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Wound healing is a complex and energy-demanding process. The relationship between nutrition and wound healing has been recognized for many centuries. Several studies have indicated that nutritional deficiencies are more prevalent among patients with chronic wounds. Malnutrition may alter the inflammatory response, collagen synthesis, and wound tensile strength, all of which are crucial for wound healing. Although the specific role of nutrition and supplementation in wound care remains uncertain, it is necessary to identify and correct nutritional imbalances to avoid any potential deterioration of the healing process. It is also important to recognize the differences in pathophysiology between acute and chronic wounds. A burn, surgical, or a traumatic wound is different from a diabetic foot ulcer, which is different from a pressure ulcer. Chronic wounds are more prevalent in the aging population, and patients often have underlying comorbidities, such as diabetes mellitus, peripheral vascular disease, connective tissue disease, or other systemic illnesses that may alter energy metabolism and contribute to impaired healing. Management approaches to acute wound care may not apply universally to chronic wounds. In this review, we discuss the available data and possible roles for nutrition in wound healing.

In this Part 1 of a 2-part continuing medical education series, we review the epidemiology and pathophysiology of cardiovascular disease, its association with cutaneous symptoms, and the diagnosis and evaluation of cutaneous features of cardiovascular syndromes, including infective endocarditis, acute rheumatic fever, Kawasaki disease, cholesterol embolization syndrome, lipid disorders, cardiac amyloidosis, and cardiac myxomas. As the incidence and prevalence of cardiovascular disease increases, dermatologists have an essential role in recognizing cutaneous manifestations of cardiovascular diseases in order to appropriately connect patients with follow up care.

Prevention has been a primary goal of pressure ulcer research. Despite such efforts, pressure ulcers remain common in hospitals and in the community. Moreover, pressure ulcers often become chronic wounds that are difficult to treat and that tend to recur after healing. Especially given these challenges, dermatologists should have the knowledge and skills to implement pressure ulcer prevention strategies and to effectively treat pressure ulcers in their patients. This continuing medical education article focuses on pressure ulcer prevention and management, with an emphasis on the evidence for commonly accepted practices.

In this Part 2 of a 2-part continuing medical education series, we review the epidemiology of peripheral vascular disease, its association with cutaneous symptoms, and the diagnosis and evaluation of cutaneous features of vascular disorders. As peripheral vascular disease becomes more prevalent globally, it is essential for dermatologists to become competent at accurately recognizing and diagnosing cutaneous manifestations and directing individuals to receive appropriate care and treatment.

Lymphedema is a localized form of tissue swelling resulting from excessive retention of lymphatic fluid in the interstitial compartment. It is caused by impaired lymphatic drainage. Lymphedema is a chronic progressive disease with serious physical and psychosocial implications. It can be challenging to diagnose, especially in obese patients and in those with coexisting venous disease. We performed PubMed and Google Scholar searches of the English-language literature (1966-2017) using the terms lymphedema, lymphedema management, and lymphatic complications. Relevant publications were manually reviewed for additional resources. There are currently no standard guidelines for the diagnosis of lymphedema. There is no cure yet for lymphedema, and the objective for management is to limit disease progression and prevent complications.

Lymphedema is a localized form of tissue swelling resulting from excessive retention of lymphatic fluid in the interstitial compartment and caused by impaired lymphatic drainage. Lymphedema is classified as primary or secondary. Primary lymphedema is caused by developmental lymphatic vascular anomalies. Secondary lymphedema is acquired and arises as a result of an underlying systemic disease, trauma, or surgery. We performed PubMed and Google Scholar searches of the English-language literature (1966-2017) using the terms lymphedema, cancer-related lymphedema, and lymphatic complications. Relevant publications were manually reviewed for additional resources. This progressive chronic disease has serious implications on patients' quality of life. It is often misdiagnosed because it mimics other conditions of extremity swelling. There is no definitive cure for lymphedema. However, with proper diagnosis and management, its progression and potential complications may be limited.

In the United States, chronic ulcers—including decubitus, vascular, inflammatory, and rheumatologic subtypes—affect >6 million people, with increasing numbers anticipated in our growing elderly and diabetic populations. These wounds cause significant morbidity and mortality and lead to significant medical costs. Preventative and treatment measures include disease-specific approaches and the use of moisture retentive dressings and adjunctive topical therapies to promote healing. In this article, we discuss recent advances in wound care technology and current management guidelines for the treatment of wounds and ulcers.

