This document describes the case of an 8-year-old girl brought to the emergency department with vomiting, breathlessness, fever, and altered mental status due to diabetic ketoacidosis (DKA). Her history of type 1 diabetes and discontinuing insulin therapy for 2 days contributed to the development of DKA. On examination, she had a low blood pressure, tachycardia, and altered mental status. Laboratory findings showed high blood glucose, low bicarbonate, and ketones in the urine, consistent with DKA. She was treated according to the Milwaukee protocol for DKA, which involves slow correction of dehydration with intravenous fluids, administration of insulin, and monitoring of electrolytes and mental status. Her

1. Fluid therapy in Diabetic
ketoacidosis
Dr. Mansoor Elahi

2. Case report

3. • A 8 yr old girl first in birth order born out of
non- consanguineous parentage brought to
casualty with
Chief complaints of Vomitings and
Breathlessness associated with fever since 3
days.
Seizure like activity 1 episode & Altered
Sensorium since 1 day.

4. Brief History
• Child was a known diabetic patient and on
insulin therapy since 2 years.
• History of discontinuation of insulin for 2 days.
• She didn’t had similar complaints previously.
• On evaluation of history, child was on 15 and
10 units of mixtard insulin in morning and
evening respectively.

5. O/E
• Child was in altered sensorium , her GCS was 6/15
• Sunken eyes
• No pallor / CY / I/ L/ O / CL
• Vitals :
• Temp 100F,
• PR = 146 / min, Low volume pulses, regular rhythm, No
radioradial / femoral delay, All peripheral pulses felt
• RR = 58 / min, deep breathing
• BP = 90/50 mmHg, Rt. Arm supine posture
• Saturation was 96% without O2

6. • Child was put on IV access and sent blood
investigations for RBS, VBG analysis.
• Correction of Dehydration :
Started on NS boluses 20ml/kg over 30min,
intially with monitoring of vitals and
proceeded to further 20 ml/kg as the child
was not improving and continued it for 1 hr.

7. On Monitoring
• Child still in altered sensorium
• Her vitals shows PR = 108/min
• RR = 56/min, Acidotic breathing
• BP = 100/60 mmHg
• Sats were 98% with Oxygen

8. • Lab reports were as follows
RBS = 340 mg/dl
Na = 145 meq/l
K = 5.3 meq/l
Cl = 116 meq/l
HCO3 = 5 meq/l
PH = 7.2, Pco2 = 22 mmHg
PO4 = 4 meq/l
Urine ketone bodies positive and glucose 3+

9. Note:
• Correct dehydration first slowly
• Never start insulin bolus
• Never administer bicarbonate until unless
indicated.
• Add potassium when K < 5
Most important don’t panic and don’t overcorrect
anything.

10. Monitoring and Investigations:
-Moderate-severe DKA- Admitted in ICU.
-Hrly HR,RR,BP, Spo2, GCS
-Monitor for warning signs of cerebral edema
-2nd hrly monitoring of blood glucose, electrolytes,
blood gases, urine ketones were done
-sent blood samples for CBC, Cultures for focus of
infection
-X-ray chest to exclude other causes

11. O/E:
At the time of admission RBS: 330 mg/dl
8:30 am- 312mg/dl
11:30 am- 304mg/dl
PR = 102 bpm
RR = 48 bpm, kussmal breathing
BP = 100/60 mmHg
CNS: altered sensorium GCS = 7/15,
Pupils NSRL, fundus normal,
Tone decreased, tendon reflexes 1+,
Plantars flexors.
CVS: S 1 S 2 +
R/S : B/L NVBS +
P/A: soft , non tender , no organomegaly
DAY 1

12. Investigations
• Hb = 8.5 g/dl
• TC = 7600 /mm3
• DC = P52, L46, E02
• ESR = 45 mm /1st hr
• Urine ketones + and glucose 2+
• Xray chest was normal
• Blood gases – Na 145 meq/l, K 5.3 meq/l, HCO3
5meq/l, Po4 3.2 meq/l, PH -7.24, Pco2 24mmHg

13. Treatment plan
• After 1 hour
• IV fluids according to Milwaukee formula
80ml/kg + maintenance – bolus
23
which gives approx. 90 ml/hr
• Started on Regular Insulin drip @ 0.1 U/kg/hr
• Started on IV Antibiotics, antipyretics
• Don’t administer bicarbornate therapy till ph drops to 7 or
cardiac instability occurs.

