Postsclerotherapy Hyperpigmentation

Cutaneous pigmentation to some degree is a relatively common occurrence after sclerotherapy with any sclerosing solution. It has been reported in 11% to 80%1-3 of patients. The true incidence of hyperpigmentation is a result of many factors, including treatment technique, sclerosing solution, and concentration, as well as how the authors define pigmentation. The definition of pigmentation should be, "any brown-black staining of the skin occurring after sclerotherapy," with persistent pigmentation being separated out to those patients whose brown staining is present after one year.

Pigmentation usually is temporary. Physicians report a 1% to 2% incidence of pigmentation persisting after one year.4-6 Pigmentation usually is linear along the course of the treated blood vessel. We use the term ghost of the blood vessel to explain to patients that it represents a resolving and not functioning vessel (see Figure 15.1).

Etiologic Factors

The cause of this pigmentation most likely results from a combination of postinflammatory hyperpigmentation (incontinence of melanin pigment) and hemosiderin deposition. However, histologic examination has demonstrated that this pigmentation is caused only by hemosiderin staining of the dermis, irrespective of the type of sclerosing solution used, pigmentation of the patient, or length of time after injection7,8 (see Figure 15.2).

Perivascular phagocytosis of RBCs occurs either by intact cells or piecemeal after fragmentation by macrophages.9 The intracellular fragments in the macrophage cytoplasm are further compartmentalized into hemoglobin-containing globules. Since hemosiderin is an indigestible residue of hemoglobin degradation, it may appear as aggregates up to 100 |im in diameter.10 Hemosiderin has a variable concentration of these aggregates. Its elimination from the area through phagocytosis may take years, if it ever occurs.

The incidence of pigmentation apparently is related to multiple factors, including (1) sclerosing solution type and concentration, (2) sclerotherapy technique, (3) gravitational and other intravascular pressures, (4) innate tendency toward cutaneous pigmentation (total body iron stores and/or altered iron transport and storage mechanisms, innate enhanced histamine release or hypersensitivity, and vessel fragility),

(5) postsclerotherapy treatment (graduated compression),

(6) vessel diameter, and (7) concomitant medication.

Solution Type and Concentration

The extent of endothelial destruction with resulting inflammation and extravasation of RBCs is thought to influence the development of postsclerotherapy hyper-

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FIGURE 15.1 Linear pigmentation along the course of a treated blood vessel. A. Before treatment. B. Eight weeks after treatment with POL 0.5%. C. Punctate pigmentation 8 weeks after treatment with Sclerodex. (From Goldman MP. Adverse sequelae of sclerotherapy treatment of varicose and telangiectatic leg veins. In Bergan JJ, Goldman MP, eds. Varicose veins: Diagnosis and treatment. 1993, St Louis: Quality Medical Publishing.)

FIGURE 15.1 Linear pigmentation along the course of a treated blood vessel. A. Before treatment. B. Eight weeks after treatment with POL 0.5%. C. Punctate pigmentation 8 weeks after treatment with Sclerodex. (From Goldman MP. Adverse sequelae of sclerotherapy treatment of varicose and telangiectatic leg veins. In Bergan JJ, Goldman MP, eds. Varicose veins: Diagnosis and treatment. 1993, St Louis: Quality Medical Publishing.)

pigmentation. The increased incidence of pigmentation with certain concentrations of sodium tetradecyl sulfate (STS) and hypertonic saline (HS) that produce a greater reaction than polidocanol (POL) and glycerin confirms this hypothesis.1,11,12 Thus the inflammatory response after treatment should be kept to a minimum, and sclerosing solutions and concentrations should be altered for each treatment session so that the minimally effective sclerosing concentration is used.

with minimal pressure. Since injection pressure is inversely proportional to the square of the piston radius, a syringe with a larger radius causes less pressure. The average piston radius is 8 mm for a 2-ml syringe and 5 mm for a 1-ml syringe. The calculated pressure with an implied force of 250 g is 180 mm Hg for a 2-ml syringe and more than 300 mm Hg for a 1-ml syringe.14 This is one reason we recommend using a 3-ml syringe for sclerotherapy.

