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34. Burnand KG , Clemenson G , Gaunt J , Browse NL . e e ect of sus-
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78 • BASIC CONSIDERATIONS
9 .
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MECHANISM AND EFFECTS OF
COMPRESSION THERAPY
Hugo Partsch
ompression therapy is a very e ective treatment
modality whose mechanisms are not yet fully
C
face pressure and sti ness.
sion device on a speci c skin area. Sti ness is de ned by the
increase of the interface pressure induced by the increase
of the circumference of a limb segment when muscles are
contracting.
understood.
e clinical e ects depend mainly on two factors, inter-
Interface pressure is the pressure exerted by a compres-
1
I N T E R F A C E P R E S S U R E
However, comparisons may also be problematic because the
given ranges are measured by di erent methods. ese facts
underline the necessity of in vivo pressure measurements on
the individual leg, at least in future clinical studies.
e unit for pressure is 1 Pascal (Pa), which is 1 Newton
(N) per square meter. In the medical eld, for example,
measuring blood pressure, the usual unit for pressure is the
weight of one cubic millimeter of mercury.
e pressure values in Table9.1 refer to the ankle region,
called the level B.Proximal measuring points on the legare:
•
B1, the point at which the Achilles tendon changes into
the calfmuscle
1
COMPRESSION HOSIERY
e pressure ranges given for compression hosiery are measured in the laboratories of the producers by determining
the force that is necessary to stretch the ankle part of the
stocking in transverse direction. e pressure values are calculated from the force-extension diagram of the elastic fabric, the so-called hysteresis curve, projected to a leg model
with de ned circular cross sections using Laplace’s law.
is formula describes the relationship between the interface pressure (P), which is directly proportional to the tension (T)of the bandage and inversely proportional to the
radius (R)of the curvature to which it is applied (P=T/R).
e proportion of stretch and force, which corresponds to
the steepness of the so-called slope in the hysteresis curve,
re ects the elasticity of the material of the stocking.
Several industrial measuring systems for obtaining hysteresis curves are used, such as the Hosy method, the Hatra
tester, the Instron method, the French ITF method, and
2
others.
ready-to-wear and custom stockings used in several countries. e range of compression pressures and the description
of these classes vary among di erent countries. erefore, it
is recommended to use the pressure range in mmHg rather
than compression classes for a better universal understanding.
Table9.1 gives a comparison of compression classes for
•
C, corresponding to the calf at its maximumgirth
•
D, just below the tibial tuberosity
•
E, over the patella
•
F, between KandE
•
G, 5cm below K in the upright position
•
H, at the greatest lateral trochanteric projections of the
buttock
•
K, at the center point of thecrotch
As the circumference of the leg progressively increases, a
compression gradient is produced, which is de ned by the
European prestandard as follows: for level B1, 70–100%;
for C and D, 50–80%; and for F or G, 20–40% for compression classIII and IV, 20–60% for the classes A–I, and
20–50% for classII.
C O M P R E S S I O N B A N D A G E S
e interface pressure of compression bandages depends on
the experience and the skill of the bandager and only rarely
is declared. For future trials it will be essential to measure
the interface pressure as a parameter characterizing the
“dosage” and hence the e cacy of the bandage.
79
Table9.1 COMPRESSION CLASSES OF COMPRESSION STOCKINGS USED IN SEVERAL COUNTRIES VALUES ARE
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MMHG, 1MMHG=1333HPA
COMPRESSION CLASS EU CEN64 USA UK BS 661265 FRANCE GERMANY66
A
I
II
III
IV
e values indicate the compression exerted by the hosiery at a hypothetical cylindricalankle
10–14 (light)
15–21 (mild)
23–32 (moderate)
34–46 (strong)
>49 (very strong)
15–20 (moderate)
20–30 (rm)
30–40 (extra rm)
40+
14–17 (light)
18–24 (medium)
25–35 (strong)
10–15
15–20
20–36
>36
18–21 (light)
23–32 (medium)
34–46 (strong)
>49 (very strong)
Several devices for measuring the interface pressure on
2,3
the individual leg have been described.
e pressure measured under static (resting) conditions is termed resting
pressure; that measured on the moving patient is known as
working pressure.
When pressure data are reported it is essential to indi-
cate the type and size of the transducer and the exact local-
4
ization on the extremity.
e ankle region, which is a reference point for stocking
manufacturers (B-segment), is not a suitable location for
reliable in vivo measurement because of the radius changes
varying widely due to the bony prominences and tendons
prevailing in this segment. is is the reason why some
reports of stocking pressures have given lower values from B
than from the more proximal segmentB1.
