Can you get paralysis after sugammadex?: A Look at Recurarization and Patient Safety

October 8, 2025 •

4 min read

While sugammadex is highly effective for reversing neuromuscular blockade during surgery, studies confirm that residual neuromuscular paralysis remains a potential complication. This rare phenomenon, known as recurarization, can result in recurrent weakness or paralysis if not managed correctly, directly addressing the question, "Can you get paralysis after sugammadex?".

Quick Summary

It is possible to experience a return of paralysis, known as recurarization, after receiving sugammadex, typically due to insufficient binding or patient-specific factors, emphasizing the importance of precise management.

Key Points

Recurarization Risk: Although rare, paralysis can recur after sugammadex, a phenomenon called recurarization, typically caused by insufficient binding to capture all rocuronium molecules.
Insufficient Binding: Inadequate availability of sugammadex can lead to a supply imbalance, allowing the muscle relaxant to return to the neuromuscular junction and cause paralysis.
Objective Monitoring is Key: Accurate, objective neuromuscular monitoring is crucial to ensure that the reversal is complete before extubation.
Patient-Specific Factors: Conditions like renal impairment, obesity, and neuromuscular diseases (e.g., myasthenia gravis) can increase the risk of residual or recurrent weakness despite sugammadex.
Managing Recurarization: If recurrent paralysis occurs, clinicians may need to provide ventilatory support and readminister a muscle relaxant, often from a different class, to achieve reliable re-paralysis.
Associated Adverse Effects: Sugammadex also carries risks of adverse effects like anaphylaxis and severe bradycardia, though paralysis itself is tied to incomplete reversal.

What is Sugammadex and How Does It Work?

Sugammadex is a selective relaxant-binding agent (SRBA), a unique modified gamma-cyclodextrin molecule designed to reverse the effects of specific muscle relaxants, namely rocuronium and vecuronium. Unlike traditional reversal agents that indirectly affect the neuromuscular junction, sugammadex works by encapsulating and inactivating the muscle relaxant molecules in the bloodstream. This creates a concentration gradient that draws the muscle relaxant molecules from the neuromuscular junction back into the blood, where they are bound by sugammadex and rendered inactive. This process rapidly restores neuromuscular function and muscle strength, allowing the patient to breathe independently after surgery.

The Phenomenon of Recurarization

Despite the advanced and generally reliable action of sugammadex, a small but clinically significant risk exists for a return of neuromuscular blockade, or paralysis, after the initial reversal appears successful. This event, termed recurarization, is often linked to specific circumstances.

Insufficient Binding and Incomplete Reversal

Recurarization most often occurs when there is an insufficient amount of sugammadex available to bind all the muscle relaxant molecules, particularly when reversing deep levels of neuromuscular blockade. The mechanism is based on pharmacodynamics:

Initial Recovery: After sugammadex is administered, free rocuronium molecules are rapidly encapsulated in the blood. This allows muscle strength to recover, and patients may appear ready for extubation.
Redistribution of Rocuronium: Over time, rocuronium molecules can redistribute from peripheral compartments (tissues and fat) back into the central compartment (the bloodstream).
Insufficient Encapsulation: If there are not enough free sugammadex molecules left in the blood to bind with this returning rocuronium, due to factors such as administration of an inadequate amount initially, there is a risk of recurarization.
Recurrence of Paralysis: The unbound rocuronium can then diffuse back to the neuromuscular junction, causing a recurrence of paralysis.

Case reports have highlighted recurarization in obese patients. This underscores the necessity of precise management.

The Importance of Objective Neuromuscular Monitoring

Subjective clinical assessment alone is not sufficient to confirm complete reversal of neuromuscular blockade. Anesthesia guidelines strongly recommend using objective neuromuscular monitoring to confirm a train-of-four (TOF) ratio of 0.9 or greater before extubation. Without this objective measure, even after sugammadex administration, a small percentage of patients may experience residual paralysis upon arriving at the Post Anesthesia Care Unit (PACU). Objective monitoring helps anesthesiologists determine the appropriate approach for the level of blockade and confirm full recovery.

