VD604R

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

ABSTRACT AND COMMENTARY BY:
David Green, MD
Bethesda, Maryland

This paper includes the results of four related studies or "phases" and reports the outcome of treatment of telangiectasias and ectatic veins (up to 0.3 mm) of the lower extremity with a 755 nm laser (PhotoGenica, Cynosure, Inc., Bedford, MA). Phases I and II included 28 participants who received single, double, or triple pulses with fluences of 15 to 30 J/sq cm, a pulse duration of 6 ms, and a circular beam 10 mm in diameter. A total of up to three treatments were administered at four-week intervals.

Phase I included all participants without regard to vessel size in order to determine the optimal overall parameters. They found that using a fluence of 20 J/sq cm, double-pulsed with a pulse duration of 5 ms, yielded as high as 42% improvement after three treatments. Phase II segregated the Phase I participants into three groups based on vessel width: less than 0.4 mm, 0.4 to 1 mm, and 1 to 3 mm, yielding improvement rates of 23%, 48%, and 32%, respectively. Phase III reported the outcome of vessels treated by a combination of laser therapy and sclerotherapy with a 23.4% saline solution 3 to 28 days later.

There were 22 sites in 12 participants with each site treated with one of the five laser protocols used in Phases I and II. The success rate for all vessel diameters ranged between 80 and 87% after only one treatment. Phase IV reported on the histopathologic changes observed in biopsy specimens of vessels treated by laser.

COMMENTARY

The authors are to be commended for objective reporting of their results. Their limited success rate, as acknowledged in the paper, is partly attributable to constraints of the laser system at the time of their study. The maximum pulse width of their system was 5 ms and a cutaneous cooling system was not available. After their study commenced, an upgraded version provided for pulse widths of up to 20 ms with a contact cooling device became available. These upgrades increased the efficacy and safety of the system. The authors recommended that all telangiectatic vessels of the lower extremity be treated with cutaneous cooling.

Regarding their Phase II results, the authors found a greater rate of success for vessels 0.4 to 1.0 mm than for those less than 0.4 mm in diameter. Grouping of small vessels into arbitrary categories can explain these seemingly anomalous results. Within the category of telangiectasias less than 0.4 mm in diameter, capillary telangiectasias (ectatic capillaries less than 0.2 mm) were not distinguished from venous telangiectasias (ectatic veins 0.2 to 2.0 mm). Capillary telangiectasias of the lower extremity are especially refractory to any form of ablative therapy, compared to veins. Any group including capillary telangiectasias would be expected to have low success rates. The authors would likely have had very different findings if they grouped capillary telangiectasias in a separate category.

In their Phase II study, the addition of sclerotherapy resulted in an overall 80% rate of improvement when administered three to seven days after laser treatment. However, there was no sclerotherapy control group and it is likely that this combined improvement rate would be similar to success rates with sclerotherapy alone. In fact, the success rates in the combination group could probably be attributed completely to sclerotherapy. The fact that sclerotherapy could be performed 3 to 28 days after laser indicates that laser did not successfully damage the telangiectasias. When laser treatment has irreversibly denatured all the mural layers of a telangiectasia, it will not be possible to perform sclerotherapy. This is because the denatured telangiectasia will not have the intraluminal patency of an undisturbed vessel (either due to obliteration of the intraluminal space or due to the presence of an intraluminal thrombus, either of which would preclude the infusion of a sclerosant). If a telangiectasia has been subjected to laser but remains patent at three days or longer, it did not respond to treatment. Certainly by 14 to 28 days, a successfully treated telangiectasia will have been partially or completely resorbed.

