JS-NG-9: PRIMARY HYPERALDOSTERONISM IN A TRIPLET PREGNANCY: CONSIDERATIONS FOR INTRA-PARTUM DIAGNOSIS AND MANAGEMENT

Abstract

Primary aldosteronism (PA) is an uncommon etiology of hypertension. We report the first known case of PA in a triplet pregnancy to describe the intra-partum considerations in diagnosis, investigation and management of PA. A 33-year-old female G3P0A2 at 10 weeks gestation with triplet pregnancy was admitted for hyperemesis gravidarum and hypertension. Her comorbidities include chronic hypertension, uterine fibroids, and two previous pregnancy losses. Home medications are labetalol 100 mg BID. On presentation, the patient complained of nausea, vomiting and epigastric pain and headache. On examination, her blood pressure was 161/90 and heart rate of 75. The rest of the cardiopulmonary exam was normal. Laboratory values were notable for potassium:2.9 mmol/L (n 3.5–5mmol/L) and bicarbonate 26 mmol/L (n 24–31mmol/L). The platelets, liver function tests and renal function tests were normal. Despite continuous high dose oral and parenteral high dose potassium supplementations, she had hypokalemic episodes (nadir 2.7mmol/L). She remained hypertensive at 140/90 on labetalol 200 mg QID and nifedipine XL 30 mg q12 hours. PA was suspected and testing revealed aldosterone 1280 (n 166–2885), renin 0.49 (n 0.10–1.10), aldosterone-renin ratio (ARR) 2615 (n < 1500), which is indeterminate. Abdominal MRI demonstrated right adrenal mass, measuring 2.7 x 5.2 x 2.9 cm. Repeat testing revealed aldosterone 11,000, renin 0.34, ARR > 30,000, which is highly suggestive of PA. The uterus was too bulky with the triplet pregnancy and uterine fibroids to safely proceed with adrenalectomy. The patient consented to receive eplerenone 25 mg BID for medical management of PA in addition to nefidipine XL 60 mg BID and oral potassium supplementation. She re-presented to hospital at 31 weeks with spontaneous rupture of membranes. She had an emergency caesarian section and delivery three healthy male infants. At one month postpartum, she was switched to spironolactone 25 mg BID from eplerenone, in addition to nefidipine and potassium supplementation, and maintained blood pressure of 130–140/80–90. At five months postpartum, she had testing on doxazosin 4 mg daily, hydralazine 10 mg TID and potassium supplementations, which revealed aldosterone 2360 pmol/L, renin < 2, ARR > 1200. Adrenal vein sampling demonstrated marked lateralization of aldosterone production to the right adrenal gland. A right laparoscopic adrenalectomy was completed and she achieved normotension on post-operative day 2. She was discharged on no antihypertensive medication or potassium supplementation. At 8 months post-adrenalectomy, her blood pressure is 120/96 potassium is 4mmol/L and her aldosterone levels remain low at 252 on no medications. In this case of triplet pregnancy, the diagnosis of PA was difficult to establish given the impact of pregnancy on the renin-angiotensin-aldosterone-system. Treatment with eplerenone resulted in improvement of hypertension and good pregnancy outcome. Postpartum, adrenalectomy resulted in rapid and sustained improvement in hypertension and reversal of hypokalemia.