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Acute Pulmonary Embolism: A Comprehensive Guide for Clinicians

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Epidemiology and risk factors of PE,
Acute pulmonary embolism (PE) is a life-threatening condition that occurs when a blood clot blocks one or more of the pulmonary arteries, reducing blood flow to the lungs and impairing gas exchange. PE can cause symptoms such as chest pain, shortness of breath, cough, hemoptysis, syncope, or sudden death. PE is often associated with deep vein thrombosis (DVT) in the lower extremities, which is the main source of emboli. The diagnosis and management of PE require a multidisciplinary approach that involves clinical assessment, risk stratification, imaging tests, laboratory biomarkers, and anticoagulant therapy. The aim of this course is to provide a comprehensive guide for clinicians on how to diagnose and treat patients with acute PE, based on the latest evidence and guidelines. The course will cover the following topics: Epidemiology and risk factors of PE, including the incidence, prevalence, mortality, morbidity, and prevention strategies. Pathophysiology and clinical presentation of PE, including the mechanisms of embolization, hemodynamic consequences, right ventricular dysfunction, and common signs and symptoms. Diagnosis and differential diagnosis of PE, including the assessment of clinical probability, D-dimer testing, computed tomographic pulmonary angiography (CTPA), lung scintigraphy, pulmonary angiography, magnetic resonance angiography (MRA), echocardiography, compression ultrasonography, and other tests. Risk assessment and prognostic factors of PE, including the evaluation of PE severity, right ventricular function, myocardial injury, comorbidity, and aggravating conditions. Treatment and follow-up of PE, including the indications, contraindications, benefits, risks, and modalities of anticoagulation therapy (oral, parenteral, or novel agents), thrombolysis (systemic or catheter-directed), surgical or percutaneous embolectomy, inferior vena cava filters (IVCFs), supportive measures (oxygen therapy, fluid management, vasopressors), and long-term management (duration of anticoagulation, recurrence prevention). Special situations and challenges in the management of PE, including pregnancy-associated PE, cancer-associated PE, chronic thromboembolic pulmonary hypertension (CTEPH), subsegmental PE, incidental PE, and COVID-19-associated PE. The course will be based on the 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism12, which were developed in collaboration with the European Respiratory Society (ERS). The course will also include relevant information from other sources3, such as recent studies and reviews. The course will provide practical recommendations and algorithms for the diagnosis and treatment of PE in different clinical scenarios. The course will also highlight the areas of uncertainty and controversy in the management of PE and discuss the future directions for research and innovation. By completing this course, you will be able to: Recognize the epidemiology and risk factors of PE and implement appropriate prevention strategies. Identify the pathophysiology and clinical presentation of PE and differentiate it from other causes of acute chest pain or dyspnea. Apply the diagnostic tests and algorithms for PE according to the clinical probability and availability of resources. Assess the risk and prognosis of PE using various parameters and scores. Choose the optimal treatment strategy for PE based on the risk assessment and patient preferences. Monitor and follow-up patients with PE according to the guidelines and best practices. Manage special situations and challenges in the management of PE using evidence-based approaches. Update your knowledge on the latest developments and innovations in the field of PE.

