Penyakit vena

VENOUS THROMBOSIS
DEEP VENOUS THROMBOSIS (DVT)
SUPERFICIAL VEIN THROMBOSIS
VARICOSE VEINS
CHRONIC VENOUS INSUFFICIENCY

DISORDERS OF THE VEINS AND LYMPHATICS

VENOUS DISORDERS
Veins in the extremities can be broadly classified as either superficial or deep. In the
lower extremity, the superficial venous system includes the greater and lesser saphenous veins
and their tributaries. The deep veins of the leg accompany the major arteries. Perforating veins
connect the superficial and deep systems at multiple locations. Bicuspid valves are present
throughout the venous system to direct the flow of venous blood centrally.

VENOUS THROMBOSIS
The presence of thrombus within a superficial or deep vein and the accompanying
inflammatory response in the vessel wall is termed venous thrombosis or thrombophlebitis.
Initially, the thrombus is composed principally of platelets and fibrin. Red cells become
interspersed with fibrin, and the thrombus tends to propagate in the direction of blood flow. The
inflammatory response in the vessel wall may be minimal or characterized by granulocyte
infiltration, loss of endothelium, and edema. The factors that predispose to venous thrombosis
were initially described by Virchow in 1856 and include stasis, vascular damage, and
hypercoagulability. Accordingly, a variety of clinical situations are associated with increased risk
of venous thrombosis (Table 232- 2). Venous thrombosis may occur in 50% of patients having
orthopedic surgical procedures, particularly those involving the hip or knee, and in 10 to 40% of
patients who undergo abdominal or thoracic operations. The prevalence of venous thrombosis is
particularly high in patients with cancer of the pancreas, lungs, genitourinary tract, stomach, and
breast. Approximately 10 to 20% of patients with idiopathic deep vein thrombosis have or
develop clinically overt cancer; there is no consensus on whether these individuals should be
subjected to intensive diagnostic workup to search for occult malignancy. The risk of thrombosis
is increased following trauma, such as fractures of the spine, pelvis, femur, and tibia.
Immobilization, regardless of the underlying disease, is a major predisposing cause of venous
thrombosis. This fact may account for the relatively high incidence in patients with acute
myocardial infarction or congestive heart failure. The incidence of venous thrombosis is
increased during pregnancy, particularly in the third trimester and in the first month postpartum,
and in individuals who use oral contraceptives or receive postmenopausal hormone replacement
therapy. A variety of clinical disorders that produce systemic hypercoagulability, including
resistance to activated protein C (factor V Leiden); prothrombin G20210A gene mutation;
antithrombin III, protein C, and protein S deficiencies; antiphospholipid syndrome;
hyperhomocysteinemia; SLE; myeloproliferative diseases; dysfibrinogenemia; and disseminated
intravascular coagulation, are associated with venous thrombosis. Venulitis occurring in
thromboangiitis obliterans, Behcets disease, and homocysteinuria may also cause venous
thrombosis.
DEEP VENOUS THROMBOSIS (DVT)
The most important consequences of this disorder are pulmonary embolism (Chap. 244)
and the syndrome of chronic venous insufficiency. DVT of the iliac, femoral, or popliteal veins is
suggested by unilateral leg swelling, warmth, and erythema. Tenderness may be present along
the course of the involved veins, and a cord may be palpable. There may be increased tissue
turgor, distention of superficial veins, and the appearance of prominent venous collaterals. In
some patients, deoxygenated hemoglobin in stagnant veins imparts a cyanotic hue to the limb, a
condition called phlegmasia cerulean dolens. In markedly edematous legs, the interstitial tissue
pressure may exceed the capillary perfusion pressure, causing pallor, a condition designated
phlegmasia alba dolens. The diagnosis of DVT of the calf is often difficult to make at the
bedside. This is so because only one of multiple veins may be involved, allowing adequate
venous return through the remaining patent vessels. The most common complaint is calf pain.
