[How to manage hypertension after an ischemic or hemorrhagic stroke?] / Hypertension artérielle après un accident vasculaire cérébral: quelle prise en charge?

The sometimes-divergent results of studies on the management of blood pressure in the acute phase of stroke have not led to strong and generalizable recommendations. Indeed, an individualized approach seems to be necessary. Depending on the etiology of the stroke, the time to introduce blood pressure lowering therapy differs. In hemorrhagic stroke, it is recommended that intensive hypotensive therapy be started immediately aiming a systolic blood pressure of 130-140mmHg, whereas in the management of ischemic stroke, no hypotensive therapy should be introduced within the first 24 hours except if thrombectomy or thrombolysis are performed. No antihypertensive agent has clearly demonstrated superiority over other classes. However, abrupt changes in blood pressure should be avoided.

Les résultats, parfois divergents, des études évaluant la prise en charge de la tension artérielle en phase aiguë d'un accident vasculaire cérébral (AVC) n'ont pas permis d'établir avec certitude les stratégies thérapeutiques optimales. Néanmoins, ces études mettent en évidence des différences majeures selon le type d'AVC. En cas d'AVC hémorragique, il est recommandé de débuter immédiatement un traitement hypotenseur intensif en visant une tension artérielle systolique (TAS) entre 130 et 140 mmHg, alors que, lors de la prise en charge d'un AVC ischémique, aucun traitement hypotenseur ne devrait être instauré, sauf en cas de thrombectomie ou de thrombolyse. Aucun agent antihypertenseur n'a clairement démontré une supériorité sur les autres classes. Il faut toutefois éviter toute variation brutale de la tension artérielle.

Safety of continuous intraoperative vagus nerve neuromonitoring during thyroid surgery.

BACKGROUND: Continuous intraoperative neuromonitoring has successfully demonstrated to predict impending damage to the recurrent laryngeal nerve, by detecting changes in electromyographic recordings. Despite the apparent benefits associated with continuous intraoperative neuromonitoring, its safety is still a debate. The aim of this study was to investigate the electrophysiological impact of continuous intraoperative neuromonitoring on the vagus nerve. METHODS: In this prospective study, the amplitude of the electromyographic wave of the vagus nerve-recurrent laryngeal nerve axis was measured both proximally and distally to the stimulation electrode placed upon the vagus nerve. Electromyographic signal amplitudes were collected at three distinct events during the operation: during the dissection of the vagus nerve, before application of the continuous stimulation electrode onto the vagus nerve and after its removal. RESULTS: In total, 169 vagus nerves were analysed, among 108 included patients undergoing continuous intraoperative neuromonitoring-enhanced endocrine neck surgeries. Electrode application resulted in a significant overall decrease in measured proximo-distal amplitudes of -10.94 µV (95 per cent c.i. -17.06 to -4.82 µV) (P < 0.005), corresponding to a mean(s.d.) decrease of -1.4(5.4) per cent. Before the removal of the electrode, the measured proximo-distal difference in amplitudes was -18.58 µV (95 per cent c.i. -28.31 to -8.86 µV) (P < 0.005), corresponding to a mean(s.d.) decrease of -2.50(9.59) per cent. Seven nerves suffered a loss of amplitude greater than 20 per cent of the baseline measurement. CONCLUSION: In addition to supporting claims that continuous intraoperative neuromonitoring exposes the vagus nerve to injury, this study shows a mild electrophysiological impact of continuous intraoperative neuromonitoring electrode placement on the vagus nerve-recurrent laryngeal nerve axis. However, the small observed differences are negligible and were not associated with a clinically relevant outcome, making continuous intraoperative neuromonitoring a safe adjunct in selected thyroid surgeries.

Improving safety of unfractionated heparin: a retrospective, quasi-experimental, observational study of the impact of a pocket card and a computerised prescription aid tool in the University Hospitals of Geneva.

BACKGROUND: Despite the rapid rise of direct oral anticoagulants, unfractionated heparin (UFH) remains the mainstay anticoagulant in specific situations such as severe renal failure, perioperative setting or in critical care units. However, its titration is often challenging. OBJECTIVES: To investigate the effect of a pocket card and a computerised prescription aid tool (CPAT) on the quality of UFH anticoagulation. DESIGN: Monocentric retrospective, quasi-experimental, observational study. SETTING: Inpatient primary care centre between 1 January 2016 and 31 December 2019. PARTICIPANTS: >18 years-old treated with therapeutic UFH for more than 24 hours. There were 819 and 1169 anticoagulation episodes before and after intervention, respectively. INTERVENTION: In October 2017, we implemented a pocket card with evidence-based recommendation for therapeutic UFH initiation, monitoring and dosing adaptation. In October 2019, we implemented a CPAT in a group subset. PRIMARY AND SECONDARY OUTCOMES: The primary outcome was the time needed to reach a therapeutic anti-Xa before and after the implementation of the pocket card. The secondary outcomes included a subgroup analysis assessing the effect of the CPAT. Other secondary outcomes were the anti-Xa status (infratherapeutic, therapeutic or supratherapeutic) at 7 and 24 hours of UFH treatment. RESULTS: We found a significant increase in the time to reach therapeutic dosing with pocket card-guided recommendations implementation (10.1 vs 14 hours, HR of 0.8, 95% CI: 0.70 to 0.93). However, the CPAT was associated with a significant decrease in the time needed to reach the therapeutic range (13.9 vs 7.1 hours, HR of 1.74, 95% CI: 1.17 to 2.60). CONCLUSION: Although we observed an increase in time to reach therapeutic anti-Xa with the pocket card, possibly due to a selection bias (use of activated partial thromboplastin time for monitoring before the pocket card), the implementation of CPAT significantly decreased the delay for effective therapy. Further studies are needed to confirm these findings, and to determine the optimal initial dose of UFH anticoagulation.

Hv1 proton channels differentially regulate the pH of neutrophil and macrophage phagosomes by sustaining the production of phagosomal ROS that inhibit the delivery of vacuolar ATPases.

Production of ROS and maintenance of an appropriate pH within the lumen of neutrophil and macrophage phagosomes are important for an effective immune response. Hv1 proton channels sustain ROS production at the plasma membrane, but their role in phagosomes is not known. Here, we tested whether Hv1 channels regulate the pHp and sustain phagosomal ROS production in neutrophils and macrophages. The presence of Hv1 channels on phagosomes of human neutrophils and mouse macrophages was confirmed by Western blot and immunostaining. Phagosomal ROS production, measured with OxyBurst-coupled targets, was reduced in neutrophils and macrophages isolated from Hv1-deficient mice. Ratiometric imaging of FITC-coupled targets showed that phagosomes acidified more slowly in Hv1-deficient macrophages and transiently alkalinized when the V-ATPase was inhibited. In WT neutrophils, 97% of phagosomes remained neutral 30 min after particle ingestion, whereas 37% of Hv1-deficient phagosomes were alkaline (pH>8.3) and 14% acidic (pH<6.3). The subpopulation of acidic phagosomes was eliminated by V-ATPase inhibition, whereas NOX inhibition caused a rapid acidification, independently of Hv1 expression. Finally, V-ATPase accumulation on phagosomes was inversely correlated to intraphagosomal ROS production in neutrophils. These data indicate that Hvcn1 ablation deregulates neutrophil pHp, leading to alkalinization in phagosomes with residual ROS production or to the early accumulation of V-ATPase on phagosomes that fail to mount an oxidative response. Hv1 channels therefore differentially regulate the pHp in neutrophils and macrophages, sustaining rapid acidification in macrophage phagosomes and maintaining a neutral pH in neutrophil phagosomes.