Diabetic KETOACIDOSIS

1. INTRODUCTION
- Diabetic Ketoacidosis is an acute metabolic complication of diabetes
characterized by hyperglycemia, hyperketonemia, and metabolic
acidosis.
- Hyperglycemia causes an osmotic diuresis with significant fluid and
electrolyte loss.
- DKA occurs mostly in type 1 diabetes mellitus (DM).
- It causes nausea, vomiting, and abdominal pain and can progress to
cerebral edema, coma, and death.
- DKA is diagnosed by detection of hyperglycemia.
- Treatment involves volume expansion, insulin replacement, and
prevention of hypokalemia.

2. DEFINITION
- Diabetic Ketoacidosis is a state of absolute or relative
insulin deficiency aggravated by ensuring hyperglycaemia,
dehydration and acidosis producing derangements in
intermediary metabolism.
- They are both associated with:
• Insulin deficiency (absolute in TlDM and relative in
T2DM) and hyperglycemia.
• Acid-base abnormalities (ketoacidosis)
• Severe volume depletion.

3. DEFINITION
- Diabetic Ketoacidosis is a state of absolute or relative
insulin deficiency aggravated by ensuring hyperglycaemia,
dehydration and acidosis producing derangements in
intermediary metabolism.
- They are both associated with:
• Insulin deficiency (absolute in TlDM and relative in
T2DM) and hyperglycemia.
• Acid-base abnormalities (ketoacidosis)
• Severe volume depletion.

4. Other hyperglycemic states
Diabetes mellitus
Hyperosmolar hyperglycemic state
Impaired glucose tolerance
Stress hyperglycemia
Other ketotic states
Ketotic hypoglycemia
Alcoholic ketosis
Starvation ketosis
H
yper
glycemia
O
K
A
Ket-. Acidosis
Other metabolic acidosis states
lactic acidosis
Hyperchloremic acidosis
Salicylism
Uremic acidosis
Drug-induced acidosis

5. ROLE OF INSULIN
Insulin
Skeletal m usc le Liver
i glycogenesis
J. gluconeogenesis
i glycogenesis
T protein synthesis
Tissue metabolic spectrum
Adipose t issue
i adipogenesis
J. lipolysis
INSULIN- .
Cat abolism Anabolism
Tissue breakdown
Glycogenolysis, gluconeogenesis,
protein catabolism, lipotysis
Tissue b uildup
Glycogen, protein,
fat synthesis

6. - - - -
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7. CAUSES CAN TRIGGER OKA:
- New diagnosis of diabetes.
- Drugs:
• Antipsychotic agents
• Others: Corticosteroids, sympathomimetic agents, thiazide diuretics...
- Inf ection :Pneumonia, sepsis, urinary tract infection (UTI)
- Lack of insulin - Most common cause of DKA.
• Insulin pump failure.
• Nonadherence to insulin treatment plans:body image issues, financial
problems, psychological factors.
• Umecognized symptoms of new-onset diabetes mellitus.
- Other physiologic stressors: MI, Stroke, Pancreatitis, Trauma.

8. PATHOPHYSIOLOGY
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9. PATHOPHYS IOLOGY
Acetoacetate P-hydroxyl bu tyrate
D-p-hydroxyl bu tyrate
dehydrogenase
NADH + H + NAO +
• Acetone isn't an acid.
• In DKA, the dominant ketoacid is p-hydroxylbu tyric acid, especially in cases
of poor tissue perfusion/ lactic acidosis .
• During recovery, the balance shifts to acetoacetic acid.

10. PATHOPHYS IOLOGY
- Secondary to insulin deficiency, and the action of counter-regulatory
hormones, blood glucose increases leading to hyperglycemia and
glucosuria. Glucosuriacauses an osmotic diuresis, leading to water &
solutes loss.
- In the absence of insulin activity the body fails to utilize glucose as fuel
and uses fats instead ketosis (acetoacetate & -hydroxyl butyrate)
- The excess of ketone bodies will cause metabolic acidosis, the later is
also aggravated by lactic acidosis caused by dehydration & poor tissue
perfusion.
- Vomiting due to an ileus, plus increased insensible water losses due to
tachypnea will worsen the state of dehydration.
- Electrolyte abnormalities are secondary to their loss in urine and trans
membrane alterations fallowing acidosis & osmotic diuresis.

11. PATHOPHYS IOLOGY
- Because of acidosis, K+ions enter the circulation leading to
hyperkalemia, this is aggravated by dehydration and renal failure.
- So, depending on the duration of DKA, serum K at diagnosis may be
high, normal or low, but the intracellular K stores are always depleted.
- Na+loss occurs secondary to the hyperosmotic state & the osmotic
diuresis.
- The dehydration can lead to decreased kidney perfusion and acute
renal failure.
- Accumulation of ketone bodies contributes to the abdominal pain and
vomiting.
- P-hydroxyl butyrate can serve as an energy source in the absence of
insulin-mediated glucose delivery, and is a protective mechanism in
case of starvation.

