Dataset Information

The preventive effect of dexmedetomidine on paroxysmal sympathetic hyperactivity in severe traumatic brain injury patients who have undergone surgery: a retrospective study.

ABSTRACT:

Background

Paroxysmal sympathetic hyperactivity (PSH) results and aggravates in secondary brain injury, which seriously affects the prognosis of severe traumatic brain injury patients. Although several studies have focused on the treatment of PSH, few have concentrated on its prevention.

Methods

Ninety post-operation (post-op) severe traumatic brain injury (sTBI) patients admitted from October 2014 to April 2016 were chosen to participate in this study. Fifty of the post-op sTBI patients were sedated with dexmedetomidine and were referred as the "dexmedetomidine group" (admitted from May 2015 to April 2016). The other 40 patients (admitted from October 2014 to May 2015) received other sedations and were referred as the "control group." The two groups were then compared based on their PSH scores and the scores and ratios of those patients who met the criteria of "probable," "possible" and "unlikely" using the PSH assessment measure (PSH-AM) designed by Baguley et al. (2014). The durations of the neurosurgery intensive care unit (NICU) and hospital stays and the Glasgow outcome scale (GOS) values for the two groups were also compared to evaluate the therapeutic effects and the patients' prognosis.

Results

The overall PSH score for the dexmedetomidine group was 5.26 ± 4.66, compared with 8.58 ± 8.09 for the control group. The difference between the two groups' PSH scores was significant (P = 0.017). The score of the patients who met the criterion of "probable" was 18.33 ± 1.53 in the dexmedetomidine group and 22.63 ± 2.97 in the control group, and the difference was statistically significant (P = 0.045). The ratio of patients who were classified as "unlikely" between the two groups was statistically significant (P = 0.028); that is, 42 (84%) in the dexmedetomidine group and 25 (62.5%) in the control group. The differences in NICU, hospital stays and GOS values between the two groups were not significant.

Conclusion

Dexmedetomidine has a preventive effect on PSH in sTBI patients who have undergone surgery.

SUBMITTER: Tang Q

PROVIDER: S-EPMC5314954 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Introduction: Progressive encephalomyelitis with rigidity and myoclonus (PERM) is a severe form of stiff-person spectrum disorder characterized by painful spasms, myoclonic jerks, hyperekplexia, brainstem dysfunction, and dysautonomia, which is sometimes resistant to γ-amino-butyric acid (GABA)-ergic agents. The response to immunotherapy varies depending on identified autoantibodies. We report a dramatic response to dexmedetomidine in a patient with glycine receptor (GlyR) antibody-positive PERM who developed intractable clusters of myoclonic jerks and paroxysmal sympathetic hyperactivity (PSH) that was highly refractory to conventional symptomatic treatment with GABAergic drugs and immunotherapy. Case Presentation: A 62-year-old Japanese man was transferred to our center for intermittent painful spasms that progressed in severity over the preceding 7 weeks. On admission, he had gaze-evoked nystagmus, and paroxysmal painful spasms/myoclonic jerks triggered by sound or touch. The myoclonic jerks rapidly worsened, along with the development of hyperekplexia, opisthotonus, and PSH, leading to prolonged apnea requiring mechanical ventilation. Brain and spinal cord magnetic resonance imaging was unremarkable. Cerebrospinal fluid (CSF) examination revealed mild pleocytosis and oligoclonal bands. Surface electromyography confirmed simultaneous agonist-antagonist continuous motor unit activity. Based on the clinico-electrophysiological features, PERM was suspected. He was initially treated with intravenous steroids, immunoglobulin, benzodiazepines, and propofol, but the symptoms persisted. On day 9, he received a continuous infusion of dexmedetomidine, which resulted in dramatic reduction in the frequency of clusters of myoclonic jerks and PSH. The effect of dexmedetomidine was confirmed by surface electromyography. The addition of plasma exchange resulted in further clinical improvement. GlyR antibodies were identified in the CSF but not the serum, leading to the diagnosis of GlyR antibody-positive PERM. Conclusions: PERM is an immune-mediated disorder, but dexmedetomidine, a highly selective α2-adrenergic agonist, may alleviate paroxysmal symptoms by decreasing noradrenergic neuronal activity, resulting in attenuation of antibody-mediated disinhibited increased motor and sympathetic activity. Dexmedetomidine may be useful as an adjunctive symptomatic therapy in PERM and related disorders.

