{"id":5184,"date":"2011-07-14T20:24:13","date_gmt":"2011-07-14T20:24:13","guid":{"rendered":"http:\/\/crashtext.org\/misc\/5184.htm\/"},"modified":"2014-09-17T13:44:55","modified_gmt":"2014-09-17T17:44:55","slug":"fat-embolis","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/trauma\/orthopedics\/fat-embolis.htm\/","title":{"rendered":"Fat Embolism Syndrome"},"content":{"rendered":"
FAT EMBOLISM SYNDROME\u0097<\/em>John E. Tetzlaff, MD, Director, Center for Anesthesiology Education, The Cleveland Clinic, Cleveland Incidence: <\/strong>microscopic fat in circulation in 100% of long bone fractures and elective manipulations; fat in circulation does not necessarily indicate fat embolism syndrome (FES; requires fat in circulation, but also 1 of 4 to 5 end-organ manifestations); some element of FES seen in 23% of young adults with high-velocity fractures (eg<\/em>, alpine skiing injuries), 5% of pelvic fractures, and 1% to 2% of long bone fractures; FES occurs in <1% of total joint replacement patients; Pell study used transesophageal echocardiography (TEE) during hip replacement and found that 40% of patients had macroscopic fat pass through right heart Pathophysiology:<\/strong> starting point for organ damage associated with embolization of fat is accumulation of fat in circulation; eventually leads to sludging in microcirculation, leading to blood vessel injury; lipases recruited to remove fat, but lipases do not recognize difference between fat globules and normal cell membranes in immediate area; creates potential for direct lipase destruction of cells; cutaneous etiologies include deposition of fat in microcirculation, release of fat into incorrect tissue, and recruitment of lipases and destruction of capillaries; central nervous system (CNS) etiologies may be related to pulmonary pathophysiology based on hypoxia; eventually leads to deposition of fat in microcirculation of cerebral tissue, recruitment of lipases, and cerebral edema by accumulation of extracellular fluid; pulmonary etiologies include clogging of microcirculation leading to sludging in macrocirculation and eventually pulmonary hypertension; gradual accumulation of fat also occurs in improper places in lung, with recruitment of lipases and destruction of lung tissue; lipases more effective at destroying alveolar structures than deposited fat; pulmonary causes are primary etiology of death in FES; primary cardiovascular manifestation of FES based on pulmonary hypertension and right heart failure Diagnosis <\/strong> Cutaneous signs: include truncal flushing of chest and upper body (related to release of cell mediators of vasodilation and to cell destruction by lipases), petechiae, and retinal funduscopic cotton-wool sign (leaking capillaries in back of eye) CNS signs: include altered level of consciousness, anxiety, lethargy, disorientation, unconsciousness, focal signs (related to embolization into CNS, ie<\/em>, stroke), fear (due to fat accumulation in limbic brain), and seizure activity (due to direct CNS reasons or cerebral hypoxia) Pulmonary signs: include alteration in respiration (tachypnea and dyspnea), hypoxemia (suggestive but not pathognomonic; assume FES in elderly patient with long bone fracture and alveolar-arterial [A-a] O2 gradient >100 mm Hg or absolute PO 2 <60 mm Hg), abnormal pulmonary reflexes (eg<\/em>, wheezing; difficult to treat; associated with poor outcome), hemoptysis (associated with worse outcome), and noncardiogenic pulmonary edema; bilateral chest x-ray \u0093not a way to make an early diagnosis of the FES\u0094 Cardiovascular signs: include tachycardia, right-sided electrocardiography (ECG) changes (eg<\/em>, right axis shift), hyperdynamic state (in early phase), compromised cardiac output (later phase), and end-stage cyanosis and hypotension (possibly disseminated intravascular coagulation [DIC]) High-risk surgical procedures:<\/strong> include high-velocity injury (particularly with open reduction and internal fixation of multiple long bone fractures), endomedullary reaming (typically long bones [eg<\/em>, femur, tibia] without pneumatic tourniquet), pelvic fracture (unstable pelvic ring), placement of endoprostheses and use of pressurized methylmethacrylate, and major joint fusion (eg<\/em>, attempted primary fusion of knee) Treatment:<\/strong> stop bony manipulation; if applicable, inflate pneumatic tourniquet; support cardiovascular system (eg<\/em>, volume, inotropes, vasopressors); pulmonary support (eg<\/em>, additional O2 therapy, endotracheal intubation, mechanical ventilation, positive end-expiratory pressure [PEEP]); <\/p>\n extracorporeal membrane oxygenation (ECMO) in extreme cases; steroids indicated with evidence of CNS damage; avoid increased intracranial pressure (\u0093this can be the absolute make or break point\u0094); support BP Conclusion:<\/strong>mobilization of fat into circulation common during surgery and almost inevitable after long bone fracture and high-velocity trauma; FES not as common as mobilization of fat; etiology of FES known; diagnosis of exclusion; treatment supportive (Audiodigest Anesthesiology 2004) | | |<\/p>\n","protected":false},"excerpt":{"rendered":" Array<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_genesis_hide_title":false,"_genesis_hide_breadcrumbs":false,"_genesis_hide_singular_image":false,"_genesis_hide_footer_widgets":false,"_genesis_custom_body_class":"","_genesis_custom_post_class":"","_genesis_layout":"","footnotes":""},"categories":[17],"tags":[],"yoast_head":"\n