CEAP Classification

C

Clinical Classification — C0 to C6 Objective signs of chronic venous disease graded by severity · Suffix (s) = symptomatic · (a) = asymptomatic · C2r & C6r denote recurrence

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Code	Classification	Severity	Clinical Findings & Features	Key Characteristic
C0	No Visible DiseaseNO SIGNS · NO SYMPTOMS	Nil	No visible or palpable signs of venous disease; patient may still have subjective symptoms such as heaviness, aching or pruritus without any objective finding on examination	Symptom Only
C1	TelangiectasiaSPIDER / RETICULAR VEINS	Minimal	Telangiectasias (intradermal venules <1 mm, spider veins) and/or reticular veins (1–3 mm, subdermal, non-palpable, dilated bluish-green vessels); may be isolated or combined	Spider Veins ≤ 3mm
C2	Varicose VeinsDILATED SUBCUTANEOUS	Mild	Tortuous subcutaneous veins ≥3 mm diameter in the standing position; includes great saphenous vein, small saphenous vein, and their tributaries; palpable and visible; may be trunk, tributary or both	≥ 3mm Tortuous
C2r	Recurrent Varicose VeinsPOST-TREATMENT RECURRENCE	Mild+	Recurrent varicose veins at a site previously treated; defined as varicose veins recurring after documented prior intervention (surgery, foam sclerotherapy, thermal ablation, or mechanical closure)	Post-Treatment
C3	OedemaVENOUS OEDEMA	Moderate	Oedema of venous origin; perimalleolar or ankle oedema that increases throughout the day and reduces with limb elevation; pitting; not caused by cardiac, renal or hepatic disease	Pitting Oedema
◆ C4 — Skin & Subcutaneous Changes (Subclassified A · B · C) — Added in Revised 2020 CEAP
C4a	Pigmentation / EczemaSKIN COLOUR CHANGES	Mod–Sev	Hyperpigmentation (brown/golden haemosiderin deposition from extravasated red cell breakdown) and/or venous eczema (stasis dermatitis): erythema, pruritic, scaling, vesicular rash in gaiter area	Stasis Dermatitis
C4b	LipodermatosclerosisSUBCUTANEOUS FIBROSIS	Severe	Lipodermatosclerosis (LDS): localised chronic inflammation and fibrous replacement of skin and subcutaneous fat, typically medial distal leg; &/or atrophie blanche (white avascular scarred plaques within areas of pigmentation)	Fibrosclerosis · LDS
C4c	Corona PhlebectaticaANKLE FLARE · NEW 2020	Severe	Fan-shaped pattern of numerous small intradermal telangiectasias & reticular veins on the medial and/or lateral aspects of the ankle and foot; recognised as a sign of advanced CVI; added as new subcategory in the 2020 revision	Ankle Flare
C5	Healed Venous UlcerHEALED SKIN BREAKDOWN	Very Sev.	Previously documented open venous ulceration that has healed; high risk of recurrence without continuous compression therapy; C4 skin changes typically persist around the healed ulcer bed	Healed Ulcer
C6	Active Venous UlcerOPEN SKIN BREAKDOWN	Critical	Full-thickness skin defect of venous origin, most commonly above the medial malleolus; may be single or multiple; spontaneous healing unlikely without treatment of underlying venous hypertension	Active Ulcer
C6r	Recurrent Active UlcerRECURRENT OPEN ULCER	Critical+	Active venous ulcer at a site of previously healed venous ulceration; requires aggressive management including endovenous intervention, compression and specialist wound care; nutritional and systemic assessment indicated	Recurrent Ulcer

E

Etiological Classification Underlying cause of chronic venous disease · Ec (Congenital) · Ep (Primary) · Es (Secondary) · En (No cause identified)

