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MICROSHUNT HISTOLOGY IN TELANGIECTASIAS
Bihari I, Magyar E.
Int J Angiol 1999; 8:98-101

COMMENTARY BY:
Marianne Vandendriessche, MD, FRCS (Belg)
Gent, Belgium

The authors studied 234 subjects. Group I (132) had telangiectasias only and Group II (102) had varicose veins. All subjects were studied with Doppler ultrasound. Group I was studied at the site of the telangiectasias. Group II was studied at similar, but unaffected, locations as in Group I.

Pulsatile sound was detected in 68.9% of Group I and in 8.8% of Group II. In 18 patients from Group I, biopsies were taken over the pulsatile-sound-positive spider veins. In 16 of the 18 biopsies, AV microshunts were demonstrated histologically. Also demonstrated was a feeding arteriole, a draining vein, and an arterialized venule. In the biopsies in Group II, no AV shunts were detected. The authors conclude that ulceration, a rare complication of injection compression treatment of venules, is due to fast injection of an excessive volume of sclerosant into the venule with backflow into the arteriole through the AV shunt.

COMMENTARY

Telangiectasias are more common in women (hormonal etiology ?) and often there is a request for treatment because of cosmetic reasons. Injection compression is still my treatment of choice over the laser. Doctors use different sclerosants with various results. Some authors have recently suggested that a perforator vein is present under most patches of venules and so they perform a duplex examination on every patient who presents with even minor venules. However, in this time of economic restrictions on healthcare, I think a duplex exam on every patient is unnecessary since it will have no influence on the treatment. A duplex exam should be performed of course if there is a suggestion of an unusual perforator vein (i.e., lateral thigh perforator) or an underlying more serious venous problem.

I disagree with the authors' statement that extravascular injection of diluted or concentrated polidocanol cannot cause ulceration. Ulceration can almost always be avoided by careful injection of small volumes of the appropriate sclerosant. The use of STD (even diluted to 0.2%) is more likely to cause ulceration than other sclerosants such as polidocanol. In my experience, Scleremo and 72% glycerine are safe and effective. However, Scleremo has the disadvantage of slight allergic risk due to its chromate content.

Extravascular injection must be avoided with all sclerosants. There is no evidence that the presence of AV shunts is a theoretical cause of ulceration when treating telangiectasias by injection compression. Arteriovenous malformations such as Klippel-Trenaunay syndrome are effectively treated by sclerotherapy when 3% sodium tetradecyl sulfate is injected into dilated veins without causing ulceration.

REDONE ENDOSCOPIC PERFORATOR SURGERY: FEASIBILITY AND FAILURE ANALYSIS
Kolvenbach R, Ramadam H, Schwierz E.
J Vasc Surg 1999; 30: 720-6

ABSTRACT AND COMMENTARY BY:
Peter Charlesworth, FRACS
Auckland, New Zealand

The stated purpose of this study was to evaluate the feasibility, efficacy, and safety of a second endoscopic perforator vein operation on patients who had previously been treated by subfascial endoscopic perforator surgery (SEPS).

A total of 24 consecutive patients to be considered for a repeat SEPS procedure were accrued over a 30-month period. Of these, the study group totalled 19 who agreed to proceed. All had healed or currently active ulcers (CEAP clinical classes 5 and 6). The original surgery had been performed at other hospitals so minimal information about the first operation was obtainable. It was known that the other institutions favored SEPS using a single-port approach without CO2 insufflation but there was no detail on the nature or number of perforators previously divided. From the findings at the second operation, the authors concluded that the deep posterior compartment had not been dissected previously in the majority of patients.

All patients were assessed preoperatively by duplex sonography and ascending phlebography. Descending phlebography was done only in selected cases. The duplex criterion for venous insufficiency was taken as a reflux time of 0.3 seconds, which is shorter than the 0.5 to 1.0 seconds considered significant by many researchers. The demographic data of the group were interesting. Only 2/19 had perforator reflux alone while 15/19 had superficial venous incompetence combined with perforator and/or deep reflux. One patient had isolated superficial reflux.

