At the start of your shift on an orthopaedic ward, you are asked to review two patients.
Elizabeth is a 70-year-old who was making a good recovery from her hip replacement 3 days ago. This morning while having breakfast, she developed sudden breathlessness. She denies any pain.
Alice is a 35-year-old woman who had an internal fixation of a femoral shaft fracture following a road traffic accident 4 days earlier. This morning she complains of pleuritic pain but no breathlessness.
Initial clinical findings for Elizabeth are blood pressure (BP) of 110/80 mmHg, heart rate (HR) 95 beats/min, respiratory rate 24 breaths/min and oxygen saturation 86%. Initial clinical findings for Alice are BP 126/80 mmHg, HR 80 beats/min, respiratory rate 18 breaths/min and oxygen saturation 97%.
In both patients, examination is otherwise unremarkable and the initial chest X-ray and electrocardiogram (ECG) are normal, although a repeat X-ray the following day shows that Alice has developed a small right-sided pleural effusion.
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1. You are worried whether either or both could have a pulmonary embolus (PE). From the history and findings so far, is this likely in either or both of these patients? If these patients had not had surgery recently but had presented with the same symptoms and signs in Accident and Emergency, would your answer be different?
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Correct answer:
Pulmonary embolism can be asymptomatic or present with a variety of different symptoms and signs including sudden death. Breathlessness and pain, which is typically pleuritic, are the most common symptoms followed by cough. Haemoptysis is relatively uncommon occurring in only about one in six patients. Other presentations and symptoms include hypotension and syncope, wheezing and sudden onset of atrial fibrillation. Symptoms and signs of a deep venous thrombosis (DVT), such as swelling and pain in the calf, may also be present, but they are often absent. Both these patients have had recent orthopaedic surgery and are in a high-risk group for DVT and pulmonary embolus. In this context, sudden onset of breathlessness and/or pleuritic pain makes pulmonary embolism a serious possibility. In patients without a history of recent surgery or fracture presenting in an Accident and Emergency department with recent onset of breathlessness or pleuritic pain, pulmonary embolus would be a less likely explanation for these symptoms but still a real possibility even in those with no other recognized risk factors (see Answer to Question 3).
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2. Which of these oxygen saturations is ‘typical’ of a pulmonary embolus?
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Correct answer:
Either of these oxygen saturations is entirely compatible with the diagnosis of pulmonary embolus. A low PaO2 and arterial oxygen saturation are common especially with the larger, more proximally lodged emboli, whereas oxygen saturation may be normal with smaller emboli that lodge more peripherally.
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3. Pulmonary emboli produce an area of lung that is ventilated but not perfused; that is, they produce alveolar dead space and therefore increase physiological dead space. Does increased physiological dead space inevitably lead to a reduced arterial PO2?
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No, with a moderately increased physiological dead-space hypoxia can be avoided if the subject increases respiratory rate and/or tidal volume sufficiently to compensate for the increased dead-space ventilation, restoring alveolar ventilation to its previous level. However, pulmonary embolism leads to other problems such as reduced surfactant production, areas of atelectasis and increased ventilation–perfusion mismatching. The effects of ventilation–perfusion mismatching may be made worse by decreased mixed venous oxygen content, resulting from a reduced cardiac output. As a result, hypoxia and an increased A–a PO2 gradient are common with pulmonary emboli. As expected with ventilation–perfusion mismatching, PaCO2 is usually reduced.
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4. What other aspects of the history might be relevant?
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Other risk factors may be revealed. These include pregnancy, oestrogen therapy, cancer, malignancy, chemotherapy, previous DVT, myocardial infarction, inflammatory bowel disease, immobilization or recent long-distance travel. A previous or family history of venous thrombosis will suggest an inherited problem with the coagulation system such as factor V Leiden. On examination a raised jugular venous pressure and/or a pleural rub would increase suspicion.
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5. D-dimer tests are a useful addition to the diagnostic armoury but false-positives are common. False-negatives also occur. Which sort of PE is most likely to be associated with a false-negative PE? How long do D-dimers remain elevated?
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Correct answer:
D-dimers are fibrin degradation products. They are not specific to pulmonary embolus or DVT but may be raised in sepsis, trauma (including surgery) and malignancy, so false positives are common. With the most sensitive assays, false negatives are less common but may occur with small peripheral emboli. Following a pulmonary embolus, they remain elevated for about 6 days following the onset of symptoms. In the clinical context of low probability of pulmonary embolus, negative D-dimers can be the end of the investigation. If D-dimers are positive or clinical probability high then further investigation is likely to be appropriate.
Small peripheral emboli may also be missed by other techniques such as computed tomography pulmonary angiogram (CTPA). They tend to cause pleuritic pain but less breathlessness and haemodynamic disturbance than larger emboli, which lodge in more proximal pulmonary arteries. There is some controversy about whether failing to detect such emboli matters. They are likely to clear without treatment but on the other hand they may herald further, more significant emboli.
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6. What is the role of chest X-ray (CXR) and ECG? How will they be affected in the presence of a pulmonary embolus?
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Both the chest X-ray (CXR) and the electrocardiogram (ECG) may show abnormalities, but none of the abnormalities are specific to pulmonary emboli. In the presence of a pulmonary embolus, the X-ray may be normal initially but abnormalities such as areas of atelectasis, parenchymal densities and pleural effusions often develop over the first day or so. Pleural effusions are usually small, often bloody and resolve over a few days. An increasing pleural effusion suggests another cause for the symptoms or recurrent emboli. The ECG may be completely normal or show non-specific changes. Other changes that may be found are associated with right ventricular strain such as the S1, Q3, T3 pattern (prominent S wave in lead I, Q wave and inverted T in lead III), right axis deviation, dominant R wave in lead V1, inverted T waves in leads V1–V3 and right bundle-branch block.
Probably the most important role of the CXR and ECG is to reveal alternative causes of symptoms such as dyspnoea and chest pain, such as pneumothorax or myocardial infarction.
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7. What other investigations are appropriate?
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Correct answer:
Diagnosing pulmonary emboli is difficult and as yet there is no single test that is highly sensitive, highly specific, non-invasive, readily available and suitable for all situations. Various algorithms and investigation strategies have been proposed that take into account risk factors and the clinical situation, but this still remains a difficult area with problems of both under- and overdiagnosis. Radionuclide ventilation–perfusion scans, spiral/helical computed tomography (CTPA) and pulmonary angiograms – all have advantages and disadvantages, which are discussed in Chapter 28. Demonstrating a DVT using Doppler imaging or venography is helpful, both because it greatly increases the likelihood that pulmonary symptoms are embolic in origin and also because the treatment is the same for both.
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8. What are the treatment options for Elizabeth and Alice?
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Correct answer:
Anticoagulation with heparin and then warfarin for 6 months is the standard treatment for proven pulmonary emboli (see Chapter 28), but for Elizabeth and Alice this option is complicated by their recent surgery, which would increase the risk of haemorrhagic complications. An inferior vena cava filter is an alternative and may be necessary to prevent further fatal emboli. This is a further reason why vigorous prophylaxis (see Chapter 28) is essential in high-risk patients. Thrombolysis is sometimes considered in large emboli with haemodynamic effects but would be contraindicated here by the recent surgery.
