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 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.
1. Fat embolism syndrome is a serious complication that can occur after long bone fractures, where fat particles travel through the blood and lodge in organs.
2. Symptoms usually develop within 24-72 hours and include respiratory issues, neurological changes, and a rash.
3. Treatment focuses on supportive care like oxygen supplementation, ventilation if needed, and intravenous fluids to maintain stability. Prevention emphasizes quick surgical fixation of fractures.
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 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 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.
This document discusses fat embolism syndrome (FES), which occurs in up to 10% of patients with severe skeletal injuries. It can lead to respiratory distress, hypoxemia, neurological abnormalities, and petechial rash. The highest risk is for patients with femur or pelvic fractures. Treatment is supportive care and prevention through early surgical fixation of long bone fractures. A multidisciplinary approach is recommended to monitor for symptoms and manage complications of FES.
This document discusses fat embolism syndrome (FES), which occurs in up to 10% of patients with severe skeletal injuries. It can lead to respiratory distress, hypoxemia, neurological abnormalities, and petechial rash. The highest risk is for patients with femur or pelvic fractures. Treatment is supportive care and prevention through early surgical fixation of long bone fractures. A multidisciplinary approach is recommended to monitor for symptoms and manage complications of FES.
Fat embolism syndrome is a condition where fat particles travel through the bloodstream and lodge in blood vessels, potentially causing organ dysfunction. It most commonly occurs after long bone fractures or pelvic fractures. While fat emboli occur in most patients with these injuries, less than 10% exhibit clinical symptoms. Symptoms usually begin 1-3 days after injury and involve the lungs, brain, and skin. Diagnosis is clinical and treatment is supportive, focusing on oxygenation, ventilation, circulation, and early surgical fixation of fractures when possible. Prognosis is generally good, though neurological deficits can occasionally persist long-term.
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.
1. Fat embolism syndrome is a serious complication that can occur after long bone fractures, where fat particles travel through the blood and lodge in organs.
2. Symptoms usually develop within 24-72 hours and include respiratory issues, neurological changes, and a rash.
3. Treatment focuses on supportive care like oxygen supplementation, ventilation if needed, and intravenous fluids to maintain stability. Prevention emphasizes quick surgical fixation of fractures.
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 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 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.
This document discusses fat embolism syndrome (FES), which occurs in up to 10% of patients with severe skeletal injuries. It can lead to respiratory distress, hypoxemia, neurological abnormalities, and petechial rash. The highest risk is for patients with femur or pelvic fractures. Treatment is supportive care and prevention through early surgical fixation of long bone fractures. A multidisciplinary approach is recommended to monitor for symptoms and manage complications of FES.
This document discusses fat embolism syndrome (FES), which occurs in up to 10% of patients with severe skeletal injuries. It can lead to respiratory distress, hypoxemia, neurological abnormalities, and petechial rash. The highest risk is for patients with femur or pelvic fractures. Treatment is supportive care and prevention through early surgical fixation of long bone fractures. A multidisciplinary approach is recommended to monitor for symptoms and manage complications of FES.
Fat embolism syndrome is a condition where fat particles travel through the bloodstream and lodge in blood vessels, potentially causing organ dysfunction. It most commonly occurs after long bone fractures or pelvic fractures. While fat emboli occur in most patients with these injuries, less than 10% exhibit clinical symptoms. Symptoms usually begin 1-3 days after injury and involve the lungs, brain, and skin. Diagnosis is clinical and treatment is supportive, focusing on oxygenation, ventilation, circulation, and early surgical fixation of fractures when possible. Prognosis is generally good, though neurological deficits can occasionally persist long-term.
Fat embolism syndrome is a complication that can occur after long bone fractures, with onset of symptoms between 12-72 hours. It involves the blockage of small blood vessels in the lungs and other organs by fat globules, and can lead to respiratory distress, hypoxemia, neurological symptoms and petechial rash. Diagnosis is clinical and supported by criteria involving respiratory, neurological and skin findings. Treatment focuses on prevention through early surgical fixation of fractures, as well as supportive care of respiratory, cardiac and neurological complications. Outcomes vary from complete resolution to long-term deficits.
