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Products for the Care of Chronic Wounds


Questions

  • Q54.1 What are the four main stages (and their general sequence) of wound healing? (Pg. 598)

  • Q54.2 What are some of the most important medical conditions to exclude (and related laboratory tests) in patients with a chronic cutaneous ulcer? (Pgs. 598, 600 Table 54.1 )

  • Q54.3 What are some of the main clinical features to distinguish the most common causes of cutaneous ulcers? (Pgs. 598, 601 Table 54.1 )

  • Q54.4 In assessing the role of bacterial commensalism versus active infection, what is the role of (1) superficial swabbing, (2) curetting tissue for culture, and (3) tissue biopsy for culture? (Pgs. 600, 601)

  • Q54.5 How does the overall rationale for the various methods of compression assist healing of venous ulcers? (Pg. 601x2)

  • Q54.6 What are the three main types of compression dressings used in chronic venous ulcers, and what is the most important contraindication to this compression therapy? (Pg. 602)

  • Q54.7 Concerning the above compression dressing options, what are the primary conclusions of clinical trials comparing these options? (Pg. 602x2)

  • Q54.8 What type of compression stockings are recommended after healing of venous ulcers, and what are some of the decisions and parameters to order these stockings? (Pg. 602)

  • Q54.9 What are the main components of the ‘TIME’ acronym for measures to prepare the wound bed in patients with chronic cutaneous ulcers and, specifically, what are some of the categories of debridement options? (Pg. 602x2)

  • Q54.10 What are the five main categories of occlusive wound dressings and representative examples of each category? (Pg. 603)

  • Q54.11 What are some of the current cellular-based dressings used in chronic venous ulcers? (Pg. 604x3)

  • Q54.12 What are three of the most common current medical and surgical options for chronic venous ulcers? (Pg. 605x3)

  • Q54.13 What are the newer antimicrobials used in wound dressings? (Pg. 605)

  • Q54.14 What are the emerging therapies in wound care? (Pg. 605)

Abbreviations used in this chapter

ABI

Ankle–brachial index

ANA

Antinuclear antibody

BMI

Body mass index

C3

Complement component 3

C4

Complement component 4

CBC

Complete blood count

CFU

Colony-forming units

CRP

C-reactive protein

CT

Computed tomography

ECM

Extracellular matrix

EGF

Epidermal growth factor

ESR

Erythrocyte sedimentation rate

Hgb

Hemoglobin

HIV

Human immunodeficiency virus

MRI

Magnetic resonance imaging

MRSA

Methicillin-resistant Staphylococcus aureus

PDGF

Platelet-derived growth factor

RCT

Randomized controlled trial

SPEP

Serum protein electrophoresis

TGFβ 1

Transforming growth factor β 1

UB

Unna boot

VRE

Vancomycin-resistant Enterococcus

Introduction

Wounds are defined as macroscopic breaks in the skin barrier. They are further classified into acute (<6 weeks) and chronic (>6 weeks or frequent recurrences). Chronic wounds are a major healthcare burden, with total annual medical costs approaching US$12 billion in the United States.

As dermatologists, we should familiarize ourselves with the various wound care dressings used to treat chronic wounds.

Wound Healing Physiology and Ideal Wound Healing Environment

Q54.1 Wound healing is a dynamic, complex interaction between different blood and tissue cells, along with extracellular matrix (ECM) molecules. It can be divided into (1) coagulation, (2) inflammatory, (3) proliferative, and (4) remodeling phases. Activated platelets together with polymerized fibrin form thrombi that stop initial blood loss. During the inflammatory phase, neutrophils recruited by complement fragments and cytokines, followed by macrophages recruited by the growth factors and ECM fragments, phagocytose bacteria and debris, killing the former and degrading the latter. In the proliferative phase, fibroblasts and blood vessels repopulate the wound bed, restoring the ECM and the microcirculation, respectively, while epidermal cells migrate and proliferate to cover the newly formed neodermis with a new epidermis. During the remodeling phase, fibroblasts evolve into myofibroblasts, which contract the wound and then, over months, remodel the neodermis through continuing ECM synthesis and degradation. Many growth factors play a critical role in regulating wound healing throughout these processes.

In addition to local endogenous factors, systemic and exogenous factors can markedly affect healing. These include cardiopulmonary and hematologic status, nutrition, metabolic disorders, immune status, local and systemic infections, mechanical forces, and desiccation.

General Approach to a Patient with Chronic Wounds

A detailed history and thorough physical examination are crucial in approaching a patient with chronic wounds, as many of the factors listed in the preceding paragraph can impede healing.

