Wound Assessment (2024)

Continuing Education Activity

Damage or disruption of living tissue's cellular, anatomical, and/or functional continuum defines a wound. Before treatment, the exact cause, location, and type of wound must be assessed to provide appropriate care. Each clinician will have widely differing and distinct opinions on wound therapy depending on prior experiences. Given that non-healing wounds affect millions of people in the United States impacting a significant percentage of persons 65 years and older, minimizing wound complications is essential in the current healthcare environment. This activity addresses protocol for wound assessment for the interprofessional team during initial and subsequent wound assessments to best classify and treat a wound to enhance outcomes.

Objectives:

• Describe the initial assessment of a wound.

• Explain the potential complications in wound care.

• Identify the two types of wounds.

• Outline optimal wound management based on the assessed type of wound.

Access free multiple choice questions on this topic.

Introduction

Damage or disruption of living tissue's cellular, anatomical, and/or functional integrity defines a wound.[1]Acute and chronic wounds are technically categorized by the time interval from the index injury and, more importantly, by the evidence of physiological impairment.[2]Accordingly, specific treatments, including biofilms, would be planned to address the management of chronic wounds with an impaired physiological outcome.[1]Before treatment, the exact cause, location, and type of wound must be assessed to provide appropriate care. Each clinician will have widely differing and distinct opinions on wound therapydepending on prior experiences. An ostomy nurse will have a completely different approach to wound care than an orthopedic surgeon dealing with an open fracture during a trauma. Both will be far different from a dermatologist who treats burn victims. Nevertheless, each of these healthcare providers is performing wound care. Since non-healing wounds affect millions of people in the United States, impacting a significant percentage of persons 65 years and older, minimizing wound complications is essential in the current healthcare environment.[3]

As non-healing wounds constituted a multi-billion dollar industry of hospital admissions, antibiotics, and local wound care and were called a silent epidemic, this topic will be presented with an emphasis on clinical quality and optimization of patient safety.[4][5][6]Moreover, the 0.3 to 0.4 % rate for wound diagnosis has been reported in the general European population.[6][7]Almost all wounds are colonized with a spectrum of microbes. However, only some of them are considered infected wounds.[8]

Community nurses usually manage patients with chronic wounds. Chronic wounds are identified as wounds persisting for greater than six weeks.[9]Considering thecomplexity of the patients' health needs and the wound, on the other hand, this is a complicated, perplexing task for the nurse. Accordingly, wound assessment tools are designed to support all qualified nurses in the wound management field in delivering safe and appropriate wound care. The wound assessment tool, TIME, has been recently revised to TIMERS (Tissue, Infection/Inflammation, Moisture, Wound edge, Repair/Regeneration, Social).[10]

Function

At the very premiseof gaining a thorough understanding of wounds is acquiring solid foundational knowledge inskin anatomy, physiology, and the biologicalcascade of normal wound healing.

• Skin layers:[11]

• • Epidermis (superficial to deep): stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, stratum basalis

  • • Primary cell: keratinocyte [11]

  • Dermis: 2 layers - papillary (superficial) and reticular (deep) dermis

  • • It contains hair follicles, sebaceous glands, sweat glands, blood vessels, and nerve fibers.[11]

• Skin offers protection from UV light and serves as a mechanical, chemical, and thermal barrier. Moreover, the skin is involved in the Vitamin D synthesis process.[12]

The series of events associated with wound healing instantaneously begins at the moment of injury. Each of the potential underlying causes must be addressed and optimized for the wound to progresssuccessfully through a complex biological healing procession of hemostasis, inflammation, proliferation, and remodeling. All four highly integrated and overlapping physiological phases must occur in the proper sequence and time frame for wound healing success.

• Hemostasis begins shortly after wound infliction.

• • Platelets are the first cells to arrive at the injury site and are critical in clot formation to establish hemostasis[13]

  • Platelets release platelet-derived growth factor(PDGF) and transform growth factor-beta (TGF-B) to stimulate chemotaxis and proliferation of inflammatory cells[13][14][15]

  • (Hemostasisis sometimes included within the inflammatory phase, depending on the source)

• Inflammation is initiated at the moment of tissue disruption (Days 1to 6)

• • Polymorphonuclear cells (PMNs) first appear during this phase, with a primary role of clearing devitalized tissue, blood clot, foreign material, and bacteria from the wound [13][16]

  • Macrophages appear within 48 hours and complete the clean-up activities. Macrophages are the most critical cell in wound healing. Theysecrete cytokines and growth factors to induce activation and recruitment of additional macrophages while stimulating angiogenesis, the proliferation of fibroblasts, and extracellular matrix (ECM) production, thus prompting the proliferative phase.[15][16]

• The defining role of the fibroproliferation/proliferative phase is ECM production (Day 4 - Week 3)

• • While the inflammatory phase is most active, proliferation lays the foundation of a transitional ECM to stabilize the wound edges and provide a healing framework.

  • Fibroblasts replace macrophages to generate new tissue and stimulate collagen production for enhanced structural integrity.[16]

  • Tensile strength begins to increase on days 4to 5

  • Angiogenesis occurs simultaneously

• Maturation/remodeling is characterized by continued synthesis and degradation of the ECM components in efforts to establish a new equilibrium and organized scar formation (Week 3 - Years) [13]

• • As the scar matures, late remodeling occurs

  • Type I collagen replaces type III collagen [13]

  • Peak tensile strength at 60 days is approximately 80% of pre-injury strength.

  • The scar eventually contracts and thins out.[17][18][19][20]

Clinicians perform wound assessments to determine the appropriate treatment for extremely diverse disease processes.

How do professionals then approach wound assessment when the causes are so diverse? Below are some basic questions for the interprofessional team during initial and subsequent wound assessments to best classify and treat a wound tooptimize outcomes.

The initial assessment is crucial.[21] It should begin with the following:

• How: How was the wound created? If chronic, why is it still open? What is the underlying etiology?[22][23]

• Where: Where on the body is it located? Is it in an area that is difficult to offload or to keep clean? Is it in a region of high skin tension? Is it near any vital structures such as a major artery?

