Contrast extravasation mimicking intracerebral and intraventricular hemorrhage after intravenous thrombolytic treatment of ischemic stroke: a case report.

BACKGROUND: Although contrast extravasation on follow-up head computed tomography (CT) is frequently visualized after endovascular treatment, this phenomenon is rare after intravenous thrombolytic treatment in patients with acute ischemic stroke (AIS). Here, we report a case of contrast extravasation mimicking intracerebral hemorrhage (ICH) with intraventricular extension after intravenous thrombolytic treatment and computed tomography angiography (CTA). CASE PRESENTATION: A 52-year-old man presented with right-sided hemiparesis and hypoesthesia. Initial non-contrast head CT was negative for intracranial hemorrhage and acute ischemic changes. He received intravenous treatment with tenecteplase 3.8 h after the onset of stroke. CTA of the head and neck was performed at 4.3 h after stroke onset. It showed no stenosis or occlusion of the carotid and major intracranial arteries. At about 1.5 h after CTA, the right-sided hemiparesis deteriorated, accompanied by drowsiness, aphasia, and urinary incontinence. Immediate head CT showed hyperdense lesions with mild space-occupying effect in the left basal ganglia and both lateral ventricles. The hyperdense lesions were reduced in size on follow-up CT after 5 h. Two days later, CT showed that the hyperdense lesions in the lateral ventricles almost completely disappeared and only a small amount remained in the infarcted area. CONCLUSIONS: Contrast extravasation into the brain tissue and lateral ventricles, mimicking ICH with intraventricular extension, could occur after intravenous thrombolytic treatment and CTA in a patient with AIS, which might lead to misdiagnosis and wrong treatment of the patient. The rapid resolution of intracranial hyperdense lesions is key to differentiate contrast extravasation from ICH on serial non-enhanced CT.

Incidence and associated in-hospital mortality of myocardial injury characterised by elevated cardiac troponin in adult patients with traumatic brain injury: protocol for a systematic review and meta-analysis.

INTRODUCTION: Myocardial injury is a relatively common complication of traumatic brain injury (TBI). However, the incidence and clinical impact of myocardial injury characterised by elevated cardiac troponin (cTn) levels after TBI are still poorly known. The objective of our study is to assess the global incidence of myocardial injury characterised by elevated cTn in adult patients with TBI and its association with in-hospital mortality. METHODS AND ANALYSIS: The protocol of our systematic review and meta-analysis is performed in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Protocols guidelines. We will search the Medline, Embase, Cochrane Library, Scopus and Web of Science databases from inception to 1 January 2024, for observational studies in any language that reported the incidence of elevated cTn and/or in-hospital mortality associated with elevated cTn among adult patients with TBI. Two reviewers will independently assess study eligibility, extract the data and assess the risk of bias. ORs and 95% CIs will be used with a random-effects or fixed-effects model according to the estimated heterogeneity among studies assessed by the I2 index. We will perform a quantitative synthesis for the incidence of elevated cTn and in-hospital mortality data. If sufficient data are available, we will perform subgroup analysis and meta-regression to address the heterogeneity. In addition, we will perform a narrative analysis if quantitative synthesis is not appropriate. ETHICS AND DISSEMINATION: Ethics approval was not required for this study. We intend to publish our findings in a high-quality, peer-reviewed journal. PROSPERO REGISTRATION NUMBER: CRD42023454686.

Traumatic subdural hygroma and chronic subdural hematoma: A systematic review and meta-analysis.

Recently, a relationship between traumatic subdural hygroma (SDG) and chronic subdural hematoma (CSDH) has been proposed. However, the role of traumatic SDG in development of CSDH has not been well characterized. This systematic review aimed to estimate the rate of evolution of traumatic SDG to CSDH, and to identify risk factors associated with traumatic SDG evolution to CSDH. We searched MEDLINE, EMBASE, and Cochrane Library databases from inception to May 26, 2021, using the combination of the terms "subdural hygroma" and "chronic subdural hematoma." Using a random-effects model, we calculated a pooled estimate of rate of evolution of traumatic SDG to CSDH. In addition, we conducted a systematic review of studies of risk factors for traumatic SDG evolution to CSDH. Nineteen studies with 1,335 patients met the inclusion criteria for meta-analysis. The pooled estimate of evolution rate was 25.0 % (95 % CI, 19.3 %-30.7 %; I2 = 85.6 %), with significant heterogeneity among studies (P < 0.01). Age ≥ 60 years was associated independently with traumatic SDG evolution to CSDH, after adjustment for study design using multivariate meta-regression. Risk factors associated with evolution of traumatic SDG to CSDH were radiological characteristics such as thicker SDG and higher SDG CT value. The rate of traumatic SDGs evolution to CSDH is approximately 25 %. Patients aged 60 or older with traumatic SDGs are at increased risk of CSDH development. Thicker SDG and higher SDG CT value, are commonly reported risk factors for traumatic SDG evolution to CSDH. However, higher quality studies are needed.