DKA vs HHS | Endocrine System (Part 4)

Summary

In this educational video, Eddie Watson from ICU Advantage explains the differences between Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycemic State (HHS), focusing on their causes, symptoms, and treatments. DKA is common in type 1 diabetics, characterized by high glucose levels, low bicarbonate, and metabolic acidosis. HHS typically affects type 2 diabetics, presenting with severe dehydration without ketosis. The video outlines the pathophysiology behind these conditions and emphasizes the importance of fluid and electrolyte management, insulin therapy, and treating underlying causes for effective patient care.

Takeaways

• 🚑 DKA (Diabetic Ketoacidosis) and HHS (Hyperosmolar Hyperglycemic State) are both hyperglycemic emergencies requiring urgent intervention.
• 🏥 DKA is more common in type 1 diabetics, whereas HHS is typically seen in type 2 diabetics.
• 📈 DKA is characterized by high blood glucose, low bicarbonate levels, and a pH less than 7.3, indicating anion gap metabolic acidosis.
• 🔍 Causes of DKA include new-onset type 1 diabetes, insufficient insulin, stress, infection, trauma, surgery, and alcohol intoxication.
• 🧬 The pathophysiology of DKA involves insulin deficiency leading to increased fatty acid metabolism, ketone production, and fluid loss.
• 🌡 Signs of DKA include fruity breath due to acetone, Kussmaul respirations, abdominal pain, and neurological symptoms like paresthesia and aphasia.
• 💧 HHS is defined by extreme hyperglycemia without ketosis, leading to severe dehydration and high osmolarity.
• 🏋️‍♂️ The onset of HHS is often slow and progressive, potentially developing over weeks to months.
• 🩺 Treatment for both DKA and HHS involves fluid replacement, insulin therapy for hyperglycemia, electrolyte replacement, and treating the underlying cause.
• ⏱ Monitoring is crucial during treatment to prevent complications like cerebral edema and hypokalemia.

Q & A

What are the two hyperglycemic emergencies discussed in the lesson?

The two hyperglycemic emergencies discussed are Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycemic State (HHS).

Who is more likely to experience DKA, type 1 or type 2 diabetics?

DKA is almost primarily experienced by type 1 diabetics, although it can rarely occur in type 2 diabetics.

What are the defining characteristics of DKA?

The defining characteristics of DKA include hyperglycemia, hypovolemia, ketone emia, anion gap metabolic acidosis, a glucose level greater than 300 milligrams per deciliter, a bicarbonate level less than 15 mEq/L, a pH less than 7.3, and the presence of ketones in the blood and urine.

What are some common causes of DKA?

Common causes of DKA include newly diagnosed type 1 diabetes, insufficient insulin administration, stressful events, infections, trauma, surgery, pregnancy, and alcohol intoxication.

How quickly can DKA develop?

DKA can develop in less than 24 hours, oftentimes developing very quickly in patients.

What is the primary difference between DKA and HHS?

The primary difference is that DKA involves the presence of ketosis, whereas HHS is characterized by hyperglycemia with profound dehydration in the absence of ketosis.

What are the typical glucose levels seen in HHS?

Glucose levels in HHS are typically in the range of 600 to 2000 milligrams per deciliter, often around 1100 milligrams per deciliter.

What is the treatment approach for both DKA and HHS?

The treatment approach for both DKA and HHS involves fluid replacement, treating hyperglycemia with IV insulin, electrolyte replacement, and treating the underlying disorder.

Why is fluid replacement a priority in the treatment of DKA and HHS?

Fluid replacement is a priority to prevent cardiovascular collapse due to the profound dehydration and hypovolemia experienced by patients with these conditions.

How do patients with HHS differ in terms of mortality risk compared to DKA?

Patients with HHS have a higher risk of death due to severe volume loss, often dealing with chronically ill patients, CNS dysfunction, and potential complications such as cerebral edema, cardiovascular collapse, renal shutdown, and vascular embolism.

Outlines

00:00

📚 Introduction to Endocrine System Lesson

Eddie Watson welcomes viewers to the fourth lesson on the endocrine system, focusing on the differences between DKA (Diabetic Ketoacidosis) and HHS (Hyperosmolar Hyperglycemic State). He introduces himself and ICU advantage, encourages viewers to subscribe for more critical care educational content, and thanks the audience for their support. DKA and HHS are described as hyperglycemic emergencies requiring quick intervention, typically managed in the ICU.