• When: How long has this wound been present? (e.g., acute or chronic)

• What: What anatomy does it involve (e.g., epidermis, dermis, subcutaneous tissue, fascia, muscle, tendon, bone, arteries, nerves)?

• What: What comorbidities or social factors does the patient have thatmight negatively impacttheir healing ability?[23]

• Is it life-threatening?

All of these factors significantly impactthe treatment plan moving forward. While there are many excellent biologics, skin grafts, and other options available, without the proper understanding of the nature of the wound, the chances of healing will decline significantly.[23][24]

Issues of Concern

While some wounds are simple, the majority of encountered wounds are caused by or become complicated by confounding patient-related issues.

Examples

• A chronic wound will have a different structure and percentage of components than an acute wound, requiring conversion for healing.[25]

• An underlying infection will impedewound healing even if the infection is subacute.[26]

• Damaged or constricted arterial supply will prevent appropriate blood flow to the wound.[27]

• Impairedvenous drainage maycause venous stasis.[25]

• Physical pressure on chronic ulceration will cause repeated damage, preventing healing.[28]

Universal Principles of Management

1. Thorough evaluation

2. Obtain source control

3. Eliminate confounding/contributing factors

4. Optimize the wound’s healing ability/environment

5. Close the wound[29]

Considering this rational algorithm, in total, is the core of successful wound healing. Similarly, there is no one-to-one correlation between a givenwoundand specific treatment. A spectrum of options must be considered for every wound encountered; selecting the best option for each patient remains challenging.

Clinical Significance

Before determining the underlying cause, it is essential to establishwhat type of wound the patient has. These subclassifications can be acute or chronic.

Types of Wounds

Acute

Clinicians assess acute wounds by the method of injury and resultant damage to soft tissues andbony structures. For example, in crush or high impact injuries, there is an area of demarcation which is not fully recognized until sometimes as much as a week or twolater. For this reason, it is important to determine the method of injury and to keep in mind that the wound seen is not necessarily the entirety of the wound which will be present in a week. In these cases, the patient and their family should be educated on this progression to prevent frustration and misunderstanding.

For all acute types of wounds, it is important to determine the length of time since injury (days or hours), the involvement of neurovascular supply, muscle, tendon, ligament, and bony structures, and the likelihood of contaminants in the wound. Also important is when the patient had their last tetanus vaccine/booster dose. Clinicians should start antibiotics if the wound is severely contaminated or if it has been longer than 3 hours since the injury. All underlying tissue should be repaired, and the wound should be irrigated to remove contaminants and bacteria.

In cases of traumatic/open fracture, the most used classification system is Gustillo-Anderson:

• Type 1: Clean wound, low energy puncture wound of less than 1 cm size, minimal contamination, minimal soft tissue damage, adequate soft tissue coverage of bone, without periosteal stripping, minimal fracture comminution[30]

• Type 2: Moderate soft tissue damage and crushing, moderate contamination, laceration of greater than 1cm in size, adequate soft tissue coverage of bone, without periosteal stripping, minimal fracture comminution[31]

• Type 3A: High-energy open injury, massively contaminated wound, extensive/significant soft tissue damage and crushing, adequate soft tissue coverage of bone, severely comminuted and/or segmental fracture, periosteal stripping is present[32]

• Type 3B: Significantlycontaminated wound, extensive soft tissue damage, unable to cover bone with soft tissue (requiring graft), severely comminuted and/or segmental fracture, periosteal stripping, and bone exposure[33]

• Type 3C: Similar to type A or B, however, associated with arterial injuries requiring repair[30]

Chronic

If a wound becomes arrested during normal stages of inflammation and healing, this classifies a chronic wound; deemed such at an untimely three months of non-progression. They often stall in the inflammatory phase.[34][35][36]Numerous factors and disease conditions impair the wound healing process, resulting in chronic, non-healing wounds. The most important concept is a persistent pro-inflammatory condition that propagates an unstable wound environment, recalcitrant to healing. Persistent hyper-inflammation is the ubiquitous pathophysiological characteristic of chronic wounds, and macrophage malfunction significantly contributes to the altered normal course.In the chronic setting, the main goal is to identify why the wound is not healing and alleviate these obstacles. Chronic wound causalities can be categorized as follows, and the related questions should be responded to accordingly.

• Arterial (Atherosclerosis, Raynaud Disease, Scleroderma)

  • Is there enough blood flow?

  • Generally, an ankle-brachial index (ABI) of less than 0.9 is diagnostic of peripheral arterial disease (PAD) and limits blood supply to the tissues while impairing antibiotic delivery to infected wounds[37]

• Venous

  • Pressure-induced changes in blood vessel wall permeability lead to leakage of fibrin and other plasma components into the perivascular space

    See Also

    Principles of Wound HealingPrinciples of Wound Management for ProfessionalsCurrent wound healing procedures and potential careWound healing assay

  • Accumulation of fibrin has direct and negative effectson wound healing as it down-regulates collagen synthesis

• Infection

  • Underlying infectious processes, including cellulitis and osteomyelitis, will inhibit wound healing

  • Culturing for aerobic, anaerobic, and fungal pathogens is recommended

• Pressure

  • Increased pressure to the area of concern will destroy new tissue growth and prevent proper perfusion of blood to the wound site[15]

  • These areas need to be offloaded to avoidundue pressure

• Radiation Therapy

  • Causes stasis/occlusion of small vessels and damages fibroblasts and nuclei

• Oncologic

  • Always biopsy areas of concern in non-healing wounds, as this can be an atypical presentation in various types of malignancies

• Systemic

  • Multiple systemic diseases inhibit wound healing, with diabetes being the most common culprit

    • It has been determined that uncontrolled blood glucose levels suppress the body's normal inflammatory response while inducing microvascular disease, which limits healing[15]

  • Obesity is also a significant risk factor that impairs wound healing, perhaps secondary to relative hypoperfusion and ischemia of subcutaneous adipose tissues[15]

