Impact of multidetector computed tomography on the diagnosis and treatment of patients with systemic inflammatory response syndrome or sepsis.

OBJECTIVES: To evaluate the impact of CT scans on diagnosis or change of therapy in patients with systemic inflammatory response syndrome (SIRS) or sepsis and obscure clinical infection. METHODS: CT records of patients with obscure clinical infection and SIRS or sepsis were retrospectively evaluated. Both confirmation of and changes in the diagnosis or therapy based on CT findings were analysed by means of the hospital information system and radiological information system. A sub-group analysis included differences with regard to anatomical region, medical history and referring department. RESULTS: Of 525 consecutive patients evaluated, 59% had been referred from internal medicine and 41% from surgery. CT examination had confirmed the suspected diagnosis in 26% and had resulted in a different diagnosis in 33% and a change of therapy in 32%. Abdominal scans yielded a significantly higher (p=0.013) change of therapy rate (42%) than thoracic scans (22%). Therapy was changed significantly more often (p=0.016) in surgical patients (38%) than in patients referred from internal medicine (28%). CONCLUSIONS: CT examination for detecting an unknown infection focus in patients with SIRS or sepsis is highly beneficial and should be conducted in patients with obscure clinical infection. KEY POINTS: • Evaluation of patients with obscure clinical infection is a challenging task. • CT examination of patients with SIRS or sepsis seems to be beneficial. • CT examination confirmed suspected diagnosis in 26% of patients. • CT examination yielded a new infection focus in 33% of patients. • CT examination changed therapy in up to 32% of patients.

[Extracorporeal CO2 removal as an alternative to tracheotomy in a patient with extubation failure]. / Extrakorporale CO2-Elimination als Alternative zur Tracheotomie bei Weaningversagen.

We report a patient with chest trauma who was admitted to the ICU after surgery. As he fulfilled protocol-based criteria, he was extubated 7 days after admission. However, despite intermittent non-invasive ventilation, the patient had to be re-intubated on day 10 owing to progressive hypercapnia. We decided to support the patient with a mid-flow veno-venous extracorporeal carbon dioxide removal (ECCO2­R) system instead of a tracheotomy. Sufficient CO2 removal was established with a blood flow of 1.5 l/min and the patient was successfully extubated within a few hours. After 5 days of ECCO2­R the patient could be weaned and transferred to a general ward in a stable condition.

The second window of desflurane-induced preconditioning is mediated by STAT3: role of Pim-1 kinase.

BACKGROUND: Late ischemic preconditioning is mediated via nuclear transcription factor signal transducer and activator of transcription 3 (STAT3). Pim-1 kinase reduces infarct size in cardiomyocytes and is regulated by STAT3. We tested the hypothesis that late desflurane-induced preconditioning (DES-SWOP) is mediated via STAT3 and Pim-1. METHODS: After institutional approval, pentobarbital-anesthetized male C57BL/6 mice were subjected to 45 min coronary artery occlusion (CAO) and 3 h reperfusion. Control animals received no additional intervention. Desflurane was administered 48 h before CAO either alone or in combination with the janus kinase/STAT3 inhibitor AG-490 (40 µg/g i.p., 20 min before desflurane administration) or the Pim-1 kinase inhibitor II (PIM-Inh.II, 10 µg/g i.p., 15 min before CAO). Infarct size (IS) and area at risk were determined with triphenyltetrazolium chloride and Evans blue, respectively. Additionally, cytosolic and nuclear fractions were separated at two different time points and expression of STAT3, phospho-STAT3(Ser727) , phospho-STAT3(Tyr705) , Pim-1, Bad and phospho-Bad(Ser112) were determined by Western Blot analysis. Data were analyzed with one-way or two-way ANOVA and post hoc Duncan test and are presented as mean ± SEM. RESULTS: IS was 47 ± 2% (n = 7-8 per group) in control animals (CON). DES-SWOP reduced myocardial infarct size to 23 ± 4%* (*P < 0.05 vs. CON). AG-490 alone did not affect myocardial infarct size (44 ± 7%), but abolished DES-SWOP (44 ± 4%). Blockade of Pim-1 did not affect the protection by DES-SWOP (34 ± 4%*). Desflurane reduced cytosolic content and enhanced nuclear content of phospho-STAT(S) (er727) . After 48 h, desflurane enhanced Pim-1 activity, whereas Pim-1 expression remained unchanged. CONCLUSION: These data suggest that DES-SWOP is mediated by activation and nuclear translocation of STAT3. The impact of Pim-1 in DES-SWOP signaling remains unclear.