Wounds are an excellent example of how the field of dermatology represents a cross-section of many medical disciplines. For instance, wounds may be caused by trauma, vascular insufficiency, and underlying medical conditions, such as diabetes, hypertension, and rheumatologic and inflammatory disease. This continuing medical education article provides an overview of wound healing and the pathophysiology of chronic wounds and reviews the broad differential diagnosis of chronic wounds. It also describes the initial steps necessary in evaluating a chronic wound and determining its underlying etiology.

Leg ulcerations are a common problem, with an estimated prevalence of 1% to 2% in the adult population. Venous leg ulcers are primarily treated in outpatient settings and often are managed by dermatologists. Recent advances in the diagnosis and treatment of leg ulcers combined with available evidence-based data will provide an update on this topic. A systematized approach and the judicious use of expensive advanced therapeutics are critical. Specialized arterial and venous studies are most commonly noninvasive. The ankle brachial pressure index can be performed with a handheld Doppler unit at the bedside by most clinicians. The vascular laboratory results and duplex Doppler findings are used to identify segmental defects and potential operative candidates. Studies of the venous system can also predict a subset of patients who may benefit from surgery. Successful leg ulcer management requires an interdisciplinary team to make the correct diagnosis, assess the vascular supply, and identify other modifiable factors to optimize healing. The aim of this continuing medical education article is to provide an update on the management of venous leg ulcers. Part I is focused on the approach to venous ulcer diagnostic testing.

Significance: Chronic wounds are a major healthcare burden.The practitioner should have an appropriate understanding of both the etiology of the wound as well as the optimal type of dressings to use. Fundamental wound characteristics may be used to guide the practitioner's choice of dressings. The identification of optimal dressings to use for a particular wound type is an important element in facilitating wound healing. Recent Advances: Researchers have sought to design wound dressings that aim to optimize each stage in the healing process. In addition, dressings have been designed to target and kill infection-causing bacteria, with the incorporation of antimicrobial agents. Critical Issues: Chronic wounds are frequently dynamic in presentation, and the numerous wound dressings available make dressing selection challenging for the practitioner. Choosing the correct dressing decreases time to healing, provides cost-effective care, and improves patient quality of life. Future Directions: Research into the mechanisms of wound healing has enhanced our ability to heal chronic wounds at a faster rate through the use of moisture-retentive dressings. Newer dressings are incorporating the use of nanotechnology by incorporating miniature electrical sensors into the dressing. These dressings are engineered to detect changes in a wound environment and alert the patient or practitioner by altering the color of the dressing or sending a message to a smartphone. Additional investigations are underway that incorporate biologic material such as stem cells into dressings.

Though preventable in most cases, pressure ulcers continue to pose a major burden to the individual and society, affecting ≤3 million adults annually in the United States alone. Despite increased national attention over the past 20 years, the prevalence of pressure ulcers has largely remained unchanged, while the associated costs of care continue to increase. Dermatologists can play a significant role in pressure ulcer prevention by becoming aware of at-risk populations and implementing suitable preventive strategies. Moreover, dermatologists should be able to recognize early changes that occur before skin breakdown and to properly identify and stage pressure ulcers to prevent delay of appropriate care. The aim of the first article in this continuing medical education series is to discuss the pathophysiology, risk factors, epidemiology, social and economic burdens, and clinical presentation of pressure ulcers.

Chronic, nonhealing ulcers are a frustrating therapeutic challenge and investigation of innovative therapies continues to be an important research pursuit. One unique and newly applied intervention is the use of ablative fractional lasers. This technology has recently been employed for the treatment of hypertrophic, disfiguring and function-limiting scars, and was first shown to induce healing of chronic wounds in patients with persistent ulcers and erosions within traumatic scars. Recent reports suggest it may be applicable for other types of chronic wounds as well. The mechanism of action for this modality remains to be elucidated but possible factors include laser-induced collagen remodeling, photomicrodebridement and disruption of biofilms, and induction of a proper wound healing cascade.

PURPOSE: The purpose of this learning activity is to provide information about the etiology and treatment of atrophie blanche. TARGET AUDIENCE: This continuing education activity is intended for physicians and nurses with an interest in skin and wound care. OBJECTIVES: After participating in this educational activity, the participant should be better able to:1. Discuss the pathophysiology of atrophie blanche.2. Explore treatment options for livedoid vasculopathy. ABSTRACT: Atrophie blanche (AB) is a porcelain-white scar that may be seen at the base of a healed ulcer or in association with livedoid vasculopathy (LV). The term AB originally had been used synonymously with LV, whereas LV is a noninflammatory thrombotic condition presenting as either a primary or secondary event (often associated with coagulation).

