Enhancing Caudal Analgesia in Pediatrics: A Comparison of Ropivacaine With and Without Clonidine for Infra-Umbilical Surgeries.

Introduction Regional anesthesia, particularly caudal blocks, is increasingly used in pediatric surgeries for effective post-operative pain management. However, the duration of analgesia with agents such as ropivacaine alone can be limited. This study investigates the effects of adding clonidine to ropivacaine in caudal blocks for pediatric patients undergoing infra-umbilical surgeries, with the purpose of enhancing the duration and quality of analgesia. Methods We conducted a randomized, double-blind study including 50 children aged one to eight years, divided equally into two groups: group R received 0.2% ropivacaine and group RC received 0.2% ropivacaine with 2 mcg/kg clonidine. Intraoperative and post-operative monitoring included heart rate, blood pressure, and respiratory parameters. Analgesia duration, sedation scores, and the need for rescue analgesia were assessed. Results Group RC exhibited significantly longer analgesia duration (18.4 ± 2.31 hours) compared to group R (10.56 ± 2.27 hours, P < 0.0001). Fewer patients in group RC required a second dose of rescue analgesia (4% vs. 32%, P = 0.023), with no significant differences in sedation scores or adverse effects between the groups. Conclusion Adding clonidine to ropivacaine in caudal blocks significantly prolongs analgesia and reduces the need for additional post-operative pain management in pediatric surgeries without increasing the risk of side effects. This study supports the use of clonidine as an effective adjuvant in pediatric pain management.

Comparative Analysis of Oral Clonidine Versus Oral Gabapentin on Subarachnoid Block Duration and Postoperative Analgesic Needs.

INTRODUCTION: Pain, an inherently subjective experience, plays a pivotal role in the body's defence mechanism by signalling tissue damage or potential harm. Thus, optimal postoperative pain management is a cornerstone of modern surgical practice, essential for improving recovery outcomes and overall patient well-being. METHODS: In this study, a total of 60 patients were randomly assigned to two groups of 30 each: Group C (clonidine) and Group G (gabapentin). Group C received oral clonidine 100 mcg and Group G received oral gabapentin 600 mg one hour prior to the subarachnoid block. Duration of sensory and motor block, hemodynamic parameters, Visual Analog Scale (VAS) scores, time to rescue analgesia and any side effect of both drugs were assessed in both groups. RESULTS: The duration of motor and sensory blockade, as well as intraoperative hemodynamics and respiratory rates, were comparable between the two groups. Group G exhibited significantly lower VAS scores from 150 minutes postoperatively up to 12 hours (p < 0.001). Additionally, Group G experienced longer duration of postoperative analgesia (16.8±3.9 hours) compared to Group C (9.27±1.7 hours). About 26.6% of the patients in Group C and 6.7% of the patients in Group G presented with postoperative nausea and vomiting (PONV). CONCLUSION: Oral gabapentin at a dosage of 600 mg demonstrates superior efficacy as a premedication compared to oral clonidine 100 mcg for patients undergoing lower abdominal and lower limb surgeries under spinal anesthesia. Group G demonstrated extended postoperative analgesia, lower VAS scores, and a reduced incidence of PONV, indicating its superiority over clonidine as an analgesic adjunct.

Efficacy and Safety of Alpha-2 Agonists in Autism Spectrum Disorder: A Systematic Review.

BACKGROUND: This analysis is a systematic literature review assessing efficacy and adverse effects of three alpha-2 agonists for the symptomatic management of autism spectrum disorder (ASD). METHODS: The present investigation involved an extensive systematic search for eligible studies in PubMed, Embase, Cochrane Library, and Google Scholar. Nine studies, collectively incorporating 226 patients, were assessed. RESULTS: The results demonstrated promising indications for use of alpha-2 agonists in the symptomatic management of autism spectrum disorders, including improvement of hyperactivity, impulsivity, attention deficit symptoms, irritability, and stereotypies in many of the participants studied. CONCLUSION: The present investigation encourages physicians to consider treatment outcomes of clonidine, guanfacine, and lofexidine to determine the most effective management of ASD-related symptoms and to minimize adverse effects. However, our review cannot provide definitive treatment protocols related to various study limitations.

