Venous Disease
ANATOMY
 A clear understanding of the anatomy of the venous
system in the legs is essential to understanding
pathophysiology as well as treatment. Venous
drainage of the legs is the function of two parallel
and connected systems: the deep and the superficial
systems connected by perforators .
Superficial Venous System
 . The dorsal venous arch, into which empty the dorsal metatarsal veins, is
continuous with the greater saphenous vein medially and the lesser
saphenous vein laterally .
 The greater saphenous vein, in close proximity to the saphenous nerve,
ascends anterior to the medial malleolus, crosses, and then ascends medial
to the knee. It ascends in the superficial compartment and empties into the
common femoral vein after entering the fossa ovalis.
 Before its entry into the common femoral vein, it receives medial and
lateral accessory saphenous veins, as well as small tributaries from the
inguinal region, pudendal region, and anterior abdominal wall. The
posterior arch vein drains the area around the medial malleolus, and as it
ascends up the posterior medial aspect of the calf, it receives medial
perforating veins, termed Cockett’s perforators, before joining the greater
saphenous vein at or below the knee.
 The lesser saphenous vein arises from the dorsal venous arch at the lateral
aspect of the foot and ascends posterior to the lateral malleolus, and it
empties into the popliteal vein after penetrating the fascia. The exact entry
of the lesser saphenous vein into the popliteal vein is variable.
Deep Venous System
 The plantar digital veins in the foot empty into a network of metatarsal
veins that comprise the deep plantar venous arch. This continues into the
medialand lateral plantar veins that then drain into the posterior tibial
veins. The dorsalis pedis veins on the dorsum of the foot form the paired
anterior tibial veins at the ankle.The paired posterior tibial veins, adjacent
to and flanking the posterior tibial artery, run under the fascia of the deep
posterior compartment. These veins enter the soleus and join the
popliteal vein, after joining with the paired peroneal and anterior
tibial veins. There are large venous sinuses within the soleus muscle—the
soleal sinuses—that empty into the posterior tibial and peroneal veins.
 The popliteal vein enters a window in the adductor magnus, at which point
it is termed the femoral vein. The femoral vein ascends and receives
venous drainage from the profunda femoris vein, or the deep femoral vein,
and after this confluence, it is called the common femoral vein. As the
common femoral vein crosses the inguinal ligament, it is called the
external iliac vein.
Perforating veins
 Perforating veins connect
the superficial venous
system to the deep
venous system at various
points in the leg—the
foot, the medial and
lateral calf, the mid- and
distal thigh .
Venous Function
 The venules, the smallest veins ranging from 0.1 to 1 mm, contain mostly
smooth muscle cells, whereas the larger extremity veins contain relatively
few smooth muscle cells. These larger caliber veins have limited contractile
capacity.
 The venous valves prevent retrograde flow, and it is the failure of the valves
that leads to reflux and associated symptoms. Venous valves are most
prevalent in the distal lower extremity, whereas as one proceeds
proximally, the number of valves decreases to the point that in the superior
and inferior vena cava, no valves are present.
 The return of the blood to the heart from the lower extremity is facilitated
by the muscle pump function of the calf—a mechanism whereby the calf
muscle, functioning as a bellows during exercise, compresses the
gastrocnemius and soleal sinuses and propels the blood toward the heart.
The normally functioning valves in the venous system prevent retrograde
flow; it is when one or more of these valves become incompetent that
symptoms of venous insufficiency can develop. During calf muscle
contraction, the venous pressure of the foot and ankle drop dramatically.
The pressures developing in the muscle compartments during exercise
range from 150 to 200 mm Hg, and when there is failure of perforating
veins, these high pressures are transmitted to the superficial system.
Varicose Veins terms
 The term varicose veins is, in the common parlance, a term that
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encompasses a spectrum of venous dilation that ranges from minor
telangiectasia to severe dilated, tortuous varicose veins. As stated earlier,
for a proper categorization, as well as for appropriate treatment options to
be considered, certain definitions must be agreed on.
Varicose veins refer to any dilated, tortuous, elongated vein of any
caliber.
Telangiectasias are intradermal varicosities that are small and tend to
be cosmetically unappealing but not symptomatic in and of themselves.
Reticular veins are subcutaneous dilated veins that enter the tributaries
of the main axial or trunk veins.
