This document discusses fat embolism syndrome, which occurs when fat globules enter the bloodstream and lungs after long bone fractures or other major trauma. It presents most commonly 24-72 hours after injury. The classic triad of symptoms includes respiratory distress, neurological abnormalities, and a petechial rash. Diagnosis is based on clinical criteria and supportive investigations. Treatment is supportive, focusing on oxygenation, ventilation, and prevention of complications. Prognosis is good with proper care, though mortality can be 5-15% in severe cases.
- Fat embolism syndrome is a serious complication that can occur after major trauma like long bone fractures, where fat globules enter the bloodstream and become lodged in the lungs and other organs. It typically presents 1-3 days after injury with respiratory issues, neurological abnormalities, and a petechial rash.
- Diagnosis is based on meeting criteria involving the clinical presentation as well as imaging and lab findings. Treatment is supportive in nature, focusing on oxygenation, ventilation, hemodynamic stability and early stabilization of fractures to prevent further fat embolization. Corticosteroids and colloids may help reduce inflammation and expand plasma volume. Prognosis can be poor, with fatality rates up to 15
Fat embolism syndrome (FES) is a serious complication that can occur after long bone fractures or other trauma involving bone marrow. Fat droplets released from the bone marrow can travel through the bloodstream and lodge in small blood vessels in the lungs, brain, and other organs. This can cause respiratory failure, neurological symptoms like confusion, and a characteristic rash. Diagnosis is based on clinical criteria involving these organ system dysfunctions. Treatment focuses on supportive care, oxygenation, ventilation if needed, and hemodynamic support. Outcomes depend on severity but mortality is typically under 10%. Prophylactic measures like early fracture fixation and steroids in high risk patients may help reduce risk of FES in trauma patients.
Fat embolism syndrome (FES) is a serious complication that can occur after long bone fractures or other trauma involving bone marrow. Fat droplets released from the bone marrow can travel through the bloodstream and lodge in small blood vessels in the lungs, brain, and other organs. This can cause respiratory failure, neurological symptoms like confusion, and a characteristic rash. FES is diagnosed clinically based on symptoms occurring within 72 hours of injury. Treatment focuses on supportive care, oxygenation, and preventing further fat emboli through early stabilization of fractures. While mortality was historically high, most cases are now successfully managed with supportive care alone.
This document discusses fat embolism syndrome, which occurs in 0.5-2% of patients following a long bone fracture. It is caused by the toxic effects of free fatty acids released into circulation from bone marrow. The syndrome is diagnosed clinically based on respiratory, cerebral and dermal manifestations appearing 12-72 hours after injury. Treatment is supportive to maintain respiratory function, as the condition is usually self-limiting. Risk is highest with multiple long bone fractures, and the pathophysiology involves mechanical obstruction of fat globules, biochemical toxicity of free fatty acids, and activation of coagulation pathways.
4 G. Hypoxia after abdominal and thigh liposuction pulmonary embolism or fat ...minhtu
This case report describes a 58-year-old woman who developed shortness of breath and chest pain after undergoing liposuction of her abdomen, flanks, and thighs. The differential diagnosis included pulmonary embolism and fat embolism syndrome. Fat embolism syndrome involves the blockage of small blood vessels by fat globules released into the bloodstream after trauma like liposuction. The woman was diagnosed with fat embolism syndrome based on clinical findings of hypoxia, fever, and bilateral lung changes seen on imaging. Treatment involves supportive care, as there is no specific treatment for fat emboli. Risks of developing fat embolism syndrome after liposuction include the volume and areas of liposuction
This document discusses geriatric anaesthesia and the age-related physiological changes that are important for anaesthesiologists to consider. It notes that aging results in a decline in organ reserve and functional capacity. Specifically, it outlines changes to the cardiovascular, respiratory, renal, neurological, and other body systems that increase perioperative risk. It emphasizes the need for thorough preoperative evaluation and optimization, careful titration of anaesthetic agents, and vigilant postoperative management given the higher risk of complications in elderly patients.
Fat embolism syndrome is a complication that can occur after long bone fractures or other trauma involving bone marrow. Fat droplets released from the bone marrow can travel through the bloodstream and lodge in the lungs and other organs. The classic triad of symptoms includes hypoxemia, neurological abnormalities, and petechial rash. Diagnosis is based on clinical criteria and there is no confirmatory lab test. Treatment is supportive and focuses on oxygenation, ventilation, hemodynamic stability, and occasionally corticosteroids are used for prevention. Prognosis depends on severity but most cases resolve without long term effects.