The repeat operation was performed using a double-port technique and CO2 insufflation without a tourniquet. The GSI Spacemaker balloon was utilized in 12 patients. The deep posterior compartment was opened and all perforators (competent and incompetent) were ligated. The mean number of perforators found was 3.4. Repeat endoscopy took 49 13 minutes which was at least half of the total operating time. In two cases, SEPS was converted to an open procedure due to bleeding and extensive scarring, respectively. Only two patients had SEPS alone. In the remainder, concurrent elimination of superficial reflux was necessary. This involved complete ligation of the saphenofemoral junction and groin tributaries (12), complete or partial stripping of the greater saphenous vein (exact number uncertain from the text but likely the majority of patients), and ligation of the lesser saphenous vein and tributaries (2). Four patients suffered minor complications including one temporary saphenous nerve neuralgia following stripping.

Clinical results of the repeat SEPS operation were classified as excellent (4), an improvement (11), and no change (4). In CEAP class 6 patients, the cumulative ulcer healing rate was 86% after a mean followup period of 9 6 months. One very longstanding ulcer was not healed but it was reduced in size. One CEAP class 5 patient suffered a recurrent ulcer 14 months following the redone SEPS procedure.

COMMENTARY

This paper raises a number of interesting issues, some of which are only indirectly inferred from the subject of the study. It is gratifying to learn that a repeat SEPS procedure is obviously practicable in the majority of cases with relatively minimal morbidity. However, it is clearly preferable that the first SEPS operation should achieve the desired result, thus making a second exploration unnecessary.

Although details of the first operation are unknown, from the number of perforators divided at the second operation (even if some were competent), it can be assumed that many incompetent perforators were initially missed. The authors imply that this was because only the superficial posterior compartment was explored in most cases, and division of an intermuscular septum and/or paratibial fasciotomy was not performed. This finding supports the contention of a number of authors that the deep posterior compartment should be dissected routinely during SEPS to avoid overlooking perforators, particularly of the Cockett II type.

Perhaps a more challenging question is whether the first (or second) SEPS procedure should have been performed at all. A striking observation is the number of patients in this study who required standard surgery for superficial venous reflux at the time of the second SEPS procedure. It is axiomatic that this was not adequately treated at the first operation. Therefore, it is interesting to speculate what the clinical outcome of this patient group might have been had superficial venous incompetence alone had been treated originally. The precise relevance of the perforator in this situation has been questioned in various careful studies1-3 leading to the conclusion that correct treatment of superficial venous reflux may be the key issue in the majority of patients. Much as SEPS is an elegant and satisfying operation to perform, there is a groundswell of opinion that it has been inappropriately overused in many published series to date.

There is a need for clinical trials on CEAP class 5 and 6 patients where significant superficial venous incompetence alone is adequately treated before SEPS is performed utilizing defined groups where respective perforator division and sparing can be properly compared. vdcha063

REFERENCES

1. Stacey MC, Burnand KG, Layer GT, Pattison M. Calf pump function in patients with healed venous ulcers is not improved by surgery to the communicating veins or by elastic stockings. Br J Surg 1988; 75:436-9.

2. Akesson H, Brudin L, Cwikiel W, Ohlin P, Plate G. Does the correction of insufficient superficial and perforating veins improve function in patients with deep venous insufficiency? Phlebology 1990; 5:113-23.

3. Campbell WA, West A. Duplex ultrasound audit of operative treatment of primary varicose veins. Phlebology 1995; 1(Suppl):407-9.

A COMPARATIVE STUDY OF STRUCTURES COMPRISING THE THORACIC OUTLET IN 250 HUMAN CADAVERS AND 72 SURGICAL CASES OF THORACIC OUTLET SYNDROME
Redenbach DM, Nelems B.
Eur J Cardiothor Sur 1998; 13:353-60

ABSTRACT AND COMMENTARY BY:
Fred A. Weaver, MD
USC Medical Center
Los Angeles, California

This comparative study provides an evaluation of the thoracic outlet in 250 human cadaver dissections compared to a thorough assessment of the thoracic outlet and anomalies in 72 surgical cases of neurogenic thoracic outlet syndrome. The authors focus on potential anatomic anomalies which may be causative for neurogenic thoracic outlet. They do not address issues referable to the vascular structures such as the subclavian artery and vein that can also be affected by thoracic outlet compression.

