Background
Venous lakes manifest as dark blue-to-violaceous compressible papules caused by dilation of venules. They were first described in 1956 by Bean and Walsh, who noted their compressibility and predilection for sun-exposed skin, especially the ears of elderly patients.[1] Although benign, venous lakes are important because of their mimicry of malignant lesions, such as melanoma and pigmented basal cell carcinoma.
Pathophysiology
A venous lake is an acquired form of vascular ectasia (vascular dilatation). A capillary aneurysm is considered a precursor or variant of a venous lake.
Epidemiology
Frequency
The worldwide incidence of venous lakes is unknown, but they are believed to be common.
Race
No racial predilection has been documented for venous lakes.
Sex
Bean and Walsh reported that 95% of venous lakes were observed in males.[1] Another review of venous lakes confirmed the same sex distribution. The disproportionate male distribution may be related to occupational sun exposure, hair length, and hairstyles. Women comprised the majority of treated patients in a large study of laser therapy for venous lakes; however, this may be related to increased concern among women regarding cosmetic appearance rather than with true incidence.
Age
Venous lakes have been reported only in adults and usually occur in patients older than 50 years. The average age of presentation for venous lakes has been reported to be 65 years.
Prognosis
The prognosis for venous lakes is excellent. Although venous lakes do not resolve on their own, patients can be reassured that venous lakes do not evolve into something more serious, such as a skin cancer. Mortality from venous lakes has not been reported. Venous lakes are usually asymptomatic, although pain, tenderness, and excessive bleeding may occur if a lesion is traumatized. Venous lakes are considered biologically harmless.
History
Venous lakes most commonly occur in adults older than 50 years with a history of long-term sun exposure. The typical presentation is a slow-growing asymptomatic lesion. Patients with venous lakes may report that the papule has been present for several years prior to presentation. Recurrent bleeding after minor trauma may also be reported.
Physical Examination
Physical examination usually reveals a soft, compressible, dark-blue or violaceous papule (slightly elevated lesion), up to 1 cm in diameter. Venous lakes usually are well demarcated, with a smooth surface. Compression often causes a emptying of the blood content. Venous lakes typically are distributed on the sun-exposed surfaces of the face and neck, especially on the helix and antihelix of the ear and the posterior aspect of the pinna, as shown in the image below. Another common site of involvement is the vermilion border of the lower lip, shown below. Sometimes, several lesions are found on the same person, and the surrounding skin reveals actinic damage, as shown below.
View Image | Venous lake on the helix of the ear. |
View Image | Venous lake on the lower lip. |
View Image | Venous lake of the lip. Note the apparent actinic damage of the surrounding skin. Courtesy of Albert C. Yan, MD. |
Causes
Two main theories regarding the development of venous lakes have been proposed. The first involves injury to the vascular adventitia and the dermal elastic tissue due to long-term solar damage permitting dilatation of superficial venous structures. The second theory involves the involvement of vascular thrombosis in the development of venous lakes. Thrombosis is commonly present in lesions of this type; however, whether the thromboses is a primary or a secondary event in the development of these lesions is unclear.
Laboratory Studies
Blood laboratory studies are not usually indicated in the evaluation of venous lakes and other lesions of this type. Pathologic examination can prove useful in confirmation of a clinical diagnosis of venous lakes.
Imaging Studies
Imaging studies are not necessary in the evaluation of venous lakes.
Other Tests
Diascopy is useful for differentiating venous lakes from other lesions. Direct pressure created by a glass microscope slide causes a vascular lesion such as a venous lake to blanch as its contents are emptied. Sometimes, blood may not be completely emptied with diascopy, but a color change ensues. Cherry angiomas and neoplasms (ie, basal cell carcinoma or nodular melanoma) do not change color with diascopy.
Epiluminescence techniques such as dermoscopy also can be used to differentiate vascular lesions (eg, venous lake) from melanocytic neoplasms. A venous lake observed under the dermatoscope has a homogenous reddish-blue to reddish-black color and no pigment network structures.
A biopsy is indicated if the diagnosis of venous lakes remains in doubt.
Procedures
Punch or shave biopsy can be used to obtain a specimen from the venous lake for pathologic confirmation of diagnosis.
Histologic Findings
In venous lakes, a single large dilated space or several interconnecting dilated spaces characteristically are observed in the superficial dermis. The dilated channels have very thin walls that are lined by a single layer of flattened endothelium and supported by a thin layer of fibrous connective tissue.
Usually, no smooth muscle or elastic tissue is found in the vessel wall. In rare cases, a thin and noncircumferential area suggestive of smooth muscle can be found instead of the fibrous tissue. Solar elastosis and other evidence of sun damage usually are found in the adjacent dermis.
