LYMPHOLOGY

PHLEBO N°23

Arm/foot venous pressure

differential test: value in chronic
venous insufficiency

Treatment of nonhealing venous

leg ulcers and lipodermatosclerosis
by shave therapy

Pathophysiology of secondary
lymphedema
 CONTENTS

EDITORIAL --------------------------------------------------------------------------------------- 2

PHLEBOLOGY --------------------------------------------------------------------------------- 3
Arm/foot venous pressure differential test:
value in chronic venous insufficiency
Seshadri Raju, MD (USA)

Treatment of nonhealing venous leg ulcers

and lipodermatosclerosis by shave therapy
Wilfried Schmeller, MD (Germany)

BOOKSHELF --------------------------------------------------------------------------------- 12
Review of 5 original studies

LYMPHOLOGY ---------------------------------------------------------------------------- 16
Pathophysiology of secondary
lymphedema
M. J. W. Husmann, MD, U. K. Franzeck, MD (Switzerland)

NEWS ----------------------------------------------------------------------------------------------- 22
 EDITORIAL
I t is an oversimplification to define edema as
the accumulation of fluids in the interstices,
that is to say outside the vessels and cells.
Clinically, it will be reflected in swelling and
accumulation of fluids in the
tissues.
Many mechanisms may give
rise to the appearance of
edema.
The lymphatic system no
doubt plays a primordial role
in the development of edema,
so Prof Földi considers that the
presence of any type of edema
represents the overflow or Prof José Antonio Jiménez Cossío
flooding of the lymphatic sys-
tem. When the lymphatic load exceeds lym-
phatic transport capacity, edema inevitably
1
appears. When an increase in lymphatic load
occurs we say that there is high-flow edema,
and when the transport capacity is reduced we
have low-flow edema.
From the greater or lesser concentration of
proteins in the edematous fluid, we can clas-
sify edema into high-protein and low-protein.
We would therefore have to consider lymphe-
dema as a low-flow and high-protein edema.
1.
2.
2
Venous blockade, hypoproteinemias, lym-
phatic blockade, or the capillary lesions pro-
duced in burns may give rise to the appear-
ance of edema, even when they affect the
microcirculation by different
mechanisms.
When faced with any clinical
manifestation of edema, it is
essential to determine its etio-
logy (central, venous, lympha-
tic, traumatic, etc) on which the
establishment of the treatment
for each case will depend.
If we consider the worldwide
incidence of edema, establi-
shed by Prof J. Casley-Smith in
1986,2 we have to accept that 50% of the popu-
lation, that is to say 1 500 million inhabitants,
present protein-rich edema each year, with
the consequent socioeconomic and health
repercussions of this disorder.
José Antonio Jiménez Cossío
 PHLEBOLOGY

Arm/foot venous pressure

differential test:
value in chronic venous
insufficiency
SESHADRI RAJU, MD (USA)

Chronic venous insufficiency may be due to reflux, obstruction, or a combination of these.

The majority of postthrombotic cases, some 70% or more, harbor some element of obstruction.1
Symptoms of pain and swelling are thought to be more frequently associated with the obstructive component,
while reflux is considered to be the major etiological mechanism in the causation of stasis ulceration.
Separate assessment of both obstruction and reflux is clearly necessary to better
understand the disease process, and for evaluation of the individual patient for appropriate therapy.

Assessment techniques with
regard to reflux are quite well-advanc-
ed, and most clinical laboratories
perform duplex and air plethysmo-
graphy for this purpose. Unfortunate-
ly, most centers still rely on duplex
information or ascending venogra-
phy to assess the obstructive com-
ponent. Since these are morpho-
logical methods, functional assess-
ment of obstruction is not provided
by these techniques2; furthermore,
obstructive lesions, particularly in
the iliac veins, may be frequently
missed by them.3
Part of the reason why functional
tests are not more frequently
employed is due to the fact that
readily employable and reliable
techniques for assessment of
obstruction have not been devel-
oped. Impedance plethysmography
may have diagnostic value in acute
venous obstruction for some weeks
after onset, but becomes unreliable
later due to the rapid develop-
ment of collaterals; as commonly
employed, it is an “all-or-none” tech-
nique unable to distinguish milder
forms of obstruction from the more
severe variety. Strain-gauge plethys-
mography has been employed for
the assessment of chronic venous
obstruction.4 In this method outflow
fractions are measured; a flatter-
than-normal curve or a 1-second frac-
tion of less than 50 mL is considered
to indicate venous obstruction.
Neglen and Raju have shown that this
assumption may be erroneous, and
the test may not be specific. In parti-
cular, poor calf vein compliance per
se without outflow obstruction can
result in a flatter curve and a dimi-
nished outflow fraction.5 Thus, an
abnormal test result with plethysmo-
graphy may be a marker of previous
deep vein thrombosis without being
diagnostic of venous obstruction.
The strain-gauge technique can be
further refined to derive flow
resistance calculations if simul-
taneous foot venous pressures are
recorded.6 Even this refinement may
be prone to errors, due to procedu-
ral artefacts introduced by the occlud-
ing cuff employed with the strain
gauge. In our laboratory, we have
employed an arm/foot venous pres-
sure technique with reactive hyper-

3
emia to diagnose and grade venous
obstruction.2 The technique appears FIGURE 1.
to be superior to the aforementioned Arm/foot venous pressure differential measurement in the supine patient.
techniques in diagnostic accuracy.6

Technique7
Simultaneous venous pressures in
an arm vein and the dorsal vein of the
foot are measured (Figure 1). A pres-
sure differential of >4 mm Hg is
considered abnormal. Patients with
normal unobstructed venous ana-
tomy have a differential of 4 mm Hg
or less. Some patients with venous
obstruction that is evident on duplex
examination or venography also have
a normal differential, ie, 4 mm Hg
or less. Obviously, collateralization
and/or recanalization has provided
functional compensation at rest in
these patients. Further testing is
required in this subset to determine
whether the collaterals will be func- FIGURE 2.
tionally adequate under the stress of Reactive hyperemia-induced foot venous pressure elevation.
increased blood flow that occurs with
exercise. To mimic exercise, we per-
form inflow occlusion with a thigh cuff
(15 cm wide) for 2 minutes to induce
reactive hyperemia while monitoring
dorsal foot vein pressure (Figure 2).
Reactive hyperemia-induced pres-
sure of 6 mm Hg or less in the dorsal
foot vein is normal. A pressure
elevation beyond 6 mm Hg is consid-
200 mmHg for 3 minutes and released
ered an abnormal response. By per-
forming both the arm/foot venous
pressure differential test and the
reactive hyperemia test in all
patients, venous obstruction can be
graded according to severity (Table I).
The arm/foot venous pressure tech-
nique with reactive hyperemia, as
described, has been incorporated in
our practice as a routine part of the
evaluation of patients with suspect- is seldom refused by patients who not require a great deal of skill to
ed chronic venous insufficiency, not are symptomatic, and we consider administer, thus allowing it to be
only for the initial evaluation but for the information provided valuable incorporated into laboratory rou-
periodic follow-up as well. Even enough to justify its routine use. The tines without on-site physician
though it is an invasive technique, it test is easily performed and does supervision. The last factor has been

4
TABLE 1.

ARM/FOOT PRESSURE REACTIVE

DUPLEX FUNCTIONAL
GRADE DIFFERENTIAL TEST HYPEREMIA TEST
OR VENOGRAM ASSESSMENT
(Normal ≤ 4 mm Hg) (Normal ≤ 6 mm Hg)

Grade 0 No obstruction Normal Normal Normal

Grade 1 Obstruction Fully compensated Normal Normal

Partially
Grade 2 Obstruction Normal Abnormal
compensated

Partially
Grade 3 Obstruction Abnormal Abnormal
decompensated

Grade 4 Obstruction Fully decompensated Abnormal Normal*

* Paradoxical response due to muted reactive hyperemia response. See Figure 3.

particularly important in increasing

its utility and application as a screen- FIGURE 3.
ing tool in patients. Photoplethysmography (PPG) tracings of toe pulse before, during,
and after ischemic thigh cuff occlusion in a patient with Grade 1 obstruction
The technique has proven to be and another patient with Grade 4 obstruction.
highly reliable, at times exposing the The reactive hyperemia response is muted in the patient
presence of venous obstruction even with high-grade obstruction. The mechanism is not understood and results
when the lesion had not been visible in the paradoxical response noted in Table I.