Wound History

Information regarding wound history should be elicited, including duration, causation, previous work-up, previous treatments, drainage, purulence, pain, and alleviating and aggravating factors.

Past Medical History

Q54.2 The patient should be questioned about pre-existing medical conditions, including metabolic disorders (diabetes, hypertension), vascular disorders (peripheral vascular disease, varicose veins, deep venous thrombosis), neuropathy, nutritional disorders, viral infections (viral hepatitis, human immunodeficiency virus [HIV]), autoimmune disorders (rheumatoid arthritis, inflammatory bowel disease), and hereditary disorders (sickle cell disease, hereditary spherocytosis). In addition, hypercoagulable states (protein C deficiency, protein S deficiency, factor V Leiden, antiphospholipid syndrome, homocysteine deficiency, thrombin gene mutation, antithrombin III deficiency) can predispose patients to chronic wounds.

Past Surgical History

The existence of any fractures, joint replacements, and vein harvest grafts compromising the circulatory system should be determined.

Medication History

Whether the patient is taking any immunosuppressive medications, chemotherapy such as hydroxyurea, or anti-inflammatory medications must be established.

Social History

Any current or previous history of smoking, alcohol intake, illicit drug use, and occupations predisposing to foreign body exposure should be elicited from the patient.

Review of Systems

The patient should be asked about any recent weight loss, edema, pain, or loss of sensation in the extremities. A history of deep venous thrombosis and miscarriages can point toward a hypercoagulable state.

Physical Examination

The location, size, depth, and color of the wound base should be assessed, as well as the color and odor of the drainage at each visit. The wound edges and formation of sinus tracts and tunnels should be noted, and the periwound area examined for maceration and/or allergic contact dermatitis.

Physical examination alone can suggest the etiology/etiologies of the ulcer. There is often more than one etiology. Table 54.1 lists the presentation and associated abnormalities for various ulcers.

