Dka, Cerebral Edema, Hhs

DIABETIC KETOACIDOSIS AND
NONKETOTIC
HYPERGLYCEMIA
GUIDE: PRESENTER:
Dr.Gayathri H Aradhya Dr.M.Narasinga Raj
Associate Professor 3rd yr Postgraduate
Dept of Pediatrics Dept of Pediatrics
JJMMC JJMMC
Overview:
• Introduction
• Definition
• Classification based on severity
• Frequency
• Risk factors
• Physiology
• Pathophysiology
• Clinical manifestations
• Investigations
• Management
• Complications
INTRODUCTION:
• Diabetic ketoacidosis (DKA) is the most severe acute complication of diabetes
mellitus.
• State of metabolic decompensation that results from
Severe Insulinopenia.
Excessive Production Of Catabolic Hormones.
Sepsis And Trauma.
• Seen in DM type 1 > DM type 2, MODY.
• Common presentation of Children with DM type 1.
• Early identification- reduction in morbidity and mortality.
Sperling Pediatric Endocrinology 5th Edition 2020 by Mark A. Sperling

DEFINITION:
Diabetic
Keto
Acidosis
Ketonemia (blood
Hyperglycemia Venous pH <7.3
ß hydroxybutyrate
(blood glucose or serum
≥3 mmol/L) or
>11 mmol/L bicarbonate <15
moderate or large
[≈200 mg/dL]) mmol/L
ketonuria

Classification of DKA:
• Venous pH - 7.2 to 7.29 OR
MILD • Serum HCO3 – 10 to 15 mmol/L
• Venous pH - 7.1 to 7.19 OR

MODERATE • Serum HCO3 – 5 to 10 mmol/L
• Venous pH – under 7.1 OR

SEVERE • Serum HCO3 – < 5
SEVERITY OF DKA DEPENDS ON DEGREE OF ACIDOSIS

Acc. to NELSON TEXTBOOK:
NORMAL MILD MODERATE SEVERE
CO2 (mEq /L 30-35 16-20 10-15 <10
venous)
pH(venous) 7.35 to 7.45 7.25-7.35 7.15-7.25 <7.15
Clinical features No Change Oriented ,alert but Kussmaul Kussmaul or

fatigued respirations, depressed
oriented but respirations;
sleepy; arousable. Sleepy to
depressed
sensorium to
coma.
Nelson Textbook of Pediatrics. Edition 21. Philadelphia, PA: Elsevier, 2020.

ISPAE Classification of DKA:
ISPAE clinical practice guidelines 2011

Frequency of DKA:
1. At Disease Onset:
There is wide geographic variation in the frequency of DKA at onset of
diabetes.
About 20-40% of children with new onset diabetes present in DKA.
Frequencies range from approximately 15% to 70% in Europe and North
America.
Approximately 30 to 50% of all children have DKA even in developed
countries.
DKA at diagnosis is more common in younger children (especially <2 years
of age), including infants with both transient and permanent neonatal diabetes
(overall frequency 66%), often the consequence of diagnostic error or
delayed treatment.
1.Sperling Pediatric Endocrinology 5th Edition 2020 by Mark A. Sperling
2.Nelson Textbook of Pediatrics. Edition 21. Philadelphia, PA: Elsevier, 2020
3.ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidosis and the hyperglycemic hyperosmolar state
ICMR – YDR INDIA
Executive Summary: ICMR- YDR Registry (Phase-1) Report:
The most common mode of presentation among patients with T1DM:

1.combination of osmotic symptoms and weight loss (28.8%).
2.DKA, one of the common modes of presentations of T1DM, was reported
by 25.2% of the patients.
3.Other common presentations for these patients were osmotic symptoms
alone (27.1%) and history of isolated weight loss (22.6 %).
Registry of Youth Onset Diabetes inIndia (YDR): Rationale, Recruitment, andCurrent Status Pradeep A.
Praveen, MPH1, Sri Venkata Madhu.
2.In children with ESTABLISHED DIABETES:
WORLDWIDE:
• The risk of DKA in established type 1 diabetes is 1% to 10% per patient per
year.
In INDIA (acc. to ICMR-YDR PHASE -1 Report):

• 56.1% of the registered patients had at least one episode of hospitalization due to
acute medical conditions related to diabetes.
• The most common reason behind hospitalization among the YDR patients was
1. Diabetic ketoacidosis /uncontrolled hyperglycemia (31.8 %)

2.Hypoglycaemia (11.0% of the YDR patients).
BCHI STATISTICS:
In last two years,
• Number of patients presented to BCHI PICU with DKA- 42 Cases
• Frequency- 3.9%
• Initial presentation – seen in 28 cases(66.6%)
• DKA in Established - 14 cases(33.3%)
Grades OF DKA FREQUENCY PERCENTAGE
MILD 3 7.1
MODERATE 12 28.6
SEVERE 27 64.3
TOTAL 42 100
Risk factors in newly diagnosed cases:
YOUNGER AGE
GROUPS(Age< 2 yrs) Delayed diagnosis
Residence in a country
Lower socio-economic
with low prevalence of
status
T1DM

Risk factors in established cases:
Children
Poor Previous episodes
who
metabolic of DKA
omits
control
insulin
Increased Insulin Sepsis Psychiatrc

Requirement and disorders
trauma
Poor Children with

Physically food limited access to
inactive control medical services

PHYSIOLOGY:
• Normal insulin secretion in response to feeding is modulated by the interplay of
neural, hormonal, and substarte related mechanisms, which permit controlled
disposition of ingested foodstuff as energy for immediate or future use in
metabolism and growth.
• Mobilization of energy during fasted state depends on low plasma levels of
insulin.
• There are regular swings between the post prandial high insulin anabolic state and
the fasted low-insulin catabolic state that affect three major tissues: Liver, Muscle
And Adipose tissue.