The effect of oral clonidine and intravenous dexmedetomidine administration on the quality of functional endoscopic sinus surgery.

BACKGROUND: Clonidine and dexmedetomidine are alpha-2 receptor blockers administered for haemorrhage control during surgery in limited settings. Functional endoscopic sinus surgery (FESS) may be associated with bleeding, thus making it challenging. This study aims to evaluate the effect of dexmedetomidine and clonidine on haemorrhage control during FESS and surgical outcomes. METHODS: This three-blinded prospective study included 102 patients who underwent FESS at the Imam Khomeini public referral hospital at the Imam Khomeini public referral hospital, in Urmia, Iran. It was either American Society of Anaesthesiologists (ASA) class I or II. They were divided into three groups (clonidine, dexmedetomidine, and placebo). The volume of blood loss, mean arterial pressure, surgical field visualisation, and surgeon satisfaction were assessed in the three groups. Data analysis was performed using SPSS version 23.0. RESULTS: Dexmedetomidine and clonidine decreased mean arterial pressure, heart rate, and blood loss volume while improving surgical field visualisation. The effect of dexmedetomidine was associated significantly statistically with surgeon satisfaction (p < 0.0001). Furthermore, dexmedetomidine improved the surgical field and reduced operating times in the dexmedetomidine group (p < 0.0001). CONCLUSION: The present clinical trial findings indicated that the administration of dexmedetomidine during FESS decreased mean arterial pressure, provided balanced anaesthesia and appropriate analgesia, and improved the visibility of the surgical field and increased surgeon satisfaction.

Low-dose clonidine infusion to improve sleep in postoperative patients in the high-dependency unit. A randomised placebo-controlled single-centre trial.

PURPOSE: Dexmedetomidine increases sleep and reduces delirium in postoperative patients, but it is expensive and requires a monitored environment. Clonidine, another α 2-agonist, is cheaper and is used safely for other purposes in wards. We assessed whether clonidine would improve sleep in postoperative high-dependency unit (HDU) patients. METHODS: The Clonidine at Low dosage postoperatively to Nocturnally Enhance Sleep (CLONES) study was a double-blind, placebo-controlled, parallel-group pilot effectiveness randomised trial involving adult elective surgery HDU patients in a single academic hospital. Patients received clonidine 0.3 µg/kg/h or saline placebo on the night of surgery. The primary outcome was total sleep time measured using a consumer actigraphy/photoplethysmography device. RESULTS: Of the 83 randomised patients, three had no data available, leaving 80 (39 clonidine, 41 placebo) in the intention-to-treat analysis, modified for missing data. Median patient ages of the groups were similar (61 and 59 years), as were other baseline characteristics. Clonidine patients had a mean of 100.8 (95% confidence interval [CI] 38.2-163.4) minutes (p = 0.002) longer total sleep time (mean 497.2 vs. 396.4 min) and reported better sleep overall. Delirium was only observed in one patient prior to study drug infusion, and none at the end of the study. Safety outcomes were not different. Four clonidine patients had their medication ceased due to bradycardia and hypotension that required no additional treatment. CONCLUSION: Among postoperative elective surgical patients admitted to HDU, low-dose non-titrated clonidine, compared to placebo, was associated with longer and subjectively better-quality sleep.

Partial chemogenetic inhibition of the locus coeruleus due to heterogeneous transduction of noradrenergic neurons preserved auditory salience processing in wild-type rats.

