(BQ) Part 2 book “Text and atlas of wound diagnosis and treatment” has contents: Flaps and skin grats, wound debridement, burn wound management, factors that impede wound healing, wound dressings, electrical stimulation, negative pressure wound therapy, pulsed lavage with suction,… and other contents.
C H A P T E R E I G H T Atypical Wounds Jayesh B Shah, MD, CWSP, FACCWS, FAPWCA, FUHM, FAHM and Rose L Hamm, PT, DPT, CWS, FACCWS CHAPTER OBJECTIVES At the end of this chapter, the learner will be able to: Recognize signs of an atypical wound Categorize an atypical wound into a basic pathology Determine the appropriate medical specialist for a given wound Develop an evidence-based care plan for an atypical wound Educate the patient and family about the wound diagnosis INTRODUCTION Most wounds are diagnosed as arterial, venous, pressure, neuropathic, surgical, or burn and are treated according to the principles that have been discussed in the previous chapters If a wound has a different appearance or does not respond to standard care, the clinician is challenged to determine either the factors that are inhibiting healing or to consider a different diagnosis This chapter reviews the basic morphology of skin disease, red flags of atypical wounds, and characteristics of different diagnostic categories The pathophysiology, clinical presentation with photographs, differential diagnosis, medical management, and wound management of each wound category are provided to assist the clinician in making sound clinical decisions CHARACTERISTICS OF ATYPICAL WOUNDS The first signal that a wound is atypical is that little signal in the clinician’s instinct that says, “This is just not quite what it looks to be.” And usually it behooves the clinician to follow those instincts, to at least rule out an atypical diagnosis, and at most to make a differential diagnosis that completely changes the care plan and results in wound healing TABLE 81 provides a list of characteristics that suggest a wound does not fall into the typical categories.1,2 MORPHOLOGY OF SKIN DISEASE Many diseases will cause changes in the skin that are predictable and/or suggestive of a certain diagnosis TABLE 82 provides a list of terms and definitions of integumentary characteristics (based on size, texture, and color) that are used to describe abnormal skin appearance.2 These terms are used in the following descriptions of atypical wound clinical presentations CATEGORIES OF ATYPICAL WOUNDS Allergic Reactions Allergic reactions can be either contact (the offending substance touches the skin) or systemic (the offending substance is injected or ingested) In either case, the substance, termed an antigen, causes an immunological response that results in the production of antibodies and a subsequent inflammatory response The reaction can actually cause wounds to develop, or in the case of existing wounds, prevent healing from progressing Contact Dermatitis Pathophysiology Dermatitis can be either contact or irritant, depending on the host immune system and the concentration of the irritant.3 In contact allergies, the irritant reacts with the skin barrier to initiate an immune response—the allergen binds to the carrier protein and creates a sensitizing antigen, the Langerhans cells carry the antigen to the T cells, and the T cells cause the release of cytokines Thus develops the inflammatory symptoms of erythema, rash, itching, and sometimes vesicular lesions (FIGURES 81, 82) The allergic response can be either immediate TABLE 81 Characteristics of Atypical Wounds Unusual locations Unusual age Asymmetric lesion Granulation extending over the wound edge Exuberant granulation tissue or callus Purple-red color around ulcer (termed violaceous) Ulcer in center of pigmented lesion History of repeated trauma Rolled out edges Fungating growth No obvious diagnosis History of radiation therapy Wound secondary to burns, trauma, and diabetes 227 Hamm_Ch08_227-254.indd 227 18/12/14 10:58 AM 228 Chapter Atypical Wounds TABLE 82 Skin Disease Morphology Macule—A circumscribed, flat, nonpalpable lesion that is flush with the level of surrounding normal skin; smaller than 10 mm in diameter Patch—A flat, nonpalpable lesion that is flush with the level of surrounding normal skin; greater than 10 mm in diameter Papule—A superficial, circumscribed dome-shaped or-flat topped palpable lesion elevated above the skin surface; less than 10 mm in diameter Plaque—A lesion that rises slightly above the surface of the skin; greater than 10 mm in diameter Nodule—A firm lesion that is thicker or deeper than the average plaque or papule; is palpable as differentiated tissue Vesicle—An elevated lesion that contains clear fluid; less that 10 mm in diameter Bulla—An elevated lesion that contains clear fluid; greater than 10 mm in diameter Pustule—An elevated lesion that contains pus Urticarial (hives)—An allergic reaction characterized by white fluidfilled blisters (termed wheals) surrounded by erythema (flares) 10 Livedo reticularis—A mottled, lace-like purplish discoloration of the skin caused by thrombotic occlusion of the capillaries that leads to swelling of the venules or delayed, and can involve both the skin and the subcutaneous tissue Usually the response increases in severity after repeated exposures due to increased numbers of antibodies The irritant type of contact dermatitis is not an immunological response, but a reaction to a caustic substance and depends on the concentration of the substance, for example, a chemical or topical liquid Patients with chronic leg wounds have an increased susceptibility to allergic contact dermatitis,4 especially if they are being treated with compression therapy This condition is sometimes referred to as stasis dermatitis If contact dermatitis FIGURE 82 Contact dermatitis This patient with a known latex allergy was being treated for a chronic venous wound using antimicrobial dressings and multilayered compression bandages After progressing well for several months, the wound and periwound tissue began to deteriorate with numerous areas of partial thickness skin loss like the one proximal to the primary wound Cessation of any dressings that contained silver resulted in an immediate reversal of the symptoms, confirming a suspicion that she had a silver allergy Infection and an allergic reaction can both cause deterioration of the wound bed, and are obviously treated quite differently Confirmation of infection is by culture and allergy by removing the suspected offending agent is suspected or if the patient reports a history of allergies to other substances, patch testing can be performed to confirm the diagnosis TABLE 83 provides a list of common allergens for patients who have wounds Clinical Presentation Signs of dermatitis include erythema, weeping, scaling of the periwound area, and itching It can occur at any age; however, in the older population it can easily TABLE 83 Common Allergens for Contact Dermatitis FIGURE 81 Contact dermatitis Characteristics of contact dermatitis seen on the lower extremity are a well-defined border of exposure, erythema, rash (at the proximal aspect of the wound), and patient complaint of itching under the bandages Some of the dressing components that can cause an allergic reaction are sulfa, silver, silicone, iodine, or latex Careful subjective history about possible allergies is important to minimize the risk of reactions that may inhibit wound healing or even extend the wound Hamm_Ch08_227-254.indd 228 Contact allergens Neomycin Bacitracin Wool Alcohol Formaldehyde Parabens Tape adhesives Latex Perfumes Metals (eg, nickel, silver) Irritant allergens Soap Detergent Cleaning solvents Poison ivy or oak Pesticides 18/12/14 10:58 AM Categories of Atypical Wounds be misdiagnosed In severe cases, shiny skin and alopecia may develop A visible determining factor is that the symptoms occur only in areas of direct contact with the irritating material TABLE 84 229 Drug-Induced Hypersensitivity Syndrome Syndrome Description Erythema multiforme Generalized rash with macular or popular skin eruptions Drug rash with eosinophilia and systemic systems DRESS Syndrome Three of the following is necessary for diagnosis: fever, exanthema, eosinophilia, atypical circulating lymphocytes, lymphadenopathy, hepatitis Medical Management The most important component of treating any dermatitis is the identification and discontinuation of the medication, dressing, or other substance that might be responsible for contact dermatitis Low-dose topical steroids may help decrease inflammation and discomfort; systemic steroids may be beneficial if there is an extensive area of contact dermatitis Stevens-Johnson syndrome Cutaneous lesions of papules, vesicles, or bullae covering 30% of the body surface area; mucosal lesions; conjunctivitis Wound Management Patients usually require only supportive care and discontinuation of the irritating topical agent and, in the case of an existing wound, substitution of a dressing that has fewer or no allergens Nonadherent hypoallergenic dressings are recommended for care of open lesions Most products that are used for wound care are available in latex-free forms, as both patients and clinicians can suffer from latex allergies The skin will usually heal in to weeks Chemotherapy-induced acral erythema Painful swelling and erythema of the palms and soles of patients on highdose chemotherapy Drug-induced lupus erythematosus Lupus-type symptoms with skin signs associated with medications; resolves when medications withdrawn Differential Diagnosis Cellulitis Vasculitis Drug-Induced Hypersensitivity Syndrome Pathophysiology Drug-induced hypersensitivity syndrome (DIHS) is an immunologic response to a drug received either orally, by injection, or by IV Although not fully understood, the process is similar to what occurs with skin allergies except that the immune response is activated by the causative agents and their metabolites rather than by a direct effect on the keratinocytes.5 There are numerous syndromes based on severity, types of lesions and underlying diseases processes; however, all of them produce generalized (rather than localized) skin lesions and systemic symptoms (TABLE 84) Some of the more common drug-hypersensitivity syndrome nomenclature and symptoms that have been reported in the literature (From Hamm RL Drug-induced hypersensitivity syndrome: diagnosis and treatment Journal of the American College of Clinical Wound Specialists 2012:3(4):77-81) progression and relieve symptoms, and supportive care is provided in an intensive care unit or a burn unit for more severe cases Wound Management In minor cases, cessation of the medication may be sufficient to reverse symptoms and no wound care is needed In more severe cases with epidermal sloughing, treatment is similar to that of a deep superficial burn except Clinical Presentation Symptoms include generalized rash (with or without vesicles) and any of the following: local eruptions, fever, lymphedema, mucosal lesions, conjunctivitis, and epidermal sloughing (FIGURE 83) Onset is usually to weeks after the first exposure to the offending drug, beginning with a fever or sore throat and progressing to the cutaneous/ mucosal involvement In the younger adult population (20 to 40 years), the syndrome is termed erythema multiforme Differential Diagnosis Infection Vasculitis Contact dermatitis Medical Management Medical management begins with identification and cessation of the causative agent, which is usually the last one that the patient has initiated taking Depending on the severity of the symptoms, corticosteroids are used to prevent Hamm_Ch08_227-254.indd 229 FIGURE 83 Drug-induced hypersensitivity syndrome Diffuse generalized rash (with or without vesicles)—with symptoms of local eruptions, fever, lymphedema, mucosal lesions, conjunctivitis, and epidermal sloughing—can occur on any part of the body as a result of an allergic or hypersensitive reaction to medications Unlike a local allergic response, DIHS involves a larger surface area without direct exposure to a specific substance 18/12/14 10:58 AM 230 Chapter Atypical Wounds FIGURE 84 Vasculitis due to SLE Vasculitis presents as dermal necrosis as a result of occluded small arteriole and is exquisitely painful, making local care very difficult Patients with autoimmune disorders, for example, systemic lupus erythematosus (SLE) are at greater risk The medications used to treat SLE further complicate and inhibit wound healing that debridement of the detached epidermal tissue is usually not advisable Nonadherent antimicrobial dressings are recommended to help prevent infection and to avoid further skin tearing with dressing changes Prevention of fluid loss and infection is paramount, and as the patient improves, dressings to promote reepithelialization are advised ing the skin The etiology is often idiopathic—it is a reaction pattern that may be triggered by certain comorbidities including underlying infection, malignancy, medication, and connective tissue diseases such as systemic lupus erythamatosus (FIGURE 84) Circulating immune complexes (antibody/antigen) deposit in the