Upper extremity arterial disease can be caused by large vessel occlusive diseases like atherosclerosis or embolism, or small vessel diseases like autoimmune disorders. Symptoms range from Raynaud's phenomenon to acute ischemia with pain and pallor. Evaluation involves vascular exams, imaging like ultrasound and angiography. Treatment depends on severity and includes medications for vasospasm, endovascular interventions for stenoses, or open surgery for severe occlusions.
This document provides an overview of infective endocarditis, including its definition, classification, epidemiology, pathogenesis, clinical manifestations, diagnosis, treatment, complications and prophylaxis. Some key points:
- Infective endocarditis is an infection of the heart valves or endocardial surface. It is classified based on location and causative organism.
- Common symptoms include fever, heart murmur, heart failure and embolic phenomena. Vegetations may be seen on echocardiography.
- Diagnosis is based on the modified Duke criteria, which consider clinical features, blood culture results and echocardiographic findings.
- Treatment involves parenteral antibiotics tailored to the causative organism. Surgery
Constrictive pericarditis is caused by scarring and thickening of the pericardium, restricting cardiac filling. It is diagnosed using echocardiography which shows septal bounce, exaggerated mitral inflow, and hepatic vein reversal. While similar to restrictive cardiomyopathy, constrictive pericarditis shows increased ventricular interaction and respiratory effects on cardiac physiology. Surgical pericardiectomy is usually required for treatment but is high risk, with post-op complications common. Long-term survival depends on the underlying cause of constriction.
Atrial septal defect (ASD) closure can be performed surgically or percutaneously. Percutaneous closure is preferred for secundum ASDs that meet criteria such as defect size less than 38mm and adequate rim tissue. Echocardiography guides device placement and confirms closure. Complications include device embolization, arrhythmias, and erosion. Most studies report high success rates with percutaneous closure and shorter hospital stays than surgery. Surgical closure is preferred for sinus venosus, primum, or coronary sinus defects.
This document provides information about a seminar on aortic dissection presented by Monika Devi. It discusses the introduction, types, causes, symptoms, risk factors, diagnosis, treatment, complications and prevention of aortic dissection. The two main types are Type A, which involves the ascending aorta, and Type B, which only involves the descending aorta. Causes include high blood pressure, genetic conditions like Marfan syndrome, and traumatic injury. Symptoms can include chest pain and symptoms of a stroke. Treatment depends on the type but may involve medications to lower blood pressure or surgery to repair the tear in the aorta. Complications can include death, organ damage or stroke if not properly treated.
1. Left bundle branch block (LBBB) is a conduction abnormality caused by impaired conduction in the left bundle branch or its fascicles.
2. LBBB can be chronic or intermittent and is often caused by coronary artery disease or hypertension.
3. On ECG, LBBB is characterized by a QRS duration ≥120ms and other abnormalities including broad R waves and abnormal ST-T wave patterns.
4. LBBB can make ECG diagnosis of myocardial infarction difficult and criteria like Sgarbossa scores are used to help identify MI in the setting of LBBB.
This document discusses coarctation of the aorta, including its embryology, nomenclature, pathophysiology, natural history, and clinical features. Some key points include:
- Coarctation of the aorta is a congenital narrowing of the aorta near the ductus arteriosus. Left untreated, 50% of patients will die within 10 years primarily due to heart failure.
- Associated anomalies include ventricular septal defects (40% of cases) and bicuspid aortic valves (46% of cases).
- Long-term complications include hypertension, aneurysm formation, dissection, and rupture.
- Natural history studies show mortality rates increase significantly from 25% at age
ARVC is a heritable heart muscle disorder that predominantly affects the right ventricle. It is caused by genetic defects in cardiac desmosomes, which are important for cell-to-cell adhesion. This leads to progressive loss of right ventricular myocardium and replacement by fibrofatty tissue. ARVC can cause dangerous ventricular arrhythmias and is a leading cause of sudden cardiac death in young people. Diagnosis involves imaging tests and electrocardiography to detect right ventricular structural abnormalities and arrhythmias.
Takotsubo cardiomyopathy (TC), also known as "broken heart syndrome", is an acute cardiac syndrome that presents similarly to acute coronary syndrome (ACS) but is caused by transient left ventricular dysfunction rather than coronary artery blockages. It often occurs in post-menopausal women in response to severe emotional or physical stress and is characterized by abnormal ventriculograms showing apical ballooning of the left ventricle. While difficult to distinguish from ACS initially, differentiating the two is important to avoid unnecessary thrombolysis in TC patients. The pathophysiology of TC involves excess catecholamine release and microvascular dysfunction resulting in reversible myocardial stunning.
This document provides an overview of infective endocarditis, including its definition, classification, epidemiology, pathogenesis, clinical manifestations, diagnosis, treatment, complications and prophylaxis. Some key points:
- Infective endocarditis is an infection of the heart valves or endocardial surface. It is classified based on location and causative organism.
- Common symptoms include fever, heart murmur, heart failure and embolic phenomena. Vegetations may be seen on echocardiography.
- Diagnosis is based on the modified Duke criteria, which consider clinical features, blood culture results and echocardiographic findings.
- Treatment involves parenteral antibiotics tailored to the causative organism. Surgery
Constrictive pericarditis is caused by scarring and thickening of the pericardium, restricting cardiac filling. It is diagnosed using echocardiography which shows septal bounce, exaggerated mitral inflow, and hepatic vein reversal. While similar to restrictive cardiomyopathy, constrictive pericarditis shows increased ventricular interaction and respiratory effects on cardiac physiology. Surgical pericardiectomy is usually required for treatment but is high risk, with post-op complications common. Long-term survival depends on the underlying cause of constriction.
Atrial septal defect (ASD) closure can be performed surgically or percutaneously. Percutaneous closure is preferred for secundum ASDs that meet criteria such as defect size less than 38mm and adequate rim tissue. Echocardiography guides device placement and confirms closure. Complications include device embolization, arrhythmias, and erosion. Most studies report high success rates with percutaneous closure and shorter hospital stays than surgery. Surgical closure is preferred for sinus venosus, primum, or coronary sinus defects.
This document provides information about a seminar on aortic dissection presented by Monika Devi. It discusses the introduction, types, causes, symptoms, risk factors, diagnosis, treatment, complications and prevention of aortic dissection. The two main types are Type A, which involves the ascending aorta, and Type B, which only involves the descending aorta. Causes include high blood pressure, genetic conditions like Marfan syndrome, and traumatic injury. Symptoms can include chest pain and symptoms of a stroke. Treatment depends on the type but may involve medications to lower blood pressure or surgery to repair the tear in the aorta. Complications can include death, organ damage or stroke if not properly treated.
1. Left bundle branch block (LBBB) is a conduction abnormality caused by impaired conduction in the left bundle branch or its fascicles.
2. LBBB can be chronic or intermittent and is often caused by coronary artery disease or hypertension.
3. On ECG, LBBB is characterized by a QRS duration ≥120ms and other abnormalities including broad R waves and abnormal ST-T wave patterns.
4. LBBB can make ECG diagnosis of myocardial infarction difficult and criteria like Sgarbossa scores are used to help identify MI in the setting of LBBB.
This document discusses coarctation of the aorta, including its embryology, nomenclature, pathophysiology, natural history, and clinical features. Some key points include:
- Coarctation of the aorta is a congenital narrowing of the aorta near the ductus arteriosus. Left untreated, 50% of patients will die within 10 years primarily due to heart failure.
- Associated anomalies include ventricular septal defects (40% of cases) and bicuspid aortic valves (46% of cases).
- Long-term complications include hypertension, aneurysm formation, dissection, and rupture.
- Natural history studies show mortality rates increase significantly from 25% at age
ARVC is a heritable heart muscle disorder that predominantly affects the right ventricle. It is caused by genetic defects in cardiac desmosomes, which are important for cell-to-cell adhesion. This leads to progressive loss of right ventricular myocardium and replacement by fibrofatty tissue. ARVC can cause dangerous ventricular arrhythmias and is a leading cause of sudden cardiac death in young people. Diagnosis involves imaging tests and electrocardiography to detect right ventricular structural abnormalities and arrhythmias.
Takotsubo cardiomyopathy (TC), also known as "broken heart syndrome", is an acute cardiac syndrome that presents similarly to acute coronary syndrome (ACS) but is caused by transient left ventricular dysfunction rather than coronary artery blockages. It often occurs in post-menopausal women in response to severe emotional or physical stress and is characterized by abnormal ventriculograms showing apical ballooning of the left ventricle. While difficult to distinguish from ACS initially, differentiating the two is important to avoid unnecessary thrombolysis in TC patients. The pathophysiology of TC involves excess catecholamine release and microvascular dysfunction resulting in reversible myocardial stunning.
This document discusses the natural history of ventricular septal defects (VSDs). It covers the incidence, classification, factors influencing outcomes, and potential complications of VSDs over time, including:
1. Cardiac failure in large VSDs due to left-to-right shunting.
2. Spontaneous closure or diminution, which is more common in smaller defects and those under 10 years of age.
3. Complications such as right ventricular outflow tract obstruction, aortic valve prolapse, pulmonary vascular disease, infective endocarditis, and arrhythmias.
The classification, mechanisms of closure, and guidelines for antibiotic prophylaxis for infective endocard
This document discusses coarctation of the aorta, including:
1. The definition and history of coarctation as a congenital narrowing of the upper descending thoracic aorta.
2. Theories on the pathogenesis of coarctation related to reduced blood flow through the left side of the heart or abnormal ductal tissue.
3. Types of coarctation including preductal and postductal, and surgical techniques for repair such as patch aortoplasty or bypass grafting.
4. Presentation varies from heart failure in neonates to hypertension in older children and adults, with complications including aneurysm and rupture.
