EPIDEMIOLOGICAL STUDY ON THE CONSEQUENCES OF LONG DISTANCE AIR FLIGHTS ON THE VENOUS
SYSTEM OF THE LOWER LIMBS
COMPARISON OF THE PHLEBOLOGICAL REPERCUSSIONS OF LONG DISTANCE AIR FLIGHTS ON THE
VENOUS SYSTEM OF THE LOWER LIMBS WITH AND WITHOUT COMPRESSION STOCKINGS
THE ECONOMY CLASS SYNDROME: LITERATURE REVIEW, PREVENTIVE TREATMENT, PROPOSITIONS
IN RELATION WITH RISK FACTORS
PROSPECTIVE EPIDEMIOLOGICAL STUDY OF THE ECONOMY CLASS SYNDROME: CLINICAL RECORD FORM
Benigni JP, Sadoun S, Auvery JF, Banet M, Demagny A, Sica M, Saurin I.
European School of Phlebology, 6 Rue G Bruno, 75014 Paris, France
COMMENTARY BY:
Georges Jantet
Paris, France
Four presentations by the European School of Phlebology of Paris at the recent XIII
World Congress of the Union Internationale de PhlÈbologie in Sydney, Australia concerns
the "economy class syndrome," venous disturbances in the legs which may be associated with venous thrombosis and pulmonary embolism following long distance air flights.
The first case was described in 1946 by J. Homans but the "syndrome" was not given
its name until 1977 and there is little in the literature on the subject.
The authors describe their findings in 50 patients (40 women, 10 men) with previous
venous symptoms before and after a flight lasting more than four hours. Before and
after the flights, the patients were examined and completed a questionnaire containing
21 phlebological items and 20 analogue scales (0 to 10). The results showed a statistically
significant rise (3.6%) in leg volume with concomitant mild pain.
A series of 103 patients (83 women, 20 men) were randomly divided into two comparable
groups, one wearing compression stockings (ankle pressure 19.6 mmHg) during the flight
and the other not. The same 21 phlebological items were analyzed and showed a statistically significant difference between the two groups. The group without compression
stockings had a 3.7% rise in leg volume whereas the group wearing compression stockings
had a 4.1% decrease in leg volume with three times less pain.
The authors conclude that the wearing of compression stockings could be good prevention
against the economy class syndrome. They note that with 600 million passengers
traveling by air each year, with a prediction of 1.6 billion in the year 2020, this
syndrome could become a public health problem. They point out the responsibility of
the airlines in instituting preventive measures and improved seating.
The European School of Phlebology is setting up a worldwide study of the epidemiology
of this syndrome on the worldwide web. They have drawn up a Clinical Record Form
obtainable from them and returnable to them upon completion.
COMMENTARY
The economy class syndrome deserves the study which the European School of Phlebology
is undertaking. This syndrome can have serious consequences but is, to a large
extent, probably preventable which further justifies more study. Published figures
by the International Air Transport Association quoted by Le Monde on September 30, 1998
suggests an even larger rise in air passengers from 1.4 billion in 1997 to 1.5 billion
in 1998 to 2 billion in 2003. Yes, a proper epidemiological study is certainly
warranted. ivdfjan
KLIPPEL-TRENAUNAY SYNDROME: SPECTRUM AND MANAGEMENT
Jacob AG, Driscoll DJ, Shaughnessy WJ, Stanson AW, Clay RP, Gloviczki P.
Mayo Clin Proc 1998; 73:28-36
COMMENTARY BY:
Dr. Ermenegildo A. Enrici
Dr. Cristobal Papendieck
Argentine Catholic University
Buenos Aires, Argentina
This paper by Dr. Gloviczki and colleagues presents an exhaustive 40-year summary
of the Klippel-Trenaunay syndrome at the Mayo Clinic Rochester. The statistical
analysis of the 252 cases allows an accurate evaluation of the frequency of the
elements of the affliction - that is, capillary malformations, atypical varicosities, and limb
osteohypertrophy.
