Alison White, ST6 Northern Ireland

12 Pages·2015·0.05 MB·English

"DESCRIBE AN EXPERIENCE YOU HAVE HAD ON LABOUR
WARD AND EXPLAIN HOW AND WHY IT CHANGED YOUR
CLINICAL PRACTICE"

Experiential learning, defined as ‘learning through reflection on doing’, is a proven approach
to learning.1,2 The Royal College of Anaesthetists promote the practice of reflective thinking;
as trainees we are encouraged to reflect on events and record this in our portfolio. The
Academy of Medical Royal Colleges has produced guidance on reflection. Reflective practice
is the essence of continuous professional development. It is an opportunity to develop
knowledge, skills and professional behaviours, consider the impact on our patients and the
services in which we work, and reinforce or improve our current practice.3 The concept of
learning through experience is ancient. Around 350 BC, the Greek philosopher Aristotle
wrote in the Nicomachean Ethics "for the things we have to learn before we can do them, we
learn by doing them".4 This holds true of our training in obstetric anaesthesia. We can devote
hours to books, journals, web-based learning, attend conferences, courses and meetings, and
pass the required Fellowship exams. However nothing can substitute for direct clinical
experience under local or distant consultant supervision on a labour ward; I will discuss a
recent personal experience. As I reflect, I will explore how this complex case has changed my
own practice and, on a larger scale, how preparations are in place for a multi-disciplinary
departmental change in clinical practice.

By way of background, a 29 year old female, gravida two para one, presented at 30 weeks
gestation to the antenatal clinic with a short history of a headache associated with visual
disturbance and vomiting. Her current pregnancy was complicated by pregnancy-induced
hypertension and she was on treatment with oral labetalol. Her medical history included a
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previous pregnancy complicated by pre-eclampsia, and migraines. She was initially admitted
to the antenatal ward for observation. She was hypertensive with a blood pressure of 154/103
mmHg but there was no proteinuria and no oedema. Labetalol dose was increased and full
pre-eclampsia screening bloods were taken. All blood results were unremarkable and serum
sodium level at this stage was 133 mmol/L.

The following day, blood tests were repeated and serum sodium level was then 125 mmol/L.
Plasma osmolality was low at 257 mOsm/kg and urine osmolality was inappropriately high
(776 mOsm/kg) given the low plasma osmolality. Urinary sodium was elevated at 77 mmol/L.
Clinically however, she had improved; her headache had resolved and blood pressure was
controlled on the increased dose of labetalol. In view of the hyponatraemia, the obstetricians
requested the advice of the medical team, clinical biochemists, endocrinologists and renal
physicians. This included a check of cortisol and thyroid function (results were within normal
limits), regular monitoring of renal function, and a fluid restriction of 1200 ml in 24 hours
with strict input/output monitoring.

Twelve hours later she became unwell with acute nausea, severe headache and a blood
pressure of 165/109 mmHg. She was treated with intravenous labetalol, a loading dose of
magnesium sulphate, and transferred to labour ward for close monitoring. The obstetricians
then contacted the obstetric anaesthetists as they wished to expedite delivery with a category
three Caesarean section.

As the anaesthetic registrar on call for labour ward, I reviewed the patient and discussed her
with the consultant obstetric anaesthetist. We had concerns about her for a number of reasons
and there were questions that required answers before an anaesthetic and Caesarean section
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could safely proceed. Due to symptoms of headache on a background of hyponatraemia, we
agreed that the patient should have imaging to exclude cerebral oedema. A computerised
tomography scan of the brain was normal. We then requested further blood tests to confirm
suitability for regional anaesthesia in view of the history suggestive of pre-eclampsia. Again,
blood results were normal aside from serum sodium which remained low at 126 mmol/L. We
discussed the patient with the consultant on the intensive care unit (ICU) and planned ICU
admission for monitoring post-operatively.