  • Immunodeficiencies/immunosuppression and renal failure are also implicated

• Nutrition

  • Although serum albumin is not a good predictor of wound healing, there is some evidence that protein malnutrition, as well as insufficient levels of certain vitamins and minerals, will hinderthe body's ability to heal chronic wounds

  • High glucose levels interfere with nutrient absorption, causing depletion of several nutrients

  • Protein and energy requirements of chronic wound patients may rise by 250% and 50%, respectively[38]

• Age and Hormones

  • It is commonly recognized that, in healthy older adults, the effect of aging causes a temporal delay in wound healing but not an actual impairment in terms of healing quality

  • A review of age-related changes in healing capacity demonstrated that every phase of healing undergoes characteristic age-related changes. Compared with females, aged males have been shown to exhibitdelayed healing of acute wounds. Studies indicate that estrogen can improve the age-related impairment in healing in both men and women, while androgens negatively regulate cutaneous wound healing.[15]

• Pharmacological

• • Hydroxyurea has been reported in multiple instances to cause non-healing ulcerations

  • Chemotherapeutic drugs delay cell migration, decrease wound matrix formation, lower collagen production, impair fibroblast proliferation, and inhibit wound contraction; furthermore, they weaken immune functions, thereby impeding the natural inflammatory phase of healing, and increasing the risk of infection[15]

  • Steroids decrease inflammation, inhibit epithelialization, and decrease collagen production[15]

    • Vitamin A reverses delayed wound healing from steroids[39]

• Self-inflicted/Psychosocial

  • There are instances where a patient causesthe ulceration, either on purpose or as a result of non-compliance[40]

  • This is often the hardest factor to spot and overcome but must always be a consideration

  • In addition, psychological stress impairs cell-mediated immunity, compromisingnormal healing processes[15]

• Genetic

  • Predisposition to hypertrophic or keloid scarring, hereditary conditions, and variousskin types (pigmentation, elasticity, thickness, sebaceous quality, and location)

• Smoking

  • Cigarette smoke contains more than 4000 constituents

  • Nicotine constricts blood vessels and increases platelet adhesiveness, carbon monoxide binds to hemoglobin and reduces oxygen delivery, and hydrogen cyanide inhibits oxygen transport[15]

Necrotizing Soft Tissue Infections

Necrotizing soft tissue infections (NSTIs)can induce and instigate widespreadnecrosis subsequent totheir aggressive nature.Despite increased understanding of their disease processes, NSTI'srarity, complexity, and occasional ambiguity of symptomatology continue to pose diagnostic dilemmas.[41]A clear approach allows rapid identification, early administration of antimicrobial agents, and immediate surgical intervention, as they are limb- and life-threatening. Failure to recognize the underlying disease process and intervene expeditiously results in extremely high mortality.

• Categorizedbased on the layer(s) of soft tissue association, these infections include skin levelnecrotizing cellulitis, necrotizing fasciitis within the superficial or deep soft tissue, and myonecrosis/necrotizing myositisindicatingmuscle involvement. Establishing the diagnosis of these infections is often the main challenge. This differentiation is critical asnecrotizing infections warrant prompt, aggressive surgical debridement.

• It should be of no surprise after reading this review that susceptible patients at most significant risk for these types of infections include elderly adults, patients with obesity, immunosuppressed individuals, patients withrenal failure ordiabetes, those who sufferfrom peripheral vascular disease, or patientswith a combination of these factors.

• When the "hard signs" of bullae, crepitus, gas/emphysema on X-ray, hypotension with systolic blood pressure less than 90 mmHg, or skin necrosis are present, establishing the diagnosis of NSTI is not challenging. However, these indicatorsare often absent on presentation, thus potentially delaying diagnosis and surgical intervention. Most commonly, the diagnosis is clinical.

• Patients mayclinically present or progress todevelop sepsis or septic shock without obvious causation. The extremities, perineum, trunk, and torso are commonly implicated. A detailed examination should be undertaken forexpression ofturbid, grayish, semi-purulent material ("dishwater fluid") from anidentifiableentry site, in addition to assessing thepresence of skin changes, blebs, or crepitus. At the site of infection, patients oftendevelop pain out of proportion to observedphysical manifestations. Any of these findings mandateimmediate surgical intervention, which should consist of exposure and direct visualization of potentially infected tissue (including deep soft tissue, fascia, and underlying muscle) and radical resection of affected areas.

• The Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score is also helpful as a laboratory aid in distinguishing necrotizing from non-necrotizing skin and soft tissue infections (SSTIs). Wong et al. originally published a score of >/= 6, yielding a positive predictive value of 92% and a negative predictive value of 96%. Developed in 2004, LRINEC displayed promise for predicting the severity of skin and soft tissue infections.[42]

• NSTIs necessitate prompt surgical debridement for satisfactory treatment following the primary initiation of antimicrobial therapy. Because of the rapidly progressive and potentially fatal outcome of this condition, if imaging cannot be performed expeditiously, delaying treatment is not justified. Radiologic studies should be consideredonly in patients in whom the diagnosis is not seriously considered.[43]

  • Plain film findings may demonstrateextensive soft tissue gas

  • CT examination can reveal asymmetric thickening of deep fascia in association with gas, or the presence of abscesses

  • MR imaging effectively differentiates between necrotizing and non-necrotizing infections; although it can be overly sensitive as well as time-consuming, thus should not delay prompt surgical intervention in the management of NSTIs[43]

• Classified into two types, NSTIs areeither polymicrobial (type I) or monomicrobial (type II), dependent upon the offending organism(s).[41]Antimicrobial therapy is an essential componentof their management. As in all serious life-threatening infections, it is important to initiate early, empiric antimicrobial therapy. Prompt and appropriate treatment improves outcomes for SSTIs, and furthermore, it is well established that aggressive and timely antibiotic therapy reduces mortality.

