Lutheran Medical Center

Department of Surgery

Morbidity & Mortality Conference

Case & Topic Presentation

Baiju C. Gohil, M.D.

April 9, 2004
FAT EMBOLISM
SYNDROME
 INTRODUCTION
• Fat emboli were first noted by F.A. Zenker in 1861 in a
railroad worker with a thoraco-lumbar crush injury
• Fat Embolism Syndrome (FES) was first described by
Von Bergman in 1873 in a diagnosis confirmed by post
mortem examination
• In the US, frequency of FES is unknown; clinical
diagnosis; dx missed because of subclinical illness or
confounding injury or illness
• Fat embolism develops in nearly all pts with fractured
bones or during ortho procedures and is asymptomatic
• In minority of pts s&s develop as a result of organ
dysfunction, notably lungs, brain, and skin; FES
• Mortality rate 10-20%

Chest Volume 123 • Number 4 • April 2003

 PATHOPHYSIOLOGY
• Two theories exist about FES:
– Mechanical theory states that large fat
droplets are released into venous system,
deposit into pulmonary capillary beds, and
through 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 sepsis
induce systemic release of free fatty acids
and chylomicrons; acute phase reactants
cause chylomicrons to coalesce and create
ischemia

Chest Volume 123 • Number 4 • April 2003

 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 and
resolve quickly
– Subconjunctival and oral hemorrhages/petechiae
• Neurologic
– CNS dysfunction initially manifests as agitated delirium; may
progress to stupor, seizures, or coma; frequently unresponsive
to correction of hypoxia
– Retinal hemorrhages with intra-arterial fat globules are visible
upon fundoscopic examination
Arch Surg 1997; 132:435–439
 CAUSES OF FES
• Blunt trauma; multiple long bone and
pelvic fxs (assoc w/ 90% of FES cases)
• Acute pancreatitis
• DM
• Burns
• Joint reconstruction
• Liposuction
• Cardiopulmonary bypass
• Parenteral lipid infusion
• Sickle cell crisis
 WORKUP
• Laboratory
– ABG
– Thrombocytopenia, anemia, and
hypofibrinogenemia are indicative of FES, but
nonspecific
– Urine, blood, sputum examination with Sudan or oil
red O staining detect fat globules
• Imaging
– CXR-diffuse b/l pulmonary infiltrates
– Head CT-nl or diffuse white matter petechial
hemorrhages
– 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
 FES: CRITERIA FOR DIAGNOSIS
• Dx of FES requires at least one sign from major criteria and at least four signs
from 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, <60 mmHg)
– central nervous system (CNS) depression disproportionate to hypoxemia, and pulmonary
edema
• Gurd's Minor Criteria:
– tachycardia (more than 110 beats per minute)
– pyrexia (temperature higher than 38.5 degrees)
– emboli present in retina on funduscopic examination
– fat present in urine
– sudden unexplainable drop in hematocrit or platelet values
– increasing sed rate
– fat globules present in sputum
• Misc:
– occurs w/in 72 hours of skeletal trauma
– shortness of breath
– altered mental status
– occasional long tract signs and posturing
– urinary incontinence

J Arthroplasty. 2000 Sep;15(6):809-13.

 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 to
minimize bone marrow embolization into
venous system
Arch Surg 1997; 132:435–439
 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
 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 provides
protection against fat embolism and pulmonary dysfunction after
skeletal trauma, the safety of this therapy requires further
evaluation
 CONTROVERSIES
• Corticosteroids as prophylaxis for FES:
Several studies have demonstrated
varying results using corticosteroids in
patients identified as high-risk for
developing FES; while the data appear
compelling, the optimal timing, duration,
and dose of steroids are undetermined