MANAGEMENT PROTOCOL OF PEDIATRICS DKA

PATIENTS IN ASELA TEACHING AND REFERAL

HOSPITAL

BY TESFA G/MESKEL

ASELA
1

ETHIOPIA
Page

JUNE 2017
1
Contents Page

1. Introduction…………………………………………………………..4

1.1. Precipitating causes……………………………………………….4

1.2. Potential pitfalls in diagnosis……………………………………..5
1.3. Pathophysiology of DKA………………………………………….5
1.4. Classification of Ketoacidosis……………………………………6

2. Management of DKA………………………………………………7

2.1. General Resuscitation / Supportive Measures: A, B, C of life…7

2.2. Fluids and Electrolytes…………………………………………….8

2.2.1. Fluid management……………………………………………………………..8

2.2.2. Electrolyte management………………………………………………………..11
2.2.3. Fluid and electrolyte Management of DKA patients in Special situations…13

2.3. Insulin…………………………………………………………………18

2.3.1. Management during Infections and sick days…………………………………20

2.3.2. Management during Surgery……………………………………………………22

2.4. Monitoring…………………………………………………………….24
2.5. Management of complications……………………………………..24
2.5.1. Treatment of Cerebral Edema…………………………………………………..24
2.5.2. Treatment of Hypoglycemia……………………………………………………..25

2.6. Transfer to Oral Fluids and Subcutaneous Insulin……………….26

2.7. Discharge Planning………………………………………………….29
2.8. Summary of Medical treatment of DKA……………………………30

3. REFERENCES………………………………………………………..31

NB:
The ideas, figures and recommendations included in this material are based on different protocols
from other different setups, from pediatrics text books and clinical studies; but no strict evidence
based recommendations are available regarding universal DKA management protocol, so this
protocol can be amended any time as far as better alternative options are available.
2
Page

2
Abbreviations:

AcAc = Acetoacetate
BG = Blood glucose
BOHB = Betahydroxybutyrate
BP = Blood pressure
DKA = Diabeticketoacidosis
DW = Dextrose in water
ECF = Extracellular
ICF = Intracellular
IV = Intravenous
NS = Normal saline
RBS = Random blood sugar
TDD = Total daily dose

Acknowledgement
This protocol was commented by the following professionals:
Dr Abebe Sorsa, Dr Dejene Lema, Dr Simenew Ambachew ,Dr Belay Shewaye , Dr
Mersha Mekonen, Dr Nuri Mama, Dr Achalu Mekutia, Dr Birhane Fiseha, Dr Tsigereda
Atumo, Dr Zemzem Niguse, Dr Ashenafi Degefa, Dr Tadese Asefa, Dr Mikael Siyum, Dr
Dawit Zena .

3
Page

3
 1. Introduction

DKA results from absolute or relative deficiency of insulin and the combined effects of increased
levels of counter-regulatory hormones. This leads to both increased production and impaired
utilization of glucose, with resultant hyperglycemia and hyperosmolality. Increased lipolysis and
ketone body production causes ketonaemia and metabolic acidosis. Hyperglycemia and acidosis
result in an osmotic diuresis, dehydration and obligate loss of electrolytes. DKA may occur at
diabetes onset or in children with established diabetes who have either omitted insulin or had
inadequate insulin therapy during intercurrent illness.

The biochemical criteria for the diagnosis of DKA are:

 Hyperglycemia (blood glucose >11mmol/L),>200mg/dl
 Venous pH <7.3 and / or bicarbonate <15mmol/L.
 Ketonaemia (indicated by blood beta-hydroxybutyrate above 3 mmol/litre)
 Ketonuria and glycosuria.
 There is also: an increased ion gap and an elevated effective serum osmolality, indicating
hypertonic dehydration.
 Anion gap = Na – (Cl + HCO3); Normal = 12 ± 2
 Corrected Na (Na correction for glucose) = Measured Na + 2x {(Glucose
– 5.5) ÷ 5.5} mmol/L = measured Na + (serum glucose-100) (1.6)/100
 Effective osmolality = 2 x (Na (uncorrected) + K) + Glucose mmol/L =
2(Na+K) + glucose/18 + BUN/2.8

Clinically they may have the following features:

 Acetone-fruity breath or Kussmaul respirations
 Dehydration, decreased peripheral perfusion/hypovolemic shock (rarely)
 Fatigued/ Depressed level of consciousness.
 Abdominal pain/vomiting
The clinical manifestations of DKA are related to the degree of hyperosmolality, volume depletion,
and severity of acidosis

1.1. Precipitating causes:

 Infection;
 Psychosocial: Stress…
 Omission of insulin;
 Drugs like Steroids
 Deficient patient/parent/school education
 Health service problems and so on.
4
Page

4
1.2. Potential pitfalls in diagnosis:
 Children may appear well despite gross metabolic imbalance
 Abdominal symptoms may mimic an acute abdomen
 DKA can occur without pronounced hyperglycemia
 Hyperglycaemia may cause false hyponatraemia
 Creatinine assay may be falsely elevated by ketones (i.e. aceto-acetate)
 Outdated reagent strips may not show ketones

1.3. Pathophysiology of DKA

5
Page

5
 1.4. Classification of Ketoacidosis:
NORMAL MILD MODERATE SEVERE
CO2 (mEq/L, 20-28 16-20 10-15 <10
venous)
pH (venous) 7.35-7.45 7.25-7.35 7.15-7.25 <7.15
Clinical No change Oriented, alert Kussmaul Kussmaul or
but respirations; depressed
fatigued oriented respirations;
but sleepy; sleepy to
arousable depressed
sensorium to
coma
Hydration NORMAL < 5% DHN 5 to 7%DHN 7 to 10% DHN
In Shock:: (>10% dehydration: shock, weak peripheral pulses, hypotension, oliguria;
which is rare in DKA)

Classification of severity of DKA based on acidosis may be difficult in our set up due to lack of the
facility to measure venous PH and Bicarbonate; but can be assumed based on Clinical condition
of the patient, i.e. : Level of consciousness, Level of DHN, Breathing pattern…

At the time of presentation, clinical estimates of the extracellular fluid volume deficit in moderate to
severe DKA are usually in the range of 5 to 10 percent.

Hypovolemic shock is a rare occurrence in DKA. The patient in shock should be evaluated for
other causes of shock.

In DKA, Clinical assessment of dehydration may be difficult especially in young children and
Severity of dehydration is often overestimated; In addition, the degree of extracellular fluid loss is
in part masked because hyperglycemia results in a shift of water from the intracellular to the
extracellular fluid compartment. The fluid losses are from both the extracellular and intracellular
spaces.

Elevations in the blood urea nitrogen and hematocrit remain useful laboratory studies to confirm
hypovolemia in DKA and to follow its correction. 6
Page

6
 2. Management of DKA:

Managementgoals:
 Restoration of circulating volume
 Replacement of fluid and electrolyte deficit evenly over 48 hours
 Correction of acidosis and hyperglycemia with insulin
 Treatment of Precipitating factors
 Avoidance of the complications of DKA and its treatment by frequent monitoring for
 Cerebral oedema
 Hypoglycemia
 Electrolyte abnormalities

Management background: Any treatment plan for DKA should be based on the underlying
Pathophysiology. Hyperglycemia and ketoacidosis induce important alterations in organ
Physiology. Hyperglycemia causes an osmotic diuresis and eventually leads to dehydration,
electrolyte depletion, and hypertonicity. Metabolic acidosis is partiallycompensated by
hyperventilation and hypocapnia. These effects in turn cause changes in Renal, CNS, and
Cardiovascular system functioning.
Considering the above, the first therapeutic step is to restore extracellular fluid volume
which has been depleted through osmotic diuresis and vomiting. Insulin must be given to
allow normal carbohydrate utilization and to stop ketogenesis. Serum hyperosmolality
should be normalized gradually and intracellular stores of potassium replenished. Severe
acid/base disturbances need to be corrected both for homeostatic reasons and to permit
optimally effective insulin action. Normal glycogen and fat stores, and protein synthesis
also need to be restored over time.

2.1. General Resuscitation / Supportive Measures: A, B, C of life:

Airway: Ensure that the airway is patent and if the child is comatose, insert an airway.
If consciousness reduced or child has recurrent vomiting, insert N/G tube, aspirate and leave on
open drainage.

