The effects of robot-assisted laparoscopic surgery with Trendelenburg position on short-term postoperative respiratory diaphragmatic function.

OBJECTIVE: To study how Pneumoperitoneum under Trendelenburg position for robot-assisted laparoscopic surgery impact the perioperative respiratory parameters, diagrammatic function, etc. METHODS: Patients undergoing robot-assisted laparoscopic surgery in the Trendelenburg position and patients undergoing general surgery in the supine position were selected. The subjects were divided into two groups according to the type of surgery: robot-assisted surgery group and general surgery group. ① Respiratory parameters such as lung compliance, oxygenation index, and airway pressure were recorded at 5 min after intubation, 1 and 2 h after pneumoperitoneum. ② Diaphragm excursion (DE) and diaphragm thickening fraction (DTF) were recorded before entering the operating room (T1), immediately after extubation (T2), 10 min after extubation (T3), and upon leaving the postanesthesia care unit (T4). ③ Peripheral venous blood (5 ml) was collected before surgery and 30 min after extubation and was analyzed by enzyme-linked immunosorbent assay to determine the serum concentration of Clara cell secretory protein 16 (CC16) and surfactant protein D (SP-D). RESULT: ① Compared with the general surgery group (N = 42), the robot-assisted surgery group (N = 46) presented a significantly higher airway pressure and lower lung compliance during the surgery(P < 0.001). ② In the robot-assisted surgery group, the DE significantly decreased after surgery (P < 0.001), which persisted until patients were discharged from the PACU (P < 0.001), whereas the DTF only showed a transient decrease postoperatively (P < 0.001) and returned to its preoperative levels at discharge (P = 0.115). In the general surgery group, the DE showed a transient decrease after surgery(P = 0.011) which recovered to the preoperative levels at discharge (P = 1). No significant difference in the DTF was observed among T1, T2, T3, and T4. ③ Both the general and robot-assisted surgery reduced the postoperative serum levels of SP-D (P < 0.05), while the robot-assisted surgery increased the postoperative levels of CC16 (P < 0.001). CONCLUSION: Robot-assisted laparoscopic surgery significantly impairs postoperative diaphragm function, which does not recover to preoperative levels at PACU discharge. Elevated levels of serum CC16 after surgery suggest potential lung injury. The adverse effects may be attributed to the prolonged Trendelenburg position and pneumoperitoneum during laparoscopic surgery.

Electroacupuncture relieves chronic pain by promoting microglia M2 polarization in lumbar disc herniation rats.

Electroacupuncture has an effective analgesia on chronic pain caused by lumbar disc herniation (LDH) clinically, however, the underlying mechanism is unclear. In this study, we investigated whether electroacupuncture alleviated pain in LDH model rats by inducing spinal microglia M2 polarization. We established a noncompression LDH rat model by implanting autologous caudal nucleus pulposus into L5/L6 nerve root. Electroacupuncture (30 min/day) treatment on the ipsilateral side was started on the 8th postoperative day, once a day for consecutive 7 days. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were tested for pain behavior. Western blotting was used to detect the protein expression in lumbar enlargement (L5/L6). Immunofluorescence was used to detect iNOS+/Iba-1+ and Arg-1+/Iba-1+ and CB2R+/Iba-1+ in lumbar enlargement (L5/L6). We show that PWT and PWL decreased in the LDH group while Iba-1, iNOS, and TNF-α expression increased significantly in lumbar spinal dorsal horn (SDH) after LDH surgery, and revealing that microglia were activated and polarized towards proinflammatory M1 phenotype. Electroacupuncture treatment significantly increased PWT and PWL while reducing Iba-1, iNOS, and TNF-α expression, interestingly, Arg-1 and IL-10 expression were significantly increased. Moreover, electroacupuncture treatment led to CB2 receptors on microglia upregulation, while NF-κB and p-NF-κB expression in lumbar SDH downregulation. Our study indicated that electroacupuncture may reduce nociceptive hyperalgesia by inhibiting microglia activation and microglia M1 polarization and promoting microglia M2 polarization in lumbar SDH of LDH rats, which may be caused by the activation of CB2 receptors on microglia and inhibition of NF-κB pathway in lumbar SDH.

Proinflammatory activation of microglia in the cerebellum hyperexcites Purkinje cells to trigger ataxia.

