DIABETIC KETOACIDOSIS IN CHILDREN

AN OVERVIEW

Dr. K. Radha Krishna

MD.,DCH

Chairman
DIABETIC KETOACIDOSIS

A child is not a miniature adult

The child differs from the adult

 More difficult it is to obtain the classical history
 The higher BMR & large surface area.

 Cerebral & auto regulatory mechanisms are not

well developed.
DIABETIC KETOACIDOSIS

 DKA is an emergency medical condition that can be

life-threatening.
 DKA results from deficiency of circulating insulin
and the combined effects of increased levels of the
counter regulatory hormones.
 DKA occurs more commonly in patients who have
Type 1 diabetes.
 DKA carries a high mortality in our country.
INCIDENCE:
 15%to 70% of all newly diagnosed DM present
with DKA.

 Younger the child more the chance.

 5% of Adult T2 DM patients present C DKA at the

time of diagnosis.

 30 % of child T2 DM patients present C DKA at

the time of diagnosis.

 The annual incidence ranges from 4.6 to 8 cases

per 1000 diabetic patients,
 Statistics from our country.
PATHOGENESIS

Acidosis Water Loss Electrolyte disturbances

DIABETIC KETOACIDOSIS –
PRECIPITATING FACTORS

Approximate frequency
Factor
(%)

Infection 35

Omission of insulin or inadequate insulin 30

Initial presentation of diabetes mellitus 20

Medical illness 10

Unknown 05
SYMPTOMS

A person developing diabetic ketoacidosis may have

one or more of these symptoms:

 Excessive thirst
 Frequent urination
 General weakness
 Vomiting
 Loss of appetite,
 Confusion
 Abdominal Pain
 Rapid breathing
CASE #1
DEFINITION OF DKA

The biochemical criteria for the diagnosis of

DKA are:

 Hyperglycemia (blood glucose ≈200 mg/dL

 Venous pH <7.3 or bicarbonate <15 mmol/L

 Ketonemia and ketonuria.

DEFINITION OF DKA

In setup where investigations are not available

 Clinical features of DKA

 Hyperglycemia,Urine-Sugar/ KBs

 Signs of dehydration

 Tachypnea
SEVERITY OF DKA

The severity of DKA is categorized by the degree

of acidosis:

Grade pH Bicarbonate

Mild pH <7.3 <15 mmol/L

Moderate pH <7.2 <10 mmol/L

Severe pH<7.1 <5 mmol/L

HYPERGLYCEMIC HYPEROSMOLAR
STATE (HHS)
May occur in young patients with T2DM , but
rarely in T1DM subjects.

The criteria for HHS include

 Plasma glucose concentration (600 mg/dL)

 Arterial pH >7.30

 Serum bicarbonate >15 mmol/L

 Small ketonuria, absent to mild ketonemia

 Effective serum osmolality >320 mOsm/kg

 Stupor or coma
MANAGEMENT OF DKA

Cases should ideally be admitted to PICU

General Resuscitation: A, B, C.
 Airway Ensure that the airway is patent

 Breathing Give 100% oxygen by face-mask.

 Circulation Insert IV cannula and take blood

samples
 Cardiac monitor for T waves
MANAGEMENT OF DKA

 Perform a clinical evaluation to confirm the

diagnosis
 Look for trigger factors.

 Record the weight of the child.

 Clinically assess the severity of dehydration.

 Assess level of consciousness. (Attach a GCS)

PHYSICAL EXAMINATION

 Signs of volume depletion

 Kussmaul respiration
 Fruity odor (exhaled acetone)
 Sensorium c or c out neuro deficits
DEGREE OF DEHYDRATION

Degree of Dehydration:
mild, 3% Is only just clinically detectable
moderate, 5% Dry mucous membranes, reduced skin
turgor
severe, 8% Above with sunken eyes, poor
capillary return
+ shock May be severely ill with poor
perfusion, thready rapid pulse
(reduced blood pressure is not likely
and is a very late sign)
BIOCHEMICAL ASSESSMENT

Obtain a blood sample for laboratory

Measurements:

 Glucose, urea, creatinine,

 ABG including electrolytes, S Osmolality

 CBC

 Urine routine and ketone bodies,

Serum ketone bodies
 Various cultures for evidence of infection

 ECG
CLINICAL AND BIOCHEMICAL MONITORING
CLINICAL AND BIOCHEMICAL MONITORING
ADDITIONAL CALCULATIONS THAT MAY BE
INFORMATIVE:

