Pneumothorax is the presence of air in the pleural space and can occur spontaneously or due to injury. It is classified as primary or secondary based on whether there is pre-existing lung disease. Clinical features include chest pain and breathlessness. Chest x-rays and CT scans are used to diagnose and monitor pneumothorax. Small primary pneumothoraces may resolve on their own while chest drains and surgery are used for larger cases or those with lung disease. Recurrent pneumothoraces often require surgical treatment to prevent future occurrences.
This document discusses pulmonary embolism (PE), including:
- PE occurs when blood clots (thrombi) block pulmonary arteries, ranging from acute massive PE to chronic PE.
- Deep vein thrombosis is the main cause of PE. Risk factors include recent surgery, oral contraceptive use, and malignancy.
- Symptoms can range from asymptomatic to sudden death. Common symptoms include dyspnea and chest pain.
- Diagnostic tests include CT pulmonary angiography, ventilation-perfusion scanning, echocardiography, and D-dimer levels. CT pulmonary angiography has high sensitivity and specificity for PE diagnosis.
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 is a blockage in the lungs caused by blood clots that travel from deep veins, usually in the legs or pelvis. It can be life-threatening and is responsible for around 100,000-200,000 deaths in the US each year. Risk factors include inherited or acquired hypercoagulability, venous stasis, or vessel wall injury. Diagnosis involves assessment of likelihood using scoring systems, blood tests like D-dimer, and imaging tests like CT pulmonary angiogram. Treatment depends on stability but generally involves anticoagulants like heparin or newer oral medications to prevent further clots. Prevention focuses on early mobilization, stockings, and blood thinners for
1. Pulmonary embolism is caused by a blood clot in the lung, usually formed in the deep veins of the lower limbs. It is a leading cause of preventable death in hospitalized patients.
2. Symptoms include shortness of breath, chest pain, increased heart rate, coughing up blood, and fainting. Diagnosis involves assessing risk factors and test like D-dimer and CT scan.
3. Treatment involves anticoagulant drugs to dissolve clots initially by injection and then orally for 3-6 months. Prevention focuses on continuing anticoagulants, lifestyle changes like exercise and diet, wearing compression stockings, and early movement after surgery.
This document summarizes pulmonary embolism (PE), including its causes, symptoms, diagnosis, and treatment. PE occurs when blood clots or other substances block arteries in the lungs, and is usually caused by deep vein thrombosis. Common symptoms include chest pain, difficulty breathing, and cough. Diagnosis involves tests like plasma D-dimer levels, ECGs, lung scans, and pulmonary angiography. Treatment focuses on anticoagulation therapy, and sometimes thrombolytic therapy or inferior vena cava filters for severe cases. Prognosis is generally good with proper diagnosis and treatment.
Diagnosis of Pulmonary Embolism is often difficult. This presentation highlights step-wise and practical approach to the diagnosis of PE in short and precise fashion.
Pulmonary thromboembolism is caused by a blood clot in the lung arteries, usually forming in the deep leg veins and then traveling to the lung. It reduces blood flow and oxygen delivery to the lungs and heart. Common symptoms include shortness of breath, chest pain, and fainting. Diagnosis involves assessing risk factors and test like D-dimer blood test and CT scan of the chest. Treatment is initially parenteral anticoagulants to dissolve clots followed by long-term oral anticoagulants to prevent future clots for at least 3 months and sometimes lifelong for high-risk patients. Prevention focuses on continued anticoagulation, lifestyle changes like diet and exercise, wearing compression
PowerPoint presentation about pulmonary embolism -- Teaching at Zagazig university cardiology department ,
Egypt in 2013 by Islam Ghanem , assistant lecturer of cardiology
This document discusses pulmonary embolism (PE), including:
- PE occurs when blood clots (thrombi) block pulmonary arteries, ranging from acute massive PE to chronic PE.
- Deep vein thrombosis is the main cause of PE. Risk factors include recent surgery, oral contraceptive use, and malignancy.
- Symptoms can range from asymptomatic to sudden death. Common symptoms include dyspnea and chest pain.
- Diagnostic tests include CT pulmonary angiography, ventilation-perfusion scanning, echocardiography, and D-dimer levels. CT pulmonary angiography has high sensitivity and specificity for PE diagnosis.
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 is a blockage in the lungs caused by blood clots that travel from deep veins, usually in the legs or pelvis. It can be life-threatening and is responsible for around 100,000-200,000 deaths in the US each year. Risk factors include inherited or acquired hypercoagulability, venous stasis, or vessel wall injury. Diagnosis involves assessment of likelihood using scoring systems, blood tests like D-dimer, and imaging tests like CT pulmonary angiogram. Treatment depends on stability but generally involves anticoagulants like heparin or newer oral medications to prevent further clots. Prevention focuses on early mobilization, stockings, and blood thinners for
1. Pulmonary embolism is caused by a blood clot in the lung, usually formed in the deep veins of the lower limbs. It is a leading cause of preventable death in hospitalized patients.
