A 63-year-old woman with cirrhosis and ascites, on spironolactone, reports leg cramps and a fluttering feeling in her chest. She's on a low-sodium, fluid-restricted diet. Exam shows 2+ pitting edema and a fluid wave. Telemetry shows peaked T waves. Labs: albumin 2.3 g/dL, Na+ 128 mEq/L, K+ 6.2 mEq/L.
Total body sodium should be up, not down, in ascites. So why is her serum sodium low, and why is her potassium dangerously high?
Peaked T waves plus a potassium of 6.2 is clinically significant hyperkalemia, and spironolactone, a potassium-sparing diuretic, is a direct contributor. Adding potassium-rich foods would worsen it, extra furosemide is outside scope, and fluid restriction alone doesn't address the acute cardiac risk right now.
Three findings, one story: low albumin lets fluid leak from vessels into the belly (ascites/edema); the kidneys sense that as low volume and activate RAAS, so serum sodium gets diluted even though total body sodium is up; and spironolactone, given to counter that same aldosterone, can push potassium too high when renal clearance is already impaired.
"Serum sodium is 128, replace it with a sodium infusion." This is usually dilutional hyponatremia from water retention, not sodium loss. Treatment is fluid restriction, not sodium replacement, giving more sodium can worsen the ascites it's tied to.
keep asking why