INTRODUCTION

Overview

This topic covers the Introduction and Assessment of venous leg ulcers (VLU) including epidemiology, risk factors, etiology, pathophysiology, history,  physical examination, diagnosis, differential diagnoses, documentation and ICD-10 coding. For VLU management including a section for clinicians on patient education, see "Venous ulcers - Treatment and Prevention". For clinical guidelines and quality measures specific to VLU, see "Venous Ulcers - Overview". For an overview of surgical interventions for management of chronic venous disease and resulting manifestations such as VLUs, see " Chronic Venous Disease - Surgical Management".

Background

Venous disease is a chronic condition that can be characterized by periods of ulceration (i.e. an open wound) followed by healing and then recurrence.[8] Patients with chronic venous disease (CVD) of the lower extremities may present with many different clinical features, ranging from reticular veins, telangiectasias, varicose veins, edema, skin pigmentation, lipodermatosclerosis, and atrophie blanche, to venous ulceration. [9][10] Venous Leg Ulcers (VLUs) are a relatively common, complex type of wound that have a negative impact on people’s lives and incur high costs for health services.[11] 

Definitions

• Venous leg ulcers: VLU can be defined as an open skin lesion of the leg or foot that occurs in an area affected by venous hypertension.[2] VLUs can result in pain, unpleasant odor, reduced mobility, sleep disturbance, reduced psychological well-being and social isolation.[11] In severe cases and when associated with arterial insufficiency, VLUs can lead to limb amputation.[12][13]
• Chronic venous disease: the term chronic venous disease (CVD) has been defined as “(any) morphological and functional abnormalities of the venous system of long duration manifest either by symptoms and/or signs indicating the need for investigation and/or care”. [14][15]
• Chronic venous insufficiency: the term “chronic venous insufficiency” (CVI) is reserved for advanced CVD, which is applied to functional abnormalities of the venous system, producing edema, skin changes, or venous ulcers, corresponding with C3 to C6 of the CEAP classification. [14] See section 'CEAP Classification System' below.
  

Relevance of VLUs

• Venous ulcers are often recurrent:
• The recurrence rate within 3 months after wound closure is as high as 70%.[1] Thirty-five percent of people with VLU experience four or more episodes during their life times.[3][4]
• Open ulcers can persist from weeks to many years:
• The first-line treatment for VLUs is compression therapy, but despite adequate compression up to 45% of people have unhealed ulcers after 6 months of treatment.[11][16] Since these figures were extracted from randomized controlled trials, the percentage of unhealed ulcers in the real world are probably higher.
• It is estimated that 93% of VLUs will heal in 12 months, and 7% remain unhealed after five years.
• Despite the relatively low prevalence, VLUs represent a significant financial burden to the healthcare system:
• In the U.S., the overall burden to Medicare and private insurers due to VLU is estimated to be around US$14.9 billion (in 2012 US$, excluding out-of-pocket payments and other indirect costs such as lost productivity).[17] Also, it has been reported that 4.6 million workdays per year are lost secondary to chronic venous insufficiency (CVI), in which VLUs are the most severe complication. [18]
• In the U.K., estimated costs to treat a person with open leg ulcer is around GBP 1700 (US$ 2122) per year at 2012 prices, mostly related to nurses' time.[19] 

Epidemiology

Prevalence

• Prevalence of ulcers of venous etiology only the UK is about 2.9 cases per 10,000 people [11][20], whereas mixed arterial/venous leg ulcers have a prevalence of 1.1 per 10,000 people.[2]
• Approximately 1% of the population in the United States, 3% of people over 80 years of age in westernized countries. [1] Prevalence is increasing, coinciding with an aging population. [18] In the U.S., VLUs affect between 500,000 to 2 million people per year. [21]
• More prevalent among women, but this gender discrepancy decreases with age. [22]
• Most common type of leg ulcer (~ 80% of leg ulcers). [23]

Incidence

• The overall incidence rate is 0.76 (95% CI, 0.71, 0.83) for men and 1.42 (1.35, 1.48) per 100 person-years for women. [24]

Risk Factors   

• Risk factors for development of VLU:
• • Presence of chronic venous insufficiency (CVI): risk factors for CVI include older age, obesity, reduced mobility, previous leg injuries, deep venous thrombosis, phlebitis, low physical activity, prolonged standing or sitting, arterial hypertension, deep venous thrombosis, family history of VLU.[22][23][25][26][27]
  • Genetic predisposition to early onset of varicose veins: Klippel-Trenaunay syndrome, CADASIL, FOXC2 gene mutation, desmulin dysregulation, and Ehlers-Danlos syndrome [26]
• Risk factors for delayed VLU healing:
• • Initial VLU location, area and duration are the most important predictors [28]: 
  • • VLU location in posterior ankle or back of calf region [7]
      