The cadaveric study involves 250 cadaver dissections in which both thoracic outlets were examined, including the incidence of anomalies such as cervical ribs, connective tissue bands, or anomalous slips of muscle. The cadavers were assumed to have no known symptoms of thoracic outlet syndrome and thus comprised the "control" group. No difference in incidence of anomalies was found between male and female cadavers. Anomalies were equally distributed between the right and left thoracic outlet and were primarily found anterior to the plexus.

In the surgical group, anomalies were much more frequent, being present in virtually every patient. A higher incidence of posterior anomalies were found in thoracic outlet patients when compared to cadaveric controls. Posterior anomalies were present in 51% of thoracic outlet patients and only 5% of cadaveric controls. As expected, cervical ribs or elongated C7 transverse processes were much more common in the thoracic outlet group. The authors also evaluated CT scan for assessment of cervical ribs or elongated C7 process and found it to be highly accurate.

COMMENTARY

This is an interesting first-stage study aimed at unraveling the clinical ambiguities in patients with thoracic outlet syndrome. The large cadaveric experience is informative and provides a baseline incidence of thoracic outlet anomalies. The importance of posterior anomalies as a causative factor in symptomatic patients is an important finding.

From a practical perspective, the diagnosis of thoracic outlet syndrome remains a clinical one. Hopefully, studies such as this one will provide objective data to guide clinical decisionmaking, specifically the timing of and indications for thoracic outlet decompression. vdwea103

EXTERNE RETRAKTIONS-TECHNIK (ERT) VERBESSERT DEN ENDOSKOPIERAUM BIE DER ENDOSKOPISCHEN SUBFASZIALEN DISZISION DER PERFORANSVENEN
(External Retraction Technique for Improvement of Visualization in the Subfascial Space During SEPS)
Duff CA, Fischer R, Linde N.
Phlebologie 1999; 28:132-34

ABSTRACT AND COMMENTARY BY:
Dr. med. Gerhard Sattler
Darmstadt, Germany

In this article, a surgical technique for creation of a subfascial space in endoscopic perforator vein surgery is described and evaluated on a prospective cohort group. In 64 of 67 endoscopies, a sufficient subfascial space could be achieved with the external retration technique using a specially designed atraumatic skin clamp (Figure 1). In three cases, insufficient results were achieved due to massive interstitial edema or failed exsanguination with the pneumatic tourniquet.

COMMENTARY

In cases where no CO2 insufflation is used, this is an excellent method of creating a subfascial space for the SEPS procedure. It is quick, easy to handle and is quickly adaptable to the individual needs of the surgeon. For sufficient exploration of the subfascial space, particularly in cases with tight skin, it is a great advantage to have a flexible method because this eliminates the need for CO2 gas insufflation. The clamp is reusable, making the method time efficient and cost effective. On the other hand, an assistant is needed to follow the diaphanoscopic light which shines through the skin of the lower calf. Although skin traumas due to chronic venous incompetence might be considered harmful, in our ten years of experience, we have had no skin infections attributed to the technique. vdsat103

VENOUS DIGEST ARTICLE LIST 1999

As the editors of the Venous Digest scan the world literature for articles which will be abstracted each month, the yearly contents become a complete summary of scientific information relating to venous disorders.

This is a listing of articles published in 1999.

COAGULATION
1. The prevalence of factor V Leiden mutation in patients with leg ulcers and venous insufficiency. Maessen-Visch MB, Hamulyak K, Tazelaar DJ et al. Arch Dermatol 1999; 135:41-44 (8/99).
2. Superficial vein thrombosis of the lower limbs: Influence of factor V Leiden, factor II G20210A, and overweight. de Moerloose P, Wutschert R, Heinsmann M et al. Thromb Haemost 1998; 80:239-41 (11/99).
3. APC resistance is a risk factors for postoperative thromboembolism in elective replacement of the hip or knee: A prospective study. Lindahl TL, Lundahl TH, Nilsson L et al. Thromb Haemost 1999; 81:18-21 (11/99).

