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40 Classification and etiology of chronic venousdisease
https://t.me/med1917
natural history of the disease process. By interval CEAP
examination, the longitudinal changes that occur over time
or aer interventions can be documented.
is classication addressed the considerations imposed
by modern diagnostic and treatment capabilities. It was
incorporated into the updated Reporting Standards for
Venous Disease in 19952 and became known as the CEAP
classication. Its acceptance has been promulgated by
venous authorities around the world, and it has been published in most native languages. is worldwide dissemination addresses the need for a universal classication system
that enables accurate communication between institutions
and countries regarding the details of CVD and the results
of dierent forms of treatment.
e CEAP classication was originally intended to be
a dynamic document that could be amended in the future
in light of experience with its usage. Several evaluations of
the clinical categories3 and of the appended scoring systems4 based upon CEAP have been published,
5–7
and provide both validity to and critique of their content. Aer the
rst 10 years of clinical usage, CEAP’s validity and usefulness underwent its rst critical review in 2004 in order to
make needed revisions by a new international subcommittee of the American Venous Forum, chaired by Professor
Bo Eklöf. In this revision,8 the fundamental structure of
the CEAP categories was armed and retained; additions
to the classication included specic denitions of terms,
clarication of details within the C class, and improvements
in the methods of recording the ndings in order to render
the classication more complete in its long form and more
user friendly in its short form. is chapter will present the
approved revised format of CEAP, and will examine the
fundamental importance of dening the etiologic basis of
the clinical problem.
4.2 “REVISED” CEAP DOCUMENT
8
e CEAP classication divides CVD into its component
parts of clinical manifestations, etiologic basis for the disease, anatomic distribution of the disease, and pathophysiologic mechanism operating in the venous segments aected
by the disease. Each of these elements of CVD is specically
dened within the classication in order to achieve uniform
reporting wherever the classication is used, and thereby
enable inter-institutional communication regarding similar
problems throughout the world. It is important to understand that the classication is a time-specic qualitative
assessment of the disease process, which requires interval
updating for follow-up assessment of the individual case or
for longitudinal studies that track the natural history of a
disease entity.
e contents of the revised tables follow:
C (Table 4.1): the clinical classication is divided into
seven classes of progressive severity ranging from C0,
representing no diagnosable venous disease, through to
telangiectasias/reticular veins, varicose veins, venous
Table 4.1 Clinical classification
Classification Description
C0 No visible or palpable signs of venous
disease
C1 Telangiectasias or reticular veins
C2 Varicose veins
C3 Edema
C4a Pigmentation and/or eczema
C4b Lipodermatosclerosis and/or atrophie
blanche
C5 Healed venous ulcer
C6 Active venous ulcer
S Symptoms including ache, pain, tightness,
skin irritation, heaviness, and muscle
cramps, as well as other complaints
attributable to venous dysfunction
A Asymptomatic
edema, mild and severe skin changes, and venous ulcer,
divided into healed ulcer and active ulcer categories.
e clinical category is amended by a notation to indicate whether the diagnosed abnormalities were accompanied by symptoms (s) or were asymptomatic (a). is
ordering of the severity of the clinical manifestations
was proposed in the initial report of the CEAP classication, and has been retained in validity studies of
disease severity scoring.
4,5
E (Table 4.2): the etiologic classication is divided into
three classes of congenital, primary, and secondary
categories, and a new designation to indicate instances
in which no etiologic basis could be determined
(En). Congenital disease refers to named, recognized
problems, where the vessels themselves are deformed
from birth, such as the Klippel–Trenaunay deformity.
Primary disease refers to cases with degeneration of
elements of the normally formed vein wall with valvular reux, typied by varicose veins. Secondary disease
refers to acquired deformities of the veins in which
elements of obstruction and reux oen coexist, as in
post-thrombotic veins.
A (Table 4.3): the anatomic classication is divided into
three categories to denote supercial, perforator, and
deep vein involvement, and a new category to indicate
that no anatomical category could be determined (An).
is simple anatomical classication is supplemented
by 18 named segments (Table 4.4) of the veins from the
infra-diaphragmatic inferior vena cava to the crural
Classification Description
Ec Congenital
Ep Primary
Es Secondary (post-thrombotic)
En No venous etiology identified
4.3 Terminology and new definitions 41
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Table 4.3 Anatomic classification
Classification Description
As Superficial veins
Ap Perforating veins
Ad Deep veins
An No venous location identified
veins, which are used in the following section to locate
the segments of reux and obstruction.
