Introduction:Aneurysmal subarachnoid hemorrhage (aSAH) primarily impacts the working-age population. We have shown that 12-month survivors of aSAH from a defined population have increased use of antipsychotic drugs (APD) after aSAH. Research question:Does familial psychiatric burden associate with the risk of APD use or having a poor outcome (mRS 3-5) after aSAH? Material and methods:In our retrospective case-control study, we included consecutive 12-month survivors of aSAH admitted to Kuopio University Hospital with a first aSAH from 1995 to 2018 from its defined catchment population. From national health registries, data were retrieved and linked to aSAH patients, relatives, and matched population controls. Results:Of 1347 aSAH patients (median age 54; 53 % females, median follow-up 11 years), a total of 187 (14 %) had started APD use only after the aSAH. Among 10 820 relatives, 1070 (10 %) with APD use were identified. In overall, 79 aSAH survivors with a family history of APD use or psychiatric diagnoses were not at increased risk of initiating APD use after aSAH (OR 0.79, 95 % CI 0.58-1.09). 84 (51 %) of 166 aSAH survivors with a 12-month poor outcome had a positive family history. Positive family history was an independent risk for poor outcome (OR 1.87, 95 % CI 1.28-2.73). Discussion and conclusion:The family history of APD use or psychiatric diagnoses was not a risk factor for APD use but was an independent risk factor for poor outcome at 12 months after aSAH. This should be considered in the rehabilitation and follow-up programs.

Purpose In aneurysmal intracerebral hemorrhage (aICH), our review showed the lack of the patient’s individual (i) timeline panels and (ii) serial brain CT/MRI slice panels through the aICH evacuation and neurointensive care until the final brain tissue outcome. Methods Our retrospective cohort consists of 54 consecutive aICH patients from a defined population who acutely underwent the clipping of a middle cerebral artery bifurcation saccular aneurysm (Mbif sIA) with the aICH evacuation at Kuopio University Hospital (KUH) from 2010 to 2019. We constructed the patient’s individual timeline panels since the emergency call and serial brain CT/MRI slice panels through the aICH evacuation and neurointensive care until the final brain tissue outcome. The patients were indicated by numbers (1.–54.) in the pseudonymized panels, tables, results, and discussion. Results The aICH volumes on KUH admission (median 46 cm 3 ) plotted against the time from the emergency call to the evacuation (median 8 hours) associated significantly with the rebleeds ( n =25) and the deaths ( n =12). The serial CT/MRI slice panels illustrated the aICHs, intraventricular hemorrhages (aIVHs), residuals after the aICH evacuations, perihematomal edema (PHE), delayed cerebral injury (DCI), and in the 42 survivors, the clinical outcome (mRS) and the brain tissue outcome. Conclusions Regarding aICH evacuations, serial brain CT/MRI panels present more information than words, figures, and graphs. Re-bleeds associated with larger aICH volumes and worse outcomes. Swift logistics until the sIA occlusion with aICH evacuation is required, also in duty hours and weekends. Intraoperative CT is needed to illustrate the degree of aICH evacuation. PHE may evoke uncontrollable intracranial pressure (ICP) in spite of the acute aICH volume reduction.

Our review of acute brain insult articles indicated that the patients’ individual (i) timeline panels with the defined time points since the emergency call and (ii) serial brain CT/MRI slice panels through the neurointensive care until death or final brain tissue outcome at 12 months or later are not presented. We retrospectively constructed such panels for the 45 aneurysmal subarachnoid hemorrhage (aSAH) patients with a secondary decompressive craniectomy (DC) after the acute admission to neurointensive care at Kuopio University Hospital (KUH) from a defined population from 2005 to 2018. The patients were indicated by numbers (1.–45.) in the pseudonymized panels, tables, results, and discussion. The timelines contained up to ten defined time points on a logarithmic time axis until death ( n=25 ; 56 n=20 ; 44