Under direct supervision of the consultant obstetric anaesthetist, the Caesarean section was
carried out uneventfully under spinal anaesthesia and a live male infant in good condition was
delivered. Certain adaptations were made in view of the clinical history. Invasive blood
pressure monitoring was used and the intravenous fluid administered was 0.9% normal saline
rather than the standard Ringer’s lactate solution. Post delivery, the usual intravenous bolus of
oxytocin was omitted and an oxytocin infusion was administered in a reduced volume at a
reduced rate. The patient was admitted to the ICU as planned post-operatively. Here, serum
sodium and fluid balance were tightly monitored and fluid restriction was continued. The
lowest recorded serum sodium (124 mmol/L) was at the time of ICU admission. The level
gradually increased without any intervention other than fluid restriction. She had an
uneventful overnight stay in ICU and was discharged back to a monitored bed on labour ward.
Serum sodium had returned to normal range two days following delivery and she was
discharged home on day five.

On reflection there are multiple learning points which I can draw from this experience on
labour ward. My own critical analysis has served to highlight such learning points and initiate
a change in my own clinical practice as an anaesthetic registrar on call for labour ward.
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Furthermore, the event has also impacted towards a change within the obstetric, anaesthetic
and midwifery departments as a whole.

Firstly, this case has allowed me to review the pathophysiology of hyponatraemia focusing
particularly on hyponatraemia occurring in pregnancy. Hyponatraemia is a disorder of sodium
and water metabolism and is defined as a serum sodium concentration of less than 135
mmol/L and is the most common electrolyte abnormality in hospitalised patients.5,6 The fall in
serum sodium is, in most patients, associated with a proportional reduction in the plasma
osmolality (true hyponatraemia) but there are exceptions. In most patients, hyponatraemia
results from the intake and subsequent retention of water. In normal circumstances, a water
load will be rapidly excreted as the dilutional fall in serum osmolality suppresses the release
of anti-diuretic hormone (ADH), thereby allowing excretion of the excess water in a dilute
urine. In contrast to this normal response, patients who develop hyponatraemia typically have
an impairment in renal water excretion, most often due to an inability to suppress ADH
secretion. An inability to suppress ADH release can be seen in a number of settings which
include true volume depletion, effective arterial volume depletion, or a primary increase in
ADH release (in the syndrome of inappropriate ADH secretion, SIADH).7 The signs and
symptoms of hyponatraemia depend critically on the rapidity of onset and the severity of the
derangement. The clinical manifestations are primarily related to central nervous system
effects and include nausea and lethargy, progressing in more severe cases to agitation,
headache, seizures, focal neurological deficits and coma.5 We must take notice as
hyponatraemia can have serious and potentially fatal consequences. In addition to maternal
consequences, as sodium equilibrates across the placenta, there is also potential for fetal
damage so extra vigilance is needed in the pregnant patient.8

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Our case looks specifically at hyponatraemia with a low plasma osmolality in pregnancy.
Normal pregnancy is characterised by profound changes in almost every organ system in
order to accommodate the demands of the fetoplacental unit. The plasma osmolality in normal
pregnancy falls to a new set point of about 270 mOsm/kg, with a proportional decrease in
serum sodium that is 4-5 mmol/L below non-pregnancy levels. The physiological responses to
changes in osmolality above or below the new set point (i.e. thirst and ADH release) are
intact. The reduced set point for plasma osmolality has been attributed to pregnancy-related
vasodilation and resultant arterial underfilling, which stimulates ADH release and thirst.
There is evidence that hyponatraemia of pregnancy is mediated by hormonal factors. The fall
in serum sodium concentration during pregnancy correlates closely with increased production
of human chorionic gonadotrophin (hCG), and hCG appears to produce these changes via the
release of relaxin. Our patient had a serum sodium level of 125 mmol/L and a plasma
osmolality of 257 mOsm/kg. These are below the normal values for the third trimester of
pregnancy (serum sodium 130-148 mmol/L, plasma osmolality 270 mOsm/kg) and therefore
cannot be dismissed solely as a normal physiological response to pregnancy, especially in a
setting of headache.9