05:01

🩺 DKA: Definition and Characteristics

DKA is defined as a state of hyperglycemia, hypovolemia, ketone emia, and anion gap metabolic acidosis. It primarily affects type 1 diabetics, with rare occurrences in type 2 diabetics. Key characteristics for identifying DKA include a glucose level greater than 300 mg/dL, a bicarbonate level less than 15 mEq/L (with severity levels going down to less than 5), a pH less than 7.3 (with severity levels down to less than 7.1), and the presence of ketones in the blood and urine. Causes of DKA include new diagnoses of type 1 diabetes, insufficient insulin administration, and stressful events such as infections, trauma, surgery, pregnancy, and alcohol intoxication.

10:04

🌡️ Pathophysiology of DKA

The pathophysiology of DKA involves a rapid development of symptoms within less than 24 hours due to insufficient or absent insulin levels. This leads to an increase in fatty acid metabolism, resulting in ketone production, and an increase in liver gluconeogenesis, contributing to higher glucose levels. Counter-regulatory hormones like glucagon and stress hormones are secreted, which decrease insulin's effectiveness and contribute to the condition. The body's response includes fluid volume deficit, electrolyte imbalance, and acid-base imbalance, leading to symptoms such as osmotic diuresis, dehydration, and neurological symptoms due to cellular dehydration.

15:08

🌡️ Signs and Symptoms of DKA

Signs and symptoms of DKA include acetone breath due to ketone production, Kussmaul respirations as a compensatory response to acidosis, abdominal pain, nausea, vomiting, altered sensorium with symptoms like paresthesia, paresis, paralysis, or aphasia, tachycardia, polyuria, polydipsia, and lethargy, stupor, or unconsciousness due to dehydration. These symptoms are a direct result of the pathophysiology discussed in the previous paragraph.

20:09

🏥 HHS: Definition, Characteristics, and Causes

HHS is defined as hyperglycemia with profound dehydration in the absence of ketosis, typically seen in type 2 diabetics. Glucose levels are usually between 600 to 2000 mg/dL, with dehydration and hyperosmolality as defining characteristics. Causes of HHS are similar to DKA, including stressful events, infections, trauma, and surgery, often occurring in undiagnosed or untreated type 2 diabetes.

25:12

💊 Treatment for DKA and HHS

Treatment for both DKA and HHS involves fluid replacement, treating hyperglycemia with IV insulin, electrolyte replacement, and treating the underlying disorder. Fluid replacement begins with 0.9% normal saline, potentially starting with a rapid bolus, followed by a switch to d5 half ns to prevent hypoglycemia. Insulin treatment protocols vary by facility but aim to reduce glucose levels by 50 to 70 mg/dL per hour. Electrolytes are replaced based on serum levels, with special attention to potassium due to the risk of hypokalemia. Bicarbonate replacement is considered for patients with a pH less than 7. The goal of treatment is to stabilize the patient hemodynamically and facilitate recovery.

🔄 Conclusion and Upcoming Lesson

The lesson concludes with a summary of the key differences and similarities between DKA and HHS, emphasizing the importance of recognizing these conditions for appropriate treatment. Eddie Watson thanks the viewers for watching and encourages them to like, comment, and subscribe for more educational content. He also previews the next lesson, which will discuss the differences between diabetes insipidus and the syndrome of inappropriate antidiuretic hormone (SIADH).

Keywords

💡Endocrine System

The endocrine system is a collection of glands that produce and secrete hormones directly into the bloodstream, regulating various bodily functions. In the video, the endocrine system is the central theme, as the educator discusses DKA and HHS, both of which are conditions related to the pancreas, an important endocrine gland.

💡DKA (Diabetic Ketoacidosis)

DKA is a life-threatening condition that occurs primarily in people with type 1 diabetes, where the body produces high levels of blood sugars and ketones due to insufficient insulin. The video describes DKA as a hyperglycemic emergency characterized by hyperglycemia, hypovolemia, ketone emia, and anion gap metabolic acidosis.

