RESUMOA síndrome de enfalopatia posterior reversível é uma síndrome neurológica caracterizada por cefaleias, confusão, alterações visuais e convulsões associada a áreas de edema cerebral identificável em exames de neuroimagem. Os autores relatam o caso de um homem, 33 anos, leucodérmico, com história de alcoolismo e tabagismo crónico, que recorre ao serviço de urgência por epigastralgia em cinturão e vómitos com cerca de seis horas de evolução e cefaleia holocraneana intensa há duas horas. Ao exame objectivo, apresentava tensão arterial de 190/100 mmHg e empastamento no epigastro. Analiticamente, amilase 193 U/L e lipase 934 U/L. Durante a observação no serviço de urgência, apresentou uma crise tónico-clónica generalizada. A ecografia abdominal realizada foi sugestiva de pancreatite, sem sinais de litíase biliar. A tomografia computorizada crânio-encefálica demonstrou hemorragia subaracnoideia e pequena hemorragia cortical frontal direita. A ressonância magnética nuclear crânio-encefálica realizada uma semana após a admissão revelou áreas de hipersinal T2/FLAIR bilaterais e simétricas na substância branca subcortical das regiões parietais e frontais superiores, sugerindo o diagnóstico de síndrome de enfalopatia posterior reversível. Na tomografia computorizada abdominal (10 dias após a admissão) visualizou-se pâncreas espessado, em relação com processo inflamatório e dois pequenos focos hipodensos na parte anterior do corpo, traduzindo pequenos focos de necrose. A investigação de defeitos trombofílicos revelou uma mutação do gene G20210A da protrombina em heterozigotia. O doente teve alta sem sequelas neurológicas, e assintomático. A ressonância magnética nuclear crânio-encefálica de controlo confirmou a reversão das lesões, confirmando o diagnóstico. Palavras-chave: Alcoolismo/complicações; Edema Cerebral; Pancreatite Alcoólica; Síndrome de Enfalopatia Posterior Reversível. ABSTRACTThe posterior reversible encephalopathy syndrome is a neurological syndrome characterized by headache, confusion, visual disturbances and seizures associated with identifiable areas of cerebral edema on imaging studies. The authors report the case of a man, 33 years-old, leukodermic with a history of chronic alcohol and tobacco consumption, who is admitted to the emergency department for epigastric pain radiating to the back and vomiting with about six hours of evolution and an intense holocranial headache for two hours. His physical examination was remarkable for a blood pressure of 190/100 mmHg and tenderness in epigastrium. His analytical results revealed emphasis on amylase 193 U/L and lipase 934 U/L. During the observation in the emergency department, he presented a generalized tonic-clonic seizure. Abdominal ultrasonography was performed and suggestive of pancreatitis without gallstones signals. Head computed tomography showed subarachnoid haemorrhage and a small right frontal cortical haemorrhage. The brain magnetic resonance imaging done one week after admission showed areas of a bilateral and symmetrical T2 / FLAIR hyperinte...