12. PATHOPHYSIOLOGY
Dehydration: 6 liters or more, 15-20%of their weight.
Osmotic Diuresis: Blood glucose exceeds the renal threshold (160-180mg/ dL)
• Vomiting
• Hyperventilation .
• Impaired consciou sness- Decreased intake.
Metabolic acidosis: Initially due to the excess ketones. Compensatory mechanisms:
• Respiratory compensation
• Intracellular buffering- excess H+goes into cells in exchange for potassium.
• Bicarbonate buffering system.
Ionic changes:
• A general loss of electrolytes due to osmotic diuresis.
• Potassiu1n:intracellular bufferin g mechanism shifts potassium out of cells so even if there
decreased total potassium in the body, serum potassium may initially be normal or even high.
This potassium is further lost through the kidneys.
Paradoxes of OKA
Hyperglycemin despite decreased intake
Polyuria despite dehydration
Catabolic state despite hyperglycemia

13. THOROUGH HISTORY is imperative!
•
New onset diabetes
Recent history of
Polyuria, polydipsia, polyphagia,
weight loss
Pass medical history
Family history of diabetes
History/Du ration of syn1
ptoms
• Headache
• Blurry vision
• Nausea/ Vomiting/ Abdominal pain.
• Difficulty in breathing
• Changes in behavior
Precipitatingfactor :
• Concurrent illness or infection
•
Preexisting diabetes
History of diabetes and duration:
• Last meal/ Carbohydrate intake
• Current and routine blood glucose
levels
- Standard insulin regimen
• Last insulin dose
• Type of insulin and route
- Past hospitalization history
- Duration of sy1nptoms
• Nausea/vomiting/ abdominal pain
- Precipitatingfactors:
• Physical exertion
• Change in eating habits/ diets
• Stress, missed insulin dose, illness

14. condition can develop in afew hours.
Early symptoms include the following:
• Thirst or a very dry mouth.
• Frequent urinary
• High blood glucose level.
• High levels of ketones in the urine.
Then, other symptoms appear:
• Constantly feeling tired.
• Dry or flushed skin.
• Nausea, vomiting, or abdominal pain .
• Difficulty breathing .
• Fruity odor on breath .
• Confusion
THE WARNING SIGNS
DKA usually develops slowly. But when vomiting occurs, this life-threatening
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15. LABORATORY EVALUATION
- Initial Labs:
• Blood glucose
• Urine ketones
• Venous blood gas
• Basic blood chemistry: Electrolytes, BUN, creatinine,
Magnesium, Calcium, Phosphorus.
- Ad ditional labs:
• CBC
• Osmolality
• Serum P-hydroxyl butyrate (p-OH)
• Hemoglobin AlC (HbAlC)
• Pancreatic antibodies.
• Additional testing as indicated: CXR, non-contrast head
CT, cultures (blood, urine, throat)
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16. LABORATORY EVALUATION
- Blood Gases:
• ABG - artery blood sample or VBG - V enous blood sample are both
adequate to determine blood pH .
• VBG is sufficient who are hemodynamically stable and without
respiratory failure.
);
;
>Metabolic acidosis is defined as a low pH and decreased HC0 3-
);
;
>Metabolic alkalosis is defined as a high pH and increased HC0 3-

17. LABORATORY EVALUATION
Calculations for the Evaluation of Diabetic Ketoacidosis
Value Purpose Formula Normal value

18. DIAGNOSIS
ADA Diagnostic Criteria for DKA
IParameter I
IPlasma glucose, mg/ dL
IArterial pH
!Serum bicarbonate (mmol/ L)
Serum ketones
Urine ketones
I : I
Effective serum osmolality(mOsm/ kg)
IAlteration in sensoria or mental
>250 >250 >250
7.25-7.3 7.0-7.24 <7.0
15-18
Positive
Positive
10 to <15
Positive
Positive
<10
Positive
Positive
Variable Variable Variable
Alert
Alert/ Drowsy Stupor/ Coma
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19. MANAGEMENT
- Initial Hospital Management:
• Fluid Replacement
• Potassium Replacement
• IV insulin therapy
• Bicarbonate and Metabolic Acidosis
• Phosphate Depletion
• Close Monitoring
• Watch for complications
- Once Resolved:
•
•
Convert to home insulin regimen
Prevent recurrence

20. BICARBONATE THERAPY
Bicarbonateadministration is also controversial.
Several potential harmful effects:
If bicarbonate infusion successfully increases the blood bicarbona te concentration, this can reduce the hyperventilatory
drive, which will raise the blood pC0 2 . Increase blood C 02 tension is more qu ickly reflected across the blood brain
barrier than the increased arterial bicarbona te. This may cause a paradoxical fall in cerebra l pH. Although neurologic
deterioration has been attributed to this mechanism, it rema ins a very controversia l effect and, if it occurs, is rare.
The ad ministra tion of alkali may slow the rate of recovery of the ketosis
Alkali administration can lead to a posttrea tment metabolic alkalosis since metabolism of ketoacid anions with insulin
results in the generation of bicarbonate and spontaneous correction of most of the meta bolic acidosis.
Source: Uptodate.com
Benef it from cautious alkali therapy:
Patients with an arterial pH 6.9 in whom d ecreased card iac contractility and vasodila tation can impair tissue perf usion.
At an arteria l pH above 7.00, most experts agree that bicarbonate therapy is not necessary, since therapy w ith insu lin and
volume expansion will largely reverse the metabolic acid osis.
Patients with potentially life-threatening hyperkalemia, since bicarbonate administra tion in academic patients may
d rive potassium into cells, thereby lowering the seru m potassium concentration.
Source: Up todate.com
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