The acoustic startle reflex (ASR) and prepulse inhibition of the ASR (PPI) assess the efficiency of salience processing, a fundamental brain function that is impaired in many psychiatric conditions. Both ASR and PPI depend on noradrenergic transmission, yet the modulatory role of the locus coeruleus (LC) remains controversial. Clonidine (0.05 mg/kg, i.p.), an alpha2-adrenoreceptor agonist, strongly reduced the ASR amplitude. In contrast, chemogenetic LC inhibition only mildly suppressed the ASR and did affect the PPI in virus-transduced rats. The canine adenovirus type 2 (CAV2)-based vector carrying a gene cassette for the expression of inhibitory receptors (hM4Di) and noradrenergic cell-specific promoter (PRSx8) had high cell-type specificity (94.4 ± 3.1%) but resulted in heterogeneous virus transduction of DbH-positive LC neurons (range: 9.2-94.4%). Clozapine-N-oxide (CNO; 1 mg/kg, i.p.), a hM4Di actuator, caused the firing cessation of hM4Di-expressing LC neurons, yet complete inhibition of the entire population of LC neurons was not achieved. Case-based immunohistochemistry revealed that virus injections distal (> 150 µm) to the LC core resulted in partial LC transduction, while proximal (< 50 µm) injections caused neuronal loss due to virus neurotoxicity. Neither the ASR nor PPI differed between the intact and virus-transduced rats. Our results suggest that a residual activity of virus-non-transduced LC neurons might have been sufficient for mediating an unaltered ASR and PPI. Our study highlights the importance of a case-based assessment of the virus efficiency, specificity, and neurotoxicity for targeted cell populations and of considering these factors when interpreting behavioral effects in experiments employing chemogenetic modulation.

The alpha2-adrenoceptor agonist clonidine protects against hypoxic-ischemic brain damage in neonatal mice through the Nrf2/NF-κB signaling pathway.

Neonatal hypoxic-ischemic brain damage (HIBD) is a severe condition closely associated with neuroinflammation and oxidative stress. Clonidine, a selective α2-adrenergic receptor agonist, is known for its anti-inflammatory and antioxidant properties. Despite these recognized therapeutic benefits, the exact mechanisms by which clonidine exerts its effects in the context of HIBD are not fully understood. This study was designed to thoroughly investigate the impact of clonidine on HIBD-induced neuronal injury and to clarify its underlying mechanism of action. We employed a neonatal mouse model of HIBD to meticulously assess the effects of clonidine on neuronal injury, apoptosis, inflammation, and oxidative stress markers. In addition, we conducted extensive in vitro studies to evaluate the neuroprotective effects of clonidine on primary hippocampal neuronal cells, utilizing advanced techniques such as the Cell Counting Kit-8 (CCK-8), flow cytometry, enzyme-linked immunosorbent assay (ELISA), immunofluorescence assay, and western blotting. Furthermore, we explored the regulatory effects of clonidine on the nuclear factor erythroid 2-related factor (Nrf2)/nuclear factor-κB (NF-κB) signaling pathway through a combination of in vivo and in vitro experiments. The results showed that clonidine significantly reduced cerebral infarction, neuronal damage, and apoptosis in HIBD mice. It also alleviated neuroinflammation and oxidative stress, improved cell viability, and reduced neuronal injury following oxygen-glucose deprivation/reoxygenation (OGD/R). The neuroprotective effects of clonidine were linked to the activation of the Nrf2/heme oxygenase-1 (HO-1) pathway and the inhibition of the NF-κB pathway. Overall, clonidine exhibited neuroprotective properties in HIBD by reducing neuroinflammation and oxidative stress, likely through the modulation of the Nrf2/NF-κB signaling pathway.

The Impact of Sedative Choice in the Management of Aneurysmal Subarachnoid Hemorrhage: A Scoping Review.

Aneurysmal subarachnoid hemorrhage (aSAH) is characterized by high mortality and morbidity. This scoping review assesses the current evidence regarding the use of sedatives and analgesics in the acute intensive care unit management of aSAH. We conducted a systematic search of Ovid MEDLINE, Ovid Embase, Ovid EmCare, APA PsycInfo, CINAHL, and the Cochrane Database of Systematic Reviews from inception to June 2023. Studies were included if they enrolled intensive care unit patients aged 18 or older with a significant proportion (> 20%) who had aSAH and evaluated the impact of one or more commonly used analgosedatives on physiological parameters in the management of aSAH. The methodological quality of the studies was assessed using the Methodological Index for Nonrandomized Studies score. Of 2,583 articles, 11 met the inclusion criteria. The median sample size was 47 (interquartile range 10-127), and the median Methodological Index for Nonrandomized Studies score was 9.5 (interquartile range 8-11). The studies' publication years ranged from 1980 to 2023. Dexmedetomidine and ketamine showed potential benefits in reducing the incidence of cortical spreading depolarization and delayed cerebral ischemia. Propofol and opioids appeared safe but lacked robust evidence for efficacy. Benzodiazepines were associated with increased delayed cerebral ischemia-related cerebral infarctions and cortical spreading depolarization events. The evidence available to guide the use of analgosedative medications in aSAH is critically inadequate. Dexmedetomidine and ketamine warrant further exploration in large-scale prospective studies because of their potential benefits. Improved study designs with consistent definitions and a focus on patient-centered outcomes are necessary to inform clinical practice.