Examination may reveal posterior calf tenderness, warmth, increased tissue turgor or modest
swelling, and, rarely, a cord. Increased resistance or pain during dorsiflexion of the foot
(Homans sign) is an unreliable diagnostic sign. DVT occurs less frequently in the upper
extremity than in the lower extremity, but the incidence is increasing because of greater
utilization of indwelling central venous catheters. The clinical features and complications are
similar to those described for the leg.
Diagnosis
D-Dimer, a degradation product of cross-linked fibrin, is often elevated in patients with
venous thrombosis. It is a sensitive, but not specific, test for venous thrombosis. The noninvasive
test used most often to diagnose DVT is duplex venous ultrasonography (Bmode, i.e., two-
dimensional, imaging, and pulse-wave Doppler interrogation). By imaging the deep veins,
thrombus can be detected either by direct visualization or by inference when the vein does not
collapse on compressive maneuvers. The Doppler ultrasound measures the velocity of blood flow
in veins. This velocity is normally affected by respiration and by manual compression of the foot
or calf. Flow abnormalities occur when deep venous obstruction is present. The sensitivity of
duplex venous ultrasonography approaches 95% for proximal DVT and 75% for symptomatic
calf vein thrombosis. Magnetic resonance imaging (MRI) is another noninvasive means to detect
DVT. Its diagnostic accuracy for assessing proximal DVT is similar to that of duplex
ultrasonography. It is useful in patients with suspected thrombosis of the superior and inferior
venae cavae or pelvic veins. DVT can also be diagnosed by venography. Contrast medium is
injected into a superficial vein of the foot and directed to the deep system by the application of
tourniquets. The presence of a filling defect or absence of filling of the deep veins is required to
make the diagnosis. DVT must be differentiated from a variety of disorders that cause unilateral
leg pain or swelling, including muscle rupture, trauma, or hemorrhage; a ruptured popliteal cyst;
and lymphedema. It may be difficult to distinguish swelling caused by the postphlebitic
syndrome from that due to acute recurrent DVT. Leg pain may also result from nerve
compression, arthritis, tendinitis, fractures, and arterial occlusive disorders. A careful history and
physical examination can usually determine the cause of these symptoms.

TREATMENT
Anticoagulants (See also Chap. 244)
Prevention of pulmonary embolism is the most important reason for treating patients with
DVT, since in the early stages the thrombus may be loose and poorly adherent to the vessel wall.
Patients should be placed in bed, and the affected extremity should be elevated above the level of
the heart until the edema and tenderness subside. Anticoagulants prevent thrombus propagation
and allow the endogenous lytic system to operate. Initial therapy should include either
unfractionated heparin or low-molecularweight heparin. Unfractionated heparin should be
administered intravenously as an initial bolus of 7500 to 10,000 IU, followed by a continuous
infusion of 1000 to 1500 IU/h. The rate of the heparin infusion should be adjusted so that the
activated partial thromboplastin time (aPTT) is approximately twice the control value.
Subcutaneous injection of heparin has been used as an alternative form of therapy. In _5% of
patients, heparin therapy may cause thrombocytopenia (heparin-induced thrombocytopenia,
HIT). Infrequently, these patients develop arterial thrombosis and ischemia.
Low-molecular-weight (4000 to 6000 Da) heparins are as effective as or better than
conventional, unfractionated heparin in preventing extension or recurrence of venous thrombosis.
