Fat embolism

Abstract

Although its original clinical description dates from 1873, 1 fat embolism syndrome remains a diagnostic challenge for clinicians. The term fat embolism indicates the often asymptomatic presence of fat globules in the lung parenchyma and peripheral circulation after long bone or other major trauma. The majority (95%) of cases occur after major trauma. Fat embolism syndrome is a serious consequence of fat emboli producing a distinct pattern of clinical symptoms and signs. It is most commonly associated with fractures of long bones and the pelvis, and is more frequent in closed, rather than open, fractures. The incidence increases with the number of fractures involved. Thus, patients with a single long bone fracture have a 1-3% chance of developing the syndrome, but it has been reported in up to 33% of patients with bilateral femoral fractures. 2 Fat embolism syndrome can also occur in relation to other trauma, for example, soft tissue injury, liposuction, bone marrow harvest (Table 1). Non-trauma-related causes (e.g. acute pancreatitis, sickling crisis) are less likely to lead to fat embolism syndrome compared with those associated with trauma. An overall mortality of 5-15% has been described. 3 Clinical presentation Fat embolism syndrome typically presents 24-72 h after the initial injury. Rarely, cases occur as early as 12 h or as much as 2 weeks later. 4 Patients present with a classic triad: (i) respiratory changes; (ii) neurological abnormalities; (iii) petechial rash.

Fat Embolism Syndrome After Femur Fracture With Intramedullary Nailing: Case Report

“…Unlike the typical fat emboli associated with traumatic injury, FES is symptomatic. Manifestations of the syndrome usually occur 24 to 72 hours after the initial injury 2,6 or following the surgical repair of the fracture, in this case, the intramedullary nailing of the femur. 1,5,7 After traumatic injuries and their surgical repair, emboli consisting of fat and bone marrow molecules migrate from the injured site via the bloodstream.…”

“…The fat emboli can lodge in various sites, including the pulmonary vasculature, and then travel systemically to neurological or cutaneous sites. 5,6 According to the biochemical theory, embolized fat is degraded into free fatty acids, which cause toxic injury and inflammation in the lungs, 5,6 including an increase in vascular permeability, hemorrhage, and edema, leading to acute lung injury and acute respiratory distress syndrome. 5 Despite the lack of consensus on the pathogenesis of FES, the syndrome consists of a defined triad of signs and symptoms.…”

“…The classic FES triad consists of pulmonary, neurological, and cutaneous manifestations. 3,6,7 Pulmonary manifestations, including dyspnea, tachypnea, and hypoxemia, are generally the first to appear and occur in approximately 75% of FES patients. 7,9 A total of 10% to 50% of patients progress to respiratory failure and acute respiratory distress syndrome, often requiring mechanical ventilation 2,3,7 because of an inflammatory process triggered by fat emboli that leads to hemorrhage and the leaking of proteins into the alveoli.…”

“…10 The neurological manifestations occur in more than 80% of patients and may include restlessness, acute confusion, altered level of consciousness, focal deficits, and seizures. 1,6,11 Neurological signs and symptoms generally occur after the onset of pulmonary signs and symptoms. 2 Cutaneous signs and symptoms occur in up to 60% of FES patients and include petechiae of the skin and mucous membranes.…”

“…2 Cutaneous signs and symptoms occur in up to 60% of FES patients and include petechiae of the skin and mucous membranes. 6,9 The petechiae are nonpalpable, generally located on the thorax, axilla, and neck, and usually disappear within 1 week. 7,9 FES is often diagnosed on the basis of clinical features and the exclusion of other disease processes.…”