Actions of remimazolam on inhibitory transmission of rat spinal dorsal horn neurons.

Remimazolam is an ultra-short benzodiazepine that acts on the benzodiazepine site of γ-aminobutyric acid (GABA) receptors in the brain and induces sedation. Although GABA receptors are found localized in the spinal dorsal horn, no previous studies have reported the analgesic effects or investigated the cellular mechanisms of remimazolam on the spinal dorsal horn. Behavioral measures, immunohistochemistry, and in vitro whole-cell patch-clamp recordings of dorsal horn neurons were used to assess synaptic transmission. Intrathecal injection of remimazolam induced behavioral analgesia in inflammatory pain-induced mechanical allodynia (six rats/dose; p < 0.05). Immunohistochemical staining revealed that remimazolam suppressed spinal phosphorylated extracellular signal-regulated kinase activation (five rats/group, p < 0.05). In vitro whole-cell patch-clamp analysis demonstrated that remimazolam increased the frequency of GABAergic miniature inhibitory post-synaptic currents, prolonged the decay time (six rats; p < 0.05), and enhanced GABA currents induced by exogenous GABA (seven rats; p < 0.01). However, remimazolam did not affect miniature excitatory post-synaptic currents or amplitude of monosynaptic excitatory post-synaptic currents evoked by Aδ- and C-fiber stimulation (seven rats; p > 0.05). This study suggests that remimazolam induces analgesia by enhancing GABAergic inhibitory transmission in the spinal dorsal horn, suggesting its potential utility as a spinal analgesic for inflammatory pain.

Developmental outcome after corpus callosotomy for infants and young children with drug-resistant epilepsy.

AIM: To examine the developmental and seizure outcomes after corpus callosotomy (CC) in early childhood. METHODS: We retrospectively identified 106 patients who underwent CC for drug-resistant epilepsy before the age of 6 years, at the Nagasaki Medical Center, between July 2002 and July 2016. Patients' developmental outcomes were evaluated one year after CC using the Kinder Infant Development Scale. RESULTS: The mean preoperative developmental quotient (DQ) was 25.0 (standard deviation [SD], 20.8), and the mean difference between preoperative DQ and one-year postoperative DQ was -1.6 points (SD, 11.6). However, 42.5% of patients had a mean DQ increase of 6.5 points (SD, 6.4), one year after CC from that before surgery. Factors related to the improvement in postoperative DQ were 'low preoperative DQ', 'developmental gain 1 month postoperatively', and 'postoperative seizure-free state'. Approximately 21.7% of patients were seizure-free 1 year after CC. INTERPRETATION: Performing CC, in infancy and early childhood for patients with drug-resistant epilepsy and severe developmental impairment, was associated with improved development in 42.5% of patients. Remission of seizures, even if only for a short period, contributed to developmental improvement. From a developmental perspective, CC for drug-resistant epilepsy in early childhood is an effective treatment.

Epidural Administration of Ropivacaine Reduces the Amplitude of Transcranial Electrical Motor-Evoked Potentials: A Double-Blinded, Randomized, Controlled Trial.

