Search

Critically ill COVID-19 patients are at high risk for venous thromboembolism (VTE), namely deep vein thrombosis (DVT) and/or pulmonary embolism (PE), and death. The optimal anticoagulation strategy in critically ill patients with COVID-19 remains unknown. This study investigated the ante mortem incidence as well as postmortem prevalence of VTE, the factors predictive of VTE, and the impact of changed anticoagulation practice on patient survival. We conducted a consecutive retrospective analysis of postmortem COVID-19 ( n = 64) and non-COVID-19 ( n = 67) patients, as well as ante mortem COVID-19 ( n = 170) patients admitted to the University Medical Center Hamburg-Eppendorf (Hamburg, Germany). Baseline patient characteristics, parameters related to the intensive care unit (ICU) stay, and the clinical and autoptic presence of VTE were evaluated and statistically compared between groups. The occurrence of VTE in critically ill COVID-19 patients is confirmed in both ante mortem (17%) and postmortem (38%) cohorts. Accordingly, comparing the postmortem prevalence of VTE between age- and sex-matched COVID-19 (43%) and non-COVID-19 (0%) cohorts, we found the statistically significant increased prevalence of VTE in critically ill COVID-19 cohorts ( p = 0.001). A change in anticoagulation practice was associated with the statistically significant prolongation of survival time (HR: 2.55, [95% CI 1.41-4.61], p = 0.01) and a reduction in VTE occurrence (54% vs. 25%; p = 0.02). In summary, in the autopsy as well as clinical cohort of critically ill patients with COVID-19, we found that VTE was a frequent finding. A change in anticoagulation practice was associated with a statistically significantly prolonged survival time.

Background: There are large uncertainties with regard to the outcome of patients with coronavirus disease 2019 (COVID-19) and mechanical ventilation (MV). High mortality (50-97%) was proposed by some groups, leading to considerable uncertainties with regard to outcomes of critically ill patients with COVID-19., Objectives: The aim was to investigate the characteristics and outcomes of critically ill patients with COVID-19 requiring intensive care unit (ICU) admission and MV., Methods: A multicentre retrospective observational cohort study at 15 hospitals in Hamburg, Germany, was performed. Critically ill adult patients with COVID-19 who completed their ICU stay between February and June 2020 were included. Patient demographics, severity of illness, and ICU course were retrospectively evaluated., Results: A total of 223 critically ill patients with COVID-19 were included. The majority, 73% (n = 163), were men; the median age was 69 (interquartile range = 58-77.5) years, with 68% (n = 151) patients having at least one chronic medical condition. Their Sequential Organ Failure Assessment score was a median of 5 (3-9) points on admission. Overall, 167 (75%) patients needed MV. Noninvasive ventilation and high-flow nasal cannula were used in 31 (14%) and 26 (12%) patients, respectively. Subsequent MV, due to noninvasive ventilation/high-flow nasal cannula therapy failure, was necessary in 46 (81%) patients. Renal replacement therapy was initiated in 33% (n = 72) of patients, and owing to severe respiratory failure, extracorporeal membrane oxygenation was necessary in 9% (n = 20) of patients. Experimental antiviral therapy was used in 9% (n = 21) of patients. Complications during the ICU stay were as follows: septic shock (40%, n = 90), heart failure (8%, n = 17), and pulmonary embolism (6%, n = 14). The length of ICU stay was a median of 13 days (5-24), and the duration of MV was 15 days (8-25). The ICU mortality was 35% (n = 78) and 44% (n = 74) among mechanically ventilated patients., Conclusion: In this multicentre observational study of 223 critically ill patients with COVID-19, the survival to ICU discharge was 65%, and it was 56% among patients requiring MV. Patients showed high rate of septic complications during their ICU stay., Competing Interests: Conflict of Interest K.R., D.J., L.T., M.B., F.S., C.F.W., U.S., C.V., H.-P.H., S.Ko., K.S., A.d.W., M.B., R.S., O.D., J.-P.R., B.S., C.B., O.B., B.B., and G.d.H. do not report any conflicts of interest. S.K. received research support from Ambu, E.T.View Ltd., Fisher & Paykel, Pfizer, and Xenios; lecture honoraria from ArjoHuntleigh, Astellas, Astra, Basilea, Bard, Baxter, Biotest, CSL Behring, CytoSorbents, Fresenius, Gilead, MSD, Orion, Pfizer, Philips, Sedana, Sorin, Xenios, and Zoll; and consultant honorarium from AMOMED, Astellas, Baxter, Bayer, Fresenius, Gilead, MSD, Pfizer, and Xenios. A.N. received research funds, lecture honoraria, and travel reimbursement within the last 5 years from CytoSorbents Europe, Biotest AG, and Thermo Fisher Scientific. D.F. reports lecture honoraria within the last 5 years from Xenios AG., (Copyright © 2020 Australian College of Critical Care Nurses Ltd. Published by Elsevier Ltd. All rights reserved.)

