This document discusses pulmonary embolism (PE). It notes that PE is a common disorder that can be deadly if left untreated. The presentation of PE is often vague and nonspecific. While the classic triad of symptoms is hemoptysis, dyspnea, and pleuritic pain, this occurs in less than 20% of patients. The document reviews risk factors, clinical features, diagnostic testing options including Wells criteria, imaging studies, D-dimer testing and their limitations. Treatment involves anticoagulation with heparin or warfarin to prevent clot extension and recurrence while educating patients.
1. Pulmonary embolism is an obstruction of the pulmonary artery or its branches by a thrombus originating in the venous system or right side of the heart.
2. The annual incidence of PE ranges from 23-69 cases per 100,000 population in India. Globally, the incidence of venous thromboembolism remains relatively constant at 117 cases per 100,000 person-years.
3. Diagnosis involves using criteria like Wells criteria and PERC rule to determine pre-test probability, D-dimer testing, and imaging like CT pulmonary angiography or lung scan if needed based on risk level and test results. Management involves anticoagulation with heparin or low molecular weight he
Pulmonary embolism occurs when a blood clot blocks an artery in the lungs, usually originating from deep vein thrombosis. Symptoms range from sudden shortness of breath to chest pain. Diagnosis involves tests like CT scans, V/Q scans, echocardiograms and blood tests. Treatment consists of oxygen, anticoagulant drugs, and sometimes fibrinolytics for massive clots. Long term prevention focuses on continued anticoagulation and devices like IVC filters for recurrent embolisms despite treatment.
This document discusses pulmonary thromboembolism (PE), which refers to blood clots (thrombi) traveling from deep veins to the lungs. Most clots originate in the lower extremities. Risk factors include inherited conditions, surgery, trauma, immobilization, cancer and pregnancy. PE can cause hypoxemia and pulmonary hypertension. Diagnosis involves clinical assessment, D-dimer testing, chest imaging like CT pulmonary angiogram (gold standard), ventilation-perfusion scanning and echocardiogram. Treatment aims to relieve symptoms and prevent complications like right heart strain.
A pulmonary embolism occurs when a blood clot forms in the deep veins of the legs or pelvis and travels through the bloodstream, lodging in the pulmonary arteries of the lungs. It can be difficult to diagnose and is a potentially life-threatening condition. Diagnostic tests may include a d-dimer blood test, CT scan, ventilation-perfusion scan, echocardiogram, and angiogram. Treatment involves anticoagulation medications to prevent further clotting and thrombolysis in some severe cases. Prevention by minimizing risk factors for deep vein thrombosis is important.
This document discusses pulmonary embolism (PE). Some key points:
- PE causes 50,000-200,000 deaths annually in the US, with an incidence of 500,000 cases.
- Risk factors include stasis, injury to veins, and coagulation issues.
- PE occurs when clots, usually from deep leg veins, travel to the lungs and block vessels. This can strain the right ventricle.
- Symptoms include sudden dyspnea, tachycardia, chest pain, hemoptysis. No single symptom confirms PE.
- Diagnosis involves CXR, blood tests, V/Q scan, CT, and angiogram. ECG may show right
Pulmonary embolism (PE) is a blockage in the lungs caused by blood clots that travel from deep veins, usually in the legs. It is the third most common cause of death in hospitalized patients, with over 650,000 cases occurring per year in the US. Risk factors include immobilization, hypercoagulability, and recent surgery or trauma. Symptoms can include chest pain, shortness of breath, cough, or fainting. Diagnosis is confirmed through imaging tests like CT angiography or ventilation-perfusion scans. Treatment involves blood thinners like heparin, warfarin, or newer oral anticoagulants to prevent further clotting. Thrombolytic drugs
Acute heart failure (AHF) is defined as rapid onset of new or worsening signs and symptoms of heart failure. It represents a life-threatening condition requiring treatment for fluid overload and hemodynamic compromise. Presentation may be initial diagnosis with symptoms and signs of AHF or acute decompensation of pre-existing cardiomyopathy. Hemodynamic instability results from disorders of the myocardium, valves, conduction system or pericardium, in isolation or combination. Potentially treatable causes, e.g. acute coronary syndromes, must be diagnosed and managed early for restoration of function.
Physiological changes associated with AHF result in reduced cardiac output and end-organ hypoperfusion. Once potentially treatable causes are managed, stratification of patients by clinical presentation guides further therapeutic intervention. AHF patients can be categorized as either ‘wet’ or ‘dry’ by clinical fluid status assessment, and either ‘cold’ or ‘warm’ according to perfusion status. In combination, these features identify four patient groups (‘warm-wet’, ‘warm-dry’, ‘cold-dry’, ‘cold-wet’) that guide therapy and facilitate prognostication. ‘Warm-dry’ patients rarely require intensive care for AHF treatment but may benefit from escalation of oral therapeutic regimen. Patients who examine as ‘cold-dry’ may benefit from fluid challenge, and/or inotropic agent infusion. ‘Warm-wet’ patients present with predominantly congestive or hypertensive symptoms which benefit from diuresis and vasodilatation. Patients who present ‘wet-cold’ with normal blood pressure (SBP >90) may benefit from vasodilators and diuretics, with inotropic agents for refractory symptoms. Hypotensive ‘wet-cold’ patients (classic cardiogenic shock) require inotropy with or without vasopressor agents, effective diuresis and early consideration of mechanical circulatory support (MCS).
Definitive therapies for AHF depend on underlying cause, and may include coronary artery intervention, valve repair, rhythm control to restore atrio-ventricular synchrony or management of pericardial tamponade. Patients with severe AHF not responsive to standard therapies should be considered for temporary MCS while candidacy for more durable option is explored by the multi-disciplinary team.
This document discusses acute pulmonary embolism (PE), which results from blood clots (deep vein thromboses or DVTs) breaking off and traveling to the lungs. PE is a leading cause of preventable hospital death. The document covers risk factors for PE like immobility, surgery, cancer, and inherited conditions. It also discusses methods for diagnosing PE like the Wells criteria, D-dimer testing, chest imaging like CT scans, and treatment including anticoagulation and thrombolysis for hemodynamically unstable patients. Poor prognostic signs of PE include hypotension, cardiac biomarkers indicating injury, and imaging findings of right ventricular dysfunction. Prevention through appropriate DVT prophylaxis is emphasized.
1. Pulmonary embolism is an obstruction of the pulmonary artery or its branches by a thrombus originating in the venous system or right side of the heart.
2. The annual incidence of PE ranges from 23-69 cases per 100,000 population in India. Globally, the incidence of venous thromboembolism remains relatively constant at 117 cases per 100,000 person-years.
3. Diagnosis involves using criteria like Wells criteria and PERC rule to determine pre-test probability, D-dimer testing, and imaging like CT pulmonary angiography or lung scan if needed based on risk level and test results. Management involves anticoagulation with heparin or low molecular weight he
Pulmonary embolism occurs when a blood clot blocks an artery in the lungs, usually originating from deep vein thrombosis. Symptoms range from sudden shortness of breath to chest pain. Diagnosis involves tests like CT scans, V/Q scans, echocardiograms and blood tests. Treatment consists of oxygen, anticoagulant drugs, and sometimes fibrinolytics for massive clots. Long term prevention focuses on continued anticoagulation and devices like IVC filters for recurrent embolisms despite treatment.
This document discusses pulmonary thromboembolism (PE), which refers to blood clots (thrombi) traveling from deep veins to the lungs. Most clots originate in the lower extremities. Risk factors include inherited conditions, surgery, trauma, immobilization, cancer and pregnancy. PE can cause hypoxemia and pulmonary hypertension. Diagnosis involves clinical assessment, D-dimer testing, chest imaging like CT pulmonary angiogram (gold standard), ventilation-perfusion scanning and echocardiogram. Treatment aims to relieve symptoms and prevent complications like right heart strain.
A pulmonary embolism occurs when a blood clot forms in the deep veins of the legs or pelvis and travels through the bloodstream, lodging in the pulmonary arteries of the lungs. It can be difficult to diagnose and is a potentially life-threatening condition. Diagnostic tests may include a d-dimer blood test, CT scan, ventilation-perfusion scan, echocardiogram, and angiogram. Treatment involves anticoagulation medications to prevent further clotting and thrombolysis in some severe cases. Prevention by minimizing risk factors for deep vein thrombosis is important.
This document discusses pulmonary embolism (PE). Some key points:
- PE causes 50,000-200,000 deaths annually in the US, with an incidence of 500,000 cases.
- Risk factors include stasis, injury to veins, and coagulation issues.
- PE occurs when clots, usually from deep leg veins, travel to the lungs and block vessels. This can strain the right ventricle.
- Symptoms include sudden dyspnea, tachycardia, chest pain, hemoptysis. No single symptom confirms PE.