Wound care dressings have evolved over time, from bandaging to the development of occlusive dressings to negative pressure wound therapy. A novel therapeutic delivery system dressing has been cleared by the United States Food and Drug Administration. This semi occlusive wound dressing has been developed to provide local, continuous delivery of aqueous topical agents, such as therapeutics (anesthetics, antiseptics, antibiotics, steroids, topical beta-blockers, immune modulatory agents, growth factors, and fibrinolytic agents, among others), at a rate of about ¾ mL per day, thus maintaining a hydrated environment and providing topical treatment. This type of system may be beneficial in situations where systemic therapies cannot be used, wounds are small and few, wounds may need frequent application of medication or moisture, or low and steady delivery of medications is needed.The authors assessed a delivery system dressing with different types of liquid medications for the management of hard-to-heal, chronic lower extremity wounds.Patients aged ≥ 18 and ≤ 90 years with stalled chronic wounds30 days' duration were selected for the use of a topical delivery system, which consists of a semi occlusive wound dressing and fluid delivery unit that can provide local application of small therapeutic quantities of medication directly to the wound.Several successful cases with the use of this device are presented in which pain relief, enhancement of epithelial migration, inflammation reduction, bacterial control, and wound size reduction were achieved.This delivery system dressing is an effective and safe treatment option for wounds. Advantages include reduced potential of systemic side effects, flexibility in what can be delivered, constant rate of medication delivery, and convenience.

Cutaneous changes are a common feature of chronic venous insufficiency and include venous eczema and lipodermatosclerosis. This review will address the presumed pathophysiology of these conditions, their clinical findings, and important management strategies.

Lymphedema is a localized form of tissue swelling resulting from excessive retention of lymphatic fluid in the interstitial compartment and caused by impaired lymphatic drainage. Lymphedema is classified as primary or secondary. Primary lymphedema is caused by developmental lymphatic vascular anomalies. Secondary lymphedema is acquired and arises as a result of an underlying systemic disease, trauma, or surgery. We performed PubMed and Google Scholar searches of the English-language literature (1966-2017) using the terms lymphedema, cancer-related lymphedema, and lymphatic complications. Relevant publications were manually reviewed for additional resources. This progressive chronic disease has serious implications on patients' quality of life. It is often misdiagnosed because it mimics other conditions of extremity swelling. There is no definitive cure for lymphedema. However, with proper diagnosis and management, its progression and potential complications may be limited.

Lymphedema is a localized form of tissue swelling resulting from excessive retention of lymphatic fluid in the interstitial compartment. It is caused by impaired lymphatic drainage. Lymphedema is a chronic progressive disease with serious physical and psychosocial implications. It can be challenging to diagnose, especially in obese patients and in those with coexisting venous disease. We performed PubMed and Google Scholar searches of the English-language literature (1966-2017) using the terms lymphedema, lymphedema management, and lymphatic complications. Relevant publications were manually reviewed for additional resources. There are currently no standard guidelines for the diagnosis of lymphedema. There is no cure yet for lymphedema, and the objective for management is to limit disease progression and prevent complications.

Diffuse dermal angiomatosis of the breast (DDAB) is an uncommon ulcerative angiomatosis, which occurs in middle aged women with large pendulous breasts, a history of cigarette smoking, and risk factors for atherosclerosis. Based on its rarity, no well-defined therapeutic regimen has been elucidated. We report a case of DDAB in a woman with no history of smoking or radiographic evidence of occluded vasculature who presented with ulceration and pain-associated breast nodularity. She had a complete reproducible response to oral corticosteroids.

Venous leg ulcers account for approximately 70% of all leg ulcers and affect 2.2 million Americans annually. After a comprehensive patient and wound assessment, compression therapy remains the cornerstone of standard care. Adjuvant care with topical or systemic agents is used for wounds that do not heal within 4 weeks. Once healed, long-term compression therapy with stockings or surgical intervention will reduce the incidence of recurrence. This continuing medical education article aims to outline optimal management for patients with venous leg ulcers, highlighting the role of a multidisciplinary team in delivering high quality care.

The management of acute and chronic wounds has drastically changed within the past 20 years. This update focuses on the most recent recommendations for acute wound care as well as new technologies that are available for chronic wounds.