If the child or young person has a reduced level of consciousness and is unable to protect their
airway, may need Anesthetic review for further mgt of the airway.

Breathing: Give 100% oxygen by face-mask.

Circulation: Vital signs (B/P, P/R…), Insert IV cannula and take blood samples, Cardiac monitor
(Hypokalemia/Hyperkalemia)

If shocked (reduced peripheral perfusion) give 10ml/kg of 0.9% sodium chloride over 10-20
minutes; repeat until circulation restored, but do not exceed 30ml/kg.
7
Page

7
 2.2. Fluids and Electrolytes

2.2.1. Fluid management

Initial fluid bolus: initial volume expansion/ Initial stabilization of the patient in the first 1 to
2hours.The volume and rate of administration depends on the circulatory status.

Patients even with an adequate blood pressure should receive a bolus infusion of 10 mL/kg of IV
NS during the initial hour. The NS bolus infusion may decrease the blood glucose by 20% solely
by dilution and improving renal perfusion, leading to enhanced urinary glucose excretion.

In moderate to severe DKA or If shocked give 10ml/kg of 0.9% sodium chloride over 10-
20minutes, this may be repeated if necessary but should not exceed 30ml/kg. Clinical
improvement should be apparent within minutes of the bolus being completed.

NB: In some patients with late presentation may have sever circulatory collapse with late signs of
shock (feeble pulse, poor capillary refill, hypotension, cold extremities…); in such patients, the
management should start with A, B C of life. The initial fluid management should stabilize the
circulatory status: such patients may be resuscitated as any shock patients and the fluid given at
this time will be reduced later on from the total calculated fluid over 48 hours. Patients should be
strictly followed for early signs of cerebral edema.

Some setups with good diabetes management team omit the Initial fluid bolus in mild DKA.

Subsequent fluid requirement: once circulating blood volume has been restored, calculate fluid
requirements as follows:

Fluid Requirement = Deficit + Maintenance

=Deficit + [(Maintenance/Day) x 2] = to be given over 48hrs

Deficit:is calculated based on the severity of DKA; Clinical assessment of dehydration may be
difficult especially in young children and Severity of dehydration is often overestimated, therefore
in moderate tosevereDKA a deficit of85 mL/kg (8.5% dehydration)can be considered for
replacement of fluid deficit.

Children with milder DKA recover in 10-20 hr and need less total IV fluid before switching to oral
intake; they can be rehydrated earlier and can be switched to oral intake.

In some setups with good Diabetes control team,children with less than 5% dehydration and
clinically well without vomiting are tried with oral fluid intake and subcutaneous insulin.

Maintenance =100 mL/kg (for the first 10 kg) + 50 mL/kg (for the second 10 kg) + 20 mL/kg (for
all remaining kg)or 1500 mL/m2 body surface area.
8
Page

8
Different methods are used to estimate maintenance fluid and electrolyte requirements in infants
and children. The two most common methods are based on either metabolic rate (the caloric or
Holliday- Segar method) or on body surface area (or square meter method).

1. The most commonly used technique to calculate maintenance fluids for children is the
Holliday Segar method. This equation estimates the amount of kilocalories expended, and
equates this with fluid requirements. For every 100 kilocalories used during metabolism,
roughly 100 mL of fluid is needed to replace losses. Thus, while the Holliday-Segar method
actually estimates kilocalories lost, it is estimated that a loss of 1 kilocalorie requires 1 mL
in replacement, so the kilocalorie estimate is an efficient target for fluid requirements.

Method 1: Maintenance fluid volume for a 24-hour period):

 Weight less than 10 kg = 100 mL/kg

 Weight >10 kg to 20 kg = 1000 mL for first 10 kg of body weight plus 50 mL/kg for any
increment of weight over 10 kg
 Weight >20 kg to 80 kg = 1500 mL for first 20 kg of body weight plus 20 mL/kg for any
increment of weight over 20 kg, up to a maximum of 2400 mL daily

Method 2: Maintenance fluid needed on an hourly basis:

 Weight less than 10 kg = 4 mL/kg per hour

 Weight >10 kg to 20 kg = 40 mL/hour for first 10 kg of body weight plus 2 mL/kg per hour
for any increment of weight over 10 kg
 Weight >20 kg to 80 kg = 60 mL/hour for first 20 kg of body weight plus 1 mL/kg per hour
for any increment of weight over 20 kg, to a maximum of 100 mL/hour, up to a maximum of
2400 mL daily

2. The body surface area method is based on the assumption that caloric expenditure is
related to body surface area. This method requires the use of Mosteller’s formula or
nomogram found in most textbooks and requires knowledge of the patient’s height.
Mosteller’s formula is surface area (m2) = Ht (cm) x Wt (kg) / 3600. Apply body surface
area to maintenance fluids = 1500 ml / m2 / 24hr.

Rate of IV fluid should be calculated to rehydrate evenly over at least 48 hours. Infuse fluid each
day at a rate rarely in excess of 1.5 to 2 times the usual daily maintenance requirement (about
3000 cc/m2/day).Unless there is objective evidence of shock; excessive fluids may increase the
risk for cerebral edema.

Neonatal patients may require larger volumes: 100-150 ml/kg/24 hours.

9
Page

9
Resuscitation fluid:

The solution used for this ongoing volume repletion should initially consist of isotonic normal
saline. For most patients, 40mEq/L of potassium salts should be added to the solution to correct
the total body potassium deficit. Subtract any additional bolus volumes (which were given initially
for stabilization) from the total fluid calculation for the 48-hour period.

Subsequent fluid management should begin with 0.9% sodium chloride with added KCl, at a rate
calculated to replace the fluid deficit evenly over 48 hours.

If IV fluids have been given elsewhere, prior to assessment, the volume should be included in the
fluid calculations
Urinary losses should not be added to the calculation of replacement fluid

When blood glucose falls to <250 - 300mg/dl, add dextrose to the IV solution. The IV solution can
be changed to 1/2 normal saline plus 5% Dextrose =5%DW + 0.45%NS (with potassium).

Fluid options that can be used in our setup:

 To make 0.9% sodium chloride with 5% glucose: Remove 100ml of 0.9% sodium chloride
from a 1000ml bag of 0.9% sodium chloride and add 100ml of 50% glucose = 200ML of
D5%0.9%NS.
 The preparation of 5%DW with 0.45%NS fluid is not available in our Hospital: but we can
use an alternative fluid by mixing: 1/3 of the fluid to be NS plus 2/3 of the fluid to be 5%
Dextrose plus 40meq/Lof potassium.
 We can use D5% 0.9%NS (DNS) instead of changing to pure 5% or 10%DW

If the blood glucose concentration falls below 150 mg/dL (8.3 mmol/L), a10%
Dextrose solution with Saline 0.45%and potassium should be given and if the Blood glucose is still
below 150 mg/dL (8.3 mmol/L) despite the addition of 10% glucose with saline, the insulin dose
can be reduced to 0.05 U/kg/hour but do not discontinue the insulin drip which is often necessary
to correct the residual ketoacidosis.

The preparation of 10%DW with 0.45%NS fluid is not available in our Hospital; but we can use an
alternative fluid by mixing: 1/3 of the fluid to be NS plus 2/3 of the fluid to be 10% Dextrose plus
40meq/Lof potassium.

Oral Fluids:
Do not give oral fluids to a child or young person who is receiving intravenous fluids for DKA until
ketosis is resolving and until there is no nausea or vomiting.

In severe dehydration and acidosis only allow sips of water or ice to suck (include in fluid balance)
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.

Oral fluids should only be offered after substantial clinical improvement and cessation of vomiting
10

(mild acidosis and ketosis may still be present).

Page

10
 2.2.2. Electrolyte management

Sodium:
Serum sodium is an unreliable measure of the degree of ECF contraction due to the dilutional
effect of the hyperglycemia and the resultant fluid shift from the ICF to the ECF. (The serum urea
and haematocrit are more useful markers of severe ECF contraction)
Calculate and monitor corrected sodium throughout therapy:
 Corrected Na = Measured Na + 2 x [(glucose – 5.5) ÷ 5.5] mmol/L
As the plasma glucose concentration falls, measured and corrected sodium should rise steadily

Hyperglycemia may cause false hyponatraemia: calculation of Corrected Na is important to

determine the actual value.

