Rocuronium is a non-depolarizing neuromuscular blocker widely used to produce muscle relaxation to help facilitate surgery and ventilation of the lungs in elective and emergent situations. It is one of the many non-depolarizing neuromuscular blockers used but has the distinct advantage of being fast-acting and reversible. The major indications for its use are:

• Provide airway muscle paralysis to facilitate endotracheal intubation in elective as well as emergent conditions
• Provide surgical paralysis to facilitate surgery
• Provide chest wall relaxation to facilitate mechanical ventilation in critically ill patients who are under adequate sedation
• Provide defasciculating dose to prevent fasciculations during depolarizing muscle paralysis to prevent myalgias. (off-label)
• Prevent shivering in patients post cardiac resuscitation after the return of spontaneous circulation during therapeutic hypothermia (off-label)

It is vital to ensure that the patients who receive a muscle relaxant like rocuronium are adequately sedated to prevent the risk of awareness. A patient can be paralyzed but awake and cannot show the motor signs of awareness.

Non-depolarizing neuromuscular blockers work at the site of nicotinic neuromuscular junction by acting on the synapse. A synapse is a specialized area where the prejunctional nerve ending interacts with a highly folded postjunctional part of the skeletal membrane. Both of these pre and post-junctional sites have a higher concentration of acetylcholine (Ach) and nicotinic acetylcholine receptors (nAchR), respectively. Normally when an electrical impulse reaches the prejunctional nerve terminal, calcium influx causes a release of Ach ligands, which then interacts at the nicotinic acetylcholine receptors located at the postjunctional membrane to cause changes in the electrical permeability of the membrane, specifically sodium and potassium. This rapid movement of ions causes a decrease in the transmembrane potential to reach threshold potential leading to the generation of an action potential that travels across the muscle membrane and causes muscular contraction.

Nondepolarizing drugs like rocuronium are quaternary ammonium compounds, which are intermediately acting, highly ionized drugs administered intravenously under controlled conditions by anesthesiologists and other critical care providers after ensuring that the patient is under the effects of anesthesia. The dose of administration can be decided based on the clinical indication versus patient characteristics. Rocuronium does not undergo metabolism into active metabolites and has very limited lipid solubility. Therefore these drugs do not pass the blood-brain barrier, placental barrier, and other lipid membrane barriers. Thus rocuronium has no effects on the central nervous system, effects on the fetus, minimal renal reabsorption as well as ineffective absorption if given orally. Rocuronium is largely excreted unchanged in bile and has around 30 % renal excretion. Factors like hypothermia, hypovolemia, concomitant volatile agents, and renal and hepatic diseases prolong the effects of rocuronium.

Rocuronium is an intermediate-acting nondepolarizing neuromuscular blocker with ED95 of 0.3 mg/kg. At a dosing range of 0.6 to 1.2 mg/kg, intubating conditions can be reached in 1 to 2 min with effects lasting until 20 to 35 min. Higher doses, like 1.0 to 1.2 mg/kg, can be used to provide intubating conditions similar to succinylcholine with a short onset time of approximately 1 minute. However, that comes with a duration of action similar to longer-acting nondepolarizing drugs like pancuronium.

Allergic reactions: Although there have been reports of cardiovascular side effects with the use of non-depolarizing neuromuscular agents like mivacurium and atracurium, rocuronium has been shown to be very cardiac stable and has no effects on heart rate or blood pressure. Rocuronium has been implicated in multiple IgE induced anaphylaxis in the perioperative setting, and one paper cites the incidence of around 1 in 2500 patients.[1] After rocuronium administration, any patient who develops sudden cardiovascular collapse along with cutaneous symptoms of allergic reactions should come under suspicion for anaphylaxis.

Residual neuromuscular weakness: Residual neuromuscular blockade is a condition where the effects of the neuromuscular blocks do not completely reverse. The adverse effects of the residual neuromuscular blockade have been proven beyond doubt to increase postoperative morbidity and mortality[2]. The inability to completely reverse the effects of the neuromuscular blockade can result in increased risks of postoperative respiratory dysfunction, including hypoxia, the need for mechanical ventilation, and increasing the length of hospital stay.[3]

Critical illness myopathy and polyneuropathy: Prolonged infusion of neuromuscular blockers can prolong skeletal muscle weakness due to the myopathy induced by critical illness in a subset of patients on steroids or who have multiple organ failure. It is advised to keep the duration of paralysis to less than 48 hrs to prevent this complication.[4]

The absolute contraindication to using rocuronium would be a documented allergic reaction to the drug. Rocuronium should also not be given to any patient who is not sedated or not under the influence of anesthesia to avoid the risk of awareness. It is advisable not to use rocuronium as an infusion to prevent critical illness myopathy and polyneuropathy. Rocuronium should not be used in patients with renal or hepatic dysfunction as it will prolong its effects by delaying elimination. Although with the use of sugammadex, rocuronium can be used in these clinical situations too with caution.