Trunk veins are the named veins, such as the greater or lesser saphenous
veins or their tributaries.
The end result of CVI can range from aching, heaviness, pain, and swelling
with prolonged standing or sitting in the case of symptomatic varicose
veins, to severe lipodermatosclerosis with edema and ulceration in the
patient with severe CVI.
Risk Factors
 A combination of risk factors, rather than any one specific risk factor, is a better
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predictor of the likelihood of a given patient developing symptomatic varicose veins.
Heredity undoubtedly plays a significant role in the development of varicose veins.
Valvular dysfunction and insufficiency
Female sex, gravitation hydrostatic force, and hydrodynamic forces due to muscular
contraction.
Hormonal Influence
Venous function is undoubtedly influenced by hormonal changes. In particular,
progesterone liberated by the corpus luteum stabilizes the uterus bycausing
relaxation of smooth muscle fibers. This effect directly influences venous function.
The result is passive venous dilation, which, in many instances, causes valvular
dysfunction. Although progesterone is implicated in the first appearance of
varicosities in pregnancy, estrogen also has profound effects. It produces the
relaxation of smooth muscle and a softening of collagen fibers. Further, the
estrogen-progesterone ratio influences venous distensibility. This ratio may explain
the predominance of venous insufficiency symptoms on the first day of a menstrual
period when a profound shift occurs from the progesterone phase of the menstrual
cycle to the estrogen phase.
Pathogenesis
 Defects in the strength and characteristics of the venous wall enter into the
pathogenesis of varicose veins.
 Furthermore, communicating veins connecting the deep with the
superficial compartment may have valve failure.
 Pressure studies show that two sources of venous hypertension exist. The
first is gravitational and is a result of venous blood coursing in a distal
direction down linear axial venous segments. This is referred to as
hydrostatic pressure and is the weight of the blood column from the right
atrium.
 The second source of venous hypertension is dynamic. It is the force of
muscular contraction, usually contained within the compartments of the
leg. If a perforating vein fails, high pressures (ranging from 150 to 200 mm
Hg) developed within the muscular compartments during exercise are
transmitted directly to the superficial venous system. Here, the sudden
pressure transmitted causes dilation and lengthening of the superficial
veins. Progressive distal valvular incompetence may occur.
Pathogenesis :
Changes occur at the cellular level.
 In the distal liposclerotic area, capillary proliferation
is seen and extensive capillary permeability occurs as
a result of the widening of interendothelial cell pores.
Transcapillary leakage of osmotically active particles,
the principal one being fibrinogen, occurs. The
extravascular fibrin remains to prevent the normal
exchange of oxygen and nutrients in the surrounding
cells.However, little proof exists for an actual
abnormality in the delivery of oxygen to the tissues.
An other factor is the protolytic enzymes from the
extravasated leukocytes
VENOUS INSUFFICIENCY
 The C-E-A-P classification is a recent scoring system that
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stratifies venous disease based on clinical presentation,
etiology, anatomy, and pathophysiology.
C Clinical signs (grade 0–6 , supplemented by “A” for
asymptomatic and “S” for symptomatic presentation
E Etilogic classification (congential, primary,
secondary)
A Anatomic distribution (superficial, deep, or
perforator, alone or in combination)
P Pathophysiologic dysfunction (reflux or obstruction,
alone or in combination)
Clinical Classification of Chronic Lower
Extremity Venous Disease
 Class 0 No visible or palpable signs of venous disease
 Class 1 Telangiectasia, reticular veins, malleolar flare
 Class 2 Varicose veins
 Class 3 Edema without skin changes
 Class 4 Skin changes ascribed to venous disease (e.g.,
pigmentation, venous eczema, lipodermatosclerosis)
 Class 5 Skin changes as defined above with healed
ulceration
 Class 6 Skin changes as defined above with active
ulceration
 Etiologic Classification of Chronic Lower Extremity Venous
Disease
 Congenital (EC ) Cause of the chronic venous disease present since birth
 Primary (EP ) Chronic venous disease of undetermined cause
 Secondary (ES ) Chronic venous disease with an associated known cause
(post-thrombotic, post-traumatic, other)
 ANATOMIC CLASSIFICATION (AS , AD , or AP )
The anatomic site(s) of the venous disease should be described as superficial
(AS ), deep (AD ), or perforating (AP ) vein(s). One, two, or three systems
may be involved in any combination. For reports requiring greater detail,
the involvement of the superficial, deep, and perforating veins may be
localized by use of the anatomic segments.
