Date post: | 31-May-2015 |
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FAT EMBOLISM SYNDROMEFAT EMBOLISM SYNDROME
FAT EMBOLISM
Indicates the presence of fat globules in lung parenchyma & peripheral circulation after # of a long bone or major trauma.
Usually occurs within 72 hrs of skeletal trauma.
Often asso with multiple #res, major bone #res, pelvic #res, multi system injuries like chest& abdomen, head injuries etc.
Causes a devastating clinical deterioration within hrs.
The overall prevalence of fat embolism syndrome is 1% to 3.5% of patients with a fracture of tibia or femur.
Patients with bilateral femoral fractures are at particular risk & have a higher risk of ARDS & death.
CAUSES Traumatic & non traumatic factors.
1. Traumatic causes are;
Fractures – long bones, pelvis Burns Surgery – IM nailing, arthroplasty Sub cutaneous adipose tissue injuries.
2. Non traumatic causes;• Diseases – DM, collagen diseases, severe
infections, c/c pancreatitis, c/c alcoholism, osteo myelitis, sickle cell anemia.
Procedures – cardio pulmonary bypass, blood transfusion, renal transplantation, liposuction.
PATHO PHYSIOLOGY Mechanical theory& Bio chemical theory
-Toxic theory
-Obstructive theory• Mechanical theory;
Suggests that fat globules are forcibly intravasated from marrow thru disrupted vessels & then they are transported to the pulmonary vascular bed & are trapped as emboli in the lung capillaries.
Some reaches systemic circulation causing embolization in areas such as brain,kidney,retina or skin.
2. Bio chemical theory;
Toxic theory – Lung lipase hydrolyzes neutral fat to chemically toxic free fatty acids. This causes severe inflammatory changes by producing endothelial damage, inactivation of lung surfactant & increase in capillary permeability leading to ARDS.
Obstructive theory –
A chemical event at the site of # releases mediators that affect the solubility of lipids, causing coalescence & subsequent embolization. Normal chylomicrons may coalesce & form fat globules which are capable of occluding the lung capillaries.
Gurd’s criteria for diagnosis
Major criteria:
- Axillary & sub conjunctival petechiae.
- Pa O2 < 60 mm Hg
- CNS depression Minor criteria:
- pulse>110/mt
- pyrexia>38.5
-retinal embolism
-fat in urine
- reduced platelet count- increased ESR- Fat globules in sputum
…..At least 1 from major criteria & 4 from minor criteria.
The classic syndrome involves pulmonary, cerebral & cutaneous manifestations.
- Pulmonary: tachypnoea,dyspnoea,cyanosis,tachy cardia,& rhonchi
Cerebral: headache,irritability,delirium, stupor,convulsions & coma.
Cutaneous and retinal: retinal exudates, edematous patches,cotton wool spots & petechial haemorrhages.
Three presentations:
1.Sub clinical fat embolism syndrome:
Lab abnormalities present..but non specific clinical symptoms.
Tachy cardia>100beats/mt, tachypnoea >25breaths/mt, temp>37.8.
Moderate hypoxemia(Pa O2< 80mm Hg)& moderate decrease in platelets is a common finding.
2.Non fulminant sub acute fat embolism syndrome
Characterised by respiratory failure, fever, tachycardia, petechiae & cerebral signs etc.
Petechial rashes are pathognomonic of fat embolism syndrome.This rashes appears between 12 to 96 hrs following injury.
Retinal lesions are described as cotton wool spots & flame like haemorrhages on fundoscopy.
PaO2 <60 mm Hg,anemia,thrombocytopenia & lung opacities on CXR.
3.Fulminant fat embolism syndrome Severe variant. Patients may present with sudden hypotension,
cerebral signs, severe hypoxemia, frank pulmonary edema or acidosis.
Petechiae arise from occlusion & distention of dermal capillaries by fat globules & increased CP.•They are present across the chest,axilla,root of neck &conjunctiva and they fades rapidly.
Laboratory investigations
Shows hypoxemia(<60mm Hg),thrombocytopenia(<1.5 lakhs), anemia & hypo calcemia.
The most useful diagnostic test is arterial blood gas analysis.
PT & ESR increases. Demonstration of fat globules in urine, sputum or
blood. Raised serum lipase level& Raised blood lipid levels.
X ray chest:
Pathognomonic snow storm appearance.
ECG:
S waves prominent.
DIAGNOSTIC TRIAD:
1. Thromboctopenia
2. PaO2 < 60 mm Hg
3. Rashes
Management Non specific: 3 vital steps.1. Keep airway patent & #
immobilized.2. Restore blood volume, fluid &
electrolyte balance.3. Avoid careless handling of the
injured.
Specific: 3 vital steps.1. Respiratory support: Can
range from O2 administration to full respiratory support with mechanical ventillation.
2.Drug therapy
Treatment of shock: Aggressive fluid resuscitation under appropriate monitoring.
Albumin is preferred because it not only restores blood volume but also binds free fatty acids.
Steroids: Helps gas exchange by decreasing inflammation
in the lungs.Methyl prednisolone appears to modify the pulmonary response to injury by relative preservaton of arterial oxgenation.
Heparin: Increases serum lipase activity &
decreases no of circulating fat globules.
Low molecular wt dextran: Useful in prophylaxis. Acts by increasing plasma
volume,decreases blood viscosity & reduces platelet adherence.
Hypertonic glucose: Decreases free fatty acid production. Improves arterial oxygenation.
Intra venous alcohol: Reduces serum lipase activity. Thus limits free fatty acid production.
3. Definitive fracture treatment: Early fixation of fractures is advocated to
prevent worsening of the situation.