Comparison of the Effect of Scalp Block With Ropivacaine vs. Ropivacaine and Clonidine on Postoperative Pain in Patients Undergoing Craniotomy Surgery Under General Anesthesia.

Introduction Clonidine, an α2 agonist known for its hypotensive and analgesic effects, has proven beneficial in various routes of administration such as oral, intravenous, and local infiltration. Scalp blocks enhance hemodynamic stability during surgery and reduce intraoperative opioid requirements compared to controls in numerous studies. Additionally, they are effective in managing postoperative pain, resulting in reduced opioid consumption. Research has shown that clonidine can enhance and prolong the effects of intrathecal, epidural, and peripheral nerve blocks (e.g., brachial plexus, peribulbar). Here, we investigated the impact of adding clonidine at a dose of 1 µg/kg to scalp blocks performed with 0.5% ropivacaine for supra-tentorial craniotomy Material and methods This study was conducted on 60 patients under the American Society of Anesthesiologists (ASA) grade I and II who were scheduled for elective supratentorial craniotomy. Patients were divided into two equal groups of 30 and received a scalp block following general anesthesia. Patients in Group A (n=30) received a scalp block of 0.5% ropivacaine plus 1 ml of normal saline (total 21 cc). Patients in Group B (n=30) received a scalp block of 0.5% ropivacaine and clonidine (1 µg/kg) combined with 0.5 ml of normal saline (total 21 cc). Blood pressure, heart rate, peripheral oxygen saturation (SpO2), visual analog score, Ramsay sedation score, duration of analgesia, and analgesia requirement in the first 24 hours were recorded from baseline and postoperatively. Results The duration of first rescue analgesia for Group A was 4.30 ± 1.5 hours and that of Group B was 9.10 ± 1.4 hours. Duration of analgesia was significantly prolonged in patients receiving ropivacaine with clonidine for scalp nerve block. The amount of tramadol given in the first 24 hours in Group A, 62.50 ± 25.00 mg, was high compared to Group B, 57.14 ± 18.89 mg. The mean arterial blood pressure differed significantly in both groups at 30 minutes, 1 hour, 3 hours, and 12 hours after scalp block postoperatively and lower in Group B. Although changes in pulse rate, and SpO2 were not statistically significant in both groups, patients were hemodynamically stable and did not require any ionotropic support. Ramsay sedation score and visual analog score postoperatively were not significant. There were no significant adverse effects noted in any groups. Conclusion Our study concluded that administering clonidine at a dosage of 1 µg/kg, in combination with 0.5% ropivacaine for scalp nerve block procedures, significantly extends the duration of analgesia and enhances its quality, all while maintaining stable hemodynamic parameters.

Role of Dexmedetomidine and Clonidine With Hyperbaric Ropivacaine in Subarachnoid Block: A Comprehensive Review.

Subarachnoid block (SAB), a fundamental technique in regional anesthesia, offers efficient anesthesia for various surgical procedures with advantages including rapid onset, reliable anesthesia, and reduced systemic effects compared to general anesthesia. Hyperbaric ropivacaine, a long-acting local anesthetic, has gained popularity due to its favorable pharmacokinetic profile and safety profile. However, to extend the duration and enhance the quality of anesthesia provided by hyperbaric ropivacaine, adjuvants such as dexmedetomidine and clonidine are frequently employed. This comprehensive review explores the roles of dexmedetomidine and clonidine as adjuvants to hyperbaric ropivacaine in SAB. It examines their pharmacological mechanisms, clinical efficacy, safety profiles, and comparative effectiveness in prolonging analgesia and enhancing anesthesia. The review synthesizes evidence from clinical studies to delineate the synergistic effects of these adjuvants, their impact on patient outcomes, and their potential advantages over traditional anesthesia techniques. Through a detailed analysis of current literature and clinical practices, this review aims to provide insights into optimizing the use of dexmedetomidine and clonidine in SAB protocols. It discusses clinical implications, offers recommendations for practice, and identifies future research directions to further enhance the efficacy and safety of SAB using these adjuvants.

