Paolo Severgnini

Protective Mechanical Ventilation during General Anesthesia for Open Abdominal Surgery Improves Postoperative Pulmonary Function

Background:The impact of intraoperative ventilation on postoperative pulmonary complications is not defined. The authors aimed at determining the effectiveness of protective mechanical ventilation during open abdominal surgery on a modified Clinical Pulmonary Infection Score as primary outcome and postoperative pulmonary function. Methods:Prospective randomized, open-label, clinical trial performed in 56 patients scheduled to undergo elective open abdominal surgery lasting more than 2 h. Patients were assigned by envelopes to mechanical ventilation with tidal volume of 9 ml/kg ideal body weight and zero-positive end-expiratory pressure (standard ventilation strategy) or tidal volumes of 7 ml/kg ideal body weight, 10 cm H2O positive end-expiratory pressure, and recruitment maneuvers (protective ventilation strategy). Modified Clinical Pulmonary Infection Score, gas exchange, and pulmonary functional tests were measured preoperatively, as well as at days 1, 3, and 5 after surgery. Results:Patients ventilated protectively showed better pulmonary functional tests up to day 5, fewer alterations on chest x-ray up to day 3 and higher arterial oxygenation in air at days 1, 3, and 5 (mmHg; mean ± SD): 77.1 ± 13.0 versus 64.9 ± 11.3 (P = 0.0006), 80.5 ± 10.1 versus 69.7 ± 9.3 (P = 0.0002), and 82.1 ± 10.7 versus 78.5 ± 21.7 (P = 0.44) respectively. The modified Clinical Pulmonary Infection Score was lower in the protective ventilation strategy at days 1 and 3. The percentage of patients in hospital at day 28 after surgery was not different between groups (7 vs. 15% respectively, P = 0.42). Conclusion:A protective ventilation strategy during abdominal surgery lasting more than 2 h improved respiratory function and reduced the modified Clinical Pulmonary Infection Score without affecting length of hospital stay.

New treatment of acute hypoxemic respiratory failure: Noninvasive pressure support ventilation delivered by helmet: A pilot controlled trial

OBJECTIVE To assess the efficacy of noninvasive pressure support ventilation (NPSV) using a new special helmet as first-line intervention to treat patients with hypoxemic acute respiratory failure (ARF), in comparison to NPSV using standard facial mask. DESIGN AND SETTING Prospective clinical pilot investigation with matched control group in three intensive care units of university hospitals. PATIENTS AND METHODS Thirty-three consecutive patients without chronic obstructive pulmonary disease and with hypoxemic ARF (defined as severe dyspnea at rest, respiratory rate >30 breaths/min, PaO2:FiO2 < 200, and active contraction of the accessory muscles of respiration) were enrolled. Each patient treated with NPSV by helmet was matched with two controls with ARF treated with NPSV via a facial mask, selected by simplified acute physiologic score II, age, PaO2/FiO2, and arterial pH at admission. Primary end points were the improvement of gas exchanges, the need for endotracheal intubation, and the complications related to NPSV. RESULTS The 33 patients and the 66 controls had similar characteristics at baseline. Both groups improved oxygenation after NPSV. Eight patients (24%) in the helmet group and 21 patients (32%) in the facial mask group (p = .3) failed NPSV and were intubated. No patients failed NPSV because of intolerance of the technique in the helmet group in comparison with 8 patients (38%) in the mask group (p = .047). Complications related to the technique (skin necrosis, gastric distension, and eye irritation) were fewer in the helmet group compared with the mask group (no patients vs. 14 patients (21%), p = .002). The helmet allowed the continuous application of NPSV for a longer period of time (p = .05). Length of stay in the intensive care unit, intensive care, and hospital mortality were not different. CONCLUSIONS NPSV by helmet successfully treated hypoxemic ARF, with better tolerance and fewer complications than facial mask NPSV.

Noninvasive positive pressure ventilation using a helmet in patients with acute exacerbation of chronic obstructive pulmonary disease : a feasibility study

BackgroundNoninvasive positive pressure ventilation (NPPV) with a facemask (FM) is effective in patients with acute exacerbation of their chronic obstructive pulmonary disease. Whether it is feasible to treat these patients with NPPV delivered by a helmet is not known. MethodsOver a 4-month period, the authors studied 33 chronic obstructive pulmonary disease patients with acute exacerbation who were admitted to four intensive care units and treated with helmet NPPV. The patients were compared with 33 historical controls treated with FM NPPV, matched for simplified acute physiologic score (SAPS II), age, Paco2, pH, and Pao2:fractional inspired oxygen tension. The primary endpoints were the feasibility of the technique, improvement of gas exchange, and need for intubation. ResultsThe baseline characteristics of the two groups were similar. Ten patients in the helmet group and 14 in the FM group (P = 0.22) were intubated. In the helmet group, no patients were unable to tolerate NPPV, whereas five patients required intubation in the FM group (P = 0.047). After 1 h of treatment, both groups had a significant reduction of Paco2 with improvement of pH; Paco2 decreased less in the helmet group (P = 0.01). On discontinuing support, Paco2 was higher (P = 0.002) and pH lower (P = 0.02) in the helmet group than in the control group. One patient in the helmet group, and 12 in the FM group, developed complications related to NPPV (P < 0.001). Length of intensive care unit stay, intensive care unit, and hospital mortality were similar in both groups. ConclusionsHelmet NPPV is feasible and can be used to treat chronic obstructive pulmonary disease patients with acute exacerbation, but it does not improve carbon dioxide elimination as efficiently as does FM NPPV.

