A middle-aged white woman was in her usual state of health a week before admission, with no significant past medical history other than high cholesterol, for which she takes lipitor. She then noted progressive weakness of her arms and legs, more each day. She woke up on the day of admission, essentially unable to move. In the ER, they found she was hypokalemic and gave her potassium. She wasted it. When she got to the floor, they gave her K, and more, and finally some of her strength returned. Her thyroid was fine. Thus, her demogaphics are not good for either hypokalemic periodic paralysis (first onset usually in adolescence) or thyrotoxic periodic paralysis (she's not Asian, and her thyroid appeared fine). She drinks A LOT of cola. About three liters a day. Caffeinated. And not diet.
Other lab results excluded other causes of muscle weakness. We saw she had CPK's at around 1000 (a sign of muscle damage). Her metabolic panel, ABG, and potassium wasting led us to suspect she had type I renal tubular acidosis. But what brought on this RTA? Could it have been triggered by statin-induced muscle damage, or cola-induced muscle damage... or both?
The literature reveals that high-dose cola by itself (ok, with the help of a fetus) can cause a hypokalemic paralysis.
Whatever the cause, she lost potassium and was transiently paralyzed. We held her lipitor and her soda. She got better over the course of a few days.
But what the heck actually happened? And could it happen again?