Abstract

We present a case of a 68 year old man who arrived at our ED manifesting fatigue, low
tolerance to mild effort as well as palpitations. Stated onset of symptoms is two months ago
with gradual worsening upon presentation. He is known to have hypertension under
hydrochlorothiazide-like and CCB treatment, non-insulin dependent diabetes mellitus,
dyslipidemia and has no blood test performed in several years.
From history we retain sustained antihypertensive treatment with indapamide 2.5 mg,
lecarnidipine 10 mg, without having conducted recent blood tests. We also mention grade 2
obesity with a BMI of 36.5 and a non-smoking status. On examination in the ED he was
hemodynamically stable with a BP of 165/94 mmHg, HR of 77 with irregular beats, no
audible heart or vascular murmurs, no signs of heart failure, oxygen saturation of 98% in
room air, denies both chest pain and syncope, complains of generalized muscular weakness
and low physical effort tolerance and palpitation. ECG reveals atrial fibrillation cu a moderate
ventricular response without any notable repolarization abnormalities. Preliminary blood tests
show negative troponin, as well as negative D-dimer, and NT-proBNP with age limits.
Further laboratory tests show severe hypokalemia (1.3 mmol/l), hypomagnesaemia (1.25
mmol/l), hypochloremia, normal renal function with an eGFR of 90 ml/min/1,73 m 2, increase
of serum myoglobin and total creatine kinase in accordance with rhabdomyolysis, hepatic
cytolysis. Heart ultrasound showed a preserved ejection fraction, with concentric LV
hypertrophy, without wall motion abnormalities, enlarged left atrium (70 ml) and moderate
mitral and tricuspid regurgitation, normal sized right chambers. Given this information,
clinical presentation was attributed to electrolyte depletion. Also not having documented atrial
fibrillation prior to this presentation it was assumed to be due to hypokalemia as well.
Of the underlying causes for this severe hypokalemia we assumed either iatrogenesis (side
effects of indapamide) or an endocrine pathology. Rapid release indapamide in 2.5 mg dosing
is known to cause more frequently hypokalemia with similar BP effects compared to its 1.5
mg SR version. To further investigate a urinary electrolyte test was obtained and showed
increased urinary potassium. Thyroid function was evaluated by TSH and fT4 values, which
were both in the normal range. Moreover, a whole-body CT scan with iv contrast was
performed and strengthened the suspicion of ectopic hormonal releasing structures, revealing
adenomatous nodules in the left suprarenal gland. We inquired an endocrinology consult,
which recommended patient stabilization firstly and subsequent testing for primary
hyperaldosteronism. Therefore the patient was taken off his initial treatment and given KCl
supplementation via central vein catheter as well as oral K and Mg supplement.
Antialdosteronic diuretic was added in maximum doses, ACE inhibitor, NOAC with a
favorable outcome including restoration of sinus rhythm on subsequent ECG strips. 24-hour
blood pressure monitor showed good systolic and diastolic pressure control under the newly
introduced medication. The patient was discharged with ICE inhibitor, antialdosteronic
diuretic, oral K and Mg supplementation for an additional week after and NOAC
anticoagulation for the next month, having attributed the atrial fibrillation episode to
hypokalemia and low cardio-embolic risk score. He was recommended to undergo periodical
blood tests in order to prevent the reoccurrence of severe electrolyte abnormalities and
redirected to an endocrinology service. It was there, where primary hyperaldesteronism was
investigated and ruled out as a cause of hypokalemia.
At 1 month follow up, asymptomatic, laboratory tests are within normal limits, systolic and
diastolic blood pressure targets are within normal range. ECG monitoring rules out atrial
fibrillation, sinus pauses or extra systolic disease.

A 68 year old man presented for generalized muscular weakness and low physical effort
tolerance and palpitation with sudden onset.
Past medical history includes: hypertension, dyslipidemia, type 2 diabetes mellitus. For his
hypertension he was recommended indapamide of 2.5 mg and lecarnidipine 10 mg.
Laboratory tests show severe hypokalemia, hypomagnesaemia and hypochloremia as well as
elevated muscular cytolysis enzymes. ECG strip shows atrial fibrillation. Having underwent
indapamide treatment without previous blood tests, we could attribute the electrolyte
unbalance to this. However an endocrine dysfunction must be excluded. We performed blood
tests for thyroid function, which came out normal, urinary electrolyte testing showing
increased urinary potassium as well as performed whole body CT scan for ectopic hormonally
active sources. Imaging revealed left suprarenal nodules of adenomatous nature, which
required further investigation in an endocrinology service. The patient recovered well with
potassium supplementation and cessation of former treatment and was discharged after 7 days
and redirected for additional tests in the endocrinology department. At 30 days follow up , he
was asymptomatic at usual effort with controlled blood pressure values and normal blood
tests.