 PATHOPHYSIOLOGIC CLASSIFICATION (PR,O )
Clinical signs or symptoms of chronic venous disease result from reflux (PR ),
obstruction (PO ), or both (PR,O ).
Symptoms
 The patient with symptomatic varicose veins relates, most often, symptoms of
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aching, heaviness, discomfort, and sometimes pain in the calf of the affected limb.
This is particularly worse at the end of the day, most likely due to prolonged sitting
or standing that results in venous distention and associated pain. The symptoms are
typically reduced or absent in the morning owing to the fact that the limb has not
been in a dependent position through the night.
In the case of women, the symptoms are often most troubling and exacerbated
during the menstrual period, particularly during the first day or two.
Primary varicose veins consist of elongated, tortuous, superficial veins that are
protuberant and contain incompetent valves.
Primary varicose veins merge imperceptibly into more severe CVI.
Swelling ,edema is moderate to severe, an increased sensation of heaviness occurs
with larger varicosities, and early skin changes of mild pigmentation and
subcutaneous induration appear.
When CVI becomes severe, marked swelling and calf pain occur after standing,
sitting, or walking.
Multiple dilated veins are seen associated with various clusters and heavy medial
and lateral supramalleolar pigmentation.
 Many causes of leg pain are possible, and most may coexist.
Therefore, defining the precise symptoms of venostasis is necessary.
Discomfort usually occurs during warm temperatures and after
prolonged standing. The pain is characteristically dull, does not
occur during recumbency or early in the morning, and is
exacerbated in the afternoon, especially after long standing. The
discomforts of aching, heaviness, fatigue, or burning pain are
relieved by recumbency, leg elevation, or elastic support.
 Cutaneous itching is also a sign of venostasis and is often the
hallmark of inadequate external support. It is a manifestation of
local congestion and may precede the onset of dermatitis. This, and
nearly all the symptoms of stasis disease, can be explained by the
irritation of superficial nerve fibers by local pressure or
accumulation of metabolic end products with a consequent pH shift.
 External hemorrhage may occur as superficial veins press on
overlying skin within this protective envelope.
DIAGNOSTIC EVALUATION OF VENOUS
DYSFUNCTION
 Clinical examination of the patient in good light provides nearly all the information
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necessary. It determines the nature of the venostasis disease and ascertains the
presence of intercutaneous venous blemishes and subcutaneous protuberant
varicosities, the location of principal points of control or perforating veins that feed
clusters of varicosities, the presence and location of ankle pigmentation and its
extent, and the presence and severity of subcutaneous induration.
Visual examination can be supplemented by noting a downward-going impulse on
coughing.
Tapping the venous column of blood also demonstrates pressure transmission
through the static column to incompetent distal veins.
The modified Perthes test for deep venous occlusion .
Brodie-Trendelenburg test ,and multible tornicheat test of axial reflux
Those testes have been replaced by in-office use of the continuouswave, handheld
Doppler instrument supplemented by duplex evaluation.The handheld Doppler
instrument can confirm an impression of saphenous reflux, and this, in turn,
dictates the operative procedure to be performed in a given patient. And it is used in
specific locations to determine incompetent valves of perforators.
Duplex technology more precisely defines which veins are refluxing by imaging the
superficial and deep veins.
Treatment
 Indications for treatment are pain, easy fatigability,
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heaviness, recurrent superficial thrombophlebitis,
external bleeding, and appearance.
Nonoperative Management
The cornerstone of therapy for patients with CVI is
external compression.
A triple-layer compression dressing, with a zinc oxide
paste gauze wrap in contact with the skin, is utilized most
commonly from the base of the toes to the anterior tibial
tubercle with snug, graded compression.
In general, snug, graded-pressure triple-layer
compression dressings effect more rapid ulcer healing
than compression stockings alone.
Venous Ablation: Sclerotherapy
 Cutaneous venectasia with vessels smaller than 1 mm in
diameter do not lend themselves to surgical treatment. Dilute
solutions of sclerosant (e.g., 0.2% sodium tetradecyl) can be
injected directly into the vessels of the blemish. Care should
be taken to ensure that no single injection dose exceeds 0.1
mL but that multiple injections completely fill all vessels
contributing to the blemish.
