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152 Chapter 15/Complications and Adverse Sequelae of Sclerotherapy
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shock fi ve minutes after injection with 1 ml despite maximal intervention. In 1994, Kreussler reported two patients with urticaria. In 1995, two additional patients were reported with urticaria, two with bronchospasm, and one with angioedema. In 1996, there were four reports of urticaria, two of anaphy­lactoid reactions, one with angioedema, one with pruritus, and one with contact allergy. Therefore POL is not free from allergy and like all sclerosing solutions, physicians must be prepared to evaluate and treat patients who have an allergic reaction to the sclerosing solution.
A detailed account of three serious cases of anaphylaxis was reported from the Netherlands.55 These patients were anaphylactic within 15 minutes after injection of POL. Two of them received the drug for the fi rst time. One patient, a 70-year-old woman with a complicated medical history of two heart operations, two cerebrovascular accidents, and hyperthyroidism, was successfully resuscitated after cardiac arrest. She was receiving multiple medications, including digoxin, carbimazole, captopril, furosemide, mebeverine, and acenocoumarol. She was treated without complications four previous times with POL. The second patient showed signs of ARDS after being treated with epinephrine and systemic methylprednisolone for shock. The third patient developed urticaria, dyspnea, paresthesia, headache, and chest pain with electrocardiographic (ECG) fi ndings of cardiac ischemia. No further studies were performed on these patients.
The Australian Polidocanol Open Clinical Trial at two years, with over 8000 treated patients, reported nine local urticarial reactions and three generalized reactions, with two patients developing a rash, for a frequency of approximately
30
0.2%. There were no cases of anaphylaxis.
After an addi­tional 8804 patients were evaluated, an additional three patients developed urticaria again without any additional signifi cant adverse sequelae.56 A fi ve-year experience in 500 patients treated with POL 3% reported fi ve cases of allergic reaction (1% incidence); one patient had nonfatal anaphylactic shock, with the other patients experiencing urticaria.
57
Two of 689 sequential patients were reported who devel­oped an immediate-type hypersensitivity reaction with sys­temic pruritus and urticaria.58 This represented an incidence of 0.3% in their patient population and 0.91% for the “true” population. These two reactions occurred without prior exposure to POL as a sclerosing agent. Since POL is used as an emulsifying agent in preprocessed foods, patients may have been exposed previously through ingestion. Both patients responded easily to either a single dose of oral diphenhydramine, 50 mg, or 0.3 ml of subcutaneous epi­nephrine plus 50 mg diphenhydramine IM.
One specifi c case report describes a 30-year-old woman who underwent four separate sclerotherapy sessions with POL. On the fourth session, 3 ml of POL 1.5% and 12 mls of POL 0.5% were administered. The patient complained of
chest heaviness and constriction, which also appeared after two of her other sessions but was not brought to the attention of the medical staff. During the fourth episode she lost con­sciousness and was found without a pulse or blood pressure with dilated pupils. Spontaneous respiration occurred after two to three minutes, she began to vomit and complained of headache and earache. She recovered and was discharged after 10 hours well but returned the next day with dysosmia, which lasted six weeks. Although a brain CT scan was normal the presumed cause was cerebral.
59
The LD50 in rabbits at two hours is 0.2 g/kg, which is three to six times greater than the LD50 for procaine hydrochlo­ride. The LD50 in mice is 110 mg/kg. The systemic toxicity level is similar to that of lidocaine and procaine.
60
Chromated Glycerin
CG 72% (Scleremo) is a sclerosing solution with a very low incidence of side effects (Scleremo product information [1987]). Hypersensitivity is a very rare complication.61 Contact sensitivity to chromium occurs in approximately 5% of the population.62 IV potassium dichromate leads to complete desensitization in chromium-sensitized guinea pigs. This effect occurs because chromium needs to bind to skin proteins to become an effective antigen. This may be related to the necessity for epidermal Langerhans’ cells to produce an allergic response, whereas T lymphocyte acces­sory cooperation is not optimal with IV injection and its resulting endothelial necrosis. Thus it is more common for a sclerotherapist to develop an allergic contact dermatitis to CG than it is for a patient to have an allergic reaction to IV use of CG. Indeed, Ouvry (personal communication, 1995) has developed an allergic contact dermatitis from CG injected without the use of protective gloves.
