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DEEP VENOUS THROMBOSIS

Farouq Muhammad 6-10-11

SYNOPSIS
Definition Risk factors Pathophysiology Clinical features Investigations Management Complications Prognosis Prevention

Definition

Deep vein thrombosis is the formation of a blood clot in one of the deep veins of the body, usually in the leg

Virchow's triad
More than 100 years ago, Virchow described a triad of factors:
1. venous stasis, 2. endothelial damage, and 3. hypercoagulable state

Venous stasis
Prolonged bed rest (4 days or more) : more time for clotting A cast on the leg Limb paralysis from stroke or spinal cord injury: small thrombi not washed away Extended travel in a vehicle

Hypercoagulability
Surgery and trauma responsible for up to 40% of all thromboembolic disease : increase in tissue factor Malignancy: Presence of activating factors Increased estrogen (due to a fall in protein S) Increased estrogen occurs during
all stages of pregnancy the first three months postpartum, after elective abortion, and during treatment with oral contraceptive pills

Inherited disorders of coagulation

deficiencies of protein S, protein C, and antithrombin III. Factor V leiden

Acquired disorders of coagulation


nephrotic syndrome results in urinary loss of antithrombin III, this diagnosis should be considered in children presenting with thromboembolic disease Antiphospholipid antibodies accelerate coagulation and include the lupus anticoagulant and anticardiolipin antibodies.

Inflammatory processes, such as


systemic lupus erythematosus (SLE), sickle cell disease, and inflammatory bowel disease (IBD),

Also predispose to thrombosis, presumably due to hypercoagulability

Endothelial Injury
Trauma, Surgery, and invasive procedure may disrupt venous integrity Iatrogenic causes of venous thrombosis are increasing due to the widespread use of central venous catheters, particularly subclavian and internal jugular lines. These lines are an important cause of upper extremity DVT, particularly in children.

Pathophysiology
The nidus for a clot is often an intimal defect When a clot forms on an intimal defect, the coagulation cascade promotes clot growth proximally. Thrombus can extend from the superficial veins into the deep system from which it can embolize to the lungs.

Opposing the coagulation cascade is the endogenous fibrinolytic system. After the clot organizes or dissolves, most veins will recanalize in several weeks. Residual clots retract as fibroblasts and capillary development lead to intimal thickening.

Venous hypertension and residual clot may destroy valves, leading to the postphlebitic syndrome, which develops within 5-10 years

Edema, sclerosis, and ulceration characterize this syndrome, which develops in 40-80% of patients with DVT.

Pulmonary embolism (PE) is a serious complication of DVT. Many episodes of pulmonary embolism go unrecognized, and at least 40% of patients with DVT have clinically silent PE on VQ scanning

Presentation and Physical Examination


Calf pain or tenderness, or both Swelling with pitting oedema Swelling below knee in distal deep vein thrombosis and up to groin in proximal deep vein thrombosis Increased skin temperature Cyanosis can occur with severe obstruction

Palpate distal pulses and evaluate capillary refill to assess limb perfusion. Move and palpate all joints to detect acute arthritis or other joint pathology. Neurologic evaluation may detect nerve root irritation; sensory, motor, and reflex deficits should be noted Homans' sign: pain in the posterior calf or knee with forced dorsiflexion of the foot

Search for stigmata of PE such as tachycardia (common), tachypnea or chest findings (rare), and exam for signs suggestive of underlying predisposing factors.

Wells Clinical Prediction Guide


The Wells clinical prediction guide incorporates risk factors, clinical signs, and the presence or absence of alternative diagnoses

Diagnostic Studies
Clinical examination alone is able to confirm only 2030% of cases of DVT Blood Tests the D-dimer INR. Current D-dimer assays have predictive value for DVT, and the INR is useful for guiding the management of patients with known DVT who are on warfarin (Coumadin)

D-dimer
D-dimer is a specific degradation product of cross-linked fibrin. Because concurrent production and breakdown of clot characterize thrombosis, patients with thromboembolic disease have elevated levels of D-dimer three major approaches for measuring D-dimer
ELISA latex agglutination blood agglutination test (SimpliRED)

False-positive D-dimers occur in patients with


recent (within 10 days) surgery or trauma, recent myocardial infarction or stroke, acute infection, disseminated intravascular coagulation, pregnancy or recent delivery, active collagen vascular disease, or metastatic cancer

Imaging Studies
Invasive venography, radiolabeled fibrinogen and. noninvasive ultrasound, plethysmography, MRI techniques

DVT Algorithm

DIFFERENTIAL DIAGNOSIS
Cellulitis Thrombophlebitis Arthritis Asymmetric peripheral edema secondary to CHF, liver disease, renal failure, or nephrotic syndrome Lymphangitis Extrinsic compression of iliac vein secondary to tumor, hematoma, or abscess Hematoma Lymphedema

Muscle or soft tissue injury Neurogenic pain Postphlebitic syndrome Prolonged immobilization or limb paralysis Ruptured Baker cyst Stress fractures or other bony lesions Superficial thrombophlebitis Varicose veins

Management

EMERGENCY DEPARTMeNT CARE


The primary objectives of the treatment of DVT are to
prevent pulmonary embolism, reduce morbidity, and prevent or minimize the risk of developing the postphlebitic syndrome.

