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In a trial involving patients with coma after out-of-hospital cardiac arrest, a strategy targeting mild hypercapnia for 24 hours did not improve neurologic outcomes at 6 months as compared with targeted normocapnia.

Background N -acetylcysteine (NAC) improves transplant-free survival in early coma grade (I–II) patients with non-acetaminophen induced acute liver failure (ALF). We determined whether the clinical benefit was associated with improvements in hepatic function. Methods In a prospective, double blind trial, 173 ALF patients without evidence of acetaminophen overdose were stratified by coma grade (I–II vs. III–IV) and randomly assigned to receive either intravenous NAC or dextrose (placebo) for 72 h, resulting in four patient groups. INR, ALT, bilirubin, creatinine, and AST obtained on admission (day 1) and subsequent days (days 2–4) were used for secondary analysis performed by fitting longitudinal logistic regression models to predict death or transplantation or transplantation alone. Results Treatment group and day of study in models including bilirubin or ALT were predictors of transplantation or death (maximum p  < 0.03). Those patients with early coma grade who were treated with NAC showed significant improvement in bilirubin and ALT levels when compared to the other three groups (maximum p  < 0.02 for NAC 1–2 vs. the 3 other treatments) when predicting death or transplantation. Treatment group, day of study, and bilirubin were predictors of transplantation (maximum p  < 0.03) in ALF patients. Conclusion The decreased risk of transplantation or death or of transplantation alone with intravenous NAC in early coma grade patients with non-acetaminophen induced ALF was reflected in improvement in parameters related to hepatocyte necrosis and bile excretion including ALT and bilirubin, but not in INR, creatinine, or AST. Hepatic recovery appears hastened by NAC as measured by several important lab values.

PurposeThe purpose of this study was to determine associations between markers of inflammation and endogenous anticoagulant activity with delirium and coma during critical illness.MethodsIn this prospective cohort study, we enrolled adults with respiratory failure and/or shock treated in medical or surgical intensive care units (ICUs) at 5 centers. Twice per day in the ICU, and daily thereafter, we assessed mental status using the Richmond Agitation Sedation Scale (RASS) and the Confusion Assessment Method-Intensive Care Unit (CAM-ICU). We collected blood samples on study days 1, 3, and 5, measuring levels of C-reactive protein (CRP), interferon gamma (IFN-γ), interleukin (IL)-1 beta (IL-1β), IL-6, IL-8, IL-10, IL-12, matrix metalloproteinase-9 (MMP-9), tumor necrosis factor-alpha (TNF-α), tumor necrosis factor receptor 1 (TNFR1), and protein C using validated protocols. We used multinomial logistic regression to analyze associations between biomarkers and the odds of delirium or coma versus normal mental status the following day, adjusting for age, sepsis, Sequential Organ Failure Assessment (SOFA), study day, corticosteroids, and sedatives.ResultsAmong 991 participants with a median age (interquartile range, IQR) of 62 [53–72] years and enrollment SOFA of 9 [7–11], higher concentrations of IL-6 (odds ratio [OR] [95% CI]: 1.8 [1.4–2.3]), IL-8 (1.3 [1.1–1.5]), IL-10 (1.5 [1.2–1.8]), TNF-α (1.2 [1.0–1.4]), and TNFR1 (1.3 [1.1–1.6]) and lower concentrations of protein C (0.7 [0.6–0.8])) were associated with delirium the following day. Higher concentrations of CRP (1.4 [1.1–1.7]), IFN-γ (1.3 [1.1–1.5]), IL-6 (2.3 [1.8–3.0]), IL-8 (1.8 [1.4–2.3]), and IL-10 (1.5 [1.2–2.0]) and lower concentrations of protein C (0.6 [0.5–0.8]) were associated with coma the following day. IL-1β, IL-12, and MMP-9 were not associated with mental status.ConclusionMarkers of inflammation and possibly endogenous anticoagulant activity are associated with delirium and coma during critical illness.