- Diagnosis involves CXR, blood tests, V/Q scan, CT, and angiogram. ECG may show right
Pulmonary embolism (PE) is a blockage in the lungs caused by blood clots that travel from deep veins, usually in the legs. It is the third most common cause of death in hospitalized patients, with over 650,000 cases occurring per year in the US. Risk factors include immobilization, hypercoagulability, and recent surgery or trauma. Symptoms can include chest pain, shortness of breath, cough, or fainting. Diagnosis is confirmed through imaging tests like CT angiography or ventilation-perfusion scans. Treatment involves blood thinners like heparin, warfarin, or newer oral anticoagulants to prevent further clotting. Thrombolytic drugs
Acute heart failure (AHF) is defined as rapid onset of new or worsening signs and symptoms of heart failure. It represents a life-threatening condition requiring treatment for fluid overload and hemodynamic compromise. Presentation may be initial diagnosis with symptoms and signs of AHF or acute decompensation of pre-existing cardiomyopathy. Hemodynamic instability results from disorders of the myocardium, valves, conduction system or pericardium, in isolation or combination. Potentially treatable causes, e.g. acute coronary syndromes, must be diagnosed and managed early for restoration of function.
Physiological changes associated with AHF result in reduced cardiac output and end-organ hypoperfusion. Once potentially treatable causes are managed, stratification of patients by clinical presentation guides further therapeutic intervention. AHF patients can be categorized as either ‘wet’ or ‘dry’ by clinical fluid status assessment, and either ‘cold’ or ‘warm’ according to perfusion status. In combination, these features identify four patient groups (‘warm-wet’, ‘warm-dry’, ‘cold-dry’, ‘cold-wet’) that guide therapy and facilitate prognostication. ‘Warm-dry’ patients rarely require intensive care for AHF treatment but may benefit from escalation of oral therapeutic regimen. Patients who examine as ‘cold-dry’ may benefit from fluid challenge, and/or inotropic agent infusion. ‘Warm-wet’ patients present with predominantly congestive or hypertensive symptoms which benefit from diuresis and vasodilatation. Patients who present ‘wet-cold’ with normal blood pressure (SBP >90) may benefit from vasodilators and diuretics, with inotropic agents for refractory symptoms. Hypotensive ‘wet-cold’ patients (classic cardiogenic shock) require inotropy with or without vasopressor agents, effective diuresis and early consideration of mechanical circulatory support (MCS).
Definitive therapies for AHF depend on underlying cause, and may include coronary artery intervention, valve repair, rhythm control to restore atrio-ventricular synchrony or management of pericardial tamponade. Patients with severe AHF not responsive to standard therapies should be considered for temporary MCS while candidacy for more durable option is explored by the multi-disciplinary team.
This document discusses acute pulmonary embolism (PE), which results from blood clots (deep vein thromboses or DVTs) breaking off and traveling to the lungs. PE is a leading cause of preventable hospital death. The document covers risk factors for PE like immobility, surgery, cancer, and inherited conditions. It also discusses methods for diagnosing PE like the Wells criteria, D-dimer testing, chest imaging like CT scans, and treatment including anticoagulation and thrombolysis for hemodynamically unstable patients. Poor prognostic signs of PE include hypotension, cardiac biomarkers indicating injury, and imaging findings of right ventricular dysfunction. Prevention through appropriate DVT prophylaxis is emphasized.
1) Pulmonary embolism is a blockage in the pulmonary artery or its branches by a blood clot that originated in the veins, causing serious health risks.
2) Risk factors include prolonged bed rest, cancer, smoking, oral contraceptive use, and pregnancy. Symptoms include dyspnea, chest pain, cough, and leg pain. Diagnosis involves tests like CT pulmonary angiography and ventilation-perfusion scanning.
3) Treatment involves oxygen, anticoagulant drugs like heparin and warfarin, and sometimes surgical embolectomy for severe cases. Prevention focuses on leg exercises, early ambulation, and compression stockings.
This document discusses acute aortic syndrome, including a case presentation of a 55-year-old female with chest pain. Key details include:
1. The patient presented with sudden onset chest pain and was found to have hypertension on examination.
2. Initial workup including ECG, labs and chest x-ray were non-diagnostic but showed a widened mediastinum.
3. Echocardiogram and CT angiogram revealed an aortic dissection involving the aortic arch and descending thoracic aorta.
4. She was referred urgently for cardiovascular surgery to treat this life-threatening condition within 24 hours of presentation.
Pulmonary arterial hypertension (PAH) is high blood pressure in the arteries connecting the heart and lungs. The document defines PAH and related types, and discusses risk factors, symptoms, diagnosis, classification, complications and treatments. PAH has no known cause in many cases, but can result from other conditions. Common symptoms include shortness of breath, chest pain and fatigue. Diagnosis involves medical tests and right heart catheterization. Treatment aims to improve symptoms and outcomes through medications, supplemental oxygen, diet changes and exercise.
1) Pulmonary embolism (PE) was first described in the 18th century and risk factors include both modifiable factors like obesity and smoking as well as non-modifiable factors like age, family history, and cancer.
2) PE is classified by size from massive to small, with massive PE affecting half the pulmonary arteries and causing shock while small PE causes few symptoms.
3) Diagnosis involves assessment of clinical probability with tools like Wells Criteria followed by tests like CT, ventilation-perfusion scan, or ultrasound depending on the patient's situation.
4) Treatment involves anticoagulation with drugs like heparin or novel oral anticoagulants, with duration depending on prov
Pulmonary embolism is a potentially deadly condition caused by blood clots in the lungs. It is difficult to diagnose due to non-specific symptoms. Imaging tests like CT scans and ventilation-perfusion scans are used to identify clots in the lungs. Prompt diagnosis and treatment are important to reduce the high mortality rate associated with untreated pulmonary embolism.
Venous thromboembolism is a condition where a blood clot forms in a vein. Deep vein thrombosis is a blood clot that forms in deep leg veins and can dislodge and travel to the lungs, called a pulmonary embolism. Risk factors include prolonged bed rest, surgery, cancer, pregnancy, oral contraceptives, and genetic conditions. Diagnosis involves a clinical assessment, D-dimer blood test, and ultrasound or venography imaging of the legs. Treatment consists of blood thinners like heparin and warfarin to prevent further clotting and embolism.
This document provides guidance on evaluating and managing patients presenting with hemoptysis. It defines hemoptysis and outlines its various classifications based on blood loss. Common causes are discussed, including tuberculosis, bronchial carcinoma, bronchiectasis, and lung abscesses. A systematic approach to evaluation is recommended, beginning with history, physical exam, chest imaging, and sputum/blood tests. Bronchoscopy can help localize the bleeding site but is usually best delayed until acute bleeding subsides. The goal is to determine the cause and initiate appropriate treatment while stabilizing patients experiencing massive hemorrhage.
This document discusses chronic coronary syndrome (CCS), previously known as stable coronary artery disease. It defines CCS and outlines the six entities it can be classified into. It discusses the natural history, pathophysiology, risk factors, diagnosis and management of CCS. Key changes from 2013 guidelines include exercise stress testing now recommended for assessing symptoms and risk rather than diagnosis, and several new second-line treatment options for angina added based on heart rate, blood pressure and tolerance. Invasive testing guidelines were also updated.
Around 50% of patients with image-documented DVT lack specific symptoms. The diagnosis of DVT relies on a pretest probability assessment using Wells Criteria followed by D-dimer testing and venous ultrasound if needed. While anticoagulation is the mainstay of treatment, newer oral anticoagulants provide efficacy comparable to heparin and warfarin but with less bleeding risk and more convenient dosing without the need for monitoring. Home treatment is sufficient for most patients.
The document discusses constrictive pericarditis, providing details on:
1) The pathology of constrictive pericarditis which involves thickening and scarring of the pericardium leading to loss of elasticity.
2) The pathophysiology of constrictive pericarditis where the inelastic pericardium constrains cardiac filling and prevents adaptation to volume changes.
3) Key diagnostic features of constrictive pericarditis seen on echocardiogram include septal bounce, rapid early diastolic mitral inflow, and increased mitral annular velocities that rise with inspiration.
This document provides information on evaluating and diagnosing chest pain. It begins by defining chest pain and noting that it is a common reason patients present for medical care. It then discusses the causes of chest pain and provides details on distinguishing ischemic from non-ischemic chest pain. Key factors for ischemic cardiac pain are discussed such as onset during exertion and relief with rest. The document provides guidance on evaluating a patient's chest pain by taking a thorough history addressing 10 specific points. Differential diagnoses for chest pain are also reviewed.
Pleural effusion results from an imbalance between pleural fluid formation and absorption, causing fluid to accumulate in the pleural space. Fluid formation occurs through capillaries in the parietal pleura, and absorption occurs via lymphatic vessels. When the rate of formation exceeds absorption, effusion occurs. Effusions are classified as transudative or exudative based on fluid characteristics. Diagnostic testing of pleural fluid aims to determine the cause of effusion. Radiography and ultrasound are used to identify and characterize pleural fluid.
Peripheral vascular diseases (PVD), also known as peripheral artery occlusive disease, refers to obstruction or deterioration of arteries other than those supplying the heart or brain, primarily caused by atherosclerosis. PVD presents as either chronic arterial insufficiency or acute arterial occlusion. Management involves risk factor modification, endovascular or surgical revascularization techniques, and exercise therapy. For intermittent claudication, cilostazol is an effective pharmacotherapy that improves walking distance. Acute limb ischemia requires immediate anticoagulation and revascularization to prevent limb loss.