PHYSIOLOGY OF CARBOHYDRATE METABOLISM:
Carbohydrates, Proteins and Lipid
METABOLISM
REGULATORY COUNTER
HORMONE: REGULATORY
HORMONES:
Insulin
Glucagon
Growth Hormone
ANABOLIC Catecholamines
Cortisol
CATABOLIC
Nelson Textbook of Pediatrics. Edition 21. Philadelphia, PA: Elsevier, 2020.
Contd….
INSULIN • Glucose used for energy substrate or stored as

glycogen
(Anabolic) • Protein formation
• Fats stored as triglycerides
Counter
regulatory • Glycogenolysis.
hormones • Proteolysis-gluconeogenesis.
• Lypolysis-FFA & ketone bodies.
(catabolic)
Nelson Textbook of Pediatrics. Edition 21. Philadelphia, PA: Elsevier, 2020

Contd..
GLYCOGENOLYSIS Glycogen Glucose
Proteins
GLUCONEOGENESIS (Amino Glucose
acids)
Fats(Free Glucose and

KETOGENESIS
Fatty acids) Ketoacids
Nelson Textbook of Pediatrics. Edition 21. Philadelphia, PA: Elsevier, 2020

What happens in T1 DM?
• T1DM, as it evolves becomes a permanent low insulin catabolic (starvation) state
in which feeding cannot reverse but rather exaggerates catabolic process.
• Consequently, with progressive failure of insulin secretion,
1.Initially postprandial hyperglycemia- initial manifestation,
2.Fasting hyperglycemia is a late manifestation that reflects severe insulin
deficiency and indicates excessive endogenous glucose production.
Although insulin deficiency is the primary defect, several secondary changes that
involves the stress hormones accelerate and exaggerate the rate and magnitude of
metabolic decompensation.

Consequences of Insulinopenia..
Increased glucose
Osmotic
production and HYPERGLYCEMIA
decreased utilization diuresis
Activation of the renin–

Fluid and angiotensin–aldosterone axis
DEHYDRATION
electrolytes loss with accelerated potassium loss.
If glucose elevation and dehydration are

severe and persist for several hours, the risk
of HYPOVOLEMIC SHOCK increases

CONSEQUENCES OF INSULINOPENIA…..
Increased release of Substrate for

FFA from peripheral hepatic ketoacid
Ketoacids Depletion of METABOLIC
accumulation buffer systems ACIDOSIS
fat production
Increased KETOTIC
catabolic LOSS OF COMA
processes SODIUM,
result in POTASSIUM
cellular PHOSPHATE
losses

Pathophysiology in DKA:
Losses of fluid and electrolytes in diabetic ketoacidosis and maintenance requirements in normal children:
Average (range) 24 hour maintenance requirements

losses per kg
Water 70 ml (30-100) ≤10 kg 100 mL/kg/24 h
11-20 kg 1000 mL + 50 mL/kg/24 h for
each kg from 11 to 20
>20 kg 1500 mL + 20 mL/kg/24 h for
each kg >20
Sodium 6 mmol (5-13) 2-4 mmol
Potassium 5 mmol (3-6) 2-3 mmol
Chloride 4 mmol (3-9) 2-3 mmol
Phosphate 0.5-2.5 mmol 2-3 mmol
• Maintenance electrolyte requirements in children are per 100 mL of maintenance IV fluid.

Clinical manifestations:
Any child without known diabetes whose h/o -
1. Dehydration
2. Nausea, vomiting, and abdominal pain that may mimic an acute abdominal condition.
3. Hurried breathing; deep, sighing(kussmaul) respiration.
4. Confusion, drowsiness, progressive obtundation and loss of consciousness.
“SUSPECT DKA”
ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidosis and the hyperglycemic hyperosmolar state
Contd…
Suspect DKA even if the blood glucose is normal in a child with known diabetes
and with any of following:
• Fever(on going Infection)

• Nausea Or Vomiting
• Abdominal Pain
• Hyperventilation
• Dehydration
• Reduced Level Of Consciousness
• Seizures, coma.
Signs on Examination..
• Fruity odour in breath (ketosis)
• Sunken eyes
• Absence of tears
• Dry lips
• Impaired skin turgor Indicate dehydration or
• Tachycardia hypovolemia
• Low volume pulses
• Hypotension
• Delayed capillary refill time
• Weight loss (if premorbid weight known)
• Rapid deep sighing breathing, Kussmaul respiration (metabolic acidosis)
INVESTIGATIONS:
IMMEDIATE INVESTIGATIONS:
When a child or young person with suspected DKA arrives at
hospital, immediately measure their
• Capillary blood glucose levels using glucometer.

