AIPG 2005 Ortho Fat Embolism

Question
A 30-year-old man had road traffic accident and sustained fracture of femur. Two days later he developed sudden breathlessness. The most probable cause can be:
1. Pneumonia
2. Congestive heart failure.
3. Bronchial asthma.
4. Fat Embolism.
Answer
4. fat Emboolism.
Reference
Harrison 15th Edition Chapter 369
Sabistorn 15th Edition Chapter 18
Quality
Reader
Status
Repeat
QTDF
All Books
Discussion
Fat emboli probably originate from the bone marrow and enter the circulation through torn venules at the fracture site. Although direct occlusion of small blood vessels in the lungs, brain, and skin by fat droplets may cause ischemic injury, the pathogenesis of the syndrome probably involves generation of toxic free fatty acids by lipase in the lungs or platelet aggregation around the fat droplets, with release of vasoactive mediators such as serotonin.
The classic triad of the fat embolism syndrome consists of respiratory insufficiency, neurologic signs, and a petechial rash, although many patients exhibit only one or two of these features. Respiratory insufficiency is associated with dyspnea, inspiratory crepitations, and hypoxemia. Neurologic disturbance ranges from mild confusion to severe impairment of consciousness, which may be accompanied by focal neurologic signs. The petechial rash characteristically occurs in the distribution of the carotid and subclavian arteries, affecting skin, mucous membranes, and conjunctiva. Pyrexia, tachycardia, retinopathy, and oliguria due to renal embolization are additional features.
Laboratory investigations may reveal fat droplets in the blood, urine, or sputum; increased serum lipase and free fatty acid levels; decreased serum albumin and calcium levels; and decreased platelet count. However, none of these tests is specific for fat embolism syndrome, and a combination of clinical and laboratory features is required to establish the diagnosis.
No specific treatment is of proven benefit after fat embolism. Heparin, low-molecular-weight dextran, aprotonin, and alcohol have all been suggested on theoretic grounds, but they may add more risks than benefits. There is anecdotal evidence that high-dose steroids, which stabilize membranes and reduce the inflammatory response, may limit the pulmonary injury. Early immobilization of fractures is a logical preventive measure, and internal fixation may be the most effective method. Measures directed at the early identification and correction of hypoxia and avoidance of hypercarbia, which may exacerbate the neurologic injury, are currently the mainstays of treatment.
Explanation
Self Explanatory
Comments
No specific treatment is of proven benefit after fat embolism. Heparin, low-molecular-weight dextran, aprotonin, and alcohol have all been suggested on theoretic grounds, but they may add more risks than benefits. There is anecdotal evidence that high-dose steroids, which stabilize membranes and reduce the inflammatory response, may limit the pulmonary injury. Early immobilization of fractures is a logical preventive measure, and internal fixation may be the most effective method. Measures directed at the early identification and correction of hypoxia and avoidance of hypercarbia, which may exacerbate the neurologic injury, are currently the mainstays of treatment.
Oxford Text book of Surgery says “that treatment with high-dose corticosteroids may reduce platelet aggregation. Other agents such as aspirin and heparin carry a significant risk of haemorrhage and are not recommended.”
Tips
Few more points : Several days after the bone fractures occur, restlessness, delirium or drowsiness progressing to coma in severe cases, seizures, generalized brain edema, and hypoxia develop. About half the patients have retinal and punctate conjunctival hemorrhages or fat that is visible in retinal vessels. A petechial rash (prominent in the anterior axillary folds and supraclavicular fossae), diffuse interstitial infiltrates on the chest x-ray, fat in the urine, and/or renal failure occur in some patients. Severe reduction in arterial oxygen content is common from widespread lung injury (ARDS). Cerebral fat embolism causes a cerebral purpura, mainly in the white matter, due to capillary occlusion by fat globules. There is evidence that patients in whom this complication is recognized and treated early have a better prognosis. Massive doses of glucocorticoids and administration of positive-pressure ventilation with high end-expiratory pressures have been claimed to be useful

Question
A 30-year-old man had road traffic accident and sustained fracture of femur. Two days later he developed sudden breathlessness. The most probable cause can be:
1. Pneumonia
2. Congestive heart failure.
3. Bronchial asthma.
4. Fat Embolism.
Answer
4. fat Emboolism.