This document discusses fat embolism syndrome, which occurs when fat globules enter the bloodstream and lungs after long bone fractures or other major trauma. It presents most commonly 24-72 hours after injury. The classic triad of symptoms includes respiratory distress, neurological abnormalities, and a petechial rash. Diagnosis is based on clinical criteria and supportive investigations. Treatment is supportive, focusing on oxygenation, ventilation, and prevention of complications. Prognosis is good with proper care, though mortality can be 5-15% in severe cases.
- Fat embolism syndrome is a serious complication that can occur after major trauma like long bone fractures, where fat globules enter the bloodstream and become lodged in the lungs and other organs. It typically presents 1-3 days after injury with respiratory issues, neurological abnormalities, and a petechial rash.
- Diagnosis is based on meeting criteria involving the clinical presentation as well as imaging and lab findings. Treatment is supportive in nature, focusing on oxygenation, ventilation, hemodynamic stability and early stabilization of fractures to prevent further fat embolization. Corticosteroids and colloids may help reduce inflammation and expand plasma volume. Prognosis can be poor, with fatality rates up to 15
Fat embolism syndrome (FES) is a serious complication that can occur after long bone fractures or other trauma involving bone marrow. Fat droplets released from the bone marrow can travel through the bloodstream and lodge in small blood vessels in the lungs, brain, and other organs. This can cause respiratory failure, neurological symptoms like confusion, and a characteristic rash. Diagnosis is based on clinical criteria involving these organ system dysfunctions. Treatment focuses on supportive care, oxygenation, ventilation if needed, and hemodynamic support. Outcomes depend on severity but mortality is typically under 10%. Prophylactic measures like early fracture fixation and steroids in high risk patients may help reduce risk of FES in trauma patients.
Fat embolism syndrome (FES) is a serious complication that can occur after long bone fractures or other trauma involving bone marrow. Fat droplets released from the bone marrow can travel through the bloodstream and lodge in small blood vessels in the lungs, brain, and other organs. This can cause respiratory failure, neurological symptoms like confusion, and a characteristic rash. FES is diagnosed clinically based on symptoms occurring within 72 hours of injury. Treatment focuses on supportive care, oxygenation, and preventing further fat emboli through early stabilization of fractures. While mortality was historically high, most cases are now successfully managed with supportive care alone.
This document discusses fat embolism syndrome, which occurs in 0.5-2% of patients following a long bone fracture. It is caused by the toxic effects of free fatty acids released into circulation from bone marrow. The syndrome is diagnosed clinically based on respiratory, cerebral and dermal manifestations appearing 12-72 hours after injury. Treatment is supportive to maintain respiratory function, as the condition is usually self-limiting. Risk is highest with multiple long bone fractures, and the pathophysiology involves mechanical obstruction of fat globules, biochemical toxicity of free fatty acids, and activation of coagulation pathways.
4 G. Hypoxia after abdominal and thigh liposuction pulmonary embolism or fat ...minhtu
This case report describes a 58-year-old woman who developed shortness of breath and chest pain after undergoing liposuction of her abdomen, flanks, and thighs. The differential diagnosis included pulmonary embolism and fat embolism syndrome. Fat embolism syndrome involves the blockage of small blood vessels by fat globules released into the bloodstream after trauma like liposuction. The woman was diagnosed with fat embolism syndrome based on clinical findings of hypoxia, fever, and bilateral lung changes seen on imaging. Treatment involves supportive care, as there is no specific treatment for fat emboli. Risks of developing fat embolism syndrome after liposuction include the volume and areas of liposuction
This document discusses geriatric anaesthesia and the age-related physiological changes that are important for anaesthesiologists to consider. It notes that aging results in a decline in organ reserve and functional capacity. Specifically, it outlines changes to the cardiovascular, respiratory, renal, neurological, and other body systems that increase perioperative risk. It emphasizes the need for thorough preoperative evaluation and optimization, careful titration of anaesthetic agents, and vigilant postoperative management given the higher risk of complications in elderly patients.
Fat embolism syndrome is a complication that can occur after long bone fractures or other trauma involving bone marrow. Fat droplets released from the bone marrow can travel through the bloodstream and lodge in the lungs and other organs. The classic triad of symptoms includes hypoxemia, neurological abnormalities, and petechial rash. Diagnosis is based on clinical criteria and there is no confirmatory lab test. Treatment is supportive and focuses on oxygenation, ventilation, hemodynamic stability, and occasionally corticosteroids are used for prevention. Prognosis depends on severity but most cases resolve without long term effects.
Cushing syndrome results from excessive cortisol secretion and is characterized by central obesity, muscle wasting, hyperglycemia, and hypertension. It can be caused by prolonged glucocorticoid use or tumors that secrete cortisol or ACTH. Diagnosis involves testing for cortisol levels, and treatment focuses on treating the underlying cause and managing complications through lifestyle changes and medications. Nursing care aims to prevent injuries and infections while promoting skin integrity and a healthy body image and thought processes.
