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Clinical Management of Pulmonary Embolism
Pulmonary embolism (PE) is a relatively uncommon condition with an annual incidence of 60-70 cases per 100,000 (1). It is a potentially life-threatening condition with an annual mortality rate of 30%, however with effective treatment mortality can be reduced to just 2-8% (1). A PE is a thrombus, usually formed in the venous circulation (deep femoral, pelvic or abdominal veins) due to one or more of the components of Virchow's triad (figure 1).
A PE can be classified according to its size: massive and non-massive. A massive PE is an emergency presentation with haemodynamic instability and circulatory collapse. A non-massive PE can be of insidious onset, with progressive dyspnoea, tachypnoea and pleuritic chest pain. There may be small, multiple emboli present that may not be evident on a chest radiograph (2). Clinicians therefore need to have a high index of suspicion of a PE particularly if the presentation is not classical. To aid clinicians, the Quantified Well's Score can be used in the acute assessment of determining the likelihood of a PE and its severity (3).
Medical Management
The initial management of both types of PE follows a common pathway and presentations should be treated as a suspected PE until excluded by subsequent investigations.
Airway, breathing and circulation must first be assessed to ensure the patient is stable. High-flow oxygen (100%) should be given via a facemask to correct hypoxia, unless contraindicated by chronic obstructive pulmonary disease (COPD). Analgesics (non-steroidal anti-inflammatory drugs - NSAIDs) can be administered to relieve pleuritic chest pain. If there is evidence of a massive PE, due to circulatory collapse (hypotension, tachycardia, tachypnoea and syncope), a 500ml bolus of intravenous fluid can be given (4,6).
Once the patient has stabilised, they can undergo appropriate investigations - such as chest X-ray, electrocardiogram, echocardiogram, blood tests and arterial blood gases, plasma D-dimer, CTPA, ventilation/perfusion (V/Q scan), spiral CT and magnetic resonance imaging to confirm the diagnosis of PE (3,4).
Heparin
Until the diagnosis is confirmed, all patients suspected of PE are initiated on low-molecular weight heparin (LMWH) such as enoxaparin or tinzaparin (5,6). Heparin is an anticoagulant that prevents clotting by enhancing the activity of antithrombin, which effectively inactivates thrombin and factor Xa in the clotting cascade (5). There are two types of heparin that can be used - LMWH and unfractionated heparin (UFH). Both have the same mechanism of action. A meta-analysis conducted in 2000, compared LMWH and UFH in the treatment of venous thromboembolism. UFH has long been studied and recent comparison studies with LMWH found that LMWH is as effective as UFH in preventing recurrent venous thromboembolism.(7) LMWH was also found to significantly reduce total mortality (7). There are advantages of using LMWH over UFH; 1) LMWH can be given as a once daily injection (has a longer duration of action than UFH) (BNF). 2) The standard dose of LMWH does not require activated partial thromboplastin time (aPTT) monitoring (8) and 3) LMWH can be administered in an outpatient setting, if the patient is suitable, which is far more cost effective than treating as an inpatient. The main advantages of UFH are that its affects can be rapidly reversed due to its shorter duration of action than LMWH and it is more cost effective than LMWH (8). Bleeding is an obvious complication of anticoagulation therapy and is directly related to a prolonged aPTT (2,12), however, haemorrhages whilst on heparin are uncommon unless an invasive procedure (such as an angiogram) is performed (2).
Thrombolysis
For those patients with signs of circulatory collapse, studies show early use of fibrinolytic agents (such as recombinant tissue plasmin activator (rtPA) and streptokinase) improve mortality when compared to heparin alone (9). Fibrinolytics act directly on the thrombus, dissolving it, to reduce the obstruction in the venous circulation. In contrast, heparin does not act on the thrombus itself but prevents new thrombus from forming. This is evident from studies that have shown thrombolysis has a faster action to improve cardiac parameters such as blood pressure, due to its direct action on dissolving the clot, whereas heparin had no effect on these parameters (6).
Thrombolysis is reserved for those patients with massive PE due to the two fold increase in risk of major bleeding compared to using heparin alone (10). Studies have concluded that the increased risk of bleeding outweighs the benefit of thrombolysis in patients with non-massive PE (2) and should therefore not be offered to those patients.
