This is the first prospective study assessing the release over time of HMGB1 in a population of patients with sepsis, severe sepsis, or septic shock. Levels remained high in the majority of patients up to 1 wk after admittance, indicating that the cytokine indeed is a downstream and late mediator of inflammation. Further studies are required to fully define the relationship of HMGB1 to severity of disease.

This is the first study assessing systemic levels of resistin in patients with septic shock/severe sepsis. We show that resistin is a marker of severity of disease and possibly a mediator of the prolonged inflammatory state seen in infected critically ill patients. Further exploration of resistin as a therapeutic target and marker of disease is merited.

Thirteen patients with healthy hearts and lungs, and with a mean age of 68 years, who were scheduled for lower abdominal surgery during isoflurane anaesthesia with muscular paralysis, were investigated with arterial blood gases, spirometry, pulmonary x-ray and computed tomography (CT) of the chest before and during anaesthesia, as well as during the first 4 postoperative days. Before anaesthesia, lung function and gas exchange were normal in all patients. Pulmonary x-ray and CT scans of the lungs were also normal. During anaesthesia, 6 of 13 patients developed atelectasis (mean 1.0% of intrathoracic transverse area in all patients). Two hours postoperatively, 11 of 13 patients had atelectasis and the mean atelectatic area was 1.8%. Pao2 was significantly reduced by 2.1 kPa to 9.8 kPa. On the first postoperative day, the mean atelectasis was unaltered (1.8%). None of the atelectasis found on CT scanning could be detected on standard pulmonary x-ray. Forced vital capacity (FVC) and forced expired volume in 1 s (FEV1) were significantly decreased to 2/3 of preoperative level. Pao2 was significantly reduced to less than 80% of the preoperative level (mean 9.4 kPa). There were significant correlations between the atelectatic area and the impairment in FVC, FEV1, and Pao2. Spirometry and blood gases improved during the succeeding postoperative days, and atelectasis decreased. No patient suffered from pulmonary complications, as judged from clinical criteria and pulmonary x-ray, in contrast to the findings of atelectasis in 85% of the patients by computed tomography.

Pulmonary gas exchange and the development of atelectasis were studied in eight essentially lung-healthy patients, awake and during halothane anaesthesia with mechanical ventilation. Gas exchange was evaluated by a multiple inert-gas elimination technique and conventional blood-gas analysis, and atelectasis was studied by computerized tomography (CT). Ventilation and lung perfusion were well matched in the majority of the patients when awake. In two patients there was low perfusion of poorly ventilated regions (low VA/Q). One patient had a shunt corresponding to 4% of cardiac output. None of the patients showed signs of atelectasis on the CT scans. After 15 min of anaesthesia, shunt had appeared in all patients, ranging from 1% in two patients (unchanged from the awake state) to 17%. The major VA/Q mode was widened and ventilation of poorly perfused regions (high VA/Q) was noted in seven patients. Densities in dependent lung regions (interpreted as atelectasis) were seen on the CT scans in six patients. The extent of atelectasis was significantly correlated both to the magnitude of shunt (r = 0.93, P less than 0.01) and to the impairment of arterial oxygenation (r = 0.99, P less than 0.001). The findings indicate that atelectasis in dependent lung regions during halothane anaesthesia creates shunting of blood flow and that atelectasis is the major or sole cause of impaired gas exchange in the lung-healthy, anaesthetized subject.

Transverse sections of lung tissue were studied in patients by computerized tomography during anaesthesia and in the postoperative period. Eight patients were studied during intravenous (thiopentone) and six during inhalational (halothane) anaesthesia. The latter patients were studied during both spontaneous and mechanical ventilation. Five of the patients who underwent surgery for inguinal hernia and five patients in whom laparotomy was performed were studied 1 h and 24 h postoperatively. No patient showed any lung changes while awake preoperatively, and all patients developed dependent, crest-shaped lung densities within 5-10 min of anaesthesia. The densities comprised 3.4% of the lung volume in the caudal (basal) 5 cm of the lung tissue. No significant differences in the size and distribution of the densities were noted between spontaneous breathing and mechanical ventilation during anaesthesia, or between intravenous and inhalational anaesthesia. The densities remained in nine of ten patients 1 h postoperatively, and they remained in five of ten patients 24 h after anaesthesia. The densities are considered to be compression atelectases which may develop as a result of relaxation of the diaphragm. They may be important contributors to postoperative pulmonary complications.

We aimed to describe the frequency of atelectasis occurring during anaesthesia, to describe the size and pattern of the atelectasis, and to standardise the method of identifying the atelectasis and calculate its area. Material and Methods: Patients (n= 109) scheduled for elective abdominal surgery were examined with CT of the thorax during anaesthesia. Results: In 95 patients (87%) dependent pulmonary densities were seen, interpreted as atelectasis. Two different types of atelectasis were foundhomogeneous (78%) and non-homogeneous (9%). Attenuation values in histograms of the lung and atelectasis were studied using 2 methods of calculating the atelectatic area. Conclusion: On the basis of the present findings, we defined atelectasis as pulmonary dependent densities with attenuation values of-100 to + 100 HU.

The extent of atelectasis was correlated to constitutional factors in 38 patients who underwent computed tomography prior to and during general anaesthesia with halothane. All patients but two developed atelectasis in dependent regions of both lungs immediately after induction of anaesthesia prior to surgery. The transverse area of the densities ranged from 0 to 27 cm2, and there were no significant differences between patients of different age or sex, or with different smoking habits. A significant linear regression was found between Broca's index weight (kg)/height (cm)-100 and the area of the densities, and also between an index describing the shape of the thorax and the density area. Thus, patients who were overweight and/or had a low and wide thorax tended to develop more extensive atelectasis during anaesthesia. This finding might partly explain why overweight patients develop postoperative pulmonary complications more often than non-obese patients.

We have studied the effects of anaesthesia on atelectasis formation and gas exchange in 45 patients of both sexes, smokers and nonsmokers, aged 23-69 yr. None of the patients showed clinical signs of pulmonary disease, and preoperative spirometry was normal. In the awake patient, partial pressure of arterial oxygen (Pa 0 J decreased with increasing age (P < 0.001) and the alveolar-arterial oxygen partial pressure difference (PA 02-Pa 0 J increased with age (P < 0.001). Shunt, assessed by the multiple inert gas elimination technique, was small (mean 0.5%) and uninfluenced by age. However, there was an increasing dispersion (log SD Q) of ventilation I perfusion ratios (Wi/Q) and increasing perfusion of regions of low S/A/Cl (\JAI<1<0.1) with increasing age {P < 0.001 and P < 0.05, respectively). No patient displayed any atelectasis as assessed by computed x-ray tomography of the chest. During inhalation anaesthesia (halothane or enflurane) with mechanical ventilation, 39 of 45 patients developed atelectasis and shunt. There was a strong correlation between the atelectatic area and the magnitude of shunt (x = 0.81, P < O.OO1). Atelectasis and shunt did not increase significantly with age, whereas log SD Q and perfusion of regions with low VA/Q. ratios did (r = 0.55, P < 0.001 and r = 0.35, P < 0.05, respectively). Awake, the major determinant of Pa Oi was perfusion of regions of low \IA/Q ratios, which increased with age. During anaesthesia shunt influenced Pa Oi most, low \IAI& being a secondary factor which, however, was increasingly important with increasing age, thus explaining the well-known age-dependent deterioration of arterial oxygenation during anaesthesia.