S T I F F N E S S
It has been shown that compression devices exerting the
same resting pressure have di erent hemodynamic e ects
on venous re ux and venous pumping function depending
5
on the elastic property of the material.
is can be characterized by the sti ness, which plays an important role
concerning the performance of a compression device during
standing and walking, and which can be measured invivo.
Sti ness is de ned by the increase of compression
per centimeter increase in the circumference of the leg,
expressed in hectopascals per centimeter and/or millime-
1
ters of mercury per centimeter.
Avery appropriate method
to measure a dynamic sti ness index during walking has
6
been described by a Dutch group.
However, this technique
requires sophisticated instrumentation and can be performed only in specialized laboratories.
We have proposed a very simple method that is able to
di erentiate inelastic from elastic material by measuring the
di erence between the standing pressure and the supine
pressure at the B1 region, which is the area where the tendinous part of the medial gastrocnemius muscle changes into
7
the muscular part.
e standing position is considered to
be a snapshot of the walking cycle. erefore pressure sensors also may be used that are not able to register continuous
pressure changes.
Especially when several textiles are combined in a multi-
layer bandage, the sti ness of the nal bandage will increase
2
because of the friction of the layers.
e same is true when
two compression stockings are donned over eachother.
Compared with in vivo measurements sti ness corre-
8
sponds to the slope of the hysteresis curve in vitro.
COMPRESSION MATERIAL
Based on the principles mentioned earlier, several textiles
used for compression therapy can be di erentiated (see
Table9.2).
PERFORMANCE OF
COMPRESSION MATERIALS
Elastic textiles exert pressure by being stretched. During
walking only small pressure peaks will occur, because the
elastic material gives way with every step. e working pressure is therefore not much higher than the resting pressure
(see Figure 9.1). Because of the retraction of the elastic
bers there is only a small reduction of interface pressure
in the sitting and lying position. Acontinuous high resting
Table9.2 COMPRESSION MATERIALS
ELASTIC, LONGSTRETCH MATERIAL INELASTIC, SHORTSTRETCH MATERIAL NONSTRETCH MATERIAL
Compression stockings
Long-stretch bandages
Extensibilty >100%
Low sti ness
Exerts pressure when applied with stretch
*Bandages consisting of several elastic components with an extensibility of the single layer >100% for example as the “four-layer bandage,” will become relatively
inelastic when applied in more layers and therefore may also be ranged into this category.
Short-stretch bandages
Multilayer short-stretch bandages*
Extensibility <100%*
Medium sti ness
Pressure increases when movement causes
calf muscle to contract
80 • BASIC CONSIDERATIONS
Zinc paste bandages, Unna boot
Velcro band devices (also short stretch)
Extensibility 0–10%
High sti ness
Pressure increases when movement causes
calf muscle to contract
90
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80
70
60
50
40
mmHg
30
20
10
0
Resting vs. Working Pressure
Elastic
Inelastic
applied with several elastic layers get similar elastic properties as short-stretch bandages.
Intermittent pneumatic compression o ers adjunctive
bene cial e ects, especially in patients with a restricted
walking ability. In addition to the decongestive e ect, an
increase of arterial ow and a release of vasoactive and anticoagulatory mediators from the endothelial cells have been
10,12
documented during the last few years.
Standing
Figure9.1 Interface pressure measured on the medial aspect of the leg
(B1) of an elastic and an inelastic bandage. Both bandages are rmly
applied and exert a pressure of 60mmHg immediately a er application
in the standing position. During walking much higher pressure peaks
are obtained with inelastic than with elastic material. When the patient
lies down and also a er 24 hours, elastic bandages show only a mild
reduction of pressure. e more intense pressure loss of the inelastic
material is the reason why these bandages also are tolerated during
nighttime, and why they should be renewed when getting tooloose.
Walking
Recumbent
After 24 h
pressure may cause unpleasant feelings during rest and is
strictly contraindicated in patients with arterial occlusive
disease. erefore elastic bandages and rm medical compression stockings should be removed over nighttime. e
main advantage of elastic material is that it can also be
handled by nonexperienced sta and even by the patients
t h em s e l v e s .
Short-stretch material and completely rigid devices
show a high working pressure with high peaks during walking that are able to occlude leg veins intermittently, thereby
9
reducing ambulatory venous hypertension.
During walking, nonyielding material will exert similar
e ects as intermittent pneumatic compression, especially
concerning the release of anti-in ammatory, anticoagulatory, and vasoactive mediators from the endothelial cells.
10
ese e ects are probably the reason for the fact that the
best healing rates of venous ulcers have been described with
11
multilayer high-pressure bandages.