Fat embolism occurs when fat particles enter the bloodstream after long bone fractures or other orthopedic injuries and procedures. This can lead to fat embolism syndrome (FES), a condition with respiratory, neurological, and dermatological symptoms. Diagnosis is based on clinical criteria like Gurd and Wilson's criteria. Treatment focuses on oxygenation, hydration, and preventing further emboli through early fracture stabilization. Outcomes are generally good, with most neurological deficits resolving.
This document discusses a 75-year-old man with chronic obstructive pulmonary disease (COPD) who requires a transurethral resection of the prostate. The main advantages of spinal anesthesia for this patient are avoiding general anesthesia and the risks it poses for someone with COPD such as airway instrumentation and barotrauma. The disadvantages include potential respiratory compromise if the spinal block spreads too high and difficulties lying flat due to COPD.
Pericardial diseases can present as pericarditis, pericardial effusion, tamponade, constrictive pericarditis, or effusive-constrictive pericarditis. The document discusses the anatomy and functions of the pericardium, pericarditis including its classification, presentations, investigations, and management. It also covers pericardial effusion and tamponade discussing their pathophysiology, clinical features, diagnostic workup including echocardiography, and management focusing on pericardiocentesis for tamponade cases. Recurrent pericarditis and its treatment strategies are also summarized.
1) The document discusses pericardial diseases, beginning with the anatomy and functions of the pericardium.
2) It then covers pericarditis, including classifications, presentations, and management. Empirical anti-inflammatory therapy including NSAIDs and colchicine is recommended for acute idiopathic pericarditis.
3) Recurrent pericarditis is identified as the most common complication, occurring in 15-30% of cases, and requiring prolonged anti-inflammatory treatment.
1. A pleural effusion is a collection of fluid in the pleural space that is usually caused by an underlying condition such as heart failure, pneumonia, or cancer.
2. Physical assessment of a patient with pleural effusion involves examining breath sounds, chest expansion, tracheal position, and vital signs. Diagnosis involves chest x-ray, CT scan, ultrasound and thoracentesis.
3. Treatment focuses on treating the underlying cause as well as draining fluid and preventing reaccumulation through procedures like thoracentesis, chest tubes, pleurodesis using chemical agents or surgery.
This document provides an overview of hyperthyroidism and its management. It discusses that Graves' disease accounts for 60-80% of cases of hyperthyroidism. The pathogenesis involves genetic and environmental factors leading to thyroid-stimulating immunoglobulins that cause excessive thyroid hormone production. Clinical features include nervousness, tremor, palpitations, and in severe cases, eye involvement. Laboratory tests can detect thyroid antibodies. Treatment options include antithyroid medications, radioactive iodine, or surgery to restore euthyroidism.
Fat embolism syndrome is a rare clinical syndrome caused by the presence of fat globules in the pulmonary circulation following trauma or other insults that release fat into the bloodstream. It is characterized by a clinical triad of hypoxemia, neurological abnormalities, and petechial rash that typically develops 24-72 hours after the initial injury. Diagnosis is clinical based on criteria sets, and treatment is supportive to address respiratory failure, shock, or other complications until it resolves spontaneously in days. Prevention focuses on early immobilization of fractures to reduce fat release and potential prophylactic corticosteroids, though their benefit is controversial.
This document provides an overview of hyperthyroidism and its management. It discusses the main causes and clinical features of hyperthyroidism, focusing on Graves' disease which accounts for 60-80% of cases. The pathogenesis involves genetic and environmental factors leading to thyroid-stimulating immunoglobulins that cause excessive thyroid hormone production. Management includes antithyroid medications, radioiodine therapy, or thyroidectomy. Antithyroid drugs are usually the first line treatment but have potential adverse effects. Radioiodine is an alternative that destroys thyroid tissue over time. Considerations for special populations like pregnant women are also covered.
This document provides information on fat embolism syndrome and pulmonary embolism. It discusses the background, causes, pathophysiology, clinical features, diagnostic criteria, investigations and treatment of fat embolism syndrome. It also covers the definition, risk factors and evaluation of pulmonary embolism. The key points are that fat embolism syndrome is a clinical diagnosis with non-specific tests, treatment is supportive, and prevention focuses on early fracture stabilization and adequate hydration and prophylaxis.
This document reviews acute respiratory distress syndrome (ARDS), fat embolism, and thromboembolic disease in orthopaedic trauma patients. It discusses the history, diagnosis, classification, epidemiology, pathophysiology, and treatment of ARDS, fat embolism, and venous thromboembolism (VTE). For ARDS, it outlines the Berlin Definition criteria and risk factors. It describes the two main theories for the pathophysiology of fat embolism. The document also reviews prevention and treatment strategies for fat embolism and VTE in orthopaedic trauma patients.
