2010/05/22
Fat Embolism
The quantity was referred to in the last program of the common ABC telly broadcast "House" and since then people somebody been really eager to cognise writer nigh the term. Considering the fact that friendly networking place Chirrup has transmute the most touristed modality of connexion, group are also tweeting on the subject.Thanks to the video periodical, fill are now conversation of modification caused by an nausea that was supposedly not regularize heard of before. According to examination history, fat embolism was rank perceived in the twelvemonth 1873. Doctors explained that the syndrome was the ending of an accruement of fat instruction globules in the rare tracts of the lungs which leads to breathing problems as the fat in the lungs coil the respiratory piece.Fat embolism according to doctors is a really extraordinary disease and is also real catchy to notice in a organism. Though the venture for the employment of such a disease may be a limited breakage, a paper unhealthiness, vaudevillian on the cutis or any respiratory disarray, more of us are quite unacquainted with the quantity. After the recent cite of fat interval by one of the characters in "House", the communal man seems to mortal turn addicted to the point and is on the track for sources which may helpfulness them to get a gambler statement of the medical statement, an statement that was not provided in the broadcast.In the closing programme of "House", the role of Hannah dies of fat embolism, which is caused by an amputation activity. Since then grouping hit been on the watch for an statement to fat interval.
2010/05/21
Fat Embolism Syndrome in a Surgical Patient: Discussion
The workup of a patient with acute onset of shortness of breath after an orthopedic operative procedure should include consideration of pulmonary thromboembolism and fat embolism as possible causes. Fat embolus is a common occurrence in many orthopedic procedures. Although it has been described extensively in the setting of long-bone fractures and multiple trauma, fat embolism syndrome has not been widely reported as a complication of total hip arthroplasty.
In the patient described above, the diagnosis of fat embolism syndrome was entertained after the possibility of pulmonary thromboembolism was ruled out. The fat embolism syndrome was first described clinically by Von Bergmann,who cared for a man with a broken femur and symptoms of the syndrome in 1873. The prevalence of fat embolism syndrome among all fracture patients is reported to be between 0.25% and 1.25%. Among patients with multiple bone fractures, the prevalence can reach 5% to 10%.
The pathophysiology of fat embolism syndrome has not yet been definitively characterized. A mechanical theory holds that the embolization event results from a transient rise in pressure in a fat-containing cavity in association with torn blood vessels, allowing escape of marrow or adipose fat cells into the circulation.Two alternative biochemical theories posit explanations for fat embolism syndrome, both of which could account for the observation of the syndrome in nontraumatic settings. In one, fat droplets already in the circulation are broken down at distal sites to free fatty acids, which then exert a local toxic effect on the tissues. This theory explains the appearance of petechiae and the histologic changes in pneumocytes in association with fat-embolism-induced acute respiratory distress syndrome (ARDS).The obstructive explanation for fat embolism syndrome proposes that free fatty acids are mobilized by circulating catecholamines. Fat droplets in the circulation eventually coalesce and embolize, causing destructive effects.
Fat embolism syndrome can occur in immediate conjunction with a precipitating factor or it can be delayed for up to 3 days, although 85% of cases are apparent within 48 hours. The diagnostic workup of a patient suspected of having fat embolism syndrome should include serial arterial blood gas measurements, as hypoxemia is one of the cardinal features. Serial chest radiographs can be used to observe the progression of ARDS infiltrates in the lungs, although it should be noted that chest radiographic changes are often not apparent in the initial stages of the syndrome. An ECG might show a new right bundle-branch block or nonspecific T-wave changes. A late laboratory marker of fat embolism syndrome is serum lipase, which becomes elevated 3 to 5 days after embolization and peaks at 5 to 8 days.
Gurd and Wilson proposed the most widely accepted guidelines for the diagnosis of fat embolism syndrome, which require at least one sign from the major and at least four signs from the minor criteria ( Table 1). An alternative set of standards was later proposed by Lindeque et al, who believed that the criteria of Gurd and Wilson were too restrictive. The criteria of Lindeque et al are seldom used among clinicians, in part because of they are unable to distinguish fat embolism syndrome from other causes of respiratory distress.
The histologic diagnosis of fat embolism syndrome relies on observing fat globules in vascular spaces. This finding is most reliably obtained by a biopsy of superficial cutaneous petechial lesions. Fat globules can also be found in sputum and urine, although this evidence is made more elusive by the fact that fat must be actively circulating at the time the sample is collected.