BACKGROUND AND OBJECTIVES:Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating form of stroke affecting the working-age population, where epilepsy is a common complication and major prognostic factor for increased morbidity in aSAH survivors. The objective of this analysis was to assess whether epilepsy in first-degree relatives is a risk of developing epilepsy after aSAH. METHODS:We used a region-specific database that includes all cases of unruptured and ruptured saccular intracranial aneurysm admitted to Kuopio University Hospital from its defined Eastern Finnish catchment population. We also retrieved data from Finnish national health registries for prescription drug purchases and reimbursement, hospital discharge, and cause of death and linked them to patients with aSAH, their first-degree relatives, and population controls matched 3:1 by age, sex, and birth municipality. Cox regression modeling and Kaplan-Meier survival curves were used for analysis. RESULTS:We examined data for 760 consecutive 12-month survivors of aSAH, born in 1950 or after, with a first aSAH from January 1, 1995, to December 31, 2018. Of the 760 patients (median age, 47 years; 53% female; median follow-up, 11 years), 111 (15%) developed epilepsy at a median of 7 months (interquartile range, 2-14 months) after admission for aSAH. Of the 2,240 population controls and 4,653 first-degree relatives of patients with aSAH, 23 (0.9%) and 80 (1.7%), respectively, developed epilepsy during the follow-up period. Among 79 patients with epilepsy in first-degree relatives, 22 (28%) developed epilepsy after aSAH; by contrast, among 683 patients with no epilepsy in first-degree relatives, 89 (13%) developed epilepsy after aSAH. Having at least 1 relative with epilepsy was an independent risk factor of epilepsy after aSAH (hazard ratio, 2.44; 95% CI 1.51-3.95). Cumulative 1-year rates by first-degree relationship were 40% with 1 or more children with epilepsy, 38% with 1 or more affected parents, 5% with 1 or more affected siblings, and 10% with no relatives with epilepsy. DISCUSSION:Patients who developed epilepsy after aSAH were significantly more likely to have first-degree relatives with epilepsy than those who did not develop epilepsy after the aSAH.

Subarachnoid hemorrhage (SAH) is a serious condition, and a myocardial injury or dysfunction could contribute to the outcome. We assessed the prevalence and prognostic impact of cardiac involvement in a cohort with SAH. This is a prospective observational multicenter study. We included 192 patients treated for non-traumatic subarachnoid hemorrhage. We performed ECG recordings, echocardiographic examinations, and blood sampling within 24 h of admission and on days 3 and 7 and at 90 days. The primary endpoint was the evidence of cardiac involvement at 90 days, and the secondary endpoint was to examine the prevalence of a myocardial injury or dysfunction. The median age was 54.5 (interquartile range [IQR] 48.0–64.0) years, 44.3% were male and the median World Federation of Neurological Surgeons (WFNS) score was 2 (IQR 1–4). At day 90, 22/125 patients (17.6%) had left ventricular ejection fractions ≤ 50%, and 2/121 patients (1.7%) had evidence of a diastolic dysfunction as defined by mitral peak E-wave velocity by peak eʹ velocity (E/eʹ) > 14. There was no prognostic impact from echocardiographic evidence of cardiac complications on neurological outcomes. The overall prevalence of cardiac dysfunction was modest. We found no demographic or SAH-related factors associated with 90 days cardiac dysfunction.