Ramalet63 has reported seven patients who developed an allergic reaction to CG. One patient had a vasculitis, and six patients had an eczematous reaction. All allergic patients demonstrated a sensitivity to topically applied chrome.
Hematuria accompanied by urethral colic has been reported to occur transiently after injection of large doses of CG. Ocular manifestations, including blurred vision and a partial visual fi eld loss, have been reported by a single author, with resolution in less than two hours. any sclerotherapy)-induced hemolysis may not be a benign event. Hemoglobin can exert direct cytotoxic, infl ammatory, and pro-oxidant effects that adversely effect endothelial function.65 Hemoglobin from destroyed red blood cells dimerizes and is rapidly bound by the serum protein hapto­globin. The haptoglobin-hemoglobin complex causes endo­cytosis and degradation, which can lead to a variety of adverse effects.
66
An additional case was reported of transient hypertension and visual disturbance after the injection of 12 ml of 50% CG into spider and “feeder” leg veins in a fourth treatment
64
Glycerin (or
References 153
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session.67 These symptoms occurred two and a half hours after treatment and lasted more than three hours without treatment. This may have represented a retinal spasm or an ophthalmic migraine.
Although transient hemoglobinuria is common in athletes and without known long-term adverse effects, hemoglobu­linemia can cause renal failure.68 More commonly, hemo­globulinemia can cause a dose-related gastrointestinal dystonia and pain including esophageal spasm and dyspha­gia. Refer to an excellent recent review that details more clinical manifestations of hemoglobinemia.
69
Since we have been using glycerin alone without chro­mium but mixed 2 : 1 with 1% lidocaine with or without 1 : 100,000 epinephrine we have yet to see an allergic reac­tion. We have also yet to see hemoglobinuria or adverse effects with the use of up to 12 ml of this glycerin mixture except for a minute or two of epinephrine-induced “rush” that can occur in rare patients who have a sensitivity to epinephrine.
Polyiodide Iodine
Polyiodide iodine (Varigloban; Sclerodine 6) is a stabilized water solution of iodide ions, sodium iodine, and benzyl alcohol. Sigg et al.
70,71
reported on their experience with over 400,000 injections with Variglobin reported an incidence of 0.13 allergic cutaneous reactions per 1000. No systemic allergic reactions were observed. Obvious contra­indications to the use of Variglobin are hyperthyroidism and allergies to iodine and benzyl alcohol.
Sodium Salicylate
Saliject (Omega Laboratories, Montreal) has not been reported in a literature review to cause allergic reactions. Dr. Beverly Kemsley has reported 1 of 6000 patients who devel­oped an anaphylactic reaction after the use of Saliject. Thirty patients developed localized erythema and urticaria that responded to the oral antihistamine terfenadine 120 mg (per­sonal communication, 1996).
Hypertonic Saline
Alone, hypertonic saline (HS) solution shows no evi­dence of allergenicity or toxicity. Complications that may arise from its specifi c use include hypertension that may be exacerbated in predisposed patients when an excessive sodium load is given, sudden hypernatremia, central nervous system disorders, extensive hemolysis, and cortical necrosis of the kidneys (Mary Helenek, written correspondence, American Regent Laboratories, Inc., May 1990). These complications among others have led one manufacturer
TABLE 15.1 Summary of Complications of Sclerosing
Agents
Allergic Solution Pigmentation reaction Necrosis Pain
Sodium morrhuate ++ ++ +++* +++ Sodium tetradecyl ++ + ++* + sulfate Ethanolamine oleate + ++ ++* ++ Polidocanol + + +* 0 Hypertonic saline + 0 +++* +++ Sclerodex (+0% + 0 + ++ saline 5% dextrose) Chromated glycerin 0 + 0 ++ Glycerin 0 0 0 + Polyiodinated iodine ++ + +++* +++
+, Minimal; ++, moderate; +++, signifi cant. *Concentration dependent.
(American Regent Laboratories) to add to its label the warning “For IV or SC use after dilution” in bold red ink.
As discussed previously, hematuria can occur with any sclerosing agent. Sometimes blood appears in the urine after one or two acts of micturition and occasionally at other times throughout the day. Usually there are no other ill effects, and the hematuria resolves spontaneously. Hematuria probably occurs because of hemolysis of RBCs during sclerotherapy.
