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PubMed1976

Induced fat embolism in rabbits by means of radioactively labelled fat. Evaluation of different treatments.

Fat embolism was induced in the rabbit by administering a suspension containing radioactively (triglyceride) labelled homologous fat. Different kinds of treatment were tested: Ringerdex, 2% dextran 70, 2.2% dextran 40 SoluMedrol, and EPL-a phospholipid mixture with detergent properties. It was sound that fat injection gave a macroscopically and histologically verifiable fat embolism with lung edema. 2% dextran 70 significantly increased edema, whereas 2.2% dextran 40 did not. SoluMedrol significantly decreased edema caused by fat injection. Of the triglyceride administered, 99.5% was recovered as such from the lungs. Practically no radioactivity was found in cerebrum and kidneys. Compared with Ringerdex, no other treatment increased elimination of fat from lungs.

Animals↗
PubMed1997

[Fat embolism--a too infrequently determined pathoanatomic diagnosis].

In 1993, pulmonary fat embolism occurred in 92 cases (17%) out of 527 clinical autopsies. It was found in 62% of patients who had suffered bone fractures, in 9% with soft tissue surgery and in 53% after resuscitation; non-traumatic fat embolism was present in 6% of the cases. The comparison group of 50 persons with lethal polytrauma revealed pulmonary fat embolism in 52% of the cases. Bone-marrow embolism and microthrombi accompanied fat embolism of the lungs; furthermore some of the persons with pulmonary fat embolism also expressed minor degrees of renal (55%) and cerebral (25%) fat emboli. A retrospective analysis of the clinical data revealed no specific symptoms: a so called fat embolism syndrome had not been discovered clinically in any of the cases with histologically proven fat embolism. The significance of pulmonary fat embolism as a cause of death with regard to histological and clinical findings is discussed.

Cause of Death↗
PubMed1975

Fat embolism: a comprehensive review.

Fat embolism as a cause or as a contributing factor to the death of injured patients is probably not diagnosed in many instances. Treatment is beneficial in moderate cases of fat at embolism; severe cases result in death and mild cases usually resolve without treatment. Awarness of the symptoms is important. Treatment should be directed to the symptoms rather than to the disease. Respiratory support seems to be the most effective treatment.

Brain↗
PubMed1990

The fat embolism syndrome. A review.

While fat embolism occurs in most (more than 90%) patients with traumatic injury, the fat embolism syndrome (FES) occurs in only 3%-4% of patients with long-bone fractures. FES involves multiple organ systems and can cause a devastating clinical deterioration within hours. The major clinical features of FES include hypoxia, pulmonary edema, central nervous system depression, and axillary or subconjunctive petechiae. Improvements have been made in supporting the respiratory compromise and adult respiratory distress syndrome that these patients develop. Aggressive measures to improve the pulmonary function, i.e., positive pressure ventilation and effective fluid management, are important and expedite fixation of bone fractures.

Embolism, Fat↗
PubMed2006

Time course of spontaneous recovery of subacute fat embolism syndrome--a case report.

Pulmonary embolism is not uncommonly encountered in orthopedic patients with high risks, such as prolonged immobility, obesity, past or family history of thromboembolism, pelvic and long bone fractures. Here we report a young male patient with a residual cerebral arteriovenous malformation post-craniotomy suffered from acute severe hypoxemia after sustaining a simple fracture of the left femur shaft from a motorcycle accident. The emergent surgery was deferred in view of suspectable pulmonary embolism. Under supportive treatment, the condition spontaneously resolved, and the surgery was later performed uneventfully. To the best of our knowledge, this was the first instance that a pulmonary embolism (suspected subacute fat embolism syndrome) which ran in a natural course to spontaneous resolution was observed. We would like to report our clinical observation, and discuss the principle of anesthetic management in the text.

Adolescent↗
PubMed1985

[Fat embolism in the spleen].

A fat embolism is seldom seen in the spleen. In some cases, fat globules lie in the central arteries and capillaries of the Malpighian bodies only and in other cases in the red pulp in capillaries or sinus. Part of the fat droplets has been phagocytosed by mononuclear cells, especially when patients die some days after injury and the beginning of fat embolism in the systemic circulation. The distribution of fat emboli described can been explained by the peculiarities of vascular structures in form of sheathed capillaries, which arise from pencil arterioles and probably do not permit fat globules to pass the capillary wall in this part of the vasculature.