Pulmonary hypertension is defined by specific hemodynamic criteria and can be categorized into 5 groups. Group 1 includes pulmonary arterial hypertension which can be caused by various genetic, medical, and environmental factors. Groups 2-5 involve pulmonary hypertension secondary to other conditions such as left heart disease, lung disease, chronic thromboembolic pulmonary hypertension, or unclear mechanisms. Diagnosis involves right heart catheterization and testing for vasodilator response. Symptoms range from exertional dyspnea to right heart failure. Treatment depends on the type and severity of pulmonary hypertension and may include vasodilator medications, endothelin receptor antagonists, phosphodiesterase-5 inhibitors, prostanoids, or surgery for chronic thromboembolic pulmonary
The discovery of malignant cells in pleural fluid
and/or parietal pleura signifies disseminated or
advanced disease and a reduced life expectancy in
patients with cancer.Median survival following
diagnosis ranges from 3 to 12 months and is
dependent on the stage and type of the underlying
malignancy. The shortest survival time is observed
in malignant effusions secondary to lung cancer
and the longest in ovarian cancer, while malignant
effusions due to an unknown primary have an
intermediate survival time.Historically, studies
showed that median survival times in effusions due
to carcinoma of the breast are 5-6 months.
However, more recent studies have suggested
longer survival times of up to 15 months. A
comparison of survival times in breast cancer
effusions in published studies to 1994 calculated
a median survival of 11 months.9
Currently, lung cancer is the most common
metastatic tumour to the pleura in men and breast
cancer in women.Together, both malignancies
account for 50- 65% of all malignant effusions. Lymphomas, tumours of the genitourinary
tract and gastrointestinal tract account for
a further 25% Pleural effusions from an
unknown primary are responsible for 15% of all
malignant pleural effusions.Few studies have
estimated the proportion of pleural effusions due to
mesothelioma: studies from 1975, 1985 and 1987
identified mesothelioma in 1/271, 3/472 and 22/592
patients, respectively, but there are no more recent
data to update this in light of the increasing incidence
of mesothelioma.
2019 ESC guidelines on pulmonary embolismSaitej Reddy
The document provides an overview of the updates in the 2019 guidelines for pulmonary embolism (PE) diagnosis and treatment. Key changes include adjusted D-dimer cut-off values based on age and probability; revised algorithms for diagnosing high-risk PE and assessing severity; recommending non-vitamin K antagonist oral anticoagulants as first-line treatment for eligible patients; classifying recurrence risk factors and extending treatment duration indications; and proposing a comprehensive post-PE patient follow-up algorithm. The guidelines aim to improve PE risk stratification, optimize acute care, determine chronic anticoagulation regimens, and ensure long-term management and surveillance for complications.
The pulmonary vascular circuit has low resistance and carries 70ml of blood normally. Blood flow is normally higher in the lung bases than apices due to gravity. The pulmonary arteries have a small diameter of 3mm or less in the upper intercostal spaces. Pulmonary hypertension is defined as a sustained elevation of pulmonary arterial pressure over 25mmHg at rest or 30mmHg during exercise, with normal pulmonary capillary wedge pressure and left ventricular end-diastolic pressure. Signs on chest X-ray include enlarged pulmonary arteries, loss of peripheral vessel markings, and enlargement of the right side of the heart in advanced disease.
This document discusses venous thromboembolism (VTE) in intensive care medicine. It covers the pathophysiology of thrombosis and pulmonary embolism, diagnostics for pulmonary embolism, and therapeutic approaches to VTE including prophylaxis, anticoagulation therapies, and thrombolytics. It highlights several key risk factors for VTE in critically ill and trauma patients.
Restrictive lung diseases can be caused by chest wall disorders like kyphoscoliosis or interstitial lung diseases such as pneumoconiosis from inhaling inorganic dusts. Pneumoconiosis includes conditions like coal worker's pneumoconiosis from coal dust inhalation, silicosis from silica exposure in occupations like mining, and asbestosis from asbestos exposure. These diseases are characterized by nodular scarring in the lungs visible on x-ray. Long-term inhalation of very small dust particles can lead to fibrotic nodule formation and restricted lung function over time. Silicosis presents as small fibrotic nodules throughout the lungs and is associated with occupations involving silica exposure
Pulmonary embolism is a blockage in the pulmonary artery or its branches, usually caused by blood clots from deep vein thrombosis. It occurs in over 600,000 patients annually in the US and contributes to 50,000-200,000 deaths per year. Common signs and symptoms include dyspnea, chest pain, tachycardia, and hypoxia. Diagnostic tests include chest x-rays, CT scans, D-dimer tests, V/Q scans, and blood gas analysis. Treatment involves anticoagulant therapy, thrombolytic therapy, bed rest, and in severe cases, surgical embolectomy.
1) Pulmonary embolism is a blockage in the pulmonary artery or its branches by a blood clot that originated in the veins, causing serious health risks.
2) Risk factors include prolonged bed rest, cancer, smoking, oral contraceptive use, and pregnancy. Symptoms include dyspnea, chest pain, cough, and leg pain. Diagnosis involves tests like CT pulmonary angiography and ventilation-perfusion scanning.
3) Treatment involves oxygen, anticoagulant drugs like heparin and warfarin, and sometimes surgical embolectomy for severe cases. Prevention focuses on leg exercises, early ambulation, and compression stockings.
This document discusses acute aortic syndrome, including a case presentation of a 55-year-old female with chest pain. Key details include:
1. The patient presented with sudden onset chest pain and was found to have hypertension on examination.
2. Initial workup including ECG, labs and chest x-ray were non-diagnostic but showed a widened mediastinum.
3. Echocardiogram and CT angiogram revealed an aortic dissection involving the aortic arch and descending thoracic aorta.
4. She was referred urgently for cardiovascular surgery to treat this life-threatening condition within 24 hours of presentation.
Pulmonary arterial hypertension (PAH) is high blood pressure in the arteries connecting the heart and lungs. The document defines PAH and related types, and discusses risk factors, symptoms, diagnosis, classification, complications and treatments. PAH has no known cause in many cases, but can result from other conditions. Common symptoms include shortness of breath, chest pain and fatigue. Diagnosis involves medical tests and right heart catheterization. Treatment aims to improve symptoms and outcomes through medications, supplemental oxygen, diet changes and exercise.
1) Pulmonary embolism (PE) was first described in the 18th century and risk factors include both modifiable factors like obesity and smoking as well as non-modifiable factors like age, family history, and cancer.
2) PE is classified by size from massive to small, with massive PE affecting half the pulmonary arteries and causing shock while small PE causes few symptoms.
3) Diagnosis involves assessment of clinical probability with tools like Wells Criteria followed by tests like CT, ventilation-perfusion scan, or ultrasound depending on the patient's situation.
4) Treatment involves anticoagulation with drugs like heparin or novel oral anticoagulants, with duration depending on prov
Pulmonary embolism is a potentially deadly condition caused by blood clots in the lungs. It is difficult to diagnose due to non-specific symptoms. Imaging tests like CT scans and ventilation-perfusion scans are used to identify clots in the lungs. Prompt diagnosis and treatment are important to reduce the high mortality rate associated with untreated pulmonary embolism.
Venous thromboembolism is a condition where a blood clot forms in a vein. Deep vein thrombosis is a blood clot that forms in deep leg veins and can dislodge and travel to the lungs, called a pulmonary embolism. Risk factors include prolonged bed rest, surgery, cancer, pregnancy, oral contraceptives, and genetic conditions. Diagnosis involves a clinical assessment, D-dimer blood test, and ultrasound or venography imaging of the legs. Treatment consists of blood thinners like heparin and warfarin to prevent further clotting and embolism.
This document provides guidance on evaluating and managing patients presenting with hemoptysis. It defines hemoptysis and outlines its various classifications based on blood loss. Common causes are discussed, including tuberculosis, bronchial carcinoma, bronchiectasis, and lung abscesses. A systematic approach to evaluation is recommended, beginning with history, physical exam, chest imaging, and sputum/blood tests. Bronchoscopy can help localize the bleeding site but is usually best delayed until acute bleeding subsides. The goal is to determine the cause and initiate appropriate treatment while stabilizing patients experiencing massive hemorrhage.
This document discusses chronic coronary syndrome (CCS), previously known as stable coronary artery disease. It defines CCS and outlines the six entities it can be classified into. It discusses the natural history, pathophysiology, risk factors, diagnosis and management of CCS. Key changes from 2013 guidelines include exercise stress testing now recommended for assessing symptoms and risk rather than diagnosis, and several new second-line treatment options for angina added based on heart rate, blood pressure and tolerance. Invasive testing guidelines were also updated.
Around 50% of patients with image-documented DVT lack specific symptoms. The diagnosis of DVT relies on a pretest probability assessment using Wells Criteria followed by D-dimer testing and venous ultrasound if needed. While anticoagulation is the mainstay of treatment, newer oral anticoagulants provide efficacy comparable to heparin and warfarin but with less bleeding risk and more convenient dosing without the need for monitoring. Home treatment is sufficient for most patients.
The document discusses constrictive pericarditis, providing details on:
1) The pathology of constrictive pericarditis which involves thickening and scarring of the pericardium leading to loss of elasticity.
2) The pathophysiology of constrictive pericarditis where the inelastic pericardium constrains cardiac filling and prevents adaptation to volume changes.