 Anion gap = Na − (Cl + HCO3): normal is 12 ± 2

(mmol/L)
 In DKA the anion gap is typically 20–30 mmol/L; an
anion gap >35 mmol/L suggests concomitant lactic
acidosis (E)
 Corrected sodium = measured Na + 2([plasma glucose
−100/100) (meq/L)
 Effective osmolality = (mOsm/kg) 2x(Na + K) +
glucose/18
GOALS OF THERAPY

 Correct dehydration
 Restore blood glucose to near normal

 Correct acidosis and reverse ketosis

 Identify and treat any precipitating

PRINCIPLES OF WATER AND SALT
REPLACEMENT

In DKA there is significant intracellular &

extracellular water loss to the tune of 5-10 %,
which has to be replaced.

Sodium is lost due to:

 Massive osmotic dieresis

 Vomiting

 Poor intake of food

WHAT IS THE IDEAL FLUID?

 NS
 RL is an alternative.
QUANTITY OF FLUID

 Requirement = Maintenance/day x 2 + Deficit

aministered over 48 hrs

 Deficit (litres) = % dehydration x body weight (kg) X

1000.
 For most children, use 5% to 8% dehydration to
calculate fluids.
MAINTENANCE REQUIREMENTS:

Weight
0-12.9 kg 80 ml/kg/24 hrs
13 – 19.9 kg 65 ml/kg/24 hrs
20 – 34.9 kg 55 ml/kg/24 hrs
35 – 55.9 kg 45 ml/kg/24 hrs

(BSPED Recommended DKA Guidelines 2009)

ISPAD RECOMMENDATION 2009
RATE OF FLOW PER HOUR:

48 hr maintenance + deficit
Hourly rate = --------------------------------------
48

 Urinary losses should not be added.

 Other losses like vomitus can be added.

 After initial resus. Replacement of above fluid equal

hourly over 48 hrs
WHEN TO ADD 5% DEXTROSE

Change to 5% dextrose + 0.45 saline once BG

touches 250 mgs/dl.

Why add 5% dextrose?

Goals of therapy
 Correct dehydration

 Restore blood glucose to near normal

 Correct acidosis and reverse ketosis

 Identify and treat any precipitating

POTASSIUM REPLACEMENT
Total body potassium deficits - 3 to 6 mmol/kg.
Major loss of K+ is from the intracellular pool
Trans cellular shifts of pool.
 Hypertonicity-solvent drag
 Glycogenolysis
 Proteolysis

Potassium is lost
 Osmotic diuresis.
 Vomiting
POTASSIUM REPLACEMENT
Depletion Total body potassium occurs Serum
potassium levels may be

 Normal
 Increased or

 Decreased

Admin. of insulin and the correction of acidosis

Abrupt K+ - cardiac arrhythmias.
POTASSIUM REPLACEMENT

 Replacement Rx regardless of S. potassium

 If S.K+ level not available

Start K+ c insulin drip stop when insulin drip is

stopped
 ECG

 Replacement fluid 40 mmol/L 20

mmol/L
 Potassium replacement should continue throughout IV
fluid therapy .
 Never ever give K+ as a bolus
ECG CHANGES IN HYPOKALEMIA
&HYPERKALEMIA
PHOSPHATE

 Depletion of intracellular phosphate occurs

 Prospective studies no clinical benefit from phosphate

replacement .

 Not available
ACIDOSIS
 Severe acidosis is reversible by fluid and insulin
replacement;

 Insulin stops further ketoacid production

 Treatment of hypovolemia improves renal function

If ABG not available..........

If ABG is available .........
COMPLICATIONS OF NA HCO3
REPLACEMENT

 Hypoglycemia

 Hypokalemia

 Hyperchloremic acidosis
 Cerebral edema
INSULIN THERAPY

 DKA is caused by a decrease in circulating insulin

 Insulin therapy is essential to normalize blood glucose

 Suppress lipolysis and ketogenesis.

