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68 The Chronically Swollen Leg: Finding the Cause
nutrients move through the interstitial fl uid largely by diffusion. Diffusion
is an effi cient transport system over short distances (micrometers), but very
ineffi cient at large distances (millimeters). Also, edema fl uid is a good
culture medium, and swollen limbs are prone to infections that can be dif-
fi cult to eradicate and are prone to recurrence. Lastly, patients want treat-
ment. Their symptoms may be minimal, often none or only a vague feeling
of heaviness. However, they know the swelling indicates that something is
wrong, and they want something done about it.
FLUID EXCHANGE IN THE
MICROCIRCULATION
The exchange of fl uids between the blood and interstitium takes place
at the capillary level of the microcirculation. A diagrammatic microcircula-
tion unit is shown in Figure 6-1. The exchange of fl uid between the intra-
vascular and interstitial spaces is the result of forces in the form of hydraulic
and osmotic pressures. Systemic arterial pressure is reduced by the arteri-
oles and precapillary sphincters to approximately 30 mmHg. The systolic-
ELUNEV ELOIRETR
A
CAPILLARY
INTERSTITIAL SPACE
LYMPH ANGION
FIGURE 6-1 Diagrammatic microcirculation unit.
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The Chronically Swollen Leg: Finding the Cause 69
diastolic variation of pressure is typically only 1–2 mmHg or 2–4 mmHg
with dilation of the precapillary sphincters. The resistance of the micro-
circulation vessels causes a further reduction in pressure such that in a
supine patient, the blood enters the arterial end of the capillaries with a
pressure of approximately 30 mmHg and leaves the venular end with a
pressure of 10 mmHg. The fl uid/hydraulic pressure of the interstitial space
in a normal subject is approximately 0 mmHg. Thus, the net effect of
hydraulic pressure is to force fl uid out of the capillaries and into the
interstitium.
Opposing these “outward” forces is an osmotic pressure gradient, which
is the result of the proteinaceous colloids in the blood and interstitium.
These colloids make up only a small percentage of the total plasma osmotic
pressure, but because they are the main molecules that cannot cross the
capillary wall, they are responsible for the osmotic pressure gradient
between the plasma and the interstitium. This colloid osmotic pressure is
usually referred to as the oncotic pressure. The oncotic pressure of the
plasma is typically 28 mmHg. Only a small fraction of the plasma is fi ltered
during a single transit through the microcirculation, and the oncotic pres-
sure remains at approximately 28 mmHg throughout the circulatory system.
The oncotic pressure of the interstitium is typically 8 mmHg. Thus, the
effect of the osmotic forces across the capillary walls is to cause fl uid to
fl ow from the interstitium into the capillary lumen.
The net effects of the hydraulic and osmotic pressures are shown in
Figure 6-2. At the arterial end of capillaries the net forces of 30 mmHg
hydraulic versus 20 mmHg oncotic causes fl uid to leave the capillary and
fl ow into the interstitium. As the blood transits the capillary, the hydraulic
forces diminish and the net effect at the venular end of the capillary is for
fl uid to pass from the interstitium into the capillary.
The net effect of these forces and the resulting fl uid fl ux were quantifi ed
by Starling in 1896.
2
The equation, known as Starling’s hypothesis, is shown
in Figure 6-3. Several modifi cations have been made to Starling’s hypoth-
esis to adjust for experimental observations and other factors; however, it
is still a very good working model.
Normally, the above-described forces maintain a good, but not perfect,
balance of fl uid between the circulation and the interstitial tissues. There
is usually a slight excess of fl uid fl owing into the interstitium with time.
This excess is normally removed by the lymphatics. Total lymphatic fl ow
in the body is, however, only about 2 liters per day.
MECHANISMS OF EDEMA
Examination of the Starling equation and Figure 6-2 reveals there are
four possible mechanisms of edema formation. They are (1) an increase in
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70 The Chronically Swollen Leg: Finding the Cause
the hydraulic pressure gradient, (2) a decrease in the oncotic pressure
gradient, (3) increased capillary permeability, and (4) decreased lymphatic
fl ow.
The result of an increased hydraulic pressure gradient (an elevation
of Pc in the Starling equation) can occur on either the arterial or venous
end of the capillary. On the arterial end, the mechanism is usually relax-
ation of the arteriolar sphincters. This can be the result of infl ammation
(from any cause) and medications. Calcium channel blockers, which cause
ARTERIOLE
VENULE
CAPILLARY
INTERSTITIAL SPACE
Hydraulic
10 – 0 = 10
Oncotic
28 – 8 = 20
Net
10 – 20 = -10
Inwards
Hydraulic
30 – 0 = 30
Oncotic
28 – 8 = 20
Net
30 – 20 = 10
Outwards
FIGURE 6-2 Effects of net forces on fl uid exchange in the microcirculation. Water
normally leaves the capillary on the arteriolar side and fl ows back into the capillary on the
venular side.