Reference
Harrison 15th Edition Chapter 369
Sabistorn 15th Edition Chapter 18
Quality
Reader
Status
Repeat
QTDF
All Books
Discussion
Fat emboli probably originate from the bone marrow and enter the circulation through torn venules at the fracture site. Although direct occlusion of small blood vessels in the lungs, brain, and skin by fat droplets may cause ischemic injury, the pathogenesis of the syndrome probably involves generation of toxic free fatty acids by lipase in the lungs or platelet aggregation around the fat droplets, with release of vasoactive mediators such as serotonin.
The classic triad of the fat embolism syndrome consists of respiratory insufficiency, neurologic signs, and a petechial rash, although many patients exhibit only one or two of these features. Respiratory insufficiency is associated with dyspnea, inspiratory crepitations, and hypoxemia. Neurologic disturbance ranges from mild confusion to severe impairment of consciousness, which may be accompanied by focal neurologic signs. The petechial rash characteristically occurs in the distribution of the carotid and subclavian arteries, affecting skin, mucous membranes, and conjunctiva. Pyrexia, tachycardia, retinopathy, and oliguria due to renal embolization are additional features.
Laboratory investigations may reveal fat droplets in the blood, urine, or sputum; increased serum lipase and free fatty acid levels; decreased serum albumin and calcium levels; and decreased platelet count. However, none of these tests is specific for fat embolism syndrome, and a combination of clinical and laboratory features is required to establish the diagnosis.
No specific treatment is of proven benefit after fat embolism. Heparin, low-molecular-weight dextran, aprotonin, and alcohol have all been suggested on theoretic grounds, but they may add more risks than benefits. There is anecdotal evidence that high-dose steroids, which stabilize membranes and reduce the inflammatory response, may limit the pulmonary injury. Early immobilization of fractures is a logical preventive measure, and internal fixation may be the most effective method. Measures directed at the early identification and correction of hypoxia and avoidance of hypercarbia, which may exacerbate the neurologic injury, are currently the mainstays of treatment.
Explanation
Self Explanatory
Comments
No specific treatment is of proven benefit after fat embolism. Heparin, low-molecular-weight dextran, aprotonin, and alcohol have all been suggested on theoretic grounds, but they may add more risks than benefits. There is anecdotal evidence that high-dose steroids, which stabilize membranes and reduce the inflammatory response, may limit the pulmonary injury. Early immobilization of fractures is a logical preventive measure, and internal fixation may be the most effective method. Measures directed at the early identification and correction of hypoxia and avoidance of hypercarbia, which may exacerbate the neurologic injury, are currently the mainstays of treatment.
Oxford Text book of Surgery says “that treatment with high-dose corticosteroids may reduce platelet aggregation. Other agents such as aspirin and heparin carry a significant risk of haemorrhage and are not recommended.”
Tips
Few more points : Several days after the bone fractures occur, restlessness, delirium or drowsiness progressing to coma in severe cases, seizures, generalized brain edema, and hypoxia develop. About half the patients have retinal and punctate conjunctival hemorrhages or fat that is visible in retinal vessels. A petechial rash (prominent in the anterior axillary folds and supraclavicular fossae), diffuse interstitial infiltrates on the chest x-ray, fat in the urine, and/or renal failure occur in some patients. Severe reduction in arterial oxygen content is common from widespread lung injury (ARDS). Cerebral fat embolism causes a cerebral purpura, mainly in the white matter, due to capillary occlusion by fat globules. There is evidence that patients in whom this complication is recognized and treated early have a better prognosis. Massive doses of glucocorticoids and administration of positive-pressure ventilation with high end-expiratory pressures have been claimed to be useful