The Basics of Wound Care

It is estimated that 6.5 million people living in the United States have a chronic wound and up to 25% of patients with diabetes will develop a foot ulcer in their lifetimes.1 Approximately 12% of diabetic foot ulcers will require an amputation, and the estimated five-year survival rate after a major lower extremity amputation is about 50%.1 Impaired quality of life and increased health care costs are a consequences of the treatment of chronic wounds.1 It is estimated that ulcerations precede 85% of lower extremity amputations.2

The basis of achieving a healed wound involves an accurate diagnosis and a collaborative treatment of multiple factors. There is an array of ulceration etiologies that will determine a characteristic treatment course. For example, ulcers of vascular etiology commonly include ulcers that result from either venous insufficiency or arterial occlusive disease (peripheral arterial disease [PAD]) (Figures 1 and 2). The basis of the treatment course between these two vascular etiologies differs greatly as the former necessitates compression and elevation while the latter often requires revascularization.3

Figure 1: Venous Stasis Ulceration With Lower Extremity Edema

Figure 1

Figure 2: Ulceration With Ischemic Etiology

Figure 2

Controlling Edema

In patients with chronic lymphedema and venous stasis ulcerations, the control of edema is essential. Interstitial edema impairs healing through several mechanisms including the accumulation of breakdown products that impair healing, inhibition of fibroblasts, and suppression of epithelial and endothelial cells.4 Therefore, it is important in patients with chronic venous insufficiency to reduce lower extremity edema to facilitate wound healing. The etiology of the patient's edema should be determined for effective treatment of the condition. The patient's history of the edema onset, possible association with illnesses, diseases, and changes in medication, and relationship to activity and time of day provide clinical clues of edema etiology. Physical examination should describe the edema distribution and pitting; identify any lymphadenopathy or masses; and evaluate skin condition, texture, color, temperature, and hydration.5 Unilateral versus bilateral involvement can also help rule out disease processes as unilateral causes of edema include status post-deep vein thrombosis (post-thrombotic syndrome), cellulitis or infection, lymphedema, complex regional pain syndrome, trauma or compartment syndrome, tumor, or factitial causes.6 Close collaboration with the patient's primary care physician can help facilitate reduction of edema secondary to a systemic etiology. Methods to reduce edema include lower extremity elevation, compression wraps, and pneumatic compression pumps. Lower extremity elevation is effectively achieved when the patient's feet are above the level of the right atrium because this decreases venous hypertension.7 Sedentary patients can perform calf muscle pump and toe crunching exercises to reduce dependent edema.5 Compression therapy modalities are dependent on the patient and include an ACE wrap, several commercial specialty compression wraps, and compression stockings.3 Elastic or compression wraps are utilized until the wound heals and compression stockings are prescribed for prophylactic maintenance of edema reduction.7 In patients who are non-compliant with their leg elevation and compression wraps, a venous pneumatic pump can be used to milk fluid out of the legs by alternating inflation of air bladders located at the foot/ankle region and the other around the calf.3 Surgical options for venous insufficiency management include sclerotherapy, phlebectomy, radiofrequency or laser thermal ablation, and foam sclerotherapy.5 Caution is advised when acutely reducing lower extremity edema in patients with congestive heart failure.8 Acutely increasing venous return may cause an increase in pulmonary blood flow resulting in possible clinical, auscultative, or oxidative worsening.8 Compression above 40 mm Hg is contraindicated in patients with PAD.9

Arterial Perfusion Optimization

A thorough history and exam will provide clinical clues if the patient's ulceration is of PAD etiology.10 It is important when taking the patient's history to identify PAD risk factors, which include diabetes mellitus, tobacco use, hypertension, age >65 years, and dyslipidemia.3,5,10 Some other red flags are iIntermittent claudication and rest pain symptoms, as well as history of revascularization procedure, cerebrovascular incident, coronary disease, and erectile dysfunction.11 The physical exam should include a comprehensive pulse exam for adequate perfusion assessment of the femoral, popliteal, and pedal pulses.12 The clinical appearance of the patient's lower extremity is thin, atrophic, tight, or shiny skin that often feels cool to the touch. In the setting of critical limb ischemia, the patient will exhibit the position dependent color changes of pallor with elevation and rubor with dependency. Ulcerations are often seen at the distal clavi of digits, have a "punched out" appearance, and have a mixed fibrous necrotic base with minimal drainage.5 These lesions are typically very painful unless masked by neuropathy, commonly present in patients with diabetes mellitus.

