DKA – Diabetic Ketoacidosis Nursing Care NCLEX® Review |
Articles Blog

DKA – Diabetic Ketoacidosis Nursing Care NCLEX® Review |

September 1, 2019

Nursing Care NCLEX Review | Okay, so let s talk about Diabetic Ketoacidosis.
This is something that you may see in your time in the hospital. If you work in an ICU,
general medical ICU, you re gonna see this often as it is fairly common but it requires
very intensive monitoring labs, frequent lab draws, cardiac monitoring, electrolyte monitoring,
so there s a lot that goes on that is involved with taking care of a Diabetic Ketoacidosis
patient. So, let s talk about it really quickly and we re gonna break it down very simply
with our nursing and what we need to know to understand these patients and take care
of them. So, first of all, this is gonna occur with
type I diabetic patients. You remember with Type I, it is an autoimmune disorder where
our immune system destroys these beta cells produced insulins, so, we have extreme insulin
deficiency or no insulin at all and this leads to, what happens is this ends up leading to
the breakdown of fat into glucose which results in ketone bodies which are acidic. Okay. That
s very simply, we re gonna get in this a little bit more here. So, we have severe insulin
deficiency or no insulin at all which leads to breakdown of fat into glucose for energy
and that results in acidic ketones in the body. So, briefly, we re gonna tell you the assessment
and then we re gonna go over it a little bit really quick. So, what happens is, it is a
sudden onset, it is usually associated with infection or stress. You re gonna notice fruity
breath on your patient and that is result of those acid bodies which have kind of that
fruity smell. Ketones are gonna be released into the urine. You re gonna have severe hyperglycemia,
generally in like the 400 – 600 range with DKA. You re gonna have dehydration and this
is due to osmotic diuresis which we will go a little bit more in the next slide. You re
also gonna have acidosis, okay. What is acidosis? Acidosis is pH of less than 7.35, right? And
then, it s gonna be also a HCO3 of less than 22. Okay. So, we re gonna have a decrease
in pH and we re gonna see a decrease in Bicarb because of this acidosis. The reason acidosis
occurs, is because these fats are broken down into glucose. These ketones are a by product
to the fat breakdown, ketones are very acidic and potassium begins to leave the cell as
a result of this acidosis. You re also gonna see these Kussmaul s respirations in your
patient, and like we said, this hyperkalemia. Hyperkalemia is associated with this acidosis.
You re also gonna see an elevated BUN and creatinine and that s a result to this osmotic
diuresis. As you begin to put out all these urine, you see an elevated creatinine associated
with that renal failure. You re also gonna want to monitor level of consciousness, cerebral
edema can occur due to this fluid shift as we become highly osmotic and your patient
s level of consciousness. Okay. So, let s look at it one more time really
quick. So, what happens is, we have a decreased level of insulin or essentially, what happens
is, the body is no longer producing insulin, okay. So, because we do not have insulin,
alright, so our cell can
use glucose and fatty acids to produce energy, right? And so, within the mitochondria, it
can breakdown glucose, it can break down fatty acids to produce ATP, right? But, in order
to use glucose, it has to have insulin, right? Okay, so, here s our cell. Glucose is outside
the cell. We ve already talked about this before, that in order to get into the cell,
it needs insulin. So, without the presence of insulin, glucose is unable to get into
the cell. So, glucose is going to remain outside the cell, alright? But the cell has another
way that it can use energy. It can actually break down fatty acids. Okay. So, when these
fatty acids are broken down, we get enough energy to kinda carry out cellular metabolism
but we still remain with this glucose outside the cell, okay. So, what happens when we do
not have insulin, is the cell starts to breakdown fatty acids, okay. This leads to acidosis
which is our pH less than 7.35 and a Bicarb of less than 22. Okay, now it s gonna be an
anion gap acidosis. If you wanna learn more about that, there s actually some really good
videos on youtube by MedCram about what anion gap is, but for our purposes, we just need
to understand this is going to lead to acidosis. Due to this acidosis, we re also gonna see
hyperkalemia. Okay, now, it also leads to, when we don t have insulin, this is also gonna
lead to an elevated glucose level, right? So, glucose is not able to get into the cell.
So, glucose is rising within our blood. So, our glucose continues to rise, continues to
rise because we are not pulling it into the cell to use it, it s the reason these fatty
acids. So, as that glucose rises, this is going to lead to osmotic diuresis, okay? Or
simply means that our osmotic pressure becomes so great, that the kidneys begin to dump it