In summary, sclerotherapy with a wide variety of scleros­ing solutions is a safe and effective procedure for the treat­ment of varicose and telangiectatic leg veins. Space does not permit a more complete discussion of other possible adverse effects. Table 15.1 summarizes the different adverse effects from a variety of available sclerosing solutions. The inter­ested reader is referred elsewhere for a complete review of adverse effects from sclerotherapy treatment.
13
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occurrence of hyperpigmentation and other local and systemical signs in the treatment of small vessels varices with different sclerotherapic agents, Acta Phlebol. 2001. 2: 43–49.
6. Georgiev M. Postsclerotherapy hyperpigmentations: A one-year
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7. Goldman MP, Kaplan RP, Duffy DM. Postsclerotherapy hyperpigmen­tation: A histologic evaluation, J Dermatol Surg Oncol. 1987. 13:
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8. Cuttell PJ, Fox JA. The etiology and treatment of varicose pigmenta­tion, Phlébologie. 1982. 35: 387.
9. Bessis M. Living blood cells and their ultrastructure. 1973. Berlin: Springer-Verlag.
10. Bessis M, Lessin LS, Beutler E. Morphology of the erythron. In: Williams WJ, et al., eds. Hematology, 3e. 1983. New York: McGraw-Hill.
11. Leach B, Goldman MP. Comparative trial between sodium tetradecyl sulfate and glycerin in the treatment of telangiectatic leg veins, Dermatol Surg. 2003. 29: 612–625.
12. Georgiev M. Postsclerotherapy hyperpigmentation: Chromated glyc­erin as a screen for patients at risk (a retrospective study), J Dermatol Surg Oncol. 1993. 19: 649.
13. Complications and Adverse Sequelae of Sclerotherapy. In: Goldman MP, Bergan JB, Guex JJ, eds. Sclerotherapy Treatment of Varicose and Telangiectatic Leg Veins, 4e. 2006. London: Elsevier.
14. Guex JJ. Indications for the sclerosing agent polidocanol, J Dermatol Surg Oncol. 1993. 19: 959.
15. Leffell DJ. Minocycline hydrochloride hyperpigmentation complicat­ing treatment of venous ectasia of the extremities, J Am Acad Derma­tol. 1991. 24: 501.
16. Leu HJ, Wenner A, Spycher MA. Erythrocyte diapedesis in venous stasis syndrome, Vasa. 1981. 10: 17.
17. Scultetus AH, Villavicencio JL, Kao TC, Gillespie DL et al. Micro­thrombectomy reduces postsclerotherapy pigmentation: Multicenter randomized trial, J Vasc Surg. 2003. 38: 896–903.
18. Weiss RA, Sadick NS, Goldman MP et al. Post-sclerotherapy compres­sion: Controlled comparative study of duration of compression and its effects on clinical outcome, Dermatol Surg. 1999. 25: 105.
19. Tafazzoli A, Rostan EF, Goldman MP. Q-switched ruby laser treat­ment for postsclerotherapy hyperpigmentation, Dermatol Surg. 2000. 26: 653.
20. Denekamp J. Angiogenesis, neovascular proliferation, and vascular pathophysiology as targets for cancer therapy, Br J Radiol. 1993. 66:
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21. Weiss RA, Sadick NS, Goldman MP et al. Postsclerotherapy compres­sion: Controlled comparative study of duration of compression and its effects on clinical outcome, Dermatol Surg. 1999. 25: 105.
22. Weiss RA, Weiss MA. Incidence of side effects in the treatment of telangiectasias by compression sclerotherapy: Hypertonic saline vs polidocanol, J Dermatol Surg Oncol. 1990. 16: 800.
23. Davis LT, Duffy DM. Determination of incidence and risk factors for post-sclerotherapy telangiectatic matting of the lower extremity: A retrospective analysis, J Dermatol Surg Oncol. 1990. 16: 327.
24. Laser treatment of telangiectasia. In: Goldman MP, Guex JJ, Bergan JB, eds. Sclerotherapy treatment of varicose and telangiectatic leg veins, 4e. 2006. London: Elsevier.
