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[Fat embolism, a frequently misunderstood disorder].
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[ON THE TREATMENT OF FAT EMBOLISM].
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Plasma levels of atrial natriuretic peptide and endothelin-1 in experimental fat embolism.
In order to understand the role of vasoactive peptides in fat embolism, arterial plasma atrial natriuretic peptide (ANP) and endothelin-1 concentrations were investigated in an experimental study. Nine anesthetized and mechanically ventilated pigs received an intracaval infusion of allogeneic bone marrow suspension at a dose of 100 mg/kg (fat embolism group); 9 control pigs received saline. The observation period was 5 h. In the fat embolism group, cardiac index and heart rate decreased within 30 min, whereas mean arterial pressure remained stationary. Pulmonary capillary wedge pressure rose transiently and central venous pressure rose slightly in time, while mean pulmonary arterial pressure, pulmonary vascular resistance and pulmonary shunt increased immediately and persistently after the bone marrow suspension infusion. Simultaneously, arterial oxygen tension and arterial hemoglobin oxygen saturation decreased markedly. Arterial plasma ANP and endothelin-1 concentrations remained stable in the fat embolism animals, whereas in the controls ANP and endothelin-1 levels decreased at 3 and 5 h. Arterial epinephrine concentrations were stable in animals receiving bone marrow suspension, while in the controls arterial epinephrine concentrations decreased towards the end of the experiment. Arterial norepinephrine concentrations remained unchanged in both groups. To conclude, impaired pulmonary function and consequent systemic hypoxemia distinguish the present fat embolism model. Unchanged arterial ANP and endothelin-1 concentrations in the fat embolism group suggest that these circulating vasoactive hormones have a minor impact on the pathogenesis of the current experimental fat embolism.
Roentgen manifestations of traumatic pulmonary fat embolism.
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FAT EMBOLISM IN DIABETES MELLITUS.
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Computed tomography for diagnosis and assessment of cerebral fat embolism.
A patient with cerebral fat embolism was followed by computed tomography (CT). For the first few days after injury, CT revealed no abnormality. About a week later, multiple low density areas appeared in the white matter of the frontal region. They disappeared within the subsequent 2 weeks while subdural effusions developed in the fronto-parieto-temporal regions. As neurologic recovery progressed, the subdural effusions gradually diminished and cerebral atrophy was seen.
The fat embolism syndrome.
The clinical fat embolism syndrome consisting of progressive pulmonary insufficiency, cerebral disfunction, and petechiae is rare. Following severe skeletal trauma, fat droplets appear in the circulating blood and embolize the capillaries of the lungs and other organs. Whether fat droplets are of mechanical or chemical origin remains controversial. These fat droplets cause mechanical occlusion of lung capillaries followed by chemical changes associated with hydrolysis of the neutral fat to free fatty acids. The free fatty acids produce a toxic and inflammatory reaction resulting in pulmonary edema, hemorrhage, and microatelectasis. The clinical and radiographic abnormalities appear after an initial latent period of 12 to 72 hours. The chest radiographic findings are nonspecific and consist of bilateral patchy or diffuse alveolar and interstitial lung densities. With aggressive management the survival has markedly improved, and mortality is now rare.
[ACUTE COR PULMONALE. 3. FAT EMBOLISM AND AIR EMBOLISM].
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[Fat embolism with lung hemorrhage].
Post-traumatic fat embolism was disclosed by a picture of alveolar hemorrhage. Acute hypoxemia associated with dense bilateral pulmonary infiltrates was observed in a 21 year-old woman, 4 days after an accident with closed tibial fracture. Cruoric pulmonary thromboembolism was ruled out, as was an acute pulmonary edema. Neither infectious nor immunologic etiology was found. The diagnosis of alveolar hemorrhage was based on bronchoalveolar lavage. Lipid droplets in macrophages stained by "Oil Red O" established the relationship with fat embolism. The outcome was favorable. The association of fat embolism and alveolar hemorrhage has already been reported, but remains rare.
Fat embolism syndrome and pulmonary microvascular cytology.
Pulmonary microvascular cytology consists of analysis of capillary blood sampled while a Swan-Ganz catheter is in the wedge position. This technique has proved to be useful in the diagnosis of lymphangitic spread of carcinoma in the lungs and there are case reports of their use in amniotic fluid embolism. Its usefulness in diagnosing fat embolism syndrome has been shown only rarely. We report a new case in which pulmonary microvascular cytologic study allowed a definite diagnosis of fat embolism syndrome. We suggest obtaining routinely samples of capillary blood when a pulmonary catheter is in place and fat embolism is suspected on a clinical basis.
[ON PULMONARY FAT EMBOLISM AFTER INJURIES WITH DIFFERENT PERIODS OF SURVIVAL].
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[Fat embolism after total hip prosthesis replacement preserving the femoral stem].
