Predictors of Unexpected Early Reocclusion After Successful Mechanical Thrombectomy in Acute Ischemic Stroke Patients.

Background and Purpose- Sustained successful reperfusion is an important prognostic factor for good clinical outcome in acute ischemic stroke. We aimed to identify the prevalence, clinical impact, and predictors of early reocclusion after initially successful thrombectomies within a prospective cohort. Methods- A total of 711 stroke patients with successful reperfusion (modified Thrombolysis in Cerebral Infarction, 2b/3) followed with magnetic resonance or computed tomographic angiography at 24 to 48 hours were included. Multivariable logistic regression analysis was used to evaluate associated factors and clinical impact. Results are displayed as adjusted odds ratio (aOR) and 95% CI. Improvement in accuracy of additional imaging findings on angiography control runs after the intervention was evaluated by area under the curve. Results- Early reocclusion was observed in 16 of 711 successfully reperfused patients (2.3%; 95% CI, 1.1-3.3; median delay: 20 hours). Suggestive predictors were higher platelets on admission (aOR, 1.01; 95% CI, 1.01-1.02), prestroke functional dependence (aOR, 7.12; 95% CI, 1.49-34.03), and stroke of undetermined or other specified pathogenesis in the TOAST classification (aOR, 7.19; 95% CI, 1.10-47.05 and aOR, 36.50; 95% CI, 4.47-298.11, respectively). When implementing residual embolic fragments or stenosis at the thrombectomy site into the logistic regression model, discrimination between patients with and without reocclusion improved significantly (area under the curve, 0.955 versus 0.854; P=0.023). Early reocclusion was an independent predictor of unfavorable outcome at 90 days (aOR for modified Rankin Scale ≤2, 0.13; 95% CI, 0.03-0.57). Conclusions- Early reocclusion within 48 hours after successful mechanical thrombectomy is rare but associated with poor outcome. Patients with high platelets on admission and residual embolic fragments or stenosis at the thrombectomy site are at high risk for reocclusion, which may be prevented or corrected after carefully re-evaluating the last angiographic run.

Stroke-heart syndrome: A case report and mini literature review.

Despite the fact that cardiac troponin (cTn) elevation is commonly seen in the acute phase of ischemic stroke, investigating its etiology represents a challenge for healthcare practitioners. Therefore, we describe the case of an 86-year-old woman with dyspnea and cTn-elevation within the first days following acute ischemic stroke and discuss potential differential diagnoses and diagnostic dilemmas.

First Case of Meningoencephalitis and Bacteraemia with Flavobacterium Lindanitolerans.

Purpose: Flavobacterium lindanitolerans is an environmental Gram-negative, non-spore-forming rod which is usually not considered to be a human pathogen. Isolation from human clinical samples has been described only once. We report the first case of meningoencephalitis and bacteraemia with Flavobacterium lindanitolerans. Case description: A 76-year-old female presented with fever, headache, alteration of mental status, marked meningism and dysarthria. A lumbar puncture demonstrated cerebrospinal fluid findings consistent with bacterial meningitis, and a broad-spectrum antibiotic therapy was initiated. Blood and cerebrospinal fluid cultures revealed a growth of Flavobacterium lindanitolerans. Based on antimicrobial susceptibilities testing, antibiotic treatment was changed to levofloxacin, resulting in a remission of the clinical symptoms after 21 days of treatment. Conclusion: Flavobacterium species are extremely rare human pathogens. However, some of them have been reported to cause opportunistic infections. We describe the first case of meningoencephalitis and bacteraemia caused by Flavobacterium lindanitolerans which was effectively treated with levofloxacin for 21 days. LEARNING POINTS: This is the first case of a meningoencephalitis and bacteraemia with Flavobacterium lindanitolerans.Levofloxacin can be given for 21 days as a treatment of F. lindanitolerans.

Clinical Reasoning: A Dizzy Architect.

