ABSTRACT
PURPOSE: Cesarean section may result in adverse psychosocial and behavioral outcomes because women put considerable emphasis on the process of birth. Virtual reality treatment has been shown by many studies to reduce anxiety and improve patient satisfaction. Therefore, we designed a randomized controlled trial to investigate whether the application of virtual reality technology during cesarean section can reduce maternal anxiety and improve satisfaction. METHODS: We recruited 128 women undergoing elective cesarean delivery with proposed spinal anesthesia and randomly assigned them to either virtual reality or routine care. The virtual reality intervention was a virtual reality program tailored specifically for women undergoing cesarean section. Primary outcome was the change in anxiety score (change = preoperative-intraoperative score). Secondary outcomes included patient satisfaction score, requirement of intraoperative sedative and analgesic drugs, and respiratory rate. RESULTS: The change in anxiety score in the virtual reality group was significantly higher than that in the routine care group (30 [20, 47.5] vs 10 [- 10, 23.8], respectively; P < 0.001, with Hodges-Lehmann median difference estimate of 20 (95% confidence interval CI, 15-30)). There were no significant differences between the two groups in patient satisfaction scores, the requirement of intraoperative sedative and analgesic drugs, and respiratory rate and side effects. CONCLUSION: Virtual reality treatment could reduce the anxiety of women undergoing elective cesarean section, which is beneficial to the mother and baby. Trial registration This study was registered at the Chinese Clinical Trial Registry (ChiCTR2200061936) on July 11, 2022, and can be reached at https://www.chictr.org.cn/showprojEN.html?proj=173329.
ABSTRACT
BACKGROUND: To study the incidence and risk factors of shivering in pregnant women during cesarean section. METHODS: We performed a prospective nested case-control study involving parturients scheduled for cesarean sections between July 2018 and May 2021. The overall incidence of intraoperative shivering and its potential risk factors were investigated. The potential risk factors evaluated were pain, anxiety, emergency surgery, transfer from the delivery room, epidural labor analgesia, membrane rupture, labor, and the timing of the surgery. Shivering and body temperature at different time points during the cesarean section were also recorded. The selected seven time points were: entering the operating room, post-anesthesia, post-disinfection, post-delivery, post-oxytocin, post additional hysterotonics, and before leaving the operating room. RESULTS: We analyzed 212 cesarean section parturients. The overall incidence of shivering was 89 (42.0%). Multivariate logistic regression showed that anxiety, emergency delivery, and transfer from the delivery room to the operating room increased the overall shivering incidence (odds ratio = 1.77, 2.90, and 3.83, respectively). The peak shivering incidence occurred after skin disinfection (63, 29.7%), and the lowest body temperature occurred after oxytocin treatment (36.24 ± 0.30 °C). Stratified analysis of surgery origin showed that emergency delivery was a risk factor for shivering (odds ratio = 2.99) in women transferred from the obstetric ward to the operating room. CONCLUSION: Shivering occurred frequently during cesarean sections, with the peak incidence occurring after skin disinfection. Anxiety, emergency delivery, and transfer from the delivery room to the operating room increased the risk of shivering development during cesarean sections. TRIAL REGISTRATION: The study protocol was registered online at China Clinical Registration Center (registration number: ChiCTR-ROC-17010532, Registered on 29 January 2017).
Subject(s)
Cesarean Section , Shivering , Case-Control Studies , Cesarean Section/adverse effects , Female , Humans , Oxytocin , Pregnancy , Prospective Studies , Risk FactorsABSTRACT
BACKGROUND: Intestinal ischemia is a common clinical critical illness. Intestinal ischemia-reperfusion (IIR) leads to acute lung injury (ALI), but the causative factors of ALI are unknown. The aim of this study was to reveal the causative factors and mechanisms of IIR-induced lung injury. METHODS: A mouse model of IIR was developed using C57BL/6 mice, followed by detection of lung injury status and plasma levels of inflammatory factors in sham-operated mice and model mice. Some model mice were treated with a tumor necrosis factor-α (TNF-α) inhibitor lenalidomide (10 mg/kg), followed by observation of lung injury status through hematoxylin and eosin staining and detection of neutrophil infiltration levels through naphthol esterase and Ly6G immunohistochemical staining. Additionally, peripheral blood polymorphonuclear neutrophils (PMNs) were cultured in vitro and then stimulated by TNF-α to mimic in vivo inflammatory stimuli; this TNF-α stimulation was also performed on PMNs after knockdown of FoxO3a or treatment with the c-Jun N-terminal kinase (JNK) inhibitor SP600125. PMN apoptosis after stimulation was detected using flow cytometry. Finally, the role of PMN apoptosis in IIR-induced lung injury was evaluated in vivo by detecting the ALI status in the model mice administered with ABT-199, a Bcl-2 inhibitor. RESULTS: IIR led to pulmonary histopathological injury and increased lung water content, which were accompanied by increased plasma levels of inflammatory factors, with the TNF-α plasma level showing the most pronounced increase. Inhibition of TNF-α led to effective reduction of lung tissue injury, especially that of the damaging infiltration of PMNs in the lung. In vitro knockdown of FoxO3a or inhibition of JNK activity could inhibit TNF-α-induced PMN apoptosis. Further in vivo experiments revealed that ABT-199 effectively alleviated lung injury and decreased inflammation levels by promoting PMN apoptosis during IIR-induced lung injury. CONCLUSION: TNF-α activates the JNK/FoxO3a pathway to induce a delay in PMN apoptosis, which promotes IIR-induced lung injury.
