Increase in optic nerve sheath diameter predicts early cerebral involvement in fat embolism syndrome.

Early diagnosis of cerebral fat embolism in a patient with contradiction to MRI is challenging. Here we report an interesting case, where the raised optic nerve sheath diameter helped us to predict the early cerebral involvement with fat emboli in a left femoral shaft fracture patient. MRI scan could not be performed due to the presence of a metallic implant in the patient from a previous surgery. He was later diagnosed as an atypical presentation of fat embolism syndrome. Optic nerve sheath monitoring also helped us to guide further management of the patient.

A 21-year-old Pregnant Trauma Patient with Asymptomatic Fat Embolism; a Case Report.

INTRODUCTION: Fat embolism syndrome (FES) is most often associated with orthopedic trauma that typically presents 24-72 hours after the trauma with a classic triad. Only few cases of fat embolism due to lower extremity venous system had been reported. CASE PRESENTATION: The current case report presents a pregnant woman who was referred to our emergency department with bilateral femoral open fracture. After detecting fetal demise by abdominopelvic ultrasound, an area of fat density in right external iliac vein was detected in abdominopelvic contrast enhanced computed tomography (CT) scan which was considered as the probable diagnosis of fat embolism. While the patient did not show signs and symptoms of FES, the fat embolism was confirmed in further evaluations. CONCLUSION: In summary, although detection of fat embolus in CT scan in the emergency department is very rare, evaluation of lower extremity venous system in a posttraumatic patient seems to be crucial because early diagnosis of fat embolism can help the clinicians to prevent FES.

Sudden death caused by Clostridium perfringens sepsis presenting as massive intravascular hemolysis.

An 80-year-old Japanese woman with diabetes mellitus was admitted with gastrointestinal symptoms and pyrexia. At presentation, liver abscesses and severe hemolytic anemia were noted. Before detailed diagnostic evaluation and adequate treatment, she suddenly died 2.5 hours after admission. The autopsy and bacteriological examinations revealed liver abscesses and massive intravascular hemolysis caused by Clostridium perfringens as well as other miscellaneous critical pathological findings, including acute renal tubular necrosis, lung edema, and pulmonary fat embolism. In this article, the detailed autopsy results are described and clinicopathologic characteristics on Clostridium perfringens-related sudden death are discussed with a review of the literature.

Sudden death caused by pulmonary fat embolism in a patient with miliary tuberculosis.

An 84-year-old Japanese woman with myelodysplastic syndrome was admitted with pyrexia and dyspnea, but died suddenly during diagnostic evaluation. The autopsy revealed miliary tuberculosis in addition to myelodysplastic syndrome in the bone marrow. The immediate cause of the patient's sudden death was pulmonary fat embolism derived from bone marrow necrosis. This case shows that the infiltration of the myelodysplastic bone marrow by tuberculosis and consequent bone marrow necrosis and fat embolism can be the cause of sudden death. In this article, we report the autopsy results of this unusual cause of sudden death, and discuss tuberculosis-related sudden death with a review of the literature.

Fat embolism: the hidden murder for trauma patients! / Embolia gordurosa: a assassina oculta para pacientes com trauma!

ABSTRACT Introduction: fat embolism syndrome (FES) is an acute respiratory disorder that occurs when an inflammatory response causes the embolization of fat and marrow particles into the bloodstream. The exact incidence of FES is not well defined due to the difficulty of diagnosis. FES is mostly associated with isolated long bone trauma, and it is usually misdiagnosed in other trauma cases. The scope of this study was to identify and search the current literature for cases of FES in nonorthopedic trauma patients with the aim of defining the etiology, incidence, and main clinical manifestations. Methods: we perform a literature search via the PubMed journal to find, summarize, and incorporate reports of fat embolisms in patients presenting with non-orthopedic trauma. Results: the final literature search yielded 23 papers of patients presenting with fat embolism/FES due to non-orthopedic trauma. The presentation and etiology of these fat embolisms is varied and complex, differing from patient to patient. In this review, we highlight the importance of maintaining a clinical suspicion of FES within the trauma and critical care community. Conclusion: to help trauma surgeons and clinicians identify FES cases in trauma patients who do not present with long bone fracture, we also present the main clinical signs of FES as well as the possible treatment and prevention options.