In this study group, there were 116 males (46%) and 136 females (54%). The age of
diagnosis ranged from birth to 83.4 years with a median of 11.9 years. Ninety-one
percent of the 252 individuals with the syndrome had evidence of this at birth.
Of these patients, 159 (63%) had all three features of the syndrome, 93 (37%) had two of the
three features, the capillary malformations were found in 246 patients (98%), varicosities
or venous malformations were found in 182 (72%) and limb hypertrophy was found in 170 (67%). The atypical lateral vein, or persistent sciatic vein, was found to
be present in 182 (72%). The authors point out the lack of family history in this
condition. However, in 74 patients (29%), concomitant congenital defects were found.
The most common of these was developmental dysplasia of the hip (10 patients), and syndactyly
(10 patients). One patient had a coexisting Sturge-Weber syndrome and another had
neurofibromatosis. Seventy percent of the patients (177) had involvement only in the lower extremity and 11% (28) had only upper extremity involvement. Additionally,
venous thromboembolism was present in a number of patients. Eleven (4%) had deep
venous thrombosis and 9 (4%) had pulmonary embolization, and this was fatal in one
patient.
In managing these patients, 54 (21%) had no treatment. The other patients had nonoperative
or surgical treatment or both. Nonoperative therapy consisted of elastic support
or heel lift as well as antibiotics for cellulitis and symptomatic support for those 11 patients who had rectal bleeding or hematuria. A total of 145 patients with
this syndrome had a surgical procedure done. In general, operations on varicose
veins or venous malformations decreased symptoms, but these recurred later. Attempted
excision of the angioma was done in 44 patients, epiphysiodesis was done in 41, with a
debulking procedure in 11. Some patients did poorly after surgical procedures.
The complications observed included massive lymphedema, nonhealing wound after debulking
done elsewhere, and limb swelling after removal of varicose veins in a patient with an
atretic superficial femoral vein.
COMMENTARY
While the cause of Klippel-Trenaunay syndrome remains obscure, we know that three
possibilities exist in its classification: 1) Klippel-Trenaunay-Servelle syndrome
where patients have lesions of the deep venous system (hypoplasias, fetal thrombosis,
fibrous constricting bands) without precapillary fistulae or macrofistulae. Limb lengthening
is dyscoordinate and there is persistence of embryonic veins that act as supplementary
circulating pathways. 2) Klippel-Trenaunay-Weber syndrome where the pathology is due to the existence of precapillary microfistulae which create deep venous
hypertension thus increasing pCO2 which is a stimulus for limb overgrowth, phlebectasias,
and varicose veins with passage of time. 3) Parkes-Weber syndrome which is due to
arteriovenous microfistulae. In the Mayo Clinic experience, there was a single proven
case that is not integrated to the statistical analysis. However, in another series
discussed in this paper, 13% of the patients experienced congestive heart failure.
This should suggest a Parkes-Weber syndrome rather than Klippel-Trenaunay syndrome.
A variety of diagnostic methods were used in this experience. Microfistulae were
not demonstrable either clinically or in contrast studies. The persistence of embryonic
veins (sciatic) was confirmed by this study. Other venous alterations such as varicose veins may be caused by reflux, or those that appear late may be caused by venous
hypertension.
Many diverse complications are discussed in this paper. We would include von Willebrand
disease among the hemorrhagic complications as it is stated in the experience that
this occurs in 20% of cases. As discussed, evaluation of treatment clearly indicates that medical therapy is the treatment of choice and that surgical intervention is
treatment of necessity. This is a fact with which there is general agreement.
To the wide range of operations listed in this paper, we would add venous banding
to compensate growth of the shortest limb in accordance with the chart of Moseley.
The growth of the femur, tibia, and possibly the radioulnar bone might be modified
with the method of Ilizarov. The longest limb overgrowth, of course, is treated with metaphyseal
staples.
