By Masood Shariff, MD, and Peter Kyunghwan Kim, MD
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All surgeons and many other physicians create and treat wounds. General surgeons were once the masters of the care of both physical and, sometimes, emotional wounds. Wound care requires an understanding of normal wound healing, causes of delays of wound healing, and the management of wounds. Every wound must be treated in regard to cause, chronicity, location and level of microbial contamination, as well as critical patient factors that greatly affect wound healing, such as age, immunosuppression, nutrition, off-loading and eradication of infection.

Too many patients of the underserved populations in the Bronx, N.Y., where we practice, are struck with the worst disease—not COVID-19 or HIV, but uncontrolled diabetes. For them and others, wound care is a common necessity that requires increasing health care attention. If appropriate care is not given early, expensive complications to the wound-healing process can lead to multiple ER visits, the development of chronic nonhealing wounds, and even amputation.

Knowledge of wound care products, negative pressure wound therapy and drain placement to manage dead space can improve outcomes with wound healing. Inappropriate product use can cause delays in healing. As wound healing progresses, management of a wound and the bandage materials must be open to innovation.

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Evolution of the Standard of Care in Wound Management

The “standard of care” in wound management is evolving and used to include a wet-to-dry gauze dressing that is performed daily until wound closure occurs, with an average time of one to 10 weeks. New biological products that provide an added layer of reinforcement and coverage on open wounds with tissue regenerative properties have been shown to increase wound healing and hasten recovery in the clinical care setting. The era of regenerative medicine has begun, but excellent, well-designed studies are lacking.

Wound care requires the achievement of an optimal environment for epidermal renewal with preservation of underlying skin and deeper tissues, with constant care and monitoring of secondary complications, such as infection or dehiscence. This process is a prolonged feat that the health care team undertakes to ensure proper healing, and it may necessitate expensive personnel and devices in the outpatient setting. The wound bed needs to be well vascularized, free of devitalized tissue, clear of infection and moist. Wound dressings should eliminate dead space, control exudate, prevent bacterial overgrowth, ensure proper fluid balance, be cost-efficient, and be manageable for the patient and any health care staff. Wounds that demonstrate progressive healing as evidenced by granulation tissue and epithelialization can undergo closure or coverage.1,2

Many topical agents and alternative therapies are available that are meant to improve the wound-healing environment. Although definitive data are lacking to support any recommendations, some may be useful under specific circumstances.3,4 Moist wound healing is the standard of care. The area in and surrounding an abscess is usually acidic in pH; thanks to the Henderson-Hasselbalch equation, antibiotics—and even local anesthetics—are inactivated due to their pKa, or acid dissociation constant. Therefore, teaching point No. 1 is this: When abscesses need to be drained and cultured, call a surgeon. Don’t forget to culture the infected fluid because of the possibility of drug-resistant organisms.

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The Importance of Debridement

Before wound healing, the area needs to be free of any foreign or dead tissue. Necrotic tissue is food for bacteria that can replicate as fast as every 20 minutes in the setting of an all-you-can-eat buffet. Therefore, when dead tissue needs to be debrided, call a surgeon. We need to sharply debride necrotic debris and hypergranulation tissue, typically in an OR, to create a wound bed that is a healthy pink-red in color. Tissue that bleeds is usually alive, and the scalpel is a handy tool that is both diagnostic and therapeutic. Vascular diseases, diabetes, pressors and sepsis can result in poor blood flow to the tissues that require revascularization and critical care. Source control is paramount, and serial excisional debridements of necrotizing skin and soft tissue infections should be the rule, not the exception.

At the end of a major debridement of necrotizing tissue, I ask myself and the residents three questions:

  1. “Did we come to the OR for the right reason, that is, was the surgery indicated?”
  2. “Did we do enough?” Hopefully, yes, but sometimes it is appropriate to schedule another good look in the OR 24 to 48 hours later where, resources willing, the wound can be evaluated and treated. This is a good time to get the reconstructive plastic surgeons involved for future wound coverage.
  3. My final question is, “Did we do too much?” Most patients do not want their feet—much less any toes—cut off unnecessarily, but source control for sepsis often demands these extreme measures. Limb salvage is a complex process that may require multidisciplinary care, but life over limb should prevail, including quality of life, salvaging a lower extremity that cannot be used for ambulation. Sometimes early amputation is the wise choice for the clinicians and the patient.
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Diabetic Foot Ulcers

On a less dramatic but more insidious note, one of the major clinical diagnostic billing codes that arises for wound care is maintenance of a diabetic foot ulcer.5 These ulcers are a major cause of morbidity and mortality, accounting for approximately two-thirds of all nontraumatic amputations performed in the United States.6,7 In these patients, chronic hyperglycemic episodes lead to neuropathy and vasculopathy causing the skin to break down and progress to an ulcerative or gangrenous process, resulting in an open wound. The wound is evaluated for vitality with sharp debridement or even amputation.

