Transurethral resection of the prostate
Transurethral resection of prostatic tumours require specific consideration for potential electrolyte disturbance throughout the perioperative period. Patients may present for surgery with an obstructive nephropathy, with elevated urea and creatinine, and are at risk of dilutional hyponatraemia, resulting in water intoxication syndrome, both during and following the procedure, due to the absorption of hypotonic 1.5% glycine irrigation fluid.
1 Recognize the post-operative transurethral resection of the prostate (TURP) syndrome
2 Differentiate other causes of post-operative neurological impairment
3 Outline the correct management plan for post-operative hyponatraemia.
2A06; 2A07
A 70 kg, 79-year-old man with benign prostatic hypertrophy has presented for an elective TURP. He was known to have glaucoma, recurrent UTIs, AF, and a mild degree of cognitive impairment. However, he lived alone in the community, with support from his daughter. He had an excellent exercise tolerance and frequently went for long walks. He managed all his activities of daily living. His medications included aspirin, digoxin, tamsulosin, oxybutynin, doxazosin, and timolol.
A preoperative ECG demonstrated AF, with a ventricular rate of 72. Preoperative investigations were as follows:
◆ Hb 134 g/L, WCC 6.5, Plt 232
◆ Na+ 132 mmol/L, K+ 4.5 mmol/L, urea 5.5 mmol/L, Cr 62 micromoles/L.
Induction of anaesthesia occurred with 50 micrograms of fentanyl and 100 mg of propofol. A size 4 LMA was placed correctly. A self-ventilating anaesthetic was maintained with sevoflurane, with 1 g of IV paracetamol, a further 50 micrograms of fentanyl, and 5 mg of morphine as intraoperative analgesia. A single slow bolus of gentamicin 2 mg/kg was given to prevent bacteraemia during instrumentation of the urinary tract.
The urology registrar struggled to resect the hyperplastic tissue and required help from his consultant. Ninety minutes later, the operation finished, and the patient entered the recovery room. A further 30 min later, the recovery nurse informs you that she cannot waken your patient.
1 Pharmacological:
• Opioids: produce sedation and respiratory depression, the intensity of which can be difficult to predict in the elderly
• Volatile anaesthetic agent: emergence from anaesthesia depends on the pulmonary elimination, MAC awake being typically 30% of MAC. Opioid-induced hypoventilation lengthens the time taken to exhale the anaesthetic agent
2 Metabolic:
• Hypoglycaemia: post-operatively most often results from poorly controlled diabetes, starvation, and alcohol consumption
• Hyperglycaemia: blood hyperosmolality and hyperviscosity predispose to cerebral oedema and thrombosis
• Hyponatraemia: <120 mmol/L causes confusion; in this context, the most likely cause would be TURP syndrome
• Hypothermia: confusion at <35°C unconsciousness at <30°C
3 Respiratory failure: resulting in hypoxia, hypercapnia, or both
4 Neurological:
• Intraoperative cerebral insult, secondary to an inadequate cerebral perfusion, due to a low MAP, thrombosis, or intracranial haemorrhage
• Central anticholinergic syndrome, antihistamines, antidepressants, and anti-parkinsonian drugs are common culprits.
◆ ABC: secure the airway, 100% oxygen, manual ventilation
◆ D: assess GCS, capillary blood glucose
◆ E: measure the temperature, and warm if <35.5°C; clinical examination with particular attention to the respiratory and nervous systems (focal or lateralizing neurology)
◆ Investigations:
• ABG: correct hypoxia, hypercapnia, or acidosis
• A point-of-care assessment of Hb values if a co-oximeter measurement is not included in the ABG, e.g. HemoCue® (blood loss is inevitable during TURP and difficult to estimate intraoperatively, due to the large amounts of irrigation fluid used)
• Blood tests: FBC, U&E, osmolality, and glucose.
After a further 15 min, your patient started to regain consciousness but was confused, complaining that he could not see properly. Over the next few minutes, he became increasingly agitated, before slipping into a self-limiting 2-min grand mal seizure. Meanwhile, the blood gas results are available, demonstrating a Na+ of 114 mmol/L (later confirmed on formal bloods).
Severe TURP syndrome.
Secure the airway, and support ventilation, as required, typically with tracheal intubation and PPV. Inotropes or vasopressors should be administered via a central line, as required, to maintain normotension for the patient, with invasive pressure monitoring via arterial access.
Further seizures can be controlled with IV diazepam, in 2 mg increments, up to 10 mg, or repeated once after 15 min. Consider a bolus of 2 g IV magnesium sulfate if seizures are uncontrolled.
You may consider administering a small dose of hypertonic saline (3% NaCl), typically in the dose of 1–1.5 mL/kg, infused over 1 hour.
The patient should be subsequently admitted to intensive care for ongoing therapy.