Abstract Rationale Acute kidney injury may contribute to distant organ dysfunction. Few studies have examined kidney injury as a risk factor for delirium and coma. Objectives To examine whether acute kidney injury is associated with delirium and coma in critically ill adults. Methods In a prospective cohort study of intensive care unit patients with respiratory failure and/or shock, we examined the association between acute kidney injury and daily mental status using multinomial transition models adjusting for demographics, nonrenal organ failure, sepsis, prior mental status, and sedative exposure. Acute kidney injury was characterized daily using the difference between baseline and peak serum creatinine and staged according to Kidney Disease Improving Global Outcomes criteria. Mental status (normal vs. delirium vs. coma) was assessed daily with the Confusion Assessment Method for the ICU and Richmond Agitation-Sedation Scale. Measurements and Main Results Among 466 patients, stage 2 acute kidney injury was a risk factor for delirium (odds ratio [OR], 1.55; 95% confidence interval [CI], 1.07–2.26) and coma (OR, 2.04; 95% CI, 1.25–3.34) as was stage 3 injury (OR for delirium, 2.56; 95% CI, 1.57–4.16) (OR for coma, 3.34; 95% CI, 1.85–6.03). Daily peak serum creatinine (adjusted for baseline) values were also associated with delirium (OR, 1.35; 95% CI, 1.18–1.55) and coma (OR, 1.44; 95% CI, 1.20–1.74). Renal replacement therapy modified the association between stage 3 acute kidney injury and daily peak serum creatinine and both delirium and coma. Conclusions Acute kidney injury is a risk factor for delirium and coma during critical illness.

To assess the association of serum glycocalyx shedding components (Heparan sulfate, HS; Hyaluronic acid, HA; Syndecan-1, Sdc-1) with outcomes after CA. Patients who were comatose for >24 h after CA in the intensive care unit (ICU) of the Affiliated Hospital of Xuzhou Medical University from 9/2021 to 04/2023 were enrolled. Serum samples were collected 24 h after CA to measure the concentrations of glycocalyx shedding components. The outcomes were the 30-day Cerebral Performance Categories (CPC) scale and 30-day mortality. The association of glycocalyx shedding with outcomes was examined by regression analysis. The area under the curve was used to evaluate the value of glycocalyx shedding for predicting outcomes. Sensitivity analysis and subgroup analysis were conducted. 111 patients were enrolled. The unfavorable group (CPC 3–5, n = 69) had significantly higher serum concentrations of HA and Sdc-1 than the favorable group (CPC 1–2, n = 42) (HA:149.7 ng/ml vs. 824.8 ng/ml, P < 0.001; Sdc-1: 303.8 ng/L vs. 447.0 ng/L, P = 0.026)but not HS. Elevated serum HA concentrations was an independent risk factor for unfavorable 30-day neurological function (OR = 2.485, 95 % CI = 1.656–3.729). For the 30-day mortality, the nonsurvivor group (n = 53) had significantly higher serum concentrations of HA, HS and Sdc-1 (HA: 177.3 ng/ml vs. 1106.7 ng/ml, P < 0.001; HS: 2403.7 ng/ml vs. 3383.3 ng/ml P = 0.030; Sdc-1: 352.1 ng/L vs. 487.8 ng/L, P = 0.005) than the survivor group (n = 58). However, only elevated serum HA and Sdc-1 concentrations are independent risk factors for 30-day mortality (HA: HR = 2.321, 95 % CI = 1.776–3.035; Sdc-1: HR = 1.702, 95 % CI = 1.038–2.792). Elevated serum HA at 24 h after CA is an independent risk factor for 30-day unfavorable neurological function or mortality and elevated serum Sdc-1 concentrations is an independent risk factor for 30-day mortality. Our results suggested the potential value of serum glycocalyx shedding components as predictors for the outcomes in post-CA patients. •An observational study assessed the link between serum glycocalyx components and prognosis after cardiac arrest.•Serum glycocalyx components are associated with poor prognosis after cardiac arrest.•The serum glycocalyx shedding components are promising predictors for the prognosis in post-CA patient.

