TURP syndrome

Reviewed and revised 16 May 2016


  • Transurethral resection of the prostate (TURP) syndrome is fluid overload and iso-osmolar hyponatraemia during TURP from large volumes of irrigation fluid being absorbed through venous sinuses
  • Irrigation fluid is required to maintain visibility despite bleeding tissue beds
  • TUPR syndrome can also occur in other procedures requiring large volumes of irrigation, such as hysteroscopy
  • True TURP syndrome is now rare, particularly as glycine-based irrigation fluids are less commonly used


No such thing exists (of course), but it would have these features:

  • transparent (for good visibility)
  • electrically non-conductive (to prevent dispersion of the diathermy current)
  • isotonic
  • non-toxic
  • non-haemolytic when absorbed
  • easy to sterilize
  • inexpensive


Glycine 1.5% in H2O is used as the irrigation fluid

  • hyposomolar at 220mmol/L
  • non-conductive, non-haemolytic and has a neutral visual density

Patients usually absorb around 20mL/min, average absorption during a case is ~ 1.5L and depends on:

  • pressure of infusion (keep bag at <60cm height)
  • venous pressure
  • exposed vascular bed
  • duration of irrigation

Mechanism of clinical manifestations

  • symptoms primarily arise from the effects of glycine, which acts as an inhibitory CNS neurotransmitter at GABA receptors and paradoxically potentiates NMDA receptors
  •  Increased plasma ammonia may also contribute
  • not (usually) from increased brain water!
  • glycine also has cardiodepressant effects and may have renal toxicity

Other irrigation fluids

  • In the past, other irrigation fluids (e.g. mannitol, sorbitol and glucose) have been used that lack the specific toxic effects of glycine
  • More recently, the increased use of bipolar resectoscopes has enabled the use of electrolyte-containing crystalloid solutions that lack glycine toxicity but may contribute to hyponatraemia.



  • it may occur within 15 minutes or be delayed for up to 24 hours post-operatively
  • typically lasts hours, but neurological manifestations may be prolonged if complications arise

Early features

  • mild cases may go unrecognised
  • restlessness, headache, and tachypnoea, or a burning sensation in the face and hands

Features of greater severity

  • respiratory distress, hypoxia, pulmonary oedema
  • nausea, vomiting
  • visual disturbance (e.g. blindness, fixed pupils)
  • confusion, convulsions, and coma
  • haemolysis
  • acute renal failure
  • reflex bradycardia from fluid absorption

Symptoms may be masked by general anaesthesia and severe cases may present with dysrhythmias and cardiovascular collapse


  • surgical time > 1 hr
  • height of bag > 70cm
  • resected > 60g
  • large blood loss
  • perforation of the bladder (leads to rapid absorption from the peritoneal cavity)
  • large amount of fluid used
  • poorly controlled CHF



  • hyponatraemia (dilutional effect of a large volume of absorbed irrigation fluid, but later due to natriuresis)
  • iso-osmolar (or mildly hypo-osmolar)
  • increased osmolar gap from absorbed glycine
  • hyperglycinaemia (up to 20 mM; normal is 0.15-0.3mmol/L)
  • hyperserinaemia (major metabolite of glycine)
  • hyperammonaemia (due to deamination of glycine and serine)
  • hyperoxaluria and hypocalcaemia (glycine is metabolised to glycoxylic acid and oxalic acid, the latter forms calclium oxalate crystals in the urinary tracts and may contribute to renal failure)
  • metabolic acidosis
  • haemodilution and haemolysis



  • Attend to ABCs and address life threats:
    • O2 +/- intubation (or airway protection) and ventilation
    • invasive monitoring

Specific Treatment

  • fluid overload: frusemide 40mg IV
  • seizures: benzodiazepines +/- other anti-epileptics; consider magnesium (stabilises NMDA receptors)
  • hyponatraemia:
    • hypertonic saline is only indicated for neurological manifestations if measured serum osmolality is < 260 mOsmol/kg
    • aim to raise Na+ by no more than 10-12 mmol/24 hours)
    • a rapid increase in plasma sodium is not concerning (this often happens with glycine metabolism), unless there is a sudden change in osmolality (measured osmolality usually changes little as the hyponatremia resolves)
  • severe cases may require renal replacement therapy
  • treat acute pulmonary oedema and dysrhythmias as required
  • treat hypocalcaemia

Treat underlying cause

  • stop surgery as soon as possible
  • coagulate bleeding points
  • stop IV fluid
  • monitor Hb


  • admission to HDU/ ICU (features may worsen due to ongoing absorption of irrigation fluid)


  • In some centres, ethanol 1% was added to the irrigation solution and the patient’s breath  tested for ethanol every few minutes: a positive test indicates a significant quantity of fluid has been absorbed.

References and Links

Journal articles

  • Beal JL, Freysz M, Berthelon G, D’Athis P, Briet S, Wilkening M. Consequences of fluid absorption during transurethral resection of the prostate using distilled water or glycine 1.5 per cent. Canadian journal of anaesthesia. 36(3 Pt 1):278-82. 1989. [pubmed]
  • Gravenstein D. Transurethral resection of the prostate (TURP) syndrome: a review of the pathophysiology and management. Anesth Analg. 1997 Feb;84(2):438-46. PMID: 9024044.
  • Hamilton Stewart PA, Barlow IM. Metabolic effects of prostatectomy. Journal of the Royal Society of Medicine. 82(12):725-8. 1989. [pubmed]
  • Hahn RG. Serum amino acid patterns and toxicity symptoms following the absorption of irrigant containing glycine in transurethral prostatic surgery. Acta anaesthesiologica Scandinavica. 32(6):493-501. 1988. [pubmed]
  • O’Donnell AM, Foo IT. Anaesthesia for transurethral resection of the prostate. Contin Educ Anaesth Crit Care Pain. 9(3):92-96. 2009. [article]
  • Rhymer JC, Bell TJ, Perry KC, Ward JP. Hyponatraemia following transurethral resection of the prostate. British journal of urology. 57(4):450-2. 1985. [pubmed]
  • Trépanier CA, Lessard MR, Brochu J, Turcotte G. Another feature of TURP syndrome: hyperglycaemia and lactic acidosis caused by massive absorption of sorbitol. Br J Anaesth. 2001 Aug;87(2):316-9. PMID: 11493513.

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Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

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