• Capillary blood ketones (beta-hydroxybutyrate) if near-
patient testing is available, or urine ketones if it is not
available.
• VBG- Venous pH and bicarbonate.
ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidosis and the hyperglycemic
hyperosmolar state
ESSENTIAL INVESTIGATIONS
* Plasma glucose
* HbA1c
IF REQUIRED
* Serum electrolytes(incld Obtain appropriate
serum bicarbonate levels) specimens for culture
NON-URGENT
* Blood urea nitrogen (blood, urine, throat) &
CXR only if there is * TSH/FT4
*Creatinine * Coeliac screen (TTG
evidence of infection
* serum osmolality IgA) and total IgA
(eg, fever)
* venous pH, pCO2 * Islet Autoantibodies (anti
* Hb, HCT,CBC, CRP GAD-65/ IA2/ICA/ZnT8)
* Albumin, calcium,
phosphate, magnesium (if
possible)
*Urinalysis
*Corrected sodium levels
*ECG
Where should the child with DKA be managed?
The child should receive care in a unit that has:
• A specialist/consultant pediatrician with training and expertise in the management
of DKA should direct inpatient management.
• Experienced nursing staff trained in monitoring and management of DKA in
children and adolescents.
• Written guidelines or, if unavailable, access to online guidelines for DKA
management in children.
• Access to a laboratory that can provide frequent and timely measurements of
biochemical variables.
• Transport teams should be knowledgeable about DKA management and should
have rescue medications available during the transport, including IV solutions and
mannitol or 3% hypertonic saline
MANAGEMENT:
GOALS OF THERAPY:
Correct Dehydration
Correct Acidosis and reverse Ketosis(by gvng INSULIN)
Correct Restore blood glucose to near normal
Monitor for complications of DKA and its treatment
Identify and treat any precipitating event
1ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidosis and the hyperglycemic hyperosmolar state.
2.BSPED guidelines for the management of children and young people under the age of 18 yrs with DKA.
1.Emergency Management:
A- AIRWAY:
Ensure that the airway is patent.
In unconscious/ severely obtunded patient, secure the airway and empty the stomach by continuous
nasogastric suction to prevent pulmonary aspiration.
Intubation should be avoided if possible.
B- BREATHING:
Give oxygen to patients with circulatory impairment or shock.
C- CIRCULATION:
Insert IV cannula and take blood samples and send for investigations.
Cardiac monitor for T waves (peaked in hyperkalemia).
Measure blood pressure and heart rate.
1.BSPED guidelines for the management of children and young people under the age of 18 yrs with DKA
2. ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidosis and the hyperglycemic hyperosmolar state
Initial fluid bolus (RESUSICATION FLUIDS)…
Volume depleted but NOT IN SHOCK:- should receive a 10 ml/kg of 0.9% sodium
chloride bolus over 60 minutes.
DKA IN SHOCK:- 20 mL/kg bolus of 0.9% sodium chloride over 15-30
mins/infused as quickly as possible.
Reassess and further boluses of 10 ml/kg may be given if required to restore adequate
circulation up to a total of 40 ml/kg at which stage inotropes should be considered.
Whilst excessive fluid should be avoided because of the risk of cerebral oedema, it is
important to ensure that the circulation is adequate and fluid should be given to
support this.
 Cerebral perfusion is dependent on both Mean Arterial Pressure and intracranial
pressure and hypotension will exacerbate the risk of brain injury.
Use crystalloids not colloids(ISPAD).
BSPED guidelines for the management of children and young people under the age of 18 yrs with DKA – Updated jan 2020 .
D-Assess severity of Dehydration:-
Estimation of the degree of dehydration is imprecise and generally shows only fair to
moderate agreement among examiners, and should be based on a combination of physical
signs.
5% 7% 10%
Dehydration Dehydration dehydration
• Prolonged CRT • Dry mucous • Presence of
• Abnormal skin membranes weak or
turgor • Sunken eyes impalpable
• Absent tears pulses
• Weal pulses • Hypotension
• Cold extremities • oliguria
BSPED comments on assessment of Dehydration:
• It is not possible to accurately clinically assess the degree of dehydration to
work out the deficit.
• Clinical methods are unreliable.
• Estimation of the fluid dehydration should be based on the initial blood pH.
Assume 5 % DEHYDRATION MILD DKA (Blood pH 7.2-7.29)
Assume 7% DEHYDRATION MODERATE DKA (blood pH of 7.1- 7.19)
Assume 10% DEHYDRATION SEVERE DKA (blood pH <7.1)
E- A second peripheral IV cathEtEr should be placed for convenient and painless repetitive
blood sampling.
 An arterial catheter may rarely, be necessary in some critically ill patients managed in an
intensive care unit.
 Unless absolutely necessary, avoid placing a central venous catheter because of the high risk
of thrombosis, especially in the very young child.
 If a central catheter has been inserted, the catheter should be removed as soon as the patient's
clinical status permits.
Insulin should preferably not be given through a central line unless it is the only
available option because its infusion may be interrupted when other fluids are given
through the same line.
2. BSPED guidelines for the management of children and young people under the age of 18 yrs with DKA – Updated jan 2020
F- Full Clinical Assessment:
• Assess and record in the notes.
1.CONSCIOUS LEVEL:-
 Institute hourly neurological observations including Glasgow Coma Score.
 conscious level is directly related to degree of acidosis, but signs of raised intracranial pressure
suggest cerebral edema.
2. FULL EXAMINATION:- looking particularly for evidence of
 Cerebral Oedema:- headache, irritability, slowing pulse, rising blood pressure, reducing
conscious level.(papilloedema is a late sign)
 Infection
 Ileus (which is common in DKA)
3. WEIGH THE CHILD:- If this is not possible because of the clinical condition, use the most
recent clinic weight as a guideline, or an estimated weight from centile charts.
F- Febrile:
DKA may be precipitated by sepsis or intercurrent infection, and fever is not part.
Infection may co-exist with DKA.
Suspect sepsis if there is fever or hypothermia, hypotension, refractory acidosis or
lactic acidosis.
A high lactate should increase concern about possible infection or sepsis.
Give antibiotics to febrile patients after obtaining appropriate cultures of body fluids.
G- Bladder catheterization usually is not necessary, but if the child is unconscious or