The Candela laser and the PhotoDerm laser are used currently in the treatment of capillary
angiomas but require multiple interventions. ivfdenr
PLASMA ENDOTHELIN-1 RELEASE IN NORMAL AND VARICOSE SAPHENOUS VEINS
Mangiafico RA, Malatino LS, Santonocito M, Spada RS, Benedetto FA
Angiology 1997; 48(9):769-74
ABSTRACT AND COMMENTARY BY:
Prof. Dr. med. Drs. h.c.K. Messmer
M¸nchen, Germany
It is assumed by some that varicose veins develop as a consequence of hypoxic activation
and damage of endothelial cells which is induced by chronic venous stasis. Based
on recent findings in vascular biology, the authors tried to elucidate characteristic features of large varicose veins by measuring the release of endothelin-1 (ET-1)
when exposed to hydrostatic stress.
Ten patients with varicose greater saphenous veins were compared to ten age-matched
controls without overt venous pathology. The stress test consisted of venous occlusion
using the individual patient's pressure between systolic and diastolic values. Venous blood samples were obtained at baseline ten minutes after induction of venous stasis.
ET-1 in plasma was determined by radioimmunoassay. Hematocrit was determined
to exclude dilutional changes.
In blood from the saphenous vein, patients with varicose veins presented higher ET-1
values when compared to their own antecubital vein blood and blood from the saphenous
vein and antecubital vein of controls. ET-1 was released from the saphenous vein
in both the controls and patients, while ET-1 release was not observed in blood from
antecubital veins of either group. ET-1 release in varicose patients was significantly
higher than in controls.
COMMENTARY
The authors suggest that venous stasis and its enhancement by venous occlusion leads
to activation and damage of venous endothelial cells. As it is known that the production
of prostacyclin is reduced when more prostaglandin E2 is formed, the balance between dilating and constrictive forces becomes disturbed. Since venous occlusion induces
low flow and hence reduces wall shear stress, nitric oxide will be released from
endothelial cells and ET-1 effects become predominant. Unfortunately, nitric oxide
release was not quantified in these studies.
ET-1 not only stimulates vasoconstriction but also stimulates smooth muscle cell proliferation
as well. It potentiates the effect of local growth factors and thereby favors changes
in vessel wall morphology. The authors caution the use of grafts prepared from varicose saphenous veins for coronary artery bypass because these vessels might
be particularly prone to accelerated atherosclerosis. ivdfmes
CUTANEOUS INFLAMMATION LIMITED TO THE REGION OF THE ULCER IN CHRONIC VENOUS INSUFFICIENCY
Hahn J, J¸nger M, Friedrich B, Zuder D, Steins A, Hahn A, Klyscz T.
VASA 1997; 26:277-81
COMMENTARY BY:
Prof. Renate Koppensteiner
Z¸rich, Switzerland
The role of inflammation processes in the pathogenesis and persistence of venous
ulceration is still under debate. To study the presence and intensity of inflammatory
reactions in patients with stage 3 chronic venous insufficiency, skin specimens were
obtained from the border of the ulcer and from clinically unaffected skin of the same
leg (12 cm mean distance from the ulcer). Specimens of the perimalleolar skin of
ten healthy subjects served as controls. The distribution of ICAM-1 expression and
the density of various inflammatory cells (B and T lymphocytes, macrophages) were studied
by immunohistochemical and histological methods to quantify the inflammatory process.
At the border of the ulcer, a strong expression of ICAM-1 and a dense infiltration
of T-lymphocytes and macrophages was seen, representing a chronic inflammatory reaction.
In contrast, the results obtained in clinically unaffected skin did not differ from the findings in healthy controls. That is, ICAM-1 expression was not increased
and only a slight perivascular infiltration of T-lymphocytes was seen in some patients.
