Systemic Fat Embolism Research Articles

The Role of Fat Embolism in the Etiology of Corticosteroid-induced Avascular Necrosis

Case reports since 1957 implicate corticosteroids in excess of physiologic requirements as a cause of nontraumatic osteonecrosis. Both laboratory and clinical studies demonstrate marked alterations in lipid metabolism with hyperlipemia, fatty liver and systemic fat embolism. Intra-arterial infusion of fat produces embolic vascular obstruction, focal marrow necrosis and osteocytic death in the femoral head of the rabbit. Induced hypercortisonism in rabbits produces severe hyperlipemia, fatty liver, systemic fat emboli, terminal vascular obstruction in bone and associated areas of osteocytic death representing avascular necrosis. Osteoporosis develops without fracture. Histologic evidence of vasculitis, thrombosis, or microfracture is lacking. The specific biochemical pathway of corticosteroid lipid alterations is unknown.

Hyperlipoproteinemia in Idiopathic Necrosis of the Femoral Head in Adults

The etiology of idiopathic necrosis of the femoral head in adults is unknown and controversial.In 1965 it was hypothesized by Jones that excessive corticosteroid and alcohol might induce the formation of fatty liver, with possible subsequent systemic fat embolism, infarction of bone and eventual aseptic necrosis. The Cholesterol, triglyceride and phospholipid levels were investigated in 65 patients with idiopathic necrosis of the femoral head to select patients with hyperlipoproteinemia. Twenty nine of the 65 patients had hyperlipoproteinemia. They were classified by disc electrophoresis. Eleven of them were in type IIa, 16 in type IIb, and 2 in type IV.A definite correlation between idiopathic necrosis of the femoral head and hyperlipoproteinemia was found, while no relationship between diseases associated with idiopathic necrosis of the femoral head and certain types of hyperlipoproteinemia was established.

Silicone embolism, fat embolism, and fibrin thrombosis in dogs after extracorporeal circulation using a bubble-oxygenator (author's transl)

Following extracorporeal circulation with a bubble oxygenator (Rygg-Kyvsgaard) silicone emboli were found in the brain-and-kidney-capillaries of all dogs evaluated. There was no obvious correlation between intensity of silicone embolism and pump time. No cellular reaction was seen around the anti-foam agent. Occasionally single small areas of embolic brain damage were found. During extracorporeal circulation and within a recovery period up to one hour no silicone excretion through the kidneys could be demonstrated. Systemic fat embolism occurred less frequent than previously reported. Use of a filter in the cardiotomy suction line reduced its intensity further. In neither of the various organs examined, disseminated intravascular thrombosis could be found.

Central nervous system complication in a patient with chronic gaucher's disease.

Central nervous system manifestations developed in a patient suffering from the chronic, adult form of Gaucher's disease. At autopsy, massive systemic fat embolism was found, involving mainly the brain and the lungs. As there was no evidence of bone fracture, or trauma to the adipose tissues, it is presumed that the severe skeletal involvement by the Gaucher's disease led to the development of the fat embolization.

Clinical, ophthalmoscopic and biological findings in systemic fat embolism. Pathogenetic theory and treatment in 30 cases.

Several clinical pictures which may allow a better understanding of the pathogenesis of fat embolism have been presented. The well-known picture of systemic embolism and vascular disease has been contrasted with those cases where emboli are not observed. Cases of petechial rash and retinal haemorrhage without other signs have been reported to illustrate that there are two phases of the disease: mechanical and metabolic. Metabolic phenomena may be the inaugurating signs or may occur secondarily, with varying degrees of severity, after petechiae and fundoscopic alterations have developed. A complete description of the different clinical pictures which may be seen in fat embolism requires that one includes the findings in the optic fundi. Ophthalmoscopic findings in our group of 30 patients have been detailed.

Systemic fat embolism. A diagnostic profile in 24 patients.

In a series of 24 patients with systemic fat embolism, clinical signs commenced within 12 hours of the trauma in one third and within 24 hours in two thirds of the cases. Impairment of consciousness was the most common finding. The neurologic manifestations usually were bilateral and symmetric, being chiefly pyramidal signs, epileptic seizures, and decerebrate rigidity. Thirty percent of the patients also had focal neurologic deficit. Sudden onset of fever, tachycardia, and tachypnea was common, whereas roentgenographic evidence of pulmonary fat embolism was noted in only one of every three patients. Petechial hemorrhages, signs of retinal fat embolism, lipuria, and a major decrease in hemoglobin level were found in half the patients. Seven of the 24 patients died, all within 96 hours and all in deep coma. Survival for longer than four days carried a good prognosis. Treatment with massive doses of steroids may be useful.