2. Symptoms include shortness of breath, chest pain, increased heart rate, coughing up blood, and fainting. Diagnosis involves assessing risk factors and test like D-dimer and CT scan.
3. Treatment involves anticoagulant drugs to dissolve clots initially by injection and then orally for 3-6 months. Prevention focuses on continuing anticoagulants, lifestyle changes like exercise and diet, wearing compression stockings, and early movement after surgery.
This document summarizes pulmonary embolism (PE), including its causes, symptoms, diagnosis, and treatment. PE occurs when blood clots or other substances block arteries in the lungs, and is usually caused by deep vein thrombosis. Common symptoms include chest pain, difficulty breathing, and cough. Diagnosis involves tests like plasma D-dimer levels, ECGs, lung scans, and pulmonary angiography. Treatment focuses on anticoagulation therapy, and sometimes thrombolytic therapy or inferior vena cava filters for severe cases. Prognosis is generally good with proper diagnosis and treatment.
Diagnosis of Pulmonary Embolism is often difficult. This presentation highlights step-wise and practical approach to the diagnosis of PE in short and precise fashion.
Pulmonary thromboembolism is caused by a blood clot in the lung arteries, usually forming in the deep leg veins and then traveling to the lung. It reduces blood flow and oxygen delivery to the lungs and heart. Common symptoms include shortness of breath, chest pain, and fainting. Diagnosis involves assessing risk factors and test like D-dimer blood test and CT scan of the chest. Treatment is initially parenteral anticoagulants to dissolve clots followed by long-term oral anticoagulants to prevent future clots for at least 3 months and sometimes lifelong for high-risk patients. Prevention focuses on continued anticoagulation, lifestyle changes like diet and exercise, wearing compression
PowerPoint presentation about pulmonary embolism -- Teaching at Zagazig university cardiology department ,
Egypt in 2013 by Islam Ghanem , assistant lecturer of cardiology
- Pulmonary embolism (PE) is a potentially life-threatening condition where one or more arteries in the lungs become blocked by blood clots.
- Virchow's triad of stasis, hypercoagulability, and endothelial injury often leads to the formation of blood clots. Inflammation also plays a key role in precipitating PE.
- PE can range from low-risk cases with no adverse effects to massive cases involving multiple blood clots that can cause heart failure or death. Diagnosis involves assessing symptoms and risk factors, blood tests, imaging like CT scans, and electrocardiograms.
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
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 is a blood clot that develops in another part of the body and travels to the lungs, obstructing blood flow. Risk factors include older age, cancer, prior history of DVT/PE, and prolonged immobility. Symptoms can include dyspnea, chest pain, and cough, though many cases are asymptomatic. Diagnosis involves tests like CT angiography, ventilation-perfusion scanning, ultrasound, and D-dimer level. Treatment consists of oxygen, anticoagulation with heparin or warfarin, and sometimes thrombolysis for large clots or right heart strain. Long-term anticoagulation aims to prevent future 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 provides an overview of acute pulmonary embolism (PE). It discusses the pathophysiology, signs and symptoms, differential diagnosis, types, investigations and treatment of PE. Regarding treatment, it describes the use of oxygen therapy, anticoagulation including unfractionated heparin, warfarin and novel oral anticoagulants. It also discusses reperfusion treatments such as thrombolytic therapy and percutaneous catheter-directed treatment, as well as the use of vena cava filters. The document provides detailed information on diagnostic testing and therapeutic approaches for acute pulmonary embolism.
Acute pulmonary embolism is a form of venous thromboembolism that occurs when a blood clot breaks off and lodges in the pulmonary arteries of the lungs. The clinical presentation of PE can be variable and non-specific, making diagnosis challenging. It is important to efficiently evaluate patients suspected of having a PE to diagnose and treat it quickly in order to reduce morbidity and mortality. Treatment involves hemodynamic and respiratory support, initial anticoagulation with drugs like heparin, and potentially reperfusion therapies for more severe cases including thrombolysis or embolectomy.
- Acute pulmonary embolism (PE) is a common cardiovascular condition caused by obstruction of the pulmonary arteries by blood clots.
- Diagnosis can be difficult as symptoms are nonspecific, but includes dyspnea, chest pain, syncope. Imaging tests like CT pulmonary angiography or ventilation-perfusion scanning are used to diagnose PE.
- Treatment involves anticoagulation to prevent further clot growth. For high risk PE with hemodynamic instability, thrombolysis or embolectomy may be used to rapidly restore blood flow. Risk stratification guides duration of anticoagulation which is typically 3-6 months or longer for recurrent PE or persistent risk factors.
Rehabilitation of patient with pleural effusionAdemola Adeyemo
1) Pulmonary embolism occurs when a blood clot blocks an artery in the lungs, and can cause pleural effusions in about 30% of cases. Physiotherapy is an important part of managing patients with pleural effusions secondary to pulmonary embolism.