    • VLU that is smaller than 10 cm2 and has a duration shorter than 12 months at first visit has a 70% change of healing by the 24th week of care, whereas a VLU larger than 10 cm2 and with a duration longer than 12 months has only 22% chance of healing by the 24th week of care [11][29].
  • Other risk factors include [7]:
  • • > 50 years, male gender
      
    • History of vascular surgery, trauma, repeat intimal venous damage or varicosities
      
    • Family history of VLU
    • BMI > 33 kg/m2 with documented nutritional deficiency
    • Multiple pregnancy
• Risk factors for recurrence [7][18]:
• • Deep venous disease
    
  • Deep venous thrombosis
  • Thrombophilia 

Etiology

VLUs are the final stage of chronic venous insufficiency (CVI) and associated venous hypertension (increased ambulatory venous pressure).[11][26]

• The term chronic venous disease is generally applied to the full spectrum of chronic venous disease (CEAP C0-6), whereas chronic venous insufficiency is reserved for more severe presentations (CEAP C4-6).[30] See section 'CEAP Classification System' below.
• It is not infrequent for leg ulcers to be associated with CVI and arterial vascular disease, in which case, these ulcers are said to be of “mixed etiology.”

Pathophysiology

• The pathophysiology of VLU is complex and healing is delayed in many patients due to a chronic inflammatory condition.[31] Patient risk factors predispose individuals to chronic venous diseases including VLU.
• CVI results in venous hypertension (ambulatory venous pressures of up to 60 to 90 mmHg, as opposed to the normal levels of 20 to 30 mmHg), which can happen due to obstruction to venous flow or venous reflux from dysfunction of venous valves, and/or failure of the "venous pump".[26][32] Reflux is much more prevalent among patients across the different stages of chronic venous disease (CVD), including VLUs. However, obstruction has a higher rate of patients who develop VLU and a much faster disease progression.[26]
• Venous hypertension and hemodynamic abnormalities caused by venous flow obstruction or venous reflux lead to inflammatory alterations with microcirculatory changes described below that can result in venous stasis and VLU (see Figure 1) [32][33]:
• Pooling of venous blood: valve dysfunction or venous obstruction leads to blood accumulation, heightening pressure against vein walls.
• Altered shear stress: increased pressure against vein walls changes the physiological shear stress, crucial for maintaining blood fluidity and preventing blood cell adherence.
• Endothelial damage: the resulting mechanical stress disrupts the endothelium's protective glycocalyx layer, leading to cell activation and increased permeability.
• Imbalance of inflammation, inflammatory modulators, oxidative stress, and proteinase activity: endothelial damage leads to activation of adhesion molecules on endothelial cells, leukocyte activation with attachment and migration into vein wall, microcirculation, and in the interstitial space. Multiple chemokines, cytokines, growth factors, proteases and matrix metalloproteinases are produced to target fibroblasts, vascular smooth muscle cells, and the extracellular matrix.[26][31]
• Skin changes: the increased permeability of endothelial cells allows red blood cells to escape, releasing hemoglobin and ferric iron into the interstitial fluid. This release contributes to increased oxidative stress and inflammation, leading to noticeable skin changes and progression of CVD. Skin changes include [34]:
• Eczema and pigmentation (CEAP stage C4a), which appear to be caused mainly by a hemosiderin deposit occurring in the early stages of CVD
• Chronic fibrosing panniculitis (inflammation of subcutaneous fat) related to CVI
• Lipodermatosclerosis (CEAP stage C4b), which eventually leads to the development of tissue breakdown and VLU.[35]

ASSESSMENT

• Primary goals of assessment are:
• • To identify risk factors for VLU, amputation, delayed healing, recurrence. See details in “Risk Factors”
  • To assess patient's and caregiver's concerns
  • To screen for significant signs and symptoms to differentiate from other types of lower extremity ulcers, which may require different treatments. See “Differential Diagnoses”
  • To categorize VLUs as "simple", "complex" or of mixed etiology (i.e., due to venous disease and peripheral arterial disease) to determine likely prognosis, so that appropriate time frames for monitoring, reassessment and specialist referral can be established [6]
  • • Peripheral arterial disease (PAD) needs to be ruled out with noninvasive arterial tests and venous disease should be documented with duplex ultrasound. See section 'Diagnosis' below 
      