P (Table 4.5): the pathophysiologic classication is divided
into two categories of reux and obstruction, and
a third category when elements of both reux and
obstruction coexist. A new category (Pn) is added in the
revised format to indicate that no determination was
made for reux and obstruction.
When reux and/or obstruction are found, the anatomic
segments aicted with each problem are identied by using
the 18 designated segments described under anatomic classication (Table 4.4).
It is recognized that post-thrombotic disease is a dynamic
process in which elements of obstruction become altered by
the process of recanalization and maturation of the thrombus to yield a variable mix of reux and obstruction in the
Table 4.4 Venous anatomic segment classification
Classification Description
Superficial veins
1 Telangiectasias/reticular veins
2 Greater saphenous vein above knee
3 Greater saphenous vein below knee
4 Small saphenous vein
5 Non-saphenous veins
Deep veins
6 Inferior vena cava
7 Common iliac vein
8 Internal iliac vein
9 External iliac vein
10 Pelvic: gonadal, broad ligament
veins, other
11 Common femoral vein
12 Deep femoral vein
13 Femoral vein
14 Popliteal vein
15 Crural veins: anterior tibial, posterior
tibial, peroneal veins (all paired)
16 Muscular veins: gastrocnemius,
soleal, other
Perforating veins
17 Thigh perforator veins
18 Calf perforator veins
Table 4.5 Pathophysiologic classification
Classification Description
Pr Reflux
Po Obstruction
Pr,o Reflux and obstruction
Pn No venous pathophysiology identifiable
later stages. is evolution of post-thrombotic changes may
present as reux, obstruction, or a mixture of both; the CEAP
system allows for segment-by-segment classication of these
ndings at the time of the examination. Serial examinations
can be used to catalogue the dynamic changes of reux and
obstruction that occur in the specic case over time.
4.3 TERMINOLOGY AND NEW
DEFINITIONS
e CEAP classication deals with all forms of chronic
venousdisorders. e term “chronic venous disorder” includes
the full spectrum of morphological and functional abnormalities of the venous system, from telangiectasias to venous
ulcers. Some of these, like telangiectasias, are highly prevalent in the normal adult population, and in many cases the
use of the term “disease” is not appropriate. Aer the revision
of CEAP in 2004, the VEIN-TERM transatlantic consensus
was organized in 2007 in order to update the terminology of
chronic venous disorders under the auspices of the American
Venous Forum, the European Venous Forum (EVF), the
International Union of Phlebology, the American College
of Phlebology, and the International Union of Angiology.
e VEIN-TERM consensus was established to complement
terms previously dened in the revision of CEAP.
4.3.1 Definitions in the revision of CEAP
of2004
Telangiectasia: A conuence of dilated intradermal venules
of less than 1 mm in caliber. Synonyms include spider
veins, hyphen webs, and thread veins.
Reticular veins: Dilated bluish subdermal veins usually
from 1 mm to less than 3 mm in diameter. ey are
usually tortuous. is excludes normal visible veins in
people with thin, transparent skin. Synonyms include
blue veins, subdermal varices, and venulectasias.
Varicose veins: Subcutaneous dilated veins equal to or more
than 3 mm in diameter measured in the upright position. ese may involve saphenous veins, saphenous tributaries, or non-saphenous supercial leg veins. Varicose
veins are usually tortuous, but tubular saphenous veins
with demonstrated reux may be classied as varicose
veins. Synonyms include varix, varices, and varicosities.
Corona phlebectatica: A fan-shaped pattern of numerous
small intradermal veins on the medial or lateral aspects
of the ankle and foot. is is commonly thought to be
an early sign of advanced venous disease. Synonyms
include malleolar are and ankle are.
8
42 Classification and etiology of chronic venousdisease
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Edema: A perceptible increase in the volume of uid in the
skin and subcutaneous tissue, which characteristically
indents with manual pressure. Venous edema refers to
edema in the leg, ankle, or foot associated with identiable reux or obstruction in the veins appropriate to the
site of swelling. It usually occurs in the ankle region, but
it may extend to the leg and foot.
Pigmentation: A brownish darkening of the skin resulting
from extravasated blood, which usually occurs in the
ankle region, but may extend to the leg and foot.
