the metablog

Posts tagged Sugammadex.

Sugammadex and rocuronium anaphylaxis

I have been intrigued since the first case reports appeared describing the use of sugammadex in rocuronium anaphylaxis. It sounds beautiful and elegant. A drug that magically mops up the offending molecule, removing it from circulation; quickly reversing the cardiovascular collapse as rapidly as it reverses muscle relaxation.

The little we know

  1. There have been case reports from 5 countries showing dramatic improvement of rocuronium-confirmed anaphylaxis after administration of sugammadex.
  2. One case study showed a dose-dependent effect of sugammadex on modifying anaphylaxis.
  3. There are not yet any published cases of rocuronium anaphylaxis where sugammadex was administered without clinical improvement (though beware).
  4. Sugammadex although incompletely encapsulating rocuronium, does prevent the rocuronium epitope from binding IgE.
  5. Cutaneous and in vitro models of hypersensitivity have shown no or limited ability of sugammadex to modify type 1 hypersensitivty after triggering.
  6. Our understanding of the pathophysiology of anaphylaxis is over-simplified and incomplete.

Unfortunately the truth is not quite as clear. Case reports showing impressive recovery of rocuronium anaphylaxis minutes after giving sugammadex are tempered by in vitro and in vivoimmunological studies suggesting an inability of sugammadex to modify a type 1 hypersensitivity reaction. The reality is likely somewhere in between, highlighting our limited understanding of anaphylaxis and our tendency to rush to over-simplified models of disease processes.

The story so far...

Jones and Turkstra first raised the possibility of using sugammadex to treat rocuronium anaphylaxis in 2010.1 One year later Nolan McDonnell and team published the first case report of a remarkable use of sugammadex to manage rocuronium anaphylaxis.2 McDonnell described a 33 year old having an elective diagnostic laparoscopy suffering anaphylaxis to rocuronium. After 19 min of conventional resuscitation, involving CPR, 3500 mL of intravenous fluids and 4 mg of epinephrine/adrenaline - 500 mg of sugammadex was given with remarkable effect:

"A dose of 500 mg (6.5 mg kg21) was given while chest compressions were in progress. The last dose of epinephrine had been given 4 min previously. Approximately 45 s after administration and while chest compressions were in progress, the patient suddenly opened her eyes and reached for her tracheal tube.

Read more...


  1. Jones PM, Turkstra TP. Mitigation of rocuronium-induced anaphylaxis by sugammadex: the great unknown. Anaesthesia. 2010 Jan;65(1):89-90; author reply 90. 

  2. McDonnell NJ, Pavy TJ, Green LK, Platt PR. Sugammadex in the management of rocuronium-induced anaphylaxis. Br J Anaesth. 2011 Feb;106(2):199-201. 

Sugammadex, suxamethonium and the rapid sequence induction

Does sugammadex mean the end of suxamethonium for rapid sequence induction?

The answer: No, not by a long shot. Let me explain...

Suxamethonium (succinylcholine) is a depolarising muscle relaxant and often the first choice for muscle paralysis when a rapid sequence induction (RSI)1 is needed. In addition to working quickly suxamethonium has a very rapid offset. For both anaesthetist and patient these are very desirable characteristics, although they come at a price. The price is suxamethonium's long list of side effects, ranging from minor to life threatening.2 Were it not for it's life-saving fast-kinetics, suxamethonium's use in modern anaesthesia would no longer be justifiable.

This article is part two in a three part series beginning with 'If sugammadex is the answer, what is the question?'.

Enter rocuronium

When rocuronium was first introduced in the 1990s it was met with excitement.3 Rocuronium's claim to fame was a very fast onset of action. Because it was less potent than other non-depolarising muscle relaxants of its generation (atracurium & vecuronium) a larger dose was required to achieve the same level of muscle paralysis. This dose created a large concentration gradient between plasma and the neuromuscular junction resulting in a faster onset of action. By giving a very large dose of rocuronium the anaesthetist could produce acceptable intubating conditions within 60 seconds, creation the first reliable modified rapid sequence induction.