Additionally, this case has raised my awareness of the potential dangers of headache in
pregnancy. When asked to review a pregnant patient with a headache, I will always be
mindful of the potential causes, the importance of a thorough clinical history, examination
and appropriate investigations, and the impact it can have upon choice of anaesthetic
technique, in addition to the potential need for ICU admission. There are multiple causes of
headache in a parturient; some relatively benign such as tension headache and migraines, and
other more serious causes such as in pre-eclampsia and subarachnoid haemorrhage. However
a headache in the setting of acute hyponatraemia is alarming. The way the brain responds to a
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changing serum sodium concentration can have serious neurological sequelae. Because
sodium does not readily cross the blood-brain barrier, water flows into or out of the brain in
response to osmotic forces. If the serum sodium concentration falls rapidly, the resulting
increase in brain water can generate cerebral oedema, increasing intracranial pressure,
potentially with a fatal outcome.6 This was a major concern for us. Our patient had a headache
on a background of hyponatraemia and therefore cerebral oedema must be excluded.
Furthermore, this had implications for our anaesthetic technique as neuraxial anaesthesia is
contraindicated in the setting of cerebral oedema. Dural puncture is not recommended in
patients with increased intracranial pressure since this will result in an acute leakage of
cerebrospinal fluid which decreases cerebrospinal fluid pressure and may provoke cerebellar
herniation.10

Our case was significantly more complex than that of a headache with hyponatraemia in a
parturient; there was also the issue of pre-eclampsia. Therefore, I investigated the available
literature to ensure optimal patient care and guide our management. Evidence based medicine
is a technique which I endeavour to incorporate into my daily clinical practice. This
experience has highlighted its benefits, particularly in the management of more infrequent
clinical scenarios. It is well recognised that pre-eclampsia is a multisystem disorder occurring
after the 20th week of pregnancy and affecting five to eight per cent of all pregnancies. It is a
disease with major anaesthetic implications. The main features are hypertension and
proteinuria that may be associated with symptoms and signs such as headache, visual
disturbances, oedema, epigastric pain and abnormalities such as thrombocytopaenia and
deranged liver function tests. Severe pre-eclampsia can progress to eclampsia which may be
difficult to distinguish from hyponatraemia-induced seizures.8,11

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Through a literature search, I aimed to determine whether there is a known association
between pre-eclampsia and hyponatraemia and how these have been managed previously. In a
retrospective study of 160 women with pre-eclampsia, five had serum sodium levels below
130 mmol/L. This suggests that the prevalence might be around three per cent.12 Camara-
Lemarroy et al identified 15 cases of pre-eclampsia-associated hyponatraemia reported in the
literature and all describe good maternal outcomes. In addition to the usual management of
pre-eclampsia, fluid restriction was implemented in 14 cases, resulting in resolution of
hyponatraemia in the puerperium within 72 hours. Hypertonic saline was administered in only
one case, with equally good results. In light of these findings, we opted to continue the
management of hyponatraemia with fluid restriction rather than administer hypertonic saline.
It would appear there is a relationship between pre-eclampsia and hyponatraemia, however
the mechanism is not entirely clear. There are two postulated mechanisms; transient SIADH
or a state of low effective plasma volume as a result of pre-eclampsia, leading to a non-
osmotic release of vasopressin.8,13 In circumstances of effective volume depletion, in addition
to impaired water excretion, sodium is usually conserved by the renal system and measured
urinary sodium is low (less than 25 mmol/L). In the case described, urinary sodium level was
77 mmol/L, making it likely that SIADH effects with salt wasting were predominant. Not
only has a literature search served to guide successful management for our patient, but it has
alerted me to an association between pre-eclampsia and hyponatraemia. Therefore my clinical
practice will change to encourage routine analysis of serum sodium levels in all patients with
pre-eclampsia and, if abnormal, I will ensure serum sodium levels are monitored closely.

In addition, this experience has highlighted the importance of effective multidisciplinary
communication and teamwork on the labour ward and this is another area in which I have
changed my practice. We only became aware of this patient when delivery was considered
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whereas other specialist teams within the hospital were involved earlier. As an anaesthetic
registrar on call for labour ward, my practice has always included attending the labour ward
handover between the obstetric team and the midwife in charge. I believe attendance at the
handover should not be optional, rather an essential requirement for safe clinical practice and
time must be set aside around workload pressures to attend. Since this experience, I ensure I
stay present at handover until every patient under the care of the obstetricians has been
discussed, not just the women on labour ward. This will facilitate early identification of
women on the wards with complications or co-morbidities that may be a cause for concern
with resulting implications for any future anaesthetic management. This should ‘flag up’
patients who can then be comprehensively assessed in a timely manner rather than in an
emergency situation. Fortunately, we had time to obtain necessary investigations and exclude
cerebral oedema before proceeding. However, had this been a category one Caesarean section,
this could have been a very different case.