RESUMO Introdução: a síndrome da embolia gordurosa (SEG) representa um distúrbio respiratório agudo que ocorre quando uma resposta inflamatória leva a uma embolização de partículas de gordura e medula na corrente sanguínea. A incidência exata da SEG não está bem estabelecida devido à dificuldade de diagnóstico. Tal síndrome está associada principalmente a traumas isolados de ossos longos e geralmente é diagnosticada erroneamente em outros casos de trauma. O escopo deste estudo foi de realizar uma pesquisa e identificar na literatura atual casos de SEG em pacientes com trauma de natureza não ortopédica com o objetivo de definir a etiologia, a incidência e as principais manifestações clínicas. Métodos: foi realizada uma pesquisa na literatura utilizando como base de dados o PubMed a fim de identificar os relatos e series de casos de embolias gordurosas em pacientes vítimas de traumas de natureza não ortopédica. A pesquisa final resultou em 23 artigos de pacientes que apresentaram embolia gordurosa/SEG devido a trauma não ortopédico. Resultados: a apresentação e a etiologia dessas embolias gordurosas são variadas e complexas, diferindo de paciente para paciente. Nesta revisão, destacamos a importância de manter uma suspeita clínica de SEG para pacientes vítimas de trauma que se encontrem sob cuidados intensivos. Conclusão: para ajudar os cirurgiões de trauma e os clínicos a identificar casos de SEG em pacientes com trauma que não apresentam fratura de ossos longos, foram destacados os principais sinais clínicos de SEG, bem como as possíveis opções de tratamento e prevenção.

Trauma Patient with Fat Embolism Detected on Computed Tomography.

Fat embolism is frequent following fractures of long bones, however the development of the clinical syndrome of fat embolism (characterized by progressive respiratory distress, mental status depression and petechial rash) is rare, but relevant because of its potential severity. We report a case of a trauma patient with multiple fractures of the right lower limb in whom an emergency computed tomography scan showed fat emboli within the lumen of the homolateral common femoral vein. The imaging detection of macroscopic fat emboli should alert the clinician to the potential for subsequent fat embolism syndrome.

A embolia gorda é frequente no contexto de fracturas de ossos longos, contudo o desenvolvimento da síndrome clínica da embolia gorda (caracterizada por dificuldade respiratória progressiva, depressão do estado de consciência e rash petequial) constitui uma ocorrência rara, embora relevante pela sua gravidade. Apresentamos o caso de um politraumatizado com fraturas múltiplas do membro inferior direito a quem foi detetada, em tomografia computorizada de urgência, a presença de êmbolos de gordura no lúmen da veia femoral comum homolateral. A visualização de êmbolos macroscópicos de gordura através de métodos de imagem deverá alertar o clínico para a possibilidade de desenvolvimento da síndrome da embolia gorda.

Síndrome de embolismo graso en fractura de huesos largos, reporte de caso / Fat embolism syndrome in long bone fractures, case report

Introducción: El síndrome de embolismo graso es una complicación severa, aun-que poco frecuente de trauma grave. Es desencadenado por el paso de partículas de grasa hacia la microcirculación en varios órganos. La tríada característica: lesión pulmonar, hemorragia petequial y disfunción neurológica. Su prevalencia varía se-gún los criterios diagnósticos y la causa desencadenante, dificultando su detección temprana. Presentación del caso: Caso 1. Paciente 22 años, masculino, sufrió accidente automovilístico con fracturas abierta de fémur, tibia y peroné derechos, resueltas quirúrgicamente, a las 5 horas del evento sufre deterioro respiratorio, petequias conjuntivales, torácicas y en extremidades; posteriormente deterioro de concien-cia, estatus epiléptico y síndrome de hiperactividad simpática paroxística. Caso 2. Paciente 29 años, masculino, sufrió volcamiento del vehículo en el que viajaba, sufriendo fracturas cerradas de tibia, peroné y fémur izquierdas, luego de la cirugía traumatológica sufrió deterioro del estado de conciencia, petequias conjuntivales e hipoxemia.Diagnósticos e intervenciones: los dos pacientes fueron operados para resolución traumatológica dentro de las primeras 24 horas, luego del aparecimiento de síntomas neurológicos se sometieron a neuroimagen encontrándose el patrón de "campo de es-trellas" y recibieron corticoides.Resultados: Caso 1 el desenlace fue estado vegetativo, Caso 2 recuperación completa.Conclusión: La detección es imprescindible para establecer el tratamiento temprano, planificar la cirugía traumatológica o diferirla y estimar el pronóstico según la evolu-ción. El síndrome de embolia grasa cerebral es una causa rara del síndrome de hipe-ractividad simpática paroxística