This document discusses fat embolism syndrome (FES), including its history, causes, mechanisms, clinical presentation, diagnosis, and treatment. Some key points:
- FES was first identified in 1862 and occurs when fat enters the bloodstream after long bone fractures or other trauma, causing respiratory, neurological and dermal symptoms.
- The exact mechanism is unknown but theories include fat globules entering blood mechanically from bone marrow or biochemically through free fatty acid release.
- Clinical diagnosis is based on respiratory issues, neurological abnormalities like confusion, and a petechial rash occurring 1-3 days post-injury. Treatment focuses on respiratory support.
This document discusses fat embolism syndrome, which refers to a clinical syndrome following an insult that releases fat into the circulation, causing pulmonary and systemic symptoms. It presents 24-72 hours after injury and has a mortality rate of 10-20%. Risk factors include long bone fractures from blunt trauma. Pathophysiology involves fat globules lodged in the pulmonary vasculature and brain. The clinical triad includes pulmonary dysfunction, neurological signs, and dermatological petechiae. Diagnosis relies on criteria from Gurd or Schonfeld. Treatment focuses on supportive care, oxygenation, hemodynamics, and occasionally steroids.
Fat Embolism Syndrome (FES) is a Syndrome characterized by: Hypoxia, Confusion and Petechiae. Presenting soon after long bone fracture and soft tissue injury. Diagnosed by exclusion of other causes 0f (Hypoxia & Confusion). It occurs in 0.9 – 8.5% of all fracture patients. Up to 35% of the multiply injured. Mortality 2.5 – 15 - 20%. Rare in upper limb injury and children.
Treatment includes prompt stabilization of long bone fractures and supportive measures which includes: 1- Oxygen Therapy to maintain PaO2. 2- Mechanical Ventilation. 3- Adequate Hydration.
This document discusses several anesthetic complications that can occur during pregnancy, including thrombocytopenia/epidural hematoma, aspiration, difficult airways, and neuraxial blockade complications. Key points include: 1) There is no minimum platelet count that absolutely contraindicates neuraxial procedures, but less than 100,000 is often quoted as a threshold. 2) Pregnancy increases the risk of aspiration due to anatomical changes, so all pregnant patients are considered at high risk of aspiration. 3) Airway management can be difficult in pregnancy due to edema and weight gain; facilities should be prepared with multiple airway devices and surgical options. 4) Neuraxial blockade commonly causes hypotension due to sympathetic blockade,
Cushing's syndrome is caused by excessive cortisol levels and can be due to exogenous glucocorticoid use or endogenous overproduction. It is characterized by central obesity, moon face, buffalo hump, skin changes, hypertension and diabetes. The diagnosis involves tests to check for cortisol suppression and circadian rhythm disturbances. Further tests are then used to determine the underlying cause as pituitary, adrenal or ectopic tumor. Treatment depends on the specific cause but may include surgery, medication or radiation. Pheochromocytomas are rare catecholamine-secreting tumors that cause hypertension and panic attacks. Diagnosis involves urine or plasma tests for metabolites and imaging to locate the tumor. Preparation with alpha-blockers is usually
This document provides background information on fat embolism syndrome (FES). It discusses that FES has a high incidence in patients with major trauma and causes multi-organ inflammation if not diagnosed and treated swiftly. While the exact mechanisms are not fully understood, FES is thought to be triggered by the release of fat emboli from bone fractures that occlude blood vessels and cause pulmonary and systemic inflammation. The diagnosis is mainly clinical based on respiratory, skin and neurological symptoms following trauma. Supportive care is the primary treatment approach through oxygenation, ventilation and symptom management while efforts focus on prevention, early diagnosis and surgical stabilization of fractures.
This document provides an overview of acute respiratory distress syndrome (ARDS) including its definition, pathophysiology, clinical presentation, diagnosis, and management. Some key points:
- ARDS is characterized by acute hypoxemic respiratory failure due to widespread inflammation and fluid buildup in the lungs.
- Treatment involves supportive care with mechanical ventilation using low tidal volumes, maintaining adequate oxygen levels, treating the underlying cause, and considering rescue therapies for severe cases like prone positioning or extracorporeal membrane oxygenation.
- Mortality remains high at around 26-58% depending on severity, with the most common causes of death being complications of the initial insult or secondary infections like pneumonia. Ongoing research focuses on
Fat embolism syndrome is a clinical diagnosis characterized by a triad of hypoxemia, neurological abnormalities, and petechial rash that develops within 24-72 hours of long bone fractures or other trauma. Fat particles released from the bone marrow can cause pulmonary and systemic complications by lodging in the lungs and other organs. While supportive care focuses on oxygenation, ventilation, and hemodynamic stability, the most effective prevention method is early surgical fixation of fractures within 24 hours to reduce risk. Outcomes range from full recovery to respiratory failure and death, depending on severity.