The treatment of fat embolism syndrome is primarily supportive. As with other causes of ARDS, maintaining adequate tissue oxygenation and an arterial oxygen saturation of more than 90% should be the clinician's goal. The patient's lung disease might necessitate the use of positive airway pressure or even mechanical ventilation. Because many patients suffer fat embolism syndrome in conjunction with multiple trauma, general supportive measures, including hemodynamic stabilization, maintenance of normal electrolyte values, and prompt attention to orthopedic and soft-tissue injury should be maintained.
The effects of steroids on patients with fat embolism syndrome have long been debated in the literature. The theoretical basis for using corticosteroids is sound; they are thought to stabilize granulocyte membranes, reduce catecholamine levels, retard platelet aggregation, inhibit the activation of complement system, and protect the capillary endothelium. Corticosteroids have been shown to reduce the incidence of fat embolism syndrome when given prophylactically in the emergency department, although data showing a therapeutic role for them once clinically apparent fat embolism syndrome has developed have remained elusive.
Orthopedic surgeons might be able to reduce their patients' risk of fat embolism syndrome. Early fracture fixation has decreased the incidence of pulmonary complications and fat embolism syndrome related to long-bone trauma. Using a distal drain hole or a proximal and distal vacuum during the cementing stage of total hip arthroplasty has been associated with markedly reduced embolization. Recent studies using ultrasound have detected embolic events in routine total hip replacement operations in 94% and 100% of patients studied. No patients in either group, however, showed clinically observable symptoms, underscoring the complexity of the factors that contribute to the genesis of the fat embolism syndrome.
It is thought that the technique used to cement the intramedullary component of the prosthesis causes embolic events during total hip arthroplasty. In the traditional method, the femoral canal is first reamed out. Next, glue is inserted into the intramedullary canal, then the stem of the prosthesis. This technique generates tremendous pressures in the canal, which might cause the extravasation of marrow or cement into the vasculature. Use of a distal drain hole or vacuum greatly reduces the intermedullary pressures during total hip arthroplasty. Although such new approaches seem to reduce a patient's risk of fat embolism syndrome, surgeons caution that operative techniques which use a distal port might be associated with increased incidence of cement failure and femoral shaft fracture.
Table 1. Criteria for Fat Embolism Syndrome by Gurd and Wilson
Major Criteria Minor Criteria
Petechiae in a vest distribution Tachycardia (heart rate > 110 beats per minute)
Hypoxemia with PaO2 <> 38.5°C)
FI02 < /= 0.4
Central nervous system depression Emboli visible in retina
disproportionate to hypoxemia
Pulmonary edema Fat in urine
Fat in sputum
Unexplained drop in hematocrit or platelet count
Increasing erythrocyte sedimentation rate
PaO
2
- arterial oxygen pressure, FIO
2
- forced inspiratory oxygen.
In the patient described above, the diagnosis of fat embolism syndrome was entertained after the possibility of pulmonary thromboembolism was ruled out. The fat embolism syndrome was first described clinically by Von Bergmann,who cared for a man with a broken femur and symptoms of the syndrome in 1873. The prevalence of fat embolism syndrome among all fracture patients is reported to be between 0.25% and 1.25%. Among patients with multiple bone fractures, the prevalence can reach 5% to 10%.
The pathophysiology of fat embolism syndrome has not yet been definitively characterized. A mechanical theory holds that the embolization event results from a transient rise in pressure in a fat-containing cavity in association with torn blood vessels, allowing escape of marrow or adipose fat cells into the circulation.Two alternative biochemical theories posit explanations for fat embolism syndrome, both of which could account for the observation of the syndrome in nontraumatic settings. In one, fat droplets already in the circulation are broken down at distal sites to free fatty acids, which then exert a local toxic effect on the tissues. This theory explains the appearance of petechiae and the histologic changes in pneumocytes in association with fat-embolism-induced acute respiratory distress syndrome (ARDS).The obstructive explanation for fat embolism syndrome proposes that free fatty acids are mobilized by circulating catecholamines. Fat droplets in the circulation eventually coalesce and embolize, causing destructive effects.