The document describes a case of a 46-year-old male who presented with sudden onset chest and back pain that progressed to weakness in his lower extremities. Imaging revealed an aortic dissection involving the ascending aorta and descending aorta. He underwent surgery to replace the dissected ascending aorta but later developed multiple complications and died. The document also reviews the classification, presentation, risk factors, diagnosis and management of aortic dissections.
This document discusses aortic aneurysms, including their anatomy, physiology, risk factors, diagnosis, and management. It provides details on:
1) The layers of the aortic wall and how they give the aorta elasticity and strength.
2) Factors that cause the aortic wall to stiffen with age like increases in collagen and calcification of elastic fibers.
3) Definitions of aortic aneurysm and classifications based on location and shape. Thoracic aortic aneurysms involve the ascending aorta while abdominal aortic aneurysms are infrarenal.
4) Screening recommendations, diagnosis using imaging like ultrasound, CT and echocardiography, and considerations for open surgical repair
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.
An aortic dissection occurs when blood tears the inner layer of the aorta, separating it from the middle layer. It is classified by location and timing of symptoms. Risk factors include hypertension, connective tissue disorders, and family history. Treatment depends on location but may include surgery, endovascular stent grafting, or medical management of blood pressure. Prognosis depends on type and treatment, with mortality rates declining with advances in surgical and endovascular techniques.
This document discusses hypertrophic cardiomyopathy (HCM), providing details on:
- Causes, including primary genetic and secondary forms
- Clinical manifestations such as asymmetrical septal hypertrophy in 70% of cases
- Prevalence of 0.2% in the population
- Risk factors for sudden cardiac death such as young age at presentation and family history
- Mechanisms of left ventricular outflow tract obstruction including systolic anterior motion of the mitral valve
- Echocardiographic findings and their implications for diagnosis and management
Single ventricle refers to congenital heart defects where there is only one functional ventricle supporting both the pulmonary and systemic circulations. There are various classifications, and the goal of treatment is to balance blood flow between the lungs and body. Initial medical management uses prostaglandins and aims for balanced pulmonary flow. Later stages involve surgical procedures like shunts, banding of arteries, and ultimately the Fontan procedure to separate circulation to the lungs and body without overloading the single ventricle. Complications can include arrhythmias, heart failure, and protein-losing enteropathy. Long term outcomes are improved with careful patient selection and multi-stage management to optimize hemodynamics at each stage.
Coarctation of the aorta is a congenital narrowing of the aorta near the site where the ductus arteriosus attaches. It can range from a localized stenosis to tubular hypoplasia of the aorta. Left untreated, it causes increased blood pressure in the upper body and heart complications due to increased workload. Surgical repair techniques include subclavian flap aortoplasty, end-to-end anastomosis, and patch angioplasty. Postoperative risks include recoarctation, spinal cord injury, and persistent hypertension. Long term follow up is needed due to risks of aneurysm and cardiovascular complications.
A 17-year-old male basketball player collapsed during practice and suffered cardiac arrest. An autopsy later revealed he had hypertrophic cardiomyopathy (HCM), a genetic heart condition where the heart muscle becomes abnormally thick. HCM is a leading cause of sudden cardiac death in young athletes. The patient had previously noticed some shortness of breath with exertion but it did not limit his activity. He was found to have a heart murmur as a child but it was never investigated. HCM causes the left ventricle to become thickened and stiff, which can obstruct blood flow out of the heart and cause heart failure, chest pain, arrhythmias, and sudden cardiac death.
A 50-year-old man presented with 3 hours of central chest pain. Initial investigations revealed a blood pressure of 90/60 and a normal ECG. A CT angiogram showed an intimal tear and dissection in the aortic arch. The patient was transferred urgently for surgical repair of a type A aortic dissection. Aortic dissection is a tear in the aortic wall that can propagate and cause complications if not treated. Diagnosis is made through imaging like CT scans. Emergent management involves stabilizing the patient's blood pressure and transferring patients with type A dissections for surgical intervention.
A 63-year-old man presented with syncope, shortness of breath, and other symptoms for 2 years. Examination found dyspnea, tachycardia, low blood pressure, a systolic thrill, and left ventricular hypertrophy. Imaging showed severe aortic stenosis. The patient underwent transcatheter aortic valve implantation and is now doing well.
Evaluation of prosthetic valve function and clinical utility.Ramachandra Barik
Many of the prosthesis-related complications can be prevented or their impact minimized through optimal prosthesis selection in the individual patient and careful medical management and follow-up after implantation.
Diagnosis, management, workup in a case of Takayasu's arteritis. Definition, synonyms, history, epidimiology, pathophysiology, etiology of Takayasu's arteritis.
The document discusses various pericardial diseases including acute pericarditis, constrictive pericarditis, pericardial effusion, and cardiac tamponade. It provides details on the anatomy and functions of the pericardium, pathophysiology, clinical features, diagnostic tests, and management of these conditions. Key points include that pericardial diseases can present with non-specific symptoms, clinical suspicion is important for diagnosis, and treatment depends on underlying etiology and presence of hemodynamic compromise. Differentiating constrictive pericarditis from restrictive cardiomyopathy is important as treatment approaches differ significantly.
This document provides an overview of acute aortic syndrome (AAS), including aortic dissection, intramural hematoma, penetrating aortic ulcer, and ruptured aortic aneurysm. It discusses the pathophysiology, imaging appearance and protocols, classification systems, and reporting considerations for each condition. CT and MRI are highlighted as the primary imaging modalities. The radiologist plays an important role in diagnosing AAS, determining treatment approaches such as endovascular intervention, and evaluating outcomes through follow up imaging. Proper technique and systematic reporting of anatomic details are essential for clinical management of these life-threatening aortic emergencies.
This document summarizes hypertrophic cardiomyopathy (HCM), an autosomal dominant genetic heart condition characterized by unexplained left ventricular hypertrophy. Key points include that it has a prevalence of 1 in 500 adults and is caused by over 200 mutations in genes involved in heart muscle proteins. Symptoms range from none to heart failure, arrhythmias, and sudden cardiac death. Diagnosis is typically made by echocardiogram showing left ventricular hypertrophy. Treatment involves managing symptoms and reducing risk of complications like sudden cardiac death.
This document discusses cardiac trauma, including traumatic aortic rupture and penetrating cardiac injuries. It provides details on:
- The pathophysiology, clinical features, diagnosis and treatment options for traumatic aortic rupture, including endovascular stenting or open surgical repair.
- The indications and techniques for emergency resuscitative thoracotomy to address penetrating cardiac injuries.
- The principles of managing blunt cardiac trauma and penetrating injuries, including decompressing cardiac tamponade, repairing lacerations, and addressing injuries to the coronary arteries.
Emergency surgical access methods like left anterolateral thoracotomy or clamshell thoracotomy are described for rapidly addressing life-threatening cardiac injuries.
The document describes the anatomy of the carotid arteries and their branches, evaluation and imaging of carotid artery disease, and treatment strategies including lifestyle modifications to reduce risk factors, carotid endarterectomy to remove plaques from significantly stenotic arteries, and outcomes data from clinical trials on endarterectomy for symptomatic and asymptomatic carotid stenosis. Imaging modalities like carotid duplex ultrasound, CTA, and MRA are described for evaluating the degree of carotid stenosis. The benefits of carotid endarterectomy are greater for symptomatic high-grade stenosis while more moderate for asymptomatic disease.
Atrial septal defect (ASD) is an abnormal opening in the wall separating the left and right atria of the heart. There are several types of ASDs including secundum, ostium primum, sinus venosus, and coronary sinus defects. ASDs are usually diagnosed through echocardiography which can determine the size and location of the defect. Small, asymptomatic ASDs may not require treatment, but larger defects with evidence of right heart strain often warrant closure either through open heart surgery or a nonsurgical approach using an implantable device delivered through catheters. Both methods effectively close the defect to prevent long-term complications like heart failure and pulmonary hypertension.
extra articular manifestation of rheumatoid arthritis.pptxGyaltsenTenzin1
Rheumatoid arthritis is a chronic inflammatory disease that causes swelling and stiffness in the joints. It can also cause extra-articular manifestations affecting various organs. The document discusses the epidemiology, etiology, clinical features, extra-articular manifestations and treatment of rheumatoid arthritis. It highlights that rheumatoid arthritis predominantly affects women aged 25-55 years and can involve the lungs, heart, blood vessels and skin. Treatment involves NSAIDs, corticosteroids, conventional DMARDs like methotrexate and biological DMARDs that target cytokines like TNF-alpha if first line treatments are inadequate.
This document discusses different types of vasculitis and disorders of blood vessel hyperreactivity. It describes how vasculitis can be caused by immune-mediated inflammation, direct infection, or physical/chemical injury. The main immunologic mechanisms are immune complex deposition, antineutrophil cytoplasmic antibodies, anti-endothelial cell antibodies, and autoreactive T cells. It also discusses Raynaud phenomenon and myocardial vessel vasospasm as examples of disorders involving exaggerated vasoconstriction.
This document discusses the natural history of ventricular septal defects (VSDs). It covers the incidence, classification, factors influencing outcomes, and potential complications of VSDs over time, including:
1. Cardiac failure in large VSDs due to left-to-right shunting.
2. Spontaneous closure or diminution, which is more common in smaller defects and those under 10 years of age.
3. Complications such as right ventricular outflow tract obstruction, aortic valve prolapse, pulmonary vascular disease, infective endocarditis, and arrhythmias.
The classification, mechanisms of closure, and guidelines for antibiotic prophylaxis for infective endocard
This document discusses coarctation of the aorta, including:
1. The definition and history of coarctation as a congenital narrowing of the upper descending thoracic aorta.
2. Theories on the pathogenesis of coarctation related to reduced blood flow through the left side of the heart or abnormal ductal tissue.