The sodium should increase by approximately 1.6 mmol/L for each100 mg/dL decline in the blood
glucose.
The corrected sodium is usually normal or slightly elevated and indicates moderate hypernatremic
dehydration. If the corrected value is greater than 150 mmol/L, severe hypernatremic dehydration
may be present and may require slower fluid replacement. If hypernatraemia is present (corrected
Na >150mmol/L) fluid management should also begin with 0.9% sodium chloride and correction of
fluid and electrolyte deficit should be over 48-72 hours.

Declining sodium may indicate excessive free water accumulation and increased risk of cerebral
edema.If the corrected sodium fails to rise, and particularly if it falls, a careful re-evaluation of the
fluid replacement is required as the concentration of sodium chloride may need to be increased.
The sodium should steadily increase with therapy.

Potassium:
Both the metabolic shift to a catabolic predominance and the acidosis move potassium and
phosphate from the cell to the serum. The osmotic diuresis, the kaliuretic effect of the
hyperaldosteronism, and the ketonuria then accelerate renal losses of potassium and phosphate.

Sodium is also lost with the diuresis, but free water losses are greater than isotonic losses. With
prolonged illness and severe DKA, total body losses can approach 10-13 mEq/kg of sodium, 5-6
mEq/kg of potassium, and 4-5 mEq/kg of phosphate. These losses continue for several hours
during therapy until the catabolic state is reversed and the diuresis is controlled. For example,
50% of infused sodium may be lost in the urine during IV therapy. Even though the sodium deficit
may be repaired within 24 hr, intracellular potassium and phosphate may notbe completely
restored for several days. Therefore Potassium replacement is always required in DKA, as total
body potassium is substantially depleted.

Serum potassium levels at presentation may be normal, increased or decreased. (Hypokalaemia

at presentation represents a significant total body potassium deficit, whereas Hyperkalaemia may
imply reduced renal function or shift of K to the ECF)
Insulin administration and the correction of acidosis will drive potassium back into the cells,
decreasing serum levels of potassium.
11
Page

11
  If the patient is normokalemic, potassium replacement should be given with the
start of insulin therapy (eg, adding 40 meq/L of potassium to the saline solution),
as insulin will reduce the serum potassium.
 If the patient is markedly hypokalemic, potassium replacement should be started
immediately, using an initial potassium concentration of 40 meq/L, concurrent with
volume expansion. The serum potassium levels should be monitored hourly and
the replacement adjusted as needed. The insulin infusion should be delayed
and/or given at a reduced rate until the serum potassium is in the normal range.
 If the patient is hyperkalemic, potassium replacement should be initiated when the
serum potassium falls to normal and after verifying urine production.

The maximum recommended rate of intravenous potassium replacement is 0.5mmol/kg/hour.

Potassium administration (concentration of 40 mEq/L; approximately double the usual

maintenance requirement) can be given as ½ potassium chloride and ½ potassium phosphate (or
K-acetate) formulations to avoid chloride overload, which can exacerbate acidosis.

Bicarbonate therapy
Is rarely necessary and may even increase the risk of hypokalemia and Cerebraledema.The rapid
correction of acidosis with bicarbonate therapy may result in hypokalemia.
Even severe acidosis is reversible by fluid and insulin replacement.

Cautious alkaline therapy may be required however in selected patients with severe acidaemia
(pH <6.9) in whom decreased cardiac contractility and peripheral vasodilatation can further impair
tissue perfusion and in patients with potentially life threatening hyperkalaemia.

The use of large amounts of 0.9% NaCl has been associated with the development of a
hyperchloraemic metabolic acidosis after the clinical status has improved and ketosis has
resolved. Treatment with NaHCO3 may be considered.

NB: In DKA, calcium, magnesium, and phosphate are also deficient. The prevalence and clinical
need for replacement of these electrolytes are not universally accepted.

Calcium:
Hyperglycemia also causes increased urinary calcium loss. Because of the large calcium reservoir
in bone, serum calcium usually remains normal.
Excessive phosphorus administration may result in hypocalcaemia due to suppressed PTH.
12
Page

12
Magnesium:

Because magnesium reabsorption is proportional to urine volume and flow, volume expansion or
osmotic diuresis can lead to magnesium wasting.

Significant magnesium depletion usually is associated with hypocalcaemia and hypokalemia,

since they have similar mechanisms.

Clinical manifestations of hypomagnesaemia are nonspecific and include weakness, dizziness,

tremors, cramps, paresthesias, and seizures. Severe hypomagnesaemia can lead to both atrial
and ventricular arrhythmias. If the patient has a magnesium level of less than 1.8 mEq/L or has
tetany, then magnesium sulfate may be started.

Phosphate:
There is a depletion of intracellular phosphate in DKA and insulin administration results in a fall in
plasma phosphate as phosphate re-enters the cells

Prospective studies have not shown clinical benefit from phosphate replacement; this aspect of
therapy is controversial. One theoretical concern against routine replacement is that it may lead to
symptomatic hypocalcaemia

KPO4 may be used as an alternative to or in combination with KCl to avoid hyperchloraemia,

provided careful monitoring for hypocalcaemia is performed.

Intravenous phosphate administration may induce hypocalcaemia and hypomagnesaemia, and is

generally not necessary or sufficient to replace the total body phosphate

The main indication for phosphate therapy is a serum phosphate concentration less than 1.0
mg/dL (0.32 mmol/L). When phosphate is given, careful monitoring of the serum calcium and
magnesium is required

It is unclear whether phosphate deficits contribute to symptoms of DKA such as generalized

muscle weakness. In pediatric patients, a deficit has not been shown to compromise oxygen
delivery via a deficiency of 2, 3-diphosphoglycerate.

13
Page

13
 2.2.3. Fluid and electrolyte Management of DKA patients in Special situations:

There is no a separate management protocol for pediatrics DKA with Sever acute malnutrition,
Acute Renal Failure, Cardiac or Pulmonary problems.

DKA and Severe Malnutrition:

Current WHO guidelines recommend that children with severe malnutrition should not routinely
receive intravenous fluids. Fluid resuscitation should be reserved for those with signs of
decompensated shock. These recommendations are based on two concerns of salt and water
overload and incipient heart failure.

Misdiagnosis and inappropriate treatment for dehydration is the commonest cause of death in the
malnourished patient.

With severe malnutrition the “therapeutic window” is narrow, so that even dehydrated children can
quickly go from having a depleted circulation to over-hydration with fluid overload and cardiac
failure. IV infusions are rarely used. In malnutrition (both marasmus and, to a greater extent,
kwashiorkor) there is a particular renal problem that makes the children sensitive to salt (sodium)
overload.

If the patient is newly admitted, it is difficult to judge the amount of fluid that has been lost. The
estimated weight deficit should be very conservative. It is better and much less dangerous to
slightly under-estimate the amount of weight deficit than to overestimate the weight deficit. In
practice, the weight loss is generally up to 5% of body weight. Do not attempt to increase body
weight by more than 5% in conscious children. Normally much less ReSoMal is sufficient to
restore adequate hydration in malnourished than normally nourished children (e.g. a total of 50ml
per kg body weight = 5% body weight).

Management of DKA with SAM:

 In patients that are assumed to be overloaded, maintenance can be reduced to

insensible loss ( about 400ml/m2/day) or 50% of the calculated maintenance/day.
 Children with severe acute malnutrition and who have dehydration but no shock
should be rehydrated slowly (up to a maximum of 12 hrs), either orally or by
nasogastric tube, using oral rehydration solution for malnourished children
(ReSoMal)
 In SAM the deficit can be given as 5ml/kg/ over 30min for 2 hours followed by 5 -
10ml/kg/hour over 10 hours
 In DKA the fluid deficit is replaced over 48 hours
 Based on this, In DKA with SAM and DHN, the fluid requirement can be calculated
as Deficit(to be given over 48 hours) plus maintenance/day plus replacement of the
ongoing loss (from vomiting, diarhoea, NGT ...)
 i.e: fluid requirement over 48 hours = 50 to 100ml/kg plus 2(50% of
maintenance) plus ongoing loss.
14
Page

14
  The rate of fluid administration should not be < 5ml/kg/hour; If there is still continued
weight loss, increase the rate of administration of ReSoMal by 10ml/kg/hour; the
feeding can be resumed in alternate hours with F-75 when the patient is stable, can
take PO with no vomiting; and this F-75 can be reduced from the maintenance .
 Signs of improved hydration status and over hydration should be checked every half
hour for the first 2 h, then hourly.
 Give re-hydration fluid until the weight deficit (measured or estimated) is corrected.
Weigh the child each hour and assess his/her liver size, respiration rate and pulse.