Fat embolism syndrome can occur in immediate conjunction with a precipitating factor or it can be delayed for up to 3 days, although 85% of cases are apparent within 48 hours. The diagnostic workup of a patient suspected of having fat embolism syndrome should include serial arterial blood gas measurements, as hypoxemia is one of the cardinal features. Serial chest radiographs can be used to observe the progression of ARDS infiltrates in the lungs, although it should be noted that chest radiographic changes are often not apparent in the initial stages of the syndrome. An ECG might show a new right bundle-branch block or nonspecific T-wave changes. A late laboratory marker of fat embolism syndrome is serum lipase, which becomes elevated 3 to 5 days after embolization and peaks at 5 to 8 days.
Gurd and Wilson proposed the most widely accepted guidelines for the diagnosis of fat embolism syndrome, which require at least one sign from the major and at least four signs from the minor criteria ( Table 1). An alternative set of standards was later proposed by Lindeque et al, who believed that the criteria of Gurd and Wilson were too restrictive. The criteria of Lindeque et al are seldom used among clinicians, in part because of they are unable to distinguish fat embolism syndrome from other causes of respiratory distress.
The histologic diagnosis of fat embolism syndrome relies on observing fat globules in vascular spaces. This finding is most reliably obtained by a biopsy of superficial cutaneous petechial lesions. Fat globules can also be found in sputum and urine, although this evidence is made more elusive by the fact that fat must be actively circulating at the time the sample is collected.
The treatment of fat embolism syndrome is primarily supportive. As with other causes of ARDS, maintaining adequate tissue oxygenation and an arterial oxygen saturation of more than 90% should be the clinician's goal. The patient's lung disease might necessitate the use of positive airway pressure or even mechanical ventilation. Because many patients suffer fat embolism syndrome in conjunction with multiple trauma, general supportive measures, including hemodynamic stabilization, maintenance of normal electrolyte values, and prompt attention to orthopedic and soft-tissue injury should be maintained.
The effects of steroids on patients with fat embolism syndrome have long been debated in the literature. The theoretical basis for using corticosteroids is sound; they are thought to stabilize granulocyte membranes, reduce catecholamine levels, retard platelet aggregation, inhibit the activation of complement system, and protect the capillary endothelium. Corticosteroids have been shown to reduce the incidence of fat embolism syndrome when given prophylactically in the emergency department, although data showing a therapeutic role for them once clinically apparent fat embolism syndrome has developed have remained elusive.
Orthopedic surgeons might be able to reduce their patients' risk of fat embolism syndrome. Early fracture fixation has decreased the incidence of pulmonary complications and fat embolism syndrome related to long-bone trauma. Using a distal drain hole or a proximal and distal vacuum during the cementing stage of total hip arthroplasty has been associated with markedly reduced embolization. Recent studies using ultrasound have detected embolic events in routine total hip replacement operations in 94% and 100% of patients studied. No patients in either group, however, showed clinically observable symptoms, underscoring the complexity of the factors that contribute to the genesis of the fat embolism syndrome.
It is thought that the technique used to cement the intramedullary component of the prosthesis causes embolic events during total hip arthroplasty. In the traditional method, the femoral canal is first reamed out. Next, glue is inserted into the intramedullary canal, then the stem of the prosthesis. This technique generates tremendous pressures in the canal, which might cause the extravasation of marrow or cement into the vasculature. Use of a distal drain hole or vacuum greatly reduces the intermedullary pressures during total hip arthroplasty. Although such new approaches seem to reduce a patient's risk of fat embolism syndrome, surgeons caution that operative techniques which use a distal port might be associated with increased incidence of cement failure and femoral shaft fracture.
Table 1. Criteria for Fat Embolism Syndrome by Gurd and Wilson
Major Criteria Minor Criteria
Petechiae in a vest distribution Tachycardia (heart rate > 110 beats per minute)
Hypoxemia with PaO2 <> 38.5°C)
FI02 < /= 0.4
Central nervous system depression Emboli visible in retina
disproportionate to hypoxemia
Pulmonary edema Fat in urine
Fat in sputum
Unexplained drop in hematocrit or platelet count
Increasing erythrocyte sedimentation rate
PaO
2
- arterial oxygen pressure, FIO
2
- forced inspiratory oxygen.