  • To determine "healability", that is, the potential of the ulcer to heal with conservative treatment only

• See Algorithm for Assessment of Venous Ulcers below (Algorithm 1)

Algorithm 1. Algorithm for Assessment of New and Recurrent Venous Ulcer (click link to enlarge)

History

Qualified professional multidisciplinary team should evaluate and perform a complete assessment of the patient. Patients with VLU frequently present with other co-morbidities that may impede healing. It is important to obtain a comprehensive patient history of the patient’s current condition, recurrence and treatment if any, medical and surgical history including past deep vein thrombosis (DVT), pulmonary embolism or malignancy, medications, and other risk factors related to VLU, CVI or non-healing leg wounds.[2][36][37]

Chief Complaint and History of Present Illness

• Time of symptom onset and duration
• Symptoms experienced by patients with VLU include extremity pain, burning aching, throbbing, cramps, heaviness, itching, tiredness, fatigue, and restless legs.[2][23][36] Venous symptoms are usually exacerbated when the patient is standing and relieved by rest or limb elevation (as opposed to pain of peripheral artery disease, which worsens with walking or that is relieved by rest, or which worsens with limb elevation). Pain is localized to the affected veins, skin changes or ulcer and does not irradiate.
• Edema of lower extremities:
• • History of medical condition resulting in edema of lower extremities, such as heart failure, hypothyroidism, hypoalbuminemia or nephrotic syndrome
  • History of lymphatic disease resulting in edema of lower extremities. It is common for chronic venous disease to be associated with chronic lymphatic insufficiency, a condition known as phlebolymphedema. See topic "Lymphedema - Introduction and Assessment".
  • Extremity swelling due to chronic venous disease can be present in 25-75% of patients, worsens with prolonged standing and improves with leg elevation and walking. In women, symptoms exacerbate with menses or pregnancy.  
• History of complications, such as DVT, embolisms, skin infections, cellulitis, osteomyelitis, and malignant change.[23]
• Assess risk factors for development of VLU. See section ‘Risk factors’ above 
  
• Past treatment history
• Comorbidities: autoimmune disorders, diabetes, immunosuppression and other conditions may delay healing.[38] 

Medications

• Medications that delay wound healing (in case patient has an ulcer) include: anticoagulants, antimicrobials (various antibiotic classes), anti-angiogenesis agents (eg, bevacizumab, aflibercept), antineoplastic drugs, anti-rheumatoid drugs (eg, methotrexate, aspirin/nonsteroidal anti-inflammatory drugs [NSAIDs]), colchicine (anti-gout drug), topical hydrogen peroxide, topical iodine, full-strength 0.5% Dakin’s solution (sodium hypochlorite), nicotine, steroids, and vasoconstrictors.[39][40]

Social History

• Injectable drugs: repeated injections of illicit or not illicit drugs into the lower limb veins results in CVI. Increased risk for VLU persists even after prolonged periods free from injecting.[38][41] 

Nutrition

• Clinical guidelines recommend nutritional assessment for patients with VLU [2][42][43], despite the relative low number of studies on nutritional supplementation on VLU healing. Poor nutrition may be a risk factor for delayed VLU healing.[44] Patients with VLUs are commonly overweight and also have a relative nutritional deficiency that needs to be addressed.[5][45] 
• • Standardized tools such as the "Nestlé MNA" and "Self-MNA®" by Nestlé can be used
  •  Medicare Quality Payment Program, Quality Measure:
  • • "Process Measure: Nutritional Screening and Intervention Plan in Patients with Chronic Wounds and Ulcers" 
    • "Patient Reported Nutritional Assessment and Intervention Plan in Patients with Wounds and Ulcers"
    • "Preventative Care and Screening: Body Mass Index (BMI) Screening and Follow-Up"

Patient's and caregivers' concerns 

• Patient's and caregiver's concerns and psychosocial aspects should be assessed and taken in consideration when creating a treatment plan:
• • Evaluate patient's concerns: pain, exudate, odor, ability to carry out daily activities
  • •  Medicare Quality Payment Program, Quality Measure: "Pain Assessment and Follow-Up"
  • Evaluate psychosocial aspects of the patient, caregiver and family: cognitive, functional, emotional status, understanding of the wound and risk factors, preference for treatment, motivation for adherence to the care plan, financial concerns
  • We recommend use of Patient-Reported Outcome Tools to assess aspects above and measure impact of interventions. See 'Patient-reported outcomes (PRO) tools' below.
    