3. Types of coarctation including preductal and postductal, and surgical techniques for repair such as patch aortoplasty or bypass grafting.
4. Presentation varies from heart failure in neonates to hypertension in older children and adults, with complications including aneurysm and rupture.
The document describes a case of a 46-year-old male who presented with sudden onset chest and back pain that progressed to weakness in his lower extremities. Imaging revealed an aortic dissection involving the ascending aorta and descending aorta. He underwent surgery to replace the dissected ascending aorta but later developed multiple complications and died. The document also reviews the classification, presentation, risk factors, diagnosis and management of aortic dissections.
This document discusses aortic aneurysms, including their anatomy, physiology, risk factors, diagnosis, and management. It provides details on:
1) The layers of the aortic wall and how they give the aorta elasticity and strength.
2) Factors that cause the aortic wall to stiffen with age like increases in collagen and calcification of elastic fibers.
3) Definitions of aortic aneurysm and classifications based on location and shape. Thoracic aortic aneurysms involve the ascending aorta while abdominal aortic aneurysms are infrarenal.
4) Screening recommendations, diagnosis using imaging like ultrasound, CT and echocardiography, and considerations for open surgical repair
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.
An aortic dissection occurs when blood tears the inner layer of the aorta, separating it from the middle layer. It is classified by location and timing of symptoms. Risk factors include hypertension, connective tissue disorders, and family history. Treatment depends on location but may include surgery, endovascular stent grafting, or medical management of blood pressure. Prognosis depends on type and treatment, with mortality rates declining with advances in surgical and endovascular techniques.
This document discusses hypertrophic cardiomyopathy (HCM), providing details on:
- Causes, including primary genetic and secondary forms
- Clinical manifestations such as asymmetrical septal hypertrophy in 70% of cases
- Prevalence of 0.2% in the population
- Risk factors for sudden cardiac death such as young age at presentation and family history
- Mechanisms of left ventricular outflow tract obstruction including systolic anterior motion of the mitral valve
- Echocardiographic findings and their implications for diagnosis and management
Single ventricle refers to congenital heart defects where there is only one functional ventricle supporting both the pulmonary and systemic circulations. There are various classifications, and the goal of treatment is to balance blood flow between the lungs and body. Initial medical management uses prostaglandins and aims for balanced pulmonary flow. Later stages involve surgical procedures like shunts, banding of arteries, and ultimately the Fontan procedure to separate circulation to the lungs and body without overloading the single ventricle. Complications can include arrhythmias, heart failure, and protein-losing enteropathy. Long term outcomes are improved with careful patient selection and multi-stage management to optimize hemodynamics at each stage.
Coarctation of the aorta is a congenital narrowing of the aorta near the site where the ductus arteriosus attaches. It can range from a localized stenosis to tubular hypoplasia of the aorta. Left untreated, it causes increased blood pressure in the upper body and heart complications due to increased workload. Surgical repair techniques include subclavian flap aortoplasty, end-to-end anastomosis, and patch angioplasty. Postoperative risks include recoarctation, spinal cord injury, and persistent hypertension. Long term follow up is needed due to risks of aneurysm and cardiovascular complications.
A 17-year-old male basketball player collapsed during practice and suffered cardiac arrest. An autopsy later revealed he had hypertrophic cardiomyopathy (HCM), a genetic heart condition where the heart muscle becomes abnormally thick. HCM is a leading cause of sudden cardiac death in young athletes. The patient had previously noticed some shortness of breath with exertion but it did not limit his activity. He was found to have a heart murmur as a child but it was never investigated. HCM causes the left ventricle to become thickened and stiff, which can obstruct blood flow out of the heart and cause heart failure, chest pain, arrhythmias, and sudden cardiac death.
A 50-year-old man presented with 3 hours of central chest pain. Initial investigations revealed a blood pressure of 90/60 and a normal ECG. A CT angiogram showed an intimal tear and dissection in the aortic arch. The patient was transferred urgently for surgical repair of a type A aortic dissection. Aortic dissection is a tear in the aortic wall that can propagate and cause complications if not treated. Diagnosis is made through imaging like CT scans. Emergent management involves stabilizing the patient's blood pressure and transferring patients with type A dissections for surgical intervention.
A 63-year-old man presented with syncope, shortness of breath, and other symptoms for 2 years. Examination found dyspnea, tachycardia, low blood pressure, a systolic thrill, and left ventricular hypertrophy. Imaging showed severe aortic stenosis. The patient underwent transcatheter aortic valve implantation and is now doing well.
Evaluation of prosthetic valve function and clinical utility.Ramachandra Barik
Many of the prosthesis-related complications can be prevented or their impact minimized through optimal prosthesis selection in the individual patient and careful medical management and follow-up after implantation.
Diagnosis, management, workup in a case of Takayasu's arteritis. Definition, synonyms, history, epidimiology, pathophysiology, etiology of Takayasu's arteritis.
The document discusses various pericardial diseases including acute pericarditis, constrictive pericarditis, pericardial effusion, and cardiac tamponade. It provides details on the anatomy and functions of the pericardium, pathophysiology, clinical features, diagnostic tests, and management of these conditions. Key points include that pericardial diseases can present with non-specific symptoms, clinical suspicion is important for diagnosis, and treatment depends on underlying etiology and presence of hemodynamic compromise. Differentiating constrictive pericarditis from restrictive cardiomyopathy is important as treatment approaches differ significantly.
This document provides an overview of acute aortic syndrome (AAS), including aortic dissection, intramural hematoma, penetrating aortic ulcer, and ruptured aortic aneurysm. It discusses the pathophysiology, imaging appearance and protocols, classification systems, and reporting considerations for each condition. CT and MRI are highlighted as the primary imaging modalities. The radiologist plays an important role in diagnosing AAS, determining treatment approaches such as endovascular intervention, and evaluating outcomes through follow up imaging. Proper technique and systematic reporting of anatomic details are essential for clinical management of these life-threatening aortic emergencies.
This document summarizes hypertrophic cardiomyopathy (HCM), an autosomal dominant genetic heart condition characterized by unexplained left ventricular hypertrophy. Key points include that it has a prevalence of 1 in 500 adults and is caused by over 200 mutations in genes involved in heart muscle proteins. Symptoms range from none to heart failure, arrhythmias, and sudden cardiac death. Diagnosis is typically made by echocardiogram showing left ventricular hypertrophy. Treatment involves managing symptoms and reducing risk of complications like sudden cardiac death.
This document discusses cardiac trauma, including traumatic aortic rupture and penetrating cardiac injuries. It provides details on:
- The pathophysiology, clinical features, diagnosis and treatment options for traumatic aortic rupture, including endovascular stenting or open surgical repair.
- The indications and techniques for emergency resuscitative thoracotomy to address penetrating cardiac injuries.
- The principles of managing blunt cardiac trauma and penetrating injuries, including decompressing cardiac tamponade, repairing lacerations, and addressing injuries to the coronary arteries.
Emergency surgical access methods like left anterolateral thoracotomy or clamshell thoracotomy are described for rapidly addressing life-threatening cardiac injuries.
The document describes the anatomy of the carotid arteries and their branches, evaluation and imaging of carotid artery disease, and treatment strategies including lifestyle modifications to reduce risk factors, carotid endarterectomy to remove plaques from significantly stenotic arteries, and outcomes data from clinical trials on endarterectomy for symptomatic and asymptomatic carotid stenosis. Imaging modalities like carotid duplex ultrasound, CTA, and MRA are described for evaluating the degree of carotid stenosis. The benefits of carotid endarterectomy are greater for symptomatic high-grade stenosis while more moderate for asymptomatic disease.
Atrial septal defect (ASD) is an abnormal opening in the wall separating the left and right atria of the heart. There are several types of ASDs including secundum, ostium primum, sinus venosus, and coronary sinus defects. ASDs are usually diagnosed through echocardiography which can determine the size and location of the defect. Small, asymptomatic ASDs may not require treatment, but larger defects with evidence of right heart strain often warrant closure either through open heart surgery or a nonsurgical approach using an implantable device delivered through catheters. Both methods effectively close the defect to prevent long-term complications like heart failure and pulmonary hypertension.
extra articular manifestation of rheumatoid arthritis.pptxGyaltsenTenzin1
Rheumatoid arthritis is a chronic inflammatory disease that causes swelling and stiffness in the joints. It can also cause extra-articular manifestations affecting various organs. The document discusses the epidemiology, etiology, clinical features, extra-articular manifestations and treatment of rheumatoid arthritis. It highlights that rheumatoid arthritis predominantly affects women aged 25-55 years and can involve the lungs, heart, blood vessels and skin. Treatment involves NSAIDs, corticosteroids, conventional DMARDs like methotrexate and biological DMARDs that target cytokines like TNF-alpha if first line treatments are inadequate.
This document discusses different types of vasculitis and disorders of blood vessel hyperreactivity. It describes how vasculitis can be caused by immune-mediated inflammation, direct infection, or physical/chemical injury. The main immunologic mechanisms are immune complex deposition, antineutrophil cytoplasmic antibodies, anti-endothelial cell antibodies, and autoreactive T cells. It also discusses Raynaud phenomenon and myocardial vessel vasospasm as examples of disorders involving exaggerated vasoconstriction.
D. Fadhil Vasculitis-7 (Muhadharaty) (1).pptxhussainAltaher
Vasculitides are a group of rare diseases characterized by inflammation and necrosis of blood vessels. They are classified based on the size of affected vessels into large, medium, and small vessel vasculitis. Some of the main types discussed in the document include giant cell arteritis/polymyalgia rheumatica, Takayasu's arteritis, polyarteritis nodosa, Churg-Strauss syndrome, Wegener's granulomatosis, and Henoch Schonlein purpura. The document provides details on clinical features, investigations, treatments, and prognosis for each type of vasculitis.
