|Year : 2017 | Volume
| Issue : 1 | Page : 54-56
Does the use of a birthing pool in labour contribute to maternal hyponatraemia? Two case reports
Chris Walmsley, Tony Wong, Julian Chilvers
Department of Anaesthetics, Sandwell and West Birmingham Hospitals NHS Trust, Birmingham, UK
|Date of Web Publication||1-Jun-2017|
Department of Anaesthetics, Sandwell and West Birmingham Hospitals NHS Trust, Birmingham
Source of Support: None, Conflict of Interest: None
Maternal hyponatraemia in labour is a recognised consequence of inappropriate fluid management, both as a result of administration of hypotonic intravenous fluid and increased maternal oral fluid intake. Other less common causes of hyponatraemia in labour include inappropriate secretion of antidiuretic hormone (ADH), exogenous administration of oxytocin, reset osmostat and sodium depletion. Patients with hyponatraemia are often asymptomatic, or display non-specific symptoms such as headache, lethargy and confusion. If hyponatraemia remains undetected, symptoms can progress to seizures, coma and death. Maternal hyponatraemia in labour may also cause a corresponding hyponatraemia in the foetus/neonate. We present two recent cases of severe symptomatic maternal hyponatraemia in labour where a birthing pool was utilised, and hypothesise how birthing pool use may increase the likelihood of developing hyponatraemia.
Keywords: Birthing pool, hyponatraemia, labour
|How to cite this article:|
Walmsley C, Wong T, Chilvers J. Does the use of a birthing pool in labour contribute to maternal hyponatraemia? Two case reports. J Obstet Anaesth Crit Care 2017;7:54-6
|How to cite this URL:|
Walmsley C, Wong T, Chilvers J. Does the use of a birthing pool in labour contribute to maternal hyponatraemia? Two case reports. J Obstet Anaesth Crit Care [serial online] 2017 [cited 2021 May 16];7:54-6. Available from: https://www.joacc.com/text.asp?2017/7/1/54/207387
| Introduction|| |
The potential adverse effects of hyponatraemia in labour for mother and neonate have been previously documented elsewhere. Hyponatraemia in labour is believed to be a more common occurrence than previously suspected. Fortunately, the proportion of these patients developing severe symptomatic hyponatraemia remains low. Oral and intravenous fluid intake is considered the main risk factor for development of hyponatraemia in labour. However, the extent to which other factors may influence the development of hyponatraemia in labour is by no means clear. Here we present two cases of symptomatic maternal hyponatraemia in labour that occurred on our unit in parturients utilising a birthing pool, and hypothesise how birthing pool use may influence the development of hyponatraemia.
| Case reports|| |
A healthy 25-year-old primiparous woman presented to triage at 41 weeks and 6 days with irregular contractions. The patient's pregnancy had been uneventful to date, with no concerns at booking and routine screening tests were unremarkable. The birth plan was for a normal vaginal delivery in the midwife-led unit with minimal intervention. On presentation at triage, the patient was noted to have ketones and blood in the urine on urine dipstick and so oral intake was encouraged. The patient was prescribed pethidine and utilised a transcutaneous electric nerve stimulator machine for contraction pain.
After approximately 10 hours on the midwifery-led unit, the patient was transferred to the obstetric-led delivery suite due to concerns over a protruding anterior lip of cervix. The patient was allowed to use the birthing room pool and remained there for the rest of her labour, during which she spent a significant amount of time in the birthing pool (estimated around 5 hours).
She had a spontaneous vaginal delivery of a healthy female infant at 12:08. One minute following delivery she had a generalised tonic-clonic seizure. The emergency alarm was activated and the full team attended. Seizure activity self-terminated after several minutes and a presumptive diagnosis of eclampsia was made. Magnesium sulphate was administered in accordance with the Trust policy.
Following the termination of the seizure, the patient was confused with a Glasgow Coma Scale score of 10 (E4V1M5). An initial arterial blood sample taken following termination of the seizure showed serum sodium of 115 mmol/L, glucose of 3.6 mmol/L and lactate of 10 mmol/L. In addition, it was observed that the patient had been polyuric, passing 4 litres of urine in 4 hours. The patient's oral intake had not been formally recorded; however, it was noted she had an isotonic sports drink and been drinking excessive amounts of water continuously since admission (approximately 19 hours before). Her laboratory bloods taken immediately post-seizure showed serum sodium of 120 mmol/L, urea 1.6 mmol/L with white cell count (WCC) of 30.3 × 109/L and a neutrophil count 25.35 × 109/L. Based on these findings, the seizure was felt to be secondary to hyponatraemia.
The patient was transferred to the high dependency area of the delivery suite. She was initially managed with an initial infusion of 0.9% normal saline (1000 mL) and subsequent fluid restriction. Despite appropriate management, she remained drowsy and became agitated, ultimately necessitating sedation and intubation. A computed tomography scan of her head and lumbar puncture were performed, but neither showed any abnormality. Serum osmolality was 251 mmol/kg (normal 275–295mmol/kg), with a urine osmolality 45 mmol/kg (normal 50–1500 mmol/kg) and urinary sodium of <20mmol/L (normal). Endocrine investigations revealed no abnormality. These results correlated with a diagnosis of hyponatraemia secondary to polydipsia.
The following morning the patient was extubated, and remained stable. Her serum sodium had returned to normal within 18 hours of the seizure.
