Background: Emergent intubation is associated with a high rate of complications. Neuromuscular blocking agents are routinely used in the operating room and emergency department to facilitate intubation. However, use of neuromuscular blocking agents during emergent airway management outside of the operating room and emergency department is controversial. We hypothesized that the use of neuromuscular blocking agents is associated with a decreased prevalence of hypoxemia and reduced rate of procedure-related complications.
Results: The use of neuromuscular blocking agents was associated with a lower prevalence of hypoxemia (10.1% vs. 17.4%, p = .022) and a lower prevalence of procedure-related complications (3.1% vs. 8.3%, p = .012). This association persisted in a multivariate analysis, which controlled for airway grade, sedation, and institution. Use of neuromuscular blocking agents was associated with significantly improved intubating conditions (laryngeal view, p = .014; number of intubation attempts, p = .049). After controlling for the number of intubation attempts and laryngoscopic view, muscle relaxant use is an independent predictor of complications associated with emergency intubation (p = .037), and there is a trend towards improvement of oxygenation (p = .07).
Conclusion: The use of neuromuscular blocking agents, when used by intensivists with a high level of training and experience, is associated with a decrease in procedure-related complications.
The widespread use of neuromuscular blocking agents (NMBA) was a significant milestone in the development of anesthesia. Before the introduction of NMBA, anesthesia was induced and maintained with intravenous and inhalational agents. The introduction of NMBA led to a significant conceptual change in the practice of anesthesia. Anesthesia was redefined to include a triad of narcosis, analgesia, and muscle relaxation. This activity outlines the indications, mechanism of action, methods of administration, important adverse effects, contraindications, monitoring, and toxicity of NMBAs, so providers can direct patient therapy to optimal outcomes in anesthesia and other conditions where NMBA have therapeutic benefit.
The widespread use of neuromuscular blocking agents (NMBA) was a significant milestone in the development of anesthesia. Before the introduction of NMBA, anesthesia was induced and maintained with intravenous and inhalational agents. The introduction of NMBA led to a significant conceptual change in the practice of anesthesia. Anesthesia was redefined to include a triad of :
Another side effect of succinylcholine is malignant hyperthermia; this is a pharmacogenetic disorder that occurs with the use of volatile inhalation anesthetic agents and succinylcholine. Clinically it can manifest with hypercarbia, hyperventilation hyperthermia, rhabdomyolysis, and metabolic acidosis. The condition has correlated with the mutation in the RYR1 and CACNA1S genes.
Neuromuscular blockade is frequently used in anesthesia to facilitate endotracheal intubation, optimize surgical conditions, and assist with mechanical ventilation in patients who have reduced lung compliance. Neuromuscular blocking agents (NMBAs) come in two forms: depolarizing neuromuscular blocking agents (e.g., succinylcholine) and nondepolarizing neuromuscular blocking agents (e.g., rocuronium, vecuronium, atracurium, cisatracurium, mivacurium). The class of NMBAs used for achieving neuromuscular blockade must be selected carefully based on patient factors, the type of procedure being performed, and clinical indication.
Nondepolarizing neuromuscular blockers: Nondepolarizing neuromuscular blockers can be divided into two classes based on their chemical structure: steroidal (e.g., rocuronium, vecuronium, pancuronium) or benzylisoquinolinium (e.g., mivacurium, atracurium, cisatracurium). Nondepolarizing neuromuscular blockers are competitive acetylcholine (ACh) antagonists that bind directly to nicotinic receptors on the postsynaptic membrane, thus blocking the binding of ACh so the motor endplate cannot depolarize.  This leads to muscle paralysis.
The AOR comparing the drug use group versus the non-drug group were calculated separately in patients with a diagnosis code of RA and psoriasis. There were not enough patients (at least one cell in a two by two table have counts lower than 10 for all the strata) to test the effect of TNF blocking agents in patients with the other inflammatory diseases. We list the number of patients that were treated with each of the drugs in each of the inflammatory disease groups in S27 Table. To assess the effects of gender, age, and race on the risk associations between the therapeutic drugs and dementia, we separately calculated the crude OR of dementia among the 2 age groups, 2 gender groups, and 2 race groups. To adjust for methotrexate prescription status in psoriasis patients, we separately calculated the crude OR for a diagnosis of AD or dementia among 16 strata (tabulation of 2 age groups, 2 gender groups, 2 race groups, and 2 methotrexate groups (history of methotrexate or no methotrexate) and then calculated the weighted average across all strata using the CMH method .