25. Yosowitz P et al. Peripheral intravenous infi ltration necrosis, Ann Surg. 1975. 182: 553.
26. Duffy DM. Cutaneous necrosis following sclerotherapy, J Aesthetic Dermatol Cosmetic Surg. 1999. 1: 157.
26. Hoffer AE. Aethoxysklerol (Kreussler) in the treatment of varices, Minerva Cardioang. 1972. 20: 601.
27. de Faria JL, Moraes IN. Histopathology of the telangiectasias associ­ated with varicose veins, Dermatologica. 1963. 127: 321.
28. Bihari I, Magyar E. Microshunt histology in telangiectasias, Int J Angiol. 1999. 8: 98.
29. Bihari I, Magyar E. Reasons for ulceration after injection treatment of telangiectasia, Dermatol Surg. 2001. 27: 133–136.
30. Conrad P, Malouf GM. The Australian polidocanol (Aethoxysklerol) open clinical trial results at two years. Presented at the Annual Meeting
of the North American Society of Phlebology, Maui, Hawaii, Feb 21,
1984.
31. Guckens J, Rabe E, Bieber T. Embolia cutis medicamendosa of the foot after sclerotherapy, Eur J Dermatol. 1999. 9: 132–133.
32. Zimmet SE. The prevention of cutaneous necrosis following extravasa­tion of hypertonic saline and sodium tetradecyl sulfate, J Dermatol Surg Oncol. 1993. 19: 641.
33. Grossman JA et al. The effects of hyaluronidase and dimethyl sulfox­ide (DMSO) on experimental fl ap survival, Ann Plast Surg. 1983. 11:
222.
34. Haire RD. Use of Alidase in prevention of painful arm in accidental perivascular injection of neoarsphenamine and mapharsen, Rocky Mt Med J. 1950. 600.
35. Lorenz HP, Adzick NS. Scarless skin wound repair in the fetus, West J Med. 1993. 159: 350.
36. Zimmet SE. Hyaluronidase in the prevention of sclerotherapy-induced extravasation necrosis: A dose response study, Dermatol Surg. 1996. 22: 73.
37. Heckler FR, McCraw JB. Calcium-related cutaneous necrosis, Plast Surg. 1976. 27: 553.
38. Adams JG Jr, Dhar A, Shukula SD et al. Effect of pentoxifylline on tissue injury and platelet-activating factor production during ischemia­reperfusion injury, J Vasc Surg. 1995. 21: 742.
39. Weithmann KU. The infl uence of pentoxifylline on interactions between blood vessel wall and platelets, IRCS J Med Sci. 1980. 8:
293.
40. Dick ET. The treatment of varicose veins, N Z Med J. 1966. 65:
310.
41. de Lorimier AA. Sclerotherapy for venous malformations, J Pediatr Surg. 1995. 30: 188–194.
42. Perakos PG, Cirbus JJ, Camara S. Persistent bradyarrhythmia after sclerotherapy for esophageal varices, South Med J. 1984. 77: 531.
43. Foote RR. Severe reaction to monoethanolamine oleate, Lancet. 1942. 1: 390.
44. Reid RG, Rothine NG. Treatment of varicose veins by compression sclerotherapy, Br J Surg. 1968. 55: 889.
45. Goldman MP, Bennett RG. Treatment of telangiectasia: A review, J Am Acad Dermatol. 1987. 17: 167.
46. Steinberg MH. Evaluation of Sotradecol in sclerotherapy of varicose veins, Angiology. 1955. 6: 519.
47. Nabatoff RA. Recent trends in the diagnosis and treatment of varicose veins, Surg Gynecol Obstet. 1950. 90: 521.
48. Fegan G. Varicose veins: Compression sclerotherapy. 1967. London: Heinemann Medical.
49. Tibbs DJ. Treatment of superfi cial vein incompetence. 2. Compression sclerotherapy. In: Tibbs DJ, ed. Varicose veins and related disorders.
1992. Oxford: Butterworth-Heinemann.
50. Clinical Case 1. Presented at the Third Annual Meeting of the North American Society of Phlebology, Phoenix, Ariz, Feb 21, 1990.
51. Passas H. One case of tetradecyl-sodium sulfate allergy with general symptoms, Soc Fr Phlebol. 1972. 25: 19.
52. Thibault PK. Sclerotherapy of varicose veins and telangiectasias: A 2-year experience with sodium tetradecyl sulphate, Aust NZ J Phlebol.
1999. 3: 25.
53. Reiner L. The activity of anionic surface active compounds in produc­ing vascular obliteration, Proc Soc Exp Biol Med. 1946. 62: 49.