💡HHS (Hyperosmolar Hyperglycemic State)

HHS is another hyperglycemic emergency, typically seen in type 2 diabetics, characterized by severe high blood sugar without ketosis. The video script explains HHS as a state of hyperglycemia with profound dehydration and hyperosmolality, often leading to worse CNS dysfunction and higher mortality rates compared to DKA.

💡Hyperglycemia

Hyperglycemia refers to a condition where there is too much glucose in the blood. It is a common feature of both DKA and HHS, as discussed in the script, and is a result of insufficient insulin or the body's inability to use insulin effectively.

💡Ketosis

Ketosis is a metabolic state where the body, lacking sufficient glucose, starts breaking down fats to produce ketones for energy. The video explains that ketosis is a key feature of DKA but not HHS, leading to symptoms like acetone breath and Kussmaul respirations in DKA patients.

💡Acidosis

Acidosis is a condition where the blood becomes too acidic. In the context of DKA, the video describes it as a metabolic acidosis caused by the accumulation of ketone acids. This is different from HHS, where acidosis, if present, is due to lactic acid buildup from hypoperfusion.

💡Anion Gap

The anion gap is a measure used to determine the cause of changes in the pH of the blood. The video script explains that in DKA, the anion gap increases due to the accumulation of negatively charged ketone bodies, leading to metabolic acidosis.

💡Insulin

Insulin is a hormone that regulates blood sugar levels by allowing glucose to enter cells. The video discusses how insufficient insulin levels lead to DKA and HHS, and how insulin therapy is a critical part of treating these conditions.

💡Osmotic Diuresis

Osmotic diuresis is a condition where excessive glucose in the blood draws fluid out of cells, leading to increased urine production. The video script describes how osmotic diuresis contributes to fluid volume deficit and electrolyte imbalance in both DKA and HHS.

💡Fluid Volume Deficit

Fluid volume deficit refers to a decrease in the body's fluid volume, which can lead to dehydration. The video explains that fluid volume deficit is a significant consequence of both DKA and HHS due to osmotic diuresis and the loss of fluids and electrolytes.

💡Electrolyte Imbalance

Electrolyte imbalance occurs when there is an abnormal amount of electrolytes in the body. The video script mentions that electrolyte imbalance is a common feature of DKA and HHS, with patients losing sodium, potassium, magnesium, calcium, and phosphorus due to osmotic diuresis.

Highlights

Introduction to the differences between DKA (Diabetic Ketoacidosis) and HHS (Hyperosmolar Hyperglycemic State).

DKA primarily occurs in type 1 diabetics, while HHS is more common in type 2 diabetics.

Definition of DKA includes hyperglycemia, hypovolemia, ketone emia, and anion gap metabolic acidosis.

Key characteristics of DKA include high glucose levels, low bicarbonate, low pH, and presence of ketones in blood and urine.

Causes of DKA can include new diagnosis of type 1 diabetes, insufficient insulin, stress, infection, and alcohol intoxication.

Pathophysiology of DKA involves insulin deficiency leading to increased fatty acid metabolism and ketone production.

Fluid volume deficit and electrolyte imbalance are significant in DKA due to osmotic diuresis.

Acid-base imbalance in DKA is characterized by metabolic acidosis due to ketone production.

Signs and symptoms of DKA include acetone breath, Kussmaul respirations, abdominal pain, and neurological issues.

HHS is defined by hyperglycemia, profound dehydration, and absence of ketosis.

Causes of HHS are similar to DKA, often seen in undiagnosed or untreated type 2 diabetes.

Pathophysiology of HHS includes progressive onset and lack of ketosis due to some insulin presence.

Signs and symptoms of HHS often include severe dehydration, altered mental status, and higher mortality rates.

Treatment for both DKA and HHS involves fluid replacement, treating hyperglycemia, electrolyte replacement, and treating the underlying cause.

Fluid replacement in DKA and HHS starts with normal saline and may switch to d5 half ns to prevent hypoglycemia.

Treating hyperglycemia involves IV insulin with the goal of decreasing glucose levels by 50 to 70 per hour.

Electrolyte replacement is crucial to avoid hypokalemia and monitor magnesium, calcium, and phosphorus levels.

Bicarbonate replacement may be necessary for patients with a pH less than 7.

Conclusion of the lesson and预告 of the next lesson on diabetes insipidus and SIADH.