Sarcoidosis is a multisystem disorder characterized by noncaseating granulomas in affected tissues. It most commonly involves the lungs but can affect other organs. The cause is unknown but genetic and environmental factors are thought to play a role. Diagnosis is made through biopsy showing granulomas and excluding other causes. Treatment involves corticosteroids for organ involvement. Prognosis is generally good with remission occurring within 3 years for over half of patients.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Cushing syndrome results from excessive cortisol secretion and is characterized by central obesity, muscle wasting, hyperglycemia, and hypertension. It can be caused by prolonged glucocorticoid use or tumors that secrete cortisol or ACTH. Diagnosis involves testing for cortisol levels, and treatment focuses on treating the underlying cause and managing complications through lifestyle changes and medications. Nursing care aims to prevent injuries and infections while promoting skin integrity and a healthy body image and thought processes.
Fat embolism occurs when fat particles enter the bloodstream after long bone fractures or other orthopedic injuries and procedures. This can lead to fat embolism syndrome (FES), a condition with respiratory, neurological, and dermatological symptoms. Diagnosis is based on clinical criteria like Gurd and Wilson's criteria. Treatment focuses on oxygenation, hydration, and preventing further emboli through early fracture stabilization. Outcomes are generally good, with most neurological deficits resolving.
This document discusses a 75-year-old man with chronic obstructive pulmonary disease (COPD) who requires a transurethral resection of the prostate. The main advantages of spinal anesthesia for this patient are avoiding general anesthesia and the risks it poses for someone with COPD such as airway instrumentation and barotrauma. The disadvantages include potential respiratory compromise if the spinal block spreads too high and difficulties lying flat due to COPD.
Pericardial diseases can present as pericarditis, pericardial effusion, tamponade, constrictive pericarditis, or effusive-constrictive pericarditis. The document discusses the anatomy and functions of the pericardium, pericarditis including its classification, presentations, investigations, and management. It also covers pericardial effusion and tamponade discussing their pathophysiology, clinical features, diagnostic workup including echocardiography, and management focusing on pericardiocentesis for tamponade cases. Recurrent pericarditis and its treatment strategies are also summarized.
1) The document discusses pericardial diseases, beginning with the anatomy and functions of the pericardium.
2) It then covers pericarditis, including classifications, presentations, and management. Empirical anti-inflammatory therapy including NSAIDs and colchicine is recommended for acute idiopathic pericarditis.
3) Recurrent pericarditis is identified as the most common complication, occurring in 15-30% of cases, and requiring prolonged anti-inflammatory treatment.
1. A pleural effusion is a collection of fluid in the pleural space that is usually caused by an underlying condition such as heart failure, pneumonia, or cancer.
2. Physical assessment of a patient with pleural effusion involves examining breath sounds, chest expansion, tracheal position, and vital signs. Diagnosis involves chest x-ray, CT scan, ultrasound and thoracentesis.
3. Treatment focuses on treating the underlying cause as well as draining fluid and preventing reaccumulation through procedures like thoracentesis, chest tubes, pleurodesis using chemical agents or surgery.
This document provides an overview of hyperthyroidism and its management. It discusses that Graves' disease accounts for 60-80% of cases of hyperthyroidism. The pathogenesis involves genetic and environmental factors leading to thyroid-stimulating immunoglobulins that cause excessive thyroid hormone production. Clinical features include nervousness, tremor, palpitations, and in severe cases, eye involvement. Laboratory tests can detect thyroid antibodies. Treatment options include antithyroid medications, radioactive iodine, or surgery to restore euthyroidism.
Fat embolism syndrome is a rare clinical syndrome caused by the presence of fat globules in the pulmonary circulation following trauma or other insults that release fat into the bloodstream. It is characterized by a clinical triad of hypoxemia, neurological abnormalities, and petechial rash that typically develops 24-72 hours after the initial injury. Diagnosis is clinical based on criteria sets, and treatment is supportive to address respiratory failure, shock, or other complications until it resolves spontaneously in days. Prevention focuses on early immobilization of fractures to reduce fat release and potential prophylactic corticosteroids, though their benefit is controversial.
This document provides an overview of hyperthyroidism and its management. It discusses the main causes and clinical features of hyperthyroidism, focusing on Graves' disease which accounts for 60-80% of cases. The pathogenesis involves genetic and environmental factors leading to thyroid-stimulating immunoglobulins that cause excessive thyroid hormone production. Management includes antithyroid medications, radioiodine therapy, or thyroidectomy. Antithyroid drugs are usually the first line treatment but have potential adverse effects. Radioiodine is an alternative that destroys thyroid tissue over time. Considerations for special populations like pregnant women are also covered.