blood vessel walls, causing inflammation that may be segmental or involve the entire vessel At the site of inflammation, varying degrees of cellular inflammation and resulting necrosis or scarring occur in one or more layers of the vessel wall, and inflammation in the media of the muscular artery tends to destroy the internal elastic lamina 6–7 Leukocytoclastic vasculitis, a histopathologic term used to describe findings in small-vessel vasculitis, refers to the breakdown of inflammatory cells that leaves small nuclear fragments in and around the vessels Vasculitic inflammation tends to be transmural, rarely necrotizing, and nongranulomatous Resolution of the inflammation tends to result in fibrosis and intimal hypertrophy, which in combination with secondary clot formation, can narrow the arterial lumen and account for the tissue ischemia or necrosis.8 Clinical symptoms (ie, tissue loss) depend on the artery or arteries that are involved and the extent of lumen occlusion Cutaneous vasculitis usually occurs in the lower extremities and feet Vasculitis Vasculitis is an inflammatory disorder of blood vessels, which can ultimately result in organ damage, includ- Clinical Presentation Clinical presentation, which varies depending on the arterial involvement, includes palpable purpura, livedo reticularis, pain, skin lesions with or without nodules, and tissue necrosis It may present as one large necrotic lesion or several small lesions, but all are full thickness after debridement Systemic systems may also be present and usually relate to kidney, lung, or gastrointestinal tract involvement On some occasions, signs of vasculitis in other organs may appear at the same time that skin lesions appear (FIGURES 85, 86) One very FIGURE 85 Vasculitis associated with other symptoms This patient with vasculitis of the posterior calf noted the onset of pain and dermal symptoms at the same time that he experienced neurological signs associated with what was diagnosed as a CVA Both maladies occurred after the stress of losing a family member Note the discoloration of the proximal periwound skin, indicating that the inflammation is still evolving FIGURE 86 Vasculitis in the remodeling phase of healing The patient in Figure 8-5 was treated with low-frequency noncontact ultrasound, nonadherent dressings to facilitate autolytic debridement, and compression therapy He progressed to full closure of the wounds without surgical intervention Topical 2% Lidocaine gel was applied prior to each treatment for assistance with pain management Autoimmune Disorders Hamm_Ch08_227-254.indd 230 18/12/14 10:58 AM Categories of Atypical Wounds distinctive characteristic for differential diagnosis from chronic venous wounds is the exquisite pain that occurs with vasculitis, making the initial local treatment very tedious Differential Diagnosis (TABLE 85) Giant cell arteritis Primary angiitis of the CNS Takayasu arteritis Churg-Strauss syndrome Immune complex–associated vasculitis Microscopic polyangiitis Polyarteritis nodosa Rheumatoid arthritis Wegener granulomatosis Henoch-Schönlein purpura Chronic venous wounds Medical Management Treatment of any vasculitis depends on the etiology, extent, and severity of the disease For secondary vasculitic disorders, treating the underlying comorbidity (eg, infection, drug use, cancer, or autoimmune disorder) is crucial Remission of life- or organ-threatening disorders is induced by using cytotoxic immunosuppressants (eg, cyclophosphamide) and high-dose corticosteroids, usually for to months, until remission occurs or until the disease activity is acceptably reduced Adjusting treatment to maintain remission takes longer, usually to years During this period, the goal is to eliminate corticosteroids, reduce the dosage, or use less potent immunosuppressants as long TABLE 85 231 as needed After tapering or eliminating corticosteroids, methotrexate or azathioprine can be substituted to maintain remission Wound Management Initial treatment of wounds caused by vasculitis is extremely difficult because of the pain The principles of standard wound care (debride necrotic tissue, treat inflammation and infection, apply moist wound dressings, nurture the edges, and ensure optimal oxygen supply, termed TIMEO2)9 are recommended Topical lidocaine helps reduce pain during treatments, noncontact low-frequency ultrasound helps mobilize cellular activity and interstitial fluids, and compression therapy helps manage the edema that occurs in the lower extremities as a result of the inflammation and decreased mobility Nonadherent dressings that promote autolysis of the necrotic tissue (eg, X-Cell, Medline, Mundelein, IL) are excellent initially, especially in reducing pain levels with dressing changes Silicone-backed foam dressings are helpful in absorbing exudate as well as in reducing pain If the patient is on steroids, local vitamin A can be used to negate the effects of steroids As the acute inflammation recedes, pain levels decrease, and wound healing progresses to proliferation, treatment can be more aggressive Antiphospholipid Syndrome Pathophysiology The antiphospholipid syndrome (APS) is characterized by elevated titres of different antiphospholipid antibodies It consists of arteriole thrombosis (and in pregnancy, fetal demise) associated with various autoimmune antibodies directed against one or more phospholipid-binding proteins (eg, anti-β2-glycoprotein I, anticardiolipin, and lupus anticoagulant).10 These proteins normally bind to phospho- Vasculitic Syndromes Name Typical Vessels Involved Symptoms Churg-Strauss syndrome Small and medium vessel Three stages: Airway inflammation, asthma, allergic rhinitis Hypereosinophilia Vasculitis with tissue necrosis Giant cell arteritis Temporal and cranial arteries Headaches, temporal pain, visual disturbances, scalp sensitivity, dry cough with respiratory symptoms, fever, upper extremity weakness, and sensory changes Henoch-Schönlein purpura Small vessels Purpura, arthritis, abdominal pain (usually in children) Immune complex associated vasculitis Small vessels to neurons Peripheral neuropathy Microscopic polyangiitis Small vessels to organs Ischemia, hemorrhage, loss of organ function Polyarteritis nodosa Small and medium arteries Subcutaneous nodules or projections of lesions; fever, chills, tachycardia, arthralgia, myositis, motor and sensory neuropathies Primary angiitis of the CNS Small and medium vessels in the brain and spinal cord Brain: headache, altered mental status, focal CNS deficits; spinal cord: lower extremity weakness, bladder dysfunction Takayasu arteritis Aorta, aorta branches, pulmonary arteries Inflammatory phase with flu-like symptoms, pulseless upper extremity, claudication, renal artery disease Wegener granulomatosis (granulomatosis with polyangiitis) Small and medium vessels Organ failure (lungs and kidneys), variable including skin, depending on the vessels involved Hamm_Ch08_227-254.indd 231 18/12/14 10:58 AM 232 Chapter Atypical Wounds lipid membrane constituents and protect them from excessive coagulation activation The autoantibodies displace the protective proteins and thus produce procoagulant endothelial cell surfaces and cause arterial or venous thrombosis In vitro clotting tests may paradoxically be prolonged because the antiprotein/phospholipid antibodies interfere with coagulation factor assembly and with activation on the phospholipid components that are added to plasma to initiate the tests The lupus anticoagulant is an antiphospholipid autoantibody that binds to protein-phospholipid complexes It was initially recognized in patients with SLE; however, these patients now account for a minority of patients with the autoantibody The lupus anticoagulant is suspected if the PTT is prolonged and does not correct immediately upon 1:1 mixing with normal plasma but does return to normal upon the addition of an excessive quantity of phospholipids (done by the hematology laboratory) Antiphospholipid antibodies in patient plasma are measured by immunoassays of IgG and IgM antibodies that bind to phospholipid-β2-glycoprotein I complexes on microtiter plates.10 Clinical Presentation The arteriole thrombosis results in venous swelling, creating the typical livedo reticularis skin appearance In addition, the lower extremities may have superficial thrombophlebitis with cutaneous infarcts As the disease progresses, skin necrosis may occur (FIGURE 87) Differential Diagnosis Disseminated intravascular coagulation Infective endocarditis Thrombotic thrombocytopenic purpura FIGURE 87 Antiphospholipid syndrome Antiphospholipid syndrome is characterized in the early stages by livedo reticularis (resulting in small brown spots on the skin) and in the later stages by ischemic skin changes (Used with permission from Lichtman MA, Shafer JA, Felgar RE, Wang N A External Manifestations In: Lichtman MA, Shafer JA, Felgar RE, Wang N eds Lichtman’s Atlas of Hematology New York: McGraw-Hill; 2007 http://accessmedicine mhmedical.com/content.aspx?bookid=368&Sectionid=40094294 Accessed November 12, 2014.) Hamm_Ch08_227-254.indd 232 Medical Management Asymptomatic individuals in whom blood test findings are positive not require specific treatment Prophylactic therapy involves elimination of other risk factors such as oral contraceptives, smoking, hypertension, or hyperlipidemia For patients with SLE, hydroxychloroquine, an anti-inflammatory which may have intrinsic antithrombotic properties, may be useful Statins are beneficial for patients with hyperlipidemia If the patient has a thrombosis, full anticoagulation with intravenous or subcutaneous heparin followed by warfarin therapy is recommended.10,11,12 Based on the most recent evidence, a reasonable target for the international normalized ratio (INR) is 2.0 to 3.0 for venous thrombosis and 3.0 for arterial thrombosis Patients with recurrent thrombotic events, while well maintained on the above regimens, may require an INR of 3.0 to 4.0 For severe or refractory cases, a combination of warfarin and aspirin may be used Treatment for significant thrombotic events in patients with APS is generally lifelong Wound Management Conservative wound care is recommended for patients with skin lesions, keeping the wound moist and following wound bed preparation principles Healing of wounds caused by other etiologies, eg trauma or spider bites, will be delayed Pemphigus Pathophysiology Pemphigus is an autoimmune blistering disease resulting from loss of normal intercellular attachments in the skin and oral mucosal membrane Circulating antibodies attack the cell surface adhesion molecule desmoglein at the desmosomal cell junction in the suprabasal layer of the epidermis, resulting in the destruction of the adhesion molecules (acantholysis) and initiating an inflammatory response that causes blistering There are three major forms of pemphigus: pemphigus foliaceus (FIGURE 88) and pemphigus vulgaris that have IgG autoantibodies against desmoglein and desmoglein 3, respectively; and paraneoplastic pemphigus that has IgG autoantibodies against plakins and desmogleins (FIGURE 89) Clinical Presentation Pemphigus vulgaris, the most common type, involves the mucosa and skin, especially of the scalp, face, axilla, groins, trunk, and points of pressure Patients usually present with painful oral mucosal erosions and flaccid blisters, erosions, crusts, and macular erythema in areas of skin involvement.10,12 The primary cell adhesion loss is at the deeper suprabasal layer (Refer to Chapter for a review of the skin anatomy.) Pemphigus foliaceus is a milder form of the disease, with the acantholysis occurring more superficial in the epidermis and usually on the face and chest Paraneoplastic pemphigus, in addition to having different autoantibodies, occurs exclusively on patients who have some type of malignancy, usually a lymphoproliferative disorder (FIGURE 89) Because of the malignancy, mortality is high in this type of pemphigus.13 Differential Diagnosis Diagnosis is confirmed by using immunofluorescence to demonstrate the IgG autoantibodies against the cell surface of intraepidermal keratinocytes 18/12/14 10:58 AM Categories of Atypical Wounds 233 FIGURE 88 Pemphigus Pemphigus foliaceous is characterized by blistering of the epidermis followed by crusting and sloughing, resulting in painful wounds and discoloration after healing Complications include bacterial and viral infections as a result of the open wounds and immunosuppression, as well as sequelae from long-term use of corticosteroids (osteoporosis, avascular necrosis) Medical Management Medical treatment of all three types consists of systemic corticosteroids and immunosuppressive therapy Wound Management Wound management is conservative with the goal of preventing infection and promoting reepithelialization if denuding occurs with the blistering Flat antimicrobial dressings (eg, Acticoat Flex, Smith & Nephew, Largo, FL) are useful over open areas, and hydrotherapy is beneficial when the disease is widespread and in the crusty phase Secondary dressings are required for most areas, and can include surgical or fish-net garments Silicone-backed foam dressings