Transcripts

[Music]

all right welcome back you guys to the

fourth lesson in our series on the

endocrine system and in this lesson

we're gonna be talking about the

differences between DKA and HHS and for

those of you who don't know my name is

Eddie Watson and this is ICU advantage

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support our channel and for that I do

want to thank you guys alright so with

that said let's go ahead and begin the

lesson and let's start to talk about DKA

and HHS and really DKA diabetic

ketoacidosis and HHS which is

hyperosmolar hyperglycemic State they're

really both hyperglycemic emergencies

that are similar in some sense but are

also quite different from one another

they essentially are both states of an

acute hyperglycaemia in decompensated

diabetic patients and what's really

important for us to know is that they

require quick intervention and close

monitoring typically in the ICU we're

gonna cover quite a bit of information

here but hopefully at the end of this

lesson you'll have a really good

understanding of what each of these are

as well as how we're gonna take care of

these patients and so with that said

let's go ahead and start right off with

diabetic ketoacidosis

so our first distinction when we talk

about DKA is that this is going to occur

almost primarily with type 1 diabetics

now it can happen but it is pretty rare

for it to occur in our type 2 diabetics

and so our DKA is really defined as

hyperglycemia hypovolemia ketone emia

anion gap metabolic acidosis

so I know that was a mouthful and we

definitely will get into explaining that

more here and just a bit but this is

really our definition of what DK is but

there really are some key

characteristics that we're going to be

looking for and identifying these

patients with DKA the first of these is

going to be a glucose level greater than

300 milligrams per deciliter we're also

gonna see a bicarb that's less than 15

mil equivalents per liter although in

moderate DKA we could see this less than

10 and in severe DK that can even be

less than 5 we're also gonna see our

patients with a pH that's less than 7.3

although once again for moderate DK this

can be less than 7.2 and in severe DKA

we're gonna often see this less than 7.1

and finally our patients are gonna have

ketone emia & ketonuria present and what

this means is that we're gonna see

ketones in the blood and ketones in the

urine so now that we know what these

defining characteristics are let's talk

about some of the causes for DK and the

first and primary one that I want to

talk about is really our patients who

are newly diagnosed with type 1 diabetes

and oftentimes that's how these patients

are first diagnosed by having some sort

of event that leads them into DKA

other causes could also be things like

insufficient administration of insulin

as well as stressful events also things

like infection trauma surgery or even

pregnancy and alcohol intoxication can

all lead our patients into decay and so

what is it about these causes that leads

our patient into the state of decay in

order to really tell you about that

we're gonna have to talk about the patho

that goes into this so as we talk about

the patho for this it's important to

know that this can develop in less than

24 hours so oftentimes this DKA will

develop very quickly in these patients

so it's gonna be initiated by having

either insufficient or absent levels of

insulin and as a result of this glucose

is not going to be able to be brought

into their cells and as a result of this

we're gonna see a couple things happen

we're gonna see an increase in our fatty

acid metabolism and as a result of this

this is where we're gonna see our

ketones

we're also gonna see an increase in our

liver gluconeogenesis and this is where

we're gonna get glucose from our

proteins and amino acids and so we're

also gonna see the secretion of our

counter regulatory hormones glucagon and

the stress hormones and these stress

hormones like we've talked about before

those catecholamines the cortisol and

growth hormone these are all released as

a result of stress and what they do is

they actually will decrease the effect

of insulin and being able to lower our

glucose levels but the important thing

to know here is that our body is going

to have more and more of this glucose in

our blood but the cells are going to be

deprived of glucose at the cellular

level and so this is where we're gonna

see the effects of these within our

pathophysiology and we can organize this

into two main components first we are

going to see a fluid volume deficit with

an electrolyte imbalance and we're also

going to see an acid-base imbalance in

our patients so first let's talk about

this fluid volume deficit and this

electrolyte imbalance so we know that

due to the lack of insulin our glucose

levels are going to be high in the blood

and like we just talked about due to the

stress response hormones we are going to

further increase this glucose that is

available as well as we're also going to

see the production of those ketones in

addition to that we also have the

catabolism of protein stores which is

again going to further elevate that

glucose level and so now because we have

all of

this glucose in the blood glucose

actually contributes to osmotic pressure

and so as a result of this osmotic