Contraindications to thrombolysis for massive PE must be weighted against the benefit. Absolute contraindications are an active internal bleed and recent spontaneous intracranial bleed (2.4). Other contraindications include recent major surgery, recent ischaemic stroke, recent gastrointestinal bleed, uncontrolled severe hypertension (systolic BP >180mmHg, diastolic BP >110mmHg), thrombocytopenia and pregnancy (2,4).
Long-term Anticoagulation
For the treatment of non-massive PE, heparin therapy is concurrent with oral anticoagulation, such as warfarin (3,4,5,6). Warfarin is an antagonist of vitamin K and consequently inhibits the synthesis of vitamin K dependent coagulation factors (VII, IX, X and prothrombin) (5). The international normalised ratio (INR) indicates a ratio of the patient prothrombin time over normal prothrombin time. It is recommended that heparin is continued until warfarin reaches the therapeutic INR range (2-3) (4,5). A high INR together with a long duration of treatment is related to an increased risk of bleeding (12). The duration of warfarin therapy is an area of considerable debate. There is some controversy regarding the optimum duration and recommendations vary between 4-6 weeks for temporary risk factors (6) and 3-6 months (3,5,11). There is agreement that if a patient suffers recurrent venous thromboembolism or has a continuous risk factor (i.e. immobilisation) - anticoagulation therapy should continue for at least 6 months and in the case of irreversible factors (i.e. coagulation disorders) anticoagulation should be lifelong (5,6). Long-term and lifelong warfarin therapy can have dramatic implications on a patients life including the increased risk of bleeding complications and inconvenience of fortnightly blood tests to monitor the INR to ensure a therapeutic level is maintained.
Anticoagulation therapy is contraindicated in patients with a history of gastrointestinal bleeding (8,12). Warfarin has many drug interactions which can potentiate its anticoagulant effect and hence further increase the risk of bleeding, such interactions include: aspirin, allopurinol, NSAIDs, amiodarone, antibiotics (cephalosporins and macrolides), St. John's wort and antidiabetic agents (8).
Surgical Management
Surgical Embolectomy Thrombolysis is the treatment of choice for massive PE causing circulatory collapse due to obstruction of the pulmonary artery. However, surgical removal of the PE can be a life-saving option in those patients with absolute contraindications to thrombolysis, or in patients with inadequate response to thrombolysis (within 3 hours) (13), however the risk of surgical mortality is reported between 20-35% (4) primarily due to pulmonary haemorrhage (14). Embolectomy can now be performed using a percutaneous approach, compared to invasive thoracic surgery; however, the surgical option is still used where catheterisation facilities are unavailable (15). Confirmation of the extent and site of the PE is needed prior to any surgical intervention and this can be achieved quickly using transoesophageal echocardiogram (TEE). Studies report patient survival rates of 71% after 8 years after surgical embolectomy (2). At present there are no randomised control trials comparing outcome of surgical and percutaneous embolectomy and hence this is an area of future research.
Inferior vena cava (IVC) filters
For the past 25 years IVC filters have been used to prevent PE. Percutaneous insertion of filters can effectively sieve blood returning to the heart via the IVC to prevent the development of a PE. A randomised control trial of patients with deep vein thrombosis (DVT) identified that patients who were treated with IVC filter and anticoagulant therapy had a better short term (12 weeks) mortality rate than those treated with anticoagulant therapy alone. However, there was no significant difference in mortality at two years between the two groups, although 4 out of 5 deaths in the anticoagulant group were attributed to PE, whereas no deaths in the filter group patients were due to PE (2). Follow up of patients with IVC filters revealed occlusion in up to 30% at 6 years (2) and a higher rate of DVT (21%) compared to those patients who were managed with anticoagulation therapy alone (12%) (2). Clearly, IVC filters do not provide an alternative to anticoagulation therapy but serve as an adjunct to significantly reduce the risk of PE in those patients with recurrent DVT, despite adequate anticoagulation for those patients with long-term risk factors.
Conclusion
Pulmonary embolism is a significant cause of mortality for which doctors need to have a high index of suspicion as presentation may not be classical. If suspected, prompt initiation of heparin prior to confirmed diagnosis, is an essential mortality reducing step in the management of acute PE. Warfarin should be started once PE is confirmed and INR maintained between 2-3. Thrombolysis should be given to all haemodynamically unstable patients with massive PE unless absolutely contraindicated. If contraindicated, surgical embolectomy via thoracic or percutaneous route should be performed if facilities are available. IVC filters can be used in patients with recurrent DVT in conjunction with anticoagulation therapy.
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