2) Physiotherapy includes techniques like incentive spirometry, chest physiotherapy, and exercises to improve cardiopulmonary function and endurance. Drainage of fluid from chest tubes is also facilitated.
3) As the patient's condition improves with physiotherapy, their ability to exercise intensifies and shortness of breath decreases, with the goal of restoring independence and fitness.
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 provides information on the anaesthetic management of surgery for Tetralogy of Fallot (TOF). It describes the key anatomical features of TOF and its variants. It outlines the natural history of untreated TOF, including risks of cyanotic spells, heart failure and early death. The document discusses the goals of palliative and corrective surgeries, including the modified Blalock-Taussig shunt. It provides guidance on preoperative evaluation, intraoperative management and goals of anaesthesia to optimize hemodynamics and oxygenation during surgery.
1. Pulmonary arteriovenous malformations (PAVMs) are rare vascular anomalies where abnormal dilated vessels provide a right-to-left shunt between the pulmonary artery and vein.
2. PAVMs are usually diagnosed through imaging like chest X-ray, CT, or MRI which show dilated vessels. Right-to-left shunting can be detected using echocardiography, oxygen studies, or pulmonary angiography.
3. Treatment involves embolization to occlude the abnormal vessels which successfully treats over 99% of PAVMs. Surgery is an alternative for cases that cannot be embolized or if embolization fails.
Imaging of Pulmonary Vascular Lesions ``Gamal Agmy
This document contains a series of questions and answers about the management of pulmonary embolism from Gamal Agmy, a professor of chest diseases. It discusses issues such as when to use thrombolysis for intermediate risk PE, the risks of thrombolysis for patients with recent surgery or stroke, and alternatives to thrombolysis if it is deemed too unsafe. It also addresses questions about managing PE in pregnant patients, PE with right atrial thrombus, and the appropriate use of IVC filters.
This document discusses pulmonary embolism (PE), including its epidemiology, disease burden, risk factors, pathophysiology, signs and symptoms, diagnostic evaluation, and treatment approaches. It notes that PE has an annual incidence of 100-200 per 100,000 people. Diagnostic evaluations discussed include assessment of clinical probability, D-dimer testing, CT pulmonary angiography, lung scintigraphy, and echocardiography. Treatment of acute PE involves hemodynamic support, anticoagulation with unfractionated heparin, low molecular weight heparin or fondaparinux, and potentially thrombolysis for high-risk cases.
The document discusses the stepwise management of hemoptysis. It defines hemoptysis and massive hemoptysis. The most common causes in Egypt are discussed. Steps in diagnosis include history, exams, labs, imaging like CXR, CT, bronchoscopy. Treatment depends on localization and cause but may include bronchoscopic interventions, bronchial artery embolization, or surgery. Disease-specific approaches are also outlined. Three case studies are presented to demonstrate tailored management of hemoptysis.
Thorax cardio adult dyspnea imaging g ferrettiJFIM
The document discusses dyspnea (shortness of breath), which is a common symptom in patients presenting to the emergency department with thoracic diseases. High-resolution computed tomography (HRCT) is highlighted as the best non-invasive tool for evaluating dyspnea, as it can identify underlying causes such as emphysema, asthma, pulmonary embolism, and interstitial lung diseases. The document presents several case examples where HRCT provided a diagnosis when other tests were nondiagnostic or revealed atypical features of diseases. HRCT is particularly useful when initial clinical exams and tests fail to identify a cause of dyspnea.
The document discusses postoperative care and monitoring of surgical patients. It covers assessing vital signs, pain, mobility and complications in various body systems. Common complications include respiratory issues like atelectasis, cardiovascular problems like hypotension, and gastrointestinal issues like nausea. It provides guidance on monitoring for and managing specific complications, as well as care aspects for different surgical specialties. Regular evaluation of patient progress and problems is emphasized.
This document provides an overview of pediatric anesthesia for congenital heart disease (CHD). It defines CHD and discusses classifications including cyanotic vs acyanotic defects. Key pathophysiology and anesthesia management are described for common defects like tetralogy of Fallot, transposition of the great arteries, atrial septal defects, ventricular septal defects, and patent ductus arteriosus. The objectives are to define CHD subtypes, discuss problems anesthesiologists may encounter, explain pathophysiology and implications for anesthesia, and how to manage CHD patients undergoing surgery.
- Pulmonary embolism (PE) is a potentially life-threatening condition where one or more arteries in the lungs become blocked by blood clots.
- Virchow's triad of stasis, hypercoagulability, and endothelial injury often leads to the formation of blood clots. Inflammation also plays a key role in precipitating PE.
- PE can range from low-risk cases with no adverse effects to massive cases involving multiple blood clots that can cause heart failure or death. Diagnosis involves assessing symptoms and risk factors, blood tests, imaging like CT scans, and electrocardiograms.
