cm to the deep venous
system has been treated surgically. However, there is no consensus in the literature as to how to treat ascending thrombophlebitis. e surgical procedure can be performed under
47
local anesthesia, and is safe and e cient.
Varicose vein thrombectomy, when performed concurrently, gives patients better postoperative pain control.
Zone
2.0
IJ
EJ
Bas
Brach
SC
Ax
1.0
3.0
4.0
5.0
6.0
Ceph
Anticoagulants have been shown to decrease the incidence
of new SVT andDVT.
Considering patients with SVT and varicose veins,
Factor V Leiden in the nonspreading group is present in
6.7%. In patients with complications it may be found in
35.7%. Prothrombin mutation is present in 4.4% of SVT
T R E A T M E N T
45
Figure50.3 Zones of reference for upper extremity venous
scanning:midline=1.0, acromion=3.0, elbow=5.0, wrist=8.0,
and ngertips=9.0.
SUPERFICIAL THROMBOPHLEBITIS • 423
From Lohr etal. J Vasc Surg 1991;14:618–23.
7.0
8.0
9.0
Zone
https://t.me/med1917
1.0
2.0
3.0
4.0
5.0
6.0
7.0
8.0
Figure50.4 In an average-sized adult, one zone equals a length of
approximately 10cm on the extremity. Zone 1 is de ned as the
intersection of the femoral vessels with the inguinal ligament. Zone 5 is
an imaginary line passing from midpatelia to the popliteal crease. Zone
8 corresponds to a line from midmedial malleolus to the midlateral
malleolus. Zone 9 corresponds to the tips of the toes. With use of the
above landmarks, the thigh and calf are subdivided into four and three
equal zones, respectively.
From Lohr etal. Am J Surg 1995;170:86–90 .
9.0
Duplex scanning a ords 100% accuracy in both determin-
48
ing the presence of thrombosis and its extent.
Treatment of super cial thrombophlebitis may be
provided by a variety of measures. ese include local
anti-in ammatory applications including gels, creams, and
sprays, local incision and expression of clots, microthrombectomy, and ligation of connecting points, compression
bandaging and stockings, immediate mobilization and
walking exercises, analgesias and anti-in ammatory drugs,
surgery with high ligation and completed varicose vein
excision, anticoagulation with unfractionated heparin,
LMWH in prophylactic or therapeutic doses, and oral
49
anticoagulants.
Treatment with a therapeutic or prophylactic dose of
LMWH or an NSAID reduces the incidence of SVT extension or recurrence but not the VTE. More randomized
control trials are needed before any evidence-based recommendations on the treatment of SVT for the prevention of
50
VTE can be given.
In a comparison of high and low doses of LMWH
for the treatment of SVT of the legs, a double-blind
randomized control trial suggested therapeutic doses of
LMWH administered for one month in patients with
SVT of the great saphenous vein did not improve results
obtained when compared with prophylactic doses administered for the same period. e patients were followed for
51
three months.
e recent CHEST guidelines stated that peripheral
vein infusion thrombophlebitis is estimated to occur in
25–35% of hospitalized patients with peripheral IV catheters. No control trials have evaluated systemic anticoagu-
52
lants for the treatment of infusion thrombophlebitis.
e CHEST guidelines suggest oral diclofenac or
another NSAID as a Grade 2B recommendation. Topical
diclofenac gel, Grade 2B, or heparin gel, Grade 2B, are recommended for resolution of symptoms for up to 2 weeks.
We recommend against the use of systemic anticoagulation in this population as a Grade 1C recommendation.
52
Super cial venous thrombosis has been less studied than
DVT; however it is more common. Treatment of super cial
thrombophlebitis has been the subject of a recent Cochrane
53
meta-analysis.
e CHEST guidelines recommend that patients with
spontaneous SVTP be treated with prophylactics or intermediate doses of LMWH or unfractionated heparin as a
Grade 2B for at least 4 weeks. ey suggest an alternative of
4 weeks of LMWH or unfractionated heparin and a vitamin
K agonist with a target INR of 2.5 with a range of 2 to 5
that can be overlapped with 5 d of LMWH or unfractionated heparin and continued for 4 weeks. is is a Grade 2C
recommendation. ey suggest oral NSAIDs not be given
in addition to anticoagulants. Anticoagulation is a 2B recommendation, and they recommend medical treatment
with anticoagulants over surgical treatment as a Grade 1B
recommendation. It is thought likely that less extensive SVT
(i.e., where the a ected venous segment is short in length
or further from the saphenofemoral junction) does not
require treatment with anticoagulation at all. It is reasonable
to use oral or topical NSAIDs for symptoms and control of
52
thesecases.