Introduction: Fat embolism syndrome is a severe, although rare complication of major trauma. It is triggered by the passage of fat particles into the microcirculation in various organs. The characteristic triad: lung injury, petechial hemorrhage and neurological dysfunction. Its prevalence varies according to the diagnostic criteria and the triggering cause, making its early detection difficult. Case presentation: Case 1. Patient 22 years old, male, suffered a car accident with open fracture of the right femur, tibia and fibula, surgically resolved, 5 hours after the event he suffered respiratory impairment, conjunctival, thoracic and extre-mity petechiae; later impaired consciousness, status epilepticus and paroxysmal sympathetic hyperactivity syndrome. Case 2. Patient 29 years old, male, suffered overturning of the vehicle in which he was traveling, suffering closed fractures of the left tibia, fibula and femur, after trauma surgery he suffered impaired consciousness, conjunctival petechiae and hypoxemia.Diagnoses and interventions: Both patients underwent surgery for trauma reso-lution within 24 hours, after the appearance of neurological symptoms they un-derwent neuroimaging finding "star field" pattern, both received corticosteroids.Results: Case 1 the outcome was vegetative state, Case 2 complete recovery.Conclusion: Detection is essential to establish early treatment, to plan trauma sur-gery or to defer it and to estimate prognosis according to evolution. Cerebral fat em-bolism syndrome is a rare cause of paroxysmal sympathetic hyperactivity syndrome.

A Case of Acute Fulminant Fat Embolism Syndrome after Liposuction Surgery.

Fat embolism syndrome (FES) is a clinical manifestation that consists of multiple organ dysfunction due to fat emboli. FES occurs as a complication after trauma or procedures such as surgery. The diagnostic criteria of FES have not yet been established, so clinical criteria are used for its diagnosis. The clinical course of acute fulminant FES can be rapid. Liposuction surgery, in which adipocytes are mechanically disrupted, is one cause of FES. As the number of liposuction surgeries increases, clinicians should be aware of the possibility of FES. This was the first report of a case of acute fulminant FES with severe acute respiratory distress syndrome after liposuction surgery, in Korea.

Sudden death caused by Clostridium perfringens sepsis presenting as massive intravascular hemolysis

An 80-year-old Japanese woman with diabetes mellitus was admitted with gastrointestinal symptoms and pyrexia. At presentation, liver abscesses and severe hemolytic anemia were noted. Before detailed diagnostic evaluation and adequate treatment, she suddenly died 2.5 hours after admission. The autopsy and bacteriological examinations revealed liver abscesses and massive intravascular hemolysis caused by Clostridium perfringens as well as other miscellaneous critical pathological findings, including acute renal tubular necrosis, lung edema, and pulmonary fat embolism. In this article, the detailed autopsy results are described and clinicopathologic characteristics on Clostridium perfringens-related sudden death are discussed with a review of the literature.

Transposition of intravascular lipid in experimentally induced fat embolism: a preliminary study.