The Cause of Death in Fat Embolism

The purpose of this retrospective study is to determine the cause of death in systemic fat embolization. This study is based on the dispute existent in the literature between the earlier hypothesis of cerebral involvement as the main cause of death and the newer concept that the primary pulmonary insufficiency is the principal cause of death in this syndrome. We found that patients diagnosed as having pure cerebral embolism recovered after supportive treatment and the only fatal case in this group had involvement of the brainstem. The other patients developed respiratory failure of different degree. Those with mild cases recovered completely, while, despite intensive therapy, those with severe conditions died. Seven patients from this group also had cerebral fat embolization without any clinical neurologic signs and all died due to their respiratory insufficiency. Our findings enhance our belief that systemic fat embolism is essentially a pulmonary disease. The purpose of this retrospective study is to determine the cause of death in systemic fat embolization. This study is based on the dispute existent in the literature between the earlier hypothesis of cerebral involvement as the main cause of death and the newer concept that the primary pulmonary insufficiency is the principal cause of death in this syndrome. We found that patients diagnosed as having pure cerebral embolism recovered after supportive treatment and the only fatal case in this group had involvement of the brainstem. The other patients developed respiratory failure of different degree. Those with mild cases recovered completely, while, despite intensive therapy, those with severe conditions died. Seven patients from this group also had cerebral fat embolization without any clinical neurologic signs and all died due to their respiratory insufficiency. Our findings enhance our belief that systemic fat embolism is essentially a pulmonary disease.

SYSTEMIC FAT EMBOLISM ASSOCIATED WITH THE TOXIC EFFECTS OF AVIATION-FUEL INHALATION AND GENERAL ANAESTHESIA

In an unusual accident the two occupants of a light aircraft were exposed to petrol vapour for different periods of time before being rescued. Both received almost identical injuries and were admitted to hospital in a satisfactory condition. Each received a general anaesthetic. They both died from systemic fat embolism, one 48 hr. after the accident with severe jaundice, the other 75 hr. after the accident with no jaundice. Necropsy findings were identical with severe fatty change in the liver and myocardial fatty degeneration, associated with fat embolism and pulmonary oedema. It was shown by experiments in mice that exposure to petrol produces severe fatty change in the liver in these animals and the formation of fat emboli was demonstrated. Exposure of mice to halothane anaesthesia for 5-10 min. caused some fatty change in the liver cells in the centrilobular area after 48 hr. When mice were given a halothane anaesthetic 2 hr. after exposure to petrol extensive fatty change was present in all liver cells after 48 hr. Assuming the incidence of fatal fat embolism after long-bone trauma to be in the vicinity of 4%, there would have been 1 chance in 1000 of both persons in the accident developing systemic fat embolism from the fractured bones alone. It is postulated that the systemic fat embolism is more likely to have resulted from the hepato-cellular damage, possibly aggravated by the subsequent anaesthetic. Supporting evidence for this hypothesis is provided by the direct correlation between the length of exposure to petrol, the degree of liver damage, the extent of the pulmonary and systemic fat embolism, and the survival period in both airmen.

Systemic fat embolism associated with the toxic effects of aviation fuel inhalation and general anaesthesia