Presentation1.pptx, radiological imaging of upper limb ischemia.Abdellah Nazeer
This document discusses radiological imaging techniques for evaluating upper limb ischemia. It begins by providing background on upper limb ischemia, noting it has varied etiologies including atherosclerosis, arteritis, and trauma. CT angiography is described as the preferred initial imaging technique, providing high-quality images of the entire arterial tree to precisely plan revascularization. Other techniques discussed include Doppler ultrasound, MRI, and invasive angiography. The document then provides several examples of upper limb CT angiography findings, demonstrating various pathologies like thrombosis, aneurysms, occlusions, and fistulas. In summary, the document outlines radiological evaluation and various pathologies of upper limb ischemia visualized on CT angiography.
Infective endocarditis is a condition where the inner lining of the heart (endocardium) becomes infected by bacteria or other microorganisms. It typically occurs where there is pre-existing heart valve damage. The infection can cause heart valve damage and formation of clumps (vegetations) that can break off and spread through the bloodstream (embolize). Presentation depends on the causative organism and can range from non-specific fever to new heart murmurs or signs of embolization. Diagnosis is based on blood cultures and echocardiography, while treatment involves prolonged antibiotic therapy and may require heart valve replacement surgery. Risk factors include rheumatic or congenital heart disease, prosthetic heart
This document discusses endocarditis and its association with stroke. There are two main types of endocarditis - infective endocarditis, caused by bacterial infection of the heart valves, and nonbacterial thrombotic endocarditis (NBTE), associated with cancer and lupus. Infective endocarditis carries risks of neurologic complications including ischemic or hemorrhagic stroke. Larger vegetations, location on the mitral valve, and certain organisms increase embolism risks. Treatment involves antibiotics but anticoagulation is generally not recommended due to bleeding risks. Neurologic complications influence management decisions.
The document summarizes various potential complications that can occur during or after cardiac catheterization. The major complications discussed include death, myocardial infarction, stroke, bleeding, vascular injury, and contrast induced nephrotoxicity. Risk factors for complications include patient demographics, cardiovascular anatomy, clinical situation, and operator experience. Local vascular complications like hematoma, pseudoaneurysm, arterial thrombosis are also described. Strategies to prevent complications involve careful technique, minimizing contrast and anticoagulation.
Vasculitis refers to inflammation of blood vessels. There are many types classified by the size of vessels involved and pathogenic mechanisms. Noninfectious vasculitis can be immune complex-mediated, associated with ANCAs, anti-endothelial cell antibodies, or autoreactive T cells. Infectious vasculitis involves direct invasion of vessels by pathogens. Common noninfectious vasculitides include giant cell arteritis, Takayasu arteritis, polyarteritis nodosa, Kawasaki disease, microscopic polyangiitis, Wegener's granulomatosis, Churg-Strauss syndrome, and Buerger's disease. Clinical manifestations depend on the organs involved. Treatment involves immunos
This document provides information about infective endocarditis:
- Infective endocarditis involves infection of the heart valves and inner lining of the heart. Common causes are bacteria entering the bloodstream from dental, respiratory, or other procedures.
- The infection can cause growths (vegetations) on the heart valves that can break off and block blood vessels in the brain, lungs, kidneys or other organs.
- Risk factors include previous heart damage, dental and surgical procedures, and some reproductive or congenital conditions. Investigations include blood tests, cultures, ECG and echocardiography. Complications may require surgery to repair or replace damaged valves.
Endocarditis presentation to internal medicine2019hospital
This document discusses infective endocarditis, including its definition, classification, common sites of involvement, risk factors, general lesions, mortality rates, and Osler's nodes and Janeway lesions as associated findings on physical examination. Key points covered include that infective endocarditis is an infection of the endocardial surface, most commonly involving the heart valves. It can be classified as acute or subacute/chronic based on temporal factors and severity. Overall mortality is around 40% usually due to heart failure from valve dysfunction. Having a prosthetic valve or previous endocarditis are major risk factors.
Superior Vena Cava Syndrome. Etiology and managementRomanusMapunda1
Superior vena cava (SVC) syndrome is a collection of clinical signs and symptoms resulting from either partial or complete obstruction of blood flow through the SVC.
This obstruction is most commonly a result of thrombus formation or tumor infiltration of the vessel wall.
Presentation about the hazards and potential complications that could happen in any cardiac or peripheral catheterization procedure and how to avoid them
This document discusses various types of arrhythmias and heart conditions including their causes, characteristics, and clinical presentations. It covers topics such as:
- Arrhythmias which can be initiated anywhere in the heart's conduction system and may present as tachycardia, bradycardia, or other irregular rhythms.
- Hypertension can lead to hypertensive heart disease over time due to increased pressure on the heart.
- Valvular heart diseases like rheumatic heart disease and degenerative valve diseases can cause stenosis or insufficiency of the heart valves.
- Infective endocarditis is a bacterial infection of the heart valves that forms vegetations and can cause embol
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Temporal arteritis (TA), also known as giant cell arteritis (GCA), is a systemic vasculitis that commonly affects medium and large arteries in adults over 50 years old. It is characterized by inflammation of the arteries, especially the temporal arteries, which can cause headaches. Left untreated, TA can lead to permanent vision loss by damaging the ophthalmic and retinal arteries. The cause is unknown but may involve a maladaptive immune response triggered by endothelial injury. Treatment involves high-dose corticosteroids to suppress inflammation.
This document provides an overview of vasculitis, including classification, pathophysiology, clinical manifestations, investigations, and management approaches. It discusses several specific large vessel vasculitides - giant cell arteritis, Takayasu arteritis, and polyarteritis nodosa. Giant cell arteritis commonly involves temporal arteries and causes headaches. Takayasu arteritis primarily affects the aorta and its branches. Polyarteritis nodosa preferentially involves the skin, nerves, gastrointestinal tract and kidneys. Diagnosis relies on tissue biopsy and imaging. Treatment focuses on glucocorticoids, with additional immunosuppressants for severe or refractory disease.
This document discusses infective endocarditis (IE), including its changing epidemiology, pathogenesis, clinical manifestations, diagnosis, complications, and management. Some key points:
- The median age of IE patients has increased to over 60 years old. Rheumatic heart disease is less common while intracardiac devices and nosocomial sources have risen.
- Vegetations form from platelet-fibrin deposition on damaged heart valves, allowing bacterial colonization and abscess formation.
- Echocardiography is important for diagnosis. Findings include vegetations, abscesses, and valve dysfunction. Blood cultures help identify causative organisms.
- Complications include heart failure, embolization, and periannular
Stanford Type A Aortic Dissection: a Complex Disease for Patients and Cardiot...Crimsonpublisherssmoaj
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1. Acute limb ischemia occurs due to a sudden decrease in blood flow to a limb, threatening the viability of the extremity. It requires prompt diagnosis and treatment to determine if the limb is viable, threatened, or irreversibly ischemic.
2. Initial management involves analgesia, oxygen, intravenous heparin, and urgent referral to a vascular specialist. Further imaging and either surgical or endovascular revascularization may be needed depending on the classification of ischemia.
3. The prognosis depends on factors like etiology and severity of ischemia. With timely treatment, limb salvage is possible in the majority of patients.
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2) Key risk factors for aneurysm rupture include diameter greater than 5.5 cm, female sex, smoking, and saccular aneurysm morphology. Imaging recommendations include ultrasound screening and CT or MRI for diagnosis.
3) Treatment is generally recommended for aneurysms greater than 5.5 cm in men or 5 cm in women, or those showing rapid growth. Immediate repair is indicated for ruptured aneurysms.
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1. Acute limb ischemia (ALI) occurs due to sudden deterioration of arterial blood supply to the limb. The main causes are thrombosis from atherosclerosis or embolism from cardiac sources.
2. ALI is clinically evaluated and classified into 3 classes based on severity of symptoms. Treatment depends on the class and involves early heparinization, catheter-directed thrombolysis, percutaneous thrombectomy, or surgical thrombectomy/bypass.
3. For less severe class I and IIA ALI, endovascular options like catheter-directed thrombolysis or pharmacomechanical thrombectomy are preferred to rapidly restore blood flow while minimizing risks. More severe class III ALI often requires emergency surgical intervention or
This document discusses penetrating aortic ulcers (PAUs), which are focal ulcerative lesions in the aortic wall. PAUs have unknown causes but are often associated with atherosclerosis. They can progress to pseudoaneurysms or ruptured aneurysms. Symptomatic PAUs usually require intervention to prevent rupture, while asymptomatic cases may be monitored. Computed tomography is the primary diagnostic tool and endovascular stent grafting is now usually the preferred treatment approach over open surgery due to lower risks, though complications can still occur.
1. Arterial aneurysms most commonly occur in the abdominal aorta and can be caused by degenerative processes, infections, trauma, or genetic conditions.
2. Abdominal aortic aneurysms are the most prevalent type of aneurysm in the United States and rupture of aneurysms is a serious complication.
3. Aneurysms can be classified by their morphology (fusiform vs. saccular), etiology (degenerative, inflammatory, infectious), and location (aortic, iliac, femoral, etc.). Management depends on the type and severity of the individual aneurysm.
Acute mesenteric arterial disease can result from occlusion of the mesenteric arteries or veins, reducing or stopping blood flow to the intestines. It has high morbidity and mortality rates of 60-70% despite aggressive treatment. Diagnosis involves clinical evaluation, lab tests, CT angiography and mesenteric angiography. Treatment depends on the severity and includes resuscitation, antibiotics, surgery to remove dead bowel and restore blood flow, and endovascular procedures in some cases. Prompt diagnosis and treatment is needed to prevent intestinal infarction and improve outcomes.