unable to void on demand (eg:infants and very ill young children) the bladder should
be catheterized.
FLUID THERAPY:
The objectives of fluid and electrolyte replacement therapy are to:
Restore circulating volume.
Replace sodium and the extracellular and intracellular water deficits.
Improve glomerular filtration and enhance clearance of glucose and
ketones from the blood.
BSPED guidelines for the management of children and young people under the age of 18 yrs with DKA – Updated jan 2020
1.Volume of fluids:
• By this stage, the circulating volume should have been restored.
• Once circulating blood volume has been restored and the child
adequately resuscitated,
• calculate fluid as follows:
REQUIREMENT = DEFICIT + MAINTENANCE
Note: It is essential that all fluids given are documented carefully, particularly the fluid which
is given in the accident and emergency department and on the way to the ward, as this is where
most mistakes occur.
(i). Fluid Deficit:
• It is not possible to accurately clinically assess the degree of dehydration to
work out the deficit.
• Clinical methods are unreliable.
• Estimation of the fluid dehydration should be based on the initial blood pH.
Assume 5 % DEFICIT MILD DKA (Blood pH 7.2-7.29)
Assume 7% DEFICIT MODERATE DKA (blood pH of 7.1- 7.19)
Assume 10% DEFICIT SEVERE DKA (blood pH <7.1)
THE FLUID DEFICIT SHOULD BE REPLACED OVER 48 HOURS

ALONGSIDE MAINTENANCE FLUIDS
Important points to be remembered:
Dehydration and fluid deficit calculation:
Dehydration Fluid Deficit
1% 10ml/kg
5% 50ml/kg
7% 70ml/kg
10% 100ml/kg
Resuscitation fluids in Fluid deficit: –

• The volume of any fluid boluses given for resuscitation in children with shock should
NOT be subtracted from the estimated fluid deficit.
• The initial 10ml/kg bolus given to all non-shocked patients requiring IV fluids
SHOULD be subtracted from total calculated fluid deficit.
BSPED guidelines for the management of children and young people under the age of 18 yrs with DKA – Updated jan 2020.
(ii).Maintenance fluids:
• should be calculated using the Holliday – Segar formula.
BODY WEIGHT(KGS) MAINTENANCE BODY WEIGHT(KGS) MAINTENANCE
FLUIDS FLUIDS
1-10 Kgs 100ml/kg/day 1-10 Kgs 4ml/kg/hr
11-20 kgs 50ml/kg/day 11-20 kgs 2ml/kg/hr
For every 1kg above 20 20ml/kg/day > 20 kgs 60ml + 1ml/kg/hr for
kgs of body weight every>20kgs
Neonatal DKA Will Require Special Consideration And Larger Volumes Of Fluid Than
Those Quoted May Be Required, Usually 100-150 ml/Kg/24 Hours
(iii). Fluid calculations:
• Calculate the fluid deficit (either 5%, 7% or 10% dehydration depending on
whether the patient has mild, moderate or severe DKA), subtract the initial
10ml/kg bolus then divide this over 48 hours and add to the hourly rate of
maintenance fluid volume , giving the total volume evenly over the next 48 hours.
i.e.
Hourly rate = ({Deficit – initial bolus} / 48hr) + Maintenance per hour
Example-1:
• A 25 kg 6 year old boy who has a pH of 7.15 (Moderate DKA => 7% Dehydrated)
will receive a 10ml/kg bolus (250mls fluid) over 60 minutes as part of his initial
management. His ongoing fluids will comprise:
Deficit 7% x 25 kgs = 1750 ml
Substract initial bolus 1750 – 250 = 1500 ml to be replaced over 48 hrs

= 31.9ml/hr.
Maintenance fluid = 10 x 100= 1000 ml per day for 1st 10 kgs
10 x 50 = 500 ml per day for next 10kgs
5 x 20 = 100 ml per day for next 5 kgs (weighs 25 kgs)
= 1600 ml per day total (over 24 hrs)
=66.6 ml/ hour
Total fluid = 31.9 ml /hr – 7% deficit

+ 66.6 ml/hr – mainatenance fluids
= 98.5 ml/hr
Example -2:
• A 60 kg 15 year old girl with a pH of 6.9 who was shocked at presentation has
received 30ml/kg of 0.9% Saline for resuscitation. These boluses are not
subtracted from ongoing maintenance fluids. Her ongoing fluids will comprise:
Deficit 10 % x 60 kg = 6000 ml to be replaced over 48 hours
= 125 ml/hr
Maintenance = 10 x 100 = 1000 ml per day for 1st 10 kg

10 x 50 = 500ml per day for next 10 kg (10-20kg)
40 x 20 = 800ml per day for next 40kg
= 2300 ml per day total (over 24 hours)
= 96 ml/hour
Total fluid = 125 ml/hour - Deficit of 10 % over 48 hours

