PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “EMBOLISM, FAT”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMed2002

Computed tomography diagnosis of macroscopic pulmonary fat embolism.

Pulmonary fat embolism probably occurs commonly after major orthopedic injuries and after orthopedic surgery. Furthermore, tiny fat emboli can often be shown by transesophageal echocardiography during orthopedic surgery. However, large macroscopic are rarely identified radiologically. Macroscopic fat emboli have been previously described in the common femoral vein and inferior vena cava on abdominal imaging. To the authors' knowledge, a macroscopic fat embolus in the pulmonary arteries has not been previously described. The authors report a case of a woman who, on computed tomography, had a large fat embolus after intramedullary rod placement for an isolated left femur fracture.

Adult↗
PubMed1972

Role of plasma lipoproteins in cortisone-induced fat embolism.

The clinical syndrome of fat embolism can be a complication in patients who have suffered long-bone fracture, and has been associated with a number of conditions in which bone fracture is not a factor. The origin of embolic fat (bone marrow or depot fat versus plasma lipoproteins) has been debated. To test the hypothesis that alterations in the composition of plasma very-low-density lipoproteins (VLDL) could lead to their coalescence and subsequent impaction in pulmonary vasculature, New Zealand white rabbits were injected intramuscularly with 25 mg of cortisone twice a day for 2, 4, 6, 11 and 12 days. Blood samples were obtained from unanesthetized animals prior to the cortisone treatment and at sacrifice. Pulmonary fat embolism that was similar histologically to that found in the human patient with the clinical syndrome was produced in all rabbits treated for 4-12 days. After the fourth day, all animals were hyperlipidemic. There was a tenfold increase in plasma VLDL concentration and the mean particle diameter of the VLDL was increased from 620 A to 1016 A. The proportion of triglyceride (TG) was increased, protein (PR) and phospholipid (PL) were decreased and total cholesterol (TC) was unaltered (untreated controls: PR, 16.4%; TG, 58.5%; PL, 19.2%; TC, 6.7% and cortisone-treated: PR, 8.4%; TG, 75.1%; PL, 11%; TC, 6.4%). The lipid composition of pulmonary embolic fat from rabbits treated with cortisone for 6 or 11 days was TG, 81%; PL, 13% and TC, 6%. VLDL from similarly treated rabbits had a lipid composition of TG, 79%; PL, 14.5% and TC, 6.6%. The TC concentration of bone marrow and depot fat from animals treated with cortisone for 11 days was <1%, and the PL concentration was <2%. These data support the hypothesis that plasma lipoproteins, primarily the VLDL, when altered in size and composition can coalesce into globules of sufficient size to occlude peripheral capillaries.

Adipose Tissue↗
PubMed1992

Bronchoalveolar lavage in trauma patients for diagnosis of fat embolism syndrome.

Fat embolism syndrome (FES) is a rare but serious complication occurring after long bone fractures. Presence of fat droplets in cells obtained by bronchoalveolar lavage has been proposed as a specific tool for FES diagnosis in trauma patients. We evaluated this technique over a 15-month period in 85 patients. Twenty-eight patients were excluded. The remaining 57 patients were divided into three groups: group 1, 26 patients without trauma as control; group 2, 22 patients with trauma but without evidence of FES; and group 3, nine patients with trauma and evidence of FES. Six of 26 patients in group 1 and nine of 22 patients in group 2 exhibited fat droplets in alveolar macrophages, whereas three of nine patients of group 3 had not. This study suggests that (1) presence of fat droplets in alveolar macrophages is not a reliable method for diagnosis of FES after long bone trauma, and (2) many conditions are associated with fat droplets in alveolar macrophages.

Adult↗
PubMed2006

Prevention of fat embolism syndrome.

Fat embolism syndrome is a condition of acute respiratory distress following long-bone trauma. This condition may involve not only the lungs but also a number of other body systems. The pathophysiology is not as yet clearly understood, however, intravasation of fat from long-bone fractures may play a role. Early recognition of the severity of injury both on clinical and biochemical grounds and early surgical stabilization of long bones may help to decrease its incidence. However, the best surgical technique with which to do this stabilization has not yet been clearly determined. Surgical and pharmacological techniques have been developed in an attempt to either decrease the intravasation of fat during long-bone stabilization or block the inflammatory cascade with varying degrees of efficacy. Ongoing research focuses on both the prevention and treatment of this condition.

Bone Nails↗
PubMed1978

Fat embolism in infancy after intravenous fat infusions.

Four cases of fat embolism are described in infants receiving prolonged intravenous infusion of fat (Intralipid 20%). This therapeutic complication has been termed 'fat overloading syndrome' but bears a clinical similarity to post-traumatic fat embolism. These 4 cases are the first to be recorded in infancy, and with histopathological proof of fat embolism. These 4 cases are the first to be recorded in infancy, and with histopathological proof of fat embolism. Transient high rates of infusion of Intralipid appears to be a factor in the aetiology of the condition.

Capillaries↗
PubMed1979

Fat embolism as a cause of idiopathic necrosis of the head of the femur. Review of forty five cases of post traumatic fat embolism.