There is an increasing body of evidence describing an association between anti-Kelch-like protein 11 (KLHL11) encephalitis and various tumors such as seminoma. However, when the diagnosis of neoplasia is uncertain and the clinical syndrome resembles those caused by other etiologies, the possibility of anti-KLHL11 encephalitis may not be obvious during early clinical evaluations. We present the case of a 68-year-old man with clinical features of anti-KLHL11 encephalitis, in whom no clear signs of an active neoplasia could be found. However, a burnt-out germ cell tumor was suspected. This case highlights the importance of having a high clinical suspicion for anti-KLHL11 encephalitis in patients who exhibit symptoms and signs, even in the absence of an active tumor.

Symptomatic and asymptomatic intracranial atherosclerotic stenosis: 3 years' prospective study.

BACKGROUND: Intracranial stenoses can cause TIA/ischaemic stroke. The purpose of this study was to assess vascular risk factors, clinical and imaging findings and outcome in Caucasians with intracranial stenosis under best prevention management. METHODS: In this prospective observational study (from 05/2012, to last follow-up 06/2017) we compared vascular risk factors, imaging findings and long-term outcome in Swiss patients with symptomatic versus asymptomatic intracranial atherosclerotic stenoses on best prevention management. RESULTS: 62 patients were included [35.5% women, median age 68.3 years], 33 (53.2%) with symptomatic intracranial stenoses. Vascular risk factors (p = 0.635) and frequency of anterior circulation stenoses (66.7% vs. 55.2%; p = 0.354) did not differ between symptomatic and asymptomatic patients, but CT/MR-perfusion deficits in the territory of the stenosis (81.8% vs. 51.7%; p = 0.011) were more common in symptomatic patients. Outcome in symptomatic and asymptomatic patients at last follow-up was similar (mRS 0-1:66.7% vs. 75%;adjp = 0.937, mRS adjp-shift = 0.354, survival:100% vs. 96.4%;adjp = 0.979). However, during 59,417 patient follow-up days, symptomatic patients experienced more cerebrovascular events (ischaemic stroke or TIA) [37.5% vs. 7.1%;adjHR 7.58;adjp = 0.012], mainly in the territory of the stenosis [31.3% vs. 3.6%;adjHR 12.69;adjp = 0.019], more vascular events (i.e. ischaemic stroke/TIA/TNA and acute coronary/peripheral vascular events) [62.5% vs. 14.3%;adjHR 6.37;adjp = 0.001]) and more multiple vascular events (p-trend = 0.006; ≥ 2:37.5% vs. 10.7%;adj OR 5.37;adjp = 0.022) than asymptomatic patients. CONCLUSIONS: Despite best prevention management, one in three patients with a symptomatic intracranial stenosis suffered a cerebrovascular event, three in five a vascular event and two in five ≥ 2 vascular events. There is an unmet need for more rigorous and effective preventive strategies in patients with symptomatic intracranial stenoses.

CO(2)-Dependent vasomotor reactivity of cerebral arteries in patients with severe traumatic brain injury: time course and effect of augmentation of cardiac output with dobutamine.

Failing cerebral blood flow (CBF) autoregulation may contribute to cerebral damage after traumatic brain injury (TBI). The purpose of this study was to describe the time course of CO(2)-dependent vasoreactivity, measured as CBF velocity in response to hyperventilation (vasomotor reactivity [VMR] index). We included 13 patients who had had severe TBI, 8 of whom received norepinephrine (NE) based on clinical indication. In these patients, measurements were also performed after dobutamine administration, with a goal of increasing cardiac output by 30%. Blood flow velocity was measured with transcranial Doppler ultrasound in both hemispheres. All patients except one had an abnormal VMR index in at least one hemisphere within the first 24 h after TBI. In those patients who did not receive catecholamines, mean VMR index recovered within the first 48 to 72 h. In contrast, in patients who received NE within the first 48 h period, VMR index did not recover on the second day. Cardiac output and mean CBF velocity increased significantly during dobutamine administration, but VMR index did not change significantly. In conclusion, CO(2) vasomotor reactivity was abnormal in the first 24 h after TBI in most of the patients, but recovered within 48 h in those patients who did not receive NE, in contrast to those eventually receiving the drug. Addition of dobutamine to NE had variable but overall insignificant effects on CO(2) vasomotor reactivity.