Technique

Optimal technique consists of limiting pressure into damaged (sclerosed) veins to prevent extravasation of RBCs. To limit the degree of intravascular pressure, larger feeding varices, incompetent varices, and points of high pressure reflux should be treated first. A greater incidence of pigmentation occurs if vessels distal to points of reflux such as reticular veins feeding into telangiectasia or vessels distal to the saphenofemoral junction (SFJ) are treated before successful closure of the junction or feeding veins.13

The degree of injection pressure is also important. Because telangiectasia and small venules are composed essentially of endothelial cells with a thin (if any) muscular coat and basement membrane, excessive intravascular pressure from injection may cause vessel rupture. In addition, endothelial pores and spaces between cells in the vascular wall dilate in response to pressure, leading to extravasation of RBCs. It is therefore important to inject intravascularly

Gravitational and Other Intravascular Pressures

Postsclerotherapy pigmentation appears most commonly in vessels treated below the knee but can occur anywhere on the leg, probably as a result of a combination of increased capillary fragility and increased intravascular pressure by gravitational effects in this location. Pigmentation has never been observed in our practice after sclerotherapy on the hands, face, or chest.

Predisposition to Pigmentation

Certain individuals appear to be predisposed to the development of pigmentation through a variety of genetic mechanisms. Vessel fragility may also result in an innate predisposition toward pigmentation.

Patients taking minocycline may have an increased risk for postsclerotherapy pigmentation.15 This propensity may

FIGURE 15.2 Section stained with hematoxylin-eosin taken 6 months after injection with POL 0.75%. Note scattered foci of golden brown pigment. A. Original magnification x50. B. Perls-stained section from the same patient as in Figure 15.1. Note scattered foci of green-blue granules within siderophages. Original magnification x200. C. Original magnification x50. D. Original magnification x 350. (From Goldman MP, Kaplan RP, and Duffy DM. J Dermatol Surg Oncol 13:547. 1987.)

FIGURE 15.2 Section stained with hematoxylin-eosin taken 6 months after injection with POL 0.75%. Note scattered foci of golden brown pigment. A. Original magnification x50. B. Perls-stained section from the same patient as in Figure 15.1. Note scattered foci of green-blue granules within siderophages. Original magnification x200. C. Original magnification x50. D. Original magnification x 350. (From Goldman MP, Kaplan RP, and Duffy DM. J Dermatol Surg Oncol 13:547. 1987.)

be related to the inflammatory effects of sclerotherapy. Unlike the golden to deep brown color characteristic of typical sclerotherapy-induced pigmentation, pigmentation from minocycline is typically blue-gray. Therefore it may be prudent to withhold minocycline therapy in sclerotherapy patients.

Postsderotherapy Coagula

Removal of postsclerotherapy coagula may decrease the incidence of pigmentation. Thrombi to some degree are thought to occur after sclerotherapy of all veins, regardless of size, because of the inability to occlude the vascular lumen completely with external pressure. Persistent thrombi are thought to produce a subacute "perivenulitis" that can persist for months.16 The perivenulitis favors extravasation of RBCs through a damaged endothelium or by an increase of the permeability of treated endothelium. This provides a rationale for drainage of all foci of trapped blood two to four weeks after sclerotherapy. Sometimes blood can be released even two months after sclerotherapy.

Thrombi are best removed by gentle expression of the liquefied clot through a small incision made with a 21-gauge needle (see Figure 15.3). A multicentered, randomized controlled study of 101 patients with varicose veins was treated at one to three weeks with microthrombectomy in half of

FIGURE 15.3 Method for evacuation of a thrombosis in a 1 mm diameter reticular varicose vein 2 weeks after sclerotherapy. A. Small incision. B. Expelling clot (see text for details). (From Complications of Sclerotherapy. In Sclerotherapy Treatment of Varicose and Telangiectatic Leg Veins, 4e. Goldman MP, Bergan JB, Guex JJ, eds. London: Elsevier. 2006.)