Most often associated with TURP, a similar phenomenon has been described with other procedures requiring irrigation fluids such as endometrial ablation and ureteroscopy.
The most common irrigation fluid used in the UK is 1.5% glycine which has an osmolality of 220 mOsmol/kg, hypotonic relative to plasma (280–300 mOsmol/kg). Rapid intravascular infusion of this hypotonic fluid can trigger a variety of pathological processes.
1 Intravascular volume shifts:
Absorption rates of irrigation fluid can approach 200 mL/min, leading to a rapid intravascular volume expansion, with consequent hypertension, reflex bradycardia, LV failure, and pulmonary oedema. This may be followed by profound hypotension, as dilutional hyponatraemia and hypertension lead to a net water flux, along osmotic and hydrostatic pressure gradients, out of the intravascular space. Fluid shifts should be anticipated in the patient with TURP syndrome, necessitating invasive monitoring and careful fluid management in a critical care setting post-operatively.
2 Hyponatraemia and plasma osmolality:
Rapid infusion of sodium-free fluid produces hyponatraemia, via an initial dilutional effect, followed by natriuresis. Although undoubtedly hyponatraemia contributes to the pathology of TURP syndrome, current thinking suggests that plasma hypo-osmolality may be the more important factor. The clinical consequences of hyponatraemia are due to water moving from a relatively hypo-osmolar ECF into the hyperosmolar cell interior, cerebral oedema being the most serious complication. The Nernst equation predicts that a decrease in the extracellular Na+ concentration, from 140 to 100 mmol/L, has only a modest effect on membrane excitability, increasing the resting membrane potentials by a modest 9 mV. Therefore, the likely explanation for TURP symptoms, such as headache, altered level of consciousness, nausea and vomiting, seizures, coma, and death, is not the low levels of Na+ per se, but the plasma hypo-osmolality resulting in cerebral oedema. Measuring and correction of plasma osmolality should be a key aspect in the management of TURP syndrome.
In practice, Na+ levels below 120 mmol/L are likely to be associated with low plasma osmolality and severe TURP syndrome, requiring treatment. Infusion of hypertonic saline, commonly 3%, is the conventional treatment used. Regimes vary, but the following has been suggested:
• Calculate total body water (TBW) as 0.6 × body weight (kg), e.g. 70 kg man = 42 L
• 2 × TBW / 1000 as the number of mL of 3% NaCl which will raise serum [Na+] by 1 mmol/L
• For example, 2 × 42 / 1000 = 84 mL of 3% NaCl
• Usually given over 1 hour.
The rate of correction has traditionally been advocated to be no more than 1 mmol/L/hour, to avoid the most feared complication of central pontine myelinolysis (CPM). Most authors suggest stopping hypertonic saline on the resolution of symptoms and not waiting for Na+ levels to be fully corrected.
3 Hyperglycinaemia:
Glycine is a known inhibitory neurotransmitter, present in the midbrain, spinal cord, and retina. These depressant effects on the CNS make hyperglycinaemia the most likely culprit for the visual aberrations described during TURP syndrome. Symptoms can range from blurred vision to complete blindness and will usually resolve within 24 hours as the glycine is metabolized. No specific treatment is required, except for reassurance.
Glycine also potentiates the action of NMDA receptors which can result in paradoxical excitatory symptoms such as seizures. Consideration of magnesium therapy for glycine-induced encephalopathy is a rational approach. In addition to its well-known membrane-stabilizing properties, magnesium exerts a negative action on NMDA receptors, and plasma levels are likely to be low, due to the dilutional effects of the irrigation fluid.
Spinal anaesthesia is regarded as the technique of choice for TURP (2.5–3.0 mL of plain 0.5% bupivacaine), despite a lack of objective evidence demonstrating clear benefit over general anaesthesia. Perceived advantages are good post-operative analgesia, reduced surgical stress response, and, most importantly, the early identification of TURP syndrome. Sedation can be provided with midazolam or propofol, though these drugs could mask the early signs of TURP syndrome. Additionally, the profound sympathetic blockade from a spinal anaesthetic can worsen the cardiovascular consequences of profound fluid shifts.
If a general anaesthetic technique is selected, a single-shot caudal epidural injection with 20–25 mL of 0.375% plain bupivacaine could be considered for post-operative analgesia. A valid criticism of this case would be the failure to consider a regional technique.
Summary
There are several benefits to the use of regional anaesthesia in urological surgery in the elderly patient group. The generic advantages of a central–neuraxial block, including reduction in post-operative respiratory complications, reduced venous thrombosis risk (particularly important in patients with prolonged lithotomy positioning), and reduced blood loss, are boosted by the benefit of the ability to continually monitor central neurological function in patients undergoing TURP, under regional anaesthesia alone.
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