Treatment of venous leg ulcers (VLU) represents a considerable challenge to the health care professional and to the patient alike. Much of the current literature regarding VLU focuses on either wound pathophysiology and treatment of chronic venous insufficiency or the patients' experience of the condition. We present two studies that examine more closely the clinicians' experience of treating VLU and reflect upon how that understanding may further enhance better outcomes for patients in the future. The first of these studies is a qualitative investigation of 49 clinicians treating VLU in the UK and USA. The second is a quantitative, online survey of 304 clinicians' beliefs, attitudes and practices in the UK, Germany and USA. Findings show that the clinicians' experience of treating VLU is often accompanied by frustration and dissatisfaction with treatment challenges and uncertain outcomes. Practices and treatment choices were found to vary widely and differ by countries. We conclude that a key aspect in improving VLU treatment is in listening to the frustrations of the clinician when considering new approaches to therapy.

Importance Treating posttraumatic lower extremity wounds can be challenging, especially in elderly patients. Recently, the use of fractional carbon dioxide laser has been shown to improve wound healing in scar-related wounds. We used this treatment modality in posttraumatic wounds that were slow to heal in 3 elderly patients. Observations Each wound underwent one fractional carbon dioxide laser treatment. The wound base was treated at 30 mJ and 5% density. The entire wound edge and 1 to 2 cm into the normal surrounding skin were treated at 50 mJ and 5% density. One pass was completed at 150 Hz per treatment. Treatments were well tolerated with only mild discomfort. Each wound healed by 60% or greater within 3 weeks. No adverse events were reported aside from mild and transient erythema at site of treatment. Conclusions and Relevance Fractional carbon dioxide laser treatment appeared to accelerate healing in each of these posttraumatic wounds. It may be a helpful adjunct in nonhealing posttraumatic wounds.

In the United States, chronic ulcers--including decubitus, vascular, inflammatory, and rheumatologic subtypes--affect6 million people, with increasing numbers anticipated in our growing elderly and diabetic populations. These wounds cause significant morbidity and mortality and lead to significant medical costs. Preventative and treatment measures include disease-specific approaches and the use of moisture retentive dressings and adjunctive topical therapies to promote healing. In this article, we discuss recent advances in wound care technology and current management guidelines for the treatment of wounds and ulcers.

A 34-year-old Haitian man presented with a 1-year history of a gradually en- larging, ulcerating nodule on the right posterior ankle that bled after trauma. The patient denied any history of prior trauma at the site of the lesion and foreign travel.There were no HIV risk factors or personal or family history of skin cancer.The patient was otherwise healthy with no additional complaints. Physical examination revealed a 1.4 cm firm, hyperpigmented nodule with a yellow crateriform center on the right posterior ankle (Figure 1).A punch biopsy was performed (Figures 2, 3). Histopathologic examination revealed a superficial and mid-dermal, multi- nodular proliferation of bland epithelioid cells with occasional foci of ductal differentiation embedded in a fibrotic stroma. Focal epidermal connection and mucinous metaplasia were noted. Immunohistochemical stains revealed diffuse positive staining of the lesional cells with cytokeratins (high and low) and variable positivity with epithelial membrane antigen (EMA), as well as negative S100P. Fungal, viral, and mycobacterial tissue cultures were negative and RPR was non-reactive. Bacterial tissue culture was positive for Prevotella oris and Staphylococcus aureus.

Wounds are an excellent example of how the field of dermatology represents a cross-section of many medical disciplines. For instance, wounds may be caused by trauma, vascular insufficiency, and underlying medical conditions, such as diabetes, hypertension, and rheumatologic and inflammatory disease. This continuing medical education article provides an overview of wound healing and the pathophysiology of chronic wounds and reviews the broad differential diagnosis of chronic wounds. It also describes the initial steps necessary in evaluating a chronic wound and determining its underlying etiology.

Both inherited and acquired hypercoagulable states can present with nonspecific clinical manifestations, such as petechiae, purpura, livedo reticularis, and ulcerations. A good history and physical examination are crucial to diagnoses of these conditions. Inherited conditions tend to present either in neonatal period or later in life, while acquired conditions typically occur later in life. Diagnostic studies are performed to identify the coagulation cascade deficiency or defect. Treatment primarily hinges on anticoagulation and wound care. In this article, we provide an in-depth analysis of the clinical manifestations, diagnostic considerations, and management options of patients in hypercoagulable states.