Eczema: An erythematous dermatitis, which may progress
to a blistering, weeping, or scaling eruption of the skin
of the leg. It is most oen located near varicose veins,
but may be located anywhere in the leg. Eczema is usually seen in uncontrolled CVD, but may reect sensitization to local therapy.
Lipodermatosclerosis (LDS): Localized chronic inammation
and brosis of the skin and subcutaneous tissues of the
lower leg, sometimes associated with scarring or contracture of the Achilles tendon. LDS is sometimes preceded
by diuse inammatory edema of the skin that may be
painful and is oen referred to as hypodermitis. is
condition must be distinguished from lymphangitis, erysipelas, or cellulitis by its characteristically dierent local
signs and systemic features. LDS is a sign of severe CVD.
Atrophie blanche or white atrophy: Localized, oen circular
whitish and atrophic skin areas surrounded by dilated
capillaries and sometimes hyperpigmentation. is nding is a sign of severe CVD and not to be confused with
healed ulcer scars. Scars of healed ulceration may also
have atrophic skin with pigmentary changes, but are distinguishable by history of ulceration and appearance from
atrophie blanche and are excluded from this denition.
Venous ulcer: Full-thickness defect of the skin, most
frequently in the ankle region, which fails to heal
spontaneously and is sustained by CVD. Dened by
Guidelines for Management of Venous Leg Ulcers as “an
open skin lesion of the leg or foot that occurs in an area
aected by venous hypertension.”
9
4.3.2 Added definitions in the VEIN-TERM
consensus of 2007
4.3.2.1 CLINICAL VENOUS TERMS
Chronic venous disease: Morphological and functional
abnormalities of the venous system of long duration
manifested either by symptoms and/or signs indicating
the need for investigation and/or care.
Chronic venous insuciency (C3–C6): A term reserved for
advanced CVD, which is applied to functional abnormalities of the venous system producing edema, skin
changes, or venous ulcers.
Venous symptoms: Complaints related to venous disease,
which may include tingling, aching, burning, pain,
muscle cramps, swelling, sensations of throbbing or
heaviness, itching skin, restless legs, leg tiredness, and/
or fatigue. Although not pathognomonic, these may be
10
suggestive of CVD, particularly if they are exacerbated
by heat or dependency in the day’s course, and may be
relieved with leg rest and/or elevation. Existing venous
signs and/or laboratory evidence are crucial in associating these symptoms with CVD. However, symptoms
without signs (C0s) are common problems. A consensus
committee on venous symptoms has been organized by
the EVF, and the report should be available in 2016.
Venous signs: Visible manifestations of venous disorders,
which include dilated veins (telangiectasias, reticular
veins, and varicose veins), leg edema, skin changes, and
ulcers, as included in the CEAP classication.
Recurrent varices: Reappearance of varicose veins in an
area previously treated successfully.
Residual varices: Varicose veins remaining aer treatment.
PREVA I T: is acronym stands for presence of varices
(residual or recurrent) aer intervention.
Post-thrombotic syndrome: Chronic venous symptoms and/
or signs secondary to deep vein thrombosis (DVT) and
its sequelae.
Pelvic congestion syndrome: Chronic symptoms which may
include pelvic pain, perineal heaviness, urgency of micturition, and post-coital pain, caused by ovarian and/or
pelvic vein reux and/or obstruction, and which may be
associated with vulvar, perineal, and/or lower leg varices.
Varicocele: Presence of scrotal varicose veins.
Venous aneurysm: Localized saccular or fusiform dilata-
tion of a venous segment with a caliber of at least 50%
greater than the normal trunk.
4.3.2.2 PHYSIOLOGICAL VENOUS TERMS
Venous valvular incompetence: Venous valve dysfunction
resulting in the retrograde venous ow of an abnormal
duration.
Venous reux: Retrograde venous ow of abnormal dura-
tion in any venous segment.
●
Primary: Caused by idiopathic venous valve
dysfunction
●
Secondary: Caused by thrombosis, trauma, or
mechanical, thermal, or chemical etiologies
●
Congenital: Caused by the absence or abnormal
development of venous valves
Axial reux: Uninterrupted retrograde venous ow from
the groin to the calf.
