Breaking the block: Sugammadex as the last resort for refractory vecuronium-induced neuromuscular blockade in a patient receiving hydroxychloroquine

Dear Editor,

Hydroxychloroquine (HCQ), a 4-aminoquinoline derivative, is commonly prescribed for autoimmune disorders such as systemic lupus erythematosus (SLE). While its immunomodulatory effects are well documented, its potential interactions with neuromuscular blocking agents (NMBAs) remain underappreciated in anaesthetic practice. We report a case of delayed recovery from neuromuscular blockade in a young female patient on chronic HCQ therapy, likely due to pharmacodynamic interaction with vecuronium.

A 26-year-old female, weighing 70 kg and diagnosed with SLE, was scheduled for elective laparoscopic cystectomy under general anaesthesia. Her pre-anaesthetic evaluation was unremarkable, with no other comorbidities or prior anaesthetic exposures. She was receiving oral HCQ 400 mg daily as part of long-term management. In the operating room, standard monitors were attached. Neuromuscular monitoring was done using the Train of Four (TOF). Anaesthesia was induced using intravenous (IV) propofol (100 mg) and fentanyl (100 µg), followed by vecuronium (6 mg, approximately 0.1 mg/kg) to facilitate tracheal intubation (TOF count 0). Anaesthesia was maintained with oxygen, air, and sevoflurane under controlled ventilation. The intra-operative period was uneventful, with stable haemodynamics. Approximately 2 L of crystalloids were administered, and the blood loss was estimated to be 250 mL. At the conclusion of surgery, IV paracetamol (1 g) and ondansetron (4 mg) were administered. Neuromuscular blockade reversal was initiated using IV neostigmine (3.5 mg) and glycopyrrolate (0.6 mg) at a TOF ratio of <0.4 and 4 twitches. Despite this, the patient exhibited inadequate recovery, with shallow respiration, poor tidal volume, and diminished muscle tone. An additional IV 1 mg dose of neostigmine with glycopyrrolate was administered, but there was no significant improvement. TOF monitoring revealed a persistently low ratio (<0.4) with four twitches and significant fade, indicating profound blockade. Given the lack of response to neostigmine, and after systematically ruling out all other causes of delayed recovery, including electrolyte imbalances, hypothermia, residual volatile anaesthetic effect, pre-existing neuromuscular disease, and renal or hepatic dysfunction, IV sugammadex (150 mg) was administered. This dose is consistent with the recommended dose for reversal of moderate blockade (defined as at least two twitches in the TOF count), as per standard guidelines.[1] Remarkably, this resulted in rapid and complete reversal of the neuromuscular blockade, as indicated by the improvement in TOF ratio to >0.9 with restoration of spontaneous respiration, normal tidal volumes, and adequate muscle strength. The patient was extubated without further complications, and the postoperative course remained uneventful.

HCQ belongs to the 4-aminoquinoline class and shares structural similarities with chloroquine and quinine. Previous reports have documented its potential for direct myopathy and rare neuromyopathy.[2] More critically, quinoline derivatives are known to potentiate non-depolarising neuromuscular blocking agents.[3,4] The proposed mechanism involves interference with presynaptic calcium channels and impairment of acetylcholine release, leading to additive or synergistic blockade when combined with agents like vecuronium.

Our case emphasises the clinical relevance of this interaction. Acetylcholinesterase inhibitors such as neostigmine, which act by increasing acetylcholine at the neuromuscular junction, may fail to reverse such potentiated blockades effectively. In contrast, sugammadex provides a unique mechanism of action by encapsulating steroidal neuromuscular blockers (e.g., vecuronium), rendering them inactive and facilitating rapid reversal independent of acetylcholine dynamics.[5]

Although few reports exist documenting the interaction of HCQ with neuromuscular blockers, chloroquine has been more widely implicated in the prolongation of blockade with both depolarising and non-depolarising agents.[6] A recent pharmacological review underlined the theoretical additive effects of HCQ with non-depolarising neuromuscular blockers, particularly vecuronium.[7]

We suggest that anaesthesiologists maintain a high index of suspicion for delayed recovery in patients on chronic HCQ therapy. In such cases, quantitative TOF monitoring should be employed routinely to assess the depth of blockade and adequacy of reversal. Additionally, consideration of sugammadex as a rescue agent may improve patient safety, especially when conventional reversal proves ineffective.

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