CHRONIC VENOUS INSUFFICIENCY
1. Cutaneous inflammation limited to the region of the ulcer in chronic venous insufficiency. Hahn J, Jã«ger M, Friedrich B, et al. VASA 1997; 26:277-81 (2/99).
2. Compression therapy. Choucair M, Phillips TJ. Dermatol Surg 1998; 24:141-48 (2/99).
3. Pericapillary fibrin cuffs in venous disease: A reappraisal. Van de Scheur M, Falanga M. Dermatol Surg 1997; 23:955-59 (3/99).
4. A novel culturing and grafting system for the treatment of leg ulcers. Villeneuve P, Hafner J, Prenosil JB et al. Br J Dermatol 1998; 138:849-51 (3/99).
5. Management of venous ulcers. Coats U. Crit Care Nursing Q 1998; 21(2):14-23 (4/99).
6. Pinch grafting of leg ulcers in primary care. Oien RF, Hansen U, Hakansson A. Acta Derm Venereol (Stockh) 1998; 78:438-39 (4/99).
7. Horse-chestnut seed extract for chronic venous insufficiency. Pittler MH, Ernst E. Arch Dermatol 1998; 134:1356-60 (5/99).
8. The safety and efficacy of a proteolytic ointment in the treatment of chronic ulcers of the lower extremity. Falabella AF, Carson P, Eaglestein WH et al. J Am Acad Dermatol 1998; 39:737-40 (5/99).
9. EMLA cream as a topical anesthetic for the repeated mechanical debridement of venous leg ulcers: A double-blind, placebo-controlled study. Loc et al. J Am Acad Dermatol 1999; 40:208-13 (5/99).
10. Endoscopic perforator vein division with ablation of superficial reflux improves venous hemodynamics. Rhodes J, Gloviczki P, Canton L et al. J Vasc Surg 1998; 28:839-47 (6/99).
11. Classic versus endoscopic perforating vein surgery: A retrospective study. Lacroix H, Smeets A, Nevelsteen A, et al. Acta Chir Belg 1998; 98:71-75 (6/99).
12. Venous leg ulcers: Modern evaluation and management. Zimmet SE. Dermatol Surg 1999; 25:236-41.
13. Mid-term results of endoscopic perforator vein interruption for chronic venous insufficiency: Lessons learned from the North American Subfascial Endoscopic Perforator Surgery (NA-SEPS) Registry. Gloviczki P, Bergan JJ, Rhodes JM, et al. J Vasc Surg 1999; 29:489-502 (7/99).
14. A clinical and hemodynamic investigation into the role of calf perforating vein surgery in patients with venous ulceration and deep venous incompetence. Scriven JM, Bianchi V, Hartshorne T, et al. Eur J Vasc Endovasc Surg 1998; 16:148-52 (7/99).
15. Color duplex ultrasound in the assessment of primary venous leg ulceration. Yamaki T, Nozaki M, Sasaki K. Dermatol Surg 1998; 24:1124-28 (7/99).
16. Squamous cell carcinoma complicating chronic venous leg ulceration: A study of the histopathology, course, and survival in 25 patients. Baldursson BT, Hedblad M-A, Beitnar H et al. Br J Dermatol 1999; 140:1148-52 (8/99).
17. Chronic leg ulcers: The impact on venous disease. Bergqvist D, Lindholm C, Nelz? O. J Vasc Surg 1999; 29:752-55 (8/99).
18. Nonoperative management of venous leg ulcers: Evolving role of skin substitutes. Moneta GL, Falanga V. Vasc Surg 1999; 33:2 (8/99).
19. Prevalence and distribution of incompetent perforating veins in chronic venous insufficiency. Delis KT, Ibegbuna V, Nicolaides AN et al. J Vasc Surg 1998; 28:815-25 (8/99).
20. Power-based color-coded duplex sonography for evaluation of calf veins. Baumgartner I, Braunschweig M, Triller J et al. Int Angio 1998; 17:43-48 (9/99).
21. Frozen allogenic human epidermal cultured sheaths for the cure of complicated leg ulcers. Bolivar-Flores YJ, Kuri-Harcuch W. Dermatol Surg 1999; 25:610-17 (10/99).
22. Leg ulcers and hydroxyurea: 41 cases. Siriex M-E, Debure C, Baudot M et al. Arch Dermatol 1999; 135:818-20 (10/99).
23. Patients with chronic leg ulcers show diminished levels of vitamin A and E, carotenes, and zinc. Rojas AI, Phillips TJ. Dermatol Surg 1999; 25:601-04 (10/99).
24. Predictors of wound healing. Belo YM, Phillips TJ. J Clin Dermatol 1999; 2:39-43 (10/99).
25. Venous insufficiency four years after an episode of deep venous thrombosis: A clinical and plethysmographic investigation. Nordstr?m M, Lindblad B, Akesson H et al. Phlebology 1998; 13:53-58 (10/99).
26. Change in microcirculation in patients with atrophie blanche visualized by laser Doppler perfusion imaging and transcutaneous oxygen measurements. Maessen-Visch MB, Sommer A, De Paepe JA et al. Phlebology 1998; 13:45-49 (10/99).
27. The postthrombotic syndrome in relation to venous hemodynamics as measured by means of duplex scanning and strain-gauge plethysmography. Haenen JH, Janssen MCH, van Langen H et al. J Vasc Surg 1999; 29:1071-76 (11/99).
28. Quality assurance in phlebography of the extremities. Weber J. VASA 1999; 28:216-22 (12/99).
29. Endothelial activation in patients with chronic venous disease. Saharay M, Shields DA, Georgiannos SN et al. Eur J Vasc Endovasc Surg 1998; 15:342-49 (12/99).

