Prevalence and risk factors related to haloperidol use for delirium in adult intensive care patients : the multinational AID-ICU inception cohort study

We assessed the prevalence and variables associated with haloperidol use for delirium in ICU patients and explored any associations of haloperidol use with 90-day mortality. All acutely admitted, adult ICU patients were screened during a 2-week inception period. We followed the patient throughout their ICU stay and assessed 90-day mortality. We assessed patients and their variables in the first 24 and 72 h in ICU and studied their association together with that of ICU characteristics with haloperidol use. We included 1260 patients from 99 ICUs in 13 countries. Delirium occurred in 314/1260 patients [25% (95% confidence interval 23-27)] of whom 145 received haloperidol [46% (41-52)]. Other interventions for delirium were benzodiazepines in 36% (31-42), dexmedetomidine in 21% (17-26), quetiapine in 19% (14-23) and olanzapine in 9% (6-12) of the patients with delirium. In the first 24 h in the ICU, all subtypes of delirium [hyperactive, adjusted odds ratio (aOR) 29.7 (12.9-74.5); mixed 10.0 (5.0-20.2); hypoactive 3.0 (1.2-6.7)] and circulatory support 2.7 (1.7-4.3) were associated with haloperidol use. At 72 h after ICU admission, circulatory support remained associated with subsequent use of haloperidol, aOR 2.6 (1.1-6.9). Haloperidol use within 0-24 h and within 0-72 h of ICU admission was not associated with 90-day mortality [aOR 1.2 (0.5-2.5); p = 0.66] and [aOR 1.9 (1.0-3.9); p = 0.07], respectively. In our study, haloperidol was the main pharmacological agent used for delirium in adult patients regardless of delirium subtype. Benzodiazepines, other anti-psychotics and dexmedetomidine were other frequently used agents. Haloperidol use was not statistically significantly associated with increased 90-day mortality.Peer reviewe

Serum fibroblast growth factor 21 levels after out of hospital cardiac arrest are associated with neurological outcome

Fibroblast growth factor (FGF) 21 is a marker associated with mitochondrial and cellular stress. Cardiac arrest causes mitochondrial stress, and we tested if FGF 21 would reflect the severity of hypoxia-reperfusion injury after cardiac arrest. We measured serum concentrations of FGF 21 in 112 patients on ICU admission and 24, 48 and 72 h after out-of-hospital cardiac arrest with shockable initial rhythm included in the COMACARE study (NCT02698917). All patients received targeted temperature management for 24 h. We defined 6-month cerebral performance category 1-2 as good and 3-5 as poor neurological outcome. We used samples from 40 non-critically ill emergency room patients as controls. We assessed group differences with the Mann Whitney U test and temporal differences with linear modeling with restricted maximum likelihood estimation. We used multivariate logistic regression to assess the independent predictive value of FGF 21 concentration for neurologic outcome. The median (inter-quartile range, IQR) FGF 21 concentration was 0.25 (0.094-0.91) ng/ml in controls, 0.79 (0.37-1.6) ng/ml in patients at ICU admission (PPeer reviewe

Near-infrared spectroscopy after out-of-hospital cardiac arrest

BackgroundCerebral hypoperfusion may aggravate neurological damage after cardiac arrest. Near-infrared spectroscopy (NIRS) provides information on cerebral oxygenation but its relevance during post-resuscitation care is undefined. We investigated whether cerebral oxygen saturation (rSO(2)) measured with NIRS correlates with the serum concentration of neuron-specific enolase (NSE), a marker of neurological injury, and with clinical outcome in out-of-hospital cardiac arrest (OHCA) patients.MethodsWe performed a post hoc analysis of a randomised clinical trial (COMACARE, NCT02698917) comparing two different levels of carbon dioxide, oxygen and arterial pressure after resuscitation from OHCA with ventricular fibrillation as the initial rhythm. We measured rSO(2) in 118 OHCA patients with NIRS during the first 36h of intensive care. We determined the NSE concentrations from serum samples at 48h after cardiac arrest and assessed neurological outcome with the Cerebral Performance Category (CPC) scale at 6months. We evaluated the association between rSO(2) and serum NSE concentrations and the association between rSO(2) and good (CPC 1-2) and poor (CPC 3-5) neurological outcome.ResultsThe median (inter-quartile range (IQR)) NSE concentration at 48h was 17.5 (13.4-25.0) g/l in patients with good neurological outcome and 35.2 (22.6-95.8) g/l in those with poor outcome, pPeer reviewe