Physical Examination

VLUs commonly present in between area mid-calf and approximately 1 inch below the malleolus.[5] The recurrence of an ulcer in the same area is highly suggestive of venous ulcer.[23] Physical examination of lower extremities should include [2]:

Inspection

• See Figures 1-9
• Limb shape and size (abnormal shape or large limbs can lead to challenges in compression therapy)
• Presence of active or healed ulcers, varicosities, telangiectasia, varicose veins, edema
• Chronic venous skin changes and dermatitis, such as skin discoloration, inflammation, eczema, hyperpigmentation, malleolar flair, corona phlebectatica (venous starburst of veins radiating distally from the medial malleolus), atrophie blanche (capillaries are virtually absent in areas of fibrotic scars, also known as livedoid vasculopathy), lipodermatosclerosis (severe fibrosing panniculitis of the subcutaneous tissue, area of indurated inflammatory tissue that binds the skin down to the subcutaneous tissue)
• Signs of infection, cellulitis

Palpation

• Varicosity, palpable venous cord, tenderness, sensation, induration
• Edema
• Peripheral pulses. See section 'Palpation' in topic "Arterial Ulcers - Introduction and Assessment".
• Percussion (or tap) test: this exam evaluates the functional status of valves in the superficial venous system. The test can be performed with or without a Doppler.
• Test: With the patient standing, place fingers of one hand on the saphenous vein. With fingers of the other hand, tap the saphenous vein about 15-20 cm proximally to the fingers previously placed on the saphenous vein. 
• Abnormal test: distally placed fingers feel a pulsatile wave as the saphenous vein is proximally tapped, which indicates that valves between the 2 points are incompetent, and thus allow for the wave to travel distally. 
• Normal test: the distally placed fingers should not feel any waves or oscillatory signals
• Trendelenburg test: this test measures how long it takes to refill the distal superficial veins on the dorsum of the foot. The goal is to assess valvular competency of the superficial, perforator and deep veins. 
• Test: With the patient supine, raise one leg for 60 seconds, then apply a tourniquet around the proximal thigh. Have the patient stand up and observe any filling of the veins of the dorsum of the foot. Release the tourniquet.
• Abnormal test: if veins are immediately filled, the perforator system is incompetent. If veins are filled after the tourniquet is removed, incompetence of the superficial veins are likely. 
• Normal: no filling is observed while the tourniquet is on or immediately after it is removed.

Auscultation

• Bruit and reflux

Other assessment

• Evaluation of ankle mobility: bony ankylosis and fibrosis may result in los off ankle function
• Assessment of foot temperature, measurement of the ankle brachial pressure index, testing for peripheral neuropathy, to look for signs of associated diseases such as arterial disease or diabetes mellitus.[5]                

Figure 2. Atrophie blanche and livedoid vasculopathy

Ulcer Exam

• Wound assessment: location, number and size of ulcers, edges, undermining, presence and type of nonviable tissue, signs of infection or biofilm, exudate type and quantity, periwound appearance (e.g., altered perfusion, maceration), edema.[38][46] 
• Common VLU characteristics: 
• • Anatomic location: often at the medial distal lower extremity and ankle, at the malleolar area
  • Margins: irregular 
  • Depth: superficial-to-deep
  • Wound bed: granulation tissue and fibrin often present, minimal to moderate aching pain at borders and middle of the wound bed
  • Exudate: frequent, moderate to heavy. 
  • • "Wet leg syndrome": occurs when large quantities of exudate exude from lower extremities, increasing risk for skin maceration, infection and wound chronicity.[38] Often seen in phlebolymphedema. See topic "Lymphedema - Introduction and Assessment".

Diagnosis

The diagnosis of VLU is predominantly clinical. Clinical assessment for the assessment of chronic venous disease is very important because diagnostic testing results and symptoms do not always correlate.[53] However, peripheral arterial disease (PAD) needs to be ruled out with noninvasive arterial tests and venous disease should be documented with duplex ultrasound. PAD can be present in up to 25% of VLU patients [3][4] and its presence affects how compression therapy, one of the main interventions to manage VLUs, is implemented. Prior to application of compression therapy, presence of other ulcer etiologies and/or co-morbid conditions that affect how compression is applied should be carefully evaluated. Failure to do so can result in adverse effects and deterioration of the patient's condition. PAD may be ruled out with evaluation of ankle brachial index ratio (ABI); for patients with diabetes or arterial calcification, audible handheld Doppler ultrasound with continuous waveform analysis is preferred. Additional tests can be ordered when necessary, as illustrated in Table 1 below. See section on 'Algorithms' in topic "How to Select Adequate Compression Therapy Pressure Levels and Products". See types and brands of noninvasive arterial testing devices in topic "Assessment and Documentation".  