A considerable fall
of pressure will occur when the patient lies down, so that
short-stretch bandages may better be tolerated in the resting
position. e pressure loss of up to 40% in the rst two hours
is caused by an immediate reduction of the limb volume
and should be taken into account by applying an inelastic
bandage with a much higher strength than an elastic bandage, which needs some experience. Due to the pressure fall,
inelastic bandages are well tolerated also during nighttime.
In patients with massive edema they should be reapplied
a er short periods of time in the initial phase when they
get loose. Later on they may be worn for one week and longer. In the presence of arterial occlusions inelastic bandages
should be applied with a very low resting pressure, which
should be adjusted to the systolic ankle pressure in order not
to interfere with the reduced arterial in ow. During movement there will be a massage of the limb, which may be compared with intermittent pneumatic compression. Bandages
THERAPY PHASE AND
MAINTENANCE PHASE OF
COMPRESSION THERAPY
In general, we prefer multilayer short-stretch or completely
nonelastic material for the therapy phase of severe stages of
chronic venous insu ciency like venous ulcers, for lymphedema, and also for acute phlebitis and deep vein thrombo-
13
When the leg ulcers are healed and when the extremity
sis.
is fairly free from edema, elastic material (preferably compression stockings) is used in order to maintain this condition (maintenance phase).
PHYSIOLOGICAL EFFECTS OF
COMPRESSION THERAPY
Some physiological e ects of compression therapy as documented in several studies are summarized in Table9.3.
e application of continuous compression is contraindicated in patients with advanced peripheral arterial disease
or severe sensory impairment.
Several e ects of compression therapy have been demonstrated in the acute experiment using intermittent pneumatic compression. It may be assumed that similar e ects
will also occur during walking with inelastic bandages.
TISSUE PRESSURE ANDEDEMA
By increasing the tissue pressure, compression works against
ltration, which is the most important mechanism to
Table9.3 EFFECTS OF COMPRESSION THERAPY
STOCKINGS AND BANDAGES
PARAMETERS EFFECT
Tissue pressure
Edema
Venous volume
Venous velocity
Blood shi into central compartments
Venous re uxes
Venous pump
Arterial ow
Microcirculation
Lymph drainage
Increase
Decrease
Decrease
Increase
Increase
Decrease
Improvement
Increase (intermittent
compression)
Improvement
Improvement
1,14
MECHANISM AND EFFECTS OF COMPRESSION THERAPY • 81
prevent or to remove edema. Occupational leg swelling in
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sitting and standing professions can be prevented by light
compression stockings, which are also able to reduce mild
15
edema.
Reduction in intradermal edema can be measured
with ultrasonography in patients with CVI and lipodermatosclerosis. Severe stages of limb swelling bene t more from
inelastic compression devices exerting higher pressure.
Compression may reveal bene cial e ects also in nonphlebological causes of edema like in ammatory edema
(arthritis, cellulitis), cardiac, dysproteinemic, renal edema,
2
lymphedema, and cyclic idiopathic edema.
VENOUS VOLUME AND VENOUS
BLOOD FLOW VELOCITY
Depending on the exerted pressure and the body position,
external compression is able to narrow or to occlude super-
16
cial and deep leg veins.
In the supine position an external pressure of
10–15mmHg is enough to decrease the venous diameter.
e resulting increase of blood ow velocity as clearly
17
shown by measuring the circulation time with isotopes
is
the rationale for recommending light compression stockings for thromboprophylaxis in bedridden patients.
Venous volume can be assessed using air-plethysmography
(APG), which shows a signi cantly more pronounced
reduction by inelastic than by elastic compression, even
5
when the resting pressure is thesame.
In the upright position elastic stockings will have only
a minor e ect on decreasing the diameter of the leg veins.
18
However, a very small decrease of venous diameter will result
in an overproportional decrease of the local blood volume
5,14
as demonstrated by several plethysmographic studies
BLOOD SHIFT INTO CENTRAL
COMPARTMENTS
Firm compression bandages applied on both lower extremities may redistribute blood toward the central parts of the
body. is can lead to an increase of the preload of the heart
by about 5% and should be avoided in patients with border-
19
line cardiac function.
DECREASE OF VENOUS REFLUXES
AND IMPROVEMENT OF THE
VENOUSPUMP
Using APG in patients with deep venous incompetence, it
could be shown that compression with increasing interface
pressure was associated with a decreasing amount of total
re ux measured by venous llingindex.
A statistically signi cant reduction of re uxes was
achieved with pressures over 30mmHg for inelastic and
5
over 40mmHg for elastic material.
e reduction of venous re uxes in patients with
chronic venous insu ciency by external compression
explains the improvement of the venous pumping function. Plethysmographic studies have shown an increasing
improvement of the venous pump with increasing stocking pressures, starting with an ankle pressure of around
9,20–23
20mmHg.
