Peri-operative SARS-CoV-2 infection increases postoperative mortality. The aim of this study was to determine the optimal duration of planned delay before surgery in patients who have had SARS-CoV-2 infection. This international, multicentre, prospective cohort study included patients undergoing elective or emergency surgery during October 2020. Surgical patients with pre-operative SARS-CoV-2 infection were compared with those without previous SARS-CoV-2 infection. The primary outcome measure was 30-day postoperative mortality. Logistic regression models were used to calculate adjusted 30-day mortality rates stratified by time from diagnosis of SARS-CoV-2 infection to surgery. Among 140,231 patients (116 countries), 3127 patients (2.2%) had a pre-operative SARS-CoV-2 diagnosis. Adjusted 30-day mortality in patients without SARS-CoV-2 infection was 1.5% (95%CI 1.4-1.5). In patients with a pre-operative SARS-CoV-2 diagnosis, mortality was increased in patients having surgery within 0-2 weeks, 3-4 weeks and 5-6 weeks of the diagnosis (odds ratio (95%CI) 4.1 (3.3-4.8), 3.9 (2.6-5.1) and 3.6 (2.0-5.2), respectively). Surgery performed ≥ 7 weeks after SARS-CoV-2 diagnosis was associated with a similar mortality risk to baseline (odds ratio (95%CI) 1.5 (0.9-2.1)). After a ≥ 7 week delay in undertaking surgery following SARS-CoV-2 infection, patients with ongoing symptoms had a higher mortality than patients whose symptoms had resolved or who had been asymptomatic (6.0% (95%CI 3.2-8.7) vs. 2.4% (95%CI 1.4-3.4) vs. 1.3% (95%CI 0.6-2.0), respectively). Where possible, surgery should be delayed for at least 7 weeks following SARS-CoV-2 infection. Patients with ongoing symptoms ≥ 7 weeks from diagnosis may benefit from further delay.
RESUMOO traumatismo cranioencefálico (TCE) é a principal causa de morte e sequela em crianças e adultos jovens nos países industrializados ocidentais. A lesão encefálica definitiva que se estabelece após o TCE é o resultado de mecanismos fisiopatológicos que se iniciam com o acidente e estendem-se por dias ou semanas. As lesões encefálicas no TCE podem ser classificadas em difusas e focais. Esses dois mecanismos costumam associar-se em um mesmo paciente, embora, geralmente exista o predomínio de um tipo. O conhecimento dos mecanismos fisiopatológicos da lesão cerebral no traumatismo cranioencefálico é fundamental para o estabelecimento de medidas terapêuticas clínicas e cirúrgicas. Neste artigo, realizamos uma revisão crítica da literatura sobre os princípios fisiopatológicos da lesão cerebral no paciente com traumatismo cranioencefálico. UNITERMOS FISIOPATOLOGIAA lesão encefálica definitiva que se estabelece após o TCE é o resultado de mecanismos fisiopatológicos que se iniciam com o acidente e se estendem por dias a semanas. Assim, do ponto de vista didático, as lesões cerebrais são classificadas em primárias e secundárias 8 . As lesões primárias são aquelas que ocorrem no momento do trauma. No paciente com ferimentos por projétil de arma de fogo ou arma branca que penetram o crânio, a lesão primária ocorre em virtude do trauma direto ao parênquima encefálico. Por outro lado, nos traumatismos fechados, caracterizados quando não ocorre contato com o conteúdo intracraniano, as lesões primárias podem resultar da movimentação cerebral associada à energia cinética do acidente. Nas lesões decorrentes de forças de aceleração e desaceleração não é necessário o impacto do crânio contra estruturas externas. Como o encéfalo e a caixa craniana possuem densidades diferentes, quando submetidos às mesmas forças inerciais, respondem de forma desigual. Esse descompasso de movimentos pode promover a ruptura de veias cerebrais que desembocam nos seios durais, bem como impacto e laceração do parênquima contra as estruturas rígidas do crânio. Somado a esse mecanismo como a região central do encéfalo é relativamente fixa em virtude da presença do tronco encefálico, as regiões periféricas do cérebro e cerebelo tendem a apresentar maior amplitude de movimento. Essa diferença na amplitude dos movimentos entre a região central e a periférica do encéfalo gera o estiramento de axônios e de vasos sanguíneos cerebrais, o que pode resultar desde uma disfunção temporária até ruptura dessas estruturas 9,10 . As lesões secundárias decorrem de agressões que se iniciam após o momento do acidente, resultantes da interação de fatores intra e extracerebrais, que se somam para inviabilizar a sobrevivência de células encefálicas poupadas pelo trauma inicial. No local do acidente, intercorrências clínicas como hipotensão arterial, hipoglicemia, hipercarbia, hipóxia respiratória, hipóxia anêmica e distúrbios hidroeletrolíticos são os principais fatores de lesão secundária. Posteriormente, são somados outros distúrbios metabólicos e infecciosos sistêmi...
We systematically reviewed the literature concerning the anterior cranial fossa schwannomas to understand their pathogenesis, determine their origin, and standardize the terminology. We performed a MEDLINE, EMBASE, and Science Citation Index Expanded search of the literature; age, gender, clinical presentation, presence or absence of hyposmia, radiological features, and apparent origin were analyzed and tabulated. Cases in a context of neurofibromatosis and nasal schwannomas with intracranial extension were not included. Age varied between 14 and 63 years (mean ¼ 30.9). There were 22 male and 11 female patients. The clinical presentation included seizures (n ¼ 15), headache (n ¼ 16), visual deficits (n ¼ 7), cognitive disturbances (n ¼ 3), and rhinorrhea (n ¼ 1). Hyposmia was present in 14 cases, absent in 13 cases (39.3%), and unreported in five. Homogeneous and heterogeneous contrast enhancement was observed in 14 and 15 cases, respectively. The region of the olfactory groove was the probable site in 96.5%. Olfactory tract could be identified in 39.3%. The most probable origin is the meningeal branches of trigeminal nerve or anterior ethmoidal nerves. Thus, olfactory groove schwannoma would better describe its origin and pathogenesis and should be the term preferentially used to name it.
Results: Overall mortality at 14 days was 22.8%. Models had a high prediction performance, with the best prediction for overall mortality achieved through Naive Bayes (area under the curve = 0.906). The most significant predictors were the GCS at admission and prehospital GCS, age, and pupil reaction. When predicting the length of stay at the intensive care unit, the Conditional Inference Tree model had the best performance (root mean square error = 1.011), with the most important variable across all models being the GCS at scene.Conclusions: Models for early mortality and hospital length of stay using Machine Learning can achieve high performance when based on registry data even in LMICs. These models have the potential to inform treatment decisions and counsel family members.Level of evidence: This observational study provides a level IV evidence on prognosis after TBI.
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