Veien inn til sykehus for pasienter innlagt ved mistanke om akutt hjerneslag

Bakgrunn: Hjerneslag er en tidskritisk tilstand, men fremdeles ankommer under halvparten av pasientene sykehus innen fire timer fra symptomdebut. En mulig forklaring på forsinkelsen kan være at første kontakt med helsevesenet er hos legevakten eller fastlegen. Hensikt: Hensikten med denne studien var å kartlegge innleggende instans for pasienter ved mistanke om akutt hjerneslag før de kom til akuttmottaket ved Oslo universitetssykehus OUS på Ullevål. Vi ville også kartlegge hvorvidt innleggelsesinstans kunne korreleres til slagdiagnose ved utskrivelse. Metode: En retrospektiv observasjonsstudie identifiserte alle pasienter der mistanke om hjerneslag var innleggelsesårsaken på akuttmottaket ved Ullevål i 2018. Vi grupperte pasientene etter innleggende instans: ambulanse, legevakt, fastlege eller direkte kontakt. Vi sammenliknet utskrivelsesdiagnoser «hjerneslag» eller «ikke hjerneslag» etter innleggende instans og fordelte på alder ved å bruke kjikvadrattest. Resultat: Totalt 1399 pasienter med mistanke om hjerneslag ble innlagt, hvorav 594 42 prosent) fikk en hjerneslagdiagnose. Medianalderen var 72 år, og 52 prosent var kvinner. Halvparten ble innlagt direkte med ambulanse, en tredel via legevakten og 12 prosent fra fastlegen. Signifikant flere pasienter av de som ble innlagt med ambulanse 51 prosent), fikk hjerneslag som utskrivelsesdiagnose sammenliknet med pasienter som kom via henholdsvis legevakt 29 prosent) eller fastlege 40 prosent) (kjikvadrat p < 0,001. Pasientene som ble innlagt med ambulanse, var signifikant eldre enn pasientene som kom via legevakten 72 år versus 65 år, p < 0,001. Konklusjon: Kun halvparten av pasientene med symptomer på mistenkt hjerneslag ble innlagt med ambulanse. Pasientene som ble innlagt direkte med ambulanse, ble oftere utskrevet med en hjerneslagdiagnose. Vi trenger mer kunnskap om årsakene til at de resterende pasientene kom via fastlegen eller legevakten.publishedVersio

No change in plasma potassium concentration during 10 minutes of apnoea: An observational study on potential organ donors

Background Acute acidosis can increase the plasma potassium concentration. However, data on the effects of acute respiratory acidosis on plasma potassium concentration are conflicting. This study aimed to determine whether acute respiratory acidosis induces an immediate increase in plasma potassium concentration. Methods This observational study was conducted on participants undergoing apnoea testing prior to final radiological examination, registered in an internal quality registry at Oslo University Hospital between 25 April 2013 and 1 May 2020. A total of 124 donors were assessed for inclusion. Sixteen donors with blood glucose concentrations exceeding 10 mmol L−1 were excluded; finally, data from 108 donors were included in the study. The apnoea test, which is a standard neurological test performed in potential organ donors prior to radiological confirmation of ceased brain circulation, induces respiratory acidosis. The arterial plasma potassium concentration, pH and PaCO2 before and after the apnoea test were compared. Statistical analysis was conducted using the paired t test. Results The pre-apnoea and post-apnoea mean plasma potassium concentrations were 3.79 (95% confidence intervals [CI] 3.70–3.87) and 3.79 mmol L−1 (95% CI 3.70–3.88), respectively. The mean difference was −0.002 mmol L−1 (95% CI −0.04 to 0.04); the difference was not significant. The pre-apnoea and post-apnoea mean pH were 7.39 and 7.21, respectively, and the mean difference was 0.175 (P < .01). The pre-apnoea and post-apnoea mean PaCO2 were 5.66 and 9.48 kPa, respectively, and the mean difference was −3.83 (P < .01). Conclusions Acute respiratory acidosis does not lead to rapid changes in plasma potassium concentration during apnoea testing in potential organ donors

Combined Inhibition of C5 and CD14 Attenuates Systemic Inflammation in a Piglet Model of Meconium Aspiration Syndrome

Background: Meconium aspiration syndrome (MAS) is a severe lung condition affecting newborns and it can lead to a systemic inflammatory response. We previously documented complement activation and cytokine release in a piglet MAS model. Additionally, we showed ex vivo that meconium-induced inflammation was dependent on complement and Toll-like receptors. Objectives: To assess the efficacy of the combined inhibition of complement (C5) and CD14 on systemic inflammation induced in a forceful piglet MAS model. Methods: Thirty piglets were randomly allocated to a treatment group receiving the C5-inhibitor SOBI002 and anti-CD14 (n = 15) and a nontreated control group (n = 15). MAS was induced by intratracheal meconium instillation, and the piglets were observed for 5 h. Complement, cytokines, and myeloperoxidase (MPO) were measured by ELISA. Results: SOBI002 ablated C5 activity and the formation of the terminal complement complex in vivo. The combined inhibition attenuated the inflammasome cytokines IL-1β and IL-6 by 60 (p = 0.029) and 44% (p = 0.01), respectively, and also MPO activity in the bronchoalveolar fluid by 42% (p = 0.017). Ex vivo experiments in human blood revealed that the combined regimen attenuated meconium-induced MPO release by 64% (p = 0.008), but there was only a negligible effect with single inhibition, indicating a synergic cross-talk between the key molecules C5 and CD14. Conclusion: Combined inhibition of C5 and CD14 attenuates meconium-induced inflammation in vivo and this could become a future therapeutic regimen for MAS