Un caso de síndrome de embolia grasa: tratamiento y rehabilitación neurológica y cognitiva / A case report off at embolism syndrome: Treatment and neurological and cognitive rehabilitation

Resumen Se reporta el proceso de recuperación y rehabilitación neurológica y cognitiva de una mujer joven que desarrolló un síndrome de embolia grasa con repercusiones neurológicas, después de sufrir un politraumatismo. La paciente era una mujer de 21 años de edad con fractura cerrada de húmero y fémur izquierdos, que presentó un síndrome de embolia grasa, neumotórax izquierdo e hipertensión pulmonar, en las primeras 24 horas después de un accidente. Estuvo hospitalizada un mes y quedó con varios déficits neurológicos centrales, como infartos 'lacunares' y necrosis cortical laminar occipital, así como limitaciones en la bipedestación, la marcha, la visión y las funciones cognitivas. A partir del primer mes después del alta hospitalaria, se comenzó un proceso integral de rehabilitación neurológica y cognitiva en casa, y posteriormente, en una unidad médica de rehabilitación. Durante los primeros dos años después del accidente, la paciente recibió estimulación sensorial, sensoperceptiva y motora, así como rehabilitación motora y visual intensiva. Una vez se recuperó físicamente, se inició un proceso de rehabilitación neuropsicológica. Seis años después del accidente, la paciente terminó sus estudios universitarios y hoy está laboralmente activa. El proceso de rehabilitación neurológica es complejo, individual y difícil, aunque no imposible, y no se puede estandarizar un patrón de recuperación para todos los pacientes. Si bien existe la recuperación espontánea, la cual se da en los primeros seis meses, el caso aquí reportado demuestra que, en la fase crónica, la recuperación se puede lograr, pero requiere de evaluaciones y técnicas coordinadas de rehabilitación neurológica.

Abstract We report the neurological and cognitive recovery and rehabilitation process in a young woman who developed a fat embolism syndrome with neurological repercussions secondary to multiple trauma. The patient was a 21-year-old woman with a closed fracture of the left humerus and femur. She developed fat embolism syndrome, left pneumothorax and pulmonary hypertension in the first 24 hours after the accident. After one month of hospitalization, the patient had several central neurological deficits such as lacunar infarcts and occipital laminar cortical necrosis, as well as limitations in standing, walking, vision, and cognitive functions. An integral process of neurological and cognitive rehabilitation--first at home and later in a medical rehabilitation unit-- was carried out from the first month after being released from the hospital. During the first two years after the accident, the patient received sensory and motor stimulation, motor rehabilitation, and intensive visual rehabilitation. Once recovered physically, a process of neuropsychological rehabilitation began. Six years after the accident, the patient finished her university studies and she is working actively. The neurological rehabilitation process is complex, individual and difficult, but not impossible, and a recovery pattern cannot be standardized for all patients. Although there is spontaneous recovery, which occurs in the first six months, the case here reported shows that in the chronic phase recovery can be achieved but requires evaluations and coordinated techniques of neurological rehabilitation.

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.

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.

Severe fat embolism in perioperative abdominal liposuction and fat grafting / Embolia gordurosa grave no peroperatório de lipoaspiração abdominal e lipoenxertia

ABSTRACT BACKGROUND AND OBJECTIVES: Fat embolism syndrome may occur in patients suffering from multiple trauma (long bone fractures) or plastic surgery (liposuction), compromising the circulatory, respiratory and/or central nervous systems. This report shows the evolution of severe fat embolism syndrome after liposuction and fat grafting. CASE REPORT: SSS, 42 years old, ASA 1, no risk factors for thrombosis, candidate for abdominal liposuction and breast implant prosthesis. Subjected to balanced general anesthesia with basic monitoring and controlled ventilation. After 45 min of procedure, there was a sudden and gradual decrease of capnometry, severe hypoxemia and hypotension. The patient was immediately monitored for MAP and central catheter, treated with vasopressors, inotropes, and crystalloid infusion, stabilizing her condition. Arterial blood sample showed pH = 7.21; PCO2 = 51 mmHg; PO2 = 52 mmHg; BE = -8; HCO3 = 18 mEq L-1, and lactate = 6.0 mmol L-1. Transthoracic echocardiogram showed PASP = 55 mmHg, hypocontractile VD and LVEF = 60%. Diagnosis of pulmonary embolism. After 24 h of intensive treatment, the patient developed anisocoria and coma (Glasgow coma scale = 3). A brain CT was performed which showed severe cerebral hemispheric ischemia with signs of fat emboli in right middle cerebral artery; transesophageal echocardiography showed a patent foramen ovale. Finally, after 72 h of evolution, the patient progressed to brain death. CONCLUSION: Fat embolism syndrome usually occurs in young people. Treatment is based mainly on the infusion of fluids and vasoactive drugs, mechanical ventilation, and triggering factor correction (early fixation of fractures or suspension of liposuction). The multiorgânico involvement indicates a worse prognosis.

