A fat embolism occurs when fat macroglobules or fat tissue circulates through the bloodstream and ultimately lodge within a blood vessel. It is most often a result of trauma to the long bones of the body (e.g., femur, humerus).
Presentation
Symptoms from a fat embolism (commonly called fat embolism syndrome) typically onset 24 to 72 hours after the insult [1] [2]. In some cases symptoms appear as soon as 12 hours and as late as 2 weeks following injury. The severity of symptoms depends on the location of the blocked vessels. Patients present with the "classic triad" of symptoms, which consists of respiratory distress, petechial rash, and neurological abnormalities.
- Respiratory related symptoms such as cyanosis, dyspnea, hypoxemia, and tachypnea onset first [3]. The severity of respiratory distress varies based on the size and location of the fat embolism; they may progress to acute respiratory failure requiring mechanical ventilation, similar in presentation to acute respiratory distress syndrome.
- Neurologic abnormalities occur after the onset of respiratory distress. They are characterized by drowsiness, confusion, and altered mental status. Some patient will also develop more severe neurological symptoms such as rigidity, seizures, and coma [4].
- A petechial rash is the last sign of the triad to occur. It often presents on the chest, axilla, conjunctiva, head and neck [5] [6]. The rash resolves in about one week in most patients.
Less common symptoms of fat embolism include: pyrexia, cardiac depression, Purtscher's retinopathy, fever, coagulopathy (resembling disseminated intravascular coagulation), and kidney dysfunction (e.g., lipiduria, oliguria, proteinuria, hematuria) [7] [8].
Workup
The diagnosis of fat embolism syndrome can be made based on clinical presentation; for example, when the "classic" petechial rash occurs alongside hypoxemia and neurologic impairment, fat embolism syndrome should be suspected. A recent history of trauma resulting in the fracture of or surgery on a large bone (e.g., femur or humerus) should raise the index of suspicion for a fat embolism [9].
Laboratory studies
- Arterial blood gas findings often demonstrate hypoxia, PaO2 <60 mmHg, and hypocapnia
- Hematologic studies may show non-specific findings such as thrombocytopenia, anemia, hypofibrinogenemia, and an elevated erythrocyte sedimentation rate.
- Cytological evaluation of urine, blood, and sputum may reflect fat globules.
Imaging
- The initial chest radiograph will be essentially normal in the majority of patients [10]. Occasionally, there may be air space disease or alveolar hemorrhages visualized [11]. Subsequent radiographs, however, will show progressive diffuse bilateral pulmonary infiltrates, fleck-like pulmonary shadows (often referred to as a 'snow storm'), and dilatation of the right heart.
- Ventilation-perfusion scans may show a mottled pattern of subsegmental perfusion defects and a normal ventilatory pattern.
- Chest computed tomography (CT) often depicts areas of ground glass opacities with interlobar septal thickening. Parenchymal changes of the lungs which are indicative of acute lung injury, pulmonary contusion, or adult respiratory distress syndrome may also be seen on CT.
- Magnetic resonance imaging (MRI) of the brain may reveal high intensity T2 signal and white matter changes along the boundary zones of major vascular territories [12] [13] [14]. Neurological findings have been correlated with a "starfield" pattern on brain magnetic resonance imaging [15].
- Transesophageal echocardiography (TEE) can be used intraoperatively to detect release of marrow contents into the bloodstream during orthopedic surgery (e.g., intramedullary reaming and nailing) [16].
Procedures
Staining of bronchoalveolar lavage (BAL) contents (alveolar macrophages for fat) will demonstrate fat droplets, allowing diagnosis of a fat embolism [17]. Findings should be interpreted with caution since fat droplets in BAL may also be present in patients with sepsis, hyperlipidemia, and patients on lipid feeding infusions. The use of BAL for diagnosis of fat embolism is controversial and its sensitivity and specificity are not well studied [18].
Treatment
There is no specific treatment for fat embolism, so management focuses on supportive care. This includes ensuring adequate oxygenation and ventilation, often requiring supplemental oxygen or mechanical ventilation in severe cases. Intravenous fluids may be administered to maintain blood pressure and hydration. In some instances, corticosteroids are used to reduce inflammation, although their effectiveness is debated.
Prognosis
The prognosis for fat embolism varies depending on the severity of the symptoms and the patient's overall health. Many patients recover fully with appropriate supportive care. However, severe cases can lead to complications such as acute respiratory distress syndrome (ARDS) or neurological damage, which can impact long-term outcomes. Early recognition and management are crucial for improving prognosis.
