Complex Wound Management
- ️Tue Jul 04 2023
Continuing Education Activity
Wound healing is a critical physiological process to maintain the integrity of the skin as a mechanical barrier after trauma. It can be generally divided into hemostatic, inflammatory, proliferative, and remodeling phases. Complex wounds classically arrest in the inflammatory phase without further progression. Many factors can lead to this, including poor systemic conditions or poor local tissue environments such as vascular compromise or infection. Proper understanding of the healing process is essential when addressing any complex wound. This activity reviews the evaluation and treatment of complex wounds and highlights the importance of the interprofessional team approach when evaluating patients with this condition.
Objectives:
Review the basic concepts of wound healing and discuss factors that affect the healing process.
Explain how to evaluate patients presenting with complex wounds.
Describe the current practice in the treatment of complex wounds.
Outline the management by an interprofessional team in dealing with complex wounds.
Introduction
Wound healing is a complex dynamic biomechanical process as the body attempts to restore the integrity of traumatized or devitalized tissues. Chronic wounds are defined as longstanding tissue injuries that cannot be treated with conventional methods of wound dressing or closure either due to local tissue factors or systemic factors.[1]
Recently, chronic wounds have been described as “complex wounds,” a term more representative of the multifactorial dynamic tissue healing process. For a wound to be classified as a complex wound, it should show one of the following features[2]:
Persistent for more than three months
Compromised vascularity or necrosis
Presence of infection
Associated comorbidities impair healing potential
There are many factors, both local and systemic, that can affect wound healing. Local factors include wound depth, infection, peripheral vascular disease, radiotherapy, sustained pressure, and excessive moisture. While systemic factors include metabolic disorders such as diabetes mellitus, immunodeficiency, and nutritional deficiencies.[3]
Complex wounds cause a huge burden on both the individual level (health-related quality of life) and the institutional level (economic cost). It is estimated that 1 to 3% of the health care expenses in developed countries go for complex wound management. This represents around the US $25 billion a year in the united states. This figure is subjected to further increase as the number of chronic morbidities rises in the community.[4][5][6][7]
Anatomy and Physiology
Skin is the largest organ in the body. It is composed of three main layers: epidermis, dermis, and subcutis. The epidermis is the outermost layer, and it is composed of five sublayers. The basal layer or stratum germinativum is formed of columnar cells which continuously divide to regenerate the skin. It also contains melanin-producing cells (melanocytes) and neuroendocrinal cells (Merkel cells). The prickle cell layer or stratum spinosum is formed of polyhedral cells, and it makes up most of the epidermis structure. It contains antigen-presenting cells, which are called Langerhans cells. The next sublayers are stratum granulosum and stratum lucidum, which are formed of big and flatter cells. These cells eventually die to form the outermost layer of the epidermis, which is the stratum corneum.
The dermis is the next layer of the skin. It accounts for 90% of the thickness of the skin. It is mainly formed of collagen and elastin and contains blood vessels, sweat glands, sebaceous glands, and hair follicles. It can be further subdivided into the papillary and reticular dermis. The innermost layer is the subcutis or hypodermis, which is mainly formed of fat and collagen. It acts as an insulator and a shock-absorbent.[8]
The skin has four principal functions: protection against the external environment, including ultraviolet rays and infection, thermal regulation through blood vessels and sweat glands, the sensation of different nerve endings, and endocrine function by producing vitamin D.[9]
Restoration of tissue integrity following an injury is a complex dynamic biological series of events. It can be categorized into four main phases: the hemostatic, inflammatory, proliferative, and remodeling phases. In the hemostasis phase, the body tries to form a coagulum by vasoconstriction, platelet aggregation, and activation of intrinsic and extrinsic coagulation pathways. While in the inflammatory phase, the polymorphonuclear leukocytes (PMNS) move from the bloodstream to the wound to clear any debris.
On days 3 to 4, macrophages predominate the wound and modulate angiogenesis and fibroblast activity by certain cytokines. Proliferation is the third phase of wound healing, mainly moderated by fibroblasts around days 5 to 7. Fibroblast controls new collagen deposition, mainly type III, angiogenesis, and epithelialization. This phase can last up to 4 weeks. Remodeling is the final phase of wound healing characterized by the replacement of collagen III by collagen I, and it may last for years. The wound exhibits its maximal tensile strength at 12 weeks. The final scar will exhibit only 80% of the tensile strength of the normal, pre-injury, skin.[10][11][12]
Contraindications
Iodine-based dressing: It is better to be avoided in patients with thyroid problems and pregnant patients.[13][14]
Negative Pressure Wound Therapy (NPWT): wound bed is suspicious for the presence of malignancy, unexplored fistula, untreated osteomyelitis, and the presence of necrotic tissue.[15]
Larval therapy is contraindicated if near a major organ, cavity, or blood vessel, if the wound is too dry, or if the wound is prone to significant bleeding.[16]
Relative contraindications for leech therapy include arterial insufficiency, bleeding tendency, Jehovah's Witness, immunosuppression, diabetic patients, previous allergy to leeches or fluoroquinolone antibiotics, and psychological aversion to leech use.[17]
Hyperbaric oxygen: pneumothorax, severe reactive airway disease, and recent chemotherapy use.[18]
Personnel
Management of complex wounds should be carried out in an interprofessional team approach. This is crucial to optimize the wound healing environment and control any pre-existing conditions. Regular communication between team members is mandatory for optimal wound healing. This team can include wound care specialists such as tissue viability nurses, plastic surgery nurse specialists, and plastic surgeons. The involvement of the diabetic team, vascular surgeons, lymphedema care team, dietitian, and microbiology should be assessed on an individual basis. Moreover, pain team and occupational therapist involvement are essential, especially in the interim phase before discharging the patient to the community.[2]
Early involvement of tissue viability or other wound-care nurse is advisable, especially in wounds that show deterioration or no improvement after the first two weeks of management. Medical photography is also important to monitor wound healing progress. Cases that require urgent surgical debridements, such as necrotizing fasciitis, or cases that may need complex reconstruction should be discussed with a plastic surgeon.[19]
The involvement of a plastic surgery nurse specialist may be helpful in the postoperative management of reconstructive surgery such as skin grafts of flap-based reconstruction. They can also provide support to the nursing team when special dressing techniques are used, such as topical negative pressure therapy or if larvae have been used for wound debridement.[20][21] All diabetic patients with complex wounds should be routinely referred to the diabetic team to optimize blood glucose levels and HbA1c. Patients with complex wounds are likely to require meal adjustment to aid the healing process. All these patients should be screened for malnutrition and referred to a dietitian accordingly. Meal adjustment is usually made by increasing caloric intake, especially proteins, along with minerals and vitamins. Frequent monitoring of albumin, prealbumin, and transferrin is helpful to monitor the progress.[22]