BACKGROUND: Liposuction is a procedure to reduce the volume of subcutaneous fat by physical force. Intracellular storage fat is composed of triglyceride, whereas circulating fat particles exist as cholesterol or triglycerol bound to carrier proteins. It is unavoidable that the storage form of fat particles enters the circulation system after these particles are physiologically destroyed. To date, however, no studies have clarified the fatal characteristics of fat embolism that occurs after the subclinical phase of free fat particles. METHODS: A mixture of human lipoaspirate and normal saline (1:100, 0.2 mL) was injected into the external jugular vein of rats, weighing 200 g on average. Biopsy specimens of the lung and kidney were examined at 12-hour intervals until postoperative 72 hours. The deposit location and transport of the injected free fat particles were confirmed histologically by an Oil Red O stain. RESULTS: Inconsistent with previous reports, free fat particles were transported from the intravascular space to the parenchyma. At 24 hours after infusion, free fat particles deposited in the vascular lumen were confirmed on the Oil Red O stain. At 72 hours after infusion, free fat particles were accumulated compactly within the parenchymal space near the perivascular area. CONCLUSIONS: Many surgeons are aware of the fatal results and undiscovered pathophysiologic mechanisms of free fat particles. Our results indicate that free fat particles, the storage form of fat that has been degraded through a physiological process, might be removed through a direct transport mechanism and phagocytotic uptake.

Sudden death caused by pulmonary fat embolism in a patient with miliary tuberculosis

An 84-year-old Japanese woman with myelodysplastic syndrome was admitted with pyrexia and dyspnea, but died suddenly during diagnostic evaluation. The autopsy revealed miliary tuberculosis in addition to myelodysplastic syndrome in the bone marrow. The immediate cause of the patient's sudden death was pulmonary fat embolism derived from bone marrow necrosis. This case shows that the infiltration of the myelodysplastic bone marrow by tuberculosis and consequent bone marrow necrosis and fat embolism can be the cause of sudden death. In this article, we report the autopsy results of this unusual cause of sudden death, and discuss tuberculosis-related sudden death with a review of the literature.

Bone marrow necrosis and fat embolism: an autopsy report of a severe complication of hemoglobin SC disease.

Sickle Cell Disease encompasses a group of disorders related with the hemoglobin S and other hemoglobin genotypes. The clinical manifestation and the severity of symptoms are dependent on the specific genotype. In this setting, homozygous genotype (HbSS) presents an early onset of symptoms and a low expectancy of lifetime. However, the SC genotype (HbSC), which apparently shows a less severe clinical course, may exhibit the same complications of HbSS. These complications are usually manifested late in the course of life, when compared with the HbSS patients. It is noteworthy that HbSC may present a normal hematocrit, and therefore stays unknown until the first complication, that may be disastrous. The authors report a case of an African-Descendant woman, aging 65 years, with no previous diagnosis of anemia who sought medical attention because of a thoracic back pain followed by fever and altered mental status. The clinical picture deteriorated very fast with multiple organ failure and death. The autopsy findings concluded by generalized vaso-occlusive crisis, bone marrow necrosis and bone marrow and fat embolism, mainly to the lungs and kidney. The authors call attention for the knowledge of this severe life threatening complication, mainly in a country with a high Afro-Descendant population.

Síndrome De Embolia Grasa Postraumática, Síntomas Neurológicos Sin Clínica Respiratoria En Ausencia De Foramen Oval Permeable / Posttraumatic Fat Embolism Syndrome, Neurological Symptoms Without Respiratory Symptoms In The Absence Of Permeable Foramen Ovale

Resumen El síndrome de embolia grasa es una complicación potencialmente catastrófica de las fracturas de huesos largos. La tríada clásica de síntomas son erupciones cutáneas petequiales, hipoxemia y anomalías neurológicas, que generalmente ocurren dentro de las 24 a 72 horas posteriores a la fractura. El componente respiratorio se presenta en prácticamente la totalidad de los reportes. Presentamos el caso de un paciente con embolia grasa postraumática con clínica neurológica preponderante, sin afectación respiratoria en ausencia de foramen oval permeable.

Abstract Fat embolism syndrome is a potentially catastrophic complication of long-bone fractures. The classic triad of symptoms are petechial skin rashes, hypoxemia, and neurological abnormalities, which usually occur within 24 to 72 hours after the fracture. The respiratory component occurs in practically all of the reports. We present the case of a patient with posttraumatic fat embolism with predominant neurological symptoms, without respiratory involvement in the absence of patent foramen ovale.