●
Supercial: Conned to the supercial venous system
●
Deep: Conned to the deep venous system
●
Combined: Involving any combination of the three
venous systems (supercial, deep, and perforating)
Segmental reux: Localized retrograde ow in venous seg-
ments of any of the three venous systems (supercial,
deep, and perforating) in any combination in the thigh
and/or calf, but not in continuity from the groin to the
calf. Explanation: the now-recognized signicance of
11
axial reux in the pathophysiology of venous ulcers
justied the distinctions made in order to clarify the denitions of dierent types of lower extremity venous reux
with axial reux, dened as uninterrupted retrograde
4.4 Writing of the CEAP 43
C2 4b S Ep Asp Pr2 3 18.,;;,;,,−
C2 4b S Ep Asp Pr2 3 18.,;;,;,,−
C4bS Ep As p Pr.− ;;,;
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venous ow from the groin to the calf in continuity. It
was accepted that axial reux might be conned to the
supercial or deep systems, but could also involve any
combination of the supercial, deep, and perforator systems. is is in contrast to “segmental reux,” dened as
localized retrograde ow in any of the three venous systems, but without continuity from the groin to the calf.
Perforator incompetence: Perforating veins with outward
ow of abnormal duration.
Neovascularization: Presence of multiple new small, tortu-
ous veins in anatomic proximity to a previous venous
intervention.
Venous occlusion: Total obliteration of the venous lumen.
Venous obstruction: Partial or total blockage to venous ow.
Venous compression: Narrowing or occlusion of the venous
lumen as a result of extra-luminal pressure.
Recanalization: Development of a new lumen in a previ-
ously obstructed vein.
Iliac vein obstruction syndrome: Venous symptoms and
signs caused by narrowing or occlusion of the common
or external iliac vein.
May–urner syndrome: Venous symptoms and signs
caused by obstruction of the le common iliac vein due
to external compression at its crossing posterior to the
right common iliac artery.
4.4 WRITING OF THE CEAP
e method of recording the CEAP classication is important. When this was addressed in the 2004 revised CEAP,
a simplied “basic CEAP” was added to the original “full
CEAP” method of recording. e revised format8 includes
three basic elements to be included in the CEAP recording:
1. e CEAP ndings
2. Date of the examination
3. Diagnostic “level” of the examination:
a. Level 1: History, physical, and Doppler examination
(hand-held)
b. Level 2: Noninvasive: duplex scan and
plethysmography
c. Level 3: Invasive: venography, venous pressure,
intravascular ultrasound (IVUS), spiral computed
tomography (CT), and magnetic resonance venography (MRV)
4.4.1 Full CEAP
e full (advanced) CEAP classication system is essential
for standardized reporting in scientic journals and for the
researcher. It enables grouping of patients so that similar
types of patients can be analyzed together for the study of
both group and sub-group elements of C, E, A, and P. is
complete classication, for example, enables any of the 18
named venous segments to be identied as the location of
venous pathology. Consider a patient with pain, varicose
veins, and LDS, where duplex scan conrms primary reux
of the greater saphenous vein (GSV) and incompetent perforators in the calf. e classication here would be:
4.4.2 Basic CEAP
is format provides simplications of the full format for
more informal usage. It is meant to replace the habit of
simply using the highest clinical class to denote the venous
problem, a practice discouraged as being too incomplete.
Basic CEAP applies two simplications:
1. e single highest descriptor can be used for clinical
classication. For example, a patient with varicose veins,
swelling, and LDS would be C4b (as opposed to the full
CEAP format of C2,3,4b).
2. e anatomic segments are deleted. For example, the
full CEAP format of:
would be simplied to:
Venous disease is oen considered to be a simple
problem undeserving of a multi-categorized classication
format. e truth is that venous disease is not so simple,
and it demands well-dened categorical descriptions in
order to be understood. In modern phlebological practice,
the majority of patients should have a duplex scan of the
leg veins in order to diagnose the E, A, and P categories
ofthe CEAP classication. is examination is in contrast
to an ultrasound survey of the limb for DVT and supercial
venous thrombosis (SVT).
4.4.3 Identifying the date and method
ofexamination
CEAP is not a static classication; it can be altered by factors
such as a corrective treatment or a more denitive test, or
simply the eect of the passage of time on the natural evolution of the disease process. For this reason, the date and the
method of testing (Doppler, duplex scan, venography, etc.)
used for a particular classication should be recorded.
Method of investigation: the accuracy of the diagnosis
increases with the addition of imaging and invasive testing
in CVD. ree “levels” of testing are outlined:
Level 1: e oce visit with history and clinical examina-
tion, which may include use of a hand-held Doppler.