 Venules larger than l mm and smaller than 3 mm in size can
also be injected with sclerosant of slightly greater
concentration (e.g., 0.5% sodium tetradecyl), but limiting the
amount injected to less than 0.5 mL.
 If their cause is saphenous or tributary venous incompetence,
these conditions can be treated surgically.
 Surgery is not indicated for the treatment of venous
insufficiency in limbs with deep venous incompetence .
Surgical Management
 Surgical treatment may be
used to remove clusters
with varicosities greater
than 4 mm in diameter.
Ambulatory phlebectomy
may be performed using
the stab avulsion
technique with
preservation of the greater
and lesser saphenous veins,
if they are unaffected by
valvular incompetence
 When greater or lesser
saphenous incompetence
is present, the removal of
clusters is preceded by
limited removal of the
saphenous vein
(stripping).
 Stripping techniques are
best done from above
downward to avoid
lymphatic and cutaneous
nerve damage.
Subfascial endoscopic perforator vein surgery
 perforating vein division using laparoscopic
instrumentation. Initial data suggested that
perforator interruption produced rapid ulcer healing
and a low rate of recurrence.
 Direct Venous Reconstruction ??
DEEP VENOUS THROMBOSIS
 Acute deep venous thrombosis (DVT) is a major cause of morbidity and
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mortality in the hospitalized patient, particularly in the surgical patient.
The triad of venous stasis, endothelial injury, and hypercoagulable state
first posited by Virchow has held true a century and a half later.
The thrombotic process initiating in a venous segment can, in the absence
of anticoagulation or in the presence of inadequate anticoagulation,
propagate to involve more proximal segments of the deep venous system,
thus resulting in edema, pain, and immobility.
The most dreaded sequel to an acute DVT is that of pulmonary embolism, a
condition of potentially lethal consequence.
The late consequence of DVT, particularly of the iliofemoral veins, can be
CVI due to valvular dysfunction in the presence of luminal obstruction.
For these reasons, understanding the pathophysiology, standardizing
protocols to prevent or reduce DVT, and instituting optimal treatment
promptly all are critical to reducing the incidence and morbidity of this
unfortunately common condition.
Etiology
 Stasis
Soleal sinuses are the most common sites for initiation of venous thrombosis. The
stasis may contribute to the endothelial cellular layer contacting activated platelets
and procoagulant factors, thereby leading to DVT.
 The Hypercoagulable State
Should any of these conditions be identified, a treatment regimen of anticoagulation is
instituted for life, unless specific contraindications exist.
Following major operations, large amounts of tissue factor may be released into the
bloodstream from damaged tissues. Tissue factor is a potent procoagulant
.Increases in platelet count, adhesiveness, changes in coagulation cascade, and
endogenous fibrinolytic activity all result from physiologic stress such as major
operation or trauma and have been associated with an increased risk of thrombosis.
 Venous Injury
It has been clearly established that venous thrombosis occurs in veins that are distant
from the site of operation; for instance, it is well known that patients undergoing
total hip replacement frequently develop contralateral lower extremity DVT.
There were multiple microtears noted within the valve cusps that resulted in the
exposure of the subendothelial matrix. The exact mechanism by which this injury at
a distant site occurs, and what mediators, whether cellular or humeral, are
responsible is not clearly understood but that the injury occurs and occurs reliably is
evident from these and other studies.
Hypercoagulable States
■ Factor V Leiden mutation
■ Prothrombin gene mutation
■ Protein C deficiency
■ Protein S deficiency
■ Antithrombin III deficiency
■ Antiphospholipid syndrome
Incidence
 Venous thromboembolism occurs for the first time in
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approximately 100 persons per 100,000 This incidence
increases with increasing age with an incidence of 0.5% per
100,000 at 80 years of age.
More than two thirds of these patients have DVT alone, and
the rest have evidence of pulmonary embolism.
The recurrence rate with anticoagulation has been noted to be
6% to 7% in the ensuing 6 months.
Aside from pulmonary embolism, secondary CVI (that
resulting from DVT) is significant in terms of cost, morbidity,
and lifestyle limitation.
If the consequence of DVT, in terms of pulmonary embolism
and CVI, is to be prevented, the prevention, diagnosis, and
treatment of DVT must be optimized.
Clinical Diagnosis
 The diagnosis of DVT requires, to use an overused phrase, a high index of
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suspicion.