  • Polymicrobial infections are more common, occursecondary to a combination of aerobic and anaerobic organisms, and primarily involvethe trunk and perineum.[43]

• Antimicrobial agents directed against gram-positive and gram-negative aerobes and anaerobes should be administered. Due to its inherent anti-toxin properties, Clindamycin is recommendedas anaddition to any empiric regimen.[34][43]Any chosen antibiotic regimencan be laterrefined based on culture and sensitivity, particularly in the case of monomicrobial (type II)infections.

• The aforementioned findings constitute a surgical emergency,the mainstay of which remains wide debridement of necrotic tissue until bleeding, viable tissue is reached. A grey serous fluid at the level of the necrotic tissue is usually noted, and as the infection spreads, thrombosed blood vessels can be visualized along the involved tissue planes.

  • Typically, patients require serial trips to the operating room for wide debridement until adequate infectious source control is obtained.

In summary, successful treatment requires early initiation ofbroad-spectrum systemic antibiotic therapy, aggressive surgical debridement of all necrotic tissue, and supportive care (fluid resuscitation, organ, and critical care support) to maintain oxygenation and tissue perfusion. Delay of definitive debridement isthe most critical risk factor for death. Early operative debridement is a significant determinant of success in NSTI treatment and an independent predictor of improved outcomes.[34][42][43]

Other Issues

A wound ensues following a breach in epithelial integrity and may be accompanied by disruption of structure and/or function of underlying normal tissue. To restore the structure of the injured tissue, a complex signaling network of biomolecular interactions must occur in a precisely programmed fashion. Along each individual wound’s course of healing, repeated thorough assessments are necessary. Once a wound has been fully evaluated, treatment should be designed to address any modifiable cause for the wound and then to achieve specific targeted goals of (a) preventingcomplications resulting from the wound, (b) preserving or restoring critical functions, (c) achieving wound closure, and (d) restoration of aesthetics.[44]

Enhancing Healthcare Team Outcomes

The current review provides a basic understanding of the common types of wounds and the underlying concerns. The takeaway is the need for appropriate assessment. Too often, wounds are not treated properly because of a lack of understanding of the underlying disease process. Most chronic wounds are complex and best managed by an interprofessional team coordinating care that includes a wound care nurse, general and/or vascular surgeon, podiatrist, plastic surgeon, hyperbaric specialist, infectious disease consultant, dietitian, and physical therapist. The key is first to find out the cause of wound breakdown. Without resolving the primary cause, wounds cannot heal.

There are hundreds of wound care dressings and solutions, and for the most part, all work similarly with the same efficacy. The second point is to ensure that the wound is clean, has ample blood supply, and is regularly debrided. Other factors that play a role in wound healing include patient nutritional status, comorbidities, state of the immune system, age, degree of ambulation, presence of a foreign body, and infection. It is important to have a team of wound experts regularly assess the wound and the patient to achievesuccessful healing.[45]

Nursing, Allied Health, and Interprofessional Team Interventions

Evaluation

Once the underlying issues and healing impediments are determined, a formal wound assessment is performed. The evaluation of patients with complex wounds is best approached systematically since wounds are rarely secondary to only one sole cause. Assessment of both local and systemic contributing factors within each portion of the work-up is critical. Generally, ongoing nursing and clinician assessments and monitoring of wounds are similar. Physical examination should be the primary criterion for the diagnosis of local wound infection:

• Identify the wound location.

• Determine the cause of the wound:

• • Evaluate for foreign bodies or neoplastic processes.[46]

  • Consider bacterial colonization versus acute/chronic infection.[47]

  • • Note that all open wounds will have bacterial colonization, yet this in itself does not constitute an infected wound.[48]

    • Diagnosis of infection is designated in the presence of erythema, pain, swelling, fluctuance, purulence, and loss of function.[13]

• Determine the stage of the wound:

• • Stage I: Superficial, involving only the epidermal layer

  • • Intact skin with non-blanchable erythema

      See Also

      Healing with Color: Green - National Solutions

  • Stage II: Partial thickness affects the epidermis and may extend into the dermis

  • Stage III: Full thickness, extends through the dermis and into the adipose tissues

  • Stage IV: Full thickness, extends through the dermis and adipose, exposing muscle, bone, fascia, or tendon[49]

  • Unstageable: Full-thickness skin and tissue loss obscured by slough or eschar; thus, the true extent of tissue damage cannot be confirmed[50]

  • • If slough or eschar are removed, a stage III or IV wound results

• Evaluate and measure the depth, length, and width of the wound[51]

• • Granulation tissue: beefy red bleeding tissue that indicates healing in progress

  • Fibrinous tissue: white-ish/yellow slough that does not bleed (not healthy)

  • Eschar: roof or rim of black/charred-appearing callous-like tissue (not healthy)

• Measure the amount of undermining and tunneling[52]

• Evaluate the wound bed for exposed bone, vessels, hardware, or subcutaneous fat[53]

• Survey for presence, type, and amount of exudate:

• • Serous, serosanguineous, sanguineous, or purulent[54]

  • Minimal, light, moderate, or heavy[54]

• Assess surrounding skin tissue for signs of injury (actinic changes), previous irradiation, arterial or venous insufficiency, lymphedema, loss of sensation, and dermal thinning (i.e., aging, steroid therapy)

• Check wound margins for tunneling, rolled edges, undermining, and fibrotic changes.

• Evaluate for warmth, pain, odor, purulence, delayed healing, or other signs of infection

• Observe pain

• For all wounds on extremities, a careful neurovascular examination ofthe entire limb is mandatory.

• Document findings and report unexpected resultsto the healthcare team

Diagnostics

• Surface swabs indicating the presence of pathogenic bacteria do not correlate with clinically significant infection. For local wound evaluation, wound swabs can be valuable for surveillance of the flora colonizing a wound but should not be used as a trigger to initiate therapy for wound infection.

• Wound biopsies can be invaluable for diagnosing invasive burn wounds; the presence of bacteria in the deep dermis on biopsy correlates with the risk of system sepsis in burn patients.