e optimal duration of treatment for SVT as well as
the best regimen is unclear. General questions about the
treatment of SVT remain unresolved. Large and adequately
designed randomized control trials are needed to assess the
actual role of NSAIDs and LMWH to ascertain whether
these drugs are actually comparable, and whether used in
combination they may be more e ective and as safe compared with a single treatment. Another important issue is
to clarify the optimal duration of SVT treatment. Current
available data suggest that LMWH given for a week is probably too short to prevent VTE in the long term. Aprolongation of LMWH or NSAID treatment for at least a month
might be considered. Whether a topical treatment might
add some bene t if given in combination with LMWH or
NSAIDs remains unclear. Finally, whether treatment needs
424 • VENOUS THROMBOEMBOLISM
to be adapted based on location and the etiology of super -
https://t.me/med1917
53
cial thrombophlebitis warrants further investigation.
e goal of treatment for SVT is to improve local
symptoms while preventing the development of complications such as VTE and PE. Topical treatment alone does
not seem a reasonable approach to treat these patients. e
most e ective approach to treat SVT may be represented
by LMWH which has been shown to prevent VTE events
and extension and/or recurrence of SVT. In addition, the
administration of LMWH does not seem to carry a high risk
53–55
of bleeding, although these data are very preliminary.
It is advisable to repeat duplex scanning to determine
whether propagation of thrombus exists as an adjuvant in
56
those patients who are not actively treated.
e three main local actions of heparin on the skin
can be de ned as (1) the anticoagulant action; (2) the
microcirculatory-modulatory action determining important control of the microcirculation in case of excessive
vasoconstriction or vasodilatation; and (3)the “facilitatory
action” on skin permeability, allowing other drugs to di use
better and faster into the skin producing a better therapeutic e ect. Observation suggests important clinical applica-
57,58
tions for local liposomal heparin action.
Exercise may reduce pain as well as decrease the possibility of deep vein extension. Bed rest should be avoided in
patients with SVT. DVT prophylaxis should be established
in patients with reduced mobility. Antibiotics usually do
not have a place in super cial vein thrombophlebitis unless
59
there are documented episodes of infection.
Extended thrombus prophylaxis may be indicated in
patients with a history of venous thrombosis and genetic
mutations due to the enhanced risk of recurrence. Patient
groups with thrombophilias might bene t from extended
oral anticoagulation or vitamin supplementation if clini-
60
cally warranted.
ere are no good data on the use of pentasaccharide for
61
use of prophylaxis or treatment.
e incidence of deep and super cial thromboembolism and symptoms was signi cantly reduced by day 12 in
all active treatment groups treated with LMWH. No episodes of death or major hemorrhage occurred in this study.
62
When high-dose and low-dose unfractionated heparin
were evaluated in patients with acute SVT of the thigh,
unmonitored high doses of unfractionated heparin were
more e ective than prophylactic doses for the prevention
of thromboembolic complications and did not enhance the
63
risk of bleeding complications.
Local treatment with Essaven Gel in comparison with
placebo showed a decrease in the analogue symptomatic
score and in the skin temperature in the placebo group that
was due to skin manipulation and massage while the SVT
treated group had improved symptoms and decreased skin
temperature faster. is would suggest an e ective symp-
64
tomatic improvement with EssavenGel.
e Belgian rombosis Guidelines Group recommends immediate mobilization in elastic compression for
all patients withSVT.
65
Dr.Jason Lee and Dr.Maziyar Kalani from Stanford in
California suggested that in patients with refractory SVT
surgical intervention such as phlebectomy, sclerotherapy,
saphenofemoral junction ligation, or saphenous vein strip-
66
ping are all potentially acceptable treatments.
Researchers at the University of Michigan in 2001 also
suggested that ligation of above-knee super cial thrombophlebitis that does not involve the deep system may be a
67
suitable alternative.