Síndrome de hiperatividade simpática paroxística causada por síndrome da embolia gordurosa / Paroxysmal sympathetic hyperactivity syndrome caused by fat embolism syndrome

RESUMO A hiperatividade simpática paroxística representa uma complicação incomum, com potencial risco à vida, de lesões cerebrais graves, mais comumente de origem traumática. Seu diagnóstico clínico se baseia na manifestação recorrente de taquicardia, hipertensão, diaforese, taquipneia e, às vezes, febre, além de posturas distônicas. Os episódios podem ser induzidos por estímulos ou ocorrer de forma espontânea. É comum que ocorra subdiagnóstico desta síndrome, e o retardamento de seu reconhecimento pode aumentar a morbidade e a incapacidade em longo prazo. Evitar os desencadeantes e a farmacoterapia podem ter muito sucesso no controle desta complicação. A síndrome da embolia gordurosa é uma complicação rara, mas grave, das fraturas de ossos longos. Sinais neurológicos, petéquias hemorrágicas e insuficiência respiratória aguda são as características que constituem seu quadro clínico. O termo "embolia gordurosa cerebral" é estabelecido quando predomina o envolvimento neurológico. O diagnóstico é clínico, porém achados específicos de neuroimagem podem confirmá-lo. As manifestações neurológicas incluem diferentes graus de alteração da consciência, défices focais ou convulsões. Seu tratamento é de suporte, porém são possíveis desfechos favoráveis, mesmo nos casos com apresentação grave. Relatamos dois casos de hiperatividade simpática paroxística após embolia gordurosa cerebral, uma associação muito incomum.

ABSTRACT Paroxysmal sympathetic hyperactivity represents an uncommon and potentially life-threatening complication of severe brain injuries, which are most commonly traumatic. This syndrome is a clinical diagnosis based on the recurrent occurrence of tachycardia, hypertension, diaphoresis, tachypnea, and occasionally high fever and dystonic postures. The episodes may be induced by stimulation or may occur spontaneously. Underdiagnosis is common, and delayed recognition may increase morbidity and long-term disability. Trigger avoidance and pharmacological therapy can be very successful in controlling this complication. Fat embolism syndrome is a rare but serious complication of long bone fractures. Neurologic signs, petechial hemorrhages and acute respiratory failure constitute the characteristic presenting triad. The term cerebral fat embolism is used when the neurological involvement predominates. The diagnosis is clinical, but specific neuroimaging findings can be supportive. The neurologic manifestations include different degrees of alteration of consciousness, focal deficits or seizures. Management is supportive, but good outcomes are possible even in cases with very severe presentation. We report two cases of paroxysmal sympathetic hyperactivity after cerebral fat embolism, which is a very uncommon association.

Síndrome de embolia grasa con predominio de síntomas neurológicos / Fat embolism syndrome with predominant neurological symptoms / Síndrome de embolia gordurosa com predomínio de sintomas neurológicos

Introducción. La embolia grasa es la obstrucción de los vasos sanguíneos de pequeño calibre por lípidos producidos durante la degradación tisular. Se presenta en individuos con fracturas de huesos largos, y es asintomático en más del 90 % de los casos. El síndrome de embolia grasa corresponde a un proceso grave poco frecuente en la práctica clínica, caracterizado por la aparición de petequias, dificultad respiratoria y alteraciones neurológicas. Reporte de caso. Se trata de una mujer adulta joven con trauma cerrado de tórax y fracturas múltiples de huesos largos de las extremidades superiores e inferiores por politraumatismo de alta energía, que fue sometida a reducción bajo anestesia de las fracturas. A las 48 horas, comenzó a presentar dificultad respiratoria, exantema petequial de predominio en la pared anterior del tórax y deterioro neurológico con convulsiones tónico-clónicas focales y bilaterales, que cedieron con un medicamento anticonvulsivo intravenoso. Se le diagnosticó síndrome de embolia grasa debido al antecedente de trauma y a las lesiones evidenciadas en la resonancia magnética. Se le brindó soporte respiratorio y terapia anticoagulante, con lo cual el cuadro clínico mejoró. Discusión. El tejido graso ingresa a la circulación cuando la presión en el lecho del drenaje venoso es superada por la presión en la médula ósea. Los ácidos grasos libres tóxicos causan edema vasogénico y citotóxico, así como hemorragia por destrucción celular. Conclusión. Es importante considerar la presencia de esta complicación en pacientes con múltiples fracturas y brindar un tratamiento oportuno con la intención de disminuir las secuelas asociadas con esta condición