Desflurane-induced and ischaemic postconditioning against myocardial infarction are mediated by Pim-1 kinase.

BACKGROUND: Anaesthetic-induced (APOST) and ischaemic postconditioning (IPOST) against myocardial infarction are mediated via phosphatidylinositol-3-kinase/Akt. Pim-1 kinase is acting downstream of Akt and has recently been demonstrated to enhance cardiomyocyte survival. We tested the hypothesis that both APOST and IPOST are mediated by Pim-1 kinase. METHODS: Pentobarbital-anaesthetized male C57BL/6 mice were subjected to 45-min coronary artery occlusion (CAO) and 3-h reperfusion. Animals received either no intervention, the Pim-1 kinase inhibitor II (10 µg/g intraperitoneally) or its vehicle dimethy sulfoxide (10 µl/g intraperitoneally). Three minutes prior to the end of CAO, 1.0 minimum alveolar concentration desflurane was administered for 18 min alone or in combination with Pim-1 kinase inhibitor II. IPOST was induced by three cycles of each 10-s ischaemia/reperfusion, and animals received either IPOST alone or in combination with Pim-1 kinase inhibitor II. Infarct size was determined with triphenyltetrazolium chloride and area at risk with Evans blue. Protein expression of Pim-1 kinase, Bad, phospho-Bad(Ser112) and B-cell lymphoma 2 was determined using Western immunoblotting analysis. RESULTS: Infarct size in control animals (CON) was 46 ± 3%. Dimethylsulfoxide (47 ± 3%) and Pim-1 kinase inhibitor II (44 ± 5%) did not significantly reduce infarct size. Desflurane (16 ± 2%*; *P < 0.05 vs. CON) and IPOST (21 ± 2%*) significantly reduced infarct size compared with CON. Inhibition of Pim-1 kinase abolished desflurane-induced postconditioning (46 ± 4%) and IPOST (44 ± 5%). Western blot analysis revealed that only desflurane enhances phosphorylation of Bad at serine 112 that was abrogated by Pim-1 kinase inhibitor II. CONCLUSION: These data suggest that Pim-1 kinase mediates both desflurane-induced postconditioning and IPOST in mice.

Desflurane-induced post-conditioning against myocardial infarction is mediated by calcium-activated potassium channels: role of the mitochondrial permeability transition pore.

BACKGROUND: Desflurane (DES)-induced preconditioning is mediated by large-conductance calcium-activated potassium channels (BK(Ca)). Whether BK(Ca) are involved in anaesthetic-induced post-conditioning is unknown. We tested the hypothesis that DES-induced post-conditioning is mediated by BK(Ca) upstream of the mitochondrial permeability transition pore (mPTP). METHODS: Pentobarbital-anaesthetized male C57Black/6 mice were subjected to 45 min coronary artery occlusion (CAO) and 3 h reperfusion. Animals received either no intervention or dimethylsulphoxide (DMSO, 10 µl g(-1)). DES (1.0 MAC, 7.5 vol%) was administered for 18 min, starting 3 min before the end of CAO. The following agents were given either alone or in combination with DES: the BK(Ca) activator NS1619 (1 µg g(-1)), the BK(Ca) inhibitor iberiotoxin (IbTx, 0.05 µg g(-1)), the mPTP opener atractyloside (ATRA, 25 µg g(-1)), and the mPTP inhibitor cyclosporine A (CYC A, 10 µg g(-1)). Infarct size (IS) was determined with triphenyltetrazolium chloride and the area at risk with Evans Blue, respectively. RESULTS: IS in control animals was 48(6)%. Neither DMSO, IbTx nor ATRA affected myocardial IS. DES alone or NS1619 alone or the combination reduced IS (P<0.05), CYC A alone or in combination with IbTx or DES also reduced IS (P<0.05). DES-induced reduction of myocardial IS was completely abolished by IbTx and was partially blocked by ATRA and ATRA partially blocked IS reduction by NS1619. CONCLUSIONS: These data suggest that DES-induced post-conditioning against myocardial infarction is mediated by BK(Ca) and mPTP. Cardioprotection by BK(Ca) activator NS1619 might occur, at least in part, independently of mPTP.

