| Telangiectasia |
| Classification and external resources |
|
| ICD-10 |
G11.3, I78.0, M34.1 |
| ICD-9 |
362.15, 448.0 |
| DiseasesDB |
27395 |
| MedlinePlus |
003284 |
| MeSH |
D013684 |
Telangiectasias // or angioectasias (also known as spider veins) are small dilated blood vessels[1] near the surface of the skin or mucous membranes, measuring between 0.5 and 1 millimeter in diameter.[2] They can develop anywhere on the body but are commonly seen on the face around the nose, cheeks, and chin. They can also develop on the legs, specifically on the upper thigh, below the knee joint, and around the ankles. Many patients who suffer with spider veins seek the assistance of physicians who specialize in vein care or peripheral vascular disease. These physicians are called phlebologists or interventional radiologists.
Some telangiectasia are due to developmental abnormalities that can closely mimic the behaviour of benign vascular neoplasms. They may be composed of abnormal aggregations of arterioles, capillaries, or venules. Because telangiectasias are vascular lesions, they blanch when tested with diascopy.
Telangiectasia is a component of the CREST variant of scleroderma (CREST is an acronym that stands for calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia.)
Contents
- 1 Causes
- 1.1 Congenital causes
- 1.2 Acquired causes
- 1.2.1 Venous hypertension
- 1.2.2 Other acquired causes
- 2 Treatment
- 3 References
- 4 External links
Causes[edit]
The causes of telangiectasia can be divided into congenital and acquired factors.
Congenital causes[edit]
Goldman states that "numerous inherited or congenital conditions display cutaneous telangiectasia".[2] These include:
- Naevus flammeus (port-wine stain)
- Klippel-Trenaunay syndrome
- Maffucci's syndrome (multiple endochondromas & hemangiomas)
- Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)
- Ataxia-telangiectasia
- Sturge-Weber syndrome, a nevus formation in the skin supplied by the trigeminal nerve and associated with facial port-wine stains, glaucoma, meningeal angiomas and mental retardation.
Acquired causes[edit]
Venous hypertension[edit]
Telangiectasia in the legs is often related to the presence of venous hypertension within underlying varicose veins. Flow abnormalities within the medium sized veins of the leg (reticular veins) can also lead to the development of telangiectasia. Factors that predispose to the development of varicose and telangiectatic leg veins include
- Age: The development of spider veins may occur at any age but usually occurs between 18 and 35 years, and peaks between 50 and 60 years.[citation needed]
- Gender: Females are affected approximately four to one to males.[citation needed]
- Pregnancy: Pregnancy is a key factor contributing to the formation of varicose and spider veins. The most important factor is circulating hormones that weaken vein walls. There's also a significant increase in the blood volume during pregnancy, which tends to distend veins, causing valve dysfunction which leads to blood pooling in the veins. Moreover, later in pregnancy, the enlarged uterus can compress veins, causing higher vein pressure leading to dilated veins. Varicose veins that form during pregnancy may spontaneously improve or even disappear a few months after delivery.[citation needed]
- Lifestyle/Occupation: Those who are involved with prolonged sitting or standing in their daily activities have an increased risk of developing varicose veins. The weight of the blood continuously pressing against the closed valves causes them to fail, leading to vein distention.[citation needed]
Other acquired causes[edit]
Acquired telangiectasia, not related to other venous abnormalities, for example on the face and trunk, can be caused by factors such as
- Acne rosacea
- Environmental damage such as that caused by sun or cold exposure
- Trauma to skin such as contusions or surgical incisions.
- Radiation exposure such as that experienced during radiotherapy for the treatment of cancer
- Chemotherapy
- Carcinoid syndrome
- Limited systemic sclerosis/scleroderma (a Scleroderma sub-type)
- Chronic treatment with topical corticosteroids may lead to telangiectasia.[3]
- Spider angiomas are a radial array of tiny arterioles that commonly occur in pregnant women and in patients with hepatic cirrhosis and are associated with palmar erythema. In men, they are related to high estrogen levels secondary to liver disease.