A combination of LMWH and an anti-in ammatory
agent is more e ective than LMWH alone as a standard
treatment for SVT with improved symptom resolution and
68
reduction of pain and tenderness.
e Cincinnati group has previously demonstrated that
ligation is a safe alternative and may be combined with compression in outpatient treatment with LMWH in the man-
37
agement ofSVT.
e use of duplex ultrasound can safely identify patients
69
who need ligation.
e exact results and treatment recommendations
need to be individualized and further trials are needed. An
article in the New England Journal of Medicine suggested a
cost-bene t analysis needs to be done to evaluate the pricing of medications and other interventions in consideration
of the range of patients being treated to identify patients in
whom treatments may be most bene cial and cost-e ective,
but rapidly expanding those to others may be less clear and
must be considered carefully. Dr.Goldman suggests phase
3.5 trials to document the cost, the e ect on quality of life,
and the cost-e ectiveness of new interventions so as to
70
reach a consensus regarding their worthiness.
Goldman suggests that the exact treatment for SVT
needs to be individualized with special care given to the
presentation, the pattern of disease, and the potential
complications. If only tributaries are involved local heat,
nonsteroidal anti-in ammatories, graduated compression,
frequent ambulation, and elevation may be appropriate.
Anticoagulation is needed if there is concomitant DVT, if
the SVT is not responding to therapy, if there is involvement
of the great saphenous vein at the saphenofemoral junction
or of the small saphenous and the saphenopopliteal junction, if there are known underlying hypercoagulable states,
or if patients have had frequent recurrences. When a healthy
vein is involved, the treatment workup should include evaluation for underlying diseases and thrombophilias, a careful
duplex evaluation to evaluate for propagation, and a hypercoagulable workup. Surgical intervention is potentially
indicated for patients with a very symptomatic SVT in varicose veins and re ux in the great saphenous vein. Timing of
surgical treatment is controversial. Ultimately the treatment
of SVT needs to be decided on an individual patient basis.
70
SUPERFICIAL THROMBOPHLEBITIS • 425
R E F E R E N C E S
https://t.me/med1917
1. Coon WW . Tecumseh Community Health Study , Circulation .
1973 . 48 : 839–846 .
2. Lewis GHG , Heckle JF . Infusion thrombophlebitis , Br J Anaesth.
1985 . 57 : 220–233 .
3. Guildyal SK , Pande RC , Mirsa TR . Histopathology and bacteriology of post-infusion phlebitis , Inter Surg. 1975 . 60 : 341–344 .
4. Decousus H , Epinat M , Cuillot K , Boissier C , Tardy B . Super cial
vein thrombosis:Risk factors, diagnosis, and treatment , Curr Opin
Pulm Med. 2003 . 9 : 393–397 .
5. Gorty S , Palton-Adkins J , DaLanno M , Starr J , Dean S , Satiana B .
Super cial venous thrombosis of the lower extremities: Analysis
of risk factors and recurrence and role of anticoagulation , Vasc
Medicine. 2004 . 9 : 1–6 .
6. Blattler W , Schwarzenbach B , Largiader J . Super cial vein
thrombophlebitis-serious concern or much ado about little?, VASA.
2008 . 37 : 31–38 .
7. Van Weert H , Dolan G , Wichers I , de Vries C , ter Riet G , Buller H .
Spontaneous super cial venous thrombophlebitis:Does it increase
risk for thromboembolism?, J Fam Practice. 2006 . 55 : 52–57 .
8. uenet S , Laport S , Decousus H , Leizorovicz A , Epinat M ,
Mismetti P . Factors predictive of venous thrombotic complications
in patients with isolated super cial vein thrombosis, J Vasc Surg.
2003 . 38 : 944–949 .
9. Ascher E , Hanson JN , Salles-Cunha S , Hingorani A . Lesser saphenous vein thrombophlebitis:Its natural history and implications for
management , Vas Endovasc Surg. 2003 . 37 : 421–427 .
10. Gorski G , Norszczyk W , Kostewicz W , etal. Progress of local symptoms of super cial vein thrombosis vs. duplex ndings , VASA. 2004 .
33 : 219–225 .
11. Chengelis DL , Bendick PJ , Glover JL , Brown OW , Ranval TJ .
Progression of super cial venous thrombosis to deep vein thrombosis , J Vasc Surg. 1996 . 24 : 745–749 .
