|
|
| Year : 2009 | Volume
: 2
| Issue : 1 | Page : 29-33 |
|
| Emergency management of fat embolism syndrome |
|
|
Nissar Shaikh
Hamad Medical Corporation, P.Box 3050, Doha, Qatar
Click here for correspondence address and email
| Date of Submission | 12-Aug-2008 |
| Date of Acceptance | 13-Aug-2008 |
|
|
 |
|
 Abstract | | |
Fat emboli occur in all patients with long-bone fractures, but only few patients develop systemic dysfunction, particularly the triad of skin, brain, and lung dysfunction known as the fat embolism syndrome (FES). Here we review the FES literature under different subheadings.
The incidence of FES varies from 1-29%. The etiology may be traumatic or, rarely, nontraumatic. Various factors increase the incidence of FES. Mechanical and biochemical theories have been proposed for the pathophysiology of FES. The clinical manifestations include respiratory and cerebral dysfunction and a petechial rash. Diagnosis of FES is difficult. The other causes for the above-mentioned organ dysfunction have to be excluded. The clinical criteria along with imaging studies help in diagnosis. FES can be detected early by continuous pulse oximetry in high-risk patients. Treatment of FES is essentially supportive. Medications, including steroids, heparin, alcohol, and dextran, have been found to be ineffective. Keywords: Brain, clinical criteria, fat emboli, imaging studies, lung
How to cite this article:
Shaikh N. Emergency management of fat embolism syndrome. J Emerg Trauma Shock 2009;2:29-33 |
| Introduction | |  |
The fat embolism syndrome (FES) is a rare clinical condition in which circulating fat emboli or fat macroglobules lead to multisystem dysfunction.
In 1862, Zenker first described this syndrome at autopsy. In 1873, Von Bergmann clinically diagnosed FES for the first time. [1] Fat embolism occurs in all patients with long-bone fractures after intramedullary nailing. It is usually asymptomatic, but a few patients will develop signs and symptoms of multiorgan dysfunction, particularly involving the triad of lungs, brain, and skin. [2]
Here we review the FES literature under systematic subheadings.
| Epidemiology | | |
The incidence of FES ranges from < 1 to 29% in different studies. It varies considerably according to the cause. The actual incidence of FES is not known, as mild cases often go unnoticed.
Bulger et al ., [3] in their retrospective study, reported an incidence of < 1%, while Fabian et al . in their prospective study, reported an incidence of 11-29%. [4] Surprisingly, the incidence was 0.9% when only clinical criteria were used to diagnose FES, whereas with the aid of postmortem examination the incidence was as high as 20%. [2]
| Etiology | | |
FES is commonly associated with traumatic fracture of femur, pelvis, and tibia, and, postoperatively, after intramedullary nailing and pelvic and knee arthroplasty. The other forms of trauma that may be rarely responsible for FES include massive soft tissue injury, severe burn, bone marrow biopsy, bone marrow transplant, cardiopulmonary resuscitation, liposuction, and median sternotomy. The non-traumatic conditions are very uncommon causes of FES; they are acute pancreatitis, fatty liver, corticosteroid therapy, lymphography, fat emulsion infusion and haemoglobinopathies. [5]
| Risk Factors | | |
The risk factors for the development of FES are young age, closed fractures, multiple fractures, and conservative therapy for long-bone fractures. [6] Factors which increase the risk of FES after intramedullary nailing are over-zealous nailing of the medullary cavity, reaming of the medullary cavity, increased velocity of reaming and increase in the gap between nail and cortical bone.
| Pathophysiology | | |
Two theories are postulated for the occurrence of FES. First, there is the mechanical theory by Gassling et al ., [7] which states that large fat droplets are released into the venous system; these droplets are deposited in the pulmonary capillary beds and travel through arteriovenous shunts to the brain. Microvascular lodging of the droplets produces local ischemia and inflammation, with concomitant release of inflammatory mediators and vasoactive amines and platelet aggregation. The biochemical theory states that hormonal changes caused by trauma and/or sepsis induce systemic release of free fatty acids as chylomicrons. Acute-phase reactants, such as C-reactive proteins, cause the chylomicrons to coalesce and create the physiologic reactions described above. Baker et al . blame the fatty acids for FES; the local hydrolysis of fat emboli by pneumocytes generates free fatty acids, which migrate to other organs via the systemic circulation, causing multiorgan dysfunction. [8] The biochemical theory helps in explaining the pathophysiology of the nontraumatic forms of FES. In an experimental study it is found that the intramedullary pressure increased up to 350 mm of Hg during reaming of the cavity. [9]
| Clinical Features | | |
The principal clinical features of FES are respiratory failure, cerebral dysfunction, and skin petechiae.
