3. BY
DR. MOUSA EL-SHAMLY

4. •Fat embolism syndrome is a
well-known cause of pulmonary
and neurologic dysfunction
secondary to a variety of
injuries.
•Its presentation vary from a sub
clinical state to fulminant
respiratory failure.

5. •The amount of manipulation of
injured tissue and degree of
hypovolemia or hypoperfusion
are thought to be factors that
predispose the patient to fat
embolism syndrome.
•Overall mortality range from 5 to
15 %.

7. Pathophysiology
•FES most commonly associated
with long bone and pelvic
fractures, and most common in
closed rather than open fracture.
•Patients with a single long bone
fracture have 1-3 % chance of
developing the syndrome .

11. Pathophysiology (Cont’d.)
•The incidence increase to 33 %
with bilateral femoral fractures.
•Other less common causes include
liposuction thrombolytic therapy
and orthopedic reconstructive
surgery.
•

12. Pathophysiology Cont’d.
•Theories about the origin of fat
deposition in the pulmonary
vasculature include venous fat
embolization originating from
traumatized bone marrow or
excessive mobilization of free fatty
acid from peripheral tissue secondary
to stress hormones.

13. Pathophysiology Cont’d.
•Those acids coalesce in the blood
and form fat aggregates.
•Regardless of the site of origin of fat
emboli the pulmonary capillaries act
as filters and the emboli are carried
to the lung where they lodge in
pulmonary capillaries and increase
resistance to blood flow.

14. Pathophysiology Cont’d.
•The lung parenchymal produce
lipase to remove emboli.
•Hydrolysis of the triglycerides to
glycerol and fatty acid occur
and chemical pneumonitis
results.

15. Pathophysiology Cont’d.
•This inflammatory response is
mediated by complement
activation platelet aggregation
and leukocyt enzymatic action.

16. Pathophysiology Cont’d.
•Morphologically there is increase
in the permeability of the
capillaries and alveolar cell
With leakage of fluid and protein
into the alveolar wall and into
alveolar space.

17. Pathophysiology Cont’d.
•Lung surfactant activity is decreased,
functional residual capacity is
reduced and there is diffusion barrier.
•This cascade of events is seen
clinically as decreased pulmonary
compliance, increase a work of
breathing and hypoxia.

18. Pathophysiology Cont’d.
•Other studies demonstrate presents of
echogenic material passing into right
heart during orthopedic and spinal
surgery, with continued emoblization
,pulmonary artery and right pressure
rise and material can pass through
patent foramen ovale into systemic
circulation resulating in paradoxical
embolism.

19. Pathophysiology Cont’d.
•Serum from acutely ill
patients has the capacity to
agglutinate chylomicrons,
low density lipoprotein and
liposomes of nutritional fat
emulsions.

20. Pathophysiology Cont’d.
•C reactive protein which
appear to be elevated in these
patient appear to be responsible
for the lipid agglutination and
may also participate in the
mechanism for non traumatic
fat embolism .

22. Clinical Manifestation
•FES typically manifest 24 to
72 hours after the initial
insult rarely occur as early
as 12 hours or as later 2
weeks after the inciting
events.

23. Clinical Manifestation (Cont’d.)
1. Pulmonary abnormalities
- Tachypnea
- Dyspnea
- Hypoxemia

24. Clinical Manifestation (Cont’d.)
1. Pulmonary abnormalities
- Diffuse bilateral inspiratory
crepitation
- Approximately one half of the
patients with FES develop
severe hypoxemia and require
mechanical ventilation

25. Clinical Manifestation (Cont’d.)
2. Neurological abnormalities
• Neurological abnormalities
occur in majority of patient
with FES and often occur
after development of
respiratory distress.

26. Clinical Manifestation (Cont’d.)
2. Neurological abnormalities
• Affected patients usually
develop a confusional state
followed by an altered level of
consciousness.
• Seizures and focal deficits also
have been described.

27. Clinical Manifestation (Cont’d.)
2. Neurological abnormalities
• In severe injured patients it
may difficult to separate
changes caused by fat
embolism from these caused
by head injury.

28. Clinical Manifestation (Cont’d.)
2. Neurological abnormalities
In general changes caused
by fat embolism are diffuse
without localization and may
change quickly.

