t h e s u r g e o n 1 3 ( 2 0 1 5 ) 1 6 3 e1 6 9

Available online at www.sciencedirect.com

ScienceDirect
The Surgeon, Journal of the Royal Colleges
of Surgeons of Edinburgh and Ireland
www.thesurgeon.net

Review

The relevance of hyponatraemia to perioperative

care of surgical patients

Martı́n 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 individ-
ualization 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.

between 2 and 5%, but in some series, up to 30% of in patients

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
have been reported to be affected.2 In comparison with pa-
tients 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: christhompson@beaumont.ie (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.
164 t h e s u r g e o n 1 3 ( 2 0 1 5 ) 1 6 3 e1 6 9
Although hyponatraemia has traditionally been viewed as
a condition relevant to internal medicine, and managed
principally by endocrinologists, nephrologists and geriatri-
cians, there is an increasing evidence base which documents
the relevance of hyponatraemia to the perioperative man-
agement of surgical patients. Firstly, hyponatraemia is com-
mon 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 pre-
senting for vascular surgery (11.2%), with lower rates in pa-
tients 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 mortal-
ity 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 repro-
duced in other small surgical studies and subgroup ana-
lyses,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 gastro-
enterological conditions.10
The second issue with hyponatraemia is the poorer
outcome when plasma sodium concentration drops peri-
operatively. Studies in surgical patients entering intensive
care units have demonstrated a clear association of worse
surgical outcomes, including excess mortality, with post-
operative hyponatraemia.11 Furthermore, symptomatic
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
Hypovolaemia Vomiting, diarrhoea,
(Dry tongue, decreased BP, burns, skin losses
increased pulse, decreased CVP,
increased urea, orthostatism)
Euvolaemia Hypothyroidism
Any cause and hypotonic fluids
Hypervolaemia Congestive cardiac failure,
(Oedema, ascites, Chirrosis, Nephrotic Syndrome
increased JVP and CVP)
BP ¼ blood pressure; CVP ¼ central venous pressure; JVP ¼ jugular venous pressure.
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 man-
agement of hyponatraemia offers the opportunity to improve
perioperative care,14 to assess surgical risk and to individu-
alize 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-, peri-
and 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 hyper-
volaemic, or fluid overloaded. However, it can be more diffi-
cult 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 pa-
tients. The next step is to classify hyponatraemia on the basis
of urine sodium concentration. Low urine sodium concen-
trations 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 post-
operatively setting, it is important to remember that potent
pathophysiological stimuli for the release of ADH, such as
Urine [Naþ]>30 mmol/L Treatment
Diuretics, salt-losing nephropathy, IV saline þ
Addison's, cerebral salt wasting syndrome Treat underlying cause
SIADH Fluid restriction
Glucocorticoid deficiency Vaptan therapy
Drugs
Renal failure, any cause with diuretics use Diuretic therapy
 t h e s u r g e o n 1 3 ( 2 0 1 5 ) 1 6 3 e1 6 9
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 sec-
ondary hyperaldosteronism, which leads to renal tubular so-
dium 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 diag-
nostic 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 disor-
ders, 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 hypopi-
tuitarism, with subsequent low plasma cortisol concentra-
tions. 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 post-
operative ventilator support.
Hypervolaemic hyponatraemia is rare pre-operatively,
though it may be seen in patients presenting for cardiotho-
racic surgery when in a state of cardiac decompensation. In
contrast, in the post-operative period, hypervolaemic hypo-
natraemia 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 hypona-
traemia, itself, the rapidity of the fall in plasma sodium con-
centration is far more important in determining the likelihood
of neurological symptoms Chronic hyponatraemia, which is
seen in many elderly patients, may have relatively few
165
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 hy-
pertonic brain, producing cerebral swelling and intracranial
hypertension.19,20 Symptoms of cerebral irritation include
headaches, nausea, decreased level of consciousness, confu-
sion 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 dis-
turbances,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 sur-
gery are particularly likely to present or to develop hypona-
traemia 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, uro-
logical tumours and head and neck tumours are particularly
likely to cause SIADH, and any intracranial lesion may pro-
duce 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 va-
riety 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 hypopituita-
rism. 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 hypona-
traemia has been treated to restore plasma sodium con-
centrations to normal, this option should be exercised.
Successful surgical outcome will be enhanced by pre-
treatment 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-
