Fat Embolism Syndrome by luckboy


Fat Embolism Syndrome

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									Fat Embolism Syndrome
A 20 year old man presented with a fractured femur after his car was involved in a head on collision while overtaking. Aside from a comminuted fracture of the femur he had no other evident injuries. He was booked to have a fixation of his femur, but developed respiratory failure within twelve hours of admission. He was transferred to the intensive care in extremis with an SpO2 of 83% on a face mask with a reservoir bag. His chest X-Ray (below) showed widespread alveolar shadowing consistent with a diagnosis of Acute Respiratory Distress Syndrome. The mechanism of injury, together with the absence of any other cause for ARDS, made the diagnosis of fat embolism syndrome likely.

Relevant management
The patient required intubation and ventilation. In view of his persistently poor oxygenation despite high PEEP, paralysis and inverse ratio ventilation he was turned prone, with immediate improvement in his oxygenation. He was ventilated prone for approximately 20 hours each day, and 3 days later he had plating of his femur, with a percutaneous tracheostomy performed simultaneously. Intramedullary nailing was avoided, as it was felt that this may precipitate further fat embolism. His course was further complicated by the development of rhabdomyolysis, with myoglobinuria and a CK rise to 17000IU. Despite this, serum creatinine remained normal. Over the next few days his condition improved. On day 6 he was commenced on methylprednisolone to diminish the fibrotic inflammatory response resulting from his ARDS.

Further information
Fat embolism syndrome Fat embolism syndrome is said to occur when symptoms result due to the inflammatory response to the presence of fat in the circulation. There are many causes, of which the most common are pelvis or long bone lower limb fractures, as in our patient. The classical picture is that of a patient with a pelvic or lower limb long

bone fracture developing a petechial rash, with progressive hypoxaemia occurring 12 to 36 hours after the insult. However, a spectrum of presentations exist, from catastrophic cardiorespiratory collapse to minor impairment in oxygenation. Neurological manifestations are frequently seen and range from confusion to coma. Thrombocytopaenia and anaemia are also common. The embolism is thought to occur when fat is forced at high pressure into the circulation during trauma. For example, marrow pressure can increase to 600mmHg during intramedullary reaming. Although the fat is physiologically inert, it has been suggested that there is in vivo hydrolysis of these neutral fats to free fatty acids. These are known to cause severe vasculitis in animal models leading to haemorrhagic oedema and destruction of the pulmonary architecture within 6 hours. This may explain the delay between the insult and respiratory symptoms developing. Treatment is supportive. The most important factors seem to be early resuscitation and monitoring for hypoxaemia. Of note, patients with a PaO2 < 9.2 kPa on admission are twice as likely to develop hypoxaemia. Between 10 and 44% of patients with fat embolism syndrome require a period of mechanical ventilation, but the pulmonary dysfunction usually resolves within 7 days. Corticosteroid use has been studied extensively, but only as a prophylactic measure in high risk patients. Studies in the 1970s suggested large reductions in the incidence of FES when steroids were used, but the numbers were small and the use of steroids has not gained widespread popularity.

How would you change your future management
We administered steroids to our patient as it was felt that it would be of benefit in reducing the incidence of long term fibrotic consequences of ARDS. However, as the lung dysfunction resulting from FES seems to be more short lived than from ARDS resulting from other insults, the use of steroids may not have been of benefit.

1. Meduri GU, Chinn AJ, Leeper KV et al. Corticosteroid rescue treatment of progressive fibroproliferation in late ARDS. Patterns of response and predictors of outcome. Chest 1994;105:1516-1527 2. Gurd AR, Wilson RI. The fat embolism syndrome British Journal of Bone and Joint Surgery 1974;56B:417-20 3. Lindique BG, Shoeman HS, Dominique GF, Boeyens MC, Vlok AL. Fat embolism and the fat embolism syndrome. A double blind therapeutic syndrome. British Journal of Bone and Joint Surgery 1987;69:128-31 4. King EG, Wagner WW Jr, Ashbaugh DG, Latham LP, Halsey DR. Alterations in pulmonary microanatomy after fat embolism. Chest 1971;59:524-30 5. Hofmann S, Huemer G, Salzer M. Pathophysiology and management of the fat embolism syndrome. Anaesthesia 1998;53(Suppl 2):35-7

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