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
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 is a blood clot that develops in another part of the body and travels to the lungs, obstructing blood flow. Risk factors include older age, cancer, prior history of DVT/PE, and prolonged immobility. Symptoms can include dyspnea, chest pain, and cough, though many cases are asymptomatic. Diagnosis involves tests like CT angiography, ventilation-perfusion scanning, ultrasound, and D-dimer level. Treatment consists of oxygen, anticoagulation with heparin or warfarin, and sometimes thrombolysis for large clots or right heart strain. Long-term anticoagulation aims to prevent future 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 provides an overview of acute pulmonary embolism (PE). It discusses the pathophysiology, signs and symptoms, differential diagnosis, types, investigations and treatment of PE. Regarding treatment, it describes the use of oxygen therapy, anticoagulation including unfractionated heparin, warfarin and novel oral anticoagulants. It also discusses reperfusion treatments such as thrombolytic therapy and percutaneous catheter-directed treatment, as well as the use of vena cava filters. The document provides detailed information on diagnostic testing and therapeutic approaches for acute pulmonary embolism.
Acute pulmonary embolism is a form of venous thromboembolism that occurs when a blood clot breaks off and lodges in the pulmonary arteries of the lungs. The clinical presentation of PE can be variable and non-specific, making diagnosis challenging. It is important to efficiently evaluate patients suspected of having a PE to diagnose and treat it quickly in order to reduce morbidity and mortality. Treatment involves hemodynamic and respiratory support, initial anticoagulation with drugs like heparin, and potentially reperfusion therapies for more severe cases including thrombolysis or embolectomy.
- Acute pulmonary embolism (PE) is a common cardiovascular condition caused by obstruction of the pulmonary arteries by blood clots.
- Diagnosis can be difficult as symptoms are nonspecific, but includes dyspnea, chest pain, syncope. Imaging tests like CT pulmonary angiography or ventilation-perfusion scanning are used to diagnose PE.
- Treatment involves anticoagulation to prevent further clot growth. For high risk PE with hemodynamic instability, thrombolysis or embolectomy may be used to rapidly restore blood flow. Risk stratification guides duration of anticoagulation which is typically 3-6 months or longer for recurrent PE or persistent risk factors.
Rehabilitation of patient with pleural effusionAdemola Adeyemo
1) Pulmonary embolism occurs when a blood clot blocks an artery in the lungs, and can cause pleural effusions in about 30% of cases. Physiotherapy is an important part of managing patients with pleural effusions secondary to pulmonary embolism.
2) Physiotherapy includes techniques like incentive spirometry, chest physiotherapy, and exercises to improve cardiopulmonary function and endurance. Drainage of fluid from chest tubes is also facilitated.
3) As the patient's condition improves with physiotherapy, their ability to exercise intensifies and shortness of breath decreases, with the goal of restoring independence and fitness.
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 provides information on the anaesthetic management of surgery for Tetralogy of Fallot (TOF). It describes the key anatomical features of TOF and its variants. It outlines the natural history of untreated TOF, including risks of cyanotic spells, heart failure and early death. The document discusses the goals of palliative and corrective surgeries, including the modified Blalock-Taussig shunt. It provides guidance on preoperative evaluation, intraoperative management and goals of anaesthesia to optimize hemodynamics and oxygenation during surgery.
1. Pulmonary arteriovenous malformations (PAVMs) are rare vascular anomalies where abnormal dilated vessels provide a right-to-left shunt between the pulmonary artery and vein.
2. PAVMs are usually diagnosed through imaging like chest X-ray, CT, or MRI which show dilated vessels. Right-to-left shunting can be detected using echocardiography, oxygen studies, or pulmonary angiography.
3. Treatment involves embolization to occlude the abnormal vessels which successfully treats over 99% of PAVMs. Surgery is an alternative for cases that cannot be embolized or if embolization fails.
Imaging of Pulmonary Vascular Lesions ``Gamal Agmy
This document contains a series of questions and answers about the management of pulmonary embolism from Gamal Agmy, a professor of chest diseases. It discusses issues such as when to use thrombolysis for intermediate risk PE, the risks of thrombolysis for patients with recent surgery or stroke, and alternatives to thrombolysis if it is deemed too unsafe. It also addresses questions about managing PE in pregnant patients, PE with right atrial thrombus, and the appropriate use of IVC filters.
This document discusses pulmonary embolism (PE), including its epidemiology, disease burden, risk factors, pathophysiology, signs and symptoms, diagnostic evaluation, and treatment approaches. It notes that PE has an annual incidence of 100-200 per 100,000 people. Diagnostic evaluations discussed include assessment of clinical probability, D-dimer testing, CT pulmonary angiography, lung scintigraphy, and echocardiography. Treatment of acute PE involves hemodynamic support, anticoagulation with unfractionated heparin, low molecular weight heparin or fondaparinux, and potentially thrombolysis for high-risk cases.