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Treating a diabetic foot ulcer.Source: Adobe Stock

Infected or ischemic diabetic foot ulcers account for approximately 25% of all hospital stays for patients with diabetes. The healing time for a diabetic foot ulcer ranges from two to 15 weeks, with an average of eight weeks.8 Appropriate local wound care can achieve 50% surface area reduction or reduction of ulcer depth in four weeks.9 If this rate of progress is not observed, further management to address glycemic control, edema, and other aspects of general health and nutrition should be considered. Ulcers that still do not improve should be reevaluated for ongoing soft tissue infection or osteomyelitis, impaired extremity vascular flow, and, most commonly, the need for more effective off-loading or surgical debridement.10

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Venous Stasis

Another clinical pathology that leads to lower extremity wounds is venous stasis. The proportion of the population suffering from obesity and chronic venous insufficiency is increasing, and obese patients are more likely to be symptomatic because of their venous disease.11 The final common pathway that leads to chronic venous insufficiency is the development of venous hypertension. In most cases, venous hypertension results from obstruction of venous flow, dysfunction of venous valves, and/or the venous flow is directed abnormally from the deep to the superficial system, producing local tissue inflammation, fibrosis and occasional ulceration. Sustained venous hypertension is associated with histologic and ultrastructural changes that lead to increased vascular permeability (edema) and the chronic release of inflammatory mediators that are the fundamental cause of cutaneous hyperpigmentation, trophic skin changes and ulceration.12 New techniques using radiofrequency ablation by vein specialists for patients with venous reflux disease have been promising for those formerly relegated to compression with weekly Unna’s boot changings and Jobst stockings.

The Ideal Dressing

The standard of care for wound healing has been wet-to-moist gauze dressings that are useful for packing large soft tissue defects until wound closure or coverage with split-thickness skin grafts can be performed. In the literature, average wound closure with wet-to-moist gauze dressings has been approximately 5.7±4.6 weeks.13-17 Acute wound fluid is rich in platelet-derived growth factor, basic fibroblast growth factor, and has a balance of metalloproteases serving as a matrix custodial function. These interact with one another and other cytokines to stimulate healing. An ideal dressing is one that absorbs excessive wound fluid while maintaining a moist environment that protects the wound from further mechanical or caustic damage. Also, the ideal wound dressing conforms to the wound shape, eliminates dead space, achieves hemostasis and minimizes edema through compression. New hydrogels and alginates pervade the toolbox for nurses and physicians who specialize in wound care.

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Negative Pressure Wound Therapy and Hyperbaric Oxygen Therapy

Larger wounds, due to various pathophysiologic conditions, could become edematous and benefit from negative pressure wound therapy or hyperbaric oxygen chamber therapy, particularly for radiated tissue and chronic, nonhealing wounds. Negative pressure wound therapy accelerates wound healing where the subatmospheric pressure improves and accelerates healing by reducing the time to wound closure.18-21 As any therapy, negative pressure wound therapy and hyperbaric oxygen chamber therapy are not always effective, have a cost associated with them, and will require the wound care team to reevaluate other possibilities.

Several studies include a standard-of-care arm measuring wound size, duration of wound, healing time in days to complete epithelization, patient characteristics, and many complications and adverse events.22-35 In a literature review, the healing time for standard-of-care wet-to-moist dressing changes was an average of 53.3±24.5 days, which is a difference of 18 days compared with negative pressure wound therapy (35.1±17.2 days).22-35

New Horizons: Biologics

In recent years, bioscaffold material has shown promising tissue regenerative properties. Bioscaffold is an artificial structure, usually derived from a biological source (xenoform or alloform), and is implanted on the open exposed wound. Tissue engineering has produced these biological products that have shown at the microscopic level to adhere, blend and act as a supporting matrix in the patient’s body to reepithelialize denuded areas and enhance tissue recovery and the healing process. The biological tissue is taken and put under multiple sterilization steps and is decellularized to maintain and retain the native extracellular matrix, which has been shown to adapt with the body’s own connective tissue cell’s matrix of type I collagen, type IV collagen and fibronectin. This allows “regenerative” remodeling of the wound instead of engaging in a process that leads to scar tissue formation.36,37 The structure allows for support, growth and proliferation of epithelial cells. This type of matrix has been derived from small intestinal submucosa and urinary bladder tissue. Uses have been numerous with repair of hernias as well as musculoskeletal, cardiovascular, urogenital and integumentary structures. We hope this review of basic ideas and concepts for practicing surgeons will spark the imagination of a new era in wound care management.