In the case of infected wounds, the choice of antibiotic should be selected in line with the antimicrobial policy and after discussion with the microbiology team to prevent unnecessary prolonged antibiotic administration. Patients with evident lymphedema should be referred to the lymphedema team to optimize and apply compression dressing if possible.[23] Vascular team involvement is also critical in the following conditions: Needing limb revascularization, urgent amputation to control sepsis, overt vascular diseases such as an ischemic limb, or deep venous thrombosis.[2]
Adequate analgesia is pivotal for patient compliance, and the early involvement of a pain management specialist is beneficial. Occupational therapists and psychological support are needed throughout the hospital admission and after discharge to the community.[24]
Preparation
Proper history taking is an essential step in the management of any wound. Pertinent data include the cause of the wound if known, nutritional status of the patient, duration of the wound, history of previous trauma or ulceration, prior treatment regimens, and if there is any allergy to certain medications or dressing. Examination of wounds should follow a systematic approach. TIMES framework provides a comprehensive and consistent way of wound assessment. The acronym stands for Tissue type in the wound, Infection or inflammation presence, Moisture balance assessment, Epithelialization assessment, and Surrounding skin.[25]
Tissue type: The type of tissue in the wound bed will influence the decision-making regarding wound management. Assessment should include assessing the viability of this tissue, specifying its type, which may be necrotic, sloughy, infected, granulating, or epithelializing, presence of a foreign body, and finally highlighting any exposed vital structures such as tendons or bones.[26]
Infection or inflammation: The presence of infection can retard wound healing as it prolongs the inflammatory phase. It is crucial to differentiate between contamination or colonization and infection. Almost all wounds are contaminated or colonized. To diagnose infection, health practitioners should look for symptoms such as fever, increased pain and swelling, erythema, and purulent discharge. A wound swab with more than >10colonies/mm3 is suggestive of infection.[27] This presentation may be subtle in immunocompromised and diabetic patients. Any systemic antimicrobial treatment should be in line with the local antimicrobial policy and after discussion with the local microbiology team.[28]
Moisture balance: The provision of adequate moisture is essential for the healing of many vascularized wounds. Nevertheless, excess moisture can provide a medium for bacterial growth. Moisture balance assessment: a holistic assessment of the patient will guide the amount of moisture needed and the dressing choice. It is imperative to document the amount, color, and odor of any exudate. Involvement of vascular team in choice of dressing is crucial in cases of vascular compromise of a limb.[29]
Epithelialization assessment: The absence of epithelial advancement is a sign of a non-healing wound. The cause of this should be investigated and treated accordingly. This may include hyper granulation, excess moisture, and the presence of infection.
Surrounding skin: It is crucial to assess any further inflammation or breakdown in the surrounding skin, indicating the extension of the initial wound.[25]
Technique or Treatment
At the end of the wound assessment, a wound management plan should be formulated, including the possible need for specialist input. This management plan's main goals should focus on optimizing the patient's general condition, infection control, cleaning of the wound, debridement of any necrotic tissues, pain management, and pressure relief measures in cases of pressure ulcers.[25] For optimal wound healing, the patient should have a blood glucose level of less than 200g/dl, albumin level of more than 3 g/dl, prealbumin level of more than 15 mg/dl, lymphocyte count of more than 1,500, well-vascularized wound bed, and a period of smoking cessation.[30]
All wounds must be managed with an aseptic, non-touch technique using personal protective equipment to prevent contamination and subsequent infection, delaying wound healing. The use of warmed saline usually does a cleansing of the wound. Use of antiseptic solution is highly recommended if there are excessive exudate or signs of infection. Debridement of debris and non-viable tissue can be done by many methods, either autolytic, larval therapy, chemical (through antiseptic use such as hydrogen peroxide or prontosan), hydrosurgery (versajet), conservative bedside sharp debridement (by scalpel or scissor), or surgical debridement.[31][32][33]
Dressing
Wounds heal quicker in a moist and clean environment as this facilitates the migration of numerous growth factors and epithelial cells to the wound bed along with wound edge contraction.[34] There are four main principles involved in dressing choice. If a wound has an excessive discharge, this exudate needs to be absorbed. If a wound is dry, hydration is needed. If a wound is infected, appropriate antimicrobial treatment should be initiated. If a wound shows necrotic tissue, debridement is needed.[35]
Dressing choice must be based on a holistic assessment of the patient's general condition, the wound bed, and an understanding of the advantage and disadvantages of each dressing type. The ideal dressing should create a moist and clean environment, prevent desiccation, remove excess exudate, be impermeable to microorganisms but allow gas exchange, be free of toxic materials, conform to the wound with minimal pain on application and removal, and be cost-effective. Regarding the frequency of dressing change, infected wounds and wounds with high exudate should be monitored closely daily and should be changed more frequently. While non-infected wounds should be changed less frequently to keep a moist wound environment and facilitate the effect of biological dressings. Continuous wound evaluation with each dressing change is essential to check the suitability of the dressing regime and the potential need for shifting to another dressing type.[30]
All dressing materials can manipulate the wound environment. There are three broad dressing categories. The first category induces autolytic debridement in the wound bed by activation of the host's proteolytic enzymes.[36] The second category ameliorates the moisture level of the wound. The third category suppresses bacterial growth. There is a lack of evidence on clinical effectiveness when comparing different types of dressing. Most of the reports are anecdotal and lack proper randomization. Different types include:
Gauze: is available in all hospitals. It is highly permeable, non-occlusive, and can be used as a primary or secondary dressing. The only drawback is that it can adhere to the bed and lead to wound trauma when removed, though this can be useful as a built-in form of debridement of any devitalized tissue in the wound bed. Its woven type can initiate granuloma formation from the remaining particles.[37] Impregnated gauze with iodine, petroleum, bismuth, or zinc is non-adherent and semi-occlusive. It is important to understand that bismuth or iodine impregnated gauze is cytotoxic and inhibits inflammatory cells, so they should be changed regularly and limited to less than five days. Iodine impregnated gauze can be used to temporarily pack foul-smelling infected wounds after debridement until the infection is fully cleared.[38]