Table 54.1
Common Presentation of Ulcers
Etiology of Ulcer Presentation Treatment Approach
Vascular
Venous Ulceration often around medial malleolus, accompanying hyperpigmentation, edema, lipodermatosclerosis, hyperkeratosis, atrophie blanche, stasis dermatitis, varicosities. Leg elevation, compression, moist dressing, pentoxifylline.
Arterial Punched-out ulcers overlying bony prominences (foot), surrounding atrophic, hairless and shiny skin, visible tendons and deep tissue, accompanying claudication/pain, poor peripheral pulses, slow capillary refill time, color change in limbs, decreased ABI. Modification of risk factors (tobacco use, hyperlipidemia, diabetes, hypertension), aspirin, ticlopidine, clopidogrel, vasodilator drugs, pentoxifylline, cilostazol, naftidrofuryl, propionyl L -carnitines, pain control, limb warmth, hyperbaric oxygen therapy.
Endocrinopathy
Diabetes Occurs at area of pressure, prior callus, accompanying peripheral neuropathy, peripheral vascular disease, foot deformities. Off-loading of mechanical stress at wound site, debridement, antibiotic treatment, glucose control.
Physical/Chemical Injury
Decubitus ulceration Ulceration at bony prominences, predisposing factors include immobility, moisture, increased age, poor nutrition. Reduction of pressure at area involved, turning and positioning of patients, specialized mattresses.
Infectious
Viral Ulceration in the setting of chronic infection with HIV/AIDS, hepatitis C, other viruses. Treatment of hepatitis C, HIV/AIDS, or other infectious or immunologic cause.
Bacterial Pyoderma secondary to beta hemolytic Streptococcus pyogenes or Staphylococcus aureus; pustule or punched-out nonhealing ulcer with overlying membrane in cutaneous diphtheria; papule, hemorrhagic blister, malignant pustule leading to shallow ulcer secondary to Bacillus anthracis. Cultures, appropriate antibiotic therapy.
Mycobacterial, fungal or other History of recent travel/exposure to pathogens such as parasites, atypical mycobacteria, fungi (sporotrichoid spread with Mycobacterium marinum, sporotrichosis or leishmaniasis). Appropriate treatment of pathogen.
Vasculitis/Vasculopathy
Calciphylaxis Occurs in patients with end-stage renal disease, high parathyroid hormone, hyperphosphatemia, high calcium × phosphorous product, hypercalcemia. Initially appears as atypical livedo reticularis with subcutaneous nodules and plaques, later becoming large, painful ulcers with necrosis. Decrease calcium in dialysate, reduce phosphate and calcium intake, discontinue vitamin D analogs, elimination of calcium-based phosphate binders, parathyroidectomy, bisphosphonates, sodium thiosulfate, hyperbaric oxygen, tissue plasminogen activator.
Antiphospholipid antibody syndrome Livedo racemosa, tender leg ulcers occurring in a variety of sizes, thromboses, anticardiolipin antibodies, lupus anticoagulant, anti-β 2 glycoprotein I antibodies, antiphosphotidylserine antibodies. Cases with widespread involvement or gangrene, consider anticoagulation.
Cryoglobulinemia Painful, symmetric, bilateral, necrotic ulceration with surrounding purpuric skin. May occur in the setting of hepatitis C. Plasma exchange, immunosuppressive medications. In hepatitis C-related cryoglobulinemia, treatment to eradicate the virus (i.e., currently lamuvidine) is indicated. Other treatments include corticosteroids, cytotoxic agents, rituximab, plasmapheresis, iloprost, colchicine.
Vasculitis Ulceration in the distribution of small and medium vessels accompanied by pustules, palpable purpura, urticaria, livedo reticularis, petechiae, subcutaneous nodules and gangrene. There may be accompanying fever, fatigue, and aches. Etiology dependent treatment. In isolated cutaneous small vessel vasculitis, conservative treatment may be sufficient. Treatment with dapsone +/− colchicine has been done in mild/moderate disease. In more severe cutaneous small vessel vasculitis particularly with systemic involvement, immunosuppressive or immune modulating medications may be indicated. Treatment with corticosteroids and cytotoxic agents is indicated in medium vessel vasculitis.
Malignancy
Squamous cell carcinoma Long-standing ulcer in sun-exposed skin, surrounding hyperkeratosis, crusting. Appropriate surgical or topical treatment for squamous cell carcinoma.
Basal cell carcinoma Long-standing, easily friable rodent ulcer in sun-exposed skin. Appropriate surgical or topical treatment for basal cell carcinoma.
CTCL Ulcerations may be accompanied by fissures, patches, plaques, nodules, erythroderma. Treatment of CTCL, spot radiation to ulcer site.
Hematologic
Sickle cell anemia Commonly seen in African-Americans, painful ulcers which may also be associated with priapism and pulmonary hypertension. Wet-to-dry dressings, blood transfusion, grafting, zinc, Unna boots, hyperbaric oxygen, arginine butyrate, topical herbal preparations, topical growth factors, pain management.
Connective Tissue Disease
Scleroderma Painful digital ulcers may develop secondary to severe sclerosis progressing to gangrene, atrophy and autoamputation. May be associated with bacterial infection. Physical therapy, intravenous iloprost, bosentan, hydrocolloid dressings, absorbent dressing, skin substitutes, antibiotics (topical/systemic).
Other Etiologies
Pyoderma gangrenosum Undermined ulcers with surrounding violaceous border, sometimes in association with underlying disease (inflammatory bowel disease, monoclonal gammopathy, hematologic malignancy or paraproteinemia, Behçet disease, Sweet syndrome, hepatitis, HIV, connective tissue disease, rheumatoid arthritis, Takayasu arteritis). Moisture retentive dressings, pain control, topical tacrolimus, topical corticosteroids, topical cyclosporine for small lesions. In larger lesions, high dose systemic corticosteroids, cyclosporine, thalidomide, methotrexate, tacrolimus, azathioprine, mycophenolate mofetil, cyclophosphamide, chlorambucil, intravenous immunoglobulin, dapsone, granulocyte apheresis, biologics including infliximab, adalimumab, etanercept.
Neurotic/psychogenic excoriations Angulated or linear erosions or superficial ulcerations with various stages with accompanying crusts, erosions within reach of digits, there may be surrounding pigmentary alteration and other scars. Seek out underlying psychiatric disease and appropriate treatment
Factitial ulceration Angulated or linear ulcerations with crusts, erosions at various stages with hyper- or hypopigmentation, may be extensive. Patients deny their role in creating ulcer. Seek out underlying motivation for creating ulcers, patients with severe self-mutilation may be suicidal.
CTCL¸ Cutaneous T-cell lymphoma; HIV/AIDS, human immunodeficiency virus/acquired immunodeficiency syndrome.

Q54.3 Venous ulcers have sloping edges, copious serosanguinous discharge, and can be associated with leg edema, atrophie blanche, hemosiderin deposition, and lipodermatosclerosis. The location is variable, based on the site of the perforator incompetence, most commonly noted near the medial malleolus.

Arterial ulcers have punched-out edges commonly located over the plantar foot and lateral malleolus, with minimal to no drainage and decreased pulses on palpation. Associated findings include slow capillary refill (>5 seconds), cool extremities, and shiny atrophic skin with loss of hair. The presence of claudication or rest pain is suggestive of arterial insufficiency. The ankle–brachial blood pressure ratio (ankle–brachial index [ABI]) measured by Doppler ultrasound can provide more information on arterial circulation. An ABI of 0.9 or higher is normal, whereas an ABI of 0.5 or less indicates severe arterial disease.