This document provides information on fat embolism syndrome and pulmonary embolism. It discusses the background, causes, pathophysiology, clinical features, diagnostic criteria, investigations and treatment of fat embolism syndrome. It also covers the definition, risk factors and evaluation of pulmonary embolism. The key points are that fat embolism syndrome is a clinical diagnosis with non-specific tests, treatment is supportive, and prevention focuses on early fracture stabilization and adequate hydration and prophylaxis.
This document reviews acute respiratory distress syndrome (ARDS), fat embolism, and thromboembolic disease in orthopaedic trauma patients. It discusses the history, diagnosis, classification, epidemiology, pathophysiology, and treatment of ARDS, fat embolism, and venous thromboembolism (VTE). For ARDS, it outlines the Berlin Definition criteria and risk factors. It describes the two main theories for the pathophysiology of fat embolism. The document also reviews prevention and treatment strategies for fat embolism and VTE in orthopaedic trauma patients.
This document discusses fat embolism syndrome (FES), including its history, causes, mechanisms, clinical presentation, diagnosis, and treatment. Some key points:
- FES was first identified in 1862 and occurs when fat enters the bloodstream after long bone fractures or other trauma, causing respiratory, neurological and dermal symptoms.
- The exact mechanism is unknown but theories include fat globules entering blood mechanically from bone marrow or biochemically through free fatty acid release.
- Clinical diagnosis is based on respiratory issues, neurological abnormalities like confusion, and a petechial rash occurring 1-3 days post-injury. Treatment focuses on respiratory support.
This document discusses fat embolism syndrome, which refers to a clinical syndrome following an insult that releases fat into the circulation, causing pulmonary and systemic symptoms. It presents 24-72 hours after injury and has a mortality rate of 10-20%. Risk factors include long bone fractures from blunt trauma. Pathophysiology involves fat globules lodged in the pulmonary vasculature and brain. The clinical triad includes pulmonary dysfunction, neurological signs, and dermatological petechiae. Diagnosis relies on criteria from Gurd or Schonfeld. Treatment focuses on supportive care, oxygenation, hemodynamics, and occasionally steroids.
Fat Embolism Syndrome (FES) is a Syndrome characterized by: Hypoxia, Confusion and Petechiae. Presenting soon after long bone fracture and soft tissue injury. Diagnosed by exclusion of other causes 0f (Hypoxia & Confusion). It occurs in 0.9 – 8.5% of all fracture patients. Up to 35% of the multiply injured. Mortality 2.5 – 15 - 20%. Rare in upper limb injury and children.
Treatment includes prompt stabilization of long bone fractures and supportive measures which includes: 1- Oxygen Therapy to maintain PaO2. 2- Mechanical Ventilation. 3- Adequate Hydration.
This document discusses several anesthetic complications that can occur during pregnancy, including thrombocytopenia/epidural hematoma, aspiration, difficult airways, and neuraxial blockade complications. Key points include: 1) There is no minimum platelet count that absolutely contraindicates neuraxial procedures, but less than 100,000 is often quoted as a threshold. 2) Pregnancy increases the risk of aspiration due to anatomical changes, so all pregnant patients are considered at high risk of aspiration. 3) Airway management can be difficult in pregnancy due to edema and weight gain; facilities should be prepared with multiple airway devices and surgical options. 4) Neuraxial blockade commonly causes hypotension due to sympathetic blockade,
Cushing's syndrome is caused by excessive cortisol levels and can be due to exogenous glucocorticoid use or endogenous overproduction. It is characterized by central obesity, moon face, buffalo hump, skin changes, hypertension and diabetes. The diagnosis involves tests to check for cortisol suppression and circadian rhythm disturbances. Further tests are then used to determine the underlying cause as pituitary, adrenal or ectopic tumor. Treatment depends on the specific cause but may include surgery, medication or radiation. Pheochromocytomas are rare catecholamine-secreting tumors that cause hypertension and panic attacks. Diagnosis involves urine or plasma tests for metabolites and imaging to locate the tumor. Preparation with alpha-blockers is usually
This document provides background information on fat embolism syndrome (FES). It discusses that FES has a high incidence in patients with major trauma and causes multi-organ inflammation if not diagnosed and treated swiftly. While the exact mechanisms are not fully understood, FES is thought to be triggered by the release of fat emboli from bone fractures that occlude blood vessels and cause pulmonary and systemic inflammation. The diagnosis is mainly clinical based on respiratory, skin and neurological symptoms following trauma. Supportive care is the primary treatment approach through oxygenation, ventilation and symptom management while efforts focus on prevention, early diagnosis and surgical stabilization of fractures.
This document provides an overview of acute respiratory distress syndrome (ARDS) including its definition, pathophysiology, clinical presentation, diagnosis, and management. Some key points:
- ARDS is characterized by acute hypoxemic respiratory failure due to widespread inflammation and fluid buildup in the lungs.