Etiology
Fat embolism is most commonly caused by trauma, particularly fractures of long bones like the femur or pelvis. It can also occur after orthopedic surgeries, such as joint replacements, or in cases of severe burns and liposuction. The exact mechanism by which fat enters the bloodstream is not fully understood, but it is believed to involve the release of fat from bone marrow or adipose tissue into damaged blood vessels.
Epidemiology
Fat embolism syndrome is relatively rare, occurring in about 1-3% of patients with long bone fractures. It is more common in young adults, likely due to the higher incidence of traumatic injuries in this age group. The condition is less frequently reported in children and the elderly, although it can occur in any age group.
Pathophysiology
The pathophysiology of fat embolism involves the release of fat globules into the bloodstream, which then travel to various organs. In the lungs, these fat droplets can obstruct small blood vessels, leading to respiratory distress. In the brain, they can cause neurological symptoms by blocking blood flow. The petechial rash is thought to result from small blood vessel blockages in the skin.
Prevention
Preventing fat embolism involves minimizing the risk of trauma and managing fractures promptly and appropriately. In surgical settings, careful handling of bone and soft tissues can reduce the likelihood of fat entering the bloodstream. Early stabilization of fractures and the use of less invasive surgical techniques may also help prevent the condition.
Summary
Fat embolism is a condition where fat droplets block small blood vessels, leading to symptoms affecting the lungs, brain, and skin. It is most commonly associated with fractures of long bones but can occur in other situations. Diagnosis is based on clinical presentation, and treatment focuses on supportive care. While the prognosis is generally good with appropriate management, severe cases can lead to complications.
Patient Information
If you or someone you know has experienced a traumatic injury, especially involving long bones, it's important to be aware of the symptoms of fat embolism. These include difficulty breathing, confusion, and a rash of small red or purple spots. If these symptoms occur, seek medical attention promptly. Early recognition and treatment can improve outcomes and reduce the risk of complications.
References
- Carr JB, Hansen ST. Fulminant fat embolism. Orthopedics. 1990;13:258.
- Carr JB, Hansen ST. Unusual forms of pulmonary embolism. Clin Chest Med. 1994;15:561.
- Jacobson DM, Terrence CF, Reinmuth OM. The neurologic manifestations of fat embolism. Neurology. 1986;36:847.
- Byrick RJ. Fat embolism and postoperative coagulopathy. Can J Anaesth. 2001;48:618–21.
- Alho A. Fat embolism syndrome, Etiology pathogenesis and treatment. Acta Chir Scand. 1980;499:75–85.
- Kaplan RP, Grant JN, Kaufman AJ. Dermatologic features of the fat embolism syndrome. Cutis. 1986; 38:52-5.
- Jones JP Jr. Fat embolism, intravascular coagulation, and osteonecrosis. Clin Orthop Relat Res. 1993.
- Murray DA, Racz GB. Fat embolism syndrome: A rational for treatment. J Bone Joint Surg Br. 1974;56:1338–49.
- King MB, Harmon KR. Unusual forms of pulmonary embolism. Clin Chest Med. 1994; 15:561-80.
- Glas WW, Grekin TD, Musselman MM. Fat embolism. Am J Surg. 1953;85:363.
- Umali CB, Smith EH. The chest radiographic examination. In: Intensive Care Medicine, Rippe, JM, Irwin, RS, Alpert, JS, Fink, MP (Eds), Little Brown, Boston 1991. p.596.
- Kellogg RG, Fontes RB, Lopes DK. Massive cerebral involvement in fat embolism syndrome and intracranial pressure management. J Neurosurg. 2013;119:1263-70.
- Takahashi M, Suzuki R, Osakabe Y, et al. Magnetic resonance imaging findings in cerebral fat embolism: correlation with clinical manifestations. J Trauma. 1999;46:324.
- Guillevin R, Vallée JN, Demeret S, et al. Cerebral fat embolism: Usefulness of magnetic resonance spectrometry. Am Neurol. 2005;57:434–9.
- Stoeger A, Daniaux M, Feiber S, Stockhammer G, Aichner F, zur Nedden D. MRI finding in cerebral fat embolism. Eur Radiol. 1998;8:1590–3.
- Wenda K, Runkel M, Degrief J, Ritter G. Pathogenesis and clinical relevance in medullary nailing demonstrated by intra-operative echocardiography. Injury. 1993;24:S73–81.
- Fourme T, Vieillard-Baron A, et al. Early fat embolism after liposuction. Anaesthesiology. 1998;89:782–4.
- Godeau B, Schaeffer A, Bachir D, et al. Am Bronchoalveolar lavage in adult sickle cell patients with acute chest syndrome: value for diagnostic assessment of fat embolism. J Respir Crit Care Med. 1996;153:1691.