Laser Treatment of Vascular Lesions

S. Bard, D. J. Goldberg

• Publisher: S. Karger
• Year: 2014
• ISBN:
  9783318023138
• Topic: Medicine
• Subtopic: Medical Technology & Supplies

Today, nearly 60 years after the invention of the first medical laser, multiple laser and light systems exist and are applied in various medical specialties such as dermatology, ophthalmology, and urology. This volume - the first in the series Aesthetic Dermatology - focuses on the laser treatment of cutaneous lesions with a vascular target. Each chapter describes a particular laser or light modality and its specific application to a variety of both vascular and nonvascular lesions. Renowned specialists in laser medicine have contributed their expertise, incorporating current evidence-based literature and their own personal treatment recommendations, as well as pearls and perils. The purpose of this book is to explore the options and parameters available to treat cutaneous lesions traditionally responsive to vascular laser therapy and to expand the application to further lesion treatments. Readers who wish to broaden their knowledge and further hone their skills in treating cutaneous vascular lesions with lasers will find this publication a valuable and comprehensive review.

Bard S, Goldberg DJ (eds): Laser Treatment of Vascular Lesions.
Aesthet Dermatol. Basel, Karger, 2014, vol 1, pp 121-142 (DOI: 10.1159/000355061)

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Complications of Vascular Laser Treatment

Lisa D. Grunebaum^a · Kyle Bartlett^b

^a Departments of Dermatology and Otolaryngology, ^b Miller School of Medicine, University of Miami, Miami, Fla., USA

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Abstract

Although in knowledgeable hands treatment of vascular lesions is unlikely to result in permanent unwanted sequelae, complications do occur. Erythema and edema are common side effects and can be treated with supportive care. Pigmentary abnormalities and scarring are among the most feared risks. In addition, vesiculation, purpura, and infection are also potential side effects, and if severe may increase the possibility of untoward permanent consequences. Ocular damage is a rare but devastating complication of laser use. In all areas, attention to detail and prevention are the best means to avoid sequelae. This chapter aims to review these possible complications with pathophysiology and common treatment options for each area.

© 2014 S. Karger AG, Basel

Laser therapy in vascular lesions is based upon the laser’s ability to supply a destructive dose of thermal energy to affected tissues. The capability to selectively target specific structures, termed ‘selective photothermolysis’, is possible based on adjustments in laser parameters of wavelength, pulse duration, fluence, irradiation, and spot size to match the therapeutic parameters required by the target tissue [1]. Unfortunately, this selectivity can be imperfect due to overlapping absorption spectra of targeted and untargeted tissues, as well as target tissue heat energy dissipation to surrounding untargeted tissues, resulting in collateral damage [1, 2] . All lasers have some risk of complication, and the complication rate further varies based on the individual patient, lesions, and operator [3, 4] . This chapter details complications that have been shown to arise with vascular laser surgery. The topics are organized by complication in order of frequency of occurrence, with pathophysiology and examples of complications, and recommendations for prevention and treatment should complications occur.

Hyperpigmentation

Definition and Etiology

Hyperpigmentation is an increase in the pigment concentration relative to the surrounding skin. Melanin is the pigment most commonly implicated in hyperpigmentation [5] . Postinflammatory hyperpigmentation (PIH) is a feared but known complication of laser treatment. PIH can arise from laser therapies for vascular cutaneous lesions, and in fact, pigmentary changes, with hyperpigmentation making up the majority, is the most common complication seen from treatment for these [6-8] . In addition, PIH can result from several disease processes involving the skin, such as infections, acne, allergic reactions, trauma, reactions to medications, lupus erythematous, atopic dermatitis, contact dermatitis, and lichen planus [7] . The physician should also be aware of noninflammatory medicinal causes of hyperpigmentation such as use of tetracycline, doxorubicin, bleomycin, 5-fluorouracil, busulfan, arsenic, gold, silver, mercury, lead, bismuth, antimalarial drugs, hormones, clofazimine, minocycline, and tinea versicolor in addition to the inflammatory causes [9].

