Introduction

Hyponatraemia is a deficiency of extracellular sodium relative to the body water. It can occur in a hypovolaemic, an euvolaemic or a hypervolaemic state. The differential diagnosis hinges both on this assessment and the urinary sodium concentration. The causes of hyponatraemia are discussed in Table 1.

Case Report

A 38 year old woman presented at 30 weeks of gestation in her second pregnancy with a BP of 140/98 (booking BP 120/78 mm Hg) mm Hg with 1+ proteinuria. Ultrasound showed foetal growth on the 3rd centile with oligohydramnios and an increased umbilical artery resistance on Doppler waveform analysis. She had 2.1 g of urinary protein in 24 hours and mild peripheral oedema. She received two doses of betamethasone to accelerate foetal lung maturity, but no anti-hypertensive drugs.

At 32 weeks she developed headache, visual disturbance and her BP was 200/94 mmHg. Her laboratory values were as follows: Serum sodium 130 mmol/L, potassium 4.4 mmol/L, urea 6.8 mmol/L, creatinine 70 mmol/L, urate 357 mmol/L, albumin 22 g/L. She was treated with two doses of hydralazine and was started on magnesium sulphate infusion. She received no other IV fluids. A baby girl weighing 1.4 kilogram was delivered by caesarean section, with the following cord blood analysis: venous pH 7.23, arterial pH 7.20, BE –3.0. At delivery the mother received one litre of isotonic saline.

Following ceaserean section, the mother developed worsening hyponatraemia with serum sodium of 128 mmol/L after the delivery, 124 mmol/L after 15 hours and 122 mmol/L after 21 hours. She was clinically euvolaemic. Her thyroid profile, renal function and serum cortisol levels were all normal. She was given isotonic saline and the sodium level dropped further to 118 mmol/L, 36 hours post-partum. Urinalysis at that time on a spot urine sample showed: urine sodium 35 mmol/L, potassium 52 mmol/L, and osmolality 659 mmol/Kg. Her serum osmolality was 250 mmol/Kg. She was commenced on fluid restriction. She remained hypertensive, but euvolaemic. She complained of headache, lethargy and jitteriness. After 36 hours she started improving clinically and her serum sodium rose to 136 mmol/L. The rest of her hospital stay was uneventful with the patient becoming normotensive and serum electrolyte values remained within normal levels. She was discharged home seven days post-partum.

The baby girl developed hyponatraemia over the first day of her life. Her serum electrolytes were: sodium 131 mmol/L (Normal neonatal range, 135-142 mmol/L), potassium 6.0 mmol/L, urea 4.7 mmol/L and creatinine 123 mmol/L. She was treated with sodium supplementation to 10% dextrose solution. On the second neonatal day her serum sodium level rose to 135 mmol/L. On the sixth neonatal day her blood biochemistry became normal with serum sodium of 141 mmol/L.

Discussion

All (Eight) reported cases of hyponatraemia with pre-eclampsia were antenatal hyponatraemia resolving spontaneously with childbirth.

1. Two cases had Syndrome of Inappropriate ADH secretion (SIADH) of pregnancy One was transient and pregnancy related.2 The other case was caused by past head injury.1
2. Five cases of dilutional hyponatraemia,reported by:

   Table 1 :Causes of hyponatraemia

   Hayslett et al3, Magriples et al1, Burrell and de Swiet4. Nephrotic syndrome was associated with three, in the other two hypervolaemia of pre-eclampsia was felt to be responsible.
3. One case of hyponatraemia with HELLP (Haemolysis, Elevated Liver enzymes, Low Platelet count) syndrome.

This patient presented with pre-eclampsia and borderline low sodium level (130 mmol/L). She developed severe hyponatraemia following childbirth with caesarean section. She had the diagnostic combination of Syndrome of inappropriate ADH secretion (SIADH): dilutional hyponatraemia (122 mmol/L), high urine osmolality 659 mosmol/Kg) with low normal serum osmolality (250 mosmol/Kg), inappropriately high urinary sodium excretion (35 mmol/L) with normal excretory renal function, and normal adrenal and thyroid function.

This is the only case where hyponatraemia developed post-partum, immediately after caesarean section. We postulate that the inappropriate ADH secretion in this patient was most likely due to non-osmolar stimulus of operative trauma and associated pain and anxiety. This is of special relevance in Obstetric setting as symptoms and signs of worsening hyponatraemia and ecclampsia are very similar and may result in adverse outcome due to missed diagnosis.

Two of the previous reports detected neonatal hyponatraemia.4,5 There is extensive bi-directional water diffusion across the placenta.6 Even though placental transfer of Anti-diuretic Hormone or Arginine Vasopressin remains unclear, maternal hypo-osmolarity due to a Syndrome of Inappropriate ADH secretion, causes foetal hyponatraemia in an effort to reduce the sodium gradient across the placenta.

Foetal hyponatraemia may occur more commonly with maternal hyponatraemia than previously thought and follows a time lag. The most dangerous effects are due to cellular swelling causing cerebral oedema, seizure and hypoxia. Although many cases resolve spontaneously, some neonates like this reported case require treatment.

References

*Specialist Registrar in Obstetrics and Gynaecology, King’s Mill Hospital, Mansfield Road, Sutton in Ashfield Notts, NG18 4EJ. **Professor of Obstetrics and Gynaecology, City Hospital, Hucknall Road, Nottingham, NG5 1PB.