• • Bone biopsy demonstrating bacteria within the bone is the gold standard for diagnosing osteomyelitis.[36]

• Laboratory studies can be a useful adjunct in managing chronic wounds; however, they are often misused, and an evidence-based, rationalized approach is necessary to utilize this expensive resource efficiently. Routine blood work is not required. Serum prealbumin may be valuable in determining nutritional status. A significantly elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) can help confirm the diagnosis of osteomyelitis or be used in monitoring response to treatment.[55]

• Ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI) may be useful for delineating fluid collections, necrotic tissue, or inflammation in select circ*mstances.

• Assessment of peripheral perfusion via ankle/brachial index and toe brachial index (ABI/TBI) should be performed as it guides further management strategies. ABI does not provide reliable results in patients with non-compressible vessels, such as patients with diabetes or renal insufficiency, so TBI is also needed.[56]Utilize monofilament examinations to assess the presence of peripheral neuropathy and pressure sensation.

Prevention

The preventative measures that should be taken for patients with open wounds depend on the setting.

• Tetanus prophylaxis should be considered for acute lacerations

• Strict adherence to pressure-relief protocol, turning bed-bound patients every 2 hours, offloading pressure points, floating heels, optimization of wheelchair seating/bedding, social support and wound care, and assessment of nutritional status take priority in pressure sores

• Prophylactic antibiotics are necessitated in human/animal bites

• Any associated medical conditions must be aggressively optimized

• Preserving joint motion must be considered for patients with open wounds of the extremities:

• • Institute aggressive physiotherapy regimens to maintain or improve joint motion

  • Utilize splinting to minimize joint contractures

Interventions

After careful adherence to preventative measures and preservation of critical function, a strategy for wound closure can be formulated with respect to multidisciplinary decision-making.

• The basic tenet of non-surgical therapy is debridement of dirty wounds and closure of clean wounds, first focusing on eliminating necrotic debris while controlling any associated infectious burden.

• • The utilization of wound dressings comprises the mainstay of non-surgical therapy, with a fundamental principle of employing debriding dressings for dirty wounds and occlusive dressings for clean wounds.

  • • A commonly used debriding dressing is the “wet-to-dry” dressing, in which gauze is dampened, then positioned into the wound base. Evaporation dries the dressing, which becomes slightly adherent to the wound surface. Necrotic debris and biofilm are removed with the dressing on subsequent exchanges, leaving healthy tissue behind. Wet-to-dry dressings work through mechanical debridement. Conceptually, establishing a clearly outlined regimen for frequency of dressing changes is most important for optimized success; generally, twice daily is recommended, although some may require heightened frequency. Debriding dressings are indicated in infected wounds or those containing necrotic debris.

  • In clean woundslackingnecrotic debris with acceptable bacterial load(s), a dressing that maintains a moist environment should be utilized to encourage healing. This technique should not be employed for infected or dirty wounds.

  • Occasionally, circ*mstances necessitate antibiotic dressings. Mupirocin ointment has the added benefit of treating methicillin-resistant staph aureus (MRSA). Burn wounds are commonly dressed with silver sulfadiazine or mafenide acetate due to their high antimicrobial activity. The low toxicity and exceptional antimicrobial properties of elemental silver have led to the development and widespread use of silver-impregnated wound dressings.

  • Although multiple commercial variations in negative pressure wound therapy exist, all utilize a similar sponge-like material connected to a suction device. When applied appropriately and for the correct wound, negative pressure wound therapy can be efficacious and cost-effective. Negative pressure therapy, through extensive experimental and clinical trials, has confirmed the promotion of tissue perfusion, reduced edema, and, furthermore, favorably alters the wound-fluid composition and stimulates the formation of healthy granulation tissue. While negative pressure systems are easy to use and decrease the number of dressing changes, they are contraindicated in acutely infectious wounds.

• For problem wounds, surgical debridement remains the gold standard. Removal of necrotic tissue to permit thorough inspection of underlying tissue while eliminating dead spaces, allowing wide drainage of infectious fluid, reducing pressure, and creating a healthy surface for subsequent topical preparations are cornerstone intentions of surgical wound care.[34]A judicious yet thorough surgical debridement can convert a dirty, necrotic, contaminated wound into a clean one. In addition, a single operative debridement is often preferred over a protracted course of debriding dressings.

• Necrotic bone segments serve as a nidus for infection in osteomyelitis, termed “sequestra,” thus, IV nor PO antibiotics alone can clear the bacteria from a focus of dead bone, and formal resection is required. Targeted antimicrobial therapy, along with source control via debridement of necrotic bone, drainage/irrigation or abscessed tissue, and optimization of medical comorbidities, are the main pillars of osteomyelitis therapy.[57]

Putting it All Together

Taking the above information into consideration, walk through a formal wound evaluation.

For instance:

• What type of tissue is present in the wound?

  • Is it normal, healthy tissue? Is it granular, necrotic, fibrotic?

  • In red, granular tissue, the treatment is generally to keep it clean and moist, and offload pressure, to allow healing.

  • If necrotic tissue is present, this should be resected (i.e., debrided) immediately to remove a potential nidus ofinfection.

  • If faced with a dry wound and compromised vascular supply, the patient may need revascularization in the hands of their vascular surgeon or interventional cardiologist prior to debridement.

    • Debriding a wound lackingadequatevascular supply will cause an increased size of the non-healing wound without addressing the underlying cause of halted healing.

  • For fibrotic tissue, debridement must be performed to create a healing wound environment.

    • This can be performed sharply, with a scalpel or curette, or via a chemical/enzymatic debridement.

• Is the wound wet or dry?

  • A simple rule of thumb is that if it is wet, dry it; if it is dry, wet it.

    • The idea is to keep the wound at an optimal moisture level for healing.

  • Hydrogels are advantageousfor keeping a relatively dry wound moist.

  • Moisture-absorbing materials such as alginates are useful for drying out a weeping ulcer.

    • Some wounds, such as venous stasis ulcerations, weep such high volumes of fluid that they require daily dressing changes simply to keep the surrounding skin from becoming maceratedor excoriated from the secretions/fluid contents.

