DVT Pulmonary Embolism

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Deep Vein Thrombosis and Pulmonary Embolism

Dr. Shatdal ChaudharySIS 12 Nov 2009

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DVT-PE – Epidemiology

• VTE-related deaths in the United States are estimated at 300,000 annually:– 7% diagnosed with VTE and treated,– 34% sudden fatal PE, – and 59% as undetected PE.

• In Europe- an estimated 370,000 per year PE-related deaths

• Approximately two-thirds of symptomatic VTE events are hospital acquired, and the remainder are community acquired.

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• DVT occurs about 3 times more often than PE.

• The major adverse outcome of DVT alone, without PE, is the development of postphlebitic syndrome.– It occurs in more than half of patients with DVT.

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• Genetic and acquired factors contribute to the likelihood of VTE.

• The two most common genetic factors are – the factor V Leiden – and the prothrombin gene mutations.

DVT – VTE Risk Factors

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DVT – VTE Risk Factors

• Acquired predispositions include– Malignancy

– Surgery

– Trauma

– Pregnancy

– Oral contraceptives or hormonal therapy

– Immobilization

– Presence of venous catheter

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– long-haul air travel, – obesity, – cigarette smoking, – and medical conditions such as

• antiphospholipid antibody syndrome,• Hyperviscosity• Nephrotic syndrome• Inflammatory bowel disease• systemic arterial hypertension, • chronic obstructive pulmonary disease, CCF• Thrombophilia contributes to the risk of venous thrombosis,

often due to an inherited risk factor in combination with an acquired predisposition.

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• About half of patients with pelvic vein thrombosis or proximal leg DVT develop PE

• Isolated calf vein thrombi pose a much lower risk of PE.

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Physiology• The most common gas exchange abnormalities are

hypoxemia and an increased alveolar-arterial O2 tension gradient.

• Anatomic and Physiologic dead space • Other pathophysiological abnormalities include:

– Increased pulmonary vascular resistance – Impaired gas exchange due to increased alveolar dead space

from vascular obstruction, – Alveolar hyperventilation due to reflex stimulation of irritant

receptors– Increased airway resistance due to constriction of airways distal

to the bronchi– Decreased pulmonary compliance due to lung edema, lung

hemorrhage, or loss of surfactant

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What are the SYMPTOMS and SIGNS of Pulmonary embolism?

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PULMONARY EMBOLISM SYMPTOMS

• Chest Pain

- pleuritic

-non pleuritic

• Dyspnea


PULMONARY EMBOLISM SYMPTOMS

• Apprehension

• Cough

• Hemoptysis

• Leg pain and Cramps in calf

• Syncope


PULMONARY EMBOLISM SIGNS

• Tachypnea • Crackles • Tachycardia • Fever• Increased “P2”• Phlebitis


Differential Diagnosis• DVT

– Ruptured Baker's cyst

– Cellulitis

– Postphlebitic syndrome/venous insufficiency

• PE – Pneumonia, asthma, chronic obstructive pulmonary disease

– Congestive heart failure Pericarditis Pleurisy: "viral syndrome,"

– costochondritis, musculoskeletal discomfort Rib fracture,

– pneumothorax Acute coronary syndrome Anxiety


Nonimaging Diagnostic Modalities

Blood Tests: D-dimer• The quantitative plasma D-dimer ELISA rises in the

presence of DVT or PE• The sensitivity is greater than 80% for DVT and

greater than 95% for PE. • The D-dimer is a useful "rule out" test. • The D-dimer assay is not specific.• Levels increase in patients with myocardial infarction,

pneumonia, sepsis, cancer, the postoperative state, and second or third trimester of pregnancy.

ECG FINDINGS• Sinus Tachycardia • “T” wave inversion V1-V4• ST segment depression • Low voltage • S1 Q3 T3 • ST elevation • R Bundle Branch Block


Noninvasive Imaging Modalities

• Venous Ultrasonography – loss of vein compressibility– direct visualization of thrombus


X-RAY FINDINGS

A normal or near-normal chest x-ray in a dyspneic

patient often occurs in PE.

• Focal oligemia (Westermark's sign)

• A peripheral wedged-shaped density above the

diaphragm (Hampton's hump),

• An enlarged right descending pulmonary artery

(Palla's sign).


P.E. atelectasis


P.E. effusion


P.E. Hampton’s Hump


P.E. subsegmental defect


Chest CT

• Multidetector-row spiral CT of the chest with intravenous contrast is the principal imaging test for the diagnosis of PE.


Pulm. Embolism CT

J. Galvin, M.D. J.Choi, B.S. The Diagnosis of P. E. Virtual Hospital:http://www.vh.org/Providers


Lung Scanning

• Lung scanning is now a second-line diagnostic test for PE.– Small particulate aggregates of albumin labeled with a gamma-

emitting radionuclide are injected intravenously and are trapped in the pulmonary capillary bed.

– The perfusion scan defect indicates absent or decreased blood flow, possibly due to PE.

– Ventilation scans, obtained with radiolabeled inhaled gases such as xenon or krypton, improve the specificity of the perfusion scan.


