Diabetic

ketoacidosis
 PARTICIPANTS

Ahmed Mahmoud abdelaty

Esmael Elsayed Khalil
Asmaa Naeem zaki
Asmaa Wael Morad
Esmael mohmed Esmael
Ashraf Abdelhameid Ibrahim
Ashraf mohamed salah
Ashraf Mohamed Ali
Asmaa Hesham Barakat

🌿Supervision : dr Mohamed hegazi

🌿Head of department : prof gehan younis
Content
Abstract
Definition
Pathophysiology
Causes
Signs and symptoms
Assessment and diagnostic
findings
Medical Management
Complications
Nursing management
Refrances
Abstract
DKA is a serious acute complications of
Diabetes Mellitus. It carries significant
risk of death and/or morbidity especially
with delayed treatment.
The prognosis of DKA is worse in the
extremes of age, with a mortality rates of
5-10%.
Definition
Biochemically, DKA is defined as
an increase in the serum concentration
of ketones greater than 5 mEq/L,
a blood sugar level greater than 250 mg/dL
(although it is usually much higher),
and a blood (usually arterial) pH less than
7.3.
Pathophysiology of DKA
Insulin deficiency and an increase in
counterregulatory hormones (glucagon,
catecholamines, cortisol) causes the body
to metabolize triglycerides and amino
acids instead of glucose for energy. Serum
levels of glycerol and free fatty acids rise
because of unrestrained lipolysis. Alanine
levels rise because of muscle catabolism.
Glycerol and alanine provide substrate for
hepatic gluconeogenesis, which is
stimulated by the excess of glucagon that
accompanies insulin deficiency.

Glucagon also stimulates mitochondrial

conversion of free fatty acids into
ketones. Insulin normally blocks
ketogenesis by inhibiting the transport of
free fatty acid derivatives into the
mitochondrial matrix, but ketogenesis
proceeds in the absence of insulin. The
major ketoacids produced, acetoacetic
acid and beta-hydroxybutyric acid, are
strong organic acids that create metabolic
acidosis. Acetone derived from the
metabolism of acetoacetic acid
accumulates in serum and is slowly
disposed of by respiration.

Hyperglycemia due to insulin deficiency

causes an osmotic diuresis that leads to
marked urinary losses of water and
electrolytes. Urinary excretion of ketones
obligates additional losses of sodium and
potassium. Serum sodium may fall due to
natriuresis or rise due to excretion of
large volumes of free water.
Potassium is also lost in large quantities.
Despite a significant total body deficit of
potassium, initial serum potassium is
typically normal or elevated because of
the extracellular migration of potassium in
response to acidosis. Potassium levels
generally fall further during treatment as
insulin therapy drives potassium into cells.
If serum potassium is not monitored and
replaced as needed, life-threatening
hypokalemia may develop.

Causes of DKA
⭐Causes of DKA in type 1 diabetes mellitus include the
following:

In 25% of patients, DKA is present at

diagnosis of type 1 diabetes due to acute
insulin deficiency (occurs in 25% of
patients)

Poor compliance with insulin through the

omission of insulin injections, due to lack
of patient/guardian education or as a
result of psychological stress,
particularly in adolescents

Missed, omitted or forgotten insulin

doses due to illness, vomiting or excess
alcohol intake

Bacterial infection and intercurrent

illness (eg, urinary tract infection [UTI])

Klebsiella pneumoniae (the leading cause

of bacterial infections precipitating
 DKA)

Medical, surgical, or emotional stress

Brittle diabetes

Idiopathic (no identifiable cause)

Insulin infusion catheter blockage

Mechanical failure of the insulin infusion

pump

⭐Causes of DKA in type 2 diabetes mellitus include

the following:
 Intercurrent illness (eg, myocardial
infarction, pneumonia, prostatitis, UTI)

Medication (eg, corticosteroids,

pentamidine, clozapine)

Signs and symptoms

General findings in diabetic ketoacidosis

Ill appearance

Dry skin

Labored respiration

Dry mucous membranes

Decreased skin turgor

Decreased reflexes

Characteristic acetone (ketotic) breath

odor
 Tachycardia

Hypotension

Tachypnea

Hypothermia

Assessment and Diagnostic Findings

▪ Blood glucose levels may vary from 300

to 800 mg/dL
▪ Some patients have lower glucose values,
and others have values of 1,000
mg/dL (55.5 mmol/L) or more (usually
depending on the degree of
dehydration).