- Treatment involves supportive care with mechanical ventilation using low tidal volumes, maintaining adequate oxygen levels, treating the underlying cause, and considering rescue therapies for severe cases like prone positioning or extracorporeal membrane oxygenation.
- Mortality remains high at around 26-58% depending on severity, with the most common causes of death being complications of the initial insult or secondary infections like pneumonia. Ongoing research focuses on
Fat embolism syndrome is a clinical diagnosis characterized by a triad of hypoxemia, neurological abnormalities, and petechial rash that develops within 24-72 hours of long bone fractures or other trauma. Fat particles released from the bone marrow can cause pulmonary and systemic complications by lodging in the lungs and other organs. While supportive care focuses on oxygenation, ventilation, and hemodynamic stability, the most effective prevention method is early surgical fixation of fractures within 24 hours to reduce risk. Outcomes range from full recovery to respiratory failure and death, depending on severity.
Sarcoidosis is a multisystem disorder characterized by noncaseating granulomas in affected tissues. It most commonly involves the lungs but can affect other organs. The cause is unknown but genetic and environmental factors are thought to play a role. Diagnosis is made through biopsy showing granulomas and excluding other causes. Treatment involves corticosteroids for organ involvement. Prognosis is generally good with remission occurring within 3 years for over half of patients.
Similar to FAT EMBOLISM SYNDROME (FES)_Dr. Mousa.ppt (20)
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
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TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kol...rightmanforbloodline
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Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
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Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
4. •Fat embolism syndrome is a
well-known cause of pulmonary
and neurologic dysfunction
secondary to a variety of
injuries.
•Its presentation vary from a sub
clinical state to fulminant
respiratory failure.
5. •The amount of manipulation of
injured tissue and degree of
hypovolemia or hypoperfusion
are thought to be factors that
predispose the patient to fat
embolism syndrome.
•Overall mortality range from 5 to
15 %.
6.
7. Pathophysiology
•FES most commonly associated
with long bone and pelvic
fractures, and most common in
closed rather than open fracture.
•Patients with a single long bone
fracture have 1-3 % chance of
developing the syndrome .
8.
9.
10.
11. Pathophysiology (Cont’d.)
•The incidence increase to 33 %
with bilateral femoral fractures.
•Other less common causes include
liposuction thrombolytic therapy
and orthopedic reconstructive
surgery.
•
12. Pathophysiology Cont’d.
•Theories about the origin of fat
deposition in the pulmonary
vasculature include venous fat
embolization originating from
traumatized bone marrow or
excessive mobilization of free fatty
acid from peripheral tissue secondary
to stress hormones.
13. Pathophysiology Cont’d.
•Those acids coalesce in the blood
and form fat aggregates.
•Regardless of the site of origin of fat
emboli the pulmonary capillaries act
as filters and the emboli are carried
to the lung where they lodge in
pulmonary capillaries and increase
resistance to blood flow.
14. Pathophysiology Cont’d.
•The lung parenchymal produce
lipase to remove emboli.
•Hydrolysis of the triglycerides to
glycerol and fatty acid occur
and chemical pneumonitis
results.
16. Pathophysiology Cont’d.
•Morphologically there is increase
in the permeability of the
capillaries and alveolar cell
With leakage of fluid and protein
into the alveolar wall and into
alveolar space.
17. Pathophysiology Cont’d.
•Lung surfactant activity is decreased,
functional residual capacity is
reduced and there is diffusion barrier.
•This cascade of events is seen
clinically as decreased pulmonary
compliance, increase a work of
breathing and hypoxia.
18. Pathophysiology Cont’d.
•Other studies demonstrate presents of
echogenic material passing into right
heart during orthopedic and spinal
surgery, with continued emoblization
,pulmonary artery and right pressure
rise and material can pass through
patent foramen ovale into systemic
circulation resulating in paradoxical
embolism.
19. Pathophysiology Cont’d.
•Serum from acutely ill
patients has the capacity to
agglutinate chylomicrons,
low density lipoprotein and
liposomes of nutritional fat
emulsions.
20. Pathophysiology Cont’d.
•C reactive protein which
appear to be elevated in these
patient appear to be responsible
for the lipid agglutination and
may also participate in the
mechanism for non traumatic
fat embolism .
21.
22. Clinical Manifestation
•FES typically manifest 24 to
72 hours after the initial
insult rarely occur as early
as 12 hours or as later 2
weeks after the inciting
events.
24. Clinical Manifestation (Cont’d.)
1. Pulmonary abnormalities
- Diffuse bilateral inspiratory
crepitation
- Approximately one half of the
patients with FES develop
severe hypoxemia and require
mechanical ventilation
25. Clinical Manifestation (Cont’d.)
2. Neurological abnormalities
• Neurological abnormalities
occur in majority of patient
with FES and often occur
after development of
respiratory distress.