+ 96 ml/hr – Maintenance fluids
= 221 ml/hour
2.Type of fluids:
• Use 0.9% sodium chloride with 20 mmol potassium
chloride in 500 ml (40 mmol per litre) until blood glucose
levels are less than 14 mmol/l (250mg/dl).
• PlasmaLyte 148 has been suggested as an alternative as it
has a lower chloride content and hyperchloraemic
acidosis is therefore less likely.
• Additional potassium will need to be added to
PlasmaLyte 148 as it only contains 5mmol/l Potassium.
ISPAD FLUID THERAPY:
1.RESUSCITATION FLUIDS- same as BSPED regimen.
2.FLUID THERAPY-
• Subsequent fluid management can be accomplished with 0.45% to 0.9% saline or
a balanced salt solution (Ringer's lactate, Hartmann's solution or Plasmalyte).
• Deficit replacement should be with a solution that has a tonicity in the range
0.45% to 0.9% saline, with added potassium chloride, potassium phosphate or
potassium acetate.
• Decisions regarding use of isotonic vs hypotonic solution for deficit replacement
should depend on clinician judgment based on the patient's hydration status,
serum sodium concentration and osmolality.
3.Oral fluids:-
• Do not give oral fluids to a child or young person
1.Who is receiving intravenous fluids for DKA until ketosis is resolving and
2.No nausea of vomiting.
3.Significant electrolyte shifts are no longer likely.
• Water in sips may be given as a minimal oral intake.
• Time required to rehydrate depends on severity of DKA
• Oral fluids that may have been given in another facility before assessment should
be factored into calculations of deficit and replacement volumes.
1.BSPED guidelines for the management of children and young people under the age of 18 yrs with DKA – Updated jan 2020
4.Fluid losses.. whether to replace or not?
• Do not give additional intravenous fluid to replace urinary losses.
• Urinary catheterization should be avoided but may be useful in the child
with impaired consciousness.
• If a massive diuresis continues for several hours, fluid input may need to be
increased; this should be isotonic to the urine.
• If large volumes of gastric aspirate continue, these will need to be replaced
with same amount of 0.45% saline with Potassium Chloride.
ISPAE Fluid Infusion Guidelines:
INSULIN THERAPY:
• Blood glucose will fall after initial fluid therapy alone by improvement of renal
perfusion and enhancing excretion.
• Insulin therapy is essential to
1.Restore normal cellular metabolism
2.To suppress lipolysis and ketogenesis, and
3.To normalize blood glucose concentrations.
• An IV bolus should not be used at the start of therapy !!!
Start an Intravenous insulin infusion 1-2 hours after beginning intravenous fluid
therapy.
Use a REGULAR INSULIN infusion at a dosage between 0.05 and 0.1
units/kg/hour.
Contd….
• Your local policy may have a particular preference for the dose, but there is no
evidence that one dose is superior to the other.
• An infusion rate of 0.05 Units/kg/hr is likely to be sufficient in most cases, and
may have a lower incidence of subsequent hypoglycemia.
• In severe DKA an infusion rate of 0.1 Units/kg/hr may be needed.
• The recommendation of the BSPED working group was that a starting dose of
0.05 Units/kg/hr should be used unless severe DKA or in adolescents.
Type of DKA INSULIN DOSE
MILD , Moderate DKA 0.05units/kg/hr.
Severe DKA 0.1units/kg/hr.
How to prepare insulin infusion?
• Use pre-filled syringes containing 50 Units of soluble insulin in 50 ml 0.9%

sodium chloride where available.
• If pre-filled syringes are not available, add 50 units of Regular insulin to
49.5ml of 0.9% sodium chloride.
• Prime the IV tubing by flushing the insulin infusion solution.
• Better to start infusion in separate iv cannula.
Contd..
• Maintain insulin infusion at 0.05 to 0.1 unit/kg/h atleast until resolution of DKA (pH
>7.30, serum bicarbonate >15 mmol/L, BOHB <1 mmol/L, or closure of the anion
gap).
• If the insulin effect is adequate
1.Serum BOHB should decrease by approximately 0.5 mmol/L/h.
2.Expect a Blood Glucose decrease at a rate of 40 to 90mg/dL/hr(2-5 mmol/L/H).
If the blood glucose rises out of control, or the pH level is not improving after 4-6
hours consult senior medical staff and re-evaluate (possible sepsis, insulin dosage
errors, blocked or leaking lines, excessive urine loss, fluid calculation error or other
conditions), and consider starting the whole protocol again.
If the blood ketone level is not falling within 6–8 hours then get senior help and advice
and consider increasing the insulin dosage to 0.1 units/kg/hour or greater.
BSPED guidelines for the management of children and young people under the age of 18 yrs with DKA – Updated jan
2020
When blood glucose levels starts to fall..
• Change the fluid to contain 5% glucose.
• Reduce insulin infusion rate to 0.05 units/kg/hr from 0.1 Units/kg/hour.
<14mmol/L
• if a higher dose of insulin necessary -10% glucose rather than 5% glucose
(250mg/dL)
• Increase the glucose concentration to 10%.

• If there is persisting ketosis, continue to give insulin at a dosage of least 0.05
<6mmol/L
units/kg/hour.
(110mg/dL)
• Give a bolus of 2 ml/kg of 10% glucose and increase the glucose

concentration of the infusion to 12.5%.
<4mmol/L
• Insulin can temporarily be reduced for 1 hour.
(72mg/dL)
Other insulin managements:
1. For children and young people on continuous subcutaneous insulin infusion (CSII)
pump therapy, stop the pump when starting intravenous insulin.
2. For children who are already on long-acting insulin, you may wish to continue this at
the usual dose and time throughout the DKA treatment, in addition to the IV insulin
infusion, in order to shorten length of stay after recovery from DKA.
3. In circumstances where continuous IV administration is not possible and in patients
with uncomplicated DKA, hourly or 2-hourly SC rapid-acting insulin analog (insulin
lispro or insulin aspart) is safe and may be as effective as IV regular insulin infusion.
but, ideally, should not be used in patients whose peripheral circulation is impaired.
4. Subcutaneous administration of short-acting insulin (regular) every 4 hours is also a
safe and effective alternative to IV insulin infusion in children with pH ≥7.0.
Examples:
Q) A 25 kg 6 year old boy who has a pH of 7.15 will receive a 10ml/kg bolus
(250mls fluid) over 60 minutes as part of his initial management. Fluid therapy has
been started. Now, How much insulin should we start?
A) Moderate DKA = 0.05Units/kg/hr
so Insulin infusion = 0.05 x 25 = 1.25 units/hr = 1.25ml/hr of insulin through
infusion pump after PRIMING.
Q) A 60 kg 15 year old girl with a pH of 6.9 who was shocked at presentation has
received 30ml/kg of 0.9% Saline for resuscitation. Fluid therapy has been started.
Now, How much insulin should we start?
A) SEVERE DKA = 0.1Units/kg/hr
so Insulin infusion = 0.1 x 60 = 6 units/hr = 6ml/hr of insulin through infusion
pump after PRIMING.
ELECTROLYTE DISTURBANCES:
DKA Impact
Na Loss K Loss PO4 Def

