Fat Embolism

Synonyms: fat embolism syndrome and FES

Fat embolism can be difficult to diagnose. It most often follows a closed fracture of a long bone but there are many other causes.

The given incidence of this complication ranges from less than 2% to 22% in different studies. It varies considerably according to the cause. Patients with fractures involving the middle and proximal parts of the femoral shaft are more likely to experience fat embolism. Age also seems to be a factor with young men at highest risk.

• Fractures: Closed fractures produce more emboli than open fractures. Long bones, pelvis and ribs cause more emboli. Sternum and clavicle furnish less. Multiple fractures produce more emboli.
• Massive soft tissue injury
• Severe burns
• Liposuction
• Bone marrow biopsy
• Fixation of cement-free hip prosthesis.
• Non-traumatic settings occasionally lead to fat embolism. These include conditions associated with:
  • fatty liver
  • Prolonged corticosteroids therapy
  • Acute pancreatitis
  • Osteomyelitis
  • Conditions causing bone infarcts, especially sickle cell disease

There is usually a latent period of 24 to 72 hours between injury and onset but a fulminant form presents as acute cor pulmonale, respiratory failure, and/or embolic phenomena leading to death within a few hours of injury.

• Symptoms There is vague pain in the chest and shortness of breath.
• Signs The onset is sudden, with
  • Restlessness
  • Fever occurs, often in excess of 38.3° C with a disproportionately high pulse rate.
  • Drowsiness with oliguria is almost pathognomonic.

• Otherwise unexplained dyspneoa, tachypnoea, arterial hypoxia with cyanosis and diffuse alveolar infiltrates on chest X-ray
• Otherwise unexplained signs of cerebral dysfunction, such as confusion, delirium or coma.
• Petechiae over the upper half of the body, conjunctive, oral mucosa and retinae.

CNS signs, including a change in level of consciousness, are common. They are usually nonspecific and have the features of diffuse encephalopathy with acute confusion, stupor, coma, rigidity, or convulsions. Cerebral oedema contributes to the neurological deterioration.
Cerebral dysfunction will occur with hypoxia or meningitis but the rash of meningococcal septicaemia is all over and spreads rapidly. It can also occur as a late feature of head injury.

Dyspnoea, hypoxia and abnormal CXR can occur with thrombo-embolism and pneumonia.

• Cytological examination of urine, blood and sputum may detect fat globules that are either free or in macrophages. This test has low sensitivity and a negative result does not exclude fat embolism
• The chest X-ray may show evenly distributed, fleck-like pulmonary shadows (Snow Storm appearance), increased pulmonary markings and dilatation of the right side of the heart.
• Blood gases will show hypoxia, pO2 usually less than 60mmHg and hypocapnia. Continuous pulse oximeter monitoring may enable hypoxia from fat embolism to be detected in at risk patients before it is clinically apparent.²
• Platelets are reduced. Decreased haematocrit occurs within 24 to 48 hours and is attributed to intra-alveolar haemorrhage. Lipase is elevated but this is not pathognomonic as it occurs in any bone trauma. Calcium is reduced.

Management of fat embolism syndrome is supportive and consists primarily of ensuring good arterial oxygenation. High flow rate of oxygen is given to maintain the arterial oxygen tension in the normal range. Restriction of fluid intake and the use of diuretics can minimize fluid accumulation in the lungs so long as circulation is maintained. On the other hand maintenance of intravascular volume is important³ because shock can exacerbate the lung injury caused by FES. Albumin has been recommended for volume resuscitation in addition to balanced electrolyte solution, because it not only restores blood volume but also binds fatty acids, and may decrease the extent of lung injury.

Mechanical ventilation and Positive End-Expiratory Pressure (PEEP) may be required to maintain arterial oxygenation.

Drugs

High dose corticosteroids⁴ have been effective in preventing development of FES in several trials, but controversy on this issue still persists. Lower doses may also be effective.⁵ There is also dispute as to whether steroids are effective at all.

Surgical

Prompt surgical stabilization of long bones fractures reduces the risk of the syndrome.

The mortality rate from fat embolism syndrome is 5 to 15%. Even severe respiratory failure associated with fat embolism seldom leads to death.

The prognosis is worse in older patients and those with more severe injury but is not affected by gender.⁶

Early immobilisation of fractures seems to be the most effective way of reducing the incidence of this condition.⁷