This event has also triggered a forthcoming multi-departmental change regarding intravenous
infusion of oxytocin post delivery at Caesarean section. As described earlier, in view of
specific concerns, we deviated from our standard hospital protocol post Caesarean section
delivery of a single infant. Currently, this is an intravenous bolus dose of five units of
oxytocin after clamping of the cord, followed by an intravenous infusion of 20 units of
oxytocin (or 40 units if requested by the obstetrician) in 1000 ml Ringer’s lactate solution to
run over eight hours. As previously discussed, we already know that a degree of
hyponatraemia is normal in pregnancy.9 However, it could be argued that a prolonged infusion
of oxytocin post Caesarean section may exacerbate this normal phenomenon due to the anti-
diuretic effect of oxytocin. In a secondary argument, our current practice of an intravenous
infusion for eight hours following operative delivery will surely prevent an early return to re-
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establishing oral diet and the early mobilisation recommended in enhanced recovery
programmes. The benefits of enhanced recovery in this population are numerous; an
improved pyschosocial experience for women and their families by de-medicalising birth by
Caesarean section, improved postnatal experience, a reduction in maternal and neonatal
nosocomial infection, not to mention the financial savings to the National Health Service of a
reduced hospital stay.14 It would therefore seem that if an infusion of oxytocin following
elective Caesarean section is not essential, then we should not employ this strategy routinely
in view of potential issues with sodium homeostasis and the patient’s recovery pathway. We
eagerly await the results of ECSSIT – Elective Caesarean Section Syntocinon Infusion Trial.
This multi-centre randomised controlled trial across five large maternity units in Ireland aims
to compare the effects of administration of an intravenous slow bolus of oxytocin and placebo
infusion with an intravenous slow bolus of oxytocin and oxytocin infusion for the control of
blood loss at elective Caesarean section.15 A national survey of practice in the use of oxytocin
for the prevention of blood loss at Caesarean section found general consistency in the use of
bolus oxytocin but a great deal of variation in the use of additional oxytocin infusions.16

Consultation between the midwifery, obstetric and anaesthetic departments is planned locally
to discuss the issue regarding oxytocin infusions. Suggestions proposed include selective use
of oxytocin infusion in patients who are bleeding or at increased risk of blood loss, and also a
neat infusion of oxytocin administered via syringe driver. This last option will clearly reduce
intake of fluid volume and may have been a useful strategy in our patient with hyponatraemia.
However an infusion via syringe driver is unlikely to be a pragmatic solution due to the
demand for multiple syringe drivers on labour/postnatal ward and the additional midwifery
training required. Furthermore, if this strategy was employed routinely it would not be in
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keeping with an enhanced recovery pathway. Perhaps the best solution is a combination of the
two proposals; a selective use of a neat infusion of oxytocin administered via syringe driver.

Finally, this event highlights a role for a maternal high dependency/critical care facility in our
hospital. This is another subject for discussion at departmental level but is by no means a
change that we can introduce in the near future. So instead, as a multi-specialist team, we
must strive together to bring excellent care to the mother, regardless of location.

In conclusion, my reflections on this case have served to change my own clinical practice, and
added to discussions in departmental practice. I have increased awareness of the mechanisms
and dangers of hyponatraemia for mother and baby, and the associated implications for
obstetric anaesthetists. I have direct experience of the benefits of literature review and critical
appraisal in the provision of safe patient care in this complex case, and I will continue to
practise this skill. Further, the importance of effective teamwork, communication and
handover has been reinforced; my attendance at obstetric handover will continue and I will
allocate time to be involved in patient care beyond labour ward. I look forward to meeting
with consultant obstetric anaesthetists and obstetric and midwifery colleagues to discuss the
future of the routine use of oxytocin infusions following elective Caesarean section. Lastly, as
a result of my reflective practice, I intend to produce a protocol for the management of
hyponatraemia in pregnancy.

References

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