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PubMed1979

[Basic studies on the pathogenesis and treatment of fat embolism. I. Fracture mechanism and fat embolism].

We examined the amount of fat that can be forced into the circulation by compression of femora and of heads of the tibia in the very moment of injury. By fractures of diaphyses no considerable reduction of the intraosseous space was achieved and no fat was expelled through the foramina nutritia before the hard cortical bone was splintered. However, considerable amounts of fat were expelled into veins, when the epiphyses of the femora or when the head of the tibia was compressed from medially and from laterally. Even by a purely manual compression some fat was forced to leave the spongiosa by the foramina nutritia. This is explained by the higher elasticity of the spongious bone, permitting a marked space reduction by compression even before a fracture sets in. The mechanism resembles the procedure of opacification of veins by contrast media, injected into the bone cavity under pressure. The significance of these findings for the pathogenesis of clinical fat embolism is discussed.

Adult↗
PubMed1995

Role of bronchoalveolar lavage in the diagnosis of fat embolism syndrome.

Fat embolism syndrome (FES) is a serious clinical disorder occurring in trauma patients. The diagnosis of fat embolism syndrome may be difficult to establish clinically. We therefore wanted to investigate the usefulness of bronchoalveolar lavage (BAL) in the diagnostic evaluation of fat embolism syndrome. We analysed the presence of fat droplets in BAL cells in 32 trauma patients (7 with full diagnostic criteria of fat embolism syndrome, 17 with incomplete diagnostic criteria, and 8 with no diagnostic criteria at the time of bronchoscopy), 9 nontrauma patients with acute respiratory failure and radiographic pulmonary infiltrates, and a control group composed of 10 individuals. An increased percentage of oil red O positive alveolar macrophages (cut-off point > 3%) in BAL was found in 6 out of 7 patients with definite clinical criteria of fat embolism syndrome, and in 6 out of 20 trauma patients without the clinical diagnosis of fat embolism syndrome. In two patients with fat embolism syndrome, sequential BAL showed that the percentage of positive macrophages decreased when the clinical manifestations disappeared. An increased number of BAL macrophages with fat droplets was also observed in two trauma patients without evidence of fat embolism syndrome after long-bone surgical intervention. By contrast, all non-trauma patients had a percentage of positive cells lower than 3%. Our findings suggest that BAL oil red O positive macrophages are frequently observed in trauma patients irrespective of the presence of fat embolism syndrome. Conceivably, a high number of oil red O positive macrophages could reflect clinically silent fat embolization.

Adult↗
PubMed2002

Fat embolism syndrome.

Fat embolization and the clinical syndrome associated with this pathology are poorly understood complications of skeletal trauma. Fat embolization is characterized by release of fat droplets into systemic circulation after a traumatic event. Fat embolism syndrome (FES) is an infrequent clinical consequence of fat embolization. Classically, FES presents with the triad of pulmonary distress, mental status changes, and petechial rash 24 to 48 hours after pelvic or long-bone fracture. FES incidence increases with the number of fractures sustained by an individual. Many clinicians believe that FES incidence has decreased over the past several decades secondary to advances in resuscitative measures. FES pathophysiology remains unclear. Current theories involve common mechanical and biochemical mechanisms that explain how fat emboli manifest as FES. Much controversy surrounds the question of whether there is a causal relation between intramedullary nailing and FES onset. Clinical diagnosis is essential, as laboratory and radiographic findings are nonspecific. Early supportive pulmonary therapy and other resuscitative measures may halt the pathophysiologic cascade and prevent clinical deterioration. Fortunately, if FES is diagnosed early, and pulmonary and cardiac functions are optimally supported, prognosis is very good.

Bone and Bones↗
PubMed1997

Fat embolism syndrome.