without adhesive borders are also recommended for easy removal of loose necrotic tissue without causing painful skin tears Bullous Pemphigoid Pathophysiology Bullous pemphigoid (BP) is associated with tissue-bound and circulating autoantibodies directed against BP antigen 180 and BP antigen 230, both components of the basement membrane.12 An immune reaction is initiated by the formation of IgG autoantibodies that target dystonin, a component of the hemidesmosomes, resulting in the infiltration of immune cells to the area The consequence is separation of the dermal/epidermal junction with fluid collection and blistering or bullae Clinical Presentation BP occurs most commonly among the elderly, and the most common sites of involvement include inner aspects of thighs, flexor aspects of forearms, axilla, groin, and Hamm_Ch08_227-254.indd 233 FIGURE 89 Paraneoplastic pemphigus Characteristics of paraneoplastic pemphigus include extensive lesions on the lips, severe stomatitis, and erythematous macules and papules that coalesce into large cutaneous lesions The lesions are diagnosed by biopsy that shows a mix of individual cell necrosis, interface change, and acantholysis (Used with permission from Anhalt GJ, Mimouni D Chapter 55 Paraneoplastic Pemphigus In: Wolff K, ed Fitzpatrick’s Dermatology in General Medicine 8th ed New York: McGraw-Hill; 2012 http://www.accessmedicine.com/content.aspx?aID=56037677 Accessed August 24, 2013.) oral cavity The extremities can also become involved Clinically, patients can present with urticarial plaques with intense pruritis to widespread tense bulla filled with clear fluid (FIGURE 810) Differential Diagnosis Histologically, BP is the prototype of a subepidermal bullous disease along with eosinophilic spongiosis The dermis shows an inflammatory infiltrate composed of neutrophils, lymphocytes, and eosinophils Diagnosis is confirmed by the presence of linear deposits of IgG and/or C3 along the dermal-epidermal junction on direct immunoflouroscence.10,12 Medical Management Medical options include systemic corticosteroids and immunosuppressive therapy 18/12/14 10:58 AM 234 Chapter Atypical Wounds FIGURE 810 Bullous pemphigoid Tense bullae filled with clear fluid (a result of the inflammatory process) are typical of bullous pemphigoid Wound Management Wound management recommendations are the same as for pemphigus, with the goal of minimizing pain, preventing infection, and promoting reepithelialization Cryoglobulinemia Pathophysiology Cryoglobulins are abnormal proteins (immunoglobulins), and cryoglobulinemia is the presence of these proteins in the blood They coagulate or become thick and gellike in temperatures below body temperature (37° C), thereby clogging the small blood vessels and causing hypoxic skin changes, ischemic wounds, or other organ damage (TABLE 86) The symptoms are reversible if the environmental temperaTABLE 86 Symptoms of Cryoglobulinemia Local/Integumentary Type I Lesions in head and mucosa Acrocyanosis Raynaud phenomenon Digital ulceration Skin necrosis Livedo reticularis Purpura Type II and III Lesions in lower extremities Erythematous macules Purpura Raynaud phenomenon Cutaneous vasculitis Peripheral neuropathy Nailfold capillary abnormalities General/Systemic Type I Retinal hemorrhage Arterial thrombosis Renal disease Type II and III Breathing difficulty Fatigue Arthralgia (PIP, MCP, knees, ankles) Myalgia Immune complex deposition Cough Pleurisy Abdominal pain Fever Hepatomegaly or signs of cirrhosis Hypertension Data from Tritsch AM, Diamond HS Cryoglobulinemia Clinical Presentation http:// emedicine.medscape.com/article/329255 Accessed July 8, 2013 Hamm_Ch08_227-254.indd 234 FIGURE 811 Cryoglobulinemia Cryoglobulinemia on the foot of a patient with hepatitis C Classic signs include purpura, loss of dermis due to occlusion of the small vessels to the skin, severe pain, and tendency to develop infections This patient’s wounds healed with the use of antibiotics and standard wound care; however, when he returned to a cold climate his symptoms recurred ture is warmed The disorder is grouped into three main types, depending on the type of antibody that is produced: Type I is most often related to cancer of the blood or immune system, for example, multiple myeloma Types II and III, also referred to as mixed cryoglobulinemia, most often occur in people who have a chronic inflammatory condition, for example, hepatitis C or systemic lupus erythematosus Type II is the most common type, and most of these patients also have hepatitis C.1,10,12 Clinical Presentation Symptoms vary depending on the type of cryoglobulinemia present and the organs that are affected Systemic signs may include difficulty breathing, fatigue, glomerulonephritis, joint pain, and muscle pain Integumentary signs may begin with purpura and Raynaud phenomenon (FIGURE 811) Meltzer triad, associated with Types II and III, includes arthralgia, purpura, and weakness.14 See TABLE 86 for a list of cryoglobulinemia symptoms Differential Diagnosis Antiphospholipid syndrome Chronic lymphocytic leukemia Churg-Strauss syndrome Cirrhosis Giant cell arteritis Systemic lupus erythematosus 18/12/14 10:58 AM Categories of Atypical Wounds 235 Medical Management Treatment of mild or moderate cryoglobulinemia depends on the underlying cause, and treating the cause will often treat the cryoglobulinemia as well Mild cases can be treated simply by avoiding cold temperatures Standard hepatitis C treatments usually work for patients who have hepatitis C and mild or moderate cryoglobulinemia However, the condition can return when treatment stops NSAIDs may be used to treat mild cases that involve arthralgia and myalgia Severe cryoglobulinemia (involving vital organs or large areas of skin) is treated with corticosteroids, immunosuppressants, interferon, or cytotoxic medications Plasmapheresis may be indicated if the complications are life threatening.15 Wound Management Wound care involves treatment of infection and pain management, especially in the early stages Nonadherent dressings such as X-Cell (Medline, Mundelein, IL), hydrogel, Acticoat (Smith & Nephew, Largo, FL), and petrolatum gauze help minimize pain with dressing changes and promote autolytic debridement A topical anesthetic is advised 10 to 15 minutes before initiating any sharp debridement; enzymatic debridement may also be beneficial but can cause stinging and burning upon application Absorbent dressings are advised if there is wound drainage, and modified compression (eg, with short stretch bandages) helps reduce edema that occurs with chronic inflammation, immobility, and lower extremity dependency Compression bandages also help keep the extremities warm and facilitate vasodilation If edema is not severe, warm hydrotherapy can help reduce precipitation of the cryoglobulins and relieve ischemic pain Patient education regarding avoidance of cold or wearing warm clothing such as thermal socks is a crucial component of long-term management FIGURE 812 Pyoderma gangrenosum Pyoderma gangrenosum on the abdomen of a female with diabetes The PD developed after an open hysterectomy The wounds were treated with nonadherent antimicrobial dressings (X-cell) in order to minimize pain, facilitate autolytic debridement and re-epithelialization, and prevent infection As the necrotic plaques loosened and new skin was visible beneath, they were removed with sterile forceps; however, aggressive debridement is contraindicated Pyoderma Gangrenosum Pathophysiology Pyoderma gangrenosum (PD) is an autoimmune disorder of unknown etiology that leads to painful skin necrosis PD is commonly associated with other inflammatory diseases such as Crohn disease, inflammatory bowel disease, arthritis, and hematologic malignancy.15 Pathergy, the development of skin lesions in the area of trauma or the enlargement of initially small lesions, is commonly seen with PD, especially if debridement of necrotic tissue is attempted Neutrophilic dermatosis occurs with altered neutrophilic chemotaxis and is thought to be part of the pathology.16 Clinical Presentation PD ulcers usually begin as small pustules or blisters and become larger with a violaceous border and surrounding erythema The first lesion may be at the site of minor trauma, but will progress and enlarge rapidly They are painful, necrotic, and usually recurring Sometimes PD will appear in groups of lesions at different stages of formation or healing They not respond to standard care if diagnosed as another wound type, and indeed may worsen if the standard TIMEO2 care is administered (FIGURES 812 to 814) Hamm_Ch08_227-254.indd 235 FIGURE 813 Pyoderma gangrenosum Some of the symptoms of PD are seen on this lower extremity wound, including the violaceous border, purulence, and necrotic tissue (Used with permission from Flowers D, Usatine RP Chapter 167 Pyoderma Gangrenosum In: Usatine RP, Smith MA, Chumley H, Mayeaux, Jr E, Tysinger J, eds The Color Atlas of Family Medicine New York: McGraw-Hill; 2009 http:// www.accessmedicine.com/content.aspx?aID=8208222 Accessed August 24, 2013.) 18/12/14 10:59 AM 236 Chapter Atypical Wounds skin grafts, along with concurrent immunosuppressive therapy to reduce the risk of pathergy, have been reported Necrobiosis Lipoidica Diabeticorum Pathophysiology Necrobiosis Lipoidica diabeticorum (NLD) is a disease of unknown etiology that is usually seen in morbidly obese patients with a strong family history of diabetes Different pathological mechanisms have been proposed and include microangiopathic and neuropathic processes, abnormal collagen degeneration, abnormal immune mechanisms, and abnormal leukocyte function NLD also results in thickening of the blood vessel walls and fat deposition, making the integumentary symptoms similar to vasculitis The disease tends to be chronic with recurrent lesions and scarring.19 FIGURE 814 Pyoderma gangrenosum The clinical appearance of PD can vary, as in this wound with both eschar and purulent subcutaneous tissue at the edges (Used with permission from Flowers D, Usatine RP Chapter 167 Pyoderma Gangrenosum In: Usatine RP, Smith MA, Chumley H, Mayeaux, Jr E, Tysinger J, eds The Color Atlas of Family Medicine New York: McGraw-Hill; 2009 http:// www.accessmedicine.com/content.aspx?aID=8208222 Accessed August 24, 2013.) Differential Diagnosis As there is no diagnostic test to confirm PD and multiple other conditions that resemble PD, a correct diagnosis relies on clinical presentation and exclusion of other causes TABLE 87 lists the systemic diseases most often associated with PD Further differentiation is made into these four subgroups: ulcerative, pustular, bullous, and vegetative.12,17 18 Medical Management Systemic management includes treatment of any underlying disease; systemic steroids are recommended for severe or widespread disease Other therapies that have been used in patients with PD include antibiotics (dapsone and minocycline), cyclosporine, clofazimine, azathioprine, methotrexate, chlorambucil, cyclophosphamide, thalidomide, tacrolimus, mycophenolate, mofetil, IV immunoglobulin, plasmapheresis, and infliximab.10,12,19 Wound Management Topical steroids, topical tacrolimus, nicotine patches, and intralesional steroids have been used for mild or moderate disease Debridement of adhered tissue is contraindicated and may cause pathergy; however, as the necrotic tissue loosens with reepithelialization, it may be gently removed with sterile forceps Keeping the lesions covered with a nonadherent mesh or silicone-backed wicking foam that will allow drainage to escape to a secondary dressing can help alleviate the pain associated with PD wound care Split-thickness TABLE 87 Clinical Presentation Lesions usually are bilateral but asymmetric on the tibial surface of the lower leg, and begin as a rash or to mm slightly raised spots They progress to irregular ovoid reddish-brown plaques with shiny yellow centers and violaceous indurated borders The edges may be raised and purple, and the wound bed may have good granulation tissue but no epithelial migration Pain and edema are also usually present Remodeling is characterized by round patches of hyperpigmentation (FIGURE 815).10,12,20 Differential Diagnosis Pyoderma gangrenosum Calciphylaxis Vasculitis Diabetic wound with peripheral vascular disease Medical Management Systemic steroids or other immunotherapy can be given in patients with severe disease Blood thinners such as pentoxifylline and aspirin may be helpful in facilitating cell migration to the damaged tissue Wound Management Topical and intralesional steroids can be beneficial in treating mild to moderate cases Other reported treatments include 0.1% topical tacrolimus ointment,20 collagen matrix dressings,21 and phototherapy.22 A combination of low-frequency noncontact ultrasound, topical steroid ointment, saline-impregnated cellulose dressings, and multilayer compression wraps, in conjunction with Systemic Diseases Associated with Pyoderma Gangrenosum Inflammatory Bowel Disease Arthritis Hematologic Abnormalities Immunologic Abnormalities Ulcerative collitis Regional enteritis Crohn disease Seronegative arthritis Rheumatoid