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Paediatric DKA.pdf
1. PAEDIATRICS AND CHILD HEALTH
• Paediatrics and Child Health
• Paediatric DKA
Dr. Chongo Shapi (Bsc.HB,MBChB)
Medical Doctor
3/20/2022 1
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
2. Diabetic Ketoacidosis (DKA)
• Is the hallmark of T1DM
• It is usually seen in the following circumstances:
1. Previously undiagnosed diabetes
2. Interruption of insulin therapy
3. Stress of intercurrent illness
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3. • The majority of cases reaching hospital could have
been prevented by:
- Earlier diagnosis
- Better communication between patient and
doctor
- Better patient education
• The most common error of management is for
patients to reduce or omit insulin because they
feel unable to eat owing to nausea or vomiting
• Insulin should NEVER be stopped
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4. Pathogenesis of DKA
• Ketoacidosis is a state of uncontrolled catabolism
caused by:
1. Insulin deficiency
2. Counter-regulatory hormone excess (stress
hormones)
3. Fluid depletion
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5. Pathogenesis of DKA
• Insulin deficiency is a necessary precondition
• This is because insulin is needed to inhibit
hepatic ketogenesis
• Stable patients do not readily develop
ketoacidosis when insulin is withdrawn
• In the absence of insulin, hepatic glucose
production (gluconeogenesis + glycogenolysis)
accelerates, and peripheral uptake by tissues
such as muscle is reduced
• Rising glucose levels lead to an osmotic diuresis,
loss of fluid and electrolytes, and dehydration
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6. • Plasma osmolality rises and renal perfusion falls
• In parallel, rapid lipolysis occurs, leading to
elevated circulating free fatty-acid levels
• The free fatty acids are broken down to fatty acyl-
CoA within the liver cells, and this in turn is
converted to ketone bodies (beta
hydroxybutyrate, acetoacetate, acetone) within
the mitochondria
• Accumulation of ketone bodies produces a high
anion gap metabolic acidosis
• Vomiting leads to further loss of fluid and
electrolytes
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7. • The excess ketones are excreted in the urine but also
appear in the breath, producing a distinctive smell
similar to that of acetone
• Respiratory compensation for the acidosis leads to
hyperventilation, graphically described as 'air hunger'.
• Progressive dehydration impairs renal excretion of
hydrogen ions and ketones, aggravating the acidosis
• As the pH falls below 7.0 ([H+] > 100 nmol/L), pH-
dependent enzyme systems in many cells function
less effectively
• Untreated, severe ketoacidosis is invariably fatal
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8. Diagnosis of DKA
Requires testing for 3 things:
1. Hyperglycaemia (Diabetic)
- Measure blood glucose
2. Ketonaemia (keto)
- Test plasma with ketostix
- Finger prick sample for β-hydroxybutyrate
3. Acidosis (acidosis)
- Measure pH and arterial blood gases (ABGs)
The words in brackets = Diabetic ketoacidosis (DKA)
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9. Classification of DKA
Normal Mild Moderate Severe
CO2 (mEq/L,
venous )
20-28 16-20 10-15 < 10
pH (venous) 7.35–7.45 7.25-7.35 7.15-7.25 < 7.15
Clinical No change - Oriented
- Alert but
fatigued
- Kussmaul
respirations
- Oriented but sleepy
- Arousable
- Kussmaul or
depressed
respirations
- Sleepy to
depressed
sensorium to coma
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11. Management of DKA
3 Phases:
Phase 1
• Admit to ICU and do your ABCs
Step 1. Rehydrate the patient (dehydration kills faster,
hyperglycaemia will not kill the patient)
- If patient is in shock, give a bolus of IVF 0.9% NS at 20ml/kg
- Calculate fluid deficit and maintenance fluid to get the total
fluid needed
- Subtract the bolus amount you gave if patient was in
shock from the total IVF
- For DKA, patients are severely dehydrated, assume losing
10% of body weight (= 100mL/kg) in 24 hrs
- Hence, fluid deficit = 100mL x pt’s weight
Give 0.9% NS with 20 mmol KCl per litre (if not able to
monitor the K+ levels, add KCl after patient passes urine)
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12. IF:
- BP is below 80 mmHg, give plasma expander
- pH is below 7.0 give 500 mL of NaHCO3 1.26% plus
10 mmol KCl. Repeat if necessary to bring pH up to
7.0
Step 2. Give insulin (to reduce hyperglycaemia)
a. Soluble insulin 0.1 U/kg/hr by infusion (IV) 6
hourly or
b. 20 U IM stat, followed by 6 U IM hourly
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13. Phase 2
• When blood glucose falls to 10-12 mmol/L
