RESUMO
BACKGROUND: Spasm control is essential in the management of tetanus. Benzodiazepines are administered as initial treatment of tetanic spasms; however, sedation may be difficult to attain among patients with methamphetamine use disorder. Neuromuscular blocking agents, which act on an entire different mechanism, can be given to induce paralysis. METHODS: We describe 2 cases of patients with methamphetamine use disorder who were diagnosed with severe tetanus and our experience in the use of rocuronium to control their spasms. We performed a systematic review of the SCOPUS and PubMed databases for case reports and case series describing the use of rocuronium in tetanus patients who also have methamphetamine use disorder. We discussed the clinical features and treatment outcomes. RESULTS: A total of 4 cases of patients with substance abuse disorder who had severe tetanus were reported in the literature, including the current cases. The mean age was 28.8 years; all of them male. Trismus, generalized limb and abdominal rigidity were the most common presentation. Three patients underwent emergency tracheostomy. Rocuronium was given as 0.008mg/kg bolus in 1 patient; 2 patients received an intravenous bolus dose of 0.6mg/kg. Infusion dose ranged from 5 to 10 mcg/kg/min. Spasms were controlled within 24-48 hours after giving rocuronium in 3 out of 4 patients. One patient died from complications of dysautonomia and immobility. CONCLUSION: Rocuronium demonstrates a potential role as neuromuscular blocking agent of choice for patients with chronic methamphetamine use disorder and severe tetanus. Management challenges and complications of severe tetanus were also highlighted in this study.
RESUMO
Wilson disease is a rare genetic disease causing pathologic deposition of copper in the liver, brain, cornea, kidney, and cardiac muscles. Presented are two cases of neurologic Wilson disease with progressive movement disorder and Kayser-Fleischer rings with low serum copper, low ceruloplasmin, and increased 24-hour urine copper against a background of normal transaminases. Cranial imaging revealed symmetric basal ganglia hyperintensities in T2/FLAIR. More often than not, these cases go unnoticed and misdiagnosed because of its rarity and varied presentation. Extensive workup is necessary to confirm the diagnosis. As for management, the earlier the intervention is initiated, the better prognosis would be for recovery. There are several treatment options which should be tailored to every patient with neurologic Wilson disease. Neurologic Wilson disease is considered as a copper toxicity; immediate diagnostic evaluation and early treatment initiation is a must.
La Enfermedad de Wilson es una enfermedad genética rara provocada por un depósito patológico de cobre en el hígado, cerebro, córnea, riñón y músculo cardíaco. Se presentan dos casos de Enfermedad de Wilson neurológica con trastorno progresivo del movimiento y anillos de Kayser-Fleischer con cobre y ceruloplasmina séricos bajos, y aumento de cobre en orina de 24 horas, con transaminasas normales. Las imágenes craneales revelan hiperintensidad simétrica en T2/FLAIR de los ganglios basales. Lo más frecuente es que estos casos pasen inadvertidos o no se realice el diagnóstico correcto debido a la rareza y variedad de sus presentaciones. Se require de un completo trabajo para poder precisar el diagnóstico. Respecto al manejo, cuanto antes se inicie la intervención, mejor será el pronóstico para la recuperación. Existen diversas opciones terapéuticas y deben adaptarse a cada paciente con Enfermedad de Wilson neurológica. La Enfermedad de Wilson neurológica se considera una toxicidad al cobre, por lo que es una necesidad la evaluación diagnóstica inmediata y el tratamiento precoz.
La maladie de Wilson est une maladie génétique rare qui provoque un dépôt de cuivre pathologique dans le foie, le cerveau, la cornée, le rein et le muscle cardiaque. Nous présentons deux cas de maladie de Wilson dans sa forme neurologique avec un trouble kinétique progressif et des anneaux de Kayser-Fleischer, avec une hypocuprémie, une hypocéruloplasminémie et une hypercuprurie des 24 h, les transaminases étant normales. L'IRM cérébrale montre des hypersignaux symétriques en FLAIR et T2 des ganglions de la base. Le plus souvent ces cas ne sont pas diagnostiqués et passent inaperçus en raison de la rareté et de la présentation variée de la maladie. Un bilan approfondi est nécessaire pour établir le diagnostic. De même que pour la prise en charge, plus tôt le traitement est instauré, meilleur est le pronostic de guérison. Plusieurs options de traitement sont disponibles qui doivent être adaptées à chaque patient atteint de la maladie de Wilson. La maladie de Wilson sous sa forme neurologique est considérée comme une toxicité au cuivre ; elle nécessite une évaluation diagnostique immédiate et un traitement précoce.