Fat Embolism Syndrome

Fat Embolism

    FAT EMBOLISM SYNDROME—John E. Tetzlaff, MD, Director, Center for Anesthesiology Education, The Cleveland Clinic, Cleveland Incidence: 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, 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: 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 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, 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, wheezing; difficult to treat; associated with poor outcome), hemoptysis (associated with worse outcome), and noncardiogenic pulmonary edema; bilateral chest x-ray “not a way to make an early diagnosis of the FES” Cardiovascular signs: include tachycardia, right-sided electrocardiography (ECG) changes (eg, 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: include high-velocity injury (particularly with open reduction and internal fixation of multiple long bone fractures), endomedullary reaming (typically long bones [eg, femur, tibia] without pneumatic tourniquet), pelvic fracture (unstable pelvic ring), placement of endoprostheses and use of pressurized methylmethacrylate, and major joint fusion (eg, attempted primary fusion of knee) Treatment: stop bony manipulation; if applicable, inflate pneumatic tourniquet; support cardiovascular system (eg, volume, inotropes, vasopressors); pulmonary support (eg, additional O2 therapy, endotracheal intubation, mechanical ventilation, positive end-expiratory pressure [PEEP]);

extracorporeal membrane oxygenation (ECMO) in extreme cases; steroids indicated with evidence of CNS damage; avoid increased intracranial pressure (“this can be the absolute make or break point”); support BP Conclusion: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)   | | |