The relevance of hyponatraemia to perioperative care of surgical patients

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Review

The relevance of hyponatraemia to perioperative care of surgical patients Martı´n Cuesta, Christopher Thompson* Academic Department of Endocrinology, Beaumont Hospital/RCSI Medical School, Dublin, Ireland

article info

abstract

Article history:

Background: Hyponatraemia is the most common electrolyte disturbance in hospitalized

Received 12 June 2014

patients. There is an increasing awareness of the impact of hyponatraemia on the peri-

Received in revised form

operative management of surgical patients.

16 September 2014

Methods: We performed a literature review. We have included relevant data from different

Accepted 22 September 2014

surgical disciplines for analysis. In this review we discuss the differential diagnosis of

Available online 15 December 2014

hyponatraemia, and explain the specific relevance of hyponatraemia to pre-, peri- and post-operative care.

Keywords:

Results: Hyponatraemia is common during the preoperative period and is associated with

Hyponatraemia

an increase in subsequent peri-operative complications, such as wound infection, pneu-

Perioperative care

monia, higher mortality rate and higher direct and indirect costs. Furthermore, data shows poorer surgical outcomes when plasma sodium concentration drops. Careful preoperative evaluation of the hyponatraemic patient enables assessment of surgical risk and individualization of the management of hyponatraemia. Conclusions: We outline a practical guide to the assessment of the cause of hyponatraemia, which dictates the correct management of hyponatraemia and the correct selection of perioperative fluids. Finally, for the therapeutic role of the new vasopressin antagonist drugs in the treatment of surgical hyponatraemia is discussed in two illustrative surgical clinical cases. © 2014 Royal College of Surgeons of Edinburgh (Scottish charity number SC005317) and Royal College of Surgeons in Ireland. Published by Elsevier Ltd. All rights reserved.

Introduction Hyponatraemia is usually defined as a serum sodium level below-135 mmol/l and it is the most common electrolyte disturbance found in clinical practice.1 The prevalence of hyponatraemia at the time of hospital admission varies

between 2 and 5%, but in some series, up to 30% of in patients have been reported to be affected.2 In comparison with patients with normal serum sodium levels, patients who develop hyponatraemia have been reported to have an increase in mortality rate,3e5 longer duration of hospital stay,4,6 higher readmission rate and increased direct and indirect costs associated with their care.6

* Corresponding author. Beaumont Private Clinic, Beaumont Hospital, Dublin 9, Ireland. Tel.: þ353 1 8376532; fax: þ353 1 8376501. E-mail address: [email protected] (C. Thompson). http://dx.doi.org/10.1016/j.surge.2014.09.005 1479-666X/© 2014 Royal College of Surgeons of Edinburgh (Scottish charity number SC005317) and Royal College of Surgeons in Ireland. Published by Elsevier Ltd. All rights reserved.

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Although hyponatraemia has traditionally been viewed as a condition relevant to internal medicine, and managed principally by endocrinologists, nephrologists and geriatricians, there is an increasing evidence base which documents the relevance of hyponatraemia to the perioperative management of surgical patients. Firstly, hyponatraemia is common in the peri-operative period. In a recent observational study of over a million patients undergoing major surgery, 7.8% of patients presented with preoperative hyponatraemia. Hyponatraemia in this large cohort was particularly common in patients undergoing cardiac surgery (11.8%), perhaps because of the high rate of diuretic therapy in cardiac patients. However, hyponatraemia was also common in patients presenting for vascular surgery (11.2%), with lower rates in patients admitted for general surgical procedures (7.5%), orthopaedic operations (7.1%), and other (6.1%) procedures. Patients with hyponatraemia tended to be older, male and with higher rates of comorbid conditions; hyponatraemia was also commoner in patients admitted for urgent surgery. The authors concluded that hyponatraemia was associated with increased morbidity, including increased risk of coronary events, pneumonia and wound infection, and higher mortality and prolonged length of stay.7 It was not clear whether the increased morbidity was related to the hyponatraemia per se, or whether hyponatraemia was simply a marker for patients with complex co-morbidities which predisposed them to worse outcomes. The results of this study have been reproduced in other small surgical studies and subgroup analyses,4,8 which emphasizes the risk of perioperative complications associated with preoperative hyponatraemia. Hyponatraemia is also common in a variety of neurosurgical conditions such as traumatic brain injury (20%), subarachnoid haemorrhage (50%) and transsphenoidal hypophysectomy (10%).9 There is also evidence that patients admitted to surgical-ICUs are at high risk of developing hyponatraemia, with higher prevalence rates following organ transplantation, cardiovascular procedures and surgery for trauma or gastroenterological conditions.10 The second issue with hyponatraemia is the poorer outcome when plasma sodium concentration drops perioperatively. Studies in surgical patients entering intensive care units have demonstrated a clear association of worse surgical outcomes, including excess mortality, with postoperative hyponatraemia.11 Furthermore, symptomatic