▪ The severity of DKA is not necessarily

related to the blood glucose level.
Some patients may have severe acidosis
with modestly elevated blood
glucose levels, whereas others may have no
evidence of DKA despite blood
glucose levels of 400 to 500 mg/dL (22.2
to 27.7 mmol/L)

▪ Low serum bicarbonate (0 to 15 mEq/L)

▪ Low PH (6.8 to 7.3) values.
▪ A low PCO2 level (10 to 30 mm Hg)
reflects respiratory compensation
(Kussmaul respirations) for the metabolic
acidosis.

▪ Accumulation of ketone bodies (which

precipitates the acidosis) is reflected
in blood and urine ketone measurements.

▪ Sodium and potassium levels may be low,

normal, or high, depending on the
amount of water loss (dehydration)

▪ Elevated levels of creatinine, blood urea

nitrogen (BUN), hemoglobin, and
hematocrit may be seen with dehydration

Management of DKA

Managing diabetic ketoacidosis (DKA) in

an intensive care unit during the first 24-
48 hours always is advisable. When
treating patients with DKA, the following
points must be considered and closely
monitored:

Correction of fluid loss with intravenous fluids

Correction of hyperglycemia with insulin

Correction of electrolyte disturbances, particularly

potassium loss
 Correction of acid-base Imbalance

1.cOrrection fluid loss

🌲Fluid resuscitation is a critical part of treating

patients with DKA. Intravenous solutions replace
extravascular and intravascular fluids and electrolyte
losses. They also dilute both the glucose level and the
levels of circulating counterregulatory hormones.
Insulin is needed to help switch from a catabolic state
to an anabolic state, with uptake of glucose in tissues
and the reduction of gluconeogenesis as well as free
fatty acid and ketone production.

🌲Initial correction of fluid loss is either by isotonic

sodium chloride solution or by lactated Ringer solution.
The recommended schedule for restoring fluids is as
follows:

Administer 1-3 L during the first hour.

Administer 1 L during the second hour.

 Administer 1 L during the following 2 hours

Administer 1 L every 4 hours, depending on the degree

of dehydration and central venous pressure readings

🌲When the patient becomes euvolemic, the physician

may switch to half the isotonic sodium chloride
solution, particularly if hypernatremia exists. Isotonic
saline should be administered at a rate appropriate to
maintain adequate blood pressure and pulse, urinary
output, and mental status.

🌲If a patient is severely dehydrated and significant

fluid resuscitation is needed, switching to a balanced
electrolyte solution (eg, Normosol-R, in which some of
the chloride in isotonic saline is replaced with acetate)
may help to avoid the development of a hyperchloremic
acidosis.

🌲When blood sugar decreases to less than 180 mg/dL,

isotonic sodium chloride solution is replaced with 5-
10% dextrose with half isotonic sodium chloride
solution.

🌲After initial stabilization with isotonic saline, switch

to half-normal saline at 200-1000 mL/h (half-normal
saline matches losses due to osmotic diuresis).

🌲Insulin should be started about an hour after IV

fluid replacement is started to allow for checking
potassium levels and because insulin may be more
dangerous and less effective before some fluid
replacement has been obtained.