Neuropathic ulcers are associated with decreased or altered sensation. They are commonly seen in patients with diabetes mellitus and have high rates of infection.

Decubitus ulcers are located at pressure points such as elbows, heels, sacrum, and ischial tuberosities. These ulcers can begin as erythematous plaques or bullae that can belie the depth of injury, which may go to bone. Deep wounds may be associated with purulent to serosanguinous drainage and sinus tract formation.

Pyoderma gangrenosum ulcers are typically very painful and have punched-out or undermined borders with cribriform bases and violaceous discoloration of the surrounding skin. They exhibit pathergy, that is, new ulcers form at the site of minimal trauma.

Factitial wounds have asymmetric, sharp, geometric borders with healthy granulation tissue at the bases.

Laboratory Evaluation

Q54.2 Laboratory evaluation can include complete blood count (CBC) with white blood cell differential counts; albumin for possible malnutrition; liver enzymes for possible hepatitis; hepatitis virus panel for detection of undiagnosed hepatitis C that can be associated with mixed cryoglobulinemia; rheumatoid factor for possible circulating immune complexes including mixed cryoglobulinemia; and other immunological work-up, including antinuclear antibody (ANA), complement component 3 (C3), complement component 4 (C4), and total hemolytic complement activity titer (CH50). In addition, evaluation of lupus anticoagulant and antiphospholipid antibodies; general markers of inflammation such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP); and hemoglobin (Hgb) A1c for status of diabetes mellitus should be carried out, and other hypercoagulable work-up performed, including protein C, protein S, factor V Leiden, homocysteine, antithrombin III, thrombin gene, and serum protein electrophoresis (SPEP) for blood dyscrasias.

Culture

Q54.4 Wound culture and sensitivities can provide invaluable information on bacterial colonization and infection. Bacterial colonization is almost universal for wounds, with the presence of skin commensals on the surface and no overt signs of infection. In lower concentrations, bacteria are known to actually hasten the healing process. Once the bacterial count reaches the critical colonization level, wound healing is impeded, without overt signs and symptoms of infection. Bacterial counts greater than 10 5 colony-forming units (CFU) per gram of tissue are known to impede wound healing.

As the bacterial count continues to rise, organisms cause overt infection accompanied by warmth, erythema, pain, swelling, and leukocytosis. Bacteria secrete a variety of enzymes that degrade the ECM, resulting in delayed healing.

Q54.4 Wound cultures can be obtained through a variety of techniques, including superficial swabs, curettes, aspiration, and tissue biopsies. Although swabs are most commonly used and are noninvasive, they often isolate surface bacteria not responsible for infection. Tissue obtained with a 3 mm curette on the advancing edge of the wound reliably elucidates the bacteria responsible for slow healing and infection. This maneuver often accelerates wound healing, possibly through biofilm disruption. In addition, it offers quantification of bacteria as well as qualitative data. It is relatively noninvasive and correlates with deep tissue biopsy more than wound fluid aspirate and culture swabs. Culture of wound fluid aspirate does not quantify bacterial burden, but it is a noninvasive technique. Deep tissue biopsy is the ‘gold standard’ and reflects the bacterial burden more accurately, but it is invasive and can contribute focally to nonhealing of wounds. In addition to culture, tissue can also be submitted for histological examination and stained for bacteria, fungi, and mycobacteria. Biopsy is also helpful to exclude squamous cell carcinomas (and rarely basal cell carcinomas) in long-standing ulcers.

Imaging Studies

Imaging includes Doppler ultrasound to evaluate venous incompetence, with particular attention to perforators. In addition to valvular insufficiency, it can also identify chronic vein wall thickening, or chronic thrombosis suggestive of postthrombotic syndrome. Doppler ultrasound can also be used to evaluate arterial supply to identify arterial stenosis. Biphasic and monophasic wave forms are seen in the setting of arterial stenosis instead of the normal triphasic wave forms. If there is a concern for osteomyelitis, plain films, computed tomography (CT) scans, magnetic resonance imaging (MRI), indium scan/indium white blood cell scan/indium leukocyte imaging/indium-111 scan, and bone biopsy can provide more diagnostic information.

In this chapter, we will be discussing primarily the standard practice and management of venous ulcers, as other ulcers (such as arterial ulcers) are beyond the scope of dermatologists and may require surgical intervention. Most of the same wound care principles (aside from debridement) apply to management of pyoderma gangrenosum ulcers; in addition, an underlying autoimmune disorder must be managed with systemic medications.

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