These data suggest that the chronic inflammatory reaction is limited to the ulcer,
representing an "injury and repair" process that might play a role in the persistence
and recurrence of venous ulceration.
COMMENTARY
The mechanisms leading to venous ulceration are still not clearly identified. According
to Coleridge Smith, venous hypertension reduces the capillary perfusion pressure
and hence the capillary flow rate.1 Low capillary flow rates have been shown to be associated with enhanced white
cell adherence leading to white cell activation that causes damage of the endothelium.2 Therefore, the upregulation of adhesion molecules, especially ICAM-1, plays an
essential role in the initiation of the inflammatory process. The results of this
study suggest that this process is not present in the clinically unaffected skin
in patients with chronic venous insufficiency and that the inflammatory reaction is only secondarily
induced. ivdfkop
REFERENCES
1. Coleridge Smith PD, Thomas PRS, Scurr JH, Dormandy JA. The etiology of venous
ulceration: A new hypothesis. Br Med J 1988; 296:1726-27.
2. Braide M, Blixt A, Bagge U. Leukocyte effects on the vascular resistance and glomeruli
of the isolated rat kidney at normal and low flow rates. Circ Shock 1986; 20:71-80.
Phlebolymphoedema: From Diagnosis to Therapy
A. Cavezzi, S Michelini (Preface by JR Casley-Smith)
Edizioni P.R. Bologna, Italy 1998
213 pages with bibliography
REVIEW BY:
John J. Bergan, MD
La Jolla, California
This attractive paperback volume has been prepared by angiologists with a special
interest in the swollen leg. In his preface, Professor Corradino Campisi describes
the authors' approach to phlebolymphoedema as being characterized by "...passion
and great skill."
For the American reader, this book is of particular value because its central elements
detail physical therapy in treatment of the swollen limb. After brief chapters on
the anatomy and physiology of the venous and lymphatic system, the pathophysiology
of phlebolymphoedema is described. This is followed by a chapter on the diagnostic
approach to lymphedema which emphasizes the use of duplex ultrasound and illustrates
CT diagnosis of the swollen limb, but, curiously omits mention of lymphoscintigraphy
in diagnosis. This has been quite popular in the United States.
Following these preliminaries, there are chapters on manual lymphatic drainage itself
and then its application to varicose vein surgery, plastic surgery, and sclerotherapy
as well as lymphedema. Of course, there is a section on compression therapy by elastic stockings and sleeves as well as sections on pneumatic compression and even
mercury pressure therapy. The brief chapter on surgical treatment of phlebolymphoedema
emphasizes venous surgery, mentions ultrasound-guided sclerotherapy, and diagrams
direct lymphovenous anastomoses. These latter procedures have been abandoned for the
most part. Curiously, no mention is made of subfascial endoscopic perforator vein
surgery for severe chronic venous insufficiency nor the application of liposuction
in debulking either the lymphedematous arm or the lymphedematous lower extremity.
The final portion of the book deals with physical rehabilitation treatment in venous
disease, lymphatic disease, and the post mastectomy arm. Completeness of the book's
coverage of phlebolymphoedema is exemplified by the chapters on nursing principles,
health and hygiene roles, and a description of recent developments in the field of phlebolymphoedema.
This last section distinguishes between primary prevention and secondary prevention
of lymphedema. The latter cites use of lymphoscintigraphy and sentinel lymph node biopsy as a method of diminishing post mastectomy lymphedema.
The final page of this interesting volume details the results of a national epidemiologic
study of lymphedema performed in Italy. This gives figures from February 1997 through
January 1998 in which 34 centers encountered 2743 patients with lymphedema. Of these, 777 were men and 1966 were women. There were 1009 cases of primary lymphedema,
only 21 of which were congenital. A further 286 were classified as lymphedema praecox
and the remaining 702, lymphedema tarda. Among the 1734 secondary lymphedemas, 880 were postoperative, 112 post radiation, 289 post trauma, and 331 post inflammatory.
