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proposed this theory for the development of fat embolism syndrome.

The release of inflammatory mediators and vasoactive amines like histamine, serotonin leads to an increase in vascular permeability and vasodilation with ensuing hypotension and hypoperfusion.īaker et al. Systemic effects on end-organs such as the brain, kidney, and skin.ĭeposition of the fat droplets in the brain produces a cascade of reactions and leads to a systemic inflammatory response syndrome, local inflammation, and ischemia as a result of disruption of microcirculation. Since early open reduction and internal fixation has become the standard of care for repairing fractures of long bones, the incidence of fat embolism and fat embolism syndrome has gradually decreased. Most recent studies show an incidence of about 1% to 11%. In the landmark study carried out by Gurd, using the established clinical criteria, an incidence of 19% of fat embolism syndrome was reported in a group of trauma patients. With a transesophageal echocardiogram, fat embolism has been detected in close to 41% of patients.įat embolism has a higher incidence than fat embolism syndrome. If the blood sample was taken from a site close to the area of the fracture, the incidence is closer to 95%.įat embolism and fat embolism syndrome also can occur intraoperatively while repairing a long bone fracture. In one study, about 67% of orthopedic trauma patients have fat globules in their blood. Clinical diagnosis of small fat embolism or mild cases of fat embolism syndrome may be missed and go away unnoticed. Variable data have been reported on the incidence of fat embolism and fat embolism syndrome. Since the majority of reported cases of fat embolism is seen in patients with orthopedic trauma,most research on this condition is in orthopedic patients.Įven though the clinical criteria proposed by Gurd et al. and Wilson can help or aid in the diagnosis, fat embolism syndrome still poses a major diagnostic challenge to most clinicians. This was later modified by Wilson in 1974 in conjunction with Gurd and is the most commonly used clinical criteria for diagnosis. In the early 70's, Gurd proposed a clinical criterion for the diagnosis of fat embolism syndrome. In 1873, Von Bergmann clinically diagnosed the condition for the first time. Since the initial description by Zenker and Von Bergmann, several articles and studies have been published on this diseases entity. Zenker first described the clinical presentation of fat embolism syndrome in 1863 in a patient suffering from crush injury. Fat embolism syndrome is a continuum of fat embolism. In most instances, diagnosis is usually established during the autopsy.įat embolism is the presence of fat globules in microcirculation whereas fat embolism syndrome is a systemic manifestation of dissemination of fat molecules or globules in microcirculation.