Umesh Yadav presented on fat embolism syndrome. Key points include:
1) Fat embolism syndrome is a serious complication of long bone fractures that can cause multi-system organ dysfunction, most commonly involving the lungs and brain.
2) The pathophysiology involves fat globules entering the bloodstream from broken bone marrow and lodging in the pulmonary vasculature and brain. This can lead to hypoxemia, neurological changes, and petechial rashes.
3) Diagnosis is clinical based on criteria like Gurd's that require respiratory symptoms plus findings in two other organ systems. Treatment focuses on fracture stabilization, ventilation, volume resuscitation and sometimes
- 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
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.
This document discusses fat embolism syndrome (FES), which occurs when fat particles travel through the bloodstream and lodge in blood vessels, potentially causing organ dysfunction. FES most commonly results from long bone fractures but can occur without trauma. It involves an initial asymptomatic period followed by pulmonary, neurological and skin manifestations. The pathophysiology may involve both mechanical obstruction of vessels by fat emboli and biochemical toxicity of free fatty acids. Diagnosis is clinical and management involves supportive care.
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.
Fat embolism occurs when fat enters the bloodstream and lodges in blood vessels, typically in the lungs. This can lead to fat embolism syndrome (FES), dysfunction of organs like the lungs and brain. FES risk factors include long bone fractures, especially those with high blood vessel density. Fat enters veins and forms emboli, which the lungs normally break down, but large numbers can overwhelm the lungs. In the lungs, emboli may plug vessels and cause injury through free fatty acids. While common clinical signs include respiratory distress, neurological changes, and petechiae rashes, laboratory findings like anemia and low platelets are not definitive for FES diagnosis.
Fat embolism syndrome is a rare complication that can occur following long bone fractures. It is caused by fat globules entering the bloodstream from broken bone marrow and causing mechanical obstruction or toxic effects. Clinically, it presents as a triad of respiratory distress, mental confusion, and petechial rash 12-72 hours after injury. Diagnosis is based on clinical criteria and treatment is supportive to maintain respiratory function. Prognosis is generally good, with most deaths due to pulmonary dysfunction or other injuries.
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.
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.
3 de 11
26/11/13 13:43
Fat embolism syndrome
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3665122/?repor...
Fat embolism syndrome is caused by fat particles entering the bloodstream and blocking small blood vessels following trauma. It most commonly occurs after orthopedic injuries like long bone fractures. Symptoms can range from mild respiratory issues to respiratory failure and involve multiple organ systems. There is no definitive test and diagnosis is based on clinical criteria. Treatment focuses on supportive care, and early surgical fixation of fractures may decrease risk.
Fat embolism syndrome is caused by fat globules entering the bloodstream after trauma like long bone fractures. It can cause respiratory failure, neurological symptoms, and a rash. Diagnosis is based on clinical criteria like hypoxemia, thrombocytopenia, and petechial rash appearing 1-4 days after injury. Treatment focuses on respiratory support, fluid resuscitation, steroids to reduce lung inflammation, and early fracture fixation to prevent worsening.
1. Fat embolism syndrome is a serious manifestation of fat embolism that can cause multi-system dysfunction, most commonly affecting the lungs and brain.
2. It occurs most often after long bone fractures, especially femur fractures, when fat droplets enter the bloodstream and lodge in the pulmonary capillaries or brain vasculature.
3. Clinical features include a triad of respiratory distress, neurological changes like confusion, and petechial rash. Diagnosis is based on clinical criteria and imaging may show changes in the lungs and brain. Treatment is supportive with oxygen, ventilation if needed, IV fluids and steroids. Prognosis is generally good if respiratory failure can be prevented.
1. Fat embolism syndrome is a serious condition caused by fat emboli obstructing blood vessels, most commonly after long bone or pelvic fractures. It typically manifests 1-3 days after injury.
2. Patients present with a classic triad of hypoxemia, neurological abnormalities, and petechial rash. The most severe cases can involve respiratory distress, restlessness, and coma.
