An 87 year-old woman on nightly CPAP status post recent left hip fracture presents from rehabilitation with weakness for 2 weeks. At rehabilitation, the patient had not had access to CPAP and had been prescribed multiple anxiolytics as well as sedating sleep aids. She had also completed a 7 day course of ciprofloxacin for urinary tract infection. On admission the patient was lethargic and using accessory muscles of respiration, she was hemodynamically stable with oxygen saturation at 96% on RA. Arterial blood gas was notable for carbon dioxide level of 78 and bicarbonate of 33. The patient improved on bi-level positive pressure ventilation. A plan was made to reinitiate nightly CPAP, wean sedating medications, and refer the patient to a new rehabilitation facility per the family’s request. However over the next few days, the patient’s respiratory status did not improve as expected. Pulmonary consultation and ENT laryngoscopy showed thick secretions, but was otherwise unremarkable. Chest PT, nebulized saline, and mucolytics did not relieve the patient’s discomfort. She began reporting pooling of saliva and an inability to swallow. Speech and swallow evaluation revealed an inability to trigger a volitional swallow. Tensilon test performed with neurology showed an increase in oropharyngeal muscle strength in response to pyridostigmine. The patient’s respiratory status did not improve despite pyridostigmine and IVIG therapy. She was not intubated due to her DNR/DNI status and was eventually made comfort care according to her wishes. She was started on a morphine drip and expired the following morning. After expiration, her acetylcholine receptor antibody returned markedly elevated.
After stopping all anxiolytics and re-initiating positive pressure ventilation the patient continued to suffer from hypercarbic and hypoxic respiratory failure. Due to anchoring and availability bias, the investigation for neuromuscular junction disorders only began when the patient developed overt bulbar dysfunctioni,ii, which further compromised the patient’s pulmonary reserve with recurrent aspirationiii. The tensilon test has a sensitivity of 71.5% to 95% for generalized myasthenia gravisiv. It uses edrophonium to demonstrate improved strength in a pre-determined muscle group, most commonly a single paretic extraocular muscle. Acetylcholine Receptor Binding Antibodies have a reported sensitivity from 70% to 95% for generalized myasthenia gravis. There are 37 case reports of fluoroquinolone-induced myasthenia exacerbations, 6 of which were related to ciprofloxacin. There are no incident cases of myasthenia gravis related to fluoroquinolone exposure reportedv.
This patient expired from hypoxic and hypercarbic respiratory failure likely secondary to a first episode of acute myasthenic crisis secondary to recent fluoroquinone use. For the practicing hospitalist, early identification of respiratory failure secondary to neuromuscular junction disorders is critical to prevent poor outcomes in this population.