Fat embolism

FAT EMBOLISM SYNDROMEFAT EMBOLISM SYNDROME

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.

 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.

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

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.

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.

 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.

 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.

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

- 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

 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.

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.

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.

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.

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

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.

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.

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.

 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.

Fat embolism

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Fat embolism