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Clinical assessment of chronic wounds

Clinical assessment of chronic wounds
Literature review current through: Jan 2024.
This topic last updated: Oct 05, 2023.

INTRODUCTION — A wound represents a disruption of the normal structure and function of the skin and soft tissue structure and may be due to a variety of mechanisms and etiologies [1,2]. The clinical assessment of a wound begins with a general determination of whether the wound is acute or chronic in nature. Acute wounds, such as from trauma or surgery, are those in which healing is anticipated to progress through an orderly physiologic sequence of inflammation, proliferation, and maturation (in the absence of risk factors for nonhealing) [3,4]. A chronic wound may be defined as one that is physiologically impaired because of inadequate angiogenesis, impaired innervation, or impaired cellular migration, among other reasons [5,6]. Examples of chronic wounds include ischemic ulcers, venous ulcers, diabetic foot ulcers, and infected wounds, including surgical site infections [7]. Even healed chronic wounds, particularly diabetic foot ulcers, should be considered "wounds in remission," because they are at very high risk for recurrence [8,9].

The clinical assessment of chronic wounds, including differentiating the most common chronic ulcers, will be reviewed. Treatment of chronic wounds is discussed separately. (See "Basic principles of wound management" and "Overview of treatment of chronic wounds".)

Complications that lead to open wounds following abdominal surgery or trauma are discussed separately. (See "Risk factors for impaired wound healing and wound complications" and "Complications of abdominal surgical incisions" and "Surgical management of sternal wound complications".)

CLINICAL ASSESSMENT — Any patient with a wound or ulceration should undergo a complete history and physical examination, including review of systems. The history should include at least the elements below and seek to identify risk factors associated with nonhealing.

Current wound history – Ask the patient about the onset and perceived causal factors for the current wound. Have there been any qualitative changes (size, drainage) to the wound over time? What is the current wound care regimen? Have any other treatments been attempted? Is the wound painful? How severe is the pain? It is important to realize that patients with neuropathy might still have pain, and this might indicate involvement of deeper tissue structures.

Prior wound history – Ask the patient about the presence of prior wounds or ulcers. What were their locations and what, if any, previous measures were used to effect wound healing?

Medical history – Determine if the patient has any medical conditions that are risk factors for nonhealing, such as diabetes, peripheral artery disease, chronic kidney disease, peripheral neuropathy, impaired nutritional status, chronic steroid use, obesity, or older age.

Social history – Does the patient have a history of smoking? Is there a supportive social environment for wound management? Can the patient adequately navigate his/her environment with or without assistive devices or help from other people? Is the patient employed? How will wound care affect their daily life?

Surgical history – Has the patient had any prior surgery? Where were the surgical wounds located? Were there any issues with healing? Has the patient undergone surgery to manage a nonhealing wound? More specifically, has there been a need for skin grafting, arterial revascularization, or vein ablation procedures?

Wound assessment — The location and number of wounds should be diagrammed, and the characteristics of each wound detailed. Photography may be helpful for documentation and can be an important part of ongoing wound assessment. The use of objective wound photography decreases interobserver variability and allows for consistent and accurate assessment of changes in wound area over time [10].

Wound location, length, width, depth, and the presence and position of undermining, dried necrotic wound surface (ie, eschar), presence of cellulitis, and drainage (amount, type, color, odor) should also be documented. A subjective assessment of the greatest depth of tissue penetration should also be performed. Has the wound penetrated the dermis or a deep fascial layer? Does the wound probe to the level of bone? Probing to bone is best performed with a metal-tipped probe, since a wooden probe (eg, cotton-tip applicator) often cannot adequately differentiate between bone and other periosseous structures.

Calculation of wound area or volume should be performed and documented at each patient visit. After sharp debridement, measure and record the longest wound length, width, and depth. The rate of wound healing, as assessed by the percent change in wound area over time, may be predictive of wound healing potential [11-14].

Wound cultures — Wound cultures should only be obtained in the presence of local signs of infection to help guide antibiotic therapy. Wound infection is a clinical diagnosis, and wound cultures should not be used as a substitute for clinical judgment. If a culture is indicated, the sample should be obtained after a wound has been thoroughly cleansed and debrided; collection of deep tissue for culture is recommended over superficially swabbing the wound base or collecting drainage [15-17].

Signs of infection — Virtually all wounds are colonized with bacteria; thus, a diagnosis of invasive infection is a clinical diagnosis and not a microbiological one. Periwound induration, cellulitis extending >2 cm beyond the margin of the wound, increased local warmth, pain on palpation, and drainage from the site are all signs of infection and may indicate an underlying abscess that would benefit from decompression, drainage, and/or debridement [18]. (See "Necrotizing soft tissue infections" and "Complications of abdominal surgical incisions", section on 'Surgical site infection' and "Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis" and "Overview of the evaluation and management of surgical site infection".)

