FAT EMBOLISM SYNDROME

1. By
Dr. Jitendra Wadhwani
PG ORTHOPAEDICS
PGIMS, ROHTAK

2.  Zenker, a pathologist,1st identified fat embolism
syndrome at autopsy 1862.
 First diagnosed in 1873 by Dr Von Bergmann
 1879 Fenger and Salisbury published description of
FES

3. Fat Emboli: Fat particles or droplets
that travel through the circulation
Fat Embolism: A process by which fat
emboli passes into the bloodstream
and lodges within a blood vessel.
Fat Embolism Syndrome (FES):
serious manifestation of fat
embolism occasionally causes multi
system dysfunction, the lungs are
always involved and next is brain

4. FAT EMBOLISM SYNDROME:
 Clinical diagnosis, No specific laboratory test is
diagnostic
 Mostly associated with long bone and pelvic #, and
more frequent in closed # then open #
 Single long bone fracture 1-5% chance of
developing FES, and increases with number of #
 Onset is 24-72 hours from initial insult
 Mortality: 5-15%

7. CAUSES CONTD..
 Blunt Trauma (90%)

8. CAUSES CONTD..
 Non Trauma: agglutination of chylomicrons and VLDL
by high levels of plasma CRP.
– disease-related
• Diabetes, acute pancreatitis, burns, SLE, sickle cell crisis
– drug-related
• parenteral lipid infusion
– procedure-related
• Orthopedic surgery, liposuction

9. Exact mechanism unknown, but two main hypothesis
• Mechanical vs. Biochemical
• MECHANICAL – Fat globules from disrupted bone
marrow or adipose tissue are forced into torn venules
in areas of trauma.
• BIOCHEMICAL – Hormonal changes caused by trauma
and/or sepsis induce systemic release of free fatty
acids (FFA) as chylomicrons which cause the systemic
FES.

10. MECHANICAL HYPOTHESIS-
 – Fractures of marrow-containing bone (Femur,
Pelvis) have the highest incidence of FES and
cause the largest volume of fat emboli, because the
disrupted venules in the marrow remain tethered open
by their osseous attachments.
 – The marrow contents enter the venous circulation
with little difficulty.

11. CONT..
This theory is supported by research on Orthopaedic
long bone (IM reaming) and spinal surgeries which
cause fat globules to enter the blood circulation
when vigorous reaming/fixation is done.
 Increased Pressure + Volume Extravasation
 Measuring fat globules pre and post reaming
shows significant difference in concentration

12. CONT..
 Fat droplets are deposited in the pulmonary capillary
beds and travel through arteriovenous shunts to the
brain. Systems affected include LUNG, BRAIN and
CIRCULATION.
 Microvascular lodging of droplets produces local
ischemia and inflammation, with concomitant release
of inflammatory mediators, platelet aggregation, and
vasoactive amines

13. BIOCHEMICAL :
 FES is dependent upon degradation of the embolized fat
into free fatty acids.
 Neutral fat does not cause an acute lung injury, it is
hydrolyzed over the course of hours to several products,
including FFA, which cause ARDS in animal models.
 CRP (acute phase reactant), which is elevated in trauma
patients, appears to be responsible in lipid agglutination
(FES) for both traumatic and non- traumatic FES.

14. CONT..
 The process of Neutral fat cells -> FFA ->
Agglutination with CRP may explain the time
sequence of clinical findings in FES.
 Onset of symptoms may coincide with
Agglutination.
 This theory is animal model based and
circumstantial at best.

15.  Diagnosis is made CLINICALLY NOT
CHEMICALLY. It does not matter how much
fat globules are in your circulation, it just matters if
you have their side effects.
 FES typically manifests 24 to 72 hours after the
initial insult. Rarely <12 hrs or >72 hrs.

16. TRIAD OF FES
 Hypoxemia
 Neurological abnormalities
 Petechial rash

17. EARLY SIGNS
 Dyspnea
 Tachypnea
 hypoxemia

18. PULMONARY:
 Hypoxia, rales, pleural friction rub
 Breath sounds: Loud harsh, Crepts & wheeze
 ARDS may develop(fat emboli obstructs lung vessel
(20microns) platelets and fibrin adhere.)
 ½ of pts with FES require mechanical ventilation (Bulger,
Archives of Surgery 1997; 132: 435-9)
 CXR usually normal early on, later may show
‘snowstorm’ pattern- diffuse bilateral infiltrates
 CT chest: ground glass opacification with interlobular
septal thickening

20. NEUROLOGICAL FINDINGS:
 Usually occur after respiratory symptoms.
 Incidence 80% patients with FES
 Minor global dysfunction most common, but ranges from
mild delirium to coma.
 Seizures/focal deficits not common but can occur
 Transient and reversible in most cases
 CT Head: general edema, usually nonspecific
 MRI brain: Low density on T1, and high intensity T2
signal, correlates to degree of impairment

21. RASH:
 Petechial
 Usually on conjuntiva , neck, axillae
 Results from occlusion of dermal capillaries by fat
globules and then extravasations of RBC
 Fleeting & last short.Resolves in 5-7 days
 PATHOGNOMONIC, but only present in 20-50% of
patients

24. OTHER FINDINGS
 Retinopathy (exudates, cotton wool spots, hemorrhage)
 Lipiduria
 Fever (to 39-40ºC)
 DIC
 Myocardial depression (prominent S, T depression, RBBB,
arrythmia)
 Thrombocytopenia/Anemia
 Hypocalcemia