Protective versus Conventional Ventilation for Surgery: A Systematic Review and Individual Patient Data Meta-analysis.

Background:Recent studies show that intraoperative mechanical ventilation using low tidal volumes (VT) can prevent postoperative pulmonary complications (PPCs). The aim of this individual patient data meta-analysis is to evaluate the individual associations between VT size and positive end–expiratory pressure (PEEP) level and occurrence of PPC. Methods:Randomized controlled trials comparing protective ventilation (low VT with or without high levels of PEEP) and conventional ventilation (high VT with low PEEP) in patients undergoing general surgery. The primary outcome was development of PPC. Predefined prognostic factors were tested using multivariate logistic regression. Results:Fifteen randomized controlled trials were included (2,127 patients). There were 97 cases of PPC in 1,118 patients (8.7%) assigned to protective ventilation and 148 cases in 1,009 patients (14.7%) assigned to conventional ventilation (adjusted relative risk, 0.64; 95% CI, 0.46 to 0.88; P < 0.01). There were 85 cases of PPC in 957 patients (8.9%) assigned to ventilation with low VT and high PEEP levels and 63 cases in 525 patients (12%) assigned to ventilation with low VT and low PEEP levels (adjusted relative risk, 0.93; 95% CI, 0.64 to 1.37; P = 0.72). A dose–response relationship was found between the appearance of PPC and VT size (R2 = 0.39) but not between the appearance of PPC and PEEP level (R2 = 0.08). Conclusions:These data support the beneficial effects of ventilation with use of low VT in patients undergoing surgery. Further trials are necessary to define the role of intraoperative higher PEEP to prevent PPC during nonopen abdominal surgery.

Association between driving pressure and development of postoperative pulmonary complications in patients undergoing mechanical ventilation for general anaesthesia: a meta-analysis of individual patient data.

BACKGROUND Protective mechanical ventilation strategies using low tidal volume or high levels of positive end-expiratory pressure (PEEP) improve outcomes for patients who have had surgery. The role of the driving pressure, which is the difference between the plateau pressure and the level of positive end-expiratory pressure is not known. We investigated the association of tidal volume, the level of PEEP, and driving pressure during intraoperative ventilation with the development of postoperative pulmonary complications. METHODS We did a meta-analysis of individual patient data from randomised controlled trials of protective ventilation during general anesthaesia for surgery published up to July 30, 2015. The main outcome was development of postoperative pulmonary complications (postoperative lung injury, pulmonary infection, or barotrauma). FINDINGS We included data from 17 randomised controlled trials, including 2250 patients. Multivariate analysis suggested that driving pressure was associated with the development of postoperative pulmonary complications (odds ratio [OR] for one unit increase of driving pressure 1·16, 95% CI 1·13-1·19; p<0·0001), whereas we detected no association for tidal volume (1·05, 0·98-1·13; p=0·179). PEEP did not have a large enough effect in univariate analysis to warrant inclusion in the multivariate analysis. In a mediator analysis, driving pressure was the only significant mediator of the effects of protective ventilation on development of pulmonary complications (p=0·027). In two studies that compared low with high PEEP during low tidal volume ventilation, an increase in the level of PEEP that resulted in an increase in driving pressure was associated with more postoperative pulmonary complications (OR 3·11, 95% CI 1·39-6·96; p=0·006). INTERPRETATION In patients having surgery, intraoperative high driving pressure and changes in the level of PEEP that result in an increase of driving pressure are associated with more postoperative pulmonary complications. However, a randomised controlled trial comparing ventilation based on driving pressure with usual care is needed to confirm these findings. FUNDING None.

Prognostic Role of Clinical and Laboratory Criteria To Identify Early Ventilator-Associated Pneumonia in Brain Injury*

BACKGROUND We investigated the role of the clinical pulmonary infection score (CPIS), serum levels of procalcitonin (PCT), C-reactive protein (CRP), and serum amyloid A (SAA) in the detection of patients with early ventilator-associated pneumonia (VAP). METHODS Observational study in a university hospital. In 58 patients with severe brain injury receiving mechanical ventilation, CPIS, PCT, CRP and SAA were evaluated at ICU entry and at days 3 to 4 of hospital stay for VAP diagnosis (confirmed by endotracheal aspirate or BAL cultures). RESULTS We found the following: (1) PCT at entry was increased in patients who later had early VAP develop (25 patients) compared to no VAP (median, 1.4 ng/mL; 25-75 percentiles, 0.14-0.78; vs median, 0.2 ng/mL; 25-75 percentiles, 0.76-2.4, p<0.001; sensitivity, 76%; and specificity, 75%); (2) CPIS increased at the day of VAP diagnosis, compared to entry (median, 6.6+/-1.1 vs 1.5+/-1.1, p<0.001; sensitivity, 97%; specificity, 100%), while other serum inflammatory markers did not change; and (3) deterioration in oxygenation and changes in tracheal secretions were the main determinants of CPIS changes. CONCLUSIONS PCT may be a useful marker to predict which patients subsequently have early VAP. The CPIS could help as an early way to detect the patients with early VAP and who need further diagnostic testing.