Symptoms and clinical signs that could suggest the presence of serious infection and warrant hospitalization, intravenous antibiotics, and debridement treatment include [19]:

Increasing erythema/cellulitis of the surrounding skin >2 cm

Lymphangitis

Increase in the size of the ulcer

Large amount of drainage

Fever

Wound odor

Larval infestation — Larval (maggot) infestation (myiasis) is a condition in which fly larvae feed off and develop in the tissues of living organisms [20-24]. Infestation associated with wounds is referred to as facultative or traumatic (wound) myiasis, in which flies opportunistically take advantage of necrotic conditions or infection to incubate their larvae [20,24]. Species that can cause wound myiasis include those from the Calliphoridae (eg, blowflies, screwworm flies), Sarcophagidae (eg, fleshflies), and Phoridae (eg, humpback fly) families [24]. Most species are not pathogenic, and some are used in larval therapy as a means to provide biologic debridement (see "Basic principles of wound management", section on 'Biologic'). It is also important not to confuse the blowfly, a common cause of wound myiasis, with botfly, a cause of furuncular myiasis. (See "Skin lesions in the returning traveler", section on 'Myiasis'.)

In a review of 42 cases from 20 United States centers, myiasis occurred within preexisting wounds. Factors associated with myiasis included male sex, older age, housing insecurity, alcohol use disorder, and peripheral vascular disease [22]. Five percent of infestations were nosocomially acquired and not necessarily associated with patient neglect. The most common species was the green blowfly (ie, Lucilia [Phaenicia] sericata).

In some cases, the patient is not aware of the infestation due to the location of the wound but may complain of itching or may sense movement in the wound. If the larvae invade rather than staying on superficial layers of exposed tissue, subcutaneous nodules can result [24]. In the review above, there were no cases of invasion [22]. Wound myiasis is self-limiting and generally not harmful, but the presence of the larvae can be alarming to the patient, which is sufficient reason to remove them. Depending on the circumstances under which myiasis develops, lawsuits can result.

Removal involves irrigation to dislodge larvae that are not well attached. Simple removal of attached larvae is hampered by larval spines and hooks. Surgical debridement of surrounding tissue and the larvae together can usually be accomplished with local anesthesia. Care must be taken to avoid larval fragmentation, which can produce subsequent inflammation, bacterial infection, or granuloma formation [24]. Alternatively, suffocation methods can be used, resulting in death of the larvae, which will then slough from the wound. Suffocation methods include use of occlusive dressings, petroleum jelly, and/or wound submersion, often in a diluted povidone-iodine solution [25].

Vascular assessment — A thorough vascular examination is essential when a patient presents with a chronic wound of the extremity [9,26]. Signs of arterial obstruction include lack of peripheral pulses with poor capillary refill, thin atrophic skin, lack of hair on the feet and lower leg, and hypertrophic deformed nails.

Noninvasive vascular testing should be performed in patients who present with a wound and have an abnormal pulse examination and in patients with a nonhealing extremity wound or ulcer. Noninvasive diagnostic options for arterial assessment include the ankle-brachial index, duplex ultrasound, segmental blood pressures, and plethysmography. (See "Noninvasive diagnosis of upper and lower extremity arterial disease".)

Laboratory studies — Routine laboratory studies are performed to evaluate for active infection, anemia, nutrition status, and medical conditions that place the patient at risk for nonhealing wounds.

Hematology – Complete blood count and differential

Chemistries – Metabolic panel, liver function tests, albumin, prealbumin, hemoglobin A1c

Microbiology – The result of previous cultures/pathology should be obtained (wound, urine, blood, Clostridioides [formerly Clostridium difficile])

Nutrition screening — Although there is not definitive evidence that supplemental nutrition will help healing of wounds, adequate nutrition is likely still important to assist in wound healing and minimize the potential for wound complications. We prefer to screen for malnourishment with prealbumin and albumin and maximize nutritional supplementation for patients with chronic wounds that do not respond as expected to appropriate intervention. Prealbumin and albumin are not perfect markers of nutritional status but should be evaluated for any patient with a nonhealing wound. (See "Overview of perioperative nutrition support".)