J = k[( Pc – Pi ) – σ(Πc – Πi )]
J – flux
k – capillary filtration coefficient
Pc – intraluminal hydraulic pressure
Pi – interstitial hydraulic pressure
σ – reflection coefficient (the effectiveness of the semipermiable membrane; 1 = perfect)
Πc – intraluminal oncotic pressure
Πi – interstitial oncotic pressure
FIGURE 6-3 Starling’s hypothesis.
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The Chronically Swollen Leg: Finding the Cause 71
smooth muscle relaxation, are often involved. Nifedipine is the most
common of the calcium channel blockers that can cause edema with an
incidence of 10%. Hydralazine, also a vasodilator, is also known to cause
edema. Cilostazol, a phosphodiesterase inhibitor used in the treatment of
claudication, has vasodilatory properties and an 8% incidence of periph-
eral edema.
It is also possible to raise the hydraulic pressure gradient on the venous
side of the microcirculation. Simple dependency of the limbs, without
movement, raises the venous pressure at the ankle level to approximately
90 mmHg when standing and 60 mmHg in the sitting position. This is due
to the vertical column of blood between the heart and the ankle. In normal
subjects, even minimal movements can reduce the venous pressure to
20 mmHg as the valve leafl ets close and negate the effects of a long column
of blood when the limbs are below heart level. In contrast, people with
chronic venous insuffi ciency (i.e., chronic obstruction or more commonly
valvular insuffi ciency) cannot relieve this venous hypertension with move-
ment. So-called fl uid retention is also a cause of venous hypertension and
edema. Causes of excess venous volume include congestive heart failure,
renal disease, hormones (especially estrogen and progesterone), secondary
aldosteronism, and drugs such as the nonsteroidal anti-infl ammatories.
Naprosyn has a 1% to 3% incidence of peripheral edema. Recently, oral
hypoglycemics such as Actos and Avandia have been shown to cause fl uid
retention by a renal mechanism.
A decrease in the oncotic pressure gradient, the force that “pulls” fl uid
back into the intravascular space, can cause edema. A decrease in plasma
oncotic pressure (Π
c
in the Starling equation) can be caused by malnutri-
tion, protein losing enteropathies such as Chron’s or celiac disease, protein
losing nephropathy, or hepatic disease with decreased production of plasma
proteins. Interstitial oncotic pressure (Πi) can be increased as a result of
decreased lymphatic fl ow, which leads to decreased clearing of macro-
molecules from the interstitium, or by a disease that causes the deposition
of osmotically active substance in the tissues. An example would be the
deposition of mucopolysaccharides that occurs in hypothyroidism leading
to myxedema.
An increase in capillary permeability will also cause edema. The hydrau-
lic pressure gradient becomes more “effective” (increased k in the Starling
equation), and the increased permeability causes the capillary wall to be
less effective as a semipermeable membrane (lower σ) decreasing the
oncotic gradient. The causes of increased capillary permeability include
endothelial damage, allergy, and infl ammation. Endothelial damage can
be caused by burns and toxins. Allergic reactions cause the release of his-
tamine. Histamine causes endothelial cells to shrink and increases the
distance between cell margins, thus increasing capillary permeability.
Infl ammation can be from any cause such as infection, or a systemic
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72 The Chronically Swollen Leg: Finding the Cause
infl ammatory condition such as lupus or vasculitis. It is also believed that
cyclic idiopathic edema, sometimes seen in premenstrual females, is the
result of increased capillary permeability on a hormonal basis.
Decreased lymphatic fl ow, either primary or secondary, will lead to
edema. Primary or idiopathic lymphedema is classifi ed as congenital,
praecox (before age 35), or tarda (after age 35). Secondary lymphedema
can be due to invasion of the lymphatic system by parasites (fi liariasis);
lymph node excision and/or radiation; tumor invasion by malignancy; or
damage to lymphatic vessels or nodes by surgery, trauma, or infection.
CLINICAL PRESENTATION
The theoretical causes of edema that have been listed will simply lead
to a long list of possible etiologies. Fortunately, recognizable clinical pat-
terns usually point an experienced clinician to a rapid diagnosis.
Edema caused by venous pathology, usually venous valvular insuffi -
ciency, may involve one or both legs. If both legs are affected, it is usually
not equal. The edema is very well relieved by overnight elevation. The feet
are usually spared. The edema may or may not pit. The symptoms range
from simple heaviness to possibly an aching pain. The presence of other
stigmata of venous disease such as varicosities and skin changes also points
to a possible venous etiology.
Lymphedema, in contrast to venous edema, is worse distally. The foot
and toes are involved and are often described as “pillow” feet and “sausage”
toes. The relief by overnight elevation is minimal to mild. The edema typi-
cally pits early in the course of lymphedema, but later, as the tissues
become more fi brotic, pitting is absent. Symptoms are often absent, or the
patient complains of only heaviness of the leg. Lymphedema can be bilat-
eral, but is usually unequal in such cases.