54. Goldman MP. Sodium tetradecyl sulfate for sclerotherapy treatment of veins: Is compounding pharmacy solution safe? Dermatol Surg. 2004. 30: 1454–1456.
55. Stricker BH, van Oijen JA, Kroon C et al. Anafylaxie na gebruik van polidocanol, Ned Tijdschr Geneeskd. 1990. 134: 240.
56. Conrad P, Malouf GM, Stacey MC. The Australian polidocanol (Aethoxysklerol) study: Results at 2 years, Dermatol Surg. 1995. 21:
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57. Tombari G et al. Sclerotherapy of varices: Complications and their treatment. In: Raymond-Martimbeau P, Prescott R, Zummo M, eds. Phlébologie ’92. 1992. Paris: John Libbey Eurotext.
58. Feied CF, Jackson JJ, Bren TS et al. Allergic reactions to polidocanol for vein sclerosis: Two case reports, J Dermatol Surg Oncol. 1994. 20:
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59. Jenkins D. Severe idiosyncratic reaction to polidocanol, Aust NZ J Phlebol. 2002. 6: 24–25.
60. Soehring K, Frahm M. Studies on the pharmacology of alkylpolyeth­yleneoxide derivatives, Arzneimittelforschung. 1955. 5: 655.
61. Ouvry P, Davy A. Le traitement sclerosant des telangiectasias des membres inferieurs, Phlébologie. 1982. 35: 349.
62. Jager H, Pelloni E. Tests epicutanes aux bichromates, posotofs dan l’eczema au ciment, Dermatologica. 1950. 100: 207.
63. Ramelet AA, Ruffi eux C, Poffet D. Complications après sclerose a la glycerine chromee, Phlebologie. 1995. 48: 377.
64. Wallois P. Incidents et accidents de la sclerose. In: Tournay R, ed. La sclerose des varices, 4e. 1985. Paris: Expansion Scientifi que Francaise.
65. Wagener F, Eggert A, Boerman OC et al. Heme is a potent inducer of infl ammation in mice and is counteracted by heme oxygenase, Blood.
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69. Rother RP, Bell L, Hillmen P, Gladwin MT. The clinical sequelae of intravascular hemolysis and extracellular plasma hemoglobin: A novel mechanism of human disease, JAMA. 2005. 293: 1653–1662.
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CHAPTER
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16
Laser Treatment of
Telangiectasias and Reticular Veins
NEIL SADICK and LIAN SORHAINDO
INTRODUCTION
The incidence of prominent venulectasias and/or telangi­ectasias on the lower extremities occurs in up to 41% of women and 15% of men within the United States.1 The current literature subdivides vascular pathology into super­fi cial “spider” veins or telangiectasias, deep reticular veins, and protuberant varicosities. Etiologies include heredity, hormonal dysregulation, prolonged periods of standing, obesity, pregnancy, and aging. Although patients may present with symptoms of fatigue, aching, swelling, throb­bing, and occasionally pain, patients seek treatment primar­ily for aesthetic concerns. With this rise in consumer demand over the past fi ve years, there has been a subsequent increase in the utilization of lasers and intense pulsed light (IPL) sources for the treatment of lower extremity veins.
IDENTIFYING THE PROBLEM
The vasculature of the lower extremity is comprised of a complex, intertwined network of superfi cial and deep venous plexuses. The superfi cial veins, as suggested by their name, lie directly underneath the skin surface. The deep veins, in contrast, traverse the muscle of the leg. The individual fl ow patterns of these two networks intertwine to such a great degree that superfi cial spider veins may be the direct result of increased hydrostatic pressure in the deep reticular veins.
In contrast to the treatment of facial veins, the varying sizes, depths, fl ow patterns, and vessel thickness of leg veins make the treatment of leg veins more challenging. Presently,
there is no gold standard of treatment for all leg veins, and lasers often are used as adjunctive therapy in patients under­going phlebectomy, sclerotherapy, or vein stripping. Laser and light source technology have become particularly useful in the treatment of small spider veins or telangiectasias, and also in the setting of vessels that are sclero-resistant that may arise from prior surgical treatment as a result of telangiec­tatic matting or angiogenic fl ushing (see Box 16.1).2 It can also be used in the treatment of large spider and reticular veins; however, sclerotherapy remains the gold standard for the treatment of these vessels. The chapter, herein, deals specifi cally with the laser treatment of telangiectasias and reticular veins; other modalities of treatment including sclerotherapy, ambulatory phlebectomy, and endovenous ablation are discussed elsewhere in the book.