OBJECTIVEThe authors set out to study whether autosomal dominant polycystic kidney disease (ADPKD), an established risk factor for intracranial aneurysms (IAs), affects the acute course and long-term outcome of aneurysmal subarachnoid hemorrhage (aSAH).METHODSThe outcomes of 32 ADPKD patients with aSAH between 1980 and 2015 (median age 43 years; 50% women) were compared with 160 matched (age, sex, and year of aSAH) non-ADPKD aSAH patients in the prospectively collected Kuopio Intracranial Aneurysm Patient and Family Database.RESULTSAt 12 months, 75% of the aSAH patients with ADPKD versus 71% of the matched-control aSAH patients without ADPKD had good outcomes (Glasgow Outcome Scale score 4 or 5). There was no significant difference in condition at admission. Hypertension had been diagnosed before aSAH in 69% of the ADPKD patients versus 27% of controls (p < 0.001). Multiple IAs were present in 44% of patients in the ADPKD group versus 25% in the control group (p = 0.03). The most common sites of ruptured IAs were the anterior communicating artery (47% vs 29%, p = 0.05) and the middle cerebral artery bifurcation (28% vs 31%), and the median size was 6.0 mm versus 8.0 mm (p = 0.02). During the median follow-up of 11 years, a second aSAH occurred in 3 of 29 (10%) ADPKD patients and in 4 of 131 (3%) controls (p = 0.11). A fatal second aSAH due to a confirmed de novo aneurysm occurred in 2 (6%) of the ADPKD patients but in none of the controls (p = 0.027).CONCLUSIONSThe outcomes of ADPKD patients with aSAH did not differ significantly from those of matched non-ADPKD aSAH patients. ADPKD patients had an increased risk of second aSAH from a de novo aneurysm, warranting long-term angiographic follow-up.

BackgroundThe long‐term effects of stress ulcer prophylaxis with pantoprazole are unknown in ICU patients. We report 1‐year mortality outcome in the Stress Ulcer Prophylaxis in the Intensive Care Unit (SUP‐ICU) trial.MethodsIn the SUP‐ICU trial, acutely admitted adult ICU patients at risk of gastrointestinal bleeding were randomised to intravenous pantoprazole 40 mg vs placebo (saline) once daily during their ICU stay. We assessed mortality at 1 year and did sensitivity analyses according to the trial protocol and statistical analysis plan.ResultsA total of 3261 of the 3291 patients with available data (99.1%) were followed up at 1 year after randomisation; 1635 were allocated to pantoprazole and 1626 to placebo. At 1 year after randomisation, 610 of 1635 patients (37.3%) had died in the pantoprazole group as compared with 601 of 1626 (37.0%) in the placebo group (relative risk, 1.01; 95% confidence interval 0.92‐1.10). The results were consistent in the sensitivity analysis adjusted for baseline risk factors and in those of the per‐protocol population. We did not observe heterogeneity in the effect of pantoprazole vs placebo on 1‐year mortality in the predefined subgroups, that is, patients with and without shock, mechanical ventilation, liver disease, coagulopathy, high disease severity (SAPS II > 53) or in medical vs surgical ICU patients.ConclusionWe did not observe a difference in 1‐year mortality among acutely admitted adult ICU patients with risk factors for gastrointestinal bleeding allocated to stress ulcer prophylaxis with pantoprazole or placebo during the ICU stay. (The SUP‐ICU trial was funded by Innovation Fund Denmark and others; ClinicalTrials.gov number, NCT02467621).

Background and Purpose- At acute phase and neurointensive care, patients with aneurysmal subarachnoid hemorrhage (aSAH) may become agitated or delirious. We found no previous studies on psychotic disorders or antipsychotic drug (APD) use by long-term aSAH survivors. We defined the APD use and its risk factors among 12-month survivors of aSAH in an Eastern Finnish population-based cohort with long-term follow-up. Methods- We analyzed APD use in 1144 consecutive patients with aSAH alive at 12 months of the Kuopio intracranial aneurysm patient and family database and their age, sex, and birth municipality matched controls (3:1; n=3432) from 1995 to 2013 and median follow-up of 9 years. Using the Finish nationwide health registries, we obtained drug purchase and hospital discharge data. Results- In total, 140 (12%) of the 1144 patients started APD use first time after aSAH (index date), in contrast to 145 (4%) of the 3432 matched population controls. The cumulative rate of starting APD was 6% at 1 year and 9% at 5 years, in contrast to 1% and 2% in the controls, respectively. The rates at 1 and 5 years were only 1% and 2% in the 489 patients with a good condition (modified Rankin Scale score, 0 or 1 at 12 months; no shunt, intracerebral hemorrhage, or intraventricular hemorrhage). Instead, the highest rate of APD use, 23% at 5 years was among the 192 patients shunted for hydrocephalus after aSAH. Eighty-eight (63%) of the 140 aSAH patients with APD use had also concomitant antidepressant or antiepileptic drug use. Conclusions- The 12-month survivors of aSAH were significantly more likely to be started on APD after aSAH than their matched population controls. These patients often used antidepressant and antiepileptic drugs concomitantly. The use of APDs strongly correlated with signs of brain injury after aSAH, with low use if no signs of significant brain injury were present.