arthritis Osteoarthritis Psoriatic arthritis Myeloid leukemia, hairy cell leukemia, myelofibrosis, myeloid metaplasia, immunoglobulin A monoclonal gammaopathy, polycythemia vera, proxysmal nocturnal hemoglobinuria, myeloma, and lymphoma Systemic lupus erythematous Complement deficiency Hypogammaglobulinemia Hyperimmunoglobulin E syndrome Acquired immunodeficiency syndrome) Hamm_Ch08_227-254.indd 236 18/12/14 10:59 AM Index Keloid scarring, 292f criteria for referral to regional burn center, 284t deep partial-thickness burn, 283f epidemiology, 281 escharotomy of circumferential burn, 289f estimating total surface burn area, 284t full-thickness burn, 283f initial evaluation and management of, 288–290 fluid requirements, 289 initial assessment, 288–289 pain control, 289–290 mechanisms of injuries, 284–288 chemical burns, 286 contact burns, 288 electrical burns, 285–286, 285f flame injuries, 285 Lichtenberg figures, 286f punctate lightning burn, 286f radiation, 286–288, 287f skin changes after, 287f scald, 284–285, 285f pathophysiology, 281 patient, formulas for nutritional requirements of, 289t rehabilitation of, 293 rule of nines, 283f superficial burns, 282f superficial partial-thickness burns, 282f treatment, 290–292 biological skin equivalent dressings, 292f deep partial-thickness and full-thickness, 291 full-thickness skin graft on hand, 291f meshed split-thickness skin graft, 291f silver-impregnated gauze, 290–291 superficial burn, 290 superficial partial-thickness burns, 290 surgical treatment, 291–292 topical antibiotic dressings, 290 zones of injury, 281 Jackson’s concentric zones of, 282f Buruli ulcers, 359 C Cadexomer iodine (CI) dressings, 374, 374f Cadherins, 3, 29 Calciphylaxis, 244–245 clinical presentation, 244 differential diagnosis, 244 early onset, 245f medical management, 244–245 pathophysiology, 244 progression of skin lesion, 245f treatment strategies, 245 wound management, 245 Calcium alginates, 355 dressings, 356f Hamm_Index_489-510.indd 491 Calf muscles, 124 dysfunction in, 136 Callous debridement, 332 Callus, 90 See also Edges, of wound, hyperkeratosis Capillary refill time (CRT), 107, 108f Capillary tube formation, 39 Cardiac cells, 310 Cardiovascular morbidity and mortality risk factor for, 100 Carville healing sandal surgical shoe with total contact heatmolded insert, 208f Carville 22° rocker sole, 208f Cataracts hyperbaric oxygen therapy, 466 CEAP classification, 130 of venous wounds, 129f Cell adherence, with desmosomes and hemidesmosomes, 5f metamorphosis, 52–57 fibroblasts, 57 macrophages, 54–57 platelets, 54 migration, 24t–25t proliferation, 24t–25t, 35f, 36f proliferation mechanisms, 21 signaling, 19t, 20t, 24t–25t Cell-to-wound matrix communication, 26 Cellular plasma membrane, 29 Cellular senescence, 319 Cellular surface hydrophobicity (CSH), 377 Cellulitis, 84f, 125, 135, 225, 239, 368 Center of gravity (COG), 205 Centers for Disease Control, 193 Centers for Medicare and Medicaid Services (CMS), 168, 363, 461 Central nervous system (CNS) hyperbaric oxygen therapy, 466 toxicity, 466 Charcot arthropathy, 213 Charcot-Marie-Tooth disease, 214 Charcot restraint orthopedic walker (CROW), 223 Charles’ law, 455–456, 456f Chemical burns, 286 Chemical messenger, 23 Chemotherapy, 311 Chemotherapy-induced peripheral neuropathy (CIPN), 311 Chicken pox, 239 See also Varicella-zoster virus (VZV) Choke vessels, 261, 262 Chronic venous insufficiency (CVI), 120 manifestation of, 123 predominant theories of, 124 risk factors for, 124t wounds, 329 491 Chronic wounds, 15–62, 57–61, 61f, 62 prevalence of, 60 growing concern, 58–60 types, 60–61 Chylous drainage, 83, 83f Circulation, efficiency, 262 Cisterna chyli, 147 Claudication, 101 Claustrophobia, 219 hyperbaric oxygen therapy, 466 Clock method, 75, 75f Closed wound, 122f Clostridium histolyticum, 327 Clostridium perfringens, 240 Coagulum, 43f, 82 in post-amputation site, 119f Cochrane-style systematic reviews, 364 Cognitive therapy, 312 Cold lasers, 483 Cold sore See Herpes virus, simplex virus (HSV), type Collagen, 28 dressing, 358f formation process, 41 synthesis, 48f triple helix, 40f Collagenases, 8, 327 use of, 328 Collectors, 144 Colonization, 189 Colonizing pathogens, 301 Colony-forming units (CFUs), 300, 364 Commercial depth shoes with heel roller toe rocker, 221f with rocker sole and total contact insert, 208f Compressed air therapy, 451–452 Compression, 131–136 bandages on an upper extremity, 160f kit, components of, 160f foam used with, 160f garments, 135f circular knit of, 161f flat-knit construction of, 161f toe, 161f principles of, 131 pumps, 160–161 intermittent, for chronic venous insufficiency, 162f stockings, 134 classification of, 136t therapy, 159–160 upper extremity compression, 161f Compression therapy, 301 algorithm for, 132f benefits of, 136 Computerized tomographic arteriography (CTA), 112, 113f Congestive heart failure, 467 exacerbation of, 466 18/12/14 12:33 PM 492 Index Connective tissue growth factor (CTGF), 38 Contact burns, 288 Contact dermatitis, 227–229, 228f allergens for, 228t clinical presentation, 228–229 differential diagnosis, 229 medical management, 229 pathophysiology, 227–228 wound management, 229 Contact layer dressings disadvantages/considerations, 350f protection of wound bed, 350f Continuous cell cycling mechanisms, 21 Corneocytes, 3, Corneodesmosomes, Corticosteroids, 304 for bullous pemphigoid (BP), 233 for cryoglobulins, 235 for debridement of detached epidermal tissue, 230 for herpes viruses, 239 side effect of, 303 Coumadin-induced skin necrosis, 245–246, 246f clinical presentation, 245 differential diagnosis, 245 medical management, 245 pathophysiology, 245 wound management, 246 C-reactive protein, 38t, 299t Critical limb ischemia (CLI), 99 natural progression of, 99, 101 Cryoglobulinemia, 234–235, 234f clinical presentation, 234 differential diagnosis, 234 medical management, 235 pathophysiology, 234 symptoms of, 234t wound management, 235 Cryoglobulins, 234 Cuboid ulcers, felted foam dressing, 219f Curling ulcers, 293 Curreri equation, 289 Custom molded shoes, 208f, 222 Cutaneous lymphoma, 249–251, 250f clinical presentation, 250 medical management, 250–251 pathophysiology, 249–250 primary, classification of, 250t wound management, 251 Cyanosis skin, 84, 85f Cytokines, 26 activity in wound healing, 55t principal sources and primary activities of, 37t–38t Cytotoxic immunosuppressants, 231 D DACC/Sorbact dressings, 378 Dalton law, 456, 456f Dark red skin discoloration, 85, 86f Hamm_Index_489-510.indd 492 Debridement, types of, 189t, 325–339 See also Enzymatic debridements; specific debridements eg, Autolytic debridements non-selective, 325 selective, 325 Deep inferior epigastric perforator (DIEP) flap, 260, 267 Defense mechanisms, 51 Delay phenomenon, 262–263, 263f Dendritic cells, 10, 52 Depression, and burnout, 201 Depth shoes with metatarsal rocker and SACH, 221f Dermagraft, 362f Dermal cells, 271 Dermal/epidermal junction, 5f Dermal papillae, Dermatome, 239, 270 Dermis, of skin, 5–7 sensory nerves within free nerve endings, 9f krause bulb, 9f Meissner corpuscle, 9f Pacinian corpuscle, 9f root hair plexus, 9f Ruffini corpuscle, 9f tactile/merkel disc, 9f vascular anatomy of, 272f Deroofed hematoma, with exposed fullthickness ulcer, 204f Desmosomes, 3, 5f Desquamation, Device-associated pressure ulcers, 185–187 Diabetes, 193–202 adults, type diagnostic criteria for, 202t annual number of U.S adults, 461f burden of, 193 care, 199 team, 199–201, 199f wound, clinician’s role, 201–202 case study, 194–197, 223–224 calcaneal eversion and toes, 196f foot examination for, 195t–196t Hubscher maneuver, 196f information, 195t plan of care, 197 plantar foot, 197f Semmes-Weinstein monofilament testing, 197f Silfverskiold test, 197f challenges in caring for patient with, 201 non-adherence, 201 depression and burnout, 201 education, 201 comprehensive management program, strategies to, 201t conclusion, 202 devastating effect, 205 diabetes mellitus (DM), 100 diagnostic criteria for, 201 diet, 200 education content, 200t epidemiology, 193–194 health care implications, 194–199 hemoglobin HbA1C and glucose critical values for, 197t impact on health, 193 impaired cellular function in, 215t impairs wound healing, mechanisms by, 199t inhibitory effects on wound healing, 305 intrinsic muscle wasting, with retraction of digits, 196f management strategies, 197f medical management, 199–201 neuropathy, 214 patients with lower-extremity wounds, 320 polyneuropathy, prevalence of, 193 in age groups, 194t statistics on, 194f treatment, annual cost of, 194, 205 type 1, 200 type (T2DM), 193 medications, 198t–199t ulceration, 212 prevention of recurrence, 222 wound evaluation, 201t Diabetes management strategies, 197 diabetes self-management education/ training (DSME/T), 200 glucose monitoring, 201 medical nutrition therapy (MNT), 200 pharmacologic management, 200 physical activity (PA), 200 Diabetes self-management education/ training (DSME/T), 200 Diabetic dyshidrosis, 204 use of emollient, 204 Diabetic foot, 202–223 AFO with double rocker sole, 222f ankle dorsiflexion knee bent— Silfverskiold test measurement of, 214f bilateral submetatarsal ulcers, 203f biomechanical changes with, 205–213 Carville healing sandal surgical shoe with total contact heat-molded insert, 208f Carville 22° rocker sole, 208f case study, 223–224 causes of wound, 212f Charcot bone destruction, X-ray of, 213f Charcot foot custom molded shoe with, 222f with dissecting sublesional hematoma, 204f 18/12/14 12:33 PM Index commercial depth shoe with heel roller toe rocker, 221f with rocker sole and total contact insert, 208f cuboid ulcer, felted foam dressing, 219f customized depth shoe with metatarsal rocker and SACH, 221f custom molded shoe, 208f deroofed hematoma with exposed full-thickness ulcer, 204f diabetes and effects on systems of foot, 203–205 diamond-shaped pixelated insole, 218f diapedia insole, 222f digital gripping with anterior imbalance, 210f dishydrosis with pre-ulcer, 213f dissecting sublesional hematoma, 215f felted foam dressing, 207f foot imbalance, eight vectors of, 210f footwear for people with, 219–223 selection, temple university classification for, 206t frontal plane forces, close-up of, 209f gait cycle, 211f glycosolation, 213–214 healing shoe with pixelated insole, 218f hexagonal pixelated insole, 218f instant total contact cast (iTCC) with ties to ensure compliance, 206f intrinsic muscle wasting with retraction, 211f limb-load removable cast walker, 208f midfoot collapse, 212f model, 212 neuropathic foot wound, 214–215 neuropathic ulcer, 215f off-loading insole, 219f off-loading the wound, 216–219 felted foam, 217–218 football dressing, 217–218 improving the removable walker, 218 off-loading devices, 217–218 transitional devices, 219 transitional off-loading, 216–217 orthowedge shoe, 217f patellar tendon bearing ankle foot orthoses, with rocker soled depth shoe, 207f brace, reinforced double upright AFO with, 223f Patient adherence, 201, 217f PressureStat pressure mat, 205f rader football dressing, 207f removable cast walkers (RCWs) with insole, 207f SACH heel insert, 221f Semmes-Weinstein monofilaments diagram of sites tested with, 204f Hamm_Index_489-510.indd 493 severe dyshidrosis before and after emollient, 204f silicone molded digital orthosis, 209f six-W biomechanical risk assessment, 216t surgical shoe with total contact molded insole, 220f TempTouch temperature sensor, 215f therapeutic shoe bill for patients, 220t total contact cast (TCC), 206f transitional off-loading devices, pictorial glossary of, 205 transmission of forces, frontal plane view of, 209f Diabetic foot ulcers (DFUs), 193, 347, 469f, 470f development of, 216 history of, 200 Diabetic foot wounds, 76, 460 classification systems for, 106t Diagnostic related group (DRG), 168 Dialkylcarbamoylchloride (DACC), 376 Diamond-shaped pixelated insole, 218f Diapedia insole, 222f Digital camera, 76 Digital deformities, 221 Digital gripping, with anterior imbalance, 210f Digital photography, 76 Digital subtraction, 112 Dihydroxyphenylalanine (DOPA), 10 Direct cutaneous perforator, 260 Dishydrosis, with pre-ulcer, 213f Distended saphenous vein, 130f DNA single-strand, 311 transcription inhibition, 370 virus, 238 Documentation, 183–185 elements of, 183 Dominant pedicles, 259 Donor site morbidity, 277 Doppler examination, 107, 108 Doppler flowmetry, 458 Doppler flow probe, 264 Doppler measured hyperemia, 465 Doppler ultrasound, 111 with color flow imaging, 111f Dorsiflexion, 135 DPP-4 inhibitors for type diabetes, 198t Drainage, for wound assessment, 81–84, 127 amount of, 82t chylous, 83, 83f definitions of, 82t enterocutaneous/enteroatmospheric fistula, 84, 84f exudate, 82, 83f infected, 84, 84f lymphatic, 83, 83f 493 purulence, 82, 83f sanguineous, 82, 82f serosanguineous, 82, 83f serous, 82, 82f Drawtex with exudate, 359f Dressings, 136 antimicrobial wound, 363–378 cadexomer iodine (CI), 374 calcium alginates, 356f DACC/Sorbact, 378 film, 350 foam, 355 gauze, 344 honey, 373f hydrocolloid, 354 hydrofiber, 355 non-adherent, 231, 290 polyhexamethylene biguanide (PHMB), 376 self-adhering, 344 silicone-backed foam, 238 