Fat embolism syndrome

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FAT EMBOLISM SYNDROME
Incidence in Plastic Surgery
 Abdominoplasty – 1%
 Liposuction – case reports
o 3 post mortems (J Forensic Sci 2002) showed 2 were due to FES, the other
from fluid overload.
2 theories
1) mechanical - large fat droplets are released into the venous system. These
droplets are deposited in the pulmonary capillary beds and travel through
arteriovenous shunts to the brain. Microvascular lodging of droplets produces
local ischemia and inflammation, with concomitant release of inflammatory
mediators, platelet aggregation, and vasoactive amines.
2) biochemical theory - circulating or hydrolyzed free fatty acids in the
pulmonary system activate acute-phase reactants, such as C-reactive proteins,
and causes damage to the endothelial cells and pneumocytes. above. The
biochemical theory helps explain delayed onset of fat embolism syndrome.
Pathogenesis
 After being trapped in the pulmonary capillaries and hydrolyzed by a pulmonary
lipase, free fatty acids cause direct toxic damage of the microvascular and
alveolocapillary units and subsequently cause release of vasoactive amines and
prostaglandins.
 The histopathology of FES is characterized by interstitial edema, transudate,
and later exudate in the alveoli, the death of type II pneumocytes, and hyaline
membrane formation.
Clinical
 Fat embolism is a clinical diagnosis.
 Characterised by fever, acute respiratory failure, global neurologic
dysfunction, and petechial rash occurring within 12-72 hours after surgery
without evidence of cardiogenic pulmonary edema or sepsis
 10-20% mortality rate
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CVS - Early persistent tachycardia
CNS – acute delirium, stupor, seizures, or coma
Resp - tachypneic, dyspneic, and hypoxic often febrile
Skin (20-50%) – reddish-brown nonpalpable petechiae developing over the upper
body, particularly in the axillae, within 24-36 hours of injury.
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Eyes - Subconjunctival and oral hemorrhages and petechiae also appear. Retinal
hemorrhages with intra-arterial fat globules are visible upon funduscopic
examination
Investigations
ABG – increased AA gradient
FBC - Thrombocytopenia, anemia, and hypofibrinogenemia
CXR - diffuse bilateral pulmonary infiltrates within 24-48 hours of onset
VQ scan - often normal
Pulmonary angiogram – rarely diagnostic
Bronchoscopy lavage – most diagnostic - fat laden macrophages
Treatment
supportive
 maintenance of adequate oxygenation and ventilation and stable
hemodynamics
 In most case reports - aggressive haemodynamic and respiratory support over
1-2 weeks required
 blood products as clinically indicated
 hydration
 prophylaxis of deep venous thrombosis and stress-related gastrointestinal
bleeding,
 nutrition.
 Consider use of steroids – may be used as prophylaxis
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