14. O/E :
No fresh complaints
Afebrile, hydration adequate
BP: 108/60mmHg, PR: 92bpm, RR : 36/min regular
CNS : GCS – E2 V2 M5 = 9/15
CVS: S 1 S 2 +
R/S : B/L NVBS +
P/A : soft
Day 2

15. Investigations
• At 5pm, RBS = 320 mg/dl
• PH 7.2, Pco2 26 mmHg, Na 142 meq/l, K 4
meq/l, HCO3 14 meq/l
• RFT were normal, Urine glucose 2+, ketones
weak positive

16. Invg. continued
• At 9 pm, RBS = 274mg/dl
• Child regains consciousness & her GCS = 13/15
• Started on 5D and ½ NS
• Reduced Insulin drip rate @ 0.05U/kg/hr with
Glucose monitoring hrly.
• Treatment started with subcutaneous regular
insulin 1U/kg/d
• Should be given 1 hr before stopping insulin drip

17. Treatment plan
• Child was conscious, alert and well oriented
• Shifted to Gen. ward on day 3.
• Continued IV saline maintenance dose i.e.,
1.5L/d
• Started her on mixtard insulin 2/3rd dose
before breakfast and 1/3rd before dinner with
gradual tapering of regular insulin doses.

18. • After 6 days, her RBS = 139 mg/dl, urine
glucose traces.
• She was now on Mixtard insulin 20 and 10
Units before breakfast and dinner respectively.

19. Insulin therapy
• Conventional &
• Intensive insulin therapy
- basal dose
- bolus dose

20. If the metabolic state is not attained correctly,
The ‘SEVENTH’S SCALE insulin regime can be
started :
Short acting insulin given Q6H with
2/7th total daily dose given before breakfast,
2/7th before Lunch,
2/7th before evening food &
1/7th without food at midnight

21. Key points to remember
• Correct dehydration first not the glucose
• Never administer Bicarbonate unless ph less than
7 associated with/ without cardiac dysfunction.
• Fluid deficit should be corrected over 48 hrs
Underhydration is somewhat helpful than
overhydration
In our case, altered mental status is bcoz of
cerebral acidosis not due to cerebral oedema or
electrolyte imbalances

22. CLASSICAL TRIAD IN DKA

23. As measurement of ketones in blood is not
readily available, ketonuria is used as a marker
of ketonemia. When measured, serum ketones
(ß hydroxybutyrate plus acetoacetate)
exceed 31 mg/dL with or without ketonuria
>80 mg/dL

27. Examination
• Fruity odour in breath (ketosis)
• Tachycardia Indicate dehydration or hypovolemia
• Low volume pulses
• Hypotension
• Impaired skin turgor
• Sunken eyes
• Delayed capillary refill time
• Absence of tears
• Weight loss (if premorbid weight known)
• Rapid deep sighing breathing, Kussmaul respiration (metabolic acidosis)
• Changes in sensorium, coma
• Bradycardia, hypertension
• Papilledema Indicate cerebral edema
• Abnormal pupillary reflexes, cranial nerve palsies
• Posturing: decerebrate, decorticate

29. Investigations

31. • Leukocytosis with leftward shift is common in DKA
due to release of cytokines and catecholamines, and
does not necessarily indicate infection
• Cultures (blood and urine) and chest radiograph are
obtained if there is suspicion of infection.
• Computed tomography to evaluate for cerebral
edema is planned in case examination suggests
raised intracranial tension.

