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Clinicians caring for a patient with venous problems review the history regarding onset and duration of symptoms and the presence of relevant medical history. On the physical exam, he or she will focus on extent of varicose veins and changes in the skin. In addition, there will be a review of the results of ultrasound or phlebogram for the presence of venous reflux or blood clot. The “CEAP” classification expresses these components of evaluation in a standardized system.

First described in 1994 by the International Consensus Committee on Chronic Venous disease, the CEAP system was revised in 2004 and again in 2012 to better reflect a more practical clinically approach [1]. While CEAP (pronounced “see AP”) may sound complex, in reality it is quite simple especially if one follows the mnemonics of the “CEAP” name. The conceptual format becomes easily adapted when one begins each evaluation with the table of CEAP classification handy for referral.

When specifically describing CEAP classification, the first letter C stands for “Clinical signs” from telangiectasia to venous ulcers and covers intermediate stages of varicose veins, leg edema and skin discoloration.

The second letter, E, refers to “Etiology” either proven or suspected and includes three groups of patients: (1) First are those who were born with venous anomalies—malformations, genetic disorders, etc.; (2) The second grouping encompasses probably the most common presentation of primary venous disorders due to “idiopathic” valvular disease and presence of reflux; and (3) Those with a history of valves damaged by trauma or clot form the last group in this category.

The letter A stands for “Anatomy” and depicts the location of veins affected by the pathology. It includes the superficial, perforating, and deep venous systems of lower extremity following the classic anatomic description of these structures (e.g., “common femoral vein,” “proximal ankle perforator vein,” “small saphenous vein”).

Finally, the letter P stands for “Pathology.” It simply deals with the etiology of obstruction leading to venous hypertension that develops below the lesion. In this grouping, two options are included: (1) the presence of valvular insufficiency leading to “physiologic” venous reflux or (2) the presence of the thrombus creating mechanical obstruction of venous return.


  • C0. No signs of venous disease by appearance or palpation

  • C1. Telangiectasias or reticular veins

  • C2. Varicose veins

  • C3. Edema

  • C4. Skin changes of venous disease

  • C4a. Pigmentation or eczema

  • C4b. Lipodermatosclerosis or atrophie blanche

  • C5. Healed venous ulcer

  • C6. Active venous ulcer

  • S. Symptoms: pain, tightness, aching, skin irritation, heaviness, muscle cramps and other symptoms attributable to venous disease

  • A. Symptomatic

  • Ec. Congenital

  • Ep. Primary

  • Es. Secondary (postthrombotic)

  • En. No venous cause identified

  • As. Superficial ...

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