Children with severe acute malnutrition and signs of shock or severe dehydration and who cannot
be rehydrated orally or by nasogastric tube should be treated with intravenous fluids. There
should never be a drip present in a malnourished child who is able to drink or is absorbing fluid
adequately from an NG-tube. The only indication for intravenous infusion in a child with severe
acute malnutrition is shock when the child is lethargic or unconscious.

The amounts given should be half or less of that used in normally nourished children:

 Give 10 - 15 ml/kg IV fluid over the first hour and reassess the child.
 If there is continued weight loss or the weight is stable, repeat the 10 - 15ml/kg IV over the
next hour. So the expected weight gain after 2 hours of fluid administration is up to 2 - 3%
of body weight). Make a major reassessment at two hours.
 Use one of the following solutions:
 Half strength Darrow’s solution
 Ringer-Lactate with 5% dextrose (this can be used in our set up if the
patient has urine output)
 Half strength Saline with 5% dextrose or 1/3 NS plus 2/3 5%DW in our
setup.

As soon as the child regains consciousness or the pulse rate drops towards a normal level
then stop the drip and treat the child orally or by NG-Tube with ReSoMal.
Continue with the above management for re-hydration of the child with DKA plus SAM
Dehydration) orally using weight change as the main indicator of progress.

NB: the above management suggestion is extrapolated from assumptions of management of

complicated patients with DKA with risk of being overloaded. This management can be be
changed when better evidence based studies are available on this issue.

Fluids and electrolytes in special clinical situations with DKA:

The two functions of maintenance fluid (heat dissipation through insensible losses and solute
excretion in urine) each can be considered as representing 50% of maintenance
needs. This simple principle is a great aid in the management of children who have anuric renal
failure. Maintenance fluid needs decrease by 50% because the only fluids needing to be replaced
are insensible losses.
15
Page

15
Maintenance fluid and electrolytes are required because of losses that stem
from basal metabolism:

Principles of management of Fluids and electrolytes in special clinical situations

The conservative approach outlined below will work for any patient; it must be used for the more
complicated patient who cannot auto regulate fluid and electrolyte status.

 Assure an adequate effective circulating volume

All patients require an adequate effective circulating volume to permit tissue perfusion. Provide
isotonic crystalloid to volume depleted patients until ECV is stabilized. Infusion volumes should be
smaller and rates slower if it is not clear that the patient can tolerate aggressive fluids. Frequent
evaluation of clinical status is mandatory. For example: It seems reasonable to give fluids to
patients with acute kidney injury secondary to volume depletion while quickly shifting to more
restrictive strategies in those who do not respond to volume and have decreasing urine output.

 Determine goals for overall fluid balance

If the patient’s overall fluid balance is appropriate, the goal is to keep it that way. The most
conservative method involves providing fluids at a baseline rate to replace insensible losses and
to replace all other measured losses on a milliliter-per-milliliter basis. By conservation of matter,
this must keep the patient balanced. Strict monitoring of input, output and weight changes is
essential. Any additional fluids, such as medications, flushes or continuous drips, must be
considered in the balance since they are not offset by a loss.

 Limit fluids for volume overloaded patients

Decrease daily input as much as possible for the volume overloaded patient. Concentrate
continuous drips and nutrition. Consider the use of diuretics to increase urine output. Do not
replace the full volume of all losses. Closely monitor input, output and weights; adjust regimen as
needed.
 Consider dialysis and ultrafiltration
16

The conservative fluid regimen may limit your ability to provide nutrition or therapy to your patient.
Dialysis or continuous ultrafiltration can remove fluid efficiently, preventing the imbalance of fluid
Page

while the patient receives the needed treatment.

16
In shocked patients who have or who may develop fluid overload (Acute Renal Failure, Cardiac or
Pulmonary problems), the initial bolus can be given in a dose of 10ml/kg over one hour while
strictly following the vital signs, input, output ,weight and status for improvement of circulatory
perfusion or deterioration; further treatment depends on the response of the patient. In a patient
with decreased urine output or deterioration despite volume replacement, fluid is restricted to the
replacement of the insensible part of the maintenance (= up to 400ml/m2/day)

Any patient with evidence of fluid deficit, the deficit should be replaced. In complicated patients
(DKA with Acute Renal Failure, Cardiac or Pulmonary problems) with evidence of fluid deficit, the
fluid requirement can be calculated as: Deficit plus insensible part of the maintenance/day minus
the bolus to be given over 48 to 72 hours, while following the condition of the patient and
adjustments of the fluid requirement can be made any time during the replacement based on the
response of the patient.

NB: Strict recommendations of fluid replacement for such patients are difficult; cautious treatment
depends on patient response with strict follow up.

17
Page

17
 2.3. Insulin:
Insulin therapy is essential to normalize blood glucose concentration and suppress lipolysis and
ketone production.

During the first 1 – 2 hrs of rehydration, the blood glucose may fall substantially (may decrease by
20%) even without insulin therapy.

Insulin therapy should be started 1 hour after the initial rehydration bolus but should not be
delayed for more than 2 hours after starting IV hydration.

Beginning insulin treatment at the same time as fluid resuscitation increases the risks of severe
hypokalemia and of rapidly and excessively decreasing the serum osmolarity

The risk of cerebral edema is decreased by delaying insulin administration for one hour or more
after initiation of fluid therapy.

A bolus dose of insulin is not indicated and may increase the risk of Cerebral Edema.

Optimal method of Insulin delivery: Continuous low-dose IV insulin infusion by syringe pump, not
by gravity controller.

Continuous IV regular insulin is given at a dose of 0.1u/kg per hour. (50units soluble insulin diluted
in 50mls of 0.9%Saline, to make 1unit = 1ml); the aim is to have blood glucose level decrease by
50-100 mg/hr.
A lower insulin dosage of 0.05u/kg/hr can be considered in children <5yrs of age (who may be
more sensitive to insulin) in children with known diabetes who have a lower blood glucose due to
partial insulin treatment prior to presentation.

Because insulin will bind to the walls of the IV tubing, the tubing is first washed with 20 ml of the
insulin solution. IV insulin provides a relatively smooth decline in blood glucose levels with a
predictable time to expect a blood sugar of less than 300mg/dl.

If intravenous administration of insulin is not possible, short- or rapid-acting insulin injected

intramuscularly or subcutaneously every 1 or 2 hours can be effective.

Alternative to insulin infusion where there are no facilities for insulin infusion, e.g. no syringe
pumps, staff constraints, etc.: Insulin short-acting, IV, 0.1 unit/kg, hourly. Do not add insulin
directly to the fluid bags.

If a syringe pump is not available for Insulin infusion, the following methods may be used:
 Mix 50 units soluble insulin in 500ml normal saline (i.e. I unit insulin / 10 ml saline) and use
infusion rate = 0.1 units/kg/hr (=1ml/kg/hr). Change the bag every 24 hr to avoid insulin
inactivation; first flush the bag and the iv line with 50 ml of the diluted insulin.

OR
18

 Give hourly bolus injections of fast acting Insulin at a rate of 0.1

units/kg/hourly IV.
Page

18
When blood glucose falls to <250 - 300mg/dl, add dextrose to the IV solution. The IV solution can
be changed to 1/2 normal saline plus 5% Dextrose =5%DW + 0.45%NS (with potassium).

If the blood glucose concentration fall below 150 mg/dL (8.3 mmol/L) a10%Dextrose solution with
Saline 0.45%and potassium should be given.

If the Blood glucose is still below 150 mg/dL (8.3 mmol/L) despite the addition of 10% glucose with
saline, the insulin dose can be reduced to 0.05 U/kg/hour but do not discontinue the insulin drip.
Continued insulin infusion is essential to inhibit gluconeogenesis and ketogenesis, promote
peripheral glucose utilization, and correct metabolic acidosis.