High Probability V/Q Scan

J. Galvin, M.D. J.Choi, B.S. The Diagnosis of P. E. Virtual Hospital:http://www.vh.org/Providers


MRI Contrast-Enhanced

• When ultrasound is equivocal, MR venography is an excellent imaging modality to diagnose DVT.

• MR imaging should be considered for suspected DVT or PE patients with renal insufficiency or contrast dye allergy.

• MR pulmonary angiography detects large proximal PE but is not reliable for smaller segmental and subsegmental PE.

Echocardiography• Echocardiography is not a reliable


Invasive Diagnostic Modalities

Pulmonary Angiography– Chest CT with contrast has virtually replaced

invasive pulmonary angiography as a diagnostic test.

– visualization of an intraluminal filling defect– abrupt occlusion ("cut-off") of vessels, segmental

oligemia or avascularity

Contrast Phlebography– Venous ultrasonography has virtually replaced


DIAGNOSIS

Based on:

• Relevant SYMPTOMS & SIGNS

• Associated RISK FACTORS

• Probability of ALTERNATIVE Diagnosis

• OBJECTIVE Confirmation


Low Clinical Likelihood of DVT If the Point Score Is Zero or Less• Clinical Variable Score• Active cancer 1• Paralysis, paresis, or recent cast 1• Bedridden for >3 days; major surgery <12 weeks 1• Tenderness along distribution of deep veins 1• Entire leg swelling 1• Unilateral calf swelling >3 cm 1• Pitting edema 1• Collateral superficial nonvaricose veins 1• Alternative diagnosis at least as likely as DVT –2

High Clinical Likelihood of PE if the Point Score Exceeds 4• Clinical Variable Score• Signs and symptoms of DVT 3.0• Alternative diagnosis less likely than PE 3.0• Heart rate >100/min 1.5• Immobilization >3 days; surgery within 4 weeks 1.5• Prior PE or DVT 1.5• Hemoptysis 1.0• Cancer 1.0


Wells Score


DVT-PE: Treatment

• Primary therapy – clot dissolution with thrombolysis – or removal of PE by embolectomy.

• Secondary prevention – Anticoagulation with heparin and warfarin – or placement of an inferior vena caval filter

constitutes


Anticoagulation• Immediately effective anticoagulation is initiated with a

parenteral drug: unfractionated heparin, low molecular weight heparin (LMWH), or fondaparinux.

• These parenteral drugs are continued as a transition or "bridge" to stable, long-term anticoagulation with a vitamin K antagonist

• The first dose of warfarin may be given as soon as several hours after the bridging anticoagulant if LMWH or fondaparinux are used. Otherwise, with UFH a therapeutic aPTT must first be documented.

• Warfarin requires 5–7 days to achieve a therapeutic effect.• Continue parenteral anticoagulation for a minimum of 5 days

and until 2 sequential INR values, at least 1 day apart, return in the target range.


Unfractionated Heparin

• anticoagulates by binding to and accelerating the activity of antithrombin III

• preventing additional thrombus formation and permitting endogenous fibrinolytic mechanisms to lyse clot that has already formed.

• intravenous bolus is 5000–10,000 units(80 units/kg) followed by a continuous infusion of 1000–1500 units/h (18 units/kg per hour).


Low Molecular Weight Heparins

• Enoxaparin 1 mg/kg twice daily

• Tinzaparin 175 units/kg once daily


Fondaparinux

• an anti-Xa pentasaccharide

• is administered by once-daily subcutaneous injection

• Patients weighing – <50 kg receive 5 mg, – 50–100 kg patients receive 7.5 mg, – >100 kg receive 10 mg.


Warfarin

• vitamin K antagonist • prevents carboxylation activation of coagulation

factors II, VII, IX, and X. • In an average-sized adult, warfarin is usually initiated

in a dose of 5 mg. Doses of 7.5 or 10 mg can be used

• The warfarin dose is titrated to achieve the target INR • The target INR is usually 2.5, with a range of 2.0–3.0.


Complications of Anticoagulants

• Hemorrhage

• Heparin-induced thrombocytopenia

• Osteopenia

• Alopecia (warfarin).

• Warfarin-induced skin necrosis

• During pregnancy, warfarin should be avoided


Duration of Anticoagulation

• Patients with PE following surgery or trauma ordinarily have a low rate of recurrence after 3–6 months of anticoagulation.

• For DVT isolated to an upper extremity or calf that has been provoked by surgery or trauma, 3 months of anticoagulation suffices.

• For provoked proximal leg DVT or PE, 6 months of anticoagulation is sufficient.

• In patients with "idiopathic," unprovoked DVT or PE : anticoagulation for an indefinite duration with a target INR between 2.0 and 3.0


Inferior Vena Caval (IVC) Filters

• active bleeding that precludes anticoagulation,

• recurrent venous thrombosis despite intensive anticoagulation.


Prevention of VTE

• Early mobilization• Graduated compression stockings • pneumatic compression devices • mini-dose unfractionated heparin (5000

units subcutaneously twice or preferably three times daily),

• Low molecular weight heparin,• fondaparinux 2.5 mg daily

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DVT Pulmonary Embolism