Iodine dressings: It was first described in 1882. Iodophors such as povidone-iodine were developed in the 1960s to overcome the side effects of iodine, such as skin irritation and pain. The mechanism of action of iodine is unclear. Several studies suggested that low-dose, slow-release iodine can kill floating bacteria by rapidly penetrating their cells, hence its efficacy as an antiseptic solution. There are some speculations that iodine may delay wound healing as being cytotoxic, especially in high doses.[39]
Transparent film dressing: These are thin, flexible sheets that are composed of polyurethane. They provide a moist environment, but they do not have any absorptive capacity. They can be used for dressing surgical wounds or the donor site of skin graft.[40]
Foam dressing: This is made of a polyurethane base and is permeable to both water vapor and gases. It can be used in wounds with moderate to high exudate, diabetic foot, and minor burns. It is not recommended in dry eschar or arterial ulcers as it can impair the healing process. It can be left in place for up to a week, and it should be changed when full of exudate.[41]
Hydrogel: It is a complex hydrophilic polymer consist of around 90% water base. This high-water content limits its capacity to absorb excess exudate. Its main application is to soften necrotic wound beds like pressure sores and vascular ulcers and dress low-exudate wounds. The surrounding skin should be protected from maceration.[42]
Hydrocolloid: It is formed of the inner layer of self-adhesive gel-forming hydrophilic colloid particles such as carboxymethylcellulose (CMC). This layer can absorb exudate, allow for a moisture healing environment, and provide thermal insulation. The outer protective layer is formed of polyurethane which acts as a mechanical barrier for bacteria and foreign bodies. It is available in many forms, including paste, granules, and powder. It can be used in low to moderate exudating wounds such as minor burns and pressure ulcers. It should be avoided in clinically infected wounds.[43][44]
Alginate: Manufactured from seaweed and covered with calcium/sodium salts. It is a highly absorbent, non-adherent, and biodegradable dressing. When applied to a wound, calcium and sodium salts interact with the host's serum to form a hydrophilic gel. It can absorb up to 20 times its original weight. It is highly effective in managing highly exudating wounds, abdominal dehiscence, pressure ulcers, sinus tract, wounds with exposed tendons, and infected wounds. In clean wounds, it can be kept in place for a week, while in infected wounds, it should be changed daily.[45][46]
Hydrofiber: It is made of 100% CMC fiber. They have similar properties and usage of alginates, so they are also suitable for use in highly exudative wounds. They can be used in partial-thickness burn and graft donor sites.[47][48] Hydrofiber has also been combined with silver which helps to maintain the antimicrobial properties for a longer period and a broader spectrum.[49]
Hydro conductive dressings: These are relatively new dressings first introduced at the Symposium on Advanced Wound Care in 2011. Data suggest that hydro conductive dressings can absorb bacteria and harmful cytokines from the wound to the dressing. This is done through the capillary action of the dressing, which moves the exudates from the wound and moves it to a second layer. It can be left in place for 3 to 7 days until it is fully saturated.[50][51]
Silicone dressing: These dressings are used in cases of abnormal wound healing such as hypertrophic and keloid scar. Several studies showed that they soften the scar and prevent progression to hypertrophic scars. The exact mechanism of action is unknown. The most popular theory is an improvement of scar hydration by decreasing vapor loss. Unfortunately, most studies have been done with small sample size, short-term follow-up, and without a control group.[52][53]
Silver dressing: Silver is a broad-spectrum antimicrobial agent that is effective against bacteria, viruses, fungi, and yeast. It has also been reported to be effective against methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant enterococci (VRE).[54] They are indicated in mild wound infections as they can not penetrate deep tissues.[55] A Cochrane review in 2007 stated that there is no sufficient evidence to recommend silver dressings for infected or contaminated wounds. [56]They are manufactured in combination with all other types of dressing, such as hydrogel, hydrocolloid, hydrofiber, and alginate.[55] Silver nitrate sticks are another entity that is effective in treating hyper granulation tissue.[57]
Polyhexamethylene biguanide and honey dressings: Manuka honey was first recognized as a topical antibacterial dressing in 1892. It is found to be effective against broad spectrum bacteria, fungi, yeast, molds, MRSA, and VRE. Its antibacterial properties are linked to its high viscosity, which forms a mechanical barrier from the environment, as well as its high sugar concentration leading to osmotic pressure changes, the production of H2O2 by peroxidase, low PH, and the presence of bioflavinoid.[57][58]
Negative pressure wound therapy (NPWT): First described in the 1990s, since then has been widely used in all wound types. NPWT applies subatmospheric pressure to the wound bed through a unit attached to a sponge and semi-occlusive dressing. The exact mechanism of action is unknown. However, it was shown to remove excess exudate, debris, enhance circulation and promote granulation tissue formation. NPWT was found to be more effective and promote faster healing of chronic wounds compared with conventional dressing.[59] Contraindications include the presence of malignancy, unexplored fistula, untreated osteomyelitis, and the presence of necrotic tissue in the wound bed.[15]
Larval therapy: Sterile larva (maggots) of the common green-bottle fly (Lucilia sericata) are used for debridement of slough and necrotic wounds and debridement of hematoma when surgical management is deemed inappropriate. It produces proteolytic enzymes that liquefy the necrotic tissue. It can be either obtained as a free-range larva or contained in a dressing named "Biobag." It can be left for 2 to 4 days according to the treatment regimen. The use of maggots should stop if the patient finds them painful, causing uncontrolled bleeding, and maggots are no longer alive or secured in the dressing.[60]
Leech therapy: In cases of venous congestion of a reconstructive flap, leeches may be used to augment venous egress from the flap. If a venous outflow problem is suspected, re-exploration should be considered first to rule out hematoma or thrombosis of the vascular supply of the flap. Leech saliva performs its action through several compounds. These include hirudin that inhibits the conversion of fibrinogen to fibrin, a histamine-like substance that causes vasodilatation, proteases like collagenase to spread the anticoagulation effect, and anesthetic. Leeches mouth and digestive tract contain Aeromonas spp., a microorganism that aids in the digestion of blood. As this bacterium can be pathogenic in humans, antibiotic prophylaxis (ciprofloxacin) should be initiated an hour before the application of leeches and continue for a day after removing the last leech. In cases of ciprofloxacin allergy, doxycycline can be used. Leeches should be applied every 4 to 6 hours to allow time for passive bleeding and feeding.[61]
Skin Substitutes
Skin substitutes can be either biological such as skin graft, or synthetic, such as Integra. Skin grafts can be either autografts from the same individual, allografts (homografts) where the skin is transferred from a different individual from the same species (from human to human), and xenografts in which skin is transferred between different species (from animal to human). The human amniotic membrane is another form of biological dressing that can be used in especially in low-resource countries. Synthetic semi-biological dressings are produced by tissue engineering technology. Some of them can be incorporated permanently into the wound. In general, they can be used to dress a superficial wound until re-epithelization occurs, optimization of the wound bed of deep wounds until grafting, and when the patient is not a candidate for surgery either due to multiple comorbidities or other factors. They are of great use when treating composite wound defects, especially in cases of high total body surface area burn due to sparsity of autologous skin graft.[62]