LYMPHEDEMA
1. Effective treatment of lymphedema of the extremities. Ko SCK, Lerner R, Klose G et al. Arch Surg 1998; 133:452-58 (12/99).

TELANGIECTASIAS
1. Laser therapy of spider veins: Clinical evaluation of a new long-pulsed Alexandrite laser. McDaniel DH, Ash K, Lord J et al. Dermatol Surg 1999; 25:52-58 (4/99).
2. Sclerosis and the Nd:YAG Q-switched laser with multiple frequency for treatment of telangiectasias, reticular veins, and residual pigmentation. Cisneros JL, Del Rio R, Palou J. Dermatol Surg 1998; 24:1119-23 (4/99).
3. Sclerotherapy for leg telangiectasia: A blinded comparative trial of polidocanol and hypertonic saline. McCoy S, Evans A, Spurrier N. Dermatol Surg 1999; 25:381-86 (10/99).
4. Three years' experience with polidocanol foam in treatment of reticular varices and varicosities. Henriet JP. Phl?ologie 1999; 52:277-82 (12/99).

THROMBOEMBOLISM
1. Occult deep venous thrombosis complicating superficial thrombophlebitis. Blumenberg RM, Barton E, Gelfand ML et al. J Vasc Surg 1998; 27:338-43 (1/99).
2. Risk of diagnosis of cancer after primary deep venous thrombosis or pulmonary embolism. Sorensen HT, Mellemkjaer L, Steffensen FH et al. New Engl J Med 1998; 338:1221 (1/99).
3. Epidemiological study on the consequences of long distance air flights on the venous system of the lower limbs. Benigni JP, Sadoun S, Auvery JF et al. Presentation from European School of Phlebology (2/99).
4. Comparison of the phlebological repercussions of long distance air flights on the venous system of the lower limbs with and without compression stockings. Benigni JP, Sadoun S, Auvery JF et al. Presentation from European School of Phlebology (2/99).
5. The economy class syndrome: Literature review, preventive treatment, propositions in relation with risk factors. Benigni JP, Sadoun S, Auvery JF et al. Presentation from European School of Phlebology (2/99).
6. Prospective epidemiological study of the economy class syndrome: Clinical record form. Benigni JP, Sadoun S, Auvery JF et al. Presentation from European School of Phlebology (2/99).
7. Long-term results of vena cava filters: Experiences with the LGM and the titanium Greenfield devices. Wittenberg G, Kueppers V, Tschammier A, et al. Cardiovasc Int Radiol 1998; 21:225-29 (2/99).
8. Acute pulmonary embolism: Assessment for helical CT for diagnosis. Drucker EA, Rivitz SM, Shepard JO et al. Radiology 1998; 209:235-41.
9. The fibrinolytic effects of intermittent pneumatic compression: Mechanism of enhanced fibrinolysis. Comerota AJ, Chouohan V, Harrada RN, et al. Ann Surg 1997; 226:306-14 (5/99).
10. Venous hemodynamics during laparoscopic surgery: A cause for concern. Scott DJA, Wyld L, Paige J et al. Min Invas Ther & Allied Technol 1997; 5/6:484-86 (5/99).
11. Outpatient treatment of acute deep venous thrombosis. Mattiasson I, Berntorp E, Bornhov S et al. Int Angiol 1998; 17:146-50 (11/99).
12. Symptomatic deep venous thrombosis of the lower limb. Giannoukas AD, Fatouros M, Batsis H et al. Int Angiol 1998; 17:151-54 (11/99).