RESUMO JUSTIFICATIVA E OBJETIVOS: A Síndrome da Embolia Gordurosa (SEG) pode acontecer em pacientes vítimas de politrauma (fratura de ossos longos) ou operações plásticas (lipoaspiração), comprometendo circulação, respiração e/ou sistema nervoso central. O presente relato mostra evolução de SEG grave após lipoaspiração e lipoenxertia. RELATO DO CASO: SSS, 42 anos, ASA 1, sem fatores de risco para trombose, candidata a lipoaspiração abdominal e implante de prótese mamária. Submetida à anestesia geral balanceada com monitorização básica e ventilação controlada. Após 45 minutos de procedimento, houve queda súbita e progressiva da capnometria, hipoxemia e hipotensão grave. Imediatamente foi monitorizada com PAM e cateter central, tratada com vasopressores, inotrópicos e infusão de cristaloides, obtendo estabilização do quadro. Amostra sanguínea arterial mostrou pH = 7,21; PCO2 = 51 mmHg; PO2 = 52 mmHg; BE = -8; HCO3 = 18 mEQ/l e lactato = 6,0 mmol/l. Ecocardiograma transtorácico mostrou PSAP = 55 mmHg, VD hipocontrátil e FEVE = 60%. Diagnóstico de embolia pulmonar. Após24 h de tratamento intensivo, a paciente evoluiu com anisocoria e coma com escala de glasgow 3. Realizada TC de encéfalo que evidenciou isquemia cerebral grave, hemisférica, com sinais de êmbolos de gordura em A. cerebral média D; o ecocardiograma transesofágico mostrou forame oval patente. Finalmente, após 72 h de evolução, a paciente evoluiu para morte encefálica. CONCLUSÃO: A SEG ocorre geralmente em jovens. O tratamento baseia-se principalmente na infusão de líquidos e drogas vasoativas, ventilação mecânica e correção do fator desencadeante (fixação precoce de fraturas ou suspensão da lipoaspiração). O comprometimento multiorgânico indica pior prognóstico.

Lipoaspiração e embolia gordurosa: revisão de literatura / Liposuction and fat embolism: a literature review

A cirurgia de lipoaspiração é com alguma frequência relacionada a consequências dramáticas ou fatais, causando grande repercussão no meio médico e principalmente na mídia leiga. Esse fato não deve fazer com que o cirurgião plástico evite essa cirurgia, mas sim estimulá-lo a conhecer profundamente a fisiopatologia inerente ao procedimento, buscando meios embasados de realizá-lo da forma mais segura possível, reduzindo ao máximo os riscos de complicações, principalmente as mais graves. Esse artigo teve o objetivo de realizar uma revisão bibliográfica a respeito especificamente da embolia gordurosa causada pela lipoaspiração, relacionada inúmeras vezes a pós-operatórios dramáticos e fatais. Além disso, ressalta alguns cuidados preventivos para uma maior segurança com esse procedimento.

Liposuction surgery is often associated with severe or fatal consequences, causing great repercussions in the medical field, and especially in the lay media . This should not cause the plastic surgeon to avoid the procedure, but rather should promote deeper knowledge of the basic pathophysiology. All means to accomplish the surgery in the safest possible way should be utilized, to minimize the risk of complications, especially the most severe risks. This article reviews the literature on liposuction-induced fat embolism, which is often associated with severe complications in the postoperative period, and even fatal outcomes. In addition, this study highlights several preventive measures that can be adopted to ensure greater safety of this procedure.

Pulmonary hemorrhagic infarction due to fat embolism and thromboembolism after maxillofacial plastic surgery: a rare case report / 法医学杂志

Pulmonary fat embolism (PFE) and pulmonary thromboembolism (PTE) are common post-operative complications of orthopedic surgical procedures, but are reported less often following maxillofacial plastic surgical procedures, especially with respect to PFE. Thrombi, or together with fat emboli in pulmonary vessels can induce hemorrhagic infarction and cause death. Herein this report introduced a death due to pulmonary hemorrhagic infarction following maxillofacial plastic surgery. The female patient underwent several osteotomies of the mandible, zygomas and autologous bone grafting within a single operation. The operative time was longer than normal and no preventive strategies for pulmonary embolism were implemented. The patient died 20 days after hospital discharge. The autopsy confirmed pulmonary hemorrhagic infarction. The fat emboli and thrombi were also noted in the pulmonary vessels, which were thought to have resulted from the maxillofacial osteotomy. Suggestions were offered to forensic pathologists that risk factors of PFE and PTE, such as the type and length of surgery, the surgical sites, and the preventive strategies, should be considered when handling deaths after maxillofacial operations.