The document discusses the stepwise management of hemoptysis. It defines hemoptysis and massive hemoptysis. The most common causes in Egypt are discussed. Steps in diagnosis include history, exams, labs, imaging like CXR, CT, bronchoscopy. Treatment depends on localization and cause but may include bronchoscopic interventions, bronchial artery embolization, or surgery. Disease-specific approaches are also outlined. Three case studies are presented to demonstrate tailored management of hemoptysis.
Thorax cardio adult dyspnea imaging g ferrettiJFIM
The document discusses dyspnea (shortness of breath), which is a common symptom in patients presenting to the emergency department with thoracic diseases. High-resolution computed tomography (HRCT) is highlighted as the best non-invasive tool for evaluating dyspnea, as it can identify underlying causes such as emphysema, asthma, pulmonary embolism, and interstitial lung diseases. The document presents several case examples where HRCT provided a diagnosis when other tests were nondiagnostic or revealed atypical features of diseases. HRCT is particularly useful when initial clinical exams and tests fail to identify a cause of dyspnea.
The document discusses postoperative care and monitoring of surgical patients. It covers assessing vital signs, pain, mobility and complications in various body systems. Common complications include respiratory issues like atelectasis, cardiovascular problems like hypotension, and gastrointestinal issues like nausea. It provides guidance on monitoring for and managing specific complications, as well as care aspects for different surgical specialties. Regular evaluation of patient progress and problems is emphasized.
This document provides an overview of pediatric anesthesia for congenital heart disease (CHD). It defines CHD and discusses classifications including cyanotic vs acyanotic defects. Key pathophysiology and anesthesia management are described for common defects like tetralogy of Fallot, transposition of the great arteries, atrial septal defects, ventricular septal defects, and patent ductus arteriosus. The objectives are to define CHD subtypes, discuss problems anesthesiologists may encounter, explain pathophysiology and implications for anesthesia, and how to manage CHD patients undergoing surgery.
Muscular dystrophy is a heterogeneous group of inherited disorders characterized by progressive muscle weakness and loss of muscle tissue. There are several classifications including sex-linked, autosomal recessive, and autosomal dominant forms that depend on the causative gene, age of onset, and symptoms. Duchenne muscular dystrophy is the most common and severe type that primarily affects males, causes muscle degeneration starting in childhood, and leads to death in the third decade without treatment. Other forms include limb-girdle, facioscapulohumeral, and congenital muscular dystrophies that have varying inheritance patterns, muscle involvement, and progression of symptoms. Treatment focuses on managing symptoms and complications to maximize quality of life.
A bone tumor is an abnormal growth of cells within a bone. There are two main types: benign tumors, which are non-cancerous, and malignant tumors, which are cancerous and can spread. Common benign bone tumors include osteochondromas, non-ossifying fibromas, and enchondromas. Primary malignant bone cancers include osteosarcoma, Ewing sarcoma, and chondrosarcoma. Secondary bone cancers spread from other parts of the body like the breast, prostate, or lungs. Diagnosis involves imaging tests, biopsies, and blood/urine tests. Treatment depends on whether the tumor is benign or malignant but may include surgery, radiation, chemotherapy, or cryos
This presentation provides an overview of cardiac failure, including its definition, types, causes, symptoms, diagnosis, and treatment options. Cardiac failure, also known as heart failure, occurs when the heart is unable to pump enough blood to meet the body's needs. It discusses the two main types - left and right cardiac failure - and covers the signs and symptoms. Common causes of cardiac failure include coronary artery disease, heart attack, high blood pressure, and heart muscle diseases. Diagnosis involves tests such as blood tests, electrocardiograms, and echocardiograms. Treatment focuses on medications and lifestyle changes, with surgery being less common except in some cases.
Neck pain is caused by abnormalities in the soft tissues or bones of the cervical spine. The most common causes are muscle strains or injuries from wear and tear. Cervical disc disease and cervical spondylosis are also common, where discs bulge or herniate, narrowing the spinal column and compressing nerves. Treatment involves physical therapy, medications like NSAIDs, and sometimes surgery to decompress the nerves.
This document discusses various chest wall deformities and conditions that affect the structure and function of the chest wall. It covers scoliosis, pectus excavatum, ankylosing spondylitis, flail chest, thoracoplasty, pectus carinatum, Poland Syndrome, and chest wall tumors. For each condition, it describes the presentation, pathophysiology, clinical features, treatment options, and relevant anatomy and imaging findings.
This document defines key terms related to orthotics and prosthetics. It describes different causes of amputation including trauma, vascular issues, infections, and tumors. The stages of rehabilitation for an amputee are outlined, including pre-amputation counseling, surgery, post-operative care, prosthetic training, and reintegration. Different levels of extremity amputation and criteria for a good stump are also defined. The roles of an interdisciplinary rehabilitation team are emphasized.