Fat embolism syndrome, an important contributor to the development of acute respiratory distress syndrome, has been associated with both traumatic and nontraumatic disorders. Fat embolization after long bone trauma is probably common as a subclinical event. Fat emboli can deform and pass through the lungs, resulting in systemic embolization, most commonly to the brain and kidneys. The diagnosis of fat embolism syndrome is based on the patient's history, supported by clinical-signs of pulmonary, cerebral and cutaneous dysfunction and confirmed by the demonstration of arterial hypoxemia in the absence of other disorders. Treatment of fat embolism syndrome consists of general supportive measures, including splinting, maintenance of fluid and electrolyte balance and the administration of oxygen. Endotracheal intubation and mechanical ventilatory assistance can be indicated. The role of corticosteroids remains controversial. Early stabilization of long bone fractures has been shown to decrease the incidence of pulmonary complications. Clinical and experimental studies suggest that the exact method of fracture fixation plays a minor role in the development of pulmonary dysfunction. As more is learned about the specifics of the various triggers for the development of fat embolism syndrome, it is hoped that the prospect of more specific therapy for the prevention and treatment of this disorder will become a reality.

Diagnosis, Differential↗
PubMedDate not supplied

[Correlation between the survival duration and trauma severity in persons who died from posttraumatic fat embolism].

INTRODUCTION: Posttraumatic fat embolism follows the injury. The fat emboli in circulation could cause death in three ways: isolated lung fat embolism, systemic fat embolism and fat embolism syndrome (FES). In forensic pathology, only two trauma scores, based on disintegration of anatomic structures, could be used for objectivization, comparison and establishment of severity of injuries. One of them is Injury Severity Score--ISS, based on Abbreviated Injury Scale--AIS. The second one is Hannover Polytrauma Score--HPTS, based on the total sum of all injuries and age of the injured person. OBJECTIVE: The objectives of this paper were to establish the correlation between outliving period and trauma severity (based on ISS and HPTS values), in persons died from posttraumatic fat embolism and/or its complications, and to establish which of these score systems could be better for prediction of development of the posttraumatic fat embolism. METHOD: The retrospective autopsy study was performed and it included the material of the Institute of Forensic Medicine in Belgrade for period 1988-2001. The autopsy reports and clinical medical data were analyzed, for persons died from posttraumatic fat embolism and/or its complications. In all cases, the fat embolism was the single cause of death, verified by autopsy. In each case, ISS and HPTS values were obtained. The sample was statistically prepared (chi2 test, correlation coefficient, regression line). RESULTS AND DISCUSSION: The sample included 50 persons: 41 males and 9 females. The proportion of men was statistically significant (chi2 = 20.480; p < 0.001). Average age of male was 55.26 years (SD = 21.39) and of female was 55.78 (SD = 17.45). There was no statistically significant disproportion among the age distribution of the sample (chi2 = 6.4; p > 0.05). The outliving period varied from 1-14 days: the average was 5.92 (SD = 3.39; Med. 5.50; Mod. 2). The average value of 1SS was 19 (SD = 7.70; Med. 19; Mod. 14), and for HPTS average value was 28.16 (SD = 12.87; Med. 26.50; Mod. 12). In literature, there have been data about critical ISS value: 12-20. HPTS value of 20 to 35 was lethal in 25%. Each injured of our sample had, at least, one long bone or pelvic fracture. There was negligible negative correlation between outliving period and 1SS and HPTS values in our sample: coefficient of linear correlation r = -0.117, t = 0.83 and r = -0.088, t = 0.59. Our sample was representative (t = 8.37). These data pointed out that the outliving period of the observed patients, died from post-traumatic fat embolism, was not in relation to general severity of injuries but to fat embolism per se and its consequences. There was low positive correlation between ISS and HPTS values: r = 0.296, t = 2.147, coefficient of determination r2 = 0.0876 and linear regression HPTS = 18.7588+0.4948 ISS. These data indicated that direct correlation between scores was only about 9% and the rest of correlation i.e. 91% depended on other factors. CONCLUSION: There was negative negligible correlation between outliving period and severity of injury based on ISS and HPTS, in patients died from posttraumatic fat embolism. So, these score systems are useless for prediction of duration of the outliving period in the injured died from fat embolism as well as for prediction of posttraumatic fat embolism as cause of death.

