Emergently planned exclusive hub-and-spoke system in the epicenter of the first wave of COVID-19 pandemic in Italy: the experience of the largest COVID-19-free ICU hub for time-dependent diseases.

BACKGROUND: Lombardy was the epicenter in Italy of the first wave of COVID-19 pandemic. To face the contagion growth, from March 8 to May 8, 2020, a regional law redesigned the hub-and-spoke system for time-dependent diseases to better allocate resources for COVID-19 patients. METHODS: We report the reorganization of the major hospital in Lombardy during COVID-19 pandemic, including the rearrangement of its ICU beds to face COVID-19 pandemic and fulfill its role as extended hub for time-dependent diseases while preserving transplant activity. To highlight the impact of the emergently planned hub-and-spoke system, all patients admitted to a COVID-19-free ICU hub for trauma, neurosurgical emergencies and stroke during the two-month period were retrospectively collected and compared to 2019 cohort. Regional data on organ procurement was retrieved. Observed-to-expected (OE) in-ICU mortality ratios were computed to test the impact of the pandemic on patients affected by time-dependent diseases. RESULTS: Dynamic changes in ICU resource allocation occurred according to local COVID-19 epidemiology/trends of patients referred for time-dependent diseases. The absolute increase of admissions for trauma, neurosurgical emergencies and stroke was roughly two-fold. Patients referred to the hub were older and characterized by more severe conditions. An increase in crude mortality was observed, though OE ratios for in-ICU mortality were not statistically different when comparing 2020 vs. 2019. An increase in local organ procurement was observed, limiting the debacle of regional transplant activity. CONCLUSIONS: We described the effects of a regional emergently planned hub-and-spoke system for time-dependent diseases settled in the epicenter of COVID-19 pandemic in Italy.

Sodium bicarbonate treatment during transient or sustained lactic acidemia in normoxic and normotensive rats.

INTRODUCTION: Lactic acidosis is a frequent cause of poor outcome in the intensive care settings. We set up an experimental model of lactic acid infusion in normoxic and normotensive rats to investigate the systemic effects of lactic acidemia per se without the confounding factor of an underlying organic cause of acidosis. METHODOLOGY: Sprague Dawley rats underwent a primed endovenous infusion of L(+) lactic acid during general anesthesia. Normoxic and normotensive animals were then randomized to the following study groups (n = 8 per group): S) sustained infusion of lactic acid, S+B) sustained infusion+sodium bicarbonate, T) transient infusion, T+B transient infusion+sodium bicarbonate. Hemodynamic, respiratory and acid-base parameters were measured over time. Lactate pharmacokinetics and muscle phosphofructokinase enzyme's activity were also measured. PRINCIPAL FINDINGS: Following lactic acid infusion blood lactate rose (P<0.05), pH (P<0.05) and strong ion difference (P<0.05) drop. Some rats developed hemodynamic instability during the primed infusion of lactic acid. In the normoxic and normotensive animals bicarbonate treatment normalized pH during sustained infusion of lactic acid (from 7.22 ± 0.02 to 7.36 ± 0.04, P<0.05) while overshoot to alkalemic values when the infusion was transient (from 7.24 ± 0.01 to 7.53 ± 0.03, P<0.05). When acid load was interrupted bicarbonate infusion affected lactate wash-out kinetics (P<0.05) so that blood lactate was higher (2.9 ± 1 mmol/l vs. 1.0 ± 0.2, P<0.05, group T vs. T+B respectively). The activity of phosphofructokinase enzyme was correlated with blood pH (R2 = 0.475, P<0.05). CONCLUSIONS: pH decreased with acid infusion and rose with bicarbonate administration but the effects of bicarbonate infusion on pH differed under a persistent or transient acid load. Alkalization affected the rate of lactate disposal during the transient acid load.

Management of mechanical ventilation during laparoscopic surgery.