Hyperbaric Oxygen
Hyperbaric oxygen (HBO) showed good promising results in managing complex wounds. The patient is placed in a special pressurized sealed room, with 100% oxygen at 1.5 to 3atm for around 3 hours. This can be repeated on several occasions according to the wound depth. Most chronic wounds will need between 20 and 40 sessions. The exact mechanism of action is unknown. It is suggested that it is mainly related to increasing the overall oxygen-carrying capacity, which helps with angiogenesis and local tissue perfusion.[63][64][65] It has certain contraindications, which include pneumothorax, severe reactive airway disease, and chemotherapy use. Potential unwanted effects include claustrophobia, ear discomfort, and potential neural toxicity due to high oxygen pressure.[65] All these can be minimized by giving enough time intervals between each session.[66][18]
Future Research
Understanding the wound healing process at the cellular level and its different modulators are the basis for future research in wound healing. Mediators such as Eicosanoid, leukotrienes, and prostaglandins can modulate the inflammatory phase, and their use showed promising results in decreasing wound size and healing time.[67][68] Cytokines such as granulocyte-macrophage colony-stimulating factors have shown encouraging results in the treatment of chronic venous ulcers.[69] Recombinant platelet-derived growth factor (PDGF) is approved by the FDA to treat diabetic foot, and there is some anecdotal evidence of its use in chronic wounds in general. Biopsy of the wound bed, especially in previously irradiated areas, may be beneficial to exclude the presence of malignancy or dysplasia. However, the potential risk of growth factors to induce malignancy is the main limitation of their wider use.[70][71] More recent studies showed that inflammatory dysregulation leads to failure of wound healing. This was evident by the high level of proteases, protease inhibitors, and other inflammatory markers. This finding encourages the potential production of targeted therapies to manage complex wounds.[72]
Complications
General complications include bleeding, failure of the treatment regime, skin maceration, and infection.
Specific Complications
Leech therapy: The mouth and digestive tract of the leech contain Aeromonas spp., which aids in the digestion of the blood. It is pathogenic to man, and the presence of venous congestion leads to localized immuno-suppression. Hence the need for antibiotic prophylaxis. Persistent, prolonged bleeding can occur, which may be significant, especially in children. Therefore, daily monitoring of the hemoglobin level is mandatory. Allergic reactions, migration to healthy tissues, and pre-renal azotemia are also reported complications.[61][73]
Hyperbaric oxygen: Potential unwanted effects include claustrophobia, ear discomfort, potential neural toxicity due to high oxygen pressure.[65]
Clinical Significance
For a complex wound to heal, optimization of both systemic and local factors is needed. Adequate debridement of the wound bed and choice of the appropriate dressing is essential. Moreover, it requires adjusting the patient's general condition, noting any comorbidities, and assessing nutritional status to aid the healing process. In most cases, an interprofessional team approach is best to achieve this goal.[71]
Special Complex Wounds
Pressure Ulcer
A pressure ulcer is a localized injury of the skin and underlying soft tissue over a bony prominence. 3 to 15% of hospitalized patients can develop pressure ulcers, and it is associated with a high mortality rate in the elderly. Common sites include sacrum, ischium, heel, trochanter, scapula, and occiput. It is usually initiated by pressure, shearing, and friction forces. The poor general condition of these patients renders the healing of the pressure ulcer.[74] American National Pressure Ulcer Advisory Panel (NPUAP) classifies pressure ulcers into four categories according to depth. Category one: non-blanching erythema, category II: partial thickness skin loss, category III: full-thickness skin loss, category IV: full-thickness tissue loss.[75]
Waterlow score is one of the most common scores used to assess the risk of developing pressure ulcers. It assesses the following skin type and risk areas: BMI, sex and age, appetite and weight loss, mobility, continence, and special risks such as malnutrition.[76] Prevention of pressure ulcers should include regular skincare, optimization of nutritional status, frequent mobilization to avoid direct contact between bony prominences, pressure dispersion by using pressure mattresses, and urinary or fecal diversion if needed. Treatment should focus on optimization of patient general condition and treatment of local infection before any reconstruction.[77]
Surgery goals should achieve adequate excision of the pressure ulcer and underlying bursa before reconstruction using durable skin flaps. Examples of the common flaps are gluteus maximus musculocutaneous flap for sacral pressure sore, posterior thigh advancement flap for ischial pressure sores, and fascia lata flap for trochanteric pressure sores.[78]
Diabetic Foot
The cause of diabetic foot is usually multifactorial, including neuropathy, ischemia, and infection. Most cases are combined neuro-ischemia.[79] According to the National Institute for Health and Clinical Excellence, management of diabetic foot should be done in an interprofessional team approach, including a general practitioner, a diabetic nurse, educator, podiatrist, orthotic specialist, and consultation of other specialists such as vascular plastic surgery, dietitian, and endocrinologist.[80] Management should focus on patient education, monitoring of blood glucose level, wound debridement, either chemical or surgical, offloading, and surgery which may be in the form of flap coverage, revascularization of a diseased limb, or even amputation.[81]
Venous Ulcer
Venous ulcer is one of the late sequelae of varicose veins and subsequent venous hypertension. It is usually difficult to heal and can significantly affect the quality of life of many patients. Treatment should focus on surgical treatment of venous incompetency, if possible, application of compression dressing, either a multi-layer compression dressing or, if not tolerated, intermittent compression, and regular wound dressing.[82] If the ulcer fails to heal, a skin graft may be needed in a combination of the artificial dermis to enhance the wound bed.[83]
Radiated Wounds
External beam radiation can significantly damage the DNA of keratinocytes, fibroblast, and endothelial cells, which will impair their ability to regenerate. Most of the radiated tissue will continue to have residual endothelial damage and endarteritis obliterans in the long term. This is the main reason why any injury in any radiated tissue will be difficult to heal. Hyperbaric oxygen can improve the wound environment to stimulate healing. However, in extensive cases, surgical excision of the affected area and coverage by vascularized flap is the most suitable option.[84]
Malignant Wounds
Early diagnosis of such cases is mandatory to improve the long-term outcome in terms of morbidity and mortality. A biopsy is essential for diagnosis, and further scans may also be needed to assess the systemic spread of the malignancy. The most common causes are basal cell carcinoma, squamous cell carcinoma, melanoma, Marjolin ulcer, or secondary malignancies. Wide local excision of the tumor along with potential lymph node surgery is the treatment of choice. In extensive non-operable cases, electrochemotherapy may be used to limit the extension of the ulcer and to decrease pain and discharge.