Sclerotherapy will likely remain the touchstone for treating most venous telangiectasias. Laser is a viable modality for removing capillary telangiectasias and some venous telangiectasias but, as this and other studies have demonstrated, it is less reproducible than sclerotherapy and usually requires multiple treatments to the same vessel. Although adverse side effects may be observed from sclerotherapy, exposure to laser light is associated with unwanted cutaneous changes which is usually more frequent than that due to sclerotherapy. Furthermore, laser is consistently more uncomfortable than carefully performed sclerotherapy with any appropriately diluted sclerosant, except for the hyperosmotic agents. vdgre067

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

ABSTRACT AND COMMENTARY BY:
David Green, MD
Bethesda, Maryland

This paper involves treatment of lower extremity telangiectatic vessels in size from 0.1 to 1.0 mm with a combination of sclerotherapy and a Q-switched Nd:YAG laser. All patients were initially treated by sclerotherapy using 0.5% polidocanol. Seven to ten days later, the previously treated and likely thrombosed, vessels were subjected to laser light. A Q-switched Nd:YAG laser was used in both the normal and frequency-doubled modes, permitting wavelengths of 1064 nm and 532 nm, respectively. In addition, colorants were used to alter the laser light output, generating wavelengths of 585 nm and 650 nm, both in Q-switched modes.

A total of 54 patients were treated (42 women, 12 men). There was no significant difference in response to treatment based on gender. The investigators reported improvement in all cases, with excellent results in 90% after up to three sessions. In only 10% did portions of treated vessels persist. In the 30% of those who developed pigmentation following sclerotherapy, the investigators successfully treated it with the 532 nm or the 650 nm Q-switched laser light. They reported that the treated sites remained free of ectatic vessels with no persistent residual lesions.

COMMENTARY

The authors stated that the basis for conducting this study was to reduce the adverse effects commonly encountered with sclerotherapy. Their methodology involved using a "minimum concentration" of sclerosant combined with a Nd:YAG laser. However, the "minimum concentration" of 0.5% polidocanol is not considered a low concentration when treating such small-caliber vessels (0.1 to 1.0 mm) as were included in this study.

While it is true that commercial polidocanol is available in concentrations from 0.5% to 5.0%, much lower concentrations can be made by diluting these stock solutions with 0.9% saline for a concentration as low as 0.1%. When treating telangiectasias as small as in this study, concentrations of 0.1% to 0.2% are more appropriate than 0.5%.

If the authors used the "minimum concentration" of 0.5% polidocanol in their combined approach to preclude adverse effects, what higher concentration did they routinely use without concomitant laser treatment? It is not surprising that unacceptably high adverse effects would be observed using solutions of polidocanol greater than 0.5% when treating vessels 0.1 to 1.0 mm in diameter. Sclerotherapy using 0.1% to 0.2% polidocanol without any additional treatment would have likely produced fewer adverse effects than these investigators observed using higher concentrations of polidocanol alone or the "minimum" 0.5% concentration in their combined approach.

In this study, seven to ten days following sclerotherapy, the injected veins were subjected to Q-switched laser light. The investigators do not provide any scientific basis or rationale for combining sclerotherapy and photothermal treatment with laser. There is no evidence that these procedures performed sequentially are synergistic, complementary, or even safe. In fact, the combined treatment is likely contraindicated when performed at such short intervals.

This can be understood when considering the pathophysiologic changes resulting from these two destructive treatment modalities. The mechanism of action of sclerotherapy is mural necrosis of the vein mediated by chemical denaturation of mural constituents. The goal of sclerotherapy is full mural necrosis. Incomplete mural injury is associated with a reconstitution and persistence of a vein. There should be no need for multiple treatments or adjuvant therapy. If a vein is not resorbed, then complete mural denaturation at the time of treatment was not accomplished. Subsequently sclerotherapy should proceed with a higher concentration and/or a greater volume of sclerosant.

Whether or not full mural denaturation has been achieved, once the intraluminal channel has been subjected to a sclerosant, intimal injury will expose subendothelial collagen which activates the coagulation cascade. Any intravascular blood will coagulate. The absorption characteristics of coagulated, denatured blood are not the same as that of non-coagulated whole blood. Therefore, subjecting a thrombosed vein to laser light in wavelengths appropriate for non-denatured hemoglobin and blood may be inappropriate. If laser initially treats ectatic vessels appropriately (i.e., clinical endpoint of treatment was achieved), then sclerotherapy shortly thereafter is contraindicated.