3) Key diagnostic features of constrictive pericarditis seen on echocardiogram include septal bounce, rapid early diastolic mitral inflow, and increased mitral annular velocities that rise with inspiration.
This document provides information on evaluating and diagnosing chest pain. It begins by defining chest pain and noting that it is a common reason patients present for medical care. It then discusses the causes of chest pain and provides details on distinguishing ischemic from non-ischemic chest pain. Key factors for ischemic cardiac pain are discussed such as onset during exertion and relief with rest. The document provides guidance on evaluating a patient's chest pain by taking a thorough history addressing 10 specific points. Differential diagnoses for chest pain are also reviewed.
Pleural effusion results from an imbalance between pleural fluid formation and absorption, causing fluid to accumulate in the pleural space. Fluid formation occurs through capillaries in the parietal pleura, and absorption occurs via lymphatic vessels. When the rate of formation exceeds absorption, effusion occurs. Effusions are classified as transudative or exudative based on fluid characteristics. Diagnostic testing of pleural fluid aims to determine the cause of effusion. Radiography and ultrasound are used to identify and characterize pleural fluid.
Peripheral vascular diseases (PVD), also known as peripheral artery occlusive disease, refers to obstruction or deterioration of arteries other than those supplying the heart or brain, primarily caused by atherosclerosis. PVD presents as either chronic arterial insufficiency or acute arterial occlusion. Management involves risk factor modification, endovascular or surgical revascularization techniques, and exercise therapy. For intermittent claudication, cilostazol is an effective pharmacotherapy that improves walking distance. Acute limb ischemia requires immediate anticoagulation and revascularization to prevent limb loss.
Pulmonary hypertension is defined by specific hemodynamic criteria and can be categorized into 5 groups. Group 1 includes pulmonary arterial hypertension which can be caused by various genetic, medical, and environmental factors. Groups 2-5 involve pulmonary hypertension secondary to other conditions such as left heart disease, lung disease, chronic thromboembolic pulmonary hypertension, or unclear mechanisms. Diagnosis involves right heart catheterization and testing for vasodilator response. Symptoms range from exertional dyspnea to right heart failure. Treatment depends on the type and severity of pulmonary hypertension and may include vasodilator medications, endothelin receptor antagonists, phosphodiesterase-5 inhibitors, prostanoids, or surgery for chronic thromboembolic pulmonary
The discovery of malignant cells in pleural fluid
and/or parietal pleura signifies disseminated or
advanced disease and a reduced life expectancy in
patients with cancer.Median survival following
diagnosis ranges from 3 to 12 months and is
dependent on the stage and type of the underlying
malignancy. The shortest survival time is observed
in malignant effusions secondary to lung cancer
and the longest in ovarian cancer, while malignant
effusions due to an unknown primary have an
intermediate survival time.Historically, studies
showed that median survival times in effusions due
to carcinoma of the breast are 5-6 months.
However, more recent studies have suggested
longer survival times of up to 15 months. A
comparison of survival times in breast cancer
effusions in published studies to 1994 calculated
a median survival of 11 months.9
Currently, lung cancer is the most common
metastatic tumour to the pleura in men and breast
cancer in women.Together, both malignancies
account for 50- 65% of all malignant effusions. Lymphomas, tumours of the genitourinary
tract and gastrointestinal tract account for
a further 25% Pleural effusions from an
unknown primary are responsible for 15% of all
malignant pleural effusions.Few studies have
estimated the proportion of pleural effusions due to
mesothelioma: studies from 1975, 1985 and 1987
identified mesothelioma in 1/271, 3/472 and 22/592
patients, respectively, but there are no more recent
data to update this in light of the increasing incidence
of mesothelioma.
2019 ESC guidelines on pulmonary embolismSaitej Reddy
The document provides an overview of the updates in the 2019 guidelines for pulmonary embolism (PE) diagnosis and treatment. Key changes include adjusted D-dimer cut-off values based on age and probability; revised algorithms for diagnosing high-risk PE and assessing severity; recommending non-vitamin K antagonist oral anticoagulants as first-line treatment for eligible patients; classifying recurrence risk factors and extending treatment duration indications; and proposing a comprehensive post-PE patient follow-up algorithm. The guidelines aim to improve PE risk stratification, optimize acute care, determine chronic anticoagulation regimens, and ensure long-term management and surveillance for complications.
The pulmonary vascular circuit has low resistance and carries 70ml of blood normally. Blood flow is normally higher in the lung bases than apices due to gravity. The pulmonary arteries have a small diameter of 3mm or less in the upper intercostal spaces. Pulmonary hypertension is defined as a sustained elevation of pulmonary arterial pressure over 25mmHg at rest or 30mmHg during exercise, with normal pulmonary capillary wedge pressure and left ventricular end-diastolic pressure. Signs on chest X-ray include enlarged pulmonary arteries, loss of peripheral vessel markings, and enlargement of the right side of the heart in advanced disease.
This document discusses venous thromboembolism (VTE) in intensive care medicine. It covers the pathophysiology of thrombosis and pulmonary embolism, diagnostics for pulmonary embolism, and therapeutic approaches to VTE including prophylaxis, anticoagulation therapies, and thrombolytics. It highlights several key risk factors for VTE in critically ill and trauma patients.
Restrictive lung diseases can be caused by chest wall disorders like kyphoscoliosis or interstitial lung diseases such as pneumoconiosis from inhaling inorganic dusts. Pneumoconiosis includes conditions like coal worker's pneumoconiosis from coal dust inhalation, silicosis from silica exposure in occupations like mining, and asbestosis from asbestos exposure. These diseases are characterized by nodular scarring in the lungs visible on x-ray. Long-term inhalation of very small dust particles can lead to fibrotic nodule formation and restricted lung function over time. Silicosis presents as small fibrotic nodules throughout the lungs and is associated with occupations involving silica exposure
Pulmonary embolism is a blockage in the pulmonary artery or its branches, usually caused by blood clots from deep vein thrombosis. It occurs in over 600,000 patients annually in the US and contributes to 50,000-200,000 deaths per year. Common signs and symptoms include dyspnea, chest pain, tachycardia, and hypoxia. Diagnostic tests include chest x-rays, CT scans, D-dimer tests, V/Q scans, and blood gas analysis. Treatment involves anticoagulant therapy, thrombolytic therapy, bed rest, and in severe cases, surgical embolectomy.
The document describes MRI findings for two patients. For the first patient, a 16-year-old male who fell from a train, the MRI shows diffuse axonal injuries with lesions in multiple areas of the brain along with a small subdural hematoma and skull fracture. For the second patient, a 47-year-old male with fever and possible seizures, the MRI reveals a small area of restricted diffusion in the splenium of the corpus callosum, which can be seen in various conditions including postictal edema, diffuse axonal injury, infections like dengue, and trauma. Clinical correlation is recommended.
This document summarizes pulmonary embolism (PE) diagnosis. It states that over 650,000 PE cases are diagnosed annually in the US, with a mortality rate of 30% that can be reduced to 3-10% with treatment. Computed tomography angiography (CTA) has become widely used as the primary diagnostic method, though some patients cannot undergo CTA due to contrast allergy or renal failure. Ventilation/perfusion (V/Q) scanning remains important and has significantly lower radiation exposure than CTA, making it preferable for some patients. Both CTA and V/Q scanning have limitations and neither has proven clearly superior to the other for PE diagnosis.
This document provides an outline and summary of various pulmonary imaging findings. It begins with an introduction by Dr. Mazen Qusaibaty and provides sections on CT halo sign (part 2), Hampton hump sign, and Westermark sign. Specific cases and images are presented to demonstrate findings of bronchiolitis obliterans with organizing pneumonia (BOOP), pulmonary endometriosis, focal traumatic lung injury, and pseudonodules. Radiographic signs of pulmonary embolism on chest x-ray and CT findings of acute pulmonary embolism on helical CT are also summarized.
Small airways disease refers to pathologies that affect the small conducting airways less than 3mm in diameter. CT scanning is the imaging modality of choice for evaluating small airways disease. On HRCT, direct signs of small airways disease include thickened airway walls, dilated or obliterated airways, and nodules. Indirect signs include air trapping, subsegmental atelectasis, centrilobular emphysema, and centrilobular nodules. Common patterns seen on HRCT include tree-in-bud, poorly defined centrilobular nodules, decreased lung attenuation, and ground glass opacities with consolidation.
Changes in Respiratory System with Various Physiological ConditionsAnand Bansal
Topics - High-Altitude Physiology, Deep Sea Diving And Effects Of Increased Barometric Pressure, Changes In Respiratory System During Pregnancy, Physiological Changes Of Repiratory System With Exercise, Physiological Changes Of Respiratory System With Aging
Pulmonary embolism (PE) is a potentially life-threatening condition with an estimated incidence between 0.5-3% in the general population. Risk factors include previous DVT, immobilization, surgery, cancer, and certain genetic conditions. Symptoms are nonspecific but commonly include dyspnea, chest pain, and cough. Diagnostic tests include D-dimer, CT pulmonary angiogram (CTPA), ventilation-perfusion scan, and pulmonary angiogram. Clinical decision rules like Wells criteria are used to determine pre-test probability to guide appropriate testing. The diagnostic algorithm involves using Wells criteria and D-dimer to determine if CTPA is needed, with CTPA used to confirm or exclude the diagnosis in
PET-MRI is a hybrid imaging technique that was approved by the FDA in 2011. It provides both the anatomical details from MRI and the functional and metabolic information from PET. There are two main types of PET-MRI scanners: simultaneous and sequential. Implementation of PET-MRI presents challenges related to PET detector elements, attenuation correction, and system corrections. PET-MRI shows potential for use in neurology, oncology, pediatrics, cardiology, and musculoskeletal imaging by providing more biological and functional data than PET-CT without radiation exposure. Examples of clinical applications include detecting tumor recurrence, evaluating treatment response, and replacing painful bone marrow biopsies for lymphoma.