BACKGROUND: An epidurally administered local anesthetic acts primarily on the epidural nerve roots and can act directly on the spinal cord through the dural sleeve. We hypothesized that epidurally administered ropivacaine would reduce the amplitude of transcranial electrical motor-evoked potentials by blocking nerve conduction in the spinal cord. Therefore, we conducted a double-blind, randomized, controlled trial. METHODS: Thirty adult patients who underwent lung surgery were randomly allocated to 1 of 3 groups, based on the ropivacaine concentration: the 0.2% group, the 0.375% group, and the 0.75% group. The attending anesthesiologists, neurophysiologists, and patients were blinded to the allocation. The epidural catheter was inserted at the T5-6 or T6-7 interspace by a paramedian approach, using the loss of resistance technique with normal saline. General anesthesia was induced and maintained using propofol and remifentanil. Transcranial electrical motor-evoked potentials were elicited by a train of 5 pulses with an interstimulus interval of 2 milliseconds by using a constant-voltage stimulator and were recorded from the tibialis anterior muscle. Somatosensory-evoked potentials (SSEPs) were evoked by electrical tibial nerve stimulation at the popliteal fossa. After measuring the baseline values of these evoked potentials, 10 mL of epidural ropivacaine was administered at the 0.2%, 0.375%, or 0.75% concentration. The baseline amplitudes and latencies recorded before administering ropivacaine were defined as 100%. Our primary end point was the relative amplitude of the motor-evoked potentials at 60 minutes after the epidural administration of ropivacaine. We analyzed the amplitudes and latencies of these evoked potentials by using the Kruskal-Wallis test and used the Dunn multiple comparison test as the post hoc test for statistical analysis. RESULTS: The data are expressed as the median (interquartile range). Sixty minutes after epidurally administering ropivacaine, the motor-evoked potential amplitude was lower in the 0.75% group (7% [3%-18%], between-group difference P < .001) and in the 0.375% group (52% [43%-59%]) compared to that in the 0.2% group (96% [89%-105%]). The latency of SSEP was longer in the 0.75% group compared to that in the 0.2% group, but the amplitude was unaffected. CONCLUSIONS: Epidurally administered high-dose ropivacaine lowered the amplitude of motor-evoked potentials and prolonged the onset latencies of motor-evoked potentials and SSEPs compared to those in the low-dose group. High-dose ropivacaine can act on the motor pathway through the dura mater.

Low-dose droperidol suppresses transcranial electrical motor-evoked potential amplitude: a retrospective study.

Low-dose droperidol has been widely used as an antiemetic during and after surgery. Although high-dose droperidol affects motor-evoked potential, the effects of low-dose droperidol on motor-evoked potential amplitude are unclear. The aim of this study was to investigate whether low-dose droperidol affects motor-evoked potential amplitude. We retrospectively reviewed the data of patients who underwent spine surgery under general anesthesia with motor-evoked potential monitoring from February 2016 to 2017. The outcome was the motor-evoked potential amplitude of the bilateral abductor pollicis brevis muscle, tibialis anterior muscle, and abductor hallucis muscle within 1 and 1-2 h after droperidol administration, compared with the baseline motor-evoked potential value. Thirty-four patients were analyzed. The median dose of droperidol was 21 µg/kg. The motor-evoked potential amplitudes of all muscles were significantly reduced after droperidol administration and recovered to baseline values within 2 h. The reduction of all motor-evoked potential amplitudes after droperidol administration was 37-45% of baseline values. There were no significant differences in other drugs administered. There were no serious adverse effects of droperidol administration. Motor-evoked potential amplitude was suppressed by low-dose droperidol. During intraoperative motor-evoked potential monitoring in spine surgery, anesthesiologists should pay careful attention to the timing of administration of droperidol, even at low doses. Based on the results of this study, we are conducting a randomized controlled trial.

Propofol reduces the amplitude of transcranial electrical motor-evoked potential without affecting spinal motor neurons: a prospective, single-arm, interventional study.

PURPOSE: Propofol inhibits the amplitudes of transcranial electrical motor-evoked potentials (TCE-MEP) in a dose-dependent manner. However, the mechanisms of this effect remain unknown. Hence, we investigated the spinal mechanisms of the inhibitory effect of propofol on TCE-MEP amplitudes by evaluating evoked electromyograms (H-reflex and F-wave) under general anesthesia. METHODS: We conducted a prospective, single-arm, interventional study including 15 patients scheduled for spine surgery under general anesthesia. Evoked electromyograms of the soleus muscle and TCE-MEPs were measured at three propofol concentrations using target-controlled infusion (TCI: 2.0, 3.0, and 4.0 µg/mL). The primary outcome measure was the left H-reflex amplitude during TCI of 4.0- compared to 2.0-µg/mL propofol administration. RESULTS: The median [interquartile range] amplitudes of the left H-reflex were 4.71 [3.42-6.60] and 5.6 [4.17-7.46] in the 4.0- and 2.0-µg/mL TCI groups (p = 0.4, Friedman test), respectively. There were no significant differences in the amplitudes of the right H-reflex and the bilateral F-wave among these groups. However, the TCE-MEP amplitudes significantly decreased with increased propofol concentrations (p < 0.001, Friedman test). CONCLUSION: Propofol did not affect the amplitudes of the H-reflex and the F-wave, whereas TCE-MEP amplitudes were reduced at higher propofol concentrations. These results suggested that propofol can suppress the TCE-MEP amplitude by inhibiting the supraspinal motor pathways more strongly than the excitability of the motor neurons in the spinal cord.