In an unusual accident the two occupants of a light aircraft were exposed to petrol vapour for different periods of time before being rescued. Both received almost identical injuries and were admitted to hospital in a satisfactory condition. Each received a general anaesthetic. They both died from systemic fat embolism, one 48 hr. after the accident with severe jaundice, the other 75 hr. after the accident with no jaundice. Necropsy findings were identical with severe fatty change in the liver and myocardial fatty degeneration, associated with fat embolism and pulmonary oedema. It was shown by experiments in mice that exposure to petrol produces severe fatty change in the liver in these animals and the formation of fat emboli was demonstrated. Exposure of mice to halothane anaesthesia for 5-10 min. caused some fatty change in the liver cells in the centrilobular area after 48 hr. When mice were given a halothane anaesthetic 2 hr. after exposure to petrol extensive fatty change was present in all liver cells after 48 hr. Assuming the incidence of fatal fat embolism after long-bone trauma to be in the vicinity of 4%, there would have been 1 chance in 1000 of both persons in the accident developing systemic fat embolism from the fractured bones alone. It is postulated that the systemic fat embolism is more likely to have resulted from the hepato-cellular damage, possibly aggravated by the subsequent anaesthetic. Supporting evidence for this hypothesis is provided by the direct correlation between the length of exposure to petrol, the degree of liver damage, the extent of the pulmonary and systemic fat embolism, and the survival period in both airmen. In an unusual accident the two occupants of a light aircraft were exposed to petrol vapour for different periods of time before being rescued. Both received almost identical injuries and were admitted to hospital in a satisfactory condition. Each received a general anaesthetic. They both died from systemic fat embolism, one 48 hr. after the accident with severe jaundice, the other 75 hr. after the accident with no jaundice. Necropsy findings were identical with severe fatty change in the liver and myocardial fatty degeneration, associated with fat embolism and pulmonary oedema. It was shown by experiments in mice that exposure to petrol produces severe fatty change in the liver in these animals and the formation of fat emboli was demonstrated. Exposure of mice to halothane anaesthesia for 5-10 min. caused some fatty change in the liver cells in the centrilobular area after 48 hr. When mice were given a halothane anaesthetic 2 hr. after exposure to petrol extensive fatty change was present in all liver cells after 48 hr. Assuming the incidence of fatal fat embolism after long-bone trauma to be in the vicinity of 4%, there would have been 1 chance in 1000 of both persons in the accident developing systemic fat embolism from the fractured bones alone. It is postulated that the systemic fat embolism is more likely to have resulted from the hepato-cellular damage, possibly aggravated by the subsequent anaesthetic. Supporting evidence for this hypothesis is provided by the direct correlation between the length of exposure to petrol, the degree of liver damage, the extent of the pulmonary and systemic fat embolism, and the survival period in both airmen.

1921. Deaths from petrol exposure: Tonge, J. I., Hurley, R. N. & Ferguson, J. (1969). Systemic fat embolism associated with the toxic effects of aviation-fuel inhalation and general anaesthesia. Lanceti, 1059

1921. Deaths from petrol exposure: Tonge, J. I., Hurley, R. N. & Ferguson, J. (1969). Systemic fat embolism associated with the toxic effects of aviation-fuel inhalation and general anaesthesia. Lanceti, 1059

An assessment of the cerebrospinal fluid and choroid plexus in relation to systemic fat embolism.

An assessment of the cerebrospinal fluid and choroid plexus in relation to systemic fat embolism.

SYSTEMIC FAT EMBOLISM ASSOCIATED WITH THE TOXIC EFFECTS OF AVIATION-FUEL INHALATION AND GENERAL ANÆSTHESIA

In an unusual aircraft accident the two occupants of a light aircraft were exposed to petrol vapour for different periods of time before being rescued. Both received almost identical injuries and were admitted to hospital in a satisfactory condition. Each received a general anæsthetic. They both died from systemic fat embolism, one 48 hours after the accident with severe jaundice, the other 75 hours after the accident with no jaundice. Necropsy findings were identical with severe fatty change in the liver and myocardial fatty degeneration, associated with fat embolism and pulmonary œdema. Experiments in mice showed that exposure to petrol produces severe fatty change in the liver in these animals, and the formation of fat emboli was demonstrated. It is postulated that the systemic fat embolism in these airmen is more likely to have resulted from the hepatocellular damage than from the bone fractures. The possible additive effect of the general anæsthesia in the production of the fatty changes is considered.

Systemic Fat Embolism in Four Combat Casualties

Collins, John A. MC, USAR; Hudson, Thomas L. Lt. Col., MC, USA; Hamacher, William R. Maj., MC, USA; Rokous, Joseph Maj., MC, USA; Williams, George CAPT., MC, USAR; Hardaway, Robert M. III, Col., MC, USA Author Information

A new clinical and experimental concept on fat embolism.

