So, let's talk about management of diabetes.
DKA is a potentially life-threatening condition.
We need to worry about this.
Patients with DKA often require ICU level of care.
We're gonna admit these children to the ICU
because we're gonna be needed to drawing their labs very frequently,
hourly perhaps to make sure that we're correcting the sodium and the sugar
and the potassium in the correct manner.
The key to the management of these patients is to provide insulin.
Typically, we'll start with an infusion of insulin at 0.1 units/kilo
and we'll continue that infusion to drive down both glucose
and to drive down ketones.
One area of confusion that happens often
when we're first experiencing how we care for these patients
is we encounter this circumstance where the ketones aren't gone
but the glucose has come down.
You might be tempted to slow down the insulin because you're thinking,
Oh no, this child is gonna develop hypoglycemia
and it will seize, so we need to stop the insulin.
No, we're gonna continue the insulin no matter what
because the problem is the ketones.
The hyperglycemia might be causing some additional dehydration
but it's not typically causing horrible body wide problem
like the ketones are.
So we continue the insulin
but we increase the glucose that's going into this patient.
Sometimes, we'll have a 2-bag system
where's there's D10 in one bag and D0 in another
and then we can wire them together
and thereby titrate exactly how much glucose is going in
so that we can keep the glucose at a safe level
while flooding this patient with the insulin
necessary to get rid of their ketones.
So, when we manage this people, one problem is usually hydration.
Remember, these people, these children have had a lot of sugar in their blood
and that sugar is spilling into the urine.
As a result, it's bringing fluid with it through osmotic forces
and these children will become profoundly dehydrated.
So when we see them, we pretty much assume that they have 10% dehydration.
We assume profound dehydration.
We'll start off with normal saline and in particular,
we're going to bolus them with normal saline 20 cc/kilo
until they have stable vital signs.
That's key. We must first stabilize the vital signs.
Then we may notice, after they're stable that patients are often hyperosmolar.
A low osmolar fluid will result in rapid shifts into the brain
and that can cause a sudden increase in cerebral pressures
and your risk is worsening edema and death.
So we're gonna avoid hyperosmolar resuscitation fluid.
We're going to replace their deficit of their fluids slowly
over 2 to 3 days to allow that brain to accommodate for their new,
less osmolar situation.
They're gonna downregulate their idiogenic osmols in their cerebellum.
Again, when their sugar starts getting low,
we'll start adding glucose to that infusion
rather than reducing the insulin.
The insulin is the medicine they need to get rid of those ketones.
We sometimes add potassium when the levels are known to be safe
and if the levels are less than 5.
Remember, it's a body deficit of potassium even if that potassium is high.
So, we wait but then we do often add potassium.
If the potassium falls below 2.5
as they're starting to recover from their acidosis,
we're gonna treat it fairly aggressively.
Remember, acidosis causes a transient hyperkalemia
through this cation exchange system but total potassium may be low.
We might also add phosphate
because too much chloride isn't good either as it can contribute to acidosis.
Let's go over again how we adjust the sodium for hypoglycemia.
Remember, the body is going to maintain
a particular osmol level that it likes.
So, if the sugar level is high, it's going to downregulate its sodium
to adjust for an appropriate amount of osmols in the blood.
So we can expect that as we lower the sugar,
that sodium is gonna come up essentially on its own.
We don't need to adjust fluid resuscitation for hyponatremia
if a patient has a very high glucose and the sodium normally would be 140
which is the normal level for sodium.
Let's go through some examples.
We're going to add 1.6 to the sodium for every 100
that the glucose is above normal which is about a hundred.
So, if a patient has a measured glucose of 200,
that's 100 above normal
and we would expect their sodium to be 138.4 rather than 140.
We've adjusted it down 1.6.
So if you measure 138.4 and we add 1.6 to it,
we get the actual sodium that we would expect
to see once that sugar comes down.
Seems like not such a big deal perhaps for a measured glucose of 400.
We're now with 300 above normal, 3 times 1.6.
So if we measure something like 135.2,
we would expect by adjusting for that,
that their actual sodium once we fix the sugar will be 140
but let's say a child has a sugar of 1000.
We absolutely see this crazy high glucoses in patients with DKA.
Now, we're taking 9 times 1.6 so you can see,
if I see patients with sodium with 125,
I would say, wow, this kid has a really low sodium.