(5-13 mmol/kg) (4-6 mmol/kg) (0.5 – 2.5 mmol/kg)
1.Sodium :
Initial serum sodium may be ‘low’ for several reasons:
1.Depletion secondary to urinary loses and vomiting.
2.Hyperlipidemia displaces sodium in most frequently used laboratory assay-

factitiously lowering sodium values - pseudohyponatremia.
3.Hyperglycemia High serum osmolarilty Water driven from

Intra to Extracellular space Dilutional hyponatremia
Contd..
• Each 100 mg/dl elevation of blood sugar above 100mg/dl lowers sodium by 1.6 mEq/dl.
• when glucose begins to fall (hydration and insulin) Plasma glucose concentration is
reduced Water leaves the ECS entering ICS Raising the extracellular
sodium concentration again Serum sodium typically rises.
• Corrected sodium levels represent the expected serum sodium concentration in the
absence of hyperglycemia.
• Corrected sodium levels should typically rise as blood glucose levels fall during
treatment.
• It has been suggested that Corrected Sodium levels give an indication of the risk of
cerebral oedema with a falling corrected sodium indicating an excess of free water and an
increased risk of cerebral oedema.
Corrected sodium (mmol/L) = measured sodium + (glucose – 5.6)
3.5
2.Potassium:
• Children with DKA suffer total body potassium deficits on the order of 3 to 6mmol/kg.
• The major loss of potassium is from the intracellular pool
 Transcellular shifts : hypertonicity, acidosis, glycogenolysis and proteolysis secondary to
insulin deficiency
 Vomiting
 Secondary Hyperaldosteronism promotes urinary potassium excretion.
• Total body depletion of potassium occurs; however, at presentation serum potassium levels
may be normal, increased, or decreased.
• Administration of insulin and the correction of acidosis further decreases serum potassium
levels.
• Replacement therapy is required regardless of the serum potassium concentration, except if
renal failure is present.
2. 2.ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidosis and the hyperglycemic hyperosmolar state
HYPOKALEMIA NORMOKALEMIA HYPERKALEMIA
(<2.5mmol/L) (3-6 mmol/L) (>6mmol/L)
• Needs vigorous • The starting potassium • DEFER potassium

replacement with concentration in the replacement therapy,
• 1.K Upto 80mmol/L infusate should be 40 until urine output is
• 2.Oral K supplementation mmol/L. noted.(to rule out AKI
• 3.REDUCE insulin • Subsequent potassium sec to Dehydration).
infusion rate. replacement therapy
• (or) delaying the start of should be based on serum
insulin till potassium> 2.5 potassium measurements.
mmol/L to avoid • Potassium replacement
cardiopulmonary should continue
/neuromuscular throughout IV fluid
compromise. therapy.
.2.ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidosis and the hyperglycemic hyperosmolar state
ECG Changes:
HYPOKALEMIA:
 Flattening T wave,
 Widening of the QT interval, and
Appearance of U waves
HYPERKALEMIA:
 Tall, peaked symmetrical, T waves and
 shortening of QT intervals
3.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,
which promotes entry of phosphate into cells.
• Decreased intracellular ATP levels impair cellular functions that depend on energy
rich phosphate compounds, and a decrease in 2,3-diphosphoglycerate (DPG) levels
increases the afﬁnity of hemoglobin for oxygen and reduces oxygen release in tissues.
• Many organ systems can be affected.
• Only severe symptomatic hypophosphatemia may be treated with potassium
phosphate in combination with potassium chloride, with careful monitoring of serum
calcium.
4.ACID BASE Management:
• Severe acidosis is reversible by fluid and insulin.
• BICARBONATE ADMINISTRATION IS NOT RECOMMENDED, except if-
pH< 6.9 with severe hemodynamic compromise.
Severe hyperkalemia (K+>6.5mEq/L with ECG changes).
• Usually avoided as there is higher risk for cerebral edema, hypokalemia.
• If bicarbonate is considered necessary, cautiously give 1–2 mmol/kg over 60 minutes.
• Anion gap to be calculated to monitor ketonemia and to check for hyperchloremia that
occurs due to prolonged administration of 0.9%NS and KCl. Continue insulin till AG
is normalized.
Anion gap = Sodium – (Chloride + Bicarbonate)
Clinical and Biochemical Monitoring
Every hour
Every 2 hours
• GCS • Blood urea, BOHB
• Serum electrolytes
• Neurological • Blood Glucose
• Lab glucose • ABG
• Saturation
Examination • Vitals
• Osmolality • Anion Gap
• Calcium, magnesium
• Fluid input and output
• Phosphate
• Corrected Na+
chart
Every 30 • Insulin administration. • Hematocrit • Urine dipstick
mins Every 2 hours
Can be switched to every 4