The cumulative age distribution for patients with a diagnosis code for rheumatoid arthritis, dementia or AD is shown in Fig 2. Given that the Explorys Cohort Discovery platform includes at least some information on patients making up over 20% of the US population, the cumulative age distribution should reasonably represent the age-dependent prevalence of these diseases in the US. As expected, the age distribution of patients with a diagnosis of RAskews younger, while patients with dementia or AD skew older. The average treatment retention time varies among the three TNF blocking agents selected for study with etanercept having a better than 50% patient retention rate at 12 years of treatment, while the 50% retention rates for adalimumab and infliximab are about 2 and 3 years, respectively [39, 40]. To comply with HIPAA compliant de-identification of EHR, the Explorys Cohort Discovery platform does not allow patient level access to prescription data. Therefore, we compared the benefit of etanercept to adalimumab and infliximab as a surrogate for duration of exposure as a modifier of treatment benefit.
Microglia activation and gliosis formerly were considered secondary to neurodegeneration in AD, however, recent genetic studies in late-onset AD implicate microglia- and astrocyte-related pathways in disease pathogenesis.[10, 48, 49] One focus of interest is TREM2, an innate immune receptor expressed on microglia and myeloid cells [50, 51]. Rare TREM2 mutations associated with AD suggest that TREM2 deficiency contributes to AD risk [52, 53]. TREM2 is a negative regulator of the release of TNF and other inflammatory cytokines through activation of the Toll-receptor pathway [8, 51, 54]. Loss of TREM2 function in monocytes or macrophages may contribute to TNF production systemically, and indeed, be a treatable risk factor for AD much as these epidemiologic data suggest that TNF production in systemic inflammatory diseases affecting the joints, gut and skin contributes to risk for AD and that risk can be lowered by a TNF blocking agent.
Neuromuscular blocking agents are commonly used to paralyze patients requiring intubation whether in an emergency as a life-saving intervention or as a scheduled surgery and procedure. The indications for intubation during an emergency can be divided into 3 categories: failure to maintain or protect the airway, failure to adequately ventilate or oxygenate, and anticipation of a decline in clinical status. This activity will highlight the mechanism of action, adverse event profile, off-label uses, dosing, pharmacodynamics, pharmacokinetics, monitoring, relevant interactions of these agents, pertinent for members of the interprofessional team in the treatment of patients where a neuromuscular blockade is needed.
Objectives:Identify the two basic mechanisms of action of depolarizing neuromuscular blockade drugs.Explain the indications where depolarizing neuromuscular blockade agents are appropriate.Outline the adverse events and monitoring necessary when using depolarizing neuromuscular blocking agents.Review the importance of improving care coordination among interprofessional team members to improve outcomes for patients undergoing procedures where depolarizing neuromuscular blocking agents are used.Access free multiple choice questions on this topic.
Neuromuscular blocking agents are commonly used to paralyze patients requiring intubation whether in an emergency as a life-saving intervention or as a scheduled surgery and procedure. The indications for intubation during an emergency can be divided into 3 categories: failure to maintain or protect the airway, failure to adequately ventilate or oxygenate, and anticipation of a decline in clinical status.
Pharmacologic paralysis is a vital aspect of rapid sequence intubation (RSI), improves visualization of the glottic anatomy, and prevents vomiting during intubation attempts. Importantly, the conjunctive use of induction agents is vital to RSI to reduce the sympathetic reflexes, improve intubating conditions, and avoid the unwarranted effect of paralyzing a conscious patient.
The most well-known depolarizing neuromuscular blocking agent is succinylcholine. It is the only such drug used clinically and is considered by many the drug of choice for emergency department RSI, although this is controversial. It provides the fastest of optimal conditions during intubation of critically ill patients.
There are 2 types of neuromuscular blocking agents that work at the neuromuscular junction: depolarizing and non-depolarizing. Depolarizing muscle relaxants act as acetylcholine (ACh) receptor agonists by binding to the ACh receptors of the motor endplate and generating an action potential. However, they are resistant to and not metabolized by acetylcholinesterase, leading to persistent depolarization of the muscle fibers, resulting in the patient's well-recognized muscle fasciculations and paralysis. This is in contrast to non-depolarizing muscle relaxants, which act as competitive antagonists. They bind (ACh) receptors but do not produce an action potential. Thus, they prevent ACh from binding, and as a result, neural endplate potentials do not develop. 041b061a72