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Nondepolarizing neuromuscular blockers prevent the membrane depolarization of muscle cells and inhibit muscle contraction. These are usually administered with anesthetics to achieve complete muscle relaxation. Upon administration, these drugs first block the small, rapidly contracting muscles of the face and hands, followed by the larger muscles of the trunk and the intercostal muscles. The diaphragm is the last muscle to be affected.
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Nondepolarizing neuromuscular blockers induce paralysis by competitively blocking nicotinic acetylcholine receptors at the muscle end plate. Examples include pancuronium, mivacurium, vecuronium, and rocuronium. These quaternary ammonium derivatives are administered intravenously, are poorly absorbed, and are excreted via the kidneys.
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The site of chemical communication between a motor neuron and a muscle fiber is called the neuromuscular junction (NMJ). The end of the motor neuron at the NMJ divides into a cluster of synaptic end bulbs. The cytoplasm of these bulbs consists of synaptic vesicles enclosing acetylcholine molecules, the principal neurotransmitter released at the NMJ. The region opposite the synaptic bulb that ends in the muscle fiber is called the motor end plate, which has acetylcholine receptors. Within the...
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All neuromuscular blocking agents are injected intravenously because they are poorly absorbed from the GI tract. Rapid onset is achieved with intravenous administration, although absorption is also adequate from an intramuscular injection. Since these agents are highly ionized, they do not readily penetrate cell membranes or cross the blood-brain barrier.
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Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
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Skeletal muscle relaxants are widely used for muscle paralysis and relieving pain following any muscle injury or stiffness. However, depending on the drug type, they can have adverse effects that range from mild to severe. Usually, nondepolarizing neuromuscular blockers have minimal side effects. For example, drugs like d-tubocurarine, cisatracurium, and rocuronium cause hypotension, whereas drugs like baclofen, when stopped abruptly, can lead to the recurrence of spastic conditions.
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Neuromuscular blocking agent induced hypersensitivity reaction exploration: an update.

Alice Dejoux1, Luc de Chaisemartin, Pierre Bruhns

  • 1From the Institut Pasteur, Université de Paris, Unit of Antibodies in Therapy and Pathology, Inserm UMR1222 (AD, LdC, PB, AGC), Immunology Department, DMU BIOGEM, Bichat Hospital, AP-HP (LdC), Université Paris-Saclay, Inserm, Inflammation, Microbiome and Immunosurveillance, Châtenay-Malabry (LdC), Anaesthesiology and Critical Care Medicine Department, DMU PARABOL, Bichat Hospital, AP-HP (DL, AGC), Université de Paris, FHU PROMICE (DL), Anaesthesiology and Critical Care Medicine Department, DMU PARABOL, Bichat-Claude Bernard and Louis Mourier Hospitals, APHP (DL), INSERM1148, Paris, France (DL), and Biostatistics Research Branch, Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA (AGC).

European Journal of Anaesthesiology
|October 27, 2022
PubMed
Summary

Acute hypersensitivity reactions during anesthesia are increasing, often caused by neuromuscular blocking agents. This review explores diagnostic challenges and novel tools for IgE and non-IgE mediated pathways to guide future anesthetic choices.

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Area of Science:

  • Anesthesiology
  • Immunology
  • Pharmacology

Background:

  • Acute hypersensitivity reactions (AHRs) during anesthesia pose severe risks and are increasing.
  • Neuromuscular blocking agents (NMBAs) are the most common cause of AHRs during anesthesia.
  • Diagnostic challenges arise in up to 30% of AHR cases, complicating subsequent anesthetic management.

Approach:

  • Reviews current diagnostic methods for IgE-mediated anaphylaxis (IgE endotype).
  • Updates on non-IgE mediated pathways involved in peri-operative AHRs.
  • Highlights novel diagnostic tools for characterizing different AHR endotypes.

Key Points:

  • Inconclusive AHR diagnostics hinder decisions on future anesthetic procedures, particularly NMBA selection.
  • Understanding diverse endotypes (IgE-mediated and IgE-independent) is crucial for accurate diagnosis.
  • New diagnostic tools are emerging to better characterize peri-operative AHR mechanisms.

Conclusions:

  • This review provides clinicians with tools to navigate incomplete AHR diagnostic work-ups.
  • Facilitates informed decision-making for anesthetic procedures following AHRs, especially concerning NMBAs.
  • Aims to reduce uncertainty and improve patient safety in anesthesia post-AHR.