| Abstract [eng] |
Although relatively underrecognized in daily clinical practice, fat embolism and its systemic manifestation, fat embolism syndrome, pose a significant threat in trauma and orthopedic surgery. Fat embolism refers to the entry of fat globules into the pulmonary or systemic circulation. In contrast, fat embolism syndrome describes the resulting clinical manifestations due to fat deposition in the microvasculature following a triggering event. Fat embolism syndrome is a potentially fatal complication most common after orthopedic surgical procedures or trauma-induced long bone fractures. While fat embolism is relatively common in cases involving long bone fractures, the progression of the clinical syndrome to fat embolism syndrome is much rarer but much more dangerous, as it has a much higher mortality rate. Despite a declining incidence over recent decades, fat embolism syndrome remains a diagnostic and therapeutic challenge. This is largely due to its highly variable clinical presentation, and that there is no possibility of using a sufficiently established biomarker routinely in standard clinical settings. The purpose of this thesis was to give an overview of the etiopathogenesis of fat embolism syndrome as understood at the current time and to critically examine evidence-based measures of prevention in orthopedic trauma care. For this purpose, an organized literature review was performed using the PubMed database, using peer- reviewed literature published in 2014 - 2024. Selection was based on relevance to pathophysiological mechanisms, risk factors, and prevention strategies in trauma- and surgery- based settings. The results highlight that the development of fat embolism syndrome involves a complex interplay of mechanical, biochemical, and coagulative factors. Clinically, fat embolism syndrome most commonly presents with a triad of respiratory distress, neurological impairment, and petechial skin manifestations. Major risk factors include multiple or bilateral long bone fractures, delayed fracture fixation, and comorbidities such as obesity or advanced age. Effective prevention strategies include early fracture stabilization, preferably within 48 hours, applying damage control orthopedics and safe definitive surgery, as well as technical measures such as intramedullary lavage and using the Reamer-Irrigator-Aspirator system. Additional strategies, including lung-protective ventilation and selective pharmacological interventions like corticosteroid therapy, remain under investigation due to limited clinical evidence. In conclusion, effective prevention of fat embolism syndrome relies on trauma management strategies tailored to the patient’s physiological status and injury pattern, particularly concerning surgical strategies and the choice of intramedullary techniques. While supportive care remains the cornerstone of fat embolism syndrome treatment, advances in intraoperative strategies have contributed to a measurable decline in incidence. Nevertheless, 2 significant gaps persist in early diagnostic capabilities and long-term outcome data. Moving forward, future research should aim to establish standardized diagnostic criteria, investigate promising molecular targets such as the renin-angiotensin system, and critically evaluate surgical innovations in prospective clinical studies. |