Objective  To assess the sensitivity/specificity of tumor detection by T1 contrast enhancement in intraoperative MRI (ioMRI) in comparison to histopathological assessment as the gold standard in patients receiving surgical resection of grade IV glioblastoma. Materials and Methods  68 patients with a primary or a recurrent glioblastoma scheduled for surgery including fluorescence guidance and neuronavigation were included (mean age: 59 years, 26 female, 42 male patients). The ioMRI after the first resection included transverse FLAIR, DWI, T2-FFE and T1 - 3 d FFE +/- GD-DPTA. The second resection was performed whenever residual contrast-enhancing tissue was detected on ioMRI. Resected tissue samples were histopathologically evaluated (gold standard). Additionally, we evaluated the early postoperative MRI scan acquired within 48 h post-OP for remaining enhancing tissue and compared them with the ioMRI scan. Results  In 43 patients ioMRI indicated residual tumorous tissue, which could be confirmed in the histological specimens of the second resection. In 16 (4 with recurrent, 12 with primary glioblastoma) cases, ioMRI revealed truly negative results without residual tumor and follow-up MRI confirmed complete resection. In 7 cases (3 with recurrent, 4 with primary glioblastoma) ioMRI revealed a suspicious result without tumorous tissue in the histopathological workup. In 2 (1 for each group) patients, residual tumorous tissue was detected in spite of negative ioMRI. IoMRI had a sensitivity of 95 % (94 % recurrent and 96 % for primary glioblastoma) and a specificity of 69.5 % (57 % and 75 %, respectively). The positive predictive value was 86 % (84 % for recurrent and 87 % for primary glioblastoma), and the negative predictive value was 88 % (80 % and 92 %, respectively). Conclusion  ioMRI is effective for detecting remaining tumorous tissue after glioma resection. However, scars and leakage of contrast agent can be misleading and limit specificity. Key points   · Intraoperative MRI (ioMRI) presents with a high sensitivity for residual contrast-enhancing tumorous tissue during glioma resection.. · Contrast leakage due to bleeding and scars with reactive contrast enhancement can cause possible misleading artifacts in ioMRI, leading to a limited specificity of ioMRI.. · Bleeding control in glioma resection is crucial for successful usage of ioMRO for glioma resection.. Citation Format · Heßelmann V, Mager A, Goetz C et al. Accuracy of High-Field Intraoperative MRI in the Detectability of Residual Tumor in Glioma Grade IV Resections. Fortschr Röntgenstr 2017; 189: 519 - 526., Competing Interests: Disclosure The authors report no conflicts of interest in this work., (© Georg Thieme Verlag KG Stuttgart · New York.)

