Peripartum Hyponatremia: A Case Report of Complications in Preeclampsia

Introduction: Preeclampsia, characterized by new-onset hypertension and end-organ dysfunction after 20 weeks of gestation, carries the potential for severe complications such as eclampsia and HELLP syndrome. Peripartum hyponatremia, associated with adverse outcomes, presents a serious concern when coupled with preeclampsia. Case Description: 39 year old with hypothyroidism, obesity (BMI 38.1), IVF pregnancy and gestational hypertension was admitted at 36 weeks for labor induction due to severe preeclampsia. At 35 weeks, she developed headaches, proteinuria (urine protein to creatinine ratio 1.1), and elevated AST levels (66 U/L). Estimated GFR and platelets were normal. Upon admission, she received misoprostol, oxytocin, and artificial rupture of membranes for labor induction. Her serum sodium decreased from 131-134 mmol/L three weeks before admission to 129 mmol/L on admission, reaching a nadir of 122 mmol/L the next day. Patient was euvolemic, with low serum osmolality (262 mOsm/kg), high urine osmolality (290 mOsm/kg), urine sodium of 29 mmol/L, normal TSH (1.44), and low morning cortisol (1.3, likely due to antenatal betamethasone). Fetal intolerance prompted a C-section. Postpartum hemorrhage from uterine atony prompted ICU transfer for hemorrhagic shock. Fluid restriction and sodium chloride tablets improved serum sodium. Treatment was continued until delivery, after which serum sodium promptly normalized. Follow-up labs at 6 weeks and 5 months postpartum showed normal electrolytes. Discussion: While rare, severe hyponatremia in preeclampsia patients can lead to maternal symptoms like nausea, headache, confusion, and seizures, with fetal manifestations including jaundice, seizures, and tachypnea. It is associated with adverse outcomes, including stillbirth and postpartum ICU admissions. Treatment in this population is challenging due to limited medication options, with fluid restriction and sodium chloride tablets typically used. Delivery of the fetus is often necessary for definitive treatment, especially in cases of moderate to severe hyponatremia. While pregnant women may have physiological alterations in sodium homeostasis causing mild hyponatremia, the exact etiology of severe hyponatremia in preeclampsia patients remains unclear. Close monitoring and timely intervention are needed to avoid adverse outcomes. Further research is needed to understand the underlying physiology contributing to hyponatremia.

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Journal
Journal of the American Society of Nephrology
Published
2024-10-01
DOI
https://doi.org/10.1681/asn.2024rgjrds30
Citations
1
Primary Topic
Pregnancy and preeclampsia studies
Type
article
Field-Weighted Citation Impact
0.58
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article

Peripartum Hyponatremia: A Case Report of Complications in Preeclampsia

Khushleen Jaggi
1 citations
Journal of the American Society of Nephrology
Pregnancy and preeclampsia studies
0.58
article

Peripartum Hyponatremia: A Case Report of Complications in Preeclampsia

Khushleen Jaggi
article en
1 citations

Abstract

Introduction: Preeclampsia, characterized by new-onset hypertension and end-organ dysfunction after 20 weeks of gestation, carries the potential for severe complications such as eclampsia and HELLP syndrome. Peripartum hyponatremia, associated with adverse outcomes, presents a serious concern when coupled with preeclampsia. Case Description: 39 year old with hypothyroidism, obesity (BMI 38.1), IVF pregnancy and gestational hypertension was admitted at 36 weeks for labor induction due to severe preeclampsia. At 35 weeks, she developed headaches, proteinuria (urine protein to creatinine ratio 1.1), and elevated AST levels (66 U/L). Estimated GFR and platelets were normal. Upon admission, she received misoprostol, oxytocin, and artificial rupture of membranes for labor induction. Her serum sodium decreased from 131-134 mmol/L three weeks before admission to 129 mmol/L on admission, reaching a nadir of 122 mmol/L the next day. Patient was euvolemic, with low serum osmolality (262 mOsm/kg), high urine osmolality (290 mOsm/kg), urine sodium of 29 mmol/L, normal TSH (1.44), and low morning cortisol (1.3, likely due to antenatal betamethasone). Fetal intolerance prompted a C-section. Postpartum hemorrhage from uterine atony prompted ICU transfer for hemorrhagic shock. Fluid restriction and sodium chloride tablets improved serum sodium. Treatment was continued until delivery, after which serum sodium promptly normalized. Follow-up labs at 6 weeks and 5 months postpartum showed normal electrolytes. Discussion: While rare, severe hyponatremia in preeclampsia patients can lead to maternal symptoms like nausea, headache, confusion, and seizures, with fetal manifestations including jaundice, seizures, and tachypnea. It is associated with adverse outcomes, including stillbirth and postpartum ICU admissions. Treatment in this population is challenging due to limited medication options, with fluid restriction and sodium chloride tablets typically used. Delivery of the fetus is often necessary for definitive treatment, especially in cases of moderate to severe hyponatremia. While pregnant women may have physiological alterations in sodium homeostasis causing mild hyponatremia, the exact etiology of severe hyponatremia in preeclampsia patients remains unclear. Close monitoring and timely intervention are needed to avoid adverse outcomes. Further research is needed to understand the underlying physiology contributing to hyponatremia.

Journal of the American Society of NephrologyVol. 35(10S)
San Mateo Medical Center (US)
Good health and well-being
Openalex Percentile: Top 27%
Pregnancy and preeclampsia studies
0.58
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