FAT EMBOLISM
Introduction
Fat embolism was first described in 1862 at autopsy by Zenker. In 1873, von Bergmann
made the first clinical diagnosis of fat embolism.
Fat embolism most commonly occurs in the setting of long bone (in particular femoral
shaft) and pelvic fractures.
The diagnosis is essentially a clinical one in the first instance and so the clinical
setting will be the most important factor in making it.
Clinically silent fat embolism is probably extremely common.
Clinically significant fat embolism (“fat embolism syndrome”) whilst uncommon is an
important condition to recognize, as it is associated with significant morbidity and
mortality.
Fat emboli are widely disseminated, but the lungs and CNS appear to be the most
affected.
Pathophysiology
There are 2 current theories about the genesis of fat embolism:
1.
Mechanical
●
2.
Embolization of fat from medullary bone into venules.
Biochemical
●
Stress response with increased levels of catecholamines and
corticosteriods leading to increased mobilization of fats that overwhelm
normal transport mechanisms resulting in fat globules coalescing. The
venous embolisation to the lungs may be explained by the mechanical
theory whilst the biochemical theory may help explain CNS involvement.
Microemboli may pass through the pulmonary into the systemic
circulation.
Causes
Fat embolism syndrome is caused by:
1.
Traumatic causes:
●
2.
Long bone, (especially shaft of femur fractures) and pelvic fractures are by
far the commonest causes.
Non-traumatic causes:
Rarely non-traumatic causes may be seen. Conditions that have been implicated
in non-traumatic cases include:
●
Diabetes
●
Pancreatitis
●
Burns
●
Lipid infusions.
●
Cardiopulmonary bypass.
Complications
1.
Respiratory
●
2.
CNS
●
3.
Hypoxia
Depressed or altered conscious state.
Release of free fatty acids from fat globules that result in toxic metabolites may
result in: 1
●
Myocardial depression
●
Vascular endothelial damage leading to hypotension
●
An ARDS type syndrome.
Clinical Features
Classically the syndrome has been described as a triad of hypoxia, neurological
disturbance and petechiae, however the syndrome can be more widespread than this and
it should be remembered that fat globules are widely disseminated.
Symptoms generally appear around 12-72 hours after injury.
1.
CVS
●
2.
3.
Persistent unexplained tachycardia will often be the first symptom.
Respiratory
●
Tachypnea and dyspnea will commonly occur early.
●
Progressive hypoxia
Neurological
CNS disturbance disproportionate to any hypoxia is characteristic.
4.
5.
●
Cerebral agitation and confusion are commonly seen.
●
In more severe cases depression of conscious state may occur progressing
to coma in some cases.
Petechiae
●
A petichial rash may develop later in the progression of the syndrome.
This is thought to be due occlusion of dermal capillaries by fat globules
and is unrelated to any platelet dysfunction.
●
Typically the petichiae appear over the upper body, including the head,
neck, chest, axillae, conjuntival and oral mucosa.
●
Petichiae resolve spontaneously within 5-7 days.
Progressive systemic involvement:
●
In severe cases symptoms may progress to an ARDS type syndrome.
●
Thrombocytopenia.
●
Hyoptension.
●
Anemia
Investigations
There are no specific diagnostic tests for fat embolism.
Investigations therefore will largely be directly to ruling out other diagnoses and
establishing how unwell a patient is.
Blood tests
●
FBE
●
U&Es/ glucose
●
CRP
●
ABGs.
CXR
●
This will be normal in the majority of cases.
●
There may be bilateral pulmonary alveolar infiltrates
ECG
●
The commonest finding will be sinus tachycardia
Fat globules
●
Contrary to some reports fat globules in urine, sputum or wedged PA catheter
blood (detected by specific staining techniques) is not diagnostic. This is a
common finding in trauma and so not helpful in making a diagnosis of fat
embolism.
CT scan
CTPA
●
This cannot make the diagnosis of fat embolism, but may need to be done when
large pulmonary embolism needs to be excluded.
CT scan brain
●
This needs to be considered for any acutely confused patient to rule out
alternative diagnoses for CNS symptoms.
Management
There is no specific treatment for fat embolism and so management is entirely
supportive.
1.
ABC issues
●
The most important initial considerations will be management of the
patient’s conscious state and oxygenation.
●
2.
Early operative fracture fixation
●
3.
Serious cases will require intubation and ventilation.
Early operative fracture fixation reduces the incidence of fat embolism
syndrome.
Any patient suspected of having fat embolism syndrome should be referred to
ICU.
Prognosis
●
Overall mortality ranges from 5 to 15%. 1
●
Multiple fractures are more likely to result in fat embolism syndrome.
●
Mortality is increased in patients with significant co-morbidities.
References
1.
Up to date Website, September 2006
Dr J. Hayes
August 2007