Comparison between remimazolam and propofol anaesthesia for interventional neuroradiology: a randomised controlled trial.

BACKGROUND: General anaesthesia can immobile patients during interventional neuroradiology to improve image quality. Remimazolam, an ultrashort-acting benzodiazepine, is advantageous for haemodynamic stability. This study compared remimazolam and propofol anaesthesia during neuroradiology procedures regarding intraoperative hypotensive events and rapid recovery. METHODS: This single-masked randomised-controlled study included 76 participants who underwent elective endovascular embolisation in a single centre. Patients were randomised between a continuous remimazolam infusion (n = 38) or a target-controlled propofol infusion group (n = 38). In the remimazolam group, flumazenil (0.2 mg) was administered at the end of the procedure. Phenylephrine was titrated to maintain the mean arterial pressure within ± 20% of the baseline value. The primary outcome was the total phenylephrine dose during the procedure. RESULTS: The total phenylephrine dose was 0.0 [0.0-30.0] µg in the remimazolam group and 30.0 [0.0-205.0] µg in the propofol group (p = 0.001). Hypotensive events were observed in 11 (28.9%) patients in the remimazolam group and 23 (60.5%) patients in the propofol group (p = 0.001). Recovery times to spontaneous breathing, eye-opening, extubation, and orientation were shorter in the remimazolam group than in the propofol group (all p < 0.001). CONCLUSIONS: Remimazolam anaesthesia showed superior haemodynamic stability compared with propofol anaesthesia during neuroradiology procedures. Systematic use of flumazenil enabled rapid recovery from remimazolam anaesthesia. REGISTRATION: University Hospital Medical Information Network Clinical Trials Registry; Registration number: UMIN000047384; URL: https://center6.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000054046.

Transcriptional regulation of Notch1 by nuclear factor-κB during T cell activation.

Notch1 plays important roles in T cell development and is highly expressed in activated CD4+ T cells. However, the underlying mechanism of Notch1 transcription in T cells has not been fully characterized. Therefore, we aimed to determine how Notch1 expression is regulated during the activation of CD4+ T cells. Both the surface expression and mRNA transcription of Notch1 were significantly higher in activated CD4+ T cells, but the inhibition of phosphatidylinositol 3-kinase (PI3K) by LY294002 or deletion of the Pdk1 gene impaired this upregulation of Notch1. Interrogation of the Notch1 promoter region using serially deleted Notch1 promoter reporters revealed that the - 300 to - 270 region is crucial for its transcription in activated T cells. In addition, we found that nuclear factor (NF)-κB subunits containing RelA bind directly to this promoter region, thereby upregulating transcription. In addition, inhibition of NF-κB by SN50 impaired upregulation of Notch1 surface protein and mRNA in activated CD4+ T cells. Thus, we provide evidence that Notch1 transcription in activated CD4+ T cells is upregulated via the PI3K-PDK1-NF-κB signaling pathway.

Direct One-Step Growth of Bimetallic Ni2Mo3N on Ni Foam as an Efficient Oxygen Evolution Electrocatalyst.

A simple and economical synthetic route for direct one-step growth of bimetallic Ni2Mo3N nanoparticles on Ni foam substrate (Ni2Mo3N/NF) and its catalytic performance during an oxygen evolution reaction (OER) are reported. The Ni2Mo3N/NF catalyst was obtained by annealing a mixture of a Mo precursor, Ni foam, and urea at 600 °C under N2 flow using one-pot synthesis. Moreover, the Ni2Mo3N/NF exhibited high OER activity with low overpotential values (336.38 mV at 50 mA cm-2 and 392.49 mV at 100 mA cm-2) and good stability for 5 h in Fe-purified alkaline electrolyte. The Ni2Mo3N nanoparticle surfaces converted into amorphous surface oxide species during the OER, which might be attributed to the OER activity.

ZIP8 exacerbates collagen-induced arthritis by increasing pathogenic T cell responses.