Subject(s)
Forkhead Box Protein O3/metabolism , MAP Kinase Signaling System/genetics , Neutrophils/metabolism , Reperfusion Injury/genetics , Tumor Necrosis Factor-alpha/metabolism , Animals , Apoptosis , Disease Models, Animal , Humans , Male , Mice , TransfectionABSTRACT
BACKGROUND: The heart is one of the most commonly affected organs during sepsis. Mitsugumin-53 (MG53) has attracted attention in research due to its cardioprotective function. However, the role of MG53 in sepsis-induced myocardial dysfunction (SIMD) remains unknown. The purpose of this study was to explore the underlying mechanism of MG53 in SIMD and investigate its potential relationship with peroxisome proliferator-activated receptor-α (PPARα). METHODS: The cecal ligation and puncture (CLP) model was created to induce SIMD in rats. Protein levels of MG53 and PPARα, cardiac function, cardiomyocyte injury, myocardial oxidative stress and inflammatory indicators, and cardiomyocyte apoptosis were measured at 18 h after CLP. The effects of MG53 on PPARα in SIMD were investigated via preconditioning recombinant human MG53 (rhMG53) and PPARα antagonist GW6471. RESULTS: The expression of MG53 and PPARα sharply decreased in the myocardium at 18 h after CLP. Compared with the sham group, cardiac function was significantly depressed, which was associated with the destructed myocardium, upregulated oxidative stress indicators and proinflammatory cytokines, and excessive cardiomyocyte apoptosis in the CLP group. Supplementation with rhMG53 enhanced myocardial MG53, increased the survival rate with improved cardiac function, and reduced oxidative stress, inflammation, and myocardial apoptosis, which were associated with PPARα upregulation. Pretreatment with GW6471 abolished the abovementioned protective effects induced by MG53. CONCLUSIONS: Both MG53 and PPARα were downregulated after sepsis shock. MG53 supplement protects the heart against SIMD by upregulating PPARα expression. Our results provide a new treatment strategy for SIMD.
Subject(s)
Muscle Proteins/metabolism , Myocardium/pathology , PPAR alpha/genetics , Protective Agents/metabolism , Sepsis/complications , Up-Regulation/genetics , Vesicular Transport Proteins/metabolism , Animals , Apoptosis , Humans , Inflammation/pathology , Models, Biological , Myocytes, Cardiac/metabolism , Myocytes, Cardiac/pathology , Oxazoles , Oxidative Stress , PPAR alpha/metabolism , Rats, Sprague-Dawley , Survival Analysis , Tyrosine/analogs & derivativesABSTRACT
The impacts of prenatal propofol on cognition and emotion of offspring remain elusive. In the present study, pregnant rats in the second trimester were anesthetized with propofol. Neuronal apoptosis and proliferation was determined in fetuses and postnatal rats by detecting caspase-3 and BrdU expression. The offspring were subjected to several behavior tests. Then the pyramidal neurons in hippocampus and the expression of NR1, NR2A, and NR2B subunits of NMDA receptor and PSD-95 in frontal cortex were examined. Propofol exposure significantly increased the number of caspase-3+ cells in lateral ganglionic eminence and hippocampus compared with control group (Pâ¯<â¯0.001). The number of BrdU+ cells in the subventricular zone (SVZ) and dentate gyrus (DG) was also reduced in propofol group (Pâ¯<â¯0.001). In propofol group, the swimming distance and time in the quadrant were shorter,but longer out of the quadrant. The number of escapes was less than those of the control group. Prenatal propofol exposure also decreased the sucrose preference, reduced the numbers of grooming, crossing, and rearing of the pups, and increased the fecal particle numbers and immobility time (Pâ¯<â¯0.05). There were fewer and shorter dendritic branches of pyramidal neurons in the CA1 and CA3 of offspring. The expression of NR1, NR2A, NR2B, and PSD-95 in the frontal cortex was downregulated by propofol exposure (Pâ¯<â¯0.001). These data suggested that prenatal propofol exposure impairs neuronal development, which may be associated with depression- and anxiety-like behaviors and cognitive disorders in offspring.
