How fat embolism occurs in fracture?
Practice EssentialsFor those who manage major trauma victims, the topic of fat embolism weighs heavily on the mind. The incidence of this problem can approach 90% in patients who have sustained major injuries. If it progresses to the rare clinical entity known as fat embolism syndrome (FES), [1] a systemic inflammatory cascade affecting multiple organ systems, morbidity and mortality are high. Accordingly, swift diagnosis and treatment of fat embolism are paramount for ensuring the survival of this patient population. [2] Show Ernst Von Bergmann, in 1873, was the first person credited with making a clinical diagnosis of fat embolism. He did this on the basis of knowledge gathered from experiments with cats 10 years previously, in which he injected them with intravenous oils. Von Bergmann later described a patient who fell off a roof and sustained a comminuted fracture of the distal femur; 60 hours after the injury, the patient developed dyspnea, cyanosis, and coma. [2] The diagnosis of FES is mainly a clinical one. It is dependent on clinical identification of dyspnea, petechiae, and cognitive dysfunction in the first few days following trauma, long bone fracture, or intramedullary surgery. Various laboratory studies and imaging modalities exist to aid in its discovery (see Presentation and Workup). Supportive measures are the mainstay of treatment; thus, efforts are targeted at prevention, early diagnosis, and symptom management (see Treatment).  PathophysiologyThe exact mechanism of fat embolism and its evolution to the entity known as FES has not been fully elucidated, but a number of experimental models have been proposed. Asymptomatic fat embolism to the pulmonary circulation almost always occurs with major trauma, including elective surgical procedures such as intramedullary nailing of long bones, which has been demonstrated with echocardiography. The development of FES is rare, occurring in 0.5-11% of cases. [3, 4] Although poorly understood, the development of FES is attributed to a series of biochemical cascades resulting from the mechanical insult sustained in major trauma. Release of fat emboli leads to occlusion of the microvasculature, triggering an inflammatory response that is clinically manifested by dermatologic, pulmonary, and neurologic dysfunction. [5, 6] (See the images below.) Pulmonary consequences of FES are clinically similar to those of acute respiratory distress syndrome (ARDS) and almost always occur. They are usually the initial manifestation of FES, typically appearing within 24 hours after the traumatic insult. They result from injury to the pulmonary capillary endothelium caused by free fatty acids that were hydrolyzed by lipoprotein lipase, releasing local toxic mediators. These mediators cause increased vascular permeability, resulting in alveolar hemorrhage and edema and causing respiratory failure and ARDS. [7, 8] Approximately 20-30% of the population have a patent foramen ovale; this may explain how fat emboli that pass through the pulmonary circulation end up with systemic manifestations of FES, particularly involving the brain and kidneys. As a result of the occluded cerebral vasculature, patients exhibit gross encephalopathy, localized cerebral edema, and white-matter changes. [7, 9, 10] EtiologyCauses of FES include the following:
In blunt trauma patients with extremity fractures, factors found to be associated with increased risk of FES include age 30 years or younger, closed femur fracture, and multiple long-bone fractures. [16] EpidemiologyFat embolism occurs in up to 90% of all trauma patients. [17, 12] Habashi et al found that FES accounted for only 2-5% of patients who have long-bone fractures. [9] Lempert et al performed a systematic review (15 articles; N = 3095) aimed at determining whether the incidence of FES decreased between 1960 and 2019 and whether specific injury patterns predispose to its development. [18] They found that the incidence of FES did decrease over time, from 7.9% in 1960-1979 to 4.8% in 1980-1999 to 1.7% in 2000-2019. They also found that the rate of FES was significantly lower for unilateral high-energy fractures (2.9%) than for pathologic fractures (3.3%) and bilateral high-energy fractures (4.6%). PrognosisThe duration of FES is difficult to predict because the syndrome is often subclinical or overshadowed by other illnesses or injuries. Increased alveolar-to-arterial oxygen gradient and neurologic deficits, including coma, may last days or weeks. Hematologic aberrations due to FES frequently are indistinguishable from those due to other causes common in these patients. As in ARDS, pulmonary sequelae usually resolve almost completely within 1 year. Residual subclinical diffusion capacity deficits may exist. FES alone has not been reported to cause global anoxic injury, but it may contribute in conjunction with other cerebral insults. Residual neurologic deficits may range from nonexistent to subtle personality changes to memory and cognitive dysfunction to long-term focal deficits. Outcomes in patients who develop FES are bleak if the syndrome is not identified early and aggressive supportive measures are not initiated. When action is taken early in the disease course, the prognosis is generally favorable, with a mortality of less than 10%. [2]
Author Coauthor(s) Rajan Gupta, MD, FACS, FCCP Associate Professor of Surgery, Chief, Division of Acute Care Surgery, Rutgers Robert Wood Johnson Medical School Rajan Gupta, MD, FACS, FCCP is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Chest Physicians, American College of Surgeons, Association for Academic Surgery, New Hampshire Medical Society, Shock Society, Society of Critical Care Medicine, Eastern Association for the Surgery of Trauma, European Society for Trauma and Emergency Surgery, Western Trauma Association, International Society of Surgery, International Association for Trauma Surgery and Intensive Care, New England Surgical Society Disclosure: Nothing to disclose. Chief Editor Vincent Lopez Rowe, MD Professor of Surgery, Program Director, Integrated Vascular Surgery Residency and Fellowship, Department of Surgery, Division of Vascular Surgery and Endovascular Therapy, Keck School of Medicine of the University of Southern California Vincent Lopez Rowe, MD is a member of the following medical societies: American College of Surgeons, American Surgical Association, Pacific Coast Surgical Association, Society for Clinical Vascular Surgery, Society for Vascular Surgery, Western Vascular Society Disclosure: Nothing to disclose. Acknowledgements Lisa Kirkland, MD, FACP, CNSP, MSHA Assistant Professor, Department of Internal Medicine, Division of Hospital Medicine, Mayo Clinic; ANW Intensivists, Abbott Northwestern Hospital Lisa Kirkland, MD, FACP, CNSP, MSHA is a member of the following medical societies: American College of Physicians, Society of Critical Care Medicine, and Society of Hospital Medicine Disclosure: Nothing to disclose. Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment How does bone fracture cause fat embolism?Smaller bones have much less fat tissue. With a broken bone, fat cells can enter the body's circulatory system and be carried by the bloodstream throughout the body. This is called fat embolism. Fat embolism is quite common after major trauma in which one or more large bones are broken.
Can fracture cause fat embolism?Fat embolism is most commonly associated with skeletal injury and is most likely to occur in patients with multiple long-bone and pelvic fractures. Some other traumatic causes include: rib fractures, massive soft tissue injury, severe burns, bone marrow biopsy, and liposuction.
How does a fat embolism form?A fat embolism happens when there is fat in the circulatory system, including the veins or arteries. It usually happens after a bone injury, when fat surrounding the bone and muscle gets into broken blood vessels. If a person develops symptoms, it means they have fat embolism syndrome.
When does fat embolism occur after fracture?The clinical manifestations may develop 24–72 h after trauma (and especially after fractures) when fat droplets act as emboli, becoming impacted in the pulmonary microvasculature and other microvascular beds such as in the brain. Embolism begins rather slowly and attains a maximum in about 48 h.
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