Level 2: e noninvasive vascular laboratory, which
includes duplex color scanning and plethysmography.
Level 3: Tnvasive investigations or more complex imag-
ing studies, including varicography, ascending and
descending venography, venous pressure measurements,
IVUS, spiral CT scan, or MRV.
44 Classification and etiology of chronic venousdisease
C2 34b6 S Ep Aspd Pr2318 13 14 (L2 52 2 15).,, ,;;,,; ,, ,, ;/ /− 00
C6 S Ep Aspd Pr (L2 5 2215).− ;;,,;. ;/ /00
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4.4.4 Recording of the date and method
is entire paragraph is presented in CEAP as follows:
used can be added in parentheses
●
after the CEAP recording as follows
Classication according to full CEAP:
Basic form: C4b–S; Ep; As,p; Pr (Level 2; 8/21/2015)
Full form: C2,4b–S; Ep; As,p; Pr2,3,18. (Level 2; 8/21/2015)
●
Classication according to basic CEAP:
4.5 CLINICAL APPLICATION OF CEAP
Example I (Figure 4.1 and Table 4.6): a patient presents with
painful swelling of the leg and varicose veins, LDS, and active
ulceration. Duplex scanning on May 17, 2015, showed axial
reux of the GSV above and below the knee, incompetent
calf perforators, and axial reux in the femoral and popliteal
veins. ere were no signs of post-thrombotic obstruction.
(a) (b) (c)
Example II (Figure 4.1 and Table 4.6): six patients pres-
ent with severe skin changes typical of advanced C4–C6
changes. From inspection alone, the clinical class of C4–C6
venous disease would be diagnosed, and many physicians
would assume that all of these are due to post-thrombotic
(d) (e) (f )
Figure 4.1 Six cases of ulceration. (a) Isolated perforator reflux, (b) GSV and perforator reflux, (c) GSV reflux, (d) no venous
disease, (e) post-thrombotic reflux: deep and superficial, and (f) primary reflux: deep, perforator, and GSV.
4.7 Comparison of primary and secondary CVD 45
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Table 4.6 CEAP classification and diagnosis of six patients
with leg ulcers (Figure 4.1)
Case CEAP
1 Isolated perforator reflux C2,3,4b,6,-s; Ep; As,p; Pr18
2 Greater and perforator
reflux
3 GSV reflux C2,3,4b,6,-s; Ep; As,p; Pr2,3
4 No venous disease C3,4b,6,-s;En; An; Pn
5 Post-thrombotic reflux:
deep and perforating
6 Primary reflux: deep,
perforating, and GSV
C2,3,4b,6,-s; Ep; As,p;
Pr2,3,18
C2,3,4b,6,-s; Es; As,p,d;
Pr2,3,11,13,14,15,18
C2,3,4b,6,-s; Ep; As,p,d;
Pr2,3,11,13,14,15,18
disease. Aer full investigation, six dierent diagnoses
emerged (Table 4.6).
ese cases illustrate that the full CEAP classication is
needed to identify the actual entity behind similar-appearing clinical conditions. e clinical class is C4–C6 in all six
cases, but the details of E, A, and P vary widely. Treatment
of these cases could range from simple ablation of the GSV
or perforator veins for cases 1, 2, and 3, through to the
potential for extensive deep vein reconstruction in cases 5
and 6, to no venous treatment at all for case 4.
4.6 IMPORTANCE OF DEFINING
ETIOLOGY
Knowledge of the etiologic basis of the CVD process is fundamental to understanding the clinical progress and treatment of the disease. e three categories within etiology are
entirely dierent in that the congenital cases represent malformation of the blood vessels, the primary cases represent
a degenerative process in the normally formed vessel walls
and valves, and the secondary cases represent an acquired
inammatory destructive process which incorporates
destructive and reparative elements in its disease progression. Congenital cases are distinctive and relatively rare and
are not further detailed in this discussion.
when he recognized, using descending venography for
diagnosis, that 58% of his cases of advanced venous insufciency were due to non-post-thrombotic disease.12 With
the later development of noninvasive imaging through
ultrasound to correctly diagnose reux and its apparent
etiologic basis, the current standard of practice should
be accuracy in diagnosis and specicity in treatment for
chronic venous conditions. Knowledge of the natural history of the clinical problem provides a guide to preventive
therapies, such as anticoagulation, or targeted sites for corrective surgery, and is essential if progress is to be made
in the interventional management of chronic venous disorders. Consideration of the dierences between PVI and
SVI follows (Tables 4.6 and 4.7).