Apligraf® is a bilayered tissue-engineered product consisting of a bovine collagen matrix with neonatal fibroblasts, overlaid by a stratified epithelium containing living keratinocytes. The United States Food and Drug Administration has approved its use for venous leg ulcers and neuropathic diabetic foot ulcers. Apligraf® provides a dermal matrix and produces cytokines similar to the human skin. However, its mechanism of action and ultimate fate in host wounds are unclear. The aim of this study was to evaluate the persistence of Apligraf® fibroblasts and keratinocytes in human acute partial-thickness wounds (split-thickness donor sites) treated with Apligraf®. In an open-label, within-patient, three-centered, controlled pilot study, 10 patients were treated with Apligraf®, Apligraf® dermis only (without epidermis), and a polyurethane film for donor site wounds of the same size, depth, and anatomical location. Apligraf® DNA persistence was the primary outcome measure. Basement membrane components, cosmetic outcome, time to wound healing, and safety parameters were secondary outcome measures. One week after the initial treatment, reverse transcription polymerase chain reaction analysis found that two Apligraf® and two Apligraf® dermis-only-treated sites had Apligraf® DNA present. Four weeks posttreatment, only one Apligraf® and one Apligraf® dermis-only sites showed the presence of Apligraf® DNA. There was no difference between the three treatment modalities in establishing basement membrane in donor site wounds. No differences in other secondary outcomes were found. Apligraf® DNA persisted in a minority of patients at 4 weeks in acute partial-thickness wounds. Apligraf®'s success in speeding healing of acute wounds appears to be related to factors other than the persistence of donor DNA or effect on basement membrane restoration.

A proportion of chronic wounds fail to heal in response to standard therapy. For venous leg ulcers, a correlation exists between longer duration before treatment initiation and poor healing response to compression therapy. Differences identified between the healing wound microenvironment and that of the non healing chronic wound suggests that many potential mechanisms exist to impair healing. One contributory mechanism may be inhibition of fibroblast proliferation and induction of a stress-induced premature senescence phenotype by the continuing inflammation found in chronic wounds. Senescent fibroblasts exhibit an extracellular matrix degradative phenotype that contributes to wound chronicity. Accumulation of greater than 15% senescent fibroblasts has been described as a threshold beyond which wounds become hard to heal. The ratio of senescent : non senescent cells is therefore critical to determining response to treatment, and adjunctive therapies that modulate this ratio in favour of non senescent cells are likely to enhance therapeutic healing rates. A number of tissue-engineered dermal replacements contain non senescent fibroblasts and can donate cells to the wound environment additional to releasing growth factors and reversing the antiproliferative activity of chronic wound exudate. Recognition of the role of fibroblast senescence in wound chronicity may allow for identification of those wounds that will respond positively to these products.

Wound-healing in the skin is a complex orchestration of cellular processes, which has been perfected throughout the eons of phylogeny. It has so many coordinated biologic processes invoked both simultaneously and in a regulated orderly fashion that it has been likened to a recapitulation of gestation. Part of the problem with studying wound healing is in analyzing the processes independently and then seeing how they fit together and influence each other. This article discusses selected and recent scientific observations that have given insight into the biology of human skin wound healing. The article then discusses selected clinical advances that are based less on evidence-based observation and more on what works in practice and promotes wound healing.