• Is the surrounding tissue healthy?

  • Friable skin (fragile and thin) is challenging to address, as any adhesive may tear the skin, increasing the size of the wound.

  • Macerated skin is found when the moisture from the wound is not well-controlled.

    • Excess moisture softens the skin until it begins to break down, therefore increasing the wound size.

• Finally, is the wound infected?

  • Cellulitic appearing skin iserythematous and edematous, with a focal increase in temperature.

  • There is often purulent discharge and, depending on the offending organism, may have a strong odor.

    • The presence of a strong odor, especially in venous stasis wounds, is not indicative of infection unless it is either noticeably worsened from normal or combined with other signs of infection, as heavy drainage will have a distinct odor by itself.

  • In the case of lower extremity erythema and edema, especially where it is seen bilaterally, this may simply be vasculitis and not an infection.

    • A useful test to employ in this scenario is to elevate the leg for 3to 5minutes; if the erythema resolves significantly during that period, it is likely vasculitis, not infectious.

  • If there is an open wound and/or other reasons to be suspicious of infection, err on the side of caution.

• If an infection is suspected, be sure to take deep cultures of the wound as just swabbing the rim will likely culture a wide variety of organisms (a.k.a. skin flora.)

  • Purulent discharge is a good source ofculture.

  • If the patient has comorbidities, is immunosuppressed, elderly or very young, an abscess cannot be completely drained, the infection does not respond to incision and drainage, or sepsis/bacteremia is suspected, the patient ought to be initiated onIV broad-spectrum antibiotic therapy, making sure to take blood cultures before antibiotics are administered.

  • For local treatment of infected wounds, debridement with copious irrigation iswarranted;if there is a concern for abscess, incision and drainage arenecessary to remove any nidus of infection.

  • Imaging in these cases is vital, as the depth and extent of infection will change the type of treatment.

    • On plain film X-ray, it is possible to see the destruction of bone, which is indicative of osteomyelitis (bone infection.)

      • Generally speaking, bone with visible destruction from an infection needs combination therapy via complete resection in conjunction with a prolonged IV antibiotic(s) course tailored to cultural sensitivities for complete clearance.

While there are many factors to consider when approaching a wound, understanding the nature and underlying factors potentiating the wound in question will lead to successful evaluation and treatment.

Nursing, Allied Health, and Interprofessional Team Monitoring

Wound checks are typically once per shift, but the clinician may vary this protocol based on concerns raised by the healthcare team. The care team must ensure that a patient with a wound does not develop complications from that wound or additional wounds from the same mechanism. This is particularly important in bedridden, obtunded, or paralyzed patients, in whom it should be possible to completely prevent pressure sores with proper care. Delays in wound healing can be perpetuated by clinicians who make poor treatment choices, fail to recognize complications, and/or do not seek timely advice. Improving patient outcomes requires a proactive methodto care that includes accurate and timely assessment and reassessment, treatment of the underlying cause using a multidisciplinary team approach, and implementationof evidence-based practice and clinical judgment to develop an appropriate therapeuticplan.

With such a broad array of possibilities, the entire interprofessional team, including all clinicians (MDs, DOs, NPs, and PAs), nurses, paramedics, and specialists, must all contribute from their specialty, document the patient's progress or lack thereof so all team members have the same patient data, and communicate any concerns to all appropriate team members so the team can implement therapeutic changes, if necessary. Utilizing this type of interprofessional paradigm will ensure that wound patients receive the best care leading to optimal outcomes. [Level 5]

Review Questions

• Access free multiple choice questions on this topic.

• Comment on this article.

References

1.

Afonso AC, Oliveira D, Saavedra MJ, Borges A, Simões M. Biofilms in Diabetic Foot Ulcers: Impact, Risk Factors and Control Strategies. Int J Mol Sci. 2021 Jul 31;22(15) [PMC free article: PMC8347492] [PubMed: 34361044]

2.

Tsegay F, Elsherif M, Butt H. Smart 3D Printed Hydrogel Skin Wound Bandages: A Review. Polymers (Basel). 2022 Mar 03;14(5) [PMC free article: PMC8912626] [PubMed: 35267835]

3.

Bonifant H, Holloway S. A review of the effects of ageing on skin integrity and wound healing. Br J Community Nurs. 2019 Mar 01;24(Sup3):S28-S33. [PubMed: 30817191]

4.

Veith AP, Henderson K, Spencer A, Sligar AD, Baker AB. Therapeutic strategies for enhancing angiogenesis in wound healing. Adv Drug Deliv Rev. 2019 Jun;146:97-125. [PMC free article: PMC6435442] [PubMed: 30267742]

5.

Leavitt T, Hu MS, Marshall CD, Barnes LA, Lorenz HP, Longaker MT. Scarless wound healing: finding the right cells and signals. Cell Tissue Res. 2016 Sep;365(3):483-93. [PMC free article: PMC5010960] [PubMed: 27256396]

6.

Lindholm C, Searle R. Wound management for the 21st century: combining effectiveness and efficiency. Int Wound J. 2016 Jul;13 Suppl 2(Suppl 2):5-15. [PMC free article: PMC7949725] [PubMed: 27460943]

7.

Jørgensen SF, Nygaard R, Posnett J. Meeting the challenges of wound care in Danish home care. J Wound Care. 2013 Oct;22(10):540-2, 544-5. [PubMed: 24142076]

8.

Valentine KP, Viacheslav KM. Bacterial flora of combat wounds from eastern Ukraine and time-specified changes of bacterial recovery during treatment in Ukrainian military hospital. BMC Res Notes. 2017 Apr 07;10(1):152. [PMC free article: PMC5384141] [PubMed: 28388920]

9.

Jirawitchalert S, Mitaim S, Chen CY, Patikarnmonthon N. Cotton Cellulose-Derived Hydrogel and Electrospun Fiber as Alternative Material for Wound Dressing Application. Int J Biomater. 2022;2022:2502658. [PMC free article: PMC8920707] [PubMed: 35295790]

10.