hyponatraemia predisposes the patient to gait instability,12 frequent falls12 and increased fracture rate,13 complications which compromise post-operative rehabilitation, particularly in the elderly. Preoperative evaluation and appropriate management of hyponatraemia offers the opportunity to improve perioperative care,14 to assess surgical risk and to individualize the treatment including type and amount of fluids used for each patient.15 For these reasons, hyponatraemia is relevant to surgical patients, and therefore to surgeons. In this review we will discuss the differential diagnosis of hyponatraemia, and explain the specific relevance of hyponatraemia to pre-, periand post-operative care.

Differential diagnosis of hyponatraemia There are a large number of different syndromes which may lead to the development of hyponatraemia. The treatment of hyponatraemia depends on the underlying aetiology so it is of paramount importance to be accurate in diagnosing the cause of the biochemical abnormality; inaccurate diagnosis leads to inappropriate and potentially damaging treatment. There are a number of clinical algorithms available to aid the approach to the patient with hyponatraemia, some of which give simple guidelines, whereas others are valuable for more complex conditions. A simple, easy to use algorithm is shown in Table 1. The first clinical step is to make an estimate of blood volume, in order to classify the patient as hypovolaemic, euvolaemic or hypervolaemic. It is usually straightforward by basic clinical examination to identify a patient who is hypervolaemic, or fluid overloaded. However, it can be more difficult to differentiate between euvolaemia and mild hypovolaemia. Nevertheless, using a combination of clinical and biochemical parameters, an experienced clinician can be accurate in assessing blood volume in hyponatraemic patients. The next step is to classify hyponatraemia on the basis of urine sodium concentration. Low urine sodium concentrations indicate appropriate renal sodium conservation, usually due to secondary hyperaldosteronism, and are nearly always indicative of hypovolaemia; elevated urine sodium usually indicate SIADH, or renal sodium losses. In the postoperatively setting, it is important to remember that potent pathophysiological stimuli for the release of ADH, such as

Table 1 e Differential diagnosis of aetiology of hyponatraemia based on the accurate assessment of the patient’s volume status and measurement of urinary [Naþ]. Urine [Naþ]>30 mmol/L

Treatment

Hypovolaemia (Dry tongue, decreased BP, increased pulse, decreased CVP, increased urea, orthostatism) Euvolaemia

Vomiting, diarrhoea, burns, skin losses

Urine [Naþ]<30 mmol/L

Diuretics, salt-losing nephropathy, Addison's, cerebral salt wasting syndrome

IV saline þ Treat underlying cause

Hypothyroidism Any cause and hypotonic fluids

Fluid restriction Vaptan therapy

Hypervolaemia (Oedema, ascites, increased JVP and CVP)

Congestive cardiac failure, Chirrosis, Nephrotic Syndrome

SIADH Glucocorticoid deficiency Drugs Renal failure, any cause with diuretics use

BP ¼ blood pressure; CVP ¼ central venous pressure; JVP ¼ jugular venous pressure.