12. Decousus H , Epinat M , Duillot K , uenet S , Boissier C , Tardy B .
Super cial vein thrombosis:Risk factors, diagnosis, and treatment ,
Curr Opin Pulm Med. 2003 . 9 : 393–397 .
13. Guex JJ . rombotic complications of varicose veins:Aliterature
review of the role of super cial venous thrombosis , Dermatol Surg.
1996 . 22 : 378–382 .
14. Marchiori A , Mosena L , Prandoni P . Super cial vein thrombosis:Risk factors, diagnosis, and treatment , Semin romb Hemost.
2006 . 32 : 737–743 .
15. Coppin T , Lebrun E , Barroy JP . Rupture of infected super cial femoral
artery aneurysm:Acase report , Acta Chir Belg. 2002 . 102 : 276–278 .
16. Rodriguez-Peralto JL , Carrillo R , Rosales B , Rodriguez-Gil Y .
Super cial thrombophlebitis, Semin Cutan Med Surg. 2007 . 26 : 71–76 .
17. Fazeli B , Modagheh H , Ravra H , Kazemzadeh G . rombophlebitis:
Migrans as a footprint of Buerger’s disease: Aprotective-descriptive
study in north-east of Iran , Clin Rheumatol. 2008 . 27 : 55–57 .
18. Evanchuk DM , Von Gehr A , Zehnder JL . Super cial venous thrombosis associated with congenital absence of the inferior vena cava and
previous episode of deep venous thrombosis , Am J Hematol. 2008 .
83 : 250–252 .
19. Griger DT , Angel TE , Grisier DB . Penile Mondor’s disease in a
22-year-old man, J Am Osteopath Assoc. 2001 . 101 : 235 .
20. Nachmann MM , Ja e J S , G i n s b e r g P C , H o r r o w M M , H a r k a w a y
RC . Sickle cell episode manifesting as super cial thrombophlebitis
of the penis , J Am Osteopath Assoc. 2003 . 103 : 102 .
21. Boehlen F . Super cial thrombophlebitis of the chest wall associated
with anticardiolipin antibodies: Antiphospholipid syndrome or
Mondor’s disease?, Lupus. 2004 . 13 : 70–71 .
22. Holzheimer RG . Laparoscopic procedure as a risk factor of deep
venous thrombosis, super cial ascending thrombophlebitis, and
pulmonary embolism:Case report and review of the literature , Eur J
Med Res. 2004 . 9 : 417–422 .
23. Micco PD . Super cial vein thrombosis in malignancy:An underestimated problem , Exp Oncol. 2008 . 30 : 4–5 .
24. Wahrenbrock M , Borsig L , Le D , Varki N , Varki A . Selectin-mucin
interactions as a probable molecular explanation for the association
of Trousseau syndrome with mucinous adenocarcinomas , J Clin
Inest. 2003 . 112 : 853–862 .
25. Kupelian AS , Huda MSB . Pregnancy, thrombophlebitis, and thromboembolism: What every obstetrician should know , Arch Gynecol
Obstet. 2007 . 275 : 215–217 .
26. Du P . Mondor disease in pregnancy , Obstet Gynecol. 1981 .
58 : 117 .
27. McCall MD , Ramsey JE , Talt RC , et al. Super cial vein thrombosis: Incidence in association with pregnancy and prevalence of
thrombophilia defects , romb Haemost.
28. Samlaska CP , James WD . Super cial thrombophlebitis:I.Primary
hypercoagulable states , J Am Acad Dermatol. 1990 . 22 : 975–989 .
29. Pereira de Godoy JM , Fernades Goday M , Batigalia F , Braile DM .
e association of Mondor’s disease with protein S de ciency:Case
report and review of literature , J romb rombolys. 2002 .
13 : 187–189 .
30. Pereira de Godoy JM , Braile DM . Protein S de ciency in repetitive
super cial thrombophlebitis , Clin Appl romb-Hem. 203 . 9 : 61–62 .
31. Schonauer V , Kyrle PA , Weltermann A , etal. Super cial thrombophlebitis and risk for recurrent venous thromboembolism , J Vasc
Surg. 2003 . 37 : 834–838 .
32. Leon LR , Labropoulos N . Super cial vein thrombosis and hypercoagulable states: e evidence , Persp Vasc Surg Endovasc er. 2005 .
17 : 43–46 .