Lumbers M. TIMERS: undertaking wound assessment in the community. Br J Community Nurs. 2019 Dec 01;24(Sup12):S22-S25. [PubMed: 31804886]

11.

Yousef H, Alhajj M, Sharma S. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Nov 14, 2022. Anatomy, Skin (Integument), Epidermis. [PubMed: 29262154]

12.

Kechichian E, Ezzedine K. Vitamin D and the Skin: An Update for Dermatologists. Am J Clin Dermatol. 2018 Apr;19(2):223-235. [PubMed: 28994020]

13.

Wilkinson HN, Hardman MJ. Wound healing: cellular mechanisms and pathological outcomes. Open Biol. 2020 Sep;10(9):200223. [PMC free article: PMC7536089] [PubMed: 32993416]

14.

Rodrigues M, Kosaric N, Bonham CA, Gurtner GC. Wound Healing: A Cellular Perspective. Physiol Rev. 2019 Jan 01;99(1):665-706. [PMC free article: PMC6442927] [PubMed: 30475656]

15.

Guo S, Dipietro LA. Factors affecting wound healing. J Dent Res. 2010 Mar;89(3):219-29. [PMC free article: PMC2903966] [PubMed: 20139336]

16.

Raziyeva K, Kim Y, Zharkinbekov Z, Kassymbek K, Jimi S, Saparov A. Immunology of Acute and Chronic Wound Healing. Biomolecules. 2021 May 08;11(5) [PMC free article: PMC8150999] [PubMed: 34066746]

17.

O'Connell RL, Rusby JE. Anatomy relevant to conservative mastectomy. Gland Surg. 2015 Dec;4(6):476-83. [PMC free article: PMC4646999] [PubMed: 26645002]

18.

Andersson T, Ertürk Bergdahl G, Saleh K, Magnúsdóttir H, Stødkilde K, Andersen CBF, Lundqvist K, Jensen A, Brüggemann H, Lood R. Common skin bacteria protect their host from oxidative stress through secreted antioxidant RoxP. Sci Rep. 2019 Mar 05;9(1):3596. [PMC free article: PMC6401081] [PubMed: 30837648]

19.

Losquadro WD. Anatomy of the Skin and the Pathogenesis of Nonmelanoma Skin Cancer. Facial Plast Surg Clin North Am. 2017 Aug;25(3):283-289. [PubMed: 28676156]

20.

Slominski AT, Manna PR, Tuckey RC. On the role of skin in the regulation of local and systemic steroidogenic activities. Steroids. 2015 Nov;103:72-88. [PMC free article: PMC4631694] [PubMed: 25988614]

21.

Rothe K, Tsokos M, Handrick W. Animal and Human Bite Wounds. Dtsch Arztebl Int. 2015 Jun 19;112(25):433-42; quiz 443. [PMC free article: PMC4558873] [PubMed: 26179017]

22.

Li S, Mohamedi AH, Senkowsky J, Nair A, Tang L. Imaging in Chronic Wound Diagnostics. Adv Wound Care (New Rochelle). 2020 May 01;9(5):245-263. [PMC free article: PMC7099416] [PubMed: 32226649]

23.

Sen CK. Human Wound and Its Burden: Updated 2020 Compendium of Estimates. Adv Wound Care (New Rochelle). 2021 May;10(5):281-292. [PMC free article: PMC8024242] [PubMed: 33733885]

24.

Liu X, Zhang H, Cen S, Huang F. Negative pressure wound therapy versus conventional wound dressings in treatment of open fractures: A systematic review and meta-analysis. Int J Surg. 2018 May;53:72-79. [PubMed: 29555530]

25.

Bowers S, Franco E. Chronic Wounds: Evaluation and Management. Am Fam Physician. 2020 Feb 01;101(3):159-166. [PubMed: 32003952]

26.

Yao K, Bae L, Yew WP. Post-operative wound management. Aust Fam Physician. 2013 Dec;42(12):867-70. [PubMed: 24324988]

27.

Johnston BR, Ha AY, Kwan D. Surgical Management of Chronic Wounds. R I Med J (2013). 2016 Feb 01;99(2):30-3. [PubMed: 26827083]

28.

Ricci JA, Bayer LR, Orgill DP. Evidence-Based Medicine: The Evaluation and Treatment of Pressure Injuries. Plast Reconstr Surg. 2017 Jan;139(1):275e-286e. [PubMed: 28027261]

29.

Quain AM, Khardori NM. Nutrition in Wound Care Management: A Comprehensive Overview. Wounds. 2015 Dec;27(12):327-35. [PubMed: 27447105]

30.

Sharma A, Gupta V, Shashikant K. Optimizing Management of Open Fractures in Children. Indian J Orthop. 2018 Sep-Oct;52(5):470-480. [PMC free article: PMC6142800] [PubMed: 30237604]

31.

Decruz J, Antony Rex RP, Khan SA. Epidemiology of inpatient tibia fractures in Singapore - A single centre experience. Chin J Traumatol. 2019 Apr;22(2):99-102. [PMC free article: PMC6488744] [PubMed: 30962125]

32.

Silluzio N, De Santis V, Marzetti E, Piccioli A, Rosa MA, Maccauro G. Clinical and radiographic outcomes in patients operated for complex open tibial pilon fractures. Injury. 2019 Jul;50 Suppl 2:S24-S28. [PubMed: 31171351]

33.

Zierenberg García C, Beaton Comulada D, Pérez López JC, Lamela Domenech A, Rivera Ortiz G, González Montalvo HM, Reyes-Martínez PJ. Acute Shortening and re-lengthening in the management of open tibia fractures with severe bone of 14 CMS or more and extensive soft tissue loss. Bol Asoc Med P R. 2016;108(1):91-94. [PubMed: 29193926]

34.

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]

35.

Martin P, Nunan R. Cellular and molecular mechanisms of repair in acute and chronic wound healing. Br J Dermatol. 2015 Aug;173(2):370-8. [PMC free article: PMC4671308] [PubMed: 26175283]

36.