Specific medications to combat cerebellar ataxias, a group of debilitating movement disorders characterized by difficulty with walking, balance and coordination, are still lacking. Notably, cerebellar microglial activation appears to be a common feature in different types of ataxic patients and rodent models. However, direct evidence that cerebellar microglial activation in vivo is sufficient to induce ataxia is still lacking. Here, by employing chemogenetic approaches to manipulate cerebellar microglia selectively and directly, we found that specific chemogenetic activation of microglia in the cerebellar vermis directly leads to ataxia symptoms in wild-type mice and aggravated ataxic motor deficits in 3-acetylpyridine (3-AP) mice, a classic mouse model of cerebellar ataxia. Mechanistically, cerebellar microglial proinflammatory activation induced by either chemogenetic M3D(Gq) stimulation or 3-AP modeling hyperexcites Purkinje cells (PCs), which consequently triggers ataxia. Blockade of microglia-derived TNF-α, one of the most important proinflammatory cytokines, attenuates the hyperactivity of PCs driven by microglia. Moreover, chemogenetic inhibition of cerebellar microglial activation or suppression of cerebellar microglial activation by PLX3397 and minocycline reduces the production of proinflammatory cytokines, including TNF-α, to effectively restore the overactivation of PCs and alleviate motor deficits in 3-AP mice. These results suggest that cerebellar microglial activation may aggravate the neuroinflammatory response and subsequently induce dysfunction of PCs, which in turn triggers ataxic motor deficits. Our findings thus reveal a causal relationship between proinflammatory activation of cerebellar microglia and ataxic motor symptoms, which may offer novel evidence for therapeutic intervention for cerebellar ataxias by targeting microglia and microglia-derived inflammatory mediators.

Dexmedetomidine Attenuates Lipopolysaccharide-Induced Sympathetic Activation and Sepsis via Suppressing Superoxide Signaling in Paraventricular Nucleus.

Sympathetic overactivity contributes to the pathogenesis of sepsis. The selective α2-adrenergic receptor agonist dexmedetomidine (DEX) is widely used for perioperative sedation and analgesia. We aimed to determine the central roles and mechanisms of DEX in attenuating sympathetic activity and inflammation in sepsis. Sepsis was induced by a single intraperitoneal injection of lipopolysaccharide (LPS) in rats. Effects of DEX were investigated 24 h after injection of LPS. Bilateral microinjection of DEX in the paraventricular nucleus (PVN) attenuated LPS-induced sympathetic overactivity, which was attenuated by the superoxide dismutase inhibitor DETC, cAMP analog db-cAMP or GABAA receptor antagonist gabazine. Superoxide scavenger tempol, NADPH oxidase inhibitor apocynin, adenylate cyclase inhibitor SQ22536 or PKA inhibitor Rp-cAMP caused similar effects to DEX in attenuating LPS-induced sympathetic activation. DEX inhibited LPS-induced superoxide and cAMP production, as well as NADPH oxidase, adenylate cyclase and PKA activation. The roles of DEX in reducing superoxide production and NADPH oxidase activation were attenuated by db-cAMP or gabazine. Intravenous infusion of DEX inhibited LPS-induced sympathetic overactivity, NOX activation, superoxide production, TNF-α and IL-1ß upregulation in the PVN and plasma, as well as lung and renal injury, which were attenuated by the PVN microinjection of yohimbine and DETC. We conclude that activation of α2-adrenergic receptors with DEX in the PVN attenuated LPS-induced sympathetic overactivity by reducing NADPH oxidase-dependent superoxide production via both inhibiting adenylate cyclase-cAMP-PKA signaling and activating GABAA receptors. The inhibition of NADPH oxidase-dependent superoxide production in the PVN partially contributes to the roles of intravenous infusion of DEX in attenuating LPS-induced sympathetic activation, oxidative stress and inflammation.

[Advances in Mechanisms of Blood Brain Barrier Impairment Induced by Sleep Deprivation].

Sleep deprivation,the process and state of partial or complete lack of normal sleep caused by various factors,is prevalent at present.Seriously impairing the physical and mental health,sleep deprivation has become a public health problem that cannot be ignored.Studies have demonstrated that blood-brain barrier impairment is the key pathophysiological process of a variety of neurological diseases.Although clinical and basic studies have suggested that sleep deprivation can induce blood-brain barrier impairment,the underlying mechanisms remain to be elucidated.This review summarizes the advances in the mechanisms of blood-brain barrier impairment induced by sleep deprivation.