All in all, this is an attractive, easily read volume which successfully introduces
the subject of phlebolymphoedema, providing a description of many of its aspects.
It is well illustrated and this reviewer is told that it will be available through
the MEDI Corporation in Bayreuth, Germany. It may also be obtained from the STD Pharmaceutical
Company in Hereford, England. That company's e-mail address is found at http://www.stdpharm.co.uk.
book-00499
LONG-TERM RESULTS OF VENA CAVA FILTERS: EXPERIENCES WITH THE LGM AND THE TITANIUM
GREENFIELD DEVICES
Wittenberg G, Kueppers V, Tschammler A, et al.
Cardiovasc Int Radiol 1998 21:225-29
ABSTRACT AND COMMENTARY BY:
Prof. dr. hab. med. Mieczyslaw Szotstek
Warszawa, Poland
Vena cava filter application is the method of choice to prevent current pulmonary
embolism in patients with deep venous thrombosis. Either temporary (LGM) or permanent
(Greenfield) devices may be used. The authors present 104 patients where vena cava
filters were introduced (87 LGM and 17 titanium Greenfield). The main indications for
filter insertion were recurrent pulmonary embolism where the patient was adequately
anticoagulated (54), pulmonary embolism in patients where anticoagulation was contraindicated (28), pulmonary embolism and heart failure (16), and other reasons (6). Patients
were examined one day, one week, one month, three months, six months, and one year
post filter placement and annually thereafter.
Early complications following vena cava placement included incomplete opening (9),
tilted filter greater than 15 degrees (12), misplaced filter (3), and access-site
thrombosis (9). Long-term complications included migration (10), apposition thrombus
(4), vena cava thrombosis (17), and pulmonary embolism (3). One patient died a few hours
following vena cava filter placement as a result of pulmonary embolism.
Long-term results were summarized in 89 patients (14 were lost to followup). The
longest followup period was 81 months; the mean observation time was 36 months.
During followup, 21 patients died. In three cases, autopsy excluded the filter as
the cause of death. In nine cases, the death certificate noted no relationship to filter placement.
The cause of death could not be elucidated in the remaining patients.
COMMENTARY
Prevention of pulmonary embolism by percutaneous vena cava filter placement is the
method of choice for patients with deep venous thrombosis in whom anticoagulation
is contraindicated or in whom pulmonary embolism occurs despite sufficient anticoagulation. Percutaneous insertion of devices designed to provide effective filtration of thromboemboli
in the vena cava offers a number of potential advantages for the patient as well
as decreased cost with use of the radiology suite instead of the operating room.
The usual route of access is the femoral vein but the jugular vein can also be used.
This avoids femoral vein trauma and subsequent postphlebitic sequelae. Because
of the serious complications, it is recommended that a permanent vena cava filter
be inserted only after strict confirmation of the indications.
The ideal filter is the one with a low complication rate where a high clot-trapping
efficiency does not exist. During the last couple of years, the temporary vena cava
filter has become very popular with placement of a temporary filter in patients
with a very high risk of thrombosis and pulmonary embolism. Such patients include those
with polytrauma, pregnancy, and perioperative state. Results and efficacy in these
patients have yet to be evaluated.
At this time, we recommend that because of the possible complications, a permanent
vena cava filter should be inserted only after strict proof of the need for the placement
has been obtained. Filter selection and insertion require experience in modern angiographic techniques with collaboration between clinicians caring for patients and
the interventional radiologists or surgeons inserting the device. ivdfszo
Suggested Reading
1. Ritchie AJ, Mitchell, L, Forty J. Migration of a vena cava filter to the pulmonary
artery. Br J Surg 1995; 82:207.
2. Becker DM, Philbrick JT, Selby JB. Inferior vena cava filters: Indications, safety,
effectiveness. Arch Intern Med 1992; 152:1985-94.