Giurato L, Meloni M, Izzo V, Uccioli L. Osteomyelitis in diabetic foot: A comprehensive overview. World J Diabetes. 2017 Apr 15;8(4):135-142. [PMC free article: PMC5394733] [PubMed: 28465790]

37.

Ugwu E, Anyanwu A, Olamoyegun M. Ankle brachial index as a surrogate to vascular imaging in evaluation of peripheral artery disease in patients with type 2 diabetes. BMC Cardiovasc Disord. 2021 Jan 06;21(1):10. [PMC free article: PMC7788706] [PubMed: 33407158]

38.

Barchitta M, Maugeri A, Favara G, Magnano San Lio R, Evola G, Agodi A, Basile G. Nutrition and Wound Healing: An Overview Focusing on the Beneficial Effects of Curcumin. Int J Mol Sci. 2019 Mar 05;20(5) [PMC free article: PMC6429075] [PubMed: 30841550]

39.

Zinder R, Cooley R, Vlad LG, Molnar JA. Vitamin A and Wound Healing. Nutr Clin Pract. 2019 Dec;34(6):839-849. [PubMed: 31697447]

40.

Leow JJ, Lingam P, Lim VW, Go KT, Chiu MT, Teo LT. A review of stab wound injuries at a tertiary trauma centre in Singapore: are self-inflicted ones less severe? Singapore Med J. 2016 Jan;57(1):13-7. [PMC free article: PMC4728696] [PubMed: 26831311]

41.

Nawijn F, Hietbrink F, Peitzman AB, Leenen LPH. Necrotizing Soft Tissue Infections, the Challenge Remains. Front Surg. 2021;8:721214. [PMC free article: PMC8458892] [PubMed: 34568417]

42.

Wong CH, Khin LW, Heng KS, Tan KC, Low CO. The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue infections. Crit Care Med. 2004 Jul;32(7):1535-41. [PubMed: 15241098]

43.

Bonne SL, Kadri SS. Evaluation and Management of Necrotizing Soft Tissue Infections. Infect Dis Clin North Am. 2017 Sep;31(3):497-511. [PMC free article: PMC5656282] [PubMed: 28779832]

44.

Rousselle P, Montmasson M, Garnier C. Extracellular matrix contribution to skin wound re-epithelialization. Matrix Biol. 2019 Jan;75-76:12-26. [PubMed: 29330022]

45.

Young S. Wound assessment. Br J Community Nurs. 2019 Sep 01;24(Sup9):S5. [PubMed: 31479330]

46.

Rupert J, Honeycutt JD, Odom MR. Foreign Bodies in the Skin: Evaluation and Management. Am Fam Physician. 2020 Jun 15;101(12):740-747. [PubMed: 32538598]

47.

Rahim K, Saleha S, Zhu X, Huo L, Basit A, Franco OL. Bacterial Contribution in Chronicity of Wounds. Microb Ecol. 2017 Apr;73(3):710-721. [PubMed: 27742997]

48.

Leaper D, Assadian O, Edmiston CE. Approach to chronic wound infections. Br J Dermatol. 2015 Aug;173(2):351-8. [PubMed: 25772951]

49.

Kim J, Simon R. Calculated Decisions: Wound Closure Classification. Pediatr Emerg Med Pract. 2018 Sep 01;14(Suppl 10):1-3. [PubMed: 30183415]

50.

Westby MJ, Dumville JC, Soares MO, Stubbs N, Norman G. Dressings and topical agents for treating pressure ulcers. Cochrane Database Syst Rev. 2017 Jun 22;6(6):CD011947. [PMC free article: PMC6481609] [PubMed: 28639707]

51.

Alsaad SM, Ross EV, Smith WJ, DeRienzo DP. Analysis of Depth of Ablation,Thermal Damage, Wound Healing, and Wound Contraction With Erbium YAG Laser in a Yorkshire Pig Model. J Drugs Dermatol. 2015 Nov;14(11):1245-52. [PubMed: 26580873]

52.

Joo J, Pourang A, Tchanque-Fossuo CN, Armstrong AW, Tartar DM, King TH, Sivamani RK, Eisen DB. Undermining during cutaneous wound closure for wounds less than 3cm in diameter: a randomized split wound comparative effectiveness trial. Arch Dermatol Res. 2022 Sep;314(7):697-703. [PMC free article: PMC9307554] [PubMed: 34546436]

53.

Eggleston RB. Wound Management: Wounds with Special Challenges. Vet Clin North Am Equine Pract. 2018 Dec;34(3):511-538. [PubMed: 30447768]

54.

Bradley P. Wound Exudate. Br J Community Nurs. 2018 Dec 01;23(Sup12):S28-S32. [PubMed: 30521362]

55.

van Asten SA, Jupiter DC, Mithani M, La Fontaine J, Davis KE, Lavery LA. Erythrocyte sedimentation rate and C-reactive protein to monitor treatment outcomes in diabetic foot osteomyelitis. Int Wound J. 2017 Feb;14(1):142-148. [PMC free article: PMC7950144] [PubMed: 26953894]

56.

AbuRahma AF, Adams E, AbuRahma J, Mata LA, Dean LS, Caron C, Sloan J. Critical analysis and limitations of resting ankle-brachial index in the diagnosis of symptomatic peripheral arterial disease patients and the role of diabetes mellitus and chronic kidney disease. J Vasc Surg. 2020 Mar;71(3):937-945. [PMC free article: PMC7203622] [PubMed: 31471230]

57.

Urish KL, Cassat JE. Staphylococcus aureus Osteomyelitis: Bone, Bugs, and Surgery. Infect Immun. 2020 Jun 22;88(7) [PMC free article: PMC7309607] [PubMed: 32094258]

Disclosure: Sean Nagle declares no relevant financial relationships with ineligible companies.

Disclosure: Kaitlyn Stevens declares no relevant financial relationships with ineligible companies.

Disclosure: Steven Wilbraham declares no relevant financial relationships with ineligible companies.