Table 1. Summary of functional/diagnostic tests for patients with venous leg ulcers

Noninvasive arterial tests 

Noninvasive arterial tests are recommended to rule out peripheral arterial disease and to determine ulcer healing potential. 

•  Medicare Quality Payment Program, Quality Measure: "Noninvasive Arterial Assessment of patients with lower extremity wounds or ulcers for determination of healing potential"
  

• Ankle Brachial index (ABI) ratio for patients with lower extremity ulcer, no diabetes and no arterial calcification (See Table 2). [18]
• • ABI testing can be completed with a hand-held Doppler machine and sphygmomanometer, or an automated ABI device. See topic "How to Perform An Ankle Brachial Index". 
  • Medicare will cover ABI and other noninvasive arterial testing if specific criteria are met.[54] 
• Audible handheld Doppler ultrasound with continuous waveform analysis, toe pressure, transcutaneous oxygen pressure (TCOM, TcPO2) are preferable for patients with diabetes or arterial calcification (See Table 2)
• • Clinicians can measure toe pressure by placing a small toe cuff around the great toe and attaching a plethysmography probe at the pulp of great toe tip. The cut-off values of toe pressure and toe brachial index (TBI) are arbitrary and vary in the literature. A toe pressure lower than 30 mmHg or TBI 0.2-0.25 is considered severely ischemic and diagnostic of critical limb ischemia (CLI). Wound healing potential drops as TBI decreases from the normal values.[55] See topic " How to Interpret Audible Handheld Doppler Ultrasound and Waveforms to Rule out PAD".
  • Microcirculation assessment  prior to primary therapy in patients can be used when concomitant arterial etiology is suspected, if arterial calcification or diabetes, or for monitoring of advanced wound therapy.[2]
  • • TCOM near VLU: if >= 30mmHg, rules out severe arterial disease and predicts VLU healing.[36]

Table 2. Arterial noninvasive bedside tests and likely interpretation 

For compression therapy according to interpretation of arterial noninvasive tests, see algorithms 'Based on ankle brachial index (ABI)' or 'Based on audible handheld Doppler ultrasound or continuous waveform analysis', and section 'Compression Therapy' in topic "Venous Ulcers - Treatment and Prevention". For details on noninvasive arterial tests, see section 'Noninvasive arterial tests' in topic "Arterial Ulcers - Introduction and Assessment".

ABI: ankle brachial pressure, AP: ankle systolic pressure, TP: toe systolic pressure, TcPO2 or TCOM: transcutaneous oxygen pressure, TBI: toe brachial index, SPP: skin perfusion pressure.( * ) ABI, toe pressure, TBI values are frequently falsely elevated in patients with diabetes. Patients with diabetes should have TP measurements [56][57]. If arterial calcification precludes reliable ABI or TP measurements, or if ABI is non-compressible (>1.3), ischemia should be documented by TcPO2, SPP, or Doppler continuous waveform analysis [56][58]. (**) Biphasic waveform may be normal in older individuals or when there is no clear transition from triphasic signal along the vascular tree .