off. Okay. And this is gonna lead to the renal failure and the elevated creatinine. Okay.
So, that s kinda what s happening here. Two things are happening and that is what we need
to understand. Two things are happening, we re breaking down fatty acids, and that s leading
to acidosis. We re also not using glucose and that s leading to hyperglycemia. Okay.
So, now that we have those two things understood, okay, now, you understand it very simply here,
right? It s very very simple once we break it down like this. We are not, we do not have
insulin available, so, out body has to get that energy from somewhere, right? The place
that is gaining that energy is from breaking down these fatty acids. And, we just said
right there, these are fatty acids. So, we re going to develop acidosis. Okay. And because
of that, we re going to develop hyperkalemia. Now, the other thing that s happening here,
we still have these glucose circulating in the cells, or in the blood. So, we still have
these glucose circulating in the blood that s leading to hyperglycemia, at the same time,
we re developing this acidosis. So, we re Diabetic Ketoacidosis. Okay. So, our blood
sugars are gonna rise, and again, they re not gonna rise as high as they are in like
HNS because we re using a little bit of this energy, okay? So, how are we gonna treat these patients,
okay. We re gonna treat these patients with very intensive insulin therapy. What insulin
is gonna do for us, is it s gonna do a couple of things. Insulin is going to help to correct
this acidosis, okay? It s also going to help to lower the glucose, okay? What our goal
here with Diabetic Ketoacidosis is to correct this acidosis. That s our primary concern
here, it s correcting this acidosis. As we correct that acidosis, our potassium is going
to improve, right? We know that insulin is one of the therapies for hyperkalemia, right?
With insulin, we can pull potassium back into the cell. And, with insulin also, we can correct
acidosis, okay? So, the other thing that is going to do at the same time, however, is
it s going to correct our glucose level. So, as we re correcting our acidosis, we re also
correcting our glucose level. Remember, our patient is also very dehydrated, and so, what
are we gonna get for dehydration? We re gonna get fluids. So, we re gonna get fluids to
our patient, that s gonna correct dehydration due to this osmotic diuresis. So, we correct
that osmotic diuresis by giving fluids and that helps to correct that patient there.
Then, we give our insulin to correct acidosis and that also brings down our blood sugars. Okay, so, we re gonna treat dehydration, we
re gonna place the patient in intensive insulin therapy, we re gonna monitor potassium and
we re going to access for and treat acidosis. If you wanna learn more about this anion gap
acidosis, you can check out the Merck Manual, it s one resource you can check out there.
But, that s really kind of the basics. But if you can draw this diagram, you get DKA,
okay? And if you get DKA, you get the treatments and you re understanding better ABG and everything
that s going on there. Okay? Okay, so that s really what s going on with DKA and that
s how you can understand why it pertains only, well, most commonly to type I Diabetics and
why it s different from HNS. Okay. So, that s what we need to understand here. If you
have any questions with that guys, please let me know.
Dj�.02ӧ����|rh^UKB90CJaJmH sH CJaJmH
sH CJaJmH sH CJo(aJmH sH CJaJmH sH CJo(aJmH sH CJo(aJmH sH CJo(aJmH sH CJo(aJmH sH CJaJmH
sH CJo(aJmH sH CJaJmH sH CJaJWB*`JphCJOJPJQJo(^[email protected]�ehr��fHq� ����;WB*`JphCJOJPJQJo(^[email protected]�ehr��fHq�
vlcYPF=CJaJmH sH CJo(aJmH sH CJaJmH sH CJo(aJmH
sH CJaJmH sH CJo(aJmH sH CJaJmH sH CJo(aJmH sH CJo(aJmH sH CJo(aJmH sH CJo(aJmH sH CJaJmH
sH CJo(aJmH sH CJo(aJH*mH sH CJo(aJmH sH CJaJmH sH CJo(aJmH sH CJaJmH sH CJo(aJmH sH CJaJmH
sH &-�8�8�8�8^9�:�:��BCCC,CfCjC�C�C|D~D�D�����Ǿ������}sj`WMC9CJo(aJmH sH CJo(aJmH sH CJo(aJmH sH CJaJmH sH CJo(aJmH
sH CJaJmH sH CJo(aJmH sH CJaJmH sH CJaJmH sH CJaJmH sH CJaJmH sH CJo(aJmH sH CJaJmH
sH CJo(aJmH sH CJaJmH sH CJo(aJmH sH CJaJmH sH CJaJmH sH CJaJmH sH CJaJmH sH CJo(aJmH
sH �DzI|I��CJo(aJmH sH CJo(aJmH sH ��>@
~D�D|I��a$$a$$,��. ��A!�#��”�$��%�����1�h/R 66666666���� [email protected]`p������6666
[email protected]`p������ [email protected]`p������ [email protected]`p������ [email protected]`p������
[email protected]`p������ [email protected]`p��[email protected]��LNormal$OJPJQJ^JmH
sH nHtH_H|@��| Heading 1a$$�d[$�d$9CJ0OJPJQJo(^JaJ05KH,mH
sH nHtH_H�[email protected]���DDefault Paragraph Font^[email protected]���^Table Normal(:V4�4�l4�4�l2&-�D|I%&'(~D|I)*�
G��z ��Times New Roman;���[SOSimSun5���(SimSun3$��*�Cx� �@��Arial7T�����@ � Calibri5���(SimSunM�RobotoSegoe
Print��HDKA – Diabetic Ketoacidosis Nursing Care NCLEX Review | NRSNGacademy.comAleixAleix
�@���hݣGg:�Gg�@Z&!),.:;?]}���� & 6″0000 00
00000��� ������=�@��]�^���([{� 0 000000��;�[���������[email protected]���P)��?��2�
����� V����� ����0�(

