[Pathophysiology of fat embolisms in orthopedics and traumatology].
It is well known that fat embolisms can occur after long bone fractures, and this has been feared for more than 100 years. Since 1970 fat embolisms have also been recognized in endoprosthetic surgery. The clinical manifestation was described as the fat embolism syndrome (FES) by Gurd in 1974. Based on reports in the literature and our own data, a concise pathophysiological model of the FES is presented in this paper. The increase in intramedullary pressure (IMP) in the long bones is the most decisive pathogenic factor for the development of an FES. Any long bone fracture, stabilization of fractures, or implantation of knee or hip endoprostheses can generate IMP peaks leading to bone marrow release into the circulation. Bone marrow itself is a tremendous stimulus for activation of the clotting system. As a result, hypercoagulation and venous stasis in the draining veins generate mixed macroemboli from the initial bone-marrow microemboli. Bone-marrow embolization of the lung in phase I leads to mechanical obstruction of pulmonary arteries. In phase II, release of local mediators, triggered by a systemic inflammatory response (SIR) of the lungs, causes damage to the pulmonary membranes. Disturbed gas exchange and respiratory insufficiency with possible cardiac and cerebral decompensation are the result. In most cases an FES may not be detected clinically, and any mild cardiorespiratory changes are treated easily with oxygen insufflation and usually disappear within 48 h. Of paramount importance for clinical manifestation of an FES are the quantity and duration of bone-marrow release and co-factors (cardiorespiratory compliance and perioperative stability of the patient). Patients with preexisting cardiorespiratory disease in combination with massive intraoperative bone-marrow release may even face a deadly FES event. Increased IMP causes local obstruction of cortical vessels with bone marrow. In combination with the damaged endosteal blood supply, avascular necrosis of the cortical bone occurs. During endoprosthetic procedures, mechanical-and mediator-triggered damage of the intima of big veins, in combination with venous stasis and hypercoagulation may be responsible for the high incidence of proximal thrombosis of femoral veins. As a delayed result of the disseminated intravascular coagulopathy, petechial bleeding in the trunk and subconjunctiva can be seen. A better understanding and recognition of the FES's pathophysiology may help to use prophylactic, diagnostic and therapeutical measures more effectively.
Hofmann
S
S
Orthopädische Abteilung, Donauspital, Wien.
Huemer
G
G
Kratochwill
C
C
Koller-Strametz
J
J
Hopf
R
R
Schlag
G
G
Salzer
M
M
D001777:Blood Coagulation; D001853:Bone Marrow / Q000503:physiopathology; D004620:Embolism, Fat / Q000209:etiology / Q000503:physiopathology*; D005593:Fracture Fixation, Internal / Q000009:adverse effects; D050723:Fractures, Bone / Q000150:complications / Q000503:physiopathology; D006801:Humans; D007595:Joint Prosthesis / Q000009:adverse effects; D008954:Models, Biological; D010020:Osteonecrosis / Q000503:physiopathology; D011183:Postoperative Complications / Q000503:physiopathology; D011312:Pressure; D011655:Pulmonary Embolism / Q000503:physiopathology*; D011659:Pulmonary Gas Exchange; D012131:Respiratory Insufficiency / Q000503:physiopathology; D013927:Thrombosis / Q000503:physiopathology
Pathophysiologie der Fettembolie in der Orthopädie und Traumatologie.