Higher compression pressure using sti material leads
to short phases of intermittent occlusion of the deep veins
with every step during muscle contraction. Such intermittent occlusions of deep veins on the leg can be visualized
16
by Duplex.
By encasing the veins in a rigid envelope
ambulatory venous hypertension may thereby be reduced
9
in patients with deep venous incompetence.
Similarly, a
progressively increasing pressure on the thigh by using a
blood pressure cu blown up to 40–80mmHg led to a progressively decreasing vein diameter and to an abolishment
of re ux when the femoral vein segment contained incom-
20
petent valves.
Reduction of venous re uxes and improvement of ambulatory venous hypertension by external cu
compression could be demonstrated even in patients without any valves (avalvulia). is e ect therefore cannot be
explained by the common explanation of a coaptation of
distended valve lea ets, but seems rather to be due to the
intermittent occlusion of the incompetent vein during
21
walking.
Con icting results have been reported concerning an
improvement of ambulatory venous hypertension by com-
2,9
pression stockings.
the pressure exerted by stockings is too low in order to su ciently compress the veins in the leg in the upright position.
is may be explained by the fact that
In addition, the elastic material gives way with every step,
whereas inelastic, short-stretch bandages with a double as
high resting pressure are able to achieve intermittently short
venous occlusions during muscle systole while walking. In
patients with severe stages of chronic venous insu ciency
a higher compression pressure is needed to improve the disturbed venous pumping function, whereas lower pressure is
22
su cient in simple varicose veins.
e key mechanism of compression therapy to reduce
ambulatory venous hypertension in patients with severe
chronic venous insu ciency is an intermittent occlusion of
the veins during walking.
In contrast, continuous obliteration of veins by external
compression may be desirable a er varicose vein surgery in
order to stop bleeding and a er sclerotherapy to prevent
re lling ofblood.
To achieve complete venous occlusion the external pressure has to be higher than the intravenous pressure, depending on the body position. By Duplex ultrasonography and
by MRI it could be demonstrated that an occlusion of
super cial leg veins can be obtained with an external pressure in the range of 20mmHg in the supine position, but
that in the sitting and standing positions the pressure has
16,24
to be between 50 and 70 mmHg.
With compression
82 • BASIC CONSIDERATIONS
stockings such pressure ranges can be achieved only when
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rolls or pads are applied over the vein. According to the law
of Laplace this will increase the local pressure due to the
25
reduction of the local radius.
ARTERIAL FLOW AND
MICROCIRCULATION
A reduction of arterial ow will occur when the external
compression pressure exceeds the intra-arterial pressure.
is may happen in patients with arterial occlusive disease with a reduced peripheral arterial pressure. In order
to avoid ischemic skin lesions from external compression
it is therefore essential to measure the peripheral arterial
pressure by a Doppler probe before strong compression
bandages or stockings are applied. It is generally accepted
that a Doppler ankle-brachial index (ABI) of less than 0.5
is a contraindication for compression therapy. However,
external compression does not invariably mean reduction of arterial ow. H.N. Mayrovitz reported on several
experiments concerning arterial blood ow and compression and was able to demonstrate an increase of the pulsatile ow below the knee in healthy volunteers using
26
nuclear magnetic resonance owmetry.
An increase of
arterial ow under the bandages could also be shown in
patients with mixed, arteriovenous ulcers and an ABPI of
>0.6 when inelastic material was applied up to a pressure
27
of 40mmHg.
Patients with edematous legs and with an ABI between
0.5 and 0.8 may bene t from inelastic or short-stretch
bandages applied with a mild resting pressure due to the
edema-removing massage e ect that will occur with every
ankle movement. In patients with mixed ulceration it could
be demonstrated that inelastic bandages applied with a pressure up to 40mmHg were able to increase arterial ow and
27
to improve the venous pumping function.
Completely
inelastic bandages together with walking have a similar
e ect as intermittent pneumatic compression. e rhythmic
pressure peaks of an inelastic bandage during walking can
be compared with those exerted by an intermittent pneumatic pressure pump. Several experiments with intermittent
pneumatic compression have demonstrated an increase of
arterial ow in patients with arterial occlusive disease.
28,29
e deciding mechanisms of action are the reduction of
edema, an increase of the arteriovenous pressure gradient,
myogenic mechanisms, and the release of vasoactive sub-
30
stances from the endothelial cells
Compression accelerates blood ow in the enlarged capillary loops and reduces capillary ltration due to enhanced
tissue pressure. Blood ow and partial oxygen tension in the
skin increase and the endothelial adhesion of leukocytes is
normalized. Di erent studies using electron microscopy
were able to show a restoration of the structural changes
in the media myocytes in stripped veins and a tightening of intercellular junctions. Increasing ow velocity
demonstrated by laser Doppler uxmetry may reduce the
likelihood of white blood cells interacting or sticking to
31
endothelium with release of various factors.