1. Autogenous vein grafts have histological properties that make them less than ideal as vascular conduits compared to arteries, such as a lack of vasa vasorum and compliance mismatch.
2. Prosthetic grafts are more standardized but have higher risk of thrombosis and intimal hyperplasia. Various modifications aim to improve patency such as heparin bonding and venous adjuncts.
3. Surveillance of vascular grafts with duplex ultrasound is important to detect failing grafts which can be treated with thrombectomy or new bypass to preserve limb.
1. Vascular surgery patients present unique challenges due to multiple comorbidities. Anesthesia aims to provide analgesia, amnesia, and muscle relaxation while minimizing physiologic stress.
2. Regional techniques like epidurals combined with light general anesthesia result in better outcomes for aortic and infrainguinal surgery compared to general anesthesia alone by reducing sympathetic activation.
3. Strict intraoperative monitoring of vital signs, oxygenation, ventilation, and neurologic function is important due to the physiologic perturbations of vascular surgery. Tight glycemic control and maintenance of normothermia and hemostasis also impact outcomes.
Graft thrombosis is a major cause of failed arterial bypass surgery. Several techniques can be used to assess grafts intraoperatively, including inspection, palpation, arteriography, ultrasonography, angioscopy, and intravascular ultrasonography. Early graft failure within 30 days is often due to technical errors, while late failure over 30 days is usually caused by atherosclerosis or intimal hyperplasia. Treatment depends on the timing and cause of failure. Early failures may be treated with thrombectomy or thrombolysis, while late failures respond better to thrombolysis or open revision. The optimal conduit depends on patient and graft factors. Close surveillance after treatment is important to monitor for recurrent stenosis.
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Preoperative evaluation and management of vascular surgery patients is important to minimize complications. It includes assessing cardiac, pulmonary, renal, and diabetic status through history, exams, labs, and testing. Patients found to be high-risk may require optimization like smoking cessation or glucose control prior to elective surgery. During surgery, prophylaxis against DVT is recommended according to patient risk factors. Postoperative care focuses on glycemic control and resuming medications appropriately.
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2. • Introduction and Epidemiology:-
• Upper extremity ischemia accounts for <5% of patients
presenting for evaluation of limb ischemia, with majority
being caused by autoimmune/connective tissue diseases.
• Upper extremity ischemia is less common than lower extremity
ischemia.
• Etiopathogenesis:- Upper extremity arterial disease can be categorized
based on:-
a) Anatomic location (large vs small vessel) and
b) Etiology (vasospastic vs occlusive).
• Occlusive disease is associated with worse prognosis with increased risk of
developing tissue loss with severe symptoms at the time of presentation.
3. • Vasospastic etiologies are more responsive to pharmacologic intervention
while occlusive etiologies demand surgical intervention.
• Palmar and digital artery occlusive disease is the most common cause of
upper extremity arterial occlusive disease, whereas large-vessel disease,
including arteries proximal to the wrist, account for less than 10%.
1) Large vessel disease:- Acute or chronic arterial occlusive disease
2) Small vessel disease:- chronic arterial occlusive disease.
Acute upper extremity ischaemia:- symptoms < 2 weeks
Chronic upper extremity ischaemia:- symptoms >2 weeks
The majority of arm emboli are cardiac in origin (75%). The most common
site for emboli is the brachial artery (60%), followed by the axillary artery
(26%).
4. Causes of upper extremity ischaemia:-
1)Arterial embolism:- 61% of cases.
Atrial fibrillation
Valvular heart diseases
Isolated ischaemiac heart disease with left ventricular hypokinesis
Infective endocarditis( vegetations)
Ventricular aneurysms
Atrial myxoma
2)Atherosclerosis:-
Diabetes mellitus
Renal failure ( arteries of hands and digits)
The subclavian artery and brachiocephalic trunk are the most common upper
extremity locations for atherosclerosis
5. 3) Traumatic injury:-
Penetrating mechanisms can cause injury to any of the named vessels and
may present with acute arm ischemia from thrombosis.
Vascular injury can be direct or indirect. Direct injury from a knife or other
implement, bullet or other projectile can cause partial or complete
transection and thrombosis. Indirect injury results when the trajectory of
a projectile is near an artery.
Eg:- 1) Subclavian artery thrombosis or avulsion is often due to severe
traction injury on the shoulder
2) Axillary artery injury can result from humeral dislocation or humeral
neck fracture.
3) Brachial artery injury can result from mid-shaft humeral fracture or
supracondylar fracture.
6. 4) Thoracic endovascular aortic repair:- Thoracic endovascular aortic repair
(TEVAR) using currently approved devices may require coverage of the left
subclavian artery in up to 40 percent of the cases.
5) Arterial access complication:- Arterial thrombosis or dissection related to
arterial access for hemodynamic monitoring or from diagnostic or therapeutic
arteriography may present with acute hand ischemia.
6) Acute arterial dissection — Acute aortic dissection (type A aortic dissection)
may present with upper extremity ischemia when the dissection extends into the
great vessels.
Spontaneous subclavian or axillary artery dissections are rare and should alert the
clinician to possible autoimmune etiology, such as Takayasu arteritis or giant cell
arteritis (GCA).
7. 7) Arterial thoracic outlet syndrome — due to arterial compression most
commonly related to a cervical rib or anamolous first rib. Symptomatic upper
extremity ischemia related to aTOS is typically due to distal thromboembolism
originating from the post-stenotic aneurysm, rather than from progressive
stenosis or thrombotic occlusion of a stenosis.
8) Aortitis/arteritis:-
a) Takayasu arteritis is a "large vessel" vasculitis affecting the aorta and its
branches typically affecting young females (<40 years old) and recognition
requires a high index of suspicion since the clinical presentation in the early
systemic inflammatory phase is often nonspecific.
The presenting symptoms of either the acute systemic inflammatory phase or the
"burnt out" or "occlusive" phase may overlap, but distinguishing between these
phases is important for determining the treatment.
8. • The clinical presentation may include diminished pulses, differential blood
pressures, and/or symptoms of upper extremity pain with exertion. Advanced
symptoms such as ischemic rest pain and tissue loss are rare.
b) GCA:- is also systemic inflammatory disease generally affecting adults over
age 50. GCA involves arteries of the head and neck, but it can also affect the
aorta and rarely lower extremity vessels.
9) Radiation therapy — Radiation therapy to the neck or upper chest may
result in accelerated atherosclerosis of the axillary or subclavian arteries.
10) Dialysis access steal syndrome- incidence is about 3 percent. patients
experiencing symptoms of "steal" have an AV access that is brachial artery
based. Ischemia related to hemodialysis AV access presents as a variant known
as Ischemic monomelic neuropathy (IMN) with profound sensory and motor
deficits in the hand. The presentation is almost immediate after the creation of
the AV access and requires immediate treatment.
9. 11) Autoimmune disease/arteritis — Digital artery occlusion causing hand or
finger ischemia is attributed to an autoimmune disease in up to 54 percent of
the cases, although this patient population also has a high prevalence of
smoking (68 percent).
• Mostly includes scleroderma, mixed connective tissue disease (MCTD),
systemic lupus erythematosus (SLE), sjogren’s syndrome and rheumatoid
arthritis.
• scleroderma accounts for majority of Raynaud’s phenomenon(80% to 90%).
• The reported prevalence of primary Raynaud’s phenomenon ranges from less
than 1% (in men) and up to 20% (in women).
10. Raynaud’s syndrome:- intermittent digital ischemia in response to
cold, caffeine or emotional stress.
Raynaud’s disease:- idiopathic Raynaud’s syndrome(80-90%).
Raynaud’s phenomenon:- Raynaud’s syndrome with identifiable arterial
pathology or associated disease.
11. Scleroderma:- Serology often reveals anti-centromere or anti-topoisomerase
(anti-Scl-70) antibodies.
Etio-pathogenesis:- mediated through these cytotoxic antibodies to endothelium.
12. Systemic Lupus Erythematosus:-
most often in young females,
Etiopathogenesis:- by immune complex deposition.
Raynaud’s syndrome is present in as many as 80% of patients.
Rheumatoid Arthritis:-
• chronic inflammatory joint disease.
• with subgroup of patients having extra-articular involvement of the skin, eyes,
lungs, spleen, and arteries.
• most severe of which is termed rheumatoid vasculitis, a systemic process
involving both arteries and veins.
• results from immune-mediated damage.
• HLA-DRW-4 allele - mark a genetic predisposition that in response to an
unknown stimulus such as infection leads to immune complex deposition and
inflammation
13.
14. Sjögren’s Syndrome :- acute necrotizing, leukocytoclastic, and
lymphocytic vasculitis.
Mixed Connective Tissue Disease :- clinically presents as an overlap syndrome
with features of two or more connective tissue diseases, such as SLE, rheumatoid
arthritis, or scleroderma.
Buerger’s Disease:- segmental thrombotic occlusions of the small- and medium-
sized arteries.
• Most commonly affects lower extremities but upper extremity is involved in as
many as 50% of these patients.
• Classically occurs in young male smokers and is often associated with both
migratory thrombophlebitis and Raynaud’s syndrome. Diagnostic
criteria include age less than 45 years, tobacco abuse, exclusion of other diseases
with similar clinical findings, normal arteries proximal to the brachial arteries.
15. • Hand-Arm Vibration Syndrome:- finding
of Raynaud’s syndrome after long-term use of vibrating
tools.
• Mostly seen in stonecutters, welders or grinders in shipyards, timber
fellers, and windshield replacement technicians in the auto-glass
industry.
• postulated that kinetic energy imparted to the small vessels and
nerves of the hand by vibrating tools with power in certain frequency
bands is harmful.
• Early on, patients have vasospastic Raynaud’s syndrome, which over a
period of time, progresses to digital artery occlusive disease.
