Question 6

College answer

Focus of the question was hyponatraemia due to TURP syndrome, with resulting neurological symptoms and seizure. Marks were weighted towards specific management, those who scored well specified the treatment and targets for sodium correction in addition to general response to a seizure on the ward, and specified indications for intubation and CT brain in this context. Some candidates appeared to misunderstand the pathogeneses of TURP syndrome and discussed glycine toxicity and hyperammonaemia interchangeably within the answer.

Discussion

a) "List three likely causes" sounds a lot like "guess what I'm thinking" but in all fairness the scenario as it has been presented does certainly send the mind into specific tunnels, and a predictable list of options does emerge if you think about it.

• TURP syndrome (obviously)
• Glycine toxicity (which is distinct from TURP syndrome)
• Cerebral oedema (body fluid becomes hypotonic after glycine is metabolised)
• Complications unrelated to TURP
  • Cerebral air embolism
  • Stroke
  • Intracranial haemorrhage
  • Idiosyncratic reaction to anaesthetic agents

TURP syndrome is just the iso-osmolar (or mildly hypo-osmolar) hyponatremia that develops as the result of absorbing a large amount of glycine-rich irrigation fluid. The glycine keeps the body fluids relatively iso-osmolar, so any osmolality measurements that are performed will be close to normal - usual glycine solutions are slightly hypotonic (200 mOsm/kg), so osmolality does drop,  just not as much as one might expect from the drop in the sodium. Yes, the sodium drop can be substantial, and seizures/coma/death may certainly result. As totally distinct from this, glycine toxicity results from metabolism of glycine by oxidative deamination, and can result in a massive excess of ammonia; which is what the examiners are talking about at the end of their comments. Still, glycine toxicity is thought to be a major contributor to the overall morbidity of TURP syndrome, so it is weird for the examiners to assert a separation between these two pathophysiologies.

b), "assessment and management plan, from the time of the tonic-clonic seizure to ICU admission" sounds dangerously like a stem that ends up producing answers with stereotypical motherhood statements about simultaneous assessment and resuscitation, two large bore cannulas, and so on. It does appear that the college wanted some of that generic material in the answer ("general response to a seizure on the ward, and specified indications for intubation and CT brain" were expected). On the basis of these considerations, a competent answer would have probably looked like this:

• Immediate management and assessment
  • Control the airway with basic manoeuvres and establish emergency vascular access
  • Terminate the seizure with IV benzodiazepines
  • Determine the need for intubation:
    • Assess the post-ictal level of consciousness
    • Test airway reflexes (eg. is the patient tolerating airway adjuncts)
  • Collect blood samples to confirm isoosmolar hyponatremia and to measure the osmolar gap
    • Glycine does not affect your anion gap as it is not ionised, and therefore TURP syndrome is one of the causes of an elevated osmolar gap without an elevated anion gap.
  • With the airways secured or assuredly self-protected, transfer to ICU via the CT scanner to exclude important intracranial causes
• Early specific management
  • Correct hyponatremia
    • Initially, consider this "symptomatic hyponatremia" and give hypertonic saline to raise the sodium level by 2-4% over 30 minutes (Spasovski et al, 2014)- eg. 150ml of 3% saline over 20 minutes
    • After this, aim for an increase of no more than 0.5 mmol/hr
    • Total daily increase no greater than 10mmol/day
  • Regular (eg. q4h) sodium measurements to guide this process
• Supportive management
  • Sedation with propofol/midazolam 
  • Diuretics to manage fluid overload
• Investigations to assess other complications
  • Continuous EEG to exclude ongoing seizures
  • Ammonia level, serum calcium and urinary oxalate to exclude glycine toxicity