Pathophysiology

Droplets of fat are released primarily from fat depots in the marrow of long bones, but also from the soft tissues and organs such as liver, enter the venous circulation, and reach the lungs, where they become lodged in the pulmonary capillaries. This behavior is similar to pulmonary embolism.

Fat embolism syndrome is characterized by pulmonary insufficiency following trauma and is a specific variant of acute lung injury. It appears to be one of a number of triggering mechanisms leading to lung pathology indistinguishable from adult respiratory distress syndrome.

The mediated inflammatory response associated with fat embolism syndrome and resulting in acute lung injury is probably the same for all variants of adult respiratory distress syndrome irrespective of etiology. The initiating event in fat embolism syndrome appears to be the release of injurious free fatty acids by pulmonary lipase. The free fatty acids result in 'injury' leading to an inflammatory cascade. Thereafter events follow a common pathway. Important initial mediators include activated complement and neutrophils. These mediate the release of oxygen free radicals and other cellular toxins such as proteases, arachidonic acid, and platelet activating factor which, in turn, directly damage vascular and respiratory endothelium, resulting in the further release of activated neutrophils, thus perpetuating the injury cycle. The final pathway is a pathological diffusion barrier and ultimately breakdown of the capillary alveolar membrane barrier, leading to leakage of protein-rich fluid through the alveolar cell wall into the alveolar sacs. This is further compounded by impaired surfactant production leading to alveolar collapse.

There are other systemic features distinguishing fat embolism syndrome. A common presenting feature is an altered mental state. The etiology may be complex. In multiple system injury it may be difficult to distinguish neurological features related to traumatic primary brain injury from hypoxia secondary to acute lung injury or hypovolemia. Where no head injury is present, neurological symptoms may present dramatically and are easily related to hypoxia from the acute lung injury or hypovolemia. Severe neurological disturbance may result from fat embolization to the brain without lung involvement. Here, arterial blood gas analysis is normal and cerebral signs are due to edema, microinfarction, and demyelination ( Scopa..et,al 1994).

Hemorrhagic shock may be one factor responsible for the entry of fat droplets into the circulation. Other factors include disseminated intravascular coagulation (DIC), sepsis, and site of injury. The incidence, morbidity, and mortality are greater with proximal than with more distal injury. Other features which characterize fat embolism syndrome as a discrete variant of adult respiratory distress syndrome include petechial hemorrhages of skin, and renal, retinal, subconjuctival, and myocardial involvement by droplet emboli.

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