UPPER EXTREMITY VENOUS PROBLEMS
1. Subclavian vein thrombosis: Outcome analysis based on etiology and modality of treatment. Beygui RE, Olcott IV C, Dalman RL. Ann Vasc Surg 1997; 11:247-55 (1/99).
2. Venous gangrene of the upper extremity. Kaufman BR, Zoldos J, Bentz M et al. Ann Plast Surg 1998; 40:370-77 (11/99).

VARICOSE VEINS
1. Of what hemodynamic significance is reflux in the femoral and popliteal veins? Recek C, Hammerschlag A. Phlebologie 1998; 27:15-28 (1/99).
2. Plasma endothelin-1 release in normal and varicose saphenous veins. Mangiafico RA, Malatino LS, Santonocito M et al. Angiology 1997; 48(9):769-74 (2/99).
3. Clinical dynamics of varicose disease in patients with high degree of venous reflux during conservative treatment and after surgery: A 7-year followup. Lurie F, Makarova NP. Int J Angiol 1998; 7:234-37 (3/99).
4. Haemodynamic pathophysiology of venous insufficiency of the lower limbs. Franceschi C. Actualit? Vasculaires Int 1997; 47:17-27 (3/99).
5. A unifying concept of primary venous insufficiency. Bergan JJ. Dermatol Surg 1998; 24:425-28.
6. Evaluation of clinical efficacy of a venotonic drug: An adreal on hemisynthesis diosmine in patients with heavy legs syndrome. Carpentier PH, Mathieu M. J des Malaides Vasculaires (Paris) 1998; 23(2):106-12 (5/99).
7. Prevalence of venous reflux in the general population on duplex scanning: The Edinburgh vein study. Evans CJ, Allan PL, Lee AJ et al. J Vasc Surg 1998; 28:767-76 (7/99).
8. Clinicopathological evidence that neovascularization is a cause of recurrent varicose veins. Nyamekye I, Shephard NA, Davies B et al. Eur J Vasc Endovasc Surg 1998; 15:412-15 (9/99).
9. Pelvic congestion syndrome: Early clinical results after transcatheter ovarian vein embolization. Cordts PR, Eclavea A, Buckley PJ et al. J Vasc Surg 1998; 28:862-68 (9/99).
10. Recurrent varicose veins: Patterns of reflux and clinical severity. Jiang P, van Rij M, Christie R et al. Cardiovasc Surg 1999; 7(3):332-39 (10/99).
11. Estrogen and progesterone receptors in normal and varicose saphenous vein. Mashiah A, Berman V, Thole HH et al. Cardiovasc Surg 1999; 7(3):312-331 (10/99).
12. Venous insufficiency of the lower limbs and working conditions. Sobaszek A, Frimat P, Tiberguent A et al. Phlebology 1998; 13:133-41 (11/99).
13. Veins of the inguinal lymph nodes. Lemasle P, Uhl JF, Lefebre-Villardebo M et al. Phl?ologie 1999; 52:263-69 (12/99).
14. Guidelines of venous diagnosis by strain-gauge occlusion plethysmography. Gerlach H, Partsch H, Rabe E et al. Phlebology 1999; 28:68-69 (12/99).