silver-impregnated gauze use of, 290 wet-to-dry, mechanical debridement, 330–331, 330f Drug-induced hypersensitivity syndrome (DIHS), 229–230, 229f, 229t clinical presentation, 229 differential diagnosis, 229 medical management, 229 pathophysiology, 229 wound management, 229–230 Dry gangrene, 104f DSME/T program, 201 Duplex ultrasound imaging, 111 Dynamic molding process, 221 Dyshidrosis, before and after emollient, 204f E Ecchymosis of the skin, 86, 86f Edema, 87, 88f, 125 chronic, effect of, 309f clinical presentation of, 154 diagnoses and recommended interventions, 158t etiology of, 126 Edges, of wound, 87–90 detached, 89–90, 90f epibole, 89, 89f epithelialization, 90, 90f even, 87–88, 88f–89f hyperkeratosis, 90, 90f rolled, 89, 89f rolling, 363 uneven, 89, 89f Efferent lymph vessels, 146 Elastic bandages, 136 Elastin, 28, 271 structure and function, 40f 18/12/14 12:33 PM 494 Index Electrical burns, 285–286, 285f complications of, 285 high voltage, 285 low voltage, 285 Electrical stimulation (ES), 392 billing codes, 391t cellular/tissue levels, effects, 389 cell charge/attracting electrod, 391t chemotaxis, 390f current of injury, 390f electrotaxis, 390f epithelialization, 391 inflammatory phase, 391 proliferation, 391 remodeling/maturation, 391 in diagnostic and treatment procedures, 387 indications, 391–392, 391t infection control guidelines, 396 lead wires, 389f manufacturers, partial list, 388t noticeable responses, 397f parameters/application, 392–396, 396t application, 394–396, 394f direct and alternating currents, 392–393, 393f LVPC, low-volt devices, 393–394 monophasic HVPC, 393 polarity, 396 pulse duration/frequency, 396 voltage, 396 portable unit, 388f precautions/contraindications, 392, 393t terminology, 387t theory of, 389 tissue healing, 389 types of electrodes, 388f unit, 388f Emollient, use in diabetic dyshidrosis, 204 Emphysema, 467 Endothelial cells, 16t, 26, 31, 39, 46, 51, 143, 237, 249, 305, 425 Endothelial progenitor cells (EPCs), 56, 306, 310 reparative function of, 310 Endovascular therapy, 117, 137 Endovenous radiofrequency, 137 Enzymatically active proteins, 36 Enzymatic debridement, 327–328, 327f collagenase, application of, 327f eschar, cross-hatching of, 328f vs autocatalytic debridements, 328 Enzyme-linked immunosorbent assay (ELISA), 244 Enzyme lysly-oxidase, 28 Epibole, 363 definition of, 319 Epidermal barrier, 290 Epidermal cells, 43 Epidermal growth factor (EGF), 43 Epidermal pegs, Hamm_Index_489-510.indd 494 Epidermis, of skin, 3–5 definition of, 271 layers of, 271f stratum basale, stratum spinosum, stratum granulosum, stratum lucidum, and stratum corneum, 4f Epithelial cells, 11, 16t, 23, 34f, 43, 89, 90f, 319, 324, 328, 367, 389, 391 Erosion, 11, 11f Erythema, 84, 84f–85f definition of, 84 Eschar on ischemic foot, 116f tissue, 79, 79f Escherichia coli, 364, 367 E-stim technology See Electrical stimulation (ES) Eucteric mixture of local anesthetic (EMLA), 377 European Pressure Ulcer Advisory Panel (EPUAP), 319 Exercise stress test (EST), 110 Expander device, 263 Extracellular matrix (ECM), 15, 26, 39f, 271 adherent components of, 29 components of, 49f liquefaction of, 36 proteins, 357 Extrinsic stressors, 202 Exudate, 82, 83f F Factitious wounds, 251, 251f clinical presentation, 251 differential diagnosis, 251 medical management, 251 pathophysiology, 251 wound management, 251 Famciclovir, for chicken pox, 239 Fascia, 120, 143, 183, 212, 239, 255–261, 324f, 410 Fasciocutaneous flap, 260 direct cutaneous perforator, 260 musculocutaneous perforators, 260 Nahai-Mathes classification, 260t septocutaneous perforator, 260 types, 260 Fasting blood glucose (FBG), 194 Felted foam dressing (FFD), 207f, 218 Fibrin, 30, 273 Fibroblasts, 16t, 29, 44, 54, 57, 271, 303 to myofibroblasts, transition of, 57f Fibroplasia, 41 overview, 48f Fibroproliferation, 263 Fibroproliferative healing mechanisms, 22 Fibrotic, hypertrophic skin, 126f Fibrous structural proteins, 28 Filaggrin, Filament-aggregating protein See Filaggrin Film dressings, 350 Filtration, 149 Fistula, 78, 78f definition of, 78 Flame injuries, 285 Flaps, 255–267 classification, 255–257 tissue composition, 256 transfer method, 256 vascular orientation, 257 vascular supply, 255–256 complications, 266–267 arterial insufficiency, 267, 267f extrinsic factors, 266 intrinsic factors, 266–267 venous insufficiency, 267, 268f definition, 255 hyperthermia, 265 monitoring, 264–267 ancillary monitoring methods, 265–266 physiological parameters, 264–265 physiology, 261–264 delay phenomenon, 262–263, 263f microcirculation regulation, 262 tissue expansion, 263–264, 263f vascular sequence following flap harvest, 261–262 vascular anatomy, 257–261 angiosome concept and choke vessels, 261 fasciocutaneous flap, 260 muscle flaps, 258–259 perforator flaps, 260–261 vascular supply of skin, 257, 258f veins and venosomes, 261 Flawed harvest technique, 267 Flexible foot imbalances, 221 Flexor carpi radialis (FCR), 260 Fluorescein dye, 266 Foam boots, with suspended heels, 173f Foam dressings, 355 Foam sclerotherapy, 137 Food and Drug Administration, 334, 336 Foot imbalance, eight vectors of, 210f muscles, dysfunction in, 136 musculoskeletal assessment of, 205 Football dressing, 218 Footwear for people with diabetes, 219–223 selection, temple university classification for, 206t Foreign debris, 23 Foreign objects, 81, 81f Fournier gangrene, 240 Fragile granulation tissue, 323 Free tissue transfer, 255 Friction, 166f forces, 165 Frontal plane forces, close-up of, 209f 18/12/14 12:33 PM Index Full-thickness injuries, 283 Full-thickness skin graft (FTSG), 270, 273 Fungal infections, 242–243 clinical presentation, 242 differential diagnosis, 242–243 evidence of, 223 medical management, 243 onychomycosis, 243f pathophysiology, 242 tinea capitis, 243f tinea pedis, 243f wound management, 243 G Gait cycle, 211, 211f Gaiter area, 126 Gas gangrene, 458 Gastrocnemius muscle, 214, 258 Gauze dressings, 344 Glabrous skin, arterioles, 10 Glucagon-like peptide-1 analog for type diabetes, 198t Glucose monitoring, 201 Glycosaminoglycans (GAGs), 5, 29, 42 Glycosolation, 213–214 Gold Dust, 360 Gram-positive bacteria, 301 Granulating wound bed, 38, 47f, 346, 358f, 414 Granulation tissue, 79, 79f, 323 Greater saphenous vein (GSV), 118, 120 Greater trochanter anatomic relationship between inferior aspects of, 178f Growth factors, 26, 50t H Hallux limitus, 223 Harris-Benedict formula, 289 Healthcare providers, 220, 221, 223 goals of, 190 Heel protection, category of, 173 protectors, 172 wound case study, 121f Hemidesmosomes, 3, 5, 7t, 233 Hemodialysis, 103f, 107, 244, 245 Hemoglobin, HbA1C and glucose, critical values for, 197t test, 195 Hemosiderin deposition in skin, 125f staining, 85–86, 86f, 124 Hemostasis, 19t, 31f clot formation, 30 Henry law, 456, 456f, 459 Herpes virus, 238–239 clinical presentation, 239 differential diagnosis, 239 medical management, 239 Hamm_Index_489-510.indd 495 pathophysiology, 238–239 simplex virus (HSV), type 1, 238–239, 238f varicella-zoster virus (VZV) chicken pox, 238, 238f shingles, 238, 238f wound management, 239 Heterotrophic ossification (HO), 293 High fevers, 467 Highly active antiretroviral therapy (HAART), 249 High-powered parallel waterjet, 334 High-volt pulsed current (HVPC), 393 Homeostasis, 10, 12, 143, 202, 203, 310 Honey dressings, 372, 373f, 432 Hubscher maneuver, 196f Hydrating cream, use in diabetic dyshidrosis, 204 Hydrocolloid dressings, 354 Hydrofiber dressings, 355, 356f dry hydrofiber, removal of, 357f Hydrostatic pressure, 149 Hydro-surgery, 115 Hydrosurgical debridement, 334, 334f clean, healthy wound bed after, 334f Hygroscopy, 10 Hyperbaric oxygen therapy, 244, 451, 452–453, 461f, 466, 467, 469–471 absolute contraindications, 468 bleomycin sulfate, 468 concomitant treatment with doxorubicin, 468 untreated pneumothorax, 468 adverse effects of, 465 cataracts, 466 central nervous system, 466 claustrophobia, 466 congestive heart failure, exacerbation of, 466 middle-ear barotrauma, 465–466 myopia, 466 pulmonary barotrauma, 466 pulmonary oxygen toxicity, 466 sinus squeeze, 466 arterial insufficiency ulcers, 462 arterial partial pressure, 460f atmospheres absolute (ATA), 453 categories of disorders, 459f in clinical practice, 459–460 angiogenesis, in irradiated tissues, 460 collagen deposition, 460 cytokine activity, mediation of, 460 HBO2 therapy, tissue oxygen levels, 459 immune response, 460 oxygen, in wound healing, 459–460 clostridial gas gangrene, 463 Clostridium perfringens, 452 compressed air therapy, 451–452 compromised skin grafts/flaps, 463–464 495 contraindications, 467 active respiratory infections/ sinusitis, 467 congestive heart failure, 467 ear surgery, history, 467 emphysema, 467 high fevers, 467 optic neuritis, 467 pregnancy, 467 seizure disorders, 467 spontaneous pneumothorax, 467 uncontrolled hypertension, 467 definition of, 453 delayed radiation injury soft tissue/bony necrosis, 462–463 diabetic wounds, of lower extremity, 460–462 double-lock chamber, 455f equipment, 453–455 hyperbaric oxygenation general principles, 453 physiologic effects, 457 blood flow to tissues, 458 gas bubble size, mechanical effects, 457 gas gangrene, Clostridium perfringens, 458–459 hypoxic wounds, 458 oxygen dissolved, in plasma mechanical effects, 457 oxygen, elevated partial pressures of, 458 skin flaps, viability of, 459 largest chamber, 452f monoplace, 453f, 454f multi-place chamber, 454f pressurization, physics of gas laws, 455 Boyle law, 455, 455f Charles’ law, 455–456, 456f Dalton law, 456, 456f Henry law, 456, 456f units of pressure, 456–457 refractory osteomyelitis, chronic, 463 safety guidelines, 468 thermal burn injury, 464–465 use of, 453f Hyperglycemia, 214 Hypergranulation tissue, 323f after treatment with PAV foam, 325f interventions, examples of, 325t before treatment with PAV foam, 325f Hypertension, uncontrolled, 467 Hypertrophic scarring with joint impairment, 293f with severe contractures and functional impairments of hand, 293f surgical excision of, 293f 18/12/14 12:33 PM 496 Index Hypodermis, of skin, Hypothermia, 262, 264 Hypovolemia, 266 I IgG autoantibodies, formation of, 233 Imbalances, chronic posterior, 211 Immune response HBO2 therapy, tissue oxygen levels, 459 Immune system, function of, 26 Immunoregulatory cell, 54 Immunosuppressive agents, 237 Incisional dehiscence, 119f Incompetent valves, 123f Incontinence-associated dermatitis, 188t Indepth shoes, 220 Indocyanine green dye (ICG), 266 Induration, 87f Infected drainage, 84, 84f Infected wounds, 239–240 Infection, 90–91, 188t causes of, 189 clinical signs of, 104 signs of, 91t treatment of, 136 wound odor, 90 Inferior vena cava (IVC), 122 Inflammation, 30–38, 32f kill and contain invader, 30–35 killing the pathogens, 32f neo-angiogenesis, 34f neo-genesis, 34f overview, 44t wound debridement, 33f, 36–37 Inflammatory mediators, 289 Inflammatory wounds, 188t Inhalation injury, 285 Inlet junction, 143 Innate immunity, 51 Innate system, 51 Inosculation, 273 “Inside-out” approach, Instant total contact cast (iTCC), 223 with ties to ensure compliance, 206f Insulin-like growth factor (ILGF-1), 303 Insulin resistance, 307 Integra, 291 Integrin, 41 Integumentary system anatomy and physiology of, 3–12 skin, anatomy of, 3–7, 4f functions of, 8–11 loss, definitions of, 11–12 physiology, Interferon gamma (IFN-γ), 51 role of, 53f Interferons, 38t Interleukins, 26 principal sources and primary activities of, 37t–38t Hamm_Index_489-510.indd 496 Intermittent pneumatic compression pumps, 136 International Consensus Committee on Chronic Venous Disease, 128 International normalized ratio (INR), 232 International Society of Lymphology, 153 Intravascular ultrasound, 131 Intrinsic minus foot, 214 Intrinsic muscle wasting with retraction, 211f of digits, 196f Invader, clearing and containing, 47–50 Invasive debridement technique, 320, 321 Invasive tests, 112, 130–131 arteriogram, 112, 114f prevention, 112–114 Invasive therapy, 137 Ischemic digits, pre-surgical protection of, 115f Ischemic limb, use of protective boots for, 115f Ischemic wounds characteristics of, 104 due to vasculitis, 102f Ischial tuberosity, 177 anatomic relationship between inferior aspects of, 178f Isograft, 270 IV Arginine butyrate for sickle cell wounds, 246 J Jaundice, 86–87, 86f–87f K Kaposi sarcoma (KS), 249, 249f clinical presentation, 249 differential diagnosis, 249 medical management, 249 pathophysiology, 249 wound management, 249 Keloid scarring, 292f Keratin matrix, Keratinocyte growth factor (KGF), 43 Keratinocytes, 3, 17t, 37, 43, 271, 276 L Lamellar granules, Langerhans cells, 10, 361 LaPlace’s law, 132 Larval therapy, 335 Laser ablation, 137 Lateral circumflex femoral artery (LCFA), 256 Lean body mass (LBM), loss of, 93 Learned immunity See Adaptive immunity Leptospermum polygalifolium, 371 Leukocyte-trapping theory, 124 Lichtenberg figures, 286f Lift pressure relief, 180f Ligation, 137 Limb-load removable cast walker, 208f Linear array of scanners, 111 Lipedema, 152, 153f Lipodermatosclerosis, 125, 125f Lipopolysaccharide (LPS), 301 Lower-extremity amputation (LEA), 205 Lower-extremity ulcers, 320 Low-frequency ultrasound (LFUS), 427 energy