The chief resident at Providence asked me to do a board review class for the third-years. They have small sessions weekly (?) in the physician lounge. This afternoon we went over fluids, electrolytes and acid-base. We did the first 14 questions. Seems like it went pretty well.
I was scheduled to just give a electrolyte lecture without any further guidance. I pulled out two interesting cases I had seen in the last few weeks. Both patients have a non-anion gap metabolic acidosis, but one is hypokalemic and the other is hyperkalemic.
Here is the native Powerpoint files for you to use or edit.
I’m working more at Providence Hospital and I find that the intensivists and cardiologists love the Bumex. This opinion is shared by some prominant nephrologists. Unfortunately bumetanide suffers from the same short pharmacokinetics as furosemide: half life of about 90 minutes after oral or IV dosing. The big advantage bumetanide has over furosemide is more predictable bioavailability after oral dosing. Torsemide trumps both of them with excellent bioavailablity and a half-life of 210 minutes.
The reason that bumex is preferred is the beleif that it is a more potent diuretic than furosemide. According to Brater, all of the loop diuretics have similar potency and decisions among the loops should be based on pharmaokinetics (as opposed to pharmacodynamics). Here is the statement in his NEJM review of diuretic therapy.
Phamacokinetics of torsemide, bumetanide and furosemide from the package inserts. And here is the table from Brater’s reveiw:
I gave my first lecture to the residents at Providence Hospital on Friday before Labor Day. I did a new lecture on calcium. I tried to base this lecture around this incredibly interesting patient I had a few years ago at St. John.
He was a young man who came in with a fracture due in part from his rip-roaring uncontrolled secondary hyperparathyroidism, which had actually progressed to tertiary hyperparathyroidism. We treated his hypercalcemia, got him a parathyroidectomy and then watched in horror as his hypercalcemia switched to hypocalcemia as part of a wicked case of Hungry Bone Syndrome. To cap it off he developed acute symptomatic hypocalcemia after meeting Alonzo Mourning.
On that one admission, in one patient my team got to see and study:
Renal osteodystrophy with skeletal complications
Diagnosis and management of Hypercalcemia
Diagnosis and management of tertiary hyperparathyroidism
Diagnosis of Hungry Bone Syndrome
Management of severe hypocalcemia
Relationship of ionized calcium to pH
I call it the greatest case report ever told and regarding calcium it probably is the best.
Again I provided the resident with a booklet and did the lecture Seder Style. This was the best use of that style yet.