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PubMed2000

Fatal fat embolism syndrome: a case report.

Fat embolism syndrome is a dire complication of long bone trauma. It is usually associated with neurological, hematological and respiratory involvement, the latter being the major cause of death. We present a case of severe fat embolism syndrome occurring 3 hours after a long bone injury, leading to permanent vegetative state and death without any respiratory signs. The diagnosis was confirmed by cytology of the bronchoalveolar lavage fluid. Clinical presentation of the puzzling fat embolism syndrome and diagnostic tests in suspected fat embolism syndrome are reviewed.

Accidental Falls↗
PubMedDate not supplied

The three syndromes of fat embolism: pulmonary manifestations.

The clinical course and radiographs of 30 patients with fat embolism syndrome were reviewed. In all cases the classic triad of neurologic dysfunction, respiratory insufficiency, and petechiae were present. Three responses to embolized fat were noted. The hyperacute response was seen in two patients with paradoxical embolization of fat to the systemic circulation. A "classic response" was noted in 18 patients with transient respiratory compromise and variable radiographic findings. The two deaths in the group responding in the classical manner were attributed to massive pulmonary emboli. The third response, noted in ten patients, consisted of a chest radiograph compatible with pulmonary edema in the clinical setting of the adult respiratory distress syndrome. In this group the degree of respiratory dysfunction and pulmonary damage correlated with the development of disseminated intravascular coagulation. Pathologic correlations are presented and the mechanisms by which embolic fat produces tissue damage are discussed.

Adolescent↗
PubMedDate not supplied

[Post-traumatic pulmonary and systemic fat embolism in forensic practice. Prospective histological study].

INTRODUCTION: The more or less subclinical presence of fat emboli in the lungs and other vital organs, without ischaemic changes in them, whose presence could be postmortem established only by microscopic examination, is termed in forensic medicine systemic fat embolism. On the other hand, Fat Embolism Syndrome (FES) is a clinical manifestation of the presence and influence of fat emboli in organs, with clearly defined neurological, respiratory and cutaneous signs and various symptoms, grouped in the so called major and minor signs [8-11]. PURPOSE: The purpose of this paper is to establish the frequency of post-traumatic occurrence of fat emboli in capillaries of the lungs and other organs in cases where the cause of death was not related to pulmonary or systemic fat embolism, but where the typical fat depot injury was established. MATERIAL AND METHOD: A prospective autopsy histological study was carried out. The sample included 56 cases. The clinical and autopsy data were analyzed and compared in order to establish the value of injury Severity Score--ISS. Histological samples of all vital organs were stained by special technique (Sudan III) and the findings in the lungs and kidneys were graded according to Sevitt's criteria [12]. All data were statistically analyzed (chi 2 test, ANOVA). RESULTS AND DISCUSSION: The sample included 38 males (average age 53.10 years) and 18 females (average age 54.84 years). The older (ANOVA; p = 0.0017) males (chi 2 = 7.14; p < 0.01), injured as pedestrians (ANOVA, p-->0) were statistically significantly more represented. The most common determined causes of death were: cerebral contusions (30), exsanguination (22), respiratory disorders (9), combustion (6), spinal cord contusions (1), and others (complication of injuries, such as inflammations or sepsis--4). These causes were singular or competitive plural. The average value of ISS was 34.59 (SD = 13.16) and that of outliving period 3.70 days (SD = 5.88). The distribution of outliving period was log-normal. Pulmonary fat embolism was established in all cases: in 14 cases pulmonary fat embolism of the first degree; in 16 of the second grade and in 26 of the third degree. Pulmonary fat embolism of the third degree could be the precipitate singular or concurrent cause of death. The presence of fat emboli in glomeruli was established in 39 cases: in 30 cases the kidney fat embolism of the first degree was established, in 6 of the second degree and in 3 cases of the third degree. In 11 cases the presence of fat globules in brain capillaries was established and in 3 cases in the capillaries of other organs (heart, liver, spleen). By analyzing the clinical and autopsy data, as well as microscopic findings, we concluded that in four cases the cause of death was associated with systemic fat embolism, what previously had been missed. CONCLUSION: In all our sample cases pulmonary fat embolism was verified, and in a great number of them systemic fat embolism. According to medicolegal principles, pulmonary and systemic fat embolism that develop a few hours after trauma can be considered as a consequence of typical body fat depot injury. The later developed FES could be considered as the complication of such an injury. Pulmonary and systemic fat embolism could complicate the basic trauma, e.g. craniocerebral, abdominal or thoracic, and could be considered as the precipitating cause of death. Because of non-specific and non-characteristic macroscopic autopsy findings, pulmonary and systemic fat embolism could be missed as the cause of death.