3. Diagnosis requires signs from both major criteria like hypoxemia and petechiae, as well as four minor criteria. Treatment focuses on supportive care like oxygenation, ventilation, hemodynamics, and early stabilization of fractures to prevent further emboli.
This document discusses fat embolism syndrome and crush syndrome. It begins by describing a case of a 24-year-old male who was in a motor vehicle accident and sustained closed femur fractures. Two days later, the patient's condition deteriorated with decreased oxygen levels and blood pressure. The document then defines fat embolism syndrome and crush syndrome and discusses their causes, presentations, diagnoses, and management, which primarily involves supportive care focused on oxygenation and hemodynamics. The key differences between fat embolism syndrome and crush syndrome (rhabdomyolysis) are also outlined.
1. The document discusses acute respiratory distress syndrome (ARDS), describing its pathophysiology, causes, diagnosis, treatment and prognosis.
2. ARDS is characterized by hypoxemia, reduced lung compliance and diffuse pulmonary infiltrates leading to respiratory failure. Common causes include sepsis, pneumonia and trauma.
3. Treatment involves treating the underlying cause, supportive care including mechanical ventilation with low tidal volumes, and managing fluid levels and oxygenation. Prognosis depends on severity of illness, with reported mortality ranging from 41-65%.
muscle diseases 4th year.F is formed by active secretionRabeaDia
1. CSF is formed by active secretion by choroids plexus in the lateral ventricles then → pass via foramen of Monro to the 3rd ventricle → then via aqueduct of Sylvius to the 4th ventricle → then via foramena of Inuscka & Magendi to the subarachnoid space.
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Similar to fatembolismsyndrome-150804111012-lva1-app6892.pdf
Fat embolism syndrome is a complication that can occur after long bone fractures, with onset of symptoms between 12-72 hours. It involves the blockage of small blood vessels in the lungs and other organs by fat globules, and can lead to respiratory distress, hypoxemia, neurological symptoms and petechial rash. Diagnosis is clinical and supported by criteria involving respiratory, neurological and skin findings. Treatment focuses on prevention through early surgical fixation of fractures, as well as supportive care of respiratory, cardiac and neurological complications. Outcomes vary from complete resolution to long-term deficits.
Umesh Yadav presented on fat embolism syndrome. Key points include:
1) Fat embolism syndrome is a serious complication of long bone fractures that can cause multi-system organ dysfunction, most commonly involving the lungs and brain.
2) The pathophysiology involves fat globules entering the bloodstream from broken bone marrow and lodging in the pulmonary vasculature and brain. This can lead to hypoxemia, neurological changes, and petechial rashes.
3) Diagnosis is clinical based on criteria like Gurd's that require respiratory symptoms plus findings in two other organ systems. Treatment focuses on fracture stabilization, ventilation, volume resuscitation and sometimes
- 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
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.
This document discusses fat embolism syndrome (FES), which occurs when fat particles travel through the bloodstream and lodge in blood vessels, potentially causing organ dysfunction. FES most commonly results from long bone fractures but can occur without trauma. It involves an initial asymptomatic period followed by pulmonary, neurological and skin manifestations. The pathophysiology may involve both mechanical obstruction of vessels by fat emboli and biochemical toxicity of free fatty acids. Diagnosis is clinical and management involves supportive care.
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.
Fat embolism occurs when fat enters the bloodstream and lodges in blood vessels, typically in the lungs. This can lead to fat embolism syndrome (FES), dysfunction of organs like the lungs and brain. FES risk factors include long bone fractures, especially those with high blood vessel density. Fat enters veins and forms emboli, which the lungs normally break down, but large numbers can overwhelm the lungs. In the lungs, emboli may plug vessels and cause injury through free fatty acids. While common clinical signs include respiratory distress, neurological changes, and petechiae rashes, laboratory findings like anemia and low platelets are not definitive for FES diagnosis.