29. Clinical Manifestation (Cont’d.)
2. Neurological
abnormalities
• The etiology of these
mental changes may
related to hypoxia or direct
fat embolism to the brain.

30. Clinical Manifestation (Cont’d.)
2. Neurological abnormalities
• The duration and severity of
the neurological
disturbances are directly
related to the degree of
hypoxemia.

31. Clinical Manifestation (Cont’d.)
2. Neurological abnormalities
• There is no relation between
the severity of neurological
signs and the prognosis for
recovery.
• The neurological finding are
reversible in most cases.

32. Clinical Manifestation (Cont’d.)
3. Petechial haemorrhage
• The classic clinical finding in patients
with fat emnbolism is petechial
haemorrhage which may appear as
early as 12 hours after injury or late
as 3 to 4 days.
• The petechiae occur in 40 % of
patient with FES.

33. Clinical Manifestation (Cont’d.)
3. Petechial haemorrhage
• They can be seen most easily in
the head, neck, anterior thorax,
axilla and subconjunctiva,
over the sclera and may
accompanied by haemorrhages
in the eye ground.

34. Clinical Manifestation (Cont’d.)
3. Petechial haemorrhage
• The petechiae come in crops
and feed over 48 hours.
• The presence of 6 to 12 classic
petechiae firmly establishes the
clinical diagnosis of fat
embolism.

35. Clinical Manifestation (Cont’d.)
3. Petechial haemorrhage
• The petechial rash result from
occlusion of dermal capillaries by fat
globules loading to extravasation of
erythrocyte or may due to increase
capillary fragility.
• The rash usually resolve in 5 to 7 days.

37. Diagnosis
• FES clinical diagnosis
usually characterized by
presence of respiratory
insufficiency, neurological
impairment and petechial
rash.

38. Diagnosis (Cont’d.)
• Chest X-Ray normal in majority
of patients
• Minority have diffuse or patchy
air space consolidation, these
changes are due to oedema or
alveolar haemorrhage and are
most prominent in the periphery
and bases.

41. Diagnosis (Cont’d.)
• Ventilation/perfusion scans
may demonstrate mottled
pattern of subsegmental
perfusion defects with normal
ventilatory pattern.

42. Diagnosis (Cont’d.)
• Focal areas of ground glass
opacification with interlobar
septal thickening are
generally seen on chest CT.

46. Diagnosis (Cont’d.)
• MRI of the brain may reveal
high intensity T2 signal which
correlate with the degree of
clinical neurological
impairment.

47. Diagnosis (Cont’d.)
• There is growing literature on
the use of bronchoscopy with
BAL to detect fat globules in
the alveolar macrophage as
mean to diagnose fat
embolism.

48. Gurd’s criteria
 Most commonly used
 1 major, plus 4 minor

51. Treatment and Prevention
1. Early immoblization of the
fractures reduce the incidence
of FES. The risk further
reduce by operative correction
rather than conservative
management (i.e. traction
alone).

54. Treatment and Prevention
2. Supportive care is the
mainstay of therapy for FES.
3. Mortality is estimated to be
between 5 and 15 %.

55. Treatment and Prevention
• Use of corticosteroid
prophylaxis. There is number
of study report decrease
incidence of FES by use of
prophylactic steroid.

56. Treatment and Prevention
• Methyl Prednisolone 7.5
mg/kg every 6 hours for 12
doses. No complication
related to steroid treatment
was observed.

60. Treatment and Prevention
• One rational, conservative approach
would be to give prophylactic steroid
therapy only to those patient at high risk
for FES as those with long bone or
pelvic fractures especially closed
fractures. Give methyl Prednisolone 1.5
mg/kg every 8 hours for six doses.

62. Treatment and Prevention
• Because hypoxemia is the
fundamental physiological
defect, its prevention by early
administration of oxygen is
reasonable.

63. Treatment and Prevention
• If it becomes impossible to
maintain Pa02 above 60
mmHg with 40 % oxygen
inhalation, intubation and use
of mechanical ventilation
must be considered.

64. Treatment and Prevention
• The use of positive end
expiratory pressure is helpful to
maintaining adequate
oxygenation with lower
concentration of oxygen.
• There is no benefit to raising
Pa02 above 100 mmHg.