Basolateral Amygdala Reactive Microglia May Contribute to Synaptic Impairment and Depressive-Like Behavior in Mice with Bone Cancer Pain.

Anxiety and depression induced by cancer-related pain disturb quality of life and willingness to survive. As a component of the limbic system, the basolateral amygdala (BLA) is critical for processing negative emotions. The reactive microglial engulfment of synapses may promote depression during adolescence. However, whether microglia phagocytose synapses to mediate cancer pain-induced depression remains unclear. The present study established a bone cancer-pain model to investigate the association between dendritic spine synapses and depressive-like behavior and explore the phagocytic function of microglia in the BLA. We found that tumor-bearing mice experienced postoperative pain-related depression, and their BLAs exhibited reactive microglia, as well as phagocytic synapses. The microglial inhibitor minocycline effectively mitigated depressive behavior, synaptic damage, and the phagocytic function of microglia. Our study implicates microglia-mediated synaptic loss in the BLA may act as the pathological basis of depressive-like behavior in bone cancer pain model.

TREM2 and CD163 Ameliorate Microglia-Mediated Inflammatory Environment in the Aging Brain.

Aging decreases cognitive functions, especially learning and memory. Neuroinflammation is mediated by microglia and occurs in age-related neurodegenerative diseases. The expression profiles in a dataset of cognitively normal controls (GSE11882) were obtained from the Gene Expression Omnibus (GEO) database. Microarray data were used to explore the expression of age-related genes in the human hippocampus. A total of 120 differentially expressed genes (DEGs) were identified and subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. A protein-protein interaction (PPI) network was constructed. A total of 18 key genes were identified by the plugin cytoHubba in Cytoscape software. Two genes with a positive impact on cognition during aging were teased out: triggering receptor expressed on myeloid cells 2 (TREM2) and a scavenger receptor (CD163). Finally, the results of reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting (WB) verified that the mRNA expression of these two genes was significantly upregulated in aged mice. Moreover, the levels of the inflammatory factors IL-1ß and IL-6 were significantly increased. TREM2 and CD163 may be upregulated to alleviate the inflammatory environment resulting from microglial activation in the aging brain, thereby delaying cognitive decline.

Risk factors of postoperative nausea and vomiting following ambulatory surgery: A retrospective case-control study.

Objective: To explore potential risk factors of postoperative nausea and vomiting (PONV) following ambulatory surgery. Method: Clinical data of 1670 cases receiving ambulatory surgery in Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School from September 2017 to December 2019 were retrospectively analyzed. They were categorized to PONV group and non-PONV group, and perioperative data in both groups were analyzed for assessing risk factors of PONV following ambulatory laparoscopy. Results: There were 156/1,670 (9.3%) PONV cases, and the female and male incidence in recruited cases was 12.0% and 6.0%, respectively. Analyses on perioperative data of them identified that female gender [adjusted odds ratio (aOR) = 2.060, P < 0.001], operation time >1 h (aOR = 1.554, P = 0.011), postoperative pain at rest (aOR = 1.909, P = 0.013) and postoperative pain during activities (aOR = 3.512, P < 0.001) were independent risk factors of PONV following ambulatory surgery. Furthermore, postoperative pain at rest and during activities were linearly, positively correlated to the incidence of PONV. Conclusion: Female gender, operation time >1 h and postoperative pain are closely related with the incidence of PONV following ambulatory surgery. Alleviating postoperative pain properly is one of the methods to reduce risk factors of PONV following ambulatory surgery.

Identification of hub genes associated with cognition in the hippocampus of Alzheimer's Disease.

Alzheimer's Disease (AD) is a neurodegenerative disease featured by cognitive impairment. This bioinformatic analysis was used to identify hub genes related to cognitive dysfunction in AD. The gene expression profile GSE48350 in the hippocampus of AD patients aged >70 years was obtained from the Gene Expression Omnibus (GEO) database. A total of 96 differentially expressed genes (DEGs) were identified, and subjected to Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses; a protein-protein interaction (PPI) network was constructed. The DEGs were enriched in synapse-related changes. A protein cluster was teased out of PPI. Furthermore, the cognition ranked the first among all the terms of biological process (BP). Next, 4 of 10 hub genes enriched in cognition were identified. The function of these genes was validated using APP/PS1 mice. Cognitive performance was validated by Morris Water Maze (MWM), and gene expression by RT-qPCR, Cholecystokinin (CCK), Tachykinin precursor 1 (TAC1), Calbindin 1 (CALB1) were downregulated in the hippocampus. These genes can provide new directions in the research of the molecular mechanism of AD.