DIFFERENTIATION OF CHRONIC ULCERS — It is important to differentiate the various types of chronic ulcers since their pathophysiology and, thus, management pathways differ. Characteristic clinical location and appearance often allow for clear distinction between venous, ischemic, pressure-related, and diabetic foot ulcers. In addition, although there are many potential etiologies of chronic wounds with varying characteristics, wound biopsy should be considered in any wound that has been present for greater than approximately three months to rule out malignancy such as squamous cell carcinoma. (See "Cutaneous squamous cell carcinoma (cSCC): Clinical features and diagnosis".)

Venous ulcers — Multiple factors can lead to the development of chronic venous insufficiency and venous ulcers, including deep vein thrombosis and venous valvular incompetence. (See "Pathophysiology of chronic venous disease" and "Clinical manifestations of lower extremity chronic venous disease" and "Overview of lower extremity chronic venous disease".)

Characteristics of venous stasis ulcers include:

Location between the knee and the ankle. The medial and lateral malleoli are the most common sites, but other sites can be involved (picture 1).

Surrounding dermatitis with venous stasis ulcers. The periwound skin is often eczematous, presenting with erythema, scaling, weeping, induration, and crusting. These contribute to intense pruritus in the region.

Pain is not usually severe. If pain is severe, it suggests invasive infection or an alternative etiology.

Hyperpigmentation, lipodermatosclerosis, and stasis dermatitis of the surrounding skin.

Variable wound bed appearance. The wound is frequently beefy red with granulation tissue. In some cases, a superficial fibrinous gelatinous necrosis may occur suddenly with healthy-appearing granulation tissue beneath [27]. Calcification in the wound base is common.

Pressure-induced skin injury — Pressure-induced skin injury includes areas of skin ulceration and/or skin and soft tissue necrosis where structures are compressed between osseous prominences and/or hard external surfaces (picture 2). They result from vertical pressure alone or vertical pressure in combination with shear. Risk factors include advanced age, impaired circulation, immobilization, ambulatory dysfunction, and incontinence. (See "Epidemiology, pathogenesis, and risk assessment of pressure-induced skin and soft tissue injury".)

Pressure-induced skin and soft tissue injury severity is frequently staged using the National Pressure Injury Advisory Panel (NPIAP) classification (table 1), which ranges from nonblanchable skin erythema to full-thickness skin/muscle necrosis with exposed structures such as muscle and bone. (See "Clinical staging and general management of pressure-induced skin and soft tissue injury", section on 'Staging'.)

Characteristics of pressure-induced injury include:

Location over osseous prominences, including the medial and lateral metatarsal heads, calcaneus, ankle malleoli, ischial tuberosities, fibular head, and sacrum. Pressure-induced injury can also develop on the anterior ankle in the setting of dressing materials applied too tightly around the ankle.

Fibrotic tissue including necrotic eschar.

Deep probing to the level of bone and undermining of skin edges.

Surrounding periwound erythema.

Diabetic foot ulcers — Chronic ulceration in patients with diabetes is multifactorial, due to a combination of diabetic neuropathy, autonomic dysfunction, and vascular insufficiency [9]. Nonischemic diabetic foot ulcers are due to a combination of foot deformities and neuropathy preventing the sensation of pain in areas of the foot that are traumatized. (See "Evaluation of the diabetic foot".)

Characteristics of nonischemic diabetic foot ulcers include:

Location at areas of repeated trauma, such as the plantar metatarsal heads (picture 3), distal toes, or dorsal interphalangeal joints.

Overgrowth of hyperkeratotic tissue (corns or calluses) on other regions of the foot. Hyperkeratotic callus formation may imply adequate vascularity.

Undermined borders.

Lack of protective sensation (distal symmetrical sensorimotor peripheral neuropathy).

Diabetic ulcers should be routinely assessed for their severity in three areas: the wound itself, the presence of ischemia, and associated foot infection. This assessment (Wound, Ischemia, Foot Infection) takes on the acronym "WIfI." Each part of the assessment can be graded as none (0), mild (1), moderate (2), or severe (3). This then provides a simple, validated method of communication between clinicians [28,29]. (See "Classification of acute and chronic lower extremity ischemia", section on 'WIfI (Wound, Ischemia, foot Infection)'.)

Once diabetic foot ulcers are healed, recurrence is not only common but likely. Up to 40 percent will recur at one year, nearly 66 percent at three years, 75 percent at five years, and 80 to 100 percent at a decade. Therefore, the term "diabetic foot remission" is used during this period, with the express goal of increasing ulcer-free and activity-rich days. This can be done with a host of technologies and treatments, including shoes, insoles, bracing, surgery, physical therapy, and home temperature monitoring [8]. (See "Management of diabetic foot ulcers", section on 'Follow-up care and ulcer prevention'.)