Functional/Diagnostics tests for chronic venous disease 

• 1BFor all patients with chronic venous disease of the lower extremities, guidelines recommend a comprehensive venous duplex ultrasound (DUS) as the diagnostic test of choice to evaluate for venous reflux. [2][5][9][37]
• • Rationale: For a leg ulcer to be classified as a VLU, objective documented evidence of venous disease is needed.[2] The correct method/type of ultrasound should be ordered to decrease chances of inconclusive results. Evaluation for both obstructive and reflux patterns of venous disease with comprehensive color flow venous duplex ultrasound including B-mode gray-scale imaging, pulsed Doppler sampling, and color flow analysis, in supine and standing positions is considered first-line.[2][5][9]
  • • Common findings in limbs with VLU are venous reflux (superficial and/or deep) and outward flow in perforators.[63][9]
    • Referral to vascular surgeon is recommended in cases with significant superficial junctional venous reflux (saphenofemoral or saphenopopliteal junction reflux >500 ms) [37][9] or superficial reflux directed to the ulcer bed [2], deep vein incompetence/obstruction [2][37], or perforator incompetence (outward flow of >500 ms duration, with a diameter of >3.5mm located beneath or associated with the ulcer bed) [2][37][9] or past history of venous surgery [37] For details on DUS diagnostic findings refer to Table 3 below. For a review on relevant anatomy of the venous system see section 'Vascular System of the Lower Extremities' in topic "Applied Anatomy and Physiology in Wound Care". 
• Venous plethysmography for routine initial evaluation of VLU is discouraged unless results of venous duplex ultrasound are inconclusive, or if patient has recurrent or recalcitrant VLU [2].
• • Rationale: Plethysmography can identify hemodynamic obstruction patterns. If venous refill time measured with below-knee tourniquet and photoplethysmography is greater than 20 mmHg after vein surgery, there is good chance of VLU healing and non-recurrence  [36].  
• Laboratory evaluation for thrombophilia for patients with a history of recurrent or recalcitrant VLU or thrombosis: these patients have a higher prevalence of thrombophilia, which is associated with recurrent and recalcitrant ulcers [2]. Laboratory evaluation includes [2]:
• • Inherited hypercoagulable factors (anti- thrombin deficiency, protein C and protein S deficiencies)
  • Factor V Leiden (resulting in activated protein C resistance)
  • Prothrombin G20210A
  • Plasminogen activator inhibitor type 1 mutations
  • Hyperhomocysteinemia,
  • Antiphospholipid antibodies (anticardiolipin and lupus anticoagulant),
  • Cryoglobulins and cryoagglutinins   
  • Factor VIII related antigen, von Willerbrand factor (VWF), D-dimer and factor V Leiden: if indicative of hypercoagulation tendency, pose a risk factor for post-thrombotic syndrome.[36]
• Routine wound culture is not advised. Instead, guidelines suggest wound culture only when VLU shows clinical signs of infection. See topic "How to Collect a Wound Swab (Levine Technique) for Culture".
• Wound biopsy is indicated in VLUs that fail standard therapy after 4 weeks of treatment or for differentiation from other possible non-venous causes for leg ulcer.[2][5] See topic "How to Perform a Wound Biopsy" 

Table 3. Summary of clinical practice guidelines on duplex ultrasound (DUS) diagnostic findings for assessing venous reflux in patients with chronic venous disease of the lower extremities [9] Abbreviations: GSV: great saphenous vein, SSV: small saphenous vein, AAGSV: anterior accessory great saphenous vein, and PAGSV: posterior accessory great saphenous vein. For a review on relevant anatomy of the venous system see section 'Vascular System of the Lower Extremities' in topic "Applied Anatomy and Physiology in Wound Care". 

Differential Diagnosis

For differential diagnosis, observing the progression of leg edema throughout the day is crucial. For instance, in venous diseases of the lower limbs, leg edema worsens in positions influenced by gravity and lessens when the limb is elevated. Symptoms are key indicators: intense pain may suggest arterial diseases, while a sense of heaviness or fatigue in the legs often points to venous disease.[64] For a comparison of clinical findings observed during physical examination of common types of lower leg ulcers, refer to section 'Physical Examination' in topic "How to Assess a Patient with Chronic Wounds" and to the 'Algorithm for Assessment of Patients with Chronic Wounds' in topic "How to Assess a Patient with Chronic Wounds". Table 4 below shows a list of differential diagnosis for VLU.[64][65]

Table 4. Differential diagnosis of venous leg ulcers

Characterization of VLUs

After differential diagnoses are ruled out and etiology is established, expert consensus recommends categorizing VLUs as "simple", "complex" or of mixed etiology to determine likely prognosis, so that appropriate time frames for monitoring, reassessment and specialist referral can be established [6]: 

• Simple VLU: 
• • Area < 100 cm2 and onset < 6 months with limited co-morbidities
• Complex VLU: 
• • Area > 100 cm2 and/or wound onset > 6 months (no other co-morbidities)
  • < 30% decrease in wound area after 4 weeks of adequate treatment
  • Lymphovenous disease
  • Associated lipedema
  • Leg/ulcer infection
  • Stable cardiac heart failure
  • History of non-adherence
• Mixed arterial venous ulcer:
• • ABI > 1.3: Non-compressible arteries
  • ABI 0.5-0.8: Mixed arterial ulcer with mild/moderate ischemia
  • ABI <0.5: Mixed arterial ulcer with severe ischemia