Fat embolism syndrome is a rare complication that can occur following long bone fractures. It is caused by fat globules entering the bloodstream from broken bone marrow and causing mechanical obstruction or toxic effects. Clinically, it presents as a triad of respiratory distress, mental confusion, and petechial rash 12-72 hours after injury. Diagnosis is based on clinical criteria and treatment is supportive to maintain respiratory function. Prognosis is generally good, with most deaths due to pulmonary dysfunction or other injuries.
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.
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.
3 de 11
26/11/13 13:43
Fat embolism syndrome
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3665122/?repor...
Fat embolism syndrome is caused by fat particles entering the bloodstream and blocking small blood vessels following trauma. It most commonly occurs after orthopedic injuries like long bone fractures. Symptoms can range from mild respiratory issues to respiratory failure and involve multiple organ systems. There is no definitive test and diagnosis is based on clinical criteria. Treatment focuses on supportive care, and early surgical fixation of fractures may decrease risk.
Fat embolism syndrome is caused by fat globules entering the bloodstream after trauma like long bone fractures. It can cause respiratory failure, neurological symptoms, and a rash. Diagnosis is based on clinical criteria like hypoxemia, thrombocytopenia, and petechial rash appearing 1-4 days after injury. Treatment focuses on respiratory support, fluid resuscitation, steroids to reduce lung inflammation, and early fracture fixation to prevent worsening.
1. Fat embolism syndrome is a serious manifestation of fat embolism that can cause multi-system dysfunction, most commonly affecting the lungs and brain.
2. It occurs most often after long bone fractures, especially femur fractures, when fat droplets enter the bloodstream and lodge in the pulmonary capillaries or brain vasculature.
3. Clinical features include a triad of respiratory distress, neurological changes like confusion, and petechial rash. Diagnosis is based on clinical criteria and imaging may show changes in the lungs and brain. Treatment is supportive with oxygen, ventilation if needed, IV fluids and steroids. Prognosis is generally good if respiratory failure can be prevented.
1. Fat embolism syndrome is a serious condition caused by fat emboli obstructing blood vessels, most commonly after long bone or pelvic fractures. It typically manifests 1-3 days after injury.
2. Patients present with a classic triad of hypoxemia, neurological abnormalities, and petechial rash. The most severe cases can involve respiratory distress, restlessness, and coma.
3. Diagnosis requires signs from both major criteria like hypoxemia and petechiae, as well as four minor criteria. Treatment focuses on supportive care like oxygenation, ventilation, hemodynamics, and early stabilization of fractures to prevent further emboli.
This document discusses fat embolism syndrome and crush syndrome. It begins by describing a case of a 24-year-old male who was in a motor vehicle accident and sustained closed femur fractures. Two days later, the patient's condition deteriorated with decreased oxygen levels and blood pressure. The document then defines fat embolism syndrome and crush syndrome and discusses their causes, presentations, diagnoses, and management, which primarily involves supportive care focused on oxygenation and hemodynamics. The key differences between fat embolism syndrome and crush syndrome (rhabdomyolysis) are also outlined.
1. The document discusses acute respiratory distress syndrome (ARDS), describing its pathophysiology, causes, diagnosis, treatment and prognosis.
2. ARDS is characterized by hypoxemia, reduced lung compliance and diffuse pulmonary infiltrates leading to respiratory failure. Common causes include sepsis, pneumonia and trauma.
3. Treatment involves treating the underlying cause, supportive care including mechanical ventilation with low tidal volumes, and managing fluid levels and oxygenation. Prognosis depends on severity of illness, with reported mortality ranging from 41-65%.
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আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
How to Manage Your Lost Opportunities in Odoo 17 CRMCeline George
Odoo 17 CRM allows us to track why we lose sales opportunities with "Lost Reasons." This helps analyze our sales process and identify areas for improvement. Here's how to configure lost reasons in Odoo 17 CRM
This slide is special for master students (MIBS & MIFB) in UUM. Also useful for readers who are interested in the topic of contemporary Islamic banking.
A review of the growth of the Israel Genealogy Research Association Database Collection for the last 12 months. Our collection is now passed the 3 million mark and still growing. See which archives have contributed the most. See the different types of records we have, and which years have had records added. You can also see what we have for the future.