32. TREATMENT OF DKA
(Milwaukee DKA PROTOCOL)

34. Electrolyte disturbances include

35. Sodium
• Initial serum sodium may be ‘low’ for several reasons:
– Depletion secondary to urinary losses / vomiting
– Hyperlipidemia displaces sodium in the most frequently
used laboratory assay, factitiously lowering sodium values.
Hyperglycemia  High serum osmolarilty 
Water driven from Intra to Extracellular space 
Dilutional hyponatremia

36. • For each 100mg% increase of serum glucose
above 100mg%, there is an expected decrease
of about 1.6mEq/L in measured sodium.
[Na] + Glucose-100 x 1.6
100
The sodium should increase by about 1.6 mmol/L
for each 100mg/dL decline in glucose.

37. • With prolonged illness & severe DKA, total body losses
can approach:
- 10-13 mEq/kg of Sodium
- 5-6 mEq/kg of Potassium
- 4-5 mEq/kg of Phosphate
• Even though Sodium deficit may be repaired within 24
hours, intracellular Potassium & Phosphate may not be
completely restored for several days.

38. Cause of hypokalemia in DKA
• During DKA, intracellular potassium is depleted
because of transcellular shifts caused by
hypertonicity and in exchange for protons that
are buffered intracellularly during metabolic
acidosis.
• In turn, this potassium is lost due to
hyperglycemia driven osmotic diuresis, and with
recurrent vomiting.
• Hyperaldosteronism secondary to volume
depletion further exacerbates potassium losses.

39. • Phosphates are reduced due to tissue
catabolism.
• Phosphate correction not needed and their
formulas are not available in india

40. IV Fluids management

42. • Our goal is to slowly decrease serum glucose
(< 100 mg/dL/hr)

43. Potassium Administration: General
Guidelines
• When initial serum potassium is <2.5 mmol/L
(hypokalemia)
Administer 0.5-1 mEq/kg of potassium chloride
in IV drip in saline
• Start potassium replacement early, even
before starting insulin therapy

44. • When initial serum potassium is 2.5 - 3.5
mmol/L
Administer potassium 40 mEq/L in IV solution
until serum potassium > 3.5 mmol/L
• Monitor serum potassium hourly
• Administer potassium 30 – 40 mEq/L in IV
solution to maintain serum potassium at 3.5 –
5.0 mmol/L

45. ECG
Hypokalemia
Flattening T wave, widening
of the
QT interval, and appearance of
U waves
Hyperkalemia
Tall, peaked symmetrical, T waves and
shortening of QT intervals

46. • When initial serum potassium is 3.5 - 5.0
mmol/L
• Administer potassium 30 – 40 mEq/L in IV
solution to maintain serum potassium at
3.5 – 5.0 mmol/L
• Monitor serum potassium hourly

47. What about bicarbonate administration?

48. BICARBONATE IS ALMOST NEVER
ADMINISTERED ?
– bicarbonate administration leads to increased
cerebral acidosis
• HCO3
- combines with H+ and dissociated to CO2 and
H2O. Whereas bicarbonate passes the blood-brain
barrier slowly, CO2 diffuses freely, thereby exacerbating
cerebral acidosis and cerebral depression

50. Complications

51. Cerebral Edema
• Occurs in less than 1% of Pediatric DKA
episodes
• Accounts for 60% to 90% of all DKA deaths
• 10% to 25% of survivors have permanent
neurological injury

54. Management of Cerebral Edema
• The head end of the bed should be elevated.
• The fluid administration rate should be reduced by 1/3
• The air way is secured; if warranted by deterioration in sensorium, the
patient should be intubated and mechanically ventilated.
• During ventilation, aggressive hyperventilation (PCO2 < 22 mm Hg) should
be avoided
• Intravenous mannitol is administered at 0.5–1 g/kg over 20 min;
alternatively 3% saline is given as 5–10 ml/kg over 30 min
• The dose is repeated if no response is perceived within 30 min to 2 h.
• Following institution of therapy, a cranial CT is ordered to rule out other
treatable causes of neurological deterioration like thrombosis or
hemorrhage.

55. Thank you for your patience