Dorsal root ganglia NR2B-mediated Epac1-Piezo2 signaling pathway contributes to mechanical allodynia of bone cancer pain.

Mechanical allodynia is a painful perception of mechanical stimuli and one of the typical symptoms in bone cancer pain (BCP). Previous studies have revealed that mice and humans lacking mechanically activated Piezo2 channels do not sense mechanical stimuli. However, the underlying mechanism of Piezo2 in BCP has not been well established. The aim of the present study was to investigate whether exchange protein directly activated by cAMP 1 (Epac1) mediated Piezo2 signaling pathway may be responsible for the mechanical allodynia of BCP and whether N-methyl-D-aspartic acid (NMDA) receptor subunit 2B (NR2B) is involved in the pathway. In the present study, a BCP model was established in C3H/HeJ mice by intramedullary injection of osteosarcoma cells. The results of the mechanical allodynia test demonstrated a markedly decreased paw withdrawal mechanical threshold in BCP mice, accompanied by a significant increase in Epac1, NR2B proteins and Piezo2 mRNA expression levels in the ipsilateral dorsal root ganglion (DRG). Compared with the sham group, intrathecal Epac1 antisense oligodeoxynucleotides (Epac1-ASODN) effectively ameliorated the mechanical allodynia and decreased the expression levels of NR2B and Piezo2 in the tumor group. Pretreatment of naïve mice with a NR2B antagonist prevented the aggravation of mechanical allodynia and DRG Piezo2 levels induced by an Epac1 agonist. However, the NR2B agonist-induced increase in Piezo2 expression levels was not reversed by pretreatment with Epac1-ASODN. In conclusion, the results of the present study demonstrated that NR2B, which is a crucial downstream regulator of Epac1, may mediate the Epac1-Piezo2 pathway contributing to the development of the mechanical allodynia of BCP. The present study may enrich the theoretical knowledge of the mechanical allodynia of BCP and provide a potential analgesic strategy for clinical treatment.

Photoacoustic treatment mitigates cognitive dysfunction in a model of sleep-wake rhythm disturbance.

Sleep-wake rhythm disturbances, which are characterized by abnormal sleep timing or duration, are associated with cognitive dysfunction. Photoacoustic treatments including light and sound stimulation have been found to be effective in modulating sleep patterns and improving cognitive behavior in abnormal sleep-wake pattern experiments. In this study, we examined whether light and sound interventions could reduce sleep-wake pattern disturbances and memory deficits in a sleep rhythm disturbance model. We established a model of sleep rhythm disturbance in C57BL/6J mice via a sleep deprivation method involving manual cage tapping, cage jostling, and nest disturbance. We used a Mini Mitter radio transmitter device to monitor motor activity in the mice and fear conditioning tests to assess cognitive function. Our results indicated that an intervention in which the mice were exposed to blue light (40-Hz flickering frequency) for 1 hour during their subjective daytime significantly improved the 24-hour-acrophase shift and reduced the degree of memory deficit induced by sleep deprivation. However, interventions in which the mice were exposed to a 40-Hz blue light at offset time or subjective night time points, as well as 2 Hz-blue light at 3 intervention time points (subjective day time, subjective night time, and offset time points), had no positive effects on circadian rhythm shift or memory deficits. Additionally, a 2000-Hz sound intervention during subjective day time attenuated the 24-hour-acrophase shift and memory decline, while 440-Hz and 4000-Hz sounds had no effect on circadian rhythms. Overall, these results demonstrate that photoacoustic treatment effectively corrected abnormal sleep-wake patterns and cognitive dysfunction associated with sleep-deprivation-induced disturbances in sleep-wake rhythm. All animal experiments were approved by the Experimental Animal Ethics Committee of Drum Tower Hospital Affiliated to the Medical College of Nanjing University, China (approval No. 20171102) on November 20, 2017.

