True about Post traumatic fat embolism syndrome is A/E
D i.e. Associated diabetes pose a risk. Fat Embolism Syndrome A syndrome caused by an inflammatory response to embolized fat globules Symptoms usually occur 1-3 days after a traumatic injury and are predominantly pulmonary (shoness of breath, hypoxemia), neurological (agitation, delirium, or coma), dermatological (petechial rash), and haematological (anaemia, low platelets). Epidemiologyincidence 3-4% with isolated long bone trauma 10-15% with polytrauma Pathophysiologyfat and marrow elements are embolized into the bloodstream during acute long bone fractures intramedullary instrumentation intramedullary nailing hip & knee ahroplasty pathophysiologytwo theories regarding the causes of fat embolism includemechanical theory embolism is caused by droplets of bone marrow fat released into venous system metabolic theory stress from trauma causes changes in chylomicrons which result in formation of fat emboli Diagnosis CriteriaMajor (1) hypoxemia (PaO2 < 60) CNS depression (changes in mental status) petechial rash pulmonary edema Minor (4) tachycardia pyrexia retinal emboli fat in urine or sputum thrombocytopenia decreased HCT Additional PCO2 > 55 pH < 7.3 RR > 35 dyspnea anxiety TreatmentNonoperative mechanical ventilation with high levels of PEEP (positive end expiratory pressure) indications acute fat emboli syndrome Preventionearly fracture stabilization indications early fracture stabilization (within 24 hours) of long bone fracture is most impoant factor in prevention of FES techniques to reduce the risk of fat emboli overreaming of the femoral canal during a TKA use of reamers with decreased shaft width reduces the risk during femoral reaming for intramedullary fixation use of external fixation for definitive fixation of long bone fractures in medically unstable patients decreases the risk
Bradycardia occur
Systemic hypoxia may occur
Fracture mobility is a risk factor
Associated diabetes pose a risk