Most are familiar with Homans’ sign, which refers to pain in the calf on
dorsiflexion of the foot. It is certainly true that although the absence of this
sign is not a reliable indicator of the absence of venous thrombus, the
finding of a positive Homans’ sign should prompt one to attempt to
confirm the diagnosis.
Certainly, the extent of venous thrombosis in the lower extremity is an
important factor in the manifestation of symptoms. For instance, most calf
thrombi may be asymptomatic unless there is proximal propagation.
Only 40% of patients with venous thrombosis have any clinical
manifestations of the condition.
Major venous thrombosis involving the iliofemoral venous system results in
a massively swollen leg with pitting edema, pain, and blanching, a
condition known as phlegmasia alba dolens. With further progression of
disease, there may be such massive edema that arterial inflow can be
compromised. This condition results in a painful blue leg, the condition
called phlegmasia cerulea dolens. With this evolution of the condition,
unless flow is restored, venous gangrene can develop.
Investigation
 Duplex Ultrasound.
 The modern diagnostic test of choice for the diagnosis of DVT is the
duplex ultrasound, a modality that combines. Real time B-mode
ultrasonography with color-flow imaging has improved the
sensitivity and specificity of ultrasound scanning. With color-flow
duplex imaging, blood flow can be imaged in the presence of a
partially occluding thrombus. The probe is also used to compress
the vein: A normal vein should be easily compressed, whereas in the
presence of a thrombus, there is resistance to compression.
Magnetic Resonance Venography.
 With major advances in technology of imaging, magnetic resonance
venography has come to the forefront of imaging for proximal
venous disease. The cost and the issue of patient tolerance due to
claustrophobia limit the widespread application, but this is
changing. It is a useful test for imaging the iliac veins and the
inferior vena cava, an area where duplex ultrasound is limited in its
usefulness.
Prophylaxis
 The patient who has undergone either major abdominal surgery, major
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orthopedic surgery, has sustained major trauma, or has prolonged
immobility (>3 days) represents a patient who has an elevated risk for the
development of venous thromboembolism.
The methods of prophylaxis can be mechanical or pharmacologic.
The simplest method is for the patient to be able to walk. Activation of the
calf pump mechanism is an effective means of prophylaxis.
A patient who is expected to be up and walking within 24 to 48 hours is at
low risk of developing venous thrombosis. The practice of having a patient
“out of bed into a chair” is one of the most thrombogenic positions that one
could order a patient into. Sitting in a chair with the legs in a dependent
position causes venous pooling, which in the postoperative milieu could be
easily a predisposing factor in the development of thromboembolism.
The most common method of prophylaxis in the surgical universe has
traditionally revolved around sequential compression devices, which
periodically compress the calves and essentially replicate the calf bellows
mechanism. This has clearly reduced the incidence of venous
thromboembolism in the surgical patient.
Heparin
 “Minidose” heparin the dose traditionally used is 5000 units of
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unfractionated heparin every 12 hours. When subcutaneous heparin
is used on an every-8-hour dosing, rather than every 12 hours, there
is a reduction in the development of venous thromboembolism.
More recently, fractionated low-molecular-weight heparin (LMWH)
for prophylaxis and treatment of venous thromboembolism.
LMWH inhibits factors Xa and IIA activity, with the ratio of
antifactor Xa to antifactor IIA activity ranging from 1:1 to 4:1.
LMWH has a longer plasma half-life and has significantly higher
bioavailability. There is much more predictable anticoagulant
response than heparin. No laboratory monitoring is necessary
because the partial thromboplastin time (PTT) is unaffected.
LMWH results less bleeding complications.
In short, LMWH should be considered the optimal method of
prophylaxis in moderate and high-risk patients.
TREATMENT
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Traditionally, the treatment of DVT centers around heparin treatment to maintain the PTT at
60 to 80 seconds, followed by warfarin therapy to obtain an International Normalized Ratio
(INR) of 2.5 to 3.0.
A widely used regimen is 80 U/kg bolus of heparin, followed by a 15 U/kg infusion. The PTT
should be checked 6 hours after any change in heparin dosing.
Warfarin is started the same day. If warfarin is initiated without heparin, the risk of a transient
hypercoagulable state exists, because proteins C and S levels fall before the other vitamin K–
dependent factors are depleted.