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Code	Etiology	Onset / Mechanism	Description & Pathogenesis	Examples
Ec	CongenitalPRESENT FROM BIRTH	Developmental venous anomaly; present since birth; may not clinically manifest until adulthood	Structural venous abnormality arising from embryological maldevelopment; venous malformations, absent or incompetent deep venous valves, vascular hamartomas; the cause is present from birth even if clinical signs appear later in life	Klippel-Trénaunay · Parkes-Weber
Ep	PrimaryUNKNOWN / IDIOPATHIC	Idiopathic; intrinsic valve weakness; likely polygenic hereditary predisposition	No definitive identifiable extrinsic cause; intrinsic valvular incompetence without history of DVT or trauma; genetic susceptibility with environmental triggers (obesity, prolonged standing, multiparity); most common etiology in primary varicose veins	Idiopathic Varices
Es	SecondaryIDENTIFIED ACQUIRED CAUSE	Acquired extrinsic cause; post-thrombotic, traumatic or compressive mechanism	Identifiable and documentable causative factor; post-thrombotic syndrome (PTS) following DVT is the most common; venous wall damage and valve destruction after thrombus organisation; also includes trauma, AV fistula, extrinsic compression (May-Thurner, pelvic masses)	Post-DVT · Trauma · Compression
En	No Cause IdentifiedUNCLASSIFIABLE	Venous disease present; no identifiable etiology after thorough investigation	Chronic venous disease is present and confirmed but no congenital, primary or secondary aetiology can be identified despite complete investigation including duplex ultrasound; 'En' is only assigned after full workup — not as a default starting category	Post-Workup Diagnosis

A

Anatomical Classification Venous system segment involved · As (Superficial) · Ap (Perforator) · Ad (Deep) · An (No venous location identified)

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Code	Segment	System Level	Anatomical Sites Included (CEAP 2020 Numbering)	Key Vessels
As	Superficial VeinsABOVE DEEP FASCIA	Superficial venous system; subcutaneous, above muscular fascia	Telangiectasias/reticular veins (1); GSV above knee (2); GSV below knee (3); small saphenous vein (4); non-saphenous veins (5); includes saphenofemoral junction (SFJ) and saphenopopliteal junction (SPJ); anterior and posterior accessory saphenous veins	GSV · SSV · SFJ · SPJ
Ap	Perforator VeinsFASCIAL PENETRATORS	Perforating veins that pierce deep fascia connecting superficial to deep system	Thigh perforators (6): Dodd, Hunterian; calf perforators (7): Cockett (paratibial/posterior tibial), Boyd, gastrocnemial, soleal; foot perforators (8); incompetent perforators (>3.5 mm, outward flow >0.5s) are haemodynamically significant	Cockett · Dodd · Boyd
Ad	Deep VeinsBELOW DEEP FASCIA	Deep venous system; beneath muscular fascia; includes axial and muscular veins	Inferior vena cava (9); common iliac (10); internal iliac (11); external iliac (12); pelvic veins (13); common femoral (14); deep femoral (15); femoral (16); popliteal (17); tibial (anterior/posterior) (18); peroneal (19); muscular veins — gastrocnemial (20), soleal (21)	IVC · Iliofemoral · Popliteal
An	No Location IdentifiedANATOMICALLY UNCLASSIFIED	Venous disease present; no anatomical venous location identifiable on investigation	No specific anatomical venous segment identified despite complete duplex ultrasound examination; assigned only after thorough imaging workup; may prompt further investigation with CT venography, MR venography or IVUS to exclude deep pelvic or iliac disease	Post-Imaging Diagnosis

P

Pathophysiological Classification Underlying haemodynamic mechanism · Pr (Reflux) · Po (Obstruction) · Pr,o (Combined) · Pn (No identifiable mechanism)

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Code	Mechanism	Haemodynamics	Pathophysiological Description	Investigation Method
Pr	RefluxVALVULAR INCOMPETENCE	Retrograde venous flow; ambulatory venous hypertension; valve leaflet failure	Incompetence of venous valves causes retrograde blood flow under gravitational or calf-pump reversal forces; reflux threshold: >0.5 seconds in superficial & perforator veins; >1.0 second in deep veins (Valsalva or calf squeeze provocation); most common mechanism in primary CVD	Duplex — Reflux Duration
Po	ObstructionOUTFLOW IMPAIRMENT	Reduced or absent venous outflow; elevated venous pressures; collateral development	Partial or complete mechanical obstruction to venous return; causes: residual thrombus/post-thrombotic synechiae (most common), extrinsic compression (May-Thurner syndrome — left iliac vein compression), intraluminal webs/spurs; venous claudication is characteristic of outflow obstruction	Duplex · IVUS · CT/MR Veno
Pr,o	Reflux + ObstructionCOMBINED MECHANISM	Mixed haemodynamic defect; most severe physiological burden; progressive	Coexisting reflux and obstruction in the same limb; most haemodynamically severe combination; classically seen in post-thrombotic syndrome (PTS) where DVT destroys valve leaflets (→ reflux) and leaves fibrotic residual thrombus (→ obstruction); worst clinical outcomes and highest recurrence risk	Multi-Modal Imaging
Pn	No Mechanism IdentifiedHAEMODYNAMICALLY SILENT	No demonstrable reflux or obstruction on complete physiological assessment	Chronic venous disease is clinically present but no pathophysiological haemodynamic mechanism is demonstrable after complete duplex assessment; 'Pn' should only be assigned after thorough investigation — not used as a default; may indicate microcirculatory or lymphatic co-pathology	Documented Full Workup