during initial venography. Repeat

venography with more careful tech- GRADE 1 OBSTRUCTION
nique usually confirms the presence
of a lesion. An abrupt deterioration
in the arm/foot venous pressure dif-
ferential on serial follow-up testing in
a patient who is being followed up
after deep venous surgery, such as GRADE 4 OBSTRUCTION
valve reconstruction, is often the first
indication that a significant interval
event, usually a silent deep venous
thrombosis, has occurred. More
detailed diagnostic measures such
as duplex and/or ascending venogra- which highlights the importance of ment of patients with venous insuffi-
phy should be ordered in such a such an objective assessment. The ciency are illustrated in Figures 3 to 5.
patient. test also helps in the selection of With the advent of newer therapeu-
Patients who have undergone patients who are being considered tic modalities, such as catheter-
venovenous bypass surgery can be for venovenous bypass. Patients directed thrombolysis for deep
objectively followed by serial test- with low-grade obstruction (grades venous thrombosis and venous
ing with this technique2 and an 1 and 2) are not candidates, as stenting for chronic occlusions, the
abnormal test result usually indi- the bypass is unlikely to stay patent arm/foot venous pressure technique
cates that the bypass has occluded. in the absence of a significant has become all the more important
Subjectively, many such patients gradient. Some examples as to how in outcome assessment and moni-
remain asymptomatic, even though the arm/foot venous pressure tech- toring of the evolution of post-
the bypass has become occluded, nique has enhanced the manage- thrombotic syndrome.

5
 FIGURE 4.
Venogram in a patient who continued to be symptomatic after a Palma bypass.
Even though the venogram shows the bypass to be open,
the patient had Grade 2 obstruction by the arm/foot and reactive hyperemia tests,
providing an objective confirmation of the symptoms.
The stenosis at the left femoral anastomoses was most likely responsible
for continuing symptoms.

FIGURE 5.
A postthrombotic patient had leg
swelling, pain, and stasis ulceration.
Grade 3 obstruction was documented
on testing, which prompted
initial iliac vein stenting above
and later valve reconstruction.
The arm/foot differential and reactive
hyperemia tests are particularly useful
in the management and follow-up
of patients with complex pathologies.

REFERENCES
1. Johnson BF, Manzo RA, Bergelin RO,
Strandness DE, Jr. Relationship between
changes in the deep venous system and
the development of the postthrombotic
syndrome after an acute episode
of lower limb deep vein thrombosis:
a one- to six-year follow-up.
J Vasc Surg. 1995;21:307-313.
of phlebographic obstruction in chronic
venous stasis.
J Cardiovasc Surg (Torino). 1990;31:173-177.
5. Neglen P, Raju S. The pressure/volume
relationship of the calf - a measurement
of vein compliance?
J Cardiovasc Surg. 1995;36:219-224.

2. Raju S. New approaches to the 6. Neglen P, Raju S. Detection of outflow

diagnosis and treatment of venous
obstruction.
J Vasc Surg. 1986;4:42-54.
3. Raju S. A pressure-based technique
for the detection of acute and chronic
venous obstruction.
Phlebology. 1988;207-216.
4. Schanzer H, Younis C, Train J,
Peirce EC II. Therapeutic implications
obstruction in chronic venous
insufficiency.
J Vasc Surg. 1993;17:583-589.
Address for correspondence
7. Raju S, Fredericks R. Venous
obstruction: Seshadri Raju, MD
an analysis of one hundred thirty-seven Professor Emeritus of Surgery
cases with hemodynamic, venographic, and Honorary Surgeon
and clinical correlations.
J Vasc Surg. 1991;14:305-313. University of Mississippi Medical Center
Jackson, Miss - USA

6

Treatment of nonhealing
venous leg ulcers
and lipodermatosclerosis
by shave therapy
Introduction
For leg ulcers caused by deep
venous insufficiency, no causal treat-
ment is available. Ulcers due to
either primary deep varicosis or
postthrombotic syndrome are often
resistant to therapy. Replacement of
insufficient vein segments by vein
valve transplants, valvuloplasties, or
venous transposition operations are
only done in highly specialized
centers.1 Compression therapy is the
treatment of choice,2,3 but is only
successful in about 80% of all venous
leg ulcers. Recurrence rates of 30%
within 1 year have been reported.4
Conventional skin grafting shows
success rates between 50% and 90%,
with recurrence rates of about 50%
within the following years.5,6 Parati-
bial fasciotomy7 and endoscopic
perforator dissection—which was
still discussed controversially some
years ago8—have proven effective
for ulcers of the inner ankle,9,10 but
not for ulcers at other locations on
the lower extremity.
Ulcers of the outer ankle, ulcers
covering the whole gaiter area,
and ulcers which recur after the
WILFRIED SCHMELLER, MD (Germany)
procedures mentioned above have
been performed, are still a big thera-
peutic problem. The common fea-
ture of these recalcitrant or “therapy-
resistant” ulcers are extensive tro-
phic changes in the form of chronic
dermatosclerosis, dermatoliposcle-
rosis, or dermatolipofasciosclero-
sis11-13; sometimes (Figures 2a, 3a,
and 5a) this is combined with acute
dermatosclerosis.14 A radical remo-
val of all areas with fibrotic changes
of skin, subcutaneous tissue, and
fascial sheets enclosing the muscular
compartments has been advocat-
ed.15-17 However, removal of ulcer
and lipodermatosclerosis without
the underlying fascia proved to be
beneficial as well.18 In the Depart-
ment of Dermatology and Venereo-
logy of the Medical University of
Lübeck, Germany, we use a surgical
procedure called shave therapy for
patients with so-called therapy-
resistant ulcers.
Patients
From January 1994 to October 1998,
124 patients with 162 nonhealing
7
PHLEBOLOGY
venous leg ulcers were treated by
shave therapy. Ten patients were
operated on in 1994, 8 in 1995, 30 in
1996, 33 in 1997, and 43 from January
to September 1998. Most of the
patients were older than 65 years
(range 42 to 87 years); the mean dura-
tion of the ulcers was 20 years (range
2 to 46 years). All ulcers had proved
to be resistant to compression
therapy and to surgical procedures
like fasciotomy, fasciectomy, dissec-
tion of perforator veins, and/or
stripping of superficial veins. In
nearly all of the cases reduced ankle
movement was noted, often with a
fixed talipes equinus.
Doppler ultrasound and duplex
sonography revealed deep venous
reflux in all patients, sometimes
combined with reflux of the superfi-
cial and/or the perforator veins. In
nearly 50% of the patients, reflux was
a result of postthrombotic syndrome.
The classification of venous disease
according to CEAP19 was: C6,S (clinical
signs: active ulceration with symp-
toms), ES or EP (etiology: due to
thrombosis or primary varicosis), AD
and AS or AD and AP (anatomy: deep
and superficial veins affected or

FIGURE 1.
Shave therapy operative procedure.

A The ulcer and most of the surrounding lipodermatosclerosis have been
removed by Schinck skin grafting knive.
B Meshed split skin graft at the end of the operation.

A 
deep and perforator veins affected;
segments affected were numbers 2
and 3 in the long saphenous veins,
11 to 15 in the deep veins, and 18 in
the perforator veins), PR (pathophy-
siology: reflux). The disability scores
in our patients were 2 (can work
8 hours daily only with support
device) or 3 (unable to work even
with support device).
Shave therapy
operative procedure
The ulcers and the surrounding lipo-
dermatosclerosis were removed
under general or spinal anesthesia
using a Schink dermatome. The indu-
rated areas, next to and underneath
the ulcers and above the fascia, were
excised in flat, horizontal layers
(Figure 1a), until palpation indicated
a less indurated tissue and until an
“improved” bleeding pattern was
B insufficiency—especially in post-
noted. The fascia was not removed.
Afterwards a meshed split skin graft
of 0.5 to 0.8 mm thickness from the
thigh was placed on the wound area
(Figure 1b). In patients with ulcers
covering the whole gaiter area
(Figures 3a and 4a), the complete cir-
cumference of the lower leg was
operated on. In some patients shave
therapy was combined with saphe-
nectomy and/or with dissection and
ligation of insufficient perforator
veins. Surgery was followed by bed
rest for 3 days. The first dressing was
done on the third, and the second
dressing on the fifth day.
Results
One week postoperatively, more
than 75% of the wound areas were
healed in all patients. From 1995, no
peri- or postoperative antibiotics
were given. Patients were discharged
8
2 to 3 weeks after surgery with
compression bandages. Follow-up
studies in 59 patients with 76 ulcers
revealed short-term healing rates
of 79% after 3 months.20 In 41 patients
with 75 ulcers, long-term healing
rates of 67% were observed after
an average period of 2 years and
5 months. Figures 2 to 5 show
some typical examples. Obvious
differences were noted according
to the etiology of chronic venous
insufficiency: ulcers caused by
primary deep varicosis showed a
healing rate of 76%; ulcers caused by
postthrombosis showed a healing
rate of 58%.21
Discussion
Chronic leg ulcers in deep venous
thrombotic syndrome—are always
surrounded by lipodermatosclero-
sis. Examinations with 20-MHz ultra-
sound revealed that sclerosis starts
in the upper dermis and proceeds to
the lower dermis; in more severe
forms it also can be found both in
the upper and in the lower subcuta-
neous fat.22 This is expressed by
the German “dermatoliposclerosis,”
which seems more appropriate than
“lipodermatosclerosis," which is
used in the international literature.
In patients with pronounced sclero-
sis the fascia may be involved as well
(dermatolipofasciosclerosis).
These areas with hyperpigmentation
and induration show extensive
trophic changes with abnormal
morphological and functional
phenomena. Morphology reveals
clusters of small vessels with thicken-
ed walls and prominent endothelial
cells, surrounded by several base-
ment membranes and amorphous
material like fibrinogen, laminine,
and type IV collagen.23 Microcircula-
tion shows an increase in laser
Doppler flow and a decrease in
transcutaneous and intracutaneous FIGURE 2.
oxygen tension.12, 24, 25 A 72-year-old man with deep venous insufficiency;
ulcer of 15 years' duration.
A close correlation between the

