diabetic ketoacidosis life-threatening problem that affects people with diabetes. It occurs when the body starts breaking down fat at a rate that is much too fast. The liver processes the fat into a fuel called ketones, which causes the blood to become acidic.

1. 300
Diabetic
Ketoacidosis
By: ANNIE MAE M. TAYOBANA
BSN 3A

2. Diabetic Ketoacidosis
DKA is associated with a relative or absolute insulin
deficiency and a severely elevated blood glucose
level, typically greater than 300 mg/dL.
• Due to the lack of insulin, tissue such as muscle, fat
and the liver are unable to take up glucose.
• Even though the blood has an extremely elevated
amount of circulating glucose, the cells are basically
starving.
• DKA occurs mostly in type 1 diabetes
ANNIE MAE M. TAYOBANA

3. 3 Major Pathophysiologic Syndromes associated with DKA
Metabolic acidosis
It is a condition in which
there is too much acid in
the body fluids.
It develops when
substances called ketone
bodies (which are acidic)
build up during
uncontrolled diabetes.
Osmotic diuresis
It is an excess of urinary
solute, typically non-
reabsorbable, that
induces polyuria and
hypotonic fluid loss.
Electrolyte disturbance
It is caused by osmotic
diuresis leading to a total
body potassium deficiency of
3 to 6 mEq/kg.
When circulating insulin is
lacking, as in DKA, potassium
moves out of cells.
ANNIE MAE M. TAYOBANA

4. Diabetic Ketoacidosis Survey
6.5
Mortality rate
2% to 5% are
emergency cases
Type II Diabetes
major surgery, severe illness
such as myocardial infarction,
or severe infection
Diagnosis
DKA is the first sign of diabetes
but 80% of cases occurred in
previously diagnosed.
Type I Diabetes
9% suffered from DKA
ANNIE MAE M. TAYOBANA

5. Lack of insulin inhibits entry of glucose to cells
with resulting hyperglycemia
ANNIE MAE M. TAYOBANA

6. Diabetic Ketoacidosis
• Without insulin, your body begins to break down fat
in attempt to get the energy it needs, a process that
ultimately results in a dangerous buildup of acids,
known as ketones, in your bloodstream.
• When this happens, your body can go into shock, and
the acid buildup causes swelling in the brain
(cerebral edema).
ANNIE MAE M. TAYOBANA

7. Pathophysiology
In the absence of insulin, glucose in blood
cannot enter tissue cells where it is needed to
provide energy, and the liver inappropriately
continues to release glucose produced from
non-carbohydrate sources and breakdown of
glycogen to the blood
The inevitable consequence is a rising blood
glucose concentration. DKA is often described as
‘starvation in the midst of plenty’ because tissue
cells deficient of their much needed energy
source, glucose, are bathed by extracellular fluid
increasingly rich in glucose.
ANNIE MAE M. TAYOBANA

8. Insulin deficiency causes
the body to metabolize
triglycerides and muscle
instead of glucose for
energy.
Serum levels of glycerol and
free fatty acids (FFAs) rise
because of unrestrained
lipolysis, as does alanine
from 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 FFAs
into ketones. Insulin normally
blocks ketogenesis by inhibiting
the transport of FFA derivatives
into the mitochondrial matrix,
but ketogenesis proceeds in the
absence of insulin.
ANNIE MAE M. TAYOBANA

9. The major ketoacids
produced, acetoacetic
acid and β-
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 caused by
insulin deficiency produces an
osmotic diuresis that leads to
marked urinary losses of water
and electrolytes.
Urinary excretion of
ketones obligates additional
losses of Na and K.
Serum Na may fall from
natriuresis or rise due to
excretion of large volumes of
free water.
ANNIE MAE M. TAYOBANA

10. K is also lost in large
quantities, sometimes >
300 mEq/24 h.
Despite a significant total body
deficit of K, initial serum K is
typically normal or elevated
because of the extracellular
migration of K in response to
acidosis.
Hyperglycemia caused by
insulin deficiency produces an
osmotic diuresis that leads to
marked urinary losses of water
and electrolytes.
K levels generally fall further
during treatment as insulin
therapy drives K into cells. If
serum K is not monitored and
replaced as needed, life-
threatening hypokalemia may
develop.
ANNIE MAE M. TAYOBANA

11. ANNIE MAE M. TAYOBANA

12. POLYPHAGIA
Excessive appetite or
eating
POLYURIA
Excessive urination
POLYDIPSIA
Excessive drinking of
fluids (constant thrist)
DYSURIA
Frequent urination
especially at night
ANNIE MAE M. TAYOBANA
Classic Signs and Symptoms of Hyperglycemia

