eMedicine Specialties > Dermatology > Diseases of the Vessels

Actinic Purpura

Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology, Professor of Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Vinay Arya, MD, Staff Physician, Department of Psychiatry and Behavioral Sciences, Johns Hopkins Medicine; George Kihiczak, MD, Clinical Associate Professor, Department of Dermatology, New Jersey Medical School and University Hospital

Updated: May 12, 2008

Introduction

Background

Actinic purpura is a benign clinical entity resulting from sun-induced damage to the connective tissue of the dermis. Actinic purpura is characterized by ecchymoses on the extensor surfaces of the forearms and the dorsa of the hands that usually last 1-3 weeks.

Bateman¹ first described the condition in 1818 when he noted dark purple blotches and determined that they were due to the extravasation of blood into the dermal tissue. Hence, it is sometimes called Bateman purpura.

It is common in elderly individuals and usually occurs after unrecognized minor trauma to the respective areas.

Clinical aspects of dermatoporosis include morphological markers of fragility, such as senile purpura, stellate pseudoscars, and skin atrophy.² The concept of the syndrome term dermatoporosis has been used to compare it to osteoporosis, implying both should be prevented and treated to avoid complications.

Pathophysiology

The purple macules and patches of this condition occur because red blood cells leak into the dermal tissue. This extravasation is secondary to the fragility of the blood vessel walls caused by ultraviolet radiation–induced dermal tissue atrophy. This atrophy renders the skin and microvasculature more susceptible to the effects of minor trauma and shearing forces. The insult to the skin is typically so minor that isolating it as a cause of the ecchymoses can be difficult.

Notably, no inflammatory component is found in the dermal tissue. The absence of a phagocytic response to the extravascular blood has been postulated to be responsible for delaying resorption for as long as 3 weeks.

Actinic purpura may be, along with osteoporosis, a sign of collagen loss in skin and bone.³ This causal loss of skin collagen has been confirmed when collagen was expressed absolutely, instead of as a percentage or ratio. That is, women have less collagen than men and it decreases by 1% a year in exposed and unexposed skin. These changes in skin collagen may correspond to changes in bone density. The hypothesis is that the changes in skin collagen also occur in bone collagen, leading to the associated changes in bone density.

Frequency

United States

Actinic purpura is an extremely common finding in elderly individuals, occurring in approximately 11.9% of those older than 50 years. Its prevalence markedly increases with years of exposure to the sun.

International

Data are not available.

Mortality/Morbidity

The ecchymoses may be cosmetically distressing and may leave dyspigmentation or scarring, but the lesions are not associated with any serious complications.

Race

The effects of chronic sun exposure with the resultant ultraviolet radiation–induced skin changes occur more often and are more pronounced in fair-skinned individuals than in others.

Sex

Both sexes are equally affected.

Age

Actinic purpura occurs almost exclusively in the elderly population, though it may sporadically occur in younger people. The incidence varies with respect to age. Approximately 2% of those aged 60-70 years and as many as 25% of those aged 90-100 years can have the purpuric lesions.

Clinical

History

Patients may report the appearance of purple blotches or bruises on their forearms, hands, face, or neck.
The macules are not associated with pain or pruritus.
Constitutional symptoms (eg, fever, malaise, weight loss) are absent.
The patient may report a history of the lesions resolving and then subsequently reappearing. Residual brown pigmentation may appear after the purpuric macules resolve.
Individual lesions usually last 1-3 weeks, and they do not undergo the color changes that occur with other types of purpuric lesions.
Patients are typically unaware of any external trauma that may have been responsible for the ecchymoses.
Individuals may report a history of chronic sun exposure to skin sites where lesions are present.
Individuals with actinic purpura are often taking blood-thinning medications such as aspirin or warfarin, which can aggravate the condition.

Physical

Purpuric patches and macules larger than 3 mm in diameter are usually present on the extensor surfaces of the forearms and on the dorsa of the hands; the lesions do not extend onto the fingers.
- Ecchymoses may also be found on the neck and face.
- Macules and patches are dark purple and irregularly shaped.
- A sharp margin is seen between the borders of the lesions and the surrounding skin.
Some macules are more deeply colored than others because the duration of the lesions varies. The color changes that are typically associated with purpura or ecchymoses due to other causes do not occur, although residual brown pigmentation may persist.
Lesions of actinic purpura occur in areas of atrophic and inelastic photodamaged skin.
- Other signs of dermatoheliosis often present include leathered wrinkling, stellate pseudoscars, and a sallow yellow hue to the skin.
- Lentigines and scars may be present.
- The skin may appear darker secondary to hyperpigmentation due to hemosiderosis.

Causes

Chronic sun exposure leads to skin changes that predispose patients to actinic purpura.
Because of the ultraviolet-induced atrophy, the connective tissue of the dermis is no longer able to adequately support the microvasculature.
As a result, even minor trauma can tear the blood vessels, leading to the extravasation of blood.

