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Unresponsive postoperative patient
  1. Keng Lam,
  2. Navdeep Sangha
  1. Department of Neurology, Kaiser Permanente LAMC, Los Angeles, California, USA
  1. Correspondence to Dr Keng Lam, Kaiser Permanente LAMC, Los Angeles, CA 90027, USA; keng.lam{at}kp.org

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Case presentation

A 53-year-old man was admitted to hospital for elective repair of a descending aortic dissection and type B intramural haematoma. He had a history of stage 3 chronic kidney disease and took aspirin for paroxysmal atrial fibrillation. At 07:00 on the morning of the operation he was awake, alert and moving all limbs. His surgery began at 09:10. He received various anaesthetic medications, including rocuronium 50 mg (0.5 mg/kg); last dose at 17:20. The surgical repair ended at 16:15, and left the operating theatre at around 20:00 after an uneventful surgery.

At midnight, he was still unresponsive despite receiving naloxone. His observations were: temperature 37°C, blood pressure 158/100 mmHg, heart rate 80/min, intubated and breathing at set respiratory rate 14/min, and oxygen saturation 100% on pressor support of 8 cmH2O, tidal volume 580 mL (8 mL/kg of his ideal body weight), FiO2 45%, and positive end-expiratory pressure of 5 cmH2O. He was not on sedation. His pupils were constricted and non-reactive to light. He had no spontaneous eye movements, even with the oculocephalic reflex. His gag reflex was absent. He did not withdraw any limb to painful stimuli. We could not elicit any deep tendon reflexes.

Serum urea and electrolytes and plasma glucose were normal. Emergency CT scan of the head showed no new findings (figure 1) and CT angiogram of the head and neck was normal.

Clinical questions

  1. What diagnoses should be considered?

  2. Would you consider trials of any medication?

Answers

The severe generalised weakness including loss of all eye movements suggested a peripheral neuromuscular weakness. Since this followed a general anaesthetic with neuromuscular blockade, the most likely explanation was a delayed recovery from this agent. The main differential diagnosis is a pontine ischaemic event (the classical cause of locked-in syndrome) where upgaze and blink are preserved, although the normal imaging is against this.

We gave sugammadex 400 mg (4 mg/kg), a neuromuscular blockade reversal agent of rocuronium, and within minutes his motor function improved. On re-examination, he was orientated to self and place, and moved all limbs. He stated that he had been awake since leaving the operating theatre and recalled everything, including the CT scan, but had been paralysed and unable to respond. Figure 2 outlines the timeline.

Non-depolarising neuromuscular blockers are competitive acetylcholine antagonists that bind to the alpha subunits of nicotinic receptors on the postsynaptic membrane. This prevents depolarisation at the neuromuscular endplate and causes muscular paralysis. Examples may include rocuronium and vecuronium, which are often used to facilitate endotracheal intubations and adjuvant sedation.1 Delayed paralysis is possible and can be difficult to diagnose despite the patient being conscious.2 The incidence of residual paralysis after emergence from anaesthesia is unclear, as the reported frequencies vary widely.3 When a patient does not respond to stimuli after surgery, neurologists are often called urgently to assess the patient.

However, the effect of neuromuscular blocking agents such as vecuronium and rocuronium rarely lasts for hours unless there is significant liver and/or kidney dysfunction. The mean clinical duration of rocuronium is usually less than 60 min; it is primarily eliminated via the liver and has no metabolite.4 One report described vecuronium’s effect lasting for 8 hours, despite no identified precipitating risk factors.5 An important differential diagnosis of coma is the locked-in syndrome, caused by a midbrain stroke, with retained vertical eye movements and blinking.6

In this patient, the effect of rocuronium lasted for at least 8 hours, and he did not recover until receiving a reversal agent. Risk factors for prolonged effect can include certain medications, autoimmune disorders, neuromuscular conditions and electrolyte abnormalities.1 7 This patient was not cooled during surgery, had no acidosis and no history of neuromuscular or autoimmune disease; we, therefore, found no explanation for this prolonged recovery. This unusual case illustrates the importance of considering the diagnosis of iatrogenic neuromuscular blockade in postoperative weakness.

Further reading

  • Non-depolarizing Neuromuscular Blocker published in May 2020 on StatPearls by Derek T. Clar and Mark Liu.

  • Kim YB, Sung TY, Yang HS. Factors that affect the onset of action of non-depolarizing neuromuscular blocking agents. Korean J Anesthesiol. 2017;70:500–51. doi: 10.4097/kjae.2017.70.5.500.

Key points

  • Neuromuscular blockade may lead to complete motor paralysis, giving an apparently comatose state.

  • Some patients have a significantly longer clinical duration of neuromuscular blockade without obvious risk factors.

  • Consider iatrogenic neuromuscular blockade as the cause of prolonged unresponsiveness after surgery, and a trial of a reversal agent.

Ethics statements

Patient consent for publication

References

Footnotes

  • Contributors KL wrote the manuscript. NS revised the manuscript. KL prepared and submitted the final version of the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed by Jon Walters, Swansea, UK.

Linked Articles

  • Editors’ commentary
    Phil E M Smith Geraint N Fuller

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