Major and Massive Pulomary Embolism
Pulmonary Embolism (PE) is often a devastating condition that can result in sudden death. This article explores the predisposing factors, clinical presentation and management strategies in PE
Pulmonary Embolism (PE) is a relatively common and potentially fatal condition that is a leading cause of death in all age groups.
Pulmonary embolism is any condition in which the pulmonary artery becomes obstructed by a foreign mass or embolus. Generally the most serious presentation is where the main pulmonary trunk or one of the main right or left branches becomes obstructed.
Causes of Pulmonary Embolism (PE)
The main cause of PE is thrombus. Thrombosis in veins is triggered by Virchows triad of:
- Vessel wall inflammation
The main sources of clot are
- Deep venous thrombosis (DVT) e.g. ileofemoral or axillary vein thrombosis
- Atrial fibrillation (Fig 1)
- Right ventricular myocardial infarction
- Central venous lines
Other potential causes of PE are:
- Fat e.g. from long bone fracture
- Amniotic fluid embolism
- Miscellaneous e.g. impure intravenously injected drugs
‘Economy Class Syndrome’
It is acknowledged that travelling for long periods of time by any transport mode may increase the risk of DVT due to immobility. Hyperbaric hypoxia in combination with immobility and dehydration may explain air travellers increased risk of thrombosis. Clearly more work needs to be done in this area in order to improve our understanding of the potential risk of air travel.
Predisposing factors for Pulmonary Embolism
- Previous thromboembolism
- Varicose veins
- Genetic coagulation defects
Patients with a major or massive pulmonary embolism may present with the following clinical signs:
- Sudden loss of cardiac output (pulseless electrical activity)
- Chest pain – the chest pain may be pleuritic in nature although it may present as acute myocardial ischaemia
- Raised jugular venous pressure
- Signs of deep venous thrombosis
Prior to any interventional procedures a pre test probability may be undertaken using the clinical model suggested by Wells. (Wells, PS et al. 1998) Table 1.The pre test probability can be used with the result of a D-Dimer blood test to decide on the next step in the management of the patient.
Diagnostic tests for PE
|Clinical Signs of DVT|
(treatment ongoing or within 6 months or palliative)
|Immobilisation (bed rest for > 3 days or surgery in past 4 weeks)|
|Previous history of PE or DVT|
|Heart rate > 100|
|PE as most likely diagnosis on clinical review|
|Probability of PE||Score|
- Nuclear scintigraphic ventilation-perfusion (V/Q) scan:
- Diagnostic patterns are classified as high probability.
- Chest x-ray:
- The chest x-ray may well appear normal initially. The presence of Westermarks sign, a darker area representing reduced perfusion, is suggestive of PE. Pleural effusions may be present.
- May demonstrate signs of right atrial and ventricular dilation and dysfunction.
- 12-Lead ECG
- May be normal although generalised T wave changes, P Pulmonale and right bundle branch block may be apparent. P Pulmonale appears as a tall, peaked P wave on the ECG and is suggestive of right atrial hypertrophy.
- Arterial Blood Gas
- Invariably demonstrate hypoxia and respiratory alkalosis in which case the PO2 will be low, the pH will be greater than 7.45 and the PCO2 will be raised
- Pulmonary Angiography
- Remains the gold standard test and will often demonstrate obstruction to pulmonary arterial blood flow
- CT Scan (computerised tomographic angiography)
- Good at detecting larger emboli but less sensitive for smaller multiple emboli that have lodged in more distal vessels
- Plasmin attacks fibrin clot producing fibrin degradation products and d-dimers hence an elevated result provides evidence of fibrinolysis but is not necessarily diagnostic for a pulmonary embolism
Management of Pulmonary Embolism
- If the patient presents as a cardiac arrest resuscitation should be initiated following the Resuscitation Council (UK) guidelines.
- High flow oxygen via a face mask will be required to maintain oxygen saturations above 90%.
- Intravenous opioid such as Morphine may be administered.
Stable and less seriously ill patients may be administered subcutaneous low molecular weight heparin as per weight. Warfarin may also be initiated with a view to longer-term anticoagulation.
However more unstable patients presenting with hypotension and signs of right ventricular failure may be commenced on intravenous thrombolysis such as tissue plasminogen activator.
Nurses are encouraged to identify patients who are potentially at risk of pulmonary embolism and introduce preventative measures:
- Early mobilisation – avoiding prolonged bed rest wherever possible will greatly assist in the prevention of immobility related complications such as pulmonary embolism
- Subcutaneous heparin – the administration of 5000iu of heparin subcutaneously is an effective preventative measure
- TED stockings (thromboembolic deterrent stockings) – these are useful in improving venous return from the lower legs
- Vena cava filters – these filters can be placed in the vena cava and may be considered in patients who cannot be anticoagulated, after surgical embolectomy or for patients with recurrent PE despite anticoagulation.
British Thoracic Society Guidelines for the management of suspected acute Pulmonary Embolism. Thorax 2003, 58: 470 – 483
Wells, PS et al Use of a clinical model for safe management of patients with suspected pulmonary embolism. Annals of internal medicine, vol 129 (12) 15 Dec 1998 997 – 1005
Anderson DR, Wells PS. Improvements in the diagnostic approach for patients with suspected deep venous thrombosis or pulmonary embolism.Thromb Haemost 1999; 82 (2) 878-886
Bendz B et al. Association between acute hypobaric hypoxia and activation of coagulation in human beings. Lancet 2000 Nov 11; 356(9242): 1657-8.
Kraaijenhagen RA et al. Travel and risk of venous thrombosis. Lancet 2000 Oct 28; 356(9240): 1492-3.