The mechanism of action of laser treatment is a photothermal response by intravascular hemoglobin when it interacts with the light. The heat generated within the blood is conducted to the surrounding mural layers with the hope that they sustain irreparable thermal denaturation. In the process, intravascular blood undergoes thermal coagulation. The two endpoints of thermal coagulation of vascular lesions are intravascular coagulation or the apparent disappearance of the vessel. Neither circumstance is conducive to the infusion of a solution into the intraluminal channel. Injection into a thrombosed vein when compared to an unobstructed intraluminal channel is likely to be associated with vessel rupture and extravasation of sclerosant.

Assuming that the combination of sclerotherapy and photothermal treatment was appropriate, the pulse duration of the Q-switched Nd:YAG used in this study would be inappropriate. The pulse duration of Q-switched lasers (measured in nanoseconds) is too short for the targeted vascular structures. Long pulse durations are required to ablate most vascular ectases. Lasers that safely and reproducibly obliterate vascular ectases have pulse durations measured in milliseconds. Q-switched lasers are more appropriately used to target minute particles such as tattoo pigment in the dermis.

Although the results on improvement of vascular lesions and dermal pigmentation (a sequel to sclerotherapy) reported in this paper are impressive, the clinical photographs do not support the findings and should clearly convince the reader as to the lack of selectivity of their light treatment. The purpose of lasers is to effect selective photothermal destruction of the targeted chromophore and structure without inflicting damage to any other chromophores or structures. Therefore, the overlying structures and the epidermis should not sustain any photothermal damage when dermal vessels or pigment depositions are targeted.

The clinical photographs in this paper reveal epidermal (and possibly dermal) devitalization (Figs. 4, 5, 6, 8, 10). Four months after treatment, Figure 11 clearly shows pigmentation alteration (and possibly textural changes) paralleling the footprint of the Q-switched laser. The legend for Figure 11 states that "the minimal residual lesions that are visible in some areas will disappear in a few weeks and there will be no remaining signs of the treatment." Although such an optimistic outcome is predicted, the authors did not present photodocumentation of such an outcome.

It has been my experience that cutaneous changes resulting from epidermal and dermal devitalization associated with non-selective photothermal injury may persist for months or years and may indeed be permanent. vdgre071

MANAGEMENT OF VENOUS ULCERS
Ursula Coats, MSN, RN, CETN
Crit Care Nurs Q 1998; 21(2):14-23

ABSTRACT AND COMMENTARY BY:
Vicki Fahey, RN, MSN, CVN
Chicago, Illinois

Readers of the Venous Digest know that 80 to 90% of lower extremity ulcers are venous in nature. These wounds represent billions of dollars in health care costs as well as significant psychosocial impact on patients and their families. Although the majority of venous ulcers are treated on an outpatient basis, occasionally admission to an intensive care unit is necessary because of comorbid conditions such as congestive heart failure, obesity, hypertension, and diabetes mellitus. These coexisting conditions need to be addressed and managed because they impact the underlying disease and compromise wound healing.

This article by a nurse clinician addresses the prevention and management of venous ulcers in a comprehensive, research-based manner. Successful management of venous ulcers includes a combination of optimal local wound care, compression therapy, and elevation. With a comprehensive approach, ulcers can be healed and prevented, allowing patients to maintain an active, productive life. This presentation underscores the role of the nurse as a part of the treatment team.

COMMENTARY

Venous disease presents a multifaceted challenge to the nurse who is often confronted with the disease in a wound care or outpatient clinic. A thorough understanding of the pathophysiology, medical management, and nursing intervention is key to successful outcome in the care of venous ulceration. In addition, there is an opportunity for nurses to make a favorable impact on the financial and psychological state of the patient. The nurse may also take an active role in deep venous thrombosis prophylaxis which may reduce the number of venous ulcers in the future.