Embolism, Fat↗
PubMed2007

Fat embolism syndrome.

Fat embolism syndrome (FES) was first described in 1862, but its frequency today is still unclear. A diagnosis of FES is often missed because of a subclinical illness or coexisting confusing injuries or disease. Fat embolism syndrome develops most commonly after orthopedic injuries, but it has also been reported after other forms of trauma such as severe burns, liver injury, closed-chest cardiac massage, bone marrow transplantation, and liposuction. Although FES usually presents as a multisystem disorder, the most seriously affected organs are the lung, brain, cardiovascular system, and skin. Fat embolism syndrome is a self-limiting disease and treatment should be mainly supportive. Many drugs have been used to treat FES, but the results are inconclusive.

Embolism, Fat↗
PubMed1995

[Neurological manifestations of fat embolism syndrome].

Fat embolism is a frequent complication of long bone trauma. Although neurological signs are key elements in the diagnosis of this syndrome, little attention to them has been paid in the spanish literature. We present a retrospective study of 13 patients with fat embolism syndrome in which we focused on neurological manifestations and alterations in computerized tomography (CT) of the head. The most frequent symptom was impairment of consciousness of varying degrees. Three patients out of the 13 also presented focal signs (hemiparesis and partial seizures). CT revealed edema (4/7) and multiple low density foci (1/7). All but one patient recovered without sequelae. Our study does not allow us to establish either the physiopathology of fat embolism syndrome or the most effective treatment.

Adolescent↗
PubMed2001

Fatal pulmonary fat embolism during humeral fracture repair in a cat.

An 11-month-old cat was referred following a road traffic accident with non-weightbearing forelimb lameness and tachypnoea. A diaphragmatic rupture was repaired two days after trauma. Six days post trauma, a further operation was performed to repair the fractured humerus. As an intramedullary pin was advanced into the bone to achieve stabilisation, acute respiratory arrest occurred. Manual extrathoracic cardiopulmonary resuscitation was immediately instigated, but the cat did not recover. Postmortem examination identified a high degree of embolic fat occluding pulmonary capillaries. A massive embolic shower was established as the cause of death.

Acute Disease↗
PubMed2004

Paradoxical cerebral embolisation. An explanation for fat embolism syndrome.

Fat embolism occurs following fractures of a long bone or arthroplasty. We investigated whether paradoxical embolisation through a venous-to-arterial circulation shunt (v-a) could lead to cerebral embolisation during elective hip or knee arthroplasty. Transcranial Doppler ultrasound (TCD), following the intravenous injection of microbubble contrast, identified the presence of a shunt in 41 patients undergoing hip (n = 20) or knee (n = 21) arthroplasty. Intra-operative cerebral embolism was detected during continuous TCD monitoring. Of the 41 patients, 34 had a v-a shunt of whom 18 had an embolism and embolism only occurred in patients with a shunt (p = 0.012). Spontaneous and larger shunts were associated with a greater number of emboli (rs = 0.67 and rs = 0.71 respectively, p < 0.01). Observations in two patients with large spontaneous shunts revealed 368 and 203 emboli and unexplained post-operative confusion and pancreatitis. Paradoxical cerebral embolisation only occurred in patients with a shunt and may explain both postoperative confusion and fat embolism syndrome following surgery.

Adult↗
PubMed1980

[Basis examinations for pathogenesis and treatment of fat embolism. III. The interface tension of blood against lipids. B. Their influence by addition of surfactants and the effect on the lipid solubility in vitro].