Risk factors of delayed awakening after aortic arch surgery under deep hypothermic circulatory arrest with selective antegrade cerebral perfusion.

BACKGROUND: To determine the risk factors of delayed awakening following aortic arch surgery under deep hypothermic circulatory arrest (DHCA) in combination with selective antegrade cerebral perfusion (SACP). METHODS: We retrospectively analyzed the clinical data of all patients who underwent aortic arch surgery under DHCA + SACP between September 2015 and September 2017 in our hospital. Delayed awakening was defined as recovery of consciousness later than 24 hours after the surgery. Risk factors of delayed awakening were evaluated using multivariate logistic regression analysis. RESULTS: A total of 168 subjects were included. In-hospital mortality of the overall sample was 19.05% (n=32). Delayed awakening occurred in 76 (45.23%) subjects. Subjects with delayed awakening had older age, hypertension, higher rate of emergency surgery and blood transfusion, and longer cardiopulmonary bypass (CPB) time and myocardial blocking time. Multivariate regression analysis showed emergency surgery (P=0.005) and CPB time >240 min (P<0.001) as risk factors for delayed awakening, even after adjusting potential confounders, including age, hypertension, aortic cross-clamp time and blood transfusion. CONCLUSIONS: In patients undergoing aortic arch surgery under DHCA + SACP, emergency surgery and CPB time >240 min are risk factors for delayed awakening.

Activation of spinal Extacellular Signal-Regulated Kinases and c-jun N-terminal kinase signaling pathways contributes to morphine-induced acute and chronic hyperalgesia in mice.

BACKGROUND: This study investigated the activation of mitogen-activated protein kinases in the spinal dorsal horn to explore the mechanisms underlying morphine-induced acute and chronic hyperalgesia in mice. METHODS: Male adult mice were given a single subcutaneous injection (SC) of morphine (1 µg/kg) or twice-daily administration of morphine (10 mg/kg/day) for 8 days. Thermal hyperalgesia and mechanical allodynia were assessed using the radiant heat and von Frey filament test. Levels of phospho (p)-extracellular signal-regulated kinases (p-ERK), p-c-Jun N-terminal kinase (p-JNK), p-p38, p-PKCγ, N-methyl-d-aspartate receptor (NMDAr), and c-Fos protein in the spinal dorsal horn were examined by Western blot assays. RESULTS: A single ultra-low dose or repeated administration of morphine induced hyperalgesia in mice and caused a significant increase in the levels of p-ERK and p-JNK, but not p-p38, in the spinal dorsal horn. The level of c-Fos protein was significantly elevated following administration of morphine. The protein levels of p-PKCγ and NMDAr subunits (NR2B and NR2A) were also altered. Pretreatment with the NMDAr antagonist MK-801 or the protein kinase C (PKC) inhibitor calphostin C (CC) suppressed the morphine-induced increase in p-ERK, p-JNK, and c-Fos. Administration of MK-801 and CC also relieved morphine-induced hyperalgesia. CONCLUSION: These findings suggest that activation of the spinal ERK and JNK signaling pathways contribute to morphine-induced acute and chronic hyperalgesia in mice.

FKBP51 is associated with early postoperative cognitive dysfunction in elderly patients undergoing hip fracture surgery.

Enhanced inflammation response was increasingly reported in association with postoperative cognitive dysfunction (POCD). Glucocorticoid receptor (GR) signal plays a key role in suppression of inflammation. This prospective cohort study aimed to evaluate GR signaling in elderly patients undergoing selective operation.One hundred twenty-six elderly patients were scheduled for hip fracture surgery with general anesthesia. Plasma cortisol levels and the expression levels of GR and FK506 binding protein 51 (FKBP51) in leukocytes were determined at 1 day preoperatively and 7 days. Postoperatively postoperative pain was assessed following surgery using visual analog pain scale (VAS). Neuropsychological tests were performed before surgery and 1 week postoperation. A decline of 1 or more standard deviations in 2 or more tests was considered to reflect POCD.POCD incidence in participants was 28.3% at 1 week after surgery. POCD patients presented significantly higher cortisol and FKBP51 levels compared with non-POCD patients (P < .05). Compared with non-POCD patients, VAS scores at 12 hours after surgery were higher in POCD patients (P < .05). No significant difference in expression levels of GR was found between groups POCD and non-POCD patients.High expression of FKBP51 in leukocytes and glucocorticoid resistance were associated with POCD in aged patients following hip fracture surgery.

