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Paroxysmal Sympathetic Hyperactivity Syndrome Caused by Fat Embolism Syndrome

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Paroxysmal Sympathetic Hyperactivity Syndrome Caused by Fat Embolism Syndrome RELATO DE CASO Daniel Agustin Godoy1,2, Jose Orquera3, Alejandro A. Rabinstein4 Síndrome de hiperatividade simpática paroxística causada por síndrome da embolia gordurosa Paroxysmal sympathetic hyperactivity syndrome caused by fat embolism syndrome 1. Unidade de Terapia Neurointensiva, Sanatório RESUMO petéquias hemorrágicas e insuficiência Pasteur - Catamarca, Argentina. respiratória aguda são as características 2. Unidade de Terapia Intensiva, Hospital San A hiperatividade simpática paro- que constituem seu quadro clínico. O Juan Bautista - Catamarca, Argentina. xística representa uma complicação in- 3. Pronto-Socorro, Hospital San Juan Bautista - termo “embolia gordurosa cerebral” é Catamarca, Argentina. comum, com potencial risco à vida, de estabelecido quando predomina o en- 4. Unidade de Terapia Intensiva de Neurociência, lesões cerebrais graves, mais comumente volvimento neurológico. O diagnóstico Mayo Clinic - Rochester, Minnesota, Estados de origem traumática. Seu diagnóstico é clínico, porém achados específicos de Unidos. clínico se baseia na manifestação recor- neuroimagem podem confirmá-lo. As rente de taquicardia, hipertensão, diafo- manifestações neurológicas incluem dife- rese, taquipneia e, às vezes, febre, além de rentes graus de alteração da consciência, posturas distônicas. Os episódios podem défices focais ou convulsões. Seu trata- ser induzidos por estímulos ou ocorrer de mento é de suporte, porém são possíveis forma espontânea. É comum que ocorra desfechos favoráveis, mesmo nos casos subdiagnóstico desta síndrome, e o retar- com apresentação grave. Relatamos dois damento de seu reconhecimento pode casos de hiperatividade simpática paro- aumentar a morbidade e a incapacidade xística após embolia gordurosa cerebral, em longo prazo. Evitar os desencadean- uma associação muito incomum. tes e a farmacoterapia podem ter muito sucesso no controle desta complicação. Descritores: Doenças do sistema A síndrome da embolia gordurosa é uma nervoso autônomo; Disautonomias complicação rara, mas grave, das fratu- primárias; Lesões encefálicas; Embolia ras de ossos longos. Sinais neurológicos, gordurosa INTRODUÇÃO Conflitos de interesse: Nenhum. A hiperatividade simpática paroxística (HSP) é uma complicação que pode Submetido em 17 de outubro de 2017 Aceito em 10 de janeiro de 2018 aumentar a morbidade e a mortalidade de pacientes graves neurológicos, espe- cialmente nos casos em que não é prontamente reconhecida e tratada.(1-5) Carac- Autor correspondente: teriza-se pelo surgimento súbito de sinais e sintomas provocados pelo aumento Daniel Agustín Godoy da descarga simpática. Hipertensão, taquicardia, taquipneia, febre e sudorese Unidade de Terapia Neurointensiva Sanatório Pasteur profusa, assim como posturas distônicas, fazem parte do quadro clínico clás- Chacabuco 675 sico.(1-5) Propuseram-se critérios diagnósticos, embora ainda não tenham sido 4700. Catamarca, Argentina validados.(6) As lesões traumáticas cerebrais graves são as causas mais frequen- E-mail: [email protected] tes de HSP,(4) embora outras lesões neurológicas também possam resultar nesta Editor responsável: Felipe Dal Pizzol complicação.(1,2) Uma causa muito incomum de HSP é a síndrome da embolia DOI: 10.5935/0103-507X.20180035 gordurosa (SEG), que ocorre em razão da passagem maciça de partículas de gordura oriundas da medula óssea para a circulação sistêmica, como resultado Rev Bras Ter Intensiva. 2018;30(2):237-243 Este é um artigo de acesso aberto sob licença CC BY (https://creativecommons.org/licenses/by/4.0/). 238 Godoy DA, Orquera J, Rabinstein AA de fraturas de ossos longos ou ossos pélvicos, ou de proce- dimentos de fixação cirúrgica intramedular.(7-9) Seus sinais clássicos são desconforto respiratório agudo, erupção de petéquias e diversas manifestações neurológicas.(7-9) Quan- do predominam sinais e sintomas neurológicos, a condi- ção é frequentemente referida como embolia gordurosa cerebral.(10-13) Em tais casos, as imagens de ressonância magnética são muito úteis para a confirmação do diag- nóstico.