Management of Diabetic Keto Acidosis (DKA) involves fluid replacement, insulin administration, electrolyte monitoring and correction, and treating any precipitating factors. DKA results from a lack of insulin causing ketone production and metabolic acidosis. Initial management focuses on intravenous fluid resuscitation and insulin therapy to lower blood glucose levels. Potassium levels must be closely monitored and supplemented as needed. While bicarbonate therapy was historically used, its benefits are now controversial. With proper management, mortality rates for DKA have decreased to 5-10%, but complications can still include cerebral edema, pulmonary edema, thromboembolism and cardiac issues.

1. Management of Diabetic
Keto Acidosis

2. PLAN
•
•
•
•
•
•
•
•
•
•
Definition
Etiology
PATHOGENESIS
Clinical manifestation
Physical examination
Differential Diagnosis
Laboratory findings
MANAGEMENT
PROGNOSIS, COMPLICATIONS
REFFERENCES

3. DIFINITION
• DKA is an acute life- threatening Sd caused by
lack Insulin and,
• it represents a derangement of the body`s
normal response to starvation, in IDDM(Type
1).
• DKA=⇑⇑⇑ glycemia+Ketonemia
+Acidosis

4. ETIOLOGY
DKA⇐ Noncompliance with insulin
Infection process,
Stress,
Pregnancy,
Trauma,
Alcohol abuse in DM-type I,
MI, CVA, GIB,
New-onset diabetic.

5. PATHOGENESIS
1.Lack Insulin ⇒ ⇓ Peripheral use of glucose and
subsequently ⇒ ⇑⇑⇑blood sugar.
⇒Glucose is unavailable for
cellular metabolism
2. Body responses by counter-regulatory
hormones(glucagons,cathecolamines,cortisol and
GH).
Stimulate the production of glucose and ⇒ ⇑⇑⇑blood
sugar.
3.In addition, hepatic gluconeogenesis is stimulated
⇒ ⇑⇑⇑blood sugar.

6. PATHOGENESIS ( CON`T)
• Source of energy is needed, thus liver begins to
break down free fatty acids i.e. LYPOLYSIS
⇒Ketoacids used by the Brain and other tissues as
substrates energy
⇒Ketonemia + Metabolic acidosis.
The acidosis ⇒ Intracellular K+ to shift to extra cellular
space ⇒ relative Hyperkalemia (despite a total body
potassium ⇓ ⇓ ⇓ ⇓).

7. PATHOGENESIS( CON`T)
• Hyperglycemia with Ketonemia ⇒
Hyperosmolar state
⇒osmotic diuresis ⇒ volume depletion,
electrolytes loss and the sequela of DKA.

8. Clinical manifestation
• HISTORY is very important !!!!!!!
A.Hyperglycemia symptom`s:
- Blurred vision
- Polyuria
- Polydipsia DM=
D’se of 3P’s
-Polyphagia
B.DKA symptoms at beginning: Nausea, Vomiting, abd
pain, fruity breath odor.
at progress DKA: Dehydration,
dizziness, weakness, altered mental status/ shock.

9. Clinical manifestation(con`t)
• Physical Examination= Dehydration(dry
mucous membranes, poor skin turgor),
hypotension, tachycardia, ± abd tenderness, ±
stretching of liver capsule, ± tachypnea or
Kusmaul breathing=a rapid, deep,and labored
breathing as compensatory response to MA=>
Air hunger, smell of acetone

10. DIFFERENTIAL DIAGNOSIS
• HHNKS( hyperosmolar hyperglycemic nonketotic
syndrome).
• Alcohol ketoacidosis
• Sepsis
• Gastroenteritis,UTI, Pancreatitis
• Uremia
• Methanol,ethylene glycol or paraldehyde
ingestion
• Starvation ketoacidosis
• Lactic acidosis

11. INVESTIGATIONS
• DKA= Glucose greater than 250mg /dl
= HCO-3 less than 15 meq / l
=pH less than 7.3
= ⇑⇑⇑ β hydroxybutyric acid and
acetoacetic acid ⇒ HAGMAK
= ⇓ Na+ by urinary loss
= Total body K+ ⇓ by renal loss, but because
of the intracellular shifts of K+ because of the
acidosis, K+ serum level is normal or ⇑.
ABG ⇒ MA with AG.
ECG ⇒ Hyperkalemia / Hypokalemia, MI
CXR ⇒ Pneumonia (precipitating factor cause
of DKA), Abd. U/S

