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Therapeutic Aspects of Fat Embolism Syndrome

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Therapeutic Aspects of Fat Embolism Syndrome Injury, Int. J. Care Injured (2006) 37S, S68—S73 www.elsevier.com/locate/injury BasicTherapeutic concepts aspects relevant of fat to embolismthe design syndrome and Naderdevelopment M Habashi1, Pennyof the L Andrews Point 2Contact, Thomas M FixatorScalea3 (PC-Fix) 1StephanMulti-Trauma M. CriticalPerren Care, and R Adams Cowley Shock Trauma Center, JoyUniversity S. Buchanan of Maryland, Baltimore, USA 2 Neuro-Trauma Critical Care, R Adams Cowley Shock Trauma Center, AO/ASIFUniversity Research of Maryland, Institute, Baltimore, Clavadelerstrasse, USA 7270 Davos, Switzerland A3 O/ASIFDepartment Research of Surgery, Institute, R AdamsClavadelerstrasse, Cowley Shock 7270 Trauma Davos, Center, Switzerland University of Maryland, Baltimore, USA KEYWORDS: Summary1 Signsbla bla and bla symptomsbla One aardvark of clinical marries fat the embolism pawnbroker, syndrome even though(FES) usu-five OneFat embolism silly fountain; bourgeoisally begin catswithin tickled 24 48 umpteen hours after Macintoshes, trauma. The but classictwo obese triad elephants involves pulmonarydrunkenly Progressivesyndrome; FES; dwarves; towedchanges, umpteen cerebral almost dysfunction, irascible and sheep. petechial Two bureauxrash. Clinical easily diagnosis telephoned is key Paul, because even Umpteenintramedullary mats; nailing; thoughlaboratory the and wart radiographic hogs gossips, diagnosis but one is elephantnot specific tastes and partlycan be putridinconsistent. wart hogs, The Fiverespiratory silly trailers; failure; becauseduration umpteenof FES is difficult purple botulisms to predict kisses because Mark, it is although often subclinical the subways or may bought be over- one ARDS; cerebral edema; extremelyshadowed byangst-ridden other illnesses lampstand, or injuries. even though five obese televisions perused cerebral fat embolism subways,Medical care then is fiveprophylactic progressive or supportive,mats auctioned including off the early bureau, fixation although and general two trail- ICU syndrome; fat emboli. ersmanagement grew up, butto ensureirascible adequate Jabberwockies oxygenation untangles and ventilation,five speedy hemodynamicfountains, yet sta-one catbility, ran prophylaxis away, then of the deep trailer venous very thrombosis, cleverly kisses stress-related two irascible gastrointestinal bureaux. bleed- ing, and nutrition. Studies support early fracture fixation as a method to reduce recurrent fat embolism and FES. The main therapeutic interventions once FES has been clinically diagnosed are directed towards support of pulmonary and neurologi- cal manifestations and management of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Introduction tological, and dermatological systems involvement is the most common. Fat embolism syndrome (FES) has been reported to In addition to fat embolization from the initial occur in several clinical conditions including bone trauma, long bone fixation may result in additional marrow transplant, pancreatitis, fatty liver and embolizations and FES. During intramedullary nail- liposuction [1, 2]. However, FES is most commonly ing, the intramedullary canal pressure can reach associated with long bone fractures. Although fat 1000 mm Hg [9]. This elevated pressure during embolism may occur in up to 90% of trauma patients reaming appears to be temporally associated with [3], FES occurs in only 2 5 % of patients with long embolization to the pulmonary circulation when bone fractures [4]. FES is characterized by both pul- studied with echochocardiography [10]. Once fat monary and systemic fat embolism [2, 5, 6, 7] and is liberated into the circulation and embolizes, the includes a spectrum of subclinical, mild to fulminate pulmonary microvasculature becomes occluded. presentations [7, 8]. Depending on the size of fat globules, smaller Clinical FES typically involves multiple organ sys- globules may traverse the pulmonary microvascu- tems; however, the pulmonary, neurological, hema- lature and reach the systemic circulation, leading to the common neurological manifestation of FES. Although the pulmonary, cerebral, retinal, and skin 1 Abstracts in German, French, Italian, Spanish, Japanese, microcirculations are typical clinical manifestations and Russian are printed at the end of this supplement. of FES, fat embolization can affect any microcir- 0020–1383/$ — see front matter # 2006 Published by Elsevier Ltd. doi:10.1016/j.injury.2006.08.042 Prevention of fat embolism syndrome S69 culatory bed. Case reports include acute coronary 33]. However, when given prophylactically, corticos- syndrome presumed to result from fat globules in teroids (methylprednisolone) may have beneficial the coronary microcirculation [11]. effects [34 38]. The mainstay of treatment for FES is supportive [32], therefore, prevention, early diagnosis, and adequate symptom management are Discussion paramount. Although long bone fracture fixation is the main Acute lung injury (ALI) and acute respiratory distress cause of fat embolism and FES, early fracture fixa- syndrome (ARDS) may result from fat emboli occlud- tion may be critical in reducing recurrent liberation ing pulmonary capillaries [2, 12 16] and biochemi- of fat into the circulation as a result of fracture cal alterations that produce lung injury that directly movement [39]. damages the pulmonary capillary endothelium Early fixation of long bone fractures within 24 [2, 12, 13, 17, 18]. hours has documented a reduction in the inci- Although many patients with long bone fractures dence of FES in patients who are stable enough to develop fat embolism, far fewer develop FES, sug- undergo surgery [40]. In addition, as patients with gesting that additional factors may be necessary polytrauma are at risk of other forms of respira- in the development of lung injury. Biochemical fat tory failure (atelectasis, pneumonia) and multiple embolization is associated with the release of free system organ failure (MSOF), early fixation and pa- fatty acids (FFAs) [19]. FFAs in the lung are locally tient mobilization may reduce complications [41]. hydrolyzed in pulmonary circulation by lipoprotein Experimentally, increasing intramedullary pressure lipase, which releases toxic substances that injure [42] has been shown to increase fat embolization. the capillary endothelium. The release of FFAs in- Methods to reduce intramedullary pressure and creases vascular permeability, producing alveolar embolization during reaming have been developed, hemorrhage, edema, and inactivate the surfactant which include venting or applying a vacuum during molecules [20 26]. Ultimately, these pulmonary reaming to limit the elevation of intramedullary alterations lead to respiratory failure, resulting in pressure and thus reduce the incidence of fat em- ALI and ARDS. bolization [43, 44]. As fat accumulates in the pulmonary microcircula- Respiratory failure from FES is characterized as tion and lipoprotein lipase liberates FFAs, dissemi- permeability edema with decreased compliance nated intravascular coagulation (DIC) and platelet similar to oleic acid lung injury [15]. Gas ex- aggregation further compound capillary disruption change abnormalities include shunt and increased and systemic inflammation. dead space from atelectasis and alveolar flooding Fat emboli that pass through the pulmonary comparable to ALI and ARDS from other causes vasculature result in systemic embolization, most [45 47]. commonly in the brain and kidneys [27]. Cerebral The general goals of ALI and ARDS management FES is a rare, yet potentially lethal, complication focus on maintaining acceptable gas exchange while of long bone fractures. Neurological symptoms vary limiting ventilator-associated lung injury (VALI). from confusion with diminished Glasgow Coma Scale Supportive pulmonary therapies may include (GCS) to encephalopathy with coma and seizures. A enhancement of spontaneous breathing and cough, clinical diagnosis may be difficult as cerebral FES early patient mobilization, utilization of positive may be masked by other clinical scenarios [28]. end-expiratory pressure (PEEP), and a reduction Diffuse encephalopathy, petichial hemorrhages, lo- in the use of sedation and neuromuscular blocking calized cerebral edema, and white matter changes agents (NMBAs). By utilizing ventilator modes that have also been seen in patients diagnosed with FES. allow spontaneous breathing and cough, patients Magnetic resonance imaging (MRI) may be necessary are not mandated to conform to a clinician-set I:E to show the characteristic cerebral lesions of the ratio; rather, the patient may spontaneously breathe acute state of FES as opposed to a CT scan, which freely and interact with the ventilator. Traditionally, appears normal [29, 30, 31]. spontaneous breathing in patients with ALI or ARDS is discouraged, forcing the patient to adapt to prede- termined ventilator settings. Controlled ventilation Treatment frequently requires heavy sedation or NMBAs to syn- chronize the patient with the ventilator, particularly A specific treatment for FES does not currently in the management of patients diagnosed with FES exist [32]. Treatments with heparin, dextran, and and associated neurological manifestations. corticosteroids have not been shown to reduce the Forms of ventilation that require excessive se- morbidity or mortality as treatments for FES [1, dation and NMBAs preclude detailed assessment S70 N M Habashi et al and the ability to perform serial neurological examination. Furthermore, the utilization of a se- examinations. In addition,
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