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.
The initial symptoms are probably caused by mechanical occlusion of multiple blood vessels with fat globules that are too large to pass through the capillaries. Unlike other embolic events, the vascular occlusion in fat embolism is often temporary or incomplete since the fat globules do not completely obstruct capillary blood flow because of their fluidity and deformability. The late presentation is thought to be a result of hydrolysis of the fat into the more irritating free fatty acids, which then migrate to other organs via the systemic circulation. It has also been suggested that paradoxical embolism occurs due to shunting. [10]
Pulmonary dysfunction is the earliest to manifest and is seen in 75% of patients; it progress to respiratory failure in 10% of the cases. The manifestations include tachypnea, dyspnea, and cyanosis; hypoxemia may be detected hours before the onset of respiratory complaints. [11] Cerebral changes are seen in 86% of patients with FES. These changes are nonspecific, ranging from acute confusion to drowsiness, rigidity, convulsions, or coma. Cerebral edema contributes to the neurological deterioration. [12]
The skin dysfunction is manifested as a nonpalpable petechial rash in the chest, axilla, conjunctiva, and neck that appears within 24-36 h and disappears within a week in 20-50% of patients. The particular distribution of the rash is related to the fact that the fat particles float in the aortic arch like oil in water and thus get embolized to the nondependent areas of the body. [13]
Several other signs are nonspecific, like tachycardia and pyrexia. Renal changes may include lipuria, oliguria, or anuria and hepatic damage may manifest as jaundice. The retina may show exudates, edema, hemorrhage, or intravascular fat globules. [14]
There may be history of orthopedic or plastic surgical procedure or parenteral lipid transfusion.
| Differential Diagnosis | | |
Dyspnea and hypoxia can also occur with pulmonary embolis and pneumonia. Cerebral dysfunction will occur with hypoxia or meningitis, but the rash of meningococcal septicemia spreads rapidly all over the body.
| Diagnosis | | |
FES is commonly diagnosed on the basis of the clinical features and by excluding other causes. Gurd's and Wilson's criteria [11] are shown in [Table 1]; diagnosis of FES requires the presence of at least one major criteria and at least four minor criteria.
Schonfeld et al . proposed [Table 2] a quantitative measure to diagnose FES; a score of more than 5 is required to diagnose FES. [15]
According to Lindeque et al ., [Table 3] FES can be diagnosed on the basis of respiratory system involvement alone. [16]
Investigations
Arterial blood gas analysis showing an unexplained increase in pulmonary shunt fraction and an alveolar-to-arterial oxygen tension difference, especially within 24-48 h of a sentinel event associated with FES, is strongly suggestive of the diagnosis. Blood gases will show hypoxia, with a paO 2 of less than 60 mmHg along with the, and presence of hypocapnia.
Thrombocytopenia, anemia, hypofibrinogenemia, and increased erythrocyte sedimentation rate (ESR) are seen in FES, but are nonspecific findings. A decrease in hematocrit occurs within 24-48 h and is attributed to intra-alveolar hemorrhage.
Cytological examination of urine, blood, and sputum may detect fat globules that are either free or within macrophages. This test is not sensitive and its absence does not rule out fat embolism. Fat globules in the urine are common after trauma. Preliminary investigations of the cytology of pulmonary capillary blood obtained from a wedged pulmonary artery catheter revealed fat globules in patients with FES and showed that this method may be beneficial in early detection of patients at risk. [17]
Imaging studies
Chest radiography: Serial radiographs reveal increasing diffuse bilateral pulmonary infiltrates [Figure 1], fleck-like pulmonary shadows ('snow storm' appearance), increased pulmonary markings, and dilatation of the right side of the heart within 24-48 h of onset of clinical findings.