  • Epidemiology and risk factors of PE
    05:03

Pathophysiology and clinical presentation of PE
Pathophysiology and clinical presentation of PE Pathophysiology of PE refers to the mechanisms and consequences of pulmonary artery obstruction by thrombus. The main factors that determine the pathophysiological effects of PE are: The size and number of emboli: Larger and more numerous emboli cause more obstruction and hemodynamic compromise. The location of emboli: Emboli that lodge in the main, lobar, or segmental pulmonary arteries cause more severe effects than those in the subsegmental branches. The rate of embolization: Rapid accumulation of emboli causes more acute and severe effects than gradual accumulation. The pre-existing cardiopulmonary status of the patient: Patients with underlying heart or lung disease have less reserve and are more susceptible to the effects of PE. The main pathophysiological effects of PE are: Pulmonary vascular resistance (PVR): PE increases PVR by mechanical obstruction, vascular constriction, and loss of capillary bed. The degree of PVR elevation depends on the extent of obstruction and the presence of pulmonary hypertension. Increased PVR impairs right ventricular (RV) function and reduces cardiac output. Right ventricular dysfunction (RVD): PE causes RVD by increasing RV afterload, reducing RV preload, and inducing RV ischemia. RVD leads to RV dilatation, hypertrophy, and failure. RVD is the main determinant of mortality in patients with acute PE. Gas exchange impairment: PE impairs gas exchange by causing ventilation-perfusion (V/Q) mismatch, intrapulmonary shunt, and hypoxic pulmonary vasoconstriction. These mechanisms result in hypoxemia, hypercapnia, and respiratory acidosis. The degree of gas exchange impairment depends on the size and distribution of emboli and the pre-existing lung function. Inflammation and coagulation: PE triggers inflammatory and coagulopathic responses that contribute to endothelial dysfunction, vascular remodeling, thrombus propagation, and fibrinolysis inhibition. These responses may lead to chronic thromboembolic pulmonary hypertension (CTEPH) in some patients. Clinical presentation of PE is variable and nonspecific, ranging from asymptomatic to shock or sudden death1. The clinical presentation depends on the size and location of emboli, the rate of embolization, the pre-existing cardiopulmonary status, and the individual response to PE. The most common presenting symptoms are: Dyspnea: This is the most common symptom of PE, occurring in up to 80% of patients2. Dyspnea may be acute or gradual in onset, mild or severe in intensity, and constant or intermittent in duration. Dyspnea may be accompanied by tachypnea, hypoxemia, or respiratory distress. Chest pain: This is the second most common symptom of PE, occurring in up to 50% of patients2. Chest pain may be pleuritic (sharp and worsened by inspiration) or nonpleuritic (dull and constant). Pleuritic chest pain suggests involvement of the pleura or pericardium by PE or infarction. Nonpleuritic chest pain suggests RV ischemia or strain. Cough: This is a common symptom of PE, occurring in up to 40% of patients2. Cough may be dry or productive. Hemoptysis may occur due to pulmonary infarction or bronchial artery rupture. Other less common symptoms of PE include: Syncope: This is a rare but serious symptom of PE, occurring in up to 10% of patients2. Syncope may be due to acute RV failure, reduced cardiac output, arrhythmia, or vasovagal reflex. Palpitations: This is a rare symptom of PE, occurring in up to 10% of patients2. Palpitations may be due to tachycardia, arrhythmia, or anxiety. Fever: This is a rare symptom of PE, occurring in up to 10% of patients2. Fever may be due to pulmonary infarction, infection, or inflammation. The clinical signs of PE are also variable and nonspecific. The most common signs are: Tachycardia: This is the most common sign of PE, occurring in up to 70% of patients2. Tachycardia may be due to sympathetic activation, hypoxemia, reduced cardiac output, or arrhythmia. Tachypnea: This is the second most common sign of PE, occurring in up to 60% of patients2. Tachypnea may be due to dyspnea, hypoxemia, respiratory acidosis, or anxiety. Hypoxemia: This is a common sign of PE, occurring in up to 50% of patients2. Hypoxemia may be mild or severe, depending on the extent of gas exchange impairment. Hypoxemia may be accompanied by cyanosis, clubbing, or polycythemia. Other less common signs of PE include: Hypotension: This is a rare but serious sign of PE, occurring in up to 10% of patients2. Hypotension may be due to RV failure, reduced cardiac output, or vasodilation. Jugular venous distension (JVD): This is a rare sign of PE, occurring in up to 10% of patients2. JVD may be due to RV dilatation, tricuspid regurgitation, or pericardial effusion. Loud P2: This is a rare sign of PE, occurring in up to 10% of patients2. Loud P2 may be due to pulmonary hypertension or RV hypertrophy. S3 gallop: This is a rare sign of PE, occurring in up to 10% of patients2. S3 gallop may be due to RV dysfunction or volume overload. Friction rub: This is a rare sign of PE, occurring in up to 10% of patients2. Friction rub may be due to pleuritis or pericarditis caused by PE or infarction. The pathophysiology and clinical presentation of PE are important topics for clinicians who deal with patients with suspected or confirmed PE. By understanding the mechanisms and consequences of pulmonary artery obstruction by thrombus, clinicians can appreciate the variability and complexity of PE. By recognizing the symptoms and signs of PE, clinicians can improve their diagnostic accuracy and initiate appropriate treatment.

