Image 1: Multiple cherry hemangiomas on the upper trunk.

Causes

Little is known about the factors that contribute to the formation of cherry hemangiomas. Most cases are idiopathic associated with aging. The gradual appearance of multiple cherry angiomas over many years is common and often is expected. Other causes include chemical exposure (mustard gas, 2-Butoxyethanol) and hormomal changes (pregnancy, increased prolactin). For multiple cherry hemangiomas that have appeared over a short period, an internal malignancy should be excluded.

History and Physical

Cherry angiomas typically present in the third or fourth decades of life, and early lesions may appear as small red macules. Lesions may be found on all body sites, but usually, the mucous membranes are spared. Most patients report an increase in number and size of individual lesions with advancing age. On physical examination, lesions may have a variable appearance, ranging from a small red macule to a larger dome-topped or polypoid papule. The color of the lesions typically is described as bright cherry red, but the lesions may appear more violaceous at times. Rarely, a lesion demonstrates a dark brown to an almost black color when a hemorrhagic plug occupies the vascular lumen, often raising concern about the possibility of a malignant melanoma.

Image 2: Various colors and shapes of cherry hemangiomas

Diagnosis

The diagnosis is usually made clinically; however, biopsy allows histopathologic confirmation in doubtful situations. A skin biopsy (shave or punch) allows histologic confirmation of the diagnosis. On scanning magnification, a sharply circumscribed vascular proliferation usually is noted, often embraced in part by a collarette of epithelium and adnexal structures. Higher magnification demonstrates numerous venules in a thickened papillary dermis. Older lesions often display prominent collagen bundles, which is an appearance suggesting septa. Rarely, some confusion may arise in determining whether a deeply violaceous or a darkly pigmented papule represents a traumatized and thrombosed cherry angioma or malignant melanoma. In any situation in which doubt exists regarding the diagnosis of a cutaneous neoplasm, a skin biopsy needs to be performed for the histopathologic analysis.

Image 3: histologic appearance of cherry hemangioma.

Treatment

Treatment for cherry hemangioma lesions is recommended in situations of irritation or hemorrhage or in instances in which the lesions are deemed by the patient to be cosmetically undesirable.

• Shave excision: This procedure allows delicate removal of the lesion by blade and histologic confirmation of the diagnosis. Hemostasis following removal may be obtained by chemical means (aluminum chloride) or by performing electrocautery.
• Curettage and electrodesiccation: These techniques permit reliable elimination of the lesion through tissue destruction. The risk of scarring usually is minimal when the technique is performed by a skilled operator.
• Pulsed dye laser - using an intense beam of light to remove the angioma. The use of a pulsed dye laser with a green light source allows selective absorption of the laser energy by the hemoglobin contained within the red blood cells and subsequent obliteration of the vascular lumen.This technique involves minimal harm to surrounding skin tissue. Unless the lesion is particularly large (1/4 inch across or more), you can expect excellent cosmetic results.

Cherry Hemangioma Images

References

1. Pembroke AC, Grice K, Levantine AV, Warin AP. Eruptive angiomata in malignant disease. Clin Exp Dermatol. Jun 1978;3(2):147-56.
2. Dawn G, Gupta G. Comparison of potassium titanyl phosphate vascular laser and hyfrecator in the treatment of vascular spiders and cherry angiomas. Clin Exp Dermatol. Nov 2003;28(6):581-3.
3. Gupta G, Bilsland D. A prospective study of the impact of laser treatment on vascular lesions. Br J Dermatol. Aug 2000;143(2):356-9.
4. Calonje E, Wilson-Jones E. Vascular tumors: tumors and tumor-like conditions of blood vessels and lymphatics. In: Elder D, Elenitsas R, Jaworsky C, Johnson B Jr, eds. Lever’s Histopathology of the Skin. 8th ed. Philadelphia, Pa: Lippincott-Raven; 1997:902.
5. Hagiwara K, Khaskhely NM, Uezato H, Nonaka S. Mast cell "densities" in vascular proliferations: a preliminary study of pyogenic granuloma, portwine stain, cavernous hemangioma, cherry angioma, Kaposi’s sarcoma, and malignant hemangioendothelioma. J Dermatol. Sep 1999;26(9):577-86.
6. Mazereeuw-Hautier J, Cambon L, Bonafé JL. [Eruptive pseudoangiomatosis in an adult renal transplant recipient]. Ann Dermatol Venereol. Jan 2001;128(1):55-6.
7. Odom RB, James WD, Berger TB. Dermal and subcutaneous tumors: cherry angiomas. In: Andrew’s Diseases of the Skin: Clinical Dermatology. 2000. 9th ed. Philadelphia, Pa: WB Saunders; 2000:751.
8. Sanchez JL, Ackerman AB. Vascular proliferations of skin and subcutaneous tissue. In: Fitzpatrick’s Dermatology in General Medicine. Vol 1. New York, NY: McGraw-Hill; 1993:1219-20.

Mechanism of Action

Digoxin binds to a site on the extracellular aspect of the ?-subunit of the Na⁺/K⁺ ATPase pump in the membranes of heart cells (myocytes) and decreases its function. This causes an increase in the level of sodium ions in the myocytes and corresponding decreased extracellular Na⁺ levels, which in turn slows down the extrusion of Ca²⁺ by the Sodium-calcium exchanger that relies on the high Na⁺ gradient.

This effect causes an increase in the length of Phase 4 and Phase 0 of the cardiac action potential, which when combined with the effects of Digoxin on the parasympathetic nervous system, lead to a decrease in heart rate.

Increased amounts of Ca²⁺ are then stored in the sarcoplasmic reticulum and released by each action potential, which is unchanged by digoxin. This leads to increased contractility of the heart.

Digoxin also increases vagal activity via its action on the central nervous system, thus decreasing the conduction of electrical impulses through the AV node. This is important for its clinical use in different arrhythmias

Adverse Effects

The occurrence of adverse drug reactions is common, owing to its narrow therapeutic index (the margin between effectiveness and toxicity). Adverse effects are concentration-dependent, and are rare when plasma digoxin concentration is <0.8 ?g/L. They are also more common in patients with low potassium levels (hypokalemia), since digoxin normally competes with K⁺ ions for the same binding site on the Na⁺/K⁺ ATPase pump.

Common adverse effects include: loss of appetite, nausea, vomiting, diarrhea, blurred vision, visual disturbances (yellow-green halos), confusion, drowsiness, dizziness, nightmares, agitation, and/or depression, as well as a higher acute sense of sensual activities. Less frequent adverse effects include: acute psychosis, delirium, amnesia, shortened QRS complex, atrial or ventricular extrasystoles, paroxysmal atrial tachycardia with AV block, ventricular tachycardia or fibrillation, heart block but when systematically sought, the evidence for this is equivocal. The pharmacological actions of digoxin usually results in electrocardiogram (ECG) changes, including ST depression or T wave inversion, which do not indicate toxicity. PR interval prolongation, however, may be a sign of digoxin toxicity. Additionally, increased intracellular Ca²⁺ may cause a type of arrhythmia called bigeminy (coupled beats), eventually ventricular tachycardia or fibrillation. The combination of increased (atrial) arrhythmogenesis and inhibited atrio-ventricular conduction (for example paroxysmal atrial tachycardia with A-V block - so-called “PAT with block”) is said to be pathognomonic (i.e. diagnostic) of digoxin toxicity.

An often described but rarely seen adverse effect of digoxin is a disturbance of colour vision (mostly yellow and green colour) called xanthopsia. It has been proposed that the painter Vincent Van Gogh’s “Yellow Period” may have somehow been influenced by concurrent digitalis therapy.