Hyponatraemia during pregnancy
J Jellema, J Balt, K Broeze, F Scheele, M Weijmer
Keywords
adh, hyponatraemia, oxytocin, preeclampsia, pregnancy
Citation
J Jellema, J Balt, K Broeze, F Scheele, M Weijmer. Hyponatraemia during pregnancy. The Internet Journal of Gynecology and Obstetrics. 2008 Volume 12 Number 1.
Abstract
Hyponatraemia during pregnancy is a problem not commonly recognised by physicians. However, it can have serious clinical consequences. Knowledge of the physiology of electrolyte disorders is necessary to distinguish between the various causes of hyponatraemia. Being able to identify the symptoms and signs of hyponatraemia is of vital importance in order to initiate the correct therapy. In this paper we present three patients with hyponatraemia during pregnancy. The various (patho)physiological mechanisms involved in hyponatraemia found in these cases are discussed. Possible iatrogenic mechanisms are outlined. The symptoms and signs of hyponatraemia are mentioned. Finally, different therapies tailored to the various causes are discussed. In conclusion, hyponatraemia during pregnancy is a complex and potentially hazardous disorder that requires optimal and swift cooperation between internist and gynaecologist.
Introduction
Hyponatraemia is a common disorder in the elderly population. Hyponatraemia in pregnancy is less well known, but can have major consequences for both the mother and child. It is important to anticipate a hyponatraemia, recognise its symptoms, and commence prompt treatment. Understanding the physiology and pathophysiology of salt and water homeostasis are therefore essential. In this article we describe three cases of pregnant women who presented with peripartum hyponatraemia.
Case Reports
Physiologic changes in salt and water homeostasis in pregnancy
During pregnancy, physiologic changes occur in volume- and osmoregulation that effect plasma osmolality and sodium concentration. In a normal pregnancy, the average plasma-osmolality is decreased by 5-10 mmol, and the sodium concentration is decreased by 5 mmol/l. 1 This drop in plasma osmolality is caused by a ‘reset osmostat’ phenomenon: the osmotic threshold above which ADH-release and a thirst stimulus occur is decreased to a lower steady state value. The mechanism that causes the reset-osmostat phenomenon is unknown, but from experimental work, it is clear that presence of the foeto-placental unit is required; a simulated pregnancy in the absence of this foeto-placental unit does not cause the reset-osmostat phenomenon. 2
Pregnancy is also characterized by an accumulation of significant amounts of sodium (approximately 900 mmol) and fluid (8-10 litres). Sodium and fluid retention is needed to accommodate the expanding maternal extracellular compartment and the fluid demands of the growing foetus. The accumulation of sodium occurs despite an increase in GFR (increased with 50% by the end of the first trimester) that causes an increase in filtered sodium of 20000 to 30000 mmol / day. 3 Consequently, this additional 10000 mmol of sodium reaches the tubules and must be absorbed to prevent sodium loss. Activation of the renin angiotensin system -that leads to an increased concentration of aldosterone- plays an important role in sodium retention despite the increased GFR. Nevertheless, pregnant women adapt less readily to low-salt than to high-salt diets.
Another important observation that influences sodium- and fluid balance is a physiological decrease in blood pressure that occurs as early as in the first 6 weeks of pregnancy, and is caused by vasodilatation, resulting in a diminished effective circulating volume, or relative underfilling. These changes trigger non-osmotic AVP release and stimulate both the sympathetic nervous system and renin angiotensin system to ensure adequate organ perfusion. Some authors have suggested that these non-osmotic factors contribute to lowering of plasma osmolality and sodium concentration. 4
Furthermore, there are several hormones that are potentially natriuretic during pregnancy, such as progesterone and nitric oxide. Estrogen and deoxycorticosterone are potentially antinatriuretic. 5,6,7 The exact contribution of the several above mentioned mechanisms on changes in salt homeostasis during pregnancy, remain unclear.
Pathophysiological mechanisms that may lead to hyponatraemia during pregnancy
More importantly, pain, nausea and fear (frequently encountered during pregnancy) can cause increased ADH-production. 8
In Patient 1, who was diagnosed with pneumonia postoperatively, a pre-existing respiratory tract infection with concurrent SIADH was considered as a cause of her hyponatraemia and seizures. However, her history and physical examination had not been suggestive of a respiratory tract infection. Excessive water-intake and ADH-secretion due to pain might have been important causative factors, in her case.
Figure 1
Figure 2
Symptoms
Symptoms of hyponatraemia are mostly caused by water shifts due to an altered plasma osmolality. Symptoms may vary from headache, nausea, dizziness, general discomfort, drowsiness, coma and seizures. Hyponatraemia can be fatal. 9 During delivery, it can be difficult to relate these symptoms to hyponatraemia, especially in patients with preeclampsia. Thus, in Patient 2 it was unclear whether her symptoms were caused by hyponatraemia or preeclampsia. Importantly, osmotic exchanges take place in the placenta, and thus the child may display hyponatraemia as well, both in utero as post-partum 15 .
Treatment
Hyponatraemia caused by SIADH or oxytocin is treated by fluid restriction and / or cessation of oxytocin infusion. If necessary, infusion of hypertonic saline can be administered, in combination with a loop-diuretic. 8 In case of polydipsia, a fluid restriction should suffice. Treatment of hyponatraemia due to preeclampsia needs to be tailored to the individual case, in which both risks and benefits of fluid restriction and iv-fluid therapy need to be considered. Absolute lack of salt is treated with sodium suppletion and treatment of the underlying cause. Detailed description of the speed of correction and frequency of laboratory measurements can be found elsewhere and are beyond the scope of this text.
Conclusion
Hyponatraemia during pregnancy is a complex problem in which many factors may play a role. As hyponatraemia is partly physiological, it may be difficult to distinguish pathological hyponatraemia from the physiological state. Measurement of plasma sodium concentration, plasma osmolality, urine sodium concentration and urine osmolality are necessary to distinguish between various pathophysiological causes. Treatment depends on the underlying cause. When iv-fluid therapy is necessary, a NaCl 0.9% solution is preferred. In case of serious hyponatraemia, hypertonic NaCl-solution may be administered. Hyponatraemia during pregnancy is complex and potentially hazardous; it requires excellent cooperation between internist and gynaecologist.