Diuretic therapy

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pain, gastrointestinal distension or nausea, may contribute to the development of euvolemic hyponatraemia.16 Surgical patients who present with vomiting may be hypovolaemic at presentation; if the vomiting is the cause of the hyponatraemia, urine sodium should be low, due to secondary hyperaldosteronism, which leads to renal tubular sodium reabsorption, in order to conserve body sodium. In contrast, patients on diuretics will present with elevated urine sodium concentrations as the kidneys are the site of sodium losses. An audit of hospital in patients in our own institution showed that 40% of elderly patients (>70 years) on thiazide diuretics have evidence of volume depletion secondary to the diuretic therapy (unpublished observations). Euvolaemic hyponatraemia is the commonest cause of hyponatraemia in hospitalized patients, and SIADH is the commonest cause of euvolaemic hyponatraemia. The diagnostic criteria for SIADH include serum hypo-osmolality (<275 mOsm/kg), inappropriately concentrated urine (>100 mOsm/kg) and urine sodium >30 mmol/l. Patients must be euvolemic with normal thyroid function, pituitary ACTH secretion and kidney function.17 SIADH may occur secondary to diseases of the central nervous system, pulmonary disorders, medication, tumours and miscellaneous causes, including the postoperative state.18 The exclusion of ACTH/ cortisol deficiency is of particular importance in neurosurgical patients. Patients with pituitary tumours who are admitted for surgery and who have biochemical and clinical evidence of euvolaemic hyponatraemia may have pre-operative hypopituitarism, with subsequent low plasma cortisol concentrations. Proper pre-operative assessment is needed to identify cortisol deficiency, which should be adequately replaced prior to surgery in order to optimize surgical stress responses. It is equally important to identify hypothyroid patients prior to surgery as patients with low serum thyroxine concentrations are unable to metabolize anaesthetic agents; in the absence of appropriate thyroxine replacement, anaesthesia may produce prolonged unconsciousness, requiring avoidable postoperative ventilator support. Hypervolaemic hyponatraemia is rare pre-operatively, though it may be seen in patients presenting for cardiothoracic surgery when in a state of cardiac decompensation. In contrast, in the post-operative period, hypervolaemic hyponatraemia may be a manifestation of excess intravenous fluid replacement, particularly if hypotonic fluids have been used. It must be highlighted that old people with high co morbidity rate, especially in those who are taking multiple drugs, some cases of hyponatraemia might not be easy to classify. In this population hyponatraemia from multifactorial origin needs to be taken into account and involving the endocrine or medical team should be considered.

Symptoms and morbidity associated with hyponatraemia Although symptoms are related to the severity of hyponatraemia, itself, the rapidity of the fall in plasma sodium concentration is far more important in determining the likelihood of neurological symptoms Chronic hyponatraemia, which is seen in many elderly patients, may have relatively few

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symptoms, as the brain adapts to hyponatraemia over time. In contrast, acute hyponatraemia, occurring over <48 h, is much more likely to develop neurological symptoms, due to osmotic movement of water from the hypotonic plasma to the hypertonic brain, producing cerebral swelling and intracranial hypertension.19,20 Symptoms of cerebral irritation include headaches, nausea, decreased level of consciousness, confusion and blurred vision. Patients may progress to toniceclonic seizures, and, in severe cases, pulmonary hypercapnic failure, with or without pulmonary oedema. Death may develop from transtentorial herniation of the brainstem.20 The risk factors for this scenario include young females, children, associated hypoxia or previous central nervous system disease, and, importantly to this review, the post-operative period.21 Although chronic hyponatraemia is associated with less in the way of neurological sequelae, recent data has shown that it is associated with increased vulnerability to falls, gait disturbances,12 fractures,13 osteoporosis22 and cognitive dysfunction.23 As the frequency of hyponatraemia increases with age, surgical procedures performed in elderly patients, such as repair of osteoporotic hip fractures or prostatic surgery are particularly likely to present or to develop hyponatraemia during hospital admission, with implications for safe post-operative rehabilitation. A wide variety of malignant conditions which may require surgical intervention are associated with hyponatraemia, predominantly secondary to the inappropriate secretion of ADH (SIADH).24 Lung cancer, haemopoietic malignancy, urological tumours and head and neck tumours are particularly likely to cause SIADH, and any intracranial lesion may produce SIADH. Hyponatraemia and SIADH have been associated with an increase in morbidity and mortality among patients with different kinds of cancer,25 which may present to a variety of branches of surgery.