If BG rises again above 15 mmol/I(> 300mg/dl), increase insulin infusion by 25%

If the acidosis is not resolving, the insulin dose should be increased to 0.15 or 0.20 units/kg per
hour. The resolution of academia invariably takes longer than normalization of blood glucose
concentrations.

If acidosis is not correcting, consider the following:

 Insufficient insulin to switch off ketones

 Inadequate resuscitation
 Sepsis
 Hyperchloraemic acidosis
 Drugs like Salicylates
 Starvation ketosis (If there is ketonuria with corrected blood glucose and negative urine
glucose)

Urine ketones maybe positive long after ketoacidosis has resolved because the nitroprusside
reaction routinely used to measure urine ketones by dipstick measures only acetoacetate. 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.
Therefore, persistent ketonuria may not accurately reflect the degree of clinical improvement and
should not be relied on as an indicator of therapeutic failure.

Once all these causes of acidosis have been excluded, and if ketones are falling gradually, then
residual acidosis is likely to be due to hyperchloraemia, and this can be left to resolve on its own,
and does not require any treatment.
19
Page

19
 2.3.1. Management during Infections and sick days:

Patients with hyperglycemia and ketonuria can be managed as DKA. And alternative
management can be as follows:
Rapid-acting insulin can be used to provide supplemental insulin during sick daysand
Recommendations include:

1 Elevated BG with an absence or only small amount of ketones:

• Give 5–10% of the total daily dose (TDD)of insulin (0.05–0.1 U/kg) as short or rapid acting
insulin subcutaneously or intramuscularly and repeat this same dose every 2–4 h according toBG
response and clinical condition.TDD of insulin is the sum of all long, intermediate and short/rapid-
acting insulin usually taken.
2 Elevated BG with moderate or large amount of ketones is more serious and reflects actual or
impending diabetic ketoacidosis (DKA) with potential for coma or death:
• Give 10–20% of the TDD of insulin (0.1–0.2 U/kg) as short or rapid-acting insulin
subcutaneously or intramuscularly and repeat this same dose every 2–4 h according to BG
response and clinical condition.

Example: A sick child has BG 14–20 mmol/L (i.e., 250–360 mg/dL)with moderate urinary ketones
and/orblood ketones of approximately 1.5 mmol/L. Advise 10–20% of total daily insulin dose (or
0.1 U/kg) asshort/rapid acting insulin every 2–4 h until BG falls to<14 mmol/L (<250 mg/dL).
Thereafter any additional doses might be 5–20% of TDD. Check urine ketones at every voiding. If
available, check blood ketones and recheck hourly if elevated (>0.6 mmol/L).
• After extra insulin has been given, the blood ketonelevel may temporarily increase by 10–20%
for the first hour or two but should be expected to decrease thereafter.
• Urine ketones often stay elevated for many hours because of the body’s conversion of blood β-
hydroxybutyrate (BOHB) into acetoacetate (AcAc) which then can be measured with urine testing.
Acetone can be stored in fat tissue during ketosis and, along with conversion of BOHB to AcAc,
may contribute to persistent urine ketones despite interruption of total ketogenesis with insulin and
fluid administration.
• Reduction of total daily insulin dose by 20–50% may be required if there is concomitant
hypoglycemia and not hyperglycemia as indicated above;
NPH should be reduced by half if blood glucose <150 mg/dL and the oral glucose intake is limited.
Oral fluids: sugar-free if blood glucose >250 mg/dL (14 mmol/L); sugar-containing if blood glucose
<250 mg/dL.
IV glucose is needed if blood glucose remains less than 70 mg/dL and child cannot take oral
supplement.

Guidelines for Sick Day Management

URINE KETONE GLUCOSE TESTING AND EXTRA RAPID-ACTING INSULIN
STATUS Insulin Correction Doses COMMENT
Negative or small q2hr q2hr for glucose Check ketones
>250 mg/dL every other void
Moderate to large q1hr q1hr for glucose Check ketones each
>250 mg/dL void; go to hospital if
emesis occurs
20

.Q2hr =every 2 hour.

NB: Mild, Moderate and Severe ketosis can be defined as: urinary ketone of + 1, + 2 and + 3
Page

respectively.
20
Sick day management in children and adolescents with diabetes
How to calculate the Amount of Extra Insulin on Sick Days
Urine Blood glucose
ketones <5.5 mmol/L 5.5–10 10–14 mmol/L 14–22 >22 mmol/L
<100 mg/dL mmol/L 180–250 mmol/L >400 mg/dL
100–180 mg/dL 250–400
mg/dL mg/dL
Negative or Do not give No need to Increase dose Give extra Give extra
trace extra insulin. worry of insulin for 5% of TDD 10% of TDD
Check BG next meal if or or
and ketones BG is still 0.05 U/kg 0.1U/kg.
again in 2 h elevated Repeat if
needed
Trace or Starvation Starvation Give extra 5% Give extra Give extra
small ketones. ketones. of TDD or 5–10% of 10% of TDD
Extra Extra 0.05 U/kg TDD or
carbohydrates carbohydrates or 0.05–0.1 0.1U/kg.
and fluid and fluid U/kg Repeat if
are needed are needed needed
Small or Starvation Starvation Extra Give extra Give extra
moderate ketones. ketones. carbohydrates 10% of TDD 10% of TDD
Extra Extra and or or
carbohydrates carbohydrates fluid are 0.1U/kg 0.1U/kg.
and fluid and fluid needed. Give Repeat if
are needed are needed 5–10% of needed
TDD or
0.05–0.1 U/kg
Moderate or High levels of High levels of Extra Give extra
large starvation starvation carbohydrates 10–20% of
ketones. ketones. and TDD
Check BG Extra fluid are or 0.1U/kg.
meter. carbohydrates needed. Give Repeat dose
Recheck BG and fluid 10% of TDD after 2 h if
and are needed. or 0.1 U/kg ketones do
ketones. Give 5% of not
Extra TDD or decrease
carbohydrates 0.05U/kg.
and fluid Repeat when
are needed. BG has
May need IV risen
glucose if
child cannot
eat or drink.
Risk of DKA
Check BG Very high Very high Extra Give extra
and ketones levels of levels of carbohydrates 10–20% of
every hour: starvation starvation and TDD
Large ketones. ketones. fluid are or 0.1U/kg.
Check BG Extra needed. Give Repeat dose
meter. carbohydrates 10% of TDD after 2 h if
Recheck BG and fluid or 0.1 U/kg ketones do
and are needed. not
ketones. Give 5% of decrease
Extra TDD or
carbohydrates 0.05U/kg.
21

and fluid Repeat when

are needed BG has
Page

risen
BG, blood glucose; TDD, total daily dose.
21
 2.3.2. Management during Surgery:
Surgery can disrupt glucose control in the same way as can intercurrent infections
May initially receive an IV infusion without dextrose for minor surgery or procedures (lasting for
less than 2 h) if treated with basal/bolus insulin regimen.
• Should initially receive an IV infusion with dextrose for major surgery or procedures (lasting for at
least 2 h) or if treated with NPH insulin.
• Require hourly capillary blood glucose monitoring to detect hypoglycemia and hyperglycemia
before the procedure. If the blood glucose exceeds 14 mmol/L (250 mg/dL), a conservative dose
of regular insulin should be administered to restore blood glucose to the target range.
◦The usual recommendation of the timing of preoperative food and fluid restrictions with the
anesthetist is no solid food for at least 6 h before surgery. Clear fluids (and breast milk) may be
allowed up to 4 h before surgery.

Major surgery
• On the evening before surgery:
◦ Give the usual evening and/or bedtime insulin(s) and bedtime snack.
• Omit the usual morning insulin dose.
• At least 2 h before surgery, start an IV insulin infusion [e.g., dilute 50 units regular (soluble)
insulin in 50mL normal saline, 1 unit=1mL] and provide IV maintenance fluids consisting of 5%
dextrose and half-normal saline (0.45% NaCl)
• Monitor blood glucose levels at least hourly before surgery and as long as the patient is
receiving IV insulin.
• Aim to maintain blood glucose between 5 and 10 mmol/L (90–180 mg/dL) by adjusting the IV
insulin dose or the rate of dextrose infusion during surgery.
• When oral intake is not possible, the IV dextrose infusion should continue for as long as
necessary.