Medical Care
Venous lakes are nonproliferative vascular lesions that are not treatable via medical means.
Surgical Care
Surgical biopsy or excision can be useful for confirmation of the diagnosis or for venous lake removal. Treatment usually is performed for cosmetic reasons or to alleviate recurrent bleeding.
Surgical treatment by cryosurgery, electrosurgery, sclerotherapy, and excision have all been reported to be successful forms of therapy for venous lakes.[2, 3, 4, 5, 6] Although all of these approaches are economical, multiple treatments may be necessary. Treatment of venous lakes may be complicated by prolonged bleeding, swelling, pain, textural changes in treated areas, and scarring.
The use of the argon laser and infrared coagulator has required up to 10-14 days for resolution of crusting and eschar formation. A tendency for scar formation with these therapies has been reported in the literature.[7]
Using the theory of selective photothermolysis, dermatologic laser surgeons have effectively used visible-light lasers such as the flashlamp pulsed dye laser at carefully chosen wavelengths, pulse durations, and doses to selectively destroy blood vessels, minimizing injury to the surrounding healthy skin. Numerous treatments may be necessary with this laser to clear the venous lake. Although scarring does not appear to be common with this laser, bleeding may occur after venous lake treatment.[8]
Other visible-light lasers include the quasicontinuous wave lasers, such as copper vapor, krypton, and potassium-titanyl-phosphate (KTP) lasers.[9, 10, 11, 12, 13] These lasers carry a slightly higher risk of scarring compared with the pulsed dye laser.
One study reported a series of 34 patients responding well to long-pulsed Nd:YAG laser, with 94% of the lesions clearing completely with one treatment and no complications reported.[14, 15] The high rate of success is attributed to the deep-penetrating 1064-nm wavelength and the longer pulse widths, which damage larger vascular structures. Authors of a recent review article stated in their experience between pulsed dye laser, intense pulsed light, and Nd:YAG, the long-pulsed Nd:YAG laser was "superior to achieve fast and safe results."[16]
A single case report describes intense pulse light source treatment with a cool thermocoupling gel to protect the epidermis. This approach has been efficacious and, similar to the visible-light lasers, requires no anesthesia. No purpura or crusting and no visible scarring were observed at 1-month follow-up visits.[17] Because only one case report has been published, more studies are needed prior to making conclusions about the effectiveness of this modality for venous lakes.
Vaporization with infrared lasers (eg, carbon dioxide laser) has been effective. One study reported that on average, only one session was needed to treat venous lakes, and the postoperative crusting resolved after 7-10 days.[18] Unlike visible-light lasers, local anesthesia is needed when venous lakes are treated with a carbon dioxide laser. Scarring, including pigmentary and textural changes, is thought to be more likely with carbon dioxide lasers compared with visible-light lasers.
An 810-nm diode laser was used on two patients in one study.[19] Both patients needed two treatments for clearance, and no atrophy or scarring was noted after treatments.
Multiwavelength laser therapy (595-nm pulsed-dye and 1064-nm Nd:YAG) have been tried with some success since the combination of lasers helps reduce pulse duration and fluence.[20] However, the studies have been small and more are needed.
With continuing advances in the technology of new lasers and intense pulsed light sources, excellent results with reduced costs, minimal pain, minimal postoperative care, and scarring will be available to an increasing patient population.
Consultations
Consultation with a dermatologist is usually appropriate for confirmation of the clinical diagnosis of venous lakes.
Diet
Diet is not relevant to the development of venous lakes.
Medication Summary
Drugs cannot be used to ameliorate or remove venous lakes.
Author
Claudia Hernandez, MD, FAAD, Associate Professor, Director of Dermatological and Clinical Studies, Department of Dermatology, University of Illinois at Chicago College of Medicine; Attending Physician, University of Illinois at Chicago Hospital
Disclosure: Nothing to disclose.
Specialty Editors
Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Disclosure: Nothing to disclose.
Rosalie Elenitsas, MD, Herman Beerman Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System
Disclosure: Received royalty from Lippincott Williams Wilkins for textbook editor.
Chief Editor
Dirk M Elston, MD, Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine
Disclosure: Nothing to disclose.
Additional Contributors
Timothy McCalmont, MD, Director, UCSF Dermatopathology Service, Professor of Clinical Pathology and Dermatology, Departments of Pathology and Dermatology, University of California at San Francisco; Editor-in-Chief, Journal of Cutaneous Pathology
Disclosure: Received consulting fee from Apsara for independent contractor.
Acknowledgements
The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors, Jining Wang, MD, and Kim Wang, MD, to the development and writing of this article.
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