Endobronchial Brachytherapy by Dr.Tinku JosephDr.Tinku Joseph
Endobronchial brachytherapy (EBBT) involves placing a radioactive source near a tumor to deliver high doses of radiation directly to it. EBBT is used palliatively to relieve symptoms from airway tumors by reducing tumor size. It can be performed using high or low dose rate brachytherapy via bronchoscopy. EBBT is effective at improving symptoms like hemoptysis and airway patency in 70% of patients for at least 6 months. It is also used to prevent restenosis in benign airway stenosis. While generally well-tolerated, risks include radiation bronchitis, stenosis, and fistula formation.
This document provides an overview of various radiographic findings related to the chest, abdomen, bones, and arthritis. Key points include:
- X-ray attenuation depends on tissue density and thickness, and abnormalities can be described based on density.
- Chest X-rays should be requested if bowel perforation is suspected to look for signs like Rigler's sign or the football sign.
- Abdominal X-rays can help identify bowel obstruction or inflammation. Findings include bowel dilation and loss of haustral markings.
- Osteomyelitis appears as bone destruction, periosteal reaction, and new bone formation. Location varies by age.
- Bone tumors like aneurysmal bone cyst, ench
Investigation of suspected pulmonary embolism in pregnancySCGH ED CME
PE in pregnancy poses significant risks but can be challenging to diagnose due to normal physiological changes and limitations of some diagnostic tests. The risk of PE increases up to 10-fold during pregnancy. Clinical evaluation alone is insufficient for diagnosis, and pre-test probability scores like Wells criteria are not validated for pregnant patients. D-dimer levels are also often elevated in normal pregnancy. Ultrasound is recommended initially to evaluate for DVT, with treatment if found. If ultrasound is negative and PE still suspected, options like VQ scan or CTPA involving limited radiation can be considered, with CTPA preferred if CXR is abnormal. Timely diagnosis and treatment are important due to risks of maternal mortality from PE.
Small Cell Lung Cancer Management by Dr.Tinku JosephDr.Tinku Joseph
Small cell lung cancer (SCLC) typically presents with widespread metastases. SCLC is classified as limited stage or extensive stage disease. Treatment for limited stage SCLC involves chemotherapy with cisplatin and etoposide plus concurrent thoracic radiation. Prophylactic cranial irradiation is also recommended. Extensive stage SCLC is treated with chemotherapy alone. The standard regimen is cisplatin and etoposide, though carboplatin-based regimens are also used. Local radiation may provide additional benefit for responsive extensive stage patients. Median survival for SCLC depends on stage but typically ranges from 10 to 24 months with treatment.
Delirium is an acute confusional state that commonly occurs in the ICU. It can be hyperactive, hypoactive, or mixed. Delirium increases mortality, length of stay, costs, and long-term cognitive impairment. It results from neurotransmitter imbalances and higher cortical dysfunction exacerbated by predisposing patient factors and precipitating insults like medications and critical illness. Screening tools like ICDSC and CAM-ICU can help diagnose delirium which non-pharmacological prevention bundles, reducing deliriogenic medications, and treatments like haloperidol or dexmedetomidine may help address.
Allergic Broncho Pulmonary Aspergillosis (ABPA) by Dr.Tinku JosephDr.Tinku Joseph
HRCT is more sensitive than CXR in detecting bronchiectasis and other pulmonary changes in ABPA. It helps establish the diagnosis and assess disease severity and response to treatment.
PowerPoint presentation describing various aspects of Pulmonary Hypertension. Please mail me your feedback on this presentation to following Email ID: tinkujoseph2010@gmail.com.
Stem cell therapy and lungs - Dr.Tinku JosephDr.Tinku Joseph
This document discusses stem cell therapy for lung diseases. It defines stem cells and describes their main types, including embryonic, adult, and adult tissue-specific stem cells. It outlines the identification of lung stem cells and controversies over their origin. Studies show lung epithelial cells and bronchoalveolar stem cells may help repair lung injury. The document also discusses applications of stem cell therapy for conditions like COPD and strategies for transplantation.
Pulmonary manifestations in immuno compromised hostMitusha Verma
This document summarizes pulmonary manifestations that are commonly seen in immuno compromised hosts. It discusses the increased risk of opportunistic and non-opportunistic infections in this population. A systematic approach is outlined including relevant history, examinations, investigations like sputum analysis and chest imaging. Specific CT findings are described for various infections like Pneumocystis jiroveci pneumonia, mycobacterial infections, viral infections like CMV, and fungal infections. CD4 counts are correlated with infection risk. Imaging patterns for various infections, diseases and entities like Kaposi's sarcoma and lymphoproliferative disorders are also summarized.
This document provides information about hepatopulmonary syndrome (HPS). It defines HPS as the presence of liver disease, impaired oxygenation, and intrapulmonary vascular abnormalities. The pathophysiology involves widespread pulmonary vasodilatation leading to ventilation-perfusion mismatching and right-to-left shunting, causing hypoxemia. Clinical features include signs of liver disease in most patients and dyspnea in some. Diagnosis requires confirming the three criteria through tests like contrast echocardiography to detect intrapulmonary shunting.
This document provides an overview of pulmonary embolism (PE). It discusses the historical context, pathophysiology, risk factors, clinical presentation, diagnostic testing and treatment of PE. Some key points include:
- PE is a common cause of preventable death, with over 600,000 cases annually in the US.
- Virchow's triad of hypercoagulability, stasis, and endothelial injury contributes to the development of PE.
- Clinical presentation is often nonspecific, and the classic triad of symptoms occurs in less than 20% of cases.
- Diagnostic testing includes D-dimer, chest CT, ventilation-perfusion scanning and pulmonary angiography. Early treatment with antico
Pulmonary embolism - Diagnosis and managementDr Vivek Baliga
Pulmonary embolism is a common problem seen in medical practice. This presentation by Dr Vivek Baliga discusses the basic aspects and evidence behind current management.
This document discusses pulmonary embolism (PE), a potentially lethal condition caused by blood clots in the lungs. PE is often missed due to nonspecific symptoms but can lead to death if untreated. Risk factors include immobilization, surgery, cancer, pregnancy, and oral contraceptives. Symptoms range from nonspecific chest pain to circulatory collapse. Diagnosis involves tests like CT scans, VQ scans, echocardiograms and D-dimer levels. Treatment involves oxygen, anticoagulants like blood thinners, and potentially thrombolytics for severe cases. Outcomes depend on early detection and treatment, but PE can still lead to complications like pulmonary hypertension if not addressed.
Pulmonary embolism (PE) is a common and potentially deadly condition where blood clots block the pulmonary arteries in the lungs. The document discusses the pathophysiology, risk factors, clinical presentation and diagnostic workup of PE. Treatment involves anticoagulation with heparin or warfarin to prevent further clotting. A simplified diagnostic algorithm is proposed utilizing pre-test probability, D-dimer testing and CT angiography to efficiently evaluate for PE.
Pulmonary embolism is a blockage of the pulmonary artery or its branches by material that has traveled from elsewhere in the body through the bloodstream. It is most commonly caused by deep vein thrombosis in the legs. Symptoms include dyspnea, chest pain, and cough. Risk factors include prolonged bed rest, cancer, oral contraceptives, and recent surgery or trauma. Diagnosis involves evaluating clinical probability and testing such as D-dimer, CT pulmonary angiography, ventilation-perfusion scanning, and pulmonary angiography. Treatment focuses on anticoagulation to prevent further clots.
This document discusses pulmonary embolism (PE), including its definition, epidemiology, risk factors, pathophysiology, clinical features, diagnosis, and management. Some key points:
- PE is an obstruction of the pulmonary artery or its branches by a thrombus originating in the venous system or right heart. It is a common cause of preventable death in hospitalized patients.
- The annual incidence of PE ranges from 23-69 cases per 100,000 people in India. Worldwide, the incidence of venous thromboembolism (which includes PE and DVT) is 117 cases per 100,000 person-years.
- Risk factors for PE include hereditary clotting disorders, immobil
This document discusses MDCT and pulmonary embolism (PE). It provides an overview of risk factors for PE, clinical signs and symptoms, diagnostic tests including CXR, V/Q scan and pulmonary CTA. It describes techniques for optimal pulmonary CTA and discusses findings of acute vs chronic PE, as well as non-thrombotic causes of PE like tumor embolism. Common pitfalls in PE CTA are outlined.