Efficacy of a novel urinary catheter for men with a local anesthetic injection port for catheter-related bladder discomfort: a randomized controlled study.

PURPOSE: The NMOC-3WAY catheter® is a novel urinary catheter for men that can be used to inject a local anesthetic into the urethra. We sought to assess whether the injection of a local anesthetic into the urethra via the NMOC-3WAY catheter® would reduce catheter-related bladder discomfort (CRBD) after endovascular aneurysm repair (EVAR). METHODS: Adult male patients who underwent elective EVAR for abdominal aortic aneurysms were randomly assigned to the 2% lidocaine group and the normal saline group (control group). CRBD was evaluated at 0, 1, 2, 4, and 6 h after surgery. The primary outcome was the incidence of CRBD at 0 h after surgery. RESULTS: Data for 37 patients (19 in the lidocaine group and 18 in the control group) were analyzed. CRBD was observed at 0 h in six patients (31.6%; mild, n = 5; moderate, n = 1) in the lidocaine group and in five patients (27.8%; mild, n = 1; moderate, n = 3; severe, n = 1) in the control group. The control group showed a tendency to have severe CRBD at 0 h, although there was no significant difference in either the incidence (P = 0.80) or severity (P = 0.21) of CRBD between the two groups. CONCLUSION: Our results suggest that the use of the NMOC-3WAY catheter® for the injection of 2% lidocaine into the urethra does not reduce the incidence of CRBD immediately after EVAR. However, it may reduce moderate or severe CRBD that may lead to postoperative distress and agitation.

Acute spatial spread of NO-mediated potentiation during hindpaw ischaemia in mice.

KEY POINTS: Neuropathic pain spreads spatially beyond the injured sites, and the mechanism underlying the spread has been attributed to inflammation occurring in the spinal cord. However, the spatial spread of spinal/cortical potentiation induced by conduction block of the peripheral nerves can be observed prior to inflammation. In the present study, we found that spreading potentiation and hypersensitivity acutely induced by unilateral hindpaw ischaemia are nitric oxide (NO)-dependent and that NO is produced by ischaemia and quickly diffuses within the spinal cord. We also found that NO production induced by ischaemia is not observed in the presence of an antagonist for group II metabotropic glutamate receptors (mGluRs) and that neuronal NO synthase-positive dorsal horn neurons express group II mGluRs. These results suggest strongly that NO-mediated spreading potentiation in the spinal cord is one of the trigger mechanisms for neuropathic pain. ABSTRACT: Cortical/spinal responses to hindpaw stimulation are bilaterally potentiated by unilateral hindpaw ischaemia in mice. We tested the hypothesis that hindpaw ischaemia produces nitric oxide (NO), which diffuses in the spinal cord to induce spatially spreading potentiation. Using flavoprotein fluorescence imaging, we confirmed that the spreading potentiation in hindpaw responses was induced during ischaemia in the non-stimulated hindpaw. This spreading potentiation was blocked by spinal application of l-NAME, an inhibitor of NO synthase (NOS). Furthermore, no spreading potentiation was observed in neural NOS (nNOS) knockout mice. Spinal application of an NO donor was enough to induce cortical potentiation and mechanical hypersensitivity. The spatial distribution of NO during unilateral hindpaw ischaemia was visualized using 4-amino-5-methylamino-2',7'-difluorofluorescein (DAF-FM). An increase in fluorescence derived from the complex of DAF-FM with NO was observed on the ischaemic side of the spinal cord. A similar but smaller increase was also observed on the contralateral side. Somatosensory potentiation after hindpaw ischaemia is known to be inhibited by spinal application of LY354740, an agonist of group II metabotropic glutamate receptors (mGluRs). We confirmed that the spinal DAF-FM fluorescence increases during hindpaw ischaemia were not observed in the presence of LY354740. We also confirmed that approximately half of the nNOS-positive neurons in the superficial laminae of the dorsal horn expressed mGluR2 mRNA. These results suggest that disinhibition of mGluR2 produces NO which in turn induces a spreading potentiation in a wide area of the spinal cord. Such spreading, along with the consequent non-specific potentiation in the spinal cord, may trigger neuropathic pain.

EEG before and after total corpus callosotomy for pharmacoresistant infantile spasms: Fast oscillations and slow-wave connectivity in hypsarrhythmia.

OBJECTIVE: We analyzed the features of fast oscillations (FOs) and connectivity in hypsarrhythmia to identify biomarkers for predicting seizure outcomes after total corpus callosotomy (TCC) in children with pharmacoresistant infantile spasms (IS). We hypothesize that the power of FOs and connectivity of slow waves in hypsarrhythmia would indicate the prognosis of IS. METHOD: We retrospectively identified 42 children with pharmacoresistant IS who underwent TCC from 2009 to 2014 at Nagasaki Medical Center. We collected preoperative hypsarrhythmia for 200 seconds from each child. Children were categorized into three groups with interictal epileptic discharges on EEG at 6 months after TCC: group A, no epileptic discharge; group B, lateralized epileptic discharges; and group C; bilateral epileptic discharges. We analyzed spectral power and phase synchronization in preoperative hypsarrhythmia among the three groups. RESULTS: We found 10 children in group A, 10 children in group B, and 22 children in group C. All group A and 1 in group B achieved seizure freedom after TCC. Six (67%) of 9 group B children who underwent further surgeries achieved seizure freedom. Ten (45%) of group C children had seizure reduction >50% after TCC, and 13 (87%) of 15 children who underwent further surgeries had residual seizures. The clinical profiles of the three groups did not differ significantly. The power of FOs (≥45 Hz) in hypsarrhythmia was significantly stronger in group C at the midline and temporal regions than in groups B and A (P = .014). The connectivity of theta (4-9 Hz) and FOs (29-70 Hz) tended to increase in group C, compared with the increased connectivity of 1-2 Hz in group A (P = .08). SIGNIFICANCE: The increased power and connectivity of FOs in hypsarrhythmia may correlate with pharmacoresistant and surgically resistant seizures in IS. The existence and connectivity of FOs are associated with unilateral/bilateral cortical epileptogenicity in hypsarrhythmia. Prominent slow waves and connectivity without FOs might correlate with seizure freedom after TCC. Modulation of the callosal system with subcortical/cortical epileptic discharges might play a role in generating hypsarrhythmia and IS.

Neurosteroid dehydroepiandrosterone sulphate enhances pain transmission in rat spinal cord dorsal horn.

BACKGROUND: The neurosteroid dehydroepiandrosterone sulphate (DHEAS) activates the sigma-1 receptor, inhibits gamma-aminobutyric acid A (GABAA) and glycine receptors, and induces hyperalgesic effects. Although its effects have been studied in various tissues of the nervous system, its synaptic mechanisms in nociceptive pathways remain to be elucidated. METHODS: The threshold of mechanical hypersensitivity and spontaneous pain behaviour was assessed using the von Frey test in adult male Wistar rats after intrathecal administration of DHEAS. We also investigated the effects of DHEAS on synaptic transmission in the spinal dorsal horn using slice patch-clamp electrophysiology. RESULTS: Intrathecally administered DHEAS elicited dose-dependent mechanical hyperalgesia and spontaneous pain behaviours (withdrawal threshold: saline; 51.0 [20.1] g, 3 µg DHEAS; 14.0 [7.8] g, P<0.01, 10 µg DHEAS; 6.9 [5.2] g, 15 min after administration, P<0.001). DHEAS at 100 µM increased the frequency of miniature postsynaptic currents in the rat dorsal spinal horn; this increase was extracellular Ca2+-dependent but not sigma-1 and N-methyl-d-aspartate receptor-dependent. DHEAS suppressed the frequency of miniature inhibitory postsynaptic currents in a GABAA receptor- and sigma-1 receptor-dependent manner. CONCLUSIONS: These results suggest that DHEAS participates in the pathophysiology of nociceptive synaptic transmission in the spinal cord by potentiation of glutamate release and inhibition of the GABAA receptor.

Subcortical axonal loss with glial reactions following partial status epilepticus with neuroradiological findings of reduced subcortical diffusion.

Hyperintensity in the subcortical white matter on the diffusion-weighted magnetic resonance image has been described recently, in association with partial status epilepticus. Although this reduced subcortical diffusion is typically seen in patients with acute encephalopathy with biphasic seizures and late reduced diffusion (AESD), the exact pathophysiological mechanism is unclear. We report the case of a 3-month-old boy who underwent surgery for intractable epilepsy associated with cortical dysplasia in the left peri-Rolandic area, coincident with the appearance of reduced subcortical diffusion. Neurohistological findings revealed that the most prominent finding was axonal loss with marked astroglial and microglial reactions in the white matter. Neither degenerated neurons nor neurophagocytic microglial accumulation was evident in the cortex. These findings confirm that white matter can be secondarily damaged in patients with partial status epilepticus, and possible pathomechanism of reduced subcortical diffusion is discussed.

Optimal Position of Inferior Vena Cava Cannula in Pediatric Cardiac Surgery: A Prospective, Randomized, Controlled, Double-Blind Study.

OBJECTIVE: To examine the authors' hypothesis that during the cardiopulmonary bypass (CPB) in children, the inferior vena cava cannula tip placed proximal to the right hepatic vein orifice would produce a higher venous drainage compared with that placed distally. DESIGN: A prospective, randomized, controlled, double-blind study. SETTING: Single university hospital. PARTICIPANTS: Thirty-two patients aged <6years, scheduled for elective cardiac surgery using CPB for congenital heart disease. INTERVENTIONS: Participants were randomized to 2 groups: the proximal group with the cannula tip placed proximally within 1cm of the right hepatic vein orifice and the distal group with the cannula placed distally within 1cm of the right hepatic vein orifice. MEASUREMENTS AND MAIN RESULTS: The primary outcome of this study was the perfusion flow rate at the time of establishment of total CPB with cardioplegia. The authors initially planned to enroll 60 patients, but before reaching the target sample size, the authors terminated this study owing to patient safety, and 18 patients in the proximal group and 14 patients in the distal group finally were analyzed. No significant differences in patient characteristics were observed between the 2 groups. The mean perfusion flow rate in the proximal group was significantly greater (2.55 ± 0.27 L/min/m2) than that in the distal group (2.37 ± 0.20 L/min/m2, p = 0.04). CONCLUSION: The inferior vena cava cannula tip placed in the proximal position was clinically superior, compared with a distal placement, in producing higher perfusion flow in children.

Surgical and developmental outcomes of corpus callosotomy for West syndrome in patients without MRI lesions.

OBJECTIVE: This retrospective study was designed to assess the impact of corpus callosotomy (CC) in patients with intractable West syndrome (WS) without lesions on magnetic resonance imaging (MRI). METHODS: This study involved 56 patients with WS who underwent CC between January 2000 and December 2014. Seizure outcomes and changes in psychomotor development were analyzed. RESULTS: Mean age at the onset of epilepsy and at the time of CC was 5.1 and 22.6 months, respectively. Mean duration of epilepsy before CC was 17.6 months. Video-electroencephalography (EEG) monitoring showed bilateral ictal and interictal abnormalities before CC. Mean follow-up duration was 36.6 months. At final follow-up, seizure outcomes after CC were seizure-free in 18 patients (32.1%), excellent (E: >80% reduction in seizure frequency) in 15 (26.8%), good (G: >50% reduction) in 10 (17.9%), and poor (P: <50% reduction) in 13 (23.2%). Epileptic spasms (ES) were eliminated in 24 patients (42.9%). However, tonic seizure (TS) outcomes were poor (P < 0.05). Of preoperative predictive factors related to seizure outcome, developmental delay before epilepsy onset correlated with poor outcome (P < 0.05). One year post-CC, 6 patients (10.7%) had no epileptic abnormality on EEG, 19 (33.9%) had lateralized epileptic abnormalities, and 31 (55.4%) had bilateral asynchronous epileptic abnormalities. All patients without epileptic discharge achieved seizure freedom. Fifteen of 19 (78.9%) patients in the lateralized group and 12 of 31 (38.7%) in the bilateral asynchronous group had worthwhile outcomes (F + E). The patterns of EEG changes after CC correlated with seizure outcome (P < 0.01). Progressive declines in developmental quotient were prevented in patients with worthwhile outcomes. SIGNIFICANCE: CC represents an important therapeutic option for patients with WS without resectable MRI lesions. Transcallosal seizure bilateralization is critical for bilateral ES generation. Early identification of potential CC candidates and surgical intervention are important for better seizure control and cognitive capacity preservation before severe developmental delay development.

Pediatric Patients with High Pulmonary Arterial Pressure in Congenital Heart Disease Have Increased Tracheal Diameters Measured by Computed Tomography.

OBJECTIVES: Determination of the appropriate tracheal tube size using formulas based on age or height often is inaccurate in pediatric patients with congenital heart disease (CHD), particularly in those with high pulmonary arterial pressure (PAP). Here, the authors compared tracheal diameters between pediatric patients with CHD with high PAP and low PAP. DESIGN: Retrospective clinical study. SETTING: Hospital. PARTICIPANTS: Pediatric patients, from birth to 6 months of age, requiring general anesthesia and tracheal intubation who underwent computed tomography were included. Patients with mean pulmonary artery pressure >25 mmHg were allocated to the high PAP group, and the remaining patients were allocated to the low PAP group. The primary outcome was the tracheal diameter at the cricoid cartilage level, and the secondary goal was to observe whether the size of the tracheal tube was appropriate compared with that obtained using predictable formulas based on age or height. MEASUREMENTS AND MAIN RESULTS: The mean tracheal diameter was significantly larger in the high PAP group than in the low PAP group (p < 0.01). Pediatric patients with high PAP required a larger tracheal tube size than predicted by formulas based on age or height (p = 0.04 for age and height). CONCLUSIONS: Pediatric patients with high PAP had larger tracheal diameters than those with low PAP and required larger tracheal tubes compared with the size predicted using formulas based on age or height.

Effect of remifentanil on postoperative nausea and vomiting: a randomized pilot study.

Opioid-related postoperative nausea and vomiting should not occur following remifentanil administration because of its relatively short time to elimination. However, studies have indicated that the incidence of postoperative nausea and vomiting associated with remifentanil is similar to that with other opioids. Hence, we aimed to determine whether intraoperative remifentanil itself is associated with postoperative nausea and vomiting when postoperative pain is managed without opioid use. In this prospective pilot study, 150 patients who underwent unilateral upper limb surgery under general anesthesia with brachial plexus block were included. Patients in the remifentanil and control groups received 0.5 µg/kg/min remifentanil and saline, respectively. Postoperative pain was managed using a brachial plexus block, non-steroidal anti-inflammatory drugs, and acetaminophen. The presence of postoperative nausea and vomiting within the first 24 h after anesthesia was assessed by an evaluator blinded to patient allocation. Eight patients were excluded from the final analysis, resulting in 72 and 70 patients in the remifentanil and control groups, respectively. Postoperative nausea and vomiting within 24 h after surgery occurred in 11 and 9 patients in the remifentanil and control groups, respectively. These data suggest that remifentanil use only minimally affects the incidence of postoperative nausea and vomiting under sevoflurane anesthesia. UMIN Clinical Trials Registry identification number: UMIN000016110.

Significant decreases in blood propofol concentrations during adrenalectomy for phaeochromocytoma.

AIM: The kinetics of propofol are influenced by cardiac output. The aim of this study was to examine changes in blood propofol concentrations during phaeochromocytoma surgery using target-controlled infusion (TCI) anaesthesia with propofol. METHODS: This is a prospective observational study. Ten patients with phaeochromocytoma who underwent unilateral adrenalectomy were included. Cardiac output was measured using an arterial pressure-based cardiac output analysis method. The target blood propofol concentrations were adjusted to maintain an approximate bispectral index (BIS) value of 40 before initiating surgery. The settings remained constant during surgery. Blood samples for propofol concentrations were collected from the radial artery at seven time points: two before tumour manipulation (T1, 2), two during tumour manipulation (T3, 4), and three after tumour vein ligation (T4-7). BIS values, the arterial pressure cardiac index (APCI) and haemodynamic parameters were measured at the same time points as the blood samples. The prop-ratio was calculated by dividing blood propofol concentrations by target concentrations of TCI. RESULTS: APCI increased during tumour manipulation and after tumour vein ligation. The prop-ratio was reduced significantly by approximately 40% and showed a significant negative correlation with APCI. BIS values increased significantly and showed a significant negative correlation with the prop-ratio. CONCLUSION: The increased APCI during tumour manipulation and after tumour vein ligation was associated with markedly reduced blood propofol concentrations. These results reveal that significant decreases in the anaesthetic effect may be observed in patients undergoing phaeochromocytoma surgery even if TCI anaesthesia is used with propofol.

Intraoperative Detection of Persistent Endoleak by Detecting Residual Spontaneous Echocardiographic Contrast in the Aneurysmal Sac During Thoracic Endovascular Aortic Repair.

Persistent endoleaks may lead to adverse events after endovascular aortic repair. We prospectively examined the relationship between intraoperative residual spontaneous echocardiographic contrast (SEC) within the aneurysmal sac and the incidence of postoperative endoleaks in 60 patients undergoing thoracic endovascular aortic repair. Patients with SEC had a higher incidence of postoperative endoleaks than did patients without SEC within a few days postoperatively (60.0% vs 12.5%, respectively; P < .001) and at 6 months postoperatively (40.0% vs 2.5%, respectively; P < .001). Intraoperative confirmation of the absence of SEC may identify patients at low risk for persistent endoleaks after thoracic endovascular aortic repair.

Anesthetic management of abdominal radical trachelectomy for uterine cervical cancer during pregnancy.

Abdominal radical trachelectomy has been identified as a surgical option for fertility preservation in cervical cancer patients, particularly in pregnant women who strongly desire to continue their pregnancy. Since this procedure requires operating in the uterus, the hardness of the uterus can affect the ease of surgery. Generally, sevoflurane is used for anesthesia in non-obstetric surgery for pregnant women because uterine relaxation is advantageous for uterine blood flow maintenance. However, the use of sevoflurane during radical trachelectomy has not been thoroughly evaluated. Here, we report on anesthesia use in three cases of abdominal radical trachelectomy during pregnancy. Propofol enabled maintenance of uterine tension while not significantly affecting fetal growth. It is important to consider maintenance of uterine tension and fetal circulation in anesthesia management. During the operation, we performed an ultrasound examination every 30 min to confirm fetal well-being. Although frequent fetal heart rate monitoring of the pre-viable fetus is not recommended, if fetal bradycardia is detected, sevoflurane may then be used to improve fetal circulation. Additionally, if the fetal heartbeat stops, a radical hysterectomy would then be required. Therefore, we consider that fetal heart rate monitoring during this procedure is necessary, and propofol is suitable as an anesthetic for this surgery during pregnancy.

Hydrogen peroxide modulates synaptic transmission in ventral horn neurons of the rat spinal cord.

KEY POINTS: Excessive production of reactive oxygen species (ROS) is implicated in many central nervous system disorders; however, the physiological role of ROS in spinal ventral horn (VH) neurons remains poorly understood. We investigated how pathological levels of H2O2, an abundant ROS, regulate synaptic transmission in VH neurons of rats using a whole-cell patch clamp approach. H2O2 increased the release of glutamate and GABA from presynaptic terminals. The increase in glutamate release involved N-type voltage-gated calcium channels (VGCCs), ryanodine receptors (RyRs), and inositol trisphosphate receptors (IP3 Rs); the increase in GABA release, which inhibited glutamatergic transmission, involved IP3 R. Inhibiting N-type VGCCs and RyRs attenuates excitotoxicity resulting from increased glutamatergic activity while preserving the neuroprotective effects of GABA, and may represent a novel strategy for treating H2O2-induced motor neuron disorders resulting from trauma or ischaemia-reperfusion injury. Excessive production of reactive oxygen species (ROS) is a critical component of the cellular and molecular pathophysiology of many central nervous system (CNS) disorders, including trauma, ischaemia-reperfusion injury, and neurodegenerative diseases. Hydrogen peroxide (H2O2), an abundant ROS, modulates synaptic transmission and contributes to neuronal damage in the CNS; however, the pathophysiological role of H2O2 in spinal cord ventral horn (VH) neurons remains poorly understood, despite reports that these neurons are highly vulnerable to oxidative stress and ischaemia. This was investigated in the present study using a whole-cell patch clamp approach in rats. We found that exogenous application of H2O2 increased the release of glutamate from excitatory presynaptic terminals and γ-aminobutyric acid (GABA) from inhibitory presynaptic terminals. The increase of glutamate release was induced in part by an increase in Ca(2+) influx through N-type voltage-gated calcium channels (VGCCs) as well as by ryanodine receptor (RyR)- and inositol trisphosphate receptor-mediated Ca(2+) release from the endoplasmic reticulum (ER). In inhibitory presynaptic neurons, increased IP3 R-mediated Ca(2+) release from the ER increased GABAergic transmission, which served to rescue VH neurons from excessive release of glutamate from presynaptic terminals. These findings indicate that inhibiting N-type VGCCs or RyRs may attenuate excitotoxicity resulting from increased glutamatergic activity while preserving the neuroprotective effects of GABA, and may therefore represent a novel and targeted strategy for preventing and treating H2O2-induced motor neuron disorders.

Ultrasound-guided ilioinguinal/iliohypogastric block did not reduce emergence delirium after ambulatory pediatric inguinal hernia repair: a prospective randomized double-blind study.

PURPOSE: Emergence delirium (ED) is a common postoperative complication of ambulatory pediatric surgery done under general anesthesia with sevoflurane. However, perioperative analgesic techniques have been shown to reduce sevoflurane-induced ED. The primary objective of this investigation was to examine whether an ultrasound-guided ilioinguinal/iliohypogastric (II/IH) nerve block for ambulatory pediatric inguinal hernia repair could reduce the incidence of sevoflurane-induced ED. METHODS: The subjects of this prospective randomized double-blind study were 40 boys ranging in age from 1 to 6 years, who were scheduled to undergo ambulatory inguinal hernia repair. The patients were randomized to either receive or not to receive an ultrasound-guided II/IH nerve block (Group B and Group NB, respectively). General anesthesia was maintained with sevoflurane and nitrous oxide. The primary outcome assessed was ED, evaluated using the Pediatric Anesthesia Emergence Delirium (PAED) scale 30 min after emergence from general anesthesia. The secondary outcomes assessed were postoperative pain, evaluated using the Behavioral Observational Pain Scale (BOPS), and the amount of intra-operative sevoflurane given. RESULTS: The median PAED scale scores did not differ between Groups B and NB at 30 min (P = 0.41). BOPS scores also did not differ significantly between the groups, but the mean amount of intraoperative sevoflurane given was significantly lower in Group B than in Group NB (P < 0.01). CONCLUSIONS: Ultrasound-guided II/IH nerve block for ambulatory pediatric inguinal hernia repair did not reduce ED, but it did decrease the amount of intra-operative sevoflurane needed. CLINICAL TRIAL REGISTRATION: UMIN000008586.

The utility of anatomic diagnosis for identifying femoral nerve palsy following gynecologic surgery.

We describe a case in which an anatomic diagnosis was useful for diagnosing and estimating the cause of femoral nerve palsy following gynecologic surgery. A 49-year-old female received general and epidural anesthesia for radical ovarian cancer surgery. Although injection pain was noted in the left medial shin with 1 % mepivacaine administered as a test dose, the catheter was left indwelling because it improved her symptoms. The surgery, which lasted 195 min, was performed in the lithotomy position, and a self-retained retractor was used to gain a good surgical field. Postoperatively, the patient complained of difficulty in stretching her knee joint and left lower limb paresthesia that did not improve after stopping continuous epidural administration. A spinal cord injury related to epidural anesthesia was suspected because the sites of sensory impairment and epidural injection pain were the same; however, the patient had greater weakness of the quadriceps muscle than the iliopsoas, and no other muscle weakness was observed. These findings and previous reports suggest that her femoral nerve palsy was caused by compression of the inguinal ligament from the self-retaining retractor and lithotomy position. Twenty months after surgery, her muscle strength had fully recovered.