Anticoagulation Thrombolytic therapy for DVT Surgery for DVT Filters for DVT Compression stockings

Anticoagulation
Heparin prevents extension of the thrombus Heparin's anticoagulant effect is related directly to its activation of antithrombin III. Antithrombin III, the body's primary anticoagulant, inactivates thrombin and inhibits the activity of activated factor X in the coagulation process.

Heparin is a heterogeneous mixture of polysaccharide fragments with varying molecular weights but with similar biological activity. The larger fragments primarily interact with antithrombin III to inhibit thrombin. The low molecular weight fragments exert their anticoagulant effect by inhibiting the activity of activated factor X. The hemorrhagic complications attributed to heparin are thought to arise from the larger higher molecular weight fragments.

The optimal regimen for the treatment of DVT is anticoagulation with heparin or an LMWH followed by full anticoagulation with oral warfarin for 3-6 months Warfarin therapy is overlapped with heparin for 4-5 days until the INR is therapeutically elevated to between 2-3.

Advantages of Low-Molecular-Weight Heparin Over Standard Unfractionated Heparin


Superior bioavailability Superior or equivalent safety and efficacy Subcutaneous once- or twice-daily dosing No laboratory monitoring* Less phlebotomy (no monitoring/no intravenous line) Less thrombocytopenia

At the present time, 3 LMWH preparations, Enoxaparin, Dalteparin, and Ardeparin

warfarin
Interferes with hepatic synthesis of vitamin Kdependent coagulation factors Dose must be individualized 2-10 mg/d PO caution in active tuberculosis or diabetes; patients with protein C or S deficiency are at risk of developing skin necrosis

Thrombolytic therapy for DVT


Advantages include
prompt resolution of symptoms, prevention of pulmonary embolism, restoration of normal venous circulation, preservation of venous valvular function, and prevention of postphlebitic syndrome.

Thrombolytic therapy does not prevent


clot propagation, rethrombosis, or subsequent embolization.

Heparin therapy and oral anticoagulant therapy always must follow a course of thrombolysis.

Thrombolytic therapy is also not effective once the thrombus is adherent and begins to organize The hemorrhagic complications of thrombolytic therapy are formidable (about 3 times higher), including the small but potentially fatal risk of intracerebral hemorrhage.

Surgery for DVT



indications when anticoagulant therapy is ineffective unsafe, contraindicated. The major surgical procedures for DVT are clot removal and partial interruption of the inferior vena cava to prevent pulmonary embolism.

These pulmonary emboli removed at autopsy look like casts of the deep veins of the leg where they originated.

This patient underwent a thrombectomy. The thrombus has been laid over the approximate location in the leg veins where it developed.

Filters for DVT


Indications for insertion of an inferior vena cava filter Pulmonary embolism with contraindication to anticoagulation Recurrent pulmonary embolism despite adequate anticoagulation

Inferior vena cava filters reduce the rate of pulmonary embolism but have no effect on the other complications of deep vein thrombosis. Thrombolysis should be considered in patients with major proximal vein thrombosis and threatened venous infarction

Compression stockings (routinely recommended

Further Inpatient Care


Most patients with confirmed proximal vein DVT may be treated safely on an outpatient basis. Exclusion criteria for outpatient management are as follows:
Suspected or proven concomitant pulmonary embolism Significant cardiovascular or pulmonary comorbidity Morbid obesity Renal failure Unavailable or unable to arrange close follow-up care

Further Inpatient Care


Platelets also should be monitored and heparin discontinued if platelets fall below 75,000. While on warfarin, the prothrombin time (PT) must be monitored daily until target achieved, then weekly for several weeks. When the patient is stable, monitor monthly. Significant bleeding (ie, hematemesis, hematuria, gastrointestinal hemorrhage) should be investigated thoroughly since anticoagulant therapy may unmask a preexisting disease (eg, cancer, peptic ulcer disease, arteriovenous malformation).

Complications
Acute pulmonary embolism Hemorrhagic complications Chronic venous insufficiency Post thrombotic syndrome
thrombolytic therapy, which has a limited use due to the risk of haemorrhage; and graduated compression stockings for 2 years after an episode of DVT: the incidence of postthrombotic syndrome was reduced from 70% to 31%.

Prognosis:
All patients with proximal vein DVT are at long-term risk of developing chronic venous insufficiency. About 20% of untreated proximal (above the calf) DVTs progress to pulmonary emboli, and 10-20% of these are fatal. With aggressive anticoagulant therapy, the mortality is decreased 5- to 10-fold.

Patient Education:

Advise women taking estrogen of the risks and common symptoms of thromboembolic disease. Discourage prolonged immobility, particularly on plane rides and long car trips

PREVENTION
Identify any patient who is at risk. During operation avoid prolonged calf compression. Passive leg exercises should be encourged whilst patient on bed. Foot of bed should be elevated to increase venous return. Early mobilization should be rule for all surgical patients.

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