Not true, as that glucose is fixed,
this child's sodium wil bounce right back up to the normal value of 140.
So, it's important to use that correction factor.
So, if we have a patient with DKA like I've said before,
we're gonna start wih a continuous insulin infusion at 0.1 units/kilo/hour.
We're flooding this patient with insulin.
We're driving down those ketones
because this is an emergency that can result in death.
If a patient doesn't have acidosis,
but has high sugar levels and ketones, this is a milder form of the illness.
It does not require the insulin infusion because while they have ketones,
there's not so many that they are in an acidotic state.
What we'll do is we'll provide insulin in regular,
routine, every-couple-hour doses
and once there's a resolution of the ketosis,
we'll then switch to a standard typical system
of taking care of them as they're healthy.
So, we start off in DKA. We're giving an infusion. Their acidosis improves.
Now, they probably can be transitioned to the general wards
instead of the ICU setting
and we're switching to every-2-hour insulin and frequent d-stick checks.
Then, as now both the dextrose and the ketones improve,
where the ketones are gone from the urine,
and the child's sugars are normal.
We're gonna put the child
on a combination of short and long-acting forms of insulin
and the regimens that people choose vary a lot
from provider to provider.
So I won't go into a specific regimens,
but often people use a long form acting of insulin like NPH
as well as short-acting like Humalog,
sometimes with large meals
and you can adjust for the number of calories.
Keep in mind for a first-time-diagnosis patient,
there is going to be this phenomenon called the 'Honeymoon'.
The 'honeymoon' happens as that pancreas is finally in its last gasp
going to give a little bit more insulin.
This means that the patient may look like they're cured.
Their need for insulin will disappear.
This can happen for several months afterwards.
Families need to be warned about this
because if they unpresume that this was a mistake
on behalf of the health professional
and they don't pay attention
and continue to follow up with their endocrinologist,
that child could go right back into DKA again the next time
and the next time, the outcome might not be so good.
So, here's an example of our short-acting/long-acting regimen.
Here's a child who's getting 3 times a day short-acting boluses
and then a long-acting one at night.
This would be a classic example.
We would say, take a dose just before breakfast,
just before lunch and just before dinner.
Some people like a snack dose.
It doesn't matter so much which kind they're going to do.
Generally, we'll do the long-acting one in the evening
to help them through their sleep
so they're maintaining a basal level of insulin as they sleep.
Another alternative that's becoming more popular is the pump.
The basal pump is a pump that's implanted.
And has a reservoir of insulin in it.
Paitients can check their sugars
and can actually dial up and down their pump.
This is usually reserved for patients
who really sort of understand their diabetes
and have figured out what's going on and again,
there's a lot of variation among both practitioners and individuals
as to what system works best for them.
The basal pump will provide a nice basal rate
while they may use boluses
for when they have a meal at breakfast, lunch, dinner or snack.
So, let's focus on the complications of diabetes.
Acutely, we can cause cerebral edema
if we don't get on this DKA setting quickly and treat it aggressively.
Cerebral edema can cause brain damage
and can result in chronic disability or death.
Patients can have hypokalemia from having body loss of potassium
and acutely, if we're treating their diabetes and we use too much insulin,
we can actually cause hypoglycemia.
Diabetics will tell you that when they take too much insulin,
they feel like a craving for sugar.
They feel jittery and they take a quick beverage.
Chronically, patients can have complications
as a result of being on insulin for long period of time.
We tend not to see this in children.
We tend to see this more commonly in adults.
This can happen because of repeated episodes of DKA
so especially in adolescents, maintaining control of their diabetes
and remembering to be responsible is very important.
Patients can develop diabetes nephritis
and eventually can result in renal failure.
Patients may develop a retinopathy over a long period of time
and develop blindness as adults.
Adults may get extremity infections especially with pseudomonas.
This can result in amputations of extremities and feet.
I'm sure you've all seen when taking care of adults, the diabetic foot.
It's a real problem.
None of these things, though, typically happen in children.
You won't expect to see it in you pediatric endocrine clinic
and don't forget about peripheral neuropathy
that can be a real problem as well.
So that's all I have to talk to you today about diabetes
especially type 1 diabetes.
We'll talk about type 2 diabetes in another lecture.
Thanks for your attention.