Adult↗
PubMed1984

Cerebral fat embolism.

An unusual presentation of fat embolism is reported. Forty-eight hours after severe trauma to her legs the patient became stuporous and her right arm weak. A computerized tomography scan showed diffuse brain swelling. Although the petechiae, thrombocytopenia and lipuria characteristic of the fat embolism syndrome were present, at no time was there any evidence of pulmonary involvement.

Accidents, Traffic↗
PubMed2004

Resuscitation of fat embolism syndrome with extracorporeal membrane oxygenation.

Embolization of marrow fat appears to be an inevitable consequence of long bone fractures. Pulmonary fat embolism (FE) with cardiovascular collapse is associated with a high mortality rate because of acute right ventricular failure and hypoxia. Immediate and appropriate resuscitation is required to prevent sudden death. Although extracorporeal membrane oxygenation (ECMO) has been used for a multitude of applications involving respiratory and circulatory collapse, its full potential as a standard conventional therapy has yet to be exploited. Herein, we describe the successful use of veno-venous (V-V) ECMO in a trauma patient who initially presented with fractures of the right ulna and femur. After surgery, the patient rapidly decompensated despite massive ventilatory support and was placed on ECMO. ECMO support lasted approximately 120 hours followed by an uneventful recovery and discharge 10 days later.

Adult↗
PubMed1994

The pulmonary artery catheter: a diagnostic adjunct for fat embolism syndrome.

Available objective tests for fat embolism are neither sensitive nor specific. We performed frozen-section analysis of blood aspirated from a pulmonary artery catheter in a trauma victim with fat embolism syndrome and found marked levels of pulmonary microvascular blood fat. The amount of fat detected in this patient with long bone fractures was higher than that observed in a pilot study of this technique in cardiopulmonary bypass patients. This technique provided diagnostic support of our clinical findings. The procedure may prove useful in patients with an equivocal diagnosis of fat embolism or when the cause of posttraumatic acute pulmonary insufficiency is unknown.

Aged↗
PubMed1991

[Is there a drug treatment approach for prevention and therapy of fat embolism syndrome?].

The pathogenesis of fat embolism has been subject to considerable debate ever since it was first described by Zenker in 1864. The clinical course, management and pathophysiology of a typical case are described. As no single causative factor has been implied in the development of fat embolism, its therapy and prevention primarily involves the adequate treatment of shock and of the underlying traumatic lesions.

Adult↗
PubMedDate not supplied

[Factors which could affect the severity of post-traumatic pulmonary fat embolism--a prospective histological study].

