Diabetic ketoacidosis (DKA) is a critical condition commonly presented in children with diabetes, characterized by hyperglycemia, metabolic acidosis, and ketonemia. The lecture outlines the definitions, diagnostic criteria, pathophysiology, and treatment protocols for DKA, emphasizing the importance of early recognition and management to reduce mortality rates. Preventive measures against recurrence include addressing insulin omission and managing psychosocial factors that contribute to non-compliance.

1. Diabetic Keto Acidosis
MBBS Lecture Series
(Paediatric Endocrinology)

2. INTRODUCTION
• Diabetes remain the commonest endocrine abnormality in children
• DKA is the commonest mode of presentation in our environment due
to poor health seeking behaviour.
• Failure to diagnose DKA at presentation invariably means mortality
• Even when diagnosed appropriate management is necessary for
survival

3. outline
• Definition
• Precipitants
• Pathophysiology
• Frequency
• Diagnosis
• Laboratory work up
• Treatment
• Complication of treatment and their management

4. OBJECTIVE
• To define DKA and know the diagnostic criteria
• To recognize clinical features of DKA
• To evaluate a child with DKA
• To plan treatment for DKA

5. DKA is characterized by triad:
• Hyperglycemia (blood glucose > 11 mmol/L or 200
mg/dl)
• Metabolic acidosis - venous pH < 7.3 or
bicarbonate < 18 mmol/L
• Ketonemia (blood B-hydroxybutyrate ≥ 3mmol/L
and ketonuria
Definition
Severity degree:
Mild ketoacidosis Venous pH < 7.3 or bicarbonate < 18
mmol/L
Moderate ketoacidosis Venous pH < 7.2 or bicarbonate < 10 mmol/L
Severe ketoacidosis Venous pH < 7.1 or bicarbonate < 5

6. Pathophysiology
DKA results from deficiency of circulating insulin and increased level of
the counterregulatory hormones.
In most case DKA is precipitated by
• New onset of diabetes
• Omission of insulin injections
• Interruption of insulin delivery in children using insulin pump
• Inadequate management of infection.

7. Counter-regulatory hormones:
Catecholamines
Glucagon
Cortisol
Growth hormone
Insulin
Absolute deficiency:
- previously undiagnosed T1DM
- patients on treatment that deliberately or
inadvertently do not take insulin
Relative insulin deficiency:
- increase concentrations of counter-regulatory
hormones in response to stress
- gastrointestinal illness
pathophysiology

8. •accelerated catabolic state
•increased glucose production
(via glycogenolysis and gluconeogenesis)
•impaired peripheral glucose utilization
(hyperglycemia and hyperosmolality)
•increased lipolysis and ketogenesis
(ketonemia and metabolic acidosis)

9. Absolute insulin deficiency OR
Stress, infection or insufficient insulin intake
Counter-regulatory hormones:  Glucagon, Cortisol,
Catecholamines, GH
Lipolysis
 FFA to liver
 Ketogenesis
 Alkali reserve
Acidosis
 Lactate
Glucose
utilization
 Proteolysis
 Protein synthesis
 Glycogenolysis
Gluconeogenic substrates
 Gluconeogenesis
Hyperglycemia
Glucosuria (osmotic diuresis)
Loss of water and electrolytes
Dehydration
Impaired renal function
Hyperosmolarity

10. Frequency of DKA
At disease onset
15-70% at onset of diabetes
>80% in series from Nig
Inversely correlate with the
regional incidence of T1DM
<5 yr of age
Families which do not have
ready access to medical care
for social or economic reasons
Poor metabolic control or previous
episodes of DKA
Peripubertal and adolescent girls
Psychiatric disorders
Difficult or unstable family
circumstances
Children who omit insulin
Children with limited access to
medical services
Insulin pump therapy
Children with
established diabetes
1-10% per patient per year

11. Diagnosis
Clinical History
• Polyuria, polydipsia, nausea, vomiting, rapid
breathing, abdominal pain, weakness, weight
loss, confusion, decreased level of
consciousness