Success in healing a venous ulcer can be achieved only if the patient is an active participant in the care plan, educated about the disease, and willing to make the necessary adjustments in lifestyle to help minimize disease complications. Nurses play a key role in the education of patients while treating the venous ulcer.

Good management of venous ulceration is dependent upon prompt recognition, accurate diagnosis, appropriate care, treatment of the underlying cause, and patient education. A team approach should include the nurse clinician. vdfah071

PINCH GRAFTING OF LEG ULCERS IN PRIMARY CARE
Oien RF, Hansen U, H”kansson A.
Acta Derm Venereol (Stockh) 1998; 78: 438-39

ABSTRACT AND COMMENTARY BY:
Jeffrey L. Ballard, MD, FACS
Associate Professor of Surgery
Loma Linda University Medical Center
Division of Vascular Surgery
Loma Linda, California

This Swedish study evaluated the pinch graft technique for coverage of chronic leg ulcers of all etiologies. A total of 84 pinch grafts in 45 patients with 55 ulcers were analyzed. A "probable" diagnosis was established for all patients with Doppler results apparently used for some patients. Etiologies of the ulcers included venous, venous and arterial, neuropathic, vasculitic, and arterial.

The technique of pinch grafting was briefly described. Postoperatively, patients were sedentary for a few days but not immobilized. After one week, the grafted wound was treated with dressings designed to avoid dryness. The overall ulcer healing rate was 40% after 12 weeks and 44% after 24 weeks. Specifically, healing occurred in 18 of 31 venous ulcers, 3 of 4 combined ulcers, 5 of 9 neuropathic ulcers, 1 of 7 vasculitic ulcers, and 1 of 4 arterial ulcers.

COMMENTARY

This study confirms the fact that poor results are to be expected if there is complete disregard for the pathogenesis of the problem. The authors suggest using pinch grafts to cover ulcers of all etiologies without a single definitive preoperative study delineating the cause of the ulcer. There is no mention of whether arteriograms were considered or whether venous imaging for reflux was obtained prior to operative intervention.

Although the article suggests the use of pinch grafts, the authors make reference to the Apligraft in the bibliography. I suspect that as articles such as this one appear, more and more clinicians will be eager to place the Apligraft on ulcers with the usual nonchalance as to the actual cause of the ulceration. If these authors had accurately uncovered the pathologic processes causing the ulceration and offered direct treatment such as arterial bypass or subfascial endoscopic perforator vein ligation in conjunction with greater saphenous vein stripping, then potentially more of the ulcers would have healed. It is likely that some would have never needed added coverage.

This is a poorly studied patient cohort with even poorer results. Thus, the study speaks for itself. In my opinion, skin grafting following an appropriate procedure designed to halt the pathologic process makes more sense and would seem to be more cost effective.

VENOUS DIGEST ARTICLE LIST 1998

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 1998.

COAGULATION
1. Activated protein C resistance and anticardiolipin antibodies in patients with venous leg ulcers. Grossman D, Heald PW, Wang Chao, et al. J Am Acad Dermatol 1997; 37:409-13. (1/98)
2. Familial thrombophilia: Genetic risk factors and management. Makris M, Rosendaal FR, Preston FE. J Intern Med 1997; 242(suppl 740): 9-15. (6/98)