hours after stabilization
Monitoring chart in DKA:
Transition to subcutaneous injection:
When ketoacidosis has resolved and oral intake is tolerated, change to SC insulin
is planned, a dose of basal (long- or intermediate-acting) insulin should be
administered in addition to rapid- or short-acting insulin.
The most convenient time to change to SC insulin is just before a mealtime.
To prevent rebound hyperglycemia the first SC injection should be given 15 to 30
minutes (with rapid-acting insulin) or 1 to 2 hours (with regular insulin) before
stopping the insulin infusion to allow sufficient time for the insulin to be
absorbed.
Subcutaneous insulin should be started according to local protocols for the child
with newly diagnosed diabetes, or the child should be started back onto their usual
insulin regimen at an appropriate time.
1.BSPED guidelines for the management of children and young people under the age of 18 yrs with DKA – Updated jan
2020
Complications of DKA:
• The mortality rate from DKA in children is 0.15% to 0.30%
• Cerebral injury is the major cause of mortality and morbidity
• Cerebral edema accounts for 60% to 90% of all DKA deaths
• Other rare causes include
Hypoglycaemia
Dyselectrolytemias
Severe hypophosphatemia
Central nervous system complications eg. dural sinus thrombosis, ICH, Infarcts.
Aspiration pneumonia
Sepsis/ Septic shock
Rhabdomyolysis
acute kidney injury including renal failure
acute pancreatitis.
CEREBRAL EDEMA:
• Occurs in less than 1% of Pediatric DKA episodes
• Accounts for 60% to 90% of all DKA deaths
• 10% to 25% of survivors have permanent neurological injury
• The cause of cerebral edema is controversial.
• Some have explained the pathogenesis as the result of rapid fluid administration
with abrupt changes in serum osmolality.
• More recent investigations, however, have found that dehydration and cerebral
hypoperfusion may be associated with DKA-related cerebral injury.
• Degree of cerebral edema that develops during DKA correlates with the degree of
dehydration and hyperventilation at presentation, but not with initial osmolality.
Risk factors:
DEMOGRAPHIC FACTORS POTENTIAL FACTORS
• Younger age. • Greater hypocapnia at presentation
• New onset diabetes. • Increased serum urea nitrogen at
presentation.
• Longer duration of symptoms. • More severe acidosis at presentation
• Bicarbonate treatment for correction of
acidosis
• A marked early decrease in serum effective
osmolality
• An attenuated rise in serum sodium
concentration or an early fall in glucose-
corrected sodium during therapy
• Greater volumes of fluid given in the first
4hours
• Administration of insulin in the first hour
of fluid treatment
Clinical features:
• Onset of headache after beginning treatment or progressively worsening
headache.
• Change in neurological status (irritability, confusion, inability to arouse,
incontinence).
• Specific neurological signs (eg, cranial nerve palsies, papilledema).
• Cushing's triad (rising blood pressure, bradycardia, and respiratory depression) is
a late but important sign of increased intracranial pressure.
• Decreased O2 saturation.
ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidosis and the
hyperglycemic hyperosmolar state
DIAGNOSTIC MAJOR MINOR
Abnormal motor or verbal response to Altered mentation, confusion, Vomiting
pain fluctuating level of consciousness
Decorticate or decerebrate posture Sustained heart rate deceleration Headache

(decrease more than 20 beats
per minute) not attributable to
improved intravascular volume or
sleep state
Abnormal neurogenic respiratory Age-inappropriate incontinence Lethargy or not easily arousable
pattern (e.g. grunting, tachypnea,
Cheyne–Stokes respiration)
Cranial nerve palsy (especially III, IV, Diastolic blood pressure >90 mm Hg
and VI)
Age <5 years
 One diagnostic criterion, two major criteria, or one major and two minor criteria have a sensitivity of 92% and a false
positive rate of only 4%.
 Signs that occur before treatment should not be considered in the diagnosis of cerebral edema
 Neuroimaging is not required for diagnosis of cerebral edema.
ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidosis and
the hyperglycemic hyperosmolar state
Treatment:
• The head end of the bed should be elevated.
• The fluid administration rate should be reduced by 1/3
• The air way is secured; if warranted by deterioration in sensorium, the patient
should be intubated and mechanically ventilated.
• During ventilation, aggressive hyperventilation (PCO2 < 22 mm Hg) should be
avoided
• Intravenous mannitol is administered at 0.5–1 g/kg over 20 min; alternatively 3%
saline is given as 2.5–5ml/kg over 20 min
• The dose is repeated if no response is perceived within 30 min to 2 h.
• Following institution of therapy, a cranial CT is ordered to rule out other treatable
causes.

2.HYPERGLYCEMIC HYPEROSMOLAR STATE
DKA HHS
Diabetes type Type – 1 Type-2
Ketosis prone type-2
Age Younger age group Older age group(often >60yrs)
Primary defect Absolute Insulin deficiency Insulin Resistance and
Relative insulin deficiency
Insulin sensitivity Normal Reduced

Serum insulin levels Very low Variable
Incidence At presentation- 30-40% At presentation- 2%
Established- 1-10% per patients/yr Established- 20-30%
Onset Rapid(hours to days) Gradual onset(weeks)

Characterised by 1.Hyperglycemia(>200mg/dL) 1.Hyperglycemia(>600 mg/dL)
2.Ketosis(BOHB> 3mmol/L) 2.Serum osmolaltity(>320mOsm/kg)
3.Acidosis(pH-<7.3) 3.Arterial pH> 7.3, venous pH>7.25
4.Bicarb> 15mEq/L
5.Small or absent to low ketonuria
6.Obtundation, seizures(50%)
Presenting complaints Polyuria, Polydipsia, Weight loss, acute abdomen, Severe dehydration with focal or global
Dehydration, Hurried breathing, altered neurological deficits.
consciousness.
DKA HHS
Precipitated by insulin omission, increased insulin requirements, Infections