Acute kidney injury (AKI) is a syndrome that frequently affects the critically ill. Recently, an increased number of dinucleotide repeats in the HMOX1 gene were reported to associate with development of AKI in cardiac surgery. We aimed to test the replicability of this finding in a Finnish cohort of critically ill septic patients. This multicenter study was part of the national FINNAKI study. We genotyped 300 patients with severe AKI (KDIGO 2 or 3) and 353 controls without AKI (KDIGO 0) for the guanine-thymine (GTn) repeat in the promoter region of the HMOX1 gene. The allele calling was based on the number of repeats, the cut off being 27 repeats in the S-L (short to long) classification, and 27 and 34 repeats for the S-M-L2 (short to medium to very long) classification. The plasma concentrations of heme oxygenase-1 (HO-1) enzyme were measured on admission. The allele distribution in our patients was similar to that published previously, with peaks at 23 and 30 repeats. The S-allele increases AKI risk. An adjusted OR was 1.30 for each S-allele in an additive genetic model (95% CI 1.01-1.66; p = 0.041). Alleles with a repeat number greater than 34 were significantly associated with lower HO-1 concentration (p<0.001). In septic patients, we report an association between a short repeat in HMOX1 and AKI risk.

Acute kidney injury (AKI) is a syndrome with high incidence among the critically ill. Because the clinical variables and currently used biomarkers have failed to predict the individual susceptibility to AKI, candidate gene variants for the trait have been studied. Studies about genetic predisposition to AKI have been mainly underpowered and of moderate quality. We report the association study of 27 genetic variants in a cohort of Finnish critically ill patients, focusing on the replication of associations detected with variants in genes related to inflammation, cell survival, or circulation. In this prospective, observational Finnish Acute Kidney Injury (FINNAKI) study, 2647 patients without chronic kidney disease were genotyped. We defined AKI according to Kidney Disease: Improving Global Outcomes (KDIGO) criteria. We compared severe AKI (Stages 2 and 3, n = 625) to controls (Stage 0, n = 1582). For genotyping we used iPLEXTM Assay (Agena Bioscience). We performed the association analyses with PLINK software, using an additive genetic model in logistic regression. Despite the numerous, although contradictory, studies about association between polymorphisms rs1800629 in TNFA and rs1800896 in IL10 and AKI, we found no association (odds ratios 1.06 (95% CI 0.89–1.28, p = 0.51) and 0.92 (95% CI 0.80–1.05, p = 0.20), respectively). Adjusting for confounders did not change the results. To conclude, we could not confirm the associations reported in previous studies in a cohort of critically ill patients.

