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Clinical assessment of wounds

Authors Section Editors Deputy Editor

David G. Armstrong, DPM, MD, PhD Hilary Sanfey, MD Kathryn A Collins, MD, PhD, FACS
Andrew J Meyr, DPM John F Eidt, MD
Joseph L Mills, Sr, MD

Disclosures: David G. Arm strong, DPM, MD, PhD Nothing to disclose. Andrew J Meyr, DPM Nothing to disclose. Hilary Sanfey, MD Nothing to disclose. John F Eidt, MD Grant/Research Support: Medtronic CEC
(drug eluting balloon). Joseph L Mills, Sr, MD Nothing to disclose. Kathryn A Collins, MD, PhD, FACS Nothing to disclose.
Contributor disclosures are review ed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence.
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All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Apr 2014. | This topic last updated: Aug 06, 2013.

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]. The clinical assessment of wounds begins with a determination of whether the wound is acute or chronic in nature. Acute wounds are those in which healing is anticipated to progress
through an orderly physiologic sequence of inflammation, proliferation and maturation [2,3]. 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 [4]. Examples of chronic wounds include ischemic ulcers, venous ulcers, neuropathic foot ulcers
and infected wounds including surgical site infections [5,6].

The clinical assessment of acute and 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".)

(See "Treatment of chronic lower extremity critical limb ischemia".)

(See "Management of diabetic foot lesions".)

(See "Medical management of lower extremity chronic venous disease", section on 'Ulcer care'.)

(See "Treatment of pressure ulcers".)

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:

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 regimen? Have any other treatments been tried? Is the wound painful? How severe is the pain? (figure 1).

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 non-healing such as diabetes, peripheral artery disease, and chronic kidney disease.
(See "Wound healing and risk factors for non-healing", section on 'Risk factors for non-healing'.)

Social history – Does the patient have a history of smoking? Is there a supportive social environment for wound management? 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 non-healing 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 inter-observer variability and allows for consistent and accurate assessment of
changes in wound area over time [7].

Wound location, length, width, depth and the presence and position of undermining, presence of cellulitis, and drainage (amount, type, color, odor) are also documented. A subjective
assessment of 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?

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 [8,9].

Acute wounds, including those from suspected surgical site infections, should be clinically assessed in the same manner with particular attention directed to the surrounding skin. Virtually
all wounds are colonized with bacteria and a diagnosis of invasive infection is a clinical diagnosis and not microbiological. Induration, cellulitis extending >2 cm beyond the margin of the
wound, increased local temperature, pain on palpation and drainage from the site are all signs of acute infection and may indicate an underlying abscess that would benefit from drainage
and debridement.

Symptoms and signs that could suggest the presence of significant infection and the need for hospitalization, intravenous antibiotics and debridement treatment include:

Increasing erythema/cellulitis of the surrounding skin

Induration of surrounding skin
Lymphangitis
Increase in the size of the ulcer
Large amount of drainage
Fever

Vascular assessment — A careful and accurate assessment of the vascular status is essential when a patient presents with a chronic wound of the extremity. A thorough vascular exam
should be performed including palpation of the radial, femoral and pedal pulses. Signs of arterial obstruction include lack of peripheral pulses with poor capillary refill, thin atrophic skin, and
hypertrophic deformed nails.

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

Laboratory studies — Routine laboratory studies are performed to evaluate for active infection, anemia, nutritional status and medical conditions that place the patient at risk for non-
healing wounds. (See "Wound healing and risk factors for non-healing", section on 'Risk factors for non-healing'.)

Hematology – complete blood count and differential

Chemistries – metabolic panel, liver function tests, albumin, prealbumin, hemoglobin A1c
 Microbiology – previous cultures/pathology (wound, urine, blood, clostridium difficile)

Although there may not be equivocal evidence that increasing nutrition will help healing of wounds, adequate nutrition is still imperative to prevent a wide variety of infections. (See "Wound
healing and risk factors for non-healing", section on 'Malnutrition'.)

We prefer to screen for malnourishment with prealbumin and albumin and maximize nutritional supplementation, if needed. Prealbumin and albumin are not perfect markers of nutritional
status, but should be evaluated for any patient with a non-healing wound.

Wound cultures should only be obtained if cellulitis is suspected to help guide antibiotic therapy. Wound infection is a clinical diagnosis and wound cultures should not be used as a
substitute for clinical judgement. If a culture is indicated, the sample should be obtained after a wound has been thoroughly cleansed and débrided; collection of deep tissue for culture is
recommended over swabbing the wound base or collecting drainage [10-12].

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 usually allows for clear distinction between ischemic, venous and neuropathic ulcers.

Ischemic ulcers — 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 dependant position, and characteristic dependant 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 including between the toes, on the tips of toes, over phalangeal
heads, at the lateral malleolus, or 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.

Venous ulcers — Venous ulcers are the most common type of chronic wound treated by practitioners. 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".)

Characteristics of venous stasis ulcers include:

Location between the knee and the ankle. The medial and lateral malleoli are the most common sites.

Surrounding dermatitis with venous stasis ulcers. The periwound skin is often eczematous, presenting with erythema, scaling, weeping, 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 [13]. Calcification in wound base is common.

Pressure ulcers — Pressure ulcers are areas of necrosis and ulceration where soft tissue structures are compressed between osseous prominences or hard external surfaces. They
result from pressure alone or pressure in combination with shearing. Risk factors include advanced age, impaired circulation, immobilization, and incontinence. (See "Pressure ulcers:
Epidemiology, pathogenesis, clinical manifestations, and staging".)

Ulcer severity ranges from nonblanchable skin erythema (stage I) to full-thickness skin loss with extensive soft-tissue necrosis (stage III) and full thickness skin/muscle necrosis with
exposed structures such as muscle and bone (stage IV). The diagnosis is clinical [14].

Characteristics of pressure ulcers include:

Location over osseous prominences including the medial and lateral metatarsal heads, calcaneus, ischial tuberosities, fibular head and sacrum.

Fibrotic tissue including necrotic eschar

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

Surrounding peri-wound erythema

Diabetic neuropathic ulcers — Chronic ulceration in patients with diabetes is multifactorial, due to a combination of diabetic neuropathy, autonomic dysfunction and vascular
insufficiency. Non-ischemic neuropathic foot ulcers in the diabetic patient 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 neuropathic diabetic ulcers include:

Location at areas of repeated trauma, such as the plantar metatarsal heads or dorsal interphalangeal joints.

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

Undermined borders.

Lack of sensation.

Signs of neuropathy are typically present on physical examination.

Malignant ulcers — 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 [15]. Rare malignancies, such as soft tissue sarcomas, have also been
documented in leg ulcers [16-18].

For this reason, skin biopsy should be considered in any non-ischemic wound that does not demonstrate signs of healing after approximately three months of treatment [19].

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 [20]. These are associated with arterial hypertension in patients with
perceptible pulses. Diabetes is present in about 60 percent of patients [21,22].

These ulcers are due to medial calcification that obliterates the small arterioles similar to calcific uremic arteriolopathy [22]. The reduction in tissue perfusion leads to local ischemia and
ulcer formation. The ulcer begins as a red patch which 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 [23]. The outcomes of treatment of this non-uremic 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'.)

SUMMARY AND RECOMMENDATIONS

Acute wounds are those in which healing progresses through normal physiologic processes, whereas a chronic wound is defined as one that is physiologically impaired. (See
'Introduction' above.)

The patient with a wound or ulcer should undergo a complete history and physical examination including vascular assessment, review of systems and comprehensive wound
assessment. (See 'Wound assessment' above.)

Further vascular testing may be indicated for patients with chronic wounds who have an abnormal pulse examination or risk factors for cardiovascular disease. (See 'Vascular
assessment' above.)

For consistent and accurate assessment of changes in wound area over time with treatment, we suggest using objective wound photography, which decreases interobserver
variability (Grade 2C). (See 'Wound assessment' above.)

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 ischemic, venous and neuropathic ulcers. (See 'Differentiation of chronic ulcers' above and "Basic principles of wound management", section on
'Management of specific wounds'.)

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REFERENCES

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