A Preoperative.
extent of morphological and func-
B 2 years and 4 months after shave therapy.
tional abnormalities and the amount
of lipodermatosclerosis could be
observed.11-13 Computed tomogra-
phic scanning and magnetic reso-
nance imaging have shown that
induration of dermis and subcuta-
neous fat is the prerequisite for the
development of ulceration; venous
leg ulcers without lipodermatoscle-
rosis have never been observed.11,12
Reduced ankle movement in
patients with recalcitrant venous leg
ulcers is called arthropathica ulce-
rosa26 or arthrogenic congestive
syndrome (Figure 4a). It is associated
with dermatoliposclerosis in the
ankle region and around the Achilles
tendon.11 The diminished efficiency 
A 
B
of the venous pump (eg, calf
muscles) aggravates the chronic
venous hypertension. Therefore,
ulcer recurrences are a common
feature in patients with ankle stiff-
FIGURE 3.
ness; this was observed after shave
A 55-year-old man with postthrombotic syndrome;
therapy as well.
ulcer of more than 12 years' duration.
In our studies, extensive changes in A Preoperative.
fascia, tendons, muscles, periostia, B 3 years after shave therapy.
and bones could be demonstrated
by computed tomographic scanning
and magnetic resonance imag-
ing.11,12,20 However, the severity and
resistance to treatment of venous
ulcers seem to depend on the extent
of trophic changes in dermis and
subcutaneous fat (dermatolipo-
sclerosis). Therefore, only the tissue
with the most extensive induration
above the fascia is removed by shave
therapy.
Although an increase in induration in
the transplanted areas could be
noticed clinically after operation,
morphological examinations with
20-MHz ultrasound showed no

A 
B
increase of dermatoliposclerosis
3 months postoperatively.27 Functio-

9
 nal examinations of the microcircula-
FIGURE 4.
tion at the ulcer edge before shave
A 72-year-old woman with ulcer of 10 years' duration. therapy and of the skin graft at iden-

A Preoperative.
tical locations 3 months after opera-
B 2 years and 9 months after shave therapy. tion revealed an improvement with
significant differences in laser Dop-
pler flow, and transcutaneous and
intracutaneous oxygen tension.28
Therefore, it is speculated that by
shave therapy the wound healing is
transferred from a superficial area
with extensive trophic changes
(upper and lower dermis) to a deep-
er area with less trophic changes
(lower subcutaneous tissue).
Compared with other surgical proce-
dures such as ulcer excision with free
tissue transfer29 or free flap valvular
transposition,30 fasciectomy,31 and
paratibial fasciotomy,7 shave therapy
is a relatively simple surgical method
with very good short-term and long-

A 
B term results.20,28 It can be used in all
ulcers caused by deep venous insuf-
ficiency, at the inner ankle as well as
at the outer ankle; it has also proved
to be enormously effective in ulcers
covering the whole circumference of
FIGURE 5. the lower leg.21
A 68-year-old man with postthrombotic syndrome;
ulcer of 8 years' duration. Shave therapy can be combined with
A Preoperative. operations for insufficient superficial

B 1 year and 2 months after shave therapy. or perforating veins. However, contin-
uous compression with elastic ban-
dages or stockings is necessary,
because it is only a symptomatic
treatment, which does not reduce
pathological reflux in the deep veins.
Therefore, the long-term results are
also very much dependent on the
patients’ compliance after successful
operation.

Conclusion
Shave therapy may be considered
as a considerable improvement in
the treatment of recalcitrant or so-

A 
B called therapy-resistant venous leg
ulcers.