PATIENT SELECTION: WHEN AND
HOW TO CHOOSE LASER/IPL
VERSUS SCLEROTHERAPY
Laser therapy is most effi cacious for treating telangiecta-
sia/venulectasia or reticular veins less than 3 mm in di-
3,4
ameter. in patients with areas of neovascularization with telangiec­tactic matting or angiogenic fl ushing, with sclero-resistant/ noncannulizable vessels, and who are needle-phobic. Rela­tive contraindications to the use of laser surgery include tanned skin, pregnancy, the use of iron supplements or anti-coagulation, history of photosensitivity disorder, or hypertrophic and keloidal scarring (see Table 16.1).
As mentioned earlier, lasers have become indicated
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157
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BOX 16.1 Indications for Laser Therapy Treatment of Leg Veins
• Refractory noncannulable vessels
• Telangiectatic matting
• Angiogenic fl ushing
• Sclero-resistance
• Needle-phobic patients
• Vessels smaller than the diameter of a 30-gauge needle are present
TABLE 16.1 Comparison of the 1064 nm Nd:YAG, 810 nm
Diode, and 755 nm Alexandrite Lasers for Leg Veins 0.3– 3 mm in Diameter
Laser Patients achieving 75% clearance at 3 months
1064 nm Nd:YAG 88% 810 nm diode 29% 755 nm Alexandrite 33%
TABLE 16.2 Vessel Thermal Relaxation Time
Vein diameter Time (seconds)
0.1 0.010
0.2 0.080
0.4 0.16
0.8 0.6
1.0 1.0
2.0 8.0
Data from Eremia 2002.
BOX 16.2 Fundamental Properties of a Laser for Leg Veins
• Must have a wavelength proportionately better absorbed by hemoglobin than the surrounding tissue.
• Penetration should reach the full depth of the target vessel.
• Suffi cient energy must be delivered to damage the vessel without damaging the overlying skin.
• Energy must be delivered over an exposure time long enough to slowly coagulate the vessel without damaging surrounding tissue.
FIGURE 16.1 Absorption spectrum of hemoglobin/deoxyhemoglobin.
FUNDAMENTALS OF LASER
TREATMENT OF LEG VEINS
Theory of Selective Thermolysis: Major
Principles and Determinants
The advent of laser technology for treatment of leg veins began with the concept of selective photothermolysis devel­oped in the late 1980s. molysis states that selective damage to a tissue structure is achieved by means of a wavelength of light preferentially absorbed by a chromophore in light-absorbing molecules and laser exposure time less than or equal to the object’s thermal relaxation time (i.e., the time required for the object to lose 50% of its thermal energy). The thermal relaxation times of leg veins vary depending upon vessel diameter (see Table 16.2).
6
A physician employing laser therapy should routinely consider the utility of laser and intense pulsed light (IPL) technologies versus that of sclerotherapy for the treatment of lower extremity vessels. for a laser or IPL source in the treatment of leg veins are delineated in Box 16.2.
5
The theory of selective photother-
7
The fundamental requirements
Laser technology and its role in leg vein reduction is rooted in the molecule hemoglobin and its absorption spec­trum, which has broad peaks at 410, 540, and 577 nm and smaller peaks at 920 and 940 nm. The spectra of oxy- and deoxyhemoglobin differ, with bluer veins responding to wavelengths targeting the deoxyspectrum; whereas red var­icosities respond more effectively to wavelengths targeting the oxyhemoglobin spectrum (see Figure 16.1). Generally speaking, any vessel that is less than 3 mm in diameter may be treated by laser and IPL technologies. However, sclerotherapy is a more effi cient modality for eradicating cannulable vessels, and when small, diffi cult to cannulate vessels are present microsclerotherapy may be implemented. Microsclerotherapy, however, is plagued by a number of adverse sequelae, increased incidence of bruising and pigment dyschromia, puncture marks from needle use, microulcerations, and inconsistent results (see Table 16.3). Given the adverse aesthetic outcomes of such procedures, the use of lasers has gained momentum in the management of cosmetic veins.
