The neuromuscular effects of 0.6 mg kg−1 rocuronium in elderly and young adults with or without renal failure*

We describe our experience of a 71-year-old patient with severe renal failure, who exhibited an unusually prolonged rocuronium-induced neuromuscular blockade (>4 h) and apparent recurarisation, following emergency rapid sequence induction (RSI). At the end of operation, 45 min post induction, train-of-four (TOF) testing had been 4/4 prior to wake up. No respiratory effort was seen 150 min postinduction, despite further neostigmine/glycopyrrolate and repeat TOF 4/4. The patient was resedated and transferred to the intensive care unit (ICU). At 180 min postinduction, fade was evident on TOF, suggestive of rocuronium reblockade. At 285 min, the patient was extubated safely following sugammadex administration and discharged uneventfully from the ICU. An important lesson to recognise is the potential for extremely prolonged neuromuscular blockade following rocuronium in patients with severe renal failure, particularly when using the higher doses (1.2 mg/kg) required for RSI, and that TOF in such cases may not be reliable in detecting residual blockade.

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“…Similar cases have been seen in the literature, where even smaller doses of rocuronium (0.6 mg/kg) resulted in NMB of over 10 h 91012…”

Section: Discussionsupporting

confidence: 86%

Sugammadex rescue following prolonged rocuronium neuromuscular blockade with ‘recurarisation’ in a patient with severe renal failure

2013

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“…Rocuronium is not dependent on renal blood flow for its major route of excretion, but is taken up by the liver and excreted into the bile in high concentrations [9]. Although hepatic uptake and biliary elimination are thought to be the main routes of elimination for rocuronium, it seems that renal failure can have a marked effect on rocuronium pharmacokinetics and pharmacodynamics, although not consistently so [16][17][18]. In patients with no or minimum renal function, the clinical duration and recovery time of rocuronium 0.6 mg/kg increased significantly [16][17][18].…”

Section: Discussionmentioning

confidence: 99%

Reversal of rocuronium-induced neuromuscular block by sugammadex is independent of renal perfusion in anesthetized cats

et al. 2011

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“…Another study showed that about 10% of the IV dose of rocuronium was excreted in urine [17,19]. Kocabas et al [20] reported that the clearance of rocuronium was reduced by 39% in patients suffering from renal failure compared with controls, with 84% increase in the mean residence time, whereas the volume of distribution was unaffected by renal failure. Therefore, the duration of action of rocuronium can be expected to be prolonged, as it undergoes organ-dependent elimination [20].…”

Section: Discussionmentioning

confidence: 99%

“…Kocabas et al [20] reported that the clearance of rocuronium was reduced by 39% in patients suffering from renal failure compared with controls, with 84% increase in the mean residence time, whereas the volume of distribution was unaffected by renal failure. Therefore, the duration of action of rocuronium can be expected to be prolonged, as it undergoes organ-dependent elimination [20]. Proost et al [3] demonstrated that rocuronium is taken up by the liver and excreted into the bile in very high concentration [3].…”

Section: Discussionmentioning

confidence: 99%

Effect of ulinastatin on the rocuronium-induced neuromuscular blockade

Kim

Park

Lim

et al. 2012

Korean J Anesthesiol

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BackgroundUlinastatin is a glycoprotein derived from human urine and a serine protease inhibitor found in human urine and blood. Ulinastatin increases both liver blood flow and urine output. Rocuronium is eliminated mainly through the liver and partly through the kidney, hepatic elimination of rocuronium might be enhanced by ulinastatin. We examined the effect of ulinastatin on the neuromuscular block caused by rocuronium.MethodsForty four adult patients were randomly divided into two groups of 22 patients each, i.e. the study group and the control group. In the study group, a bolus dose of ulinastatin 5,000 U/kg was administered 2 min before the injection of rocuronium 0.6 mg/kg. In the control group, normal saline was administered instead of ulinastatin. For the monitoring of both onset and recovery from neuromuscular blockade, train-of-four (TOF) and post-tetanic count were used with TOF-Watch Sx. All patients underwent general anesthesia with total intravenous anesthesia (TIVA) of remifentanil and propofol, using the effect site target infusion system.ResultsIn the study group, the onset of neuromuscular block was significantly slower than in the control group (P < 0.05). The recovery time from the rocuronium injection to the return of PTC was also significantly shorter in the study group than in the control group (P < 0.05). Similarly, times to the return of T1, T2, T3, and T4 (i.e. the first, second, third, and fourth response of TOF) were significantly shorter in the study group than in the control group (P < 0.05).ConclusionsUlinastatin significantly delays the onset of neuromuscular block and accelerates the recovery from the block caused by rocuronium.

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The neuromuscular effects of 0.6 mg kg−1 rocuronium in elderly and young adults with or without renal failure*

Abstract: The neuromuscular effects of 0.6 mg kg(-1) rocuronium under propofol anaesthesia were markedly prolonged in young and elderly renal failure patients compared to patients with normal renal function, and also in elderly patients with normal renal function compared with young adults.

Cited by 29 publications

References 28 publications

Sugammadex rescue following prolonged rocuronium neuromuscular blockade with ‘recurarisation’ in a patient with severe renal failure

Sugammadex rescue following prolonged rocuronium neuromuscular blockade with ‘recurarisation’ in a patient with severe renal failure

Reversal of rocuronium-induced neuromuscular block by sugammadex is independent of renal perfusion in anesthetized cats

Effect of ulinastatin on the rocuronium-induced neuromuscular blockade

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