Maurizio Chiaranda

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.

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.

How to ventilate brain-injured patients in respiratory failure

It is common knowledge that in brain-injured patients the principal morbidity and mortality are most frequently caused by the primary disease, i.e. cerebral nervous system injury and its neurological consequences [1]. Nevertheless, extracerebral organ dysfunctions are frequent in brain-injured patients, in creasing morbidity and mortality [2, 3]. Among them, the most frequent complication is respiratory dysfunction including pulmonary oedema and pneumonia. It is now clear that there is an entire spectrum of pulmonary abnormalities caused either directly or indirectly by acute brain injury. Although respiratory problems seem to play a relevant role in the clinical management of brain-injured patients, very few studies have investigated respiratory function abnormalities in this category of patients [4].