Minor surgery
• Morning operations:
◦ On the morning of the procedure, give 50% of the usual morning dose of intermediate acting
insulin (NPH)
◦ Omit the short -acting insulin unless it is needed to correct hyperglycemia.
◦ Commence IV fluids containing dextrose 5–10%, as necessary, to prevent hypoglycemia.
• Afternoon operations (if unavoidable):
◦ On the morning of the procedure, give 50% of the usual dose of intermediate-acting insulin
(NPH)
◦ The dose of short- or rapid-acting insulin will depend on whether the child is permitted to eat
breakfast.
◦ If the anesthetist allows the child to eat a light breakfast and to consume clear liquids up to 4 h
before the procedure, IV fluid administration (and IV insulin infusion, if applicable) should
commence 2 h before surgery or no later than midday

Intraoperative care:

Monitor blood glucose measurements at least hourly during and immediately after GA. If
necessary, begin dextrose infusion or increase dextrose concentration of IV fluids from 5 to 10%
to prevent hypoglycemia. Adjust dextrose infusion and insulin dose (by subcutaneous injection of
22

rapid-acting insulin for minor surgery) to maintain blood glucose in the range 5–10 mmol/L (90–
Page

180 mg/dL).

22
Infusion guide for surgical procedures:

(i) Maintenance fluid guide

• Dextrose (for major surgery and any surgery when NPH has been given) 5% dextrose; 10% if
there is concern about hypoglycemia. If blood glucose is high (>14 mmol/L, 250 mg/dL), use half-
normal saline (0.45% NaCl) without dextrose and increase insulin supply but add 5% dextrose
when blood glucose falls below 14 mmol/L (250 mg/dL).

(ii) Insulin infusion

Guidelines for Intravenous Insulin Coverage During Surgery

BLOOD GLUCOSE INSULIN INFUSION BLOOD GLUCOSE URINE KETONES
LEVEL (mg/dL) (units/kg/hr) MONITORING MONITORING
<120 0.00 1 hr
121-200 0.03 2 hr
200-300 0.06 2 hr
300-400 0.08 1 hr Check
400 0.1 1 hr check

• Aim to maintain blood glucose between 5 and 10 mmol/L (90–180 mg/dL) by adjusting insulin
infusion hourly
• Blood glucose must be measured at least hourly when the patient is on IV insulin
• Do not stop the insulin infusion if blood glucose <5–6 mmol/L (90 mg/dL) as this will cause
rebound hyperglycemia. But the rate of insulin may be reduced.
When surgery is elective, it is best performed early in the day, allowing the patient maximal
recovery time to restart oral intake and subcutaneous insulin therapy.
When elective surgery is brief (less than 1 hr) and full oral intake is expected shortly afterward,
one may simply monitor the blood glucose hourly and give a dose of insulin analog according to
the child’s home glucose correction scale.

If NPH is used, one half of the morning dose is given before surgery. The child should not be
discharged until blood glucose levels are stable and oral intake is tolerated.

An infusion of 5% glucose and 0.45% saline solution (DNS in our setup) with 20 mEq/L of
potassium acetate is given at 1.5 times maintenance rate.
23
Page

23
 2.4. Monitoring

There should be documentation of hour-by-hour clinical observations, IV and oral medication,

fluids, and laboratory results during the entire treatment period with DKA flow shit.
Monitoring should include:
 Clinical parameters including heart rate, respiratory rate, blood pressure, oxygen
saturation, and neurologic status should be monitored continuously.
 Hourly heart rate, respiratory rate, and blood pressure.
 Twice daily weight; can be helpful in assessing fluid balance
 Hourly (or more frequent), accurate fluid input and output.
 In severe DKA, electrocardiogram monitoring may be helpful to assess for evidence of
Hyperkalemia/hypokalemia.
Monitor blood glucose hourly during the initial 4 to 6 hours of fluid and insulin therapy.If
capillary blood glucose is monitored hourly (It should be cross-checked against venous
glucose, because capillary methods may be inaccurate in the presence of poor peripheral
circulation and acidosis).
 Laboratory tests: electrolytes, urea, hematocrit, and blood gases should be repeated every
2 to 4 hours. (However, electrolytes should be monitored hourly as clinically indicated in the
more-severe cases.) An elevated white blood cell count may be due to stress and cannot
be taken as a sign of infection.
 Capillary blood ketone levels every 1-2 hours (if available) otherwise urine ketone testing
every 2 hourly.
 Hourly or more-frequent neurologic observations for warning signs and symptoms of
cerebral edema.

2.5. Management of complications

2.5.1. Treatment of Cerebral Edema

Be aware of the risk of cerebral oedema, which usually occurs 6-24 hours after initiation of
therapy; rehydration, which is too rapid, has been implicated.

Warning signs of cerebral oedema include:

 Headache
 Inappropriate slowing of pulse rate
 Recurrence of vomiting
 Change in neurological status or specific neurological signs
 Rising BP
 Decreased oxygen saturation
 Fall in serum sodium concentration

Effective osmolality = 2(Na uncorrected + K) + glucose mmol/L may be a useful guide to fluid and
electrolyte therapy. A fall in serum osmolality of >3mosm/kg/hr has been suggested as a risk
factor for cerebral oedema.

A fall in serum sodium is one of the few biochemical correlates of impending cerebral oedema.
24

Excessive fluids may increase the risk for cerebral edema.

Page

24
Bicarbonate therapy has not been shown to confer clinical benefit in DKA and may increase the
risk of cerebral edema.

A bolus dose of insulin is not indicated and may increase the risk of Cerebral Edema.
Management of cerebral oedema:
 Halve the rate of IV fluid administration until the situation has stabilized; fluids should be
restricted to ½ maintenance rates.
 Give IV Mannitol 0.5 to 1 gm/kg over 20 minutes; a repeated dose of Mannitol may be
required after 2 hours if no response.
 Consider continuation of mannitol infusion 0.25g/kg/hour to prevent rebound increase in
intracranial pressure, or repeat boluses every 4-6 hours. Hypertonic Saline (3%), 5-10
ml/kg over 30 minutes may be an alternative to Mannitol
 Elevate head
 Intubation and ventilation may be necessary; however aggressive hyperventilation has
been associated with poor outcome. If assisted ventilation is required maintain pCO2
above 3.5kPa

2.5.2. Treatment of Hypoglycemia

Itis safe to define hypoglycemia for DKA in pediatric age group as random blood sugar levels
become below 70 mg/dl (although some references use blood glucose less than 60 mg/dL)with or
without symptoms or signs of hypoglycemia. In the emergency room, the management of diabetic
patients with severe hypoglycemia is to give 2 to 5 ml/kg of D10% IV followed by D10 in 1/2
normal saline at the maintenance rate and monitor the RBS. The dose can be repeated an
addition time of the blood sugar did not increase to more than100 mg/dl.

General and supportive measures:

 Determine underlying cause.
 Patient education on diabetes and its complications.
 If patient is fully alert and conscious, give sugar-containing drink and/orsnack
(carbohydrate).
 Monitor blood glucose every 15 minutes until blood glucose is >100mg/dl

Medical Treatment:

Asymptomatic hypoglycemia:
 Immediate oral rapidly absorbed simple carbohydrate, e.g.: Glucose, oral, 5–15 g or 1-3
level teaspoons of sugar in a small amount of water; Wait 10–15 minutes.
 If no response, repeat above.
 As symptoms improve, the next meal or oral complex carbohydrate should be ingested,
e.g. fruit, bread, cereal, milk, etc.
Symptomatic hypoglycemia:
If there is an unsatisfactory response or inability to take oral carbohydrate and signs of
disorientation, stupor, convulsions and coma:
 Dextrose IV, 2–5 mL/kg of 10% glucose (200 to 500mg/kg). In glucose 10% solution, the
concentration has 100g/Liter; which means, each ml contains 100mg of glucose.
25

 IV fluid with concentration of > 10% glucose (glucose concentration = 12%) can be given if
no response.
Page

 Monitor blood glucose every 15 minutes until stable, then repeat 1–2 hourly.
25
 2.6. Transfer to Oral Fluids and Subcutaneous Insulin

Any child can be easily transitioned to oral intake and subcutaneous insulin when DKA has
resolved:

 Serum anion gap reduced to normal (12 ± 2 meq/L)

 Venous pH is >7.30 or serum HCO3 is >15 meq/L
 Plasma glucose <200 mg/dL (11.1 mmol/L)
 Tolerating oral intake, no emesis

Fluids and food

 Start oral fluids when there is a clinical improvement and nausea has settled
 Begin with water or flavoured oral “cell repair fluid" (50g glucose + 4g K2HPO4 in 1L
water); then milk, reducing IV fluids accordingly
 Add solids - diabetes diet! - when fluids tolerated

The first dose of short acting subcutaneous insulin is given before meals or with a meal, and the
insulin infusion should be discontinued 30 – 60 minutes after the 1st injection of short acting
insulin is given).Subcutaneous insulin injection can be started when IV fluids are no longer
needed.IV fluids can be stopped 1-2 hours after substantial consumption of oral fluids without
vomiting.