13. (3)DPOTH
Osmotic diuresis leads to dehydration and a potential hypovolemic state from fluid loss
• Dry and warm skin
• Dry mucous
membranes
• Decreased sweating
• Poor skin turgor
• Orthostatic vital signs
• Tachycardia
• Hypotension
ANNIE MAE M. TAYOBANA

14. Other signs and symptoms
CONFUSION
FATIGUE
LETHARGY
NAUSEA & VOMITING
WEAKNESS
ABDOMINAL PAIN - (especially in children due to
gastric distention or stretching of the liver capsule)
ANNIE MAE M. TAYOBANA

15. • Stress, trauma, sickness, or drug and alcohol abuse can also
alter insulin intake, triggering DKA.
• Acute cerebral edema, 1% of DKA patients & occurs primarily
in children (cause is not well understood but may be related to
too-rapid reductions in serum osmolality or to brain ischemia)
• Fruity breath smell due to exhaled acetone
• Kussmaul’s respirations are present (deep and rapid
respirations); less carbon acid produced thereby increasing pH
value allowing more ketoacids to accumulate.
• ECG changes and dysrhythmias may also result from the
electrolyte disturbance.
ANNIE MAE M. TAYOBANA

16. Diagnosis
• ARTERIAL pH (pH < 7.30 )
• SERUM KETONES (ketone concentration of 3.0 mmol/l)
• CALCULATION OF ANION GAP (>12 mEq/L { (Na+ + K+) –
(Cl- + HCO3-) = Anion Gap})
DKA is diagnosed by an arterial pH with an anion
gap and serum ketones in the presence of hyperglycemia.
• ECG (to screen Acute MI for Adults)- to help determine the
significance of abnormalities in serum potassium.
ANNIE MAE M. TAYOBANA

17. Diagnosis
• Hyperglycemia may cause dilutional hyponatremia (a
serum sodium level of lower than 130 mEq/L)
• As acidosis is corrected, serum potassium drops. An initial
potassium level (potassium ions move out of the cells. To
maintain neutrality, hydrogen ions move into the
intracellular space.)
• Serum amylase and lipase are often elevated, (which may
be present in patients with alcoholic ketoacidosis and in
those with coexisting hypertriglyceridemia).
ANNIE MAE M. TAYOBANA

18. Treatment of DKA
• IV 0.9% saline
• Correction of
hypokalemia
• IV insulin (as long as
serum potassium is ≥
3.3 mEq/L [3.3
mmol/L])
• Rarely IV sodium
bicarbonate (if pH < 7
after 1 hour of
treatment)
Intravascular volume should be restored rapidly to
raise blood pressure and ensure glomerular perfusion;
once intravascular volume is restored, remaining total
body water deficits are corrected more slowly,
typically over about 24 hours
Initial volume repletion in adults is typically
achieved with rapid IV infusion of 1 to 3 L of 0.9% saline
solution, followed by saline infusions at 1 L/hour or faster
as needed to raise blood pressure, correct hyperglycemia,
and keep urine flow adequate.
Adults with diabetic ketoacidosis typically need
a minimum of 3 L of saline over the first 5 hours.
ANNIE MAE M. TAYOBANA

19. ANNIE MAE M. TAYOBANA

20. • IV 0.9% saline
• Correction of
hypokalemia
• IV insulin (as long as
serum potassium is ≥
3.3 mEq/L [3.3
mmol/L])
• Rarely IV sodium
bicarbonate (if pH < 7
after 1 hour of
treatment)
When blood pressure is stable and urine flow
adequate, normal saline is replaced by 0.45% saline.
ANNIE MAE M. TAYOBANA
Treatment of DKA (volume repletion)

21. • IV 0.9% saline
• Correction of
hypokalemia
• IV insulin (as long as
serum potassium is ≥
3.3 mEq/L [3.3
mmol/L])
• Rarely IV sodium
bicarbonate (if pH < 7
after 1 hour of
treatment)
When plasma glucose falls to < 200 mg/dL (<
11.1 mmol/L), IV fluid should be changed to 5% dextrose
in 0.45% saline.
ANNIE MAE M. TAYOBANA
Treatment of DKA (volume repletion)

22. • IV 0.9% saline
• Correction of
hypokalemia
• IV insulin (as long as
serum potassium is ≥
3.3 mEq/L [3.3
mmol/L])
• Rarely IV sodium
bicarbonate (if pH < 7
after 1 hour of
treatment)
For children, (for ongoing losses), initial fluid therapy
should be 0.9% saline (20 mL/kg) over 1 to 2 hours,
followed by 0.45% saline once blood pressure is stable
and urine output adequate.
The remaining fluid deficit should be replaced
over 36 hours, typically requiring a rate (including
maintenance fluids) of about 2 to 4 mL/kg/hour,
depending on the degree of dehydration.
ANNIE MAE M. TAYOBANA
Treatment of DKA (volume repletion)