Adult↗
PubMed1991

Fat embolism--a review.

The subject of fat embolism is of recurring interest to those managing trauma. This article covers the topic of fat embolism in general, and presents a case of fulminant fat embolism syndrome which highlights the importance of clinical expertise, and whatever technological aids are available to diagnose and appropriately treat this relatively rare, but highly significant form of the syndrome. Fulminant fat embolism syndrome has a very high mortality and should be watched for in patients who have experienced major trauma.

Adult↗
PubMed1972

Fat embolism in patients with fractured hips.

Fat embolism was assessed at necropsy and correlated with clinical findings in the patients who died among 854 with fractured hips admitted to hospital between 1967 and August 1971. Sixteen cases of clinical importance were found, eight of which were judged to have been fatal or to have seriously contributed to death. Frequencies were as follows: 2.4 to 3.3% among 424 patients with subcapital fractures; 0.7 to 0.8% in the 405 with trochanteric fractures; 4.1 to 7% among subjects treated without operation, representing 30% of those who died within seven days; and 0.9 to 1.1% among patients treated by pinning, nailing, or nail-plating. The higher frequency in the conservatively treated group is probably related to selection of poor-risk subjects. Fat embolism was found in 6.8 to 8.0% of those with subcapital fractures treated by primary Thompson's arthroplasty which utilizes acrylic cement, and in none of those given Moore's prostheses for which cement is not used. Study of a larger group after Moore's prosthesis is required to establish its lack of special risk. Fat embolism accounted for all the deaths within seven days of Thompson's arthroplasty and for most within 14 days; it was clearly related to surgery in some cases.A possible explanation of the hazard of Thompson's arthroplasty is that fat globule entry is enhanced by a rise of intramedullary pressure due to proximal occlusion of the reamed marrow cavity. A controlled trial of the effect of venting the marrow cavity on the frequency of fat embolism is warranted. It is possible that the acrylic monomer may also contribute to venous entry of medullary fat. The higher-age group of those with subcapital fractures and associated chronic cardiac and pulmonary disease might make them more susceptible to fat embolization than those in whom arthroplasty is also carried out for chronic hip disease.

Acrylates↗
PubMed1999

Fat embolism.

OBJECTIVE: To review the pathophysiology and management of patients with clinical manifestations of fat embolism. DATA SOURCES: A review of studies reported from 1976 to 1998 and identified through a MEDLINE search of the literature on fat embolism and fat embolism syndrome. SUMMARY OF REVIEW: Fat embolism occurs when bony or soft tissue trauma has caused fat to enter the circulation, or in atraumatic disorders where circulating fat particles have coalesced abnormally within the circulation. The fat particles deposit in the pulmonary and systemic circulations, although only 1 - 2% develop a clinical disorder with respiratory, cerebral and dermal manifestations known as the fat embolism syndrome. Rarely, fat embolism produces a fulminant fat embolism syndrome due to mechanical obstruction within the pulmonary circulation causing a severe right heart failure. The fat embolism syndrome is believed to be caused by the toxic effects of free fatty acids liberated at the endothelial layer which cause capillary disruption, perivascular haemorrhage and oedema. The clinical manifestations of respiratory failure, petechiae and a diffuse or focal cerebral disturbance, are characteristic but not pathognomonic of the syndrome. The syndrome is largely self limiting with treatment being symptomatic. Therapy is directed at maintaining respiratory function and largely follows the same principles of management used in patients who have the acute respiratory distress syndrome. Early immobilization of fractures and methods to reduce the intramedullary pressure during total hip arthroplasty have reduced the incidence of operative fat embolisation. Corticosteroids either before or after the development of respiratory or cerebral symptoms have not been shown to be of any benefit. CONCLUSIONS: Fat embolism occurs in many traumatic and atraumatic conditions and is largely asymptomatic. Preventative measures include early immobilization of fractures and methods to reduce intramedullary pressure during surgical manoeuvres. Treatment is largely symptomatic with therapy for respiratory failure similar to that used in management of acute respiratory distress syndrome. Corticosteroids have not been found to be of significant benefit.