Infections, psychological illness
Dehydration Moderate to severe Severe to Profound
Electrolyte disturbances Hypokalemia, hyponatremia, hypophosphatemia, HYPERNATREMIA, Hypokalemia,

hypocalcemia hypophosphatemia, Hypomagnesemia
Anion gap Elevated(20-30) Usually Normal
Mortality Rate 1% 40-60%
Cerebral Edema common Very rare
Treatment IV FLUIDS and IV INSULIN and Potassium IV FLUIDS and IV INSULIN

supplementation.
Resolution Anion gap normalized, Normal sugar levels, Alert, serum osmolality< 315mOsm/kg
Ketosis resolved, clinical improvement
Discharge plan Subcuatneous Insulin Sub cutaneous Insulin

PREVENTION:
• Monitor blood sugar level
• Adjust insulin dose
• Check ketone level
• Do not skip insulin doses even during illness
• Hydrate adequately
• Follow meal plan and exercise programme
• Maintain a diary
• Seek emergency care

TAKE HOME MESSAGE-
• Successful management and early intervention for complication requires close
monitoring.
• Fluid infusion should precede insulin administration
• Potassium should be replaced early and sufficiently
• Bicarbonate administration is neither necessary nor safe.
• In case of cerebral edema intervene rapidly with mannitol or hypertonic saline

infusion.
• Prevention of DKA with intensive family education esp sick day management.

Dka, Cerebral Edema, Hhs

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DIABETIC KETOACIDOSIS AND

Sperling Pediatric Endocrinology 5th Edition 2020 by Mark A. Sperling

Sperling Pediatric Endocrinology 5th Edition 2020 by Mark A. Sperling

• Venous pH - 7.1 to 7.19 OR

• Venous pH – under 7.1 OR

SEVERITY OF DKA DEPENDS ON DEGREE OF ACIDOSIS

pH(venous) 7.35 to 7.45 7.25-7.35 7.15-7.25 <7.15

Clinical features No Change Oriented ,alert but Kussmaul Kussmaul or

Nelson Textbook of Pediatrics. Edition 21. Philadelphia, PA: Elsevier, 2020.

ISPAE clinical practice guidelines 2011

The most common mode of presentation among patients with T1DM:

In INDIA (acc. to ICMR-YDR PHASE -1 Report):

1. Diabetic ketoacidosis /uncontrolled hyperglycemia (31.8 %)

Sperling Pediatric Endocrinology 5th Edition 2020 by Mark A. Sperling

Increased Insulin Sepsis Psychiatrc

Poor Children with

Sperling Pediatric Endocrinology 5th Edition 2020 by Mark A. Sperling

Sperling Pediatric Endocrinology 5th Edition 2020 by Mark A. Sperling

INSULIN • Glucose used for energy substrate or stored as

Nelson Textbook of Pediatrics. Edition 21. Philadelphia, PA: Elsevier, 2020

GLYCOGENOLYSIS Glycogen Glucose

Fats(Free Glucose and

Nelson Textbook of Pediatrics. Edition 21. Philadelphia, PA: Elsevier, 2020

Sperling Pediatric Endocrinology 5th Edition 2020 by Mark A. Sperling

Activation of the renin–

If glucose elevation and dehydration are

Sperling Pediatric Endocrinology 5th Edition 2020 by Mark A. Sperling

Increased release of Substrate for

Sperling Pediatric Endocrinology 5th Edition 2020 by Mark A. Sperling

Average (range) 24 hour maintenance requirements

• Maintenance electrolyte requirements in children are per 100 mL of maintenance IV fluid.

Sperling Pediatric Endocrinology 5th Edition 2020 by Mark A. Sperling

• Fever(on going Infection)

• Capillary blood glucose levels using glucometer.

Assume 5 % DEHYDRATION MILD DKA (Blood pH 7.2-7.29)

Assume 7% DEHYDRATION MODERATE DKA (blood pH of 7.1- 7.19)

Assume 10% DEHYDRATION SEVERE DKA (blood pH <7.1)

G- Bladder catheterization usually is not necessary, but if the child is unconscious or

REQUIREMENT = DEFICIT + MAINTENANCE

Assume 7% DEFICIT MODERATE DKA (blood pH of 7.1- 7.19)

Assume 10% DEFICIT SEVERE DKA (blood pH <7.1)

THE FLUID DEFICIT SHOULD BE REPLACED OVER 48 HOURS

Resuscitation fluids in Fluid deficit: –

1-10 Kgs 100ml/kg/day 1-10 Kgs 4ml/kg/hr

11-20 kgs 50ml/kg/day 11-20 kgs 2ml/kg/hr

Hourly rate = ({Deficit – initial bolus} / 48hr) + Maintenance per hour

Substract initial bolus 1750 – 250 = 1500 ml to be replaced over 48 hrs

Total fluid = 31.9 ml /hr – 7% deficit

Maintenance = 10 x 100 = 1000 ml per day for 1st 10 kg

Total fluid = 125 ml/hour - Deficit of 10 % over 48 hours

MILD , Moderate DKA 0.05units/kg/hr.

Severe DKA 0.1units/kg/hr.

• Use pre-filled syringes containing 50 Units of soluble insulin in 50 ml 0.9%

• Increase the glucose concentration to 10%.

• Give a bolus of 2 ml/kg of 10% glucose and increase the glucose

Na Loss K Loss PO4 Def

1.Depletion secondary to urinary loses and vomiting.

2.Hyperlipidemia displaces sodium in most frequently used laboratory assay-

3.Hyperglycemia High serum osmolarilty Water driven from

• Needs vigorous • The starting potassium • DEFER potassium

Can be switched to every 4

Decorticate or decerebrate posture Sustained heart rate deceleration Headache

Age <5 years