By

Dr Nethiya Vengataraman
Fat Embolism Syndrome
Fat embolism can occur due to the
migration of fat particles from the bone
marrow at the time of trauma or during
reaming of the intramedullary canal. This
causes the release of inflammatory
mediators ,with endothelial lung damage
and hypoxemia.



First diagnosed in 1873 by Dr Von Bergmann

Published in 1879 Fenger and Salisbury.
Fat Embolism:
Traumatic fat embolism occurs in up to 90% of
individuals with severe skeletal injuries, but < 10% of
such patients have any clinical symptoms / signs

Fat Embolism Syndrome:
FE with clinical manifestation .
Incidence: 1-3% femur #, 5-10% if bilateral or multiple.

Mortality: 5-15%

Clinical diagnosis :No specific laboratory test is
diagnostic

Mostly associated with long bone/pelvic #s, and more
frequent in closed fractures.

Onset is 24-72 hours from initial insult

A high index of suspicion is needed for diagnosis is to
be made.

An asymptomatic latent period - 12-48 hours.

The fulminant form presents as acute cor pulmonale,
respiratory failure, - death within a few hours of injury.

Mechanical and biochemical Theory
1. Two theories about fat embolism exist. First, the mechanical theory states
that large fat droplets are released into the venous system. These droplets are
deposited in the pulmonary capillary beds and travel through arteriovenous
shunts
to the brain. Micro vascular lodging of droplets produces local ischemia and
inflammation, with concomitant release of inflammatory mediators, platelet
aggregation, and vasoactive amines.

2. Second, the biochemical theory states that hormonal changes caused by
trauma and/or sepsis induce systemic release of free fatty acids as chylomicrons.
Acute-phase reactants, such as C-reactive proteins, cause chylomicrons to coalesce
and create the physiologic reactions described above. The biochemical theory
helps explain nontraumatic forms of fat embolism syndrome.
[1]




The biochemical theory


Circulating FFAs -directly toxic to Pneumocytes / capillary
Endothelium in the lung - interstitial hemorrhage, edema
& chemical pneumonitis.

Coexisting shock, hypovolemia and sepsis - reduce liver
flow exacerbate the toxic effects of FFAs.

H/E stain lung

- blood vessel with
fibrinoid material and

-optical empty space -lipid
dissolved during the
staining process.
TRAUMA
Hypoxemia
Neurological
abnormalities
Petechial
rash


Dyspnea,

Tachypnea

Hypoxemia PaO2 < 60 mm Hg
Clinically Tachpnea, Dyspnea, Hypoxia, rales, pleural
friction rub & ARDS.
High spiking temperatures.
Hypoxemia - ventilation-perfusion mismatch &
intrapulmonary shunting. Acute cor pulmonale -
respiratory distress, hypoxemia, hypotension and
elevated CVP.
of pts require mechanical ventilation
CXR normal early on - later may show snowstorm
pattern- diffuse bilateral infiltrates
CT chest: ground glass opacification with interlobular
septal thickening
CNS signs usually occur after respiratory symptoms -
nonspecific - features of diffuse encephalopathy

Acute confusion, stupor, coma, rigidity, or convulsions
- Transient and reversible in most cases

CT Head: general edema nonspecific

MRI brain: Low density on T1 & High intensity T2
signal - correlates to degree of impairment

Reddish-brown non-palpable Petechial rash - upper
anterior body, chest, neck, upper arm, axilla, shoulder,
oral mucous membranes and conjunctivae in 20 - 50%
patients.

Pathognomonic, however, it appears late and
disappears within hours.

Results from occlusion of dermal capillaries by fat
globules - extravasations of RBC

Retinopathy (exudates, cotton wool spots,
hemorrhage)
Lipiduria(fat globulin in the urine)
Fever
DIC
Myocardial depression (R heart strain)
Thrombocytopenia
Anemia, Decreased Hematocrit
Hypocalcemia
Gurds criteria

Most commonly used

1 major, plus 4 minor
The most effective prophylactic measure - operative
reduction/rigid fixation of long bone fractures as soon
as possible. Higher incidence (5 fold) when fixation
delayed greater than 24 hours.

Supportive care includes maintenance of adequate
oxygenation and ventilation, stable hemodynamics,
blood products as clinically indicated, hydration,
prophylaxis of DVT and stress-related GI bleeding.
Continuous pulse oximetry monitoring - at-risk
patients ( those patients with long bone fractures) -
detecting desaturations early.

Consultations recommended include orthopedists,
neurologists/ neurosurgeons, trauma care specialists,
critical care specialists, pulmonologists,
hematologists, and nutritionists.
Albumin has been recommended - not only restores
blood volume / binds fatty acids - may decrease the
extent of lung injury.

High dose corticosteroids have been effective in
preventing development of FES in several trials, but
controversy on this issue still persists.

Heparin has also been proposed as it activates lipase,
but no evidence exists for its use in FES.


DURATION OF FES
Difficult to predict FES is frequently subclinical or
overshadowed by other illnesses or injuries.

Increased alveolar-to-arterial oxygen gradient and
neurologic deficits, including coma, may last days or
weeks.

SEQUELAE
As in ARDS, pulmonary sequelae usually resolve
almost completely within 1 year.

Residual subclinical diffusion capacity deficits may
exist.

Residual neurologic deficits may range from
nonexistent to subtle personality changes to memory
and cognitive dysfunction to long-term focal deficits.

SUMMARY FES
Clinical diagnosis so high index of suspicion.

Most effective management is prevention with rigid
fixation of fractures within 24 hours

When developed management is supportive.