26. Clinical Manifestation (Cont’d.)
2. Neurological abnormalities
• Affected patients usually
develop a confusional state
followed by an altered level of
consciousness.
• Seizures and focal deficits also
have been described.
27. Clinical Manifestation (Cont’d.)
2. Neurological abnormalities
• In severe injured patients it
may difficult to separate
changes caused by fat
embolism from these caused
by head injury.
28. Clinical Manifestation (Cont’d.)
2. Neurological abnormalities
In general changes caused
by fat embolism are diffuse
without localization and may
change quickly.
29. Clinical Manifestation (Cont’d.)
2. Neurological
abnormalities
• The etiology of these
mental changes may
related to hypoxia or direct
fat embolism to the brain.
30. Clinical Manifestation (Cont’d.)
2. Neurological abnormalities
• The duration and severity of
the neurological
disturbances are directly
related to the degree of
hypoxemia.
31. Clinical Manifestation (Cont’d.)
2. Neurological abnormalities
• There is no relation between
the severity of neurological
signs and the prognosis for
recovery.
• The neurological finding are
reversible in most cases.
32. Clinical Manifestation (Cont’d.)
3. Petechial haemorrhage
• The classic clinical finding in patients
with fat emnbolism is petechial
haemorrhage which may appear as
early as 12 hours after injury or late
as 3 to 4 days.
• The petechiae occur in 40 % of
patient with FES.
33. Clinical Manifestation (Cont’d.)
3. Petechial haemorrhage
• They can be seen most easily in
the head, neck, anterior thorax,
axilla and subconjunctiva,
over the sclera and may
accompanied by haemorrhages
in the eye ground.
34. Clinical Manifestation (Cont’d.)
3. Petechial haemorrhage
• The petechiae come in crops
and feed over 48 hours.
• The presence of 6 to 12 classic
petechiae firmly establishes the
clinical diagnosis of fat
embolism.
35. Clinical Manifestation (Cont’d.)
3. Petechial haemorrhage
• The petechial rash result from
occlusion of dermal capillaries by fat
globules loading to extravasation of
erythrocyte or may due to increase
capillary fragility.
• The rash usually resolve in 5 to 7 days.
36.
37. Diagnosis
• FES clinical diagnosis
usually characterized by
presence of respiratory
insufficiency, neurological
impairment and petechial
rash.
38. Diagnosis (Cont’d.)
• Chest X-Ray normal in majority
of patients
• Minority have diffuse or patchy
air space consolidation, these
changes are due to oedema or
alveolar haemorrhage and are
most prominent in the periphery
and bases.
42. Diagnosis (Cont’d.)
• Focal areas of ground glass
opacification with interlobar
septal thickening are
generally seen on chest CT.
43.
44.
45.
46. Diagnosis (Cont’d.)
• MRI of the brain may reveal
high intensity T2 signal which
correlate with the degree of
clinical neurological
impairment.
47. Diagnosis (Cont’d.)
• There is growing literature on
the use of bronchoscopy with
BAL to detect fat globules in
the alveolar macrophage as
mean to diagnose fat
embolism.
51. Treatment and Prevention
1. Early immoblization of the
fractures reduce the incidence
of FES. The risk further
reduce by operative correction
rather than conservative
management (i.e. traction
alone).
52.
53.
54. Treatment and Prevention
2. Supportive care is the
mainstay of therapy for FES.
3. Mortality is estimated to be
between 5 and 15 %.
55. Treatment and Prevention
• Use of corticosteroid
prophylaxis. There is number
of study report decrease
incidence of FES by use of
prophylactic steroid.
56. Treatment and Prevention
• Methyl Prednisolone 7.5
mg/kg every 6 hours for 12
doses. No complication
related to steroid treatment
was observed.
57.
58.
59.
60. Treatment and Prevention
• One rational, conservative approach
would be to give prophylactic steroid
therapy only to those patient at high risk
for FES as those with long bone or
pelvic fractures especially closed
fractures. Give methyl Prednisolone 1.5
mg/kg every 8 hours for six doses.
61.
62. Treatment and Prevention
• Because hypoxemia is the
fundamental physiological
defect, its prevention by early
administration of oxygen is
reasonable.
63. Treatment and Prevention
• If it becomes impossible to
maintain Pa02 above 60
mmHg with 40 % oxygen
inhalation, intubation and use
of mechanical ventilation
must be considered.
64. Treatment and Prevention
• The use of positive end
expiratory pressure is helpful to
maintaining adequate
oxygenation with lower
concentration of oxygen.
• There is no benefit to raising
Pa02 above 100 mmHg.