pressure and hyper osmolality that we're

gonna see fluid shift from the

intracellular to the extracellular space

essentially pulling fluid into our

vasculature and because of this osmotic

pressure this is going to lead to

osmotic diuresis and because we have

this hypotonic loss of fluid due to this

diuresis that this is going to cause

this intracellular and extracellular

fluid volume deficit and the electrolyte

loss that goes along with it and so as

we lose this water through the urine

we're also going to lose our sodium our

magnesium calcium and phosphorus in our

patients potassium may either be low or

high depending on a few different

factors depending on if our patient is

experiencing nausea or vomiting how

their fluid status is as well as their

acid-base imbalance which we're going to

talk about here in a minute now for this

volume deficit if this progresses far

enough this can even lead our patients

into hypovolemic shock in addition to

this we're gonna see a decrease in the

GFR rate in our kidneys for glucose

which means we're gonna have a difficult

time clearing glucose via the kidneys

which is going to contribute to this

cycle of progression that we see and

then finally due to this volume deficit

we could see the dehydration of cells in

our brain which are going to lead us to

the neurological symptoms that we see

and we will talk about those signs and

symptoms that we'll see in our patients

here in a minute but next I want to move

on and talk about this

acid-base imbalance that we're going to

see and so we know with our cells that

they're gonna starve without glucose and

so the body is going to attempt to use

fats and proteins to produce glucose

thinking that's what the cells need and

so specifically as we're metabolizing

these

it's we're gonna see the production of

ketone acids and this is going to cause

a metabolic acidosis you're also going

to see the production of acetone which

will play an important role in one of

the signs and symptoms that will pick up

on here in a minute but if you remember

we were just talking about the fluid

volume deficit and the hypovolemia that

our patients are going to be

experiencing which this is going to lead

to decreased tissue perfusion causing

our cells to switch into a anaerobic

metabolism to which a byproduct of that

is going to be our lactic acid which is

going to further worsen our metabolic

acidosis and so because of this

metabolic acidosis that this is where

we're going to see an increase in our

anti n gap and normally our anion gap

we're gonna see is between 12 and 14 and

what's happening is our body is normally

maintaining a ratio of our sodium and

potassium to our chloride and bicarb and

so our calculation for this we normally

add together our sodium and potassium

then we add up our chloride and bicarb

and we subtract that from the total of

the sodium and the potassium and this is

what gives us our anion gap oftentimes

because of the low number you'll see the

potassium eliminated from this

calculation and we'll just subtract the

chloride and bicarb

our sodium and this calculation is how

we determine our anion gap but once

again because of this osmotic diuresis

we're gonna see a low bicarb and we're

not going to have the bicarb available

to buffer this metabolic acidosis that

we have going on and we'll see this

reflected in an increase in this anion

gap and so as a result of this decreased

bicarb in this metabolic acidosis

the respiratory system is going to

attempt to compensate and so what it's

going to do is attempt to blow off co2

by increasing our respiratory rate and

increasing our tidal volume to try and

bring that pH back up into a normal

level if you want to understand this

a little bit more I'm gonna link to a

lesson that I did on our arterial blood

gases which will explain this a little

bit more for you guys this acidosis

we're also gonna see spillover into an

intracellular acidosis

so the insides of our cells are going to

be acidotic which is going to lead to a

potassium shift and so it's going to

move potassium from inside the cell

outside and attempt to lower the pH of

the cell and then because of this level

of potassium in the blood the kidneys

are going to work to excrete this as

well as we're gonna lose that potassium

as a result of that fluid volume loss

and so this can become a problem later

because as we administer insulin and

these patients that we can induce a

shift of potassium back into the cell

and lead to a state of hypokalemia in

these patients because we've excreted

that potassium out at this point all

right so this was a pretty complicated

but interconnected pathology between

this fluid volume deficit and

electrolyte imbalance as well as this

acid-base imbalance that we're going to

see in our patients so next let's talk

about some of the signs and symptoms

that we are going to see in these

patients the first thing I'm going to

mention is acetone breath and that's a

fruity smelling breath because of this

acetone production which has a fruity

smell to it we're also going to see

something called Kussmaul respirations

and essentially this is rapid deep

breathing and this is a result of that

respiratory system attempting to

compensate for the acidosis these

patients oftentimes are going to have

abdominal pain and nausea and vomiting