CT (computerized tomography) head: Findings may be normal or may reveal diffuse white-matter petechial hemorrhages consistent with microvascular injury. CT will also rule out other causes for deterioration in consciousness level.
Ventilation/perfusion imaging of the lungs: Performed for suspicion of pulmonary embolus, the findings from this scan may be normal or may demonstrate subsegmental perfusion defects.
Spiral chest CT for pulmonary embolism: As the embolic particles are lodged in the capillary beds, findings of spiral chest CT may be normal. Parenchymal changes consistent with lung contusion, acute lung injury, or adult respiratory distress syndrome (ARDS) may be evident. [17]
Magnetic resonance imaging (MRI) brain: Scanty data exist regarding MRI findings in patients with this syndrome; however, in one small patient group, multiple, nonconfluent, hyperdense lesions were seen on proton-density and T2-weighted images. [18]
Magnetic resonance imaging brain is more sensitive than CT scan and diagnosis can be made earlier. It will show typical white matter changes along the boundary zones of major vascular territories [Figure 2]. [19]
Transcranial Doppler sonography: In a small case study, five patients with trauma were monitored with intracranial Doppler sonography during intraoperative nailing of long-bone fractures. Cerebral microembolic signals were detected as late as 4 days after injury. [20]
Transesophageal echocardiography (TEE): This procedure may be of use in evaluating intraoperative release of marrow contents into the bloodstream during intramedullary reaming and nailing. The density of the echogenic material passing through the right side of the heart correlates with the degree of reduction in arterial oxygen saturation. Repeated showers of emboli have been noted to increase right heart and pulmonary artery pressures. Embolization of marrow contents through a patent foramen ovale has also been noted. [21]
Procedures
Bronchoalveolar Lavage (BAL) staining of alveolar macrophages for fat will demonstrate fat droplets thus enabling a rapid and specific diagnosis of FES. [22] But one has to be careful, as fat droplets in BAL may be present in patients with sepsis and hyperlipidemia. They may also be seen in patients on lipid infusions. Presently, the use of BAL to aid in the diagnosis or to predict the likelihood of FES is controversial. [23]
| Treatment | | |
Treatment of FES consists of ensuring good arterial oxygenation. High flow rate oxygen is given to maintain the arterial oxygen tension in the normal range. Additionally, maintenance of intravascular volume is important, because shock can exacerbate the lung injury caused by FES. Albumin has been recommended for volume resuscitation in addition to balanced electrolyte solution, because it not only restores blood volume but also binds with the fatty acids and may thus decrease the extent of lung injury. Mechanical ventilation and PEEP may be required to maintain arterial oxygenation. [24] Medications, including steroids, heparin, alcohol, and dextran, have been found to be ineffective. [25]
| Prevention | | |
Continuous pulse oximetry monitoring in high-risk patients may help in detecting desaturation early, allowing early institution of oxygen (and possibly steroid) therapy; it would thus be possible to decrease the chances of hypoxic insult and the systemic complications of FES. [26] The early fixation of long-bone fracture is important to prevent or to decrease the severity of FES. [27] External fixation or fixation with plate and screw produces lesser lung injury than nailing the medullary cavity and venting the medullary canal during nailing, reduces the number of emboli. [28] Preoperative use of methylprednisolone may prevent the occurrence of FES. [15] Smaller-diameter nails and unreamed nailing have been mentioned as being useful in the prevention of FES.
| Prognosis | | |
The fulminant form presents as acute cor pulmonale, respiratory failure, and/or embolic phenomena, leading to death within a few hours of injury. Patients with increased age, multiple underlying medical problems, and/or decreased physiologic reserves have worse outcomes. [29]
The duration of FES is difficult to predict because FES is often subclinical or overshadowed by other illnesses or injuries. Increased alveolar-to-arterial oxygen gradient and neurology deficits, including altered consciousness, may last days or weeks. As in ARDS, the pulmonary sequelae usually resolve almost completely within a year. Residual subclinical diffusion capacity deficits may persist.
