To treat a case of pre-eclampsia, medical professionals at Shanghai First Maternity and Infant Hospital administered calcium channel blockers and magnesium sulfate to their patient, a 32-year-old pregnant woman [1]. By interacting with nicardipine and prior dose of magnesium sulfate that the patient had ingested before her emergency cesarean delivery, these medications prolonged rocuronium activity, extending the controlled paralysis event known as neuromuscular block [1]. In a case report analyzing this phenomenon, Song and colleagues noted how magnesium sulfate can bolster the effect of neuromuscular blockers [1]. This is not uncommon: other substances and medications that are unintended to operate as neuromuscular blocking drugs (NMBDs) can extend the duration of neuromuscular block [1, 2].
NMBDs are often used during anesthesia to facilitate endotracheal intubation and make conditions optimal for surgery [2]. Despite the advantages of this blockade generally, medications that extend neuromuscular block can be cause for concern. For one, prolonged block can result in weakness that lasts anywhere from multiple hours to multiple days [3]. Patients with pseudocholinesterase deficiency, whose bodies have trouble clearing out certain neuromuscular blocking agents, may require mechanical ventilation following surgery due to extended effects [2]. And for neonates, prolonged blockade can exacerbate the difficulty of weaning patients off the ventilator [4].
With these consequences in mind, we can now turn to two other examples of medications that extend neuromuscular block. One of the classes of medications that can extend neuromuscular block is antibiotics, most of which can not only extend blockade, but also potentiate it independently of NMDBs [5, 6]. The mechanisms through which antibiotics achieve blockade differ according to the type of antibiotic [5]. For instance, while aminoglycoside antibiotics operate both by inhibiting acetylcholine release and making postjunctional neuronal nicotinic acetylcholine receptors less receptive to the neurotransmitter that triggers muscle contraction, tetracyclines only have postjunctional effects [5]. Additionally, penicillins and cephalosporins are rare exceptions among antibiotics in that they do not appear to potentiate blockade [5]. Because of the various side effects associated with antibiotics —including end-organ damage and allergic reactions, not to mention the aforementioned harms of neuromuscular block— anesthesiologists should be cautious when treating patients currently taking or slated to take antibiotics [6].
Inhaled anesthetics can also prolong neuromuscular block [7]. For instance, Ye et al. found that inhaled sevoflurane increases skeletal muscle’s sensitivity to neuromuscular blockers. [8]. However, not all inhaled anesthetics prolong neuromuscular block, meaning that anesthesiologists typicaly have pathways to provide general anesthesia without increasing the risk of prolonged paralysis.
Besides magnesium sulfate, some antibiotics, and some inhaled anesthetics, other medications such as anti-seizure drugs and lithium can also extend a neuromuscular block [2]. Taking note of these medications’ ability to potentiate blockade independently or enhance the effects of NMDBs is key to creating the optimal duration of blockade and avoiding unnecessary complications.
References
[1] Y. Song, X. Qian, and W. Du, “Postoperative residual neuromuscular block in a woman with severe preeclampsia treated with magnesium sulfate and nicardipine: A case report and literature review,” Frontiers in Surgery, pp. 1-4, February 2023. [Online]. Available: https://doi.org/10.3389%2Ffsurg.2023.1093969.
[2] D. Cook and D. J. Simons, “Neuromuscular Blockade,” Stat Pearls, Updated September 24, 2022. [Online]. Available: https://www.ncbi.nlm.nih.gov/books/NBK538301/.
[3] J. L. Gooch, “Prolonged paralysis after neuromuscular blockade,” Journal of Toxicology: Clinical Toxicology, vol. 33, no. 5, pp. 419-26, September 1995. [Online]. Available: https://doi.org/10.3109/15563659509013750.
[4] B. T. Darras and H. Royden Jones Jr., “Neuromuscular Problems of the Critically Ill Neonate and Child,” in Neuromuscular Disorders of Infancy, Childhood, and Adolescence, 2nd ed. Amsterdam: Elsevier, 2014, ch. 43, pp. 885-903.
[5] S. J. Brull and C. Meistelman, “Pharmacology of Neuromuscular Blocking Dates,” in Miller’s Anesthesia, 9th ed. Amsterdam: Elsevier, 2019, ch. 27, pp. 792-831.
[6] J. Kang, “Antibiotics and muscle relaxation,” Korean Journal of Anesthesiology, vol. 64, no. 2, pp. 103-04, February 2013. [Online]. Available: https://doi.org/10.4097%2Fkjae.2013.64.2.103.
[7] M. Paul et al., “Characterization of the interactions between volatile anesthetics and neuromuscular blockers at the muscle nicotinic acetylcholine receptor,” Anesthesia & Analgesia, vol. 95, no. 2, pp. 362-67, August 2002. [Online]. Available: https://doi.org/10.1097/00000539-200208000-00022.
[8] L. Ye et al., “Sevoflurane enhances neuromuscular blockade by increasing the sensitivity of skeletal muscle to neuromuscular blockers,” International Journal of Physiology, Pathophysiology and Pharmacology, vol. 7, no. 4, pp. 172-77, December 2015. [Online]. Available: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4788726/.