Fat embolism is a known complication of traumatology, especially in long bone fractures. It may also occur in liposuction and articular surgery (0.1%). Fat embolic events are most often clinically insignificant and difficult to recognize since clinical manifestations are varied and there is no routine laboratory or radiographic diagnosis. Classically, fat embolism syndrome presents with the triad of pulmonary distress, mental status changes, and cutaneous manifestations. We report the case of a 33-year-old woman who developed acute respiratory distress 10 days after hip arthroplasty. Several aetiologies such as fibrinocruoric pulmonary embolism, pulmonary aspiration and bacterial pneumonia were discussed. Fat embolism was diagnosed, based on suggestive clinical manifestations, radiographic and laboratory findings, although fat embolism after hip arthroplasty without intramedullary pressurization is infrequent.
Fat embolism: a clinical diagnosis.
Fat embolism causes a distinctive clinical syndrome usually seen in trauma victims with long bone fractures. Clinical findings include hyperthermia, respiratory distress, petechiae and retinal fat emboli. Neurologic changes include decreased sensorium, decerebrate posturing and seizure activity. Chest radiographs commonly demonstrate bilateral fluffy infiltrates. Laboratory abnormalities include hypoxemia, respiratory alkalosis, anemia and hypocalcemia. Treatment consists of general supportive care with vigorous pulmonary therapy. Most patients have a good recovery.
Pathophysiological effect of fat embolism in a canine model of pulmonary contusion.
BACKGROUND: The objective of this study was to determine the individual and combined effects of pulmonary contusion and fat embolism on the hemodynamics and pulmonary pathophysiology in a canine model of acute traumatic pulmonary injury. METHODS: After a thoracotomy, twenty-one skeletally mature dogs were randomly assigned to one of three groups. Unilateral pulmonary contusion alone was produced in Group 1 (seven dogs); pulmonary contusion and fat embolism, in Group 2 (seven dogs); and fat embolism alone, in Group 3 (seven dogs). Pulmonary contusion was produced by standardized compression of the left lung with a piezoelectric force transducer. Fat embolism was produced by femoral and tibial reaming followed by pressurization of the intramedullary canals. Cardiac output, systolic blood pressure, peak airway pressure, pulmonary arterial pressure, pulmonary capillary wedge pressure, partial pressure of arterial oxygen, and partial pressure of carbon dioxide were monitored for all groups. From these data, several outcome parameters were calculated: total thoracic compliance, alveolar-arterial oxygen gradient, and ratio of partial pressure of arterial oxygen to fractional inspired oxygen concentration. All of the dogs were killed after eight hours, and tissue samples were obtained from the brain, kidneys, and lungs for histological analysis. Lung samples were assigned scores for pulmonary edema (the presence of fluid in the alveoli) and inflammation (the presence of neutrophils or hyaline membranes, or both). The percentage of the total area occupied by fat was determined. RESULTS: Pulmonary contusion alone caused a significant increase in the alveolar-arterial oxygen gradient but only after seven hours (p = 0.034). Fat embolism alone caused a significant transient decrease in systolic blood pressure (p = 0.001) and a significant transient increase in pulmonary arterial pressure (p = 0.01) and pulmonary capillary wedge pressure (p = 0.015). Fat embolism alone also caused a significant sustained decrease in the ratio of partial pressure of arterial oxygen to fractional inspired oxygen concentration (p = 0.0001) and a significant increase in the alveolar-arterial oxygen gradient (p = 0.0001). The combination of pulmonary contusion and fat embolism caused a significant transient increase in pulmonary capillary wedge pressure (p = 0.0013) as well as a significant sustained decrease in partial pressure of arterial oxygen (p = 0.0001) and a significant decrease in systolic blood pressure (p = 0.001) that lasted for an hour. Pulmonary contusion followed by fat embolism caused a significant increase in peak airway pressure (p = 0.015), alveolar-arterial oxygen gradient (p = 0.0001), and pulmonary arterial pressure (p = 0.01), and these effects persisted for five hours. Total thoracic compliance was decreased 6.4 percent by pulmonary contusion alone, 4.6 percent by fat embolism alone, and 23.5 percent by pulmonary contusion followed by fat embolism. The ratio of partial pressure of arterial oxygen to fractional inspired oxygen concentration was decreased 23.7 percent by pulmonary contusion alone, 52.3 percent by fat embolism alone, and 65.8 percent by pulmonary contusion followed by fat embolism. The mean pulmonary edema score was significantly higher with the combined injury than with either injury alone (p = 0.0001). None of the samples from the lungs demonstrated inflammation. Fat embolism combined with pulmonary contusion resulted in a significantly greater mean percentage of the area occupied by fat in the noncontused right lung than in the contused left lung (p = 0.001); however, no significant difference between the right and left lungs could be detected with fat embolism alone. The mean percentage of the glomerular and cerebral areas occupied by fat was greater with fat embolism combined with pulmonary contusion than with fat embolism alone (p = 0.0001 and p = 0.01, respectively). (ABSTRACT TRUNCATED)