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At least 19 recordsLinked to original sources
PubMed1976

[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.

Animals↗
PubMed1996

Bronchoalveolar lavage in adult sickle cell patients with acute chest syndrome: value for diagnostic assessment of fat embolism.

Fat embolism of necrotic bone marrow could be a frequent cause of acute chest syndrome (ACS) in sickle cell syndromes (SC), as suggested by postmortem findings. To check this hypothesis in living patients, we evaluated the presence of fatty macrophages recovered by bronchoalveolar lavage (BAL) in ACS. We investigated 20 consecutive cases of ACS by BAL, and identification of alveolar cells containing fat droplets was performed using oil red O (ORO), a specific neutral fat stain. The specificity of the method was determined on control groups, including eight SC patients without acute chest syndrome and 15 non-SC patients. A cut-off of > 5% of alveolar macrophages containing fat droplets was determined from the control groups to assess the diagnosis of fat embolism. In 12 ACS episodes, BAL exhibited > 5% of fatty macrophages, ranging from 10% to 100% (median value 46.5%). In 11 cases, fat embolism was associated with proven (n = 8) or probable (n = 3) bone marrow infraction, which mostly predated ACS. Eight ACS episodes were associated with a low percentage (< or = 5%) of fatty alveolar macrophages and could be related to a cause other than fat embolism in six episodes, such as sepsis, in-situ thrombosis, or rib infarcts generating hypoventilation. This study supports the diagnostic yield of BAL for fat embolism, which can be incriminated in 60% of cases of ACS in this adult population.

Adolescent↗
PubMed1995

The pathogenesis of fat embolism.

Fat embolism is a common autopsy finding in patients with or without a history of trauma. There are two basic mechanisms causing fat to embolize. Depot-derived fat embolism arises by disruption of depot fat, usually as a result of trauma, allowing direct entry into the bloodstream. Plasma-derived fat embolism is caused by agglutination of endogenous or infused exogenous fat such as Intralipid, with consequent embolism. Chylomicrons and Intralipid liposomes are known to undergo calcium-dependent agglutination by C-reactive protein (CRP), and this may play a role in vivo in this type of fat embolism.

Bone Marrow↗
PubMed2001

Fat embolism.

Fat embolism syndrome is a collection of respiratory, haematological, neurological and cutaneous symptoms and signs associated with trauma and other disparate surgical and medical conditions. The incidence of the clinical syndrome is low (< 1% in retrospective reviews) whilst the embolisation of marrow fat appears to be an almost inevitable consequence of long bone fractures. There is debate over the pathogenesis of fat embolism syndrome and it seems a variety of factors interact to produce a spectrum of end organ damage. Many therapeutic interventions and prophylactic strategies have been tried with varying success. Current treatments are supportive and the condition is usually associated with a good outcome. The literature on fat embolism syndrome is extensive and this review aims to discuss the incidence, aetiology, pathophysiology, diagnosis and treatment of fat embolism.

Anemia, Sickle Cell↗
PubMed1994

The incidence, pathogenesis, diagnosis, and treatment of fat embolism.

Fat embolism syndrome is a potentially serious and life threatening complication of long bone trauma, blunt trauma, and intramedullary manipulation. In long bone fractures, fat embolism is encountered in 0.9% to 2.2% of cases. During intramedullary manipulations, such as prosthetic stem insertion or reaming, the incidence is typically lower (range, 0.5% to 0.8%). Diagnosis is dependent upon the clinical recognition of dyspnea, petechiae, and cognitive dysfunction in the first several days following fracture, trauma, or intramedullary surgery. Treatment consists of pulmonary support and aggressive resuscitation. Studies support early fracture fixation, but the role of systemic steroids, heparin, and other modalities remains speculative.

Brain Diseases↗
PubMed2002

[Fat embolism].

Fat embolism syndrome remains a rare, but potentially life-threatening complication of long bone fracture and other surgical conditions. The true incidence is difficult to assess as many cases remain undiagnosed. This review aims to discuss the incidence, etiology, mechanical and biochemical theories of pathogenesis, clinical features, diagnosis, treatment, outcome and prophylactic strategies of fat embolism.

Diagnosis, Differential↗
PubMed1986

Fat embolism.

Fat embolism is a condition that is underdiagnosed clinically and at autopsy. This paper reviews the causes and pathogenesis of the condition and indicates possible modes of therapy.

Animals↗
PubMed1994

[Intramedullary pressure in the femur during boring and nailing with modern compression interlocking nails--risk of fat embolism?].

Fat embolism syndrome occurs in only 0.9-4% of patients with long bone fractures and especially with intramedullary nailing. Earlier publications have shown that intramedullary manipulation, e.g. reaming and nailing, can produce high pressures of up to 1 bar. The design of the new non-slotted interlocking compressions nails seems to increase the pressure in the femoral cavity. We measured the intramedullary pressure during reaming of the marrow cavity and insertion of compression nails (OSTEO), using cadaver femora and a piezo pressure transducer. We simulated a proximal fracture and performed 30 drilling and 20 nailing procedures. On average we detected a maximum pressure of 0.26 bar during drilling and 0.63 bar during nailing. During reaming the pressure increased when the reamer had passed the narrow diaphysis and reached the metaphysis. When the tried to enlarge the femoral canal by pushing and pulling the reamer repeatedly we measured high pressure peaks. During nailing we detected short impulses lasting a few milliseconds. The results show that the new compression nail do not produce higher intramedullary pressure than slotted nails. It is possible to avoid a dangerous pressure level by using a careful operative technique.

Biomechanical Phenomena↗
PubMed1987

Fat embolism and the fat embolism syndrome. A double-blind therapeutic study.

Fifty-five adults who had sustained a tibial fracture, or a femoral fracture, or both, were subjected to a double-blind randomised study to determine the efficacy of methylprednisolone in treating the fat embolism syndrome. This drug maintained arterial oxygen levels, stabilised or reduced the serum level of free fatty acids, and decreased the risk of the fat embolism syndrome in a statistically significant proportion of patients. Gurd's criteria for the diagnosis of the fat embolism syndrome were found inadequate. Other more sensitive criteria for early diagnosis and effective management were determined. There were no deaths or serious morbidity in our series.

Adolescent↗
PubMed1982

[Study of principles in pathogenesis and therapy of fat embolism. IV. In vivo studies of drug-induced mobilization of embolized lung fat].

Pluronic F 108 added to serum in a concentration of 1 g/dl proved as the optimal means to increase the fat emulgatory capacity. Similar concentrations were achieved in living rabbits by infusing 4.5 g per kg body weight. In spite of this higher dosage we failed to mobilize 131 J labelled fat, embolized into the lungs of the animals. It is concluded that also in humans there exists no possibility to mobilize fat emboli from the lungs by the application of tensides (non-ionic detergents, lecithin-preparations, bile salts) or of organic solvents (alcohol, ether). All these agents are capable to emulsify fat in vitro, however, only under vigorous shaking.--Because of the side effects of those agents their application on patients, suffering from posttraumatic fat embolism seems not to be justified.

Animals↗
PubMed1977

Diagnosis and treatment of fat embolism.

Fat emboli syndrome is one of the major causes of early posttraumatic respiratory distress. Careful attention to the multiple factors associated with the early resuscitative period can minimize this lethal complication of multisystem injury. The use of high-dose steroids and appropriate ventilatory support will decrease the high mortality rate associated with this disease syndrome once it has developed.

Adrenal Cortex Hormones↗