INTRODUCTION: Each fracture of long or pelvic bones as well as large contusions of subcutaneous fat tissue cause releasing of fat globules that rapidly penetrate into circulation through the ruptured veins of the injured tissue, and reach the lung circulation [1,2]. During the first phase, fat emboli block the functional lung circulation by their mechanical effect in capillaries producing so called isolated post-traumatic lung fat embolism [3]. The surface layer of a fat embolus, which is practically in liquid state, behaves as a membrane of very high density, i.e., as it is under high pressure which obstruct the blood stream [4] that is finally stopped at the level of lung blood vessels with diameter of approximately 20 mu [5]. This pathophysiological mechanism produces cor pulmonale acutum, with poor pathological findings [8]. Nowadays, the post-mortem diagnosis of lung fat embolism is based on microscopical examination of tissue specimens, usually prepared with special histological staining (Sudan III) [9]. The grading of fat embolism according to Sevitt's criteria is generally accepted [10]. Taking of slices from apicoventral areas of the lungs has been recommended [11]. With longer outliving period, the total number of fat emboli in the lung circulation gradually decreases, due to their disintegration and resorption. It has been stated that fat globules completely disappear about 4-6 weeks after injury, and that they should not be searched for microscopically in this post-traumatic phase [11]. OBJECTIVES: The aim of our work was to determine whether the age of injured, their gender, total severity of trauma, outliving period, and hypovolemic shock that develops after injuring, may induce development of more severe forms of post-traumatic lung fat embolism. MATERIAL AND METHODS: A prospective histological study was performed on the autopsy material of the Institute of Forensic Medicine in Belgrade. The analyzed sample consisted of individuals with injuries that might be a source of fat emboli (fractures of long bones, large contusions of subcutaneous fat tissue). The lung slices were systematically taken and stained with special fat staining (Sudan III). In each particular case, the grade of lung fat embolism was counted on the basis of microscopical appearance, according to Sevitt's criteria. The total severity of trauma was estimated by calculation of the Injury Severity Score (ISS) [13, 14]. In no cases from the analyzed sample, the fat embolism was mentioned as either singular or plural cause of death. The obtained results were analyzed by means of appropriates statistical methods (ANOVA, LSD-test, chi 2 test. Man-Whitney test, Fischer's test of correct probability). RESULTS AND DISCUSSION: The analyzed sample included 58 fatally injured individuals, 39 males and 19 females. The average age was 54.10 years (SD = 16.56), the average value of ISS was 34.69 (SD = 5.88), and the average outliving period was 3.74 days (SD = 5.88). However, all these data look differently when the analyzed sample has been stratified and analyzed according to the estimated grade of lung fat embolism. It was not showed that severity of lung fat embolism depends on sex of the injured (chi 2 = 0.842; p > 0.05). The groups with the slightest and the most severe grade of lung fat embolism are statistically significantly different in relation to age of individuals (ANOVA, p = 0.017). By means of LSD test, it has been showed that the group with the most severe grade of lung fat embolism (grade III) is statistically significantly different comparing to other two groups (with grade I and II) in relation to the age of injured (the values are p = 0.16 and p = 0.19 respectively, and the both groups are less than p = 0.05). In the group with the most severe grade of lung fat embolism, the older individuals are statistically significantly represented comparing to other two groups. CONCLUSION: The analysis of our sample showed that the most severe grade of post-traumatic lung fat embolism (microscopical grade III according to Sevitt's criteria) was determined in older individuals, more severely injured, and with shorter outliving period. The severity of fat embolism depends neither on sex of the injured, nor on development of post-traumatic hypovolemic shock. The obtained results related to the influence of hypovolemic shock on severity of fat embolism should be accepted with a caution. Namely, sometimes there is an intention to simplify a procedure of creating of autopsy conclusion about the cause of death, so that loss of blood is not mentioned at all, in spite of fact that it could have been a concurrent cause of death, while in other cases exsanguination is designated as a sole cause of death, forgetting the possibility that fat embolism could have really been the immediate cause of death.

Adult↗
PubMed1992

[Fat embolism and fracture, a review of the literature].

The reasons of fat embolism as well as the following fat embolism syndrome are most likely long bone fractures, especially if the femur is participated. On the other hand there are cases, where a severe concussion of the entire body caused fat embolism. But it is also supposed, that intramedullary reaming as well as the insertion of knee- and hip-prostheses could be a releasing factor, because the applicated pressure on the medullary canal can cause a fat release in the systemic blood system. The morbidity depends on age and fracture, which is on fractures between 0.9 and 2%. The most affected group are people between 18 and 28 years of age. The fat embolism is manifesting at 46-60% of the patients in the first 24 hours and over 90% of the patients are affected in the first three days. If you look at the metabolic changes, you will find shortly after the fracturing process a rapid increase of free fatty acids (FFA), as well as an increase of the plasmatic enzyme levels (lipase, GPT, GOT, GLDH, LDH, etc.), catecholamines and glucocorticoids. In order to discuss the pathogenesis in a fairly complete way, you have to take different theories into consideration, because several parallel running processes--which are influencing each other--are leading to the syndrome. Infloating theory: Proceeding on the assumption that contents of the bone marrow are floating out of the fracture gap into the venous system and are leading to fat embolism in the lungs. Lipase theory: You can diagnose in 50-70% of the fracture patients an increase of the lipase level, which is correlating with the manifestation of the fat embolism. The lipase releases fat from the body depositories in addition to the fat, who is coming out of the fracture gap. Shock and coagulation theory: During shock the microcirculation is decelerated, the blood viscosity is increased and the suspension stability of the cellular blood components is decreased, which is leading to the sludging phenomenon. So the capillaries of the lungs and the brain are a kind of sludge filter of the blood, that is changed in its suspensions stability. Free fatty acids theory: Primary existing capillary defects are reasonable caused by free fatty acids (FFA). They are hydrolyzed of the neutral fats and are histotoxic for the walls of the blood vessels.(ABSTRACT TRUNCATED AT 400 WORDS)

Embolism, Fat↗
PubMed1988

An application of a quantitative analytical system for the grading of pulmonary fat embolisms.