166 t h e s u r g e o n 1 3 ( 2 0 1 5 ) 1 6 3 e1 6 9
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 hypona-
traemia may develop as a result, leading to raised intra-
cranial 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 neuro-
logical disability and even death in TURP syndrome.27 Pre-
operative 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 poly-
ethylene 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 prepar-
ing 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 hypona-
traemia can arise and the use of 3% hypertonic intrave-
nously 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 hypona-
traemia 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
Table 2 e Drugs producing hyponatraemia as side effect
commonly used in clinical practice.
SSRI
Tricyclic antidepressants
Antipsychotic drugs
Carbamazepine
Oxycarbazepine
Valproate
Chlorpropamide
Cyclophosphamide
Narcotics
ACE inhibitors
Ciprofloxacin
Ethionamide
Omeprazole
Thiazides
Amiodarone
AVP analogues
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 acti-
vation of renin-angiotensin-aldosterone axis, corticotro-
phin 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 hydrocorti-
sone to cover any surgical intervention, from benign pro-
cedures 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 infu-
sion 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.
Postoperative management
Post-operative hyponatraemia is common and the patho-
physiology is often multifactorial and complex. Surgery is
associated with non-osmotic release of the anti-diuretic hor-
mone, vasopressin, and in conjunction with intravenous hy-
potonic 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 in-
crease the tendency for plasma sodium concentration to fall.
A study performed by Chung and colleagues, showed a prev-
alence of 4.4% of hyponatraemia (<130 mmol/L) during the
first post-operative week in different surgical units. Plasma
 t h e s u r g e o n 1 3 ( 2 0 1 5 ) 1 6 3 e1 6 9
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 dis-
cussion. Between 10 and 50% of patients, depending on the
underlying condition, may develop hyponatraemia; post-
operative hyponatraemia occurs in 10% of patients undergo-
ing 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 inju-
dicious intravenous fluids and SIADH still cause plasma so-
dium 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, hypona-
traemia resolves with hydrocortisone therapy.39 Other causes
of hyponatraemia, such as cerebral salt wasting are rarely
seen.
Subarachnoid hemorrhage (SAH) is associated with hypo-
natraemia 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 hypona-
traemia were due to SIADH, and 10% of these cases had acute
ACTH/cortisol deficiency.41 Although other groups have sug-
gested that cerebral salt wasting is the main cause of hypo-
natraemia in following SIADH43 this paper found no evidence
of this condition in 50 patients with hyponatraemia, studied
prospectively with sequential hormonal measurements. Ce-
rebral 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 aware-
ness of the likely differential diagnosis are necessary to
accurately identify the underlying mechanisms and institute
appropriate therapy. As SIADH is the commonest cause of
167
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 hypopi-
tuitarism, with cortisol deficiency, can occur after SAH35,41
plasma cortisol concentrations should be checked and intra-
venous hydrocortisone started if plasma cortisol concentra-
tions 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 re-
ceptor 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 de-
cision will be determined in each case depending on the
presence or absence of vasospasm and the severity of hypo-
natraemia. 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 accu-
rately 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 hypona-
traemia 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, involve-
ment of the endocrinology or medical team on call should be
done. In this high risk population for ODS, natraemia correc-
tion 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
168 t h e s u r g e o n 1 3 ( 2 0 1 5 ) 1 6 3 e1 6 9
hyponatraemia with normal saline infusion, the use of thia-
zides, 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 subse-
quently an increase in water excretion is found in the kidneys
correcting hyponatraemia. If natraemia correction is excee-
ded, 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 insta-
bility and falls may prevent full integration with physio-
therapy 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 hypona-
traemia 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 peri-
operative 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, en-
docrinologists 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 sei-
zures. They recommended discharge and readmission after
two months of fluid deprivation. Endocrine consultation rec-
ommended 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 perioper-
atively. 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 post-
procedure 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 hypona-
traemia 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 dis-
charged seven days later, with normal plasma sodium con-
centration 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.
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