This document discusses several hand disorders and conditions, including ulnar nerve injuries, Dupuytren's contracture, and Volkmann's ischemic contracture. It notes the anatomical structures involved in ulnar nerve injuries, such as the ulnar nerve, medial epicondyle, and flexor carpi ulnaris arcade. Dupuytren's contracture involves thickening of the palmar aponeurosis. Volkmann's ischemic contracture can result from a supracondylar humeral fracture causing reduced blood flow to the forearm muscles.
Varicose veins are dilated, tortuous veins caused by valve incompetence allowing blood to pool. Key risk factors include aging, family history, pregnancy, obesity, and occupations requiring long periods of standing. Patients present with darkened, bulging veins and symptoms like aching, heaviness, and cramping. Diagnosis involves physical exam and ultrasound, with treatment ranging from compression stockings to sclerotherapy, laser ablation, and surgery depending on severity. Self-care like exercise, weight loss, and elevation can help prevent worsening.
A gamma camera detects gamma rays emitted by radiotracers introduced into the body and uses this information to create images. It consists of a collimator, NaI(Tl) crystal, photomultiplier tubes, preamplifier, amplifier, pulse height analyzer, data analysis computer, and display. The gamma rays are detected by the crystal and converted to light, which is converted to electrical signals by photomultiplier tubes and processed by the computer to produce anatomical images showing the distribution of radioactive tracer in the body. Gamma cameras are used to detect medical problems like cancer tumors, bone fractures, and abnormal organ function.
This document discusses Raynaud's disease, which causes some areas of the body to feel numb and cold in response to stress or cold temperatures. There are two main types - primary Raynaud's disease, which has no underlying cause, and secondary Raynaud's, which is caused by an associated condition. Symptoms include fingers and toes turning white then blue. Diagnosis involves medical history and physical exam, and sometimes tests like nail fold capillaroscopy or blood tests. Treatment options for more severe cases include calcium channel blockers, vasodilators, nerve surgery, or chemical injections.
This document discusses several types of soft tissue injuries and arthritis conditions. It provides information on closed soft tissue injuries like contusions and hematomas. It also outlines general wound treatment concepts and essential nutrients for healing. Several common forms of arthritis are then described, including osteoarthritis, spondylosis, juvenile arthritis, tuberculous arthritis, gout, hemophilic arthritis, neuropathic arthritis, ankylosing spondylitis, and psoriatic arthritis. For each condition, it discusses causes, symptoms, and typical treatment approaches.
MRI uses strong magnets and radio waves to produce detailed images of the inside of the body without using ionizing radiation. It has important applications in neurology and musculoskeletal imaging. The MRI machine consists of a powerful magnet that aligns hydrogen atoms, gradient coils to vary the magnetic field, and RF coils used to transmit pulses and receive signals. During an MRI scan, the patient lies within the magnet while RF pulses are used to alter the hydrogen atom alignment and produce signals used to create images, with different sequences like T1-weighted and T2-weighted yielding different tissue contrasts.
This document discusses the management of soft tissue injuries in different parts of the body. It defines soft tissues as muscles, ligaments, tendons, bursae and fascia. It describes the symptoms and degrees of injuries to these tissues like strains, sprains and tears. It discusses the non-operative and operative management of soft tissue injuries in the shoulder, elbow, wrist, hand, hip, knee, ankle and foot regions. The management involves educating patients, controlling pain and edema, maintaining joint mobility and muscle integrity, and progressing from passive to active range of motion exercises. Precautions to prevent further injury are also outlined.
This document summarizes various shoulder injuries including sprains, dislocations, instability, tendon injuries, and bursitis. It describes the mechanisms of injury, signs and symptoms, special tests used for diagnosis, and diagnostic procedures for sternoclavicular joint sprain, acromioclavicular joint sprain, glenohumeral dislocations, glenohumeral instability, rotator cuff injuries, bicep tendon injuries, and subacromial/subdeltoid bursitis.
The document discusses tertiary and quaternary protein structures. It defines tertiary structure as the specific 3D shape of a protein based on interactions between amino acid side chains. Tertiary structure results from disulfide bonds, hydrophobic interactions, hydrogen bonds, ionic interactions, and Van der Waals forces. Quaternary structure refers to the assembly of multiple polypeptide subunits into a single functional protein. Protein folding and molecular chaperones facilitate proper tertiary and quaternary structure formation.
This document discusses several clinically important gram positive cocci including Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae, Enterococcus faecalis and Enterococcus faecium. It describes their characteristic morphology, hemolysis patterns on culture, identification tests and the diseases they commonly cause. Diagnosis involves gram stain, culture and identification of colonies based on catalase, bile solubility and sensitivity to specific antibiotics. These bacteria are a major cause of community and hospital-acquired infections.
This document provides an overview of the Physical Agents & Electrotherapy II course. It discusses the course structure, including lectures, labs, assessments, and textbooks. It then defines electrotherapy and provides examples like ultrasound, TENS, EMS. The document covers various types of currents, safety guidelines, the healing process, electrical charges in the body, and different electrotherapy modalities like ultrasound, traction, compression, laser therapy. Risks, indications and contraindications are discussed for each modality.
