Rocuronium

Clinical use & dosing (adult)

Intubation (routine): 0.6 mg/kg IV
- Typical onset ~60–90 s; duration ~30–40 min (dose-dependent)
Rapid sequence induction (RSI): 1.0–1.2 mg/kg IV
- Onset often comparable to suxamethonium; duration longer (often 60–90 min)
Maintenance bolus: 0.1–0.2 mg/kg IV; or infusion ~5–12 micrograms/kg/min (titrate to monitoring)
- Aim for 1–2 twitches (TOF) intra-op; ensure full reversal/TOF ratio ≥0.9 before extubation
Paediatrics: similar mg/kg dosing; onset may be faster in infants/children; always titrate to monitoring

Reversal strategy (practical)

Neostigmine + glycopyrrolate: for shallow/moderate block with evidence of recovery (e.g., TOF count ≥2 and improving)
- Typical neostigmine 40–50 micrograms/kg with glycopyrrolate 10 micrograms/kg (local practice varies)
- Ceiling effect: ineffective for profound block; requires some spontaneous recovery
Sugammadex: specific binding reversal for aminosteroids (rocuronium > vecuronium)
- 2 mg/kg for moderate block (TOF count 2); 4 mg/kg for deep block (PTC 1–2); 16 mg/kg for immediate rescue (e.g., cannot intubate/cannot ventilate soon after RSI dose)
- Recurarisation risk if under-dosed; always confirm recovery with quantitative monitoring

When to choose rocuronium

Alternative to suxamethonium for RSI when sux is contraindicated (e.g., hyperkalaemia risk, MH susceptibility, pseudocholinesterase deficiency, raised IOP/ICP considerations depending on context)
When predictable reversal with sugammadex is desirable (short cases, high aspiration risk, difficult airway planning)

Class, structure, presentation

Aminosteroid non-depolarising neuromuscular blocker; quaternary ammonium compound → poor oral absorption; does not cross BBB/placenta significantly
Usually supplied as aqueous solution (commonly 10 mg/mL); store per local guidance; check compatibility (avoid mixing with alkaline solutions in same line)

Mechanism of action (NMJ pharmacology)

Competitive antagonism at post-junctional nicotinic ACh receptors (Nm) → prevents depolarisation and muscle contraction
- Block is surmountable by increasing ACh (anticholinesterases) once some recovery has occurred
Produces fade on TOF/tetanus due to presynaptic effects reducing ACh mobilisation (feature of non-depolarising block)

Pharmacokinetics

Onset: relatively rapid for a non-depolariser (dose-dependent); faster with larger dose (RSI dosing)
Distribution: hydrophilic; Vd approximates extracellular fluid; high protein binding is not a dominant feature clinically
Elimination: predominantly hepatic uptake and biliary excretion; some renal excretion
- Prolonged duration in hepatic impairment and cholestasis; may be prolonged in renal failure (less than some agents but clinically relevant)
Metabolism: minimal; active metabolites are not a major clinical issue (contrast with vecuronium)

Pharmacodynamics & clinical effects

Produces skeletal muscle paralysis including respiratory muscles; no analgesia, amnesia or sedation
Cardiovascular: generally stable; minimal histamine release; mild vagolytic effect may cause small ↑HR in some patients
Histamine release: low compared with atracurium/mivacurium; anaphylaxis remains possible

Factors altering effect (exam-friendly list)

Potentiation: volatile agents, aminoglycosides, magnesium, lithium, local anaesthetics (high dose), hypothermia, acidosis (variable), hypokalaemia, hypocalcaemia
Resistance/shorter duration: chronic anticonvulsants (enzyme induction), burns (after ~24–48 h), denervation/upper motor neuron lesions (upregulation of ACh receptors), hyperkalaemia (variable clinical relevance)
Organ dysfunction: hepatic dysfunction/cholestasis prolongs; renal failure may prolong; critical illness can cause unpredictable sensitivity/resistance