10
 Address for correspondence
Prof Dr med Wilfried Schmeller
Department of Dermatology and Venereology
Medical University of Lübeck
REFERENCES
1. Masuda EM, Kistner RL. Long-term results
of venous valve reconstruction:
a four- to twenty-one-year follow-up.
J Vasc Surg. 1994:19:391-403.
2. Falanga V. Venous ulceration. J Dermatol
Surg Oncol. 1993;19:764-771.
3. Douglas WS, Simpson NB. Guidelines for
the management of chronic venous leg
ulceration. Report of a multidisciplinary
workshop. Br J Dermatol. 1995;132:446-452.
4. Mayer W, Jochmann W, Partsch H. Ulcus
cruris: Abheilung unter konservativer
Therapie. Wien Med Wschr. 1994;144:192-195.
5. Sebastian G. Die Rolle der
Hauttransplantation im Behandlungsplan
venöser (postthrombotischer) Ulzera cruris.
Wien Med Wschr. 1994;144:269-272.
6. Kirsner RS, Mata SM, Falanga V, Kerdel FA.
Split-thickness skin grafting of leg ulcers.
The University of Miami Department
of Dermatology´s experience (1990-1993).
Dermatol Surg. 1995;21:701-703.
7. Vanscheidt W, Peschen M, Kreitlinger J,
Schöpf E. Paratibial fasciotomy. A new
approach for treatment of therapy-resistant
venous leg ulcers. Phlebology. 1994;23:45-48.
8. Coleridge Smith P. Calf perforating veins -
time for an objective appraisal? Phlebology.
1996;25:135-136. Editorial.
9. Wolters U, Schmitz-Rixen T. Die
Behandlung insuffizienter Perforansvenen
bei Ulcus cruris venosum durch
endoskopische Dissektion. Phlebology.
1997;26:92-94.
10. Pierik EGJM, van Urk H, Wittens CHA.
Efficacy of subfascial endoscopy in
eradicating perforating veins of the lower leg
and its relation with venous ulcer healing.
J Vasc Surg. 1997;26:255-259.
11. Schmeller W, Rosenthal N, Gmelin E,
et al. Computertomographische
Untersuchungen der Unterschenkel bei
Patienten mit chronischer Veneninsuffizienz
und arthrogenem Stauungssyndrom.
Hautarzt. 1989;40:281-289.
12. Schmeller W, Roszinski S, Tronnier M,
et al. Combined morphological and
physiological examinations in
lipodermatosclerosis. In: Raymond-
Martimbeau P, Prescott R, Zummo M,
eds. Phlebology. 1992. Paris: John Libbey
Eurotext; 1992:172-174.
13. Kirsner RS, Pardes JB, Eaglstein WH,
Falanga V. The clinical spectrum of
lipodermatosclerosis. J Am Acad Dermatol.
1993;28:623-627.
14. Greenberg AS, Hasan A, Montalvo BM, et
al. Acute lipodermatosclerosis is associated
with venous insufficiency. J Am Acad
Dermatol. 1996;35:566-568.
15. Pflug JJ. Operative Behandlung
des supramalleolären medialen
Konstriktionssyndroms bei nicht oder
schlecht heilenden Ulcera cruris venosa.
Phlebology. 1995;24:36-43.
16. Dunn RM, Fudem GM, Walton RL, et al.
Free flap valvular transplantation for
refractory venous ulceration. J Vasc Surg.
1994;19:525-531.
17. Langer C, Fuhrmann J, Grimm H, et al.
Orthostatische Kompartmentdruckmessung
nach endoskopischer Fasziotomie.
Phlebology. 1995;24:163-167.
18. Galli KH, Wolf H, Paul E. Therapie des
Ulcus cruris venosum unter Berücksichtigung
neuerer pathogenetischer Gesichtspunkte.
Phlebology. 1992; 21:183-187.
19. Beebe HG, Bergan JJ, Bergqvist D, et al.
Classification and grading of chronic venous
disease in the lower limbs: A consensus
statement. Phlebology. 1995;10:42-45.
20. Schmeller W, Gaber Y, Gehl HB. Shave
therapy is a simple, quick and effective
surgical treatment for persistent venous leg
ulcers. J Am Acad Dermatol. 1998;39:232-238.
21. Schmeller W, Gaber Y. Long-term results
after shave therapy of non-healing venous
leg ulcers. Br J Dermatol. In press.
22. Welzel J, Schmeller W, Plettenberg A.
A 20 MHz ultrasound examination
of lipodermatosclerosis. In: Altmeyer P,
11
Ratzeburger Allee 160
D-23538 Lübeck - Germany
Tel: 0049 – 451 500 2512 or 2513
Fax: 0049 – 451 500 2981
Hoffmann K, el Gammal S, et al, eds.
Wound Healing and Skin Physiology. Berlin:
Springer;1995:945-948.
23. Tronnier M, Schmeller W, Wolff HH.
Morphological changes in
lipodermatosclerosis and venous ulcers:
light microscopy, immunohistochemistry
and electron microscopy. Phlebology.
1994;9:48-54.
24. Roszinski, S, Schmeller W. Influence of
erythema and sclerosis on skin oxygenation
and microcirculation around venous ulcers.
In: Negus D, Jantet G, Coleridge Smith PD,
eds. Phlebology ´95. Berlin: Springer;
1995:781-783.
25. Roszinski S, Schmeller W. Differences
between intracutaneous and transcutaneous
skin oxygen tension in chronic venous
insufficiency. J Cardiosvasc Surg.
1995;36:407-413.
26. Helliwell PS, Cheesbrough MJ.
Arthopathica ulcerosa: A study of reduced
ankle movement in association with chronic
leg ulceration. J Rheumatol.
1994:21:1412-1414.
27. Schmeller W, Wunderle U, Welzel J.
20 MHz-Sonographie zur Verlaufskontrolle
nach Shave-Therapie venöser Ulzera.
Phlebologie. 1998;27:1-8.
28. Schmeller W, Roszinski S. Shave-Therapie
zur operativen Behandlung persistierender
venöser Ulzera mit großflächiger
Dermatoliposklerose. Hautarzt.
1996;47:676-681.
29. Weinzweig N, Schuler J. Free tissue
transfer in treatment of the recalcitrant
venous ulcer. Ann Plast Surg. 1997;38:611-619.
30. Dunn RM, Fudem GM, Walton RL, et al.
Free flap valvular transplantation for
refractory venous ulceration. J Vasc Surg.
1994;19:163-167.
31. Schwahn-Schreiber Ch, Kirschner P, Hach
W. Die stadiengerechte operative Therapie
des chronisch venösen Stauungssyndroms.
Vasomed. 1997;9:134-142.
 BOOKSHELF
Daflon 500 mg:
a major benefit in leg edema
Daflon 500 mg is a potent venotro-
pic drug used in the treatment of
venous insufficiency and whose pro-
perties have been demonstrated in
pharmacological as well as clinical
studies.1,2 Previous controlled studies
demonstrated the comprehensive
mode of action of Daflon 500 mg: it
increases venous tone, it improves
lymph drainage,3,4 and protects
microcirculation.5,6
The onset of venotropic activity is
rapid (1 hour) and persists for sever-
al hours (between 4 and 24 hours,
depending on the method of admin-
istration),7 and there is a dose-effect
relationship between the phlebo-
tonic activity and the logarithm of the
administered dose.8
The clinical activity of Daflon 500 mg
has been verified after a single
administration of 2 tablets and after
two administrations of 1 tablet per
day.7,9
However, no study on Daflon 500 mg
had been carried out so far to deter-
mine which method of administra-
tion gives the best improvement of
signs and symptoms of chronic
venous insufficiency.
Aim of the study, The duration of the treatment was
2 months.
patients and method The following evaluations were
performed on entry into the trial
Thus, to assess the chronobiological
(D0), and during the treatment after
effect on therapeutic activity of
15 days (D15), 30 days (D30), and at
Daflon 500 mg, Prof Menyhei10
the end of treatment (D60):
carried out a randomized, double-
blind, controlled-study in 320 pa- • Functional discomfort evaluated by
tients with symptoms of chronic the patient on a visual analog scale;
venous insufficiency randomized to • Symptoms of venous insufficiency
3 groups, each receiving oral admi- assessed by the investigator using a
nistration of 1000 mg of Daflon 4-point scale;
500 mg in three different ways: • Signs (edema, trophic disorders)
evaluated by recording their evolu-
GROUP 1 tion and by taking photographs;
• Morning: • Ankle and calf circumferences.
2 Daflon 500 mg tablets
• Evening:
2 placebo tablets
GROUP 2
Results
• Morning:
1 Daflon 500 mg tablet Whatever the schedule
+ 1 placebo tablet of administration
• Evening: of Daflon 500 mg, patients
1 Daflon 500 mg tablet obtain significant relief
+ 1 placebo tablet from their symptoms
GROUP 3 In each group, the results of the study
shows a significant improvement
• Morning:
2 placebo tablets (P<0.001) between D0 and D60
• Evening: concerning functional discomfort and
2 Daflon 500 mg tablets intensity of symptoms, but without
12
statistically significant difference
between the three groups. The over-
all assessment of activity and accep-
tability both by the patients and by
the investigators was excellent in
each group.
Whatever the schedule
of administration
of Daflon 500 mg, leg edema
is significantly reduced
Of the 263 fully documented patients
who presented leg edema at inclu-
sion (93, 87, and 83 patients in groups
1, 2, and 3, respectively), clinical exa-
mination disclosed a disappearance
of edema during the 2-month treat-
ment in a mean percentage of
patients ranging between 28% and
43.4% according to the group and the
side affected (P<0.01). However,
there was no significant difference
between the three groups.
This clinical improvement was
confirmed by circumference measu-
rement: between D0 and D60, a
decrease in ankle circumference was
noticed ranging from 7.2 mm
(P<0.001) in group 2 to 8.8 mm
(P<0.001) in group 1 (Figure 1). Once
again, there was no significant diffe-
rence between the three groups of
patients.
REFERENCES
1. Bakri F. Interaction d’une fraction
flavonoïque avec la noradrenaline
sur la veine saphène humaine isolée.
Phlébologie. 1989;2:669-671.
2. Ibegbuna V, Nicolaides AN, Sowade O,
et al. Venous elasticity after treatment
with Daflon 500 mg. Angiology.
1997;48:45-49.
3. Cotonat J. Lymphalogue and pulsatile
activities of Daflon 500 mg on canine
thoracic lymph duct. Int Angiology.
1989;8(suppl 4):15-18.
FIGURE 1.
Mean decrease in ankle circumference
after 2 months’ treatment with Daflon 500 mg.
Whatever the dosage regimen, Daflon 500 mg fights edema
in patients suffering from CVI.
Conclusion the evening, significantly relieves
patients from their symptoms and
This double-blind, randomized reduces leg edema. No influence of
controlled- trial shows that, whatever chronobiology on therapeutic acti-
the dosage regimen of Daflon vity of Daflon 500 mg was observed.
500 mg, patients are significantly Daflon 500 mg relieves patients
relieved from signs and symptoms of regardless of the therapeutic
chronic venous insufficiency. schedule, and therefore, to fight
Daflon 500 mg, 2 tablets daily in the edema, Daflon 500 mg can be
morning, or in the evening, or prescribed at a once daily dosage
1 tablet in the morning and in (2 tablets a day).
4. Gargouil YM, Perdrix L, Chapelain B, 7. Barbe R, Amiel M. Pharmacodynamic
Gaborieau R. Effects of Daflon 500 mg on properties and therapeutic efficacy of
bovine vessel contractility. Int Angiology. Daflon 500 mg. Phlebology. 1992;7(suppl 2):
1989;8(suppl 4):19-22. 41-44.
5. Korthuis RJ, Gute DC. Postischemic 8. Tsouderos Y. Efficacy of Daflon 500 mg
leukocyte/endothelial cell interactions and in the treatment of chronic venous
microvascular barrier disruption in skeletal insufficiency. Phlebology. 1992;7(suppl 2):45-49.
muscle: Cellular mechanisms and effect
of Daflon 500 mg. Int J Microcirc. 1997; 9. Laurent R, Gilly R, Frilleux C. Clinical
17(suppl 1):11-17. evaluation of a venotropic drug in man.
Int Angiol. 1998;7(suppl 2):39-43.
6. Friesenecker B, Tsai AG, Allegra C,
Intaglietta M. Oral administration of purified 10. Menyhei G, Acsady G, Hetenyi A,
micronized flavonoid fraction suppresses Dubeaux D, Rado G. Chronobiology and
leukocyte adhesion in ischemia-reperfusion clinical activity of Daflon 500 mg in chronic
injury: in vivo observations in the hamster venous insufficiency. Phlebology. 1994;
skin fold. Int J Microcirc. 1994;14:50-54. (suppl 1):15-18.
13
 BOOKSHELF
ABSTRACTS
Treatment of chronic postmastectomy
lymphedema with low-level laser therapy:
a 2.5-year follow-up.
N. B. PILLER, A. THELANDER.
Lymphology. 1998;31:74-86.
Ten women with unilateral lymphedema of the arm after
extirpation of axillary lymph nodes (radical mastectomy)
and radiotherapy for breast cancer were given 16 ses-
sions of treatment with low-level laser therapy for
10 weeks, and there was a 36-week follow-up period in
7 patients.
The effect of the laser treatment was monitored by mea-
surement of the circumference of the arm, plethysmo-
graphy, tonometry, bioimpedance, and a questionnaire
on subjective symptoms.
After the treatment the volume of the edema was reduc-
ed, the tissues became softer, and an improvement in
pain, pressure, heaviness, cramps, pricking sensation,
and mobility was observed.
The data obtained suggest that laser treatment provides
objective and subjective improvement, at least at the
beginning, in the parameters of lymphedema of the arm.
14
Krossektomie als Embolieprophylaxe
S. STRATMENN, P. DEKER, A. HIRNER.
Phlebologie. 1998;27;70-73.
Generally speaking, cases of superficial thrombophle-
bitis recover without complications, but in some cases
they may have serious consequences. Propagation of the
thrombi in the deep venous system may give rise to a
pulmonary embolism.
Within the space of 2 years, we observed progression of
the thrombus from the great saphenous vein to the
common femoral vein in 5 cases. Thrombectomy of the
latter, and crossectomy and partial resection of the
saphenous vein, were carried out in order to prevent a
pulmonary embolism.
The thrombus may travel upwards by three anatomical
routes: saphenofemoral, saphenopopliteal, and perforat-
ing veins.
 ABSTRACTS
A randomized study comparing manual
lymph drainage with sequential pneumatic
compression for treatment
of postoperative arm lymphedema.
K. JOHANSSON, E. LIE,
C. EKDHAL, J. LINDFELDT.
Lymphology. 1998;31:56-64.
A prospective study is presented which was carried out
in 28 women with unilateral postmastectomy lymphe-
dema from dissection of axillary lymph nodes, followed
up for a period of 2.5 years.
Treatment by manual lymph drainage was compared with
sequential pneumatic compression.
After 2 weeks of treatment, each patient was randomized
to one of the two therapeutic regimens.
Manual lymph massage was carried out with Vodder’s
technique (45 min/day) and a pressure of 40 to 60 mm Hg
was used for the sequential pneumatic compression
treatment (2 h/day).
Both treatments lasted 2 weeks. The volume of the arm
was measured by means of displacement of water.
The reduction in lymphedema was 49 mL (7% reduction)
(P=0.01) in the group as a whole. In the lymph drainage
massage group the reduction was 75 mL (15%) (P<0.001)
and in the pneumatic compression group it was 28 mL
(7%) (P=0.03).
Separately, lymph drainage massage and intermittent
pneumatic compression produced a significant differ-
ence in the volume of the arm, but no significant differ-
ence could be detected between the two methods of
treatment.
15
Genexpresion von Matrix
Metalloproteinasen
und deren Inhibitoren bei
Dermatoliposklerose
Y. HEROUY, A. E. MAY, T. HEISTERKAMP,
M. HARTMENN, E. SCÖPF, N. NORGAUER, W. VANSCHEIDT.
Phlebologie. 1997:26;150-154.
Lipodermatosclerosis is characterized by an increase in
deposits of the matrix components, such as the mole-
cules of collagen in the reticular dermis, producing
hardening of the skin similar to that observed in
scleroderma.
The pathophysiological mechanisms of the etiology of
venous ulcers of the lower limbs have not yet been
elucidated.
The authors studied collagen-degraded proteolytic
enzyme from the gene family of the matrix metallopro-
teinases and its expression in extracts of skin from
patients suffering from lipodermatosclerosis.
To identify the specific mRNA transcriptors, they used
the technique of inverse transcription and amplification
in a chain of polymerases (RT-PCR). In all the skin
samples (N=20) a significant increase was found in mRNA
expression of MMP-1, MMP-2, and TIMP-1, compared
with normal skin (N=10). However, no significant differ-
ence was found for the mRNA transcriptor of MMP-9 and
TIMP-2.
Lipodermatosclerosis is characterized by a transcription
imbalance between interstitial collagenase MMP-2 and
its specific inhibitor TIMP-2. Transcription induction of
proteolytic enzyme MMP-2 may play an important role in
the pathogenesis of ulcer formation.
 LYMPHOLOGY
Pathophysiology of secondary
lymphedema
M. J. W. HUSMANN, MD, U. K. FRANZECK, MD (Switzerland)
Introduction
The functional lymphatic system is
capable of draining the lymph fluid
from the interstitial space back to the
blood vessels in physiological quan-
tities. The lymph time volume
increases to compensate an enhanc-
ed lymph fluid accumulation. The
maximum lymph fluid time volume is
called the "transport capacity"and is
capable of managing 10 times the
amount of the lymph fluid that is pro-
duced under physiological condi-
tions. Lymphedema is caused by
low-volume insufficiency of the lym-
phatic system. An underlying patho-
logical process has diminished the
transport capacity and therefore the
lymph fluid is not drained in suf-
ficient quantities. Other additional
pathological processes increasing
the amount of interstitial lymph fluid
may lead to an overload of the maxi-
mum transport capacity of the lym-
phatic system.
Secondary lymphedemas are caused
either by obstruction of the proximal
lymph nodes and collectors, by
impaired flow of the lymph, or by
involvement of the initial lymphatics.
Mechanical insufficiency leads to
lymph stasis, and hence to valvular
insufficiency, as a consequence of
the lymphatic hypertension dilating
the lymphatic vessels. Impaired
initial lymphatics cannot provide
drainage of the capillary ultrafiltrate,
or have increased permeability.
Physiology and
pathophysiology
Capillary filtration rate Jv is describ-
ed by the Landis-Starling expres-
sion1:
Jv = Lp A {(Pc – Pi) – σ (πp - πi)}
where Lp is capillary wall hydraulic
conductance, A is area, P is hydraulic
pressure, π is colloid osmotic pres-
sure (oncotic pressure), subscripts
“c”, “i”, and “p” refer to capillary
blood, interstitial fluid, and plasma,
respectively, and σ is the protein
reflection coefficient.
16
In active hyperperfusion the Jv
increases due to the increased blood
capillary pressure Pc . The increased
ultrafiltrate is regulated by two pas-
sive mechanisms that prevent
edema formation. The increased
ultrafiltrate raises the interstitial
fluid pressure Pi. Hence, the result-
ing filtrating pressure Pc – Pi is
decreased again.2-6 The accumula-
tion of interstitial fluid dilutes the
interstitial proteins and πi drops.
Consequently the effective reabsorb-
ing forces improve.
Additionally, the lymph fluid drain-
age increases due to the enhanced
accumulation of interstitial fluid, and
regulates the disturbed Starling
balance caused by hyperperfusion.7-9
This active edema-preventing
function is impaired in lymphedema,
either by impaired uptake of the
capillary ultrafiltrate by the inital
lymphatics or by insufficent lymph
fluid drainage. Reduced flow or
stasis of lymph can result from lym-
phatic hypoplasia or aplasia, from
obliteration of lymphatic trunks or
lymph nodes, from the absence or
insufficiency of lymphatic valves, or
from impaired lymphatic contrac-
tility.10
Mechanical insufficiency leads to
lymph stasis and hence to valvular
insufficiency as a consequence of the
lymphatic hypertension dilating the
lymphatic vessels.
Due to the reflux, cysts and fistulas
may develop. Further, infections
erupt more easily, as lymphangitis or
lymphnoditis, and may result in even
further decreased capacity of lymph
transport.11
Increased accumulation of extracel-
lular lymph fluid results in increased
concentration of protein in the inter-
stitial tissue, hyperkeratosis in the
epidermis, inflammatory cell infiltra-
tions, and hypertrophy of the cuta-
neous fibroblastic tissue. The high
concentration of proteins in the
capillary ultrafiltrate in lymphedema
of 1 to 4 g/100 mL (the interstitial
protein concentration in cardiac and
venous edema is 0.1 to 0.9 g/100 mL)
serves as a very good nutritional
basis for the fibrogenesis.12,13 Fat
TABLE 1.
Causes of secondary lymphedema.
1. Posttraumatic
2. Lymphangitis
• Infectious
– bacteria
– viruses
– parasites
(filaria)
– mycosis
• Chemical
environmental
accumulation and abundant fibro-
blasts cause degeneration of the
musculature and result in the clini-
cally typical firm lymphedema with
fibrosis.
Clinical stages
of lymphedema
Secondary lymphedema has a huge
variety of causes (Table I) and differ-
ent stages. Generally, there is a time
interval between the trauma to the
lymphatics and the onset of swelling
in secondary lymphedema. During
this latency stage (stage 0) there is no
edema, but a decreased transport
capacity for lymph fluid.11
The manifestation of lymphedema is
caused by:
• organic or functional disorder of the
overloaded lymphatic pumps;
• the appearance of accompanying
diseases that enhance the lymph
fluid accumulation;
• combination of these two possibili-
ties.
3. Malignancy
4. Iatrogenic
5. Artificial
6. Retroperitoneal fibrosis
(M.Ormond)
7. Various
17
Stage 0 may endure for a lifetime or
progress to lymphedema after
months or years.
Stage I is characterized by a soft
edema. Fibrosclerotic changes lead
to firm tissue swelling (stage II). The
development of stage III (lympho-
static elephantiasis) is accelerated
by recurrent erysipelas. Chronic lym-
phedema may end in angiosarcoma
(Stewart-Treves Syndrome).14
Advances
in assessment of
the pathophysiology
of secondary
lymphedema
New microcirculatory techniques
such as fluorescence microlympho-
graphy15 and microlymphatic pres-
sure measurements16 allow further
investigation and understanding of
secondary lymphedema. Both are
relatively atraumatic investigations
and are easily applicable in humans
in vivo.
Fluorescence
microlymphography
This technique has been developed
for visualization of lymph microves-
sels of the superficial skin.
The lymphatic capillaries are visual-
ized using FITC-dextran (fluores-
cein isothiocyanate-labelled dextran
150'000; Sigma Chemical Co, St
Louis, MO, USA) as a contrast
medium. FITC-dextran (0.01 mL; 25%
solution) is injected into the subepi-
dermal layer of the skin using a steel
microneedle (A. Bott, Zurich, Swit-
zerland) connected to a microsyringe
(Hamilton, Bonaduz, Switzerland).
The injection is performed under
microscopic control by means of
videomicroscopy. From the deposit,