23. Treatment of DKA
Correction of
Hypergycemia and Acidosis
Insulin 0.1 unit/kg/hour
%5 of Dextrose
Insulin reduced to 0.02 to 0.05
20 to 30 mEq potassium
Used in IV infusion in 0.9% saline solution.
Insulin should be withheld until serum
potassium is ≥ 3.3 mEq/L (≥ 3.3 mmol/L).
plasma glucose becomes < 200 mg/dL
(< 11.1 mmol/L); to reduce the risk of
hypoglycemia
Continuous IV infusion of regular insulin
should be maintained until the anion gap has
narrowed and blood and urine are consistently
negative for ketones.
insulin should be withheld and
potassium given at 40 mEq/hour until
serum potassium is ≥ 3.3 mEq/L
Potassium phosphate, 1 to 2 mmol/kg of
phosphate, can be infused over 6 to 12 hours.
If potassium phosphate is given, the serum
calcium level usually decreases and should
be monitored.
ANNIE MAE M. TAYOBANA
Hypokalemia Prevention
Hypophosphatemia

24. Treatment of DKA
Treatment of suspected cerebral edema
• Hyperventilation
• Corticosteroids
• mannitol
but these measures are often ineffective after
the onset of respiratory arrest.
ANNIE MAE M. TAYOBANA

25. NURSING CARE (Primary Assessment)
Assess air patency.
If the patient is not able
to breathe on his own
insert an oral or
nasopharyngeal airway.
01
Oral Suctioning
It is required when
vomiting occurred.
02
Assess patient
neurological status
Alert and responsive to
verbal or painful stimuli
06
Insert endotracheal tube
To protect airway if
breathing is ineffective
(ex. comatose &
vomiting)
03
Fluid bolus
Must be given if patient
is hypotensive.
05
Assess circulation,
obtain vascular assess,
and start a 0.9% NS
infusion.
04
ANNIE MAE M. TAYOBANA

26. NURSING CARE (Secondary Assessment)
Undress the patient, and
if there's hypothermia,
control temperature
(warmed blankets,
overhead heating lamps,
and warmed IV fluids).
01
Insert nasogastric tube
It is required when
vomiting occurred.
02
Administer analgesia
or antiemetics
To make the patient
comfortable.
06
Insert an indwelling urinary
catheter
To monitor output and
obtain urinalysis.
03
Initiate cardiac monitoring
To check for arrhythmia,
which may result from
electrolyte imbalances.
05
If the patient has been
intubated, place a
nasogastric tube to
decompress the stomach
04
ANNIE MAE M. TAYOBANA

27. • Obtain a thorough history from the patient and family
in order to identify what may have precipitated the
DKA episode.
• Perform a head-to-toe exam to identify
abnormalities, establish a baseline assessment, and
help identify root causes and squeal of the condition.
• The frequency of follow-up assessments will vary
depending on the baseline assessment and stability of
the patient.
• Reassessment includes examination of ABC, and
assessment of neurologic status and vital signs.
ANNIE MAE M. TAYOBANA

28. • Once the patient is extubated, he will need education
in diabetes management in order to prevent
recurrence and sequelae.
• Advise patients to seek professional medical
assistance for uncontrolled fevers, urinary frequency
or discomfort, persistent cough, or ulcerations.
• If antibiotics have been prescribed for these illnesses,
explain the importance of using the entire
prescription, even after symptoms have improved or
subsided.
ANNIE MAE M. TAYOBANA
EDUCATING THE PATIENT

29. • Registered dietitians can reinforce the importance
of proper diet planning and self-management of
diabetes. Patients may also benefit from advice on
how to accommodate dietary modifications when
grocery shopping or dining out.
• Encourage patients to continue their insulin
therapy and medications even when they're
experiencing nausea and vomiting from other
illnesses.
• To prevent DKA and dehydration, instruct patients
to drink liquids containing carbohydrates (such as
sodas, juices, and gelatins) and salt (such as
bouillon)
ANNIE MAE M. TAYOBANA
EDUCATING THE PATIENT

30. • If patients can't keep these fluids down, or if nausea
and vomiting persist for more than a day, they will
need to consult a health care professional.
• Finally, remind patients to tell family members or
friends when they become ill, and to ask family
members to check on them every four hours to
make sure the condition hasn't worsened.
ANNIE MAE M. TAYOBANA
EDUCATING THE PATIENT

31. When To Seek Help
• Altered mental status
• Dyspnea
• Respiratory distress
• Abnormal vital signs
• Unresponsive
ANNIE MAE M. TAYOBANA

32. 300
THANK YOU

ANNIE MAE M. TAYOBANA