Project description:Severe TBI, defined as a Glasgow Coma Scale???8, increases intracranial pressure and activates the sympathetic nervous system. Sympathetic hyperactivity after TBI manifests as catecholamine excess, hypertension, abnormal heart rate variability, and agitation, and is associated with poor neuropsychological outcome. Propranolol and clonidine are centrally acting drugs that may decrease sympathetic outflow, brain edema, and agitation. However, there is no prospective randomized evidence available demonstrating the feasibility, outcome benefits, and safety for adrenergic blockade after TBI.The DASH after TBI study is an actively accruing, single-center, randomized, double-blinded, placebo-controlled, two-arm trial, where one group receives centrally acting sympatholytic drugs, propranolol (1?mg intravenously every 6?h for 7?days) and clonidine (0.1?mg per tube every 12?h for 7?days), and the other group, double placebo, within 48?h of severe TBI. The study uses a weighted adaptive minimization randomization with categories of age and Marshall head CT classification. Feasibility will be assessed by ability to provide a neuroradiology read for randomization, by treatment contamination, and by treatment compliance. The primary endpoint is reduction in plasma norepinephrine level as measured on day 8. Secondary endpoints include comprehensive plasma and urine catecholamine levels, heart rate variability, arrhythmia occurrence, infections, agitation measures using the Richmond Agitation-Sedation Scale and Agitated Behavior scale, medication use (anti-hypertensive, sedative, analgesic, and antipsychotic), coma-free days, ventilator-free days, length of stay, and mortality. Neuropsychological outcomes will be measured at hospital discharge and at 3 and 12?months. The domains tested will include global executive function, memory, processing speed, visual-spatial, and behavior. Other assessments include the Extended Glasgow Outcome Scale and Quality of Life after Brain Injury scale. Safety parameters evaluated will include cardiac complications.The DASH After TBI Study is the first randomized, double-blinded, placebo-controlled trial powered to determine feasibility and investigate safety and outcomes associated with adrenergic blockade in patients with severe TBI. If the study results in positive trends, this could provide pilot evidence for a larger multicenter randomized clinical trial. If there is no effect of therapy, this trial would still provide a robust prospective description of sympathetic hyperactivity after TBI.ClinicalTrials.gov NCT01322048.

Project description:ObjectiveDexmedetomidine is a medication that has analgesic, sedative, and anti-anxiety properties. In the clinical, it is often used to prevent common complications associated with strabismus surgery, including postoperative delirium, postoperative nausea and vomiting, postoperative pain, and oculocardiac reflex. However, its effectiveness and side effects of the present studies are different. The sample sizes of the present studies on the prevention of complications of dexmedetomidine are small. Therefore, this study evaluates the efficacy of dexmedetomidine in preventing anesthesia-related complications in strabismus surgery through a systematic review and meta-analysis.MethodsLiterature was retrieved from 10 commonly used databases and randomized controlled trials published up to May 2022 were sought. The included studies compared the intervention effects of dexmedetomidine versus placebo on anesthesia-related complications in surgery. The occurrence rates of postoperative delirium, postoperative nausea and vomiting, postoperative pain, and oculocardiac reflex in patients undergoing strabismus surgery were evaluated. Statistical analyses and forest plots were generated using Review Manager and STATA software. Binary outcomes were measured using relative risk (RR) with a 95% confidence interval for each outcome. The Cochrane risk of bias tool was used to assess the bias and risk in the studies that met the inclusion criteria.ResultsA total of 13 articles were ultimately included in the analysis, comprising 1,018 patients who underwent strabismus surgery. The dexmedetomidine group, compared to the placebo group, demonstrated significant reductions in the incidence of postoperative delirium (RR = 0.73, P = 0.001), severe postoperative delirium (RR = 0.45, P = 0.005), postoperative nausea and vomiting (RR = 0.48, P < 0.0001), and the need for supplemental analgesia postoperatively (RR = 0.60, P = 0.004). Additionally, subgroup analysis revealed that intravenous administration of dexmedetomidine significantly reduced the incidence of oculocardiac reflex (RR = 0.50, P = 0.001). In contrast, intranasal administration of dexmedetomidine did not have a significant effect on the incidence of oculocardiac reflex (RR = 1.22, P = 0.15). There was a significant difference between the subgroups (P = 0.0005, I2 = 91.7%).ConclusionAmong patients undergoing strabismus surgery, the use of dexmedetomidine can alleviate postoperative delirium and reduce the incidence of postoperative nausea and vomiting, as well as postoperative pain. Moreover, intravenous administration of dexmedetomidine can lower the occurrence rate of the oculocardiac reflex.