With the advent of LMWH, it is no longer necessary to admit the patient for intravenous
heparin therapy. It is now accepted practice to administer LMWH to the patient as an
outpatient, as a bridge to warfarin therapy.
A minimum treatment time of 3 months is advocated in most cases.
If, however, the patient has a known hypercoagulable state or has experienced episodes of
venous thrombosis, then lifetime anticoagulation is required, in the absence of
contraindications.
The accepted INR range is 2.0 to 3.0.
Oral anticoagulants are teratogenic and thus cannot be used during pregnancy. In the case of
the pregnant woman with venous thrombosis, LMWH is the treatment of choice, and this is
continued through delivery and can be continued postpartum if needed.
Thrombolysis
 The advent of thrombolysis has resulted in increased interest in
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thrombolysis for DVT. The purported benefit is preservation of
valve function with subsequently lesser chance of developing CVI.
However, to date, little definitive, convincing data exist to support
the use of thrombolytic therapy for DVT.
One exception is the patient with phlegmasia in whom thrombolysis
is advocated for relief of significant venous obstruction. In this
condition, thrombolytic therapy probably results in better relief of
symptoms and less long-term sequelae than heparin anticoagulation
alone.
The alternative for this condition is surgical venous thrombectomy.
No matter which treatment is chosen, long-term anticoagulation is
indicated.
The incidence of major bleeding is higher with lytic therapy.
Vena Caval Filter
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The most worrisome and potentially lethal complication of DVT is pulmonary embolism.
The symptoms of pulmonary embolism, ranging from dyspnea, chest pain, and hypoxia to acute
cor pulmonale are nonspecific and require a vigilant eye for the diagnosis to be made.
The gold standard remains the pulmonary angiogram, but increasingly this is being displaced
by the computed tomographic angiogram.
Adequate anticoagulation is usually effective in stabilizing venous thrombosis, but if a patient
should develop a pulmonary embolism in the presence of adequate anticoagulation, a vena cava
filter is indicated. The modern filters are placed percutaneously over a guide wire. The
Greenfield filter, with the most extensive use and data, has a 95% patency rate and a 4%
recurrent embolism rate.
This high patency rate allows for safe suprarenal placement if there is involvement of the
inferior vena cava up to the renal veins or if it is placed in a woman of childbearing potential.
The device-related complications are wound hematoma, migration of the device into the
pulmonary artery, and caval occlusion due to trapping of a large embolus. In the latter
situation, the dramatic hypotension that accompanies acute caval occlusion can be mistaken for
a massive pulmonary embolism. The distinction between the hypovolemia of caval occlusion
versus the right heart failure from pulmonary embolism can be arrived at by measuring filling
pressures of the right side of the heart. The treatment of caval occlusion is volume resuscitation.
Indications for a Vena Cava Filter
 ■ Recurrent thromboembolism despite “adequate”
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anticoagulation
■ Deep venous thrombosis in a patient with
contraindications to anticoagulation
■ Chronic pulmonary embolism and resultant
pulmonary hypertension
■ Complications of anticoagulation
■ Propagating iliofemoral venous thrombus in
anticoagulation
Pulmonary Thromboembolism
 • DVT is most common source of PE; <10% of PE cases cause pulmonary infarction
 • Symptoms and signs include dyspnea and chest pain (present in 75%);
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tachycardia, tachypnea, altered mental status; classic triad of dyspnea, chest pain,
and hemoptysis in only 15%; pleural rub and S1Q3T3 rarely found
• V˙ /Q˙ scan has sensitivity and specificity of 90%, but 67% of studies are
inconclusive; spiral computed tomography is more accurate
Differential Diagnosis
• Other causes of chest pain and hypoxia, such as pneumonia
Treatment
• Stabilize initially with pressors and ventilatory support; start heparin or lowmolecular-weight heparin quickly
• Surgery: consider IVC filter if risk of embolus is ongoing and anticoagulation
is risky
• Open surgical thrombectomy (Trendelenburg procedure): high mortality, rarely
clinically useful for massive saddle embolus
• Prevention: DVT prophylaxis in perioperative period
Superficial Thrombophlebitis
Can occur spontaneously in varicose veins, post traumatic, pregnant or
postpartum women, thromboangiitis obliterans, Behçet disease; superficial
migratory phlebitis (Trousseau) suggests abdominal carcinoma
Symptoms and signs include local extremity pain, redness; indurated,
erythematous, tender areas indicate thrombosed superficial veins; well
localized over superficial vein
Differential Diagnosis
 • Ascending lymphangitis
 • Cellulitis
Treatment
 • Primary treatment includes nonsteroidal anti-inflammatory drugs, heat,
elevation, support stockings, elastic wrap; ambulation is encouraged
 • Surgery: excise vein if condition persists >2 weeks or recurs; ligate and
resect vein at saphenofemoral or cephalic-subclavian junction
Prognosis: uncomplicated superficial thrombophlebitis responds well to
conservative therapy; extension into DVT may be associated with PE
Leg ulcer
An ulcer is defined as an area of discontinuity of the surface epithelium.