‘low dose’ IV insulin administration - ideal

INSULIN THERAPY
 Start insulin infusion 1–2 hours after starting fluid
replacement therapy;
 Dose: 0.1 unit/kg/hour IV

 An IV bolus is unnecessary

 Cont. Insulin drip till acidosis is corrected

 Rarely 10% Dextrose may be necessary

 Aim to keep blood glucose at about 200 mg/dL until

resolution of ketoacidosis.
 2-hourly SC -last resort

 Change to Mixed insulin /Basal –Bolus regimen on 3rd

day
ORAL FLUIDS:

 Day 1
 Day 2

 Day 3
MORBIDITY AND MORTALITY

 The mortality < 1 %

 The commonest cause of mortality is CEREBRAL
OEDEMA .
 There is a high morbidity in survivors

 Mortality in our country

OTHER RARE CAUSES
 Hypokalemia
 Hyperkalemia
 Severe hypophosphatemia
 Hypoglycemia
 Other central nervous system complications (disseminated intravascular
coagulation, dural sinus thrombosis, basilar artery thrombosis)
 Peripheral venous thrombosis
 Sepsis
 Rhinocerebral or pulmonary mucormycosis
 Aspiration pneumonia
 Pulmonary edema
 Adult respiratory distress syndrome (ARDS)
 Pneumothorax, pneumomediastinum and subcutaneous emphysema
 Rhabdomyolysis
 Acute renal failure
 Acute pancreatitis
Classical CASE 8:45 AM

o 10 yrs M child brought to NH with typical features of DKA

o H/O Polyuria, Polydipsia, Weakness, etc., at 8:45 AM

O/E : Child is conscious

Wt - 20 kg RR 44/m Pulse 120/m BP 110/70 Temp - N
 Hydration status –

Dry mucous membranes,

Reduced skin turgor
CRF time 1.5 sec
 H/L : NAD, P/A : soft
Classical CASE 8:45 AM
10 yrs M child brought to Casuality with typical features of
DKA
H/O Polyuria, Polydipsia, Weakness, etc., at 8:45 AM

O/E : Child is conscious

Wt - 20 kg RR 44/m Pulse 120/m BP 110/70 Temp - N
 Hydration status –Mod dehydration

Dry mucous membranes,

Reduced skin turgor
CRF time 1.5 sec
 H/L : NAD, P/A : soft
ADMITTED TO PICU
 Airways
 Breathing : SPO2 98 %
 Circulation : Procure 2 IV line
 Blood sample for investigations for DKA / INFECTION
 X-ray chest PA view
 Glucometer – blood sugar – high ( >500 )
 Urine-sugar – 4+ , ketone bodies +
 ABG – PH : 7.2
PCo2: 30
HCO3:12
Anion gap: 18
S.Na :131
S.K :4.1 mEq

o Attach monitoring charts

9:00 am

 NS
 5% Dextrose + 0.45 NaCl

 5% Dextrose + 0.9 NaCl

 RL

 Isolyte –P
9:00 am

NS
 5% Dextrose + 0.45 NaCl

 5% Dextrose + 0.9 NaCl

 RL

 Isolyte –P
9:00 am
NS

How much
Mod. Dehydration – 5% wt loss ( water loss )
Actual wt 20kg , Expected wt is 30kg.
Rate of flow per hour:
48 hr maintenance + deficit
Hourly rate = -----------------------------------
48
9:00 am
NS

Does he require a rapid push/bolus?

9:00 am
NS

Does he require a rapid push/bolus?

Degree of Dehydration:
mild, 3% Is only just clinically detectable
moderate, 5% Dry mucous membranes, reduced skin
turgor
Above with sunken eyes, poor
severe, 8%  capillary return
May be severely ill with poor
+ shock  perfusion, thready rapid pulse
(reduced blood pressure is not likely
and is a very late sign)
9:00 am

30 kg Child = [(55x30)x2]+1500 = 4800 = 100

48 48

20kg Child = [(55x20)x2]+1000 = 3200 = 67

48 48
9:00 am

30 kg Child = [(55x30)x2]+1500 = 4800 = 100

48 48

20kg Child = [(55x20)x2]+1000 = 3200 = 67

48 48

Start with NS (0.9% NaCl ) 60 ml / hr

9:00 am

Weight
0-12.9 kg 80 ml/kg/24 hrs
13 – 19.9 kg 65 ml/kg/24 hrs
20 – 34.9 kg 55 ml/kg/24 hrs
3035kg Child = [(55x30)x2]+1500
– 55.9 kg
= 4800 = 100
45 ml/kg/24 hrs
48 48

20kg Child = [(55x20)x2]+1000 = 3200 = 67

48 48

Start with NS (0.9% NaCl ) 60 ml / hr

10:00 am 1 hr

 Plain insulin , ACTRARID, RAPITARD 40units / 1ml

 Syringe pump available

1.2 ml+48.8 ml NS =50ml

( 1ml = 1 unit of insulin )
0.1unit /kg = 2 units / hr = 2ml / hr

 Syringe pump not available

2cc to 400ml NS
( 5ml = 1 unit of insulin )
10ml/ hr by burette set.
10:00 am 1 hr