Abdominal Wound Dehiscence
Causes of abdominal wound dehiscence include resection of abdominal wall tumor, e.g., sarcoma or desmoid tumor, or secondary to laparotomy (e.g., trauma, aortic artery aneurysm, sepsis, or necrotizing pancreatitis).In primary cases, reconstruction should be done immediately by a skin flap. While in secondary cases, management is usually staged.[85] Initially, temporary wound closure is achieved by a skin graft. This is followed by optimization of the patient's general condition before the definitive reconstruction, which is usually in the form of component separation.[86][87]
Enhancing Healthcare Team Outcomes
Complex wounds are challenging clinical situations. An interprofessional team approach that provides holistic assessment and evaluation of each patient and addresses their different needs is the cornerstone in managing such cases. Regular communication between the team members is a key element for a better outcome. Thus should include wound care specialists such as tissue viability nurses, dietitians, microbiology, occupational therapists, and other specialists, such as diabetic team, vascular or plastic surgeons. The primary goal should be wound closure if possible. In some cases, this may not be achievable. Thus, optimization of the quality of life should be the aim.[88][1] [Level 4]
Review Questions
References
- 1.
Tricco AC, Antony J, Vafaei A, Khan PA, Harrington A, Cogo E, Wilson C, Perrier L, Hui W, Straus SE. Seeking effective interventions to treat complex wounds: an overview of systematic reviews. BMC Med. 2015 Apr 22;13:89. [PMC free article: PMC4406332] [PubMed: 25899006]
2.Ferreira MC, Tuma P, Carvalho VF, Kamamoto F. Complex wounds. Clinics (Sao Paulo). 2006 Dec;61(6):571-8. [PubMed: 17187095]
3.Han G, Ceilley R. Chronic Wound Healing: A Review of Current Management and Treatments. Adv Ther. 2017 Mar;34(3):599-610. [PMC free article: PMC5350204] [PubMed: 28108895]
4.Frykberg RG, Banks J. Challenges in the Treatment of Chronic Wounds. Adv Wound Care (New Rochelle). 2015 Sep 01;4(9):560-582. [PMC free article: PMC4528992] [PubMed: 26339534]
5.Kinmond K, McGee P, Gough S, Ashford R. 'Loss of self': a psychosocial study of the quality of life of adults with diabetic foot ulceration. J Tissue Viability. 2003 Jan;13(1):6-8, 10, 12 passim. [PubMed: 12599984]
6.Posnett J, Franks PJ. The burden of chronic wounds in the UK. Nurs Times. 2008 Jan 22-28;104(3):44-5. [PubMed: 18293879]
7.Sen CK, Gordillo GM, Roy S, Kirsner R, Lambert L, Hunt TK, Gottrup F, Gurtner GC, Longaker MT. Human skin wounds: a major and snowballing threat to public health and the economy. Wound Repair Regen. 2009 Nov-Dec;17(6):763-71. [PMC free article: PMC2810192] [PubMed: 19903300]
8.McLafferty E, Hendry C, Alistair F. The integumentary system: anatomy, physiology and function of skin. Nurs Stand. 2012 Sep 19-25;27(3):35-42. [PubMed: 23248884]
9.Dąbrowska AK, Spano F, Derler S, Adlhart C, Spencer ND, Rossi RM. The relationship between skin function, barrier properties, and body-dependent factors. Skin Res Technol. 2018 May;24(2):165-174. [PubMed: 29057509]
10.Singer AJ, Clark RA. Cutaneous wound healing. N Engl J Med. 1999 Sep 02;341(10):738-46. [PubMed: 10471461]
11.Furie B, Furie BC. Mechanisms of thrombus formation. N Engl J Med. 2008 Aug 28;359(9):938-49. [PubMed: 18753650]
12.Redd MJ, Cooper L, Wood W, Stramer B, Martin P. Wound healing and inflammation: embryos reveal the way to perfect repair. Philos Trans R Soc Lond B Biol Sci. 2004 May 29;359(1445):777-84. [PMC free article: PMC1693361] [PubMed: 15293805]
13.Patil VP, Kulkarni AP, Jacques T. Iodine induced thyrotoxicosis following povidine-iodine dressings: a case report. Crit Care Resusc. 2003 Sep;5(3):186-8. [PubMed: 16573481]
14.Thaker VV, Leung AM, Braverman LE, Brown RS, Levine B. Iodine-induced hypothyroidism in full-term infants with congenital heart disease: more common than currently appreciated? J Clin Endocrinol Metab. 2014 Oct;99(10):3521-6. [PMC free article: PMC4184078] [PubMed: 25004248]
15.Wild T, Otto F, Mojarrad L, Kellner M, Götzinger P. [Vacuum therapy--basics, indication, contraindication and cost listing]. Ther Umsch. 2007 Sep;64(9):495-503. [PubMed: 18075142]
16.Mohd Zubir MZ, Holloway S, Mohd Noor N. Maggot Therapy in Wound Healing: A Systematic Review. Int J Environ Res Public Health. 2020 Aug 21;17(17) [PMC free article: PMC7504313] [PubMed: 32825736]
17.Whitaker IS, Oboumarzouk O, Rozen WM, Naderi N, Balasubramanian SP, Azzopardi EA, Kon M. The efficacy of medicinal leeches in plastic and reconstructive surgery: a systematic review of 277 reported clinical cases. Microsurgery. 2012 Mar;32(3):240-50. [PubMed: 22407551]