you could also see an altered sense

aureum these are going to be things like

paresthesia which is the tingling

prickling chilling burning sensation

they could experience paresis or muscle

weakness pleasure or paralysis or even

aphasia which is the loss of an ability

to either understand or express speech

you're also going to see tachycardia

polyuria

which is excessive urination polydipsia

which is going to be an excessive thirst

and depending on the extent of our

dehydration

they could be lethargic stupor Asst or

unconscious and so hopefully all these

signs and symptoms make sense as a

result of what we just talked about

within this pathophysiology all right so

we talked about quite a bit so far here

for DKA but I actually want to move on

right now and talk about our HHS and so

like we talked about what DK that that's

primarily going to be seen in our type 1

diabetics HHS is typically going to be

seen in our type 2 diabetics but unlike

type 1 which is oftentimes first

diagnosed in children it's going to be

pretty rare for us to see type 2

diabetes and children although lately we

have been seeing an increase in our

childhood obesity rates and this is

actually leading to an increase in our

seeing HHS and children now our HHS is

really defined as a hyperglycemia with a

profound dehydration in the absence of

ketosis and we also have a set of

defining characteristics for this as

well and for HHS we're gonna see glucose

levels that are usually in the range of

600 to 2,000 although typically they're

around 1,100 you're also gonna see

profound dehydration and that hyper

osmolality and so the defining

characteristic of this glucose level

you're gonna see is going to be

oftentimes much higher than what we see

in DKA now for our causes they're

actually going to be very similar to

what we see in DKA

so again stressful events infection

trauma surgery but this is where you're

often gonna have undiagnosed or

untreated type 2 diabetes so now let's

move in and talk about some of the paths

though

we're gonna see in HHS and a lot of it

is actually going to be very similar to

what we see in DKA with a few

differences now the first is that the

onset is often progressive and it's not

quick like we see in dk and in fact we

can even see this happen over weeks to

months now in these patients because

they have some insulin that's being

secreted we're not gonna see that

lipolysis and thus no overproduction of

ketones and ketosis and so that means

we're not gonna see the acetone breath

we're not going to see koo smalls

respirations and we're often not going

to see abdominal pain and nausea and

vomiting in these patients and because

of the lack of these symptoms this often

is going to keep our patients from

seeking treatment earlier now because of

the extremely high glucose levels that

we talked about we're gonna see much

higher osmotic pressure and therefore

significantly higher diuresis than what

we see in DKA and this is what's going

to lead to that profound dehydration

oftentimes our volume deficit in these

patients is going to be 9 to 10 liters

we are also going to see those decreased

electrolytes due to the diaeresis and

dehydration but more often than not

we're gonna see a normal pH in these

patients if we do see acidosis or the

patients are acidic this is going to be

due to lactic acid buildup from

hypoperfusion not ketoacidosis like we'd

see in DKA and those are essentially the

differences in the path that we're going

to see with HHS here now we already

talked about some of the differences

that we're going to see and our signs

and symptoms but it is important to know

that the CNS dysfunction and our

mortality rates are often going to be

worse with HHS due to that severe volume

loss that they're experiencing and the

fact that we're often dealing with

chronically ill patients here and so

that's going to contribute to this

increase in mortality and so our concern

for our patients dying is going to be a

result of either CNS depression of

either our cardiac

respiratory centers cerebral edema

cardiovascular collapse due to that

profound dehydration

we could see renal shutdown or even

there at a high risk for vascular

embolism

so our risk of death in these patients

is definitely increased compared to that

of DKA all right so that pretty much

gives you a good overview of DKA and HHS

and some of the similarities as well as

some of the key differences that we see

with this and so now let's talk about

our treatment for these hyperglycemic

emergencies so our treatment for DKA and

HHS it's almost identical and it

revolves around four main areas the

first is our fluid replacement next is

treating the hyperglycemia the third is

our electrolyte replacement and the last

is treating the underlying disorder and

so we'll start with this last one

because it's the simplest as we really

need to just determine whatever the

precipitating event was and treat that

oftentimes for both DK and HHS this

event is going to be some sort of

infection so now let's talk about our

fluid volume replacement and both in DK

and HHS that this is going to be our

priority because we want to prevent that

cardiovascular collapse and so initially

we're going to treat this with our 0.9%

normal saline and often we're going to

start this with a rapid bolus of one to