Project description:ObjectivesThis study aimed to investigate the application status of preventive measures for feeding intolerance in patients with severe traumatic brain injury (STBI) in China and analysis the differences and their causes.MethodsA cross-sectional survey was conducted. From December 2019 to January 2020, ICU nurses and physicians of 89 hospitals in China were surveyed by using a questionnaire on preventive strategies for feeding intolerance in patients with STBI. The questionnaire included two parts: the general information of participants (10 items) and application of preventive measures for feeding intolerance in STBI patients (18 items).ResultsTotally 996 nurses and physicians completed the questionnaire. Among various methods, gastrointestinal symptoms(85.0%) and injury severity (71.4%) were mostly used to assess gastrointestinal functions and risk of feeding intolerance among STBI patients, respectively. Initiating enteral nutrition (EN) within 24-48 h (61.5%), nasogastric tubes (91.2%), 30°-45° of head-of-bed elevation (89.5%), continuous feeding by pump (72.9%), EN solution temperature of 38-40 °C (65.5%), <500 ml initial volume of EN solution (50.0%), monitoring gastric residual volume with a syringe (93.7%), and assessing gastric residual volume every 4 h (51.5%) were mostly applied for EN delivery among STBI patients. Prokinetic agents (73.3%), enema (73.6%), probiotics (79.0%), antacid agents (84.1%), and non-nutritional preparations as initial EN formula (65.6%) were commonly used for preventing feeding intolerance among STBI patients.ConclusionsThe survey showed that nurses and clinicians in China have a positive attitude towards preventive strategies for feeding intolerance. However, some effective new technologies and methods have not been timely applied in clinical practice. We suggest that managers, researchers, clinicians, nurses, and other health professionals should collaborate to explore effective and standard preventive strategies for feeding intolerance among patients with STBI.

Project description:Traumatic brain injury induces potent inflammatory responses that can exacerbate secondary blood-brain barrier (BBB) disruption, neuronal injury, and neurological dysfunction. Dexmedetomidine is a novel α2-adrenergic receptor agonist that exert protective effects in various central nervous system diseases. The present study was designed to investigate the neuroprotective action of dexmedetomidine in a mouse traumatic brain injury model, and to explore the possible mechanisms. Adult male C57BL/6J mice were subjected to controlled cortical impact. After injury, animals received 3 days of consecutive dexmedetomidine therapy (25 µg/kg per day). The modified neurological severity score was used to assess neurological deficits. The rotarod test was used to evaluate accurate motor coordination and balance. Immunofluorescence was used to determine expression of ionized calcium binding adapter molecule-1, myeloperoxidase, and zonula occluden-1 at the injury site. An enzyme linked immunosorbent assay was used to measure the concentration of interleukin-1β (IL-1β), tumor necrosis factor α, and IL-6. The dry-wet weight method was used to measure brain water content. The Evans blue dye extravasation assay was used to measure BBB disruption. Western blot assay was used to measure protein expression of nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3), caspase-1 p20, IL-1β, nuclear factor kappa B (NF-κB) p65, occluding, and zonula occluden-1. Flow cytometry was used to measure cellular apoptosis. Results showed that dexmedetomidine treatment attenuated early neurological dysfunction and brain edema. Further, dexmedetomidine attenuated post-traumatic inflammation, up-regulated tight junction protein expression, and reduced secondary BBB damage and apoptosis. These protective effects were accompanied by down-regulation of the NF-κB and NLRP3 inflammasome pathways. These findings suggest that dexmedetomidine exhibits neuroprotective effects against acute (3 days) post-traumatic inflammatory responses, potentially via suppression of NF-κB and NLRP3 inflammasome activation.