16. Fibromuscular Disease:- often present with finger ischemia because of
arterial embolization and occlusion.
• postulated that the condition known has hypothenar hammer syndrome, in
which patients have the acute onset of hand ischemia after using the heel of
their hand as a hammer,
• This is actually due to trauma to a pre-existing fibromuscular disease lesion.
Hypersensitivity Angitis:- acute onset significant digital ischemia, usually with
ulceration, with no demonstrable underlying abnormality.
• immune-mediated arterial wall injury has been hypothesized as the
underlying etiology.
• Benign disease with progressive improvement.
17. • Malignancy:- tumor-based immunologic process, including both small
vessel arteritis and immune complex deposition, including
cryoglobulins.
• Frostbite :- Freeze injury of the small vessels of the digits.
Mild disease presents as vasospastic Raynaud’s syndrome, while
significant freezing injury may result in occlusive disease of the digital
arteries.
19. Other causes:-
Accidental intra-arterial injection is often related to substance abuse
disorder.
congenital AV malformations (eg, Parkes-Weber syndrome)
hypercoagulable states (eg, heparin-induced thrombocytopenia, malignancy,
disseminated intravascular coagulation, coronavirus disease 2019 [COVID-
19])
20. Clinical features:-
1) Acute arm Ischaemia:-
• Mc cause:- thromboembolic disease (usually of cardiac origin),
• second mc cause - iatrogenic (1.5%).
• 6 P’s:- pain,
pallor,
poikilothermia,
pulselessness,
paresthesia, and
paralysis
21. Chronic Ischemia:-
• Manifest as upper limb claudication, ulcers or gangrene in the upper
extremity.
Isolated hand symptoms — With small vessel disease, often caused by
autoimmune diseases and arteritides. ischemic symptoms (coolness,
pain) are limited to the hand. In a review of hand ischemia, the
pathophysiologic mechanism responsible was emboli in 6 percent,
vasospasm in 10 percent, thrombosis or "sludging" in 28 percent,
occlusive disease in 26 percent, and occlusive disease associated with
vasospasm or external compression in 30 percent
Isolated subclavian stenosis is often asymptomatic and may be
suspected because of unequal arm blood pressures (BPs) (≥ 20 mmHg
difference in systolic BP).
•
22. • However, once obstructive disease progresses or affects vertebral vessels
and flows, the likelihood of ischaemia or steal symptoms—due to flow
reversal in the vertebral artery worsened by arm exercise—increases
significantly. Subclavian steal syndrome may be suspected in cases of visual
disturbances, syncope, ataxia, vertigo, dysphasia, dysarthria, and facial
sensory deficits occurring during efforts made by the arms.
• Brachiocephalic occlusive disease can cause a stroke or transient ischaemic
attack in carotid and vertebral territories.
• Ischaemic symptoms may include exercise-induced fatigue, pain, and arm
claudication. In severe cases, especially in distal disease, rest pain and digital
ischaemia with necrosis can develop.
23. • PHYSICAL EXAMINATION:-
• Pulse examination
• Bilateral upper extremity blood pressures
• Evaluation of capillary refill, tissue loss
• Neurologic examination assessing sensation and muscle strength
• Doppler insonation of the radial, ulnar, palmar, and digital arteries is performed
to evaluate the quality of Doppler waveforms.
• Fingers should be examined for clubbing- s/o COPD
• Nail beds should be checked for splinter hemorrhages- seen in embolic disease
• Telangiectasia and sclerodactyly - seen in scleroderma and other connective
tissue diseases.
• Clinical signs of "steal" syndrome
24. • Auscultation of the supraclavicular and infraclavicular fossa may reveal a
bruit, indicating possible subclavian artery stenosis.
• Vascular Laboratory Evaluation:-
• allows differentiation of large artery disease (reduced wrist arterial pressure
with no further reduction at the finger level) from small artery disease
(normal upper extremity examination, abnormal finger pressures)
• Cold Challenge test:- Raynaud’s phenomenon is made clinically.
The most basic test for cold sensitivity is finger temperature recovery after
ice-water immersion.
• In case the above battery of tests are non significant, then pt is subjected to
hypercoagulable screening:- antithrombin III, protein C,
and protein S levels, which are tests for the presence of anticardiolipin and
antiphospholipid (lupus inhibitor) antibodies.
• Lp(a) levels in patients with hyperlipidemia, and tests for familial
hypercoagulable states such as factor V Leiden
25. • Imaging studies:-
• DUPLEX ULTRASONOGRAPHY:-
• detection of high-velocity flows indicating >50% stenosis.
• Monophasic post-stenotic flow and altered flow in the ipsilateral vertebral artery
are seen in > 70% proximal subclavian stenosis.
• In c/o subclavian steal syndrome - flow reversal should be assessed in the
ipsilateral extracranial vertebral artery by hyperaemia testing.
• Severe stenosis or occlusion of the right brachiocephalic trunk is associated with
reduced flow velocities in the ipsilateral subclavian artery and the common carotid
artery.
• In c/o abnormal or doubtful duplex ultrasound anatomical imaging both computed
tomographic arteriography (CTA) and magnetic resonance arteriography (MRA)
provide excellent resolution and are less invasive.
• In c/o embolic disease 2D echocardiography are recommended.
• Invasive arteriography is generally reserved for patients with unexplained digital
artery occlusion in an asymmetrical distribution to rule out a surgically correctable
proximal lesion.
• both upper extremities should be imaged. The presence of significant bilateral
disease with unilateral symptomsis s/o a systemic disease.
26. • Treatment:- Medical
• Idiopathic Raynaud’s syndrome:- best treated with cold and tobacco
avoidance.
• calcium channel blocker Nifedipine:- vasodilator:- 20% to 30% of
patients do not tolerate nifedipine because of ankle swelling, headache
or fatigue.
• Losartan- ARB’s- Angiotensin II inhibitory action and production of
Aldosterone.
• Fluoxetine, a selective serotonin uptake inhibitor.
• Prazosin- alpha-1 adrenergic receptor antagonist
• sildenafil, cilostazol- PDE-III Inhibitors
• Bosentan, an endothelin receptor blocker, special benefits in patients
with scleroderma
27. • Indications for Revascularization:- in cases of severe/disabling
symptoms, bilateral stenosis, stenosis with ipsilateral arteriovenous
fistula for dialysis, patients planned for coronary artery bypass graft
surgery or those already operated on with ipsilateral internal
mammary artery grafted to coronary arteries with evidence of
myocardial ischaemia.
28. • Surgical:- Thoracic sympathectomy :- has been used both for
treatment of
• digital artery vasospasm and as an adjunct for healing of digital
ischemic ulceration.
• usually initially successful with symptom recurrence within 3 to 6
months attributed to the rich network of collateral nerve pathways in
the upper extremity.
• periarterial digital sympathectomy performed in the common digital
arteries has been suggested as a superior strategy and a number of
small series claim long-lasting benefit.
• The second, third, fourth and fifth thoracic ganglia of sympathetic
chain are identified and excised.
• Techniques :- open, laparoscopic and chemical.
29. Other options:- Endovascular therapy and open bypass surgery
a) angioplasty and/or stenting for subclavian artery occlusive disease:-
primary patency of 90% at 1 year and 81% at 5 years.
b) Most institutional reviews describe treatment of occlusions in the
axillary, brachial, radial and ulnar arteries which involve surgical
bypass or embolectomy.
30. • ACUTE UPPER LIMB ISCHAEMIA:-
• TRANSBRACHIAL EMBOLECTOMY:-
performed under local anesthesia with monitored anesthesia care.
occlusion of the distal brachial artery, important to expose the origins of both
forearm arteries because the embolectomy catheter must be passed down each
artery. Transverse arteriotomy at brachial artery. Clots encountered at the
bifurcation, are readily removed.
The majority of brachial embolectomies, the brachial artery may be pulseless,
indicative of an embolus lodged more proximally.
Concerns:- with proximal passage of an embolectomy catheter dislodgment of
debris that may embolize the vertebral artery near the origin of the subclavian
artery
Once inflow is established, a size 2 or 3 French embolectomy catheter is passed
distally down each forearm vessel.
arteriotomy closure primarily - running fine polypropylene suture if the artery is
sufficiently large or the artery should be closed with a vein patch.
31. Immediate completion angiography to be performed if the hand still appears
ischemic, especially if extensive thrombus has been extracted from forearm
arteries.
If there is any suspicion of an inflow lesion, intraoperative arteriography can
be performed by either the femoral or brachial route to diagnose and treat
such lesions.
Italian study by Zaraca et al. demonstrated a significant reduction in 2-year
reocclusion rates in patients undergoing angiography after embolectomy.
ALTERNATIVE THERAPY:- Thrombolysis of acutely occluded axillary or brachial
arteries has been described with reasonable outcomes. 8 of 55 patients
required surgical thrombectomy. Thrombolysis has also been described as a
treatment option for acute finger ischemia with disease distal to the wrist.
32.
33. CHRONIC ISCHAEMIA:- The innominate and subclavian arteries are the most
common location of upper extremity artery disease.
• Symptomatic patients are typically younger patients than in ilio‐femoral
atherosclerotic disease with mean ages of 49 years to 69 years.
• Subclavian or innominate artery stenosis is caused by a number of
conditions with atherosclerosis being the most common cause followed by
Takayasu’s arteritis.
• In 1956 Davis et al. performed the first trans‐thoracic innominate artery
endarterectomy, and prosthetic bypass grafting was introduced by DeBakey
and co‐workers in 1958. Because of a considerably high operative mortality
rate extra‐anatomic procedures were developed. Extra‐ anatomic bypass
grafts were reported to bring down the mortality rate from 22% with
transthoracic repair to 5.6% with carotid‐subclavian bypass grafting.