33. De Moerloose P , Wutschert R , Heinzmann M , Perneger T ,
Reber G , Bounameaux H . Super cial vein thrombosis of lower
limbs:In uence of factor V Leiden, factor II G20210A and overweight , romb Haemost. 1998 . 80 : 239–241 .
34. Martinell I , Cattaneo M , Tailoi E , de Stefano V , Chusolo P ,
Mannucci PM . Genetic risk factors for super cial vein thrombosis ,
romb Heamost. 1999 . 82 : 1215–1217 .
35. Terrier B , Piette AM , Kerob D , etal. Super cial venous thrombophlebitis as the initial manifestation of hypereosinophilic syndrome ,
Arch Dermatol. 2006 . 142 : 1606–1610 .
36. Raulin S , Raulin C , Greve B . Free- oating thrombus in the femoral
vein:Achallenge in phlebologic diagnostics , Eur J Dermatol. 2001 .
11 : 564–568 .
37. Lohr JM , McDevitt DT , Lutter KS , etal. Operative management of
greater saphenous thrombophlebitis involving the saphenofemoral
junction , Am J Surg. 1992 . 164 : 269–275 .
38. Kabnick LS , Ombrellino M , Agis H , etal. Endovenous heat induced
thrombus (EHIT) following endovenous vein obliteration:To treat or
not to treat? Anew perioperative thrombolic classi cation . Presented at
the 18th Annual Meeting of the American Venous Forum , Miami,
Florida , February 23, 2006 .
39. Villani C , Johnson DH , Cunha BA . Bilateral suppurative thrombophlebitis due to Staphylococcus aureus
24 : 342–344 .
40. Katz SC , Pachter L , Cuschman JG , etal. Super cial septic thrombophlebitis , J Trauma. 2005 . 59 : 750–753 .
41. Murray CK , Beckius ML, McAllister K . Fusarium proliferatum super cial suppurative thrombophlebitis , Mil Med. 2003 .
168 : 426–427 .
42. Jerkic Z , Karic A , Karic A . Clinically silent deep vein thrombosis in
patients with super cial thrombophlebitis and varicose veins at legs ,
Med Arh. 2009 . 63 : 284–287 .
43. Decousus H , uéré I , Presles E , et al. Super cial venous thrombosis and venous thromboembolism , Ann Intern Med. 2010 .
152 : 218–224 .
44. Gorty S , Patton-Adkins P , DaLanno M , Staar J , Dean S , Satiana B .
Super cial venous thrombosis of the lower extremities:Analysis of
risk factors, and recurrence and role of anticoagulation , Vasc Med.
2004 . 9 : 1–6 .
45. Milio G , Siragusa S , Minà C , et al. Super cial venous thrombosis: Prevalence of common genetic risk factors and their role on
spreading to deep veins , romb Res. 2008 . 123 :194–199 .
1998 . 79 : 741–742 .
, Heart Lung. 1995 .
426 • VENOUS THROMBOEMBOLISM
46. Zierler BK , Meissner MH , Cain K , Strandness DE . A survey of phy-
https://t.me/med1917
sicians’ knowledge and management of venous thromboembolism ,
Vas Endovasc Surg. 2002 . 36 : 367–375 .
47. Rohrbach N , Mouton WG , Naef M , Otten KT , Zehnder T , Wagner
HE . Morbidity in super cial thrombophlebitis and its potential surgical prevention , Swiss Surg. 2003 . 9 : 15–17 .
48. Murgia AP , Cisno GC , Manfredini R , Liboni A , Zamboni P .
Surgical management of ascending saphenous thrombophlebitis , Int
Angiol. 1999 . 18 : 343–347 .
49. De Maeseneer MGR . Super cial thrombophlebitis of the lower
limb:Practical recommendations for diagnosis and treatment , Acta
Chir Belg. 2005 . 105 : 145–147 .
50. Wichers IM , Di Nisio M , Miller HR , Middeldorp S . Treatment of
super cial vein thrombosis to prevent deep vein thrombosis and
pulmonary embolism: A systematic review , Haematolgica. 2005 .
90 : 672–677 .
51. Vesalio Investigators Group . High vs. low doses of low-molecularweight heparin for the treatment of super cial vein thrombosis of
the legs:Adouble-blind, randomized trail , J romb Haemost. 2005 .