INTRODUÇÃO: No acidente vascular cerebral isquémico agudo, a terapia endovascular indicada na oclusão de grande vaso cerebral suscita preocupações quanto à exposição adicional a radiocontraste. Procuramos caracterizar a evolução renal visando identificar nefropatia induzida por contraste e estudar o impacto da doença renal preexistente.MATERIAL E MÉTODOS: Estudámos retrospetivamente admissões na Unidade de Doenças Cerebrovasculares do Hospital Central do Funchal entre março 2017 e fevereiro 2020 com necessidade de terapia endovascular neste contexto. Obtivemos características demográficas e semiológicas. Registámos creatinina plasmática em três momentos. Apurámos como desfechos: nefropatia induzida por contraste, índices neurofuncionais e óbito intra-hospitalar. Comparamos aqueles com taxa de filtração glomerular estimada (TFGe) < 60 mL/min/1,73 m2 com os restantes.RESULTADOS: Na amostra de 62 casos (32 homens [51,6%], idade 69,6 ± 10,9 [média ± desvio-padrão] anos, National Institutes of Health Stroke Scale [NIHSS] à admissão 15,0 ± 5,9), descrevemos a creatinina plasmática: admissão 0,98 ± 0,23; 48 horas 0,86 ± 0,21; 5º-7º dia 0,87 ± 0,22 mg/dL. Nenhum cumpriu critérios de nefropatia induzida por contraste. Aqueles com TFGe < 60 mL/min/1,73 m2 (16 casos, 25,8%) não diferiram na evolução nefrológica (variação da creatinina plasmática às 48 horas: -0,17 ± 0,13 versus -0,11 ± 0,11 p=0,067) ou neurológica (modified Rankin Scale ? 2: 31,3% versus 23,9% p=0,563; ? NIHSS: -0,94 ± 9,6 versus -2,9 ± 9,0 p=0,479; óbito: 18,8% versus 19,6% p=0,943).CONCLUSÃO: Nesta amostra, não se detetaram casos de nefropatia induzida por contraste. Aqueles com TFGe < 60 mL/min/1,73 m2 pré-procedimento, também não demonstraram pior desfecho.

Neurotoxicity is an unusual iatrogenic effect associated with carbapenems, typically manifested as seizures or hyperactive delirium. We present an 89-year-old female patient with a medical history of hypertension and chronic kidney disease who was admitted for acute tracheobronchitis and anemia related to diverticular disease. As a complication, she developed acute cystitis caused by extended spectrum ß-lactamases producing Klebsiella pneumoniae, so intravenous ertapenem was started. On the second day of antibiotic therapy, the patient manifested visual hallucinations followed by an inattentive and lethargic state suggestive of a hypoactive delirium. An ertapenem-induced neurotoxicity was suspected. Upon substitution by meropenem, the patient improved, and symptom reversal occurred after 72 hours. We present a review of ertapenem-induced hallucinations and address pharmacokinetics aspects namely renal dysfunction and hypoalbuminemia that could potentiate encephalopathy. Although rare, clinicians should be aware of non-seizure ertapenem related neurotoxicity. Ready recognition can lead to rapid improvement and prevent dire outcomes.

Introduction: Tetanus is a vaccine-preventable disease caused by a neurotoxin produced by Clostridium tetani that proliferates in wound sites. Toxin interference with neuromuscular function leads to spasms. Trismus, risus sardonicus and opisthotonus are classic features, but tetanus can begin with subtler symptoms. Case Description: An 80-year-old man presented with dysarthria. His medical history included hypertension and dyslipidaemia. No other neurological compromise was apparent on admission. Cranioencephalic computed tomography suggested pontine and mesencephalic ischaemia and stroke treatment was implemented. Two days later, the patient displayed dysphagia that required nasogastric intubation. The next day, he developed an apparent tonic seizure with respiratory distress refractory to diazepam and phenytoin, which required sedation and invasive mechanical ventilation. Ultimately, he manifested trismus and generalized spasms. Once the diagnosis of tetanus was established, he was given anti-tetanus immunoglobulin, tetanus toxoid vaccine and metronidazole. Magnetic resonance imaging did not reveal any brain injury. During his intensive care stay, he showed cardiovascular instability, developed nosocomial pneumonia, and required prolonged ventilator support and tracheostomy. He gradually improved during a 70-day hospital stay and regained his previous functional status. Discussion: Dysarthria in an older patient with known cerebrovascular risk factors in addition to possible brainstem ischaemia contributed to an incorrect diagnosis of acute ischaemic stroke. Early manifestations of tetanus can mimic focal deficits. The limitations of brainstem computed tomography should be kept in mind. Conclusion: Older patients present a broader range of signs suggesting tetanus, including a higher frequency of bulbar symptoms, on presentation. A careful anamnesis including previous vaccination history is key for identifying high-risk patients and to widen the differential diagnosis to include tetanus.

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