COMPRESSION THERAPY
Choucair M, Phillips TJ
Dermatol Surg 1998; 24:141-48
ABSTRACT AND COMMENTARY BY:
Prof. MichaÎl F–ldi
Fachklinik f¸r Lymphologie
R–þlehofweg, Germany
It is recognized that compression therapy is fundamental in the care of venous insufficiency
in its severe chronic forms. This is also true of chronic lymphedema. The objective
of compression is to reverse underlying pathology and restore functioning pumping mechanisms in the extremity. The objective of this article was to review the
pathophysiology of severe chronic venous insufficiency and to enumerate the different
types of compression devices which are available. It is understood that the choice
of compression should be individualized and tailored to the needs of each patient.
Trained nurses and skilled physicians are necessary to provide the appropriate prescriptions.
COMMENTARY
The authors are quite right in stressing the fact that compression therapy is, and
has to be, the standard care for venous insufficiency ulcers. In addition, they
recommend home compression pumps for lymphedema patients who have not responded
to other compression modalities (bandages and stockings) in "recalcitrant cases." In this respect,
I have to stress that the adequate treatment of lymphedema is complex decongestive
physiotherapy. This is a tetrad which consists of skin care, manual lymph drainage, compression, and remedial exercises.
In the first phase of complex decongestive physiotherapy, bandages are used for compression
and, in the second phase, premeasured elastic hosiery are used. However, I feel that
one should not employ elastic stockings in lymphedema or in venous edema to remove edema fluid. This has always to be done by means of bandages. Elastic stockings/hosiery
are not for edema evacuation but instead for maintenance of an edema-free state.
I believe that if complex decongestive physiotherapy is applied in an adequate manner, there are no recalcitrant cases unless lymph vessels and nodes are blocked
by malignancy.
I think that employing pumps in the treatment of lymphedema of the lower extremity
is dangerous. In an excellent paper written by Partsch1 et al., one reads that lymph kinetics improve in cases where isotopic lymphography
has shown an intact or decreased lymph transport. However, in severe indurated cases
where no lymph transport was present, the pump had no effect whatsoever on lymph
kinetics. The treatment decreased the albumin content of the tissues. However, an increase
of the tissue albumin concentration occurred because of water reduction. An increase
of the albumin concentration induces increased fibrosclerotic alterations. Moreover, they observed an increase of swelling in the area of the root of the limb.
Every experienced physician who treats lymphedema of the lower extremities is aware
that the pump sometimes causes genital lymphedema. Boris2 et al. analyzed 128 consecutive patients with lower limb lymphedema. They separated
the patients for analysis on the basis of those who did or did not use pump therapy.
Of the 128 patients with lower limb lymphedema, 75 were not treated by pump and
53 patients were. Of the 53 who used pumps, 23 (43%) developed genital lymphedema. This
difference was statistically highly significant (p < 0.0001). I stress that in contrast
to lymphedema of the extremities, lymphedema of the genitalia cannot be treated
with the same success by complex decongestive physiotherapy. Development of a genital
lymphedema is a tragedy.
In 1987 at the 2nd International Symposium of the Swiss Society of Phlebology in Z¸rich,
St–berl reported her studies concerning the mechanism of compression treatment.
It is well known in severe cases, permeability of plasma proteins is increased.
This increase can be diminished by compression in a statistically significant manner.
In the postthrombotic syndrome, lymph flow is decreased in the subfascial lymphatics
and may be increased in the suprafascial lymphatics. St–berl reported that under
compression the decreased deep lymph transport increased and, if a pathologically increased
lymph flow in the suprafascial compartment was present, this decreased.
The authors are quite right in saying that an important effect of compression in
chronic venous insufficiency is restoration of the calf pump function.