Residual neurological deficits may range from subtle personality changes to memory loss, cognitive dysfunction and long term focal deficits. FES alone has not yet been reported to cause global anoxic injury, but it may play a contributory role, acting along with other cerebral insults. The mortality rate from FES is 5-15%. Even severe respiratory failure associated with fat embolism seldom leads to death.
| Conclusion | | |
A high index of suspicion is needed to diagnose FES. A combination of clinical criteria and MRI brain will enable early and accurate diagnosis of FES.
| References | | |
| 1. | Von Bergmann E. Ein fall todlicher fettenbolic. Berl Klin Wochenscher 1873;10:385.  |
| 2. | Georgopoulos D, Bouros D. Fat embolism syndrome clinical examination is still the preferable diagnostic method. Chest 2003;123:982-3. [PUBMED] [FULLTEXT] |
| 3. | Bulger EM, Smith DG, Maier RV, Jurkovich GJ. Fat embolism syndrome: A 10 years review. Arch Surg 1997;132:435-9. [PUBMED] |
| 4. | Fabian TC, Hoots AV, Stanford DS, Patterson CR, Mangiante EC. Fat embolism syndrome, prospective evaluation in 92 fractured patients. Crit Care Med 1990;18:42-6. [PUBMED] |
| 5. | Shapiro MP, Hayes JA. Fat embolism in sickle cell disease: Report of a case with brief review of literature. Arch Intern Med 1984;14:181-2. |
| 6. | Dillerud E. Abdominoplasty combined with suction lipoplasty: A study of complications, revision and risk factors in 487 cases. Ann Plast Surg 1990;25:333-8. [PUBMED] |
| 7. | Glossing HR, Pellegrini VD Jr. Fat embolism syndrome: A review of pathology and physiological basis of treatment. Clin Orthop Relat Res 1982;165:68-82. |
| 8. | Baker PL, Paxel JA, Pettier LF. Free fatty acids, catecholamine and arterial hypoxia in patients with fat embolism. J Trauma 1971;11:1026-30. |
| 9. | Kropfl A, Davies J, Berger U. Intra-medullary pressure and bone marrow fat embolization in reamed and undreamed femoral nailing. J Orthop Res 2005;17:261-8. |
| 10. | Riding G, Daly K, Hutchinson S, Rao S, Lovell M, McCollum C. Paradoxical cerebral embolization: An explanation for fat embolism syndrome. J Bone Joint Surg Br 2004;86:95-8. [PUBMED] [FULLTEXT] |
| 11. | Guard AR, Wilson RE. The FES. J Bone Joint Surg Br 1974;56:408-16. |
| 12. | Byrick RJ. Fat embolism and postoperative coagulopathy. Can J Anaesth 2001;48:618-21. [PUBMED] [FULLTEXT] |
| 13. | Alho A. Fat embolism syndrome, Etiology pathogenesis and treatment. Acta Chir Scand 1980;499:75-85. |
| 14. | Murray DA, Racz GB. Fat embolism syndrome: A rational for treatment. J Bone Joint Surg Br 1974;56:1338-49. |
| 15. | Schonfeld SA, Ploysongsang Y, DiLisio R, Crissman JD, Miller E, Hammerschmidt DE, et al . Fat embolism prophylaxis with corticosteroid: A prospective study in high-risk patients. Ann Int Med 1983;99:438-43. |
| 16. | Lindeque BG, Schoeman HS, Dommissen GF, Boeyens MC, Vlok AL. Fat embolism syndrome: A double blind therapeutic study. J Bone Joint Surg Br 1987;69:128-31. |
| 17. | Van den Brande FG, Hellemans S, De Schepper A, De Paep R, Op De Beeck B, De Raeve HR, et al . Post-traumatic severe fat embolism syndrome, with uncommon CT findings. Anaesth Intensive Care 2006;34:102-6. [PUBMED] |