Hyponatraemia in the preoperative evaluation Plasma sodium concentrations between 130 and 135 mmol/l are unlikely to be associated with serious perioperative sequelae, unless they are a mild biochemical manifestation of a more serious problem such as undiagnosed hypopituitarism. However, lower plasma sodium concentrations (<130 mmol/l) should prompt clinical questions regarding the safe management of the patient around surgery. 1. Is the patient symptomatic? If the patient has symptoms of cerebral irritation, such as diminished conscious level, drowsiness etc, anaesthesia is likely to enhance the development of serious neurological sequelae such as seizures. If the operation can be deferred until hyponatraemia has been treated to restore plasma sodium concentrations to normal, this option should be exercised. Successful surgical outcome will be enhanced by pretreatment of symptomatic hyponatraemia. 2. Will surgery worsen hyponatraemia? Some operations, particularly TURP, are associated with hyponatraemia; Transurethral Resection of the Prostate (TURP) Syndrome is a rare but life-threatening condition. Many centers routinely use large volumes of glycine or sorbitol-

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containing intra-cavitary irrigating solutions; these fluids can be absorbed into the prostatic venous sinuses while the bladder is irrigated during the surgery.26 Acute hyponatraemia may develop as a result, leading to raised intracranial pressure. The expansion of intravascular volume can cause hypertension and tachycardia, and in patients with impaired left ventricular function, congestive heart failure can arise. Finally, the decrease in oncotic pressure can lead to pulmonary and worsen cerebral oedema. Acute severe hyponatraemia has been reported to cause neurological disability and even death in TURP syndrome.27 Preoperative hyponatraemia increases the vulnerability to this syndrome; we have used vasopressin antagonist drugs to reverse hyponatraemia prior to TURP, with safe surgery, avoidance of the TURP syndrome, and minimal anaesthetic risk (case 1). A similar scenario has been reported in other procedures, such as hysteroscopy28 or colonoscopic screening. Concern in the use of oral sodium phosphate and polyethylene glycol for bowel preparation has been raised. The prevalence of hyponatraemia following polyethylene glycol has been recently established in a clinical trial where 3.9% of patients developed hyponatraemia.29 Although the need for hospitalization in this situation is thought to be small, several serious adverse events with seizures and coma have been reported.30 Patients preparing for colonoscopy are generally told to increase the amount of oral fluids prior to colonoscopy and the stomach or bowel distension is likely to produce non-osmotic ADH release predisposing to severe hyponatraemia. In addition, the stress of surgery or the injection of carbon dioxide during laparoscopy into the abdomen might contribute to ADH release. As a result, acute life-threatening hyponatraemia can arise and the use of 3% hypertonic intravenously is vigorously needed. 3. Should the patient's drugs be changed? Many drugs can produce SIADH (Table 2,31), and some of them might be suspended before surgery, if drug-induced hyponatraemia is suspected. As an example, a patient with mild hyponatraemia who is treated with SSRIs may have the drugs suspended perioperatively, if the psychiatrist feels the clinical risk is acceptable. Thiazide diuretics are widely used in the treatment of hypertension, and commonly