The blood supply to the wound can be assessed through a variety of methods including an ankle brachial index (ABI), toe brachial index (TBI), pulse volume recordings with segmental pressures, microvascular testing (including transcutaneous oxygen pressure), and arteriograms. An ABI may be falsely elevated in the presence of calcified vessels (commonly in patients with diabetes or renal disease) but has been correlated with an increased risk of amputation.13 Any vascular intervention that could be considered helpful should be undertaken to promote healing. Therefore, collaboration between podiatrists and dedicated peripheral vascular interventionists (e.g., vascular surgeons, interventional cardiologists, interventional radiologists) is highly recommended. Debridement in the presence of inadequate perfusion could potentiate tissue loss.3 If a PAD patient is not a candidate for surgical revascularization, amputation to a level of adequate perfusion may be indicated to allow healing. Wound healing closes a potential external portal for infection which could result in sepsis, hematogenous osteomyelitis, and mortality.14 Amputation to an effective prosthetic level instead of a lengthy burdensome hospital course of wound care with this morbidity and mortality potential may not a course for the severely immunocompromised patient.14 A patient's quality of life is greatly improved with a functional prosthetic.15


A moist wound bed is widely accepted for chronic wound management and re-epithelialization, but prolonged overhydration can lead to maceration and tissue slough.16,17 An optimal wound bed moisture balance is crucial to enhance the optimal effects of growth factors and cytokines within the wound to stimulate production of keratinocytes, endothelial cells and fibroblasts necessary for healing.17 Therefore, maintenance of an optimally moisturized wound bed can be achieved by proper dressing product selection and balanced with frequency of dressing change. There are a variety of wound care products available and only a few groupings are described in this article. Alginates and foam products are primary used for absorption (i.e., highly exudative wounds such as venous stasis ulcerations).18 Hydrogels or hydrocolloids facilitate autolytic debridement and maintain a moist wound environment but also absorb some exudate. Cochrane review studies in 2015 reveal that there is no evidence to suggest that either alginate dressings or hydrogel dressings are more or less effective in the healing of venous stasis ulcers and pressure ulcers, respectively, than other types of dressings.19,20 Collagen products provide a scaffold for granulation and epithelialization in ulcerations with large tissue defects.21 Negative pressure wound therapy is now a widely accepted therapy and promotes the development of a healthy, granular wound bed in acute and chronic wounds.17 Advanced wound care products that contain growth factors and fibroblasts, are often utilized after failed duration of standard topical therapy.5,22 Newer products include stem cells and regenerative therapy.23

Dressings impregnated with silver are antimicrobial and decrease the bioburden of the wound, although they are not a substitute for antibiotic therapy.24 Silver is found to be effective against a broad spectrum of bacteria including staphylococcus, streptococcus, pseudomonus, and methicillin resistant staphylococcus aureus (MRSA). Silver products are contraindicated for patients with a silver sensitivity.

Treatment of Infection

The treatment of infection is essential for wound healing.25 Infection results in prolonged elevation of inflammatory cytokines and transitions wounds into a healing impaired, chronic state.25 Infection also increases matrix metalloproteases, which degrade extracellular matrix and decrease protease inhibitors that cause growth factor degradation.25 Chronic wounds are often polymicrobial, with bacteria creating a biofilm on superficial wounds giving them an optimal environment for colonization. Proper wound management should, thus, include cleansing, sharp debridement, and the use of antimicrobial dressings that conform to the topography of the wound to maximize exposure between bacteria and the antimicrobial agent. Clinical signs of wound infection include erythema, calor, edema, malodor, purulent drainage, and lymphangiitis.14 Patients with impaired immunities may have blunted clinical infection signs, such as persons with diabetes mellitus.5 Plain film radiographs are ordered as an initial standard screening tool for bone integrity assessment and soft tissue emphysema.5 Further suspicion of deep soft tissue infection warrants ordering magnetic resonance imaging (MRI).5 Suspected infection will present as high signal intensity on a T2 weighted image.26 The selection of an effective antibiotic is essential for successful treatment. Superficial wound swabs are inaccurate secondary to contamination with the patient's normal skin flora.27 Accuracy of obtaining the infective organism is increased when the swab includes purulent drainage from the wound or is a deep wound culture.5 Bone biopsy is the gold standard for diagnosing osteomyelitis.28 Patients should be treated empirically with a broad spectrum antibiotic prior to culture results, and then antibiotic therapy is appropriated based on sensitivities.28 Many patients will require debridement or amputation to completely eradicate infection and non-viable tissue. Debridement should aim to remove all nonviable material, reduce the bacterial load, and achieve "clear" margins to prevent any nidus for infection recurrence.27,29,30