Near-infrared spectroscopy after out-of-hospital cardiac arrest

BackgroundCerebral hypoperfusion may aggravate neurological damage after cardiac arrest. Near-infrared spectroscopy (NIRS) provides information on cerebral oxygenation but its relevance during post-resuscitation care is undefined. We investigated whether cerebral oxygen saturation (rSO(2)) measured with NIRS correlates with the serum concentration of neuron-specific enolase (NSE), a marker of neurological injury, and with clinical outcome in out-of-hospital cardiac arrest (OHCA) patients.MethodsWe performed a post hoc analysis of a randomised clinical trial (COMACARE, NCT02698917) comparing two different levels of carbon dioxide, oxygen and arterial pressure after resuscitation from OHCA with ventricular fibrillation as the initial rhythm. We measured rSO(2) in 118 OHCA patients with NIRS during the first 36h of intensive care. We determined the NSE concentrations from serum samples at 48h after cardiac arrest and assessed neurological outcome with the Cerebral Performance Category (CPC) scale at 6months. We evaluated the association between rSO(2) and serum NSE concentrations and the association between rSO(2) and good (CPC 1-2) and poor (CPC 3-5) neurological outcome.ResultsThe median (inter-quartile range (IQR)) NSE concentration at 48h was 17.5 (13.4-25.0) g/l in patients with good neurological outcome and 35.2 (22.6-95.8) g/l in those with poor outcome, pPeer reviewe

Neurofilament light as an outcome predictor after cardiac arrest : a post hoc analysis of the COMACARE trial

Purpose Neurofilament light (NfL) is a biomarker reflecting neurodegeneration and acute neuronal injury, and an increase is found following hypoxic brain damage. We assessed the ability of plasma NfL to predict outcome in comatose patients after out-of-hospital cardiac arrest (OHCA). We also compared plasma NfL concentrations between patients treated with two different targets of arterial carbon dioxide tension (PaCO2), arterial oxygen tension (PaO2), and mean arterial pressure (MAP). Methods We measured NfL concentrations in plasma obtained at intensive care unit admission and at 24, 48, and 72 h after OHCA. We assessed neurological outcome at 6 months and defined a good outcome as Cerebral Performance Category (CPC) 1-2 and poor outcome as CPC 3-5. Results Six-month outcome was good in 73/112 (65%) patients. Forty-eight hours after OHCA, the median NfL concentration was 19 (interquartile range [IQR] 11-31) pg/ml in patients with good outcome and 2343 (587-5829) pg/ml in those with poor outcome,p <0.001. NfL predicted poor outcome with an area under the receiver operating characteristic curve (AUROC) of 0.98 (95% confidence interval [CI] 0.97-1.00) at 24 h, 0.98 (0.97-1.00) at 48 h, and 0.98 (0.95-1.00) at 72 h. NfL concentrations were lower in the higher MAP (80-100 mmHg) group than in the lower MAP (65-75 mmHg) group at 48 h (median, 23 vs. 43 pg/ml,p = 0.04). PaCO(2)and PaO(2)targets did not associate with NfL levels. Conclusions NfL demonstrated excellent prognostic accuracy after OHCA. Higher MAP was associated with lower NfL concentrations.Peer reviewe

GFAp and tau protein as predictors of neurological outcome after out-of-hospital cardiac arrest: A post hoc analysis of the COMACARE trial

Aim: To determine the ability of serum glial fibrillary acidic protein (GFAp) and tau protein to predict neurological outcome after out-of-hospital cardiac arrest (OHCA). Methods: We measured plasma concentrations of GFAp and tau of patients included in the previously published COMACARE trial (NCT02698917) on intensive care unit admission and at 24, 48, and 72 h after OHCA, and compared them to neuron specific enolase (NSE). NSE concentrations were determined already during the original trial. We defined unfavourable outcome as a cerebral performance category (CPC) score of 3-5 six months after OHCA. We determined the prognostic accuracy of GFAp and tau using the receiver operating characteristic curve and area under the curve (AUROC). Results: Overall, 39/112 (35%) patients had unfavourable outcomes. Over time, both markers were evidently higher in the unfavourable outcome group (p < 0.001). At 48 h, the median (interquartile range) GFAp concentration was 1514 (886-4995) in the unfavourable versus 238 (135-463) pg/ ml in the favourable outcome group (p < 0.001). The corresponding tau concentrations were 99.6 (14.5-352) and 3.0 (2.2-4.8) pg/ml (p < 0.001). AUROCs at 48 and 72 h were 0.91 (95% confidence interval 0.85-0.97) and 0.91 (0.85-0.96) for GFAp and 0.93 (0.86-0.99) and 0.95 (0.89-1.00) for tau. Corresponding AUROCs for NSE were 0.86 (0.79-0.94) and 0.90 (0.82-0.97). The difference between the prognostic accuracies of GFAp or tau and NSE were not statistically significant. Conclusions: At 48 and 72 h, serum both GFAp and tau demonstrated excellent accuracy in predicting outcomes after OHCA but were not superior to NSE. Clinical trial registration: NCT02698917 (https://www.clinicaltrials.gov/ct2/show/NCT02698917).Peer reviewe

Optimum Blood Pressure in Patients With Shock After Acute Myocardial Infarction and Cardiac Arrest