DEEP VENOUS THROMBOSIS
1. Popliteal venous aneurysm leading to massive pulmonary embolus in a child: A case report and literature review. Carlin RE, McGraw DJ, Xenos ES, Villavicencio JL. Vasc Surg 1997; 31:463-68. (4/98)
2. Superficial thrombophlebitis and deep vein thrombosis: A controversial association. Bounameaux H, Reber-Wasem MA. Arch Intern Med 1997; 157-1822-24. (5/98)
3. Lower limb deep venous thrombosis and meteorological factors. Esquenet P, Boudet J, Sevestre-Pietri M, Ganry O, Pietri J. J Malad Vasc (Paris) 1997; 22:244-48. (6/98)
4. Thrombosis of the proximal greater saphenous vein: Ultrasonographic diagnosis and clinical significance. Sover ER, Brammer HM, Rowedder AM. J Ultrasound Med 1997; 16:113-16. (6/98)
5. Effect of immobilization of patients during treatment of thromboembolic disorders with low-molecular-weight-heparin. Partsch H, Kechavarz B, Kohn H, Mostbeck A. Int Angiol 1997; 16:189-92. (6/98)
6. Saphenous vein thrombophlebitis (SVT): A deceptively benign disease. Hanson JN, Ascher E, DePippo P, et al. J Vasc Surg 1998; 27:677-80. (10/98)
7. Prevention of deep venous thrombosis associated with superficial thrombophlebitis of the leg by early saphenous vein ligation. Krause U, Kock HJ, Kr–ger K, Albrecht K, Rudofsky G. VASA 1998; 27:34-38. (10/98)
8. Guidelines on diagnosis and treatment of superficial thrombophlebitis. Blattler W, Bulling B, Hertel T, Rabe E. Phlebologie 1998; 27:58-9. (10/98)
9. Lower extremity venous thrombosis and cancer: Evaluation of risk factors in a medical environment. Giauffret F, Pottier P, Pistorius MA, Planchon B. J des Malaides Vasculaires 1997; 22(4)234-38. (10/98)
10. Surgical treatment of phlebitis. Shamiyeh F. Phlebology 1997; 26:157-60. (3/98)

DIAGNOSIS, REFLUX
1. Role of color-coded duplex ultrasonography in a vascular surgical/phlebological practice. Kr¸nes U, Holzapfel R, Knipp H. PhlÈbologie 1998; 27:1-6. (7/98)
2. Anatomical patterns in varicose vein disease: A duplex scanning study. Guex JJ, Hiltbrand B, Bayon JM, et al. Phlebology 1995; 10:94-97. (7/98)
3. Pre- and postoperative contribution of duplex scan in superficial venous surgery of the popliteal fossa (French). Gillet JL, Perrin M, Hiltbrand B, et al. J Mal Vasculaires 1997; 22(5):330-335. (9/98)
4. Duplex assessment of venous reflux and chronic venous insufficiency: The significance of deep venous reflux. Welch HJ, Young CM, Semegran AB, et al. J Vasc Surg 1996; 24:755-62. (10/98)
5. Duplex ultrasound exploration for diagnosis and evaluation of chronic venous diseases. Myers KA. Arteres et Veins 1997 16(5):190-201. (10/98)
6. Duplex Doppler classification of postoperative recurrent varicose veins in internal saphenous territory. Vin F, Chleir F. Presse Med 1998; 27:148-52. (10/98)
7. The role of air plethysmography in the diagnosis of chronic venous insufficiency. Criado E, Farber MA, Marston WA et al. J Vasc Surg 1998; 27:660-70. (12/98)
8. Foot venous pressure measurement for evaluation of lower limb venous insufficiency. Fukuoka M, Okada M, Sugimoto T. J Vasc Surg 1998; 27:671-76. (12/98)
9. Correlation of the anatomical distribution of venous reflux with clinical symptoms and venous hemodynamics in primary varicose veins. Sakurai T, Gupta PC, Matsushita M, Nishikimi N, Nimura Y. Br J Surg 1998; 85:213-16. (12/98)