2010/05/19
fat embolism syndrome
Emboli composed of fat are common, relatively innocuous and may occur in alcoholism, BM biopsy, cardiopulmonary bypass, compression injury, DM, lymphangiography, pancreatitis, sickle cell anemia, corticosteroid therapy; contrarily, the FES is neither common nor trivial; clinically significant FE may be endogenous or exogenous in origin; most are due to major fractures, especially of long bones, and trauma to parenchymal organs–eg, the liver–most deaths in the immediate post-trauma period have significant fat embolism, burns, blast injury, severe infections, especially α-toxin-producing Clostridium spp Clinical Hypoxia–50% of femoral shaft fractures have ↓ arterial PO2 within the first few days, acute onset of dyspnea, tachypnea, cyanosis, tachycardia with sudden onset of right-sided cardiac failure, showers of petechiae, thrombocytopenia, cerebral embolism–with changes in personality, confusion, drowsiness, weakness, agitation, spasticity, defects of the visual field, and rarely, extreme pyrexia Diagnosis It had been reported that fat droplets in a BAL was indicative of fat embolism, a finding which in one small–34 group of Pts proved to have a low specificity of 26.5%; > 3% oil red O positive macrophages in the BAL are often found in trauma Pts, and may indicate FES or silent FE Treatment No therapy is effective.
2010/05/18
fat embolism
embolism /em·bo·lism/ (em´bŏ-lizm) the sudden blocking of an artery by a clot or foreign material which has been brought to its site of lodgment by the blood current.
air embolism that due to air bubbles entering the veins from trauma, surgical procedures, or severe decompression sickness.
cerebral embolism embolism of a cerebral artery.
coronary embolism embolism of a coronary artery.
fat embolism obstruction by a fat embolus, occurring especially after fractures of large bones.
miliary embolism embolism affecting many small blood vessels.
paradoxical embolism blockage of a systemic artery by a thrombus originating in a systemic vein that has passed through a defect in the interatrial or interventricular septum.
pulmonary embolism obstruction of the pulmonary artery or one of its branches by an embolus.
fat embolism n.
a circulatory condition characterized by the blocking of an artery by a plug of fat. The plug enters the circulatory system after the fracture of a long bone or, less commonly, after traumatic injury to adipose tissue or to a fatty liver. Fat embolism usually occurs suddenly 12 to 36 hours after an injury and is characterized by symptoms related to the site occluded, such as severe chest pain, pallor, dyspnea, tachycardia, delirium, prostration, and in some cases coma. Anemia and thrombocytopenia are common. Systemic fat embolism may occur after extensive trauma, since lipid metabolism is altered by the injury and free fatty acids are released, resulting in vasculitis with obstruction of many small pulmonary and cerebral arteries. Classic signs of systemic fat embolism are petechial hemorrhages on the neck, shoulders, axillae, and conjunctivae that appear 2 or 3 days after the injury. Radiographic findings include patchy diffuse opacities throughout the lungs. There is no specific therapy for systemic fat embolism. The patient is placed in a high Fowler's position and given oxygen, corticosteroids, blood transfusion, respiratory assistance, or other supportive care as needed.
air embolism that due to air bubbles entering the veins from trauma, surgical procedures, or severe decompression sickness.
cerebral embolism embolism of a cerebral artery.
coronary embolism embolism of a coronary artery.
fat embolism obstruction by a fat embolus, occurring especially after fractures of large bones.
miliary embolism embolism affecting many small blood vessels.
paradoxical embolism blockage of a systemic artery by a thrombus originating in a systemic vein that has passed through a defect in the interatrial or interventricular septum.
pulmonary embolism obstruction of the pulmonary artery or one of its branches by an embolus.
fat embolism n.
a circulatory condition characterized by the blocking of an artery by a plug of fat. The plug enters the circulatory system after the fracture of a long bone or, less commonly, after traumatic injury to adipose tissue or to a fatty liver. Fat embolism usually occurs suddenly 12 to 36 hours after an injury and is characterized by symptoms related to the site occluded, such as severe chest pain, pallor, dyspnea, tachycardia, delirium, prostration, and in some cases coma. Anemia and thrombocytopenia are common. Systemic fat embolism may occur after extensive trauma, since lipid metabolism is altered by the injury and free fatty acids are released, resulting in vasculitis with obstruction of many small pulmonary and cerebral arteries. Classic signs of systemic fat embolism are petechial hemorrhages on the neck, shoulders, axillae, and conjunctivae that appear 2 or 3 days after the injury. Radiographic findings include patchy diffuse opacities throughout the lungs. There is no specific therapy for systemic fat embolism. The patient is placed in a high Fowler's position and given oxygen, corticosteroids, blood transfusion, respiratory assistance, or other supportive care as needed.