 Blood glucose : 410mg /dl

 EEG in monitor shows relatively flat T wave & appearance of U
waves
Start KCl
 If K+ monitoring not available.
Start KCl with insulin
Replacement :
20-40 mEq / l
5-10 ml KCl/Bottle

o Start with insulin & stop when insulin drip stops

o Replacement equal over 48 hrs
o Never –a bolus
Inj: NaHCO3

Wt. in kg x Base deficit x constant

20 kg x 8 x 0.4
160 x 0.4 = 64 mEq
Inj: NaHCO3

Wt. in kg x Base deficit x constant

20 kg x 8 x 0.4
160 x 0.4 = 64 mEq
Inj: NaHCO3

Wt. in kg x Base deficit x constant

20 kg x 8 x 0.4
160 x 0.4 = 64 mEq


12 noon 3 hrs

 Blood sugar is 350 mg .

 0.9% NaCl ( NS ) has to be continue for the 1st 12 hrs.

3 pm (6 hrs)

 Blood Sugar: 240 mg

 Change to NS+5% Dextrose (0.9 NaCl),

 Continue insulin

 Why add 5% Dextrose in Diabetes?

3 pm (6 hrs)

 Blood Sugar: 240 mg

 Change to NS+5% Dextrose (0.9 NaCl),

 Continue insulin

 Why add 5% Dextrose in Diabetes?

Acidosis not corrected

9:00 pm (12 hrs)
Blood sugar 140
Na : 136
K : 3.6
 0.45 NaCl + 5% Dextrose
 5 ml KCl / bottle
 Insulin – 0.1 units / kg – 2ml / hr
8 ml/ hr
 No NaHCO3
 No K. Phosphates
 Nil by mouth
 Monitoring to continue
 Passed I L of urine in 12 hrs
 Vomited 50 ml in first hr of admission.
 Urine ketone bodies +ve
9:00 am (24 hrs)

 Blood sugar -50 mg

 Ketosis & Acidosis corrected partially but not completed

 Insulin dose
9:00 am (48 hrs)

 Blood Sugar : 98

 ABG : Ph :7.3
HCO3 : 18
Anion gap : 9
Basal bolus insulin
ORAL FLUIDS & DIET

 Day I
 DayII

 DayIII
SUM & SUMMARY
 CASE # 3

 16 yrs M child was admitted to PICU with typical

features of DKA for the 3rd time in 2 yrs .
CASE # 4

 4yrs F child admitted with DKA & fever

Fever in DKA

INFECTION
CASE # 5

 6 yrs M child with typical DKA has a

 TC of 24000

 DC of P 60, L28, E2, M0,

 CRP- 6 mg/l (Normal )

 ESR – 12mm 1st hr

Please comment
CASE # 6

 7 yrs F child admitted to PICU with a GCS of 8/15 has

coarse creps on auscultation.
CASE # 7
 An 8 yr old K/C/O T1DM presented to PICU with typical
features DKA

 Inv. Confirmed the diagnosis

 Was rehydrated with NS at 20 ml/kg bolus followed by 10

ml kg /hr in view of severe dehydration along with iv
Insulin infusion.

 20 cc NaHCO3 given over 10 min.

 The pt transiently recovered, but later developed seizures,

headache followed by altered sensorium.

WHAT could be the CAUSE ?

CEREBRAL EDEMA

o A complication in about 1% of DKA patients, occurs

primarily in children.

o Causes are multifactorial but may include

 Too-rapid infusion of fluids and elctrolytes,
 Overly aggressive correction of acidosis or
 Administration of insulin in the 1st hour of fluid Rx

oTreatment includes intubation, hyperventilation, and

IV mannitol 0.25-1 g/kg or 3% saline.
CASE # 8

 A Pediatrician started ----treating a case of DKA with IV

fluids –NS & Insulin infusion.

 By 12 hrs the child who came walking to the PICU became

floppy, full abdomen & normal consciousness.

What is your diagnosis ?

HYPOKALEMIA

 To prevent hypokalemia start KCl c insulin infusion

CASE # 9

 7 yrs M child with DKA started on correct treatment.

Sugar is not dropping by 12 hrs.

 ABG is not improving.

 What could be the causes ?

 Wrong calculation of insulin infusion.

 Infection some where.