Background Disordered amino acid metabolism is observed in cerebral malaria (CM). This study sought to determine whether abnormal amino acid concentrations were associated with level of consciousness in children recovering from coma. Twenty-one amino acids and coma scores were quantified longitudinally and the data were analysed for associations. Methods In a prospective observational study, 42 children with CM were enrolled. Amino acid levels were measured at entry and at frequent intervals thereafter and consciousness was assessed by Blantyre Coma Scores (BCS). Thirty-six healthy children served as controls for in-country normal amino acid ranges. Logistic regression was employed using a generalized linear mixed-effects model to assess associations between out-of-range amino acid levels and BCS. Results At entry 16/21 amino acid levels were out-of-range. Longitudinal analysis revealed 10/21 out-of-range amino acids were significantly associated with BCS. Elevated phenylalanine levels showed the highest association with low BCS. This finding held when out-of-normal-range data were analysed at each sampling time. Conclusion Longitudinal data is provided for associations between abnormal amino acid levels and recovery from CM. Of 10 amino acids significantly associated with BCS, elevated phenylalanine may be a surrogate for impaired clearance of ether lipid mediators of inflammation and may contribute to CM pathogenesis.

Previous episodes of hypoglycemic coma are not associated with permanent cognitive brain dysfunction in IDDM patients on intensive insulin treatment. L Kramer , P Fasching , C Madl , B Schneider , P Damjancic , W Waldhäusl , K Irsigler and G Grimm Department of Medicine, University of Vienna, Austria. ludwig.kramer@akh-wien.ac.at Abstract Intensive insulin treatment of IDDM is associated with increased frequency of hypoglycemic coma. The extent of possible cerebral sequelae after recovery is still unknown. We studied the impact of previous hypoglycemic coma on neurophysiological measures of cognitive brain function in 108 patients with adult-onset IDDM receiving intensive insulin treatment. In the study, 55 IDDM patients (age 38 +/- 14 years, mean +/- SD) who had a history of > or =1 (median 3, range 1-35) comatose hypoglycemic event were compared with 53 IDDM patients (age 34 +/- 12 years) with no history of hypoglycemic events using P300 event-related potentials and psychometric tests (the Mini-Mental State Exam and trailmaking test, part A). Findings on these patients were compared with those from 108 matched healthy control subjects. No difference was observed in P300 latencies and psychometric tests between patients with and without a history of hypoglycemic coma (P300 latency, 346 vs. 342 ms; trailmaking test, 31 vs. 30 s; Mini-Mental State Exam, 29.5 vs. 29.6; NS). In diabetic patients, however, P300 latencies were delayed compared with those of healthy control subjects (344 vs. 332 ms; P < 0.001) and were correlated to diabetes duration but not to total hypoglycemic episodes. Scores on the Mini-Mental State Exam (29.5 vs. 29.6; P = 0.59) and trailmaking test (31 vs. 28 s; P = 0.10) were not different between patients and control subjects. In conclusion, previous episodes of hypoglycemic coma are not associated with permanent impairment of cognitive brain function in patients with adult-onset IDDM receiving intensive insulin treatment compared with patients without such episodes. Cognitive brain function, however, is subclinically impaired in relation to duration of diabetes.

