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Sacha et al (1) showed that vasopressin was utilized in 42.6% of acute kidney injury (AKI) before and increased to 54.6 % after rebranding, which seems to be high despite the cost increase. We reviewed potential justifications for the vasopressin increased use in AKI during septic shock (SS) after rebranding (2). Just after rebranding in 2016, Gordon et al (2) reported the results of the multicenter trial Vasopressin vs Norepinephrine as Initial Therapy in Septic Shock (VANISH), which compared the effect of these two vasopressors on AKI in adult patients with SS. Rationale for this study was the landmark Vasopressin and Septic Shock Trial (VASST), done in 2014 before rebranding. This study found an association between low-dose vasopressin (0.01-0.03 U/min) and decreased mortality in less severe SS but no difference between vasopressin and norepinephrine on global mortality or organ dysfunction rates (3). Post hoc analysis of the VASST study suggested that vasopressin treatment is associated with reduced progression to AKI, decreased need for renal replacement therapy (RRT), and reduced mortality in SS patients at risk of AKI (4). This concurred with earlier small clinical studies, demonstrating improvement in creatinine clearance (CCL) in vasopressin-treated patients (4). In the VANISH study, there were fewer RRTs in the vasopressin group (2).Unfortunately, the VANISH study did not find a difference in the number of kidney failure-free days in surviving patients receiving vasopressin or norepinephrine (2). The reduction in the number of RRTs in the vasopressin group but without any difference in the number of kidney failure-free days in survivors between groups had procured only some meager scientific solace (4). Many meta-analyses, however, did not reveal any significant improvements with vasopressin regarding AKI (4). Since rebranding, only one study has shown a favorable effect of vasopressin on AKI risk in sepsis. This was a study performed in an ovine model of sepsis by Okazaki et al (5). This study showed that vasopressin infusion did not significantly affect renal medullary perfusion or Po 2 and induced a sustained (6 hr) ~2.5-fold increase in CCL (5). Vasopressin reduced sepsis-induced mesenteric hyperemia (+61 ± 13 to +9% ± 6%) (5). Norepinephrine transiently (2 hr) improved CCL (by ~3.5-fold) but worsened renal medullary ischemia (to -64% ± 7%) and hypoxia (to -71% ± 6%) (5). Therefore, clearly, low-dose vasopressin (0.03 international units [IU]/min [0.03-0.05 IU/min]) as first vasopressor

L ee et al (1) addressed hyperbaric oxygenation (HBO 2 ) treatment for carbon monoxide (CO) poisoning in their recent study, concluding that early treatment improved neurocognitive prognosis at 6 months. However, they stated that no other current therapy could be expected to prevent cognitive sequelae due to cellular injuries sustained during CO exposure (1). Though we do not dispute the role of early HBO 2 therapy in CO intoxication (1), its use remains controversial as evidence for efficacy is sparse, as confirmed by the authors themselves (1, 2). Side effects derived from oxygen toxicity may play a role (2).A number of alternative (or possibly adjuvant) therapies have been described (2). A study by Feldman et al (3) described a combined therapy of HBO 2 with therapeutic hypothermia with a successful result. Neurologic sequelae were mitigated by initial intravascular cooling and subsequent HBO 2 treatment, whereas hypothermia was sustained by using ice bags inside the chamber (3). Potent anti-inflammatory steroids such as dexamethasone may limit severe inflammation in the case of CO poisoning (4). A patient with a case of CO poisoning was revived by a series of 3 HBO 2 sessions and steroid treatment from a semicoma state, without signs or symptoms of cognitive sequelae (4). Erythropoietin, a glycoprotein hormone that produces RBCs, may a have a protective role to play (5). In hypoxic states such as stroke, erythropoietin may protect neuronal cells by reducing S100B, limiting neurologic sequelae (5). Erythropoietin has been demonstrated to ameliorate cardiac complications because of CO poisoning (5), and similarly, neuronal damage was prevented by erythropoietin (5). In conclusion, it seems likely that early HBO 2 therapy alone may not suffice. In the light of the evidence described above (2-5), a new critical care neuroprotection therapy bundle for CO poisoning seems timely. Further studies, based on this new bundle, could be the next step to reduce dramatically the cognitive sequelae associated with severe CO intoxication. ACKNOWLEDGMENTWe thank Prof. David De Bels for his contribution.