Pulmonary Embolism

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Pathophysiology

PE is an obstruction of the pulmonary artery (PA) or its branches. PE most commonly occurs when a thrombus or part of a thrombus dislodges, forming an embolus, and travels through the venous system via the right ventricle (RV) into the lung. Although they may occur in any part of the venous system, most thrombi originate in the lower extremity.14, 15 Partial or total occlusion of the pulmonary circulation may also be caused by nonthrombotic agents such as cells (adipocytes, hematopoietic,

Epidemiology and risk factors

The overall incidence of first-time VTE is estimated to be between 70 and 113 cases/100,000/year.19, 20 Given the possibility of asymptomatic and atypical presentation, it is generally accepted that many cases of PE go unrecognized. In fact, some investigators estimate that up to 1 in 3 cases are not identified.6, 21 Early autopsy studies and pooled data suggested that over 60% of hospitalized patients had PE.4, 22 In addition, 60% to 80% of patients with DVT also have PE, but more than half

Clinical Features

The combination of classic findings of chest pain, dyspnea, and hemoptysis are present in fewer than 20% of patients.56 Any complaints related to pain, shortness of breath, nonspecific malaise or functional deterioration, extremity discomfort, weakness, dizziness, or syncope could be a presentation of PE.23 Indeed, most clinical manifestations in the diagnosis of acute PE are not sensitive, and none are specific.12 PIOPED I and II found dyspnea, tachypnea, or pleuritic chest pain in 92% and 97%

Diagnostic Clinical Assessment and Pretest Probability

The clinical evaluation and diagnosis of PE is challenging, thus clinicians need a method to determine when and how to evaluate the appropriate patients. In addition, it is estimated that a considerable number of CT angiographic examinations and radiation exposure could be avoided with the proper use of a clinical history and D-dimer assay.73 The diagnosis depends on an accurate determination of clinical pretest probability.13, 38 Determining the PTP encourages good clinical assessment and

Electrocardiogram

Most routine investigations, including basic blood work, chest radiograph, electrocardiogram (ECG), cardiac troponins, brain natriuretic peptide (BNP), and arterial blood gas (ABG), are of limited value. The ECG is neither sensitive nor specific. A normal ECG can be seen in 30% of patients with PE, whereas the classic S1Q3T3 occurs in only 20% of patients with angiographically proven PE, and has a sensitivity and specificity of 54% and 62% respectively.67, 106 The most common ECG change is

Approach to the diagnosis of PE

The first step is to suspect PE in the differential diagnosis, and then make an implicit or explicit determination of PTP. Physicians may find it beneficial to categorize patients as low risk (<15%), intermediate or moderate risk (15%–40%), or high risk (>40%) because these determinations may alter the diagnostic pathway at various stages of investigation (see Figs 1 and 2). Both the PERC rule and the Wells criteria may be used to categorize risk of PE because each is independently validated in

Treatment of Acute PE

The treatment of acute PE is systemic anticoagulation with or without thrombolysis. Anticoagulation halts clot progression and allows endogenous fibrinolysis to occur. Clot resolution occurs over weeks to months, and may be incomplete in some individuals.64, 197 Typically, an initial short-term therapy using unfractionated heparin, LMWH (eg, enoxaparin, dalteparin), or fondaparinux is used and bridges the transition to the vitamin K antagonist warfarin.198, 199 Initial anticoagulation should be

PE in the Pregnant Patient

Pregnancy is associated with an increased risk of VTE.230 PE is the most common non-traumatic cause of death in pregnancy and the leading cause of mortality in developed countries.43, 231 Overall, the prevalence of PE in the pregnant population is quite low.14 A meta-analysis found that more than 60% of DVTs occurred in the antepartum period, distributed equally among all trimesters, whereas 43% to 60% of PEs occurred in the postpartum period.232, 233 This increased risk is hypothesized to

Summary

The presentation of PE ranges from incidentally discovered asymptomatic emboli to massive embolism causing an immediate threat to life. Despite an ever-expanding body of literature describing various aspects of this disease, it continues to be a challenging diagnosis to make, particularly in the ED. EPs use a combination of risk factors and clinical features to estimate a patient's PTP of having PE. Although a number CDRs are available to physicians, evidence continues to support the notion

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    • Mechanisms underlying the sensation of dyspnea

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      Citation Excerpt :

      In patients with acute pulmonary embolism, increased pulmonary arterial pressure and interstitial tissue edema stimulate J-receptors juxtaposed to pulmonary capillaries, which amplifies afferent signals to the higher brain and increases motor command and ventilation [1,40]. The disturbance in lung gas exchange leads to decreased arterial Po2 increasing the afferent discharge from peripheral chemoreceptors, which magnifies the integrated chemical respiratory sensation [17,133]. An increase in motor command corollary discharge beyond the increase in ventilation results in dyspnea.

    • Clinical presentation and diagnostic work up of suspected pulmonary embolism in a district hospital emergency centre serving a high HIV/TB burden population

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      This also presents the problem of looking at vital signs in patients with co-morbidities and suspected PE. Many symptoms of PE also mimic those of other cardiopulmonary diseases such as congestive heart failure and chronic obstructive pulmonary disease (COPD) [3]. In our study, 68% of confirmed PE patients had one or more co-morbidities and 46% had current or previous lung pathology.

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