Abstracts for the 2019 Scandinavian Society of Anaesthesiology and Intensive Care Medicine Congress in Copenhagens for the 2019 Scandinavian Society of Anaesthesiology and Intensive Care Medicine Congress in Copenhagen ACTA COMPETITION (5 ABSTRACTS) ABSSUB125 | Does nonsedation affect quality of life following critical illness? Hanne T. Olsen1,2,*; Helene K. Nedergaard1,3; Hanne I. Jensen3,4; Thomas Strøm5; Palle Toft1,5 1Department of Clinical Research, University of Southern Denmark, Odense, 2Department of anesthesiology and intensive care, Odense University Hospital, Svendborg, 3Department of anesthesiology and intensive care, Lillebaelt Hospital, Kolding, Kolding, 4Department of Regional Health Research, University of Southern Denmark, 5Department of anesthesiology and intensive care, Odense University Hospital, Odense, Denmark Background: Critical illness can severely impair healthrelated quality of life (HRQL) for years following discharge. The NONSEDAtrial was a Scandinavian multicenter randomised trial in critically ill, mechanically ventilated patients, with eight participating Intensive Care Units (ICU). The main aim was to assess if nonsedation vs sedation with a daily wakeup trial improved survival. The aim of this substudy was to assess the effect of nonsedation on HRQL. Method: Patients participating in the NONSEDAtrial were randomised to nonsedation or sedation within the first 24 hours of mechanical ventilation. Nonsedated patients received no sedatives; sedated patients received propofol (first 2 days) and then midazolam. Bolus doses of morphine were used in both groups for pain and discomfort. All survivors from the NONSEDAtrial were asked to complete the Medical Outcomes Study ShortForm 36 questionnaire (SF36) 3 months post ICUdischarge. SF36 is validated within critical care. To limit missing data, reminders were sent by mail. If unsuccessful, telephone interviews could be used. Outcomes were assessed blinded. Results: In total, 700 patients were included between 2014 and 2017, and 412 survived to followup. A total of 339 survivors participated (82%). Baseline data were equal between nonsedated (n = 167) and sedated (n = 172) patients, with regard to age (median 72.5 vs 70.0 years), APACHEIIscore (median 26 vs 25) and gender (36% females vs 42%). Mean SF36 scores for the nonsedated vs sedated patients were: Physical Function 50 vs 40, P = .22, Bodily Pain: 53 vs 56, P = .55, General Health: 52 vs 50, P = .22, Vitality: 44 vs 38, P = .32, Social Function: 75 vs 63, P = .18, Role Emotional: 58 vs 50, P = .50, Mental Health: 75 vs 70, P = .40, Role Physical: 31 vs 25, P = .11. Conclusion: Nonsedation had no significant effect on HRQL 3 months post ICUdischarge, although nonsedated patients scored better within seven of the eight SF36 domains. Disclosure of Interest: None Declared.

To analyze the organ donation action in population-based neurointensive care of acute aneurysmal subarachnoid hemorrhage (aSAH) and to seek factors that would improve the identification of potential organ donors (PODs) and increase the donor conversion rate (DCR) after aSAH.

BACKGROUND:Normobaric hyperoxia is used to alleviate secondary brain ischaemia in patients with traumatic brain injury (TBI), but clinical evidence is limited and hyperoxia may cause adverse events.METHODS:An open label, randomised controlled pilot study comparing blood concentrations of reactive oxygen species (ROS), interleukin 6 (IL-6) and neuron-specific enolase (NSE) between two different fractions of inspired oxygen in severe TBI patients on mechanical ventilation.RESULTS:We enrolled 27 patients in the Fi O2 0.40 group and 38 in the Fi O2 0.70 group; 19 and 23 patients, respectively, completed biochemical analyses. In baseline, there were no differences between Fi O2 0.40 and Fi O2 0.70 groups, respectively, in ROS (64.8 nM [22.6-102.1] vs. 64.9 nM [26.8-96.3], P = 0.80), IL-6 (group 92.4 pg/ml [52.9-171.6] vs. 94.3 pg/ml [54.8-133.1], P = 0.52) or NSE (21.04 ug/l [14.0-30.7] vs. 17.8 ug/l [14.1-23.9], P = 0.35). ROS levels did not differ at Day 1 (24.2 nM [20.6-33.5] vs. 29.2 nM [22.7-69.2], P = 0.10) or at Day 2 (25.4 nM [21.7-37.4] vs. 47.3 nM [34.4-126.1], P = 0.95). IL-6 concentrations did not differ at Day 1 (112.7 pg/ml [65.9-168.9) vs. 83.9 pg/ml [51.8-144.3], P = 0.41) or at Day 3 (55.0 pg/ml [34.2-115.6] vs. 49.3 pg/ml [34.4-126.1], P = 0.95). NSE levels did not differ at Day 1 (15.9 ug/l [9.0-24.3] vs. 15.3 ug/l [12.2-26.3], P = 0.62). There were no differences between groups in the incidence of pulmonary complications.CONCLUSION:Higher fraction of inspired oxygen did not increase blood concentrations of markers of oxidative stress, inflammation or neurological injury or the incidence of pulmonary complications in severe TBI patients on mechanical ventilation.