Postoperative hypoxemia due to fat embolism

Although the reported incidence of fat embolism syndrome [FES] is low [approximately 1%], it is likely that microscopic fat emboli are showered during manipulation of long bone fractures. Even though there continues to be debate regarding the etiology and proposed mechanism responsible for FES, significant systemic manifestations may occur. Treatment is generally symptomatic based on the clinical presentations. We report a 10-year-old girl who developed hypoxemia following treatment of a displaced Salter-Harris type II fracture of the distal tibia. The subsequent evaluation and hospital course pointed to fat embolism as the most likely etiology for the hypoxemia. We discuss the etiology for FES, review the proposed pathophysiological mechanisms responsible for its clinical manifestations, present currently accepted diagnostic criteria, and discuss its treatment

Síndrome de embolismo graso: manejo anestésico: a propósito de un caso / Fat embolism syndrome: anesthetic management: a purpose of a case

El síndrome de embolismo graso se produce por las fracturas de los huesos largos. La presentación clásica consiste en un intervalo asintomático seguido de manifestaciones pulmonares y neurológicas, combinadas con hemorragias petequiales. El síndrome sigue un curso clínico bifásico. Los síntomas iniciales son probablemente causados por un mecanismo de oclusión de múmtiples vasos sanguineos por glóbulos rojos que son de demasiado tamaño para pasar a través de los capilares. El otro acontecimiento de la embolia, es que la oclusión vascular del embolismo graso es frecuentemente temporal o incompleta, porque los globulos no obstruyen completamente el flujo de sangre de los capilares por su fluidez y deformidad. El cao que se presenta a continuación es un paciente masculino de 32 años quien posterior a accidente de tránsito presentó fractura de femur derecho, y quien durante la inducción anestésica posterior a la movilización del paciente se desarrollo el embolismo graso, el cual se diagnóstico por los antecedentes del paciente, signos clínicos y hallazgos de laboratorio.

Chest radiographic evolution in fat embolism syndrome.

OBJECTIVE: To characterize the temporal chest radiographic findings of fat embolism syndrome. MATERIAL AND METHOD: Twenty-nine patients with clinically diagnosed fat embolism syndrome between 1988-1999 were retrospectively identified from the Trauma Registry of Haborview Medical Center, University of Washington. In twenty-two patients, complete medical records and serial chest radiographs were available. All images were reviewed by a dedicated thoracic radiologist. RESULTS: Two of 22 patients had normal radiographs throughout hospitalization, while 20/22 developed abnormal chest radiographs. The radiographic findings were consistent with non-specific diffuse pulmonary edema in all abnormal cases. The time to appearance of evident radiographic lung injury was < 24 hours of initial trauma in 10/20 (50%), between 24-48 hours in 4/20 (20%), between 48-72 hours in 5/20 (25%), and 1 patient (1/20, 5%) developed an abnormal chest radiograph after 72 hours. Ten of 20 patients (50%) with abnormal radiographs had complete resolution of the edema pattern within 1 week of development of opacities, 3/20 (15%) cases showed complete radiographic resolution between 1-2 weeks, 2/20 (10%) cases showed complete radiographic resolution between 2-3 weeks, 1/20 (5%) showed complete radiographic resolution between 3-4 weeks, and 4/20 (20%) died without resolution of the radiographic finding. CONCLUSION: The chest radiographic appearance of fat embolism syndrome is non-specific. Normal radiographs can also be seen. Most patients presenting with a normal initial radiograph develop radiographic evident abnormalities within 72 hours of injury and most cases showed radiographic resolution within 2 weeks of hospitalization. Although chest imaging play a little role in the clinical management of fat embolism syndrome, understanding of temporal presentation and evolution of the otherwise non-specific pulmonary opacities may help to avoid unnecessary evaluation in selected patients.

Síndrome de embolia grasa : A propósito de un caso / Fatty clot syndrome : Case report

Las complicaciones en los pacientes politraumatizados con fracturas de huesos son muy variadas. Se presenta a un paciente de sexo femenino con politraumatismo, con fractura de fémur, tibia y peroné, a la que se le realiza un bloqueo epidural para la reducción de sus fracturas utilizándose bupivacaína al 0,5 por ciento más fentanilo. A los 75 minutos del intraoperatorio la paciente en forma súbita comienza con disnea, taquipnea, taquicardia, hipotensión e hipoxemia acompañada por posterior deterioro del sensorio. Se procede a soporte ventilatorio con oxígeno al 100 por ciento y máscara, para luego trasladarla a la unidad de cuidados intensivos donde se le diagnostica, mediante elementos clínicos y pruebas de laboratorio, síndrome de embolia grasa seguido de falla multiorgánica.

Etiopatogenia de la necrosis avascular: importancia en reumatología / Avascular necrosis etiopathogenesis: rheumatology importance

La necrosis avascular (NA) es un problema importante que enfrenta el reumatólogo con mayor frecuencia. Su impacto es mayor en población joven con trascendentes implicaciones sociales y económicas. En la actualidad, quizás la mejor estrategia para disminuir esta patología es la prevención de los factores de riesgo. En este trabajo se presentan los conceptos etiopatogénicos más relevantes para lograr un mejor conocimiento que lleve a la prevención y manejo racional por parte del reumatólogo