Introduction: Fatty embolism is the obstruction of small blood vessels by lipid product of tissue degradation. It occurs in individuals with long bone fractures, being asymptomatic in more than 90% of cases. The fat embolism syndrome corresponds to a severe and rare process in clinical practice, characterized by the appearance of petechiae, respiratory stress and neurological disorders. Case report: Young adult with high energy-polytrauma and closed chest trauma with multiple fractures of long bones of the upper and lower extremities who was taken to operating theater for redu-cing them under anesthesia. Forty-eight hours after, she began to present with respiratory distress, petechial rash predominantly in the anterior thorax and neurological deterioration with focal seizure activity to bilateral tonic-clonic, which yielded with intravenous anticonvulsant. A fat embolism syndrome was diagnosed due to the history of trauma and the lesions evidenced in the magnetic resonance. She was given respiratory support and anticoagulant therapy, with which the clinical picture improved. Discussion: The fatty tissue enters the circulation when the venous drainage bed pressure is overcome by the pressure inside the bone marrow. The toxic free fatty acids cause vasogenic and cytotoxic edema, as well as hemorrhage by cell destruction. Conclusion: It is important to consider the presence of this complication in patients with multiple fractures and to offer timely treatment with the intention of reducing the sequelae associated with this condition.

Introdução. Embolia gordurosa é a obstrução dos vasos sanguíneos de diâmetro reduzido pelos lipídios produzidos durante a degradação tecidual. Ocorre em indivíduos com fraturas de ossos longos e é assintomática em mais de 90% dos casos. A síndrome da embolia gordurosa corresponde a um processo grave, pouco frequente na prática clínica, caracterizado pelo aparecimento de petéquias, dificuldade respiratória e alterações neurológicas. Relato de caso. Trata-se de uma mulher adulta jovem, com trauma de tórax fechado e múltiplas fraturas de ossos longos dos membros superiores e inferiores por politraumatismos de alta energia, que foi submetida a redução sob anestesia. Às 48 horas, ela começou a ter dificuldade em respirar, exantema petequial predominantemente sobre a parede torácica anterior e dano neurológico com convulsões tónico-clónicas e bilateral focal, que cedeu com uma medicação anticonvulsivante intra-venosa. Ela foi diagnosticada com síndrome de embolia gordurosa devido a uma história de trauma e às lesões evidenciadas na ressonância magnética. Ela recebeu suporte respiratório e terapia anticoa-gulante, com o qual o quadro clínico melhorou. Discussão. O tecido adiposo entra na circulação quando a pressão no leito da drenagem venosa é superada pela pressão na medula óssea. Os ácidos graxos livres tóxicos causam edema vasogênico e citotóxico, além de hemorragia por destruição celular. Conclusão. É importante considerar a presença dessa complicação em pacientes com múltiplas fraturas e fornecer tratamento oportuno com a intenção de reduzir as sequelas associadas a essa condição

Profilaxia da síndrome de embolia gordurosa: uma análise atual / Prophylaxis of fat embolism syndrome: a current analysis

INTRODUÇÃO: Analisar dados da internet relacionados a mortes por embolia gordurosa, inicio da doença, e outras informações podem determinar a realidade atual no Brasil relacionada à incidência da síndrome de embolia gordurosa e qualquer repercussão na mídia, e também revisar as metodologias de prevenção e quais são os melhores métodos disponíveis para tratar a doença. MÉTODOS: Uma pesquisa no google foi conduzida de Janeiro de 2000 a Janeiro de 2014 utilizando os descritores "cirurgia plástica" e "morte". Foram incluídos e revisados artigos contendo as palavras "embolia", "embolia gordurosa" e "complicações em (ou de) cirurgia plástica". RESULTADOS: Incluiu-se 235 matérias novas relevantes ao longo dos 14 anos. Houve 45 casos de óbito relacionados com cirurgia plástica que ofereceu poucos dados para individualização. Desses pacientes, 44 eram mulheres. As causas possíveis mencionadas foram embolia pulmonar (cinco casos), perfuração das vísceras (cinco casos), hipertermia maligna (três casos), anestesia (dois casos), choque anafilático (dois casos), embolia gordurosa (um caso confirmado), e "outros" (cinco casos). CONCLUSÃO: Diretrizes de prevenção para embolia gordurosa em cirurgia plástica são requeridas, porém, há também necessidade de mais estudos baseados em evidência para entender mais claramente quais são os melhores métodos.