BACKGROUND In patients with shock after acute myocardial infarction (AMI), the optimal level of pharmacologic support is unknown. Whereas higher doses may increase myocardial oxygen consumption and induce arrhythmias, diastolic hypotension may reduce coronary perfusion and increase infarct size. OBJECTIVES This study aimed to determine the optimal mean arterial pressure (MAP) in patients with AMI and shock after cardiac arrest. METHODS This study used patient-level pooled analysis of post-cardiac arrest patients with shock after AMI randomized in the Neuroprotect (Neuroprotective Goal Directed Hemodynamic Optimization in Post-cardiac Arrest Patients; NCT02541591) and COMACARE (Carbon Dioxide, Oxygen and Mean Arterial Pressure After Cardiac Arrest and Resuscitation; NCT02698917) trials who were randomized to MAP 65 mm Hg or MAP 80/85 to 100 mm Hg targets during the first 36 h after admission. The primary endpoint was the area under the 72-h high-sensitivity troponin-T curve. RESULTS Of 235 patients originally randomized, 120 patients had AMI with shock. Patients assigned to the higher MAP target (n = 58) received higher doses of norepinephrine (p = 0.004) and dobutamine (p = 0.01) and reached higher MAPs (86 +/- 9 mm Hg vs. 72 +/- 10 mm Hg, p <0.001). Whereas admission hemodynamics and angiographic findings were all well-balanced and revascularization was performed equally effective, the area under the 72-h high-sensitivity troponin-T curve was lower in patients assigned to the higher MAP target (median: 1.14 mu g.72 h/l [interquartile range: 0.35 to 2.31 mu g.72 h/l] vs. median: 1.56 mu g.72 h/l [interquartile range: 0.61 to 4.72 mu g. 72 h/l]; p = 0.04). Additional pharmacologic support did not increase the risk of a new cardiac arrest (p = 0.88) or atrial fibrillation (p = 0.94). Survival with good neurologic outcome at 180 days was not different between both groups (64% vs. 53%, odds ratio: 1.55; 95% confidence interval: 0.74 to 3.22). CONCLUSIONS In post-cardiac arrest patients with shock after AMI, targeting MAP between 80/85 and 100 mm Hg with additional use of inotropes and vasopressors was associated with smaller myocardial injury. (C) 2020 by the American College of Cardiology Foundation.Peer reviewe

Seurantakäsikirja Suomen merenhoitosuunnitelman seurantaohjelmaan vuosille 2020–2026

Tämä merenhoidon seurantakäsikirja käsittää merenhoitosuunnitelman seurantaohjelman kuvauksen kokonaisuudessaan. Se päivittää vuoden 2014–2020 seurantaohjelman ja sitä sovelletaan vuoden 2020 heinäkuusta vuoden 2026 heinäkuuhun. Seurantaohjelma on osa merenhoidon suunnittelua, jota tehdään vesienhoidon ja merenhoidon järjestämisestä annetun lain (272/2011) ja merenhoidon järjestämisestä annetun valtioneuvoston asetuksen (980/2011) toteuttamiseksi. Tämä laki ja asetus on annettu meristrategiadirektiivin (Euroopan parlamentin ja neuvoston direktiivi 2008/56/EY yhteisön meriympäristöpolitiikan puitteista) kansallista toimeenpanoa varten. Suomessa meristrategiadirektiivin mukaista meristrategiaa kutsutaan merenhoitosuunnitelmaksi. Suomen seurantaohjelma koostuu 13:sta ohjelmasta, joiden alla on yhteensä 44 alaohjelmaa. Tähän päivitettyyn seurantaohjelmaan lisättiin kuusi uutta alaohjelmaa ja useita alaohjelmia muokattiin joko muuttuneiden vaatimusten, kehittyneempien menetelmien tai muuttuneen toimintaympäristön takia. Merenhoidon uusia vaatimuksia ovat meristrategiadirektiivin liitteen 3 päivitys (EU/2017/845), Euroopan komission päätös EU/2017/848 merivesien hyvän ekologisen tilan vertailuperusteista ja menetelmästandardeista sekä seurantaa ja arviointia varten tarkoitetut täsmennykset standardoiduista menetelmistä. Seurantakäsikirja koostuu kolmesta osasta: seurantaohjelman tausta, varsinainen seurantaohjelma, ja kolmas osa, joka käsittelee seurannan kehitystarpeita, kustannuksia ja riittävyyttä. Seurantaohjelma kattaa ekosysteemilähestymistavan mukaisesti erilaisia muuttujia, jotka kuvaavat toisaalta veden ominaisuuksia ja laatua ja toisaalta ekosysteemin osia ja niiden tilaa sekä niihin kohdistuvia ihmisestä johtuvia paineita. Seurannan alaohjelmissa on kuvattu mitattavat meriympäristön ominaisuudet tai paineet, niiden seurantatiheys, indikaattorit, joihin seurantatietoa käytetään, seurannalla kootun tiedon hallinta ja yhteydet meristrategiadirektiivin hyvän tilan laadullisiin kuvaajiin ja kriteereihin