In regard to laser-induced hyperpigmentation, no preponderance for any age or gender has been shown; however, it is more common in those with Fitzpatrick skin types III-VI [6, 10] . Pigmented races are more likely to develop PIH and are also more likely to have longer-lasting hypermelanosis [5] . A review of 3,143 laser hair removal procedures on 480 patients performed with a ruby laser illustrates this. It was found that only 1.0% of those with Fitzpatrick skin types I and II had treatment resulting in hyperpigmentation, while the rate was 9.9% in those with Fitzpatrick skin types IV-VI [11] . The type of laser selected for patients plays a role in the variation in hyperpigmentation incidence among differing skin types [11] . The changes in pigmentation usually resolve on their own, but can persist for months to years without treatment and usually resolve in 6-12 months with treatment [6, 9, 12, 13].

Pathophysiology

In epidermal hypermelanosis of PIH, the process begins with an inflammatory response in the epidermis leading to keratinocyte release of prostaglandins, leukotrienes, and cytokines. These mediators cause an increase in melanocyte proliferation and production of melanin, which is then transferred to the surrounding keratinocytes [10] . The degree of hyperpigmentation is thought to depend on a number of factors. Some believe that the degree of inflammation affects the degree of hyperpigmentation in the sense that severe inflammation may lead to death of melanocytes causing hypopigmentation, whereas less severe inflammation may lead to hyperpigmentation through the inflammation-mediated induction of, but not destruction of, melanocytes [14] . This is illustrated in a study using black guinea pigs. Q-switched (QS) ruby laser 40-ns pulses that were greater than 0.4 J/cm² were found to cause depigmentation, whereas those less than 0.3 J/cm² induced melanogenesis [15].

Ruiz-Maldonado and Orozco-Covarrubias [5] proposed ‘individual chromatic tendency’ as the reasoning behind why the same inflammatory influence may induce hypopigmentation is some people while others develop hyperpigmentation. The tendency is based on the resilience of ‘weak’ versus ‘strong’ melanocytes to insults. The weak melanocytes respond to inflammation with death, but the strong melanocytes respond with excess production of melanin. They further postulated that this tendency was genetically driven in an autosomal dominant manner, and could be used to predict which type of dyspigmentation, if any, a person awaiting laser treatment may develop. Long-term or recurrent inflammation can lead to greater degrees of hyperpigmentation, showing that the duration of inflammation is an important factor. It has also been observed that those dermatoses disrupting the basal layer of the epidermis lead to a more severe degree of hypermelanosis than the inflammation associated with them would suggest [5].

Prevention

Management of PIH is best achieved by prevention of inflammation. If inflammation cannot be avoided, resolution of the underlying disorder may help prevent further progression [9] . Although NSAIDs may help prevent generalized inflammation, studies have shown that they may actually increase the risk of hyperpigmentation as well as purpura and scarring that result as side effects of laser therapy [11] . Avoidance of sun exposure both before and after treatment has been shown in multiple studies to decrease the incidence of PIH. Sun exposure will induce the formation of the epidermal chromophore, melanin, and also causes an increase in epidermal thickness. Both of these change the absorption properties of the skin [10] . Sun exposure can also reverse the effects of depigmenting agents such as hydroquinone [9] . Topical sunscreens that protect against UVA and UVB should be worn for at least 6 weeks prior to the treatment [10] . Even visible light has been shown to induce melanin formation and darkening of melanin already present [16] . Use of topical bleaching agents such as hydroquinone prior to laser treatment remains controversial [10], but some experts feel that use 2 weeks prior to therapy lowers the rate of posttreatment hyperpigmentation [17].

Epidermal cooling therapy of the treated area during the procedure is also commonly employed. When used during laser treatment, cooling has multiple benefits including decreasing procedure related pain, allowing use of higher fluences, greater clinical effectiveness, safer use in patients with darker skin types, and decreased pig-mentary changes, erythema, blistering, scarring, and purpura [3, 10, 11, 18, 19]. Three methods have been developed for epidermal cooling: contact, cooled air, and cryogen spray cooling. However, the temperature decrease associated with a 50-ms spray has been shown to decrease the skin surface from its normal temperature of 30 to 6 °C, while the basal layer of the epidermis, where two thirds of the melanin is, remains at 18-22 °C [11, 20] . Longer time periods allow for greater cooling, but run the risk of freezing the skin. Other errors can be made if there is misalignment of the laser/cryogen spray combination. Additionally, if the handpiece is not held perpendicular to the area to be treated, adequate cooling may not be achieved and crescent-shaped burn patterns may result [11, 18] . Humidity in the air can lead to formation of an epidermal ic...