INTRODUCTION: To analyze data from the internet on deaths from fat embolism, time of onset, and other information that could determine current reality in Brazil regarding fat embolism syndrome incidence and any ,media repercussions, and also to review methods of prevention and what are the best methods available to treat this disease. METHODS: A Google search was conducted from January 2000 to January 2014 using the keywords "plastic surgery" and "death." We included and reviewed articles containing the words "embolism", "fat embolism" and "complications in (or of) plastic surgery". RESULTS: We included 235 relevant news stories over the 14 included years. There were 45 cases of death related with plastic surgery that offered few data for individualization. Of these patients, 44 were women. Possible causes mentioned were pulmonary embolism (five cases), perforation of viscera (four cases), malignant hyperthermia (three cases), anesthesia (two cases), anaphylactic shock (two cases), fat embolism (one confirmed case), and "other" (five cases). CONCLUSION: Guidelines to prevent fat embolism in plastic surgery are needed, however, there is also the need of more evidence based studies to understand more clearly what methods are best.

Embolia gordurosa encefálica / Cerebral fat embolism

A embolia gordurosa é constituída pela presença de glóbulos de gordura dentro da microcirculação periférica e pulmonar, com ou sem quadro clínico. Há uma fase precoce, representada por uma obstrução mecânica, e uma fase tardia, representada por um fenômeno inflamatório, que se inicia aproximadamente 48 a 72 horas após a obstrução mecânica. O diagnóstico clínico da síndrome de embolia gordurosa pode ser auxiliado pelos critérios de Gurd-Wilson e deve ser suspeitado em doentes com traumatismo e fraturas de ossos longos e deterioração neurológica de forma inexplicada. É necessário no mínimo um critério maior (insuficiência respiratória, sinais neurológicos não relacionados ao traumatismo craniano e manifestações dermatológicas) e quatro menores ou dois maiores. Exames complementares são geralmente inespecíficos. A tomografia de crânio pode estar normal. A ressonância magnética de encéfalo pode mostrar áreas puntiformes que costumam desaparecer em 20 dias, sugerindo que a lesão pode ser predominantemente inflamatória, e não necrótico-isquêmica. Um tratamento específico para a síndrome de embolia gordurosa não existe. Ele consiste no suporte cardiopulmonar e neurológico, além de prevenção e diagnóstico precoce, auxiliando nos cuidados com o doente.

Fat embolism is constituted by the presence of fat globules in the peripheral microcirculation and lung with or without symptoms. There is an early stage, represented by a mechanical obstruction, and a late phase, represented by an inflammatory process, which begins approximately 48-72 hours after the mechanical obstruction. The clinical diagnosis of the syndrome of fat embolism can be aided by the criteria of Gurd-Wilson, and must be suspected in patients with trauma and long bone fractures and unexplained neurological deterioration. It is necessary at least one major criteria (respiratory failure, neurological signs unrelated to head trauma and skin lesions) and four small or two larger ones. Additional tests are usually nonspecific. CT scan may be normal. MRI may show punctate areas that usually disappear in 20 days, suggesting that the inflammatory lesion may be predominantly necrotic and non-ischemic. Specific treatment for fat embolism syndrome does not exist. It is the neurological and cardiopulmonary support, and prevention and early diagnosis, assisting in patient care.