debridements, 331 advantages of, 331 ankle wound after contact, 331f ankle wound before contact, 331f positive effects to wound closure and healing, 331 Low-level laser therapy (LLLT), 483, 484t application parameters for, 485 techniques for, 485–486, 486t cellular/tissue levels, effects, 485 comparison between, 484t indications/precautions/ contraindications/adverse reactions, 485 laser, properties, 484f monochromatic light emitted, 483f terminology, 484t theory of, 483–484 transparent film, 486f Low-volt pulsed current (LVPC), 393 Lupus anticoagulant, 232 Lymph capillaries, 143 nodes, 144f, 146 anatomy of, 147f clusters of, 146f transport, 158 Lymphatic drainage, 83, 83f Lymphatic flow, physiology of, 147–151 lymphatic trunks and territories, 148f venous angle, 148f Lymphatic fluid, 147 Lymphatic pumps, 160 Lymphatic system, 143 Lymphatic trunks, 144 Lymphedema, 143–164 abdominal lymph nodes, as result of occlusion to, 155f case study, 149, 163 clinical presentation of, 153–154 differential diagnosis of, 154–155 late stages, anatomic changes in, 156f lipedema, 153f lymphatic flow, physiology of, 147–151 lymphatic trunks and territories, 148f venous angle, 148f lymph system, anatomy of, 143–147 oncology-related, 152 pathophysiology of, 151–155 pitting edema, 156f praecox, 151f 18/12/14 12:33 PM Index primary, 145t, 151, 151f as result of cancer and radiation, 153f risk factors for, 153 secondary, 145t, 151, 152f causes of, 152 chronic venous insufficiency with, 152f due to orthopedic surgery, 154f due to systemic disorder, 154f due to trauma, 154f risk factors for, 155t stages of, 155t skin changes, 157f stages of, 153 Starling’s law of equilibrium, 149f physiological components, definitions for, 150t Stemmer sign, 156f treatment of, 155–159 bandage systems and indications, types of, 160t compression bandage kit, components of, 160f bandages on an upper extremity, 160f circular knit of garments, 161f flat-knit construction of garments, 161f foam used with, 160f intermittent pump for chronic venous insufficiency, 162f pumps, 160–161 therapy, 159–160 toe garment, 161f upper extremity compression, 161f exercise, 161–162 during manual lymphatic drainage, flow of, 159f manual lymphatic drainage mobilization (MLD mob), 159, 159f skin care, 162–163 upper and lower extremities, exercise programs for, 162t venous and lymphatic flow, strategies to, 158t Lymph system, anatomy of, 143–147, 144f bone marrow, 144f collectors, 144 full-body lymphatic system, 144f lymphangion, 146f lymphatic capillaries, 145f anchoring filaments of, 146f lymphatic trunks, 144 lymphatic watersheds, 146f lymph nodes, 144f anatomy of, 147f clusters of, 146f Peyer’s patches, 144f thymus, 144f Hamm_Index_489-510.indd 497 M Macrocirculation, definition of, 101 Macrophages, 17t, 31, 52 function, 54t functions of, 56t phagocytic activity of, 56f role in antigen presentation, 53f role in transition and differentiation, 55f transition, 54 wound-activated, functions, 46f Macular erythema, 232 Mafenide acetate (Sulfamylon) topical antimicrobial agent, for burns, 290 Maggot debridement therapy (MDT), 335–336, 335f, 336f actions of, 335 benefits of, 335 veil removed after therapy, 337f wound after cleansing of slough and debris, 337f Magnetic resonance arteriography, 112, 113f disadvantages, 112 Major histocompatibility complex class II (MHC class II), 54, 56 Malignancy, 188t Malignant wounds, 247–251 basal cell carcinoma, 247, 247f cutaneous lymphoma, 249–251, 250f primary, classification of, 250t Kaposi sarcoma (KS), 249, 249f melanoma, 248f Breslow depth scale for, 248t types of, 248t Merkel cell carcinoma (MCC), 249, 250f signs and symptoms of, 250t squamous cell carcinoma (SCC), 247–248 early stage, 248f late stage, 248f Manual lymphatic drainage mobilization (MLD mob), 159, 159f Marjolin ulcers, 293 Mast cells, 31 structure and function, 46f Material safety data sheets (MSDS), 286 Matrix deposition, 42 Matrix metalloproteinases (MMPs), 26, 327, 357 Maturation process, 44–47, 275 and remodeling, 51f Mechanical debridement, 328–331 hydrotherapy, 328 low-frequency ultrasound (LFU) energy, 331 pulsatile lavage with suction (PLWS), 329–330, 329f soft abrasion debridement, 328 wet-to-dry dressings, 330–331, 330f whirlpool (WP), 328, 328f contraindications to, 329t Mechanoreceptors, 8, 9f Medical nutrition therapy (MNT), 200 497 Medicare therapeutic shoe bill, 220 Medications, for venous wounds, 136–137 Medi-sol, for scald, 285 Meglitinides, for type diabetes, 198t Melanocytes, 10 Melanoma, 248f Breslow depth scale for, 248t clinical presentation, 248 medical management, 249 pathophysiology, 248 types of, 248t wound management, 249 Merkel cell carcinoma (MCC), 249, 250f clinical presentation, 249 differential diagnosis, 249 medical management, 249 pathophysiology, 249 signs and symptoms of, 250t wound management, 249 Merkel cells, 3, Metalloprotease-1 (MMP-1), 43 Metatarsophalangeal joint (MPJ) See Hallux limitus Methicillin-resistant Staphylococcus aureus (MRSA), 300f, 335, 371 Methylene blue-gentian violet polyvinyl alcohol foam (MBGV-PVA), 375 Meticulous technique, 275 Microcirculation, 261 definition of, 101 regulation, 262 local regulation, 262–263 systemic regulation, 262 Middle-ear barotrauma, 465f hyperbaric oxygen therapy, 465–466 Midfoot collapse, 212f Minimal erythema dose (MED), 477 Mölnlycke health care, 417 Morbid endovascular techniques, 139 Motor and sensory systems, 179 Muscle, 79, 80f, 324f non-viable, 80f Muscle flaps, 258–259 vascular anatomy of, 259f patterns of, 259t type I, 258 type II, 258–259 type III, 259 type IV, 259 type V, 259 Muscular atrophy, 93 Musculocutaneous perforators, 260 Musculoskeletal assessment, of wound, 92–94 Mycobacteria, 241 cause integumentary disorders, 242t clinical presentation, 241 differential diagnosis, 241 medical management, 241 pathophysiology, 241 wound management, 241 18/12/14 12:33 PM 498 Index Myofibroblasts, apoptosis of, 46 Myonecrosis (gas gangrene), 240–241, 240f, 240t clinical presentation, 240 medical management, 240–241 pathophysiology, 240 wound management, 241 Myopia, hyperbaric oxygen therapy, 466 N National health system budget, 165 National Indian Health Bureau, 203 National Pressure Ulcer Advisory Panel (NPUAP), 69, 131, 170, 183, 319 staging system, 183–185, 186t, 187 Natural killer (NK) cells, 15 Natural moisturizing factors, 10 Necrobiosis lipoidica diabeticorum (NLD), 236–237, 237f clinical presentation, 236 differential diagnosis, 236 medical management, 236 pathophysiology, 236 wound management, 236–237 Necrotic burden, definition of, 319 Necrotic tissue, 322 Necrotizing fasciitis (NF) clinical presentation, 239 differential diagnosis, 239 medical management, 240 pathophysiology, 239 risk factors for, 239 wound management, 240 Negative pressure wound therapy (NPWT), 23, 116, 274–275, 274f, 346, 401, 401f amputation site not appropriate for, 116f application, 415–418, 415t parameters/techniques for, 410 amount of pressure, 414–415 Bio-Dome™ Easyrelease™, 414f compressed foam, 411f frequency of dressing change, 415 initiation/discontinuation, 415 mode of delivery, 411–412, 412t puffy foam, 411f types of foam, 413f V.A.C., 412f wound fillers, advantages and disadvantages, 412–414, 413t tips for, 417t basic components, 402t case study wound, 419f cellular/tissue levels, effects, 404, 404t appropriate for, 405f, 406f bioburden, 405 cellular deformation, 404 circulation, 405 contraction, 405 fluid removal, 404–405 Hamm_Index_489-510.indd 498 infected wounds, 405t occlusion, 404 granulation tissue, protection of, 410f indications, 405, 406t abdominal wound, 406f incisional, 406f biological dressing, 407f lower extremity compartment syndrome, 407f medial and lateral lower extremity fasciotomies, 407f palliative care, 408f silver-impregnated foam, 407f special populations, 408–409 surgical incisions, 408f traumatic wound, 407f wounds acute, 405–408 chronic, 408 ischial tuberosity, 417f multiple pieces of foam, 416f partial vendor list, 403t patient education list, 418t pediatric patients, guidelines, 409t precautions contraindications, 409–410, 410t measures, 410 for pediatric patients, 409t pressure guidelines for pediatric patients, 409t recommendations, 415t pump connector, 417f recommendations for discontinuation, 415t reducing pain at dressing change, 418t theory of, 402 thin foam, 416f treatment with, 121f wound deterioration, signs of, 410t Neo-angiogenesis, 23, 34f, 54 Neo-genesis, 34f Neosporin, for scald, 285 Neuropathic foot classic model of, 193 wound, 214–215 Neuropathic ulcer, 215f Neuropathy, 216 Neutrophil extracellular traps (NETs), 31, 51 Neutrophils, 31 extracellular traps, 52f migration and adherence, factors to, 45f Non-adherent dressings, 231, 235, 290 Non-atherosclerotic/vasculitic disorders, 103 Non-healing pressure ulcer, 105f Non-healing wound, 101 Non-invasive vascular studies for arterial wounds, 105–112 arterial duplex, 110–112 capillary refill time (CRT), 107, 108f computerized tomographic arteriography, 112 Doppler examination, 107, 108 exercise stress test (EST), 110 pulses, 105–107 segmental limb pressure, 109, 109f toe pressures, 108–109 transcutaneous oxygen perfusion (TcPO2), 110, 110f rubor of dependency test, 107–108 for venous wounds, 130 venous duplex examination, 130 Nonsteroidal anti-inflammatory drugs (NSAIDs), 290, 303 affect wound healing, 304t for cryoglobulinemia, 235 stalled wound on patient taking, 304f Normal foot biomechanics, 212 Nutritional supplements, 308 O Off-loading insole, 219f Off-loading, the wound, 216–219 felted foam, 218 football dressing, 218–219 improving the removable walker, 218 off-loading devices, 217–218 transitional devices, 219 transitional off-loading, 216–217 Opsonization, 52 Optic neuritis, 467 Organ transplantation, 303 Orthowedge shoes, 217f Oscillating veins, 261 Osmotic pressure, 151 Osteomyelitis, 203 chronic, 463, 464f Osteomyofasciocutaneous flap, 260 Osteoradionecrosis, 462 P Pain, 91, 127 control in burn wound management, 289–290 descriptions and causes, 91t visual analog scale, 91t Patellar tendon bearing (PTB), 218 bearing ankle foot orthoses, with rocker soled depth shoe, 207f bearing brace, reinforced double upright AFO with, 223f Pathergy, definition of, 321 Pathogen-associated molecular patterns (PAMPs), 300, 301 Pathogens, definition of, 300 Patient adherence, 201, 217f Patient-centered approach, 217 Pattern recognition receptors (PRRs), 300 Peak systolic velocity (PSV), 112 Pemphigus, 232–233, 233f clinical presentation, 232 differential diagnosis, 232 18/12/14 12:33 PM Index medical management, 233 paraneoplastic, 233f pathophysiology, 232 wound management, 233 Peptidoglycan (PGN), 301 Perforator artery to skin, 257 Perforator flaps, 260–261 Gent classification of, 261f, 261t simplified classification of, 261f, 261t standardize nomenclature of, 261 Peripheral arterial occlusive disease (PAOD) causes of, 101 prevalence of, 100, 101 severe cases of, 107 surgical intervention for, 118 Peripheral edema, 164 medications for, 157t treatment of, 156 Peripheral vascular disease, 58 Periwound characteristics, 184f skin, 127 Perpendicular method, 73–75, 75f Personal protective equipment (PPE), 330, 445 Phagocytose, pathogen to, 162 D-phenylalanine derivatives for type diabetes, 198t Phlebography, 130 Photography, 76, 77f guidelines for, 76t Physical activity (PA), 200 Physiological parameters, of flaps monitoring, 264–265 capillary refill time (CRT), 264 color, 264–265 flap temperature, 265 needle prick, 265 vital signs, 264 Pie crusting, 275 Pillows, used to off-load the heels, 174f Pitting edema, 156f Pivotal cells, 15 Pixelated insole healing shoe with, 218f hexagonal, 218f Planimetry, 76 Plantar flexed ankle, 173f Plantar flexion contraction, 172 Plastic surgery procedures, 270 Platelet-derived growth factor receptor (PDGFR), 30, 362, 460 expression, 305 Platelets, 18t binding and activation, 43t plug, formation of, 50 Polyhexamethylene biguanide (PHMB), 360, 375 dressings, 376 irrigations, 367 Hamm_Index_489-510.indd 499 Polymerase chain reaction (PCR) sequencing, 366 Polymorphonuclear cells, 45t Polymorphonuclear leukocyte (PMN), 18t, 30, 459 extravasation of, 51 Polypeptides, 26 Polysaccharides biofilm, 58 matrix, 58 Polytetrafluoroethylene (PTFE), 118 Polyvinylalcohol (PVA) foam, 375, 413 Positioning cushions, 178–179, 178f Posterior interosseus artery (PIA), 257 Post-healing care, for wounds, 139 Post-phlebitic syndrome, 124 Post-thrombotic syndrome, 123, 124f signs and symptoms of, 124t Praecox, 151f Prayer sign, 213 Precollectors, 143 Pregnancy, 467 Premarket approval (PMA), 361 Pressure redistribution surfaces, 168 PressureStat device, 204, 205f Pressure ulcers, 165–190 abscess, 188t areas of body at risk for, 167f Braden scale, for predicting pressure sore risk, 169t case study, 170, 189 complications of, 189–190 debridement, for types, 189t definitions of, 165 device-associated, 187t foam boots with suspended heels, 173f friction, 166f full-forward lean to accomplish weight shift, 182f incontinence-associated dermatitis, 188t infection, 188t inflammatory wounds, 188t interventions to, reduce duration of loading, 179–182 device-associated