Laparoscopy is widely used in the surgical treatment of a number of diseases. Its advantages are generally believed to lie on its minimal invasiveness, better cosmetic outcome and shorter length of hospital stay based on surgical expertise and state-of-the-art equipment. Thousands of laparoscopic surgical procedures performed safely prove that mechanical ventilation during anaesthesia for laparoscopy is well tolerated by a vast majority of patients. However, the effects of pneumoperitoneum are particularly relevant to patients with underlying lung disease as well as to the increasing number of patients with higher-than-normal body mass index. Moreover, many surgical procedures are significantly longer in duration when performed with laparoscopic techniques. Taken together, these factors impose special care for the management of mechanical ventilation during laparoscopic surgery. The purpose of the review is to summarise the consequences of pneumoperitoneum on the standard monitoring of mechanical ventilation during anaesthesia and to discuss the rationale of using a protective ventilation strategy during laparoscopic surgery. The consequences of chest wall derangement occurring during pneumoperitoneum on airway pressure and central venous pressure, together with the role of end-tidal-CO2 monitoring are emphasised. Ventilatory and non-ventilatory strategies to protect the lung are discussed.

Static and dynamic components of esophageal and central venous pressure during intra-abdominal hypertension.

OBJECTIVE: To investigate the effects of intra-abdominal hypertension on esophageal and central venous pressure considering values obtained at end-expiration (i.e., in static conditions) and during tidal volume delivery (i.e., in dynamic conditions). DESIGN: Retrospective (pigs) and prospective, randomized, controlled (rats) trial. SETTING: Animal laboratory of a university hospital. SUBJECTS: Six female pigs and 15 Sprague Dawley male rats. INTERVENTIONS: During anesthesia and paralysis, animals' abdomens were inflated with helium. MEASUREMENTS AND MAIN RESULTS: Abdominal pressure was measured by intraperitoneal catheter. In pigs, esophageal pressure and central venous pressure were continuously measured while inflating the abdomen together with hemodynamic assessment. In rats, the abdomen was inflated after the random application of three levels of positive end-expiratory pressure. Data are shown as mean +/- SD. At end-expiration, esophageal pressures were similar before and after abdominal inflation (p = .177). In contrast, the dynamic component significantly rose after intra-abdominal hypertension, from 3.2 +/- 0.7 cm H2O to 10.0 +/- 2.3 cm H2O (p < .001), and was correlated with peritoneal pressure (linear regression, R2 = .708, p < .001). Positive end-expiratory pressure significantly influenced static esophageal pressure during intra-abdominal hypertension (p = .002) but not dynamic pressures. Static central venous pressure rose with intra-abdominal hypertension from 4.1 +/- 1.5 cm H2O to 6.7 +/- 1.8 cm H2O (p = .043), more so the dynamic component (from 2.9 +/- 0.8 cm H2O to 9.3 +/- 3.1 cm H2O, p = .02). Dynamic changes of esophageal pressures correlated with dynamic changes of central venous pressure (linear regression, R2 = .679, p < .001). Mean values of central venous pressure significantly increased with intra-abdominal hypertension from 7.7 +/- 1.5 cm H2O to 12.7 +/- 2.6 cm H2O (p = .006), whereas transmural central venous pressure and intrathoracic blood volume did not change significantly. CONCLUSIONS: Dynamic changes of esophageal pressure occurred during intra-abdominal hypertension, whereas end-expiratory pressure was affected by high positive end-expiratory pressure levels. Provided that central venous pressure changes reflect esophageal pressure, central venous pressure itself cannot be relied on to guide resuscitation in patients with intra-abdominal hypertension, particularly when abdominal pressures are changing over short periods of time.

Lactate as a marker of energy failure in critically ill patients: hypothesis.

Lactate measurement in the critically ill has been traditionally used to stratify patients with poor outcome. However, plasma lactate levels are the result of a finely tuned interplay of factors that affect the balance between its production and its clearance. When the oxygen supply does not match its consumption, organisms such as man who are forced to produce ATP for their integrity adapt in many different ways up to the point when energy failure occurs. Lactate, being part of the adaptive response, may then be used to assess the severity of the supply/demand imbalance. In such a scenario, the time to intervention becomes relevant: early and effective treatment may allow the cell to revert to a normal state, as long as the oxygen machinery (i.e. mitochondria) is intact. Conversely, once the mitochondria are deranged, energy failure occurs even in the presence of normoxia. The lactate increase in critically ill patients may therefore be viewed as an early marker of a potentially reversible state.