FIGURE 1.
Increased spread of the dye in the inital lymphatics of the skin
in a patient with secondary lymphedema.
FIGURE 2.
Cutaneous backflow of the fluorescent contrast medium.
There is no visible microlymphatic junction between the initial deposit
and lymphatic network and these meshes.
18
the dye fills the lymph capillaries
and, acting as a contrast medium,
makes them visible in fluorescent
light (450-490 nm).
This technique is very useful for
assessing the lymph capillary mor-
phology, the extension of the dye in
the network in terms of the maximum
distance in one direction measured
from the border of the dye deposit or
of the area of the lymphatic network,
the lymph capillary diameters, and
the permeability.
Fluorescence
microlymphographic findings
The morphology in secondary lym-
phedema may present an increased
area of microlymphatic network. The
normal maximum distance between
deposit edge and the most distant
meshes filled by FITC-dextran
150'000 is below 12 mm.17 In
secondary lymphedema the mean
maximum distances are greater than
12 mm (Figure 1).
There are changes in capillary
diameters, capillary fragments, and
“cutoffs” of single capillaries that are
obstructed or evaginated lymph
capillaries. Refilling of microlympha-
tic network that is independent of
the original dye deposit is called a
cutaneous backflow, and is caused by
insufficient valves of deeper lym-
phatic pathways (Figure 2). All these
signs are found in generalized or
localized secondary lymphedema as
well as in primary lymphedema, and
hence do not allow differentiation
of primary and secondary lymphe-
dema.18
Microlymphatic pressure
measurements
Subsequent to the staining of the
initial lymphatics, microlymphatic
and interstitial pressure is measured
using the servo-nulling pressure