Subject(s)
Anesthetics, Intravenous/pharmacology , Cognition/drug effects , Hypnotics and Sedatives/pharmacology , Mood Disorders/chemically induced , Prenatal Exposure Delayed Effects , Propofol/pharmacology , Receptors, N-Methyl-D-Aspartate/metabolism , Animals , Down-Regulation , Female , Maternal-Fetal Exchange , Pregnancy , Rats, Sprague-DawleyABSTRACT
The aim of this paper is to evaluate the efficacy and safety of three different norepinephrine dosing regimens for preventing spinal hypotension in cesarean section. In this randomized double-blinded controlled study, 120 parturients scheduled for elective section delivery under spinal anesthesia were assigned to 1 of 4 groups. In the control group, patients received saline infusion. In three norepinephrine groups, the infusion dosage regimens were 5, 10, and 15 µg/kg/h, respectively. Hypotension was treated with a rescue bolus of 10 µg norepinephrine. The study protocol was continued until the end of surgery. The primary outcome was the proportion of participants that underwent hypotension. The proportion of hypotension participants was significantly reduced in the norepinephrine groups (37.9%, 20%, and 25%, respectively) compared to that in the control group (86.7%). However, the highest dose of norepinephrine (15 µg/kg/h) resulted in more hypertension episodes. In addition, blood pressure was better maintained in the norepinephrine 5 µg/kg/h and 10 µg/kg/h groups than in the control group and 15 µg/kg/h group. No significant differences in other hemodynamic variables, adverse effects, maternal and neonatal blood gases, or Apgar scores were observed among the groups. In summary, for patients who undergo cesarean delivery under spinal anesthesia, infusion of 5-10 µg/kg/h norepinephrine was effective to reduce hypotension incidence without significant adverse effects on maternal and neonatal outcomes. Clinical Trial Registration Number is ChiCTR-INR-16009452.
Subject(s)
Anesthesia, Spinal , Cesarean Section , Hypotension/prevention & control , Norepinephrine/therapeutic use , Adult , Anesthesia, Obstetrical , Double-Blind Method , Female , Humans , Phenylephrine , PregnancyABSTRACT
PURPOSE: Postpartum depression is a common complication of childbirth. In the last decade, it has been suggested that subdissociative-dose ketamine is a fast-acting antidepressant. We aimed to investigate the efficacy of low-dose ketamine administered during caesarean section in preventing postpartum depression. METHODS: Using a randomized, double-blind, placebo-controlled design, 330 parturients who were scheduled to undergo caesarean section were enrolled in this trial. The parturients were randomly assigned to receive intravenous ketamine (0.25 mg/kg diluted to 10 mL with 0.9% saline) or placebo (10 mL of 0.9% saline) within 5 min following clamping of the neonatal umbilical cord. The primary outcome was the degree of depression, which was evaluated using the Edinburgh Postnatal Depression Scale (EPDS) (a threshold of 9/10 was used) at 3 days and 6 weeks after delivery. The secondary outcome was the numeric rating scale score of pain at 3 day and 6 week postpartum. RESULTS: No significant differences were found in the prevalence of postpartum depression between the two groups at 3 days and 6 weeks after delivery. The pain scores measured at 3 days postoperatively were not significantly different between the groups, whereas the scores measured at 6 week postpartum were significantly reduced in the treatment group compared with the saline group (P = 0.014). CONCLUSIONS: Intra-operative low-dose ketamine (0.25 mg/kg) does not have a preventive effect on postpartum depression.
Subject(s)
Depression, Postpartum/prevention & control , Ketamine/administration & dosage , Adult , Cesarean Section , Double-Blind Method , Female , Humans , Pain/drug therapy , Pregnancy , Prospective StudiesABSTRACT
To compare the effects of intrathecal dexmedetomidine and intrathecal morphine as supplements to bupivacaine in cesarean sections under spinal anesthesia. Full-term parturients (n=120) undergoing elective cesarean sections under spinal anesthesia were randomly allocated into three groups: Group B received 10 mg bupivacaine, Group BD received 10 mg bupivacaine plus 5 µg dexmedetomidine, and Group BM received 10 mg bupivacaine plus 100 µg morphine. The onset and regression time of sensory and motor blockade, postoperative analgesia, and side effects were recorded. Group BD showed quicker onset time and a longer sensory and motor blockade than other groups (BD vs. B and BD vs. BM, p<0.05). The mean time of sensory regression to the S1 segment was 253.21±42.79 min in group BD, 192.50±40.62 min in group BM and 188.33±37.62 min in group B (p<0.001). Group BD showed an analgesia duration (time to requirement of first rescue analgesic) (17.59±6.23 h) similar to that of group BM (16.78±5.90 h) but longer than that of group B (3.53±1.68 h) (p<0.001). The incidence of pruritus was significantly higher in group BM compared with groups BD and B (p<0.001). Less shivering was observed in group BD than in groups BM and B (p=0.009). So intrathecal dexmedetomidine (5 µg) prolonged the motor and sensory blockade, provided a similar analgesic effect and reduced pruritus and shivering compared with morphine (100 µg) in cesarean sections.