3 : 1152–1157 .
52. Kearon C , Kahn SR , Agnelli G , Goldhaber S , Raskob GE , Comerota
AJ . Antithrombotic therapy for venous thromboembolic disease ,
Chest. 2008 . 133 : 454S–545S .
53. De Nisio M , Wishers IM , Middledorp S . Treatment for super cial
thrombophlebitis of the leg (review) . e Cochrane Library 2010 ; 6 .
54. Decousus H , Leizorovicz A . Super cial thrombophlebitis of the
legs:Still a lot to learn , J romb Haemost. 2005 . 3 : 1149–1151 .
55. Bounameaux H , Righini M , Gal GL . Super cial thrombophlebitis
of the legs:Still a lot to learn:Arebuttal , J romb Haemost. 2006 .
4 :289.
56. Hill SL , Hancock DH , Webb TL . rombophlebitis of the great
saphenous vein:Recommendations for treatment , Phlebology. 2008 .
23 : 35–39 .
57. Cesarone MR , Belcaro G , Corsi M , etal. Local heparin, super cial
vein thrombosis . Angiology. 2007 . 58 (Suppl 1): 36S–40S .
58. Katzenschlager R , Ugurlouglu A , Sipos G , et al. E cacy and tolerability of liposomal heparin spray-gel as an add-on treatment in
the management of super cial venous thrombosis , Angiology. 2007 .
58 ( Suppl 1 ): 27S–35S .
59. Cesarone MR , Belcaro G , Agus G , etal. Management of super cial
vein thrombosis and thrombophlebitis: Status and expert opinion
document , Angiology. 2007 . 59 ( Suppl 1 ): 7S–15S .
60. Kyrle PA , Eichinger S . e risk of recurrent venous thromboembolism: e Austrian study on recurrent venous thromboembolism ,
Wiener Klinische Wochenschri . 2003 . 115 : 471–474 .
61. Kalodiki E , Nicolaides N . Super cial thrombophlebitis and
low-molecular-weight heparins , Angiology. 2002 . 53 : 659–663 .
62. Decousus H . A pilot randomized double-blind comparison of a
low-molecular weight heparin, a non-steroidal anti-in ammatory
agent, and placebo in the treatment of super cial vein thrombosis ,
Arch Intern Med. 2003 . 163 : 1657–1663 .
63. Marchiori A , Verlato F , Sabbion P , etal. High versus low doses of
unfractionated heparin for the treatment of super cial thrombophlebitis of the leg:Aprospective, uncontrolled, randomized study,
Haemotolgica. 2002 . 87 : 523–527 .
64. De Sanctis MT , Cesarone MR , Incandela L , Belcaro G , Gri n M .
Treatment of super cial vein thrombosis with standardized application of Essaven Gel, Angiology. 2001 . 52 ( Suppl 3 ): S57–S62 .
65. De Maeseneer MG , rombosis Guidelines Group of the
Belgian Society and Haemostasis and Belgian Working Group on
Angiology. Super cial thrombophlebitis of the lower limb:Practical
recommendation for diagnosis and treatment , Acta Chir Belg. 2005 .
105 : 145–147 .
66. Lee JT , Kalani MA . Treating super cial venous thrombophlebitis , J
Natl Compr Canc Netw. 2008 . 6 : 760–765 .
67. Sullivan V , Denk PM , Sonnad SS , Eagleton MJ , Wake eld TW .
Ligation versus anticoagulation: Treatment of above-knee super cial thrombophlebitis not involving the deep venous system , J Am
Coll Surg. 2001 . 193 : 556–562.
68. Uncu H . A comparison of low-molecular-weight heparin and
combined therapy of low-molecular-weight heparin with an
anti-in ammatory agent in the treatment of super cial vein thrombosis , Phlebology. 2009 . 24 : 56–60 .
69. Beatty J , Fitridge R , Benveniste G , Greenstein D . Acute super cial
venous thrombophlebitis:Does emergency surgery have a role?, Int
Angiol. 2002 . 21 : 93–95 .
70. Goldman L , Ginsberg J . Super cial phlebitis and phase 3.5 trials , N
Engl J Med. 2010 . 363
: 1278–1280 .
SUPERFICIAL THROMBOPHLEBITIS • 427
Соседние файлы в папке Библиотека им академика М.И. Перельмана