4.7.1 Primary venous insufficiency
PVI is a degenerative condition of the venous walls and
valves. It usua lly begins as mi ld reux in the supercial veins
of the lower extremity.13 In early stages, veins retain their
fundamental elements of valves and intima. e supercial
and perforator veins that are aected early are expendable
because of their location and function. esole pathophysiologic process in PVI is reux. e condition is widespread
in the population (20%–30% of the adult population
and signicantly more prevalent than post-thrombotic disease. e distribution of the aected veins in PVI begins
in supercial veins of the lower extremity and progresses
to involve perforator and ultimately deep veins in more
advanced cases. Progression of PVI in the supercial veins
can be tracked by using the anatomic elements of the full
CEAP classication, which detail the patency and competence of all of the venous segments. Consecutive recording
of these details over time details the progression of reux
and obstruction in additional segments of the leg veins.
Reux advances longitudinally up and down the extremity
with the passage of time until it becomes axial. At this stage,
Table 4.7 Comparative features of primary versus
post-thrombotic disease
14,1 5
)
4.7 COMPARISON OF PRIMARY AND
SECONDARY CVD
In primary and secondary CVD, the natural history and
the treatment alternatives have major dierences, but
the clinical manifestations can be similar to the point of
being indistinguishable (Figure 4.1). For too long, it has
been accepted that the dierence between primary venous
insuciency (PVI) and post-thrombotic secondary venous
insuciency (SVI) disease is of little relevance, since practical treatment of the two conditions is largely limited to
providing external support for the duration of active life.
An early report of the striking clinical similarities and the
marked pathological dierences between primary and secondary disease was beautifully described by Bauer in 1948
Primary venous
insufficiency
Degenerative Acquired (inflammatory)
Reflux only Obstruction–reflux
Intima retained Intima destroyed
Valves stretched and
atrophied
Primarily superficial veins Primarily deep veins
Widespread occurrence Limited occurrence
Slow progress to C4–C6
of decades
Treatment: support and
superficial surgery
Early surgery for quality
of life
Secondary venous
insufficiency
Valves scarred and destroyed
Faster to C4–C6 of years
Treatment: anticoagulant and
support
Late surgery for C4–C6
complications
46 Classification and etiology of chronic venousdisease
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continuous reux may develop from the groin or upper
thigh level to the lower calf or ankle level. Investigators have
long been impressed with the importance of axial reux in
cases of PVI that have progressed to the advanced stages of
11,14,16,17
CVI.
Deep vein reux is a late development in PVI; it is seen in
fewer than 10% of early C1–C2 cases compared to about 70%
of advanced (ulcerative) PVI cases in some series.18 Large
demographic studies of CVI demonstrate a preponderance
of PVI over SVI as the etiology of the venous stasis syndrome and venous leg ulcers.
14,17
Smaller studies of venous
ulcers have reported variable percentages of PVI versus SVI,
reecting the fact that either can cause ulceration.
18,19
In its milder forms (CEAP C2), PVI aects >20% of
the total adult population from 18 to 80 years of age, but
the incidence rises to 50% of those from 50 to 70 years
20–23
of age.
With the advent of large-scale imaging studies to track the natural history of PVI, there is clear evidence that it is a slowly progressive disorder which may
advance to C4–C6 manifestations over time.
23,24–26
e frequency of its progression from clinical class 2 through to 6
remains under investigation,24 although evidence is accumulating that the occurrence of progression is predictable
in a high percentage of PVI cases. For those aicted with
early-stage PVI, the risk of advancing to ulceration rises
as the individual progresses from C2 through to C4. is
risk appears to rise to the range of 20%–40% for those with
progressive changes.
14,16,17
In its far-advanced presentation,
when it aects the deep veins, primary disease can be as
devastating as late post-thrombotic disease, but the medical and surgical treatment considerations are distinctly
dierent.
27–29
Medical management of primary disease is limited to
external support or limitation of activity. Drug treatment of
symptomatic venous disorders is popular in Europe, but not
recommended in the United States. Surgical management
in primary disease varies from ablation of the oending
segments of the supercial and perforator veins in the early
stages to denitive repair of deep valve reux in late stages.
e results of denitive surgical treatment have been found
to be long-lasting in 70%–90% of supercial and perforator cases
30–32
and 70% of deep vein valve repairs.