Ischemic ulcer/wound — Ischemic ulcers are the result of inadequate perfusion due to arterial obstruction. Obstruction may be caused by atherosclerosis (ie, peripheral artery disease, patients with diabetes) affecting the large or medium arteries or from a variety of other disorders that affect the small vessels (eg, thromboangiitis obliterans, vasculitis, scleroderma).

The patient often complains of pain in the extremity at rest and increased pain with elevation of the extremity and activity. Patients will typically experience some relief of symptoms with the extremity in a dependent position, and characteristic dependent rubor may be seen. (See "Clinical features and diagnosis of lower extremity peripheral artery disease".)

Characteristics of ischemic ulcers include:

Location over prominent osseous areas and other areas where there is a potential for pressure and skin shearing (picture 4), including between the toes, on the tips of toes, over phalangeal heads, at the lateral malleolus, or at sites subjected to repetitive trauma, such as contact points with footwear.

Even, sharply demarcated and punched-out wound margins.

Appearance that may be superficial or deep.

A wound bed that may be pale, gray, or yellow with little evidence of new tissue growth or granulation tissue. Tissue necrosis or cellulitis may be present and is commonly accompanied by dry necrotic eschar. Exposed tendons or bone may be present.

Associated minimal exudate.

Surrounding blanched or purpuric periwound skin that is often shiny and tight. A loss of hair at ankle or foot may be seen.

Associated with pain that may be localized to the ulcer or more generalized to the foot. Pain may be relieved by dependent leg position and aggravated by elevation.

Ulcers associated with malignancy — Tumors can present with features similar to chronic wounds and may not be easily distinguished from a venous ulcer. In one report, 43 of 981 patients (2448 ulcers) had squamous cell or basal cell carcinoma within the ulcer, with a frequency of 2.2 malignancies per 100 leg ulcers [30]. Rare malignancies, such as soft tissue sarcomas, have also been documented in leg ulcers [31-33]. (See "Cutaneous squamous cell carcinoma (cSCC): Clinical features and diagnosis" and "Basal cell carcinoma: Epidemiology, pathogenesis, clinical features, and diagnosis".)

For this reason, skin and/or wound biopsies should be considered in any nonischemic wound that does not demonstrate signs of healing after approximately three months of treatment [34].

Hypertensive ulcers — Hypertensive ulcers (ie, Martorell hypertensive ulcer) are uncommon and thus can be easily confused with other types of chronic ulcers. The typical hypertensive ulcer is located in the supramalleolar region of the anterolateral leg or Achilles tendon, and bilateral ulcers are common [35]. These are associated with arterial hypertension in patients with palpable pulses. Diabetes is present in approximately 60 percent of patients with these wounds [36,37].

These ulcers are due to medial calcification that obliterates the small arterioles similar to calcific uremic arteriolopathy [37]. The reduction in tissue perfusion leads to local ischemia and ulcer formation. The ulcer begins as a red patch that becomes cyanotic, forming a painful ulcer with an ischemic wound bed.

Management consists of controlling hypertension and local wound care, although adequate control of hypertension alone does not appear to reverse these lesions. A randomized trial did not show any benefit for treatment with becaplermin gel over routine care with hydrogel for these ulcers [38]. The outcomes of treatment of this nonuremic form of calciphylaxis using cinacalcet, sodium thiosulfate, or sevelamer are unknown. (See "Basic principles of wound management", section on 'Growth factors' and "Calciphylaxis (calcific uremic arteriolopathy)", section on 'Treatment'.)

Mixed etiology — While the clinical characteristics can typically assist the clinician in differentiating ulcer etiology, it is not unusual to have wounds of mixed etiology. This is most frequent in diabetic foot ulcers with concomitant peripheral artery disease. For this reason, classification of the wound's characteristics is very helpful for assessment, treatment planning, and prediction of outcome (table 2).

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Chronic wound management".)

SUMMARY AND RECOMMENDATIONS

Chronic wounds – A chronic wound is defined as one that is physiologically impaired. Healed chronic wounds, particularly diabetic foot ulcers, should be considered "wounds in remission" and at very high risk for recurrence. (See 'Introduction' above.)

Clinical assessment – The patient with a wound or ulcer should undergo a complete history and physical examination including comprehensive wound assessment, vascular assessment, and review of systems. Vascular testing may be indicated for patients with chronic wounds who have an abnormal pulse examination or risk factors for cardiovascular disease. (See 'Clinical assessment' above.)

Differential diagnosis – Differentiation of the various types of chronic ulcers is important since pathophysiology, and thus management, differs. Characteristic clinical location and appearance usually allow clear distinction between venous ulcers, diabetic foot ulcers, and ischemic ulcers. (See 'Differentiation of chronic ulcers' above.)

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