Zinc is a trace element that is essential for immune responses. Therefore, changes in cellular zinc levels in specific immune cells may influence inflammatory autoimmune diseases, such as rheumatoid arthritis (RA). However, the regulation of zinc mobilization in immune cells and its role in the pathogenesis of RA are not fully understood. Thus, we investigated the roles of zinc transporters in RA pathogenesis. We demonstrated that ZIP8 was specifically upregulated in CD4+ T cells that infiltrated the inflamed joint and that ZIP8 deficiency in CD4+ T cells abrogated collagen-induced arthritis. ZIP8 deficiency dramatically affected zinc influx in effector T cells and profoundly reduced T cell receptor (TCR)-mediated signaling, including NF-κB and MAPK signaling, which are pathways that are involved in T helper (Th) 17 cell differentiation. Taken together, our findings suggest that ZIP8 depletion in CD4+ T cells attenuates TCR signaling due to insufficient cellular zinc, thereby reducing the function of effector CD4+ T cells, including Th17 cells. Our results also suggest that targeting ZIP8 may be a useful strategy to inhibit RA development and pathogenesis.

High-throughput epitope profiling of antibodies in the plasma of Alzheimer's disease patients using random peptide microarrays.

The symptoms of Alzheimer's disease (AD), a major cause of dementia in older adults, are linked directly with neuronal cell death, which is thought to be due to aberrant neuronal inflammation. Autoantibodies formed during neuronal inflammation show excellent stability in blood; therefore, they may be convenient blood-based diagnostic markers of AD. Here, we performed microarray analysis of 29,240 unbiased random peptides to be used for comprehensive screening of AD-specific IgG and IgM antibodies in the blood. The results showed that (1) sequence-specific and isotype-specific antibodies are regulated differentially in AD, and combinations of these antibodies showing high area under the receiver operating characteristic curve values (0.862-0.961) can be used to classify AD, (2) AD-specific IgG antibodies arise from IgM antibody-secreting cells that existed before disease onset and (3) target protein profiling of the antibodies identified some AD-related proteins, some of which are involved in AD-related signalling pathways. Therefore, we propose that these epitopes may facilitate the development of biomarkers for AD diagnosis and form the basis for a mechanistic study related to AD progression.

BATF regulates collagen-induced arthritis by regulating T helper cell differentiation.

BACKGROUND: We recently demonstrated that BATF, a member of the activator protein-1 (AP-1) family, regulates osteoarthritic cartilage destruction. Here, we explored the roles and regulatory mechanisms of BATF in collagen-induced arthritis (CIA) in mice. METHODS: CIA and K/BxN serum transfer were used to generate inflammatory arthritis models in wild-type (WT) and Batf-/- mice. RA manifestations were determined by examining CIA incidence, clinical score, synovitis, synovial hyperplasia, angiogenesis in inflamed synovium, pannus formation, bone erosion, and cartilage destruction. Immune features in RA were analyzed by examining immune cell populations and cytokine production. RESULTS: BATF was upregulated in the synovial tissues of joints in which inflammatory arthritis had been caused by CIA or K/BxN serum transfer. The increases in CIA incidence, clinical score, and autoantibody production in CIA-induced WT mice were completely abrogated in the corresponding Batf-/- DBA/1 J mice. Genetic ablation of Batf also inhibited CIA-induced synovitis, synovial hyperplasia, angiogenesis in synovial tissues, pannus formation, bone erosion, and cartilage destruction. Batf knockout inhibited the differentiation of T helper (Th)17 cells and the conversion of CD4+Foxp3+ cells to CD4+IL-17+ cells. However, BATF did not modulate the functions of fibroblast-like synoviocytes (FLS), including the expressions of chemokines, matrix-degrading enzymes, vascular endothelial growth factor, and receptor activator of NF-κB ligand (RANKL). CONCLUSION: Our findings indicate that BATF crucially mediates CIA by regulating Th cell differentiation without directly affecting the functions of FLS.

Myeloid-Derived Suppressor Cells Are Controlled by Regulatory T Cells via TGF-ß during Murine Colitis.

Myeloid-derived suppressor cells (MDSCs) are well known regulators of regulatory T cells (Treg cells); however, the direct regulation of MDSCs by Treg cells has not been well characterized. We find that colitis caused by functional deficiency of Treg cells leads to altered expansion and reduced function of MDSCs. During differentiation of MDSCs in vitro from bone marrow cells, Treg cells enhanced MDSC function and controlled their differentiation through a mechanism involving transforming growth factor-ß (TGF-ß). TGF-ß-deficient Treg cells were not able to regulate MDSC function in an experimentally induced model of colitis. Finally, we evaluated the therapeutic effect of TGF-ß-mediated in-vitro-differentiated MDSCs on colitis. Adoptive transfer of MDSCs that differentiated with TGF-ß led to better colitis prevention than the transfer of MDSCs that differentiated without TGF-ß. Our results demonstrate an interaction between Treg cells and MDSCs that contributes to the regulation of MDSC proliferation and the acquisition of immunosuppressive functions.

