To compare the prognostic value of blood lactate concentrations, gastric intramucosal pH, and their combination in patients with severe sepsis. Prospective, noninterventional study. Medical/surgical intensive care unit of a university hospital. The study included 35 consecutive patients (44 to 82 yrs) with severe sepsis as defined by fever or hypothermia (rectal temperature > 38.3 degrees or < 35.5 degrees C), tachycardia (heart rate > 100 beats/min), tachypnea (respiratory rate > 20 breaths/min) or mechanical ventilation, abnormal white blood cell count (> 10 or < 6 x 10(3) cells/mm3), hypotension (systolic arterial pressure < 90 mm Hg), and evidence of organ dysfunction (oliguria or deterioration of mental status). Arterial lactate concentration and intramucosal pH were measured at the time of study entry, and at 4 and 24 hrs later. Hemodynamic data and oxygen-derived variables were determined at the time of study entry and 24 hrs later. Arterial blood and balloon saline gases were also determined to obtain the pH gap (arterial pH-intramucosal pH) and the PCO2 gap (intramural PCO2-PaCO2). Of the 35 patients, 19 survived the intensive care unit stay. At the time of study admission, 23 (66%) patients had an increased lactate concentration (> 2 mEq/L) and 26 (74%) had a low intramucosal pH (< 7.32). Initially, there were no significant differences in blood lactate concentrations between nonsurvivors and survivors (3.2 +/- 1.5 vs. 2.8 +/- 2.3 mEq/L). Lactate concentrations remained high in nonsurvivors and progressively decreased in survivors (4 hrs: 3.3 +/- 1.1 mEq/L in nonsurvivors vs. 2.2 +/- 0.9 mEq/L in survivors [p < .01]; 24 hrs: 3.5 +/- 2.0 mEq/L in nonsurvivors vs. 1.9 +/- 1.1 mEq/L in survivors [p < .05]). Intramucosal pH was lower in the nonsurvivors than in the survivors initially (7.19 +/- 0.15 in nonsurvivors vs. 7.30 +/- 0.14 in survivors [p < .05]), at 4 hrs (7.18 +/- 0.17 in nonsurvivors vs. 7.29 +/- 0.13 in survivors [p = .06]), and at 24 hrs (7.19 +/- 0.31 in nonsurvivors vs. 7.30 +/- 0.17 in survivors [p < .05]). Of the 23 patients with initially high lactate concentrations, 12 (60%) of the 20 patients with low intramucosal pH died, as compared with one (33%) of the three patients with normal intramucosal pH (p = .052). Of the 14 patients with persistently high lactate concentrations at 24 hrs, all nine (100%) patients with low intramucosal pH, but only two (40%) of five patients with normal intramucosal pH died (p < .001). No significant relationship was found between lactate or intramucosal pH and oxygen-derived variables. Intramucosal pH correlated better with gastric intramural PCO2 (r2 = .58) than with arterial bicarbonate or base deficit/excess. Intramural PCO2 was a more specific predictor of mortality than intramucosal pH. When compared with patients with normal lactate concentrations, those patients with high lactate concentrations had a higher pH gap (0.22 +/- 0.22 vs. 0.07 +/- 0.13 [p < .01]) and PCO2 gap [21.0 +/- 33.9 vs. 1.8 +/- 9.8 torr [2.79 +/- 4.5 vs. 0.24 +/- 1.34 kPa]; p < .01). Both lactate concentrations and intramucosal pH represent reliable prognostic indicators in severe sepsis, and their combination improves the prognostic assessment in these patients. Both variables are better prognostic indicators than oxygen-derived variables. Intramural PCO2 appears to be a more specific variable than intramucosal pH, which partially reflects systemic metabolic acidosis. Combined determinations of blood lactate concentrations and intramucosal pH or intramural PCO2 may help to predict outcome from severe sepsis.

We compared retrospectively four similar groups of patients with multiple organ failure (MOF) due to sepsis. All of them were treated initially with conventional therapy, aprotinin as protease inhibitor and vitamin C with allopurinol as possible scavengers of oxygen-free radicals, were also added. After 24 h of no clinical progress, continuous arteriovenous hemofiltration (CAVH), CAVH/dialysis (CAVH/D), and sequential plasmafilter-dialysis with slow continuous hemofiltration (CAVHP/D) were respectively added to groups 2 (n = 14), 3 (n = 6), and 4 (n = 11). Mortality was 87% for group 1, 71% for group 2, 50% for group 3, and 36% for group 4. In the latter we were able to remove possible MOF-inducing mediators from the bloodstream, to give fluids without restriction (even in oliguric patients), and to improve removal of metabolic waste products. It is possible that these extracorporeal supports, associated with conventional therapy, and pharmacologic drugs such as protease inhibitors and possible scavengers of oxygen-free radicals, helped to reduce the mortality rate. We conclude that, although the number of study patients was too small to reach firm conclusions, the good results observed with CAVHP/D suggest clinical trials to assess the efficacy of this technique.