A SURVEY on the study of fat embolism conducted in all traumatologic departments of the teaching hospitals and of the other large hospitals, as well as in all Böhler Hospitals for the treatment of cases of injury in Austria covered 263,861 hospitalized patients. The overall mortality rate was 2 per cent (5,265 cases). In all these cases an autopsy was performed as required by Austrian law. In 5 per cent of these fatal injuries (289 cases) systemic fat embolism was the principal cause of death. In 566 additional cases (10.8 per cent) fat embolism, mostly of pulmonary nature, was considered . . .

Systemic Fat Embolism Following Acute Primary Osteomyelitis

THE SYNDROME of systemic fat embolism has been recognized for many years and several reviews of the subject have recently been published.1-4The principle underlying etiology is trauma, especially fracture of long bones. There are, however, other much less common predisposing conditions in which the associated fat embolism is usually not recognized. A partial list of these would include severe burns, acute fatty liver of the alcoholic, extracorporeal circulation, corticosteroid therapy, sickle cell and sickle-C crises with bone marrow infarction, following oil lymphography, and pancreatitis. We wish to report what we believe is the first fully documented case in the American literature of systemic fat embolism following acute primary osteomyelitis. Report of a Case A 15-year-old white boy was admitted to the Los Angeles County General Hospital on Aug 13, 1965. There had been a slight headache, some malaise, and left shoulder pain of two to three days duration.

Systemic fat embolism after renal homotransplantation and treatment with corticosteroids

MANY clinical and experimental studies have been performed to study the etiology, diagnosis and treatment of traumatic fat embolism. Recently, a less well understood counterpart, termed nontraumatic fat embolism, has been recognized. In documenting the first case of pulmonary and systemic fat embolism as a complication of hypercortisonism in man, Hill,1 in 1961, suggested that corticosteroids administered in high dosages were a major factor in the evolution of systemic fat emboli. Another case of fat embolism as a possible complication of hypercortisonism is reported. This potentially fatal entity is particularly important because of the increasing interest in homotransplantation and the . . .

Diagnosis and Treatment of Fat Embolism

The occurrence of fat embolism as a complication of skeletal trauma has been of interest for more than a century. The controversy in regard to the source of the embolic fat has still not been resolved. The incidence of fat embolism is relatively high both on the battlefield and in civilian life (Table 1).^1-7The severity of this complication in association with multiple injuries, especially with fractures of long bones, is not generally appreciated. Systemic fat embolism produces a clinical syndrome with characteristic findings and pertinent laboratory results. With a better understanding of the underlying pathophysiological mechanisms, treatment has become more specific and less empirical. <h3>Pathogenesis</h3> The pathogenesis of fat embolism is still subject to conjecture and controversy. The genesis of the embolic fat is postulated as being either mechanical or physiochemical. Although it is possible that intravasation of fat into vascular channels can occur after trauma, recent studies⁸

Fatal systemic fat embolism

<h2>Summary</h2> A case is presented of massive post-traumatic systemic fat embolism with significant embolic lesions demonstrated at autopsy in the brain, heart, and lungs. Attention is called to the need for consideration of the phenomenon of fat embolization in the post-trauma patient showing unexplained central nervous system, cardiac, and/or pulmonary symptoms, especially in the presence of skin petechiae.

The electroencephalogram in cerebral fat embolism

In six patients with traumatic systemic fat embolism electroencephalography was carried out at the earliest possible moment after confirmation of impaired consciousness, and again on repeated occasions during subsequent treatment. In five cases there was considerable generalized dysrhymia, coupled with loss of the physiological, normal rhythm and the appearance of polymorphic delta and theta waves. One patient's EEG consisted of a rhythmic pattern showing some similarity to that seen in certain stages of Nevin-Jones' disease. In three patients who recovered without neurological aftermath the tracings resumed the normal physiological pattern in the course of a few weeks or moths. No strict relationship between changes in the EEG and quantitative impairment of consciousness was found. Three patients died in the acute stage of the disease.

INHIBITION OF LIPASE ACTIVITY OF LUNG AND ADIPOSE TISSUE BY PHENOTHIAZINE DERIVATIVES.

AN increase in lipolysing activity of the blood has been recorded in some patients after injury of adipose tissue1,2. This increase is found to begin about three days after wounding. In the course of an investigation of the source of this lipase, we examined lung as well as adipose tissue, since lung is involved not only in the early complications of ‘fat embolism’, but also in ‘systemic fat embolism’, the signs of which appear after three days.