Chronic wounds are stalled in a hostile microenvironment comprised of bacterial contaminants and nonviable tissue which inhibit healing.5 Therefore, wound debridement aims to remove any foreign body or devitalized tissue.17 Wound bed preparation can be accomplished by surgical or sharp, mechanical, chemical, autolytic, biosurgical, and ultrasonic debridement.5 Surgical debridement, after vascular optimization in the arterial compromised patient, of all nonviable tissue is the most effective method to promote healing.5 Mechanical debridement can be achieved with pulse lavage, moistened dressings, or ultrasound debridement.5 Caution should be undertaken with surgical and mechanical debridement of accidental removal of viable with nonviable tissue. Enzymatic or chemical debridement is useful in the removal of fibrotic slough in the sensate patient whom sharp debridement may be painful.5 Enzymatic debridement ointments dissolve nonviable collagen and should not be used in combination with silver products because the metal ions inactivate the lytic enzyme. Autolytic debridement with hydrocolloids and hydrogels trap local wound fluid with endogenous proteolytic enzymes that promote debridement but should be avoided in the presence of infection.5 Biosurgical debridement with sterile blowflies or housefly larvae is performed in insensate patients to selectively digest nonviable tissue.5 Ultrasonic debridement by contact or non-contact are used to remove nonviable tissue, reduce biofilms and metalloproteinases, and increase angiogenesis and collagen deposition.31,32


Decubitus or pressure ulcers are common in neuropathic patients, especially common in diabetics.33 Pressure offloading is essential in the management of all chronic wounds but vital to heal decubitus ulcerations.22 Offloading allows for discontinued mechanical trauma and shearing forces, which would impair wound healing.17 A variety of durable medical equipment is available for offloading including pressure relief boots, wedges, braces, rocker bottom shoes, and Charcot Restraint Orthotic Walker.34 Modifications to offload focal pressure areas by a "drill and fill" method, or other shoe modifications can be achieved by a local pedorthotist. Total contact casting and non-removable walking cast boots have been the gold standard treatment of diabetic foot ulcerations.35,36 Fleischli et al. revealed that there is six times the amount of peak pressure absorbed to the plantar foot in a surgical shoe than in a total contact cast.37 In 2005, Nabuurs-Franssen et al. found that 90% of nonischemic diabetic ulcers healed in a total contact cast, and the average time to healing was 34 days.38 Wheelchair, crutches, and recommendations to remain out of work and bed-ridden can also be offered.5 However, in patients who fail chronic offloading equipment who have severe deformity that precludes recurrence, corrective surgery may be required (Figure 3).5

Figure 3: Total Contact Cast: Gold Standard for Offloading

Figure 3

Multidisciplinary Collaboration

As previously stated, it is important to stress multidisciplinary collaboration in chronic wound management. Vascular intervention should be utilized for arterial perfusion optimization. Endocrinology should be consulted in patients with diabetes for blood glucose management. In one study published in 2011, Christman et al. revealed that for each 1.0% increase in HbA1c, there was an associated decreased wound area healing rate by 0.028 cm2/day.33 A nutritionist and personal trainer could also assist with proper diet, hydration, and monitored exercise programs for patients with diabetes mellitus. Malnutrition or nutrient deficiencies can have a significant impact on wound healing.25 The literature states that poor healing risk factors include anemia, low albumin and pre-albumin levels, and vitamin deficiencies.39 Lymphedema and impaired glucose metabolism may also delay wound healing in obese patients.5 Obesity also causes relative hypoperfusion and ischemia in areas of dense subcutaneous adipose tissue.25 Referrals for smoking cessation counselling programs are highly recommended. Smoking decreases calcium absorption and increases bone resorption. Nicotine releases catecholamines causing vasoconstriction. Carbon monoxide binds to hemoglobin to form carboxyhemoglobin resulting in tissue hypoxia. Also, hydrogen cyanide inhibits cellular respirator enzymes necessary for healing.25 Lastly, facilitating skilled nursing care for patients who do not have the social support or personal capability to perform their own dressing changes must also be coordinated.


A multifactorial, multidisciplinary collaborative approach is essential in management and treatment of chronic wounds. Frequent follow-up care and dressing changes, depending on the patient and ulceration type, are recommended to ensure proper treatment and prevention of morbidity and mortality.