VARICOSE VEINS, SCLEROTHERAPY
1. Long cotton wool rolls as compression enhancements in macrosclerotherapy for varicose veins. Tazelaar DJ, Neumann HAM, De Roos KP. Dermatol Surg 1999; 25:38-40 (5/99).
2. Complications of varicose sclerotherapy of the lower limb. Vin F. Phl?ologie 1999; 52:53-59 (7/99).

VARICOSE VEINS, SURGERY
1. A century of varicose vein surgery. van der Strict JP. Ann Chir 1997; 51(7):707-709 (1/99) .
2. High ligation and stripping of the long saphenous vein using tumescent technique for local anesthesia. Proebstle TM, Paepcke U, Weisel G et al. Dermatol Surg 1998; 24:149-53 (1/99) .
3. Stripping the long saphenous vein reduces the rate of recurrent varicose veins: Five-year results of a randomized trial. Dwerryhouse S, Davies B, Harradine K et al. J Vasc Surg 1999; 29:589-92 (7/99).
4. Inadvertent arterial injury during saphenous vein stripping. Ramsheyi A, Soury P, Saliou C et al. Arch 1998; 133:1120-23 (8/99).
5. Technical details on excision of the short saphenous vein. Creton D. Phl?ologie 1999; 52(2):169-74 (8/99).
6. Preoperative digital photoplethysmography predicts improvement in venous function after superficial venous surgery for chronically ulcerated limbs. Sullivan JG, Ghauri ASK, Whyman MR et al. Phlebology 1998; 13:142-47 (9/99).
7. Preoperative evaluation in primary varicose veins. Pfyffer M. Schweiz Med Wochenschrift 1998; 128:1772-80 (9/99).

VENOUS PATHOPHYSIOLOGY
1. Etiology and diagnosis of bilateral leg edema in primary care. Blankfield RP, Finkelhor RS, Alexander J et al. Am J Med 1998; 105:192-97 (8/99).
2. The effect of compression on venous hemodynamics assessed by quantitative photoplethysmography. Fronek A, Goldman M, Fronek K. Phlebology 1998; 13:98-101 (12/99).

VENA CAVA SURGERY
1. Radiologic versus surgical placement of vena cava filters: A comparative study of cost, time and complications. Bhatia RS, Collingwood P, Bartlett P. Can Assoc Radiol J 1998; 49:79-83 (6/99).
2. Five-year followup of prophylactic vena cava filters in high-risk trauma. Rogers FB, Strindberg G, Shackford SR et al. Arch Surg 1998; 133:406-11 (6/99).

VENOUS MALFORMATIONS
1. Klippel-Trenaunay syndrome: Spectrum and management. Jacob AG, Driscoll DJ, Shaughnessy WJ et al. Mayo Clin Proc 1998; 73:28-36 (2/99).

VENOUS RECONSTRUCTION
1. Axial transformation of the profunda femoris vein. Raju S, Fountain T, Neglen P et al. J Vasc Surg 1998; 27:651-59 (2/99).
2. Results of treatment of inferior vena cava syndrome with expandable metallic stents. Fletcher WS, Lakin PC, Pommier RF et al. Arch Surg 1998; 133:935-38 (6/99).
3. May-Thurner syndrome: Three patients treated with catheter-directed thrombolysis and stent placement. Henderson AM, McIntyre KE, Hunter GC et al. Vasc Surg 1998; 32(5):439-46 (6/99).
4. Angioscopic external valvuloplasty in the treatment of varicose veins. Satokawa H, Hoshino S, Igari T et al. Phlebology 1997; 12:136-41 (9/99).
5. Management of upper extremity central venous obstruction using interventional radiology. Kalman PG, Linsday TF, Clarke K et al. Ann Vasc Surg 1998; 12:202-206 (11/99).