The severity of pulmonary fat embolism in 5 autopsied cases has been measured using a quantitative image analytical system. With reference to the mean size of the fat emboli, the cases were divided into 2 groupings regardless of the number of the emboli. The mean sizes of the emboli in 3 cases of the first group were significantly larger (about 490-600 microns 2) than those found in the 2 cases of the other group (about 220 and 235 microns 2). An investigation into the localization of fat emboli revealed that more were lodging in the small arteries and arterioles in the first group than in the second. Our results have indicated that a reliable grading of pulmonary fat embolism can not be established without a quantitative image analysis of the size and localization of the fat emboli, and that this quantitative analytical method is useful in achieving this reliable grading.

Adolescent↗
PubMed1990

Nonfracture-associated fatal fat embolism in a case of child abuse.

Fatal fat embolism is usually thought of as a sequel to long-bone fracture, although cases secondary to soft tissue injury and atraumatic conditions have been infrequently reported. In this case of a two-year-old child-abuse victim who sustained multiple blunt traumatic injuries without skeletal fractures, pulmonary and systemic (brain and kidney) fat emboli were identified. At autopsy, all thoracic and abdominal viscera were intact; cranial contents exhibited only diffuse symmetrical petechial hemorrhages of the white matter. Because of the severe and widespread nature of soft tissue hemorrhage, and the absence of a grossly discernible cause of death, fat embolism was suspected. Using a combination of frozen section with oil red O staining and formalin-fixed osmium stained tissues, the immediate cause of death was determined to be diffuse fat embolism. Review of the literature reveals a pathophysiologic basis for fat embolism in the absence of fracture, both as a consequence of an acute increase in local pressure at the site of trauma and an alteration of the emulsification of blood lipids during shock. In light of these findings, we present this case to remind the forensic science community to consider fat embolism as the cause of death in cases of blunt-force injury without fracture.

Cause of Death↗
PubMedDate not supplied

[Diagnostics of traumatic fat embolism].

The article deals with diagnosis and treatment of fat embolism concomitant with trauma. A new term is suggested, i.e. liqoroglobulism, which is concomitant with the cerebral form of fat embolism. The results of investigations of patients, who endured fat embolism, are presented. A new method is suggested for the treatment of fat embolism, i.e. a combination of hemosorption and liquosorption. A thesis on that the blood-brain barrier is damaged in the cerebral form of fat embolism is formulated.

Embolism, Fat↗
PubMed1996

Splanchnic and peripheral tissue perfusion in experimental fat embolism.

OBJECTIVE: To investigate the acute effects of experimental fat embolism on splanchnic and peripheral perfusion and oxygenation in pigs. DESIGN: Randomized, controlled trial. SETTING: Animal laboratory. SUBJECTS: Eighteen domestic pigs, weighing 25 to 31 kg. INTERVENTIONS: The 18 pigs were randomized to either the fat embolism or control groups. Nine anesthetized and mechanically ventilated pigs were intracavally infused with a 10% allogeneic bone marrow suspension at a dose of 100 mg/kg over 5 mins (the fat embolism group); nine control pigs received normal saline in the same volume and speed (control group). MEASUREMENTS AND MAIN RESULTS: Mean pulmonary arterial pressure, pulmonary vascular resistance, and pulmonary shunt increased, and PaO2 decreased immediately after the bone marrow suspension infusion. In the fat embolism animals, oxygen delivery decreased, oxygen content difference widened, and total oxygen consumption remained high, indicating enhanced oxygen extraction. Further, superior mesenteric artery blood flow and mesenteric oxygen delivery decreased, while intramucosal pH in the small bowel was stable. Subcutaneous PO2 decreased in both groups, whereas transcutaneous PO2 decreased only in the animals receiving bone marrow suspension. Skin red cell flux showed no significant changes. CONCLUSIONS: The present model of fat embolism results in significant impairment in systemic oxygenation. Despite this fact, the intestinal oxygenation remains unaffected probably due to sufficient compensatory mechanisms. Transcutaneous PO2 measurements may provide a useful index for early detection of fat embolism.

Animals↗
PubMed1963

[Fat embolism].

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Embolism↗