FIGURE 3.
The glass micropipette is inserted into a lymph capillary
for pressure measurement.
The tip of the micropipette is filled with dye.
FIGURE 4.
The glass micropipette is inserted into a lymph capillary-free area
for interstitial fluid pressure measurement.
19
system (Model 5A; IPM, San Diego,
CA, USA), a counterpressure pump
(Typ 203; Lung Dynamics Systems,
Royston, UK), a pressure transducer
(Spectra Med P 23 XL, Statham, USA),
and a pressure amplifier (Biophysi-
cal Universal Amplifier 13-4615-58;
Gould, Cleveland, OH, USA). A glass
micropipette with a tip diameter of 7
to 9 µm is inserted into a lymphatic
capillary (Figure 3) as well as into a
lymph capillary-free area (Figure 4),
which was well-delineated by lym-
phatic capillaries, by means of a
micromanipulator (Leica, Glattbrugg,
Switzerland) and under microscopic
control (Figure 5).
Traumatic and
iatrogenic secondary
lymphedema
Traumatic or iatrogenic lymphedema
may be localized, as in distorsion of
the ankle or by scars, or be generaliz-
ed, involving the whole limb, as in
postmastectomy edema or inguinal
lymphnodectomy.
Postmastectomy edema
Surgery for breast cancer and axillary
lymphadenectomy are well-known
causes of secondary lymphedema.
Microlymphography reveals an
increased spread of the dye in the
superficial microlymphatic network
and a pathological morphology after
inflammatory skin damage.19,20 In
cases with recurrent erysipelata, only
the deposit, without any staining of
microlymphatics, has been found.
This may be due to a local destruc-
tion and obliteration of the lymph
capillaries by recurrent inflamma-
tion19 (Husmann et al, unpublished
data, 1998).
In another study, using fluorescence
microlymphography and stereolo-