E ects on
mediators involved in the local in ammatory response may
explain both the immediate pain relief that occurs with
good compression, and ulcer healing.
Model experiments with intermittent pneumatic compression were able to demonstrate that there is an increased
release of brinolytic mediators and of the endothelial
relaxing factor (EDRF) nitrogen oxide from the endothelial
cells depending on the amount of shear stress produced by
10,30
the compression waves.
L Y M P H D R A I N A G E
Several bene cial mechanisms of compression therapy on
the swollen extremity may be explained by its e ects on the
32
lymphatic system:
•
Reduction of capillary ltration
•
Shi of uid into noncompressed parts of thebody
•
Increase of lymphatic reabsorption and lymphatic
transport
•
Breakdown of brosclerotictissue
•
Downregulation of proin ammatory cytokines and
receptors for growth factors.
External compression increases the interstitial pressure and prevents uid from ltering out of the capillary
network. e amount of the lymphatic load is thereby
decreased.
Compression removes more water than protein from
the tissue, thereby increasing oncotic tissue pressure and
reinforcing the need for sustained compression. erefore
in chronic edema, success is dependent on continued
compression.
Compression together with movement enhances the
contraction of the lymphangion.
It has been demonstrated that both compression bandaging and exercise stimulate the movement of stagnating lymph through the lymph collector in lymphedema
patients, in which the lymphatic trunks are lled. is is
probably one explanation for the reduction of intralymphatic hypertension by complex decongestive therapy.
Intermittent pneumatic compression enhances prefascial lymph drainage. Unna boots are able to increase subfascial lymph transport, which is reduced in postthrombotic
syndrome.
Consequent compression leads to a morphological
improvement of pathological initial lymphatics in patients
with lipodermatosclerosis, which can be demonstrated by
indirect x-ray lymphography.
MECHANISM AND EFFECTS OF COMPRESSION THERAPY • 83
CLINICAL EFFECTS OF
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COMPRESSION THERAPY
e use of compression therapy in various clinical indications is based mainly on experience.
Only a few randomized controlled trials (RCTs) are
available that prove the e cacy of compression treatment
33
on the level of evidence-based medicine.
Table9.4 summarizes the outcome of an international
consensus meeting in which all RCTs and systematic
reviews have been scored.
ere are only three areas for which evidence-based
medicine data show clear clinical bene ts of compression
therapy:active venous ulceration, prevention of postthrombotic syndrome a er deep vein thrombosis, and prevention
of thromboembolic events a er surgery when combined
with anticoagulatory prophylaxis.
In venous ulcers several RCTs have shown that compression is better than no compression and that high pressure is more e ective than low pressure. Con icting results
are coming from studies comparing di erent compression
materials, mainly due to the fact that frequently, good bandages have been compared with poor bandages applied by
inadequately trained sta . is underlines the need to measure pressure and sti ness of the compression products in
future trials.
Compression stockings a er proximal deep vein thrombosis are able to reduce the incidence of a postthrombotic
syndrome some years a er the acute event to one half.
Immediate mobilization of mobile patients with deep vein
thrombosis using compression has been shown not only
to reduce pain and swelling in the acute stage but also to
achieve less postthrombotic changes a er someyears.
e overview given in Table 9.4 does not mean that
compression is less or not e ective in areas with recommendation levels B and C, but that we need more trials in order
to improve the scienti c evidence for compression devices
in the future.
R E F E R E N C E S
1. CEN European Prestandard . Medical compression hosiery . Brussels:
European Committee for Standardization . 2001 . 1–40 .
2. Partsch H , Rabe E , Stemmer R . Compression therapy of the extremities .
Paris : Editions Phlébologiques Francaises . 1999 .
3. Partsch H , Mosti G.Comparison of three portable instruments to
measure compression pressure , Int Angiol . 2010. 29 ( 5 ): 426–430.
4. Partsch H , Clark M , Bassez S , etal. Measurement of lower leg com-
pression in vivo:Recommendations for the performance of measurements of interface pressure and sti ness: A consensus statement ,
Dermatol Surg . 2006 . 32 : 229–238 .
5. Partsch H , Menzinger G , Mostbeck A . Inelastic leg compression is
more e ective to reduce deep venous re uxes than elastic bandages ,
Dermatol Surg . 1999 . 25 : 695–700 .