SEVERE CHRONIC VENOUS INSUFFICIENCY
1. Activated protein C resistance and anticardiolipin antibodies in patients with venous leg ulcers. Grossman D, Heald PW, Wang Chao, et al. J Am Acad Dermatol 1997; 37:409-13. (1/98)
2. The notion and substrate of fascial sclerosis in chronic venous insufficiency. Staubesand J, Li Y. PhlÈbologie 1997; 26:72-79. (1/98)
3. Increased arterial inflow in extremities with chronic venous insufficiency: An important and unappreciated hemodynamic parameter. Skladany M, Schanzer H. Surgery 1996; 120:30-33. (1/98)
4. The microcirculatory effects of intermittent sequential compression in chronic venous hypertension. Belcaro GV, Nicolaides AN. Int Angiol 1996; 15:37-41. (1/98)
5. The home use of external pneumatic compression for the management of chronic venous insufficiency. Arcelus JI, Caprini JA. Int Angiol 1996; 15:32-36. (2/98)
6. The use of endoscopic technology for interruption of the communicating veins of the leg in Chronic venous insufficiency. Chernyshev VN, Krygin SG. Angiol & Vasc Surg 1997; 2:94-104. (4/98)
7. Leg ulceration with associated thrombocytosis: Healing of ulceration associated with treatment of the raised platelet count. Wirth K, Schoetse E, Mertelsmann R, Lindemann A. Br J Dermatol 1998; 138:533-35. (7/98)
8. Popliteal vein reflux reduces the healing of chronic venous ulcer. Brittenden J, Bradbury AW, Allan PL, et al. Br J Surg 1998; 85:60-62. (7/98)
9. Safety, feasibility, and early efficacy of subfascial endoscopic perforator surgery: A preliminary report from the North American Registry. Gloviczki P, Bergan JJ, Menawat SS, et al. J Vasc Surg 1997; 25:94-105. (8/98)
10. Efficacy of subfascial endoscopy in eradicating perforating veins of the lower leg and its relation with venous ulcer healing. Pierik EGJM, van Urk H, Wittens CHA. J Vasc Surg 1997; 26:255-59. (8/98)
11. Surgical reconstruction for deep venous insufficiency. Iafrati M, O'Donnell TF. J des Mal Vasculaires 1997; 22(3):193-97. (8/98)
12. Anatomic investigation of the deep posterior compartment of the leg. Cheney PA, Melaragno PG, Prayson MJ, Bennett GL, Njus GO. Foot & Ankle Int'l 1998; 19:98-101. (8/98)
13. Surgery of the perforating veins of the leg: Open and endoscopic techniques (French). Juhan C, Alimi Y, DiMauro P. J des Mal Vasculaires 1997; 22(5):348-51. (9/98)
14. Guidelines on diagnosis and treatment of venous ulcer. Schwahn-Schreiber C. Phlebologie 1998; 27:58-9. (10/98)
15. Light reflection rheography and clinical course of patients with advanced venous disease before and after endoscopic subfascial division of perforating veins. Proebstle TM, Weisel G, Paepcke U, Gass S, Weber L. Dermatol Surg 1998; 24:771-76. (11/98)
16. Long-term prognosis for patients with chronic leg ulcers: A prospective cohort study. NelzÈn O, Bergqvist D, Lindhagen A. Eur J Vasc Endovasc Surg 1997; 13:500-08. (12/98)
17. Intraoperative duplex scan evaluation for the assessment of perforator vein ligation surgery. Ragno I, Wengerter KR, Coyle AD, et al. J Vasc Technology 1998; 22(2):65-68. (12/98)
18. Characteristics of chronic venous insufficiency in 895 patients followed in general practice. Boccalon H, Janbon C, Shaumet J, Tafani A, et al. Int Angiol 1997; 16:226-34. (12/98)
19. Initial rate of healing predicts complete healing of venous ulcers. Tallman P, Muscare E, Carson P, et al. Arch Dermatol 1997; 133:1231-34. (12/98)

UPPER EXTREMITY VENOUS PROBLEMS
1. "Above-under" exposure of the first rib: A modified approach for the treatment of thoracic outlet syndrome. Robicsek F, Eastman D. Ann Vasc Surg 1997; 11:304-6. (4/98)
2. Surgical treatment of thoracic outlet syndrome compression syndromes: Diagnostic considerations and transaxillary first rib resection. Thompson RW, Petrinec D. Ann Vasc Surg 1997; 11:315-23. (4/98)