cause hypovolaemic and euvolaemic hyponatraemia.32,33 Patients treated with diuretics before surgeries are at high risk of dehydration and hypovolaemia, particularly if there is significant intra-operative blood loss. Generally a cardiological review will be needed to take the decision to discontinue diuretics. 4. Is the patient hypovolaemic? Low effective intravascular volume as a result of prolonged fasting or acute bleeding is a potent stimulus for neurohormonal changes, with activation of renin-angiotensin-aldosterone axis, corticotrophin stress axis and release of ADH. The potent release of ADH in this situation worsens hyponatraemia especially if low osmolality intravenous fluids are concomitantly used. Intravenous isotonic fluids should be used to replace blood volume prior to surgery where possible. 5. Is the patient on pre-operative steroids? If a patient is on corticosteroid therapy, whether as replacement therapy for pituitary or adrenal disease, or as immunosuppression for rheumatoid arthritis, polymyalgia rheumatica, or following organ transplantation, hyponatraemia may indicate incipient adrenal crisis. This is particularly likely if the patient has been unable to continue oral steroids because of vomiting, or if the patient has not doubled his/ her steroid, as part of the “sick day rules”. All patients on long term steroid therapy need intravenous hydrocortisone to cover any surgical intervention, from benign procedures like endoscopy, to cardiothoracic operations. However, if patients are hyponatraemic, hypotensive and have been vomiting prior to presentation, they will need emergency high dose intravenous hydrocortisone to resuscitate them, and endocrine review prior to surgery, where possible. 6. What is the optimum peri-operative intravenous fluid? This should always be discussed pre-operatively with the anaesthetist, who should be appraised of the presence of hyponatraemia. Hypotonic fluids such as dextrose should be avoided and isotonic saline is almost always the infusion fluid of choice. The surgical interns will need to organise regular post-operative electrolyte measurements and liaise with the physician on-call team, or the endocrine unit. We believe that in difficult cases, discussion with the local hospital hyponatraemia expert should be encouraged.

Table 2 e Drugs producing hyponatraemia as side effect commonly used in clinical practice.

Postoperative management

SSRI Tricyclic antidepressants Antipsychotic drugs Carbamazepine Oxycarbazepine Valproate Chlorpropamide Cyclophosphamide Narcotics ACE inhibitors Ciprofloxacin Ethionamide Omeprazole Thiazides Amiodarone AVP analogues

Post-operative hyponatraemia is common and the pathophysiology is often multifactorial and complex. Surgery is associated with non-osmotic release of the anti-diuretic hormone, vasopressin, and in conjunction with intravenous hypotonic fluid administration or excess isotonic fluids, this can cause dilutional hyponatraemia. Potent non-osmotic stimuli, like positive pressure ventilation, stress, nausea and vomiting, hypoglycemia, fever, or a decrease in intravascular volume are commonly found in postoperative period and may increase the tendency for plasma sodium concentration to fall. A study performed by Chung and colleagues, showed a prevalence of 4.4% of hyponatraemia (<130 mmol/L) during the first post-operative week in different surgical units. Plasma