Differential Diagnoses

Amyloidosis, Primary Systemic
Pseudoxanthoma Elasticum

Workup

Laboratory Studies

The diagnosis of actinic purpura is usually obvious at clinical examination. Laboratory investigation is not required unless the diagnosis is not readily apparent.
Findings of the following tests are in the reference ranges:
- Complete blood cell count
- Coagulation studies
- Platelet count determination
- Liver function studies
- Urinalysis
- Stool guaiac test

Histologic Findings

Biopsy reveals a thinned epidermis with many abnormal keratinocytes in a disorderly pattern. The upper dermis contains extravasated red blood cells and hemosiderin without evidence of inflammatory cells. At histologic evaluation, solar elastosis can be appreciated in the surrounding skin as faintly blue homogenized elastotic material lying just below a layer of normal connective tissue at the base of the epidermis. The amount of abnormal elastic fibers is markedly increased, and the amount of collagen is decreased.

Treatment

Medical Care

Actinic purpura does not require extensive medical care.
- To prevent further ultraviolet-induced damage to the skin, sunscreens that provide both UV-A and UV-B protection should be applied daily, especially to areas affected by the purpuric lesions.
- Patients should also use barrier protection (eg, clothing).
- Inform patients that sunscreens help prevent but do not reverse the photodamage.
Tretinoin has been observed to reverse many changes that occur with photodamage.
- The use of tretinoin may be beneficial in actinic purpura because photodamage is ultimately responsible for this disorder.
- Tretinoin increases the amount of dermal collagen and decreases the amount of abnormal elastin when applied topically. However, to the authors' knowledge, no results demonstrate that actinic purpura lesions improve with the topical application of tretinoin.

Activity

Advise patients with actinic purpura to limit their sun exposure by applying sunscreen daily or by avoiding sun exposure altogether.
Instruct patients to minimize any trauma to the skin where the purpuric lesions are present.

Follow-up

Inpatient & Outpatient Medications

Recommend the use of sunscreens that provide both UV-A and UV-B protection.

Deterrence/Prevention

Actinic purpura can be prevented by using lifelong sun protection.
Advise patients to adhere to the following precautions, starting at the earliest possible age.
- Avoid sun exposure when the most damaging rays are present (ie, from 10 am to 3 pm).
- Wear clothing at all times while outdoors to serve as barrier protection from the sun's UV rays.
- Apply sunscreens that protect against UV-A and UV-B radiation daily, especially to areas of the skin that are not covered by barrier protection.

Complications

Actinic purpura is a benign condition and does not have serious complications.
The lesions may be emotionally distressing to patients because of the cosmetic disfigurement of the skin.

Prognosis

Individual lesions of actinic purpura generally resolve within 1-3 weeks.
Residual hemosiderosis may occur. Purpuric lesions usually continue to occur during the individual's life.

Patient Education

Reassure the patient that this condition is benign.
Emphasize the absolute necessity of using sunscreen and barrier protection to prevent further photodamage.
Inform patients that sunscreens do not reverse photodamage.
Instruct patients to minimize any trauma to the skin where the purpuric lesions are present.

Miscellaneous

Medicolegal Pitfalls

The clinical sign of purpura is not necessarily benign.
- Although actinic purpura does not have serious sequelae, other causes of purpura can be serious.
- An incorrect diagnosis as to the etiology of purpuric lesions can be medically and legally disastrous.

References

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Keywords

Bateman actinic purpura, solar purpura, senile purpura, ultraviolet radiation–induced skin changes, chronic sun exposure

Contributor Information and Disclosures

Author

Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology, Professor of Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi
Disclosure: Nothing to disclose.

Coauthor(s)

Vinay Arya, MD, Staff Physician, Department of Psychiatry and Behavioral Sciences, Johns Hopkins Medicine
Vinay Arya, MD is a member of the following medical societies: Sigma Xi
Disclosure: Nothing to disclose.

George Kihiczak, MD, Clinical Associate Professor, Department of Dermatology, New Jersey Medical School and University Hospital
George Kihiczak, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, and Medical Society of New Jersey
Disclosure: Nothing to disclose.

Medical Editor

Julie R Kenner, MD, PhD, Consultant, Clinical Research, Medical Affairs, VaxGen, Inc; Private Practice, Kenner Dermatology Center
Julie R Kenner, MD, PhD is a member of the following medical societies: American Academy of Dermatology and American Society of Tropical Medicine and Hygiene
Disclosure: Nothing to disclose.

Pharmacy Editor

David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Director, Division of Dermatology, Scott and White Clinic; Director Dermatology Residency Training Program, Scott and White Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: 3M Pharmaceutical Grant/research funds Other; Graceway Pharmaceuticals Grant/research funds Other

Managing Editor

Jeffrey J Miller, MD, Associate Professor, Department of Dermatology, Penn State University, Milton S Hershey Medical Center
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System
William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology
Disclosure: elsevier Royalty Other; american college of physicians Honoraria Other

Further Reading