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1. Pneumothorax
DR.M.Shahid Shabbir
DPT.MS,NMPT
( NEUROMUSCULAR REHAB SPECIALIST )
DPT lecturer and clinical incharge ZIHS
Pneumothorax is the presence of air in the pleural space, which can
either occur spontaneously, or result from iatrogenic injury or trauma
to the lung or chest wall. Primary spontaneous pneumothorax
occurs in patients with no history of lung disease. It principally
affects males aged 15–30 in whom smoking, tall stature and the
presence of apical subpleural blebs are additional risk factors.
Secondary pneumothorax affects patients with pre-existing lung
disease, especially COPD, bullous emphysema and asthma. It is
most common in older patients and is associated with the
highest mortality rates.
2. Clinical features
• There is sudden-onset unilateral pleuritic chest pain or breathlessness (those
with underlying chest disease may have severe breathlessness).
• With a small pneumothorax the physical examination may be normal; a larger
pneumothorax (>15% of the hemithorax) results in decreased or absent breath
sounds and a resonant percussion note.
• A tension pneumothorax occurs when a small communication acts as a one-way valve
allowing air to enter the pleural space from the lung during inspiration but not
to escape on expiration; this causes raised intrapleural pressure which leads to
mediastinal displacement, compression of the opposite lung and impaired systemic
venous return and cardiovascular compromise.
Investigations
CXR shows the sharply defined edge of the deflated lung with complete lack of
lung markings between this and the chest wall. CXR also shows any mediastinal
displacement and gives information regarding the presence or absence of pleural
fluid and underlying pulmonary disease. Care must be taken to differentiate
between a large pre-existing emphysematous bulla and a pneumothorax to avoid
misdirected attempts at aspiration; where doubt exists, CT is useful in distinguishing
bullae from pleural air.
3. Management
• Primary pneumothorax, where the lung edge is <2 cm from the chest wall and the
patient is not breathless, normally resolves without intervention.
• In young patients presenting with a moderate or large spontaneous primary
pneumothorax an attempt at percutaneous needle aspiration of air should be
made in the first instance, with a 60–80% chance of avoiding the need for a chest drain.
• Patients with chronic lung disease always require a chest tube and inpatient
observation, as even a small pneumothorax may cause respiratory failure.
Intercostal drains should be inserted in the 4th, 5th or 6th intercostal space in
the mid-axillary line, following blunt dissection through to the parietal pleura, or
by using a guidewire and dilator (‘Seldinger’ technique). The tube should be advanced
in an apical direction, connected to an under-water seal or one-way Heimlich valve, and
secured firmly to the chest wall. Clamping of the drain is potentially dangerous and
never indicated. The drain should be removed 24 hrs after the lung has fully
reinflated and bub-bling stopped. Continued bubbling after 5–7 days is an
indication for surgery. Supplemental oxygen is given, as this accelerates the rate at
which air is reabsorbed by the pleura. Patients with a closed pneumothorax should not
fly until the pneumothorax has resolved, as the trapped gas expands at altitude.
Patients should be advised to stop smoking and be informed about the risks of a
recurrent pneumothorax (25% after primary spontaneous pneumothorax).
4. Recurrent spontaneous pneumothorax:
Surgical pleurodesis, with thoracoscopic pleural abrasion or
pleurectomy, is recommended in all patients following a second
pneumothorax (even if ipsilateral), and should be considered following
the first episode of secondary pneumothorax if low respiratory
reserve makes recurrence hazardous. Patients who plan to continue
activities where pneumothorax would be particularly dangerous
(e.g. diving) should also undergo definitive treatment after the first
episode of a primary spontaneous pneumothorax.
5. Pulmonary Embolism
VENOUS THROMBOEMBOLISM
Deep venous thrombosis (DVT) and pulmonary embolism (PE) can be considered
under the heading of venous thromboembolism (VTE). The majority (75%) of PEs
arise from the propagation of lower limb DVT. PE is common, occurring in ∼1% of all
patients admitted to hospital and accounting for ∼5% of in-hospital deaths. Amniotic
fluid, placenta, air, fat, tumour (especially choriocarcinoma) and septic emboli (from
endocarditis affecting the tricuspid/pulmonary valves) are rare.
Clinical features
The varied clinical presentation, non-specific nature of the physical signs and the
lack of sensitive and specific diagnostic tests can make the diagnosis of PE difficult. It is
helpful to consider three questions:
• Is the clinical presentation consistent with PE?
• Does the patient have risk factors for PE?
• Is there any alternative diagnosis that can explain the patient’s
presentation? A recognized risk factor for PE is present in 80–90% of patients.
The clinical features depend largely upon the size of embolism and comorbidity.
6. Investigations
CXR: PE may give rise to a variety of non-specific appearances but may be normal. A
normal CXR in an acutely breathless and hypoxaemic patient should raise the
suspicion of PE, as should bilateral changes in a patient with unilateral pleuritic
chest pain. CXR can also exclude alternatives such as heart failure, pneumonia or
pneumothorax.