6. Stolk R , Wegen van der-Franken CPM , Neumann , HAM . A method
for measuring the dynamic behavior of medical compression hosiery
during walking , Dermatol Surg . 2004 . 30 : 729–736 .
7. Partsch H . e static sti ness index:Asimple method to assess the
elastic property of compression material in vivo , Dermatol Surg . 2005 .
31 : 625–630 .
8. Partsch H , Partsch B , Braun W . Interface pressure and sti ness of
ready made compression stockings: Comparison of in vivo and in
vitro measurements . J Vasc Surg . 2006. 44 ( 4 ): 809–814 .
Table9.4 RCTS AND SYSTEMATIC REVIEWS ON COMPRESSION THERAPY
FIRST COLUMN:INDICATIONS, FOLLOWING THE CEAP CLASSIFICATION; SECOND COLUMN:NUMBER
OF RCTS IDENTIFIED; COLUMNS 37:LEVELS OF RECOMMENDATION A, B, C SEE LATER FOR BANDAGES
COLUMN 3OR DIFFERENT STOCKINGS WITH THEIR PRESSURE RANGES COLUMNS47
INDICATION REF # BANDAGE STOCKING 1014 STOCKING 1521 STOCKING 2332 STOCKING 3446
C0S, C1S
C1 Sclerother
C2A
C2S
C2 Pregnancy
C2 Surgery
C2 Sclerother
C3
C4b (LDS)
C5
C6
DVT
Prevention
Flight
DVT erapy
PTS
Prevention
Lymphedema
Levels of Recommendation:
A:Large RCTs, meta-analysis of homogeneous results
B:Only one or smallerRCTs
C:Observational studies, consensus among participants of the consensus meeting
3
2
1
1
1
7
3
1
1
Multiple
Multiple
Multiple
2
3
3
5
C
C
A
B
B
B
C
A–B
B
B
B
C
B
A-B
B
B
B
C
B
C
B
B
B
B
A
C
B
C
C
C
B
A
C
84 • BASIC CONSIDERATIONS
9. Partsch H . Improvement of venous pumping function in chronic
https://t.me/med1917
venous insu ciency by compression depending on pressure and
material , VA S A . 1984 . 13 : 58–64 .
10. Dai G , Tsukurov O , Orkin RW , Abbott WM , Kamm RD , Gertler
JP . An in vitro cell culture system to study the in uence of external
pneumatic compression on endothelial function , J Vasc Surg . 2000 .
32 : 977–987 .
11. O’Meara S , Cullum NA , Nelson EA. Compression for venous leg
ulcers, Cochrane Database Syst Rev . 2009 . 1 : CD000265.
12. Kessler CM , Hirsch DR , Jacobs H, etal. Intermittent pneumatic
compression in chronic venous insu ciency favorably a ects brinolytic potential and platelet activation , Blood Coagul Fibrinolysis .
1996 . 7 : 437–446 .
13. Blättler W , Partsch H . Leg compression and ambulation is better
than bed rest for the treatment of acute deep vein thrombosis , Int
Angiol . 2003 . 22 : 393–400 .
14. Vin F , Benigni JP . Compression therapy:International Consensus
Document Guidelines according to scienti c evidence , Int Angiol .
2004 . 23 : 317–345 .
15. Partsch H , Winiger J , Lun B . Compression stockings reduce occupational swelling , J Derm Surg . 2004 . 30 : 737–743 .
16. Partsch B , Partsch H . Pressure dose for leg vein compression therapy?, J Vasc Surg . 2005 . 42 : 734–738 .
17. Partsch H , Kahn P . Venöse Strömungsbeschleunigung in Bein
und Becken durch “Anti- rombosestrümpfe,” Klinikarzt . 1982 .
11 : 609–615 .
18 Lord RS , Hamilton D . Graduated compression stockings (20–
30mm Hg ) do not compress leg veins in the standing position , ANZ
J Surg . 2004 . 74 : 581–583 .
19. Mostbeck A , Partsch H , Peschl L . Änderungen der
Blutvolumenverteilung im Ganzkörper unter physikalischen und
pharmakologischen Maßnahmen , VA S A . 1977 . 6 : 137–141 .
20. Partsch H , Menzinger G , Borst-Krafek B , Groiss E . Does thigh compression improve venous hemodynamics in chronic venous insu ciency?, J Vasc Surg. 2002 . 36 : 948–952 .
21. Partsch B , Mayer W , Partsch H . Improvement of ambulatory venous
hypertension by narrowing of the femoral vein in congenital absence
of venous valves , Phlebology . 1992 . 7 : 101–104 .
22. Stöberl C , Gabler S , Partsch H . Indikationsgerechte
Bestrumpfung:Messung der venösen Pumpfunktion ,
18 : 35–39 .
