Well, in hypocalcemia we have a low serum calcium.
Mild diseases usually asymptomatic,
but severe hypocalcemia can cause a variety of symptoms.
Patients may develop seizure,
they may develop tetany or diffuse muscle spasms
and they may develop arrhythmias.
There's a great physical exam finding
that you'll probably be asked about on a test.
Actually, two physical exam findings.
One being Chvostek sign and the other one being Trousseau?s sign.
Chvostek sign is elicited when you tap on the facial nerve of a patient.
These patients will have an involuntary twitching of their facial muscles.
It's reliable and you can definitely see it
in patients with significant hypocalcemia.
Trousseau?s sign is a more subtle finding
where you inflate a blood pressure cuff and simply leave the cuff inflated.
That patient will have a carpopedal spasm just like those hand there
where the hand really comes together
and it's an uncontrollable spasm as a result of very low calcium levels.
For a hypocalcemia in a patient,
whe need to think about what might be causing it.
And there could be a wide variety of causes.
It's important to get a few labs.
One lab is the 1,25-hydroxy vitamin D level.
This will tell you if the body stores are adequately transferred into 1,25.
You might see a low 1,25-hydroxy vitamin D level
in a patient with renal disease for example.
25-hydroxy vitamin D is more reflective of the body?s overall stores.
We might see a low 25-hydroxy level in a patient
with primary vitamin D deficiency or Rickets.
The serum PTH is important in patients who have hypoparathyroidism.
Those children, they'll check the PTH.
They'll discover it's low
and there maybe a problem with the parathyroid hormone.
A basic metabolic panel is important because you want to understand
not only the various electrolytes that maybe relating to calcium
but also for renal function and other general processes of the body.
And magnesium, as phosphate as you recall
can directly affect low calcium levels
especially a high phosphate level or a low magnesium level.
Alkaline phosphatase is a marker of bony turnover.
In patients with high bony turnover,
it'll be elevated in patients with low bony turnover it will not.
So in a patient who's not accessing their bone.
We should not have a high Alk phos level.
Urine calcium to creatine ratio is helpful
in patients with primary hypercalciuria.
So patients who have hypocalciuric hypercalciuria
are gonna have a high calcium to creatine ratio,
then that maybe telling you what's going on.
So let?s take a look very carefully at condition where patients have
hypocalcemia in childhood and what these lab results might be
and on like under which common circumstances
might be presenting with a low calcium.
Let?s go one at a time here.
The first condition we'll consider is having a low vitamin D level
or vitamin D deficiency.
In vitamin D deficiency, the calcium levels drop
which stimulate parathyroid hormone,
so parathyroid hormone should be up.
Parathyroid increases fast absorption from the bone
but the extra phos is lost in the urine.
Because of high PTH levels of 1,25-hydroxy are normal.
As PTH stimulates conversion into 1,25.
So the 1,25 levels of vitamin D will be normal
but the 25-hydroxy level which are indicative
of body supplies will be low.
Alk phos is high because of bony break down
and urine calcium is low because of body deficit
and reclamation of calcium by parathyroid hormone in the urine.
In the hypoparathyroidism, this is the next condition
PTH levels are obviously quite low, 25-hydroxy levels are normal
because diet and sunlight exposure is normal
and so the body levels are normal, but 1,25-hydroxy is low
because PTH facilitates turning 25-hydroxy into 1,25-hydroxy vitamin D.
Normally parathyroid retains calcium from the urine
and causes increase urine loss of phos.
Because now there's a low PTH
the urine calcium will be high and the blood phos level will be high.
Albright?s hereditary osteodystrophy
is a horrible condition in children
where the parathyroid hormone receptor doesn't work.
It's called pseudohypoparathyroidism.
So it looks just like hypoparathyroidism
except the PTH level is through the roof
because there's no negative feedback on the parathyroid gland,
because remember PTH receptors don't work.
So you'll see very high PTH levels, a high phos,
in normal total body supply of vitamin D.
In other words, a normal 25-hydroxy and a low 1,25-hydroxy vitamin D.
Also you'll see increase urine calcium
because this patient is effectively hypoparathyroid
just like in the previous example.
In patients with renal failure these kids can get low calcium too.
The phos is elevated because of an elevated parathyroid hormone.
1,25-hydroxy is low because the kidney is not doing a good job
of converting 1,25 from 25-hydroxy.
Well, because the kidney is failing.
Creatinine is obviously elevated as well.
The phos is up because increased PTH
causes increased phos absorption from the intestine.
In hypocalcemia we'll need to check an EKG
to see if there's prolonged QRS interval
which puts children at risk for arrhythmias.
For hypoparathyroidism you should consider DiGeorge syndrome.
That's the 22q11 deficiency you see where they have
generally central defects, such as defects of the parathyroid,
the thyroid, maybe the brain, and certainly they can have
abnormalities of the heart.
We'll often check an exam on an x-ray of the chest
and extremities to look for signs of Rickets.
This is a common cause of hypocalcemia in children with dark skin
who have little vitamin D in their diet.
These children will get out bowing of bones
particularly around the wrist as you can see in this slide
and they will also get expansion of bones as the ribs insert into the sternum.
This is called the Rachitic rosary.
In hypocalcemia, we're going to manage it by giving in severe cases
an IV infusions of 10% calcium gluconate.
This will prevent the arrhythmias.
Additionally, orally we will supplement calcium and give vitamin D as needed.
Calcitriol or 1,25-hyroxy vitamin D is really for patients
who can?t metabolize the 25-hyroxy into 1,25.
So we'll specifically use this for patients in renal failure,
patients with hypoparathyroidism
and in patients with Albright?s hereditary osteodystrophy