References

  1. Atiyeh BS, Ioannovich J, Al-Amm CA, et al. Management of acute and chronic open wounds: the importance of moist environment in optimal wound healing. Curr Pharm Biotechnol. 2002;3(3):179-195.
  2. Schultz GS, Sibbald RG, Falanga V, et al. Wound bed preparation: a systematic approach to wound management. Wound Repair Regen. 2003;11(suppl 1):S1-28.
  3. Brem H, Jacobs T, Vileikyte L, et al. Wound-healing protocols for diabetic foot and pressure ulcers. Surg Technol Int. 2003;11:85-92.
  4. Rennert R, Golinko M, Kaplan D, et al. Standardization of wound photography using the Wound Electronic Medical Record. Adv Skin Wound Care. 2009;22(1):32-38.
  5. Rice JB, Desai U, Cummings AK, et al. Burden of diabetic foot ulcers for Medicare and private insurers. Diabetes Care. 2014;37(3):651-658.
  6. Ramsey SD, Newton K, Blough D, et al. Incidence, outcomes, and cost of foot ulcers in patients with diabetes. Diabetes Care. 1999;22(3):382-387.
  7. Gregg EW, Sorlie P, Paulose-Ram R, et al. Prevalence of lower-extremity disease in the US adult population >=40 years of age with and without diabetes: 1999-2000 national health and nutrition examination survey. Diabetes Care. 2004;27(7):1591-1597.
  8. Robertshaw L, Robertshaw DA, Whyte I. Audit of time taken to heal diabetic foot ulcers. Practical Diabetes Int. 2001;18(1):6-9.
  9. Sheehan P, Jones P, Giurini JM, et al. Percent change in wound area of diabetic foot ulcers over a 4-week period is a robust predictor of complete healing in a 12-week prospective trial. Plast Reconstr Surg. 2006;117(7 suppl):239S-244S.
  10. Wietlisbach CM. Cooper’s Fundamentals of Hand Therapy. 3rd ed. Mosby; 2014.
  11. Davies HO, Popplewell M, Singhal R, et al. Obesity and lower limb venous disease - the epidemic of phlebesity. Phlebology. 2017;32(4):227-233.
  12. Tretbar LL. Deep veins. Dermatol Surg. 1995;21(1):47-51.
  13. Lavery LA, Boulton AJ, Niezgoda JA, et al. A comparison of diabetic foot ulcer outcomes using negative pressure wound therapy versus historical standard of care. Int Wound J. 2007;4(2):103-113.
  14. Sajid MT, Mustafa Qu, Shaheen N, et al. Comparison of negative pressure wound therapy using vacuum-assisted closure with advanced moist wound therapy in the treatment of diabetic foot ulcers. J Coll Physicians Surg Pak. 2015;25(11):789-793.
  15. Mody GN, Nirmal IA, Duraisamy S, et al. A blinded, prospective, randomized controlled trial of topical negative pressure wound closure in India. Ostomy Wound Manage. 2008;54(12):36-46.
  16. Karatepe O, Eken I, Acet E, et al. Vacuum assisted closure improves the quality of life in patients with diabetic foot. Acta Chir Belg. 2011;111(5):298-302.
  17. McCallon SK, Knight CA, Valiulus JP, et al. Vacuum-assisted closure versus saline-moistened gauze in the healing of postoperative diabetic foot wounds. Ostomy Wound Manage. 2000;46(8):28-32, 34.
  18. Orgill DP, Manders EK, Sumpio BE, et al. The mechanisms of action of vacuum-assisted closure: more to learn. Surgery. 2009;146(1):40-51.
  19. Pollak AN. Use of negative pressure wound therapy with reticulated open cell foam for lower extremity trauma. J Orthop Trauma. 2008;22(10 suppl):S142-S145.
  20. Scherer ss, Pietramaggiori G, Mathews JC, et al. The mechanism of action of the vacuum-assisted closure device. Plast Reconstr Surg. 2008;122(3):786-797.
  21. Kairinos N, Voogd AM, Botha PH, et al. Negative-pressure wound therapy II: negative-pressure wound therapy and increased perfusion. Just an illusion? Plast Reconstr Surg. 2009;123(2):601-612.
  22. Margolis DJ, Kantor J, Santanna J, et al. Risk factors for delayed healing of neuropathic diabetic foot ulcers: a pooled analysis. Arch Dermatol. 2000;136(12):1531-1535.