23. Mosti G , Partsch H . Measuring venous pumping function by
strain-gauge plethysmography , Int Angiol . 2010. 29 ( 5 ): 421–425.
24 Partsch H , Mosti G , Mosti F . Narrowing of leg veins under com-
pression demonstrated by magnetic resonance imaging (MRI), Int
Angiol . 2010. 29 ( 5 ): 408–410.
25 Partsch B , Partsch H . Which pressure do we need to compress
the great saphenous vein on the thigh?, Dermatol Surg . 2008.
34 ( 12 ): 1726–1728.
26. Mayrovitz HN . Compression-induced pulsatile blood ow changes
in human legs, Clin Physiol . 1998 . 18 : 117–124 .
27 Mosti G , Iabichella ML , Partsch H . Compression therapy in mixed
ulcers increases venous output and arterial perfusion , J Vasc Surg .
2012. 55 ( 1 ): 122–128.
28. Delis KT , Nicolaides AN . E ect of intermittent pneumatic compression of foot and calf on walking distance, hemodynamics, and
quality of life in patients with arterial claudication:Aprospective
randomized controlled study with 1-year follow-up , Ann Surg . 2005 .
241 ( 3 ): 431–441 .
29 Labropoulos N , Wierks C , Su oletto B . Intermittent pneumatic
compression for the treatment of lower extremity arterial disease:Asystematic review , Vasc Med. 2002. 7 ( 2 ): 141–148.
30 Chen AH , Frangos SG , Kilaru S , Sumpio BE . Intermittent pneu-
matic compression devices:Physiological mechanisms of action , Eur
J Vasc Endovasc Surg . 2001. 21 ( 5 ): 383–392 .
31. Abu-Own A , Shami SK , Chittenden SJ , Farrah J , Scurr JH , Smith
PD . Microangiopathy of the skin and the e ect of leg compression
in patients with chronic venous insu ciency , J Vasc Surg . 1994 .
19 : 1074–1083 .
32. Földi E , Jünger M , Partsch H . e science of lymphoedema bandag-
ing, EWMA Focus Document:Lymphoedema bandaging in practice .
London : MEP . 2005 . 2–4 .
33. Partsch H , Flour M , Smith PC , International Compression Club.
Indications for compression therapy in venous and lymphatic disease
consensus based on experimental data and scienti c evidence , Int
Angiol . 2008. 27 ( 3 ): 193–219.
VA S A
. 1989 .
MECHANISM AND EFFECTS OF COMPRESSION THERAPY • 85
10.
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CLASSIFYING VENOUS DISEASE
Bo Eklöf
he Swedish physician and scientist Carl von Linné
published a classi cation of plants based on the num-
T
Today, classi cation of diseases is a basic instrument for uniform diagnosis and meaningful communication about disease.
In chronic venous disorders (CVD), reliance for too long has
been placed on the clinical appearance of the super cial e ects
of CVD, such as spider veins, varicose veins, swelling, skin
changes, and ulcerations, without requiring accurate objective testing of the venous system to substantiate the diagnosis.
is practice has caused errors of diagnosis and has been largely
responsible for the poor correlation of results between treatment methods. ere have been several classi cations in the
past that have added to our understanding of CVD, but all lack
the completeness and objectivity needed for scienti c accuracy.
e most commonly used classi cation, particularly in
Europe, was Widmer’s 1978
venous insu ciency:
ber of stamina and pistils in 1735 in Systema Naturae .
P R E V I O U S
CLASSIFI CATIONSOFCVD
1
classi cation of chronic
Stage I :Edema and dilated subcutaneous veins with
corona phlebectatica
Grade III :Re ux to just below theknee
Grade IV :Total re ux to theankle
Hach’s thesis was that in severe re ux of the GSV, a
vicious internal circle developed because of the large venous
blood volume with dilatation of the popliteal and femoral veins leading to deep venous incompetence if the GSV
incompetence was not treated.
In 1980,
one could achieve further improvement from other means
a er compression therapy. Could surgery or sclerotherapy
be helpful? He recommended a classi cation based on
involvement of super cial, perforator, and deep veins using
objective measures such as foot volumetry and ambulatory venous pressure to discriminate between “betterable”
( bess-erbare ) and “not betterable” ( nicht besserbare ) patients.
In 1985,
to the present CEAP (clinical, etiological, anatomic, pathophysiologic) classi cation, as follows.
Stages of regional circulatory-trophic disorders:
•
Compensation
3
Partsch asked whether in patients with CVD
4
Sytchev published a classi cation very similar
CLINICAL CLASSES
Stage II :Trophic lesions of the skin with hyper- or
depigmentedareas
Stage III :Healed or activeulcer
is clinical classi cation was criticized for the nonspeci city of Stage Iand the absence of di erentiation between
trophic changes in StageII.
