Let’s talk about central diabetes insipidus.
What’s my problem?
I don’t have enough ADH, I just don’t.
Before we get there, urine osmolality - low;
plasma osmolality - high; ADH level - decreased;
receptor activity – well, even if the receptors
are perfectly normal, which they are in central,
it does not matter, the patient does not have
May follow head injury, now, be very careful
We talk about head injury.
That’s interesting, right?
You would think-You would think by having
head injury that you would lose ADH, that’s
Or what if there is head injury and initially,
you may actually release too much ADH?
“So, Dr. Raj, you’re telling me both instances
That’s exactly what I’m telling you.
We see… we’re going to see this concept
again in thyroid disorder.
In thyroid gland, with the colloid, initially
when you destroy it, you might have too much
T3, T4, as we shall see.
So, with head injury, the trauma depletes
the posterior pituitary gland of ADH stores.
Sure, that could happen.
Posterior pituitary, it cannot-it cannot properly
secrete your ADH, your patient is central
diabetes insipidus, but the receptors?
Perfectly normal, keep that in mind because
that’s important for us to manage your patient.
Because circulating levels of ADH are low,
the entire DT/CD, by that we mean distal convoluted
tubule and collecting duct are impermeable
So, what kind of urine are you producing?
Good, diluted urine.
What’s my plasma osmolality?
Large volume, polyuria, look how much urine
you’re losing per day, 15 litres per day,
So, what’s your next step of management?
IV fluids, but “Dr. Raj, I’m already losing
Correct, you are, but my goodness gracious,
you’re losing 15 litres of water per day,
you need to hydrate your patient or your patient
Plasma osmolality, obviously increased, high
values, extremely excessive.
Normally, when you have plasma osmolality
that’s increased, what’s those receptors
up in the hypothalamus?
Good, osmoreceptors that we stimulated so
that you normally secrete ADH.
So, how do you manage your patient with central
I told you over and over again, the receptors
are perfectly normal, so go ahead and administer
ADH and analogue such as, here you go, d-arginine
Keep arginine in mind, big time please.
Arginine is going to be a precursor for creating
or synthesizing your vasopressin.
And as soon as you give this, what happens
to urine osmolality?
Initially, it was low, it starts rising; your
plasma osmolality was high, it starts lowering.
Please, from henceforth, keep your two compartments
completely separate and be able to do it as
quickly as I’m doing it on your boards,
you have to be able to.
Let’s talk about central more.
Most common cause would be, MC stands for
most common, idiopathic autoimmune.
We have something called Wolfram syndrome;
So, congenitally, the posterior pituitary
was not present.
Tumors, primary or secondary, infiltrating
the disease or infiltrating the posterior
Let me give you an example.
What if your patient was the following?
The patient had a “rash”, the-the patient
was then given cortisol, but didn’t work.
The patient goes on to develop, let’s say
couple of years later, arthritis type of issues.
NSAIDs and ibuprofen didn’t seem to work,
years went by and now, the patient is polyuria.
Upon electron microscopy, you find birbeck
Oh, I pretty much gave it away.
These tennis racket-type of structures and
the patient comes back to be positive for
CD1A, who is my patient?
Good, Langerhans cell histiocytosis.
In Langerhans cell histiocytosis, do you remember
when we talked about a cancer in WBC pathology?
A cancer that is then, if left unimpeded,
at some point in time, can infiltrate the
posterior pituitary resulting in central diabetes
Keep that in mind because Langerhans cell
histiocytosis many times goes unnoticed for
years upon years upon years until you get
these bizarre symptoms such as polyuria, important
causes of central diabetes insipidus.
Let’s talk about what happens.
Neurosurgery and trauma with typical triphasic
response, what do you mean?
Initial… anytime that you wish to choose
any type of surgical answer for dealing with
ADH in the posterior pituitary, you want to
keep the triphasic response in mind.
What do you mean triphasic?
It is possible that you might then destroy
the posterior pituitary, initial polyuria
phase begins within 24 hours.
ADH phase on, well, let’s keep that approximately
a week, then permanent central diabetes insipidus
once the ADH stores are completely, completely
Keep the triphasic in mind.
This theme or concept can also be used for
thyroid, as you shall see.
So, if there’s neurosurgery being a cause
of central diabetes insipidus, initially,
you might actually release too much ADH.
Your patient looks and presents as SIADH.
Worst case scenario, if there is enough damage,
you might completely deplete your patient,
your patient presents with central diabetes
Hypoxic encephalopathy, what does that mean?
If there’s enough hypoxia taking place,
especially of the brain region, understand
the posterior pituitary is not going to function
and nor is it going to release ADH.
These are all causes that you want to keep
in mind for CDI, central diabetes insipidus.
Your patient presents with polyuria, nocturia
is a big point and polydipsia.
Remember, this could be any age of a patient,
it could be congenital or it could be an adult.
So, if you find the symptoms that we talked
about along with the labs that I’ve given
you and there’s nocturia highly differential
should be CDI.
May present with neurologic deficit from hypernatremia.
Remember with dehydration because of polyuria,
there will be hypernatremia and that is not
good for the CNS.
May develop a decreased bone mineral density
at the lumbar spine and femoral neck, so think
about where you are, lower back or by the
Even when managed with desmopressin, the unfamiliar
mechanism of V1 could be responsible for some
of the issues that we’re seeing here for
proper bone density.
You’re going to find this quite a bit with
central diabetes insipidus, important clinical
symptoms of your patient.
What I wish to show you here more so than
the cranial nerves, this is not a review of
neuroscience, but what I do want to show you
immediately is the sphenoid sinus.
The manner in which you are then going to
approach, take a look at the pituitary gland
please and take a look at the sphenoidal sinus,
the manner in which you will be then approaching
the pituitary gland will be transsphenoidal
surgery and as you pass through here, you
are very close to a number of cranial nerves
that you see here on the left.
And so, therefore, during transsphenoidal
surgery and you have internal carotid artery,
you want to keep all this in mind.
For example, anytime that you do surgery with
a gland, things that you want to keep in mind
is, well, let’s say that I’m trying to
pass through the parotid gland, well, you
know about the facial nerve.
As you are trying to reach up into the pituitary
gland for whatever reason, maybe your patient
has issues with an adenoma, there’s every
possibility that you might have collateral
Sphenoidal sinus and transsphenoidal surgery
and often times, when you are doing neurosurgery,
look for immediate release of ADH resulting
in polyuria, SIADH or as I told you earlier
permanently resulting in complete depletion
and so, therefore, may result in central diabetes
Triphasic, triphasic, triphasic.