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Ropivacaine, a recently introduced local anesthetic of the amide family (1), seems to show less toxicity than bupivacaine (2-4). Nevertheless, both neurologic and cardiovascular toxicities are possible. Six cases of ropivacaine-induced convulsions have previously been reported (5-10), of which three cases also showed cardiovascular toxicity. In three cases, total plasma concentrations were measured (Table 1).

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Fluoroquinolones are known to cause rhabdomyolysis. Levofloxacin is a recent fluoroquinolone and its muscular toxicity is not well documented. We describe the case of a 77-year-old female patient, who presented with an acute rhabdomyolysis after treatment with levofloxacin. She had a background of serious cardio-pulmonary disease. She received an oral ambulatory treatment with levofloxacin for pulmonary infection. After 6 days, she presented with severe rhabdomyolysis, resulting in complete anuria with hyperkalaemia, complicated with acute liver cytolysis and respiratory failure. The treatment was a daily repeated haemodialysis. She presented with a fatal myocardial infarction 13 days after admission. The medical history inclines us to strongly suspect levofloxacin as the cause of this severe adverse drug reaction. We also reviewed 27 other suspect cases reported in the database provided by the World Health Organization Collaborating Centre for Drug Monitoring (Uppsala, Sweden). We conclude that rhabdomyolysis can be a rare, severe adverse effect of levofloxacin, as well as the other fluoroquinolones.

Finally, 1) the low mortality (n = 47, ∼8.5%; Table 1) does not compare with the mortality observed in young patients elsewhere (Seattle: 37% [17]; Wuhan: 38% [18]; New York: 76% [19]): our cohort is biased toward young patients with little comorbidities and single-organ failure (median: 62 yr old; range: 54-67); 2) dexmedetomidine presents advantages (U.S. Food and Drug Administration approval, IV preparation, shorter time to steady state cooperative sedation, no contraindication in the setting of acute kidney injury); and 3) patient's care was designed mid-March 2020, that is, before a switch emphasizing noninvasive ventilation. Dr. Quintin holds U.S. Patent 8,03,697, April 22, 2014: Method for treating early severe diffuse acute respiratory distress syndrome. He is a retired anesthesiologist from Service de Santé des Armées (reserve list). Drs. Danguy des Deserts,

The second part of this overview on early severe ARDS delineates the pros and cons of the following: a) controlled mechanical ventilation (CMV: lowered oxygen consumption and perfect patient-to-ventilator synchrony), to be used during acute cardio-ventilatory distress in order to "buy time" and correct circulatory insufficiency and metabolic defects (acidosis, etc.); b) spontaneous ventilation (SV: improved venous return, lowered intrathoracic pressure, absence of muscle atrophy). Given a stabilized early severe ARDS, as soon as the overall clinical situation improves, spontaneous ventilation will be used with the following stringent conditionalities: upfront circulatory optimization, upright positioning, lowered VO 2 , lowered acidotic and hypercapnic drives, sedation without ventilatory depression and without lowered muscular tone, as well as high PEEP (titrated on transpulmonary pressure, or as a second best: "trial"-PEEP) with spontaneous ventilation + pressure support (or newer modes of ventilation). As these propositions require evidence-based demonstration, the reader is reminded that the accepted practice remains, in 2016, controlled mechanical ventilation, muscle relaxation and prone position. Anestezjologia Intensywna Terapia 2016, tom 48, nr 5, 354-366Key words: acute respiratory distress syndrome, ARDS, severe ARDS; acute hypoxic non-hypercapnic respiratory failure; driving pressure; tidal volume, Vt, low tidal volume, ultra-low tidal volume; positive end-expiratory pressure, PEEP; transpulmonary pressure; controlled mechanical ventilation; spontaneous ventilation; spontaneous breathing; pressure support, airway pressure release ventilation; sedation, cooperative sedation; alpha-2 adrenergic agonist, clonidine, dexmedetomidineThe previous chapter overviewed, for residents rotating through the critical care unit (CCU), basic pathophysiology required to analyze early severe acute respiratory distress syndrome (ARDS). An emphasis was placed on spontaneous ventilation both in the setting of the healthy volunteer and of severe ARDS. This chapter will address the pros and cons of controlled mechanical ventilation, with the help of muscle relaxation, as opposed to the putative advantages of spontaneous ventilation. So far, spontaneous ventilation has not achieved evidence-based demonstration: thus, as in part I, conjectures are within [….], following [1]. i. MUSCLE RELAXATiON VERSUS SPONTANEOUS VENTiLATiON?When muscle relaxation is considered, the overall picture appears to be simplified with 48 h of muscle relaxation [2]. A sober interpretation may be considered. a. Muscle relaxationIn severe ARDS (P/F < 120), muscle relaxation [2] lowered the mortality (45 to 31%; difference of −32%; P = 0.04), multiple organ failure (MOF), and barotrauma and led to more ventilator-free days and identical CCU-acquired paresis. Muscle relaxation was hypothesized to minimize excessive transpulmonary pressure, patient-to-ventilator asynchrony [2], ventilator-induced lung injury (VILI), atelectrauma, overdistension,...