X-ray Image of Fat Embolism
Fat embolism in a 58-year-old woman who presented with sudden dyspnea. The patient had undergone intramuscular injection of some fatty materials into the buttock several days earlier. (a) Radiograph shows bilateral ground-glass areas of increased opacity. (b) Thin-section (1-mm collimation) CT scan obtained at the level of the aortic arch shows widespread patchy ground-glass attenuation and consolidation. A follow-up radiograph obtained 10 days later (not shown) revealed complete resolution of the ground-glass patterns.
But what is Fat Embolism?
Fat Embolism is an infrequent complication of long bone fracture, occurring in 1%–3% of patients with simple tibial or femoral fractures but in up to 20% of individuals with more severe trauma. Less common causes include hemoglobinopathy, major burns, pancreatitis, overwhelming infection, tumors, blood transfusion, and liposuction. The mechanisms are not completely understood but presumably are twofold. The first mechanism is the production of free fatty acids, which initiates a toxic reaction in the endothelium. The process is further complicated by the accumulation of neutrophils and other inflammatory cells, which causes damage to the vasculature. The second mechanism is the mechanical obstruction of the pulmonary vasculature by fat globules and aggregates of red blood cells and platelets.
But what is Fat Embolism?
Fat Embolism is an infrequent complication of long bone fracture, occurring in 1%–3% of patients with simple tibial or femoral fractures but in up to 20% of individuals with more severe trauma. Less common causes include hemoglobinopathy, major burns, pancreatitis, overwhelming infection, tumors, blood transfusion, and liposuction. The mechanisms are not completely understood but presumably are twofold. The first mechanism is the production of free fatty acids, which initiates a toxic reaction in the endothelium. The process is further complicated by the accumulation of neutrophils and other inflammatory cells, which causes damage to the vasculature. The second mechanism is the mechanical obstruction of the pulmonary vasculature by fat globules and aggregates of red blood cells and platelets.
Fat Embolism: The News
Fat obstruction: mean? - Many people now look for the word "fat clogged" after seeing last season House '. After searching it seems that obstruction in the lipid environment into the circulatory system of physical injury or surgery. One of the most common examples of fats clog occurs when the fracture Fat obstruction that occurs when the body fat in the blood flow and cause difficulties. Symptoms fatty obstruction of medical education, including lung, skin and nervous system, hematology I think this is one of the consequences is fat We will take care of their health, especially broken bones or injuries, or our Below is a picture of fatty blockages. You can see clearly the accumulation of fat in the blood drops causing serious disease.
Fat Embolism: Things to Know About Fat Embolism
Fat Embolism: What Does It Mean? – A lot of people are now looking for the phrase “Fat Embolism” after watching House’ season finale.
After researching for it, it turns out that Fat Embolism is a condition where in fats enter the circulatory system because of a physical trauma or a surgery. One of the most common examples of a fat embolism happens when a bone was fractured. The Fat Embolism here happens when fatty bone marrow enters the blood stream and causes blockage to the continuous blood flow.
Symptoms of Fat Embolism according to medical studies include pulmonary, neurological, dermatological, and haematological conditions. I guess this is one of the consequences of being fat. Therefore, we should then take good care of our health most especially our bones not to have fractures or trauma.
Below is an picture of a Fat Embolism. You can clearly see the accumulation of fat globules in the blood stream which can cause severe health conditions.
After researching for it, it turns out that Fat Embolism is a condition where in fats enter the circulatory system because of a physical trauma or a surgery. One of the most common examples of a fat embolism happens when a bone was fractured. The Fat Embolism here happens when fatty bone marrow enters the blood stream and causes blockage to the continuous blood flow.
Symptoms of Fat Embolism according to medical studies include pulmonary, neurological, dermatological, and haematological conditions. I guess this is one of the consequences of being fat. Therefore, we should then take good care of our health most especially our bones not to have fractures or trauma.
Below is an picture of a Fat Embolism. You can clearly see the accumulation of fat globules in the blood stream which can cause severe health conditions.
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