FRCA Notes

TURP Syndrome

The curriculum is fairly explicit here, asking us to describe 'the anaesthetic management of common surgical procedures and their complications...including the TURP syndrome'.

A CRQ from March 2021 was on TURP (80% pass rate) and although TURP syndrome isn't explicitly mentioned in the feedback, I'd hazard it formed part of the question.

Resources

  • TURP syndrome is an iatrogenic complication of urological surgery due to absorbance of the fluid used to distend and irrigate the bladder
  • It has an incidence of 1-8%, and has also been reported after endometrial ablation or ureteroscopic procedure
  • Can occur within 15mins of start of surgery or up to 24hrs post-operatively

  • It arises due to changes in:
    • Intravascular volume
    • Plasma sodium concentration
    • Plasma osmolality

  • Overall mortality is low (0.2 - 0.8%) but severe cases can have a mortality of up to 25%

The Ideal Irrigating Fluid
Transparent
Non-electrically conductive
Isotonic
Non-haemolytic
Non-toxic
Sterile (or easy to sterilise)
Cheap
  • Examples include:
    • 1.5% glycine (osmolality 220mOsm/kg i.e. hypo-osmolar)
    • 3.5% sorbitol
    • 5% mannitol

Fluid Absorption

  • Typically 10-30ml/min of fluid absorbed, although this is dependent on several factors:
Factor increasing absorption Notes
↑ hydrostatic pressure Ideally <70cm height
↓ venous pressure Maintain normovolaemia
Prolonged duration of surgery Ideally <1hr
Large blood loss Increases with ↑ prostate size
Capsule or bladder perforation (≤10%) Leakage of irrigating fluid into peritoneal cavity


Cardiovascular

  • Fluid can be rapidly absorbed, leading to an increased preload and therefore systolic & diastolic blood pressures
    • This leads to a reflex bradycardia
    • In due course there is circulatory overload and cardiac failure

  • Eventually cardiac contractility fails at the tail end of the Starling curve, causing hypotension
    • This is exacerbated by fluid egress into the interstitial space following dilution of serum proteins and a fall in oncotic pressure
    • This leads to pulmonary oedema, and cerebral oedema

  • I.e. low cardiac output is eventually due to poor contractility and relative hypovolaemia

Hypo-osmolality and hyponatraemia

  • Hypo-osmolality is more important in the disturbance of membrane and fluid function than hyponatraemia per se
    • Acute hypo-osmolality causes free water absorption in the brain parenchyma, leading to nausea and agitation from cerebral oedema
    • Although initial symptoms may be mild, it can eventually lead to seizures and coma

  • Mechanisms of hyponatraemia:
    1. Firstly there is absorption of large volumes of hypo-osmolar fluid, causing a dilutional drop in serum sodium levels
    2. Secondly, sodium is lost into either irrigation fluid which gets drained or into the fluid accumulating in the retroperitoneal/peri-prostatic spaces
    3. Lastly, glycine stimulates supra-normal ANP release causing excessive natriuresis

  • As [Na+] falls to below 120mmol/L, cardiac signs start to manifest
    • Myocardial contractility is impaired further, exacerbating hypotension and bradycardia from fluid overload
    • ECG changes occur e.g. broadened QRS
    • Eventually cardiac arrest will ensue, particularly if [Na+] is <100mmol/L

Glycine

  • Glycine is an inhibitory neurotransmitter with a terminal half-life of 45mins - 3hrs
  • It is metabolised by oxidative deamination to glyoxylic acid and ammonia by the liver & kidneys
  • TURP syndrome typically occurs when glycine concentration is >60mmol/L
  • Leads to nausea, headache, weakness and visual disturbances

  • Glycine itself causes cardiac myocyte oedema, depressed myocardial contractility and ischaemic ECG changes, further exacerbating cardiac failure
  • It also enhances NMDA pathway activity, adding to the encephalopathy and eventual seizures of TURP syndrome
    • Ammonia from glycine metabolism exacerbates the encephalopathy
  • It causes retinal toxicity, leading to transient blindness

Cardiovascular

  • Bradycardia
  • Initial hypertension with wide pulse pressure and raised CVP
  • Subsequent hypotension as the cardiovascular system is pushed along the Starling curve into cardiac failure
  • Angina
  • ECG changes: broadened QRS, ST elevation, U-waves
  • Cardiovascular collapse and VF/VT

Neurological

  • Mild symptoms such as apprehension, disorientation, restlessness, confusion
  • Nausea and vomiting from hyponatraemia and cerebral oedema
  • Visual disturbance; transient blindness is a feature of glycine toxicity
  • Seizures and coma

Other

  • Respiratory distress from pulmonary oedema
  • Abdominal pain

TURP syndrome is an anaesthetic emergency and I would seek senior anaesthetic support as well as making a rapid but thorough assessment of the patient

Immediate management

  • Stop surgery and fluids (irrigation and IV)
  • Apply 100% oxygen
  • Call for senior help
  • ABCDE approach:
  1. Maintain airway, may require I&V

  2. Apply 100% oxygen

  3. Treat bradycardia (glycopyrrolate) and hypotension (vasopressors, adrenaline)

  4. Treat seizures with anticonvulsants (e.g. IV lorazepam 4mg) and IV magnesium (Mg2+ inhibits glycine-induced potentiation of NMDA receptor activity)

  5. Can use diuretics e.g. furosemide 40mg to treat hypervolaemia/pulmonary oedema although may cause worsening of hyponatraemia, mannitol causes less hyponatraemia
    • Severe hyponatraemia (<120mmol/L) or severe symptoms can be treated by increasing intravascular fluid tonicity to reduce cerebral oedema
    • E.g. hypertonic saline (2.7%), 8.4% NaHCO3 or haemofiltration (in patients with CKD in whom large fluid volumes wish to be avoided)
    • Aim to increase Na+ by 0.5 - 1mmol/L/hr for the first 24hrs to reduce risk of worsening oedema/central pontine myelinolysis

Subsequent management

  • HDU/ICU as may need invasive monitoring to monitor fluid shifts, frequent blood sampling
  • Document in patient's notes
  • Duty of candour - explain events to patient
  • Critical incident form