🌲Although the incidence of life-threatening

hypokalemia due to aggressive insulin
administration is very low, there is little
to no advantage in starting insulin prior
to rehydration and evaluation of serum
potassium levels. Initial bolus of insulin
does not change overall management of
DKA. [30]
🌲Protocols to minimize the risk of
cerebral edema by reducing the rate of
fluid repletion vary. The International
Society for Pediatric and Adolescent
Diabetes (ISPAD) Clinical Practice
Consensus Guidelines suggest initial fluid
repletion in pediatric patients should be
10-20 mL/kg of normal saline (0.9%)
solution during the first 1-2 hours
without initial bolus, and then, after 1-2
hours

Insulin Therapy

⬆️When insulin treatment is started in

patients with DKA, several points must
be considered. A low-dose insulin
regimen has the advantage of not
inducing the severe hypoglycemia or
hypokalemia that may be observed with a
high-dose insulin regimen.

⬆️Only short-acting insulin is used for

correction of hyperglycemia.
Subcutaneous absorption of insulin is
reduced in DKA because of dehydration;
therefore, using intravenous routes is
preferable.

⬆️SC use of the fast-acting insulin analog

(lispro) has been tried in pediatric DKA
(0.15 U/kg q2h). The results were shown
to be comparable to IV insulin, but
ketosis took 6 additional hours to
resolve. Such technically simplified
methods may be cost-effective and may
preclude admissions to intensive care
units in patients with mild cases. Use of
subcutaneous insulin analog (aspart) has
been shown to be effective as well in
adults.

⬆️The initial insulin dose is a continuous

IV insulin infusion using an infusion pump,
if available, at a rate of 0.1 U/kg/h. A
mix of 24 units of regular insulin in 60
mL of isotonic sodium chloride solution
usually is infused at a rate of 15 mL/h (6
U/h) until the blood glucose level drops
to less than 180 mg/dL; the rate of
infusion then decreases to 5-7.5 mL/h
(2-3 U/h) until the ketoacidotic state
abates.
⬆️Larger volumes of an insulin and
isotonic sodium chloride solution mixture
can be used, providing that the infusion
dose of insulin is similar. Larger volumes
may be easier in the absence of an IV
infusion pump (eg, 60 U of insulin in 500
mL of isotonic sodium chloride solution
at a rate of 50 mL/h).

⬆️The optimal rate of glucose decline is

100 mg/dL/h. Do not allow the blood
glucose level to fall below 200 mg/dL
during the first 4-5 hours of treatment.
Hypoglycemia may develop rapidly with
correction of ketoacidosis due to
improved insulin sensitivity.
⬆️Allowing blood glucose to drop to
hypoglycemic levels is a common mistake
that usually results in a rebound ketosis
derived by counter-regulatory hormones.
Rebound ketosis necessitates a longer
duration of treatment. The other hazard
is that rapid correction of hyperglycemia
and hyperosmolarity may shift water
rapidly to the hyperosmolar intracellular
space and may induce cerebral edema.

⬆️Although DKA was a common problem

in patients with diabetes who were
treated with continuous subcutaneous
insulin infusion through insulin infusion
pumps, the incidence of DKA was
reduced with the introduction of pumps
equipped with sensitive electronic alarm
systems that alert users when the
infusion catheter is blocked.

Electrolyte Correction

💯if the potassium level is greater than 6

mEq/L, do not administer potassium
supplement. If the potassium level is 4.5-
6 mEq/L, administer 10 mEq/h of
potassium chloride. If the potassium
level is 3-4.5 mEq/L, administer 20
mEq/h of potassium chloride.

💯Monitor serum potassium levels hourly,

and the infusion must be stopped if the
potassium level is greater than 5 mEq/L.
The monitoring of serum potassium must
continue even after potassium infusion is
stopped in the case of (expected)
recurrence of hypokalemia.

💯In severe hypokalemia, not starting

insulin therapy is advisable unless
potassium replacement is under way; this
is to avert potentially serious cardiac
dysrhythmia that may result from
hypokalemia.