Research indicates that glial fibrillary acidic protein (GFAP), part of the astroglial skeleton, could be a marker of traumatic brain injury (TBI). S100B, an astroglial protein, is an acknowledged marker of TBI. Our goal was to analyze the relationship of GFAP/S100B to brain damage and outcome, and to compare the accuracy of GFAP/S100B for prediction of mortality after TBI. Our prospective study included 92 patients admitted <12 h after TBI (median injury severity score 25, median Glasgow Coma Scale 6). TBI was verfied by computerized tomography. GFAP/S100B were measured immunoluminometrically at admission and daily in the intensive care unit (average 10 days, range 1–21 days). We compared GFAP/S100B in non-survivors versus survivors, accuracy for mortality prediction according to receiver operated characteristic curve analysis, correlation between GFAP and S100B, relationship of GFAP/S100B to computerized tomography, cerebral perfusion pressure (CPP), mean arterial pressure (MAP) and 3-month Glasgow Outcome Score (GOS). GFAP (p < 0.005) and S100B (p < 0.0005) were higher in non-survivors than survivors. Both GFAP and S100B were accurate for mortality prediction (area under curve 0.84 versus 0.78 at <12 h after TBI). GFAP and S100B release correlated better later than 36 h after TBI (r = 0.75) than earlier(r = 0.58). GFAP was lower in focal lesions of <25 mL than in shifts of >0.5 cm (p < 0.0005) and non-evacuated mass lesions of >25 mL (p < 0.005). S100B was lower in focal lesions of <25 mL than in non-evacuated mass lesions (p < 0.0005) and lower in swelling than in shifts of >0.5 cm(p < 0.005). GFAP and S100B were lower in ICP < 25 than ICP ≥ 25 (p < 0.0005), in CPP ≥ 60 than CPP < 60 (p < 0.0005), in MAP > 70 than MAP ≤ 70 mm Hg, and in GOS 4–5 than GOS 1(p < 0.0005). Both measurement of GFAP and S100B is a useful non-invasive means of identifying brain damage with some differences based on the pattern of TBI and accompanying multiple trauma and/or shock.

Traditionally, basal rate profiles in continuous subcutaneous insulin infusion therapy are individually adapted to cover expected insulin requirements. However, whether this approach is indeed superior to a more constant BR profile has not been assessed so far. This study analysed the associations between variability of BR profiles and acute and chronic complications in adult type 1 diabetes mellitus. BR profiles of 3118 female and 2427 male patients from the \"Diabetes-Patienten-Verlaufsdokumentation\" registry from Germany and Austria were analysed. Acute and chronic complications were recorded 6 months prior and after the most recently documented basal rate. The \"variability index\" was calculated as variation of basal rate intervals in percent and describes the excursions of the basal rate intervals from the median basal rate. The variability Index correlated positively with severe hypoglycemia (r = .06; p<0.001), hypoglycemic coma (r = .05; p = 0.002), and microalbuminuria (r = 0.05; p = 0.006). In addition, a higher variability index was associated with higher frequency of diabetic ketoacidosis (r = .04; p = 0.029) in male adult patients. Logistic regression analysis adjusted for age, gender, duration of disease and total basal insulin confirmed significant correlations of the variability index with severe hypoglycemia (β = 0.013; p<0.001) and diabetic ketoacidosis (β = 0.012; p = 0.017). Basal rate profiles with higher variability are associated with an increased frequency of acute complications in adults with type 1 diabetes.

Objective To establish whether diabetic ketoacidosis (DKA) or HbA1c at onset is associated with year‐three HbA1c in children with type 1 diabetes (T1D). Methods Children with T1D from the SWEET registry, diagnosed <18 years, with documented clinical presentation, HbA1c at onset and follow‐up were included. Participants were categorized according to T1D onset: (a) DKA (DKA with coma, DKA without coma, no DKA); (b) HbA1c at onset (low [<10%], medium [10 to <12%], high [≥12%]). To adjust for demographics, linear regression was applied with interaction terms for DKA and HbA1c at onset groups (adjusted means with 95% CI). Association between year‐three HbA1c and both HbA1c and presentation at onset was analyzed (Vuong test). Results Among 1420 children (54% males; median age at onset 9.1 years [Q1;Q3: 5.8;12.2]), 6% of children experienced DKA with coma, 37% DKA without coma, and 57% no DKA. Year‐three HbA1c was lower in the low compared to high HbA1c at onset group, both in the DKA without coma (7.1% [6.8;7.4] vs 7.6% [7.5;7.8], P = .03) and in the no DKA group (7.4% [7.2;7.5] vs 7.8% [7.6;7.9], P = .01), without differences between low and medium HbA1c at onset groups. Year‐three HbA1c did not differ among HbA1c at onset groups in the DKA with coma group. HbA1c at onset as an explanatory variable was more closely associated with year‐three HbA1c compared to presentation at onset groups (P = .02). Conclusions Year‐three HbA1c is more closely related to HbA1c than to DKA at onset; earlier hyperglycemia detection might be crucial to improving year‐three HbA1c.