VARICOSE VEINS
1. Comparison of saphenous vein removed for primary venous insufficiency with cadaver saphenous vein. Ortega F, Mompeo B, Sarmiento L, et al. Vasc Surg 1997; 31:633-70. (3/98)
2. The prevalence of venous disease in primary lymphedema. Chaudhry HL, Mortimer PS, Evans JE, Dormandy JA. Phlebology 1997; 12:31-35. (7/98)

VARICOSE VEINS, SCLEROTHERAPY
1. Sclerosant treatment of saphenous trunks and their large-caliber collaterals by the MUS method. Monfreux A. PhlÈbologie 1997; 50:351-53. (1/98)
2. One year of daily use of sclerotherapy (reticular veins and telangiectasias) using polidocanol foam: Feasibility, results and complications. Henreit JP. PhlÈbologie 1997; 50:355-60. (1/98)
3. International inquiry on the practice of sclerotherapy. Baccaglini U, Stemmer R, Partsch H. PhlÈbologie 1997; 26:129-42. (1/98)
4. Aethoxysklerol (polidocanol) and FDA approval. Informational material. (5/98)
5. Progressive ascending telangiectasias treated with the 585 nm flashlamp-pumped pulsed-dye laser. Perez B, Nunez M, Bolxeda P, et al. Lasers in Surg & Med 1997; 21:413-16. (5/98)
6. Treatment of essential telangiectasias with an intense pulsed-light source (PhotoDerm VL). Raulin C, Weiss RA, Schonermark MP. Dermatol Surg 1997; 23:941-46. (5/98)
7. Optimizing a varicose vein service to reduce recurrence. Turton EPL, Berridge DC, McKenzie S, et al. Ann R Coll Surg Engl 1997; 79:451-54. (5/98)
8. Does a varicose saphenous vein exist? Zamboni P, Cappelli M, Marcellino MG, et al. Phlebology 1997; 12:74-77. (5/98)
9. A survey of current attitudes of British and Irish vascular surgeons to venous sclerotherapy. Galland RB, Magee TR, Lewis MH. Eur J Endovasc Surg 1998; 16:43-46. (11/98)

VARICOSE VEINS, SURGERY
1. Complications of ambulatory phlebectomy. Ramelet A-A. Dermatol Surg 1997; 23:947-54. (2/98)
2. Psychological tolerance to local block anesthesia for saphenous vein surgery: Study of 160 consecutive cases. Ouvry PAG, Perrott P, Amarouche A, Ouvry P. Vasc Surg 1997; 31:751-55. (2/98)
3. Complications of varicose vein surgery. Critchley G, Handa A, Maw A, et al. Ann R Coll Surg Engl 1997; 79:105-10. (2/98)
4. Duplex scanning for recurrent varicose veins. Englund R. Aust NZ J Surg 1996; 66:618-20. (3/98)
5. Reparative surgery of valves in the treatment of superficial venous insufficiency: External banding valvuloplasty versus high ligation or disconnection. A prospective multicenter trial. Corcos L, De Anna D, Zamboni P, et al. J des Mal Vasc 1997; 22:128-36. (4/98)
6. Muller's ambulatory phlebectomy for varicose veins of the foot. DeRoos KP, Neumann HAM. Dermatol Surg 1998; 24:465-70. (7/98)
7. Tumescent anesthesia in ambulatory phlebectomy. Smith SR, Goldman MP. Dermatol Surg 1998; 24:453-56. (7/98)
8. Recurrence of varicosities following surgery in the popliteal fossa: Anatomical data to ultrasonography and surgery. Rettori R. J Des Mal Vasculaires 1998; 23(1):54-60. (7/98)
9. Combined high ligation and stab avulsion for varicose veins in an outpatient setting. Sadick NS, Schanzer H. Dermatol Surg 1998; 24:475-79. (9/98)
10. Ambulatory phlebectomy: Principles & evolution of the method. Ricci S. Dermatol Surg 1998; 24:459-64. (9/98)
11. High ligation and stripping of the long saphenous vein using tumescent technique for local anesthesia. Proebstle TM, Paepcke U, Weisel G, Gass S, Weber L. Dermatol Surg 1998; 24:149-53. (9/98)
12. Prevention of saphenofemoral and saphenopopliteal recurrence of varicose veins by forming a partition to contain neovascularization: How I do it. Glass GM. Phlebology 1998; 13:3-9. (11/98)
13. Preliminary results of PTFE patch saphenoplasty to prevent neovascularization leading to recurrent varicose veins. Earnshaw JJ, Davies B, Harradine K, Heather BP. Phlebology 1998; 13:10-13. (11/98)
14. Saphenous vein-sparing surgery: Principles, techniques, and results. Zamboni P, Marcellino MG, Cappelli M, et al. J Cardiovasc Surg 1998; 39:151-62. (11/98)

