1.
Dr Amit Shekharay

2.
 Diabetic ketoacidosis (DKA) is the end result of the metabolic
abnormalities resulting from a severe insulin deficiency or
ineffectiveness.
 DKA at diagnosis is more common in young children near the age
of five years.

3.
The risk increases gradually in children with
 Poor metabolic control
 Previous episodes of DKA
 Young age
 Children with psychiatric and eating disorders
 Low socioeconomic status
 Low parental education and
 Stressful lifestyles.

4.
 Infection (viral fever, pneumonia, UTI etc.), Insulin omission
either inadvertently or deliberately, is the cause in most cases.

5.
PATHOPHYSIOLOGY OF DKA

6.
CLINICAL FEATURES
 Children and young people without known diabetes who have
increased thirst, polyuria, recent unexplained weight loss or
excessive tiredness and any of the following:
Nausea or vomiting
Abdominal pain
Hyperventilation
Dehydration
Reduced level of consciousness.

7.
 Suspect DKA even if the blood glucose is normal in a child with
known diabetes and having above mentioned complains.

8.
DIAGNOSIS
1. Acidosis (indicated by blood pH below 7.3 or plasma
bicarbonate below 18 mmol/litre), and
2. Ketonaemia (indicated by blood beta-hydroxybutyrate above 3
mmol/litre) or ketonuria (++ and above on the standard strip
marking scale).

9.
 Blood glucose levels are generally high (above 11 mmol/l or 198
mg/dl) but DKA may develop with normal blood glucose.
 Urine ketones may be positive long after ketoacidosis has
resolved because the nitroprusside reaction routinely used to
measure urine ketones by dipstick measures only acetoacetate.

10.
 During DKA, most excess ketones are β- hydroxybutyrate, which
increases the normal ratio to acetoacetate from 3 : 1 to as high as 8 : 1.
 With resolution of the acidosis, β- hydroxybutyrate converts to
acetoacetate,which is excreted into the urine and detected by the
dipstick test.

11.
 Therefore, persistent ketonuria may not accurately reflect the
degree of clinical improvement and should not be relied on as an
indicator of therapeutic failure.

12.
CLASSIFICATION OF DKA
 pH ≥7.1 - MILD or MODERATE DKA
 pH ˂7.1 - SEVERE DKA.

13.
MANAGEMENT
FULL CLINICAL ASSESSMENT
1. Consciousness Level-Directly related to degree of acidosis. Hourly
GCS monitoring.
2. Full Examination- Look for signs of
 cerebral oedema (headache, irritability, bradycardia,
rising blood pressure, reducing conscious level, N.B.
papilloedema is a late sign.
 infection
 Ileus
3. Weigh the child-If this is not possible then use the most recent
clinic weight as a guideline, or an estimated weight from centile charts.

14.
INITIAL INVESTIGATIONS
 Blood glucose
 Urea
 Electrolytes
 Blood gases (venous or capillary)
 Near patient blood ketones (beta-hydroxybutyrate) if available (superior to
urine ketones).
 + /- other investigations only if indicated e.g. PCV and full blood count
(leucocytosis is common in DKA and does not necessarily indicate sepsis),
CXR, CSF, throat swab, blood culture, urinalysis, culture and sensitivity etc.

15.
 Sepsis should be suspected, if there is
 Fever or hypothermia
 Hypotension
 Refractory acidosis
 Lactic acidosis.

16.
GENERAL CARE
Secure airway,
Give 100% oxygen by face-mask
Insert IV cannula and take blood samples
Cardiac monitor for T wave
Measure blood pressure and heart rate.

17.
 If Reduced level of consciousness and vomiting present think
about inserting a NG tube to reduce the risk of aspiration.

18.
Fluid management
 Indications for starting fluid
 Fluid bolus
 Fluid calculations
 Type of fluid
 insulin

19.
FLUIDS: Children who are alert, not clinically dehydrated, not
nauseated or vomiting, do not always require IV fluids, even if their
ketone levels are high.

20.
 INITIAL FLUID BOLUS: If child is in shock give 10 ml/kg 0.9%
sodium chloride as a bolus.
 Do not give further boluses to a child with severe DKA without
discussion with the responsible senior paediatrician.

21.
Volume of fluid
 Once circulating blood volume has been restored (child is no
more in shock), calculate fluid requirements as follows:
Requirement = Deficit + Maintenance

22.
Volume of fluid
Assume a 5% fluid deficit in mild or moderate DKA (pH>7.1).
Deficit –
Assume a 10% fluid deficit in severe DKA (pH<7.1).
Weight (kg) Maintenance fluid
<10 2 ml/kg/hour
10-40 1 ml/kg/hour
>40 40 ml/hour
Maintenance – Calculate by using the following
'reduced volume' rules

23.
If more than 20 ml/kg NS bolus has been given
Subtract any additional bolus volumes from the total fluid
calculation for the 48-hour period
ie, if 30 ml/kg bolus has been given then subtract 10 ml/kg from the
calculations.

24.
Fluid Calculation
 Hourly rate = (deficit / 48hr) + maintenance per hour
Weight Hourly rate
20 kg, with pH 7.18 without any fluid bolus
Deficit= 5% x 20 kg = 1000 mls
Rate = 1000÷48= 21ml/hr
Maintenance 1ml/kg/hr = 20 ml/hr
Total rate= 41ml/hr
50 kg, with pH of 6.8 and required 30 ml/kg 0.9%
sodium chloride bolus for circulatory collapse
Deficit= 10% x 50 kg= 5000 mls
10 ml/kg bolus fluid = -500mls=4500 mls
rate=4500÷48= 93.7 ml/hr
Maintenance= 40ml/hr
Total rate=133.7 ml/hr

25.
Type of fluid
 0.9% sodium chloride with 20 mmol potassium chloride in 500
ml (40 mmol per litre) till blood glucose ˃14 mmol/l (252 mg/dl).
 Do not give oral fluids to a child who is receiving intravenous
fluids for DKA until ketosis is resolving and there is no nausea or
vomiting.
 .