Background: Suppression of nociceptive signalling in the thalamus is considered to contribute significantly to the anaesthetic state. Assuming additivity of anaesthetic mixtures, our study assessed the effects of corresponding minimum alveolar concentrations (MACs) of isoflurane and isoflurane/nitrous oxide on thalamic nociceptive signalling., Methods: Nociceptive response activity (elicited by controlled radiant heat stimuli applied to cutaneous receptive fields) of single thalamic neurons was compared in rats anaesthetized at approximately 1.1 and approximately 1.4 MAC isoflurane with that at approximately 1.1 and approximately 1.4 MAC isoflurane/nitrous oxide., Results: Under baseline anaesthesia ( approximately 0.9 MAC isoflurane), noxious stimulation elicited excitatory responses in all neurons (n = 19). These responses were uniformly suppressed at approximately 1.1 and approximately 1.4 MAC isoflurane. In contrast, at approximately 1.1 and approximately 1.4 MAC isoflurane/nitrous oxide, excitatory responses no different to baseline were still present in 64 and 37% of the neurons, respectively., Conclusions: These data demonstrate a pronounced nitrous oxide-induced response variability. It appears that, with respect to thalamic transfer of nociceptive information, the interaction of isoflurane and nitrous oxide may not be compatible with the concept of additivity and that the antinociceptive potency of nitrous oxide is considerably less than previously reported.

Indications for a pivotal role of the thalamocortical network in producing the state of anesthesia have come from in vivo animal studies as well as imaging studies in humans. We studied possible synaptic mechanisms of anesthesia-induced suppression of touch perception in the rat's thalamus. Thalamocortical relay neurons (TCNs) receive ascending and descending glutamatergic excitatory inputs via NMDA and non-NMDA receptors (AMPAR) and are subjected to GABA(A)ergic inhibitory input which shapes the sensory information conveyed to the cortex. The involvement of these synaptic receptors in the suppressive effects of the prototypic volatile anesthetic isoflurane was assessed by local iontophoretic administration of receptor agonists/antagonists during extracellular recordings of TCNs of the ventral posteromedial nucleus responding to whisker vibration in rats anesthetized with isoflurane concentrations of approximately 0.9 vol.% (baseline) and approximately 1.9 vol.% (ISO high). ISO high induced a profound suppression of response activity reflected by a conversion of the sustained vibratory responses to ON responses. Administration of NMDA, AMPA, or GABA(A)R antagonists caused a reversal to sustained responses in 88, 94 and 88% of the neurons, respectively, with a recovery to baseline levels of response activity. The data show that the block of thalamocortical transfer of tactile information under ISO high may result from an enhancement of GABA(A)ergic inhibition and/or a reduction of glutamatergic excitation. Furthermore, they show that the ascending vibratory signals still reach the thalamic neurons under the high isoflurane concentration, indicating that this input is resistant to isoflurane while the attenuation of excitation may be brought about at the corticothalamic glutamatergic facilitatory input.

Background: We compared recovery from high-dose propofol/low-dose remifentanil ('propofol-pronounced') compared with high-dose remifentanil/low-dose propofol ('remifentanil-pronounced') anaesthesia., Methods: Adult patients having panendoscopy, microlaryngoscopy, or tonsillectomy were randomly assigned to receive either propofol-pronounced (propofol 100 microg x kg(-1) min(-1); remifentanil 0.15 microg x kg(-1) min(-1)) or remifentanil-pronounced (propofol 50 microg x kg(-1) min(-1); remifentanil 0.45 microg x kg(-1) min(-1)) anaesthesia. In both groups, the procedure was started with remifentanil 0.4 microg x kg(-1), propofol 2 mg x kg(-1), and mivacurium 0.2 mg x kg(-1). Cardiovascular measurements and EEG bispectral index (BIS) were recorded. To maintain comparable anaesthetic depth, additional propofol (0.5 mg x kg(-1)) was given if BIS values were greater than 55 and remifentanil (0.4 microg x kg(-1)) if heart rate or arterial pressure was greater than 110% of pre-anaesthetic values., Results: Patient and surgical characteristics, cardiovascular measurements, and BIS values were similar in both groups. There were no differences in recovery times between the groups (time to extubation: 12.7 (4.5) vs 12.0 (3.6) min, readiness for transfer to the recovery ward: 14.4 (4.4) vs. 13.7 (3.6) min, mean (SD))., Conclusions: In patients having short painful surgery, less propofol does not give faster recovery as long as the same anaesthetic level (as indicated by BIS and clinical signs) is maintained by more remifentanil. However, recovery times were less variable following remifentanil-pronounced anaesthesia suggesting a more predictable recovery.