Depending on the specific preparation, low-molecular-weight heparin is administered
subcutaneously, in fixed doses, once or twice daily; for example, the dose of enoxaparin is 1
mg/kg subcutaneously bid. The incidence of thrombocytopenia is less with low-molecular-
weight heparin than with conventional preparations. A direct thrombin inhibitor, such as
lepirudin or argatroban, may be used as initial anticoagulant therapy for patients in whom
heparin is contraindicated because of HIT. Warfarin is administered during the first week of
treatment with heparin and may be started as early as the first day of heparin treatment if the
aPTT is therapeutic. It is important to overlap heparin treatment with oral anticoagulant therapy
for at least 4 to 5 days because the full anticoagulant effect of warfarin is delayed. The dose of
warfarin should be adjusted to maintain the prothrombin time at an international normalized ratio
(INR) of 2.0 to 3.0. Anticoagulant treatment is indicated for patients with proximal DVT, since
pulmonary embolism may occur in _50% of untreated individuals. The use of anticoagulants for
isolated DVT of the calf is controversial. However, approximately 20 to 30% of calf thrombi
propagate to the thigh, thereby increasing the risk of pulmonary embolism. The overall incidence
of pulmonary embolism in patients presenting initially with deep calf vein thrombosis is 5 to
20%. Also, isolated calf vein thrombosis has been identified as a cause of embolic stroke via a
patent foramen ovale. Therefore, patients with calf vein thrombosis should either receive
anticoagulants or be followed with serial noninvasive tests to determine whether proximal
propagation has occurred. Anticoagulant treatment should be continued for at least 3 to 6 months
for patients with acute idiopathic DVT and for those with a temporary risk factor for venous
thrombosis to decrease the chance of recurrence. In a recent study of patients with idiopathic
venous thromboembolism, long-term management with low-intensity warfarin using a targeted
INR of 1.5 to 2.0, following at least 3 months of therapy with full-dose anticoagulation, reduced
the risk of recurrent DVT and pulmonary embolism. The duration of treatment is indefinite for
patients with recurrent DVT and for those in whom associated causes, such as malignancy or
hypercoagulability, have not been eliminated. If treatment with anticoagulants is contraindicated
because of a bleeding diathesis or risk of hemorrhage, protection from pulmonary embolism can
be achieved by mechanically interrupting the flow of blood through the inferior vena cava.
Inferior vena cava plication generally has been replaced by percutaneous insertion of a filter.
Thrombolytics
Thrombolytic drugs such as streptokinase, urokinase, and tPA may also be used, but there
is no evidence that thrombolytic therapy is more effective than anticoagulants in preventing
pulmonary embolism. However, early administration of thrombolytic drugs may accelerate clot
lysis, preserve venous valves, and decrease the potential for developing postphlebitic syndrome.

Prophylaxis
Prophylaxis should be considered in clinical situations where the risk of DVT is high.
Low-dose unfractionated heparin (5000 units 2 h prior to surgery and then 5000 units every 8 to
12 h postoperatively), warfarin, and external pneumatic compression are all useful. Low-dose
heparin reduces the risk of DVT associated with thoracic and abdominal surgery and with
prolonged bed rest. Low-molecularweight heparins have been shown to prevent DVT in patients
undergoing general or orthopedic surgery and in acutely ill medical patients. They are said to be
more effective than conventional heparin and to cause an equal or lower incidence of bleeding.
Danaparoid, a lowmolecular- weight heparinoid, may be used for prophylaxis in patients
undergoing hip surgery. Fondaparinux, a synthetic pentasaccharide capable of catalysing
antithrombin-mediated inhibition of factor Xa, may be used for prophylaxis in patients
undergoing major orthopedic surgery. Warfarin in a dose that yields a prothrombin time
equivalent to an INR of 2.0 to 3.0 is effective in preventing DVT associated with bone fractures
and orthopedic surgery. Warfarin is started the night before surgery and continued throughout the
convalescent period. External pneumatic compression devices applied to the legs are used to
prevent DVT when even low doses of heparin or warfarin might cause serious bleeding, as
during neurosurgery or transurethral resection of the prostate.
232
SUPERFICIAL VEIN THROMBOSIS
Thrombosis of the greater or lesser saphenous veins or their tributariesi.e., superficial
vein thrombosis does not result in pulmonary embolism. It is associated with intravenous
catheters and infusions, occurs in varicose veins, and may develop in association with DVT.
Migrating superficial vein thrombosis is often a marker for a carcinoma and may also occur in
patients with vasculitides, such as thromboangiitis obliterans. The clinical features of superficial
vein thrombosis are easily distinguished from those of DVT. Patients complain of pain localized
to the site of the thrombus. Examination reveals a reddened, warm, and tender cord extending
along a superficial vein. The surrounding area may be red and edematous.