Effect of neuromuscular blockade on transcranial electric motor evoked potentials during surgical correction for idiopathic scoliosis under total intravenous anesthesia.

Transcranial electric motor evoked potentials (TCeMEPs) play an important role in reducing the risk of iatrogenic paraplegia. TCeMEPs could be obviously suppressed by neuromuscular blockade (NMB). The aims of this study were to examine the effects of NMB on TCeMEPs and to determine an appropriate level of partial neuromuscular blockade (pNMB) for TCeMEPs during surgical correction of idiopathic scoliosis under total intravenous anesthesia (TIVA). All patients were maintained with TIVA. The pNMB levels were classified into five phases: one or two train-of-four (TOF) counts (TOF1); three TOF counts, or T4/T1 (TOFR, T1,4, first or four twitch height of TOF) ≤ 15% (TOF2); TOFR at 16-25% (TOF3); TOFR at 26-50% (TOF4); and TOFR at 51-75% (TOF5). No neuromuscular blockade (nNMB) was achieved when TOFR was more than 75%. The absolute and relative latency, amplitude and area under curve (AUC), efficacy of TCeMEPs and rate of unexpected movement were compared among these phases. Neither the amplitude and AUC nor the efficacy of TCeMEPs were affected at TOF4-5 of abductor halluces muscles TCeMEPs (AH-TCeMEPs) or at TOF3-5 of tibialis anterior muscles TCeMEPs (TA-TCeMEPs) compared with nNMB. However, the rate of unexpected movement was increased significantly at TOF5 and nNMB compared with TOF1 and TOF4. The application of pNMB with TOFR aimed at 26-50% for AH-TCeMEPs or 16-50% for TA-TCeMEPs seems to be an appropriate regimen for TCeMEPs during surgical correction for idiopathic scoliosis under TIVA.

Restrictive Versus Liberal Strategy for Red Blood-Cell Transfusion: A Systematic Review and Meta-Analysis in Orthopaedic Patients.

BACKGROUND: Current guidelines recommend restrictive criteria for red blood-cell transfusion in most clinical settings. However, patients undergoing orthopaedic surgery may require distinct transfusion criteria since benefits and potential harm often vary considerably based on patient characteristics and surgical procedures. We aimed to assess the efficacy and safety of restrictive transfusion in patients undergoing orthopaedic surgery, especially in important subgroups. METHODS: Electronic databases were searched to identify randomized controlled trials investigating restrictive (mostly a hemoglobin level of 8.0 g/dL or symptomatic anemia) versus liberal (mostly a hemoglobin level of 10.0 g/dL) transfusion in patients undergoing orthopaedic surgery. For the primary outcome of cardiovascular events, we performed random-effects meta-analyses to synthesize the evidence and to assess the effects in different subgroups according to patient characteristics (with versus without preexisting cardiovascular disease) and surgical procedures (hip fracture surgery versus elective arthroplasty). RESULTS: Ten trials involving 3,968 participants who underwent hip or knee surgery were included. Mean participant age ranged from 68.7 to 86.9 years. Compared with liberal transfusion, restrictive transfusion increased the risk of cardiovascular events (8 trials; 3,618 participants; relative risk [RR], 1.51; 95% confidence interval [CI], 1.16 to 1.98; p = 0.003; with no heterogeneity across all trials), irrespective of preexisting cardiovascular disease (pinteraction = 0.63). In a subgroup analysis, the increase was observed in patients undergoing hip fracture surgery (RR, 1.51; 95% CI, 1.08 to 2.10; p = 0.02), but did not reach significance in those undergoing elective arthroplasty (RR, 1.53; 95% CI, 0.96 to 2.44; p = 0.07). To minimize the bias caused by variations in transfusion threshold, we conducted an analysis that only included trials using 8.0 g/dL hemoglobin or symptomatic anemia as the threshold for restrictive transfusion and obtained identical results (6 trials; 2,872 participants; RR, 1.51; 95% CI, 1.09 to 2.08; p = 0.01; I = 0%). The 2 arms did not differ with respect to the rates of all infections, 30-day mortality, thromboembolic events, wound infection, pulmonary infection (mainly pneumonia), and cerebrovascular accidents (mainly stroke). CONCLUSIONS: In patients undergoing orthopaedic surgery, when compared with liberal transfusion, restrictive transfusion increases the risk of cardiovascular events irrespective of preexisting cardiovascular disease. Importantly, the increased risk was observed in patients undergoing hip fracture surgery but did not reach significance in those undergoing elective arthroplasty. LEVEL OF EVIDENCE: Therapeutic Level I. See Instructions for Authors for a complete description of levels of evidence.