During treatment for DKA, correction of the ketoacidosis does not necessarily result in complete
correction of the metabolic acidosis. The residual acidosis is associated with a normal anion gap
that is due to urinary loss of ketoacid anions. In this setting, insulin therapy will have no further
effect on the acidosis. Thus, a persistent normal anion gap acidosis is not a contraindication for
switching the patient to subcutaneous insulin, since there are no circulating ketoacids remaining.

For patient safety reasons, it is advisable to keep serum glucose concentrations around 150 to
200 mg/dL (8.3 to 11.1 mmol/L) for younger children; or 100 to 150 mg/dL in older children (5.5 to
8.3 mmol/L), before switching to subcutaneous insulin.

The SC insulin dosage and regimen will vary with the patient’s age and circumstances. Once DKA
has resolved in the newly diagnosed child, therapy is transitioned to that described for children
with nonketotic onset. Children with previously diagnosed diabetes who develop DKA are usually
transitioned to their previous insulin regimen.

Several factors influence the initial daily insulin dose per kilogram of body weight. The dose is
usually higher in pubertal children. It is also higher in those who are in DKA at the time of
presentation.
26
Page

26
The optimal insulin dose can only be determined empirically, with frequent self-monitored blood
glucose levels and insulin adjustment by the diabetes team.

Recommended starting dose of Insulin after resolution of DKA (units/kg/hr):

Age group No DKA DKA

Pre pubertal 0.25 – 0.50 0.75 – 1.0
Pubertal 0.50- 0.75 1.0 – 1.2
Post pubertal 0.25 – 0.50 0.8 – 1.0

Standard insulin regimens in newly diagnosed patients: Twice daily injections of a mixture of short
and intermediate-acting insulin: Mix regular and intermediate insulin 1:2; give ⅔ TDD at breakfast,
⅓ TDD at supper.

Usually commence with total daily dose (TDD) based on the Age and clinical condition of the
patient:

This is given as 2/3 of TDD in morning, 1/3 of TDD at night. 2/3 of each dose as intermediate-
acting insulin, 1/3 as short-acting insulin.

Recommended starting dose of Insulin for after resolution of DKA (units/kg/hr) =

maintenance dose of Insulin:

Time Insulin Regimen

Dayly  TDD = Based on Age & clinical condition
 2/3 of TDD is NPH; 1/3 of TDD is
Regular Insulin

Morning 2/3 of TDD will be given in the morning

2/3 of the morning dose is NPH, 1/3 of the
morning dose is Regular Insulin
Evening  1/3 of TDD will be given in the evening
 ½ to 2/3 of the evening dose is NPH and
1/3 to ½ of the evening dose is Regular
Insulin 27
Page

27
During follow up, ideally, the blood glucose concentration should range from approximately80
mg/dL in the fasting state to 140 mg/dL after meals. In practice, however, a range is acceptable
based on age of the patient.

Target Premeal and 30-Day Average Blood Glucose Ranges and the Corresponding
Hemoglobin A1c forEach Age Group
Age group Target Pre meal BG 30 day average BG Target HbA1c(%)
Range mg/dl Range mg/dl
<5 100 – 200 180 – 250 7.5 – 9.0
5 – 11 80 – 150 150 – 200 6.5 – 8.0
12 – 15 80 – 130 120 – 180 6.0 – 7.5
16 - 18 70 - 120 100 - 150 5.5 – 7.0

Blood glucose measurements that are consistently at or outside of the set limits, in the absence of
an identifiable cause such as exercise or dietary indiscretion, are an indication for a change in the
insulin dose.
If the patient is on conventional insulin therapy with regular insulin and NPH, insulin dose
adjustment depends on blood glucose monitoring.

 If the majority of morning blood glucose (the fasting blood glucose) readings are elevated,
the evening NPH may be increased by 10-15%.
 If the majority of pre-lunch (noon) blood glucose readings are elevated, the morning regular
insulin may be increased by 10-15%.
 If the majority of the evening blood glucose readings are elevated, the morning NPH may
be increased by 10% - 15%.
 If the bedtime glucose is high, the pre supper (evening) dose of regular insulin is increased
by 10-15%.

One unit of rapid acting insulin is required for each 50 - 75 mg/dl of blood glucose above the
target as a correction bolus.

Standard recommended values for blood glucose control

Blood sugar control, clinical- Healthy Metabolism Metabolism fair Metabolism
chemical assessment subjects good (measures poor
recommended) (measures
required)
preprandial or fasting BG 3.6 – 5.6 5–8 >8 >9
(mmol/L or mg/dL) 65 – 100 90 – 145 > 145 > 162
postprandial BG 4.5 – 7.0 5 – 10 10 – 14 > 14
80 – 126 90 – 180 180 – 250 > 250
nocturnal BG 3.6 – 5.6 4,5 – 9 < 4.2 or > 9 < 4.0 or > 11
65 – 100 80 – 162 < 75 or > 162 < 70 or > 200
HbA1c level (standardized < 6.05 < 7.5 7.5 – 9.0 > 9.0
measurement in %)
28

BG= blood glucose.

Page

28
2.7. Discharge Planning:
 Patient well and stable tolerates oral feeding and on SC insulin regime that will be used at
home safely by patient or care giver.
 Parents and/or child and/or other caregiver proficient in injection technique, dose
accuracy, monitoring: blood glucose, urine glucose, ketones
 Follow-up appointment has been made with diabetes clinic
 Medic-Alert badge inscribed: Information like "diabetes on insulin- give sugar if confused"
 Dietary advice and exercise
 Advice on recognizing and treating hypoglycemia/ ketoacidosis.

29
Page

29
 2.8. Summary of Medical treatment of DKA
Treatment objective/ Medicatio Dose Time period/sequence
Indication n
Initial stabilization ABC of life, Airway, Breathing(100%  Over 1 –2 hours
NaCl O2), Circulation=10 ml/kg i.  If shocked Over 20 – 30
v., may be repeated up to minutes per dose
30ml/kg
Administration of fluids NaCl 0.9 % Deficit plus Maintenance Over 48 hours
after initial stabilization solution with for 48 hrs (at most iv. daily
of circulation potassium dose should not be > 1.5
to 2
times maintenance
requirements)
To lower the blood glucose Regular 0.1 U/kg/h iv. Beginning of insulin administration 1 - 2
insulin For Insulin sensitive hours after beginning of volume
children (like < 5 years of administration
age) =0.05 u/kg/hr

