Venous Thromboembolism And Pulmonary Embolism - pediagenosis
Article Update

Tuesday, May 21, 2019

Venous Thromboembolism And Pulmonary Embolism

Venous Thromboembolism And Pulmonary Embolism
Venous thromboembolism and its most significan complication, pulmonary embolism (PE), are common clinical disorders that have a substantial impact on patient morbidity and mortality; Fig. 28c shows major risks. PE is most often a complication of deep venous thrombosis (DVT). Both disorders are commonly underdiagnosed and require appropriate clinical suspicion and a systematic diagnostic approach. About 5 million patients develop DVT in the USA each year; approximately 500 000 subsequently develop PE and approximately 10% of these die. Prophylactic therapy in patients at risk is essential (Fig. 28d); in its absence up to 70% of patients undergoing hip or knee replacement surgery develop DVT.

Venous Thromboembolism And Pulmonary Embolism

Deep venous thrombosis
Nearly all clinically significan cases of PE (  ̴90%) arise from DVT in the lower extremities, with thrombi typically originating in the calves and propagating above the knee. Approximately 15-25% will propagate into the femoral and iliac veins and have a 50% risk of embolizing to the lung. Thrombi may develop in the axillary and subclavian veins, usually due to surgery or intravenous catheters, but emboli are usually smaller, with less risk of catastrophic consequences. Soon after thrombus formation, the intrinsic fibrinolyti cascade begins to organize the thrombus. The risk of a thrombus embolizing is greatest early during ongoing proliferation and decreases once it is organized.

Pulmonary embolism
When a thrombus embolizes to the lung, respiratory or circulatory abnormalities occur due to sudden occlusion of a pulmonary artery or arteriole. Occlusion of regional perfusion causes an increase in dead space, necessitating an increase in minute ventilation to maintain normal Paco2. Surfactant production distal to the embolus may be reduced after 24 hours, resulting in atelectasis. Hypoxaemia is common and mostly due to VA/Q mismatch (Chapter 14). Pulmonary infarction occurs in less than 25% of cases of PE. Circulatory complications arise from obliteration of the pulmonary vascular bed and a reduction of cardiac output. Severity is related to the amount of lung embolized and the pre-existing state of the pulmonary vasculature and right ventricle (RV). A single large embolus can be catastrophic, whereas multiple small emboli can cause 'pruning' of smaller arteries. Circulatory collapse may occur with more than 50% obstruction of the pulmonary vascular bed. Less severe emboli may be fatal to patients with pre- existing lung or heart disease.

Clinical features
Clinical features of DVT are non-specific with lower extremity pain, swelling and erythema. Homan's sign (pain in the calf on dorsifl xion of the foot) occurs in a minority of patients. Fifty per cent of DVTs are undetected.
Most patients with PE have dyspnoea, pleuritic chest pain, haemoptysis, apprehension and tachypnoea. With severe PE, signs related to RV failure (e.g. hypotension and jugular venous distension) may occur. Most patients with PE have non-specifi abnormalities on chest X-ray, including atelectasis. The electrocardiogram (ECG) may show non-specifi ST segment changes, and rarely, with significan RV strain, an S1Q3T3 pattern (prominent S in lead I, Q and inverted T in lead III), right axis deviation (RAD) or right bundle-branch block (RBBB). Arterial blood gas abnormalities are common, including widened A–a gradient, hypoxaemia and hypocapnia (despite increased dead space).

Deep venography or pulmonary angiography is the diagnostic standard, although V/Q scanning is usually the initial investigation as it is less invasive (Fig. 28a; Chapter 21). A negative perfusion scan effectively rules out PE and a 'high probability' scan (multiple segmental perfusion defects with normal ventilation) has a more than 85% probability of PE (Fig. 28a). With a high clinical suspicion, a high-probability V/Q scan has a positive predictive value of more than 95%. Unfortunately, most V/Q scans are non-diagnostic or indeterminate, with a 15-50% likelihood of PE, necessitating further imaging. Non-invasive imaging of the lower extremity deep veins with Doppler imaging or impedance plethysmography is useful, because the presence of thrombosis requires treatment similar to PE. In patients with underlying cardiac or pulmonary disease, pulmonary angiography is indicated if the above tests are non-diagnostic. Absence of DVT and a low probability V/Q scan permit treatment to be withheld. Spiral/helical computed tomography (CT) has a sensitivity for PE of 70-95% (higher for more proximal emboli) and a specificit of more than 90%. It also allows visualization of parenchymal abnormalities and is used in patients with chronic obstructive pulmonary disease (COPD) or extensive chest X-ray abnormalities, where V/Q scanning is indeterminate. Echocardiography may reveal RV dysfunction in PE and rule out pericardial tamponade or severe left ventricular (LV) dysfunction. Transoesophageal echocardiography may visualize thromboemboli in the main pulmonary arteries, but not in lobar or segmental arteries.

The cornerstone of therapy for DVT/PE is anticoagulation, which stops propagation of existing thrombus and allows organization. Immediate therapy in patients with a high suspicion of PE may prevent further life-threatening embolization. Standard therapy is to give unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) for 5-7 days, followed by warfarin for 3-6 months. UFH and warfarin must be monitored as subtherapeutic levels increase the risk of recurrent thromboembolism. LMWH is more bioavailable and does not require monitoring. Patients with inherited or acquired hypercoagulability may require lifelong therapy.
In patients with contraindications to anticoagulation (recent surgery, haemorrhagic stroke, central nervous system metastases, active bleeding) or recurrent PE while on therapeutic anticoagulation, an inferior vena cava (IVC) filter may prevent fatal PE.
Although activation of fibrinolysis with thrombolytics hastens resolution of perfusion defects and RV dysfunction, convincing benefi is lacking. As thrombolytics cause increased bleeding complications, including a 0.3-1.5% risk of intracerebral haemorrhage, they are only recommended for life-threatening PE with compromised haemodynamics.

Share with your friends

Give us your opinion
This is just an example, you can fill it later with your own note.