pressure ulcers, 185–187 documentation, 183–185 reclined positions, 180–181 recumbent postures, 179 supine position, 179 turning frequency, 181 wheelchair weight shifts and pressure reliefs, 181–182 ischial tuberosity and greater trochanter anatomic relationship between inferior aspects of, 178f lift pressure relief, 180f location of, 165 malignancy, 188t 499 manage tissue loading, interventions to, 168–179 heels and lower extremities, protection, 173–174 positioning cushions, 178–179, 178f skin protection cushions, 177–178 support surfaces beds, mattresses, and overlays, 170–172 evaluating the effectiveness of, 172 wheelchairs cushions, 175–177 positioning and fitting, 174–175 and wheelchair cushions, 174 moisture on skin, 166f causative factors, 165 partial forward lean, 182f partial weight shifts, 182f pathophysiology, 165–166 periwound characteristics, 184f pillows used to off-load the heels, 174f plantar flexed ankle, 173f position of, patient in bed to prevent sliding, 180f prevention, 166–168 rigid ankle-foot orthotic with heel, 173f risk evaluation, 171 sacral area, anatomic nomenclature of, 185f scale for healing, 69 semi-reclined/Fowler’s position, 180f shear, 166f sitting-acquired, 174 skin tear, 188t stages, 186t support surfaces active, 171f air-fluidized bed, 171f alternating-pressure, low-air-loss, 171f categories and features of, 170t cross-section of, 171f thirty-degree side-lying posture, 174f time/pressure curve for, 168f time to tissue destruction, 167t tissue characteristics, 184f treatment of, 187–189 use of biophysical technologies for, 190t user-worn heel protector, 173f wheelchairs (See Wheelchairs) Pressure wound therapy, 240, 331 Prevena, 407 Procellera, 359, 393 Procollagen, 41 Progenitor endothelial cell adhesion molecule (PECAM-1), 39 Programmed cell death See Apoptosis Proinflammatory cytokines, 23, 26, 54, 58 Proliferation, 20t, 24t–25t, 35f, 36f, 38–44 Prominent cells, phenotypical changes in, 15 18/12/14 12:33 PM 500 Index Prophylactic therapy, 232 Prosit technology, 393 Prostaglandin, 38t Proteases, Protein energy malnutrition (PEM), 307 Proteoglycans, 5, 29, 42 structure, 41f Proud flesh See Hypergranulation tissue Provider-centered approach, 217 Pseudoequinus, 211 Pseudomonas aeruginosa, 371, 374, 375 Psoralen+UVA (PUVA) phototherapy for cutaneous lymphoma, 250 Pulmonary barotrauma, hyperbaric oxygen therapy, 466 Pulmonary oxygen toxicity, 466 Pulsatile lavage with suction (PLWS), 439 application personal protective equipment/ environmental guidelines, 445–446 techniques for, 444 frequency/duration, 445 irrigation fluid, temperature of, 445 irrigation force, 444 suction force, 444 treatment preparation, 446–448 case study, treatments, 448f cavities, 444f clinician in PPE, 445f components of, 440f debridement, 329–330, 329f benefits of, 330t equipment requirements, 441t handpiece photo of, 440f with splash shield, 446f indications, 443 infection control guidelines, 445t irrigation bag with the tubing tip, 447f negative pressure, benefits, 441t parameters for, 444t positive pressure, benefits, 441t precautions, 443–444 psi controls, handpiece photo, 441f pulsed lavage with suction, 443f right lower abdominal wound, 442f sacral ulcer patient, 446f sacral wound, 443f suction canister, 447f theory of, 439 negative pressure, 439–441 positive pressure, 439 tissue/cellular levels, effects, 442–443 whirlpool comparison, 449t turbine, photo of, 441f wound with adhered fibrous tissue, 442f Pulses, 105–107 oximetry, 266 Punctate lightning burn, 286f Purulent drainage, 82, 83f Hamm_Index_489-510.indd 500 Pyoderma gangrenosum (PD), 235–236, 235f, 236f, 322f clinical presentation, 235 differential diagnosis, 236 medical management, 236 pathophysiology, 235 systemic diseases associated with, 236t wound management, 236 R Rader football dressing, 207f Radiation, 286–288, 287f chronic, wound, 463f induced skin injury, 286 injury chronic, phenotypic characteristics of, 287 skin changes after, 287f wounds, treatment of, 311 Radiotherapy, 311 Raynaud phenomenon, 84, 89f, 237 Reabsorption, 149 Reactive oxygen species (ROS), 60t, 305 Reclined positions, 180–181 Rectus femoris muscles, 256 Recumbent postures, 179 Red blood cells (RBCs), 52, 124 Re-epithelialization, 43, 49f, 49t, 51f, 277 Regeneration mechanisms, 21 REGRANEX Gel, 362, 363 Remodeling, 44–47 Removable cast walkers (RCWs) with insole, 207f Revascularization, 101, 273 Rigid ankle-foot orthotic with heel, 173f RNA transcription inhibition, 370 Rubor of dependency test, 107–108 S SACH heel insert, 221f SACH-style heel, 221 Sacral area, anatomic nomenclature of, 185f Sacral ulcers, 75 pressure ulcer, 321f Sagittal gait cycle, 211 Sanguineous drainage, 82, 82f Saphenous vein, 120 Scald, 284–285, 285f Scalp skin expansion, 263 Schwann cell, Scleroderma, 237–238, 237f clinical presentation, 237 CREST, symptoms of, 237t differential diagnosis, 237 medical management, 237 pathophysiology, 237 wound management, 237–238 Sclerotherapy, 137 Secondary segmental pedicles, 259 Segmental limb pressure, 109, 109f Seizure disorders, 467 Self-adhering dressings, 344 Semi-reclined/Fowler’s position, 180f Semmes-Weinstein monofilaments diagram of sites tested with, 204f testing, 197f Senescent cells, 58 post-mitotic cells, definition of, 309 Sensation, 9–10, 9f Sensory receptors, Septocutaneous perforator, 260 Septum, 256, 260–261 Seropurulence drainage, 82 Serosanguineous drainage, 82, 83f Serous drainage, 82, 82f Serpentine, 89 See also Edges, of wound, uneven Serum imbibition, 273 Sharp/surgical debridement, 331–334 analgesics, examples of, 333f callus debridement, 333f currettes, 332f curved and straight iris scissors, 332f of pressure ulcer eschar, 333f scalpels, 332f serrated and standard forceps, 332f Shear, 166f forces, 215 strain, 180 Sickle cell ulcers See Sickle cell wounds Sickle cell wounds, 246–247, 246f clinical presentation, 246 differential diagnosis, 246 medical management, 246 pathophysiology, 246 wound management, 246–247 Silfverskiold test, 197f, 214 Silicone-backed foam dressings, 168, 238 Silicone molded digital orthosis, 209f Silver-impregnated gauze dressings use of, 290 Silverlon, 417 Silver sulfadiazine (Silvadene), for burns, 290 Sinus extensions, 77, 78f squeeze, 466 hyperbaric oxygen therapy, 466 Six-W biomechanical risk assessment, 216t Skeletal malalignments, 210 Skin, anatomy of, 3–7, 271–272 appendages, 271–272 blood supply, 271 dermis, 5–7, 271 epidermis, 3–5, 271 hypodermis, appendages, 271 autograft harvesting, morbidity of, 271 care, 162–163 18/12/14 12:33 PM Index cellular components of, 6t functions of, 8–11 aesthetics and communication, 11 fluid loss, prevention of, 10 protection from environment, 8–9 protection from ultraviolet rays, 10 sensation, 9–10 thermoregulation, 10 vitamin D, synthesis and storage of, 10–11 health, nutrients for maintenance, 8t loss, 445 definitions of, 11–12 full thickness, 11f, 12f partial thickness, 11f melanin, noncellular components of, 7t perforator arteries to, 258f pH of, 10 physiology, nerve supply, skin nutrition, skin renewal, vascular supply, prior to injury, baseline state of, 30f protection cushions, 177–178 protector wand, 349f wipes, 348f re-epithelialization, tear, 188t temperature sensors, 214 (See also TempTouch temperature sensor) vascular supply of, 257, 258f Skin graft, 267–278 anatomy, 269f, 271–272 areas of, 273f case study, 268–269 classification, 270–271 by full-thickness skin graft (FTSG), 270 by origin, 270–271 by split-thickness skin graft (STSG), 270, 270t definition of, 267 donor site selection and morbidity, 276–277 complications, 277f hypopigmented/reddish healed donor site, 277f dressing, 274 expansion, 276 expanded mesh skin graft, 276f meshed skin graft, 276f failure, 275–276 skin failure, factors of, 275–276, 275f healed STSG and FTSG, 273f healing, 273 immobilization, 274–275 bolster dressing, 274, 274f negative pressure therapy, 274–275, 274f Hamm_Index_489-510.indd 501 mesher, 276 physiology, 272–273 inosculation, 273 revascularization, 273 serum imbibition, 273 Slough, 323 tissue, 79, 79f Small vessel disease, 102 α-Smooth muscle actin (αSMA), 44, 57 Smooth muscle cells characteristics of, 23 Soft tissue necrosis, 463f Soft-tissue radionecrosis, 462f Spider bites, 243–244 bull’s eye sign of, 244f clinical presentation, 243 differential diagnosis, 244 medical management, 244 pathophysiology, 243 red, white, and blue sign of, 244f wound management, 244 Split-thickness skin graft (STSG), 270, 270t, 406 free latissimus dorsi muscle flap covered with, 270f Spontaneous pneumothorax, 467 Sporotrichosis, 241–242, 242f clinical presentation, 242 differential diagnosis, 242 medical management, 242 pathophysiology, 241 wound management, 242 Spot radiotherapy, for cutaneous lymphoma, 249 Squames, Squamous cell carcinoma (SCC), 247–248, 304 clinical presentation, 247 differential diagnosis, 247 early stage, 248f late stage, 248f medical management, 247 pathophysiology, 247 wound management, 247–248 Stable fibrin clot, 43f Stable heel ulcers, 320 Staphylococcus aureus, 273, 364, 367 Staphylococcus epidermidis, 367 Starling’s law of equilibrium, 149f physiological components, definitions for, 150t Stemmer sign, 156f Stratification, Stratum basale, of epidermis, 4f Stratum corneum of epidermis, 4f function of, 10 Stratum granulosum, 3, Stratum lucidum, of epidermis, 4f Stratum spinosum, of epidermis, 4f 501 Streptococcus infection, 276 Stress, 312 Stripping, 137 Sublesional hematoma, dissecting, 215f Sulfonylureas for type diabetes, 198t Superficial burns, 282f treatment, 290 Superficial injuries, 281 Superficial partial-thickness burns, 282, 282f treatment, 290 Superficial venous system, 120 Superior vena cava (SVC), 122 Superoxide dismutase (SOD), 459 Supine position, 179 Support surfaces active, 171f air-fluidized bed, 171f alternating-pressure, low-air-loss, 171f beds, mattresses, and overlays, 170–172 categories and features of, 170t cross-section of, 171f evaluating the effectiveness of, 172 Surgical debridement, form of, 334 Surgical incision, 464f Surgical shoe with total contact molded insole, 220f Surgical site infection (SSI), 370 Surgical wound, closure of, 255 Suspected deep tissue injury (SDTI), 354 Systemic sclerosis See Scleroderma Systemic steroids for necrobiosis lipoidica diabeticorum, 236 T Table top test, 213 Tactile, TempTouch temperature sensor, 215f Tendons, 80–81, 80f–81f, 324f non-viable, 81f viable, 80f Tension, 132, 468 Tensor fascia lata, 258 Therapeutic shoe bill for patients, 220t Thermal injury, 281 Th2 helper cells, 52 Thiazolidinediones, for type diabetes, 198t Thoracodorsal artery perforator flap (TAP flap), 261 Thromboemboli, 102f Thromboxane A2, 303 Tinea capitis infection, 243f Tinea pedis infection, 243f Tissue, 256 composition of, 256 expansion, 263–264, 263f perfusion, assessment of, 266 single tissue, 256 Tissue growth factor alpha (TGF-α), 43 T-lymphocytes, 10, 51 18/12/14 12:33 PM 502 Index Toe brachial index (TBI), 205 Toes post-amputation of, 121f pressures, 108–109 with diabetes assessed before, 322f Tonofibrils, 3, 4, 7t Topical negative pressure therapy (TNP), 401 Total body surface area (TBSA), 281 Total contact cast (TCC), 206f, 217, 223 Tracing, 76, 76f TRAM flap, 264 Trans-Atlantic Inter-Society Document on Management Peripheral Arterial Disease (TASC), 116 Transcutaneous oximetry, 266 Transcutaneous oxygen perfusion (TcPO2), 110, 110f interpretation of, 110t Transfer method, 256 advancement flap, 256, 256f interpolation flap, 256, 257f rotational flap, 256, 257f transposition flap, 256, 257f Transforming growth factor–β (TGF-β), 54 Transfusion therapy, for sickle cell wounds, 246 Transient ischemic attacks, 104 Transitional off-loading devices, pictorial glossary of, 205 Transmission of forces, frontal plane view of, 209f Transudate, 82 Transverse rectus abdominis flap (TRAM), 256 Trauma, 9, 46, 58, 83, 86, 88f, 102f Traumatic injury healthy tissue exposed to hydrogen peroxide (H2O2), 69 iodine, 69 ionic soaps and detergents, 69 TrueContour diabetic insoles, 222 Trunks, 147 Tumor necrosis factor (TNF), 36 Tunneling extensions, 78, 78f Turning frequency, 181 U Ulcerations etiology of, 126 risks for, 204 Ulcers arterial insufficiency, 462 bilateral submetatarsal, 203f Ultrasonic debridement, 187 Ultrasound, 110, 434–436 acoustic cavitation, 423 application techniques, 431–433, 433t high frequency, 432 low frequency, 432 Hamm_Index_489-510.indd 502 cellular/tissue levels, effects, 425–428, 426t high-frequency, 426–427 low-frequency, 427–428 continuous mode of delivery, 428f diagnostic and therapeutic purposes, 423 high/low-frequency, comparison, 426t indications/precautions/ contraindications, 428–430 infection control guidelines, 433 low-frequency/noncontact bacteria, 429f microstreaming, stable cavitation, and unstable cavitation, 425f noncontact, low-frequency ultrasound, 428f, 433f parameters for application, 430–431 periwound application, 432 precautions and contraindications, 431t pulsed mode of delivery, 428f sound waves standing, 432f transmission of, 425f theory, 423–425 transducer and head, 433 vascular occlusion, detection, 423 wound diagnoses, 430f Ultraviolet