Targeting α1- and α2-adrenergic receptors as a countermeasure for fentanyl-induced locomotor and ventilatory depression.

This study assessed the ability of α1 and α2-adrenergic drugs to decrease fentanyl-induced locomotor and ventilatory depression. Rats were given saline or fentanyl, followed by: (1) naltrexone, (2) naloxone, (3) nalmefene, (4) α1 agonist phenylephrine, (5) α1 antagonist prazosin, (6) α1D antagonist BMY-7378, (7) α2 agonist clonidine, (8) α2 antagonist yohimbine or (9) vehicle. All µ-opioid antagonists dose-dependently reversed fentanyl-induced locomotor and ventilatory depression. While the α1 drugs did not alter the effects of fentanyl, clonidine dose-dependently decreased locomotion and respiration with and without fentanyl. Conversely, yohimbine given at a low dose (0.3-1 mg/kg) stimulated ventilation when given alone and higher doses (>1 mg/kg) partially reversed (∼50 %) fentanyl-induced ventilatory depression, but not locomotor depression. High doses of yohimbine in combination with a suboptimal dose of naltrexone reversed fentanyl-induced ventilatory depression, suggestive of additivity. Yohimbine may serve as an effective adjunctive countermeasure agent combined with naltrexone to rescue fentanyl-induced ventilatory depression.

A historical perspective on clonidine as an alpha-2A receptor agonist in the treatment of addictive behaviors: Focus on opioid dependence.

Clonidine operates through agonism at the alpha-2A receptor, a specific subtype of the alpha-2-adrenergic receptor located predominantly in the prefrontal cortex. By inhibiting the release of norepinephrine, which is responsible for withdrawal symptoms, clonidine effectively addresses withdrawal-related conditions such as anxiety, hypertension, and tachycardia. The groundbreaking work by Gold et al. demonstrated clonidine's ability to counteract the effects of locus coeruleus stimulation, reshaping the understanding of opioid withdrawal within the field. In the 1980s, the efficacy of clonidine in facilitating the transition to long-acting injectable naltrexone was confirmed for individuals motivated to overcome opioid use disorders (OUDs), including physicians and executives. Despite challenges with compliance, naltrexone offers sustained blockade of opioid receptors, reducing the risk of overdose, intoxication, and relapse in motivated patients in recovery. The development of clonidine and naltrexone as treatment modalities for OUDs, and potentially other addictions, including behavioral ones, underscores the potential for translating neurobiological advancements from preclinical models (bench) to clinical practice (bedside), ushering in innovative approaches to addiction treatment.

Identification of Catecholamine and Drug Target α2A-Adrenoceptor in Human Testis and Human Testicular Peritubular Cells.

Background: Clonidine has been used in clinical medicine, e.g., to treat high blood pressure and other conditions. Animal studies have linked its use to impairments of male reproductive functions, and although only a few reports exist for the human species, such actions may exist in man as well. The underlying reasons and, specifically, possible actions of clonidine at the level of the testis are not known. Introduction: Clonidine is an agonist at the α2A-adrenoceptor (ADRA2A), which, as data bank mining indicated, is expressed by several cells of the human testis. The human testis and most of its cells are, however, not readily accessible to experimental testing. Cells from the peritubular wall compartment (human testicular peritubular cells; HTPCs) are the exception. Methods and Results: As shown by immunohistochemical/immunocytochemical and PCR techniques these cells express ADRA2A and retain expression upon isolation and culture. When tested over a concentration range (1-1000 µM) and 24 h, clonidine did not visibly affect HTPC morphology but significantly stimulated IL6 mRNA levels in a concentration-dependent manner. ELISA measurements of cell culture supernatants confirmed a stimulatory action of clonidine (10 µM) on secreted IL6. When examined in collagen gel contraction assays of HTPCs, clonidine (10 µM) exerted a slight relaxing action, while a proteomic study revealed that clonidine (10 µM) did not significantly change cellular protein abundance of HTPCs after 24 h (data available via ProteomeXchange with identifier PXD052220). Conclusion: Thus, ADRA2A-bearing cells in the human testis are targets for catecholamines and drugs such as clonidine. The results of this HTPCs-focused study only show the tip of the iceberg. It is likely that catecholamines/catecholaminergic drugs have the potential to interfere with human testicular functions.