FIGURE 15.3 Method for evacuation of a thrombosis in a 1 mm diameter reticular varicose vein 2 weeks after sclerotherapy. A. Small incision. B. Expelling clot (see text for details). (From Complications of Sclerotherapy. In Sclerotherapy Treatment of Varicose and Telangiectatic Leg Veins, 4e. Goldman MP, Bergan JB, Guex JJ, eds. London: Elsevier. 2006.)

the treated veins.17 Photographs of the sclerotherapy treated areas were evaluated at 16 weeks. Veins < 1 mm in diameter had less pigmentation when drained but veins > 3 mm did not show any benefit from microthrombectomy.

Treatment

Treatment of pigmentation, once it occurs, often is unsuccessful unless you have access to a Q-switched laser. Because this pigmentation is caused primarily by hemosiderin deposition and not melanin incontinence, bleaching agents that affect melanocytic function usually are ineffective. Exfoliants (trichloroacetic acid) may hasten the apparent resolution of this pigmentation by decreasing the overlying cutaneous pigmentation or promoting the exfoliation of hemosiderin, but they carry a risk of scarring, permanent hypopigmentation, and postinflammatory hyperpigmentation.

Haemosiderin After Scelerotherapy
FIGURE 15.4 Absorption spectra for hemosiderin (freshly frozen, average of two determinations). (From Wells CI, Wolken JJ. Biochemistry: microspectophotomotry of haemosiderin granules, Nature. 1962. 193:977.)

It seems reasonable to promote the wearing of graduated support stockings after treatment. A study on the use of 20 to 30 mm Hg compression stockings after sclerotherapy treatment of telangiectasia and reticular veins 0.4 to 3 mm in diameter found a decreased incidence of pigmentation when compression was used. Compression for three days resulted in a 20% decrease of pigmentation; compression for one week resulted in a 60% decrease in pigmentation versus no compression and compression for three weeks demonstrated limited pigmentation in only two of 10 patients.18 This follows the logic of compression reducing vessel lumen size, resulting coagula, and reducing hydrostatic pressure.

The Q-switched ruby laser (694 nm) is effective in removing recalcitrant pigmentation.19 Hemosiderin has a peak at 694 nm, and the Q-switching impulse at 20 to 30 nsec is effective in removing tattoo granules. In addition, 694 nm is not absorbed to a significant extent by epidermal melanin or hemoglobin and thus has a relative specificity for dermal hemosiderin (see Figure 15.4). In a study of eight patients with pigmentation present one to two years after sclero-therapy, 92% of the lesions lightened with treatment; 58% of lesions demonstrated significant (75% to 100%) resolution after one to three (average 1.7) treatments. The ruby laser was used with a 4 mm beam size, and fluence range of 5.6 to 10.5 J/cm2. We now use a Q-switched ruby laser (Sinon) from WaveLight Laser Technologies AG (Erlangen, Germany) at 5-7 J/cm2 with a 20-ns pulse and 4 to 5 mm diameter spot size. Treatments are performed every four weeks until resolution. Care is taken to use the minimal fluence required to produce a whitening of the skin without

Varicose Veins Spots

FIGURE 15.5 A. Resolution 2 months after the second of two treatments with the Q-switched ruby laser at 8.0 J/cm2. B. Pigmentation from sclerotherapy lasting over 1 year. (Courtesy David Duffy, MD; from Goldman MP, Weiss RA, Bergan JJ, eds. Varicose veins and telangiectasias: Diagnosis and treatment. 1999. St Louis: Quality Medical Publishing.)

FIGURE 15.5 A. Resolution 2 months after the second of two treatments with the Q-switched ruby laser at 8.0 J/cm2. B. Pigmentation from sclerotherapy lasting over 1 year. (Courtesy David Duffy, MD; from Goldman MP, Weiss RA, Bergan JJ, eds. Varicose veins and telangiectasias: Diagnosis and treatment. 1999. St Louis: Quality Medical Publishing.)

causing bleeding. Our patients require one to two treatments for complete resolution (see Figure 15.5).

Interestingly, we have not found satisfactory results using a variety of Alexandrite lasers either in long pulse or Q-switched mode. This may be due the decreased interaction of the 755-nm wavelength with hemosiderin.

The simplest treatment is flashbulb therapy or chromo-therapy. Since pigmentation usually resolves within one year in the majority of patients, time and photographic documentation to demonstrate resolution are usually all that is necessary for the understanding patient.

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