Increased microlymphatic and interstitial pressures
40
Pressure
20
(mm Hg)
Inspiration
Expiration
35 seconds
gical methods, an increased density
of microlymph vessels and increased
total length of filled vessels was
found.20 The authors speculate that
there is rerouting of collaterals in the
skin or angiogenesis. Bates et al21,22
found increased net pressure of the
interstitium opposing capillary
blood pressure. This should reduce
filtration rate, if capillary pressure is
unaltered, which should hence raise
interstitial protein concentration and
interstitial oncotic pressure. Unex-
pectedly, they found a decreased
interstitial protein concentration and
suggest that the pathophysiology of
postmastectomy edema involves
additional mechanisms besides
reduced lymphatic damage, such as
increased blood capillary filtration
and impaired venous outflow from
the extremities.
FIGURE 5.
in a patient with secondary lymphedema.
LYMPHATIC PRESSURE
New findings
in secondary forms
of lymphedema
Systemic sclerosis
A recent study in our microcirculation
laboratory in 16 patients with
systemic sclerosis showed a signifi-
cantly enlarged network extension
at the dorsum of the fingers with
8.1±6.0 mm vs 2.0±0.8 mm in controls
(n=16; P<0.01).23 Cutaneous backflow
was found in 3 patients versus none
in controls (P<0.05). Also, at the
dorsum of the hand, network exten-
sion differed significantly between
patients and controls (3.8±2.4 mm vs
1.2±0.8 mm; P<0.01). It is concluded
that patients with systemic sclerosis
20
INTERSTITIAL PRESSURE
and secondary Raynaud phenome-
non show a distinct microangiopathy
of the skin lymph capillaries in clini-
cally affected areas, with swelling of
the fingers and hands. The changes
increase from proximal to distal at
the hand and may be an important
factor for the edema in these
patients.
Psoriasis
Patients with psoriasis show com-
plete absence of well-delineated
microlymphatics in the center of the
skin lesion. Furthermore, an enlarged
network of microlymphatics could
be visualized in perilesional skin,
extending in the direction of normal
skin, and a marked reduction in
microlymphatics extending into the
lesion. In unaffected skin areas the
patients showed normal superficial
lymph capillaries.24 The presence of
lymph capillaries has been describ-
ed in biopsies from active psoriatic
lesions.25 This findings suggest
impaired function of the lymph
capillaries in the psoriatic lesion and
compensation via the inital lympha-
tics in the surrounding skin. Several
studies confirmed an increased
leakage of blood capillaries in
psoriatic lesions resulting in increas-
ed net filtration.26 Together with the
impaired function of the initial lym-
phatics, local edema develops.
REFERENCES
1. Starling EH. On the absorption of fluids
from the connective tissue spaces.
J Physiol (Lond). 1896;19:312.
2. Guyton AC, Granger HJ, Taylor AE.
Interstitial fluid pressure. Physiol Rev.
1971;51:527-563.
3. Michel CC. Fluid movement through
capillary walls. In: Renkin EM, Michel CC,
eds. Microcirculation. Part I. Handbook of
Physiology. Section 2 - The Cardiovascular
System; vol IV. Bethesda, MD: American
Physiological Society; 1984;375-409.
4. Pippard CJ, Roddie IC. Lymph flow in
sheep limbs during local exposure to
subatmospheric pressure. J Physiol (Lond).
1989;419:45-57.
5. Landis EM, Gibbon JH. The effect
of temperature and tissue pressure on
the movement of fluid through the human
capillary wall. J Clin Invest. 1933;12:105-138.
6. Bates DO, Levick JR, Mortimer PS.
Subcutaneous interstitial fluid pressure and
arm volume in lymphedema. Int J Microcirc
Clin Exp. 1992;11:359-373.
7. Wiederhielm CA, Weston BV.
Microvascular, lymphatic and tissue pressure
in the unanaesthetized mammal.
Am J Physiol. 1973;225:992-996.
8. Hogan RD, Gibson WH, Granger HJ,
Guyton AC. The initial lymphatics as sensors
of interstitial fluid volume. Microvasc Res.
1986;31:317-324.
9. Taylor AE, Gibson WH, Granger HJ,
Guyton AC. The interaction between
intracapillary and tissue forces in the overall
regulation of interstitial fluid volume.
Lymphology. 1973;6:192-208.
Conclusion
The functioning lymphatic system is
capable of managing increased
extracellular fluid accumulation. In
secondary lymphedema, the lym-
phatic clearance is disordered,
either by impaired uptake of the
capillary ultrafiltrate or by reduced
lymph flow. If a distal area is affected,
localized edema arises. If proximal
lymph vessels or lymph nodes are
affected, generalized lymphedema
may develop. Additionally, increas-
ed capillary filtration may accelerate
and sustain edema formation.
10. Szuba A, Rockson SG. Lymphedema:
anatomy, physiology and pathogenesis.
Vasc Med. 1997;2:321-326.
11. Földi M, Casley-Smith JR.
Lymphangiology. Schattauerverlag;1983.
12. Olszewski WL, Engeset A. Immune
proteins and other biochemical constituents
of peripheral lymph in patients with
malignancy and postradiation lymphedema.
Lymphology. 1978;11:174-180.
13. Olszewski WL, Ningfei L. Immune events
in human skin-changes produced by local
microwave hyperthermia in lymph stasis.
Eur Surg Res. 1990;22:90-91.
14. Enzinger FE, Weiss SW. Angiosarcoma
associated with lymphedema. In: Soft Tissue
Tumors. 3rd ed. St. Louis: Mosby;
1995;650-652.
15. Bollinger A, Jäger K, Sgier F, Seglias J.
Fluorescence microlymphography.
Circulation. 1981;64:1195-1200.
16. Spiegel M, Vesti B, Shore A, Franzeck UK,
Becker F, Bollinger A. Pressure of lymphatic
capillaries in human skin. Am J Physiol.
1992;262:H1208-1210.
17. Isenring G, Franzeck UK, Bollinger A.
Fluorescence microlymphography at the
ankle in healthy and in patients with primary
lymphedema. Schw Med Wochenschr. 1982;
112: 225-231.
18. Jäger K, Isenring G, Bollinger A.
Fluorescence microlymphography in patients
with lymphedema and chronic venous
incompetence. Int Angiol. 1983;2:129-136.
21
Therapy consists of combined
decongestive physical therapy and
the treatment of diseases that
increase capillary filtration.
Address
for correspondence
Prof U. K. Franzeck, MD
Department of Medicine
Division of Vascular Medicine
(Angiology)
University Hospital Zurich
Raemistrasse 100
CH-8091 Zurich - Switzerland
E-mail: ukfranzeck@angiology.ch
19. Baer-Suryadinata C, Clodius L,
Isenring G, Bollinger. Lymphcapillaries
in postmastectomy lymphedema.
In: Bollinger A, Partsch H, Wolfe JHN. The
Initial Lymphatics: New Methods and Findings.
Stuttgart, Germany: Thieme;1985:158-181.
20. Stanton AWB, Kadoo P, Mortimer PS,
Levick JR. Quantification of the initial
lymphatic network in normal human forearm
skin using fluorescence microlymphography
and stereological methods. Microvasc Res.
1997;54:156-163.
21. Bates DO, Levick JR, Mortimer PS. Change
in macromolecular composition of interstitial
fluid from swollen arms after breast cancer
treatment, and its implication. Clin Sci
(Colch). 1993;85:737-746.
22. Bates DO, Levick JR, Mortimer PS. Starling
pressures and their alteration in
postmastectomy edema. J Physiol (Lond).
1994;477:355-363.
23. Leu AJ, Gretener SB, Enderlin S.
Lymphatic microangiopathy of the skin in
systemic sclerosis. Br J Rheumatol. In press.
24. Cliff S, Bedlow A, Läuchli S, Mortimer P,
Franzeck UK. Skin microlymphatics in
patients with psoriasis. Int J Microcirc Clin
Exp. 1996;16(S1):164.
25. Bacharch-Buhles M, Gammal-El S, Panz B,
Altmeyer P. In psoriasis the epidermis,
including the subepidermal vascular plexus,
grows downwards into the dermis.
Br J Dermatol. 1997;136:97-101.
26. Bull RH, Bates DO, Mortimer PS. Intravital
video-capillaroscopy for the study of the
micorcirculation in psoriasis. Br J Dermatol.
1992;126:436-445.
 NEWS
Announcements
• One of the pioneers of lymphology, Dr Carlos
Granval, died last year in Buenos Aires (Argentina).
He was the organizer of the Vth International
Lymphology Congress in 1995, together with Prof
Ruben Carlos Mayall. He founded the Lymphology
Association of Argentina, contributing, with his work
on onco-lymphology, to raising the status of Latin
American lymphology.
• One of the most distinguished German phlebo-
logists, Dr Freye Heid-Fischer, who established the
Fischer School, died in February 1998 after a long
illness. Her book Venenerkrankungen, Phlebologie für
Klinik und Praxis, made six editions, one of which was
in Spanish. Despite being engaged in private prac-
tice, she established a large school, and the “Fischer”
method of compression is known throughout the
world.
• The German Phlebology Society has recently
published the Rules of Conduct for various venous
diseases, in the journal Phlebologie (1998): diagnosis
FORTHCOMING CONGRESSES
 INTERNATIONAL SOCIETY ON
THROMBOSIS AND HAEMOSTASIS (ISTH)
XVIIth BIENNAL CONGRESS, SCIENTIFIC
AND STANDARDIZATION COMMITTEE
XVTH ANNUAL MEETING
This congress will be held in Washington (USA)
from August 15 to 21, 1999.
• For further information, please contact:
CB 7035, UNC Medical School
Chapel Hill, NC 27599-7035, USA
Tel: 1 919 929 387
Fax: 1 919 929 3935
22
and treatment of pelvic DVTs; methods of
compression; pressure bandages; methods of
prophylaxis of venous thromboembolic disease;
intermittent compression; and thromboembolic
prophylaxis.
We consider this initiative of great value both to
specialists and to general practitioners.
• The Joint Meeting of the German Society of Clinical
Microcirculation and Haemorrheology, the German
Society of Microcirculation, and the Tübigne Study
Group for Vascular diseases was held in Tübingen
from September 30 to October 3, 1998, under the
aegis of the European Society of Microcirculation.
Dr Michael Jünger, President of the Congress, has
focused his program on four major topics: diabetes
angiopathy, lipid disorders in cardiovascular
disease, angiogenesis, and wound healing. More
than 200 researchers attended this congress where
120 papers and 70 posters were presented.
 XXIVth WORLD CONGRESS
OF THE INTERNATIONAL SOCIETY
FOR CARDIOVASCULAR SURGERY
This congress will be held in Melbourne (Australia)
from September 12 to 16, 1999.
• For further information, please contact:
The International Society for Cardiovascular Surgery
World Congress
13 Elm Street
Manchester, MA 01944, USA
Tel: 1 508 526 8330
Fax: 1 508 526 7521
 INTERNATIONAL SOCIETY OF Centre, Cardiology Department
LYMPHOLOGY (ISL) Klinik Cardio, Jl.
XVIIth BIENNAL INTERNATIONAL Ciniru VI N°13, Jakarta, Indonesia
Tel: 62 21 568 40 85 ext. 1426
CONGRESS
Fax: 62 21 910 12 25
This congress will be held in Chennai (India) E-mail: rilant@indosat.net.id
from September 19 to 25, 1999.
• For further information, please contact:
President: Prof S. Jamal  FORUM VENOSO LATINOAMERICANO
Organizing Secretary: Dr G Manokaran
This congress will be held in Cancun (Mexico)
Lymphology Society of India
from October 31 to November 4, 1999.
Registered Office: 30 B, II Street
Rajappanager, Thanjavur 613007, India • For further information, please contact:
Tel: 91 44 826 7864 President: Dr Jorge Ulloa Domínguez
Fax: 91 44 826 6781 Calle 47 # 22 -59
E-mail: ahel.apollo@gems.vsnl.net.in Bogota, Colombia
Tel: 571 320 25 11
Fax: 571 288 75 59
E-mail: julloa@usa.net
 CONGRESS OF THE UNION
INTERNATIONALE DE PHLEBOLOGIE -
EUROPEAN CHAPTER
 XIXth WORLD CONGRESS OF THE
This congress will be held in Bremen (Germany)
from September 26 to October 1, 1999.
INTERNATIONAL UNION OF ANGIOLOGY
This congress will be held in Gent (Belgium)
• For further information, please contact:
from May 1 to 5, 2000.
President: Prof W. Lechner
Fax: 49 49 32 805 20 • For further information, please contact:
Prof E. Rabe Prof D. Clement
Universität-Hautklinik Bonn University Hospital
Sigmund Freud Strasse, 25 Cardiology-Angiology Department
D-53105 Bonn, Germany De Pintelaan, 185
Tel: 49 22 82 87 53 70 or 66 30 B-9000 Gent, Belgium
Fax: 49 22 82 87 43 33 Tel: 32 92 40 34 80
E-mail: congress partner.bremen@tonline.de Fax: 32 92 40 34 62
Congress Partner GmbH
Birkenstrasse 37
D28195 Bremen, Germany
 IXth CONGRESO PANAMERICANO
Tel: 49 421 30 31 30
DE FLEBOLOGIA Y LINFOLOGIA
Fax: 49 421 30 31 33
This congress will be held in Córdoba (Argentina)
from May 31, June 3, 2000.
• For further information, please contact:
 IVth ASIAN CONGRESS
President: Dr Never Rosli/ Sociedad Panamericana
FOR MICROCIRCULATION (ACM)
de Flebologia
This congress will be held in Yogyakarta (Indonesia) Alvear 327
from October 23 to 25, 1999. (5000) Córdoba, Argentina
• For further information, please contact: Tel: 54 51 241 515
President: Prof Dr Lily Ismudiati Rilantono SpJP Fax: 54 51 241 515
Head of Research & Development, National Cardiac E-mail: fleborosli@powernet.com.ar