Novel drug treatments for pain in advanced cancer and serious illness: a focus on neuropathic pain and chemotherapy-induced peripheral neuropathy.

Drugs that are commercially available but have novel mechanisms of action should be explored as analgesics. This review will discuss haloperidol, miragabalin, palmitoylethanolamide (PEA), and clonidine as adjuvant analgesics or analgesics. Haloperidol is a sigma-1 receptor antagonist. Under stress and neuropathic injury, sigma-1 receptors act as a chaperone protein, which downmodulates opioid receptor activities and opens several ion channels. Clinically, there is only low-grade evidence that haloperidol improves pain when combined with morphine, methadone, or tramadol in patients who have cancer, pain from fibrosis, radiation necrosis, or neuropathic pain. Miragabalin is a gabapentinoid approved for the treatment of neuropathic pain in Japan since 2019. In randomized trials, patients with diabetic neuropathy have responded to miragabalin. Its long binding half-life on the calcium channel subunit may provide an advantage over other gabapentinoids. PEA belongs to a group of endogenous bioactive lipids called ALIAmides (autocoid local injury antagonist amides), which have a sense role in modulating numerous biological processes in particular non-neuronal neuroinflammatory responses to neuropathic injury and systemic inflammation. Multiple randomized trials and meta-analyses have demonstrated PEA's effectiveness in reducing pain severity arising from diverse pain phenotypes. Clonidine is an alpha2 adrenoceptor agonist and an imidazoline2 receptor agonist, which is U.S. Federal Drug Administration approved for attention deficit hyperactivity disorder in children, Tourette's syndrome, adjunctive therapy for cancer-related pain, and hypertension. Clonidine activation at alpha2 adrenoceptors causes downstream activation of inhibitory G-proteins (Gi/Go), which inhibits cyclic Adenosine monophosphate (AMP) production and hyperpolarizes neuron membranes, thus reducing allodynia. Intravenous clonidine has been used in terminally ill patients with poorly controlled symptoms, in particular pain and agitation.

Comparison of the Efficacies of Dexmedetomidine and Clonidine in Preventing Postoperative Nausea and Vomiting in Paediatric Patients Undergoing Abdominal Surgeries.

Background Postoperative nausea and vomiting (PONV) is a common complication in paediatric patients undergoing abdominal surgeries. Dexmedetomidine and clonidine, both α2-adrenergic agonists, have been proposed as potential treatments for PONV due to their antiemetic properties. This study aimed to compare the efficacies of dexmedetomidine and clonidine in the prevention of PONV in paediatric patients following abdominal surgeries Methods Eighty patients, aged five to 12 years undergoing abdominal surgeries under general anaesthesia were enrolled in this study. Patients were randomly assigned to receive either a single intravenous dose of 0.5 µg/kg of dexmedetomidine (Group D; n=40) or 1 µg/kg of clonidine (Group C; n = 40) 10 minutes before extubation. PONV was recorded for the next 24 hours. Results The baseline characteristics of patients were comparable. A higher proportion of patients in the clonidine group developed PONV as compared to the dexmedetomidine group (27.5% vs 20.0%, p=0.189). The visual analogue scale (VAS) score of group C was higher than that of group D (1.38±1.55 vs 1.00±1.26) but was not statistically significant. The Paediatric Anaesthesia Emergence Delirium (PAED) scale score or emergence agitation (EA) score was higher in group C during recovery time. The mean arterial pressures and the heart rates were comparable in both groups. No significant side effects were reported. Conclusion Our study concludes that dexmedetomidine and clonidine effectively control PONV in paediatric abdominal surgery, with no significant difference in incidence or severity. Dexmedetomidine significantly reduced PAED scale scores during recovery, indicating better control of EA. The two treatments showed comparable mean arterial pressures and heart rates without significant side effects.