Deep vein thrombosis (DVT) and pulmonary embolism (PE), collectively known as venous thromboembolism (VTE), represent a major global health problem. VTE has significant morbidity and mortality but is also potentially treatable. The incidence of VTE is increasing due to factors like population aging and higher rates of comorbidities. Risk factors for VTE include hypercoagulability, stasis, vascular injury, cancer, immobilization, and surgery. Diagnosis involves assessment of clinical probability with tools like the Wells criteria and D-dimer testing. Imaging options include ultrasound, CT, ventilation-perfusion scanning, and pulmonary angiography. Treatment involves anticoagulation with drugs like heparin or
Diagnosis and treatment of acute pulmonary embolism (VTE)Usama Ragab
By Dr. Usama Ragab, Zagazig Faculty of Medicine
PE may account for up to 15% of all post-operative deaths.
It is the commonest cause of death following elective surgery, and the commonest cause of maternal death.
Venous thromboembolism, THROMBOPROPHYLAXIS and managementmauryaramgopal
1) Venous thromboembolism (VTE), which includes deep vein thrombosis (DVT) and pulmonary embolism (PE), is a common cardiovascular disease among hospitalized patients, especially critically ill patients in the ICU.
2) Risk factors for VTE include surgery, trauma, cancer, immobilization, and factors related to the underlying critical illness. Several clinical prediction models can assess a patient's risk.
3) Diagnosis involves blood tests, imaging like ultrasound and CT, and assessment of right ventricular function. Treatment involves supportive care, anticoagulation with heparin or low molecular weight heparin, and consideration of thrombolysis for hemodynamically unstable patients.
Deep vein thrombosis (DVT) is a common and potentially fatal condition. It can lead to pulmonary embolism (PE), which is a leading cause of preventable hospital death. While DVT often has no symptoms, it puts patients at risk for long-term complications. Standard diagnostic tests include ultrasound, CT scans, and D-dimer tests. Risk factors include surgery, trauma, immobility, and cancer. Prophylaxis with blood thinners, compression devices, and stockings can significantly reduce the risk of DVT, especially in high-risk hospitalized patients. Early diagnosis and treatment are important to prevent fatal PE and long-term issues.
This document discusses the pathophysiology and treatment of acute pulmonary embolism (PE). It covers:
- The pathophysiological effects of PE on right ventricular function and hemodynamics.
- Clinical prediction rules and diagnostic strategies for PE including D-dimer testing and imaging modalities like CT, VQ scan, and angiography.
- Treatment options for PE including anticoagulants like heparin, low molecular weight heparin, fondaparinux, and newer oral agents; as well as thrombolytics, vena cava filters, and embolectomy. LMWH is recommended as first-line treatment due to superior safety compared to unfractionated heparin
This document provides an overview of pulmonary embolism (PE), including its causes, risk factors, presentation, diagnosis, and treatment. It notes that PE is a leading cause of morbidity and mortality, with many cases being missed or misdiagnosed. The diagnosis involves assessing risk factors and symptoms, then pursuing testing like D-dimer, chest imaging like CTPA, and ultrasound. Treatment involves starting anticoagulation like heparin or warfarin to prevent further clots and death.
The document discusses acute pulmonary embolism (PE). PE is common but difficult to diagnose, with nonspecific symptoms. It describes a case of a 48-year-old woman presenting with sudden dyspnea, tachycardia, and leg swelling who may have PE. Risk factors for PE include recent surgery or trauma, prolonged immobilization, and inherited or acquired hypercoagulable states. Diagnosis involves clinical scoring, D-dimer, imaging like CTPA, and treatment includes anticoagulation with heparin or warfarin.
Pulmonary embolism (PE) is a common and potentially fatal condition where blood clots block arteries in the lungs. An estimated 5 million venous thromboses occur annually worldwide, with 10-30% of PE cases correctly diagnosed. Risk factors include cancer, obesity, pregnancy, prolonged immobility, and genetic hypercoagulable states. Diagnosis involves assessing clinical probability, d-dimer testing, imaging like CT scans or V/Q scans, and echocardiography. Treatment consists of anticoagulants like heparin or warfarin to prevent further clotting while the body breaks down existing clots.
Pulmonary embolism (PE) is a common and potentially fatal condition where blood clots block arteries in the lungs. An estimated 5 million venous thromboses occur annually worldwide, with 10-30% of cases resulting in PE. Risk factors include immobilization, surgery, cancer, and estrogen use. Diagnosis involves assessing clinical probability based on symptoms and risk factors, followed by tests like D-dimer, chest imaging, ultrasound, V/Q scan, CT, or angiogram. Treatment aims to prevent further clotting with anticoagulants like heparin and warfarin, provide supportive care, and in some severe cases utilize thrombolysis or embolectomy.
Pulmonary embolism (PE) is a common and potentially fatal condition where blood clots block arteries in the lungs. An estimated 5 million venous thromboses occur annually worldwide, with 10-30% of PE cases correctly diagnosed. Risk factors include older age, cancer, obesity, surgery, trauma, and genetic or acquired hypercoagulable states. Diagnosis involves assessing clinical probability, blood tests like D-dimer, imaging like CT scans or ventilation-perfusion scans, and echocardiography. Treatment focuses on anticoagulation to prevent further clotting and allow natural lysis, along with supportive care and thrombolysis or embolectomy in severe cases.
Pulmonary embolism (PE) is a common and potentially fatal condition where blood clots block arteries in the lungs. An estimated 5 million venous thromboses occur annually worldwide, with 10-30% of PE cases correctly diagnosed. Risk factors include cancer, obesity, pregnancy, prolonged immobility, and genetic predispositions. Diagnosis involves evaluating symptoms, physical exam findings, blood tests like D-dimer, imaging like CT scans and V/Q scans, and echocardiograms. Treatment focuses on anticoagulation with heparin or warfarin to prevent further clotting while the body breaks down existing clots.
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2. Perspective
A Common disorder and potentially
deadly
650,000 cases occurring annually
Highest incidence in hospitalized
patients
Autopsy reports suggest it is commonly
“missed” diagnosed
3. Perspective
Presentation is often “atypical”
Signs and symptoms are frequently
vague and nonspecific and rarely
“classic”
Untreated mortality rate of 20% 30%, plummets to 5% with timely
intervention
3
4. So What Do We Do ???
Confusing
for Emergency
Physician
Do we under diagnose/over
diagnose?
4
6. Venous Thromboembolism
“ The detachment of larger or smaller fragments from the
end of the softening thrombus are carried along by the
current of blood and driven in remote vessels. This
gives rise to the very frequent process upon which I
have bestowed the name EMBOLIA.”
Vessel Injury
Acquired
Stasis
Hyper-coagulability
Inherited
7. Risk Factors
Hypercoagulability
Malignancy
Nonmalignant thrombophilia
Pregnancy
Postpartum status (<4wk)
Estrogen/ OCP’s
Genetic mutations (Factor V Leiden, Protein C & S deficiency, Prothrombin
mutations, anti-thrombin III deficiency)
Venous Statis
Bedrest > 24 hr
Recent cast or external fixator
Long-distance travel or prolong automobile travel
Obesity
Stroke
Venous Injury
Recent surgery requiring endotracheal intubation
Recent trauma (especially the lower extremities and pelvis)
8. Clinical Presentation
NOTORIOUSLY DIFFICULT
1)SIZE 0f clot and pre-existing cardiopulmonary
status
2) COMMON s/s of P.E are not specific to it
The Classic Triad: (Hemoptysis, Dyspnea, Pleuritic Pain)
Not very common!
Occurs in less than 20% of patients with documented PE
10. Clinical Features
Signs with Angiographically Proven PE
Sign
Percent
Tachypnea > 20/min
Rales
Accentuated P2
Tachycardia >100/min
Fever > 37.8
Diaphoresis
S3 or S4 gallop
Thrombophebitis
Lower extremity edema
92
58
53
44
43
36
34
32
24
10
11. IMPORTANT DEFINITIONS
Provoked
VTE
VTE which occurred in the presence of
an antecedent (within 3 months) and transient major clinical risk
factor for VTE (for example surgery, trauma, significant immobility
and pregnancy or puerperium). The GDG also considered VTE that
occurred in association with hormonal therapy (oral contraceptive or
hormone replacement therapy) to be provoked as it
UNPROVOKED
DVT or PE in a patient with no antecedent
major clinical risk factor for VTE who is not having hormonal therapy
(oral contraceptive or hormone replacement therapy). Patients with
active cancer, thrombophilia or a family history of VTE should also be
considered as having an unprovoked episode because these
underlying risks will remain unchanged in the patient
11
12. Who do we work up?
- Pretest Probability
Definition: “The probability of the target disorder (PE)
before a diagnostic test result is known”.
Used to decide how to proceed with diagnostic testing
and final disposition
“Gestalt”
This is really what it boils down to!
12
13. WELL’S CRITERIA FOR P.E
Clinical feature
Clinical
Points
signs and symptoms of DVT (minimum of leg swelling and
pain with palpation of the deep veins)
An
3
alternative diagnosis is less likely than PE
3
Heart
rate greater than 100 beats per minute
Immobilisation
Previous
1.5
(for more than 3 days) or surgery in the previous four weeks 1.5
DVT/PE
1.5
Haemoptysis
Malignancy
Clinical
(on treatment, treated in the last 6 months, or palliative)
probability simplified score
PE likely More than 4 points
PE unlikely 4 points or less
1
1
15. Diagnostic Testing
- CXR’s
Chest X-Ray Myth:
“You have to do a chest x-ray so you can
find Hampton’s hump or a Westermark
sign.”
