Year in review in intensive care medicine, 2004. I. Respiratory failure, infection, and sepsis

Measurement of lung volume has always been a concern in patients receiving mechanical ventilation (MV), and complex methods have been proposed for clinical investigation. Patroniti et al. [1] described a simplified helium dilution technique to measure end-expiratory lung volume and compared it to computed tomography (CT) in 21 MV patients. The authors specifically studied the accuracy and precision of the method. A simple rebreathing gas was used to deliver at least ten usual tidal volumes. The agreement between the two methods was found very acceptable for clinical purposes. It was noted, however, that the higher the amount of hyperinflated tissue, the greater was the underestimation of lung volume by the helium dilution method. It has been well demonstrated that a frequent cause of repeated lung volume loss is endotracheal suctioning. This can induce derecruitment in patients with acute respiratory distress syndrome (ARDS). The effects of such maneuver were tested in ten patients with only mild to moderate lung failure by Fernandez et al. [2]. Three techniques were compared with or without preoxygenation. The authors found that reduction in lung volume during suctioning was similar with the quasiclosed and closed systems but significantly higher with the open system. They also observed that in these patients without severe lung disease these changes were transient and rapidly reversible within 10 min.

Alveolar consolidation is best diagnosed by CT. Lichtenstein et al. [3], continuing their assessment of the usefulness of lung ultrasound examination in the ICU, assessed its value in 65 patients in whom CT had confirmed alveolar consolidation. Only 6 were not diagnosed by ultrasound; conversely, ultrasound was positive in only one of 52 control patients without alveolar consolidation on CT. At least in the author’s hands, this technique seems to constitute a reliable tool for this diagnosis.

Measurement of respiratory mechanics usually describes the respiratory system in terms of elastance, compliance and time constant. In an elegant study, Kondili et al. [4] divided tidal expiration in different phases based on the analysis of expiratory flow-volume curves in ten patients with acute exacerbation of chronic obstructive pulmonary disease (COPD). They showed that the end of expiration is characterized by a lengthening of time constants, and that the addition of external positive end-expiratory pressure decreases resistance at the end of expiration and shortens time constants, thus facilitating equilibration between the external pressure and the alveolar pressure. Although we already knew the effects of external positive end-expiratory pressure in such patients, this new method of exploration sheds new light on its mechanisms. A part of expiratory resistances can be caused by the endotracheal tube itself. In many cases its contribution is not huge. However, more and more studies suggest that over the course of MV the inner diameter of the tube may progressively decrease due to the permanent deposits of secretions. Using the acoustic reflectometry method Boqué et al. [5] prospectively assessed the inner volume reduction of 94 endotracheal tubes, used in 80 patients, and found this reduction to be extremely frequent. In almost one-fourth of the patients the real diameter of the tube was smaller than 7 mm. The clinical implications of such findings may be important, and further studies are needed on this topic.

Intra-abdominal hypertension may have important clinical consequences in terms of both respiratory function and intra-abdominal organs function Its prevalence, however, is not known. It is thus the great merit of this multicenter collaborative 1-day prevalence study by Malbrain et al. [6] in 13 ICUs of six countries to evaluate its frequency in a cohort of 97 patients. Based on a definition of abnormal intra-abdominal pressure of 12 mmHg or higher, its prevalence was 50%, while 8% of the patients had abdominal compartment syndrome with a pressure of 20 mmHg or higher. The only risk factor was the body mass index, while the effects of massive fluid resuscitation and renal and coagulation impairment were at the limit of statistical significance.

Last, intrahospital transport poses an important risk to ICU patients. Continuous monitoring as well as presence of qualified staff and well maintained equipment are probably essential to minimize incidents. The Australian Incident Monitoring Study in Intensive Care received 176 reports describing 191 incidents over a 6-year period [7]. They tried to identify all contributing factors, of which 46% were system-based and the others were human-based. In 31% of the incidents there were significant adverse outcomes. A number of factors were also identified as having prevented or limited harm. These problems are often underestimated or underreported and deserve great attention. An editorial by Shirley and Bion [8] accompanied this paper.

Epidemiological characteristics and outcomes from acute lung injury (ALI) vary across studies. This variability depends on definitions, subpopulations included in studies, comorbidities, and the severity of the disease per se. Brun-Buisson and coworkers [9] studied the current occurrence and causes of ALI and ARDS, the relationships and respective outcome of mild ALI (PaO₂2/FIO₂ between 200 and 300 mmHg) and ARDS (PaO₂/FIO₂ equal to or below 200 mmHg), and the factors associated with survival. A 2-month inception cohort (February–March 1999) of 463 individu