Let's talk about the
management of hypocalcemia.
Due to severe neuromuscular complications of
hypocalcemia in the absence of prodromal muscle tetany,
there is a requirement for urgent treatment with
intravenous calcium for severe hypocalcemia
usually in the range of less than 7.5 mg/dL.
Slow administration through a central venous catheter
and electrocardiographic monitoring is preferred.
Alternatively, Teriparatide at 20 mcg twice per
day rapidly eliminates hypocalcemic symptoms
in the acute postsurgical hypoparathyroidism state.
This however is an off-label indication for this drug.
Vitamin D supplementation of 1000 to 4000 IU
per day and oral calcium carbonate or citrate
at doses of 1-3 grams/day in divided doses may normalize
or sufficiently treat mild or chronic hypocalcemia.
Calcitriol may be needed in the setting of
hypothyroidism with undetectable PTH and kidney failure.
Because 1,25-dihydroxyvitamin D activation
requires both PTH and sufficient renal function
Let's talk about the chronic
management of hypoparathyroidism.
The goals of therapy are to eliminate symptoms
while avoiding complications namely, hypercalcemia
A reasonable goal is to keep serum calcium concentration
at or just below the reference range without hypercalciuria.
Monitoring of urine calcium excretion is mandatory
because hypercalciuria often limits therapy.
Correction of coexisting
hypomagnesemia is also required.
Thiazide diuretics are commonly used because
they reduce urine calcium excretion.
Let's go through a table that summarize
the different causes of hypocalcemia.
We talked about hypoparathyroidism in which case
parathyroid hormone is low, phosphorous is high
and vitamin D levels may be either low or
high, magnesium levels are usually normal
and clinical clues here are invariably
some form of neck surgery or irrradiation
or an autoimmune disorder that has
affected the parathyroid glands
In vitamin D deficiency, we note
that the PTH is high or normal.
The phosphorous is usually low and
the vitamins D levels are low.
Magnesium again is usally normal and these patients may
manifest with bone tenderness, weakness and osteomalacia.
The hungry bone syndrome that we've discussed will have a low
PTH and a low phosphorous and invariably a low magnesium.
Here the acute uptake by the bone of calcium
and phosphorous as well as magnesium
occurs after parathyroidectomy
and causes this condition.
Magnesium deficiency from impaired PTH secretion or PTH
resistance can manifest with a normal or low parathyoid,
normal phosphorous and vitamin
D, obviously a low magnesium.
And the clinical clues here are patients who have
diarrhea, or taking loop and thiazide diuretics,
those who abuse alcohol and have dietary
limitations in their magnesium intake
and is also often associated with hypokalemia
particularly where one is trying to replete the potassium
but is unable to get anywhere
because serum magnesium is also low.
And then finally, in chronic kidney disease where the PTH
is high, phosphorous is high, vitamin D level is low.
Here the clinical clues are creatinine and BUN elevations
and other features associated with renal insufficiency.