Epigenetic regulation of Kcna3-encoding Kv1.3 potassium channel by cereblon contributes to regulation of CD4+ T-cell activation.

The role of cereblon (CRBN) in T cells is not well understood. We generated mice with a deletion in Crbn and found cereblon to be an important antagonist of T-cell activation. In mice lacking CRBN, CD4(+) T cells show increased activation and IL-2 production on T-cell receptor stimulation, ultimately resulting in increased potassium flux and calcium-mediated signaling. CRBN restricts T-cell activation via epigenetic modification of Kcna3, which encodes the Kv1.3 potassium channel required for robust calcium influx in T cells. CRBN binds directly to conserved DNA elements adjacent to Kcna3 via a previously uncharacterized DNA-binding motif. Consequently, in the absence of CRBN, the expression of Kv1.3 is derepressed, resulting in increased Kv1.3 expression, potassium flux, and CD4(+) T-cell hyperactivation. In addition, experimental autoimmune encephalomyelitis in T-cell-specific Crbn-deficient mice was exacerbated by increased T-cell activation via Kv1.3. Thus, CRBN limits CD4(+) T-cell activation via epigenetic regulation of Kv1.3 expression.

Perioperative lung-protective ventilation strategy reduces postoperative pulmonary complications in patients undergoing thoracic and major abdominal surgery.

The occurrence of postoperative pulmonary complications is strongly associated with increased hospital mortality and prolonged postoperative hospital stays. Although protective lung ventilation is commonly used in the intensive care unit, low tidal volume ventilation in the operating room is not a routine strategy. Low tidal volume ventilation, moderate positive end-expiratory pressure, and repeated recruitment maneuvers, particularly for high-risk patients undergoing major abdominal surgery, can reduce postoperative pulmonary complications. Facilitating perioperative bundle care by combining prophylactic and postoperative positive-pressure ventilation with intraoperative lung-protective ventilation may be helpful to reduce postoperative pulmonary complications.

Effect of coenzyme Q10 on spinal cord ischemia-reperfusion injury.

OBJECT: Spinal cord ischemia remains a serious complication of thoracoabdominal aortic aneurysm surgery. Coenzyme Q10, a potent antioxidant, has been reported to exert a neuroprotective effect. In the present study, we evaluated the effect of coenzyme Q10 pretreatment on spinal cord ischemia-reperfusion injury. METHODS: Male Sprague-Dawley rats were treated with either 300 mg/kg coenzyme Q10 (CoQ10 group, n = 12) or saline (control and sham groups, n = 12 for each group) for 5 days before ischemia. Spinal cord ischemia was induced in the control and CoQ10 groups. Neurological function was assessed using the Basso-Beattie-Bresnahan (BBB) motor rating scale until 7 days after reperfusion, and then the spinal cord was harvested for histopathological examinations and an evaluation of malondialdehyde level. RESULTS: On post-reperfusion Day 1, the CoQ10 group showed higher BBB scores compared with those in the control group, although the difference was not significant. However, on Day 2, the CoQ10 group showed a significantly higher BBB score than the control group (14.0 [10.3-15.0] vs 8.0 [5.0-9.8], median [IQR], respectively; p = 0.021), and this trend was maintained until Day 7 (17.5 [16.0-18.0] vs 9.0 [6.5-12.8], respectively; p < 0.001). Compared with the control group, the CoQ10 group had more normal motor neurons (p = 0.003), fewer apoptotic changes (p = 0.003) and a lower level of tissue malondialdehyde (p = 0.024). CONCLUSIONS: Pretreatment with 300 mg/kg coenzyme Q10 resulted in significantly improved neurological function and preservation of more normal motor neurons.

Cardiopulmonary resuscitation with assisted extracorporeal life support during cardiac arrest caused by drug-eluting stent thrombosis: a case report.