In 1979
vein (GSV) incompetence:
Grade I :Re ux in thegroin
Grade II :Re ux to above theknee
2
Hach suggested a grading of great saphenous
•
Decompensation (cyanosis, edema, cruralgia, or legpain)
Degrees:
•
By the end of theday
•
Bymidday
•
At the beginning of theday
Phases:
•
Functional trophic disorders (hyper-, hypo-, and
anhidrosis of theskin)
86
• Preulcer condition of tissues
https://t.me/med1917
•
Trophiculcers
Etiology:
•
Primary venous dilatation
•
Secondary (postthrombotic) occlusion and
recanalization
•
Congenital dysplasias
9
In 1993,
Miranda etal. published a clinical classi cation:
Stage I :Dilatation of GSV 7mm by duplex scanning
Stage II :Dilatation of GSV > 7mm without skin
changes
Stage III :Stage II plus skin changes
Stage IV :Stage III plus active or healedulcer
Central hemodynamics
•
Compensation
•
Decompensation
— Underloaded
— Overloaded
5
e same year,
Pierchalla and Tronnier suggested differentiation between primary and secondary (postthrombotic) disease, and between super cial, perforator, and deep
venous disease using objective measures.
6
In 1988,
Porter etal. published reporting standards for
venous disease developed by an ad hoc committee for the
Society for Vascular Surgery (SVS) and the North American
chapter of the International Society for Cardiovascular
Surgery (ISCVS). is was similar to and based on the
Widmer classi cation with the addition of etiology and
anatomic distribution. is was the stimulus for the CEAP
classi cation that followedlater.
7
In 1991,
Cornu- énard etal. published a clinical classi cation of the severity of varicose veins by inspection and
palpation and calculated the sum of maximum diameter at
seven sites of theleg.
8
In 1992,
Enrici and Caldevilla published a clinical classi cation on the evolution of the postthrombotic syndrome:
Stage 1 :Early postthrombotic syndrome with painful
swelling of the leg with distal venous hypertension and
venographically demonstrating residual obstruction of
the deep veins with competent perforators
THE CREATION OF THE CEAP
CLASSIFIC AT ION
At the h annual meeting of the American Venous Forum
(AVF) in 1993, John Porter suggested using the TNM classi cation for cancer as a model to develop a classi cation
system for venous diseases. Following a year of intense
discussions a consensus conference was held at the sixth
annual meeting of AVF in February 1994 on the island of
Maui, Hawaii, at which an international ad hoc committee,
chaired by Andrew Nicolaides, and with representatives
from Australia, Europe, and the United States, developed
10
the rst CEAP consensus document.
It contained two
parts, a classi cation of CVD and a scoring system of the
severity of CVD. e classi cation was based on clinical
manifestations (C), etiologic factors (E), anatomic distribution of disease (A), and the underlying pathophysiologic
ndings (P), thus the name CEAP. e severity scoring
system was based on three elements:the number of anatomic segments a ected, grading of symptoms and signs,
and disability. e CEAP consensus statement was published in 26 journals and books in nine languages, truly a
universal document for CVD. It was endorsed by the Joint
Councils of the SVS and the North American Chapter
of the ISCVS, and its basic elements were incorporated
11
into venous reporting standards.
Today most published
clinical papers on CVD use all or portions of the CEAP
classi cation.
Stage 2 :Compensatory hypertrophy of the
musculovenous calf musclepump
Stage 3 :Stage 2 plus appearance of secondary varicose
veins. Venography shows recanalization with
varying re ux with incompetent perforators;
Stage 4 :Advanced chronic venous insu ciency with
development of a vicious venous recirculation with
lipodermatosclerosis and ulceration due to venous
hypertension
Stage 5 :Phleboarthrotic syndrome with
immobilization of theankle.
Stage 6 :Secondary, postthrombotic lymphedema
REVISION OFCEAP
Diagnosis and treatment of CVD were developed rapidly in the 1990s, and the need for an update of the classi cation logically followed. Now, it is important to stress
that CEAP is a descriptive classi cation. Venous Severity
12
Scoring (VSS)
was developed to allow longitudinal outcomes assessment, but it became apparent that CEAP itself
required updating and modi cation. In April 2002, the
AVF appointed an ad hoc committee on CEAP to review
the classi cation and make recommendations for change
by 2004, 10years a er its introduction (see Table10.1).
An International ad hoc committee was also established
to assure continued universal utilization (see Table10.2).
CLASSIFYING VENOUS DISEASE • 87
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