25. DIAGNOSIS
 FES is CLINICAL diagnosis, not biochemical.
 A high degree of suspicion is needed to make diagnosis
.
-Common misconception that the presence of fat
globules, either in sputum, urine, or a wedged PA
catheter, is necessary to confirm the diagnosis of FES
In 50% of fracture patients, fat globules was
demonstrated in the serum, without symptoms of FES.
HOWEVER
 Growing literature on the use of bronchoscopy with
bronchoalveolar lavage to detect fat droplets in alveolar
macrophages as a means to diagnose fat embolism.
Sensitivity and specificity are unknown, being studied in
Trauma patients

26.  FES = 1 major + 4 minor + fat microglobulinemia
 Still widely used today

27.  FES = femur fracture ± tibia fracture + 1 feature
 Based on respiratory parameters

28. 3 TYPES- In 1962
 SUBCLINICAL FES
 NON FULMINANT FES
 FULMINANT FES

29. SUBCLINICAL FES:
 Around 3 days post trauma
 Probably occurs in almost all long bone
fractures of the lower extremity and fractures of
the pelvis
 Characterised by decreased PaO2, decreased
Hb% and decreased platelets. No clinical signs
and symptoms of respiratory insufficiency.

30. NONFULMINANT FES:
- Any time ,upto 6 days post trauma
-Clinical signs and symptoms are clearly evident.
 Petechiae, tachycardia, respiratory failure, and signs of CNS
embolism.
 Thrombocytopaenia, anaemia, and coagulation
abnormalities can be found, as can pulmonary alveolar and
interstitial opacities on chest x ray

31.  There is no definitive test for this version of the
syndrome, as most of the changes described can
occur as a result of trauma as well as a result of fat
embolism, the diagnosis remains a clinical one,
and the significance is uncertain

32. FULMINANT FES:
 Occurs very suddenly and rapidly after injury, and
progresses very quickly, often resulting in death within a
few hours of the initial trauma.
 Clinical features are acute respiratory failure, acute
cor pulmonale and embolic neurological changes.
 These occur shortly after injury and often result in the
death of the patient.

33.  Pats. with multiple fractures are particularly
susceptible to this form of the syndrome, which,
although it is relatively rare, is of immense clinical
significance because of its high mortality.

35. TREATMENT IS LARGELY SUPPORTIVE
 Constant Positive Airway pressure(CPAP)
 Mechanical Ventilation
 Antibiotics
 Nutritional support
 Corticosteroids
 Heparins
Have all been used

36. INITIAL TREATMENT
 Adequate airway
 Start IV line – correct fluid deficit
 Basic investigation – including baseline chest X-ray
and ABG assay (v. imp).
 Nasogastric tube – should be inserted in patient
with severe trauma and gastric contents suctioned
to prevent aspiration and ARDS

37. MONITORING
 TPR, BP
 I/O chart – maintain output 50-100cc/hr
 CVP – to correct fluid deficit
 If overload  pulmn. Edema (4-8cm H2O)
 Pulmonary haemodynamics– PCWP for accurate mean
of deficit correction (5-12mm of Hg)
 Arterial blood gas monitoring

38. SPECIFIC DRUG THERAPY:
 Many drugs have tried, most without demonstrable
benefit in established ARDS except Corticosteroids
but with some prophylactic benefit.

39. Drugs which may be tried in Fat embolism associated
ARDS are:
 1.Ethanol : Lipase inhibitor, low incidence when level
>20mg.
 2.Heparin :  PL aggregation useful in DIC assoc
ARDS also.Controversial in trials.10000-15000 iu stat &
10000 iu 4-6hly with PTT at 1.5-2.5 INR.
 3.Hypertonic glucose: block post traumatic
mobilization of FFA – may improve oxygenation.

40.  4.Corticosteroids – stabilize cell member, PMN
adhesion, prevent surfactant reduction, protect
capillary endothelium, compliment activation and
minimize transudation.

41. CORTICOSTEROIDS –
Value in ARDS of Fat embolism, aspiration,
sepsis, shock and cerebral edema.
Helpful in late stage in recovering patients in
reducing fibrotic change.
Improve and preserve arterial oxygenation and
stimulate proliferation and maturation of Type II
pneumocyte.

42. CORTICOSTEROIDS -
Prophylactic dose 10mg/Kg Q8H
Or
80mg/kg bolus
Or
1-2gm IV over 24 hrs. & maintain for 48-96 hrs by
gradual reduction

43. ATLS Protocol :
 1. Early immobilization of fracture and early definitive
reduction (open or closed).
 2. Maintain intravascular volume to maintain
cardiovascular stability (hypovolemic shock
resuscitation), may use colloids (albumin) as it can
expand fluid and bind FFA.
 3. Mechanical ventilation with PEEP

44.  4. IV Ethanol has been used in Russia, Europe and
some American centres to decrease rate of FES.
J Bone Joint Surg Am. 1977 Oct;59(7):878-80
 “A raised level of alcohol in the blood was
associated with a lower incidence of fat embolism” all
other variables controlled.
- Other studies
- Can J Surg. 1970 Jan;13(1):41-9
- Br Med J. 1978 May 13;1(6122):1232-4

45. ROLE OF FRACTURE STABILIZATION
 Highly debated issue
 - Accumulated evidence over past decade support
early fixation within 24 hours of injury.

46.  Early IF – decompress # hematoma as ongoing
source of fat emboli and retained necrotic debris,
eliminate pain and physiologic stress with continued
# motion, optimize pulmn function, contributes to
reduced ventilatory dependence and improve
survival.

47.  But transient increasing pulmn Ar pressure and
worsening pulmn gas exchange observed during
reaming of medullary canal. So undreamed nailing
is suggested for femoral fixation in multiple #
patients.

48. PROGNOSIS
 Mild -undetected
 Mod -low mortality
 Severe -fatal unless if treatement
instituted early. Survivors have pulmonary sequele.