��6 �S�����������?�@

Only registered users can comment.

  1. Thank you this helped a lot! And yes this is what we are struggling more in! But this broke it down to simpler terms.

  2. My mother had ketoneacidocis, type two diabetes me had her own doctor out at home the night before who diagnosed fall stones, less than 24 hours later she collapsed and had a heart attack, her doctor knew she was type two diabetes and did not check her blood sugar levels which were At 24.2 when she went into hospital and hey keytones were 10.8, she was hours from death, and had a heArt attack in the ambulance, most these videos talk about type 1 but this can happen with type 2 diabetes too

  3. Just another THANKYOU! I love your med master podcast as well! /do you cover the Meds more in depth anywhere?

  4. For fluid resuscitation, why does a patient transition from receiving NS to D5W while he/she is still hyperglycemic? I had a patient I took care of in my critical care clinical and I couldn't figure out why the NS was replaced with D5W. Why would you want to increase a hyperglycemic patient's blood glucose?

  5. My husband died this January due to a heart attack. But as a diabetic type 2 he had an kidney infection and ketones in his urine, before he passed.Finding out if they missed he had Ketoacidosis, when they discharged him from the acute outpatients, two days before his heart attack.

  6. Can you get DKA fasting for 21 days.. Drinking fresh water and salt water with baking soda.. Sugars in the range of 65 to 120.. But only using 1.2 units of insulin per day via an omnipod..?

Leave a Reply

Your email address will not be published. Required fields are marked *