Venous ulcers
• Venous hypertension secondary to DVT or varicose veins: ulceration on the
medial side of the leg, above the ankle, any size, shallow with sloping edges,
bleeds after minor trauma, weeps readily, surrounded by pigmentation
associated dermatoliposclerosis.
Arterial ulcers
Occlusive arterial disease: painful ulcers, do not bleed, nonhealing, lateral
ankle, heel, metatarsal heads, tips of the toes, associated features of
ischaemia, e.g. claudication, absent pulses, pallor. Elderly patients may
present with ‘blue toe’ syndrome.
Diabetic ulcers
• Ischaemic: same as arterial ulcers.
• Neuropathic: deep, painless ulcers, plantar aspect of foot or toes, associated
with cellulitis and deep tissue abscesses, warm foot, pulses may be present.
Lymphatic Disorders
Lymphedema
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Excessive and persistent accumulation of
extravascular and extracellular fluid and proteins
in tissue spaces
Caused by a disturbance of the water and
protein balance across the capillary membrane
Increased concentration of proteins draws
greater amount of water into interstitial spaces
Exceeds transport capacity of the lymphatic
system, leading to lymphedema
Disorders of the Lymphatic System
Leading to Lymphatic Insufficiency
Primary
 Congenital Malformation(congenita, praecox &tarda)
Secondary:
 Infection and Inflammation
 Obstruction or Fibrosis
Trauma, Surgery, Neoplasms
Radiation Therapy
 Surgical Dissection of Lymph Nodes
 Chronic Venous Insufficiency
Clinical Signs and Symptoms of
Lymphedema
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Edema of the dorsum of the foot or hand
Decreased range of motion, flexibility and
function
Usually unilateral
Worse after prolonged dependency
No discomfort or a dull, heavy sensation; sense
of fullness
Clinical Manifestations of Lymphatic
Disorders
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Lymphedema
Increased girth and weight of the limb
Sensory disturbances
Stiffness and limited range of motion
Decreased resistance to infection
Lymphedema Location
Severity of Lymphedema
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Mild lymphedema: One to two cm increase in
girth measurements between the involved and
non-involved limb
Moderate lymphedema: Two to five cm increase
in girth measurement
Severe lymphedema: Greater than five cm
increase
Components of a Decongestive
Lymphatic Therapy Program
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Elevation
Manual lymphatic drainage
Compression
Exercise
Skin care
Daily living precautions
Elevation
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Elevate the involved limb when using a
sequential compression pump
Elevate limb when sleeping, resting, and
during sedentary activities
Compressive bandages or garment should
be worn during periods of elevation
Manual Lymphatic Drainage
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Slow, very light, repetitive stroking and circular
massage movements performed in a specific
sequence, limb elevated whenever possible
Proximal congestion in the trunk, groin, buttock,
or axilla is cleared first
Direction of massage is towards specific lymph
nodes
Usually involves distal to proximal stroking
Manual Lymphatic Drainage
Manual Lymphatic Drainage
Exercise
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Active range of motion, stretching, and
low-intensity resistance exercise is
incorporated with manual drainage
techniques
Exercises should be performed with
compressive bandages or garment
Exercise
Compression
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No-stretch, non-elastic or low-stretch elastic
bandages are used
Sports bandages, such as ACE wraps, are NOT
recommended in the treatment of lymphedema
Compressive garments are available
Use of a sequential, pneumatic compression
pump on a daily basis may be recommended
Bandages
Compressive Bandages
Skin Care and Hygiene
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Lymphedema increases risk of skin
breakdown, infection, and delayed wound
healing
Proper skin care
Inspection
Protection