[Extracorporeal membrane oxygenation and severe traumatic brain injury. Is the ECMO-therapy in traumatic lung failure and severe traumatic brain injury really contraindicated?]. / Extrakorporale Membranoxygenierung und schweres Schädel-Hirn-Trauma : Ist der ECMO-Einsatz bei polytraumatisierten ARDS-Patienten mit schwerem SHT wirklich noch kontraindiziert?

Veno-venous extracorporeal membrane oxygenation (ECMO) may be lifesaving in multiple injured patients with acute respiratory distress syndrome (ARDS) due to chest trauma. To prevent circuit thrombosis or thromboembolic complications during ECMO systemic anticoagulation is recommended. Therefore, ECMO treatment is contraindicated in patients with intracranial bleeding. The management of veno-venous ECMO without systemic anticoagulation in a patient suffering from traumatic lung failure and severe traumatic brain injury is reported.

Comparison of the Glidescope and Airtraq optical laryngoscopes in patients undergoing direct microlaryngoscopy.

Optical laryngoscopes have been developed to facilitate difficult airway management. The Airtraq is a single-use device and the GlideScope is reusable. In this study, the Airtraq and the Glidescope were compared in 60 ASA I-III patients with tumours of the upper airway undergoing direct endoscopic microlaryngoscopy. Patients were randomly assigned to the Airtraq or the Glidescope group and the Cormack and Lehane grade was assessed by Macintosh laryngoscopy prior to tracheal intubation. There were no differences in tracheal intubation success rates or duration of intubation attempts between both devices. The Cormack and Lehane grade was improved in 77% and 82% of cases in the Airtraq and Glidescope group, respectively. Blood traces on the device and traumatic pharyngeal lesions were found more frequently in the Airtraq group. The Airtraq and Glidescope laryngoscopes are valuable tools for the management of patients with potentially difficult airways with the Glidescope appearing to be less traumatic.

Ischemia-induced increase of stiffness of alphaB-crystallin/HSPB2-deficient myocardium.

The two small heat shock proteins (sHSPs), alphaB-crystallin and HSPB2, have been shown to translocate within a few minutes of cardiac ischemia from the cytosol to myofibrils; and it has been suggested that their chaperone-like properties might protect myofibrillar proteins from unfolding or aggregation during stress conditions. Further evidence of an important role for HSPs in muscle function is provided by the fact that mutations of the alphaB-crystallin gene cause myopathy and cardiomyopathy. In the present study, we subjected isolated papillary muscles of alphaB-crystallin/HSPB2-deficient mice to simulated ischemia and reperfusion. During ischemia in alphaB-crystallin/HSPB2-deficient muscles, the development of contracture started earlier and reached a higher value compared to the wildtype mice. The recovery of contracture of alphaB-crystallin/HSPB2-deficient muscles was also attenuated during the simulated reperfusion period. However, twitch force was not significantly altered at any time of the experiment. This suggests that during ischemic insults, alphaB-crystallin/HSPB2 may not be important for the contraction process itself, but rather serve to maintain muscular elasticity.