A previously healthy 71-year-old Caucasian woman presented with an ulcer on her left leg. She had a 5-month history of bilateral, indurated erythematous, and had purplish nodules and plaques on both lower extremities. One of the plaques on the right leg had ulcerated and healed spontaneously. The present ulceration began as a small opening at an incisional biopsy site. Later, she developed two adjacent ulcers that coalesced into a larger ulcer. She was not taking any medication, and there was no history of exposure to tuberculosis. Examination of the right leg demonstrated two hyperpigmented, indurated plaques, one on the calf and one over the medial malleolus. On the left posterior calf there was another hyperpigmented, indurated plaque with a central area of ulceration measuring 9 × 2 cm. The ulcer bed had a mixture of fibrinous adherent tissue and granulation tissue. (Fig. 1) There was no peripheral edema, varicose veins, nor signs of peripheral neuropathy. Peripheral pulses and capillary refilling were within normal limits. The ankle brachial index was greater than 1.0 bilaterally. Biopsy of a subcutaneous nodule revealed a superficial and deep perivascular lymphocytic infiltrate with an admixture of neutrophils and numerous extravasated red blood cells. Mixed septal and lobular panniculitis consisting of an inflammatory infiltrate of histiocytes, giant cells, and neutrophils was observed. Focal neutrophilic microabscesses in the deep dermis and fibrinoid necrosis of small blood vessels were present in the deep dermis and subcutaneous tissue (Figs 2 and 3). A smear was negative for acid fast bacilli. Figure 1. A hyperpigmented, indurated plaque with a central area of ulceration measuring 9 × 2 cm on the left posterior calf. The ulcer bed has a mixture of fibrinous adherent tissue and granulation tissue Download figure to PowerPoint Figure 2. A scanning magnification Download figure to PowerPoint Figure 3. Mixed septal and lobular panniculitis consisting of an inflammatory infiltrate of histiocytes, giant cells, and neutrophils. Focal neutrophilic microabscesses in the deep dermis and fibrinoid necrosis of small blood vessels in the deep dermis and subcutaneous tissue Download figure to PowerPoint A diagnosis of nodular vasculitis was made. A complete blood count with differential and platelets was within normal limits, tuberculin testing was negative twice, and antineutrophil cytoplasmic antibodies (p-ANCA, c-ANCA) were also negative. Fungal, mycobacterial and bacterial cultures were negative. Chest X-rays were normal. The patient received supersaturated potassium iodide (SSKI) 15 drops per day with good response. With rapid tapering of SSKI, the ulcerations on the lower legs reappeared. Therapy was reinstituted with a more gradual taper. Two years after the initial diagnosis of nodular vasculitis the patient presented with new complaints of increased urinary frequency, increased abdominal girth, and weight gain. The patient was found to be borderline anemic, and a computer tomography scan revealed ascites, a normal liver, a normal uterus, and a soft tissue density in the region of the cecum. After an exploratory laparotomy she was found to have a moderately differentiated mucinous adenocarcinoma of the colon with metastases to periaortic lymph nodes, abdominal wall, and both ovaries. She is currently receiving adjuvant chemotherapy for stage IV colon carcinoma. Only one lesion of nodular vasculitis has remained active, and the patient is continuing treatment with SSKI at a low dose.

BACKGROUND. Recent studies indicate that exogenous estrogens may promote wound healing. Many laser skin resurfacing (LSR) patients use hormone replacement therapy (HRT) or oral contraceptive pills (OCPs). OBJECTIVE. To evaluate the effect of exogenous estrogen on LSR postoperative healing. METHODS. This is a retrospective case control study of 44 female patients who underwent combination CO2/Er:YAG full-face LSR. Sixteen postmenopausal patients using oral HRT during procedure and follow-up were compared with 16 controls. Six premenopausal patients on estrogen-containing OCPs during the procedure and follow-up were compared with six controls. Case and control groups were matched by age, skin type, and treatment technique. Premenopausal and postmenopausal groups were compared. The variables evaluated included erythema, swelling, crusting, purpura, pain, pruritus, reepithelialization, complications, and patient assessment of outcome. RESULTS. For premenopausal and postmenopausal women, there were no significant differences in outcome measures of postoperative morbidity between groups receiving and not receiving estrogen. The incidence of complications, time until re-epithelialization, and patient assessment of outcome were similar between groups. CONCLUSION. Our findings suggest that exogenous estrogen in the form of HRT or OCPs does not clinically alter postoperative progress in combination CO2/Er:YAG LSR patients. Premenopausal women heal comparably to postmenopausal women after LSR.

A31-year-old man who worked as a landscape gardener was seen because of painful ulcers on his left lower leg that had been recurrent for 3 years. His history included multiple episodes of bilateral deep venous thrombosis in his upper and lower extremities and two episodes of pulmonary embolism during the previous 6 years. His father had a history of recurrent deep venous thrombosis, cerebrovascular accident at the age of 47 years, and seropositivity for lupus anticoagulant. On physical examination, several painful ulcers ranging in diameter from a few millimeters to 2 cm were seen on his left lower leg. A purplish area of livedo over the left fifth toe and scars from previous ulcers also were noted. Laboratory results included: platelets 118×10 3 /μL, a negative antinuclear antibody screen, and a positive antiphospholipid antibody test (138 IgG phospholipid [GPL] units [normal

With aging, there is a decrease in the level of hormones, such as estrogen, testosterone, dehydroepiandrosterone sulfate, and growth hormone. The effect of this decrease on the skin has been poorly documented, although more data are available for estrogen than for other hormones. This article reviews the effect of decreasing hormone levels on the skin and the possible cutaneous benefits of hormone replacement therapy.