- Tempi syndrome
Treatment[edit]
Sclerotherapy is the "gold standard" and is preferred over laser for eliminating telangiectasiae and smaller varicose leg veins.[4] A sclerosant medication is injected into the diseased vein so it hardens and eventually shrinks away. Recent evidence with foam sclerotherapy shows that the foam containing the irritating sclerosant quickly appears in the patient's heart and lungs, and then in some cases travels through a patent foramen ovale to the brain.[5] This has led to concerns about the safety of sclerotherapy for telangectasias and spider veins. In some cases stroke and transient ischemic attacks have occurred after sclerotherapy.[6] Varicose veins Varicose and reticular veins are often treated before treating telangiectasia. Although treatment of these larger veins in advance of sclerotherapy for telangiectasia may not guarantee better results.[7][8][9] Varicose veins can be treated with foam sclerotherapy, endovenous laser treatment, radiofrequency ablation or open surgery. The biggest risk, however, seems to occur with sclerotherapy, especially in terms of systemic risk of DVT, pulmonary embolism, and stroke.
Another issue that arises with the use of sclerotherapy to treat spider veins is staining, shadowing, telangetatic matting and ulceration. In addition, incompleteness of therapy is common, requiring multiple treatment sessions.
Telangiectasias on the face are often treated with a laser. Laser therapy uses a light beam that is pulsed onto the veins in order to seal them off, causing them to dissolve. These light-based treatments require adequate heating of the veins. These treatments can result in the destruction of sweat glands, and the risk increases with the number of treatments.
References[edit]
- ^
‹ The template below (DorlandsDict) is being considered for deletion. See templates for discussion to help reach a consensus.›
"telangiectasia" at Dorland's Medical Dictionary
- ^ a b Goldman, Mitchel P (1995). Sclerotherapy treatment of varicose and telangiectatic leg veins (2nd ed.). St. Louis: Mosby. ISBN 0-8151-4011-8.
- ^ Johnson BA, Nunley JR (May 2000). "Treatment of seborrheic dermatitis". Am Fam Physician 61 (9): 2703–10, 2713–4. PMID 10821151.
- ^ Sadick N, Sorhaindo L (2007). "16. Laser Treatment of Telangiectatic and Reticular Veins". In Bergan, John J. The Vein Book. Amsterdam: Elsevier Academic Press. p. 157. ISBN 0-12-369515-5.
- ^ Ceulen RP, Sommer A, Vernooy K (April 2008). "Microembolism during foam sclerotherapy of varicose veins". N. Engl. J. Med. 358 (14): 1525–6. doi:10.1056/NEJMc0707265. PMID 18385510.
- ^ Forlee MV, Grouden M, Moore DJ, Shanik G (January 2006). "Stroke after varicose vein foam injection sclerotherapy". J. Vasc. Surg. 43 (1): 162–4. doi:10.1016/j.jvs.2005.09.032. PMID 16414404.
- ^ Duffy DM Sclerotherapy for Telangiectasia – The impact of small changes in vessel size on treatment outcomes. Cosmetic Dermatology March 2012. Vol. 25, No. 3.
- ^ Treatment of Leg Veins. Procedures in Cosmetic Dermatology Series. Editors Murad Alam, Sirunya Silapunt. Second Edition Saunders Elsevier Inc. 2011
- ^ Schuller-Petrovic S, Pavlovic MD, Schuller S, Schuller-Lukic B, Adamic M. Telangiectasias resistant to sclerotherapy are commonly connected to a perforating vessel. Phlebology. 2013;28(6):320-3.
External links[edit]
- "Varicose Veins and Spider Veins - FAQs". Womenshealth.gov. December 2005. Archived from the original on 6 Oct 2008.
- "Varicose veins and spider veins fact sheet". Womenshealth.gov. 2 June 2010.