(14,15) No presente artigo, apresentamos dois casos de SEG que se manifestaram com HSP e formulamos uma hipóte- Figura 1 - Imagens do paciente 1 no momento da admissão no pronto-socorro. se para a fisiopatologia desta rara associação clínica. (A) fraturas cominutivas no terço inferior da tíbia e fíbula, perna direita. (B) A tomografia computadorizada revelou imagens hipodensas bilaterais em região RELATOS DE CASO frontal, sem desvio da linha média. Não havia evidência de hemorragia, e as cisternas da base e o sulco permaneciam visíveis. (C) Imagem de ressonância magnética mostrou lesões múltiplas em ambos os hemisférios cerebrais, Caso 1 hipointensas em T1 e hiperintensas em T2 e FLAIR, na substância branca periventricular de ambas as regiões frontoparietais. Homem de 25 anos de idade, saudável, foi trazido ao pronto-socorro com fraturas cominutivas do terço distal C-reativa (PCR) 141mg/L. Observou-se também trombo- da tíbia e fíbula em decorrência de acidente motociclístico citopenia (110.000/mm3). Fez-se o diagnóstico de SEG, (Figura 1A). Quando da admissão ao hospital, encontra- com estabelecimento de terapia de suporte e administra- va-se alerta, coerente, e não tinha qualquer défice motor. ção de metilprednisolona 10mg/kg/dia, por 3 dias. Devido Seus sinais vitais e os demais dados do exame físico eram à estabilidade clínica, 2 dias mais tarde, foram suspensas a normais. Foi admitido ao hospital para ser submetido à sedação e a analgesia para avaliação da condição neurológi- estabilização cirúrgica. Depois de 48 horas de sua admis- ca. Após 10 minutos, observou-se postura espontânea em são, ele desenvolveu confusão mental e agitação, seguidas extensão bilateral, juntamente de assincronia da ventilação por rápido declínio do nível de consciência, que progre- mecânica, taquipneia (46/min), sudorese profusa genera- diu para coma, com postura bilateral em extensão. O pa- lizada, hipertensão arterial (215/112mmHg) e taquicardia ciente se apresentava taquipneico (44/min), taquicardíaco (137/min). Tais manifestações foram recorrentes e leva- (137/min), febril (39,3ºC) e hipertenso (147/101mmHg). ram ao diagnóstico de HSP. Consequentemente, acrescen- A oximetria de pulso era de 92% com ar ambiente. Obser- taram-se ao regime terapêutico propranolol 120mg/dia e varam-se petéquias hemorrágicas na esclera, conjuntiva, morfina 3 mg a cada 4 horas, além de a sedação/analgesia mucosa bucal e porção superior do tórax. Deu-se início ter sido restituída. Dois dias mais tarde, RM do crânio a ressuscitação com fluidos, suplementação de oxigênio, revelou múltiplas pequenas lesões hipointensas em T1 e intubação traqueal e ventilação mecânica, com utilização hiperintensas em T2, e FLAIR em ambos os hemisférios de sedoanalgesia profunda. Uma tomografia computado- cerebrais, sem acentuação com injeção de gadolínio, e com rizada (TC) do crânio revelou múltiplas áreas hipodensas localização na substância branca periventricular de ambas bilaterais em região subcortical frontal, sem desvio da li- as regiões frontoparietais (Figura 1C). nha média. Não se evidenciou qualquer sinal de hemorra- Os episódios de HSP tiveram duração que oscilou en- gia, e as cisternas da base e os sulcos permaneciam visíveis tre 20 e 35 minutos, com frequência de três a quatro vezes (Figura 1B). ao dia, e foram principalmente associados com estímu- A TC do tórax foi normal, exceto quanto a pequenas los como mobilização, banho, aspiração de secreções ou atelectasias basais bilaterais, sem evidências de embolia dor. No oitavo dia na unidade de terapia intensiva (UTI), pulmonar. A ecocardiografia transtorácica revelou ventrí- suspendeu-se o uso de remifentanil e propofol, mudando culos normais, função valvar normal e ausência de forame para dexmedetomidina e mantendo o uso de proprano- oval aberto ou sinais de hipertensão pulmonar. O eletro- lol e morfina nas mesmas doses. Os episódios de descarga encefalograma revelou lentificação difusa sem descargas simpática se tornaram cada vez mais curtos e menos gra- epileptiformes. Os parâmetros laboratoriais se encontra- ves, com frequência não superior a duas vezes por dia. A vam dentro da faixa normal, exceto pela elevação de mar- resposta motora melhorou para localização dos estímulos cadores de inflamação: leucocitose 17.300/mm3 e proteína nociceptivos. Rev Bras Ter Intensiva. 2018;30(2):237-243 Síndrome de hiperatividade simpática paroxística causada por síndrome da embolia gordurosa 239 No 12º dia de UTI, o paciente foi extubado. Depois de 16 dias da admissão, o paciente estava alerta, com resposta motora normal e capaz de comunicar-se com seus fami- liares. As doses de propranolol e morfina foram reduzidas para a metade, sem piora dos episódios de HSP. Depois de 22 dias da admissão, a fratura foi tratada cirurgicamen- te. A evolução pós-operatória decorreu sem complicações. Após 3 dias da cirurgia, o paciente teve alta para o do- micílio, para dar continuidade ambulatorialmente à sua reabilitação. Um ano após o evento, as lesões descritas na RM tinham desaparecido, e os exames neuropsicológicos mostraram leve comprometimento das funções executivas, com alteração da memória de curto e longo prazo. Figura 2 - Imagens na admissão do paciente 2. (A) Fratura fechada no terço Caso 2 inferior da tíbia. (B) Tomografia computadorizada mostrando lesões hipodensas subcorticais nas regiões frontal e parietal esquerda. (C-D) Ressonância magnética revelou múltiplas lesões hiperintensas em T2 localizadas na substância branca Homem com 21 anos de
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