Diagnosis and differential diagnosis of PE
Diagnosis and differential diagnosis of PE. **Diagnosis and differential diagnosis of PE** **Diagnosis** of PE is the process of confirming or ruling out the presence of pulmonary artery obstruction by thrombi. The diagnosis of PE is challenging because the symptoms and signs are nonspecific and can mimic many other conditions. Therefore, the diagnosis of PE requires a combination of clinical assessment, risk stratification, imaging tests, laboratory biomarkers, and sometimes invasive procedures. The main steps in the diagnosis of PE are: - **Clinical assessment**: This involves obtaining a detailed history and physical examination of the patient, focusing on the presence and severity of symptoms, risk factors, and comorbidities. The clinical assessment helps to estimate the pretest probability of PE, which is the likelihood of having PE before any diagnostic test is done. The pretest probability can be calculated using validated clinical decision rules, such as the Wells score or the revised Geneva score¹². The pretest probability can be categorized into low, intermediate, or high, depending on the score. The pretest probability guides the choice and interpretation of further diagnostic tests. - **D-dimer testing**: This is a blood test that measures the level of D-dimer, which is a degradation product of cross-linked fibrin. D-dimer is elevated in conditions that involve activation of coagulation and fibrinolysis, such as PE. D-dimer testing is useful to exclude PE in patients with low or intermediate pretest probability, as a negative result has a high negative predictive value¹². However, D-dimer testing is not specific for PE, as it can be elevated in many other conditions, such as infection, inflammation, trauma, surgery, malignancy, pregnancy, or advanced age. Therefore, D-dimer testing is not useful to confirm PE in patients with high pretest probability or to differentiate PE from other causes of elevated D-dimer. - **Imaging tests**: These are tests that visualize the pulmonary arteries and detect the presence or absence of thrombi. The most commonly used imaging test for PE is computed tomographic pulmonary angiography (CTPA), which is a type of CT scan that uses contrast material to enhance the pulmonary vessels¹². CTPA has a high sensitivity and specificity for PE and can also provide information about alternative diagnoses or complications. CTPA is indicated for patients with high pretest probability or positive D-dimer test. CTPA may not be available or feasible in some situations, such as renal impairment, contrast allergy, pregnancy, or hemodynamic instability. In these cases, alternative imaging tests may be considered, such as lung scintigraphy (also known as ventilation-perfusion scan or V/Q scan), which evaluates the mismatch between lung ventilation and perfusion¹², magnetic resonance angiography (MRA), which uses magnetic fields to generate images of the pulmonary vessels³, echocardiography, which assesses the right ventricular function and pressure¹², or compression ultrasonography, which detects deep vein thrombosis (DVT) in the lower extremities¹². - **Laboratory biomarkers**: These are blood tests that measure the level of substances that reflect the pathophysiology or prognosis of PE. Some examples are troponin, which indicates myocardial injury¹², brain natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP), which indicate right ventricular dysfunction¹², or lactate, which indicates tissue hypoxia⁴. Laboratory biomarkers are not diagnostic for PE but can help to assess the severity and risk of adverse outcomes in patients with confirmed or suspected PE. - **Invasive procedures**: These are procedures that involve direct access to the pulmonary arteries or the heart. Some examples are pulmonary angiography, which is a catheter-based technique that injects contrast material into the pulmonary arteries and allows direct visualization and