A (UVA), 475 Ultraviolet B (UVB), 475 Ultraviolet C (UVC), 475–481, 477t alters, 477f application parameters for, 477 techniques for, 477–479 cellular/tissue levels, effects, 476–477 Derma-Wand, 478f indications/precautions/ contraindications/possible adverse events, 477 light source, 478f theory of, 475 Thera-wand, 478f treatment parameters, 477t ultraviolet A, B, comparison, 476t wound and apply protective ointment, 478f Ultraviolet light, 476f, 476t Undermining, 77, 77f Undersea Medical Society (UMS), 452 Unit pulmonary toxic dose (UPTD), 466 User-worn heel protector, 173f V Vacuum assisted closure (VAC) therapy system, 412f, 413, 414 Valacyclovir, for chicken pox, 239 Valsalva maneuver, 465 Valve reconstruction, 137–139 reflux, 130 Vancomycin-resistant Enterococcus (VRE), 371 Varicella, 238 Varicella-zoster virus (VZV) chicken pox, 238, 238f shingles, 238, 238f Varicose veins, 123f, 125 Vascular diseases chronic venous insufficiency (CVI), 99 peripheral arterial occlusive disease (PAOD), 99 Vascular endothelial growth factor (VEGF), 38, 56, 311, 374 Vascular orientation, 257 anterograde flow flap, 257 flow-through flap, 257 retrograde flow flap, 257 venous flap, 257 Vascular pedicle, 258–259 Vascular supply, 255–256 axial flap, 256 fasciocutaneous flap, 256 musculocutaneous flap, 256 random flap, 255–256, 256f septocutaneous, 256 Vascular Surgical Society, 100 Vascular system, 99 anatomy of, 99f Vascular wounds, 99–139, 158 arterial wounds, 100–120 lower extremity wounds, differential diagnosis of, 100t venous wounds, 120–139 Vasculitic wounds, on patient with systemic lupus erythematosus, 127f Vasculitis, 230, 231t associated with other symptoms, 230f due to SLE, 230f leukocytoclastic, 230 in remodeling phase of healing, 230f Vashe therapy, 367 Vasoconstriction, 42f, 267 by smoking, 313 Vasodilation, 262 Veins, 261 Venosomes, 261 Venous hypertension, 122 Venous insufficiency, 122, 267, 268f chronic, 309 Venous leg ulcers (VLUs), 359 Venous phlebectomy, 137 Venous ulcers, 60, 120 guideline documents, 131 Venous valves, 122 Venous valvuloplasty, 137 Venous wounds, 120–139 algorithm for, 132f anatomy case study, 121–122 deep system, 120 superficial veins, 120 of veins, 122f appearance, 127 atrophie blanche, 125f 18/12/14 12:33 PM Index Brawny edema, 126f case study, 138 left lower extremity of, 128f right lateral lower extremity of negative pressure, 138f right lower extremity of, 128f right medial lower extremity of negative pressure, 138f CEAP classification of, 129f “champagne-bottle” lower extremity, 134f chronic venous insufficiency, risk factors for, 124t Circ-Aid, 135f classification of, 128–130 clinical presentation, 125–128 closed wound, 122f compression garments, 135f compression stockings, classification of, 136t differential diagnosis of, 128t distended saphenous vein, 130f drainage, 127 epidemiology, 120 etiology, 122 fibrotic, hypertrophic skin, 126f figure-8 wrap, 133f graded compression garments, 134f heel wound case study, 121f hemosiderin deposition in skin, 125f history of formation, 127 incompetent valves, 123f invasive testing, 130–131 lipodermatosclerosis, 125f location of, 126–127 lower extremity spiral wrap of, 133f multilayer compression systems, 135f noninvasive vascular studies, 130 venous duplex examination, 130 non-surgical treatment, 131–137 adjunctive therapy, 137 compression, 131–136 dressings, 136 invasive therapy, 137 medications, 136–137 treatment of infection, 136 normal venous physiology, 122 NPWT, treatment with, 121f pain, 127 pathophysiology, 122–125 patient examination, 130 periwound skin, 127 post-amputation of toes, 121f post-healing care, 139 post-thrombotic syndrome, 124f signs and symptoms of, 124t prevention, 131 surgical intervention, 137–139 endovascular therapy, 137 endovenous radiofrequency and laser ablation, 137 Hamm_Index_489-510.indd 503 ligation and stripping and venous phlebectomy, 137 sclerotherapy, 137 valve reconstruction, 137–139 varicose veins, 123f vasculitic wounds on patient with systemic lupus erythematosus, 127f zinc oxide paste and gauze boots, 134f Vi-Drape Isolation Bag, 446 Vitamin D, 10 synthesis and storage of, 10–11 W Warfarin (coumadin) therapy for coumadin-induced skin necrosis, 245 Water-hydrated gels, 28 Weight-shifting, 181 Wet gangrene, 115 Wet-to-dry dressing, 343, 344, 344f debridements, 330–331, 330f caution to use, 331 disadvantages, 330 Wet-to-moist dressing, 344 Wheelchairs, 174 measurements, 175 poorly-fitting, 175 positioning and fitting, 174–175 problems in, 174 weight shifts and pressure reliefs, 181–182 Wheelchairs cushions, 174, 175–177, 177f with cutout/reliefs to redirect loading, 178f dimensions to consider when fitting chair for individual, 175f materials used in cushion construction, 177t positioning features of, 179 postural changes in poorly fitting, 176t vulnerable areas when patient is sitting in, 175f Whirlpool (WP) debridement, 328, 328f contraindications to, 329t Windlass mechanism, 211 World Health Organization, 281 World Union of Wound Healing Societies (WUWHS), 380 Wound assessment of (See Wound assessment) care clinician’s role, 201–202 guidelines, 319 case study, 91–92, 93 distal medial wound, 92f right lateral lower leg fasciotomy, 92f right medial lower leg fasciotomy, 92f chronic, 320 classification systems, 105 contraction, 471f etiologies, 165 characteristics of, 74t 503 evaluation, 201t full thickness, 11 goals of removing necrotic tissue from, 319 neurologic testing, 94 with osteomyelitis, 366f partial thickness, 11 patient evaluation with, 67–94 position in in-patient setting, 68f out-patient setting, 68f signs and symptoms, 68t subjective history, 67–94, 68t systems, review of, 92–94 cardiovascular/pulmonary, 92 musculoskeletal, 92–94 Wound-activated macrophages (WAMs), 36, 62, 305 Wound assessment, 67–91 Bates-Jensen tool (See Bates-Jensen wound assessment tool) dimensions, 73–76 clock method, 75, 75f perpendicular method, 73–75, 75f photography, 76, 77f guidelines for, 76t planimetry, 76 tracing, 76, 76f drainage, 81–84 amount of, 82t chylous, 83, 83f enterocutaneous/enteroatmospheric fistula, 84, 84f exudate, 82, 83f infected, 84, 84f lymphatic, 83, 83f purulent, 82, 83f sanguineous, 82, 82f serosanguineous, 82, 83f serous, 82, 82f edema, 87, 88f edges (See Edges, of wound) infection, 90–91 signs of, 91t location on dorsal foot, 74f on hand, 74f lower extremity, 74f on sacrum, 74f odor, 90 pseudomonas, 90 pain, 91 descriptions and causes, 91t visual analog scale, 91t periwound skin, 84–87 blanched, 86, 86f cyanosis, 84, 85f dark red discoloration, 85, 86f ecchymosis, 86, 86f erythema, 84, 84f–85f hemosiderous staining, 85–86, 86f jaundice, 86–87, 86f–87f 18/12/14 12:33 PM 504 Index Wound assessment (Cont.) subcutaneous extensions, 76–78 clinical consideration, 77 fistula, 78, 78f sinus, 77, 78f tunneling, 78, 78f undermining, 77, 77f suspicious condition, 68t tissue type, 78–81 adipose, 81, 81f bone, 79–80, 80f eschar, 79, 79f foreign objects, 81, 81f granulation tissue, 79, 79f muscle, 79, 80f slough, 79, 79f tendons, 80–81, 80f–81f tools for objective wound documentation, 73t Wound debridement, 36, 319–339 bone in wound bed, 324f case study, 337–339 wound presentation, 338f wound with contact, low-frequency ultrasound, 337f closure and healing, necrotic/devitalized tissue impairs and impedes, 321t as component of wound bed preparation, 319, 320f debride chronic wounds, reasons to, 320t decision to debride, 319–325 case study, 321 epibole, 320f eschar, 323f demarcation and separation, 322f factors for consideration, 321t friable granulation, 323f healthy granulation, 322f hypergranulation tissue, 323f after treatment with PAV foam, 325f interventions, examples of, 325t before treatment with PAV foam, 325f muscle/fascia, 324f with necrotic tissue, 320f pyoderma gangrenosum, 322f sacral pressure ulcer, 321f tendons, 324f toe pressures with diabetes assessed before, 322f types of, 325–339 (See also Enzymatic debridements etc.; specific debridements eg, Autolytic debridements) non-selective, 325 selective, 325 wound bed, vessel in, 324f Wound dressings, 348 amorphous gels, 351f, 352f antimicrobial dressings, 363–378 antibiofilm agents, 367 Hamm_Index_489-510.indd 504 antibiotics, 367 antimicrobial peptides (AMPs), 367 antiseptics, 367–368 biofilm, 365–366 categories/considerations, 366 disinfectants, 368 use of, 364 apligraf, 361–362 assessment of wound, 345f categories, 348 absorbent dressings calcium alginate, 355 hydrofiber dressings, 355–356 collagen dressings, 357–358 contact layer dressings, 348–349 drawtex hydroconductive dressings, 359 enluxtra self-adaptive wound dressing, 360 film dressings, 349–351 foam dressings, 354–355 gold dust, 360–361 hydrocolloid dressings, 352–354 hydrogels/hydrogel dressings, 351–352 procellera, 359 skin protectants, 348 specialty absorptive dressings, 356–357 x-cell, 360 cellular therapies, 361 characteristics of, 347, 347t dermagraft, 362 film dressings, advantages of, 351t foam dressing on sacral wound, 354f secondary dressing, 354f foam, skin protection, 355f goal-based wound management, 344 bacterial burden, 346 location of wound, 344–346 pain, 346–347 periwound condition, 346 quality of life, 347 size of wound, 346 support needs, 347 tissue type, 346 type of exudate, 346 growth factors (GFs), 362–363 HCT/Ps process, 363 historical perspective, 343–344 hydrocolloid discoloration of, 353f dressing, 353f gelling, 353f hydrogels advantages, 352t sheet, on wound, 352f multiple dressing options, 346 premarket approval (PMA), 361, 510(k), 363 protect fragile tissue, 349f protective covering, 349f topical-antimicrobial wound dressings, 368 cadexomer iodine, 373–374 dialkylcarbamoylchloride (DACC), 376–378 medicinal honey, 371–373 polyhexamethylene biguanide (PHMB), 375 polyvinylalcohol (PVA) foam with gentian violet and methylene blue, 375–376 silver dressings, 368–371 transparent film, 350f Wound healing process abdominal wound on postsurgical patient, 307f acute wounds, phases of, 30–52 autoimmune diseases, 312, 312f biofilm, on wound surface, 301f cancer/radiation, 310–311 chemotherapy, 311 decline in general health, 311 immediate, acute, and chronic effects of, 311t radiation, 311 with cardiac insufficiency, 310f case study, 297, 312 wound, closed and remodeling, 312f cell migration, 24t–25t proliferation, 24t–25t, 35f, 36f signaling, 24t–25t chronic wounds, 57–61 clinical signs, 21t comorbidities, 305–310 arterial insufficiency, 308–309 cardiac disease, 309–310 chronic edema, 309 diabetes, 305–306 obesity, 306–307 protein energy malnutrition, 307–308 delayed primary intention, 23, 28f diabetes diabetic foot ulcer, 305f recommendations for glycemic control for, 306t skin on lower extremity of, 306f differences in complicated by drugs, aging, infection/disease, 59t–60t divisions of, 26f growth factor, in cell source and function, 39t impedance, 297–314 infections, 300–301, 300f bacterial infection, 300–301 biofilms, 301 definition of, 300 fungus infections, 301, 302f laboratory values with implications for, 298t–299t liver transplant, dehisced incision on patient with, 307f 18/12/14 12:33 PM Index loss of lean body mass relative to, 308t medications, 301–305 antirejection medications, 303–304 nonsteroidal anti-inflammatory drugs, 303 steroids, 301–303 micronutrients needed for, 308t microorganisms present in chronic wounds, 301t migratory cell, arrival and departure of, 44t NSAIDs affect wound healing, 304t stalled wound on patient taking, 304f nutritional requirements, 308t organ transplantation, antirejection medications used for, 304t partial-thickness wounding, 23, 29f patient with loss of lean body mass, 308f polymorphonuclear cells in, 45t Hamm_Index_489-510.indd 505 presence of bacteria, 300t primary intention, 23, 26f psychosocial behaviors, 313–314 alcohol abuse, 313t, 313f, 313 smoking, 313, 313t response in, 21–29 cells, 16t–18t activity levels, 22f metamorphosis during, 52–57 classifications of, 23 endothelial cells, 16t epithelial cells, 16t fibroblasts, 16t keratinocytes, 17t macrophage, 17t overview of, 23–30 phases of, 19–21t platelets, 18t polymorphic neutrophilic leukocytes (PMNs), 18t secondary intention, 23, 28f 505 signaling in, 15 steroids skin on patient taking, 303f wound on patient, 302f stress, 312 surgical incision on transplant patient, 305f surgical wound, 305f Wound Healing Society, 131, 136 Wound healing trajectory, 303 X Xenografts, 270, 291 tissue transplantation, 271 Xeroform, 410 Y Yankauer suction tip, 444 Z Zero G brace, 218 18/12/14 12:33 PM ... Dunitz Ltd; 20 01 :24 7 26 3 Hamm_Ch08 _22 7 -25 4.indd 25 2 12 Falanga V, Phillips T, Harding K, Moy R, Peerson L Text Atlas of Wound Management London, UK: Martin Dunitz Ltd; 20 00:61–97, 189 22 7 13 Anhalt... Correction of hypoxia, a critical element for wound bed preparation guidelines: TIMEO2 principles of wound bed preparation Journal of the American College of Certified Wound Specialists 20 11;3 (2) :26 – 32. .. The Color Atlas of Family Medicine New York: McGraw-Hill; 20 09 http:// www.accessmedicine.com/content.aspx?aID= 820 822 2 Accessed August 24 , 20 13.) 18/ 12/ 14 10:59 AM 23 6 Chapter Atypical Wounds skin