| 18. | 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. |
| 19. | Guillevin R, Vallιe JN, Demeret S, Sonneville R, Bolgert F, Mont'alverne F, et al . Cerebral fat embolism: Usefulness of magnetic resonance spectrometry. Am Neurol 2005;57:434-9. |
| 20. | Forteza AM, Koch S, Romano JG, Zych G, Bustillo IC, Duncan RC, et al . Transcranial Doppler detection of fat emboli. Stroke 1999;30:2687-91. [PUBMED] [FULLTEXT] |
| 21. | 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. |
| 22. | Fourme T, Vieillard-Baron A, Loubiθres Y, Juliι C, Page B, Jardin F. Early fat embolism after liposuction. Anaesthesiology 1998;89:782-4. |
| 23. | Vedrinne JM, Guillaume C, Gagnieu MC, Gratadour P, Fleuret C, Motin J. Bronchoalveolar lavage in trauma patients for diagnosis of fat embolism syndrome. Chest 1992;102:1323-7. |
| 24. | Jawed M, Naseem M. An update on fat embolism syndrome. Pak J Med Sci 2005;21:2-6. |
| 25. | Enneking FK. Cardiac arrest during total knee replacement. J Clin Anaesth 1995;7:253-63. |
| 26. | Wong MV, Tsui HF, Young SH, Chan KM, Cheng JC. Continuous pulse oximeter, for in apparent hypoxemia after long bone fractures. J Trauma 2004;56:356-62. |
| 27. | Behrman SW, Fabian TC, Kudsk KA, Taylor JC. Improved outcome with femur fracture: Early VS delayed fixation. J Trauma 1990;30:792-7. [PUBMED] |
| 28. | Wheelwright EF, Byrick RJ, Wigglesworth DF, Kay JC, Wong PY, Mullen JB, et al . Hypotension during cemented arthoplasty, relationship with cardiac output and fat embolism. J Bone Joint Surg Br 1993;75:715-23. [PUBMED] [FULLTEXT] |
| 29. | Nikoliζ S, Miciζ J, Saviζ S, Gajiζ M. Factors which could affect the severity of post-traumatic pulmonary fat embolism: A prospective histological study. Srp Arch Celok Lek 2003;131:244-8. |
Correspondence Address:
Nissar Shaikh
Hamad Medical Corporation, P.Box 3050, Doha
Qatar
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0974-2700.44680
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3] |
|
| This article has been cited by | | 1 |
Practice Advisory on Gluteal Fat Grafting |
|
| Daniel Del Vecchio, Jeffrey M Kenkel | | Aesthetic Surgery Journal. 2022; | | [Pubmed] | [DOI] | | | 2 |
Risk Stratification Algorithm for Orthopedic Trauma Patients at Risk for Fat Embolism Syndrome |
|
| Andrew Lowery, Vineet Naran, Robert Ames, Akul Patel, Frederick Ramsey, Bridget Slattery, Theresa Pazionis | | Indian Journal of Orthopaedics. 2021; 55(4): 879 | | [Pubmed] | [DOI] | | | 3 |
Post-traumatic cerebral fat embolism syndrome with a favourable outcome: a case report |
|
| Wei Wang, Weibi Chen, Yan Zhang, Yingying Su, Yuping Wang | | BMC Neurology. 2021; 21(1) | | [Pubmed] | [DOI] | | | 4 |
Microbleeds show a characteristic distribution in cerebral fat embolism |
|
| Omar Giyab, Bendegúz Balogh, Péter Bogner, Orsi Gergely, Arnold Tóth | | Insights into Imaging. 2021; 12(1) | | [Pubmed] | [DOI] | | | 5 |
Cerebral fat embolization with paroxysmal sympathetic hyperactivity syndrome and septic shock at high altitude: a case report and literature review |
|
| Min Li, Gang Zhu, Hao Guo, Shun Nan Ge, Guo Dong Gao, Yan Qu | | Chinese Neurosurgical Journal. 2021; 7(1) | | [Pubmed] | [DOI] | | | 6 |
