///2017 Abstract Details
2017 Abstract Details2019-08-02T15:54:53-06:00

Profound hyponatremia as a cause of prolonged postoperative lethargy in a pre-eclamptic parturient.

Abstract Number: SUN-60
Abstract Type: Case Report/Case Series

Jim Nguyen MD1 ; Sonya Randazzo MD2; Katherine Gelber MD3; Jeffrey Grewal MD4; Mark Zakowski MD5

Introduction: Hyponatremia has a high risk of perioperative complications including nausea, confusion, lethargy, muscle spasms, weakness, seizures, and coma. We present an interesting case of acute hyponatremia as a cause of prolonged lethargy after cesarean section.

Case: A 35 y.o. primip at 34 weeks presented for medical induction of labor for pre-eclampsia (BP 160/90) and HA. PMH negative except for gestational hypertension, A1DM and intrauterine growth retardation. She was induced with dinoprostone and started on magnesium for seizure prophylaxis. Fetal bradycardia was noted 4 hrs after induction. The OB proceeded with emergent cesarean delivery under general anesthesia, with Apgars of 7/ 8 and signs of abruption. Oxytocin 40 units was administered in normal saline over 30 minutes after delivery per protocol. OR fluids were lactated ringers 3L, EBL 800 mL and urine 100 ml. In PACU, the patient was noted to be lethargic, briefly awakening to voice and maintaining eye opening for <10 seconds at a time (RASS score -2. VS BP 140/95 P74 R 12 Sat 99% on 4L O2). Four hours later, full reversal of benzodiazepines and opioids with flumazenil and naloxone were given with only mild improvement of her mental status and with still having brief apneic episodes. Neurologic status was non-focal. Work-up in PACU showed Mg 6.6mg/dL and Na 123; other electrolytes and LFTs WNL. Oral fluid intake was restricted and 3% sodium chloride was slowly administered to correct her hyponatremia in ICU. On postoperative day one, her sodium returned to 135 with no complications and resolution of her altered mental status. Discussion with the obstetrician revealed that the patient had copious excessive free water intake during her preoperative course. Preeclampsia with severe features may also predispose to hyponatremia.

Discussion: Primary polydipsia has been described but remains a rare cause of acute hyponatremia. Parturients are at risk of developing dilutional hyponatremia due to a reduction in the osmotic threshold for release of antidiuretic hormone (ADH) and the ADH-like effects of endogenous and synthetic oxytocin. In addition, parturition causes pain, stress, and nausea which stimulate the secretion of ADH. Oral fluid intake was not recorded in the fluid balance and may have played a role in diagnosing this complication. Our case emphasizes the need for an increased awareness of the potentially harming effects of primary polydipsia in the parturient and vigilance in PACU with an unusual cause of post-cesarean lethargy.

References:

Graham K. Severe hyponatraemia as a result of primary polydipsia in labour. Aust N Z J Obstet Gynaecol. 2004 Dec;44(6):586-7.

Hayslett JP. Dilutional hyponatremia in pre-eclampsia. Am J Obstet Gynecol. 1998 Nov;179(5):1312-6.

Ophir E. Water intoxication-a dangerous condition in labor and delivery rooms. Obstet Gynecol Surv. 2007 Nov;62(11):731-8.

SOAP 2017