CEAP Classification System

• Clinical guidelines recommend documenting the level of venous insufficiency with a standardized score such as the CEAP (Clinical-Etiology-Anatomy-Pathophysiology) classification system (Table 5). The clinical or basic CEAP classification can be used for clinical practice, and the full CEAP classification system should be used for clinical research.[36][9]
• Relevant chronic venous disease classification systems such as CEAP criteria can guide the assessment of CVD.[5] Developed by an international consensus, CEAP classifies lower extremity venous disease based upon clinical signs, etiology, anatomic location, and pathophysiologic abnormality. It is an internationally accepted standard for describing patients with chronic venous disorders and it has been used for reporting clinical research findings in scientific journals.[74] 
• In 2020, the CEAP classification was updated.[74] These changes include adding Corona phlebectatica as the C4c clinical subclass, introducing the modifier "r" for recurrent varicose veins and recurrent venous ulcers, and replacing numeric descriptions of the venous segments by their common abbreviations.[74]
• CEAP limitations include the fact that it was designed as a descriptive classification and does not attempt to measure disease severity or outcomes of therapy.[74]

Table 5. The 2020 revision of CEAP: Abbreviations and Descriptions of Clinical, Etiologic, Anatomic and Pathophysiologic Classification of Chronic Venous Disease [74]

Venous Clinical Severity Score (VCSS)

• Clinical guidelines recommend the use of the revised Venous Clinical Severity Score (VCSS) for patients with chronic venous disorders for grading of clinical severity and for assessment of post treatment outcome.[9][10][15]
• Rationale: The Venous Clinical Severity Score (VCSS) complements the CEAP classification’s descriptive nature and static categorical classification scheme by providing a dynamic measure of venous disease severity, reflecting changes over time and treatment response. The VCSS includes 9 parameters of venous disease with a symptom severity scale from 0 to 3 (0–1=mild; 2=moderate; and 3=severe). The scored parameters include pain, varicose veins, edema, skin pigmentation, inflammation, induration, ulcers (number, size, and duration), and compression therapy.[9][10][15]  add table

Ulcer healability 

This step involves assessing whether the ulcer can be healed with conservative management only (healable) or not (non-healable), or if co-existing medical conditions, drugs or circumstances will likely impede wound healing (maintenance). Ulcer healability classification helps in determining an adequate treatment plan.[48] A summary is provided below; for more details see topic "How to Determine Healability of a Chronic Wound". After determining ulcer healability, see "Venous ulcers - Treatment and Prevention"

Table 6: Determining ulcer healability 

( * ) As determined by comprehensive patient assessment. Maintenance wounds have healing potential but patient or health system barriers compromise healing (**) For persons without diabetes, inadequate blood supply is objectively confirmed by ankle-brachial index (ABI) < 0.5, monophasic doppler waveform, skin perfusion pressure < 30mmHg, transcutaneous oxygen < 30mmHg, absolute systolic ankle pressure < 50 mmHg OR toe pressure < 30mmHg. For persons with diabetes, perform any other testing listed above besides ABI as ABI can be falsely elevated 

Modified from Sibbald RG et al. 2011[48].

• If patient has any of the conditions below, consider a non-healing program. VLU will likely not heal with conservative treatment only:
• • Co-morbidities that impede healing: 
  • • Ulcer is malignant tumor, 
    • Major organ failure
    • Blood supply to the VLU is inadequate as determined by non-invasive vascular arterial tests (ABI, Doppler, TCOM, other exams)
• If patient has any of the conditions that impede wound healing below, consider a maintenance-healing program until element impeding healing is mitigated:
• • Co-morbidities:
  • • Uncontrolled diabetes
    • Immunosuppression
    • Obesity: BMI > 40
    • Inadequate nutrition (abnormal serum protein, unintended weight loss)
    • Cognitive, emotional, psychological dysfunction
    • Calf muscle pump disfunction (arthritic conditions, paralysis, etc)
  • Drugs and interventions :
  • • Steroids
    • Chemotherapy/ radiation
    • Immunosuppressants
  • Lifestyle:
  • • Regular smoking
    • Impaired mobility
    • Financial or resource constraints

Experimental Diagnostics

• Ulcer exudate biomarkers measurement with Multiplex ELISA: a single center study found the biomarkers granulocyte macrophage-colony stimulating factor (GM-CSF) and matrix metalloprotease-13 (MMP-13) to be accurate predictive biomarkers of VLU healing. Results suggested that VLUs with GM-CSF values greater than 29.5 pg/mL or with MMP-13 values greater than 962.2 pg/mL in their exudate will not decrease in size (that is, the the VLU is nonhealing), and thus treatment plan should be reassessed.[75] While results are promising, further validation and development of a point-of-care test are needed before use in clinical practice.