28,29,33,34
e
very-long-term question relates to how many of these cases
are permanently rescued from progression to ulceration,
and how long the favorable course aer surgical repair
remains eective.
4.7.2 Secondary venous insufficiency
In contrast to primary disease, post-thrombotic secondary
disease is an acquired inammatory venous problem that
begins as a purely obstructive phenomenon and evolves
into a mixture of reux and obstruction in the deep veins.
It begins in supercial veins infrequently compared to its
occurrence in deep veins.
vessel linings and contained valve structures in at least
35,36
Its eect is to interrupt the
half of the cases of proximal DVT in the lower extremity.
In the majority of cases, the obstructive process undergoes
recanalization of the obstructed lumina during the rst
6–12 months,37 and this process leads to a combination of
partial obstruction and variable degrees of reux in the diseased lumen due to synechiae, septae, and multi-channeled
lumina in the deep veins. e ultimate result is variable
destruction of venous valves, the development of collateral
pathways around persistent obstructions, and tendencies to
recurrent episodes of venous thrombosis.
35–37
None of these
events are seen in primary disease.
e dierences in pathologic development between primary and secondary post-thrombotic disease are outlined in
Table 4.7. Since a competent saphenous system can provide
compensating venous outow in cases where the deep system has a signicant obstructive element, the pre-existing
status of the saphenous veins is of importance in the future
course of DVT. When major DVT occurs in an individual
who has pre-existing primary reux of the saphenous veins,
the venous return from the extremity is exposed to the double jeopardy of both reux and obstruction, and the clinical
condition may deteriorate more rapidly.
For advanced stages of post-thrombotic reux and
obstruction, there are highly individualized surgical techniques for providing substitute valves,
erating the iliac vein
39,40
or shorter distal segments.41 Bypass
28,29,38
or for disoblit-
procedures are useful in secondary disease on a highly
selective basis (e.g., short segment bypass with endophlebectomy),41 while they have no role in primary disease,
since there is no obstructive component except in the iliac
vein syndrome, where angioplasty and stenting is now the
treatment of choice. Various forms of valve substitution33
or autogenous valve reconstruction38 have been successful,
although they require major surgery and can be attended by
a signicant rate of recurrent disease. Repair of valves that
were not deformed by the thrombotic process can be very
successful.
39,40
ing
28,33,34
Recent experience with endovenous stent-
has been highly successful in the iliac veins for both
PVI (iliac vein syndrome) and SVI (post-thrombotic webs
or obstruction).
4.7.3 Influence of knowledge of etiology on
the management in CVD
Clinical similarities between primary and secondary disease
lead to confusion regarding the natural history and proper
treatment of the clinical problem. ese similarities include:
1. Both etiologies aect the veins in the beginning and
cause similar complications in the skin in their later
stages.
2. Both etiologies are attended by swelling and aching in
the legs.
3. e clinical sequelae that cause late suering and
disability in CVD are largely due to similar skin and
subcutaneous tissue complications in both entities. is
4.8 Conclusions 47
https://t.me/med1917
explains why the estimation of disease etiology based
upon clinical examination of the skin is unreliable.
4. External support leads to clinical improvement in both
etiologies, since it clearly helps to control swelling, and
this is crucial to the health of the extremity. e support
appears to act by improving the micro-circulation in
the supercial tissues, but it is yet to be demonstrated
whether it materially improves venous ow.
42,43
Given the great dierences in the disease process between
primary and post-thrombotic etiologies, important advantages in case management accrue from classication systems that dierentiate these two entities in terms of:
1. e ability to dene the natural history of the disease
process in terms of complications and length of time to
development of complications (i.e., 2–10 years in secondary disease and 5 years to lifetime in primary disease).
2. e realization that the major involvement is of super-
cial veins in primary cases versus deep veins in secondary post-thrombotic cases.
3. e appreciation that early proximal thrombus removal
and anticoagulation are key to the successful prevention
of post-thrombotic secondary disease and have no role
in primary disease.