12. Diagnosis
Clinical Signs
• Dehydration
• Deep sighing respiration (Kussmaul)
• Smell of ketones
• Drowsiness

13. Diagnosis
Biochemical
• Hyperglycaemia
• Ketonuria
• Ketonaemia
• Acidemia - Plasma bicarbonate < 18 mmol/l

14. Laboratory measurement:
 Glucose
 Blood urea nitrogen
 Creatinine
 Hemoglobin and complete blood count
 Venous pH, pCO2
 Electrolytes
 Osmolality
 Calcium
 Phosphorus
 Magnesium
 HbA1c
 Urinalysis for ketones
 Blood β-hydroxybutyrate concentration

15. Specimens for culture (blood, urine, throat)
Electrocardiogram (ECG)
Serum free insulin concentration

16. Secure the airway and
Empty the stomach by continuous nasogastric
suction of to prevent pulmonary aspiration in the
unconscious or severely obtunded patient.
Peripheral intravenous (IV) catheter
Arterial catheter (critically ill patients
managed in an intensive care unit)
Treatment-Supportive measures

17. Cardiac monitor
Oxygen to patients with severe circulatory
impairment or shock
Antibiotics
Catheterization of the bladder

18. Goals of therapy
• Correct dehydration
• Correct acidosis and reverse ketosis
• Restore blood glucose to near normal
• Monitor for complications of DKA and its therapy
• Identify and treat any precipitating event

19. Fluids and salt
• Patients with DKA have a deficit in body fluid that
usually is in the range 5–10% of body weight.
• Clinical estimates of degree of dehydration based on
physical examination and vital sign are inaccurate.
Therefore
Mild DKA – 5%
Moderate DKA – 7%
Severe DKA – 10%
• Increase Urea and anion gap at presentation
correlates well with volume deficit
• Begin with fluid replacement before insulin therapy.

20. Fluids and salt
Resuscitation fluid
• Expand intravascular volume with isotonic 0.9%
saline: 10–20 ml/kg body weight over 20 – 30
min
• For those in shock 20ml/kg of 0.9% saline
boluses as rapid as possible with reassessment
of circulatory status after each bolus.

21. Fluids and salt
Deficit Replacement fluid
• Deficit is replaced over 24 – 48 hrs using 0.9%
saline or 0.45% saline or ringers
• Maintenance is also giving along with deficit
• Typical fluid calculation =
Deficit – Resuscitation fluid + 2xMaintenance
• The fluid is given evenly over 48 hours

22. Insulin therapy
• DKA is caused by either relative or absolute
insulin deficiency
• Begin with 0.1 U/kg/h 1–2 h AFTER starting
fluid replacement therapy
• An IV bolus is unnecessary, may precipitate
shock and exercabate hypokalaemia and should
not be used at the start of therapy
• The dose of insulin should usually remain at 0.1
U/kg/h at least until resolution of DKA

23. Insulin therapy
If the patient demonstrates marked sensitivity
to insulin (e.g., some young children with DKA,
patients with HHS, and some older children with
established diabetes), the dose may be
decreased to 0.05 unit/kg/h, or less.

24. Insulin therapy
To prevent any rapid decrease in plasma glucose
concentration and hypoglycemia, 5% glucose should be
added to the IV fluid (e.g., 5% glucose in 0.45% saline)
when the plasma glucose falls to approximately 14–17
mmol/L (250–300 mg/dL), or
sooner if the rate of fall is precipitous.
It may be necessary to use 10% or even 12.5%
dextrose to prevent hypoglycemia while continuing
to infuse insulin to correct the metabolic acidosis.