An integrated approach to prevent and treat respiratory failure in brain-injured patients.

Purpose of review Brain-injured patients are at increased risk of extracerebral organ dysfunction, in particular ventilator-associated pneumonia. The purpose of this review is to discuss functional abnormalities, clinical treatment, and possible prevention of respiratory function abnormalities in brain-injured patients. Recent findings Ventilator-associated pneumonia worsens the neurologic outcome and increases the intensive care unit and hospital stay, costs, and risk of death. The respiratory dysfunction can be due to several causes, but atelectasis and/or consolidation of the lower lobes predominates in the most severe cases. Strategies should be implemented to prevent lung infections and accelerate weaning from mechanical ventilation to reduce the incidence of respiratory dysfunction and ventilator-associated pneumonia. Summary An integrated approach including appropriate ventilatory, antibiotic, and fluid management could be extremely useful, not only to prevent and more rapidly treat respiratory failure but also to improve neurologic outcome and reduce hospital stay. Further studies are warranted to better elucidate the pathophysiology and clinical treatment of respiratory dysfunction in brain-injured patients.

In vitro and in vivo evaluation of a new active heat moisture exchanger

IntroductionIn order to improve the efficiency of heat moisture exchangers (HMEs), new hybrid humidifiers (active HMEs) that add water and heat to HMEs have been developed. In this study we evaluated the efficiency, both in vitro and in vivo, of a new active HME (the Performer; StarMed, Mirandola, Italy) as compared with that of existing HMEs (Hygroster and Hygrobac; Mallinckrodt, Mirandola, Italy).MethodsWe tested the efficiency by measuring the temperature and absolute humidity (AH) in vitro using a test lung ventilated at three levels of minute ventilation (5, 10 and 15 l/min) and at two tidal volumes (0.5 and 1 l), and in vivo in 42 patients with acute lung injury (arterial oxygen tension/fractional inspired oxygen ratio 283 ± 72 mmHg). We also evaluated the efficiency in vivo after 12 hours.ResultsIn vitro, passive Performer and Hygrobac had higher airway temperature and AH (29.2 ± 0.7°C and 29.2 ± 0.5°C, [P < 0.05]; AH: 28.9 ± 1.6 mgH2O/l and 28.1 ± 0.8 mgH2O/l, [P < 0.05]) than did Hygroster (airway temperature: 28.1 ± 0.3°C [P < 0.05]; AH: 27 ± 1.2 mgH2O/l [P < 0.05]). Both devices suffered a loss of efficiency at the highest minute ventilation and tidal volume, and at the lowest minute ventilation. Active Performer had higher airway temperature and AH (31.9 ± 0.3°C and 34.3 ± 0.6 mgH2O/l; [P < 0.05]) than did Hygrobac and Hygroster, and was not influenced by minute ventilation or tidal volume. In vivo, the efficiency of passive Performer was similar to that of Hygrobac but better than Hygroster, whereas Active Performer was better than both. The active Performer exhibited good efficiency when used for up to 12 hours in vivo.ConclusionThis study showed that active Performer may provide adequate conditioning of inspired gases, both as a passive and as an active device.

Impact of mechanical ventilation and fluid load on pulmonary glycosaminoglycans.

The combined effect of mechanical ventilation and fluid load on pulmonary glycasaminoglycans (GAGs) was studied in anaesthetized rats ((BW 290±21.8 (SE)g) mechanically ventilated for 4h: (a) at low (∼7.5mlkg(-1)) or high (∼23mlkg(-1)) tidal volume (V(T)) and zero alveolar pressure; (b) at low or high V(T) at 5cmH(2)O positive end-expiratory pressure (PEEP); (c) with or without 7mlkg(-1)h(-1) intravenous infusion of Phosphate Buffer Solution (PBS). Compared to spontaneous breathing, GAGs extractability decreased by 52.1±1.5% and 42.2±7.3% in not-infused lungs mechanically ventilated at low V(T) or at high V(T) and PEEP, respectively. In contrast, in infused lungs, GAGs extractability increased by 56.1±4.0% in spontaneous ventilation and PEEP and up to 81.1% in all mechanically ventilated lungs, except at low V(T) without PEEP. In the absence of an inflammatory process, these results suggest that PEEP was protective at low but not at high V(T) when alveolar structures experience exceedingly high stresses. When combined to mechanical ventilation, fluid load might exacerbate edema development and lung injury.

Impact of respiratory pattern on lung mechanics and interstitial proteoglycans in spontaneously breathing anaesthetized healthy rats.

Aim:  The aim of this study was to investigate the effect of different pattern of spontaneous breathing on the respiratory mechanics and on the integrity of the pulmonary extracellular matrix.