Monitoring

Use peripheral nerve stimulator; prefer quantitative monitoring (acceleromyography/EMG) to confirm TOF ratio ≥0.9
Deep block assessment: post-tetanic count (PTC) when TOF = 0

Adverse effects & safety

Residual neuromuscular blockade → hypoventilation, airway obstruction, aspiration risk; common if no quantitative monitoring and/or inadequate reversal
Anaphylaxis: rocuronium is among the more commonly implicated NMBDs; cross-reactivity can occur due to quaternary ammonium epitopes
Injection site pain/withdrawal movement can occur (notably with rapid bolus in awake/semi-awake patients)

Comparisons (high-yield)

Vs suxamethonium: rocuronium has slower onset at standard dose but RSI dose approaches sux onset; duration much longer; can be rapidly reversed with sugammadex
Vs atracurium/cisatracurium: rocuronium relies on hepatic/biliary elimination (not Hofmann); less histamine; useful when avoidance of histamine desired but caution in hepatic dysfunction
Vs vecuronium: rocuronium faster onset; vecuronium has active metabolite (3-desacetyl) which can accumulate in renal failure; both reversed by sugammadex

Describe rocuronium: class, mechanism, onset and duration.

Structure your answer: classification → NMJ mechanism → time course → key determinants (dose, co-administered agents, physiology).

Class: aminosteroid non-depolarising neuromuscular blocker
Mechanism: competitive antagonism at post-junctional nicotinic (Nm) receptors → prevents ACh-mediated depolarisation; causes fade on TOF/tetanus
Onset: relatively rapid; ~60–90 s after 0.6 mg/kg; faster with 1.0–1.2 mg/kg (RSI dosing)
Duration: dose-dependent; ~30–40 min after 0.6 mg/kg; often 60–90 min after RSI dose

How would you perform RSI with rocuronium and what are the implications for rescue reversal?

Examiners want: correct dose, expected onset, longer paralysis than sux, and a clear plan for failed intubation including sugammadex dosing and limitations.

Dose for RSI: 1.0–1.2 mg/kg IV (with appropriate induction agent and cricoid/RSI technique per local policy)
Implication: paralysis lasts much longer than sux → if airway difficulty occurs, cannot rely on spontaneous recovery within minutes
Rescue reversal: sugammadex 16 mg/kg for immediate reversal soon after large-dose rocuronium (e.g., cannot intubate/cannot ventilate scenario)
- Still must follow difficult airway algorithm; reversal is not a substitute for oxygenation/ventilation
Post-reversal: confirm recovery with quantitative monitoring; plan for re-paralysis if surgery must proceed (consider non-steroidal NMBD such as cisatracurium if sugammadex used, depending on timing and dose)

Outline the pharmacokinetics of rocuronium and how organ failure affects it.

Hit: distribution (hydrophilic), elimination (hepatic/biliary), and the clinical consequence (prolongation).

Hydrophilic quaternary ammonium compound → limited CNS/placental transfer; Vd approximates extracellular fluid
Elimination predominantly hepatic uptake and biliary excretion; some renal excretion
Hepatic impairment/cholestasis: prolonged duration and slower recovery; increased variability
Renal failure: may prolong effect (less reliance than some drugs but clinically relevant); use monitoring and consider alternative agents (e.g., cisatracurium) if prolonged paralysis undesirable

How do volatile anaesthetics and magnesium affect rocuronium block? Explain the mechanism and clinical implications.

This is a common FRCA physiology–pharmacology crossover: potentiation and monitoring/reversal implications.

Volatile agents potentiate non-depolarising block (greater depth and duration for a given dose), especially with longer exposure
Magnesium potentiates block by reducing presynaptic ACh release and decreasing postsynaptic excitability
Clinical implications: reduce maintenance dosing, use neuromuscular monitoring, anticipate delayed recovery and need for reversal

Discuss reversal of rocuronium with neostigmine versus sugammadex (indications, dosing, limitations).