18.Abidia A, Laden G, Kuhan G, Johnson BF, Wilkinson AR, Renwick PM, Masson EA, McCollum PT. The role of hyperbaric oxygen therapy in ischaemic diabetic lower extremity ulcers: a double-blind randomised-controlled trial. Eur J Vasc Endovasc Surg. 2003 Jun;25(6):513-8. [PubMed: 12787692]
19.Hodgins N, Damkat-Thomas L, Shamsian N, Yew P, Lewis H, Khan K. Analysis of the increasing prevalence of necrotising fasciitis referrals to a regional plastic surgery unit: a retrospective case series. J Plast Reconstr Aesthet Surg. 2015 Mar;68(3):304-11. [PubMed: 25444278]
20.Huang C, Leavitt T, Bayer LR, Orgill DP. Effect of negative pressure wound therapy on wound healing. Curr Probl Surg. 2014 Jul;51(7):301-31. [PubMed: 24935079]
21.Sherman RA. Maggot therapy takes us back to the future of wound care: new and improved maggot therapy for the 21st century. J Diabetes Sci Technol. 2009 Mar 01;3(2):336-44. [PMC free article: PMC2771513] [PubMed: 20144365]
22.Medlin S. Nutrition for wound healing. 2012 Jun 28-Jul 11Br J Nurs. 21(12):S11-2, S14-5. [PubMed: 22875371]
23.Macdonald JM, Sims N, Mayrovitz HN. Lymphedema, lipedema, and the open wound: the role of compression therapy. Surg Clin North Am. 2003 Jun;83(3):639-58. [PubMed: 12822730]
24.Hollinworth H, Hawkins J. Teaching nurses psychological support of patients with wounds. Br J Nurs. 2002 Nov;11(20 Suppl):S8, S10-S12, S14, S16, S18. [PubMed: 12476148]
25.Schultz GS, Barillo DJ, Mozingo DW, Chin GA., Wound Bed Advisory Board Members. Wound bed preparation and a brief history of TIME. Int Wound J. 2004 Apr;1(1):19-32. [PMC free article: PMC7951422] [PubMed: 16722894]
26.Harries RL, Bosanquet DC, Harding KG. Wound bed preparation: TIME for an update. Int Wound J. 2016 Sep;13 Suppl 3(Suppl 3):8-14. [PMC free article: PMC7949772] [PubMed: 27547958]
27.Robson MC, Krizek TJ, Heggers JP. Biology of surgical infection. Curr Probl Surg. 1973 Mar;:1-62. [PubMed: 4571495]
28.Bates-Jensen BM. Chronic wound assessment. Nurs Clin North Am. 1999 Dec;34(4):799-845, v. [PubMed: 10523437]
29.Gray M, Black JM, Baharestani MM, Bliss DZ, Colwell JC, Goldberg M, Kennedy-Evans KL, Logan S, Ratliff CR. Moisture-associated skin damage: overview and pathophysiology. J Wound Ostomy Continence Nurs. 2011 May-Jun;38(3):233-41. [PubMed: 21490547]
30.Sood A, Granick MS, Tomaselli NL. Wound Dressings and Comparative Effectiveness Data. Adv Wound Care (New Rochelle). 2014 Aug 01;3(8):511-529. [PMC free article: PMC4121107] [PubMed: 25126472]
31.Courtenay M, Church JC, Ryan TJ. Larva therapy in wound management. J R Soc Med. 2000 Feb;93(2):72-4. [PMC free article: PMC1288068] [PubMed: 10740573]
32.Shimada K, Ojima Y, Ida Y, Matsumura H. Efficacy of Versajet hydrosurgery system in chronic wounds: A systematic review. Int Wound J. 2021 Jun;18(3):269-278. [PMC free article: PMC8244081] [PubMed: 33759367]
33.Stephen-Haynes J, Thompson G. The different methods of wound debridement. Br J Community Nurs. 2007 Jun;12(6):S6, S8-10, S12-14, S16. [PubMed: 17577156]
34.Attinger CE, Janis JE, Steinberg J, Schwartz J, Al-Attar A, Couch K. Clinical approach to wounds: débridement and wound bed preparation including the use of dressings and wound-healing adjuvants. Plast Reconstr Surg. 2006 Jun;117(7 Suppl):72S-109S. [PubMed: 16799376]
35.Morin RJ, Tomaselli NL. Interactive dressings and topical agents. Clin Plast Surg. 2007 Oct;34(4):643-58. [PubMed: 17967620]
36.Ayello EA, Cuddigan JE. Debridement: controlling the necrotic/cellular burden. Adv Skin Wound Care. 2004 Mar;17(2):66-75; quiz 76-8. [PubMed: 15021091]
37.Ovington LG. Hanging wet-to-dry dressings out to dry. Home Healthc Nurse. 2001 Aug;19(8):477-83; quiz 484. [PubMed: 11982183]
38.Ubbink DT, Vermeulen H, Goossens A, Kelner RB, Schreuder SM, Lubbers MJ. Occlusive vs gauze dressings for local wound care in surgical patients: a randomized clinical trial. Arch Surg. 2008 Oct;143(10):950-5. [PubMed: 18936373]
39.Durani P, Leaper D. Povidone-iodine: use in hand disinfection, skin preparation and antiseptic irrigation. Int Wound J. 2008 Jun;5(3):376-87. [PMC free article: PMC7951395] [PubMed: 18593388]
40.Dinner MI, Peters CR, Sherer J. Use of a semipermeable polyurethane membrane as a dressing for split-skin graft donor sites. Plast Reconstr Surg. 1979 Jul;64(1):112-4. [PubMed: 377328]
41.Seaman S. Dressing selection in chronic wound management. J Am Podiatr Med Assoc. 2002 Jan;92(1):24-33. [PubMed: 11796796]