Background: Mechanosensory thalamocortical relay neurones (TCNs) receive glutamatergic excitatory input and are subjected to gamma-aminobutyric acid (GABA)Aergic inhibitory input. This study assessed the effects of an increase in concentration of isoflurane on thalamic excitatory and inhibitory mechanisms., Methods: TCNs (n = 15) of the thalamic ventral posteromedial nucleus responding to mechanical stimulation of whiskers were investigated in rats anaesthetized with end-tidal concentrations of isoflurane of approximately 0.9% (ISOlow, baseline) and approximately 1.9% (ISOhigh). Response activity induced by controlled vibratory movement of single whiskers was recorded before, during and after iontophoretic administration of the GABAA receptor antagonist bicuculline to the vicinity of the recorded neurone., Results: The increase in concentration of isoflurane induced a suppression of vibratory responses to 14 (4)% [mean (SEM)] of baseline activity. Blockade of GABAA receptors by bicuculline during ISOlow and ISOhigh caused increases in response activity to 259 (32)% and 116 (25)% of baseline activity, respectively. The increase in isoflurane concentration enhanced overall inhibitory inputs by 102 (38)%, whilst overall excitatory inputs were reduced by 54 (7)%., Conclusions: These data suggest that doubling the concentration of isoflurane doubles the strength of GABAAergic inhibition and decreases the excitatory drive of TCNs by approximately 50%. The isoflurane-induced enhancement of GABAAergic inhibition led to a blockade of thalamocortical information transfer which was not accomplished by the effects of isoflurane on glutamatergic synaptic transmission alone. Thus, it appears that, with respect to transmission of information in the thalamus, the most prominent action of isoflurane is an enhancement of GABAAergic synpatic inhibition, and that effects on glutamatergic neurotransmission may contribute to a lesser extent.

The neuronal mechanisms underlying the electroencephalographic (EEG) burst-suppression pattern are not yet understood, however, they are generally attributed to interactions within thalamocortical networks. In contrast, we report that the sensory cortex and the thalamus are disconnected, with thalamic sensory processing being unaffected by cortical EEG bursts. We studied the activity of single neurons of the somatosensory thalamocortical system in rats during burst-suppression EEG induced by the volatile anesthetic, isoflurane. In neurons of the thalamic ventrobasal complex, the discharge rate in response to tactile stimulation of their receptive fields did not differ significantly during EEG bursts and isoelectric periods. In contrast, in neurons of the primary somatosensory cortex, the response magnitude was significantly greater during EEG bursts as compared with isoelectric periods (mean increase to 293%). The results suggest that the profound suppression of cortical sensory information processing by isoflurane is suspended during EEG burst-induced elevated cortical excitation.

Many in vitro effects of volatile anesthetics are known, but the mechanisms of action are still under debate. Because suppression of sensory perception is one of the major goals of general anesthesia, we studied the effects of isoflurane on the processing of somatosensory information in anesthetized rats. Local iontophoretic administration of the gamma-aminobutyric acid-A (GABA(A)) receptor antagonist bicuculline in the thalamic ventral posteromedial nucleus reversed suppressive effects of isoflurane on thalamocortical relay neurons (TCNs). The action potential discharges of TCNs (n = 23) in response to defined mechanical stimulation of receptive fields seen with small concentrations of isoflurane (0.79% +/- 0.01%, mean +/- SEM) were suppressed under large concentrations (1.44% +/- 0.04%). In addition, the tonic response pattern was lost, which initially encoded the information about the stimulus features. In 70% of TCNs, bicuculline administration reestablished the initially present tonic response pattern under large isoflurane concentrations. These results indicate that isoflurane suppresses somatosensory information transfer at the thalamic level in vivo, apparently by enhancing thalamic GABA(A) receptor-mediated inhibition.