Lasers and intense pulse light (IPL) have not become replacements for sclerotherapy, primarily because hydro­static pressure considerations are not addressed by light endothelial interactions. It is also more diffi cult to have
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suffi cient penetration of photons safely through the thick epidermal-dermal wall surrounding the lower extremity vessels when utilizing noninvasive treatment modalities like laser technology; direct injection into the target chro­mophore is intuitively more effi cient. Furthermore, an altered pattern of cytokine release may be observed when using laser technology, resulting in injury to the vessel that may lead to increased incidence of postinfl ammatory hyperpigmentation.
Wavelength, pulse duration, and spot size are the pa­rameters that are most infl uential during the treatment and management of individual vessels (see Table 16.4). The larger vessels tend to respond to longer wavelengths or the ratio of vessel to epidermal heating increases the probability of achieving complete vessel coagulation.8 Shorter wave­lengths, in contrast, partially coagulate the vessel ultimately increasing the incidence of treatment failures, and subse­quent epidermal damage including hyperpigmentation.9 Maximum effi ciency of vessel clearance is achieved when the penetration depth of the beam equals the vessel diameter.
TABLE 16.3 Microtelangiectasia <0.5 mm: Comparison of
Microsclerotherapy and Laser Technology
The spot size should be as large as possible, at least on the order of 4× the optical penetration depth. An adequate spot size minimizes scattering losses in addition to maximizing beam penetration, which increases the probability that pan endothelial destruction will be achieved. The disadvantage to this, however, is that the use of larger spot sizes increases the pain and discomfort subjectively reported by the patient.
These parameters have infl uenced and spurred the devel­opment of a bimodal, dual-wavelength approach for the treatment of both red and blue lower extremity veins (see Figure 16.2). For the treatment of small, reddish telangiec­tasias with a high degree of oxyhemoglobin, short wave­lengths (500–600 nm) were found to be most effective; longer wavelengths (800–1100 nm) were found to be most effective for the treatment of deeper, blue telangiectasias and reticular veins.
With continuing advances, laser technology can now address both variations in vessel size and depth with a single long wavelength 1064 nm Nd:Yag laser utilizing a varied pulse width as the monomodal approach (see Table 16.5).
TABLE 16.4 Optimal Laser Parameters for the Treatment of
Leg Veins
Microsclerotherapy Laser
Number of Treatments
Bruising + Discomfort + Clinical Effi ciency + Purpura + Pigmentation
Ulceration + Cost + Patient Satisfaction + Physician Skill
Wavelength 530–1064 nm Pulse Duration 2–100 ms Fluence 30–150 J/cm Spot Size 1.5–10 mm
Adapted from Sadick 2002.
TABLE 16.5 Monomodal Approach to the Treatment of Leg
Veins Using the 1064 nm Nd:YAG Laser
Vessel size Spot size Fluence Pulse duration
<1 mm red Small High Short 1–3 mm (blue) Large Moderate Long
Adapted from Sadick 2003.
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FIGURE 16.2 Pre- and post-clinical pictures of lower extremity veins using biomodal technique.
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Delicate, red vessels <1 mm in diameter are superfi cial, having high oxyhemoglobin saturation. Consequently, they can be treated effectively with small spot sizes (<2 mm), higher fl uences (350–600 J/cm2), and short pulse durations (15–30 s). Larger blue vessels, in contrast, are typically 1– 4 mm in diameter, deeper, and possess a lower oxygenated hemoglobin component. As a result, these veins are effec­tively treated with larger spot sizes (2–8 mm), moderate fl uences (100–350 J/cm2), and long pulse durations (30– 50 ms). With the use of the Nd:YAG rapidly gaining momen­tum, the transition from a bimodal wavelength technique to a monomodal approach has evolved.
TREATMENT APPROACH
Candidates for Laser Therapy
Laser therapy may be considered appropriate in patients who are needle phobic, cannot tolerate sclerotherapy, are plagued by legs veins that are sclero-resistant, and/or are susceptible to telangiectatic matting (see Box 16.1). Ideal candidates for laser treatment of leg veins previously have undergone appropriate surgery or sclerotherapy for the treat­ment of varicosities, incompetent perforators, and reticular veins, as well as sclerotherapy to clear the majority of super­fi cial vessels.