Uso de corticoide na profilaxia para síndrome de embolia gordurosa em pacientes com fratura de osso longo / The use of corticosteroid for the prophylaxis of fat embolism syndrome in patients with long bone fracture

A reunião de revista "Telemedicina Baseada em Evidência - Cirurgia do Trauma e Emergência" (TBE-CiTE) realizou uma revisão crítica da literatura e selecionou três artigos recentes sobre o uso de corticoide para a profilaxia da síndrome de embolia gordurosa. O foco desta revisão foi a indicação ou não do uso de corticoide nos pacientes admitidos na unidade de terapia intensiva (UTI) com risco de desenvolverem embolia gordurosa pós traumática. O primeiro artigo foi um estudo prospectivo com o objetivo de estabelecer fatores preditivos confiáveis, precoces e úteis associados ao aparecimento da síndrome da embolia gordurosa (SEG) em pacientes traumatizados. O segundo artigo foi uma revisão de literatura sobre o papel do corticoide como medida profilática à síndrome de embolia gordurosa. O último artigo foi uma meta-análise sobre a capacidade do corticoide em reduzir o risco de síndrome da embolia gordurosa nos pacientes com fraturas de ossos longos. As principais conclusões e recomendações foram que pacientes traumatizados devem ser monitorizados na UTI com oximetria de pulso e medida do lactato já que estes fatores podem predizer o aparecimento de SEG e que não existe evidência suficiente para recomendar o uso de corticoide para a profilaxia desta síndrome.

The "Evidence-based Telemedicine - Trauma & Acute Care Surgery" (EBT-TACS) Journal Club conducted a critical review of the literature and selected three recent studies on the use of corticosteroids for the prophylaxis of fat embolism syndrome. The review focused on the potential role of corticosteroids administration to patients admitted to the intensive care unit (ICU) at risk of developing post-traumatic fat embolism. The first study was prospective and aimed at identifying reliable predictors, which occurred early and were associated with the onset of fat embolism syndrome in trauma patients. The second manuscript was a literature review of the role of corticosteroids as a prophylactic measure for fat embolism syndrome (FES). The last manuscript was a meta-analysis on the potential for corticosteroids to prophylactically reduce the risk of fat embolism syndrome in patients with long bone fractures. The main conclusions and recommendations reached were that traumatized patients should be monitored with non-invasive pulse oximetry and lactate levels since these factors may predict the development of FES, and that there is not enough evidence to recommend the use of steroids for the prophylaxis of this syndrome.

Fat embolism in liposuction and intramuscular grafts in rabbits / Embolia gordurosa na lipoaspiração e enxertia intramuscular em coelhos

PURPOSE: To evaluate the effects of fat embolism in organs such as lung and liver. METHODS: Twenty rabbits underwent autologous intramuscular fat grafting in the right thigh after liposuction. The groups were determined according to the postoperative day that occurred in euthanasia: 60, 90 and 120 day. Then, lung and liver were excised and sent to the histopathology laboratory for analysis in search of late injury secondary to a prior event of fat embolism in the tissues. RESULTS: The results showed a change in the macroscopic sample with discoloration of the liver tissue heterogeneously. There were no changes consistent with embolic effect under the microscope. CONCLUSION: The option of performing a technique of fat grafting with a less traumatic surgical procedure can be considered protective against embolic events, with no impact to late embolic events on the tissues.

OBJETIVO: Avaliar a repercussão da embolia gordurosa em órgãos como pulmão e fígado. MÉTODOS: Vinte coelhos foram submetidos à enxertia autóloga intramuscular de gordura em coxa direita após lipoaspiração. Os grupos foram determinados conforme os dias pós-operatórios (DPO) em que ocorreu a eutanásia: 60 DPO, 90DPO, 120 DPO. Em seguida, o pulmão e o fígado foram ressecados e encaminhados ao laboratório de histopatologia para análise em busca de lesão tardia secundária a evento de embolia gordurosa prévia nos tecidos. RESULTADOS: Foi evidenciada uma alteração na amostra a analise macroscópica com alteração da coloração do tecido hepático de forma heterogênea. Não houve alterações compatíveis com repercussão de processo embólico à microscopia. CONCLUSÃO: A opção pela realização de uma técnica de lipoenxertia menos traumática e com pequeno tempo cirúrgico pode ser considerada protetora para eventos embólicos, não havendo repercussão embólica a tardiamente.