Examiners look for: depth of block matters; neostigmine ceiling; sugammadex dose by TOF/PTC; monitoring and recurarisation risk.

Neostigmine: indirect reversal by increasing ACh; effective only when some spontaneous recovery present (e.g., TOF count ≥2); ceiling effect
Sugammadex: encapsulates free rocuronium in plasma → rapid reduction in free concentration → drug diffuses away from NMJ
Sugammadex dosing: 2 mg/kg (TOF count 2), 4 mg/kg (deep block PTC 1–2), 16 mg/kg (immediate rescue after RSI dose)
Limitations: under-dosing risks recurarisation; confirm TOF ratio ≥0.9; consider cost and availability; be aware of rare anaphylaxis to sugammadex

A patient has prolonged paralysis after rocuronium. Give a differential diagnosis and management plan.

A classic FRCA viva: think drug, patient, physiology, interactions, and monitoring error; then manage airway/ventilation and reverse appropriately.

Confirm: ensure adequate ventilation/sedation; check quantitative TOF; exclude equipment/monitoring error and wrong drug/dose
Drug factors: large dose/infusion, accumulation; potentiation by volatiles, magnesium, aminoglycosides; recent local anaesthetic toxicity/high dose
Patient factors: hypothermia, electrolyte disturbance (low K/Ca), acid–base disturbance; hepatic dysfunction/cholestasis; renal failure; critical illness/ICU weakness
Management: correct physiology (warm, correct electrolytes), stop potentiating drugs where possible; consider reversal (sugammadex if rocuronium and significant block; neostigmine only if partial recovery); continue ventilatory support until TOF ratio ≥0.9 and clinically strong

Discuss anaphylaxis to rocuronium: recognition, immediate management, and implications for future anaesthesia.

Common exam scenario: NMBDs are a leading cause of perioperative anaphylaxis; rocuronium is frequently implicated.

Recognition: sudden hypotension, bronchospasm, difficulty ventilating, rash/urticaria (may be absent), angioedema; consider differential (haemorrhage, high spinal, embolus)
Immediate management: call for help; stop suspected trigger; 100% O2; airway/ventilation; adrenaline titrated IV for severe reactions; large-volume IV fluids; adjuncts (antihistamine, steroid, bronchodilator) after adrenaline
Investigations: timed mast cell tryptase samples (per local protocol) and documentation of all drugs/exposures
Future: referral to specialist allergy clinic for testing; avoid culprit and consider cross-reactivity among NMBDs; provide patient information and anaesthetic alert

Compare rocuronium with atracurium/cisatracurium in a patient with severe liver disease.

This tests elimination pathways and choice of agent in organ failure.

Rocuronium: predominantly hepatic uptake/biliary excretion → prolonged and variable effect in liver disease/cholestasis
Atracurium/cisatracurium: organ-independent elimination (Hofmann ± ester hydrolysis) → more predictable in hepatic failure
Practical: if rocuronium used, reduce dose, avoid long infusions, monitor quantitatively, and plan reversal (sugammadex available) but still expect variability

Explain train-of-four fade with non-depolarising block and how you would use TOF/PTC to guide dosing and reversal for rocuronium.

A frequent FRCA viva theme: link physiology to clinical monitoring decisions.

Fade: non-depolarising agents reduce safety margin at NMJ and impair presynaptic ACh mobilisation → successive stimuli produce diminishing responses
Intra-op: titrate boluses/infusion to desired depth (often TOF 1–2); avoid unnecessary deep block unless specifically required
Deep block: if TOF=0, use PTC to estimate depth and guide sugammadex dosing (e.g., PTC 1–2 suggests deep block → 4 mg/kg)
Extubation: confirm TOF ratio ≥0.9 on quantitative monitor; clinical tests alone are insufficient