Following delivery, her baby was found to be hyponatraemic and transferred to the neonatal unit for further management.
Follow-up at 5 months found that the mother and baby are doing well with no residual adverse effects.
A healthy 26-year-old 38 weeks and 6 days low risk primiparous woman presented to triage with small amounts of per vaginal bleeding and early contractions, following spontaneous rupture of membranes at home. She was noted to have swollen hands and feet on admission, but no history of headache or visual disturbances. Urine testing demonstrated the presence of protein, blood and ketones. Her blood pressure on arrival to triage was 129/78 mmHg. She was admitted to the midwife-led unit where she used the birthing pool intermittently over 12 hours. She was eventually transferred to labour ward at 13:10. After re-assessment, the patient was found to be fully dilated and so taken to theatre for trial of forceps for prolonged labour. This was unsuccessful and so a category 2 caesarean section under spinal anaesthesia was performed.
Following surgery, the patient was febrile at 38°C, tachycardic at 105 bpm and had a blood pressure of 90/55. She was also noted to be drowsy and so routine blood testswere performed. These showed a serum sodium of 119 mmol/L, with WCC of 29.0 × 109/L and lactate 3.0 mmol/L. Reviewing her fluid intake over the previous 24 hours, it was found that she had 3 litres of water orally and 4 litres of Hartmann's intravenously. The patient was transferred to high dependency unit on delivery suite, antibiotics commenced and fluid restriction established. Subsequent analysis of the plasma showed an osmolality of 253 mmol/kg, with a urine osmolality 168 mmol/kg and urinary sodium <20mmol/L. Endocrine investigations revealed no underlying abnormality. Within 24 hours, the patient's sodium had returned to normal values and she was transferred to the post-natal ward.
| Discussion|| |
Hyponatraemia in labour is not a rare occurrence, with one study demonstrating 26% of mothers who receive more than 2500 ml fluid during labour developing biochemical hyponatraemia (defined as serum sodium ≤130 mmol/L. Pregnancy itself predisposes to hyponatraemia due to the physiological changes that effect osmo/voluregulation; in a normal pregnancy, plasma osmolality decreases by 5–10 mmol/L and plasma sodium concentration decreases by 5 mmol/L secondary to the reset osmostat phenomenon where ADH release and thirst stimulus occur at a lower level. Pregnancy also reduces the maximum capacity for excreting a water load from 900 ml/h in healthy women to 600 mL/h in late pregnancy.
Hyponatraemia can have deleterious effects for the mother and her neonate, and correlation between maternal and foetal sodium levels is demonstrated. Both foetal and maternal seizures secondary to maternal fluid intake have been reported.,,, While seizures are obviously a serious consequence, there may be more subtle effects. One study demonstrated significant correlation between hyponatraemia and longer duration of second stage, instrumental delivery and emergency caesarean section.
Currently, it is not known, nor been discussed whether the degree to which immersion in a birthing pool affects the risk of developing hyponatraemia. It may be a coincidence that both cases involved use of a birthing pool. However, exercise-associated hyponatraemia is a well-recognised condition in athletes undertaking significant exercise, and prolonged exercise (>4 hours) and a hot environment have been identified as major risk factors. Labour could certainly be considered as significant exercise, often in a warm environment. These risk factors were present in the above cases owing to prolonged labour and the use of a birthing pool maintained at a temperature of 37°C. Increasing body temperature through water immersion has been noted to increase subjective thirst, and hence, water intake. It also increases ADH secretion, which can compound the situation.
Whilst early symptoms of hyponatraemia may be absent or non specific (drowsiness, headache, irritability, nausea), increased awareness that these changes may signal underlying pathology may help in earlier recognition and treatment. However, these symptoms are common in women that are in active labour and so may be difficult to differentiate without investigation further with serum analysis of electrolyte levels.
In light of the serious consequences, we feel that maternal fluid intake and output should be documented meticulously in labour. There is no specific evidence that demonstrates the use of a birthing pool affecting the risk of hyponatraemia. However, until more research has been conducted it would be prudent to suggest particular vigilance with patients having a water birth, especially those experiencing or likely to experience prolonged labour.
Difficulties in monitoring fluid intake in patients who are not catheterised and taking on fluids independently are evident, but this should not justify failing to monitor fluid balance or moderate intake. If the importance of this is outlined to patients and their families, then their acquiescence and collaboration is far more likely.
It is important to note that the type of fluid intake is appropriate to reduce the risk of hyponatraemia. For oral intake, water is evidently hypotonic; however, some popular sports drinks may not contain adequate amounts of sodium and can also be considered hypotonic.
In summary, maternal hyponatraemia is a potentially serious complication in labour and can result in deleterious effects for both the mother and neonate. The role that birthing pools may play in the development of hyponatraemia has not been investigated in any robust fashion, but certainly merits further attention in a larger study. All staff involved in caring for parturients should be aware that hyponatraemia during active labour is possible, and be cognisant that monitoring fluid balance is important in its prevention. Co-ordinating with patients and their families should assist in good reporting of intake/output and in preventing excess oral intake of hypotonic fluids. All staff should be cognisant of the symptoms that may herald the development of hyponatraemia, and have a low threshold for seeking medical input and/or checking sodium levels in those at risk.
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Conflicts of interest
There are no conflicts of interest.
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