  1. Sen CK, Gordillo GM, Roy S, et al. Human skin wounds: a major and snowballing threat to public health and the economy. Wound Repair Regen 2009;17:763-71.
  2. Rao N, Ziran BH, Lipsky BA. Treating osteomyelitis: antibiotics and surgery. Plast Recontr Surg 2011;127(1 suppl):177-187S.
  3. Grey JE, Harding KG. Venous and arterial leg ulcers. BMJ 2006;332:347-50.
  4. Venous Ulcers. Eds. Bergan JJ, Shortell CK. Amsterdam: Elsevier Academic; 2007.
  5. Bumpus K, Maier MA. The ABC's of wound care. Curr Cardiol Rep 2013;15:346.
  6. Young JR. The swollen leg. Clinicial signficiance and differential diagnosis. Cardiol Clin 1991;9:443-56.
  7. Douketis JD. Chronic Venous Insufficiency and Postphlebitic Syndrome (Merck Manual Professional Version website). 2014. Available at: , Accessed on 10/5/2015.
  8. Bickel A, Shturman A, Sergeiev M, Ivry S, Eitan A, Atar S. Hemodynamic effect and safety of intermittent sequential pneumatic compression leg sleeves in patients with congestive heart failure. J Cardiac Fail 2014;20:739-46.
  9. Peripheral Artery Disease. Harvard Health. Harvard Health Publications. 1 April 2012.
  10. Selvin E, Erlinger TP. Prevalence of and risk factors for peripheral arterial disease in the United States: results from the National Health and Nutrition Examination Survey, 1999-2000. Circulation 2004;110:738-43.
  11. Polonsky TS, Taillon LA, Sheth H, Min JK, Archer SL, Ward RP. The association between erectile dysfunction and peripheral arterial disease as determined by screening ankle-brachial index testing. Atherosclerosis 2009;207:440-4.
  12. Dormandy JA, Rutherford RB. Management of peripheral arterial disease (PAD). TASC Working Group. TransAtlantic Inter-Society Consensus (TASC). J Vasc Surg 2000;31(1 Pt 2):S1-S296.
  13. Lew E, Nicolosi N, Botek G. Lower extremity amputation risk factors associated with elevated ankle brachial indices and radiographic arterial calcification. J Foot Ankle Surg 2015;54:473-7.
  14. Kirsner RS, Vivas AC. Lower-extremity ulcers: diagnosis and management. Brit J Dermatol 2015;173:379-90.
  15. Carroll K. Adaptive prosthetics for the lower extremity. Foot Ankle Clin 2001;6:371-86.
  16. Hopf HW, Ueno C, Aslam R, et al. Guidelines for the treatment of arterial insufficiency ulcers. Wound Repair Regen 2006;14:693-710.
  17. Migonis A and Rosenblum B. Wound bed preparation: what works best and when. Podiatry Today 2015;28:30-6.
  18. Parkes J. A clinical in-market evaluation of an alginate fibre dressing. Br J Nurs 2015;24 Supple 15:S28-35.
  19. O'Meara S, Martyn-St James M, Adderley UJ. Alginate dressings for venous leg ulcers. Cochrane Database Sys Rev 2015;8:CD010182.
  20. Dumville JC, Stubbs N, Keogh SJ, Walker RM, Liu Z. Hydrogel dressings for treating pressure ulcers. Cochrane Database Syst Rev 2015;2:CD011226.
  21. Doillon CJ, Silver FH. Collagen-based wound dressing: effects of hyaluronic acid and fibronectin on wound healing. Biomaterials 1986;7:3-8.
  22. Tsourdi E, Barthel A, Rietzsch H, Reichel A, Bornstein SR. Current aspects in the pathophysiology and treatment of chronic wounds in diabetes mellitus. Biomed Res Int 2013;2013:385641.
  23. Mulder GD, Lee DK, Jeppesen NS. Comprehensive review of the clinical application of autologous mesenchymal stem cells in the treatment of chronic wounds and diabetic bone healing. Int Wound J 2012;9:595-600.
  24. Leaper DJ. Silver dressings: their role in wound management. Int Wound J 2006;3:282-94.
  25. Guo S, DiPietro LA. Factors affecting wound healing. J Dent Res 2010;89:219-29.
  26. May DA, Disler DG, Jones EA, Balkissoon AA, Manaster BJ. Abnormal signal intensity in skeletal muscle at MR imaging: patterns, pearls, and pitfalls. Radiographics 2000;20:S295-315.
  27. Mutluoglu M, Uzun G, Turhan V, Gorenek L, Ay H, Lipsky BA. How reliable are cultures of specimens from superficial swabs compared with those of deep tissue in patients with diabetic foot ulcers? J Diabetes Complications 2012;26:225-9.
  28. Lipsky BA, Berendt AR, Cornia PB, et al. 2012 Infectious Diseases Society of America clinical practice guideline for the diagnosis and treatment of diabetic foot infections Clin Infec Dis 2012;54:e132-73.
  29. Pineda C, Espinosa R, Pena A. Radiographic imaging in osteomyelitis: the role of plain radiography, computed tomography, ultrasonography, magnetic resonance imaging, and scintigraphy. Semin Plast Surg 2009;23:80-9.
  30. Neville RF, Attinger CE, Bulan EJ, Ducic I, Thomassen M, Sidawy AN. Revascularization of a specific angiosome for limb salvage: does the target artery matter? Ann Vasc Surg 2009;23:367-73.
  31. Kavros SJ, Liedl DA, Boon AJ, Miller JL, Hobbs JA, Andrews KL. Expedited wound healing with noncontact, low-frequency ultrasound therapy in chronic wounds: a retrospective analysis. Adv Skin Wound Care 2008;21:416-23.
  32. Medrano S, Beneke MJ. Acoustic pressure wound therapy to debride unstageable pressure ulcers in the acute care setting: a case series. Ostomy Wound Manag 2008;54:54-8.
  33. Christman AL, Selvin E, Margolis DJ, Lazarus GS, Garza LA. Hemoglobin A1c is a predictor of healing rate in diabetic wounds. J Invest Dermatol 2011;131:2121-27.
  34. Frykberg RG, Bailey LF, Matz A, Panthel LA, Ruesch G. Offloading properties of a rocker insole: A preliminary study. J Am Podiatr Med Assoc 2002;92:48-53.
  35. Armstrong DG, Nguyen HC, Lavery LA, van Schie CH, Boulton AJ, Harkless LB. Offloading the diabetic foot wound: a randomized clinical trial. Diabetes Care 2003;24:1019-22.
  36. Katz IA, Harlan A, Miranda-Palma B, , et al. A randomized trial of 2 irremovable off-loading devices in the management of plantar neuropathic diabetic foot ulcers. Diabetes Care 2005;28:555-9.
  37. Fleischli JG, Lavery LA, Vela SA, Ashry H, Lavery DC. Comparison of strategies for reducing pressure at the site of neuropathic ulcers. J Am Podiatr Med Assoc 1997;87:446-72.
  38. Nabuurs-Franssen MH, Sleegers R, Huijberts MSP, et al. Total contact casting of the diabetic food in a daily practice: a prospective follow-up study. Diabetes Care 2005;28:243-7.
  39. Kavalukas SL, Barbul A. Nutrition and wound healing: an update. Plast Reconstr Surg 2011;127 Suppl 1:38S-43S.