In this study the effects of gamma-hydroxybutyrate/fentanyl on cerebral blood flow velocity (CBFV) (as measured in the middle cerebral artery by transcranial Doppler ultrasonography) and on cerebrovascular carbon dioxide reactivity were investigated. Mean CBFV (Vmean) and haemodynamic responses were recorded in 12 non-neurosurgical patients before, during and after induction of general anaesthesia with gamma-hydroxybutyrate (GHB) (20 min constant rate infusion of 100 mg kg-1). Two patients were excluded, one because of bradycardia and the other because of severe myoclonia. During the infusion of GHB, normocapnia was maintained by manually assisting ventilation as necessary. The infusion of GHB did not affect Vmean [awake: 57 +/- 12 cm s-1 (mean +/- SD); 22.5 min: 62 +/- 15 cm s-1, NS difference] or mean arterial blood pressure (MAP) (awake: 97 +/- 12 mmHg; 22.5 min: 89 +/- 10 mmHg, NS). This suggests that cerebral blood flow velocity is unaltered by an anaesthetic dose of GHB. Twenty-five minutes after the start of GHB, fentanyl 3 micrograms kg-1 and vecuronium 0.1 mg kg-1 were given, the trachea was intubated and the lungs were mechanically ventilated to maintain end-tidal PCO2 of 4.6 +/- 0.4 kPa (30 min). At 30 min after the start of the GHB infusion, Vmean and MAP decreased to 38 +/- 10 cm s-1 and 76 +/- 12 mmHg (both P < 0.05 vs 22.5 min) respectively. After adjusting the ventilation to achieve hypocapnia (40 min: end-tidal PCO2 3.5 +/- 0.2 mmHg), Vmean decreased to 29 +/- 7 cm s-1, while MAP did not change. This allowed the relative vasoreactivity (percentage change in Vmean/0.133 kPa change in the end-tidal PCO2 from normocapnia to hypocapnia) to be estimated as 2.7 +/- 1.6% 0.133 kPa-1. This suggests that cerebrovascular response to CO2 during gamma-hydroxybutyrate/fentanyl anaesthesia is maintained.

The primary aim of anesthesia is the prevention of pain perception (analgesia), intraoperative awareness (hypnosis), and postoperative recall (amnesia) (anesthetic trade). Analgesia would be a component of the anesthetic state. Pain is the conscious perception of a noxious stimulus and analgesia is the abolished perception of pain in an otherwise conscious patient. During general anesthesia pain can not be experienced, since the patient is unconscious. However, there is no certainty that during anesthesia a blockade of the nociceptive system is reliably provided in all circumstances. The impact of insufficient blockade of nociceptive pathways during anesthesia on mental status and implicit memory are largely unknown. Therefore, the anesthetic trade should consist of hypnosis, amnesia and antinociception.

Unlabelled: alpha 2-Agonists are being used increasingly in anaesthesia and intensive care medicine because of their antihypertensive, analgesic and sedative properties. Platelets bear alpha 2-receptors on the cell surface. Stimulation of these receptors by agonists induces platelet aggregation. The present study examined whether in vitro incubation of blood with the alpha 2-agonists clonidine and dexmedetomidine decreases alpha 2-receptor density and hereby influences platelet aggregation., Methods: Whole blood of 20 healthy volunteers was incubated over 24 h at 37 degrees C with 1 ng/ml clonidine or 1 or 10 ng/ml dexmedetomidine. Induced platelet aggregation was determined by means of turbidometry. Epinephrine (22 mumol/l) or collagen (20 mg/l) served as inductors. The density of alpha 2-receptors was measured in radioligand assays with 3H-Yohimbine. Phentolamine was used to assess unspecific binding. The data were analyzed with an analysis of variance., Results: Neither 1 ng/ml clonidine nor 1 ng/ml dexmedetomidine altered platelet aggregation or alpha 2-receptor density in comparison with the control sample. As a major result we found that 10 ng/ml dexmedetomidine caused a significant (P < 0.05) reduction in epinephrine-induced platelet aggregation (16.0 +/- 5.4%, n = 20, mean +/- SEM) compared with the control (46.0 +/- 1.3%, n = 20). alpha 2-Receptor density was not any different from the control., Conclusions: This in vitro study showed that clinically relevant concentrations of 1 ng/ml clonidine or dexmedetomidine did not alter platelet aggregation or alpha 2-receptor density, even after 24 h exposure. However, 10 ng/ml dexmedetomidine was found to diminish significantly epinephrine-induced platelet aggregation, but did not change alpha 2-receptor density. This result showed that desensitization of platelet aggregation can occur without quantitative changes in alpha 2-receptors.