💯Potassium replacement should be

started with initial fluid replacement if
potassium levels are normal or low. Add
20-40 mEq/L of potassium chloride to
each liter of fluid once the potassium
level is less than 5.5 mEq/L. Potassium
can be given as follows: two thirds as
KCl, one third as KPO4.
Correction of Acid-Base Balance

Sodium bicarbonate only is infused if

decompensated acidosis starts to
threaten the patient's life, especially
when associated with either sepsis or
lactic acidosis. If sodium bicarbonate is
indicated, 100-150 mL of 1.4%
concentration is infused initially. This
may be repeated every half hour if
necessary. Rapid and early correction of
acidosis with sodium bicarbonate may
worsen hypokalemia and cause
paradoxical cellular acidosis.
Diabetic Ketoacidosis Complications

Low blood sugar or hypoglycemia

Low potassium or hypokalemia

Brain swelling (cerebral edema) if your

blood sugar levels are adjusted too
quickly

Loss of consciousness

Death
Nursing interventions

➡️Monitor Blood Glucose Levels:

Consistently elevated blood glucose

levels, exceeding 400 mg/dL, serve as
the primary indicator of ketone
production in DKA. Regular monitoring of
blood glucose levels is imperative to
gauge the effectiveness of treatment
and to guide insulin administration.
Hourly blood glucose checks may be
required for the patient who is critically
ill or on an insulin drip.

➡️Maintain fluid balance:

Preventing dehydration and related

complications, such as sodium, potassium,
calcium, and magnesium imbalances, is
crucial in DKA management. Excessive
blood glucose levels can lead to nausea
and vomiting, exacerbating fluid losses.
Electrolyte deficiencies can ensue,
heightening the risk of cardiac
arrhythmias and other complications.
Close monitoring of fluid intake and
output, as well as electrolyte levels,
informs necessary interventions such as
intravenous (IV) fluid replacement and
electrolyte supplementation.

➡️Monitor for and Treat Signs/Symptoms of

Infection:
In many cases, DKA is precipitated by an
underlying infection, such as a
respiratory infection, urinary tract
infection, or flu. Recognizing signs and
symptoms of infection, including fever, is
vital. Prompt administration of
appropriate antibiotics is essential to
combat the infection effectively and
reduce the overall stress on the body,
which can contribute to hyperglycemia
and ketone production.
➡️Administer Medications as Appropriate:

Various medications play a pivotal role in

managing DKA, addressing its underlying
causes and symptoms:

💊Insulin: Administered to lower blood

glucose levels, insulin therapy is a
cornerstone in DKA treatment. It
reduces the need for fat breakdown and
subsequently decreases ketone
production. Insulin may be administered
SQ or by IV drip.
💊Antibiotics: When an infection is
identified or suspected, antibiotics
should be administered promptly to
combat the infection and reduce stress
on the body.

💊IV Fluids: Intravenous fluids are

crucial for maintaining hydration and
restoring fluid balance. They help
correct dehydration, enhance blood
pressure, and support overall
cardiovascular function.

💊Electrolyte Replacement: Electrolyte

imbalances are common in DKA.
Replacement of deficient electrolytes,
such as potassium, is essential for
preventing complications like cardiac
arrhythmias.

💊Antiemetics: Nausea and vomiting are

common symptoms of DKA. Antiemetic
medications can alleviate these
symptoms, facilitating the patient’s
ability to tolerate oral intake and maintain
hydration.

Refrances

https://www.diabetes.org.uk/guide-to-
diabetes/complications/diabetic_ketoacidosis
https://medlineplus.gov/ency/article/000320.ht
m
https://www.ems1.com/ems-
products/ambulance-disposable-
supplies/articles/understanding-the-
presentation-of-diabetic-ketoacidosis-
NekpEYII8WCE32Jn/
https://emedicine.medscape.com/article/118361-
overview?
form=fpf&scode=msp&st=fpf&socialSite=googl
e&icd=login_success_gg_match_fpf#a2
https://www.mayoclinic.org/diseases-
conditions/diabetic-ketoacidosis/symptoms-
causes/syc-20371551