This presentation includes basic of PCOS their pathology and treatment and also Ayurveda correlation of PCOS and Ayurvedic line of treatment mentioned in classics.
it describes the bony anatomy including the femoral head , acetabulum, labrum . also discusses the capsule , ligaments . muscle that act on the hip joint and the range of motion are outlined. factors affecting hip joint stability and weight transmission through the joint are summarized.
Chapter wise All Notes of First year Basic Civil Engineering.pptxDenish Jangid
Chapter wise All Notes of First year Basic Civil Engineering
Syllabus
Chapter-1
Introduction to objective, scope and outcome the subject
Chapter 2
Introduction: Scope and Specialization of Civil Engineering, Role of civil Engineer in Society, Impact of infrastructural development on economy of country.
Chapter 3
Surveying: Object Principles & Types of Surveying; Site Plans, Plans & Maps; Scales & Unit of different Measurements.
Linear Measurements: Instruments used. Linear Measurement by Tape, Ranging out Survey Lines and overcoming Obstructions; Measurements on sloping ground; Tape corrections, conventional symbols. Angular Measurements: Instruments used; Introduction to Compass Surveying, Bearings and Longitude & Latitude of a Line, Introduction to total station.
Levelling: Instrument used Object of levelling, Methods of levelling in brief, and Contour maps.
Chapter 4
Buildings: Selection of site for Buildings, Layout of Building Plan, Types of buildings, Plinth area, carpet area, floor space index, Introduction to building byelaws, concept of sun light & ventilation. Components of Buildings & their functions, Basic concept of R.C.C., Introduction to types of foundation
Chapter 5
Transportation: Introduction to Transportation Engineering; Traffic and Road Safety: Types and Characteristics of Various Modes of Transportation; Various Road Traffic Signs, Causes of Accidents and Road Safety Measures.
Chapter 6
Environmental Engineering: Environmental Pollution, Environmental Acts and Regulations, Functional Concepts of Ecology, Basics of Species, Biodiversity, Ecosystem, Hydrological Cycle; Chemical Cycles: Carbon, Nitrogen & Phosphorus; Energy Flow in Ecosystems.
Water Pollution: Water Quality standards, Introduction to Treatment & Disposal of Waste Water. Reuse and Saving of Water, Rain Water Harvesting. Solid Waste Management: Classification of Solid Waste, Collection, Transportation and Disposal of Solid. Recycling of Solid Waste: Energy Recovery, Sanitary Landfill, On-Site Sanitation. Air & Noise Pollution: Primary and Secondary air pollutants, Harmful effects of Air Pollution, Control of Air Pollution. . Noise Pollution Harmful Effects of noise pollution, control of noise pollution, Global warming & Climate Change, Ozone depletion, Greenhouse effect
Text Books:
1. Palancharmy, Basic Civil Engineering, McGraw Hill publishers.
2. Satheesh Gopi, Basic Civil Engineering, Pearson Publishers.
3. Ketki Rangwala Dalal, Essentials of Civil Engineering, Charotar Publishing House.
4. BCP, Surveying volume 1
2. History
First diagnosed in 1873 by Dr Von Bergmann
In 1879 Fenger and Salisbury published description of
Fat embolism syndrome
3. Fat Emboli: Fat particles or droplets that
travel through the circulation
Fat Embolism: A process by which fat
emboli passes into the bloodstream and
lodges within a blood vessel.
Fat Embolism Syndrome (FES): serious
manifestation of fat embolism occasionally
causes multi system dysfunction, the lungs are always
involved and next is brain
4. FE vs. FES
Fat embolization is a well-known complication of
skeletal trauma and surgery involving
instrumentation of the femoral medullary canal.
Fat embolism syndrome (FES) is a physiological
response to fat within the systemic circulation.
Fat embolization and FES are not synonymus.
The embolization of fat can be detected in almost all
patients who sustain a pelvic or femoral fracture, but
the incidence of FES is less than 1%.
5. Fat Embolism Syndrome
Mortality: 10-20%
Clinical diagnosis, No specific laboratory test is
diagnostic.