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vasopressin concentrations were detectable in all patients in whom it was measured; most of them (>90%) were receiving hypotonic fluids.10 Fluid overload is one of the main factors that must be taken into account in postoperative period and hypotonic saline infusion and dextrose infusion should be used with great caution. It should also be noted, that in those patients with hyponatraemia secondary to ADH release postoperatively who have high urine osmolality (>600 mOsm/ kg), intravenous isotonic (0.9%) sodium chloride infusion can worsen hyponatraemia. Hyponatraemia is so commonly observed in neurosurgical units that post-operative management needs particular discussion. Between 10 and 50% of patients, depending on the underlying condition, may develop hyponatraemia; postoperative hyponatraemia occurs in 10% of patients undergoing hypophysectomy for pituitary adenomas,9 50% of patients admitted with subarachnoid haemorrhage (SAH) and 20% of patients with traumatic brain injury.34,35 Patients admitted for pituitary surgery may present with hyponatraemia prior to surgery due to glucocorticoid deficiency, and it is mandatory therefore that a thorough preoperative endocrine assessment should occur. Intravenous hydrocortisone during surgery prevents hyponatraemia due to steroid deficiency, but injudicious intravenous fluids and SIADH still cause plasma sodium concentration to fall in 10% of cases.9 Traumatic brain injury causes hyponatraemia in 20% of cases,36,37 with almost all resolving spontaneously on long term follow up.38,39 Almost all cases are due to SIADH but a significant proportion of these cases have inappropriately low plasma cortisol concentrations; in these patients, hyponatraemia resolves with hydrocortisone therapy.39 Other causes of hyponatraemia, such as cerebral salt wasting are rarely seen. Subarachnoid hemorrhage (SAH) is associated with hyponatraemia in 50% of cases.40,41 Because hypovolaemia is believed to predispose to cerebral vasospasm established practice is to aggressively manage SAH patients with vigorous intravenous fluids, though there is little evidence to indicate that this is either necessary or effective.42 A retrospective study of over 300 patients recovering from SAH, showed that 57% developed mild hyponatraemia (<135 mmol/l), with 20% of them being moderate to severe hyponatraemia (<130 mmol/l). Over 60% had features most typical of SIADH. In this cohort of patients, those developing hyponatraemia had a double the length of hospital stay than those who maintained normal plasma sodium levels.40 A subsequent prospective study showed that over 80% of cases of hyponatraemia were due to SIADH, and 10% of these cases had acute ACTH/cortisol deficiency.41 Although other groups have suggested that cerebral salt wasting is the main cause of hyponatraemia in following SIADH43 this paper found no evidence of this condition in 50 patients with hyponatraemia, studied prospectively with sequential hormonal measurements. Cerebral salt wasting does occur, but we believe it is a rare condition, which is frequently erroneously diagnosed. As hyponatraemia following subarachnoid haemorrhage is multifactorial, good clinical examination and a keen awareness of the likely differential diagnosis are necessary to accurately identify the underlying mechanisms and institute appropriate therapy. As SIADH is the commonest cause of

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hyponatraemia associated with SAH, so fluid restriction of 1200 ml/day,34 would be considered first line therapy, though most neurosurgical units will not permit this because of concerns about cerebral vasospasm. Acute symptomatic hyponatraemia can be treated with hypertonic (3%) saline, either by intravenous infusion, or by bolus intravenous doses, as recommended by recent guidelines.44 As anterior hypopituitarism, with cortisol deficiency, can occur after SAH35,41 plasma cortisol concentrations should be checked and intravenous hydrocortisone started if plasma cortisol concentrations are below 300 nmol/l.41 There have been uncontrolled, retrospective reports of the successful use of urea therapy in the treatment of SIADH following SAH, but urea is not licensed for use in the treatment of hyponatraemia and there is no readily available preparation of the compound.45 In situations where a patient has been drowsy and hyponatraemic following SAH, we have used tolvaptan, the vasopressin receptor antagonist, to elevate plasma sodium concentration, and distinguish whether altered conscious levels were due to hyponatraemia or neurosurgical complications (case 2) and this seems an extremely useful situation in which to use this new class of drugs. However, the use of vaptans in patients with SAH needs to be individualized and always discussed with the neurosurgeon in charge of the patient. The final decision will be determined in each case depending on the presence or absence of vasospasm and the severity of hyponatraemia. It is critically important to avoid hypovolaemia in this situation, so an accurate clinical and biochemical assessment needs to be performed before prescribing vaptans in patients with SAH. In other words, SIADH must be accurately diagnosed in this situation before prescribing this new group of treatment. Although the correct treatment of hyponatraemia might improve surgical outcomes, it is of paramount importance to prevent from exceeding natraemia correction. If hyponatraemia is corrected too fast, the brain ability to capture extracellular organic osmolytes is exceeded and osmotic demyelination syndrome (ODS), a terrible and potentially disabling complication might occur.46 This is a complication from the rapid correction of natraemia, and not from this electrolyte disturbance itself. There is a classic clinical biphasic pattern in ODS, with an initial neurological improvement following correction of hyponatraemia whereas some days later, usually 2e6 days after natraemia correction, new progressive and potentially permanent neurological damage can arise. This terrible complication can be diagnosed with magnetic resonance image several weeks after the onset of symptoms. The risk of ODS is very low for patients with a duration of less than 24 h with hyponatraemia, and for those with hyponatraemia whose nadir sodium is >120e125 mmol/l. If other coexisting risk factors for ODS such as malnutrition, alcoholism, liver disease or concomitant hypokalemia are present, ODS might be at higher risk to happen. For this reason, in this population the natraemia should be carefully monitored every 4e6 h and if overcorrection occurs, involvement of the endocrinology or medical team on call should be done. In this high risk population for ODS, natraemia correction should not exceed 6e8 mmol/l in any 24 h period.44 Different factors associated with natraemia overcorrection reported in literature are the treatment of hypovolaemic