Keywords: Air Sacs, Albumins, Alginates, Amputation, Aneurysm, Anemia, Ankle Brachial Index, Ankle, Anti-Bacterial Agents, Anti-Infective Agents, Avitaminosis, Bacterial Load, Biofilms, Biopsy, Blood Glucose, Bone Resorption, Calcium, Carbon Monoxide, Carboxyhemoglobin, Catecholamines, Cellulitis, Collagen, Compartment Syndromes, Complex Regional Pain Syndromes, Coronary Disease, Counseling, Cytokines, Debridement, Diabetic Foot, Diet, Dyslipidemias, Edema, Emphysema, Endothelial Cells, Erectile Dysfunction, Erythema, Extracellular Matrix, Fibroblasts, Foot Ulcer, Foreign Bodies, Glucuronic Acid, Health Care Costs, Heart Atria, Heart Failure, Hexuronic Acids, Hydrogels, Hydrogel, Polyethylene Glycol Dimethacrylate, Hydrogen Cyanide, Hypertension, Immunocompromised Host, Keratinocytes, Larva, Leg, Lymphatic Diseases, Lymphedema, Magnetic Resonance Imaging, Malnutrition, Metalloproteases, Methicillin, Methicillin-Resistant Staphylococcus aureus, Negative-Pressure Wound Therapy, Neoplasms, Nicotine, Nutritionists, Obesity, Ointments, Osteomyelitis, Oxygen, Pain, Pallor, Peptide Hydrolases, Peripheral Arterial Disease, Physicians, Primary Care, Pressure Ulcer, Protease Inhibitors, Pulse, Quality of Life, Radiology, Interventional, Re-Epithelialization, Referral and Consultation, Risk Factors, Sclerotherapy, Sepsis, Smoking, Smoking Cessation, Social Support, Soft Tissue Infections, Staphylococcus, Stem Cells, Stockings, Compression, Streptococcus, Subcutaneous Fat, Survival Rate, Temperature, Therapeutic Irrigation, Toes, Ulcer, Ultrasonics, Varicose Ulcer, Vasoconstriction, Venous Insufficiency, Venous Thrombosis, Walking, Wound Infection

< Back to Listings