To test the effects of positive expiratory pressure on the leakage of fluid around cuffs of different tracheal tubes, in mechanically ventilated patients and in a benchtop model. Randomized clinical trial and experimental in vitro study. Intensive care unit of a university hospital. Forty patients recovering in the intensive care unit were ventilated in volume-controlled mode. Twenty patients were randomly intubated with Hi-Lo tubes (HL group), whereas the remaining 20 subjects were intubated with SealGuard tubes (SG group). Immediately after intubation and cuff inflation with 30 cm H2O, Evans blue was applied onto the cephalic surface of the tracheal tube cuff. A 5-cm H2O positive expiratory pressure was used during the first 5 hrs of stay, and thereafter it was removed. Bronchoscopy verified whether the dye leaked around the cuff. The experiment lasted 12 hrs. Leakage was also tested in vitro with the same tracheal tubes with incremental level of positive expiratory pressure. At 1 hr, 5 hrs, and thereafter hourly until 12 hrs, bronchoscopy was used to test the presence of dye on the trachea caudal to the cuff. At the fifth hour, two patients of the HL group failed the test. One hour after positive expiratory pressure removal, all subjects in group HL exhibited a dyed lower trachea. On the other hand, one patient in group SG presented a leak at the eighth hour, and at the 12th hour three of them were still sealed. In vitro, the same level of positive expiratory pressure delayed the passage of dye around the cuff; after 30 mins positive expiratory pressure was removed, and in 10 mins all dye leaked only in the Hi-Lo tube. We found that 5 cm H2O positive expiratory pressure was effective in delaying the passage of fluid around the cuffs of tracheal tubes both in vivo and in vitro. The SealGuard tube proved to be more resistant to leakage than Hi-Lo.

During bronchoscopy hypoxemia is commonly found and oxygen supply can be delivered by interfaces fed with high gas flows. Recently, the high-flow nasal cannula (HFNC) has been introduced for oxygen therapy in adults, but they have not been used so far during bronchoscopy in adults. Forty-five patients were randomly assigned to 3 groups receiving oxygen: 40 L/min through a Venturi mask (V40,N=15), nasal cannula (N40,N=15), and 60 L/min through a nasal cannula (N60,N=15) during bronchoscopy. Gas exchange and circulatory variables were sampled before (FiO₂= 0.21), at the end of bronchoscopy (FiO₂= 0.5), and thereafter (V40, FiO₂= 0.35). In 8 healthy volunteers oxygen was randomly delivered according to V40, N40, and N60 settings, and airway pressure was measured. At the end of bronchoscopy, N60 presented higher PaO₂, PaO₂/FiO₂, and SpO₂than V40 and N40 that did not differ between them. In the volunteers (N60) median airway pressure amounted to 3.6 cmH₂O. Under a flow rate of 40 L/min both the Venturi mask and HFNC behaved similarly, but nasal cannula associated with a 60 L/min flow produced the better results, thus indicating its use in mild respiratory dysfunctions.

To evaluate the effectiveness and potential complications of simple thoracostomy, as first described by Deakin, as a method for prehospital treatment of traumatic pneumothorax. Prospective observational study of all severe trauma patients rescued by our Regional Helicopter Emergency Medical Service and treated with on-scene simple thoracostomy, over a period of 25 months, from June 1, 2002 to June 30, 2004. Fifty-five consecutive severely injured patients with suspected pneumothorax and an average Revised Trauma Score of 9.6+/-2.7 underwent field simple thoracostomy. Oxygen saturation significantly improved after the procedure (from 86.4+/-10.2% to 98.5%+/-4.7%, P<0.05). No difference exists in the severity of thoracic lesions between patients with systolic arterial pressure and oxygen saturation below and above or equal to 90. A pneumothorax or a haemopneumothorax was found in 91.5% of the cases and a haemothorax in 5.1%. No cases of major bleeding, lung laceration or pleural infection were recorded. No cases of recurrent tension pneumothorax were observed. Forty (72.7%) patients survived to hospital discharge. Prehospital treatment of traumatic pneumothorax by simple thoracostomy without chest tube insertion is a safe and effective technique.