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hyponatraemia with normal saline infusion, the use of thiazides, administration of glucocorticoids in central adrenal insufficiency, the treatment of transitory SIADH causes (such as nausea in postoperative period) and discontinuation of drugs that cause SIADH. All these situations reverse the excessive secretion of ADH in the hypothalamus and subsequently an increase in water excretion is found in the kidneys correcting hyponatraemia. If natraemia correction is exceeded, the use of subcutaneous or intravenous Desmopressin and intravenous dextrose infusion to prevent from ODS is usually needed.47 If ODS is documented or suspected, decreasing natraemia and producing plasma hyposmolality is recommended as this has been shown in animal models and isolated human clinical reports to diminish the permanent neurological damage.48 Finally, hyponatraemia may impair patient rehabilitation and full recovery. Decreased cognitive function, gait instability and falls may prevent full integration with physiotherapy and post-operative rehabilitation. As a result, hospital stay is longer in hyponatraemic patients,9 and hospitalization costs are higher in this population.6 Patients with hyponatraemia are also more likely to be discharged to a short or long term care facility after hospitalization.49 In addition, a study of 295 patients with cancer, in an acute rehabilitation centre, found that 41% were hyponatraemic, and that those with a plasma sodium less than 130 mmol/l were admitted for a longer length of stay than those with normal plasma sodium levels.50 Whether correction of hyponatraemia in patients attending rehabilitation will shorten length of stay needs further investigation.

Summary Hyponatraemia has been underestimated as a cause of morbidity and mortality in surgical patients. We believe that improved surgical outcomes will arise from appropriate perioperative management of hyponatraemia, though there is a paucity of intervention data to confirm this statistically. Management of hyponatraemia in surgical wards needs good collaboration between surgical teams and anaesthetists, endocrinologists and nephrologists. Greater understanding of the relevance of hyponatraemia to surgical patients is the key first step.

Case 1 A 70 year old man with stable mild hyponatraemia due to idiopathic SIADH was admitted for TURP. The anaesthetist cancelled surgery because of concerns that intravenous fluids perioperatively would worsen hyponatreamia and risk seizures. They recommended discharge and readmission after two months of fluid deprivation. Endocrine consultation recommended Tolvaptan therapy; administration of 15 mg day caused a steady rise in plasma sodium from 124 to 133 mmol/l over two days; Tolvaptan therapy was continued perioperatively. Surgery was successful and uneventful during the same admission and plasma sodium was maintained at 133e136 mmol/l perioperatively, despite IV fluids and bladder

irrigation. The use of vasopressin antagonists allowed prompt, safe conduct of surgery without the need for patient discharge, and with normal use of peri-operative intravenous fluids.

Case 2 A 28 year old man underwent coiling for an anterior communicating artery aneurysm which had ruptured, causing subarachnoid haermorrhage. On day three postprocedure his GCS had fallen to 9/15 and the patient could not engage with physiotherapy. Plasma sodium had fallen acutely from 142 mmol/l on admission to 121 mmol/l three days post-op. The neurosurgeons were unsure whether the diminished conscious level was attributable to hyponatraemia or further subarachnoid bleed. Tolvaptan, 30 mg daily caused a rise in plasma sodium concentration from 121 to 136 mmol/l over two days, with a rise in GCS to 15/15; the patient was able to engage with rehabilitation and was discharged seven days later, with normal plasma sodium concentration and discontinuation of Tolvaptan. The use of Tolvaptan enabled the patient to rehabilitate and discharge from hospital, while avoiding the potential for further neurosurgical intervention.

references

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