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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.
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
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
.
2
• 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
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
.
3
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
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
.
4
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ketoacidosis when insulin is withdrawn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
3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. 5
• 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
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
.
6
• 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
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
.
7
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)
3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. 8
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
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
.
9
Investigations In DKA
• RBS
• Septic screen:
- Urinalysis
- FBC/DC
- Blood/urine for MCS
- Chest X-ray
• ABGs
• U/Es + Creatinine
• ECG
• Cardiac enzymes
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
.
10
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)
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
.
11
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
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
.
12
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
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
.
13
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
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
.
14
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
3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. 15
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
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
.
16
- 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
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
.
17
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
3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. 18
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
3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. 19
Presentation of Cerebral Oedema
• Alteration sensorium
• Dilated or unequal pupils
• Hypertension
• Headache
• Projectile vomiting
• Convulsions
• Diminished responsiveness to painful stimuli
• Diminished reflexes
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
.
20
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
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
.
21
• 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
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
.
22
3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. 23
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
3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. 24
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
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
.
25
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
.
26
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
3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. 27
The End!
3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. 28

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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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. . 2
  • 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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. . 3
  • 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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. . 4
  • 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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. 5
  • 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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. . 6
  • 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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. . 7
  • 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) 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. 8
  • 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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. . 9
  • 10. Investigations In DKA • RBS • Septic screen: - Urinalysis - FBC/DC - Blood/urine for MCS - Chest X-ray • ABGs • U/Es + Creatinine • ECG • Cardiac enzymes 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. . 10
  • 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) 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. . 11
  • 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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. . 12
  • 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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. . 13
  • 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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. . 14
  • 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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. 15
  • 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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. . 16
  • 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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. . 17
  • 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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. 18
  • 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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. 19
  • 20. Presentation of Cerebral Oedema • Alteration sensorium • Dilated or unequal pupils • Hypertension • Headache • Projectile vomiting • Convulsions • Diminished responsiveness to painful stimuli • Diminished reflexes 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. . 20
  • 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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. . 21
  • 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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. . 22
  • 23. 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. 23
  • 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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. 24
  • 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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. . 25
  • 26. 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. . 26
  • 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 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. 27
  • 28. The End! 3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. 28