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Tromboza venoasa

Tromboza venoasa

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Published by: Daniela on Jan 27, 2011
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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
5
; myeloproliferative diseases; dysfibrinogenemia; and
 
disseminated intravascular coagulation, are associated with venous thrombosis.
 
Venulitis occurring in thromboangiitis obliterans, Behcet's 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
6
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 cerulea 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 ofDVT
7
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
8
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 inpatients with venous thrombosis. It is a sensitive, but not specific, test for venous
 
thrombosis. The noninvasive test used most often to diagnoseDVT
9
is duplex venous
 
ultrasonography (B-mode, 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 detectDVT
10
. 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
11
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
12
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 withDVT
13
, 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 eitherunfractionated heparin or low-molecular-weight 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 proximalDVT
14
, 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 acause 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 targetedINR
15
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

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