Discontinuation of dual antiplatelet therapy within 12 months after drug-eluting stent (DES) implantation increases the possibility of stent thrombosis. We now report the case of a 66-year-old man who suffered a cardiac arrest due to stent thrombosis after an elective laparoscopic anterior resection. Ten month ago, he underwent DES implantation and then had been taking dual antiplatelet therapy. Nine days prior to the surgery, he discontinued dual antiplatelet therapy. Forty minutes after intensive care unit admission, cardiac arrest occurred. However, his cardiac rhythm did not restore in spite of resuscitation, so immediately veno-arterial extracorporeal membrane oxygenation (ECMO) was implanted. Four days after the surgery, he was weaned from ECMO support, recovered completely, with no cardiopulmonary or neurological sequelae.

Remifentanil dose for laryngeal mask airway insertion with a single standard dose of propofol during emergency airway management in elderly patients.

BACKGROUND: This study determined the dose of remifentanil to use during insertion of a Classic™ laryngeal mask airway (LMA, The Laryngeal Mask Co., Nicosia, Cyprus) in elderly patients during emergency airway management when combined with a single dose of propofol. METHODS: Patients aged 65-80 years were enrolled. Anesthesia was induced with propofol 1 mg/kg, and then a blinded dose of remifentanil was infused over 30 s after confirming the patient's loss of consciousness. The dose of remifentanil was determined using Dixon's up-and-down method, starting at 0.5 µg/kg (a step size of 0.1 µg/kg). Insertion of the LMA was attempted 60 s after loss of consciousness. RESULTS: In total, 23 patients were recruited and the mean age ± standard deviation was 72 ± 3 years. The effective dose for successful LMA insertion in 50% of the patients (ED50) was 0.20 ± 0.05 µg/kg. No patient needed more than 0.3 µg/kg. CONCLUSIONS: Remifentanil 0.20 ± 0.05 µg/kg with propofol 1 mg/kg resulted in excellent LMA insertion in 50% of elderly patients without significant hemodynamic changes during emergency airway management.

NF-κB Activation in T Helper 17 Cell Differentiation.

CD28/T cell receptor ligation activates the NF-κB signaling cascade during CD4 T cell activation. NF-κB activation is required for cytokine gene expression and activated T cell survival and proliferation. Recently, many reports showed that NF-κB activation is also involved in T helper (Th) cell differentiation including Th17 cell differentiation. In this review, we discuss the current literature on NF-κB activation pathway and its effect on Th17 cell differentiation.

Predicting the appropriate uncuffed endotracheal tube size for children: a radiograph-based formula versus two age-based formulas.

STUDY OBJECTIVES: To determine whether a radiograph-based formula using the tracheal diameter from a chest radiograph predicted the appropriate endotracheal tube (ETT) size in children, and to compare these results with those produced using age-based formulas. DESIGN: Retrospective, observational study. SETTING: Medical record review. MEASUREMENTS: Data from 537 pediatric patients, aged 3 to 6 years, who underwent orotracheal intubation with an uncuffed ETT, were randomly divided into two datasets: one was used to derive a formula and the other was for validation. A radiograph-based formula was obtained by linear regression modeling between the tracheal diameter at the seventh cervical vertebra (C7) on chest radiography and the appropriate ETT size from the estimation dataset (n=268). The appropriate size was defined as the ETT size when air leak pressure was 10 to 30 cmH2O. The predictive ability of this equation was evaluated using the validation dataset (n=269). The primary outcome was the success rate of the prediction. MAIN RESULTS: The following radiograph-based formula was obtained: ID = 3 + 0.3 × (tracheal diameter at C7). The success rate of the radiograph-based formula was 57%, which is higher than the 32% (P < 0.001) of the standard age-based formula (ID = 4 + age/4) or 43% (P = 0.002) of Penlington's formula (ID = 4.5 + age/4). An underestimation of the actual tracheal size occurred in 65% of cases using the age-based formulas, but in only 19% with the radiograph-based formula (P < 0.001). CONCLUSIONS: The radiograph-based formula may be useful for predicting the appropriate ETT size in children aged 3 to 6 years.

Does intraocular pressure increase during laparoscopic surgeries? It depends on anesthetic drugs and the surgical position.