TABLE 16.6 Lasers and Light Sources for the Treatment of
Leg Veins
Laser Wavelength
Pulsed Dye 585–605 nm KTP 532 nm Alexandrite 755 nm Diode 810 nm Nd:YAG 1064 nm Intense Pulsed Light 515–1200 nm
session. Laser and light therapy should be utilized in the treatment of any residual vessels including those that are too small in diameter to undergo sclerotherapy with a 30–32­gauge needle.
LASER TREATMENT SYSTEMS
A compilation of laser and intense pulsed light sources utilized in the setting of laser treatment of legs veins are presented herein and summarized in Table 16.6. The wave­lengths of light range from 515 nm to 1064 nm, depending on the treatment system employed. As mentioned earlier in the chapter, the longer the wavelength, the greater the depth of penetration, as illustrated in Figure 16.4.
Patient Interviews
Diagnosis of spider or varicose veins begins with a thor­ough medical history detailing potential risk factors or eti­ologies for vascular pathology such as hormones, prolonged standing associated with occupation, obesity, pregnancy, heredity, or aging.
Physical Examination
All potential candidates for laser treatment of leg veins should undergo a thorough physical examination. During the exam, the physician should evaluate the type and size of the leg veins, and the presence/absence of refl ux or incompetent valves. The treatment algorithm (see Figure 16.3) suggests that larger varicose veins with refl ux should be treated fi rst in an effort to avoid the unsuccessful treatment of smaller telangiectasias and complications such as dyspigmentation and telangiectatic matting.
In keeping with the treatment algorithm in Figure 16.3, initial treatment should include surgical removal, stripping, or ambulatory phlebectomy of varicosities and large feeder vessels. Sclerotherapy should then follow proceeding from large to small vessels. Adhering to this treatment strategy will obliterate, on average, 80 to 90% of vessels in a single
578 nm Copper Bromide (CuBr)
Yellow Light Laser
A new yellow light laser employing a copper bromide medium has demonstrated effi cacy in the treatment or red lower extremity telangiectasia that are less than 2 mm in size. An average of 1.7 patient sessions produced signifi cant clearing of 75% to 100% in 71.8% of patients. The positive results have been confi ned to the treatment of red vessels (1 mm).
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PULSED LASERS AND LIGHT SOURCES
Potassium-Titanyl-Phosphate Laser
For small telangiectatic leg veins in fair-skinned patients, the pulsed KTP laser has become the treatment of choice. The Versapulse KTP laser (Lumenis, Santa Clara, Califor­nia, U.S.) uses the following parameters: a spot size of 3– 5 mm, pulse duration of 10–15 ms, and fl uences of 14–20 J/cm2, which have proven to be effective. A 4ºC chilled tip provides epidermal protection. Side effects include transient erythema, crusting superfi cially, and purpura. When administering the pulsed KTP laser, lower fl uences must be employed in the
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Physical Examination
Varicose Veins
Non-invasive Testing
Doppler / Duplex / Plethysmography
Reflux
Incompetent Perforators
or
Saphenofemoral Junction
Surgical Ligation
or
Compression Sclerotherapy
Treat Varicosities and Reticular Veins with Compression
Sclerotherapy or Ambulatory Phlebectomy
No Reflux
Spider Telangiectasia
FIGURE 16.3 Systematic approach to the treatment of leg veins.
FIGURE 16.4 Wavelength and depth of penetration.
Superficial Sclerotherapy or
Laser or Light Therapy of
Superficial Telangiectasia,
Residual Vessels and of Sclerotherapy Induced Matting
darker skinned or tanned patient because of their increased melanin and its absorption of green light. This increased absorption is more likely to increase the risk of epidermal damage. Treatment failure, consequently, is higher in this subset of patients because the lower fl uences are not very effective in coagulating the target vessel. Patient acceptance of this laser treatment system is high with minimal treatment discomfort of the longer penetrating wavelengths and a relatively uncomplicated postoperative course.
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Other technologies including the Aura (Laserscope, San Jose, California, U.S.) have produced comparable results.
Flashlamp-Pumped Pulsed Dye Laser
The pump pulsed dye laser was the fi rst laser to achieve notable results in the treatment of leg veins in the 1980s. This treatment system utilizes short wavelength technology, at a wavelength of 577 nm. This has become acceptable for treatment of leg vessels <1.0 mm, but cannot be