Today, the most authors do not agree with the idea of pericapillary fibrin cuffs acting
as a barrier to the diffusion of oxygen. Although pericapillary fibrin cuffs exist,
there appears to be no evidence that they provide a barrier to oxygen. Small molecules can be expected to diffuse through these cuffs.3,4 ivdffol
REFERENCES
1. Partsch H, Mostbeck A, Leitner G. Experimentelle untersuchungen zur wirkung einer
druckwellenmassage (Lymphapress) beim lymphoedema. Phlebol u Proktol 1980; 9:124-28.
2. Boris M, Weindorf S, Lasinski BB. The risk of genital lymphedema after external
pump compression for lower limb lymphedema. Lymphology 1998; 31:15-20.
3. Scurr JH, Coleridge Smith PD. The microcirculation in venous disease. Angiology
1994; 45:537-42.
4. Leu HJ. Morphology of chronic venous insufficiency: Light and electron microscopic
examinations. VASA 1991; 20:330-42.
AXIAL TRANSFORMATION OF THE PROFUNDA FEMORIS VEIN
Raju S, Fountain T, Neglen P, Devidas M
J Vasc Surg 1998; 27:651-59
ABSTRACT AND COMMENTARY BY:
Gy–rgy Acsady, M.D.
Budapest, Hungary
The case records and phlebograms of 500 consecutive patients with venous stasis were
analyzed by Raju et al. A profunda-popliteal connector was identified in 57 cases
(11.4%). Based on the morphologic findings, the authors divided this collateral
system into four grades. The process was called axial transformation of the profunda femoris
vein. They found that the profunda femoris vein dilates considerably in grades
3 and 4, compensating for the lack of function of the stenotic or occluded superficial
femoral vein. The profunda-popliteal connector was present in 55% of grades 1 and
2, 36% of grade 3, and 9% of grade 4. Clear postthrombotic changes were identified
in the superficial femoral vein in 96%.
Cases were characterized according to the CEAP classification as follows:
- Clinical Features: Class 3 = 8%, class 4 = 4%, class 5 = 18%, class 6 = 70%.
- Etiology: Primary 4%, secondary 96%.
- Anatomic Distribution: Superficial 0%, deep 100%
- Pathophysiology: Reflux 69%, reflux with obstruction 31%
Patient conditions were classified as fully or partially compensated (obstructive
grades 1 and 2) or decompensated (obstructive grades 3 and 4). Detailed laboratory
assessment included ambulatory venous pressure measurement, air plethysmography,
and quantitative duplex examination in the recumbent and erect positions. Ascending and
descending phlebograms were obtained. Reflux in the profunda femoris vein was detected
with duplex scanning in 56%, with descending venography in 86%, and with a strip
test at operation in 91%.
Surgical treatment was considered only when conservative therapy failed or if complications
developed (recurrent cellulitis, infection, recurrent phlebitis). The primary indications
for surgery included stasis ulceration (88%), stasis dermatitis (4%), and pain (8%). In 44 of the 57 patients, an antireflux procedure was performed
on the profunda femoris vein (valve reconstruction 43, ligation 1). Valve reconstruction
in the patent superficial femoral vein was performed in 17 patients. All patients received intraoperative and long-term postoperative anticoagulation.
During followup, a full laboratory assessment, including duplex scanning, was done
three to six months after the operation and at one- to two-year intervals thereafter.
Clinical outcomes were considered good to excellent with the primary indication
resolved in 90% of patients at one year. For patients with ulceration, complete and sustained
healing without recurrence was required for these categories. No difference in outcome
was discerned on the basis of axial transformation grade or type of valve reconstruction used in the profunda femoris or superficial femoral vein.
COMMENTARY
The profunda-popliteal connector provides excellent outflow function. A valve in
the proximal profunda femoris vein normally is present in approximately 84% of patients.
This would become incompetent following axial transformation of the profunda femoris vein. Once this vein has been reconstructed to abolish reflux, the surgical approach
to the recannalized postthrombotic superficial vein is a matter of debate. Valve
repair in the profunda femoris vein in this setting appears durable. ivdfacs