Edema-caused cardiac, renal, endocrine, GI, and hepatic etiologies are
referred to as edema with a “central” cause. Both legs are involved equally,
and the edema is very well relieved by elevation. The distribution is similar
to lymphedema (i.e., worst distally); however, often the toes are not
involved. The edema typically pits. The symptoms are none or minimal.
Dependent edema of a limb is often indistinguishable from centrally caused
edema by simple clinical appearance. The clue in these cases is the patient’s
activities. It is seen in subjects with minimal activities who sit most of the
day, often in a wheelchair.
Edema caused by medication is virtually always bilateral and equal.
Relief by elevation and the distribution in the legs, however, can be variable
but usually acts and looks like central or dependent edema. Symptoms are
little or none. Common medications that can cause edema are listed in
Table 6-1.
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The Chronically Swollen Leg: Finding the Cause 73
TABLE 6-1 Commonly Used Drugs That Can Cause
Edema
Calcium channel blockers Clonidine
Hydralazine Minoxidil
Estrogen Cilostazol
Progesterone Gabapentin
Nonsteroidal anti-infl ammatories Glucocorticoids
COX2 inhibitors
TABLE 6-2 Clinical Patterns of Lower Extremity Edema
Cause Venous Lymph Central* Depend. Medication
Bilateral
Occasional / ≠ Occasional / ≠
Always Always
Relief by
Elevation
Complete Minimal Complete Varies
Distribution
Foot usually
spared
Worst distally Worst distally Varies
Pitting
±− + +
Symptoms
Heavy/ache None or heavy Little or none Little or none
* Central causes include cardiac, renal, hepatic, GI, and endocrine etiologies.
The summary of the clinical appearance of the limbs of various etiolo-
gies is shown in Table 6-2. A fl ow diagram for the likely etiology of a
chronically swollen limb or limbs is shown in Figure 6-4. This fl ow diagram
works in approximately 90% of cases. The other 10% require a more
careful history with possible laboratory and imaging studies.
Chronically
Swollen
Leg(s)
Unilateral or
Unequal
Bilateral and
Equal
Foot Spared
Relief by Elevation
Venous
Lymphedema
Dependency
Central*
Medication
Worst Distal
Elevation Min.
FIGURE 6-4 Flow diagram for diagnosis of common causes of chronic leg swelling.
*Central causes include cardiac, renal, hepatic, GI, and endocrine etiologies.
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74 The Chronically Swollen Leg: Finding the Cause
Lastly, vascular specialists may occasionally be presented with patients
with swollen legs who do not have true edema. These patients have an
unusual fat distribution in the legs called lipedema. The patients are female,
and the condition often runs in families. These patients will describe
having developed “tree trunk” legs or “thick ankles” in their teenage years.
The feet are not involved. Elevation, diuretics, and compression have
minimal effects on limb size. The tissues have a doughy consistency distinct
fro m t rue ed ema. T he sympto ms are m inim al , t houg h p atie nts m ay de sc ri be
increased skin sensitivity to touch.
REFERENCES
1. Rutherford RB. Initial patient evaluation: The vascular consultation. In: Rutherford RB,
ed. Vascular Surgery, 5th ed. Philadelphia: W.B. Saunders Company, 2000:9–11.
2. Starling EH. Physiologic forces involved in the causation of dropsy. Lancet. 1896;I;
1267–1270.
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SECTION
II
Nonoperative
Management of
Chronic Venous
Insuffi ciency
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77
7
Compression Therapy in
Venous Leg Ulcers
Hugo Partsch
INTRODUCTION
Compression therapy is the basic treatment modality in venous leg ulcers
that has been shown to be effective for healing ulcers and also for keeping
them healed.
1,2
In every single case, the underlying venous pathology
has to be ascertained, preferably by Duplex investigation, and methods
to correct pathophysiology by surgery or sclerotherapy have to be
considered.
COMPRESSION DEVICES
Different devices can be used for compression therapy of venous ulcers
(Table 7-1).
MEDICAL COMPRESSION STOCKINGS
Medical compression stockings exerting interface pressures in the gaiter
area up to 40 mmHg are effective in preventing and reducing edema.
3
For treating venous ulcers, the use of compression stockings may be
considered, if the ulcers are not too large (less than 5 sq cm) and not too
long-standing (history shorter than 3 months).
4
Even unskilled patients are
able to handle this kind of treatment, producing a constant degree of pres-
sure and allowing the patient to change the dressing, clean the ulcer, and
have a shower. One of the disadvantages is that the exudates may soil the
Venous Ulcers
Copyright © 2007 by Academic Press, Inc.
All rights of reproduction in any form reserved.
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