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Fat- Emb Death Conf

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    Lutheran Medical Center

    Department of Surgery

    Morbidity & Mortality Conference

    Case & Topic Presentation

    Baiju C. Gohil, M.D.April 9, 2004

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    FAT EMBOLISM

    SYNDROME

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    INTRODUCTION

    Fat emboli were first noted by F.A. Zenker in 1861 in arailroad worker with a thoraco-lumbar crush injury

    Fat Embolism Syndrome (FES) was first described by

    Von Bergman in 1873 in a diagnosis confirmed by postmortem examination

    In the US, frequency of FES is unknown; clinicaldiagnosis; dx missed because of subclinical illness or

    confounding injury or illness Fat embolism develops in nearly all pts with fracturedbones or during ortho procedures and is asymptomatic

    In minority of pts s&s develop as a result of organdysfunction, notably lungs, brain, and skin; FES

    Mortality rate 10-20%

    Chest Volume 123 Number 4 April 2003

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    PATHOPHYSIOLOGY

    Two theories exist about FES: Mechanical theory states that large fat

    droplets are released into venous system,deposit into pulmonary capillary beds, andthrough a-v shunts to the brain;microvascular lodging of droplets causes

    local ischemia and inflammation Biochemical theory states that hormonal

    changes caused by trauma and/or sepsisinduce systemic release of free fatty acids

    and chylomicrons; acute phase reactantscause chylomicrons to coalesce and createischemia

    Chest Volume 123 Number 4 April 2003

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    CLINICAL SIGNS OF FES

    Cardiopulmonary

    Early persistent tachycardia

    Tachypnea, dyspnea, and hypoxia due to V-Q abnormalities

    12-72 hrs after insult High temperature spikes

    Dermatological

    Reddish-brown nonpalpable petechiae over upper body, esp

    axillae, 24-36 hrs after insult; occur in 20-50% of pts andresolve quickly

    Subconjunctival and oral hemorrhages/petechiae

    Neurologic

    CNS dysfunction initially manifests as agitated delirium; mayprogress to stupor, seizures, or coma; frequently unresponsiveto correction of hypoxia

    Retinal hemorrhages with intra-arterial fat globules are visibleupon fundoscopic examination

    Arch Surg 1997; 132:435439

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    CAUSES OF FES

    Blunt trauma; multiple long bone andpelvic fxs (assoc w/ 90% of FES cases)

    Acute pancreatitis DM

    Burns

    Joint reconstruction Liposuction

    Cardiopulmonary bypass

    Parenteral lipid infusion

    Sickle cell crisis

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    WORKUP

    Laboratory ABG

    Thrombocytopenia, anemia, andhypofibrinogenemia are indicative of FES, butnonspecific

    Urine, blood, sputum examination with Sudan or oilred O staining detect fat globules

    Imaging CXR-diffuse b/l pulmonary infiltrates

    Head CT-nl or diffuse white matter petechialhemorrhages

    Chest CT-parenchymal changes c/w lung contusion,acute lung injury, or ARDS

    V/Q scan-nl or subsegmental perfusion defects

    Procedures BAL-staining of alveolar macrophages for fat

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    FES: CRITERIA FOR DIAGNOSIS

    Dx of FES requires at least one sign from major criteria and at least four signsfrom the minor criteria category

    Gurd's Major Criteria: axillary or subconjuctival petechia; occurs transiently (4-6 hours) in 50-60 % of the cases

    hypoxemia (PaO2,

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    TREATMENT

    Medical care Supportive in nature

    Maintain oxygenation and ventilation Stabilize hemodynamics

    Blood products as needed

    Hydration DVT & stress related GI bleed prophylaxis

    Nutrition

    Surgical care Early stabilization of long bone fractures tominimize bone marrow embolization intovenous system

    Arch Surg 1997; 132:435439

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    CONTROVERSIES

    Surg Gynecol Obstet. 1978 Sep;147(3):358-62

    Corticosteroids in patients with a high risk of fat embolism

    syndrome

    Alho A, Saikku K, Eerola P, Koskinen M, Hamalainen M. Effects of methylprednisolone on clinical FES were studied in

    series of 60 pts. who had at least two fractures of the pelvis, femur

    and tibia and who did not have any other significant injuries

    31 controls; 29 pts. given 10 mg/kg methylprednisolone 3 times,once at admission and, at 8 and 16 hrs post-trauma

    FES defined as combination of hypoxemia, bilateral "snow storm"

    infiltrations of the lungs, petechial rash, mental disturbances,

    pyrexia, anemia and thrombocytopenia

    Varying degrees of FES observed in 2 steroid pts. And in 15

    controls

    Methylprednisolone in an early pharmacologic dosage is effective

    in fulminant instances of fat embolism that occur in spite of

    adequate respiratory care and the proper treatment of fractures

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    CONTROVERSIES

    J Trauma. 1987 Oct;27(10):1173-6.

    'Low-dose' corticosteroid prophylaxis against fat embolism.

    Kallenbach J, Lewis M, Zaltzman M, Feldman C, Orford A, Zwi

    S. 82 skeletal trauma pts. Identified as high risk for FES

    42 control subjects given placebo and 40 steroid-treated subjects (9

    mg/kg methylprednisolone)

    Fat embolism occurred in ten controls (23.8%) and one steroid-treated subject (2.5%)

    Hypoxemia was severe (PaO2 less than 50 mm Hg) in 12 controls

    (28.6%) and two (5%) of the steroid-treated subjects

    Although methylprednisolone in a relatively low dose providesprotection against fat embolism and pulmonary dysfunction after

    skeletal trauma, the safety of this therapy requires further

    evaluation

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    CONTROVERSIES

    Corticosteroids as prophylaxis for FES:Several studies have demonstrated

    varying results using corticosteroids inpatients identified as high-risk fordeveloping FES; while the data appearcompelling, the optimal timing, duration,

    and dose of steroids are undetermined

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