What is Fat Embolism?
First of all, one should understand the difference between the fat embolism and fat embolism syndrome (FES).
Presence of fat globules in pulmonary and peripheral circulation usually following a long bone fracture or major trauma.
Fat Embolism Syndrome (FES)
A serious consequence of fat embolism producing a distinct pattern of symptoms and signs.
CAUSES OF FAT EMBOLISM
- Trauma-related – 95%
- Fractures and orthopaedic related
- Long bone fractures – tibia and femur
- Pelvic fractures
- Vertebral fractures‣ IM nailing and arthroplasty
- Non-orthopaedic related
- Soft tissue trauma
- BM harvesting and transplant
- Non-trauma related – 5%
RISK FACTORS FOR FAT EMBOLISM
- Young age
- Multiple fractures
- Conservative management of long bone fractures
- Overzealous nailing◦ Reaming the medullary cavity
- Increased gap between nail and cortical bone
PATHOGENESIS OF FAT EMBOLISM
Following trauma, fat cells in the bone marrow enter into damaged veins and venous sinusoids → reach femoral vein and IVC → reach the pulmonary circulation → obstruct pulmonary capillaries → interstitial haemorrhages and oedema → alveolar collapse → reactive hypoxaemic vasoconstriction → pulmonary symptoms.
Some fat cells reach the systemic circulation through the patent foramen ovale → neurological and dermatological manifestations.
Fat globules in the plasma are broken down to FFA by the trauma-related hormonal mechanism → FFA intermediaries form (chylomicrons, VLDL etc.) → CRP causes chylomicrons to coalesce → larger chylomicrons go and obstruct capillaries as above.
When they go and obstruct pulmonary capillaries, FFA induce capillary endothelial damage → ARDS.
The same may happen to cerebral circulation → encephalopathy and neurological deﬁcit.
Sometimes, the capillaries of skin is obstructed, conjunctiva and oral mucosa get obstructed → thin walled capillaries rupture → petechiae.
Fat globules are proinﬂammatory and prothrombotic → they cause the generation of thrombin and ﬁbrin, platelet aggregation, consumption of coagulative factors → thrombocytopaenia, anaemia and DIC.
CLINICAL FEATURES OF FAT EMBOLISM
Since it takes time for this pathological process to occur, symptoms and signs appear within 24-72 hours of the primary injury.
Respiratory Symptoms (First to Appear)
- Hypoxaemia – Occur in 75%
- ARDS develops – Occur in about 10%
Neurological Symptoms (After Respiratory Symptoms)
- Focal neurological signs (hemiplegia, aphasia etc.)
- Petechiae of skin of axilla and upper neck and chest
- Petechiae of Conjunctivae and oral mucosa (emboli shooting from the ‣ aortic arch to non-dependent areas)
- Retinal changes – Purtscher’s retinopathy, fat globules seen on retina on fundoscopy
- CVS – myocardial depression
- Coagulopathy – mimicking DIC
- Renal – oliguria, lipiduria, haematuria
DIAGNOSIS – GURD’S CRITERIA
At least 1 major and 4 minor should be present to the diagnosis of fat embolim syndrome.
- Axillary skin and subconjunctival petechiae
- Hypoxaemia – PaO2 <60
- CNS depression disproportionate to hypoxemia
- Pulmonary oedema
- Fat globules in retina on fundoscopy
- Fat globules in urine
- Fat globules in sputum
- FBC – thrombocytopenia, anaemia/drop of haematocrit
- High ESR
INVESTIGATING FAT EMBOLISM
- FBC – anaemia, thrombocytopenia, low haematocrit
- ESR – high
- Serum Lipase – elevated
- Coagulopathy screening – DIC like picture
- Serum Calcium – hypocalcaemia due to calcium binding to FF
Congo red/oil red O test
Urine, sputum, serum (specially pulmonary arterial wedge blood sample) – fat globules
- CXR – snowstorm appearance in ARDS
- CT chest – ground glass appearance
- Pulmonary artery wedge pressure – increased → this is an early way to diagnose this condition.
- MRI Brain – at the boundaries of major arterial territories there will be hyperintense punctate diffuse lesions “star ◦ ﬁeld appearance” – petechiae in the white matter!
- Transoesophageal Echocardiogram
MANAGEMENT OF FAT EMBOLISM
- Early immobilisation of the fractures
- Early operative ﬁxation of fractures
- When reaming the BM for IM nailing, make sure not to increase the intraosseous pressure
- Respiratory support – oxygenation, ventilation
- Neurological support – the aim is to prevent secondary brain damage by maintaining cerebral perfusion and, oxygenation and minimise cerebral oedema
- Renal support – proper ﬂuid management with IP/OP monitoring and renal function assessment
- CVS support – maintain stable haemodynamics, inotropes if necessary
- DVT prophylaxis
- Stress ulcer prophylaxis
- Heparin – increases lipase activity and clears the lipaemic serum
- Corticosteroids – limit FFA generation
- Aspirin – prevents gas exchange abnormalities