Let's switch gears and talk about SIADH.
Instead of too little ADH, there is too much ADH.
This excessive ADH in the blood
cause an excessive insertion of this aquaporin channels
which results an increased water retention.
Thus, the urine is excessively concentrated.
This results in a low sodium, as the water is more prevalent in the serum.
ADH can be secreted by not just your pituitary,
it secreted by a host of other cells as well
and usually in certain pathologic settings.
For example, the brain will secrete ADH
when there is irritation of the meninges so, we may see ADH in meningitis.
In the lung, the type II pneumocyte produces ADH.
We commonly see patients with a bad pneumonia
having low sodiums as a result of too much SIADH.
The GI tract also can create SIADH
typically in patients with gastroenteritis
this is probably an evolutionary way of protecting ourselves
from becoming dehydrated in the sense of a sick child.
Additionally, some drugs can cause an excessive secretion of ADH.
Let's go through one of these things that cause it.
In the CNS, tumors, meningitis, encephalitis,
hemorrhage, vasculitis and surgical trauma.
All of these things can result in a transient or more permanent SIADH.
In lung tissue, certainly pneumonias
but also even bronchiolitis can cause SIADH.
Patients with cystic fibrosis may develop SIADH
and certainly certain long malignancies
although exceptionally rare in children can cause SIADH.
Gastroenteritis can cause a mild SIADH
which can cause problems if unrecognize or if rarely severe.
Also, certain medications can cause SIADH
and we typically think of some of the psychiatric medications.
The tricyclic antidepressants,
the serotonin specific re-uptake inhibitors or SSRIs.
But also, PPIs or Protein Pump Inhibitors
as well as ACE inhibitors can cause SIADH.
So, we may sometimes simply find a patient
where we check a Chem-7 and say,
hey look at that they have a low sodium
and this how we make the diagnosis.
This is usually on patients with fairly mild disease.
And by mild, typically these patients are asymptomatic,
if their sodium is low but still above 125.
A patient with a sodium of 130 isn't really gonna notice.
They're gonna be accommodating that okay.
However, in these severe cases where the sodium gets low and below 125
these patients can develop lethargy, confusion,
you may see papilledema on the exam
as their brain is swelling or they may develop seizure.
Some of these symptoms depend on the speed
at which that sodium has been falling.
We'll talk about brain accommodation at the end
but if that sodium has been falling very gradually over time
the brain can accommodate that
and they can have fewer symptoms.
If the sodium fell very rapidly
patients can get in trouble in terms of CNS disease very quickly.
The diagnosis of SIADH can be somewhat complicated.
Typically, we will see as low sodium,
a sodium in the blood should be really less than 135.
The serum osmolarity should be also low and the urine osms should be high.
The urine sodium is going to be high.
Remember the reason the patient is having a high water in the blood
is because of an insertion of those aquaporins.
So, the sodium is still coming out.
The urine sodium will be high and the fractional excretion of sodium
which is determined by this equation here is more than 0.5%.
So, let's think about how we fix sodium.
When we're fixing sodium be at high or low
we need to it slowly and that's because sodium shifts that are rapid
can cause problems in the brain.
Let's look at this closely because I think people tend to get confused
about which problem causes which problem in the brain.
Imagine here we have a brain cell and a blood vessel.
These two compartments need to have the same osms in them.
They need to have the same osms
so that there aren't fluid shifts one way or the other.
If fluid shifts into the brain, one would get cerebral edema.
If fluid shifts out of the brain what we typically see
is central pontine myelinolysis which is really bad.
It's a disturbance of the pons which can cause problems
with the basic functions of the body.
So, now let's imagine we have a certain number of sodiums in the blood.
This would be let's say a normal number of sodiums.
Likewise, the brain will create small proteins
that exist a longer surface of the brain cell
and we'll call those idiogenic osmoles.
So these small tiny proteins are providing an osmotic force
that bounces out the sodium
and allows a prevention of fluid shifts one way the other.
Now, if a patient were to get hypernatremic,
let's say they had diabetes insipidus
and they were gradually becoming more and more hypernatremic.
The brain could adjust by creating more osms,
this osm would balance things out
and would allow that patient to continually function
even the presence of a high sodium.
We would see this for example in a profoundly dehydrated state.
However, if we would have go in and try and fix this problem quickly.
Let's say the patient had a sodium 180
that have been there for a long time.
And we went in and gave them very hypertonic fluid
and rapidly removed the sodium from the blood space.
What would happen now is fluid would flow out of the blood space
and into the brain and that would cause cerebral edema.
So, an overly rapid correction of a long-standing hypernatremia
leads to cerebral edema.
Let's go back to this brain again now,
here we have a patient with a normal sodium
and a normal number of idiogenic osmoles.
Let's say this patient now develops hyponatremia
the brain will accommodate accordingly
and downregulate the idiogenic osmoles.
So that we have an equal amount of osmotic particles
in both compartments and no fluid shift.
If we see this patient with a sodium of 120,
let's say they have SIADH
and we were to rapidly correct the problem
by bringing up their sodium too quickly.
We would have suddenly fluid shifting out of the brain into the blood
and there is one we would be at risk for central pontine myelinolysis.
I hope that clarifies that whole thing for you nicely and easily.
So if we have a patient with SIADH, we want to bring up their sodium slowly.
We may initially give 3% saline injection
but only in cases with a patient has symptomatic hyponatremia for example seizure.
If this child is actively seizing
we're going to give 3% saline boluses until the child is stabilized.
This would prevent further brain edema.
However, now we have to play our things fairy slowly
and we're gonna gradually give fluids such that there is a slow sodium rise
of about 0.5 milliequivalents per hour
or no more than 12 milliequivalents per day.
That means if the patient has a sodium of 120.
We should be taking several days bringing that sodium back up.
We may need to free water restrict the patient
to about 1 liter per meter square per day
to achieve an appropriate water stasis for this patient.
In patients where restrictions of fluid is not possible
we can use Demeclocycline.
Demeclocycline inhibits renal activity of ADH,
so it may inhibit the activity of the excessive ADH in the blood.
Ultimately, the goal for SIADH is to treat the underlying disease.
The reality is that for cases like pneumonia or meningitis
treatment of the condition,
usually results in a resolution of problems.
I hope this lecture is clarified for you the differences
between diabetes insipidus and ADH.
Thanks for your attention.