34. • Percutaneous trans‐luminal angioplasty (PTA) of the aortic arch
branches was introduced in 1980, and has subsequently evolved as an
effective and safe treatment modality for occlusive lesions of the
subclavian and innominate arteries.
• Stenting has been introduced for the management of the subclavian
and innominate arterial occlusive lesions in the early 1990s to treat
failures or complications of PTA, to increase the initial success of the
recanalization of occlusions, to improve long‐term patency, and to
protect from atheromatous debris or thrombus dislodgement during
PTA leading to cerebral embolization. Based on these improvements
endovascular treatment became the preferred first line technique for
the treatment of obstructive innominate/subclavian artery disease.
35. • For subclavian and innominate artery revascularization a dedicated fix C‐arm
unit with a digital detector with a large field‐of‐view providing high quality
imaging, road map or image overly options and sufficient magnification is
strongly recommended.
• 4‐5 Fr catheters and 0.035”, 0.018” and 0.014” (hydrophilic) guide‐wires.
• semi‐compliant balloons (diameter: 6‐12 mm, length: 20‐40mm) either in
over‐the‐ wire (OTW) or rapid exchange (Rx) technology.
• Various 4‐7F sheath with up to 90 cm length (0.035” guidewire compatible) for
the transfemoral approach as well as micropuncture sets (0.018” guidewire
compatible) for a transbrachial or transradial access.
• 8‐12 mm stents with variable lengths (12‐40mm). For treating ostial lesion
balloon expandable stents should be available as they can be placed more
precisely and have higher hoop strength. In self expandable stents, stent size
should exceed the target vessel size by 1‐ 2 mm.
36. • availability of stent grafts and balloons for vessel occlusion is indispensable for
the management of bleeding complications.
A) Innominate Artery and subclavian artery:- lesions are best depicted in LAO
projections.
femoral artery access was used. The axillary artery and the brachial artery were
used less frequently. The brachial artery approach offers a better pushability
with increased chance of crossing a complex lesion, but is associated with more
access site complications.
Alternatively:- (enabling the use of smaller sheaths) is to cross the lesion from
the ipsilateral brachial artery and snare the guidewire from the groin, in order to
place the stent from the femoral approach.
Typically a long sheath is placed in the aortic arch, so that the lesion can be
visualized by DSA or by road mapping. Mostly balloons with diameters of 6 mm
to 12 mm are used for angioplasty.
37. • Previously stents were used for unsatisfactory PTA results, but nowadays
primary stenting is the method of choice.
• Usually balloon expandable stents are used for short and/or ostial lesions.
Care should be exercised to place the stent, so that it does not protrude
more than 2 mm into the aorta, or into the orifice of the right carotid
artery.
• No specific recommendation can be made regarding the situation of the
bovine arch variation. In such a situation care should be taken not to stent
across the origin of the left carotid artery.
• It is recommended to avoid PTA or stenting across the vertebral artery
origin.
38. • Medication and Peri‐procedural Care:-
• pre‐interventional antiplatelet therapy is strongly recommended. It should
include clopidogrel (75 mg/day) and aspirin (100 mg/day) starting 3 days prior
to the procedure.
• Alternatively clopidogrel can be administered with a loading dose of 300 mg.
During the procedure, 3000‐5000 IU of heparin are administered
intra‐arterially in order to maintain an activated clotting time (ACT) of 200 to
250 s.
Post‐procedural Follow‐up Care:-
prior to discharge from hospital the local access site needs to be inspected.
Distal pulses need to be checked, particularly if closure devices were used.
Except for a completion angiogram no routine imaging is needed after the
procedure.
39. • post‐procedural antiplatelet therapy is needed with a double platelet
therapy for as described above for about 6 weeks followed by life‐ long
single antiplatelet therapy.
• Follow‐up should be performed in 6 months intervals, including blood
pressure measurement at both arms and DUS. Further imaging studies are
only recommended in symptomatic patients with CTA being the method
of choice after stenting.
40. Surgical techniques:-
A) Innominate artery:-
• include direct reconstruction and extra‐anatomic bypass. The former
may be accomplished by endarterectomy and aortic origin grafting.
Extra‐ anatomic methods include subclavian‐subclavian artery
bypass, axillary‐axillary artery bypass, or contralateral
carotid‐carotid artery bypass. The extra‐anatomic methods were
advocated to reduce the high morbidity and mortality rates.
• The two largest series of innominate artery bypass including 246
patients reported that the probability of freedom from stroke was
87% to 88.8% at 5 years, and 80.4% to 81% at 10 years. Primary graft
patency was 94% to 98.4% at 5 years, and 88% to 96.3% at 10 years.
peri‐operative stroke and mortality rates of 5.4% to 8%.
41. B) Subclavian Artery :- include carotid‐subclavian bypass using
synthetic grafts or saphenous vein, and transposition of the subclavian
artery unto the common carotid artery. Perioperative mortality is low
(0‐0.8%), and stroke rate ranges from 0‐5%. Five‐year primary patency
rates range from 92% to 95%, and eight to ten year primary patency
from 83% to 95%.
there is neither level 1 evidence to support stenting over angioplasty or
surgical over endovascular treatment. Considering the low morbidity of
endovascular therapy it should be the treatment of first choice for
innominate artery and subclavian artery occlusive disease.
42. • Bypass Conduit and Tunneling:-
• The autogenous vein is the conduit of choice for upper extremity
reconstructions. The great saphenous vein is preferable, although use
of the in situ cephalic vein has been described.
• The more joints that the bypass crosses, the lower the patency rate.
• The excised conduit may be used in either reversed or orthograde
(nonreversed) orientation.
• If orthograde orientation is used, the proximal anastomosis is
performed, the conduit is distended, and the valves are rendered
incompetent by the passage of a retrograde valvulotome.
43. • Bypasses originating from the axillary artery are preferably tunnelled
anatomically along the axis of the axillary and brachial arteries
because they are then less prone to movement or distortion (as seen
in subcutaneous tunnelling).
• Bypasses based on brachial artery inflow are most often tunnelled in
the subcutaneous plane. This facilitates physical examination for
evaluation of bypass patency, ensure surveillance of the bypass with
duplex and avoids manipulation of the rich forearm nerve network.
• Alternatively, if good-quality basilic or cephalic veins are present, an
in situ bypass may be performed.
44. • In the case of distal radial sided reconstructions, the graft is tunnelled
subcutaneously over the extensor pollicis tendons towards the
anatomic snuff-box onto the dorsum of the hand.
• The bypass ends between the thumb and index finger, where the
deep palmar arch is exposed.
• In case of ulnar-sided reconstructions, the course of the vein graft is
more direct and it passes superficial to the flexor retinaculum in the
subcutaneous plane at the wrist lateral to the pisiform bone to join
the superficial palmar arch.
45. UPPER EXTREMITY AMPUTATION:-
Incidence in USA:- 1,85,000 patients undergo amputation each year.
• 10% to 25% of these amputations involve the arm and hand . (93%) involve minor
amputation at the wrist or within the digits.
• Incidence in developing countries:- total of 2.4 million arm amputees. Of which
58% are amputee below the elbow.
1.below elbow:- 1.4million
2.Above elbow & elbow disarticulation:0.7million
3.Shoulder:- 0.2million
4.Hand/wrist:- 0.1million
46. • Etiology:-
• trauma (80%-90%):- vibration-induced white finger, hypothenar hammer
syndrome and arterial thoracic outlet compression resulting in subclavian
aneurysm. Trauma and Military Injuries.
• Vascular disease(7%) and tumors(0.6%) are the next most common
• less frequent causes:-
infections, congenital anomalies and iatrogenic reasons such as
complications related to catheterization, vasopressor administration and
vascular access.
• vasospastic disorders (e.g., Raynaud disease), small-vessel diseases
(e.g., Buerger disease) and radiation-induced arteritis
47. • GENERAL OPERATIVE CONSIDERATIONS:-
• an upper extremity amputation must be both functional and cosmetically
acceptable.
• healing will occur at the hand level when digital pressure is >40 mm Hg and wrist
Doppler pressure is >60 mm Hg
• At the forearm and arm levels, healing will almost always take place when wrist or
brachial pressure is at least 60 mm Hg or when tcPo2 is 40 mm Hg or greater.
• Preservation of length
• Soft Tissue Coverage
48. skin grafts, free flaps and composite tissue transfer have dramatically
changed this approach
• Nerves:-
Prevention of neuroma:-
proximal ligation, coagulation, chemical ablation of the end, simple division,
traction and division, nerve repair to other divided nerves and immediate
burial of the transected nerve end have all been attempted with varying
degrees of success.
locating the divided free nerve end as far from external stimuli as possible
and placing it in a healthy, non-scarred bed of tissue –best preventive
measures.
In addition, early postoperative therapy (desensitization or sensory re-
education) is an extremely important determinant of the patient’s ability to
tolerate the dysesthesias post amputation.
49. • Bone and Cartilage:-
The bony prominences must be optimally contoured.
• SPECIFIC AMPUTATIONS :-
• Fingertip Amputation:- crushing blow, such as from a closing door
• proximal portion of the distal phalanx if not severely injured, preservation of that
portion of bone is indicated for functional length.
• If these areas are damaged beyond repair, disarticulation through the distal
interphalangeal joint is indicated.
• The bone of the distal phalanx should be of adequate length to support the nail bed
and nail growth.
• The digital nerves are identified, distracted distally and divided so they will be at
least 1 cm from the fingertip stump to avoid neuroma formation in this location.
50. • If the final cutaneous defect is then less than 1 cm2, simply allowing the wound to close
by secondary intention is acceptable.
• If the cutaneous defect is greater than 1 cm2, with no exposed bone, a skin graft is
possible.