Unfortunately the result of using such a large dose of rocuronium is a prolonged blockade. Even at lower doses (0.6 mg/kg 2x ED95) rocuronium produces a block that lasts at least five times longer than suxamethonium. At the 1.2 mg/kg (4x ED95) modified-RSI-dose of rocuronium the block duration stretches out even longer, reaching the duration of pancuronium. In the event of being unable to intubate, or worse unable to ventilate, prolonged blockade is disastrous. At this point rocuronium only provided half a solution for the replacement of suxamethonium.

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  1. The rapid sequence induction, as the name suggests, involves very fast induction of general anaesthesia with rapid intubation of the trachea in order to protect the airway quickly, often in emergency situations. 

  2. Most significantly, anaphylaxis, hyperkalaemia and malignant hyperthermia, and also including suxamethonium apnoea and various cardiac arrythmias. Not to mention the 'minor' side effect of feeling run over by a truck after recovering from a suxamethonium paralysis. Suxamethonium adverse effects - wikipedia 

  3. Hunter JM. Rocuronium: the newest aminosteroid neuromuscular blocking drug. Br J Anaesth. 1996 Apr;76(4):481-3. 

If sugammadex is the answer what is the question?

Sugammadex (Bridion®) is a remarkable drug. It also has a cool name. The anaesthesia community has moved very quickly to embrace the potential of this first and only 'selective relaxant binding agent' (SRBA), despite it's considerable cost.

"Sugammadex is likely the most exciting drug in clinical neuromuscular pharmacology since the introduction of atracurium and vecuronium in the middle 1980s." - Miller RD 1

Novel pharmacology and a cool name are however insufficient reasons alone to alter our practice. There is a certain lack of clarity in the community and literature as to where sugammadex fits into anaesthesia practice and to what extent it should alter how we currently manage muscle relaxation and reversal. There has also been very limited discussion of the unintended consequences of a shift to rocuronium-sugammadex based techniques over other neuromuscular drugs.

There is no doubt that sugammadex offers a new and improved way of reversing aminosteroid muscle relaxation, in particular that from rocuronium.  The speed at which it reverses even profound neuromuscular blockade is incredible and potentially life saving. Sugammadex‘s onset is 10 times faster than neostigmine and three times faster than edrophonium.2

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  1. Miller RD. Sugammadex: an opportunity to change the practice of anesthesiology? Anesth Analg. 2007 Mar;104(3):477-8. 

  2. Sacan O, White PF, Tufanogullari B, Klein K. Sugammadex reversal of rocuronium-induced neuromuscular blockade: a comparison with neostigmine-glycopyrrolate and edrophonium-atropine. Anesth Analg. 2007 Mar;104(3):569-74. 

Neuromuscular myths: We need to do better

The rise of sugammadex has lead me down a path looking into wider aspects of my own neuromuscular blocking drug (NMBD) use. The evidence for NMBD use, monitoring and reversal is interesting, both for how consistently the same messages have been repeated over the past three decades – and for how little we have improved our practice in spite of mounting evidence demanding that we should.1

I need to do better and you probably also need to do better with how we manage NMBDs.

What is PORC?

Post-operative residual curarisation (PORC) or residual paralysis, refers to persisting neuromuscular blockade in a patient after extubation. It is considered present when the Train-of-four (TOF) ratio is less than 0.9, usually measured in recovery or the post anesthesia care unit (PACU).

The historical comparison of studies investigating PORC is difficult because for many years a TOF ratio of 0.7 was considered the cutoff value for PORC. Volunteers given d-tubocurarine had normal vital capacity and inspiratory force when the TOFR recovered above 0.7. Then in the mid-1990s a TOF ratio of 0.8 was used in studies investigating PORC.

Now in the 21st century a TOFR 0.9 is considered the cut-off for defining PORC. A TOFR 0.9 has been chosen because consequences of residual paralysis, such as pharyngeal dysfunction and impairment of respiratory function have been shown below this TOF ratio.

Read more...


  1. Case in point: Donati F. Neuromuscular monitoring: what evidence do we need to be convinced? Anesth Analg. 2010 Jul;111(1):6-8. (pubmed

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