VENA CAVA SURGERY
1. Endovascular treatment of chronic superior vena cava syndrome associated with hemodialysis access. Laronga C, Ciocca R, Warner S, Nosher J, Graham AM. Vasc Surg 1998; 32(2):207-213. (6/98)
2. Guidelines on operative treatment of venous disease. Schimmelpfenning L. Phlebologie 1998; 27:58-9. (10/98)

VENOUS PATHOPHYSIOLOGY
1. Perfused human saphenous vein for the study of the origin of varicose veins: Role of the endothelium and of hypoxia. Michiels C, Arnould Th, Thibaut-Vercruyssen R, et al. Int Angio 1997; 16:135-41. (1/98)
2. Hemodynamic assessment of femoropopliteal venous reflux in patients with primary varicose veins. Sakurai T, Matsushita M, Nishikimi N, Nimura Y. J Vasc Surg 1997; 26:260-64. (3/98)
3. Change of diameter in the greater saphenous vein during the hormonal cycle in young women. Drazkiewicz T, Ziaja K, Simka M, Urbanek T. Phlebologie 1997; 26:155-56. (6/98)
4. Monocyte infiltration into venous valves. Ono T, Bergan JJ, Schmid-Sch–nbein GW. J Vasc Surg 1998; 27:158-66. (8/98)
5. Primary varicose disease: Pathophysiological aspects and their implications in surgical therapy. Horstmann R, Hillejan L, Holzgreve A, Hohlbach G. PhlÈbologie 1995; 24:132-38. (9/98)
6. A unifying concept of primary venous insufficiency. Bergan JJ. Dermatol Surg 1998; 24:425-28. (11/98)

VENOUS INSUFFICIENCY - THERAPY
1. Pressure differences of elastic compression stockings at the ankle region. Veraart JCJM, Pronk G, Neumann HAM. Dermatol Surg 1997; 23:935-39. (3/98)
2. Effect of lightweight compression stockings on venous hemodynamics. Ibegbune V, Delis K, Nicolaides AN. Int Angiol 1997; 16:185-88. (6/98)
3. Limitation of movement in the ankle and talocalcaneonavicular joints caused by compression bandages. Lentner A, Spath F, Wienert V. Phlebology 1997; 12:25-30. (6/98)
4. Rapid healing of venous ulcers and lack of clinical rejection with an allogenic-cultured human skin equivalent. Falanga V, Margolis D, Alvarez O, Auletta M, et al. Arch Dermatol 1998; 134:293-300. (8/98)
5. Treatment of pelvic venous spur (May-Thurner syndrome) with self-expanding metallic endoprostheses. Binkert CA, Schoch E, Stuckmann G, et al. Cardiovasc Interv Radiol 1998; 21:22-26. (11/98)

TRAUMA
1. Outcome of complex venous reconstructions in patients with trauma. Pappas PJ, Haser PB, Teehan EP, et al. J Vasc Surg 1997; 25:398-404. (4/98)
2. Long-term results of common/external iliac vein reconstruction using internal jugular vein: A case report. Bergamini TM, Henke PK, Wilson MA, Bock RW. Vasc Surg 1997; 31:483-87. (4/98)