Journal Article↗
PubMed1962

Fat embolization.

Explore the source record for details and available documents.

Embolism↗
PubMed1976

[Fat-embolic vascular occlusions in avian lungs. Research of histologically determinable neutral fats in parrotlike birds (Psittaciformes)].

In 50 flying birds (49 parrot-like, one peacock), the content of fat-embolic vascular occlusions was determined. In 22 cases, fat-embolic occlusions of low intensity were found in pulmonary capillaries. There were no occlusions in renal vessels. The fat embolies had no influence on a lethal outcome. There was no statistically significant correlation between the fatty infiltration of the liver, the fat content of the bone marrow, and the frequency of fat-embolic occlusion of blood vessels. In 18 cases, mycoses were the cause of death. These infections did not influence the number of fat-embolic vascular occlusions.

Animals↗
PubMed2000

Prolonged coma due to cerebral fat embolism: report of two cases.

Fat embolism syndrome remains a rare, but potentially life threatening complication of long bone fractures. The true incidence is difficult to assess as many cases remain undiagnosed. Cerebral involvement varies from confusion to encephalopathy with coma and seizures. Clinical symptoms and computed tomography are not always diagnostic, while magnetic resonance imaging is more sensitive in the detection of a suspected brain embolism. Two cases of post-traumatic cerebral fat embolism, manifested by prolonged coma and diffuse cerebral oedema, are presented. The clinical course of the disease as well as the intensive care unit management are discussed.

Adolescent↗
PubMed1984

[Fat embolism of retinal arteries following acute pancreatitis].

Fat embolism is well known in traumatic skull fractures, chest compression and long bone fractures. Inkeles and Walsh (1975) first described fat embolism of retinal vessels following acute pancreatitis. Fat embolism of ocular vessels in this disease is presumably due to enzymatic destruction of omental tissue. The patient described here fell ill with acute pancreatitis after years of alcohol abuse; he noticed a considerable deterioration in vision. This was a result of fat embolism of the retinal arteries. Multiple cotton wool spots around the optic nerve and in the macular area, combined with some intraretinal hemorrhages, were seen at ophthalmoscopic examination. The pathogenesis of fat embolism of choroidal and retinal vessels following acute pancreatitis is discussed in brief.

Acute Disease↗
PubMed1977

Experimental fat embolism: a dynamic assessment of pulmonary fat-handling characteristics.

Injection 125I-glyceryl trioleate (0-5 mg/kg) into the right atrium of anaesthetized greyhounds caused the following changes: sequestration of far in the right side of the heart; 95 per cent removal by the lungs in a single passage through the pulmonary circulation; subsequent release of fat into the systemic circulation; rapid overall turnover of fat trapped in the lungs and slow removal of recirculating fat by other tissues. We believe that if there is release of unemulsified fat into the circulation in traumatic fat embolism these findings are of significance in interpreting the subsequent pulmonary events.

Animals↗
PubMed1978

Fat embolism in children.

Clinical fat embolism in children is rare. An 11-year-old myelodysplastic child with an apparently insignificant tibial fracture illustrates the risk of this potentially fatal complication in children with osteoporotic bone.

Child↗