ECG: ECG changes in PE are common but usually non-specific. The most common
findings are a sinus tachycardia and anterior T-wave inversion; larger emboli may
cause right heart strain revealed by an S1Q3T3pattern, ST-segment and T-wave
changes, or right bundle branch block. The ECG may also suggest an alternative
diagnosis such as myocardial infarction and pericarditis.
ABG: Typically show a reduced PaO2 and a normal or low PaCO2, but are occasionally
normal. Metabolic acidosis may occur in acute massive PE with cardiovascular
collapse.
D-dimer: This is a specific degradation product released into the circulation when
cross-linked fi brin undergoes endogenous fibrinolysis. A low D-dimer level has a high
negative predictive value and is a useful screening test. However, a suggestive clinical
picture in a high-risk patient must be investigated further even when the D-dimer level
is normal. Non-specific elevation of the D-dimer is observed in a number of
conditions other than PE, including myocardial infarction, pneumonia and sepsis.
7. CT pulmonary angiography (CTPA): The development of rapid acquisition helical CT
scanners has popularised the use of CTPA. It not only may exclude PE but may also
reveal an alternative diagnosis. Limited resolution may hinder the detection of small
peripheral emboli but further advances in CT are likely to improve this.
Ventilation–perfusion scanning: The sensitivity and specificity of V./Q. scanning
are enhanced by a clinical probability assessment. A normal V./Q. scan virtually
excludes PE, and a low-probability scan in the presence of a low clinical probability
makes PE unlikely. Similarly, the presence of a high-probability scan in a patient
with a high clinical probability almost certainly establishes the diagnosis of PE.
However, V./Q. scanning is of limited value when PE is suspected in patients with
pre-existing cardiopulmonary pathology (e.g. COPD or cardiac failure) because in
these cases 70% of scans are indeterminate.
Doppler USS of the leg veins: This is the investigation of choice in patients
with clinical DVT, but may also be applied to patients in whom PE is suspected,
particularly if there are clinical signs in a limb, as many will have identifiable
proximal thrombus in the leg veins.
8. Echocardiography: This is helpful in the differential diagnosis and assessment of
acute circulatory collapse. Acute dilatation of the right heart is usually present in
massive PE, and thrombus (embolism in transit) may be visible. Alternative diagnoses,
including left ventricular failure, aortic dissection and pericardial tamponade, can
usually be established with confidence.
Pulmonary angiography: This has largely been superseded by CTPA.
Management
• Oxygen should be given to all hypoxaemic patients in a concentration
necessary to restore SpO2 to >90%.
• Hypotension should be treated by giving i.v. fluid or plasma expander; diuretics
and vasodilators should be avoided.
• Opiates may be necessary to relieve pain and distress but should be used with
caution.
• Resuscitation by external cardiac massage may be successful in the moribund
patient by dislodging and breaking up a large central embolus
9. Anticoagulation: Should be commenced immediately in patients with a high or
intermediate probability of PE, but can usually be safely withheld from patients with a
low clinical probability pending further investigation. Low molecular weight heparin
administered subcutaneously is as effective as i.v. unfractionated heparin and easier
to administer. The dose is standardised for the weight of the patient and does
not require monitoring by tests of coagulation. Heparin is effective in reducing
mortality in PE by reducing the propagation of clot and the risk of further
emboli. It should be administered for at least 5 days and anticoagulation continued
using oral warfarin. Heparin should not be discontinued until the international
normalised ratio (INR) is >2. The optimum duration of warfarin therapy is not clear.
Current guidelines suggest that patients with an underlying prothrombotic risk or a
history of previous emboli should be anticoagulated for life. Those with a reversible
risk factor require 3 mths of therapy, although 6 wks may be sufficient for some.
Six mths of therapy is currently recommended for idiopathic VTE.
Thrombolytic therapy: Thrombolysis appears to improve outcome when acute
massive PE is accompanied by shock, but it is not clear whether there is any advantage
of thrombolysis over heparin in patients with a normal BP. Patients with PE appear
to have a high risk of intracranial haemorrhage and must be screened carefully for
haemorrhagic risk.
10. Caval filters: Selected patients with recurrent PE despite adequate anti-coagulation,
or those in whom anticoagulation is contraindicated, may benefit from insertion of
a filter in the inferior vena cava below the origin of the renal vessels.
Prognosis
Patients who develop PE after an operation have the lowest recurrence rate; in other
groups, recurrence rates may be as high as 9%/yr. Echocardiographic evidence of
right ventricular dysfunction identifies patients at risk of developing cardiogenic
shock and an increased risk of death. Persistent pulmonary hypertension and right
ventricular dysfunction 6 wks after PE identify high-risk patients with an increased
likelihood of developing overt right ventricular failure over the next 5 yrs.