Brain hypoxia can occur after non-traumatic subarachnoid hemorrhage (SAH), even when levels of intracranial pressure (ICP) remain normal. Brain tissue oxygenation (PbtO₂) can be measured as a part of a neurological multimodal neuromonitoring. Low PbtO₂ has been associated with poor neurologic recovery. There is scarce data on the impact of PbtO₂ guided-therapy on patients’ outcome. This single-center cohort study (June 2014–March 2020) included all patients admitted to the ICU after SAH who required multimodal monitoring. Patients with imminent brain death were excluded. Our primary goal was to assess the impact of PbtO₂-guided therapy on neurological outcome. Secondary outcome included the association of brain hypoxia with outcome. Of the 163 patients that underwent ICP monitoring, 62 were monitored with PbtO₂ and 54 (87%) had at least one episode of brain hypoxia. In patients that required treatment based on neuromonitoring strategies, PbtO₂-guided therapy (OR 0.33 [CI 95% 0.12–0.89]) compared to ICP-guided therapy had a protective effect on neurological outcome at 6 months. In this cohort of SAH patients, PbtO₂-guided therapy might be associated with improved long-term neurological outcome, only when compared to ICP-guided therapy.

While sudden loss of perfusion is responsible for ischemia, failure to supply the required amount of oxygen to the tissues is defined as hypoxia. Among several pathological conditions that can impair brain perfusion and oxygenation, cardiocirculatory arrest is characterized by a complete loss of perfusion to the brain, determining a whole brain ischemic-anoxic injury. Differently from other threatening situations of reduced cerebral perfusion, i.e., caused by increased intracranial pressure or circulatory shock, resuscitated patients after a cardiac arrest experience a sudden restoration of cerebral blood flow and are exposed to a massive reperfusion injury, which could significantly alter cellular metabolism. Current evidence suggests that cell populations in the central nervous system might use alternative metabolic pathways to glucose and that neurons may rely on a lactate-centered metabolism. Indeed, lactate does not require adenosine triphosphate (ATP) to be oxidated and it could therefore serve as an alternative substrate in condition of depleted energy reserves, i.e., reperfusion injury, even in presence of adequate tissue oxygen delivery. Lactate enriched solutions were studied in recent years in healthy subjects, acute heart failure, and severe traumatic brain injured patients, showing possible benefits that extend beyond the role as alternative energetic substrates. In this manuscript, we addressed some key aspects of the cellular metabolic derangements occurring after cerebral ischemia-reperfusion injury and examined the possible rationale for the administration of lactate enriched solutions in resuscitated patients after cardiac arrest.

Whether the risk of multidrug-resistant bacteria (MDRB) acquisition in the intensive care unit (ICU) is modified by the COVID-19 crisis is unknown. In this single center case control study, we measured the rate of MDRB acquisition in patients admitted in COVID-19 ICU and compared it with patients admitted in the same ICU for subarachnoid hemorrhage (controls) matched 1:1 on length of ICU stay and mechanical ventilation. All patients were systematically and repeatedly screened for MDRB carriage. We compared the rate of MDRB acquisition in COVID-19 patients and in control using a competing risk analysis. Of note, although we tried to match COVID-19 patients with septic shock patients, we were unable due to the longer stay of COVID-19 patients. Among 72 patients admitted to the COVID-19 ICUs, 33% acquired 31 MDRB during ICU stay. The incidence density of MDRB acquisition was 30/1000 patient days. Antimicrobial therapy and exposure time were associated with higher rate of MDRB acquisition. Among the 72 SAH patients, 21% acquired MDRB, with an incidence density was 18/1000 patient days. The septic patients had more comorbidities and a greater number of previous hospitalizations than the COVID-19 patients. The incidence density of MDRB acquisition was 30/1000 patient days. The association between COVID-19 and MDRB acquisition (compared to control) risk did not reach statistical significance in the multivariable competing risk analysis (sHR 1.71 (CI 95% 0.93–3.21)). Thus, we conclude that, despite strong physical isolation, acquisition rate of MDRB in ICU patients was at least similar during the COVID-19 first wave compared to previous period.

OBJECTIVES: Anemia is common after acute brain injury and can be associated with brain tissue hypoxia. RBC transfusion (RBCT) can improve brain oxygenation; however, predictors of such improvement remain unknown. We aimed to identify the factors associated with PbtO₂ increase (greater than 20% from baseline value) after RBCT, using a generalized mixed model. DESIGN: This is a multicentric retrospective cohort study (2012–2020). SETTING: This study was conducted in three European ICUs of University Hospitals located in Belgium, Switzerland, and Austria. PATIENTS: All patients with acute brain injury who were monitored with brain tissue oxygenation (PbtO₂) catheters and received at least one RBCT. INTERVENTION: Patients received at least one RBCT. PbtO₂ was recorded before, 1 hour, and 2 hours after RBCT. MEASUREMENTS AND MAIN RESULTS: We included 69 patients receiving a total of 109 RBCTs after a median of 9 days (5–13 d) after injury. Baseline hemoglobin (Hb) and PbtO₂ were 7.9 g/dL [7.3–8.7 g/dL] and 21 mm Hg (16–26 mm Hg), respectively; 2 hours after RBCT, the median absolute Hb and PbtO₂ increases from baseline were 1.2 g/dL [0.8–1.8 g/dL] (p = 0.001) and 3 mm Hg (0–6 mm Hg) (p = 0.001). A 20% increase in PbtO₂ after RBCT was observed in 45 transfusions (41%). High heart rate (HR) and low PbtO₂ at baseline were independently associated with a 20% increase in PbtO₂ after RBCT. Baseline PbtO₂ had an area under receiver operator characteristic of 0.73 (95% CI, 0.64–0.83) to predict PbtO₂ increase; a PbtO₂ of 20 mm Hg had a sensitivity of 58% and a specificity of 73% to predict PbtO₂ increase after RBCT. CONCLUSIONS: Lower PbtO₂ values and high HR at baseline could predict a significant increase in brain oxygenation after RBCT.