BACKGROUND: Pneumoperitoneum in the pelvic laparoscopic surgery induces a rise in the intraocular pressure (IOP). This study investigated whether IOP changes were different depending on the surgical position (Trendelenburg vs. reverse Trendelenburg) and the anesthetic drugs (propofol vs. desflurane). METHODS: : A total of 100 patients scheduled for pelvic laparoscopy or laparoscopic cholecystectomy were enrolled. They were randomly allocated into the propofol group or the desflurane group. In the desflurane group, anesthesia was given with thiopental and desflurane. The propofol group was anesthetized with propofol. IOP, mean blood pressure, heart rate, and peak airway pressure were measured at the following time points: awake-supine position, induction of anesthesia, after position change, 5, 10, and 20 minutes after pneumoperitoneum. IOP was measured with the handheld tonometer (Tono-penXL). RESULTS: : In all the groups, IOP decreased after anesthesia was initiated (17 ± 2 to 11 ± 2 mm Hg). In laparoscopic cholecystectomy, a low IOP was maintained during the period of pneumoperitoneum, independent of anesthetic drugs. In pelvic laparoscopy, the head-down position produced a rise in IOP (11 ± 2 to 14 ± 3 mm Hg). Further, pneumoperitoneum in addition to the head-down position raised the IOP highly in the desflurane group, and the average IOP value was over the normal limit (22 ± 4 mm Hg). In contrast, propofol kept IOP similar to the preoperative level during the whole period of pneumoperitoneum (18 ± 3 mm Hg, P<0.001 vs. desflurane). CONCLUSIONS: : Impact of anesthetics on IOP during laparoscopic surgery may change depending on the surgical position. For the laparoscopic surgery performed in the head-down position, propofol may be more helpful in preventing ocular hypertension.

Optimal remifentanil dose for lightwand intubation without muscle relaxants in healthy patients with thiopental coadministration: a prospective randomised study.

CONTEXT: Muscle relaxants used to facilitate tracheal intubation have disadvantages. OBJECTIVE: This study was designed to evaluate the dose requirements for remifentanil combined with thiopental for optimal lightwand intubation without muscle relaxants. DESIGN: Prospective randomised controlled study. SETTING: A tertiary care teaching hospital. PATIENTS: Ninety-six patients requiring general anaesthesia for elective surgery. INTERVENTIONS: Patients received remifentanil 1, 2, or 3 µg kg(-1) (group R1, R2, R3, each n = 32) as a slow bolus infusion over 60 s, followed by thiopental 5 mg kg(-1). Ninety seconds after remifentanil administration, lightwand intubation was attempted and intubation time was recorded. Intubating conditions were considered excellent if there was no patient movement or cough, good if coughing occurred once or twice after intubation and poor if persistent movement or cough occurred after intubation. Excellent or good intubating conditions were regarded as clinically acceptable. The duration of apnoea was recorded. MAIN OUTCOME MEASURES: Intubating conditions and the duration of apnoea. RESULTS: Lightwand intubation was successful at the first attempt in all patients except for two in group R1. The intubating conditions were more acceptable in groups R2 and R3 than in group R1 (97 and 100 vs. 63%, P < 0.01). Intubation time was shorter in group R3 than in group R1 (22 ± 8 vs. 33 ± 18 s, P < 0.01). There was no significant difference in intubation time and conditions between groups R2 and R3. The mean duration of apnoea was prolonged in group R3 compared with group R2 (10.2 ± 2.1 vs. 4.6 ± 1.6 min, P < 0.01). CONCLUSION: Our results suggest that remifentanil 2 or 3 µg kg(-1) combined with thiopental 5 mg kg provides acceptable conditions for lightwand intubation without muscle relaxants. Spontaneous ventilation returns more rapidly following remifentanil 2 µg kg(-1) than with remifentanil 3 µg kg(-1).

Expression of SOCS1 and SOCS3 is altered in the nasal mucosa of patients with mild and moderate/severe persistent allergic rhinitis.