Identification of a Conversion Factor for Dexmedetomidine to Clonidine Transitions.

OBJECTIVE: To determine a conversion factor for use when switching from dexmedetomidine infusion to enteral clonidine in critically ill neonates. METHODS: This was an observational, retrospective review of conversions from dexmedetomidine to -clonidine, performed in a neonatal intensive care unit (NICU) between January 2020 and December 2021. Both initial conversion factors and those resulting after a 48-hour titration period were examined. Sedation and withdrawal scores were measured, and doses were titrated based on a standardized practice within the unit. RESULTS: A total of 43 dexmedetomidine to clonidine conversions were included. The median (IQR) dexmedetomidine dose prior to conversion was 17.4 (11.3-24.0) mcg/kg/day (0.7 mcg/kg/hr) and the median (IQR) enteral clonidine dose post titration was 7.8 (4.7-9.3) mcg/kg/day (2 mcg/kg every 6 hours). This equated to a post-titration conversion factor of approximately 0.42. All neonates had also received opioid infusions while on dexmedetomidine and 60% were on concurrent opioids at the time of the clonidine conversion. CONCLUSIONS: Neonatal clinicians may find the conversion factor identified in this study a useful starting point when converting from dexmedetomidine infusion to enteral clonidine in practice and should be -reminded of the most important steps in conversions (monitoring and follow-up) owing to the variability in this patient group. More studies are needed to elucidate the impact of patient-specific factors on this -conversion process.

A Comparative Study Between Intravenous Esmolol and Oral Clonidine in Attenuating Hyperdynamic Cardiovascular Response to Laryngoscopy and Endotracheal Intubation.

Background In today's era of anesthesia, balanced anesthesia is the main basis of patient care and pain management. Of all the medications given during general anesthesia, premedication, induction agents, and muscle relaxants play a major role in keeping the hemodynamics properly under control. When laryngoscopy is performed to intubate, a pain stimulus will be generated, leading to a rise in blood pressure and heart rate. This stimulus can be avoided without any complications if appropriate premedication is given to the patient at the appropriate dosage. In this research, we compare the influence of injection esmolol and oral clonidine during the time of induction as premedications to suppress the hemodynamic response. Material and methods In a prospective randomized controlled trial, 90 patients were divided into three groups: Group E (esmolol) received 2 mg/kg IV esmolol diluted in 0.9% NS two minutes pre-anesthesia; Group C (clonidine) received oral clonidine 4 mcg/kg 90 minutes pre-anesthesia; and Group P (placebo) received IV normal saline and oral water. Blood pressure, heart rate, and mean arterial pressure were measured at baseline and seven subsequent time points. Results The study compared systolic blood pressure (SBP), mean arterial pressure (MAP), and diastolic blood pressure (DBP) changes over seven minutes in three groups, clonidine (Group C), placebo (Group P), and esmolol (Group E). At one minute, Group E showed a consistent MAP decrease from 95.21 mmHg to 85.92 mmHg, while Group C and Group P exhibited fluctuating trends. DBP decreased across all groups, with Group P ending highest (77.7 mmHg) and Group C lowest (66.8 mmHg). Group E's SBP decreased steadily from 126.2 mmHg to 118.0 mmHg, Group C decreased from 128 mmHg to 116.1 mmHg, and Group P showed more erratic fluctuations in SBP, DBP, and MAP. Conclusion These findings suggest that intravenous esmolol shows a good hemodynamic response having superior control over heart rate and getting the pressure under control quickly without major drop compared with the clonidine and placebo groups.

Comparative Study of the Effects of Clonidine and Tranexamic Acid on Intraoperative Bleeding in Rhinoplasty: A Clinical Trial.