Various surfactants such as Pluronic L 61, L 64, F 68 and F 108, Tween 80 und Triton WR 1339 as well as bile acids and sodium taurocholate were tested for their capacity to reduce the interface tension against neutral lipids and for their capacity to induce stable emulsions of triglycerides in rabbit sera. No positive correlation was found to exist between the interface activity against neutral lipids and the lipid emulsifying capacity of rabbit sera, added with the surfactants. When ether was added to serum, the lipid emulsifying capacity was increased most at concentrations of about 0,0075 g ether per 100 ml serum. This is about 1/10 of the ether concentration, achieved during anesthesia at the stage of tolerance. Pluronic F 108 in non toxic concentrations was the agent increasing the lipid emulsifying capacity of rabbit (and human) sera most efficiently. It proved superior also to ethanol and ether and appears to be the most suitable agent for mobilization of embolized fat in lung vessels.

Animals↗
PubMed1979

The fat embolism syndrome.

The fat embolism syndrome is a symptom complex of acute respiratory failure after long-bone fractures. It is thought to be caused by deposition of embolic fat within the pulmonary capillaries, resulting in a capillary leak within the lung. The source of the embolic fat appears to be marrow fat. Alterations in circulating free fatty acids, increases in fibrin split products, and increases in platelet adhesiveness have been observed to occur in this syndrome and probably play an important part in the production of the pulmonary lesion. The signs and symptoms of the syndrome are hypoxemia, tachypnea, petechiae, fever, altered sensorium, and chest roentgenograms similar to signs of the adult respiratory distress syndrome (ARDS). Early recognition is facilitated by monitoring of arterial blood gas levels for hypoxemia. Treatment is directed at ARDS using graduated oxygen therapy and steroids.

Blood Coagulation Disorders↗
PubMed1979

The role of embolic fat in post-traumatic pulmonary insufficiency. An evaluation of the pulmonary haemodynamics and blood gas levels.

Pulmonary haemodynamic and arterial blood gas changes were measured in dogs subjected to either an intravenous injection of triolein or external trauma, which produced fractures of the ipsilateral femur, tibia and fibula. Musculoskeletal trauma resulted in pulmonary vasoconstriction followed by vasodilatation, arterial hypoxia with a pulmonary shunt of 30% and a 20% decrease in systemic oxygen delivery. Lipid injection produced an increased pulmonary vascular resistance, but no significant hypoxia, pulmonary shunting or inadequate tissue oxygenation. We therefore suggest that pulmonary fat embolism does not account for the pulmonary insufficiency following musculoskeletal trauma.

Animals↗
PubMed1976

Post-traumatic blood lipid changes and fat embolism. Relation of post-traumatic blood lipid changes and fat embolism syndrome.

Serum cholesterol, triglycerides, phospholipids, and lipoprotein levels were studied by electrophoresis in 43 trauma patients with multiple fractures of the lower extremities and pelvis. Ten healthy volunteers were used for control studies. The fat embolism syndrome was diagnosed in eight of the 43 patients. The lipid values of all the trauma patients were lower than the control values. A decrease in cholesterol and phospholipids was observed in the fat embolism patients during 4 days; these changes were not observed in the other trauma patients. The triglycerides of all the trauma patients increased slowly over a period of 4 days. Changes in the lipoprotein fractions after the trauma were minor. An early increase in the alpha1 lipbrotein fraction was noted in the fat embolism patients simultaneously with a decrease in the pre-beta lipoprotein fraction; the values of the other trauma patients were at the control levels. Normalization was observed in 6 hours. The lipid concentrations of plasma and serum did not change with filtration with 1.2, 5, and 8mum Millipore filters. No differences were noted between the femoral and cubital vein samples.

Adult↗
PubMed1986

Dermatologic features of the fat embolism syndrome.

Fat embolism syndrome is a life-threatening disease with cutaneous manifestations that occur most commonly after fractures of a long bone. The syndrome consists of a triad of dermatologic, pulmonic, and neurologic involvement. Because no major dermatologic journal has reviewed this syndrome in more than five years, we present a case and discuss the current approaches to the pathogenesis, diagnosis, and treatment of this often overlooked syndrome.

Adult↗