Monday, 29 December 2014

Fat Embolism

Just now, I shared something I gained from a ward round, there was an ortho team came and taught me something which is

2 most common causes of chest pain among hospitalised  patient
1. Pneumonia
2. Pulmonary embolism.
In case of mva cases for example  if the chest pain develop veeeeryyy suddent, may suspect fat embolism  in case of fractured bone. So the discussion went on with my colleagues and senior on fat embolism when she said that in ortho, lecturers love to ask 

  • how to diagnose fat embolism? 
  • What are the criteria? 
  • What is the definitive way to diagnose fat embolism?

Kak Maliya asked us but answered them herself. LOL. because we are not posted to ortho yet. Butt, this is important isn't it to know the pathology as a whole. Here are the discussion

FAT EMBOLISM SYNDROME

Fat embolism is a common phenomenon following limb fractures. Circulating fat globules larger than 10 μm in diameter occur in most adults after closed fractures of long bones and histological traces of fat can be found in the lungs and other internal organs. A small percentage of these patients develop clinical features similar to those of ARDS; this was recognized as the fat embolism syndrome long before ARDS entered the medical literature. Whether the fat embolism syndrome is an expression of the same condition or whether it is an entirely separate entity is still uncertain. The source of the fat emboli is probably the bone marrow, and the condition is more common in patients with multiple fractures.


Clinical features

Early warning signs of fat embolism (usually within 72 hours of injury) are a slight rise of temperature and pulse rate. In more pronounced cases there is breathlessness and mild mental confusion or restlessness. Pathognomonic signs are petechiae on the trunk, axillae and in the conjunctival folds and retinae. In more severe cases there may be respiratory distress and coma, due both to brain emboli and hypoxia from involvement of the lungs. The features at this stage are essentially those of ARDS. There is no infallible test for fat embolism; however, urinalysis may show fat globules in the urine and the blood PO2 should always be monitored; values below 8 kPa (60 mmHg or less) within the first 72 hours of any major injury must be regarded as suspicious. A chest x-ray may show classical changes in the lungs.


Management

Management of severe fat embolism is supportive. Symptoms of the syndrome can be reduced with the use of supplemental high inspired oxygen concentrations immediately after injury and the incidence appears to be reduced by the prompt stabilization of long-bone fractures. Intramedullary nailing is not thought to increase the risk of developing the syndrome. Fixation of fractures also allows the patient to be nursed in the sitting position, which optimizes the ventilation–perfusion match in the lungs.

Reference: Apley (aka Ortho Bible in UIA)


From the "clinical features" in the text above, what are the things you monitor in ward? Keep an eye on the body temperature and pulse rate, and also respiratory rate. Also, GCS, SpO2. KIV arterial blood gas, urinalysis, and CXR (nak ambik tapi tak tau wajib ke tak, takut bazir duit kerajaan). Document whether any petechiae seen on trunk, axillae, and conjunctival folds.

Mortality rate of fat embolism : 5-15% which is high 

Petechiae tu dah late/severe stage.
Management is supportive, mcm patient acute pancreatitis, banyak fluid, avoid dehydration. And oxygen

Diagnosis is clinical. Kalau nak definitive diagnosis, kena buat autopsy. Seperti amniotic fluid embolism masa O&G tu.

pathogenesis of petechia in fat embolism?

"The characteristic petechial rash may be the last component of the triad to develop. It occurs in up to 60% of cases and is due to embolization of small dermal capillaries leading to extravasation of erythrocytes. This produces a petechial rash in the conjunctiva, oral mucous membrane, and skin folds of the upper body, especially the neck and axilla. It does not appear to be associated with any abnormalities in platelet function. The rash appears within the first 36 h and is self-limiting, disappearing completely within 7 days."

Source: http://m.ceaccp.oxfordjournals.org/content/7/5/148.full

Is is Gurd's criteria
photo courtesy : kak Maliya

No comments:

Post a Comment