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A letter to the editor is presented on the delivery of premature girl during veno-venous extracorporeal membrane oxygenation of H1N1 influenza A related acute respiratory failure of the mother.

Aim: The skeletal muscle Cl - channels, the ClC-1 channels, stabilize the resting membrane potential and dampen muscle fibre excitability. This study explored whether ClC-1 inhibition can recover nerve-stimulated force in isolated muscle under conditions of compromised neuromuscular transmission akin to disorders of myasthenia gravis and Lambert-Eaton syndrome., Methods: Nerve-muscle preparations were isolated from rats. Preparations were exposed to pre-or post-synaptic inhibitors (ω-agatoxin, elevated extracellular Mg 2+ , α-bungarotoxin or tubocurarine). The potential of ClC-1 inhibition (9-AC or reduced extracellular Cl - ) to recover nerve-stimulated force under these conditions was assessed., Results: ClC-1 inhibition recovered force in both slow-twitch soleus and fast-twitch EDL muscles exposed to 0.2 µmol/L tubocurarine or 3.5 mmol/L Mg 2+ . Similarly, ClC-1 inhibition recovered force in soleus muscles exposed to α-bungarotoxin or ω-agatoxin. Moreover, the concentrations of tubocurarine and Mg 2+ required for reducing force to 50% rose from 0.14 ± 0.02 µmol/L and 4.2 ± 0.2 mmol/L in control muscles to 0.45 ± 0.03 µmol/L and 4.7 ± 0.3 mmol/L in muscles with 9-AC respectively (P < .05, paired T test). Inhibition of acetylcholinesterase (neostigmine) and inhibition of voltage-gated K + channels (4-AP) relieve symptoms in myasthenia gravis and Lambert-Eaton syndrome, respectively. Neostigmine and 9-AC additively increased the tubocurarine concentration required to reduce nerve-stimulated force to 50% (0.56 ± 0.05 µmol/L with 9-AC and neostigmine) and, similarly, 4-AP and 9-AC additively increased the Mg 2+ concentration required to reduce nerve-stimulated force to 50% (6.5 ± 0.2 mmol/L with 9-AC and 4-AP)., Conclusion: This study shows that ClC-1 inhibition can improve neuromuscular function in pharmacological models of compromised neuromuscular transmission., (© 2021 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.)

Objectives/hypothesis: Perform a systematic literature search to provide an overview of today's literature regarding the different aspects that can cause dysphagia after supracricoid laryngectomy., Study Design: A systematic literature review., Review Methods: The inclusion criteria were laryngeal cancer, supracricoid laryngectomy, and swallowing. Thirty-one qualifying articles were included and analyzed describing swallowing after supracricoid laryngectomy., Results: Included studies examined the incidence of dysphagia and discussed various factors that will or will not contribute to dysphagia after supracricoid laryngectomy, type of reconstruction, swallow training, radiation, arytenoid cartilage resection, extended procedures, and age., Conclusion: A high incidence of dysphagia was reported after supracricoid laryngectomy. However, good recovery rates were observed with low incidence of severe complications. The included studies used different methods and standards to start oral intake, remove the nasogastric feeding tube, and observe swallow function. Homogenous study population and standardized guidelines on how to handle the pre- and postoperative course after supracricoid laryngectomy and how to measure swallow function could improve further research., (© 2015 The American Laryngological, Rhinological and Otological Society, Inc.)