Mostly associated with long bone and pelvic
fractures, and more frequent in closed fractures.
Single long bone fracture has 1-3% chance of
developing FES, and increases with number of
fractures.
Onset is 24-72 hours from initial insult.
6. Causes of fat embolism
TRAUMA RELATED:
Blunt trauma: Long bone (Femur, tibia, pelvic) factures
orthopedic procedures
Soft tissue injury(chest compression with or without rib
fracture)
Burn
Liposuction
Bone marrow harvesting and transplant.
7. NON TRAUMA RELATED
Pancreatitis
Diabetes mellitus
Osteomyelitis and panniculitis
Bone tumor lysis
Steroid therapy
Sickle cell hemoglobinopathy
Alcoholic liver disease
Fat infusion
8. Most common cause of FES is blunt trauma.
90 % occursafter blunt trauma complicated by long-
bone fractures
Closed fractures had higher incidence compared to
open fractures. The intramedullary bone pressure is
lower in case of open fractures, which reduces the
bulk of fat emboli propelled into the blood stream.
9. Non-traumatic fat embolism
It occurs due to the process of fat or marrow necrosis
or by the increased concentration of lipids in the
blood.
It may be caused by agglutination of chylomicrons
and VLDL by high levels of plasma CRP.
As in Acute pancreatitis in patients with types I, IV,
and V hyperlipidaemia and avascular necrosis of bone
in patients with corticosteroid-induced
hyperlipidaemia.
10. Drug-related causes of FES
Infusion of lipids at rates greater than the normal
clearance capacity of lipids.
Agglutination of lipid emulsion particles with fibrin.
Agglutination of endogenous or infused exogenous
fat such as Intra lipid.
11. FES can occur in SC
crisis.
Bone marrow necrosis
as a result of hypoxia
may release fat.
13. Pathophysiology of FES
Exact mechanism unknown, but two main hypothesis
1. Mechanical Hypothesis
2.Biochemical Hypothesis
14. Mechanical Hypothesis
Obstruction of vessels and capillaries
Increase in inter medullary pressure forces fat and
marrow into bloodstream.
Bone marrow contents enter the venous system
and lodge in thelungs as emboli.
15. Smaller fat droplets travel through the pulmonary
capillaries into the systemiccirculation: Embolization to
cerebral vessels or renal vessels also leads to central
nervous system and renal dysfunction
16. Biochemical Hypothesis
Toxicity of free fatty acids
Circulating free fatty acids directly affectthe
pneumocytes, producing abnormalities in gas
exchange.
Coexisting shock, hypovolemia and sepsis impair liver
function and augment toxic effects of free fatty acids.
17. Hormonal changes caused by trauma or sepsis
induce systemic release of free fatty acids as
chylomicrons.
Acute-phase reactants( C-reactive proteins) cause
chylomicrons to coalesce.
It explains non traumatic forms of fat embolism
syndrome and why symptoms take 12 hours to
develop.
18. FE in ARDS
Fat emboli obstructs
lung vessel (20microns),
platelets and fibrin
adhere to it
Lipase increases FFA
Inflammatory changes-
>endothelial damage-
>ARDS
20. Pulmonary
Hypoxia, rales, pleural friction rub
ARDS may develop.
CXR usually normal early on, later may show
‘snowstorm’ pattern- diffuse bilateral infiltrates
CT chest: ground glass opacification with interlobular
septal thickening.
21. Neurological findings
Usually occur after respiratory symptoms
Incidence- 80% patients with FES
Minor global dysfunction is most common-ranges
from mild delirium to coma.
Seizures/focal deficits
Transient and reversible in most cases.
CT Head: general edema, usually nonspecific
MRI brain: Low density on T1, and high intensity T2
signal, correlates to degree of impairment.
22. Dermatological findings
Petechie
Usually on conjunctiva, neck, axilla, upper limbs.
Results from occlusion of dermal capillaries by fat
globules and then extravasations of RBC.
Resolves in 5-7 days. Usually fast resolving.
Pathognomic, but only present in 20-50% of patients.