26.
 If oral fluids are given before the 48hr rehydration period is
completed, the IV infusion needs to be reduced to take account
of the oral intake.

27.
INSULIN
 0.05 to 0.1 units/kg/hour, 1-2 hours after beginning intravenous
fluid therapy (cerebral oedema is more likely if insulin is started
early).
 Once the blood glucose has fallen to 14 mmol/l (252mg/dl), add
glucose to the fluid and think about the insulin infusion rate, as
follows –

28.
 If ketone levels are < 3 mmol/l
 change the fluid to contain 5% glucose
 Reduce to or maintain at an insulin infusion rate of 0.05
units/kg/hr
 If ketone levels are > 3 mmol/l
 Maintain the insulin infusion rate at 0.05 to 0.1
units/kg/hour to switch off ketogenesis
 Change the fluid to contain 10% glucose

29.
 Blood glucose ˂ 6 mmol/l (108mg/dl)- increase the glucose
concentration of ivf, and if there is persisting ketosis, continue
insulin with at least 0.05 units/kg/hour.
 Blood glucose ˂ 4 mmol/l (72 mg/dl), give a bolus of 2 ml/kg of
10% glucose and increase the glucose concentration of the
infusion. Insulin can temporarily be reduced for 1 hour.

30.
 If the blood beta-hydroxybutyrate level is not falling within 6–8
hours in a child with DKA, think about increasing the insulin
dosage to 0.1 units/kg/hour or greater.

31.
 Once the pH is > 7.3, ketones are <3, the blood glucose is down to
14 mmol/l (252 mg/dl), and a glucose-containing fluid has been
started, reduce the insulin infusion rate, to 0.05 units/kg/hour.

32.
 If acidosis is not correcting, consider the following
 Insufficient insulin to switch off ketones
 Inadequate resuscitation
 Sepsis
 Hyperchloraemic acidosis
 Salicylate or other prescription or recreational drugs

33.
 Think about stopping intravenous fluid therapy when ketosis is
resolving and oral fluids are tolerated without nausea or
vomiting.
 Start subcutaneous insulin at least 30 minutes before stopping
intravenous insulin.
 If the child was using insulin pump therapy, restart the pump at
least 60 minutes before stopping intravenous insulin.

34.
POTASSIUM
 All fluids (except any initial bolus) contain 40 mmol/l potassium
chloride, unless there is evidence of renal failure.
 Hypokalaemia (potassium below 3 mmol/litre): think about
temporarily suspending the insulin infusion

35.
SODIUM
“True,” serum sodium=
[ Na+] + (1.6 mEq/L Na+ for every 100 mg/dL glucose in excess of
100)
Corrected sodium levels should rise as blood glucose levels fall
during treatment.
If the child is becoming hypernatraemic, this is not generally a
problem, and is protective against cerebral oedema.

36.
BICARBONATE
 Not required.

37.
MONITORING
CONTINUOUS EVERY 30 MINUTES
(in children under 2
years with DKA and
children with severe
DKA) [high risk of
cerebral oedema]
HOURLY 2 HRS AFTER
STARTING AND
THEN 4 HOURLY
ECG (to detect
signs of
hypokalaemia)
Level of
consciousness
(using the modified
Glasgow coma scale)
Capillary blood
glucose
Glucose
(laboratory
measurement)
Heart rate (to
detect bradycardia)
Vital signs
(heart rate,
blood pressure,
temperature,
respiratory rate
[look for
Kussmaul
breathing])
Blood pH and
pCO2
Fluid balance,
with input and
output charts
Plasma sodium,
potassium and
urea
Level of
consciousness
Beta-
hydroxybutyrate.

38.
COMPLICATIONS
 Headache,
 Agitation or irritability
 Unexpected fall in heart rate
 Increased blood pressure and
 Signs such as deterioration in
level of consciousness
 Abnormalities of breathing
pattern, for example
respiratory pauses
 Oculomotor palsies
 Abnormal posturing
 Pupillary inequality or
dilatation
 CEREBRAL OEDEMA

39.
COMPLICATIONS
 Treat immediately with the most readily available
 Mannitol (20% 0.5-1 g/kg over 10-15 minutes), or
 Hypertonic saline (2.7% or 3% 2.5-5 ml/kg over 10-15
minutes).
 A repeated dose of Mannitol may be required after 2 hours if
there is no response, In addition fluids should be restricted to ½
maintenance rates and inform senior staff immediately.

40.
COMPLICATIONS
 Hypoglycaemia and hypokalaemia
 Systemic Infections: Antibiotics are not given as a routine unless
a severe bacterial infection is suspected.
 Aspiration pneumonia- Insert NG tube in vomiting child with
impaired consciousness

41.
AVOIDING FUTURE EPISODES OF
DIABETIC KETOACIDOSIS
 Discuss with family members or carers (if appropriate) the
factors that may have led to the episode.
 Think about the possibility of non-adherence to therapy in
children and young people with established type 1 diabetes who
present with DKA, especially if the DKA is recurrent.

42.
 Advise how to reduce the risk of future episodes. In particular, advise
them of the importance of managing intercurrent illnesses.
 Provide appropriate diabetes education and practical information
 Emotional and psychological well-being assessment who present
with frequent episodes of diabetic ketoacidosis over a relatively
short time (previously known as 'brittle diabetes').