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FAT EMBOLISM
SYNDROME
SAIF ALI 121
Intro
• Indicate the presence of fat globals in lung parenchyma and
peripheral circulation after fracture of a long bone on major trauma
• Usually occurs within 72 hours of skeleton trauma
• Often associated with multiple fractures. Major bone fractures, pelvic
fracture multi system injury like chest and abdomen, head injury.
• Causes a devastating, clinical deterioration within hours
• Patience with bilateral similar fractures are at particular risk and have
a higher risk of ARDS and death
Causes
• Traumatic
• Fractures-longbone ,pelvis
• Burns
• Surgery- intramedullary nailing,arthroplasty
• Subcutaneousadipose Surgery
• non-traumaticcauses
• Diseases-DM, Collagen diseases,severe infections,
pancreatitis,alcoholism, sicklecell anaemia,
osteomyelitis
• Procedures-cardio pulmonarybypass,blood
transfusion,renal transplantation,liposuction
Pathophysiology
• Mechanical theory
• Biochemical theory
• toxic theory
• Obstructive theory
Mechanical theory
• Suggest that fat globules are
forcibly intravasated from marrow
through disrupted vessels, and
then they are transported to the
pulmonary vascular bed and are
trapped as emboli in the lung
capillaries
• Some reaches systemic circulation,
causing embolisation in areas such
as brain, kidney, retina or skin
Biochemical theory
• Toxic theory –lung lipase hydrolysis neutral
fat to chemically toxic free fatty acids. This
causes severe inflammatory changes by
producing endothelial damage, inactivation
of lung surfactant and increase in capillary
permeability leading to ARDS
• Obstructive theory-a chemical event at site
of fracture releases, mediators that affect
the solubility of lipids, causing coalescence
and subsequent embolisation. Normal
chylomicrons may coalesce and form fat
globules which are capable of occluding the
lung capillaries
Clinical features
• The classical syndrome involves pulmonary
,cerebral and cutaneous manifestations
• Pulmonary-
Tachypnoea,dyspnoea,cyanosis,tachycardia
• Cerebral-headache, irritable, delirium,
stupor, convulsions and coma
• Cutaneous and retinal-retinal exudate
,edematous patches, cotton wool spots
and patechial haemorrhages
Gurd’s
Diagnostic
criteria
Lab investigations
• Shows hypoxia, thrombocytopenia, anaemia and hypocalcaemia
• Arterial blood gas analysis
• PT &ESR
• Fat globes in urine or blood or sputum
• Raised serum lipase level
• Raised blood lipid level
X-ray
Snowstorm appearance
Management
• Non-specific
1. keep airway patent
and immobilise the
fracture
2. Restore blood,
volume fluid and
electrolyte balance
3. Avoid careless
handling of the
injured
Specific
1. respiratory support- O2 administration to full
respiratory support
2. Drugs –
i. steroids-methylprednisolone
ii. Heparin –decrease s.lipase activity and no. Of
circulating fat globules
iii. Low molecular wt dextran-useful in prophylaxis,act
by inc pl vol,dec blood viscosity nd reduce platelet
adherence
iv. Hypertonic glucose-dec FFA production,imp art
oxygenation
v. I/V Alcohol-dec s.lipase activity
3. Definitive fracture treatment
Thank you

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fat Embolism jsjsjakakakksjdhdhdhbdjdjdjdjdjjd

  • 2. Intro • Indicate the presence of fat globals in lung parenchyma and peripheral circulation after fracture of a long bone on major trauma • Usually occurs within 72 hours of skeleton trauma • Often associated with multiple fractures. Major bone fractures, pelvic fracture multi system injury like chest and abdomen, head injury. • Causes a devastating, clinical deterioration within hours • Patience with bilateral similar fractures are at particular risk and have a higher risk of ARDS and death
  • 3. Causes • Traumatic • Fractures-longbone ,pelvis • Burns • Surgery- intramedullary nailing,arthroplasty • Subcutaneousadipose Surgery • non-traumaticcauses • Diseases-DM, Collagen diseases,severe infections, pancreatitis,alcoholism, sicklecell anaemia, osteomyelitis • Procedures-cardio pulmonarybypass,blood transfusion,renal transplantation,liposuction
  • 4. Pathophysiology • Mechanical theory • Biochemical theory • toxic theory • Obstructive theory
  • 5. Mechanical theory • Suggest that fat globules are forcibly intravasated from marrow through disrupted vessels, and then they are transported to the pulmonary vascular bed and are trapped as emboli in the lung capillaries • Some reaches systemic circulation, causing embolisation in areas such as brain, kidney, retina or skin
  • 6. Biochemical theory • Toxic theory –lung lipase hydrolysis neutral fat to chemically toxic free fatty acids. This causes severe inflammatory changes by producing endothelial damage, inactivation of lung surfactant and increase in capillary permeability leading to ARDS • Obstructive theory-a chemical event at site of fracture releases, mediators that affect the solubility of lipids, causing coalescence and subsequent embolisation. Normal chylomicrons may coalesce and form fat globules which are capable of occluding the lung capillaries
  • 7.
  • 8. Clinical features • The classical syndrome involves pulmonary ,cerebral and cutaneous manifestations • Pulmonary- Tachypnoea,dyspnoea,cyanosis,tachycardia • Cerebral-headache, irritable, delirium, stupor, convulsions and coma • Cutaneous and retinal-retinal exudate ,edematous patches, cotton wool spots and patechial haemorrhages
  • 10. Lab investigations • Shows hypoxia, thrombocytopenia, anaemia and hypocalcaemia • Arterial blood gas analysis • PT &ESR • Fat globes in urine or blood or sputum • Raised serum lipase level • Raised blood lipid level
  • 12. Management • Non-specific 1. keep airway patent and immobilise the fracture 2. Restore blood, volume fluid and electrolyte balance 3. Avoid careless handling of the injured
  • 13. Specific 1. respiratory support- O2 administration to full respiratory support 2. Drugs – i. steroids-methylprednisolone ii. Heparin –decrease s.lipase activity and no. Of circulating fat globules iii. Low molecular wt dextran-useful in prophylaxis,act by inc pl vol,dec blood viscosity nd reduce platelet adherence iv. Hypertonic glucose-dec FFA production,imp art oxygenation v. I/V Alcohol-dec s.lipase activity 3. Definitive fracture treatment