To avoid hypoglycemia Add 1/3 NS plus 2/3 5% DW (or starting at blood sugar < 300mg/dL
Glucose to DNS); If still Blood
the fluid Glucose is < 150mg/dl
change fluid to 1/3 NS plus
2/3 10%DW; If no
improvement reduce
Insulin dose from 0.1 to
0.05u/kg/hr
potassium balance KCl 40 meq/ L  Immediately if hypokalemia:
 At start of insulin administration
if normokalemia;
 Not until urine production has
resumed if hyperkalemia;
 Continual administration until
termination of volume
administration
Transfer to Oral fluids and NPH and  For prepubertal  BID regimen of a mixture of
Subcutaneous Insulin Regular 0.75 – 1.0 NPH and Regular:
when, patient is out of DKA: Insulin  For pubertal age  2/3 of TDD in morning, 1/3 of
u/kg/day 1.0 – 1.2 TDD at night.
 Serum anion gap  For post pubertal  2/3 of each dose as NPH, 1/3 as
reduced to normal 0.8 – 1.0 Regular Insulin.
(12 ± 2 meq/L)  2/3 of the morning dose as NPH
 Venous pH is and 1/3 as regular
>7.30 or serum  ½ to 2/3 of the evening dose is
HCO3 is >15 NPH and 1/3 to ½ of the evening
meq/L dose is Regular Insulin
 Plasma glucose
<200 mg/dL (11.1
mmol/L)
 Tolerating oral
intake,
 No emesis
30
Page

30
3. REFERENCES:

1. Arlan L., The Management of Diabetic Ketoacidosis in Children, Diabetes Ther (2011)
1(2):103-120. DOI 10.1007/s13300-010-0008-2
2. A. Neu, P. Beyer, J. Bürger-Büsing, T. Danne, J. Etspüler, B. Heidtmann; Diagnosis,
Therapy and Control of Diabetes Mellitus
in Children and Adolescents , German Diabetes Association: Clinical Practice Guidelines
(Neu A et al.) Diagnosis, Therapy and… ExpClinEndocrinol Diabetes 2014; 122: 425–434
3. Bonadio W., an evidence based approach to pediatrics emergency medicine,Pediatric
Diabetic Ketoacidosis: An Outpatient Perspective On Evaluation and Management,
www.ebmedicine.net • ;March 2013Volume 10, Number 3
4. Beck J.K., PharmD., Fran R.,CogenJ.R.; Outpatient Management of Pediatric Type 1
Diabetes; PediatrPharmacolTher 2015;20(5):344–357
5. Cooke D.W.,Plotnick L., Management of DiabeticKetoacidosis in Children
andAdolescentsPediatrics in Review Vol.29 No.12 December 2008
6. ThomasD. Et al.;European Society for Paediatric Endocrinology/Lawson Wilkins Pediatric
Endocrine Society Consensus Statement on Diabetic Ketoacidosis in Children and
Adolescents, AAP, Pediatrics 2004;113;e133-e140, DOI: 10.1542/peds.113.2.e133
7. BC CHILDREN’S HOSPITAL; DIABETIC KETOACIDOSIS PROTOCOL FOR CHILDREN
UP TO AGE 19 YEARS,WWW.BCCHILDRENS.CA/ENDOCRINOLOGY-DIABETES
SITE/DOCUMENTS/DKAPRT, OCTOBER 7, 2015
8. Edge J.,BSPED Recommended Guideline for the Management of Children and Young
People under the age of 18 years with Diabetic Ketoacidosis, based on the NICE guideline;
Oxford: Approved by BSPED Clinical Committee 26/8/20152015
9. KileanM.,Helman A, Episode 63 – Pediatric DKA,University of Toronto Divisions of
Emergency Medicine. April 2015
10. South AustralianPaediatric Clinical Guidelines: Management of Diabetic Ketoacidosis
(DKA) in Children, 1 July 2013
11. WOLFSDORF J., GLASER N., SPERLING M.A., Diabetic Ketoacidosis in Infants,
Children,and Adolescents,A consensus statement from the American Diabetes Association,
DIABETES CARE, VOLUME 29, NUMBER 5, MAY 2006
12. Bin-Abbas B.S., Al Qahtani M.A., Clinical guidelines for the management oftype 1 diabetes
in children in Saudi Arabiaendorsed by the Saudi Society of Endocrinology and
Metabolism, (SSEM), International Journal of Pediatrics and Adolescent Medicine (2014) 1,
97e101
13. Rull G., Tidy C.; Childhood Ketoacidosis,patient.info/doctor/childhood-ketoacidosis,
Paediatric Diabetic Ketoacidosis calculator; British Society for Paediatric Endocrinology
and Diabetes12/03/2014
14. DKA TREATMENT PROTOCOL-DENVER, Barbara Davis Center for Childhood Diabetes,
University of Colorado & Children’s Hospital Colorado, 2015-2016
15. Shenoy G, Carrihill G., Paediatric Management of Diabetic Ketoacidosis (DKA)Guideline
No: 13 University Hospitals of Leicester NHS Trust, Children’s Services Medical Guideline,
UK,May 2008
16. The Royal Children's Hospital Melbourne, Clinical Practice Guidelines; Diabetes mellitus,
Australia, 2012
31

17. Imam Hj H., Ismail M., Phak N.H., Thomas T.; PAEDIATRIC PROTOCOLS For Malaysian
Hospitals3rd Edition, 2014
Page

31
18. PROVINCE OF KWAZULU-NATAL HEALTH SERVICES;P a e d ia t r i c G u i d e l i n e
DIABETIC KETO-ACIDOSIS Guidelines, for hospital management, South Africa, 2012
19. South Africa Ministry of Health; Standard Treatment Guideline and Essential Medicines List
for South Africa, Hospital level Pediatrics; 2013
20. Rachel S. Meyer S, PharmD;Pediatric Fluid and Electrolyte Therapy; J
PediatrPharmacolTher (JPPT) 2009;14:204–211
21. The Harriet Lane Hand Book, a manual for pediatrics house officers; chapter on DKA and
Fluids - Electrolytes, 18thed.
22. NELSON TEXT BOOK OF PEDIATRICS, 20THed.
23. UPTODATE 21.6
24. Ambalavanan N.; Fluid, Electrolyte, and Nutrition Management of the Newborn, Medscape;
Feb 28, 2014
25. Roberts K.; Fluid and Electrolytes: Parenteral Fluid Therapy Pediatrics in Review Vol.22
No.11 November 2001
26. Gangaraj S., Das G., Madhulata S.; Electrolytes and Blood Sugar Changes in Severely
Acute malnourished Children and Its Association With Diarrhea and Vomiting; International
Journal of Pharmaceutical Science Invention ISSN (Online): 2319 – 6718, ISSN (Print):
2319 – 670X www.ijpsi.org Volume 2 Issue 5 ‖ May 2013 ‖ PP.33-36
27. WHO. Guideline: Updates on the management of severe acute malnutrition in infants and
children. Geneva: World Health Organization; 2013
28. FEDERAL MINISTRY OF HEALTH; PROTOCOL FOR THE MANAGEMENT OF SEVERE
ACUTE MALNUTRITION, ETHIOPIA MARCH 2014
29. Hursh B., Ronsley R.,Islam N, et al; Acute Kidney Injury in Children With Type 1 Diabetes
Hospitalized for Diabetic Ketoacidosis, JAMA Pediatr. 2017;171(5):e170020.
doi:10.1001/jamapediatrics.2017.0020
30. Woodrow G, Brownjohn AM, Turney JH. Acute renal failure in patients with type 1 diabetes
mellitus. Postgrad Med J. 1994;70:192-194.
31. Symons D.; Clinical Fluid and Electrolyte Management, Conservative Fluid Management
for Complicated Patients, Seattle Children Hospital,Rev. 4/05)
32. Rhodes ET, Gong C, Edge JA, Wolfsdorf JI, Hanas R.; ISPAD Clinical Practice Consensus
Guidelines 2014 Compendium, Management of children and adolescents with diabetes
requiring surgery; Pediatric Diabetes 2014: 15 (Suppl. 20): 224–231.
33. Brink S, Joel D, Laffel L, LeeWWR, Olsen B, PhelanH, Hanas R., ISPAD Clinical Practice
Consensus Guidelines 2014 Compendium, Sick day management in children and
adolescents with diabetes; Pediatric Diabetes 2014: 15 (Suppl. 20): 193–202.
34. Rhodes ET, Ferrari LR, Joseph I. Wolfsdorf JI.; Perioperative Management of Pediatric
Surgical Patients with Diabetes Mellitus, the International Anesthesia Research Society,
ANESTH ANALG 2005;101:986–99
35. UMMCH: University of Minesota Masonic Childrens Hospital; Emergency Department
Guideline, Pediatric Diabetic Ketoacidosis (DKA, Division of Pediatric Emergency Medicine,
M. HEALTH July 2016.
32
Page

32