change infusion fluid to 1L ½ NS in 5% dextrose
plus 20 mmol KCl 6-hourly
• Adjust the insulin infusion rate accordingly
• Changing the fluid plus adjusting the insulin
infusion rate avoids hypoglycaemia
• Continue insulin with dose adjusted according to
hourly blood glucose test results
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14. Monitoring
1. ECG
2. Glucose levels hourly
3. In/out fluid chart (urine output, catheter if not
passing urine in 2 hrs)
4. Clinical status
5. Urinalysis
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15. Special measures
• Broad-spectrum antibiotic if infection likely
• Bladder catheter if no urine passed in 2 hours
• NG tube if drowsy
• Consider CVP pressure monitoring if shocked or if
previous cardiac or renal impairment
• Give s.c. prophylactic LMW heparin in comatose,
elderly or obese patients
Subsequent management
• Monitor glucose hourly for 8 hours
• Monitor electrolytes 2-hourly for 8 hours
• Adjust K replacement according to results
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16. Phase 3
• Once stable and able to eat and drink normally:
- Transfer patient to SC insulin QID daily based on
previous 24 hours' insulin consumption, and
trend in consumption
• If new patient: calculate the total amount of
insulin that brought the patient out of DKA and
multiply by 4 to get the total required in a day
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17. - E.g if pts weight was 32 kg (32x0.1x6 = 19.2 U),
then 19.2 x 4 = 80 U
- Home: 1-1.5 IU/kg/d of SC insulin
• Then divide by 2/3 to give in morning, 1/3 to give
in the evening (remember patients usually eat
during the day)
• Then, again divide to give 1/3 short acting
(soluble) and 2/3 long acting (lente) for each
morning and evening dose
• Counsel patient on special diabetic diet
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18. Summary: Principles of Management of DKA
1. Fluid replacement with normal saline
2. IV Insulin therapy
3. Control the electrolytes (K+, pH)
4. When blood glucose falls to 10-12 mmol/L
change infusion fluid to 1L ½ NS in 5% dextrose
plus 20 mmol KCl 6-hourly
5. Search for the precipitating cause e.g. infection
6. Once stable and able to eat and drink normally,
transfer patient to SC insulin
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19. Complications of management of DKA:
1. Hypotension (renal shut down)
2. Coma
3. Cerebral oedema (give mannitol)
4. Hypothermia
5. Late complications: pneumonia and DVT
6. Complications of therapy:
- Hypokalemia (Inverted T waves on ECG, cardiac
arrhythmias )
- Hypoglycaemia
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20. Presentation of Cerebral Oedema
• Alteration sensorium
• Dilated or unequal pupils
• Hypertension
• Headache
• Projectile vomiting
• Convulsions
• Diminished responsiveness to painful stimuli
• Diminished reflexes
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21. Paediatric DKA Diet
• Children need to grow
• The nutrition care should:
a. Normal growth and development
b. Control of blood glucose
c. Maintenance of optimal nutritional status
d. Prevention of complications
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22. • The caloric mixture should comprise
approximately:
1. 55% carbohydrate
2. 30% fat
3. 15% protein
• Approximately 70% of the carbohydrate content
should be derived from complex carbohydrates
such as starch
• Intake of sucrose and highly refined sugars
should be limited
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24. Dawn and Somogyi Effects
• Are effects which cause blood glucose levels increase
in the early morning hours before breakfast
• Dawn phenomena
- Is thought to be due mainly to increased counter-
regulatory hormones overnight
- These include GH, cortisol, glucagon, and epinephrine
- Also partly caused by increased insulin clearance
- Is different from Somogyi effect in that it is not
associated with nocturnal hypoglycaemia
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25. Somogyi Phenomenon
• Also called chronic Somogyi rebound or post-
hypoglycaemic hyperglycaemia
• This is hyperglycaemia in the morning due to a
theoretical rebound from late night or early
morning hypoglycemia
• Thought to be due to an exaggerated counter-
regulatory response
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27. Brittle Diabetes
• Is unexplained wide fluctuations in blood
glucose due to large doses of insulin
• Patient is usually an adolescent female and
has recurrent DKA
• Psychosocial or psychiatric problems, including
eating disorders, and dysfunctional family
dynamics are usually present
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