three liters within the first hour

depending on the patient's blood

pressure and their serum sodium level

and then from there we're going to

continue infusing fluids until that

volume is restored and so once our

patient serum glucose begins to come

back down we'll often switch this normal

saline to a d5 half ns and we're really

doing this to prevent hypoglycemia in

these patients typically for DK once we

reach about 250 is when we're going to

do this although we may do this higher

in patients with HHS in order to prevent

that cerebral edema risk now as we talk

about our next one here the treating of

the hyperglycemia that

is gonna involve IV insulin and this is

one of the big reasons why these

patients may require frequent monitoring

and therefore care in the ICU now with

this insulin treatment we're typically

going to be requiring more for these

patients that are in HHS due to the

really high glucose that we see and we

are gonna see different protocols that

really vary from facility to facility

for these insulin infusions but ideally

our goal is to decrease our glucose

level by 50 to 70 per hour once again

like we just talked about we're gonna

switch the patient to the d5 half an s

but we're also going to decrease our

insulin and rate at that time again

trying to prevent hypoglycemia and it's

really important that we do keep the

insulin infusion going until we have a

normal pH and this is really to avoid

that intracellular hypokalemia which

we'll talk about more as we talk about

our electrolyte replacement so once

again we're typically going to see these

deficits present both in our patients

with dk and HHS and if you remember this

is a result of that osmotic diuresis

like I said earlier who might see a

worsening of our patients hypokalemia

due to an acidosis that they have going

on while we're treating them and the

reason for this is like I talked about

with that intracellular acidosis the

cells are going to shift that potassium

outside in order to maintain a normal pH

within the cell and so typically what

you'll see in your patients for every

point one drop in their pH that you're

gonna see their potassium level rise by

0.6 as a result of this potassium shift

and so once again the body is going to

be excreting this excess potassium as

well as we're going to be losing it due

to that osmotic diuresis and so as we

administer our insulin that that

actually draws potassium back into the

cell which can cause a hypokalemia for

our patients and so it's going to be

really important that we

monitoring our patients potassium level

frequently as well as administering

potassium and our goal here is to avoid

those cardiac arrhythmias that are going

to be associated with that hypokalemia

we're also going to be monitoring their

magnesium level calcium level and

phosphorous level because as we

rehydrate them it could further dilute

those levels and so typically we're

gonna be administering and replacing our

magnesium and calcium based on our

patient serum level but typically our

foss is going to correct on its own with

our volume replacement but sometimes we

are going to be giving foss to them as

well important to remember though in our

renal patients we want to be avoiding

this phosphorus replacement finally

based on our patient's bicarb level and

the severity of their acidosis we also

need to be assessing for replacing their

bicarb this is going to be primarily for

our patients with a pH less than 7 and

again as we give the bicarb and raise

that pH that's going to cause that

potassium to go back into the cells and

so we're going to really need to monitor

for that hypokalemia again all right so

that pretty much sums up our treatment

here like I said it's pretty much the

same for DKA and HHS and it's really

revolving around making sure we get the

fluids back controlling their

hyperglycemia replacing the electrolytes

and really treating whatever the

underlying disorder was if we can do all

that we can get our patients back into a

much better more hemodynamically stable

picture and ultimately get them on their

way to recovery alright well we covered

quite a bit of information here the

pathways for DK and HHS are pretty

complex but I hope in talking through

this that some of this make sense for

you guys and you can see how these signs

and symptoms really are a result of

what's happening within this

pathophysiology that we see with these

processes along with that hopefully

you're able to really distinguish

between DK

in HHS because while they are similar in

a lot of ways there are some very key

differences that hopefully you'll be

able to pick up on and recognize all

right and with that said that's gonna

conclude this lesson and I do want to

thank you guys so much for watching I

really hope that you guys found this

lesson useful and if you did please

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series we're actually going to take a

look at the differences between diabetes

insipidus and the syndrome of

inappropriate antidiuretic hormone di

versus SIADH so if you haven't already

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becomes available and in the meantime

head on over and check out the last

series of lessons that we did in which

we did a great review of heart failure

as always thank you guys so much for

watching and you have a great day