scholarly journals Use of Dexmedetomidine in a Patient Allergic to Clonidine Presenting for an Awake Craniotomy: A Case Report

2022 ◽  
Author(s):  
Yasmin Srita ◽  
Brett Cornell ◽  
Brittany Maggard
Keyword(s):  
Adrenergic Receptor ◽  
Chemical Structure ◽  
Awake Craniotomy ◽  
Chronic Obstructive ◽  
Monitored Anesthesia Care ◽  
Obstructive Pulmonary Disease ◽  
Case Presentation ◽  
Obstructive Sleep ◽  
Scalp Block ◽  
Dose Dependent

Abstract Introduction: The use of dexmedetomidine with concurrent scalp block is increasingly being utilized as an effective and safe anesthetic approach for awake craniotomy (AC). Dexmedetomidine is an alpha-2 adrenergic receptor (α2-AR) agonist with dose-dependent sedative, analgesic, and anxiolytic properties while preserving respiratory function. The challenge with the use of dexmedetomidine arises when the patient in question has a clonidine allergy that is also an α2-AR agonist. Currently there aren’t any published literature regarding the use of dexmedetomidine in a patient allergic to clonidine. Case Presentation: A 48-year-old male with chronic obstructive pulmonary disease, obstructive sleep apnea, and body mass index of 54 with clonidine allergy presents for an AC. Given the goals of the surgery and patient comorbidities, we planned for monitored anesthesia care with intravenous (IV) dexmedetomidine, remifentanil, and propofol. We discussed the use of dexmedetomidine with the patient and the potential risk of allergic reaction given his allergy to clonidine. Patient understood the risk and consented to the anesthetic plan. AC was successfully performed with IV dexmedetomidine, remifentanil, and propofol.Conclusion: Although both dexmedetomidine and clonidine have some functional similarities in terms of acting on the central and peripheral nervous system, there are marked differences between the two based on chemical structure, receptor affinity, and metabolism of the drug. This case highlights the successful use of dexmedetomidine in a patient with known allergy of rash to clonidine.

scholarly journals β2-Adrenergic genotypes and risk of severe exacerbations in COPD: a prospective cohort study

Thorax ◽  
2019 ◽  
Vol 74 (10) ◽  
pp. 934-940 ◽  
Author(s):  
Truls Sylvan Ingebrigtsen ◽  
Jørgen Vestbo ◽  
Line Rode ◽  
Jacob Louis Marott ◽  
Peter Lange ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Vital Capacity ◽  
Genetic Factors ◽  
Forced Expiratory Volume ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
General Population Study ◽  
Heart Study ◽  
Acute Admissions

BackgroundIndividual susceptibility to exacerbations in chronic obstructive pulmonary disease (COPD) is likely influenced by genetic factors; however, most such variance is unexplained. We hypothesised that β2-adrenergic receptor genotypes, Gly16Arg (rs1042713, c.46G>A) and Gln27Glu (rs1042714, c.79C>G) influence risk of severe exacerbations in COPD.MethodsAmong 96 762 individuals in the Copenhagen General Population Study, we identified 5262 with COPD (forced expiratory volume in one second divided by forced vital capacity, FEV1/FVC, below 0.7, FEV1 less than 80% of predicted value, age above 40 years and no asthma) who had genotyping performed. Severe exacerbations were defined as acute admissions due to COPD during 5 years of follow-up (mean 3.4 years). 923 individuals with COPD diagnosed similarly in the Copenhagen City Heart Study (CCHS) were used for replication analyses.ResultsWe recorded 461 severe exacerbations in 5262 subjects. The HRs for severe exacerbations were 1.62 (95% CI 1.30 to 2.03, p=0.00002) for 16Gly/Arg heterozygotes and 1.41 (1.04 to 1.91, p=0.03) for 16Arg homozygotes, compared with 16Gly homozygotes. HRs were 1.35 (1.03 to 1.76, p=0.03) for 27Gln/Glu heterozygotes and 1.49 (1.12 to 1.98, p=0.006) for 27Gln homozygotes, compared with 27Glu homozygotes. Similar trends were observed in the CCHS. Among 27Gln homozygotes only, HRs were 5.20 (1.81 to 14.9, p=0.002) for 16Gly/Arg heterozygotes and 4.03 (1.40 to 11.6, p=0.01) for 16Arg homozygotes, compared with 16Gly homozygotes.ConclusionCommon β2-adrenergic receptor genotypes influence risk of severe exacerbations in COPD, potentially mainly by genetic influence of the 16Arg allele in rs1042713.

scholarly journals Risk for Cardiovascular Disease and One-Year Mortality in Patients With Chronic Obstructive Pulmonary Disease and Obstructive Sleep Apnea Syndrome Overlap Syndrome

2021 ◽  
Vol 12 ◽  
Author(s):  
Manyun Tang ◽  
Yidan Wang ◽  
Mengjie Wang ◽  
Rui Tong ◽  
Tao Shi
Keyword(s):  
Risk Factors ◽  
Heart Failure ◽  
Cardiovascular Diseases ◽  
Overlap Syndrome ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Obstructive Sleep ◽  
Increased Risk ◽  
All Cause Mortality ◽  
Independent Risk Factors

Background: Patients with chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSAS) overlap syndrome (OS) are thought to be at increased risk for cardiovascular diseases.Objective: To evaluate the burden of cardiovascular diseases and long-term outcomes in patients with OS.Methods: This was a retrospective cohort study. The prevalence of cardiovascular diseases and 1-year mortality were compared among patients diagnosed with OS (OS group), COPD alone (COPD group) and OSAS alone (OSAS group), and Cox proportional hazards models were used to assess independent risk factors for all-cause mortality.Results: Overall, patients with OS were at higher risk for pulmonary hypertension (PH), heart failure and all-cause mortality than patients with COPD or OSAS (all p < 0.05). In multivariate Cox regression analysis, the Charlson comorbidity index (CCI) score [adjusted hazard ratio (aHR): 1.273 (1.050–1.543); p = 0.014], hypertension [aHR: 2.006 (1.005–4.004); p = 0.048], pulmonary thromboembolism (PTE) [aHR: 4.774 (1.335–17.079); p = 0.016] and heart failure [aHR: 3.067 (1.521–6.185); p = 0.002] were found to be independent risk factors for 1-year all-cause mortality.Conclusion: Patients with OS had an increased risk for cardiovascular diseases and 1-year mortality. More efforts are needed to identify the causal relationship between OS and cardiovascular diseases, promoting risk stratification and the management of these patients.

Sign in / Sign up

Export Citation Format

Share Document