measurement of pressure¹², right heart catheterization, which is a catheter-based technique that measures the hemodynamic parameters of the right heart chambers and pulmonary circulation¹², or endobronchial ultrasound (EBUS), which is a bronchoscopic technique that uses ultrasound to visualize the mediastinal structures and lymph nodes⁵. Invasive procedures are not routinely used for the diagnosis of PE but may be indicated in selected cases when noninvasive tests are inconclusive or contraindicated, or when an intervention is planned. **Differential diagnosis** of PE is the process of distinguishing PE from other conditions that can cause similar symptoms and signs. The differential diagnosis of PE is broad and depends on the clinical presentation and risk factors of the patient. Some common conditions that can mimic PE are: - **Pneumonia**: This is an infection and inflammation of the terminal airways and alveoli, caused by various microorganisms, such as bacteria, viruses, or fungi. Pneumonia can cause symptoms such as dyspnea, chest pain, cough, hemoptysis, fever, and chills. Pneumonia can also cause signs such as tachypnea, tachycardia, hypoxemia, cyanosis, and abnormal breath sounds. Pneumonia can be differentiated from PE by the presence of infiltrates on chest X-ray, elevated white blood cell count, and positive microbiological tests. - **Acute exacerbation of congestive heart failure (CHF)**: This is a worsening of the cardiac function due to increased preload or afterload, reduced contractility, or arrhythmia. CHF can cause symptoms such as dyspnea, chest pain, cough, orthopnea, paroxysmal nocturnal dyspnea, and edema. CHF can also cause signs such as tachypnea, tachycardia, hypoxemia, cyanosis, jugular venous distension, loud P2, S3 gallop, crackles, and bilateral peripheral edema. CHF can be differentiated from PE by the presence of cardiomegaly on chest X-ray, elevated BNP or NT-proBNP levels, and abnormal echocardiographic findings. - **Pneumothorax**: This is a collection of air in the pleural space that causes collapse of the lung. Pneumothorax can cause symptoms such as dyspnea, chest pain, cough, and hemoptysis. Pneumothorax can also cause signs such as tachypnea, tachycardia, hypoxemia, cyanosis, decreased breath sounds, hyperresonance to percussion, and tracheal deviation. Pneumothorax can be differentiated from PE by the presence of air in the pleural space on chest X-ray or ultrasound. - **Pleuritis**: This is an inflammation of the pleura that causes friction between the visceral and parietal layers. Pleuritis can cause symptoms such as dyspnea and pleuritic chest pain. Pleuritis can also cause signs such as tachypnea, tachycardia, hypoxemia, cyanosis, and friction rub. Pleuritis can be differentiated from PE by the identification of the underlying cause of pleural inflammation, such as infection, malignancy, autoimmune disease, or trauma. - **Pericarditis**: This is an inflammation of the pericardium that causes irritation of the cardiac receptors. Pericarditis can cause symptoms such as dyspnea and chest pain that is worse with inspiration or lying down and relieved by sitting up or leaning forward. Pericarditis can also cause signs such as tachypnea, tachycardia, hypotension Source: (1) Differential Diagnoses | Pulmonary Embolism - U.OSU. https://u.osu.edu/smoot.43/differential-diagnoses/. (2) Pulmonary Embolism (PE) - Pulmonary Disorders - Merck Manuals .... https://www.merckmanuals.com/professional/pulmonary- disorders/pulmonary-embolism-pe/pulmonary-embolism-pe. (3) PULMONARY EMBOLISM (PE): DIAGNOSIS - Thrombosis Canada. https://thrombosiscanada.ca/wp-uploads/uploads/2021/11/4.-Pulmonary-Embolism-Diagnosis_14November2021.pdf. (4) Pleuritic Chest Pain: Sorting Through the Differential Diagnosis. https://www.aafp.org/pubs/afp/issues/2017/0901/p306.html. (5) When to suspect | Diagnosis | Pulmonary embolism | CKS | NICE. https://cks.nice.org.uk/topics/pulmonary-embolism/diagnosis/when-to-suspect/.