12. INVESTIGATIONS
•
•
•
•
•
Urea, creatinine,
URINALYSIS for MCS & KETONES PROTEIN,PROTEIN
ELECTROLYTES,
B/CULTURES
CARDIAC ENZYMES (PRN)

13. MANAGEMENT OF DKA
I.ABC evaluation
II.TWO LARGE VEINS ACCESES
III.Fluid replacement
IV.INSULIN
V.Potassium
VI.BICARBONATE
VII.ADDITIONAL
PROCEDURES

14. MANAGEMENT OF DKA
1.ABC evaluation
2.Fluid replacement
. N. saline 0.9% (NaCl)
1litre/30 mins
1L / 2 hrs
1l over next 2-4hrs
When blood glucose<
15mmoll(250mg/dl)
switch to 5% dextrose 1
litre 8- hourly.
If dehydration is still +,
continue 0.9% saline and
add 5%dextrose 1 litre /
12hrs
Fluid requirement=6-8
L/24hrs except in
elderly people where a
fluid overload is
avoided.
∆ Fluid requirement
should be based on
clinical response
including urinary
output

15. MANAGEMENT OF DKA
3.INSULIN
a. STANDARD PROTOCOL
. 50u soluble insulin in 50ml 0.9%
saline iv via infusion pump:
6u/hr initially
3u/hr if BG
<250mg/dl(12mmoll)
2u / hr if BG<180mg
/dl(10mmoll)
• Check B/Sugar hourly
initially, if no ⇓ Insulin
infusion ⇒ ⇑.
• Aim= to fall 55-110mg (36mmol / l) / hr

16. B.If IV INFUSION OF INSULIN IS NOT
POSSIBLE
1.A loading dose of 10-20 units of soluble insulin in IM
injection, immediately thereafter 5 U/hr.
2. Alternatively, a fast acting insulin
10 -20 u/h in subcutneous injection ( initially 0.3 u/kg body
weight, then 0.1u/kg/hr.
The concentration of BG should ↓ 55-110mg/hr.
If BG does not ↓ after 2 hrs of the commencing TTT, the dose
of insulin can be doubled, still a good response is obtained .
When BG has follen to 180-270mg/dl, the dose of insulin
should be
reduced to 1-4 units/hr ,then consider iv
Glucose
NB: AVOID S/C INSULIN IN Pts WITH LOW BP (SBP<90mmHg).

17. CONT
Restoration of the usual insulin regimen, by SC
injection, should not be instituted untill the
patient is not able to eat , drink normally.

18. MANAGEMENT OF DKA
4.Potassium
.None in first litre of iv fluid
unless < 3.0 mmol / L
. If plasma K+ <3.5mmol give 40
mmol added potassium in
1L fluid
.Avoid infusion rate>
20mmol / hr
.If plasma K+ is 3.5-5.0 mmol,
give 20 added K+
. If >5.0mmol/L or anuric
patient, no added K+
Avoid K+ within the first
6hrs if no K+ monitoring

19. 5.BICARBONATE
Severely acidotic where pH <7.0
TTT =300ml of 1.26% of NaHCO3- infusion /
30min into elarge vein.
∆ but its use is nowdays contreversial.

20. 6.ADDITIONAL PROCEDURES IN MGMNT
OF D KA
. Catheterisation if anuric
status in 3hrs
.NGT to keep stomach empty if
sub / or coma state,
vomiting+++
. CV line if CVS is
compromised for allowing
fluid replacement to be
adjusted accuretely
. Plasma expander
(macromolecular fluid) if
SBP<90mmHg or not rise
with IV saline
. ATB if infection or suspected.
. ECG monitoring in severe
case
. TTT according to the
complications.

21. PROGNOSIS
↑ Mortality = 5 -10%
↑ in elderly
↑ complications

22. COMPLICATION OF DKA
1 CO due to ↑ blood glucose or use hypertonic fluid
and / or Bicarbonate =↑mortality.
2. ARDS.
3. Thromboembolism
4. DIC.(DISSEMINATED INTRAVASC COAG.)
5.ACF. (ACUTE CARDIAC FAILURE)
6.ACUTE GASTRIC DILATATION
7.REBOUND KETO ACIDOSIS
_

23. REFFERENCES
• HARRISSON’S 16th edition-2006
• DAVIDSON’s 20th edition-2006
• EMERGENCY MEDICINE 31th edition