Sir, Vancomycin is a commonly prescribed antibiotic for the treatment of severe Gram-positive infections and is the drug of choice for severe infections caused by MRSA.1 Vancomycin is cited as having the potential to exacerbate myasthenia gravis, based upon reports of neuromuscular blockade potentiation when administered in combination with neuromuscular blocking agents.2,3 However, the exact mechanism by which vancomycin potentiates neuromuscular blockade is unknown. We report a case of probable vancomycin-induced myasthenic crisis in the absence of neuromuscular blocking agents. A female patient with myasthenia gravis was directly admitted to the hospital with complaints of sore throat, subjective low-grade fevers, cough and weakness. Her maintenance regimen for myasthenia gravis is rituximab, intravenous immunoglobulin, prednisone and pyridostigmine. She has had several myasthenia gravis exacerbations in the past, including those requiring intubation. She reports that they were commonly associated with her menses and characterized by diffuse body aches, proximal muscle weakness, left-sided facial droop and ptosis. Upon admission, her physical examination was notable for ptosis of the left eye, abdominal distension and abdominal pain. Her chest port site was not tender to palpation, erythematous or purulent. Additionally, she did not complain of shortness of breath, wheezing or chest tightness. Her vital signs were blood pressure of 126/82 mm Hg, pulse of 91 beats/min, respiratory rate of 18 breaths/min and pulse oximetry on room air of 97%. Her negative inspiratory force (NIF) was −40 cm H2O and her vital capacity (VC) was 1300 mL. She was diagnosed with myasthenia gravis exacerbation. Two additional doses of intravenous immunoglobulin over the course of 2 days were administered and her maintenance myasthenia gravis regimen was continued. Regarding her infectious diseases management, ceftriaxone and metronidazole were started and the Infectious Diseases service was consulted. The patient was subsequently de-escalated to amoxicillin/clavulanate and also received a dose of doxycycline for a possible upper respiratory tract infection. On hospital day 2, blood cultures drawn from admission revealed MRSA and daptomycin was initiated. On hospital day 3, the port was removed and a transthoracic echocardiogram revealed no vegetations. By hospital day 5, she was stable for discharge. Her vital signs were blood pressure of 116/68 mm Hg, pulse of 67 beats/min, respiratory rate of 18 breaths/min and pulse oximetry on room air of 98%. Her NIF was −40 cm H2O and her VC was 2400 mL. The Infectious Diseases service recommended completing a 2 week course of daptomycin for uncomplicated MRSA bacteraemia with the presumed source being the central venous catheter. However, the patient refused discharge due to the high cost of home health intravenous antibiotics. She reported receiving and tolerating a 2 week course of vancomycin in the past for a line infection. After extensive discussion, she elected to trial vancomycin, understanding the potential risk for myasthenic crisis. Nine hours after the last daptomycin dose, vancomycin was initiated. After 1 h, during the vancomycin infusion, the patient became lethargic and she was unable to speak. Her NIF and VC dropped to −18 cm H20 and 600 mL, respectively. Vancomycin was discontinued and she was transferred to the neurological ICU and was intubated. Pyridostigmine was held and daptomycin was restarted. She was given another dose of intravenous immunoglobulin. On hospital day 9, she was extubated, her NIF was −50 cm H2O and her VC was 2511 mL. She was transferred back to the acute care ward for continued neurological monitoring. She completed the course of daptomycin and was discharged after 17 days of hospitalization. Myasthenic crisis, defined as the worsening of myasthenic weakness requiring intubation, can be precipitated by a variety of factors, including infection, surgery and certain medications.4 Vancomycin is frequently listed as a medication with a low, but potential, risk of exacerbating myasthenia gravis. This is based on a few case reports of neuromuscular blockade potentiation when used in combination with other high-risk agents, such as vecuronium and succinylcholine.2,3 To our knowledge, we report the first case of probable vancomycin-induced myasthenic crisis in the absence of other known aggravating medications. Utilizing the Naranjo Adverse Drug Reaction Probability Scale for estimating the probability of adverse drug reactions,5 it is probable that the myasthenic crisis was secondary to vancomycin. However, it is unclear whether the recent myasthenia gravis exacerbation or infection may have increased the risk of myasthenic crisis with vancomycin and no acetylcholine receptor antibody levels were obtained. Additionally, it is notable that the patient tolerated vancomycin in the past with no adverse event, though details of her previous clinical course are lacking. Overall, the timing of onset and recovery of drug-induced myasthenic crisis can vary and our case is consistent with previous publications.6,7 Removal of the offending agent(s) is important to the recovery process and resolution is dependent on the ability of the patient to demonstrate improved VC and subsequently be weaned off the ventilator.8,9 As vancomycin is among the most commonly prescribed antimicrobials, it is important to recognize the potential for myasthenic crisis with this antibiotic. Though the probability of exacerbation with vancomycin is often described as low, we describe a severe presentation of probable vancomycin-induced myasthenic crisis. The benefits of utilizing vancomycin among patients with myasthenia gravis should be weighed against the risk of this severe adverse reaction. Funding This study was carried out as part of our routine work. Transparency declarations None to declare. References 1 Liu C, Bayer A, Cosgrove SE et al. Clinical practice guidelines by the Infectious Diseases Society of America for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clin Infect Dis 2011; 52: e18– 55. Google Scholar CrossRef Search ADS PubMed 2 Albrecht RF2nd, Lanier WL. Potentiation of succinylcholine-induced phase II block by vancomycin. Anesth Analg 1993; 77: 1300– 2. Google Scholar CrossRef Search ADS PubMed 3 Huang KC, Heise A, Shrader AK et al. Vancomycin enhances the neuromuscular blockade of vecuronium. Anesth Analg 1990; 71: 194–6. Google Scholar CrossRef Search ADS PubMed 4 Sanders DB, Wolfe GI, Benatar M et al. International consensus guidance for management of myasthenia gravis: executive summary. Neurology 2016; 87: 419– 25. Google Scholar CrossRef Search ADS PubMed 5 Naranjo CA, Busto U, Sellers EM et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther 1981; 30: 239– 45. Google Scholar CrossRef Search ADS PubMed 6 Cadisch R, Streit E, Hartmann K. Exacerbation of pseudoparalytic myasthenia gravis following azithromycin (Zithromax). Schweiz Med Wochenschr 1996; 126: 308– 10. Google Scholar PubMed 7 May EF, Calvert PC. Aggravation of myasthenia gravis by erythromycin. Ann Neurol 1990; 28: 577– 9. Google Scholar CrossRef Search ADS PubMed 8 Wendell LC, Levine JM. Myasthenic crisis. Neurohospitalist 2011; 1: 16– 22. Google Scholar CrossRef Search ADS PubMed 9 Thomas CE, Mayer SA, Gungor Y et al. Myasthenic crisis: clinical features, mortality, complications, and risk factors for prolonged intubation. Neurology 1997; 48: 1253– 60. Google Scholar CrossRef Search ADS PubMed © The Author(s) 2018. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please email: email@example.com.
Journal of Antimicrobial Chemotherapy – Oxford University Press
Published: Apr 1, 2018
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