FRCA Notes

Fat Embolism Syndrome

Resources

  • Fat embolism describes fat within the pulmonary or peripheral circulations
  • It is often asymptomatic, but may lead to fat embolism syndrome
  • It carries a 5 - 15% mortality

Traumatic

  • It most commonly arises following fractures of the long bones or pelvis
    • 98% of patients with femoral shaft factures have evidence of fat emboli
    • During medullary reaming, 88% of patients have echocardiographic evidence of fat emboli
    • 1/3rd of patients with bilateral femoral fractures will develop fat embolism syndrome

  • There is a higher incidence with a greater number of fractures
    • Incidence 1 in 111 - 385 after isolated long bone injuries
    • Rises to 1 in 78 after multiple closed fractures
    • It is rare in children

  • Other traumatic causes include:
    • Any orthopaedic intervention
    • Soft tissue injuries
    • Burns

Non-traumatic

  • Acute illness e.g. pancreatitis, osteomyelitis, sickle cell disease, DM, bone tumour lysis syndrome, alcoholic liver disease
  • Iatrogenic intervention e.g. extended steroid therapy, liposuction/cosmetic surgeries, TPN

  • Three main theories:
    1. Mechanical theory
    2. Biochemical theory
    3. Coagulation theory

Mechanical theory

  • Physical disruption forces adipose marrow into the venous system, and embolise into pulmonary vasculature
  • Supported by the fact that bones with high marrow content are most associated with the syndrome

  • However studies have demonstrated fat embolism in patients who haven't developed fat embolism syndrome
  • Also does not explain why symptoms peak at 24 - 72hrs when embolic load is highest at time of injury

Biochemical theory

  • Hydrolytic degradation of neutral marrow fat into FFA
  • These FFA induce acute lung injury in animal models by inducing endothelial inflammation

Coagulation theory

  • The fat emboli trigger an inflammatory response
  • Combined with hypotension and endothelial damage from trauma, a prothrombotic state emerges
  • Clotting cascade activation increases the size of the fat embolus, causing greater physical obstruction in vascular beds
  • May explain thrombocytopaenia ± DIC seen in some cases

  • Typically presents 24 - 72hrs post-injury; rarely presents at the time of surgery

  • Described as a classic triad of:
    1. Respiratory: hypoxia (98%)
    2. CNS: neurological dysfunction (59%)
    3. Dermatological: petechial rash (33 - 60%)

  • Various diagnostic criteria exist, of which the most commonly used is Gurd's criteria (also: Lindeque's criteria, Schonfeld's criteria)

Respiratory

  • The most common presenting feature
  • Initial dyspnoea and reflex tachypnoea due to increased alveolar dead space + direct irritation of lung parenchyma
  • Followed by an hypoxemic phase arising due to impaired gas exchange, pulmonary oedema/haemorrhage

  • There may be ABG or clinical features of profound T1RF + raised A-a gradient clinical ± respiratory distress
  • Can progress to respiratory failure requiring mechanical ventilation (44%) or ARDS

Neurological

  • A spectrum of neurological disturbance can occur
    • Acute confusion (most common)
    • Altered conscious level
    • Tonic-clonic seizures
    • Focal neurological deficits
    • Cerebral oedema
  • Neurological signs usually closely follow the onset of respiratory features

Dermatological

  • A late sign
  • Typically occurs in the conjunctiva, oral mucous membranes and skin folds of the neck and axillae

Other

  • FBC: marked anaemia and thrombocytopaenia
  • Raised ESR
  • Fever >38.5°C
  • Tachycardia >110bpm
  • Myocardial ischaemia
  • Fat present in the:
    • Urine - microscopy may demonstrate lipo-uria
    • Sputum
    • Alveoli - alveolar macrophages as seen on BAL
    • Eyes - emboli on fundoscopy

Imaging

  • Findings on CXR and CT may be variable and non-specific
  • MRI may be the imaging modality of choice - fat micro-emboli cause a classic 'starfield' appearance

Prevention

  • Early immobilisation and operative fixation of high-risk fractures
  • Reduce intraosseous pressure during drilling or reaming
  • Use of venting holes intra-operatively
  • Avoid intra-medullary nailing
  • Some evidence to support steroid prophylaxis with methylprednisolone, but not routinely used due to concerns the negative sequelae of steroids outweigh benefit

Management (largely supportive)

  1. May need I&V to facilitate mechanical ventilation

  2. Oxygen therapy
    • 10 - 44% of patients require mechanical ventilation; use lung-protective strategies as in ARDS

  3. Standard management of cardiovascular instability ± use of pulmonary vasodilators
    • Correction of blood indices
    • Some evidence that aspirin reduces time to platelet recovery but not routinely recommended

  4. General principles of preventing secondary brain injury ± seizure prophylaxis

  5. No evidence for steroids as treatment of fat embolism syndrome
  • Admission to a critical care environment