  23. Blume PA, Walters J, Payne W, et al. Comparison of negative pressure wound therapy using vacuum-assisted closure with advanced moist wound therapy in the treatment of diabetic foot ulcers: a multicenter randomized controlled trial. Diabetes Care. 2008;31(4):631-636.
  24. O’Brien DP, Friedman ND, McDonald A, et al. Wound healing: natural history and risk factors for delay in Australian patients treated with antibiotics for Mycobacterium ulcerans disease. PLoS Negl Trop Dis. 2018;12(3):e0006357.
  25. de Laat EH, van den Boogaard MH, Spauwen PH, et al. Faster wound healing with topical negative pressure therapy in difficult-to-heal wounds: a prospective randomized controlled trial. Ann Plast Surg. 2011;67(6):626-631.
  26. Joseph E, Hamori CA, Bergman S, et al. A prospective randomized trial of vacuum-assisted closure versus standard therapy of chronic nonhealing wounds. Wounds. 2000;12(3):60-67.
  27. Armstrong DG, Lavery LA; Diabetic Foot Study Consortium. Negative pressure wound therapy after partial diabetic foot amputation: a multicentre, randomised controlled trial. Lancet. 2005;366(9498):1704-1710.
  28. Braakenburg A, Obdeijn MC, Feitz R, et al. The clinical efficacy and cost effectiveness of the vacuum-assisted closure technique in the management of acute and chronic wounds: a randomized controlled trial. Plast Reconstr Surg. 2006;118(2):390-397.
  29. Vuerstaek JD, Vainas T, Wuite J, et al. State-of-the-art treatment of chronic leg ulcers: a randomized controlled trial comparing vacuum-assisted closure (V.A.C.) with modern wound dressings. J Vasc Surg. 2006;44(5):1029-1037; discussion 1038.
  30. Thompson CB, Wiemken TL, Brown TS. Effect of postoperative dressing on excisions performed on the leg: a comparison between zinc oxide compression dressings versus standard wound care. Dermatol Surg. 2017;43(11):1379-1384.
  31. Ubbink DT, Vermeulen H, Goossens A, et al. Occlusive vs gauze dressings for local wound care in surgical patients: a randomized clinical trial. Arch Surg. 2008;143(10):950-955.
  32. Zelen CM, Orgill DP, Serena T, et al. A prospective, randomized, controlled, multicentre clinical trial examining healing rates, safety and cost to closure of an acellular reticular allogenic human dermis versus standard of care in the treatment of chronic diabetic foot ulcers. Int Wound J. 2017;14(2):307-315.
  33. Cazzell S, Vayser D, Pham H, et al. A randomized clinical trial of a human acellular dermal matrix demonstrated superior healing rates for chronic diabetic foot ulcers over conventional care and an active acellular dermal matrix comparator. Wound Repair Regen. 2017;25(3):483-497.
  34. Zelen CM, Orgill DP, Serena TE, et al. An aseptically processed, acellular, reticular, allogenic human dermis improves healing in diabetic foot ulcers: a prospective, randomised, controlled, multicentre follow-up trial. Int Wound J. 2018;15(5):731-739.
  35. Lavery LA, Boulton AJ, Niezgoda JA, et al. A comparison of diabetic foot ulcer outcomes using negative pressure wound therapy versus historical standard of care. Int Wound J. 2007;4(2):103-113.
  36. Badylak SF. Xenogeneic extracellular matrix as a scaffold for tissue reconstruction. Transpl Immunol. 2004;12(3-4):367-377.
  37. Hodde JP, Record RD, Tullius RS, et al. Retention of endothelial cell adherence to porcine-derived extracellular matrix after disinfection and sterilization. Tissue Eng. 2002;8(2):225-234.

Dr. Shariff is a research fellow in New York City. Dr. Kim is a general surgeon in the Bronx, N.Y.

The authors reported that they have no relevant relationships.