Fat embolism syndrome is caused by fat globules entering the bloodstream after trauma like long bone fractures. It can cause respiratory failure, neurological symptoms, and a rash. Diagnosis is based on clinical criteria like hypoxemia, thrombocytopenia, and petechial rash appearing 1-4 days after injury. Treatment focuses on respiratory support, fluid resuscitation, steroids to reduce lung inflammation, and early fracture fixation to prevent worsening.

1. FAT EMBOLISM SYNDROMEFAT EMBOLISM SYNDROME

2. FAT EMBOLISM
 Indicates the presence of fat globules in lung
parenchyma & peripheral circulation after # of a long
bone or major trauma.
 Usually occurs within 72 hrs of skeletal trauma.
 Often asso with multiple #res, major bone #res, pelvic
#res, multi system injuries like chest& abdomen, head
injuries etc.
 Causes a devastating clinical deterioration within hrs.

3.  The overall prevalence of fat embolism
syndrome is 1% to 3.5% of patients with a
fracture of tibia or femur.
 Patients with bilateral femoral fractures are at
particular risk & have a higher risk of ARDS &
death.

4. CAUSES
 Traumatic & non traumatic factors.
1. Traumatic causes are;
 Fractures – long bones, pelvis
 Burns
 Surgery – IM nailing, arthroplasty
 Sub cutaneous adipose tissue injuries.

5. 2. Non traumatic causes;
• Diseases – DM, collagen diseases, severe
infections, c/c pancreatitis, c/c alcoholism,
osteo myelitis, sickle cell anemia.
 Procedures – cardio pulmonary bypass,
blood transfusion, renal transplantation,
liposuction.

6. PATHO PHYSIOLOGY
 Mechanical theory&
 Bio chemical theory
-Toxic theory
-Obstructive theory
• Mechanical theory;
Suggests that fat globules are forcibly
intravasated from marrow thru disrupted
vessels & then they are transported to the
pulmonary vascular bed & are trapped as
emboli in the lung capillaries.

7.  Some reaches systemic circulation causing
embolization in areas such as
brain,kidney,retina or skin.
2. Bio chemical theory;
 Toxic theory – Lung lipase hydrolyzes neutral
fat to chemically toxic free fatty acids. This
causes severe inflammatory changes by
producing endothelial damage, inactivation of
lung surfactant & increase in capillary
permeability leading to ARDS.

8.  Obstructive theory –
A chemical event at the site of # releases
mediators that affect the solubility of lipids,
causing coalescence & subsequent
embolization. Normal chylomicrons may
coalesce & form fat globules which are
capable of occluding the lung capillaries.

9. Gurd’s criteria for
diagnosis
 Major criteria:
- Axillary & sub conjunctival petechiae.
- Pa O2 < 60 mm Hg
- CNS depression
 Minor criteria:
- pulse>110/mt
- pyrexia>38.5
-retinal embolism
-fat in urine

10. - reduced platelet count
- increased ESR
- Fat globules in sputum
…..At least 1 from major criteria & 4 from minor
criteria.
The classic syndrome involves pulmonary, cerebral
& cutaneous manifestations.
- Pulmonary: tachypnoea,dyspnoea,cyanosis,tachy
cardia,& rhonchi

11.  Cerebral: headache,irritability,delirium,
stupor,convulsions & coma.
 Cutaneous and retinal: retinal
exudates, edematous patches,cotton
wool spots & petechial haemorrhages.
Three presentations:
1.Sub clinical fat embolism syndrome:
Lab abnormalities present..but non
specific clinical symptoms.
Tachy cardia>100beats/mt,
tachypnoea >25breaths/mt,
temp>37.8.
Moderate hypoxemia(Pa O2< 80mm
Hg)& moderate decrease in platelets
is a common finding.

12. 2.Non fulminant sub acute fat embolism
syndrome
 Characterised by respiratory failure, fever,
tachycardia, petechiae & cerebral signs etc.
 Petechial rashes are pathognomonic of fat embolism
syndrome.This rashes appears between 12 to 96 hrs
following injury.
 Retinal lesions are described as cotton wool spots &
flame like haemorrhages on fundoscopy.
 PaO2 <60 mm Hg,anemia,thrombocytopenia & lung
opacities on CXR.

13. 3.Fulminant fat embolism syndrome
 Severe variant.
 Patients may present with sudden hypotension,
cerebral signs, severe hypoxemia, frank
pulmonary edema or acidosis.
Petechiae arise from occlusion & distention of
dermal capillaries by fat globules & increased
CP.
•They are present across the chest,axilla,root of
neck &conjunctiva and they fades rapidly.

14. Laboratory investigations
 Shows hypoxemia(<60mm
Hg),thrombocytopenia(<1.5 lakhs), anemia &
hypo calcemia.
 The most useful diagnostic test is arterial blood
gas analysis.
 PT & ESR increases.
 Demonstration of fat globules in urine, sputum or
blood.
 Raised serum lipase level&
 Raised blood lipid levels.

15. X ray chest:
Pathognomonic snow storm appearance.
ECG:
S waves prominent.
DIAGNOSTIC TRIAD:
1. Thromboctopenia
2. PaO2 < 60 mm Hg
3. Rashes

16. Management
 Non specific: 3 vital steps.
1. Keep airway patent & #
immobilized.
2. Restore blood volume, fluid &
electrolyte balance.
3. Avoid careless handling of the
injured.
 Specific: 3 vital steps.
1. Respiratory support: Can
range from O2 administration
to full respiratory support with
mechanical ventillation.

17. 2.Drug therapy
Treatment of shock: Aggressive fluid resuscitation
under appropriate monitoring.
 Albumin is preferred because it not only restores
blood volume but also binds free fatty acids.
Steroids:
 Helps gas exchange by decreasing inflammation
in the lungs.Methyl prednisolone appears to
modify the pulmonary response to injury by
relative preservaton of arterial oxgenation.

18. Heparin:
 Increases serum lipase activity &
decreases no of circulating fat globules.
Low molecular wt dextran:
 Useful in prophylaxis.
 Acts by increasing plasma
volume,decreases blood viscosity &
reduces platelet adherence.
Hypertonic glucose:
 Decreases free fatty acid production.
 Improves arterial oxygenation.

19.  Intra venous alcohol:
 Reduces serum lipase activity.
 Thus limits free fatty acid production.
3. Definitive fracture treatment:
Early fixation of fractures is advocated to
prevent worsening of the situation.