Sugammadex selectively binds rocuronium and vecuronium (collectively known as the aminosteroid neuromuscular blocking agents). It causes a swift, reliable fall in their free plasma concentration and a corresponding end to their paralytic effect.
When it came out in 2008, it cost an astounding one dollar per milligram. Its steep price precluded its use in all but the most critical situations.
Prices have come down but a dose of sugammadex is still much more expensive than conventional reversal. So what should persuade an anaesthetist to spend the extra cash when conventional agents might just do the trick?
Some Good Reasons 👌
Deep Block
Conventional reversal is unable to overcome deep paralysis and, when given too early, wears off before the underlying NMBA is cleared. Residual blockade and re-paralysis are under-recognised causes of post-operative badness.
How deep is too deep? The answer lies in the train of four. In the beginning, sugammadex was reserved for urgent reversal of a TOF count ≤ 1. The most recent guidelines from The American Society of Anaesthetists are far more liberal…
TOF Count | TOF Ratio | Reversal |
---|---|---|
0 | 🚫 | Sugammadex 4 mg/kg |
1 | ||
2 | ||
3 | ||
4 | ≤ 0.4 | Sugammadex 2 mg/kg |
> 0.4 | Conventional |
Swift, Complete Reversal
Conventional reversal takes about ten minutes to work properly and doesn’t always achieve a satisfactory TOF count. There are many situations where immediate and unequivocal reversal is desired, for example…
- Severe neurological disease (e.g. myasthenia gravis) where a complete restoration of diaphragmatic tone is required for adequate ventilation
- Morbidly obese patients who must be able to protect their airway immediately after extubation
- A failed rapid-sequence intubation (maybe)1
Anticholinesterase Side-Effects
The anticholinesterase component of conventional reversal causes some unwanted side-effects that might be very poorly tolerated, for example…
- Bronchospasm
- Bradycardia, junctional escape rhythms, and complete heart block
- Patients with rate-dependent output will not tolerate these
- Hypotension
- Postoperative nausea and vomiting
- Increased gut motility
These effects are usually attenuated by simultaneous administration of an anti-muscarinic (glycopyrrolate or atropine), but not always.
Failure of Conventional Reversal
Conventional reversal has a ceiling effect. Once you have given 70mcg/kg of neostigmine and 20mcg/kg of atropine, there is no benefit to giving more.
Times Are Changing 🍁
Sugammadex continues to get cheaper and recent uptick in registration of generic alternatives only promises to accelerate that trend. This is great news.
Don’t go dancing on the grave of neostigmine just yet, though. The necessity of non-aminosteroid NMBAs (e.g. cisatracurium) means that conventional reversal is unlikely to disappear completely from the modern anaesthetist’s repertoire.
The sugammadex dose for reversal of a just-administered NMBA is a whopping 16 mg/kg, but using it at all is controversial. The patient will still be apnoeic because of the induction agent (for which there is no reversal) and removing the paralysis only stands to make further attempts at intubation more difficult. ↩