⑤

Associated Severity Scoring Tools Adjunct validated scoring instruments used alongside CEAP to quantify severity and quality of life impact

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Score / Tool	Full Name	Domain Assessed	Description & Clinical Use
VCSSSEVERITY SCORE	Venous Clinical Severity Score	Clinical Severity	10-item validated tool scoring pain, varicose veins, oedema, skin pigmentation, inflammation, induration, ulcer number, duration, size, and compression use; each item 0–3; max score 30; used to monitor treatment response over time; more sensitive to change than CEAP alone
AVVQQUALITY OF LIFE	Aberdeen Varicose Vein Questionnaire	Patient-Reported QoL	Disease-specific patient-reported outcome measure; 13 items covering pain, ankle swelling, cosmesis, itching, support stocking use, and interference with daily activities; score 0–100 (higher = worse); commonly used in clinical trials for varicose vein interventions
CIVIQQUALITY OF LIFE	Chronic Venous Insufficiency Questionnaire	Psychosocial QoL	20-item (CIVIQ-2) patient-reported questionnaire covering pain, physical, social and psychological domains; score 20–100 (lower = better); designed for chronic venous insufficiency from C2 upward; validated in multiple languages across international trials
rVCSSREVISED SEVERITY	Revised Venous Clinical Severity Score	Revised Clinical Score	Updated 2010 version of VCSS with refined pain descriptors, standardised compression category, and modified ulcer scoring; recommended by American Venous Forum as preferred objective severity measure alongside CEAP in clinical research and outcomes reporting

⑥

Clinical Pearls, Pitfalls & Special Considerations Key points for accurate CEAP assignment and safe clinical application in practice

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Type	Topic	Detail
Pearl	CEAP is Descriptive, Not Prognostic	CEAP classifies the current state of chronic venous disease; it does not predict progression, guide treatment directly, or assess treatment response over time. Use VCSS/rVCSS alongside CEAP for longitudinal outcome tracking.
Pearl	Both Limbs Assessed Separately	CEAP classification is applied independently to each limb. A patient may have C2,s Ep As Pr in the right leg and C4b,s Es Ad Po in the left leg. Report each limb separately; do not combine or average bilateral findings.
Pearl	Suffix (s) and (a) Matter	The symptomatic (s) and asymptomatic (a) suffixes should always be recorded. C2,s indicates varicose veins with symptoms (pain, heaviness, cramps); C2,a indicates asymptomatic varices. This distinction influences treatment urgency and commissioning eligibility.
Caution	May-Thurner Syndrome	Extrinsic compression of the left common iliac vein by the right common iliac artery (May-Thurner) can cause secondary CVD (Es) with obstruction (Po) in the left iliofemoral system (Ad). Standard duplex may miss this — IVUS or cross-sectional imaging is required for diagnosis.
Caution	Pelvic Congestion Syndrome	Pelvic venous insufficiency may manifest as perineal, vulval or posterior thigh varicosities with or without pelvic pain. Standard CEAP assessment may be incomplete without pelvic duplex or CT/MR venography. Classify the visible lower limb findings plus document pelvic origin (Es, Ad).
Pitfall	Confusing C3 with Non-Venous Oedema	C3 requires oedema to be of venous origin. Bilateral pitting oedema due to cardiac failure, hypoalbuminaemia, hypothyroidism or calcium channel blockers must be excluded. Venous oedema is characteristically unilateral, peri-malleolar, worsens with dependency, and improves with elevation and compression.
Pitfall	Atrophie Blanche vs Ulcer	Atrophie blanche (white, stellate, porcelain-like avascular scars surrounded by pigmentation and telangiectasias) is classified as C4b — not C5 or C6. It represents healed microvascular ischaemia and is not a healed ulcer per CEAP definition, though it indicates high ulcer risk.
Limitation	CEAP Does Not Grade Ulcer Size/Duration	All active venous ulcers are C6 regardless of size, duration or number. A 1mm ulcer and a circumferential 15cm ulcer are both C6. Use VCSS ulcer subscores or MEASURE wound assessment tools to document ulcer dimensions and monitor healing progress.