BACKGROUND: The aim of this study was to evaluate the role of suppressor of cytokine signaling (SOCS) molecules, SOCS1 and SOCS3, which act as negative regulators of cytokine signaling in various allergic diseases, in patients with mild and moderate/severe persistent allergic rhinitis. METHODS: The expression and distribution pattern of SOCS1 and SOCS3 were analyzed in nasal mucosa and peripheral blood mononuclear cells (PBMC) of healthy controls, and patients with mild and moderate/severe persistent allergic rhinitis using RT-PCR, immunohistochemistry and Western blotting. IL-4, IL-13, IL-15 and IFN-γ expression was also analyzed in the nasal mucosa of each individual using RT-PCR and Western blotting. RESULTS: SOCS1 and SOCS3 mRNA and protein expression was significantly increased in the nasal mucosa and PBMC of patients with mild and moderate/severe persistent allergic rhinitis compared with healthy controls. In healthy and allergic nasal mucosa, they were commonly localized to the epithelium, submucosal glands and endothelium, showing stronger staining intensity in mild and moderate/severe persistent allergic nasal mucosa than in healthy nasal mucosa. Tissue levels of IL-4 and IL-13 were increased in moderate/severe persistent allergic nasal mucosa whereas IL-15 and IFN-γ were decreased in moderate/severe persistent allergic nasal mucosa. CONCLUSIONS: Upregulation of SOCS1 and SOCS3 in mild and moderate/severe persistent allergic rhinitis suggests that SOCS proteins may be important regulators in the pathogenesis of allergic rhinitis and play a role as molecular determinants of allergic rhinitis persistence.

Optimal headrest height for the best laryngoscopic view: by anatomical measurements.

BACKGROUND: We hypothesized that the oro-pharyngolaryngeal axes, occipito-atlanto-axial extension (OAA) angle and intubation distance would be influenced by the height of headrests. METHODS: Twenty patients were enrolled. The Macintosh 3 blade was used for direct laryngoscopy without a headrest or with the headrest of 6 or 12 cm high in randomized order, whereas a lateral radiograph of the neck was taken when the best laryngoscopic view was obtained. The following measurements were made: (1) the axis of the mouth (MA), the pharyngeal axis (PA), the laryngeal axis (LA), and the line of vision (LV). The various angles between these axes were defined: α angle between MA and PA, ß angle between PA and LA, and δ angle between LV and LA. (2) Intubation distance, (3) mentovertebral distance, and (4) OAA angle. RESULTS: Compared with 12-cm and no headrest, the δ angle decreased significantly with 6-cm headrest (19.4°/29.2°/29.2° in 6-cm/12-cm/no headrest, respectively; P < .001), and the intubation distance increased significantly (46.2/37.3/38.7 mm in 6-cm/12-cm/no headrest, respectively; P < .001). Mentovertebral distance was smallest (107.0/106.7/98.5 mm; P < .05) at 12-cm headrest. Occipito-atlanto-axial extension angle was largest significantly (40.7°/35.2°/34.5°; P < .05) at 6-cm headrest. CONCLUSION: We conclude that compared with no or 12-cm headrest, 6-cm headrest could facilitate more alignment of these axes, increase the OAA angle, and enlarge the intubation distance.

Feasibility of continuous glucose monitoring in critically ill emergency department patients.

BACKGROUND: Glucose control is important in the management of critically ill patients. However, strict glucose control requires a large amount of nursing resources, especially in overcrowded emergency departments (EDs). OBJECTIVES: A continuous glucose monitoring system (CGMS) may be beneficial for glucose control in the ED. The objective of this study was to determine the test characteristics of CGMS in critically ill ED patients. METHODS: A prospective observational study of critically ill ED patients was conducted. During a patient's visit to the ED, a CGMS sensor measured their interstitial fluid glucose levels continuously. Capillary glucose was measured every hour and used for glucose control and as a reference value. CGMS values were recorded in real time and compared with capillary glucose values. RESULTS: A total of 122 pairs of capillary and CGMS glucose values in 12 patients were analyzed. The correlation coefficient was 0.87, and Bland-Altman analysis showed that 117 pairs (95.9%) were within a 95% confidence interval. A Clarke Error Grid Analysis indicated an overall accuracy of 96.8% (Zones A and B). However, the mean absolute relative difference (MARD) was significantly higher in the hypoglycemic range than in a normo- or hyperglycemic range (p = 0.001). The sensitivity and positive predictive value of CGMS for detecting hypoglycemia were 33.3% and 16.7%, respectively. The CGMS specificity and negative predictive value were 95.8% and 98.3%, respectively. There was no linear correlation between MARD and body mass index, axillary temperature, inotrope score, and base deficit (all p-value >0.05). CONCLUSION: CGMS demonstrated good clinical accuracy by Clarke Error Grid Analysis. There also was high agreement between CGMS and capillary glucose levels. However, CGMS demonstrated only limited real-time hypoglycemia detection ability in critically ill ED patients.