Documentation

• Documentation of VLU is important to assess healing progress, as they determine whether a treatment plan should be continued or not. VLU progress should be recorded weekly or sooner if significant change.
• All wound care services provided need to be documented in a way that supports the Medical Necessity requirements, and facilitate evaluation and subsequent care of VLUs. Many VLUs are refractory to healing or have complicated healing cycles either because of the nature of the wound itself or because of complicating metabolic and/or physiological factors.  
• Documentation should include number and position of ulcers on the leg. Wound measurements should be made for each VLU, including area, perimeter, and depth, description of wound edge, peri-wound area, wound base quality, amount and type of drainage, and infection, history of debridement. [2]
• • Wound measurement methods include manually measuring length and width (the longest length with the greatest width at right angles), manual tracing, digital photography, and software programs that calculate wound dimensions from a photograph of the lesion. Wound tracings that calculate the area via digital software are slightly better than linear measurement [5].

Documenting signs of VLU improvement to support medical necessity (Medicare):

• Reimbursement for wound care services on a continuing basis for a particular wound in a patient requires documentation in the patient's record that the wound is improving in response to the wound care being provided. 
• It is not medically reasonable or necessary to continue a given type of wound care if evidence of wound improvement cannot be shown. 
• Medicare expects that with appropriate care, wound volume or surface dimension should decrease by at least 10 percent per month or wounds will demonstrate margin advancement of no less than 1 mm/week. 
• Medicare expects the wound-care treatment plan to be modified in the event that appropriate healing is not achieved.
• Such evidence must be documented with each date of service provided.
• Evidence of improvement includes measurable changes (decreases) of some of the following: 
• • Drainage 
  • Inflammation
  • Swelling
  • Pain
  • Wound dimensions (diameter, depth) 
  • Necrotic tissue/slough 

Documentation tools: 

• Tools that facilitate standardized assessment should be used:
• • Wound Reference Wound Prep & Dress Tool creates notes to help support medical necessity that can be copied and pasted to electronic medical records
  • Validated wound assessment tools such as Bates-Jensen Tool.[46] 
  • The CEAP classification system and the VCSS scoring system may be used to describe chronic venous disorders in a standardized fashion. See section 'CEAP Classification System' above. 

• Patient reported outcome (PRO) Tools: as part of a patient-centered approach, it is recommended that clinicians adopt PRO tools to assess patient’s Quality of Life (QOL), pain, and depression [7] PROM provide a comprehensive picture of patient’s health [76], which can be used to optimize plan of care.
• • QOL tools validated for VLU patients: the Nottingham Health Profile (NHP) and Venous Leg Ulcer Quality of Life (VLU-QoL) questionnaire  seem to be the most suitable PROM for use by clinicians.[76] Others include VEINES - QoL/Sym tool, the Medical Outcomes Survey 12 item Short-Form (SF-12) the Short-Form Health Survey, 36 items (SF-36).[7] 
  • •  Medicare Quality Payment Program, Improvement Activity "Promote Use of Patient-Reported Outcome Tools" suggests use of Wound-Quality of Life (QoL) and patient-reported Wound Outcome.[77]
  • Pain measurement tools validated for VLU patients:  include the Medical Outcomes Survey 12-item Short- Form (SF-12), the Visual Analogue Scale, and the McGill Pain Questionnaire, a subscale of the Nottingham Health Profile. [7]
  • Depression measurement / assessment tools validated for VLU patients: include the Hospital Anxiety and Depression Scale (HADS), the Euroqol 5 dimensions (EQ-5D), and the Nottingham Health Profile. [7]

CODING

ICD-10

• Identify and document first any documented underlying condition (ICD-10-CM documentation)  
• • Chronic venous hypertension with ulcer  (I87.31-, I87.33-)
  • Post-phlebitic syndrome with ulcer (I87.01-, I87.03-)
  • Post-thrombotic syndrome with ulcer (I87.01-, I87.03-)
  • Varicose ulcer (I83.0-, I.83.2-)
• Specify laterality
• • Right, left or unspecified
• Specify ulcer severity: Select code for non-pressure chronic ulcer of the calf [78]
• • Limited to breakdown of skin
  • With fat layer exposed
  • With necrosis of muscle
  • With necrosis of bone
  • Unspecified severity

APPENDIX 

ICD-10 Coding