Risk assessment and prognostic factors of PE
Risk assessment and prognostic factors of PE Risk assessment of PE is the process of evaluating the likelihood of having PE before any diagnostic test is done, and the severity and prognosis of PE after the diagnosis is confirmed. Risk assessment of PE is important for guiding the choice and interpretation of diagnostic tests, the selection and duration of treatment, and the level and location of care. The main steps in risk assessment of PE are: Pretest probability assessment: This involves estimating the probability of PE based on the clinical presentation, risk factors, and comorbidities of the patient. The pretest probability can be calculated using validated clinical decision rules, such as the Wells score or the revised Geneva score12. The pretest probability can be categorized into low, intermediate, or high, depending on the score. The pretest probability guides the choice and interpretation of further diagnostic tests, such as D-dimer testing or imaging tests. PE severity assessment: This involves evaluating the impact of PE on the cardiopulmonary system and the risk of early death or complications. The PE severity can be assessed using various parameters and scores, such as hemodynamic status, right ventricular function, myocardial injury, gas exchange impairment, comorbidity, and aggravating conditions. The PE severity can be categorized into low-risk (or non-massive), intermediate-risk (or submassive), or high-risk (or massive), depending on the presence or absence of these parameters or scores12. The PE severity guides the selection and duration of treatment, such as anticoagulation, thrombolysis, or mechanical intervention. Long-term prognosis assessment: This involves estimating the risk of recurrence, chronic complications, or mortality after the acute phase of PE. The long-term prognosis can be assessed using various factors and scores, such as residual thrombus burden, chronic thromboembolic pulmonary hypertension (CTEPH), functional capacity, quality of life, bleeding risk, and adherence to treatment. The long-term prognosis guides the level and location of care, such as outpatient or inpatient management, home or hospital follow-up, or referral to specialized centers12. Prognostic factors of PE are variables that influence the outcome or course of PE. Prognostic factors can be classified into two types: determinants and predictors3. Determinants are prognostic factors that have a causal relationship with the outcome. They are modifiable by intervention and can change the outcome. For example, anticoagulation therapy is a determinant of PE outcome, as it reduces the risk of recurrence and mortality. Predictors are prognostic factors that have a statistical association with the outcome. They are not modifiable by intervention and do not change the outcome. They can be used to identify patients at high or low risk of adverse outcomes. For example, troponin level is a predictor of PE outcome, as it reflects myocardial injury and correlates with mortality. Some examples of prognostic factors for PE are: Hemodynamic status: This is a determinant and predictor of PE outcome. Hemodynamic instability (defined as systolic blood pressure <90 mmHg or shock) is associated with a high risk of early death (up to 30%) and indicates a need for immediate reperfusion therapy12. Right ventricular dysfunction: This is a determinant and predictor of PE outcome. Right ventricular dysfunction (defined as dilatation, hypokinesis, or pressure overload) is associated with a high risk of early death (up to 15%) and indicates a need for close monitoring and possible escalation of therapy12. Right ventricular dysfunction can be assessed by echocardiography, computed tomography pulmonary angiography (CTPA), magnetic resonance imaging (MRI), or biomarkers (such as troponin or BNP). Myocardial injury: This is a predictor of PE outcome. Myocardial injury (defined as elevation of cardiac biomarkers such as troponin or heart-type fatty acid binding protein) is associated with a high risk of early death (up to 10%) and indicates a need for close monitoring and possible escalation of therapy12. Gas exchange impairment: This is a predictor of PE outcome. Gas exchange impairment (defined as hypoxemia, hypercapnia, or respiratory acidosis) is associated with a high risk of early death (up to 10%) and indicates a need for supportive measures such as oxygen therapy or mechanical ventilation12. Comorbidity: This is a predictor of PE outcome. Comorbidity (defined as the presence of chronic diseases such as heart failure, chronic obstructive pulmonary disease, renal failure, liver failure, or malignancy) is associated with a high risk of early and late death and indicates a need for comprehensive care and adjustment of therapy12. Aggravating conditions: This are predictors of PE outcome. Aggravating conditions (defined as the presence of factors that increase the risk of recurrence or bleeding such as active cancer, recent surgery, trauma, or infection) are associated with a high risk of early and late death and indicate a need for comprehensive care and adjustment of therapy12. Residual thrombus burden: This is a predictor of PE outcome. Residual thrombus burden (defined as the persistence of thrombi in the pulmonary arteries or deep veins after the acute phase of PE) is associated with a high risk of recurrence and chronic complications such as CTEPH and indicates a need for long-term anticoagulation and follow-up12. Residual thrombus burden can be assessed by imaging tests such as CTPA, lung scintigraphy, or compression ultrasonography. The risk assessment and prognostic factors of PE are important topics for clinicians who deal with patients with PE. By performing risk assessment of PE, clinicians can optimize the diagnostic and therapeutic strategies for individual patients. By identifying prognostic factors of PE, clinicians can stratify patients according to their risk level and provide appropriate care and follow-up.

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