Cerebral Fat Embolism That Was Initially Negative on DiffusionWeighted Magnetic Resonance Imaging |
|
| Seung Je Go, Yun Su Mun, Seung Ho Bang, Yong Han Cha, Young Hoon Sul, Jin Bong Ye, Jae Guk Kim | | Journal of Trauma and Injury. 2021; 34(2): 126 | | [Pubmed] | [DOI] | | | 7 |
The diagnostics of fat embolism syndrome at multitrauma |
|
| A. M. Naimov, A. A. Razzokov | | Health care of Tajikistan. 2021; (2): 75 | | [Pubmed] | [DOI] | | | 8 |
Plastic Surgery Complications: A Review for Emergency Clinicians |
|
| Tim Montrief, Kasha Bornstein, Mark Ramzy, Alex Koyfman, Brit Long | | Western Journal of Emergency Medicine. 2020; 21(6) | | [Pubmed] | [DOI] | | | 9 |
Acute Kidney Injury Patterns Following Transplantation of Steatotic Liver Allografts |
|
| Caroline Jadlowiec, Maxwell Smith, Matthew Neville, Shennen Mao, Dina Abdelwahab, Kunam Reddy, Adyr Moss, Bashar Aqel, Timucin Taner | | Journal of Clinical Medicine. 2020; 9(4): 954 | | [Pubmed] | [DOI] | | | 10 |
Posttraumatic subarachnoid fat embolism: Case presentation and literature review |
|
| Rahul Chaturvedi, Ashley Williams, Nikdokht Farid, Tara Retson, Edward Smitaman | | Clinical Imaging. 2020; 68: 121 | | [Pubmed] | [DOI] | | | 11 |
A rare case of fat embolism syndrome secondary to abdominal liposuction and gluteal fat infiltration |
|
| Salvador Recinos, Sabrina Barillas, Alejandra Rodas, Javier Ardebol | | Journal of Surgical Case Reports. 2020; 2020(12) | | [Pubmed] | [DOI] | | | 12 |
Clinical significance of increased peripheral venous blood adipocyte-specific protein FABP4 after joint replacement |
|
| Zhuo Wang, Na Buqi, Pingji Zhang, Yanxun Wang, Yanwei Lv, Guisheng An | | Medicine. 2020; 99(27): e20649 | | [Pubmed] | [DOI] | | | 13 |
The intersection of cerebral fat embolism syndrome and traumatic brain injury: a literature review and case series |
|
| Taron Davis, Alan Weintraub, Michael Makley, Eric Spier, Jeri Forster | | Brain Injury. 2020; 34(8): 1127 | | [Pubmed] | [DOI] | | | 14 |
Duplex ultrasound evidence of fat embolism syndrome |
|
| Abdallah Naddaf, Jason Andre, Stanley J. Bly, Douglas Hood, Kim J. Hodgson, Sapan S. Desai | | Journal of Vascular Surgery Cases, Innovations and Techniques. 2016; 2(4): 155 | | [Pubmed] | [DOI] | | | 15 |
Does Intramedullary Canal Irrigation Reduce Fat Emboli? A Randomized Clinical Trial With Transesophageal Echocardiography |
|
| Jiaqi Zhao,Jianquan Zhang,Xiufeng Ji,Xuemei Li,Qirong Qian,Qi Xu | | The Journal of Arthroplasty. 2014; | | [Pubmed] | [DOI] | | | 16 |
Dehydroepiandrosterone modulates the inflammatory response in a bilateral femoral shaft fracture model |
|
| Philipp Lichte,Roman Pfeifer,Britta Werner,Petra Ewers,Mersedeh Tohidnezhad,Thomas Pufe,Frank Hildebrand,Hans-Christoph Pape,Philipp Kobbe | | European Journal of Medical Research. 2014; 19(1): 27 | | [Pubmed] | [DOI] | | | 17 |
Cytological detection of fat globules after embolism |
|
| J. Lie,K. Beswick,B. Saha,C. Veerappan,T. Watt | | Anaesthesia. 2014; 69(12): 1406 | | [Pubmed] | [DOI] | | | 18 |
Essex and Herts Air Ambulance: a focused case series for pre-hospital practice Case 3: a femoral shaft fracture |
|
