Update - intoxications in critical care medicine

While monitoring and symptomatic care is sufficient for most intoxicated patients, some develop life threatening symptoms. We present recent changes in the recommendations of the treatment in patients with calcium channel blocker, beta blocker and high dose paracetamol intoxications. Additionally, new insights in the efficacy and safety of the use of physostigmine in anticholinergic patients and beta blockers in cocaine intoxication are discussed as well as the specific considerations in the resuscitation of intoxicated patients

Long lie trauma patients: retrospective analysis of a patient cohort presenting to a university hospital emergency department

Background Patients discovered recumbent, helpless and incapacitated, awake or unresponsive are referred to as long lie trauma (LLT) in the German medical jargon. Yet, a characterization of this cohort is missing. Methods We retrospectively analyzed all LLT patients admitted to the emergency department of the University Hospital Cologne from July 2018 to December 2020. Results A total of 50 LLT patients (median age 76 years, median time on the ground 13.5 h) were identified. The FD was most often attributed to primary cerebral causes in 40% of the cases (20% ischemic stroke, 16% intracranial hemorrhage, 4% epilepsy), intoxication/overdose (12%), and trauma (10%). It was often associated with infection (52%), injury (22%), hypovolemia (66%), acute kidney injury (20%), and severe rhabdomyolysis (creatine kinase >= 5000 U/l, 21%) as well as severe hypothermia < 32 degrees C (20%). Overall, 69% of the patients were admitted to an intensive care unit and in-hospital mortality was 50%. Conclusion The term long lie trauma describes a complex clinical situation, in which various conditions lead to an incapacitated state with acute onset, which then causes further adverse health effects. Trauma or tissue damage were no obligatory requirement in this syndrome. Considering the high morbidity and in-hospital mortality, patients should initially be treated in the emergency room by an interdisciplinary team

Higher chance of survival in patients with out-of-hospital cardiac arrest attributed to poisoning

Aim of the study: Description and comparison of cohort characteristics and outcome of adult patients with out-of-hospital cardiac arrest (OHCA) attributed to poisoning (P-OHCA) versus patients with OHCA attributed to other medical causes (NP-OHCA). Methods: We included all patients who received cardiopulmonary resuscitation after OHCA between January 2011 and December 2020 from German emergency medical services with good data quality in the German Resuscitation Registry. Exclusion criteria: patients < 18 years of age or OHCA attributed to trauma, drowning, intracranial bleeding or exsanguination. Results: Patients with P-OHCA (n = 574) were significantly younger compared to NP-OHCA (n = 40,146) (median age of 43 (35-54) years vs. 73 (62-82) years; p < 0.001). Cardiac arrest in P-OHCA patients was significantly less often witnessed by bystanders (41.8 % vs. 66.2 %, p < 0.001). Asystole was the predominant initial rhythm in P-OHCA patients (73.5% vs. 53.7%, p < 0.001) while ventricular fibrillation (VF) and pulseless electrical activity (PEA) were less common (9.2% vs. 25.1% and 16.2 % vs. 20.5%, p < 0.001). P-OHCA had a higher chance of survival with good neurological outcome at hospital discharge (15.2 vs. 8.8 % p < 0.001) and poisoning was an independent protective prognostic factor in multivariate analysis (OR 2.47, 95%-CI [1.71-3.57]). P-OHCA patients with initial PEA survival with good neurological outcome was comparable to initial VF (34.3 % vs. 37.7%). Conclusion: Patients in the P-OHCA group had a significantly higher chance of survival with good neurological outcome and PEA as initial rhythm was as favourable as initial VF. Therefore, in P-OHCA patients resuscitation efforts should be extended

Impairment of Neurocognitive Functioning, Motor Performance, and Mood Stability in Hospitalized Patients With Euvolemic Moderate and Profound Hyponatremia

BACKGROUND: The impact of chronic moderate and profound hyponatremia on neurocognitive performance, motor skills, and mood stability has not been investigated systematically so far, and results regarding mild to moderate hyponatremia are inconsistent. Furthermore, it is not known whether treatment has an effect on outcome in these patients. METHODS: A total of 130 hospitalized patients with confirmed euvolemic hyponatremia (< 130 mEq/L) were subjected to a test battery (Mini-Mental State Examination, DemTect, Trail-Making Tests A and B, Beck Depression Inventory, Timed-up-and-go Test) before and after treatment; additionally, 50 normonatremic group-matched patients served as reference group. RESULTS: The scores of all tested domains were significantly worse in the hyponatremia group (median serum sodium [Na+] 122 (119-126) mEq/L) as compared to the reference group (P < 0.001), and the odds of obtaining a pathological test result increased markedly with more profound hyponatremic states (odds ratios between 5.0 and 21.8 in the group with Na+ <120 mEq/L compared to reference group). Inversely, treatment led to a significant amelioration of all test results with medium to large effect sizes. Linear regression models revealed the increment of Na+ as an important predictor of test outcome. CONCLUSION: We demonstrate a clear association between lower levels of Na+ beyond mild hyponatremia and impairment of neurocognitive and motor performance as well as mood disorders. Our analysis further suggests a causal role of hyponatremia in this context. However, there are apparent differences between the distinct tested domains warranting further investigations. (C) 2020 Elsevier Inc. All rights reserved

Reduced mitochondrial resilience enables non-canonical induction of apoptosis after TNF receptor signaling in virus-infected hepatocytes

Background & Aims: Selective elimination of virus-infected hepatocytes occurs through virus-specific CD8 T cells recognizing peptide-loaded MHC molecules. Herein, we report that virus-infected hepatocytes are also selectively eliminated through a cell-autonomous mechanism. Methods: We generated recombinant adenoviruses and genetically modified mouse models to identify the molecular mechanisms determining TNF-induced hepatocyte apoptosis in vivo and used in vivo bioluminescence imaging, immunohistochemistry, immunoblot analysis, RNAseq/proteome/phosphoproteome analyses, bioinformatic analyses, mitochondrial function tests. Results: We found that TNF precisely eliminated only virus-infected hepatocytes independently of local inflammation and activation of immune sensory receptors. TNF receptor I was equally relevant for NF-kB activation in healthy and infected hepatocytes, but selectively mediated apoptosis in infected hepatocytes. Caspase 8 activation downstream of TNF receptor signaling was dispensable for apoptosis in virus-infected hepatocytes, indicating an unknown non-canonical cell-intrinsic pathway promoting apoptosis in hepatocytes. We identified a unique state of mitochondrial vulnerability in virus-infected hepatocytes as the cause for this non-canonical induction of apoptosis through TNF. Mitochondria from virus-infected hepatocytes showed normal biophysical and bioenergetic functions but were characterized by reduced resilience to calcium challenge. In the presence of unchanged TNF-induced signaling, reactive oxygen species-mediated calcium release from the endoplasmic reticulum caused mitochondrial permeability transition and apoptosis, which identified a link between extrinsic death receptor signaling and cell-intrinsic mitochondrial-mediated caspase activation. Conclusion: Our findings reveal a novel concept in immune surveillance by identifying a cell-autonomous defense mechanism that selectively eliminates virus-infected hepatocytes through mitochondrial permeability transition. Lay summary: The liver is known for its unique immune functions. Herein, we identify a novel mechanism by which virus-infected hepatocytes can selectively eliminate themselves through reduced mitochondrial resilience to calcium challenge. (C) 2020 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved