A novel method using a single lumen tube and extraluminal bronchial blocker for one-lung ventilation in severe tracheal stenosis: a case report.

Double-lumen tubes (DLT) and bronchial blockers (BB) are usually used to functionally isolate the lungs during thoracic surgery. However, for patients with tracheal stenosis, management of one lung ventilation (OLV) in the anesthesia is still full of challenges due to mismatching between the trachea lumen and tracheal tube diameter. In the past, a small single-lumen tube (SLT) combined with an endobronchial pediatric BB or extraluminal detached BB of a uninvent obtained successful OLV in patients with tracheal stenosis. Additionally, nonintubated tracheal and surgical pneumothorax may work. We first report an interesting case of a 65-year-old man with a history of an upper left lobe nodule in the lung and tracheotomies. A chest computed tomographic (CT) scan showed the middle of the trachea was severely narrowed. We used a minor SLT and extraluminal BB and acquired optimal collapse of the left lung. He accepted video-assisted thoracoscopic lobectomy of an upper left lobe under general anesthesia. After both BB and SLT were removed, the patient did not present dyspnea or airway injury. The patient recovered well and was discharged from the hospital a week after surgery. This method, a minor SLT combined with extraluminal BB, is convenient for sputum suction and fiber optic bronchoscope examination, moreover, it is an option for OLV in severe tracheal stenosis cases.

Postoperative 24-h Acute Sleep Deprivation Improves Learning and Memory Through Inhibition of Tau Phosphorylation in the Hippocampal Neurons of Splenectomized Rats.

PURPOSE: As tau pathology is involved in impaired postoperative learning and memory in rats, we attempted to identify the possible mechanisms by which tau pathology affects postoperative sleep deprivation. METHODS: Adult male Sprague-Dawley rats were randomly assigned into six groups as follows: the Control group, Anaesthesia group, Surgery group, Sleep deprivation (SD) group: 24-h SD with the modified multiple platform method (MMPM), Anaesthesia and SD (ASD) group, and Surgery and SD (SSD) group. Tau396 and FOXQ1 protein expression levels in the hippocampal neurons of all groups were analysed. Changes following co-culture of hippocampal neurons with IL-6 were detected by flow cytometry. RESULTS: Twenty-four hours of acute SD decreased the error scores on postoperative day 5 in the ASD and SSD groups compared with the Anaesthesia and Surgery groups. Compared with the tau levels in the Control group, tau levels in the Anaesthesia and Surgery groups were increased, but SD decreased the expression of tau in the ASD and SSD groups. The expression levels of tau and FOXQ1 were inversely regulated. When hippocampal neurons were co-cultured with IL-6, the same changes were observed. CONCLUSION: Postoperative 24-h acute SD improves learning and memory through inhibition of tau phosphorylation and increases IL-6-induced expression of FOXQ1 in the hippocampal neurons of splenectomized rats.

Inhibiting aberrant p53-PUMA feedback loop activation attenuates ischaemia reperfusion-induced neuroapoptosis and neuroinflammation in rats by downregulating caspase 3 and the NF-κB cytokine pathway.

BACKGROUND: Ischaemia reperfusion (IR) induces multiple pathophysiological changes. In addition to its classical role in regulating tumourigenesis, the feedback loop formed by p53 and its driven target p53-upregulated modulator of apoptosis (PUMA) was recently demonstrated to be the common node tightly controlling various cellular responses during myocardial IR. However, the roles of the p53-PUMA feedback loop in the spinal cord remain unclear. This study aimed to elucidate the roles of p53-PUMA feedback interactions in the spinal cord after IR, specifically investigating their regulation of caspase 3-mediated apoptosis and nuclear factor (NF)-κB-mediated cytokine release. METHODS: SD rats subjected to 12 min of aortic arch occlusion served as IR models. Neurological assessment as well as p53 and PUMA mRNA and protein expression analyses were performed at 12-h intervals during a 48-h reperfusion period. The cellular distributions of p53 and PUMA were determined via double immunofluorescence staining. The effects of the p53-PUMA feedback loop on modulating hind-limb function; the number of TUNEL-positive cells; and protein levels of caspase 3, NF-κB and cytokines interleukin (IL)-1ß and tumour necrosis factor (TNF)-α, were evaluated by intrathecal treatment with PUMA-specific or scramble siRNA and pifithrin (PFT)-α. Blood-spinal cord barrier (BSCB) breakdown was examined by Evans blue (EB) extravasation and water content analyses. RESULTS: IR induced significant behavioural deficits as demonstrated by deceased Tarlov scores, which displayed trends opposite those of PUMA and p53 protein and mRNA expression. Upregulated PUMA and p53 fluorescent labels were widely distributed in neurons, astrocytes and microglia. Injecting si-PUMA and PFT-α exerted significant anti-apoptosis effects as shown by the reduced number of TUNEL-positive cells, nuclear abnormalities and cleaved caspase 3 levels at 48 h post-IR. Additionally, p53 colocalized with NF-κB within the cell. Similarly, injecting si-PUMA and PFT-α exerted anti-inflammatory effects as shown by the decreased NF-κB translocation and release of IL-1ß and TNF-α. Additionally, injecting si-PUMA and PFT-α preserved the BSCB integrity as determined by decreased EB extravasation and spinal water content. However, injecting si-Con did not induce any of the abovementioned effects. CONCLUSIONS: Inhibition of aberrant p53-PUMA feedback loop activation by intrathecal treatment with si-PUMA and PFT-α prevented IR-induced neuroapoptosis, inflammatory responses and BSCB breakdown by inactivating caspase 3-mediated apoptosis and NF-κB-mediated cytokine release.

MicroRNA-125b mimic inhibits ischemia reperfusion-induced neuroinflammation and aberrant p53 apoptotic signalling activation through targeting TP53INP1.

BACKGROUND: Ischemia reperfusion (IR) injury affects neuronal function through multiple pathogeneses that induce neuroinflammation and cellular apoptosis. The important roles of microRNAs (miRs) in the regulation of spinal cord IR have been recently reported. Among these roles, we investigated whether miR-125b and its downstream targets regulated the p53 signalling network and participated in both inflammation and apoptosis. METHODS: An IR model was established via 12-min occlusion of the aortic arch. The direct interaction between miR-125b and TP53INP1 was demonstrated by Western blotting and luciferase assays. The cellular distributions of TP53INP1 were visualised by double immunofluorescence labelling. The effects of miR-125b on the expression of TP53INP1, p53 and release of proinflammatory cytokines were evaluated by synthetic miRs. Additionally, the detection of hind-limb motor function in vivo and motor neuronal apoptosis in vitro were evaluated to explore the potential mechanisms. RESULTS: IR-induced alterations in hind-limb motor function were closely related to the temporal changes in miR-125b and TP53INP1 expression. The miR-125b/TP53INP1 gene pair was confirmed by luciferase assay. Compared with Sham controls, IR treatment resulted in increased TP53INP1 immunoreactivity that was primarily distributed in neurons. Treatment with miR-125b mimic markedly decreased the protein levels of TP53INP1, p53 and cytokines interleukin (IL)-1ß and tumour necrosis factor (TNF)-α, whereas miR-125b control or inhibitor did not have the above-mentioned effects. Moreover, miR-125b mimic improved motor function in vivo and attenuated neuronal apoptosis in vitro, as demonstrated by the increased average Tarlov scores in lower limbs and lower percentages of neurons in the A4 and A2 quadrants of flow cytometry. Fluorescent staining and quantification further indicated that miR-125b mimic decreased the immunoreactivities of p53 and cleaved caspase 3 in neurons and simultaneously reduced the number of double-labelled cells with TP53INP1. CONCLUSIONS: miR-125b mimic partially protected neurons against neuroinflammation and aberrant p53 network activation-induced apoptosis during IR injury through downregulation of TP53INP1.

Preoperative versus postoperative ultrasound-guided rectus sheath block for improving pain, sleep quality and cytokine levels in patients with open midline incisions undergoing transabdominal gynecological surgery: a randomized-controlled trial.

BACKGROUND: Nerve block is usually performed before surgery because it inhibits reflection of the skin incision and reduces the amount of intraoperative anesthetic used. We hypothesized that performing rectus sheath block (RSB) after surgery would result in a longer duration of the analgesic effects and have a subtle influence on sleep time after surgery but that it would not decrease the perioperative cytokine levels of patients undergoing gynecological surgery. METHODS: A randomized, double-blinded, controlled trial was conducted from October 2015 to June 2016. Seventy-seven patients undergoing elective transabdominal gynecological surgery were randomly assigned to the following two groups: a general anesthesia group who received 0.5% ropivacaine hydrochloride RSB preoperatively and saline RSB postoperatively, and another group who received the opposite sequence. The objective of the trial was to evaluate the postoperative pain, sleep and changes in cytokine levels of patients during the postoperative 48 h. RESULTS: A total of 61 female patients (mean age: 50 years; range: 24-65 years) were included in the final study sample. There was no significant difference in the pain, consumption of oxycodone, or time to first administration of patient-controlled intravenous analgesia between the two groups. The postoperative sleep stages N2 and N3 were increased by 52.9 and 29.1 min per patient, respectively, in the preoperative RSB group compared with those in the postoperative group. The preoperative IL-6 concentration in the preoperative RSB group was lower than that in the same group at the end of surgery and 24 h postoperatively. CONCLUSIONS: We concluded that preoperative RSB might preserve postoperative sleep by inhibiting the increase of IL-6 without shortening the analgesia time compared with postoperative RSB in female patients undergoing elective midline incision transabdominal gynecological surgery. TRIAL REGISTRATION: ClinicalTrials.gov , NCT02477098 , registered on 15 June 2015.

Changes in the first postoperative night bispectral index of patients after thyroidectomy with different types of primary anesthetic management: a randomized controlled trial.

Despite major advances in anesthesia management and developments in anesthetic agents, postoperative sleep disturbances remain dissatisfactory for many patients. We hypothesized that propofol might have a subtle influence on sleep after thyroidectomy compared to sevoflurane. A randomized, single-blinded, controlled trial was conducted at the First Hospital of China Medical University from October 2014 to October 2015. One hundred and twenty-four patients undergoing thyroidectomy were enrolled and received sevoflurane (sevoflurane group) or propofol (propofol group) as anesthesia maintenance. Major assessments were made during the operation (different types of anesthetic management) and on the first postoperative night (sleep status). The primary outcome was postoperative sleep status, measured by the BIS-Vista monitor on the first night after surgery between propofol and sevoflurane groups. A total of 105 patients (79 women, 26 men; mean age 49 years; range 18-65 years) were included in the final study sample. All patients in both groups showed one of the five sleep patterns classified by this trial. The BIS-area under the curve was decreased, the sleep efficiency index was significantly increased, and the durations of postoperative sleep and sleep stage N3 were increased by 110.5 and 36.5 min per patient, respectively, in the propofol compared to the sevoflurane group. Propofol might preserve sleep time immediately after thyroidectomy. Clinical Trials.gov identifier: NCT 02146976.

Effects of ultrasound-guided stellate-ganglion block on sleep and regional cerebral oxygen saturation in patients undergoing breast cancer surgery: a randomized, controlled, double-blinded trial.

Numerous factors could contribute to sleep disturbances in women with breast cancer. We hypothesized that stellate ganglion block (SGB) during surgery would preserve sleep after surgery and increase intraoperative regional cerebral oxygen saturation (rSO2) on the blocked side in patients undergoing breast cancer surgery. A randomized, double-blinded, controlled trial was conducted at the First Hospital of China Medical University from January 2016 to September 2016. Ninety-six patients who underwent radical breast cancer surgery requiring general anaesthesia were randomly assigned to one of two study groups: a control group that received a saline SGB and a block group that received a 0.25% ropivacaine hydrochloride SGB. The primary outcome measure was the postoperative sleep profile, which was assessed using the bispectral index on the first postoperative night. The secondary outcome measure was the intraoperative rSO2, monitored was throughout surgery using near-infrared spectroscopy. A total of 91 female patients (mean age: 45 years; range 24-51 years) were included in the study. The duration of sleep was significantly increased by 66.3 min in the ropivacaine-SGB group compared with the saline-SGB group. No differences in rSO2 were observed on either the left or right side of the patients in either group 50 min after anaesthesia induction. We conclude that ropivacaine-SGB combined with general anaesthesia might increase the first postoperative sleep duration without influencing the intraoperative rSO2 in female patients undergoing elective breast cancer surgery. Clinical trials.gov identifier NCT02651519.

Elevated microRNA-129-5p level ameliorates neuroinflammation and blood-spinal cord barrier damage after ischemia-reperfusion by inhibiting HMGB1 and the TLR3-cytokine pathway.

BACKGROUND: Ischemia-reperfusion (IR) affects microRNA (miR) expression and causes substantial inflammation. Multiple roles of the tumor suppressor miR-129-5p in cerebral IR have recently been reported, but its functions in the spinal cord are unclear. Here, we investigated the role of miR-129-5p after spinal cord IR, particularly in regulating high-mobility group box-1 (HMGB1) and the Toll-like receptor (TLR)-3 pathway. METHODS: Ischemia was induced via 5-min occlusion of the aortic arch. The relationship between miR-129-5p and HMGB1 was elucidated via RT-PCR, western blotting, and luciferase assays. The cellular distribution of HMGB1 was determined via double immunofluorescence. The effect of miR-129-5p on the expression of HMGB1, TLR3, and downstream cytokines was evaluated using synthetic miRs, rHMGB1, and the TLR3 agonist Poly(I:C). Blood-spinal cord barrier (BSCB) permeability was examined by measuring Evans blue (EB) dye extravasation and the water content. RESULTS: The temporal miR-129-5p and HMGB1 expression profiles and luciferase assay results indicated that miR-129-5p targeted HMGB1. Compared with the Sham group, the IR group had higher HMGB1 immunoreactivity, which was primarily distributed in neurons and microglia. Intrathecal injection of the miR-129-5p mimic significantly decreased the HMGB1, TLR3, interleukin (IL)-1ß and tumor necrosis factor (TNF)-α levels and the double-labeled cell count 48 h post-surgery, whereas rHMGB1 and Poly(I:C) reversed these effects. Injection of miR-129-5p mimic preserved motor function and prevented BSCB leakage based on increased Basso Mouse Scale scores and decreased EB extravasation and water content, whereas injection rHMGB1 and Poly(I:C) aggravated these injuries. CONCLUSIONS: Increasing miR-129-5p levels protect against IR by ameliorating inflammation-induced neuronal and BCSB damage by inhibiting HMGB1 and TLR3-associated cytokines.

Down-Regulation of CXCL12/CXCR4 Expression Alleviates Ischemia-Reperfusion-Induced Inflammatory Pain via Inhibiting Glial TLR4 Activation in the Spinal Cord.

Toll-like receptor 4 (TLR4) is important for the pathogenesis of inflammatory reactions and the promotion of pain processing after ischemia/reperfusion (IR) in spinal cord. Recently, C-X-C chemokine ligand 12 (CXCL12) and its receptor, C-X-C chemokine receptor 4 (CXCR4), were demonstrated to be simultaneously critical for inflammatory reactions, thereby facilitating glial activation. However, whether CXCL12/CXCR4 expression can contribute to IR-induced inflammatory pain via spinal TLR4 remained unclear. A rat model was established by 8 min of aortic arch occlusion. The effects of CXCL12/CXCR4 expression and TLR4 activation on inflammatory hyperalgesia were investigated by pretreatments with CXCL12-neutralizing antibody, CXCR4 antagonist (AMD3100) and TLR4 antagonist (TAK-242) for 5 consecutive days before surgery. The results indicated that IR induced significant and sustained inflammatory pain, observed as decreases in paw withdrawal threshold (PWT) and paw withdrawal latency (PWL), throughout the post-injury period. The increased levels of TLR4 and proinflammatory chemokine CXCL12, as well as its receptor, CXCR4, were closely correlated with the PWT and PWL trends. Double immunostaining further suggested that TLR4, which is mainly expressed on astrocytes and microglia, was closely co-localized with CXCL12 and CXCR4 in spinal dorsal horn. As expected, intrathecal pretreatment with the TLR4 antagonist, TAK-242 markedly ameliorated pain by inhibiting astrocytic and microglial activation, as shown by decreases in TLR4 immunoreactivity and the percentage of double-labeled cells. These protective effects were likely due in part to the reduced production of the downstream cytokines IL-1ß and TNF-α, as well as for the recruitment of CXCL12 and CXCR4. Additionally, intrathecal pretreatment with CXCL12-neutralizing antibody and AMD3100 resulted in similar analgesic and anti-inflammatory effects as those receiving TAK-242 pretreatment. These results suggest that intrathecal blockade of CXCL12/CXCR4 expression may attenuate IR-induced pain sensation and the release of inflammatory cytokines by limiting glial TLR4 activation in spinal cord.

Role of autophagy in the bimodal stage after spinal cord ischemia reperfusion injury in rats.

Autophagy plays an important role in spinal cord ischemia reperfusion (I/R) injury, but its neuroprotective or neurodegenerative role remains controversial. The extent and persistence of autophagy activation may be the critical factor to explain the opposing effects. In this study, the different roles and action mechanisms of autophagy in the early and later stages after I/R injury were investigated in rats. Thespinal cord I/R injury was induced by 14-min occlusion of the aortic arch, after which rats were treated with autophagic inhibitor (3-methyladenine, 3-MA) or agonist (rapamycin) immediately or 48h following the injury. Autophagy markers, microtubule-associated protein light chain 3-II (LC3-II) and Beclin 1 increased and peaked at the early stage (8h) and the later stage (72h) after spinal cord I/R injury. Beclin 1 was mostly expressed in neurons, but was also expressed to an extent in astrocytes, microglia and vascular endothelial cells. 8h after injury, rats treated with 3-MA showed a decrease in the hind-limb Basso-Beattie-Bresnahan (BBB) motor function scores, surviving motor neurons, and B-cell lymphoma-2 (Bcl-2) expression, and increase in the terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL)-positive cells, Bcl-2-associated X protein (Bax), tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß) expression, and activation of microglia, while those treated with rapamycin showed opposing effects. However, 72h after injury, rats treated with 3-MA improved the BBB scores, and the surviving motor neurons, and reduced the autophagic cell death, while those treated with rapamycin had adverse effects. These findings provide the first evidence that early activated autophagy alleviates spinal cord I/R injury via inhibiting apoptosis and inflammation; however later excessively elevated autophagy aggravates I/R injury through inducing autophagic cell death.

Changes in First Postoperative Night Bispectral Index After Daytime Sedation Induced by Dexmedetomidine or Midazolam Under Regional Anesthesia: A Randomized Controlled Trial.

BACKGROUND AND OBJECTIVES: Supplementation of spinal anesthesia with various sedatives is a standard protocol to alleviate patient anxiety associated with the surgical procedure. We hypothesized that, compared with dexmedetomidine, midazolam might have a subtle influence on sleep quality after surgery following elective transurethral prostatic resection (TURP) in elderly male patients. METHODS: A randomized, double-blind, controlled trial was conducted at the First Hospital of China Medical University from July 2014 to January 2015. One hundred eleven patients undergoing TURP were enrolled and received intravenous saline infusion (control group), dexmedetomidine (dexmedetomidine group), or midazolam (midazolam group) for sedation during the spinal anesthesia procedure. The intraoperative sedative state and postoperative sleep quality were evaluated using a Bispectral Index (BIS)-Vista monitor. The primary outcome was postoperative sleep quality, as measured by the BIS-Vista monitor on the first night after surgery. RESULTS: The intraoperative BIS area under the curve value was significantly lower in the dexmedetomidine group (54.1%) compared with those in the other 2 groups (control group, 94.1%; midazolam group, 77.2%).The postoperative BIS area under the curve value was highest in the dexmedetomidine group at 88.7%. The BIS sleep efficiency index showed a significant 33.1% increase in the midazolam group compared with the dexmedetomidine group. The duration of sleep in the midazolam group was 237.8 minutes longer than that in the dexmedetomidine group. CONCLUSIONS: We conclude that midazolam combined with spinal anesthesia might preserve the sleep quality of elderly male patients immediately after TURP.

miR-320a affects spinal cord edema through negatively regulating aquaporin-1 of blood-spinal cord barrier during bimodal stage after ischemia reperfusion injury in rats.

BACKGROUND: Spinal cord edema is a serious complication and pathophysiological change after ischemia reperfusion (IR) injury. It has been demonstrated closely associated with bimodal disruption of blood-spinal cord barrier (BSCB) in our previous work. Aquaporin (AQP)1 plays important but contradictory roles in water homeostasis. Recently, microRNAs (miRs) effectively regulate numerous target mRNAs during ischemia. However, whether miRs are able to protect against dimodal disruption of BSCB by regulating perivascular AQP1 remains to be elucidated. RESULTS: Spinal water content and EB extravasation were suggested as a bimodal distribution in directly proportion to AQP1, since all maximal changes were detected at 12 and 48 h after reperfusion. Further TEM and double immunofluorescence showed that former disruption of BSCB at 12 h was attributed to cytotoxic edema by up-regulated AQP1 expressions in astrocytes, whereas the latter at 48 h was mixed with vasogenic edema with both endothelial cells and astrocytes involvement. Microarray analysis revealed that at 12 h post-injury, ten miRs were upregulated (>2.0 fold) and seven miRs were downregulated (<0.5 fold) and at 48 h, ten miRs were upregulated and eleven were downregulated compared to Sham-operated controls. Genomic screening and luciferase assays identified that miR-320a was a potential modulator of AQP1 in spinal cord after IR in vitro. In vivo, compared to rats in IR and negative control group, intrathecal infusion of miR-320a mimic attenuated IR-induced lower limb motor function deficits and BSCB dysfunction as decreased EB extravasation and spinal water content through down-regulating AQP1 expressions, whereas pretreated with miR-320a AMO reversed above effects. CONCLUSION: These findings indicate miR-320a directly and functionally affects spinal cord edema through negatively regulating AQP1 of BSCB after IR.

Changes in postoperative night bispectral index of patients undergoing thoracic surgery with different types of anaesthesia management: a randomized controlled trial.

This study hypothesized that different types of anaesthesia management would result in similar postoperative sleep quality. In this prospective single-blind investigation, 219 patients undergoing elective thoracic surgery were randomized into three arms: general anaesthesia, as the control group (group C); general anaesthesia combined with thoracic epidural anaesthesia (TEA) (group E); and general anaesthesia combined with infusion of 1 µg/kg dexmedetomidine (group D). Plasma samples were obtained to measure the amine and inflammatory cytokine concentrations. All patients underwent assessment with the bispectral index (BIS) for sleep quality and the visual analogue scale (VAS) for pain. The primary outcomes were inflammatory cytokine [interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α)] secretion and postoperative sleep quality on the first and second postoperative nights. The secondary outcomes were amine (adrenaline and noradrenaline) secretion during the surgical period and haemodynamic stability. The postoperative BIS area under the curve was significantly lower in group E (75.7%) than in group C (87.3%) or group D (86.5%). Patients in group E had the highest BIS of sleep efficiency index (29.2%, P < 0.05) and the lowest VAS scores (3.5, P < 0.05). Group E had lower IL-6 levels than the other two groups 24 h after surgery (P < 0.05). Patients given TEA may show reduced sleep disturbances on the first night after surgery, perhaps due to better pain management and inhibition of IL-6 release.

Preoperative versus postoperative ultrasound-guided rectus sheath block for improving pain, sleep quality and cytokine levels of patients with open midline incisions undergoing transabdominal gynaecological operation: study protocol for a randomised controlled trial.

BACKGROUND: Rectus sheath block (RSB) is used for postoperative pain relief in patients undergoing abdominal surgery with midline incision. Preoperative RSB has been shown to be effective, but it has not been compared with postoperative RSB. The aim of the present study is to evaluate postoperative pain, sleep quality and changes in the cytokine levels of patients undergoing gynaecological surgery with RSB performed preoperatively versus postoperatively. METHODS/DESIGN: This study is a prospective, randomised, controlled (randomised, parallel group, concealed allocation), single-blinded trial. All patients undergoing transabdominal gynaecological surgery will be randomised 1:1 to the treatment intervention with general anaesthesia as an adjunct to preoperative or postoperative RSB. The objective of the trial is to evaluate postoperative pain, sleep quality and changes in the cytokine levels of patients undergoing gynaecological surgery with RSB performed preoperatively (n = 32) versus postoperatively (n = 32). All of the patients, irrespective of group allocation, will receive patient-controlled intravenous analgesia (PCIA) with oxycodone. The primary objective is to compare the interval between leaving the post-anaesthesia care unit and receiving the first PCIA bolus injection on the first postoperative night between patients who receive preoperative versus postoperative RSB. The secondary objectives will be to compare (1) cumulative oxycodone consumption at 24 hours after surgery; (2) postoperative sleep quality, as measured using a BIS-Vista monitor during the first night after surgery; and (3) cytokine levels (interleukin-1, interleukin-6, tumour necrosis factor-α and interferon-γ) during surgery and at 24 and 48 hours postoperatively. DISCUSSION: Clinical experience has suggested that RSB is a very effective postoperative analgesic technique, and we will answer the following questions with this trial. Do preoperative block and postoperative block have the same duration of analgesic effects? Can postoperative block extend the analgesic time? The results of this study could have actual clinical applications that could help to reduce postoperative pain and shorten hospital stays. TRIAL REGISTRATION: Current Controlled Trials NCT02477098 15 June 2015.