Introduction: The present study was conducted to compare the effects of clonidine and tranexamic acid on the volume of bleeding and quality of the surgical field in terms of bleeding in candidates who underwent rhinoplasty. Methods: In this two-sided clinical trial, candidates eligible for rhinoplasty were randomly assigned to two treatment groups: tranexamic acid and clonidine. The first group received tranexamic acid at a dose of 700 µg/kg of body weight 2 hours before the surgical procedure, whereas the second group received clonidine orally at a dose of 2 mg/kg of body weight, 90 minutes before surgery. Subsequently, the volume of bleeding was calculated based on the amount of blood collected via suction and in blood-soaked gauze, which was previously weighed. Results: Among the 92 patients who underwent rhinoplasty, 82% were women. The mean age and standard deviation (SD) of individuals who underwent rhinoplasty were 29.22 ± 8.50 years. There were no significant differences between the two treatment groups in terms of age, gender, and body mass index. The volume of blood collected via suction during rhinoplasty, categorized into surgery duration <63 minutes and ≤63 minutes, showed a significant difference between the 2 treatment groups. Conclusion: The use of tranexamic acid, compared with clonidine, resulted in lesser intraoperative bleeding and better surgical field quality. Considering the superior effectiveness of tranexamic acid in reducing intraoperative bleeding, it is recommended to use tranexamic acid instead of clonidine in rhinoplasty.

Comparison of alpha-2 agonist versus alpha-1 antagonist for post-traumatic stress disorder-associated nightmares in pediatric patients.

Introduction: Posttraumatic stress disorder (PTSD) in children and adolescents has a high prevalence of accompanying sleep disturbances. Currently, pediatric treatment of PTSD-related nightmares is extrapolated from adult studies. This study aims to determine the effectiveness and safety of clonidine and guanfacine compared with prazosin for the treatment of PTSD-related nightmares. Methods: This was a retrospective, single-center, medical record review of patients 5 to 17 years old admitted to an inpatient psychiatric unit from January 2015 to September 2021. Patients with a new initiation of an alpha-2 agonist (clonidine or guanfacine) or an alpha-1 antagonist (prazosin) with a diagnosis of PTSD, other trauma- or stressor-related disorder or unspecified anxiety disorder were included. The primary endpoint was the percentage of patients with a decrease in the frequency of nightmares. Results: A total of 59 patients were included in the study: 37 in the alpha-2 agonist group and 22 in the alpha-1 antagonist group. There was no statistically significant difference in reduction of nightmares with both groups having a high percentage of patients showing response (alpha-2 agonist: 91.9%, alpha-1 antagonist: 86.4%). Time to decrease in nightmares was comparable between groups with a relatively quick onset. Within the alpha-2 agonist group, clonidine (1.59 ± 1.06 days) compared with guanfacine (3.18 ± 1.74 days) had a statistically significant faster time to reduction in nightmares (p = .005). Discussion: Both pharmacologic classes of medications were effective treatment options for pediatric PTSD-associated nightmares with a low incidence of adverse effects. There was a quick time to onset seen with all agents.

Topical Clonidine Accelerates Cutaneous Wound Healing in Diabetic Rats by Regulating the Expression of Related Cytokine Signaling.

Based on the analgesic and anti-inflammatory effects of clonidine in previous studies, we hypothesized that clonidine could accelerate wound healing in rats by regulating the expression of related cytokines. In this study, the wound healing effect of clonidine was evaluated using an excision wound model in diabetic rats and a HaCaT cell model. The wounds were treated daily with topical clonidine. The results analyzed by ImageJ2 software show that the wounds of the rats that were treated with 15 ng/mL clonidine recovered faster, and the wound size was also significantly reduced compared to the control group. Western blot assays determined that clonidine induced an increase in the expression of vascular growth factors, namely, Ang-1, Ang-2, and VEGF. Moreover, clonidine demonstrated a rescuing effect on JAK2 within the JAK/STAT pathway by inhibiting SOCS3 expression, leading to decreased SOCS3 levels and increased expression of JAK2 and phospho-STAT3. Histopathological analysis revealed that clonidine promoted complete epithelial repair and minimized inflammation in skin tissue. Additionally, clonidine stimulated HaCaT cell proliferation in vitro and enhanced cellular energy levels in the presence of AGEs. In conclusion, clonidine promoted vascular growth and wound healing by stimulating the expression of cytokines that are beneficial for wound healing.