TREATMENT
Treatment is primarily supportive. Initially, patients can be placed at bed rest with leg
elevation and application of warm compresses. Nonsteroidal anti-inflammatory drugs may
provide analgesia but may also obscure clinical evidence of thrombus propagation. If a
thrombosis of the greater saphenous vein develops in the thigh and extends toward the
saphenofemoral vein junction, it is reasonable to consider anticoagulant therapy to prevent
extension of the thrombus into the deep system and a possible pulmonary embolism.
VARICOSE VEINS
Varicose veins are dilated, tortuous superficial veins that result from defective structure
and function of the valves of the saphenous veins, from intrinsic weakness of the vein wall, from
high intraluminal pressure, or, rarely, from arteriovenous fistulas. Varicose veins can be
categorized as primary or secondary. Primary varicose veins originate in the superficial system
and occur two to three times as frequently in women as in men. Approximately half of patients
have a family history of varicose veins. Secondary varicose veins result from deep venous
insufficiency and incompetent perforating veins or from deep venous occlusion causing
enlargement of superficial veins that are serving as collaterals. Patients with venous varicosities
are often concerned about the cosmetic appearance of their legs. Symptoms consist of a dull ache
or pressure sensation in the legs after prolonged standing; it is relieved with leg elevation. The
legs feel heavy, and mild ankle edema develops occasionally. Extensive venous varicosities may
cause skin ulcerations near the ankle. Superficial venous thrombosis may be a recurring problem,
and, rarely, a varicosity ruptures and bleeds. Visual inspection of the legs in the dependent
position usually confirms the presence of varicose veins. Varicose veins can usually be treated
with conservative measures. Symptoms often decrease when the legs are elevated periodically,
when prolonged standing is avoided, and when elastic support hose are worn. External
compression stockings provide a counterbalance to the hydrostatic pressure in the veins. Small
symptomatic varicose veins can be treated with sclerotherapy, in which a sclerosing solution is
injected into the involved varicose vein and a compression bandage is applied. Surgical therapy
usually involves extensive ligation and stripping of the greater and lesser saphenous veins and
should be reserved for patients who are very symptomatic, suffer recurrent superficial vein
thrombosis, and/or develop skin ulceration. Surgical therapy may also be indicated for cosmetic
reasons.
CHRONIC VENOUS INSUFFICIENCY
Chronic venous insufficiency may result from DVT and/or valvular incompetence.
Following DVT, the delicate valve leaflets become thickened and contracted so that they cannot
prevent retrograde flow of blood; the vein becomes rigid and thick-walled. Although most veins
recanalize after an episode of thrombosis, the large proximal veins may remain occluded.
Secondary incompetence develops in distal valves because high pressures distend the vein and
separate the leaflets. Primary deep venous valvular dysfunction may also occur without previous
thrombosis. Patients with venous insufficiency often complain of a dull ache in the leg that
worsens with prolonged standing and resolves with leg elevation. Examination demonstrates
increased leg circumference, edema, and superficial varicose veins. Erythema, dermatitis, and
hyperpigmentation develop along the distal aspect of the leg, and skin ulceration may occur near
the medial and lateral malleoli. Cellulitis may be a recurring problem. Patients should be advised
to avoid prolonged standing or sitting; frequent leg elevation is helpful. Graduated compression
stockings should be worn during the day. These efforts should be intensified if skin ulcers
develop. Ulcers should be treated with applications of wet to dry dressings and, occasionally,
dilute topical antibiotic solutions. Commercially available dressings comprising antiseptic
solutions and compressive bandages may be applied and should be changed weekly until healing
occurs. Recurrent ulceration and severe edema may be treated by surgical interruption of
incompetent communicating veins. Rarely, surgical valvuloplasty and bypass of venous
occlusions are employed.
(Harrisons principles of Internal Medicine)