- Cardiovascular disease: vascular disease
- Circulatory system pathology
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|
Arteries, arterioles
and capillaries |
|
Inflammation
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- Arteritis
- Buerger's disease
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Arterial occlusive disease /
peripheral vascular disease
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Arteriosclerosis
|
- Atherosclerosis
- Foam cell
- Fatty streak
- Atheroma
- Intermittent claudication
- Monckeberg's arteriosclerosis
- Arteriolosclerosis
- Hyaline
- Hyperplastic
- Cholesterol
- LDL
- Oxycholesterol
- Trans fat
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Stenosis
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- Carotid artery stenosis
- Renal artery stenosis
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Other
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- Aortoiliac occlusive disease
- Degos disease
- Erythromelalgia
- Fibromuscular dysplasia
- Raynaud's phenomenon
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Aneurysm / dissection /
pseudoaneurysm
|
- torso: Aortic aneurysm
- Abdominal aortic aneurysm
- Thoracic aortic aneurysm
- Aortic dissection
- Coronary artery aneurysm
- head / neck
- Intracranial aneurysm
- Intracranial berry aneurysm
- Carotid artery dissection
- Vertebral artery dissection
- Familial aortic dissection
|
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Vascular malformation
|
- Arteriovenous fistula
- Arteriovenous malformation
- Telangiectasia
- Hereditary hemorrhagic telangiectasia
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Vascular nevus
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- Cherry hemangioma
- Halo nevus
- Spider angioma
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| Veins |
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Inflammation
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Venous thrombosis /
Thrombophlebitis
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- primarily lower limb
- abdomen
- Hepatic veno-occlusive disease
- Budd–Chiari syndrome
- May–Thurner syndrome
- Portal vein thrombosis
- Renal vein thrombosis
- upper limb / torso
- Mondor's disease
- Paget–Schroetter disease
- head
- Cerebral venous sinus thrombosis
- Post-thrombotic syndrome
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Varicose veins
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- Gastric varices
- Portacaval anastomosis
- Caput medusae
- Esophageal varices
- Hemorrhoid
- Varicocele
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Other
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- Chronic venous insufficiency
- Chronic cerebrospinal venous insufficiency
- Superior vena cava syndrome
- Inferior vena cava syndrome
- Venous ulcer
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| Arteries or veins |
- Angiopathy
- Macroangiopathy
- Microangiopathy
- Embolism
- Pulmonary embolism
- Cholesterol embolism
- Paradoxical embolism
- Thrombosis
- Vasculitis
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| Blood pressure |
|
Hypertension
|
- Hypertensive heart disease
- Hypertensive emergency
- Hypertensive nephropathy
- Essential hypertension
- Secondary hypertension
- Renovascular hypertension
- Benign hypertension
- Pulmonary hypertension
- Systolic hypertension
- White coat hypertension
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Hypotension
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anat (a:h/u/t/a/l,v:h/u/t/a/l)/phys/devp/cell/prot
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noco/syva/cong/lyvd/tumr, sysi/epon, injr
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proc, drug (C2s+n/3/4/5/7/8/9)
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Clinical and histological nomenclature for skin lesions
|
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| Macroscopic |
| Primary lesions |
- flat
- elevated
- fluid
- Ulcer
- Erosion
- Telangiectasia
- Special initial lesions : Burrow
- Comedone
- Scutulum
- Target lesion
- Herald patch
- Wheal
|
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| Secondary lesions |
- Scale
- Crust
- Lichenification
- Excoriation
- Induration
- Atrophy
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| Microscopic |
- keratin: Hyperkeratosis
- Parakeratosis
- Dyskeratosis
- Hypergranulosis
- Acanthosis
- Papillomatosis
- Acantholysis
- Spongiosis
- Hydropic swelling
- Exocytosis
- Vacuolization
- Erosion
- Ulceration
- Lentiginous
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