2 DIABETES KETOACIDOSIS (DKA) presentation

Lectures note on Diabetes Ketoacidosis

1. DIABETES DIABETES
KETOACIDOSIS (DKA)KETOACIDOSIS (DKA)
Lt Col G SandalaLt Col G Sandala
Ref: Dr. I. A. Lyaruu MD, Msc, MmedRef: Dr. I. A. Lyaruu MD, Msc, Mmed

2. IntroductionIntroduction
•Is an acute complication of diabetes mellitus (DM) and most
frequently occurs in Type 1 DM. It is rare in Type 2 DM, but
can occur
•Mortality increases with age and is usually due to an
associated catastrophic illness (MI, CVA, sepsis etc) or acute
complications.

3. IntroductionIntroduction
•Precipitating factors for DKA (in a diabetic pt)
–Infections
–Reduction in insulin dosage
–Missed injections
–Failure to ↑ insulin dose during illness

4. PATHOLOGYPATHOLOGY
•Hyperglyceamia
•Hyperketoneamia
–The above are usually secondary to severe insulin
deficiency and ↑ secretion of the counerregulatory
hormones

5. PATHOLOGYPATHOLOGY
Resulting effects of the above
•↑ mobilization and delivery of substrates from
muscles (aa, lactate, pyruvate) and adipose
tissue (FFA, glycerol) to the liver
•↑ gluconeogenesis resulting into increased
glucose production and hence hyperglycemia (
usually > 300 mg/dl)

6. Resulting effects;Resulting effects;
•Increased ketogenesis leading to increased
production of ketone bodies (β-
hydroxybutyrate and acetoacetate) →
Hyperketonemia. → acidosis (pH < 7.35)
•Both hyperglycemia and Hyperketonemia
contributes to increase the osmolarity of blood
resulting to osmotic diuresis ultimately leading
to dehydration.

7. Mechanisms of AcidosisMechanisms of Acidosis
•Hyperketoneamia
•Loss of Na
+
with ketones and its replacement
with H
+
•Kussmaul breathing → loss of CO
2 →
decrease in HCO
3 → increase in pH of blood.

8. CLINICAL FEATURES OF DKACLINICAL FEATURES OF DKA
•Polyuria and polydypsia
•Dehydration (dry skin and mucous
membranes)
•Abdominal pain (usually periumbilical
mimicking an acute abdomen), anorexia,
nausea and vomiting.
•Paralytic ileus in severe cases

9. CLINICAL FEATURES OF DKACLINICAL FEATURES OF DKA
•Tachycardia
•Orthostatic hypotension
•Depressed mental function
•Deep and rapid respiration (Kussmaul).
•Sweet sickly smell on the patient’s breath
(acetone breath)

10. DIAGNOSIS OF DKADIAGNOSIS OF DKA
•Clinical features above
•↑ serum glucose levels (250 – 1000 mg/dl)
•↑ Serum ketone levels (qualitative assessment
using ketostix (strips) or acetest (tablets).
These tests are based on the reaction between
nitroprusside and acetoacetate.
•Presence of ketonuria.

11. Other laboratory testsOther laboratory tests
•Serum pH
•Na
+
or K
+
anions
•Serum HCO3 → decreased

12. Other laboratory testsOther laboratory tests
•Serum Na
+
→ decreased 2
o
to hyperosmolarity
→ shift of water from extra vascular space into
the intravascular space.
•↑ serum creatinine
•Serum potassium, phosphate and magnesium
may be low normal or high

13. –In elderly death is associated with presence
of infection in many cases
–In children death is associated with cerebral
edema as a complication of DKA

14. MANAGEMENT OF DKA MANAGEMENT OF DKA
(GOALS)(GOALS)
•Correction of fluid and electrolyte imbalance
•Reversal of metabolic abnormalities (insulin
treatment)
•Detection and treatment of precipitating
illnesses (infection)

15. TREATMENTTREATMENT
1. Restoration of vascular volume;
•Fluid deficit is approx. 5 – 12 L
•Sodium deficit

16. TREATMENTTREATMENT
•Regime for fluid administration
–1 L in 30 mins
–1 L in the following 1 hr.
–1 L every 2 hrs (to be adjusted in 6 hrs depending
on the response to fluid therapy)
•When glycemia falls to levels ≤ 11.1 mmol/L
dextrose solutions are introduced to avoid
hypoglycemia and minimize the risk of
cerebral edema.

17. TREATMENTTREATMENT
2. Insulin Therapy
•Short acting insulin is used
–0.1 U/kg of insulin given as a bolus i.v.
–0.1 U/kg of ins. actrapid sc. every 1 – 2 hrs till
glycemia is approx. 11 mmol/L, then adjust the
dose and frequency for the insulin injections

18. TREATMENTTREATMENT
3. Electrolyte (K
+
) Replacement Therapy
•how ever serum K
+
levels may be low, normal or high at
presentation
•insulin + fluid replacement → ins-mediated shift of K
+
into the
intracellular space + extracellular dilution of K+ →
hypokalemia

19. TREATMENTTREATMENT
4. Correction of acidosis
•In most patients acidosis disappears with
standard therapeutic measures (Fluids and
insulin).
•Correction with alkali (bicarbonate) is
unnecessary.

20. TREATMENTTREATMENT
Note:
–Insulin reduces lipolysis → ↓ FFA flux to the liver →
decrease ketogenesis and hence lowers the acidosis.
–Keto acids are oxidized leading to regeneration of HCO3
→ decrease acidosis
•Correction with bicarbonate is indicated in severe
cases of acidosis (pH < 7.0)
•Therapy should be discontinued when pH rises to
above 7.1

21. TREATMENTTREATMENT
5. Treat any associated infection (s) with
appropriate antibiotics.

22. THANK YOUTHANK YOU