Association between intraoperative hypotension and 30-day mortality, major adverse cardiac events, and acute kidney injury after non-cardiac surgery: A meta-analysis of cohort studies.

BACKGROUND: The association between intraoperative hypotension (IOH) and postoperative outcomes is not fully understood. We performed a meta-analysis to determine whether IOH is associated with increased risk of 30-day mortality, major adverse cardiac events (MACEs) and acute kidney injury (AKI) after non-cardiac surgery. METHODS: We searched PubMed and Embase through May 2016 to identify cohort studies that investigated the association between IOH and risk of 30-day mortality, MACEs, or AKI in adult patients after non-cardiac surgery. Ascertainment of IOH and assessment of outcomes were defined by the individual study. Considering the level of clinical heterogeneity, adjusted odds ratios (ORs) with 95% confidence interval (CIs) were pooled using a random-effects model. This meta-analysis is registered on PROSPERO (CRD42016049405). RESULTS: We included 14 cohort studies that were heterogeneous in terms of definition of IOH. IOH alone was associated with increased risk of 30-day mortality (OR 1.29 [95% CI, 1.19-1.41]), MACEs (OR 1.59 [95% CI, 1.23-2.05]), especially myocardial injury (OR 1.67 [95% CI, 1.31-2.13]), and AKI (OR 1.39 [95% CI, 1.09-1.77]). Triple low (IOH coincident with low bispectral index and low minimum alveolar concentration) also predicts increased risk of 30-day mortality (OR 1.32 [95% CI, 1.03-1.68]). CONCLUSIONS: IOH alone significantly increases the risk of postoperative 30-day mortality, MACEs, especially myocardial injury, and AKI in adult patients after non-cardiac surgery. Triple low also predicts increased risk of 30-day mortality after non-cardiac surgery. These findings provide evidence that IOH should be recognized as an independent risk factor for postoperative adverse outcomes after non-cardiac surgery.

Effects of Inhalation Anesthesia vs. Total Intravenous Anesthesia (TIVA) vs. Spinal-Epidural Anesthesia on Deep Vein Thrombosis After Total Knee Arthroplasty.

BACKGROUND The objective of the present study was to evaluate the varying efficacy of general anesthesia (GA), combined spinal-epidural anesthesia (CSEA), and total intravenous anesthesia (TIVA) on the occurrence of deep vein thrombosis (DVT) following total knee arthroplasty (TKA). MATERIAL AND METHODS From July 2013 to May 2015, a total of 197 cases of patients who had undergone TKA treatment at either the Drum Tower Hospital or Nanjing General Hospital of Nanjing Military Command were recruited to participate in the study. The patients in the study were separated into 3 groups depending on the anesthesia approach received: the GA group, the CSEA group, and the TIVA group. The baseline characteristics and relative parameters of patients were monitored before and after surgery for analytic purposes. A 3-month follow-up after surgery was conducted to observe the rate of DVT occurrence and any DVT-related complications. RESULTS The TIVA group exhibited significant decreases in relation to the swallowing time reflex, extubation, and consciousness recovery in comparison to other groups in the study. Additionally, platelet count was significantly decreased and there was drastic extension of the activated partial thromboplastin time (APTT) in the CSEA group and the TIVA group. There were clear differences in the incidence of DVT and its complications among the 3 groups. The TIVA group displayed the lowest incidences of DVT and DVT-related complication during the study. Based on logistic regression analysis, the type of anesthesia was utilized as an independent correlative factor for the occurrence of DVT after surgery. CONCLUSIONS The results obtained during the study established a clinical basis for comparative analysis of various anesthesia methods. We found that, compared with GA and CSEA, patients undergoing TIVA had a reduced rate of risk in relation to the occurrence of DVT following TKA.