28. Schonfeld Fat Embolism Syndrome
Index
It ranks signs and symptoms of FES in relation to
their incidence of presentation.
Score >5 required for diagnosis of fat embolism
syndrome
32. Imaging
• Chest x-ray
– shows multiple flocculent shadows (snow storm
appearance). picture may be complicated by infection
or pulmonary edema.
33. Imaging contd.
MRI Brain
- Image showing minimal hypodense changes
in periventricular region, which are more evident in
DWI and T2WI as areas of high signals.
34. Treatment and management
Prophylaxis
Immobilization and early internal fixation of
fracture.
Fixation within 24 hours has been shown to yield
a 5 fold reduction in the incidence of ARDS.
Continuous pulse oximeter monitoring in high-
risk patients may help in detecting desaturation
early, allowing early institution of oxygen and
possibly steroid therapy.
High doses of corticosteroids.
35. Supportive Medical Care
Maintenance of adequate oxygenation and ventilation
Maintenance of hemodynamic stability.
Administration of blood products as clinically
indicated.
Hydration
Prophylaxis of deep venous thrombosis .
Nutrition.
Treatment and management contd.
36. Treatment and management contd.
Oxygenation and ventilation
High flow rate oxygen is given to maintain the
arterial oxygen tension in the normal range.
Mechanical ventilation and PEEP may be required to
maintain arterial oxygenation.
37. Treatment and management contd.
Hemodynamic stability
Maintenance of intravascular volume is important,
because shock can exacerbate the lung injury caused
by FES.
Albumin has been recommended for volume
resuscitation in addition to balanced electrolyte
solution, because it not only restores blood volume
but also binds with the fatty acids and may decrease
extent of lung injury
38. Steroids
Steroid prophylaxis is controversial to prevent FES.
It causes blunting of inflammatory response and
complement activation
Prospective studies suggests prophylactic steroids
benefit in high risk patients.
Preoperative use of methylprednisolone may prevent
the occurrence of FES
Once FES established, steroids have not shown
improved outcomes.
39. Results of Randomized, Controlled Trials of Corticosteroids for Prevention of Fat
Embolism Syndrome
Dose Model Timing Duration of
study
Effect on
disease
incidence
30mg/kg Dog Before event 60min None
10mg/kg q8h
for 24 hrs
Human
trauma
At admission No data Declining
7.5mg/kg q6h
for 12hrs or
placebo
Human
Trauma
Within 12hrs 2 days Declining
40. Heparin
Heparin has also been proposed for treatment as it
"clears" lipemic plasma in vivo by causing the release
of lipoprotein lipase into the circulation, but no
evidence exists for its use in FES.
41. Prognosis
The fulminant form presents as acute cor pulmonale,
respiratory failure or embolic phenomena, leading to
death within a few hours of injury.
Most death contributed to pulmonary dysfunction
Hard to determine exact mortality rate
Estimated less than 10%
42. The incidence of FES ranges from < 1 to 29% in
different studies.
Actual incidence of FES is not known, as mild cases
often go unnoticed.
A high index of suspicion is needed to diagnose FES.
A combination of clinical criteria and MRI brain will
enable early and accurate diagnosis of FES.
43. Refrences
Altaf Hussain: “A Fatal Fat Embolism.” The Internet Journal of Anesthesiology,
2004. Volume 8 Number 2.
Fabian T. “Unraveling the fat embolism syndrome”. N Engl J Med 1993;329:961–
63
U. Galway, J. E. Tetzlaff & R. Helfand : “Acute Fatal Fat Embolism Syndrome In
Bilateral Total Knee Arthroplasty – A Review Of The Fat Embolism
Syndrome”. The Internet Journal of Anesthesiology. 2009 Volume 19 Number
2
Latif, A., Bashir, A., Aurangzeb. "Fat Embolism and Fat Embolism Syndrome;
Management Trends." Professional Med J 15.4 (2008): 407-413.
Harrisons principles of Internal medicine 18th
edition.
Nissar Shaikh, Emergency management of fat embolism syndrome.” J Emerg
Trauma Shock. 2009 Jan-Apr; 2(1): 29–33