It has been postulated in recent years that idiopathic necrosis of the head of the femur may possibly be caused by arteriolar obstruction by fat emboli emanating from a fatty liver, which would act as a reservoir, due to various causes such as alcoholism and prolonged steroid therapy. A similar situation has been found in human pathology in post traumatic fat embolism. The writers have reviewed forty five cases of post traumatic fat embolism which had passed the pulmonary filter. All the cases were reviewed after a minimum of two years, since this is considered the minimum time within which necrosis can manifest itself radiologically. In none of these cases was there any evidence of necrosis of the head of the femur. These findings, supported by other critical considerations. do not lend support to the theory of fat embolism as a case of idiopathic bone necrosis.

Embolism, Fat↗
PubMed1977

[Excessive generalized fat embolism in acutely dystrophic fat liver (author's transl)].

We have reported about a 63 year old woman, who, 1 to 2 hours after a meal containing mushrooms, became acutely ill, sank into uncontrollable shock, and died 24 hours later. Autoptically was found an acute yellow liver dystrophy in a previously existing fatty liver. Etiologically an intoxication by Amanita phalloides could be excluded as well as any other exogenic intoxication. The cause of the acute liver dystrophy was most probably a fulminant virus hepatitis. The decay of the fatty liver cells led to an unusally severe generalized fat embolism, which morphologically is regarded as the cause of death.

Acute Disease↗
PubMed1989

Subarachnoid fat embolism complicating autologous fat grafting following translabyrinthine excision of acoustic neuroma.

A 64-year-old man had complete excision of an acoustic schwannoma via the translabyrinthine route and the mastoid cavity was packed with fat. Post-operatively there were two episodes of aseptic meningitis and CT scanning demonstrated migration of fat into the basal subarachnoid CSF spaces. This unusual complication should be recognized and differentiated from both true infective meningitis and aseptic meningitis from other causes.

Adipose Tissue↗
PubMed1997

Pulmonary effects of fixation of a fracture with a plate compared with intramedullary nailing. A canine model of fat embolism and fracture fixation.

UNLABELLED: Fat-embolism syndrome and pulmonary dysfunction may develop in multiply injured patients who have a fracture of a long bone. Although early fixation of a fracture is beneficial, intramedullary nailing may exacerbate pulmonary dysfunction by causing additional embolization of marrow fat. We examined the pulmonary effects of the timing and method of fixation of a fracture in a canine fat-embolism model. Fat embolism was induced in forty-one adult dogs by reaming the ipsilateral femur and tibia followed by pressurization of the intramedullary canal. The animals were divided into a control group of eight dogs that had induction of fat embolism alone and an experimental group of thirty-three dogs that had induction of fat embolism and internal fixation of a transverse fracture of the middle of the contralateral femoral shaft. In the control group, four dogs each were killed four hours and twenty-four hours after induction of fat embolism. In the experimental group, a femoral fracture was created and fixation was performed four hours after embolic showering in fifteen animals and twenty-four hours after embolization in eighteen animals. The two experimental groups were subdivided according to the method of fixation of the fracture: eleven dogs each had application of a plate, nailing without reaming, and nailing with reaming. The pulmonary arterial pressure and the alveolar-arterial gradient were measured preoperatively, during induction of fat embolism, and as long as one hour after fixation of the fracture but before the animal was killed. The lungs, brain, and kidneys were examined for pathological and physiological evidence of intravascular fat. The intravascular fat persisted for twenty-four hours after induction of pulmonary fat embolism. Pulmonary arterial pressure remained elevated at four hours after the embolic showering, before creation and fixation of the fracture. By twenty-four hours after the induction of fat embolism, pulmonary arterial pressure had returned to the baseline level. Neither the creation nor the fixation of the fracture affected pulmonary arterial pressure. In the animals that had fixation of a fracture four hours after embolization, both nailing with reaming and nailing without reaming produced alveolar-arterial gradients that were higher than the baseline values, whereas fixation with a plate did not change the alveolar-arterial gradient significantly from the baseline value. In addition, the alveolar-arterial gradients in the animals that had nailing with reaming and nailing without reaming four hours after embolization were, respectively, four and 3.5 times higher than that in the animals that had fixation of the femur with a plate. In the animals that had fixation twenty-four hours after embolization, none of the methods for fixation affected the alveolar-arterial gradient. The amount of embolic fat in the lungs, brain, and kidneys was not affected by fixation of the fracture when it was performed at either the four-hour or the twenty-four-hour time-interval. Scores for pulmonary edema were increased by fixation of the fracture, but there was no difference among the scores associated with the three methods of fixation. CLINICAL RELEVANCE: The findings of the present study indicated that the amount of intravascular fat persisting in the lungs, kidneys, and brain twenty-four hours after pressurization of the intramedullary canal is not affected by the method of fixation of the fracture. Fixation of a fracture is associated with minimum evidence of acute inflammation and has no effect on pulmonary artery pressure. The development of pulmonary dysfunction from fat emboli depends on other factors, not just on the presence of fat in pulmonary vessels. It appears that the method of fracture fixation has little influence on the outcome of treatment.

Animals↗