23
 XXIst EUROPEAN CONGRESS Medical School, Chapel Hill
OF MICROCIRCULATION (ESM) NC 27599-7035, USA
Tel: 1 919 929 3807
This congress will be held in Stockholm (Sweden)
Fax: 1 919 929 3935
from June 4 to 7, 2000.
• For further information, please contact:
President: Prof B. Fagrell  INTERNATIONAL COLLEGE OF ANGIOLOGY
Karolinska Hospital (ICA) XLIIIrd ANNUAL MEETING
Department of medicine This congress will be held in Vienna (Austria)
S-171 76 Stockholm from July 2001.
Sweden
• For further information, please contact:
Tel: 46 8 5177 5402
D. M. Rossignol
Fax: 46 8 34 42 93
5 Daremy Court
E-mail: befa@divmed.ks.se
Nesconset NY 11767, USA
Tel: 1 516 366 1429
Fax: 1 516 366 3609
 INTERNATIONAL COLLEGE
OF ANGIOLOGY (ICA)
LXIIth ANNUAL MEETING  VIIth WORLD CONGRESS
This congress will be held in Las Vegas (USA) FOR MICROCIRCULATION
in July 2000. The VIIth World Congress for Microcirculation will be
• For further information, please contact: held from19 to 23 August 2001 in Sydney (Australia).
D. M. Rossignol • For further information, please contact:
5 Daremy Court, Nesconset 7th WCM - 13 Jeffrey Street
NY 11767, USA Mt Waverley, Victoria 3149, Australia
Tel: 1 516 366 1429 Fax: 61 3 9887 8773
Fax: 1 516 366 3609 E-mail: ca@netwide.com.au
• For information regarding the scientific program,
please contact:
 INTERNATIONAL LIAISON GROUP Michel Perry
FOR MICROCIRCULATION (ILGM) School of Physiology and Pharmacology
This congress will be held in Sydney (Australia) University of New South Wales
in 2001. Sydney, NSW 2052, Australia
Fax: 61 2 9385 1059
• For further information, please contact:
E-mail: M. Perry@unsw.edu.au
Clinical Research Centre
Web page for the 7th WCM:
University Hospital, 581 85 Linköping, Sweden
http://som.flinders.edu.au/amcirc/world.htm

 INTERNATIONAL SOCIETY ON  THE XIVth CONGRESS OF UNION

THROMBOSIS & HAEMOSTASIS (ISTH)
XVIIIth CONGRESS & SCIENTIFIC AND
STANDARDIZATION COMMITTEE (SSC)
XLVIITH ANNUAL MEETING
This congress will be held in Paris (France)
from June 30 to July 6, 2001.
• For further information, please contact:
ISTH, CB 7035
University of North Carolina.
INTERNATIONALE DE PHLEBOLOGIE
Rome (Italy), 14 to 16 September, 2001
• For further information, please contact:
Prof C. Allegra
Ospedale S. Giovanni
Via S. Giovanni Laterano, 155
00184 Rome, Italy
Fax: 39 6 77055582/70493570
E-mail: angiolsg@pronet.it or c.allegra@pronet.it

24
 ADVISORY BOARD
President

J. A. JIMÉNEZ COSSÍO, MD
Head, Dept of Angiology and
Vascular Surgery
La Paz Hospital
28043 Madrid, Spain

Members

C. ALLEGRA, MD A. N. NICOLAIDES, MD
Head, Dept of Angiology Professor of Vascular Surgery
Hospital S. Giovanni Honorary Consultant Vascular Surgeon
Via S. Giovanni Laterano, 155 Academic Vascular Surgery
00184, Rome, Italy St Mary’s Hospital
London W2 1NY, UK

P. COLERIDGE SMITH, MD
Senior Lecturer and Consultant Surgeon H. PARTSCH, MD
University College London Medical School Head, Dept of Dermatology
The Middlesex Hospital Dermatologische Abteilung
Mortimer Street Wilhelminenspital der Stadt Wien
London W1N 8AA, UK Montleart str. 37
1160 Vienna, Austria

M. COSPITE, MD M. PERRIN, MD
Head, Dept of Angiology
Chirurgie Vasculaire
University Clinic Past President of the Société de Chirurgie Vasculaire
Palermo, Italy de Langue Française
President of the Société Française de Phlébologie
G. JANTET, MD 2, avenue Léon Blum
69150 Décines Charpieu, France
Professor of Vascular Surgery
Consultant Vascular Surgeon
President of the Union Internationale de Phlébologie L. THIERY, MD
14, rue Duroc, Angiologist & Surgeon
75007 Paris, France Consultant, University Hospital Gent
Korte Meer 12, 900 Gent, Belgium
P. S. MORTIMER, MD
Consultant Skin Physician & Senior Lecturer V. WIENERT, MD
in Medicine (Dermatology) Head, Dept of Phlebology
St George’s Hospital University Clinic
Black Shaw Road Pauwelstrasse
London SW 17 OQT, UK 51000 Aachen, Germany
 99 DN 059 BA

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