42.Darkovich SL, Brown-Etris M, Spencer M. Biofilm hydrogel dressing: a clinical evaluation in the treatment of pressure sores. Ostomy Wound Manage. 1990 Jul-Aug;29:47-60. [PubMed: 2202317]
43.Varghese MC, Balin AK, Carter DM, Caldwell D. Local environment of chronic wounds under synthetic dressings. Arch Dermatol. 1986 Jan;122(1):52-7. [PubMed: 3079991]
44.Mulder G, Jones R, Cederholm-Williams S, Cherry G, Ryan T. Fibrin cuff lysis in chronic venous ulcers treated with a hydrocolloid dressing. Int J Dermatol. 1993 Apr;32(4):304-6. [PubMed: 8486467]
45.Qin Y, Gilding DK. Alginate fibres and wound dressings. Med Device Technol. 1996 Nov;7(9):32-41. [PubMed: 10163676]
46.Cannavo M, Fairbrother G, Owen D, Ingle J, Lumley T. A comparison of dressings in the management of surgical abdominal wounds. J Wound Care. 1998 Feb;7(2):57-62. [PubMed: 9543974]
47.Barnea Y, Amir A, Leshem D, Zaretski A, Weiss J, Shafir R, Gur E. Clinical comparative study of aquacel and paraffin gauze dressing for split-skin donor site treatment. Ann Plast Surg. 2004 Aug;53(2):132-6. [PubMed: 15269581]
48.Vloemans AF, Soesman AM, Kreis RW, Middelkoop E. A newly developed hydrofibre dressing, in the treatment of partial-thickness burns. Burns. 2001 Mar;27(2):167-73. [PubMed: 11226656]
49.Barnea Y, Weiss J, Gur E. A review of the applications of the hydrofiber dressing with silver (Aquacel Ag) in wound care. Ther Clin Risk Manag. 2010 Feb 02;6:21-7. [PMC free article: PMC2817785] [PubMed: 20169033]
50.Wolcott RD. The effect of a hydroconductive dressing on the suppression of wound biofilm. Wounds. 2012 May;24(5):132-7. [PubMed: 25874355]
51.Alkhalil A, Day A, Monger KW, Zhang J, Carney BC, Hoffman HN, Moffatt LT, Shupp JW. Hydroconductive and silver-impregnated foam dressings: a comparison. J Wound Care. 2017 Jul 01;26(Sup7):S15-S22. [PubMed: 28704172]
52.Poston J. The use of silicone gel sheeting in the management of hypertrophic and keloid scars. J Wound Care. 2000 Jan;9(1):10-6. [PubMed: 10827662]
53.O'Brien L, Pandit A. Silicon gel sheeting for preventing and treating hypertrophic and keloid scars. Cochrane Database Syst Rev. 2006 Jan 25;(1):CD003826. [PubMed: 16437463]
54.Warriner R, Burrell R. Infection and the chronic wound: a focus on silver. Adv Skin Wound Care. 2005 Oct;18 Suppl 1:2-12. [PubMed: 16220035]
55.Tomaselli N. The role of topical silver preparations in wound healing. J Wound Ostomy Continence Nurs. 2006 Jul-Aug;33(4):367-78; quiz 379-80. [PubMed: 16932118]
56.Vermeulen H, van Hattem JM, Storm-Versloot MN, Ubbink DT. Topical silver for treating infected wounds. Cochrane Database Syst Rev. 2007 Jan 24;(1):CD005486. [PubMed: 17253557]
57.Eberlein T, Haemmerle G, Signer M, Gruber Moesenbacher U, Traber J, Mittlboeck M, Abel M, Strohal R. Comparison of PHMB-containing dressing and silver dressings in patients with critically colonised or locally infected wounds. J Wound Care. 2012 Jan;21(1):12, 14-6, 18-20. [PubMed: 22240928]
58.Blair SE, Cokcetin NN, Harry EJ, Carter DA. The unusual antibacterial activity of medical-grade Leptospermum honey: antibacterial spectrum, resistance and transcriptome analysis. Eur J Clin Microbiol Infect Dis. 2009 Oct;28(10):1199-208. [PubMed: 19513768]
59.Philbeck TE, Whittington KT, Millsap MH, Briones RB, Wight DG, Schroeder WJ. The clinical and cost effectiveness of externally applied negative pressure wound therapy in the treatment of wounds in home healthcare Medicare patients. Ostomy Wound Manage. 1999 Nov;45(11):41-50. [PubMed: 10687657]
60.Shi E, Shofler D. Maggot debridement therapy: a systematic review. Br J Community Nurs. 2014 Dec;Suppl Wound Care:S6-13. [PubMed: 25478859]
61.Herlin C, Bertheuil N, Bekara F, Boissiere F, Sinna R, Chaput B. Leech therapy in flap salvage: Systematic review and practical recommendations. Ann Chir Plast Esthet. 2017 Apr;62(2):e1-e13. [PubMed: 27427444]
62.Halim AS, Khoo TL, Mohd Yussof SJ. Biologic and synthetic skin substitutes: An overview. Indian J Plast Surg. 2010 Sep;43(Suppl):S23-8. [PMC free article: PMC3038402] [PubMed: 21321652]
63.Hunt TK, Linsey M, Grislis H, Sonne M, Jawetz E. The effect of differing ambient oxygen tensions on wound infection. Ann Surg. 1975 Jan;181(1):35-9. [PMC free article: PMC1343711] [PubMed: 804296]
64.Uhl E, Sirsjö A, Haapaniemi T, Nilsson G, Nylander G. Hyperbaric oxygen improves wound healing in normal and ischemic skin tissue. Plast Reconstr Surg. 1994 Apr;93(4):835-41. [PubMed: 8134443]
65.Thom SR. Hyperbaric oxygen: its mechanisms and efficacy. Plast Reconstr Surg. 2011 Jan;127 Suppl 1(Suppl 1):131S-141S. [PMC free article: PMC3058327] [PubMed: 21200283]