25. Even with normal or high levels of serum
potassium at presentation, there is always a
total body deficit of potassium (3-6 mmol/kg).
The major loss of potassium is from the
intracellular pool.
Potassium replacement

26. Hypokalemic
Normal K+
concentration
Hyperkalemic
Start potassium replacement at
the time of initial volume
expansion and before starting
insulin therapy.
Start after initial volume
expansion
and concurrent with starting
insulin therapy
Defer potassium replacement
therapy until urine output is
documented
20 mmol/l KCl + 20 mmol/l K phosphate =
40 mmol/l

27. Phosphate
• Depletion of intracellular phosphate occurs in DKA and phosphate is lost as a result
of osmotic diuresis
• Plasma phosphate levels fall after starting treatment and this is exacerbated by
insulin
BUT
• Administration of phosphate may induce hypocalcemia
• Potassium phosphate salts may be safely used as an alternative to or combined with
potassium chloride
• No clinical benefit from phosphate replacement

28. Acidosis
Severe acidosis is reversible
by fluid and insulin
replacement.

29. There is no evidence that
bicarbonate is either necessary
or safe in DKA:
• paradoxical CNS acidosis
• hypokalemia

30. Cautious alkali therapy for:
 pH < 6.9
 decreased cardiac contractility and
peripheral vasodilatation
 life-threatening hyperkalemia
If bicarbonate is considered necessary,
cautiously give
1–2 mmol/kg over 60 min

31. Oral fluids
Oral fluids should be introduced only when
substantial clinical improvement has occurred
When oral fluid is tolerated, IV fluid should
be reduced

32. Change to SC insulin just before a mealtime
First SC injection should be given
15–30 min (with rapidacting insulin)
1–2 h (with regular insulin)
before stopping the insulin infusion
After transitioning to SC insulin, frequent
blood glucose monitoring is required to avoid
marked hyperglycemia and hypoglycemia
SC insulin injections

34. Complications of therapy
• Inadequate rehydration
• Hypoglycemia
• Hypokalemia
• Hyperchloremic acidosis
• Cerebral edema
Mortality rate from DKA is 0.15–0.30%; first cause is
cerebral edema

35. Cerebral edema
Increased risk of cerebral edema include:
• Younger age (age <5 years)
• New onset diabetes
• Longer duration of symptoms
• Hypocapnia (pCO2 <21mmHg)
• Increased serum urea nitrogen (>20mg/dl)
• Severe acidosis (PH <7.1)
• Bicarbonate treatment for correction of acidosis
• An attenuated rise in measured serum sodium concentrations during therapy
• Greater volumes of fluid given in the first 4 h
• Administration of insulin in the first hour of fluid treatment

36. Warning signs and symptoms
• Headache & slowing of heart rate
• Change in neurological status (restlessness,
irritability, increased drowsiness, incontinence)
• Specific neurological signs (e.g., cranial nerve
palsies)
• Rising blood pressure
• Decreased O2 saturation

37. Diagnostic
criteria
Major criteria Minor criteria
Abnormal motor or
verbal response to
pain
Decorticate or
decerebrate posture
Cranial nerve palsy
Abnormal
neurogenic
respiratory pattern
(e.g., grunting,
tachypnea, Cheyne-
Stokes respiration,
apneusis)
Altered mentation/
fluctuating level of
consciousness
Sustained heart
rate deceleration
(decrease more than
20 bpm) not
attributable to
improved
intravascular volume
or sleep state
Age-inappropriate
incontinence
Vomiting
Headache
Lethargy or not
easily arousable
Diastolic blood
pressure >90 mm Hg
Age < 5 yr
1 Diagnostic Criteria or 2 Major Criteria or 1 Major + 2 Minor Criteria

38.  Elevate the head of the bed
 Intubation but not aggressive hyperventilation
 After treatment for cerebral edema has been
started, a cranial CT scan should be obtained

39. Treatment of cerebral edema
 Initiate treatment as soon as the condition is
suspected.
 Mannitol 0.5–1 g/kg IV over 20 min and
repeat if there is no initial response in 30 min
to 2 h
 Reduce the rate of fluid administration by
one-third.
 Hypertonic saline (3%), 5–10 mL/kg over 30
min, may be an alternative to mannitol

40. Prevention of recurrent DKA
All cases of recurrent DKA are preventable
Inadvertently
or deliberately
insulin omission
Psychosocial reason
(lose weight,
depression, …)
Infection ± vomiting

41. THANK YOU