About 600,000 people in the United States are estimated to be affected by venous ulcers. The cornerstone of care of chronic venous ulcers involves the application of compression bandages. Other therapies include treatment of associated infection, treatment for edema and inflammation, and debridement when necessary. Repifermin, a recombinant human KGF-2 (fibroblast growth factor-10), exerts a proliferative effect on epithelial cells, in vitro and in vivo, and has been shown to accelerate wound healing in several experimental animal models. A randomized, double-blind, parallel-group, placebo-controlled, multicenter study was conducted to evaluate the safety and efficacy of topical repifermin treatment, for 12 weeks, in the healing of chronic venous ulcers in 94 patients. Repifermin was shown to accelerate wound healing, with significantly more patients achieving 75% wound closure with repifermin than with placebo. The treatment effect appeared more marked for a subgroup of patients with initial wound areas < or = 15 cm2 and wound ages of < or = 18 months. A longer duration of treatment (e.g., 26 weeks) may allow better differentiation of the benefit of repifermin compared with placebo, particularly with respect to complete wound closure. The safety assessment showed that repifermin was well tolerated.

Background. Venous ulcers affect as many as 2.5 million people in the United States and can cause substantial pain and loss of function. Objective. To review current approaches to venous ulcers and compression. Method. Treatment options that have been proposed in the literature are discussed utilizing the Cochrane library database, Medline, and the author's clinical experience. Results. Diagnostic findings and management strategies for venous ulcers are reviewed. Conclusion. Good wound care and compression therapy will heal the majority of small venous ulcers of short duration. For ulcers that are slow to heal, other approaches such as venous surgery and grafting with conventional or bioengineered skin substitutes should be considered.

Purpose: Fibroblasts (fb) play an important role in wound healing involving motility, contraction, fibrosis, and expression of the cytoskeletal protein α-smooth muscle actin (α-sma). Patients with chronic venous insufficiency (CVI) are known to have dermal changes and impaired venous ulcer healing. To investigate whether these dermal-fb have an altered ability to migrate and whether chronic wound fluid from venous ulcers alters neonatal fb motility, we examined cell migration and α-sma. Methods: Fibroblasts were cultured from the margin of venous ulcers (du-fb, n=4, CEAP 6), from patients with venous reflux without ulcer (dr-fb, n=5, CEAP 2), and from the ipsilateral thigh of the same patients with (pu-fb) and without (pr-fb) ulcer, respectively. The abbreviations used are p and d, which represent proximal and distal, respectively; u and r represent ulcer and reflux, respectively. Neonatal foreskin fibroblasts (nf-fb) were exposed to chronic venous ulcer wound fluid (CVUWF, 300 μg protein/mL, n=3) or bovine serum albumin (BSA, control). Fibroblast motility was determined by means of time-lapse photo-images, and the rate (micrometer per hour) was calculated. Immunohistochemistry for α-sma was analyzed with confocal laser microscopy. Results: The rate of motility (micrometer per hour ± SEM) was decreased for both du-fb (11.4 ± 0.7) and dr-fb (13.8 ± 0.6), when compared with pu-fb (21.9 ± 0.9) and pr-fb (24.7 ± 1.1), respectively. The motility rate for nf-fb was lower in CVUWF (24.7 ± 2.0) than in BSA (37.1 ± 6.7). An elevated level of microfilament bundles of α-sma for both du-fb and dr-fb, compared with those of pu-fb and pr-fb, and also in nf-fb treated with CVUWF was demonstrated by means of immunohistochemistry. Conclusion: These data demonstrate a reduced motility in the dermal fb of patients with CVI. Patients with reflux disease without ulcer are predisposed to these changes. Furthermore, it appears that CVUWF causes changes in motility and α-sma expression in nf-fb as demonstrated in du-fb. These findings suggest that reduced motility and CVUWF, representing the microenvironment of venous ulcers, play a significant role in impaired wound healing. (J Vasc Surg 2001;33:1233-41.)

The goals of this study were to analyze the 2010 update of the Association for the Advancement of Wound Care (AAWC) Venous Ulcer Guideline (VUG) and examine recommendations with less than A-level evidence to identify important research questions.The AAWC VUG may be found at http://aawconline.org/professional-resources/resources and at the National Guideline Clearinghouse, http://www.guideline.gov. Supporting references for each recommendation, compiled by the AAWC Guideline Task Force from MEDLINE, CINAHL, and EMBASE databases, may be viewed at the first website.The literature identified in support of the AAWC VUG recommendations with less than A-level evidence was evaluated and is summarized below.Questions requiring further research in venous ulcer (VU) care were developed from recommendations having less than A-level support and that fall under the following topics: diagnosis, documentation, prevention, wound care, adjunctive interventions, and palliation.Practitioners lack strong evidence for several generally accepted recommendations of this synthesis of VU guidelines concerning the following: diagnostic or screening validity of varicosities, timing of biopsies for differential diagnosis, clinic visit frequency, criteria for changing VU care plans, and effective VU preventive parameters. Bedside surgical debridement, several biologic interventions, certain types of grafting, and the comparative efficacy of intravascular surgical procedures also require rigorous examination. Adjunctive interventions to be investigated include systemic pain management, topical biophysical treatments, novel devices, pharmaceuticals, timing, methods and procedures for some surgical interventions.Better evidence for recommendations with less than A-level support may improve the quality and consistency of VU care, reduce costs, and improve resource use.