NEUTROPHIL ACTIVATION AND MEDIATORS OF INFLAMMATION IN CHRONIC VENOUS INSUFFICIENCY
Coleridge Smith PD
J Vasc Res 1999; 36(suppl 1)24-36

ABSTRACT AND COMMENTARY BY:
Prof. dr. hab. med. Mieczyslaw Szotstek
Warszawa, Poland

This presentation summarizes many of the past and current theories of etiology of venous ulceration. The condition has been diagnosed since the time of Hippocrates but the cause of the condition is incompletely understood.

Many factors are involved in the development of venous ulceration. Venous hypertension has been implicated as part of the etiology of venous ulceration and recently an association has been shown between the factor V Leiden gene and venous ulceration. This is not surprising since that condition induces a prothrombotic state. Venous thrombosis is one cause of valvular incompetence. This leads to calf pump failure and failure of reduction of venous hypertension during exercise. More recently, white cell trapping has been introduced as a cause of venous ulceration. Moyses and others have found that white cells are being lost from the veins at ankle level when subjects are studied in the sitting position. Patients with venous insufficiency trap 30% of the white cells while controls trap only 5%. Bolinger has shown that capillaries in venous disorders are much more permeable than normal, and Franczek has described the appearance of capillary loops filled with red blood cells but which seem not to be perfused. Franczek and his coworkers have suggested that this may be due to capillary thrombosis. If that were true, this could result in a heterogenous perfusion and tissue hypoxia and ischemia as has been suggested by a number of other authors as the cause of venous ulceration.

The presence of a perivascular "fibrin cuff" which we know now exists with other components is a reflection of the inflammatory process and is seen in other chronic inflammatory conditions. The disordered state of endothelium in this condition allows passage of large molecules through the endothelium, permitting their perivascular accumulation which explains the presence of the fibrin cuff.

Vascular proliferation seen in the skin of patients with venous disease has been known for many years but in recent years, many angiogenic factors have been recognized which stimulate blood vessel growth. Histology has demonstrated no evidence of upregulation of transforming growth factor ?in the skin of patients with venous disease but, in contrast, there has been some increase in platelet-derived growth factor subtype BB in patients with venous disease. This has been found in the capillary wall in vessels of the dermal papillae. Considerable upregulation of the vascular endothelial growth factor in the epidermis of patients with venous disease has been seen and this is most marked in those with skin changes of hyperpigmentation and lipodermatosclerosis. This particular growth factor is also responsible for increased vascular permeability of large molecules which is a feature of skin microangiopathy. This has been reported from capillary microscopy studies.

Sahony found evidence of leukocyte activation and raised levels of endothelial adhesion molecules in these areas. The most likely explanation of his observations is that venous disease is associated with a systemic inflammatory response and a proinflammatory state of the endothelium. These workers have also observed an increase in endothelial and leukocyte inflammatory mediators in response to venous hypertension produced by the subject standing for a period of 30 minutes. This occurred both in patients with venous disease and in control subjects. This suggests that venous hypertension provides some form of endothelial challenge which is mediated, in part, by leukocytes. In persons free of venous disease, this type of challenge must be very infrequent since the calf muscle pump normally maintains a low pressure in leg veins. On the other hand, in patients with venous valvular incompetence, venous hypertension occurs more frequently and may result in skin damage. In some patients, such an insult can cause venous ulceration.

Patients who suffer more severe forms of venous disease are apparently particularly sensitive to venous hypertension. Either the inflammatory response produced by venous hypertension is greater or the protected mechanisms that normally prevent endothelial injury are inadequate.

COMMENTARY

Despite considerable investigative work which has been accomplished in the last 5000 years, neither the pathological mechanisms at work in venous ulceration nor the exact sequence of events which lead to leg ulcer have been established. This author emphasizes that the most effective nonsurgical treatment remains compression bandaging. This method has been used for centuries and is still accepted. Compression therapy can be augmented by pharmacologic treatment but compression is the cornerstone of therapy for treating venous ulcer.

Some surgical procedures such as correction of superficial reflux, perforator vein division, and venous valve reconstructions have been more widely accepted in the recent past. In cases of complete valvular incompetence, the only hope is venous valvular transplantation to reduce ambulatory venous hypertension.