Patient-Specific Risk Factors for Post-Sugammadex Weakness

Certain patient factors can contribute to prolonged or recurrent weakness, even with appropriate sugammadex use:

Renal Impairment: Because the sugammadex-NMBA complex is eliminated primarily by the kidneys, severe renal impairment can delay its clearance, although the complex remains stable. Careful monitoring is required, and its use is not recommended for severe renal failure.
Neuromuscular Disorders: Patients with conditions like myasthenia gravis may be more susceptible to residual weakness and require special attention, including monitoring both peripheral and facial muscles, as recovery can be delayed.
Drug Interactions: In rare instances, other medications like toremifene can displace the NMBA from its binding with sugammadex, potentially leading to recurarization.

Sugammadex vs. Neostigmine: A Comparison

For many years, neostigmine was the standard for reversing neuromuscular blockade. However, sugammadex has several advantages and distinct differences that affect the risk of postoperative paralysis.


Feature	Sugammadex	Neostigmine
Mechanism	Encapsulates NMBA molecules in plasma.	Inhibits acetylcholinesterase, increasing acetylcholine at the neuromuscular junction.
Reversal Speed	Rapid and predictable, even for deep block.	Slower and less predictable, ineffective for deep block.
Side Effects	Rare hypersensitivity/anaphylaxis, bradycardia; no muscarinic effects.	Significant muscarinic side effects (bradycardia, salivation, nausea), requiring co-administration of an anticholinergic.
Safety Margin	A lower incidence of postoperative residual paralysis when used correctly with monitoring.	Higher rates of residual paralysis if not managed appropriately or if monitoring is inadequate.

Adverse Effects Beyond Paralysis

While the primary concern related to paralysis is recurarization, sugammadex is associated with other adverse events that anesthesiologists must consider. These include hypersensitivity reactions, such as anaphylaxis, which can occur within minutes of administration, and marked bradycardia, which in rare cases can lead to cardiac arrest. Though uncommon, clinicians must be prepared for these possibilities, and treatment with anticholinergic agents like atropine may be necessary for bradycardia.

Conclusion

In conclusion, the answer to the question "Can you get paralysis after sugammadex?" is yes, but it is a rare and typically avoidable event. The risk of recurrent or persistent paralysis (recurarization) after sugammadex administration is primarily linked to insufficient binding, especially in deeply blocked or obese patients. It can also be influenced by patient-specific factors such as renal function or pre-existing neuromuscular disorders. Unlike older reversal agents, sugammadex offers a significantly faster and more reliable reversal of neuromuscular blockade, but its safe and effective use relies on careful management guided by objective neuromuscular monitoring. By adhering to these practices, anesthesiologists can minimize the risk of recurarization, ensuring a safer and more predictable recovery for surgical patients. For more detailed information on sugammadex and its use in clinical practice, consult authoritative sources such as the National Institutes of Health.

Frequently Asked Questions

Recurarization is a rare but serious event where neuromuscular blockade (paralysis) returns after a successful initial reversal with sugammadex. It typically occurs when there is an insufficient amount of sugammadex to permanently bind all the muscle relaxant molecules.

The risk is minimized through precise, appropriate management of sugammadex based on the depth of neuromuscular blockade. Anesthesiologists use objective neuromuscular monitoring to ensure the reversal is complete and the patient is fully recovered before extubation.

Yes. Patients with severe renal impairment may have delayed clearance of the sugammadex-muscle relaxant complex, and those with neuromuscular disorders like myasthenia gravis may have an altered response to reversal agents.

Sugammadex works by directly encapsulating and inactivating muscle relaxants, offering a faster and more predictable reversal, especially for deep block. Neostigmine indirectly works by increasing acetylcholine and is slower, less effective for deep block, and has more side effects.

Anaphylaxis is a severe allergic reaction to sugammadex and is a separate adverse event from recurrent paralysis. While it can cause respiratory distress, it is a hypersensitivity reaction rather than a failure of the reversal mechanism.

If recurarization occurs, the patient will need re-ventilation. A clinician may administer a further amount of sugammadex (if appropriate) or use a different type of muscle relaxant to ensure continuous paralysis.

No, sugammadex is a selective binding agent and only works effectively for aminosteroidal, non-depolarizing NMBAs, primarily rocuronium and vecuronium. It does not reverse the effects of non-steroidal NMBAs like succinylcholine.