BACKGROUND:Targeting hyperoxemia is common practice in neurocritical care settings, but the safety of hyperoxemia has been questioned.OBJECTIVE:To investigate the independent effect of hyperoxemia on outcome in patients with aneurysmal subarachnoid hemorrhage (SAH).METHODS:We included 432 patients with aneurysmal SAH on mechanical ventilation for at least 24 hours after intensive care unit (ICU) admission. Arterial blood gas levels were calculated as time-weighted averages (TWAs) of all blood gas measurements during the first 24 hours in the ICU. Patients were categorized into 3 TWA-PaO2 bands (low, <97.5 mm Hg; intermediate, 97.5-150 mm Hg; high, ≥150 mm Hg). Outcome measures were unfavorable outcome at 3 months (Glasgow Outcome Scale score 1-3) and mortality. Multivariate logistic regression analysis was used to assess the independent effect of oxygen on outcome.RESULTS:Overall, 28% of patients died, and a total of 53% had an unfavorable outcome at 3 months. Patients with an unfavorable outcome had significantly higher TWA-PaO2 levels compared with patients with a favorable outcome (137 mm Hg vs 118 mm Hg, P < .001). Multivariate analysis demonstrated no significant association between TWA-PaO2 bands and unfavorable outcome (with intermediate PaO2 as a reference, odds ratio [OR] for low PaO2 1.05, 95% confidence interval [CI]: 0.52-2.12, P = .89; OR for high PaO2: 1.09, 95% CI: 0.61-1.97, P = .77) or mortality (with intermediate PaO2 as reference, the OR for low PaO2 was 0.67 (95% CI: 0.30-1.46, P = .31), and the OR for high PaO2 was 0.73 (95% CI: 0.38-1.40, P = .34).CONCLUSION:Early moderate hyperoxemia may not increase or decrease the risk of a poor outcome in mechanically ventilated aneurysmal SAH patients.

Introduction: The relationship between hyperoxemia and outcome in patients with traumatic brain injury (TBI) is controversial. We sought to investigate the independent relationship between hyperoxemia and long-term mortality in patients with moderate-to-severe traumatic brain injury.Methods: The Finnish Intensive Care Consortium database was screened for mechanically ventilated patients with a moderate-to-severe TBI. Patients were categorized, according to the highest measured alveolar-arterial O-2 gradient or the lowest measured PaO2 value during the first 24 hours of ICU admission, to hypoxemia (<10.0 kPa), normoxemia (10.0 to 13.3 kPa) and hyperoxemia (>13.3 kPa). We adjusted for markers of illness severity to evaluate the independent relationship between hyperoxemia and 6-month mortality.Results: A total of 1,116 patients were included in the study, of which 16% (n = 174) were hypoxemic, 51% (n = 567) normoxemic and 33% (n = 375) hyperoxemic. The total 6-month mortality was 39% (n = 435). A significant association between hyperoxemia and a decreased risk of mortality was found in univariate analysis (P = 0.012). However, after adjusting for markers of illness severity in a multivariate logistic regression model hyperoxemia showed no independent relationship with 6-month mortality (hyperoxemia vs. normoxemia OR 0.88, 95% CI 0. 63 to 1.22, P = 0.43; hyperoxemia vs. hypoxemia OR 0.97, 95% CI 0.63 to 1.50, P = 0.90).Conclusion: Hyperoxemia in the first 24 hours of ICU admission after a moderate-to-severe TBI is not predictive of 6-month mortality.