Reality:
Most chest x-rays in patients with PE are
nonspecific and insensitive
15
16. Chest X-ray Eponyms of PE
Westermark's sign
A dilation of the pulmonary vessels
proximal to the embolism along with
collapse of distal vessels, sometimes with
a sharp cutoff.
Hampton’s Hump
A triangular or rounded pleural-based
infiltrate with the apex toward the hilum,
usually located adjacent to the hilum.
16
18. Diagnostic Testing
– EKG’s
EKG
Most Common Findings:
Tachycardia or nonspecific ST/T-wave changes
Acute cor pulmonale or right strain patterns
Tall peaked P-waves in lead II (P pulmonale)
Right axis deviation
RBBB
S1-Q3-T3 (occurs in only 20% of PE patients)
19. Diagnostic Testing
- Pulse Oximetry
The Pulse Oximetry Myth:
“ You must do a pulse oximetry reading, since
patients with pulmonary embolism are
hypoxemic!”
Reality:
Most patients with a PE have a normal pulse
oximetry, and most patients with an abnormal
pulse oximetry will not have a PE.
19
20. Diagnostic Testing
- ABG’s
The ABG/ A-a Gradient myth:
“You must do an arterial blood gas and calculate
the alveolar-arterial gradient. Normal A-a
gradient virtually rules out PE”.
Reality:
The A-a gradient is a better measure of gas
exchange than the pO2, but it is nonspecific and
insensitive in ruling out PE.
20
21. Diagnostic Testing
Echocardiography
Consider
in every patient with a documented
pulmonary embolism
EKG
Early
maybe helpful in demonstrating right heart strain
fibrinolysis can reduce mortality by 50%!
21
22. Ancillary Test
WBC
Poor sensitivity and nonspecific
Can
Hgb/Hct
be as high as 20,000 in some patients
PTE does not alter count but if extreme,
consider polycythemia, a known risk factor
ESR
Don’t get one, terrible test in regard to
any predictive value
22
23. D-dimer Test
Fibrin split product
Circulating half-life of 4-6 hours
Quantitative test have 80-85% sensitivity, and 93-100% negative
predictive value
False Positives:
Pregnant Patients
Malignancy
Advanced age > 80 years
Hemmorrhage
AMI
Hepatic Impairment
Post-partum < 1 week
Surgery within 1 week
Sepsis
CVA
23
Collagen Vascular Diseases
24. Diagnostic Testing
D-dimer
Qualitative
Bed side RBC agglutination test
“SimpliRED D-dimer”
Quantitative
Enzyme linked immunosorbent asssay “Dimertest”
Positive assay is > 500ng/ml
VIDAS D-dimer, 2nd generation ELISA test
25. Ventilation/Perfusion Scan
- “V/Q Scan”
A
common modality to image the lung
And its use still stems from the PIOPED study.
Relatively
noninvasive and sadly most often
nondiagnostic
In
many centers remains the initial test of choice
26. V/Q Scan
Technique
Interpretation
Low probability/”nondiagnostic” (most common)
Normal
High Probability
Simplified approached to the interpretation of results:
High probability
Treat for PE
Normal Scan
If low pre-test, you’re done
Everything else
Pursue another study (CT, Angio)
27. Spiral (Helical) Chest CT
Advantages
Noninvasive and Rapid
Alternative Diagnosis
Disadvantages
Costly
Risk to patients with borderline renal function
Hard to detect subsegmental pulmonary emboli
29. Patient with signs or
symptoms of PE
Other causes excluded by assessment of general medical history, physical examination and chest X-ray
PE suspected
Two-level PE Wells score
PE likely (> 4 points)
PE unlikely (≤ 4 points)
Is CTPA* suitable** and available immediately?
no
yes
Offer CTPA(or V/QSPECT or planar scan)
Contd.. On next slide
Immediate interim parenteral anticoagulant therapy
Was CTPA (or V/Q SPECT or planar scan) positive?
CTPA (or V/Q SPECT or planar scan)
N
o
Is deep vein thrombosis suspected?
Y
e
s
NO
Consider a proximal leg vein ultrasound scan
Yes
Advise the patient it is not likely they have PE. Discuss
with them the signs and symptoms of PE, and when and
where to seek further medical help. Take into
consideration alternative diagnoses
Diagnose PE and treat
29
30.
PE unlikely (≤ 4 points)
D-dimer test
Yes
No
Was the D-dimer test positive?
Is CTPA* suitable** and available immediately?
No
Immediate interim parenteral
anticoagulant therapy
Offer CTPA (or V/Q SPECT or planar
scan)
CTPA (or V/Q SPECT or planar scan)
Was the CTPA (or V/Q SPECT or planar scan) positive?
No
Yes
Diagnose PE and treat
Advise the patient it is not likely
they have PE. Discuss with them
the signs and symptoms of PE,
and when and where to seek
further medical help. Take into
consideration alternative diagnosis
30
31. Treatment:
Goals:
Prevent death from a current embolic event
Reduce the likelihood of recurrent embolic
events
Minimize the long-term morbidity of the event
32. PATIENT EDUCATION
Give patients having anticoagulation treatment verbal and written
information about:
how to use anticoagulants
duration of anticoagulation treatment
possible side effects of anticoagulant treatment and what to do if these
occur
the effects of other medications, foods and alcohol on oral
anticoagulation treatment
monitoring their anticoagulant treatment
how anticoagulants may affect their dental treatment
taking anticoagulants if they are planning pregnancy or become
pregnant
how anticoagulants may affect activities such as sports and travel when
and how to seek medical help.
32
33. Treatment
Anticoagulants
Heparin
Provides
immediate thrombin inhibition, which prevents
thrombus extension
Does
Will
not dissolve existing clot
not work in patients with antithrombin III def.
In this case use hirudins
Few
absolute contraindications
35. Offer a choice of low molecular weight heparin (LMWH) or fondaparinux to
patients with confirmed proximal DVT or PE, taking into account comorbidities,
contraindications and drug costs, with the following exceptions:
For patients with severe renal impairment or established renal failure
(estimated glomerular filtration rate [eGFR] < 30 ml/min/1.73 m2) offer
unfractionated heparin (UFH) with dose adjustments based on the APTT
(activated partial thromboplastin time) or LMWH with dose adjustments based
on an anti-Xa assay.
For patients with an increased risk of bleeding consider UFH.
For patients with PE and haemodynamic instability, offer UFH and consider
thrombolytic therapy
Start
the LMWH, fondaparinux or UFH as soon as possible and continue it for at
least 5 days or until the international normalised ratio (INR) (adjusted by [VKA];
is 2 or above for at least 24 hours, whichever is longer.
35
36.
Offer LMWH to patients with active cancer and confirmed
proximal DVT or PE, and continue the LMWH for 6 months
At 6 months, assess the risks and benefits of continuing
anticoagulation
For patients with an increased risk of bleeding consider
UFH.
36
37. Treatment
Anticoagulants
Warfarin (Coumadin)
Interferes
with the action of Vit-K dependent factors: II, VII, IX,
and X, as well as protein C & S
Causes
temporary hypercoagulable state in first 5 days of
treatment
Important a patient is anticoagulated with heparin before initiating
warfarin therapy
Target
INR is 2.0 – 3.0
38.
Offer a VKA to patients with confirmed proximal DVT or
PE within 24 hours of diagnosis and continue the VKA for 3
months. At 3 months, assess the risks and benefits of
continuing VKA treatment
Offer a VKA beyond 3 months to patients with an
unprovoked PE taking into account the patient’s risk of
VTE recurrence and whether they are at increased risk of
bleeding. Discuss with the patient the benefits and risks
of extending their VKA treatment.
38
39. Treatment
Fibrinolytic
Therapy (Alteplase)
Indications:
Documented
PE with:
Persistent hypotension
Syncope with persistent hemodynamic compromise
Significant hypoxemia
+/- patient with acute right heart strain
Approved
infusion.
Altivase regimen is 100mg as a continuous IV
40. Treatment
Embolectomy
Prefibrinolytic therapy this was only therapy for massive
PE
Carries a 40% operative mortality
Alternative is Transvenous Catheter Embolectomy
Consider catheter-directed thrombolytic therapy for
patients with
symptomatic iliofemoral DVT who have:
symptoms of less than 14 days’ duration and
good functional status and
a life expectancy of 1 year or more and
a low risk of bleeding.
40
41. VENA CAVAL FILTERS
Offer temporary inferior vena caval filters to patients with
proximal DVT or PE who cannot have anticoagulation
treatment, and remove the inferior vena caval filter when the
patient becomes eligible for anticoagulation treatment.
Consider inferior vena caval filters for patients with recurrent
proximal DVT or PE despite adequate anticoagulation
treatment only after considering alternative treatments such
as:
increasing target INR to 3-4 for long-term high-intensity oral
anticoagulant therapy or switching treatment to LMWH.
Ensure that a strategy for removing the inferior vena caval
filter at the earliest possible opportunity is planned and
documented when the filter is placed, and that the strategy is
reviewed regularly.