4. e usefulness of specic surgical treatment
alternatives:
a. Saphenous vein ablation is essential to the manage-
ment of primary disease and usually not needed or
advisable in secondary disease.
b. e results of direct deep vein valve repair are supe-
rior in primary disease. In post-thrombotic disease,
newer techniques of neo-valve reconstruction are
favorably reported and undergoing validation studies. Attempts to create neo-valves and valve substitutes are underway. At present, there are cases of
post-thrombotic disease where valve reconstruction
is not yet feasible.
c. Other forms of deep vein reconstruction are selec-
tively useful in secondary disease and play no or
little role in primary disease below the iliac level,
since PVI has no obstructive component.
4.7.4 Influence of knowledge of anatomical
and pathophysiologic classifications
on the management of CVD
Knowledge of the anatomic and physiologic details is fundamental to understanding the clinical progress and management options in both PVI and SVI. It is within these
details that opportunities for the surgical correction of all
disease components (reux and obstruction) can be developed. In addition, the natural course of progressive venous
reux and obstructive phenomena is played out in the segments of the venous tree. For instance, there are no valves in
the inferior vena cava and the common iliac veins, so reux
does not play a role in these segments. Likewise, obstructions are not of clinical relevance in pelvic veins other than
the iliac veins or in distal tibial veins, since there are many
opportunities for collateral circulation in these areas.
e progressive involvement of the supercial veins of the
leg is important in PVI. e development of axial reux in
the supercial veins is a key pathway leading to progression
in the severity of disease reected by clinical classes, and the
progression of PVI from the involvement of the supercial to
the perforator veins and ultimately to the deep veins, appears
to be important in the development of venous leg ulcers.
ese changes are readily identied by segmental recording
of the reux and obstruction within the full CEAP classication. Longitudinal studies of these pathways leads to a
better understanding of the progression of PVI. Such studies
can identify anatomic segments in the supercial, perforator, and deep veins that constitute the course of axial reux
from the upper thigh to the ankle, as well as determine the
segments to be addressed by the surgeon during ablation
procedures in order to treat or prevent venous ulcers.
ese are some of the reasons that the determination of
overall etiology with segmental anatomy and pathophysiology is fundamental to the management of CVD and needs
to be an integral part of classication. To make progress
possible in CVD management, clinical diagnosis has to be
complete and accurate, and the many variations of pathologic processes have to be organized in a manner that enables
the analysis of variables. e full CEAP system is the current
best approach for this ideal. In clinical practice, the basic
CEAP may be chosen as a simpler but adequate compromise.
4.8 CONCLUSIONS
●
e CEAP classication and its scoring systems have
been validated and critiqued by an international audi-
ence (3[1-B], 5[1-B], 6[1-B], 7[1-B]).
●
e principle weakness of the original CEAP classica-
tion was identied as being inadequate for the dieren-
tiation of clinical class C1 (telangiectasia and reticular
disease) (3[1-B]).
●
e revised CEAP classication retains the basic
formatand contains important revisions; it replaces
theoriginal format (8[1-B]).
●
It is necessary that the full CEAP presentation be
followed in chronic venous publications in order to
adequately describe the venous state (2[1-A], 3[1-B],
8[1-B]).
●
Primary disease is a slowly progressive degenerative
vein disorder that results in vein wall weakness,
producing pure valve reux, usually beginning in
supercial veins (22[1-B], 13[1-B], 12[1-B], 19[1-C]).
●
Post-thrombotic secondary disease is a more rapidly
progressive inammatory disease that results in vein
valve and wall distortion, producing combinations of
obstruction and reux, usually beginning in deep veins
(12[1-B], 35[1-B], 33[1-B]).
48 Classification and etiology of chronic venousdisease
https://t.me/med1917
Guidelines 1.3.0 of the American Venous Forum on the classification and etiology of chronic venous disease
Grade of
recommendation
(1: strong;
No. Guideline
1.3.1 We recommend using the CEAP (clinical class,
2:weak)
1 B
etiology, anatomy, and pathophysiology)
classification to describe chronic venous disorders.
The system has been validated.
1.3.2 We recommend using the basic CEAP classification to
1 B
aid clinical practice and the full CEAP classification
for clinical research.
1.3.3 We recommend distinguishing between primary and
1 B
secondary venous insufficiency, because the two
conditions distinctly differ in pathophysiology and
management.
Grade of
evidence (A: high
quality; B:
moderate quality;
C: low or very
low quality)
●
Primary and secondary post-thrombotic diseases
require identication in classication because of the
manifold dierences in their morphologic and physiologic eects and their clinical management (12[1-B],
35 [1-B], 27[1-B], 28[1-B], 30[1-B] 3 2[1-B]).
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