Síndrome de Lance-Adams depois de parada cardiorrespiratória prolongada: relato de caso

2012 
JUSTIFICATIVA E OBJETIVOS: A sindrome de Lance-Adams (SLA) e caracterizada por mioclonias pos-hipoxicas cronicas, podendo surgir dias, semanas ou meses apos grave lesao isquemica ao sistema nervoso central. Sua incidencia e muito baixa, sendo uma doenca rara, com poucos casos descritos na literatura mundial. O objetivo desse estudo foi relatar um caso de SLA apos parada cardiorrespiratoria, discutindo algumas hipoteses de sua fisiopatologia e terapeutica. RELATO DO CASO: Paciente do sexo feminino, 50 anos, evoluiu com parada cardiorrespiratoria por 30 minutos, durante a recuperacao pos-anestesica, apos submeter-se a gastroplastia redutora. Evoluiu em coma profundo por um mes, ficando em estado vegetativo persistente por quatro meses apresentando mioclonias generalizadas de dificil controle que melhoravam apenas durante o sono. Sua recuperacao neurologica era evidente, escala de coma de Glasgow 11, quando evoluiu a obito por hipertermia de origem central nao responsiva as medicacoes, apos 120 dias de internacao. CONCLUSAO: A SLA ainda possui fisiopatologia desconhecida, as medicacoes atuais podem como no presente caso, nao atenuar os movimentos involuntarios. Com a melhora das manobras de reanimacao cardiorrespiratoria podem ocorrer mais casos de SLA, exigindo maior conhecimento clinico desta doenca. BACKGROUND AND OBJECTIVES: The Lance-Adams syndrome (LAS) is characterized by a chronic myoclonus state after central nervous system hypoxemia that appears days, weeks or months after the insult. Its incidence is very low, being a rare disease, with few cases report in the world-wide literature. The aim of this study is to report a case of LAS after cardiac arrest, discussing some therapeutics hypotheses and physiopathological pathways.CASE REPORT: Female patient, 50 years old, presented a thirty minutes cardiac arrest during post-anesthetic recovery after a successful gastric bypass. Evolved into a deep coma for a month, progressing to vegetative persistent state for four months, during which she presented chronic generalized myoclonus, difficult to control with classical pharmacological agents. His neurological recovery was evident, Glasgow coma score 11 when she evolved to death by central origin hyperthermia unresponsive to medications, after 120 days of hospitalization. CONCLUSION: The Lance-Adams syndrome has yet an unknown pathophysiology mechanism that impairs our clinical approaches. Classical pharmacological agents may be ineffective, as in our case, does not alleviate completely the involuntary movements. With the improvement of cardiopulmonary resuscitation techniques, more cases of LAS should be faced, requiring more clinical knowledge of this disease.
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