| Tim Webb, Erica Ley, Adam Chesters | | Journal of Paramedic Practice. 2014; 6(10): 502 | | [Pubmed] | [DOI] | | | 19 |
Late recovery in cerebral fat embolism |
|
| K. P. Srikanth, S. R. Sundararajan, S. Rajasekaran | | Indian Journal of Orthopaedics. 2014; 48(1): 100 | | [Pubmed] | [DOI] | | | 20 |
Percutaneous compression plate versus proximal femoral nail anti-rotation in treating elderly patients with intertrochanteric fractures: a prospective randomized study |
|
| Qingshan Guo,Yue Shen,Zhaowen Zong,Yufeng Zhao,Huayu Liu,Xiang Hua,Hui Chen | | Journal of Orthopaedic Science. 2013; | | [Pubmed] | [DOI] | | | 21 |
Fat Embolism Syndrome following minor trauma in Duchenne muscular dystrophy |
|
| Laura C. McAdam,Anjali Rastogi,Kathleen Macleod,W. Douglas Biggar | | Neuromuscular Disorders. 2012; 22(12): 1035 | | [Pubmed] | [DOI] | | | 22 |
Variability in intraosseous pressure induced by saline flush of an intraosseous cannula by multiple practitioners |
|
| Bernard J. Rubal,Kathleen McKay,Kevin R. Armstrong,Mark P. Rubal,Melissa J. Marbach | | Lab Animal. 2012; 41(8): 224 | | [Pubmed] | [DOI] | | | 23 |
A Case of Multiple Cerebral Infarction Caused by Fat Embolism after Total Hip Arthroplasty |
|
| Masanori KAWASAKI,Sunao HATASHIMA,Tomio MATSUDA | | THE JOURNAL OF JAPAN SOCIETY FOR CLINICAL ANESTHESIA. 2012; 32(3): 395 | | [Pubmed] | [DOI] | | | 24 |
Fat Embolism Syndrome After Femur Fracture With Intramedullary Nailing: Case Report |
|
| K. A. Powers, L. A. Talbot | | American Journal of Critical Care. 2011; 20(3): 267 | | [Pubmed] | [DOI] | | | 25 |
Fat embolism syndrome after shoulder hemiarthroplasty |
|
| Juan Carlos S. Paredes, Jose Fernando C. Syquia, Ann Margaret V. Chang, Jaime T. Zamuco | | Journal of Shoulder and Elbow Surgery. 2011; 20(5): e1 | | [VIEW] | [DOI] | | | 26 |
Diagnosis of fatal pulmonary fat embolism with minimally invasive virtual autopsy and post-mortem biopsy |
|
| Laura Filograna, Stephan A. Bolliger, Danny Spendlove, Corinna Schön, Patricia M. Flach, Michael J. Thali | | Legal Medicine. 2010; 12(5): 233 | | [VIEW] | [DOI] | | | 27 |
Détresse respiratoire aiguë aprčs un accident de la voie publique |
|
| G. Pouessel,S. Flammarion,D. Romero,H. Giard,A. Liesse,P.S. Ganga-Zandzou,H. Ythier,C. Santos | | Archives de Pédiatrie. 2010; 17(8): 1228 | | [Pubmed] | [DOI] | | | 28 |
Anesthetic Considerations in Orthopedic Patients With or Without Trauma |
|
| Amandeep S. Chohan | | Topics in Companion Animal Medicine. 2010; 25(2): 107 | | [Pubmed] | [DOI] | | | 29 |
Peracute manifestation of fat embolism : Letters to the editor |
|
| Jaromir Koci, Martin Slanina | | ANZ Journal of Surgery. 2010; 80(10): 757 | | [VIEW] | [DOI] | | | 30 |
Cerebral fat embolism after bilateral total knee replacement arthroplasty -A case report- |
|
| Ri-Na Chang, Jong-Hak Kim, Heeseung Lee, Hee-Jung Baik, Rack Kyung Chung, Chi Hyo Kim, Tae-Hu Hwang | | Korean Journal of Anesthesiology. 2010; 59(suppl): S207 | | [VIEW] | [DOI] | |
|
|
|
|
|
|
|
|
|
|
|
|
| Article Access Statistics | | | Viewed | 58664 | | | Printed | 1882 | | | Emailed | 50 | | | PDF Downloaded | 1415 | | | Comments | [Add] | | | Cited by others | 30 | | |
|
|