66.Kranke P, Bennett M, Roeckl-Wiedmann I, Debus S. Hyperbaric oxygen therapy for chronic wounds. Cochrane Database Syst Rev. 2004;(2):CD004123. [PubMed: 15106239]
67.Lineen E, Namias N. Biologic dressing in burns. J Craniofac Surg. 2008 Jul;19(4):923-8. [PubMed: 18650713]
68.Rosenbaum AJ, Banerjee S, Rezak KM, Uhl RL. Advances in Wound Management. J Am Acad Orthop Surg. 2018 Dec 01;26(23):833-843. [PubMed: 30180089]
69.Da Costa RM, Ribeiro Jesus FM, Aniceto C, Mendes M. Randomized, double-blind, placebo-controlled, dose- ranging study of granulocyte-macrophage colony stimulating factor in patients with chronic venous leg ulcers. Wound Repair Regen. 1999 Jan-Feb;7(1):17-25. [PubMed: 10231502]
70.Hom DB, Manivel JC. Promoting healing with recombinant human platelet-derived growth factor--BB in a previously irradiated problem wound. Laryngoscope. 2003 Sep;113(9):1566-71. [PubMed: 12972935]
71.Shokri T, Kadakia S, Ducic Y. Complex Wound Management. Facial Plast Surg. 2019 Dec;35(6):672-677. [PubMed: 31783426]
72.Hahm G, Glaser JJ, Elster EA. Biomarkers to predict wound healing: the future of complex war wound management. Plast Reconstr Surg. 2011 Jan;127 Suppl 1:21S-26S. [PubMed: 21200268]
73.Sig AK, Guney M, Uskudar Guclu A, Ozmen E. Medicinal leech therapy-an overall perspective. Integr Med Res. 2017 Dec;6(4):337-343. [PMC free article: PMC5741396] [PubMed: 29296560]
74.Coleman S, Gorecki C, Nelson EA, Closs SJ, Defloor T, Halfens R, Farrin A, Brown J, Schoonhoven L, Nixon J. Patient risk factors for pressure ulcer development: systematic review. Int J Nurs Stud. 2013 Jul;50(7):974-1003. [PubMed: 23375662]
75.Edsberg LE, Black JM, Goldberg M, McNichol L, Moore L, Sieggreen M. Revised National Pressure Ulcer Advisory Panel Pressure Injury Staging System: Revised Pressure Injury Staging System. J Wound Ostomy Continence Nurs. 2016 Nov/Dec;43(6):585-597. [PMC free article: PMC5098472] [PubMed: 27749790]
76.Thompson D. An evaluation of the Waterlow pressure ulcer risk-assessment tool. 2005 Apr 28-May 11Br J Nurs. 14(8):455-9. [PubMed: 15924028]
77.McInnes E, Jammali-Blasi A, Bell-Syer SE, Dumville JC, Middleton V, Cullum N. Support surfaces for pressure ulcer prevention. Cochrane Database Syst Rev. 2015 Sep 03;2015(9):CD001735. [PMC free article: PMC7075275] [PubMed: 26333288]
78.Lyder CH. Pressure ulcer prevention and management. JAMA. 2003 Jan 08;289(2):223-6. [PubMed: 12517234]
79.Prompers L, Huijberts M, Apelqvist J, Jude E, Piaggesi A, Bakker K, Edmonds M, Holstein P, Jirkovska A, Mauricio D, Ragnarson Tennvall G, Reike H, Spraul M, Uccioli L, Urbancic V, Van Acker K, van Baal J, van Merode F, Schaper N. High prevalence of ischaemia, infection and serious comorbidity in patients with diabetic foot disease in Europe. Baseline results from the Eurodiale study. Diabetologia. 2007 Jan;50(1):18-25. [PubMed: 17093942]
80.Wraight PR, Lawrence SM, Campbell DA, Colman PG. Creation of a multidisciplinary, evidence based, clinical guideline for the assessment, investigation and management of acute diabetes related foot complications. Diabet Med. 2005 Feb;22(2):127-36. [PubMed: 15660728]
81.Yazdanpanah L, Nasiri M, Adarvishi S. Literature review on the management of diabetic foot ulcer. World J Diabetes. 2015 Feb 15;6(1):37-53. [PMC free article: PMC4317316] [PubMed: 25685277]
82.O'Meara S, Cullum NA, Nelson EA. Compression for venous leg ulcers. Cochrane Database Syst Rev. 2009 Jan 21;(1):CD000265. [PubMed: 19160178]
83.Bevis P, Earnshaw J. Venous ulcer review. Clin Cosmet Investig Dermatol. 2011;4:7-14. [PMC free article: PMC3108280] [PubMed: 21673869]
84.Bennett MH, Feldmeier J, Hampson NB, Smee R, Milross C. Hyperbaric oxygen therapy for late radiation tissue injury. Cochrane Database Syst Rev. 2016 Apr 28;4(4):CD005005. [PMC free article: PMC6457778] [PubMed: 27123955]
85.Eke N, Jebbin NJ. Abdominal wound dehiscence: A review. Int Surg. 2006 Sep-Oct;91(5):276-87. [PubMed: 17061674]
86.Ramirez OM, Ruas E, Dellon AL. "Components separation" method for closure of abdominal-wall defects: an anatomic and clinical study. Plast Reconstr Surg. 1990 Sep;86(3):519-26. [PubMed: 2143588]
87.O'Donoghue N, Mowatt D, Sykes AJ. Electrochemotherapy and Ablative Therapies in Non-melanoma Skin Cancer. Clin Oncol (R Coll Radiol). 2019 Nov;31(11):e1-e9. [PubMed: 31543301]
88.Vowden K. Complex wound or complex patient? Strategies for treatment. Br J Community Nurs. 2005 Jun;Suppl:S6, S8, S10 passim. [PubMed: 15944506]
Disclosure: Amir Labib declares no relevant financial relationships with ineligible companies.
Disclosure: Ryan Winters declares no relevant financial relationships with ineligible companies.