41
42. THROMBOPHILIA TESTING
Consider testing for hereditary thrombophilia in patients who
have had unprovoked DVT or PE and who have a first-degree
relative who has had DVT or PE if it is planned to stop
anticoagulation treatment.
Do not offer thrombophilia testing to patients who have had
provoked DVT or PE.
Do not routinely offer thrombophilia testing to first-degree
relatives of people with a history of DVT or PE and
thrombophilia.
Consider testing for antiphospholipid antibodies in patients
who have had unprovoked DVT or PE if it is planned to stop
anticoagulation treatment.
42
43. TAKEAWAY MESSAGE
Pulmonary Emboli remain a potentially deadly and common
event which may present in various ways
Don't be fooled if your patient lacks the “classic” signs and
symptoms!
Consider PE in any patient with an unexplainable cause of
dyspnea, pleuritic chest pain, or findings of tachycardia, tachpnea,
or hypoxemia
D-Dimers have NPV of 93-99%
Heparin remains the mainstay of therapy with the initiation of
Warfarin to follow
Pulmonary embolism is the most serious complication of venous thrombosis
It is the third most common cause of death in the US
As many as 60% of deaths in hospitalized patients are found to have pulmonary emboli
So, generally speaking it is a hard diagnosis to make….
As clinicians we must consider the diagnosis in patients to put us on the right path
PE It has a wide spectrum of patient presentation, which leads us to do suboptimal testing. This can stand in the way of a timely diagnosis
It’s important, because prompt diagnosis and treatment can dramatically reduce the mortality rate and morbidity of this disease.
Unfortunately, the diagnosis is missed far more than it is made. I want to offer you a historical perspective of the disorder
Do we under diagnose or over diagnose?
If we over diagnose, is it such a big deal? It’s just a few month of inconvenience of heparin and warfarin.
Aside from the potential morbidity of the anticoagulants,there are other problems.
The diagnoses carries a stigma which will contaminate all future medical encounters. Women may be barred from oral contraceptives, future pregnancies will be considered high risk. Elective surgery may be denied.
So, really after all these years, we are still left in the dark. We still don’t have a collective conscience on a standard approach to this problem.
Before we can answer any questions we have to understand the condition and this take us to virchow.
Everyone I’m sure is familiar with Virchow’s triad. It was first described by this German pathologist.
If we think of risk factors, we should think of them as the embodiment of the triad: hypercoagulability, stasis, and vessel injury.
So, essentially, under normal conditions, microthrombi are continually formed and lysed with the venous circulatory system.
When any one of the “risk states” exists, potential microthrombi may escape the normal fibrinolytic system and grow and propagate.
Pulmonary Emboli occurs when fragments of thrombus break loose and are carried through the right side of the heart into the pulmonary arterial tree.
Cancers of primarily adenocarcinoma and CNS tumors most often cause thrombosis.
We need to make special mention about patients with a prior history of DVT or PE.
Studies have revealed these patients have between a 5 to 30 times increased risk of a new DVT in response to a triggering event compared to those who have not had prior episodes.
All the above symptoms are a manifestation of cardiopulmonary stress caused by the cloth in the lung.
These produce symptoms perceived by the patient and the signs observed by you!
There are three common clinical presentations that you should be aware of:
1. Patient’s with pulmonary infarction may have pleuritic chest pain and can be hard to distinguish between that patient with infection pneumonitis
2. Submassive embolism are the hardest of all. By definition, they have an angiographically defined blockage of flow to an area served by less than two lobar arteries.
These patients have acute or unexplained dyspnea with exertion or at rest. So, they can be easily confused with infection, asthma, CHF and the like.
3. Finally, Massive PE, or a clot which obstructs two lobar arteries, so-called “Saddle Embolus”. These patients have acute cor pulmonaly often with syncope. You might think there having an MI or look septic!
These are the common symptoms that are associated with PE
As we mentioned in the previous slide, dyspnea and chest pain are not always preset.
The explanation is that with a small V/Q mismatch, the adaptive physiology of the pulmonary vasculature and bronchi produce intermittent shortness of breath. Because of this, we are easily distracted and looking for a cardiogenic cause of the dyspnea.
What about pleuritic chest pain, still not a home run!
In fact, up to 25% of patients ultimately diagnosed with a PE, never had any chest pain!
This is what makes the diagnosis so difficult!
Lets look a t a couple of these:
Tachycardia!
Myth #2 We are all taught this is a key component of the diagnosis. Right?
In fact, actually not having tachycardia is more commonly seen in patients who are found to have a PE!
What about fever? If a patient has a fever, it must not be a PE, right?
Not true.
Although not common, Among patients with PE and no other source of fever, fever was present in one study in 43 of 311 patients (14%).
For example
This could represent the likelihood that a specific patient , say a middle-aged man, with a specific past history, say hypertension and tobacco smoking who presents with a specific symptom complex: Chest pain, Dsypnea, or Diaphoresis has a specific diagnosis.
Final Statement:
Because PE can present with or with any of the “classic signs and symptoms” and even the risk factors which contribute to PE are varied in frequency, we are left with a intuition at best!
As you can see there are a variety of test that we use to arrive at a diagnosis.
Some better than others!
So, lets talk about these individually.
Granted that most are abnormal, but certainly not diagnostic.
It is true that in the original PIOPED study it was recommended but the main value is to exclude diagnoses the mimic PE and to aid in the interpretation of the V/Q scan
Here we see the dilated vessels and oligemia of westermark’s sign
And below Hampton’s Hump
A brief mention about the classic S1-Q3-T3, its appearance on the EKG may suggest PE, but study after study has shown it has no predictive value what so ever!
But you got to know it because question writers for the boards love it!
Actually, it is opposite of what you might think!
As with most dogma, we are taken back by what we thought was truth.
About 15% of patients with proven pulmonary embolism have a pO2 of 85mmHg or higher!
In one study, researches drew from there data various combinations of the PaO2 of 80mm Hg or more, the PaCO2 of 35mmHg or higher, and the A-a gradient of 20 mmHg or less.
They found that PE could not be excluded in more than 30% of patients with no prior cardiopulmonary disease.
Moreover, PE could not be excluded in more than 14% of patients with prior cardiopulmonary disease.
Conclusion, Blood gas levels are poor discriminate value to permit the exclusion of PE.
Diagnosing of early right ventricular strain is important because it is a strong predictor of subsequent death
Important to recommend echocardiogram with your admitting internist if a pattern of right heart strain is suggested by EKG.
Studies have documented that lives are saved with early fibrinolysis is considered in these patients.
Well, what is it?
Basically, the assay is enzyme-linked monoclonal antibody test used to identify the protein, D-Dimer.
D-Dimer itself is a unique degradation product that is produced by a plasmin mediated breakdown of cross-linked fibrin
Good test with respect to its negative predictive value.
The drawbacks are some of the false positives that we commonly see in the ER.
Two types,
Qualitative RBC agglutination assay, low sensitivity and specificity and not good enough to comfortably rule out PE.
Quantitative, which measure the accurately the amount using a spectrophotometer.
Our lab uses the 2nd generation VIDAS d-dimer with a negative predictive value of 99.3%!
Essentially, a patient is injected with a radioisotope that travels through the pulmonary microcirculation and are detected by a gamma camera over the patient
A normal Perfusion study will have evenly distributed blood flow.
Then a patient inhales a radioactive gas and it is viewed as it washes over the bronchopulmonary tree.
A mismatch, areas of blocked perfusion and normal ventilation is interpreted by the radiologist and given reading as normal (never), high probability, or non-diagnostic/low-probability
The reason the low probability or non diagnostic scan category is so suspect is because in the PIOPED study this group had terrible inter-reader reliability. So, just beware.
The entire lung can be scanned while the patient holds there breath.
Advantages:
CT most useful benefit is in providing evidence for an alternative diagnosis or excluding it entirely.
Disadvantages:
The clinical significance for subsegmental PE are not well
known, but may be a marker for a larger PE
Given that the majority of V/Q studies are non-diagnostic, I prefer the CT as the initial test of choice in place of V/Q scan.
Right now there is no better test on the horizon of the immediate present to virtually rule out or in PE.
.
So what are our goals???
Heparin is the most frequently used drug in the treatment of PE.
Because heparin works by activating antithrombin III, this genetic mutation makes heparin ineffective.
FDA approved dose for Unfractionated heparin is 80units/kg IV bolus, then 18 units/kg/hr infusion to maintain the INR at 2.5-3
Lovenox is dosed at 1mg/kg every 12 hours or 1.5 mg/kg per day.
LMWH in pregnancy only preferred for convenience sake.
This is because the anticoagulants protein C and S have short half-lives compared with the procoagulant vitamin K-dependent proteins.
So, this gives rise to the clinical importance that heparin must be continued for at least five days after beginning Coumadin
The incidence of progressive thrombosis and embolization is 40% when starting warfarin directly, compared to only 8% when beginning after a patient has been anticoagulated with heparin.
Treatment is usually for 6 months, but may continue lifelong
For critically ill patients, a very rapid infusion of 100mg over 10 minutes is preferred.
Alternative is Retavase, you can give it as two IV doses of 10 units, each over two minutes.
This is a procedure where a suction tip catheter is placed in contact with the thrombus under fluoroscopy and sucked out while catheter is withdrawn