Pulmonary embolism

Chapter 30 Pulmonary embolism



Pulmonary embolism (PE) is a commonly considered, but relatively uncommonly diagnosed, condition. It is important to have an adequate understanding of the pathophysiology, as well as a rapid and reliable strategy of investigation and management. This is particularly important in critically ill patients where diagnosis can be difficult and PE may be life-threatening.



AETIOLOGY


Deep venous thrombosis (DVT) and PE are components of a single disease termed venous thromboembolism (VTE). Embolisation of DVT to the pulmonary arteries leads to PE, which is the most severe and life-threatening manifestation. VTE occurs in the population at a rate of about 1 in 1000 per year and is more common both with advancing age and in males.


Most PE results from DVT of the lower limbs, pelvic veins or inferior vena cava (IVC), although DVT of the upper limbs, right atrium or ventricle does also occur. Up to 40% of patients with DVT develop PE, although if the DVT is isolated to below the knee, clinically obvious PE is rare.


Predisposing risk factors for VTE involve one or more components of Virchow’s triad: (1) venous stasis; (2) vein wall injury; and (3) hypercoagulability of blood. The main factors are immobility (from any cause), surgery, trauma, malignancy, pregnancy and thrombophilia (Table 30.1).


Table 30.1 Risk factors for venous thromboembolism













































Primary hypercoagulable states (thrombophilia)
Antithrombin III deficiency
Protein C deficiency
Protein S deficiency
Resistance to activated protein C resistance (inherited factor V Leiden mutation)
Hyperhomocysteinaemia
Lupus anticoagulant (antiphospholipid antibody)
Secondary hypercoagulable states
Immobility
Surgery
Trauma
Malignancy
Pregnancy and the puerperium
Obesity
Smoking
Oestrogen-containing oral contraception or hormone replacement therapy
Indwelling catheters in great veins and the right heart
Burns
Patients with limb paralysis (e.g. spinal injuries)
Heart failure
Increasing age

VTE can be recurrent, which should prompt investigation for thrombophilia, which describes a group of conditions which are inherited and associated with a high incidence of VTE. The most important of these is activated protein C resistance, which is mediated by the factor V Leiden mutation. Up to 50% of patients with recurrent VTE episodes (as well as 20% of patients with a single episode) have this condition; however, its association appears to be greater with DVT than with PE.1 Up to 5% of patients with VTE develop chronic pulmonary hypertension.2




CLINICAL PRESENTATION


PE is relatively uncommon in critically ill patients despite the frequent presence of risk factors for VTE. However, when PE does occur, the diagnosis is frequently overlooked or is difficult to confirm because of the presence of coexistent cardiorespiratory disease. Clinical assessment raises the suspicion of PE but is neither sensitive nor specific. A number of clinical prediction systems have been developed, the most widely reported of which are the Wells’ score and the Geneva score.4 The differential diagnosis is listed in Table 30.2.


Table 30.2 Differential diagnosis of pulmonary embolism



























Acute myocardial infarction
Acute pulmonary oedema
Pneumonia
Asthma or exacerbation of chronic obstructive pulmonary disease
Pericardial tamponade
Pleural effusion
Fat embolism
Pneumothorax
Aortic dissection
Rib fracture
Musculoskeletal pain
Anxiety




INVESTIGATIONS


The diagnosis of PE requires a high level of clinical suspicion and the appropriate use of investigations. The aim of these investigations is to confirm or exclude the presence of PE and then to stratify treatment accordingly. The optimal investigation strategy depends upon the individual patient and institution as a number of investigations are available. Pulmonary angiography has traditionally been considered the ‘gold standard’ for the diagnosis of PE. The advent of multidetector row computed tomography (CT) scanning (which compares well with standard pulmonary angiography5) has led to the emergence of this as the ‘first-line’ test in many centres. A suggested investigation algorithm is shown in Figure 30.1.






ARTERIAL BLOOD GASES


A normal arterial blood gas profile does not rule out the diagnosis; however hypoxaemia (with a widened alveolar–arterial oxygen gradient), hypocapnia and an increased end-tidal CO2 gradient13 should raise the suspicion of PE, even though there are many other causes of these findings in critically ill patients.14 Metabolic acidosis may be present if shock from a large PE occurs.





COMPUTED TOMOGRAPHY


As CT technology has improved, CT angiography (CTA) has emerged as a cost-effective and clinically reliable alternative to the V/Q scan.16 The single-detector row CT has been superseded by multidetector row CT, which allows imaging of the entire chest with high-resolution images in ‘in-plane’ and ‘through-plane’ resolution. High-resolution images to the level of segmental and in some cases subsegmental pulmonary arteries can be obtained in a short time period (often a single breath-hold).


When CTA is compared to conventional angiography it appears reliable, with sensitivity, specificity and accuracy of 100%, 89% and 91% respectively.5 Adding venography of the leg veins to the CTA (CTA-CTV) further increases the diagnostic certainty.17 It is therefore recommended that CTA or CTA-CTV should be the principal radiological test for patients with high and moderate probability of PE.18


Although the ability of many CT scanners to detect PE at the subsegmental level is limited, it is debatable whether this is of clinical significance. Patients who have negative or indeterminate CT scans and in whom anticoagulation is withheld have low subsequent rates of thromboembolic events.19


The advantage of CT is that it can not only diagnose PE but can also be used to assess severity of the condition. Increased RV/LV ratio (> 0.9)20 and clot in the proximal branches of the pulmonary artery21 correlate with the clinical severity of PE. Severity stratification is further increased by combining CT with other tests such as troponin9 and BNP or NT-terminal ProBNP.11 CT scanning may also identify the causative DVT in the veins of the legs, pelvis and abdomen or detect alternative or additional diagnoses such as a pulmonary mass, pneumonia, emphysema, pneumothorax, pleural effusion or mediastinal adenopathy (Figure 30.2).







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Jul 7, 2016 | Posted by in CRITICAL CARE | Comments Off on Pulmonary embolism

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