Background: Venous ulcers can be difficult to heal, and prognostic factors for healing have not been fully elucidated. Objective: The objective of this study was to analyze the results of a large multicenter venous ulcer trial to retrospectively establish prognostic factors for venous ulcer healing. Methods: This study examined data from a previously published prospective randomized placebo-controlled trial of an oral medication versus placebo treatment for venous ulcers. Local leg ulcer care involved the use of a moisture-retentive dressing and sustained graduated compression with a paste bandage and a self-adherent wrap. The oral medication or placebo was administered on a daily basis with the same dressings and bandage system in both groups for 12 weeks. A total of 165 patients completed the full 12-week treatment period; 83 received ifetroban, 82 received placebo. Results: There was no statistically significant difference in outcome between the two groups. The study showed that consistent local ulcer treatment with a clearly defined system of care was associated with an unexpectedly high percentage (55%) of long-standing large venous ulcers (mean duration, 27 months; mean area, 15.9 cm 2 ) being healed in both groups. Baseline ulcer area and duration of leg ulcer were found to be important in predicting outcome. Ulcers of short duration were found to be most likely to heal. Percent healing and ulcer area at week 3 were good predictors of 100% healing. Ulcers that had at least 40% healing by week 3 predicted more than 70% of the outcomes correctly. Conclusion: From this large study it was determined that baseline ulcer area and ulcer duration are significant predictors of 100% healing and time to heal. Percent healing and ulcer area at week 3 are good predictors of complete ulcer healing. Ulcers that are large, long-standing, and slow to heal after 3 weeks of optimal therapy are unlikely to heal rapidly, and might benefit from alternative therapies. (J Am Acad Dermatol 2000;43:627-30.)

Background: Acute and chronic skin damage occurs as a consequence of solar UV radiation exposure. To diminish such skin damage, the dermatologic community advocates the daily use of sunscreens as part of a sun avoidance strategy. Objective: We determined the effectiveness of a sunscreen product with a sunscreen protection factor (SPF) of 15 applied daily in preventing UV-induced histologic damage in human skin compared with the protection afforded by sunscreens with equal or higher SPF applied intermittently. Methods: Twenty-four subjects were exposed to 2 minimal erythema doses of solar-simulated UV on 4 consecutive days. Three sunscreen products were applied to the buttock of each subject. One SPF 15 product was applied daily before exposure to UV and, to simulate intermittent product use, an SPF 15 or SPF 29 product was applied on 3 of 4 days, with one missed application on days 2, 3, or 4. Skin biopsy specimens were taken and processed for routine and immunohistochemical staining. Changes in number of sunburn cells and Langerhans cells as well as degree of inflammatory infiltrate and lysozyme immunostaining were determined. Results: There was a statistically significant increase in the number of sunburn cells, degree of inflammation, and intensity of lysozyme staining, and there was a decrease in the number of Langerhans cells at sites where sunscreen application was missed as compared with unirradiated control and daily SPF 15 sunscreen-treated sites. Conclusion: Our data suggest that daily use of a sunscreen reduces the skin damage produced by UV exposure compared with intermittent use of equal or higher SPF products. The daily application of sunscreens in appropriate quantities reduces the harmful effects of solar UV radiation on skin. Compliance is essential for maximal benefit of sunscreens. (J Am Acad Dermatol 2000;43:610-8.).

(2000). Combined classic and iatrogenic Kaposi's sarcoma. Postgraduate Medicine: Vol. 108, No. 2, pp. 103-106.

This report reflects the best data available at the time the report was prepared, but caution should be exercised in interpreting the data; the results of future studies may require alteration of the conclusions or recommendations set forth in this report.

Disorders of the arteries, veins, or nerves, alone or in combination, can result in leg ulcers. The presentation in these cases varies with the cause, which in turn guides management. A differential diagnosis is critical, because treatment that is essential for one type of ulcer may be contraindicated in another.