What is Fat Embolism?

7/04/2020

What is Fat Embolism?

First of all, one should understand the difference between the fat embolism and fat embolism syndrome (FES).

DEFINITIONS

Fat Embolism

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
    • Liposuction
    • BM harvesting and transplant
• Non-trauma related – 5%
  • Acute pancreatitis
  • Diabetes Mellitus
  • Sickle cell disease
  • Osteomyelitis
  • Alcoholic liver disease

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

Mechanical theory

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.

Biochemical theory

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)

• Dyspnoea
• Tachypnoea
• Hypoxaemia – Occur in 75%
• ARDS develops – Occur in about 10%

Neurological Symptoms (After Respiratory Symptoms)

• Drowsiness
• Confusion
• Focal neurological signs (hemiplegia, aphasia etc.)

Dermatological Signs

• 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)

Other Signs

• Fever
• Tachycardia
• 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.

Major Criteria

• Axillary skin and subconjunctival petechiae
• Hypoxaemia – PaO2 <60
• CNS depression disproportionate to hypoxemia
• Pulmonary oedema

Minor Criteria

• Tachycardia
• Fever
• 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

Blood Tests

• 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

Pulmonary Tests

• CXR – snowstorm appearance in ARDS
• CT chest – ground glass appearance
• Pulmonary artery wedge pressure – increased → this is an early way to diagnose this condition.

Other Tests

• MRI Brain – at the boundaries of major arterial territories there will be hyperintense punctate diffuse lesions “star ◦ field appearance” – petechiae in the white matter!
• ECG
• Transoesophageal Echocardiogram

MANAGEMENT OF FAT EMBOLISM

Prevention

• 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

Supportive therapy

• 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

General Measures

• Physiotherapy
• DVT prophylaxis
• Skincare
• Stress ulcer prophylaxis
• Nutrition

Unproven Medication

• Heparin – increases lipase activity and clears the lipaemic serum
• Corticosteroids – limit FFA generation
• Aspirin – prevents gas exchange abnormalities