• Non-traumatized skin graft donor sites that may be considered
are:
• The ulnar border of the palm (within the operative field and a good colour match).
• The forearm (the medial portion of the forearm or the elbow crease)
• The groin (a well-hidden donor area, although the colour match is not good)
51. • Local Flap Closure :- more common flaps include:
1)The Kutler flap, a lateral V-Y flap for closure of a central tip defect = For fingers or
toes in which the tips are destroyed but the nail matrix is still intact or only slightly
injured.
52. • 2) The Atasoy flap, a palmar V-Y flap
• The palmar flap, based on both digital neurovascular bundles in which
the entire soft tissue coverage of the digit above the tendon sheath is
elevated and advanced to cover the tip of the finger.
53. • Digit-Level Amputations:-
• Midfinger Amputation :-
Amputations that leave more than half the proximal phalanx
may be functional for the patient
• Amputation proximal to the midportion of the proximal phalanx is not
typically a functional amputation.
• If enough digit remains, it may be possible for patients to wear a cosmetic
prosthesis that may allow some functional restoration; however, most
patients find the remaining digit a nuisance.
54. • Ray Amputation:- includes removal of the injured finger to the metacarpal base.
• often provides a far more cosmetically acceptable hand.
• dorsal longitudinal incision over the index metacarpal along with a palmar skin
incision over
the proximal phalangeal level.
• Alternatively, a circumferential racket incision may be used.
• Risks:- 1) the procedure narrows the palm by 20% to 25%, which reduces the hand’s
ability to stabilize objects.
• 2) more extensive procedure that produces more proximal postoperative pain,
edema, and stiffness.
55. • Thumb Amputation :- THUMB accounts for 40% of the function of the
hand.
• It deserves special attention in any amputation.
• standard of care is now to attempt reimplantation of the thumb if
possible, and encouraging results have been achieved even after avulsion
injuries.
• Non-reimplantable amputations at the level of the interphalangeal joint
are functional.
• More proximal thumb amputations can be reconstructed by pollicization
(CREATING A FUNCTIONAL THUMB using a remaining finger, usually the
index finger and myodesic techniques), osteoplasty, bone-lengthening
techniques)
56. • Wrist Amputations :-
• A transcarpal amputation allows supination and pronation of the forearm, as well as
flexion and extension of the wrist.
• Wrist disarticulation is preferred to more proximal forearm amputation because it
has the same advantages of a transcarpal amputation except that wrist flexion and
extension are lost.
• Wrist disarticulation is performed by creating a long palmar and short dorsal flap;
ligating the radial and ulnar arteries proximal to the wrist.
• identifying the median, radial, and ulnar nerves and distracting and dividing them;
dividing all tendons; disarticulating the joint; and resecting the tips of the radial and
ulnar styloid processes. The resultant smooth contour can easily be fitted for a
prosthesis.
57. FOREARM AMPUTATION:-
• The optimal level for a forearm amputation is the junction of the middle and
distal third of the forearm. The issue with the distal third of the forearm is the
relative paucity of padding in this area because of the thin skin and
subcutaneous tissue.
• This factor can be more evident in patients with ischemia because this area is
notably prone to skin breakdown.
• The technique is as follows: creation of equal anterior and posterior skin flaps;
ligation of the radial and ulnar arteries; distraction and division of the median,
radial and ulnar nerves; transection of the muscle bellies; division of the radius
and ulna; and closure of the deep fascia followed by the skin.
58. • However, as described by Tubiana, bilateral upper extremity amputations
can be functionally improved with the Krukenberg procedure, in which a
sensate pincer is created between the radius and ulna.
• The pincer is motorized by the pronator teres muscle, and this procedure
allows preservation of proprioception and stereognosis.
• Although cosmetic result is far from desirable, the functional improvement
is great, and the procedure should be given serious consideration
in the rare instances of bilateral injuries, in blind individuals,
or when prosthetic reconstruction is not practical
59. • ELBOW DISARTICULATION :-
If the elbow joint is not salvageable, elbow disarticulation is preferred over distal
humeral transection. In addition to maintaining length, humeral rotation can be
transmitted to the elbow, and the broad flare of the condyles makes for a good
prosthetic fit.
Procedure:- anterior and posterior skin flaps are created; the brachial artery is
ligated; the median, ulnar, and radial nerves are distracted and divided; the joint
capsule is opened and the forearm removed; and a muscle flap (brachialis or
triceps) is then used to cover the humerus.
there has been an emphasis on retaining all of the humerus if possible. However, in
doing so, the upper part of the arm may appear longer than the normal
(unamputated) arm when fitted with an internal elbow joint prosthesis.
It is possible to use an external elbow joint option, but these joints are substantially
less durable.
60. • UPPER ARM AMPUTATIONS:-
• A transcondylar amputation functions essentially the same as an elbow
disarticulation.
• Taking into account the location of the elbow lock, which extends 4 cm from
the distal amputation site, the transhumeral amputation should be made 4 cm
proximal to the elbow.
• The use of free flaps can provide additional soft tissue and bone length for a
short upper arm amputation. Functional restoration of the glenohumeral joint
may be accomplished with a free fibular transfer.
• One final technique used to achieve adequate bony length
is distraction osteogenesis (Ilizarov’s technique).
61. • Shoulder Disarticulation and Forequarter Amputations or scapulothoracic,
amputation
most complex and difficult procedures from a prosthetic and functional
standpoint.
Considerations are
• (1) loss of potential motor units as drivers of the prosthetic device
and (2) difficulty fitting the prosthesis to contours.
• The shoulder disarticulation (after rounding off any bony prominences) leaves
a contour adequate to provide a snug fit for the prosthesis.
• In addition, scapular functionis retained and can be used (with some difficulty)
as a motor unit for the prosthetic device
62. • surgical techniques:- The shoulder disarticulation may be modified by
retention of the humeral head to assist in contouring or may be a true
disarticulation with complete removal of the humerus.
• Regardless, the deltoid and pectoral muscles, along with their overlying
myofasciocutaneous tissue, provide the flap coverage. Occasionally, if the
deltoid is not available, an inferior axillary fasciocutaneous flap may be
necessary.
• The latissimus dorsi and pectoralis major are reattached to either the glenoid
capsule or the humeral head remnant. The tendinous components
of the rotator cuff are also attached to the glenoid capsule.
• There are two approaches to forequarter amputation. The anterior approach,
described by Berger, and the posterior approach, described by Littlewood,
differ only in exposure of the vascular structures hidden behind the clavicle.
63. • POSTOPERATIVE MANAGEMENT AND COMPLICATIONS :-
1) Wound Treatment:-
low threshold for the use of drains in areas of potential space (hematoma, seroma
formation.
Early physical activity and rehabilitation
Compressive dressings
Full range-of-motion exercises of the elbow and shoulder should be started
immediately when these structures are preserved.
Poor wound healing and the concerns of flap ischemia/stump necrosis, are less
well appreciated in upper extremity amputation.
The threat of rhabdomyolysis and myoglobinuria - less than in the lower extremity
because of smaller muscle mass, shorter arm length
64. 2) Revision amputation:-
Patients undergoing transradial amputation were 4.7 times more likely to have phantom
pain. Revisions of these amputations resulted in an increase in prosthetic use from 19%
preoperatively to 87% post revision.
3) Phantom pain:- occurs in 40% to 80% of patients. loss of the dominant hand is an
independent predictor for the development of more significant phantom
limb pain.
Treatment methods:- categorized as pharmacologic, surgical, psychological and
neurostimulatory
65. • Psychosocial Rehabilitation:-
• compared with lower extremity amputees, those losing part of the arm or the hand
suffer from a higher rate of psychological disorders, such as depression, anxiety,
and PTSD. 30% to 40% of upper extremity amputees will require psychological
care.
• Physical Rehabilitation:-
• Rehabilitation for those with upper extremity amputation is
complex compared to lower extremity because of the intricate movements
and fine sensorimotor function in the native arm and hand. Replicating these has
been difficult.
• Principles of upper extremity amputees rehabilitation include:- residual limb soft
tissue shrinkage and shaping, desensitization, maximization of range of motion,
skin health and mobility, muscle strength, augmentation of self-reliance and daily
activities and exploration of prosthetic options.
66. • Prostheses :-
• three categories:-
1. purely aesthetic,
2. body powered, and
3. myoelectrically powered.
1) Aesthetic Prosthesis:- usually consist of silicone and are made to produce a lifelike
appearance so the amputee can have a relatively normal body habitus. very minimal function.
2) Body-powered prostheses:-
• are simple mechanical devices that are controlled by residual body motion and function.
• most durable of prostheses and are used for most significant physical activity by amputees.
Mostly used for for swimming, rock climbing and performing most athletic activities
67. 3) Myoelectrically controlled prostheses:-
• use electrodes to convert the electrical stimulation of residual muscle groups into a
current used to power the prosthesis.
• wrist rotation and finger movement is a reality and many terminal devices may be
attached to the prosthesis to allow various functions.
• much more complex, more expensive and less durable for hard physical activity.
• Advances:-
The residual muscles are surgically re-innervated, for the maintenance of cortical
functioning to enable muscle contraction and thus application of the myoelectric
prosthesis. This allows amputees to simultaneously open and close the hand and flex and
extend the elbow.
68. • Hand Transplantation:-
• first hand transplantation was performed in 1964 and it failed secondary to acute
rejection. Since then 70 hand transplantations have been performed as at 2013.
• In a review of 5 bilateral hand transplant patients with a mean follow up of 7.6
years, Bernardon et al., found that the physical results achieved were considered
“fair” and the functional results were considered “good.”
• The ethical dilemma is weighing the perceived benefit of hand transplantation in
regard to expected quality-adjusted life years (QALY) versus the effects of long-
term immunosuppression.