Background Anemia of inflammation (AI) is common in critically ill patients. Although this syndrome negatively impacts the outcome of critical illness, understanding of its pathophysiology is limited. Also, new therapies that increase iron availability for erythropoiesis during AI are upcoming. A model of AI induced by bacterial infections that are relevant for the critically ill is currently not available. This paper describes the development of an animal model for AI that is relevant for critical care research. Results In experiments with rats, the rats were inoculated either repeatedly or with a slow release of Streptococcus pneumoniae or Pseudomonas aeruginosa . Rats became ill, but their hemoglobin levels remained stable. The use of a higher dose of bacteria resulted in a lethal model. Then, we turned to a model with longer disease duration, using pigs that were supported by mechanical ventilation after inoculation with P. aeruginosa. The pigs became septic 12 to 24 h after inoculation, with a statistically significant decrease in mean arterial pressure and base excess, while heart rate tended to increase. Pigs needed resuscitation and vasopressor therapy to maintain a mean arterial pressure > 60 mmHg. After 72 h, the pigs developed anemia (baseline 9.9 g/dl vs. 72 h, 7.6 g/dl, p = 0.01), characterized by statistically significant decreased iron levels, decreased transferrin saturation, and increased ferritin. Hepcidin levels tended to increase and transferrin levels tended to decrease. Conclusions Using pathogens commonly involved in pulmonary sepsis, AI could not be induced in rats. Conversely, in pigs, P. aeruginosa induced pulmonary sepsis with concomitant AI. This AI model can be applied to study the pathophysiology of AI in the critically ill and to investigate the effectivity and toxicity of new therapies that aim to increase iron availability. Electronic supplementary material The online version of this article (10.1186/s40635-019-0261-2) contains supplementary material, which is available to authorized users.

Summary Leakage of colonised oropharyngeal secretions across the tracheal tube cuff may cause iatrogenic pulmonary infection. We studied a novel ‘add‐on’ cuff, which can be inserted over an existing tracheal tube and advanced into the subglottic region. The physical properties of the novel silicone cuff (BronchoGuard, Ciel Medical, USA) were evaluated in comparison with the Hi‐Lo® tracheal tube. In a bench study, we identified saline inflation volumes required to transmit pressures between 15 and 30 cmH2O against artificial tracheas of 18, 20 and 22 mm internal diameter. We computed cuff compliance, and minimal inflation volume to achieve air sealing during mechanical ventilation. Finally, we compared the leakage flow rate of artificial saliva across the novel cuff. On average, the mean (SD) inflation volumes necessary to transmit tracheal pressures of 15, 20, 25 and 30 cmH2O were 4.1 (2.2), 4.4 (2.3), 4.6 (2.4) and 4.8 (2.4) ml for the novel cuff and 7.7 (2.5), 8.0 (2.6), 8.4 (2.6) and 8.7 (2.7) ml for the Hi‐Lo tube, respectively (p < 0.001). The minimal inflation volumes to achieve air sealing were 3.8 (0.9) and 10.5 (2.1) ml (p < 0.001), which resulted in transmitted tracheal pressures of 8.3 (9.8) and 27.6 (34.8) cmH2O (p < 0.001). Compliance was 0.026 (0.004) and 0.616 (0.324) ml.cmH20−1, respectively (p < 0.001). Although massive leak was found when the novel cuff transmitted pressures ≤ 20 cmH2O against the trachea, leakage was avoided with pressures ≥ 25 cmH2O, owing to optimal contact between the cuff and the tracheal wall. In contrast, the standard cuff consistently leaked irrespective of the pressure. We conclude that the novel cuff has advantageous properties that warrant clinical corroboration.

reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. carbon dioxide 30 [27][28][29][30][31][32][33][34][35] mmHg and median temperature 37.1 [36.8-37.3]°C. After removal of artefacts, the mean monitoring time was 22 h08 (8 h54). All patients had impaired cerebral autoregulation during their monitoring time. The mean IAR index was 17 (9.5) %. During H 0 H 6 and H 18 H 24 , the majority of our patients; respectively 53 and 71 % had an IAR index > 10 %. Conclusion According to our data, patients with septic shock had impaired cerebral autoregulation within the first 24 hours of their admission in the ICU. In our patients, we described a variability of distribution of impaired autoregulation according to time. ReferencesSchramm P, Klein KU, Falkenberg L, et al. Impaired cerebrovascular autoregulation in patients with severe sepsis and sepsis-associated delirium. Crit Care 2012; 16: R181. Aries MJH, Czosnyka M, Budohoski KP, et al. Continuous determination of optimal cerebral perfusion pressure in traumatic brain injury. Crit. Care Med. 2012.

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