This document summarizes diabetic ketoacidosis (DKA), including its diagnosis, pathophysiology, clinical manifestations, treatment goals, and management. DKA is characterized by severe dehydration and electrolyte depletion due to insulin deficiency and increased counterregulatory hormones. Its treatment involves intravenous fluid resuscitation and insulin therapy to correct dehydration, acidosis, and ketosis. Careful monitoring is required to watch for complications like cerebral edema. Recent studies have found subcutaneous insulin and lower-dose intravenous insulin to be effective alternatives to standard intravenous insulin therapy for mild-moderate DKA.

1. DIABETIC KETOACIDOSIS
DR.R.SHELLY
POST GRADUATE

2. DIAGNOSIS
• Acidosis - Venous pH <7.3
OR
• Sr bicarbonate <15mmol/L
AND
• Ketonemia ( blood Beta HB >3mmol/L)
• Blood glucose levels are generally high (above 11
mmol/l)
but children and young people with known diabetes
may develop DKA with normal blood glucose levels

3. • International Society for Paediatric and Adolescent
Diabetes (ISPAD) 2018
• British society of Paediaric Endocrinology &
Diabetes(BSPAD ) 2020
• DKA occurs from deficient circulating insulin
• increased counter regulatory hormones: catecholamines,
glucagon, cortisol, growth hormones.
• Failed insulin pump
• Stress like Sepsis, trauma, febrile illness
• gastroenteritis

4. PATHOPHYSIOLOGY OF DKA
• Accelerated catabolic state with increased glucose
production by liver and kidney- glycogenolysis,
gluconeogenesis
• Impaired peripheral glucose utilisation –
hyperglycemia, hyperosmolality
• Increased lipolysis, and ketogenesis- ketonemia &
met.acidosis
• Hyperglycemia+hyperketonemia cause osmotic
diuresis, dehydration & loss of electrolytes
• DKA is characterized by severe depletion of water
and electrolytes from both the intra- and
extracellular fluid (ECF) compartments
• Lactic acidosis from sepsis – further acidosis

6. CLINICAL MANIFESTATION
• Dehydration, tachycardia, tachypnea,
• deep sighing respiration, breath smells of
acetone
• Nausea vomiting abdominal pain _ mimic
acute abdomen
• blurry vision,Confusion, drowsiness, LOC,coma

7. • CBG
• BOHB conc-for diagnosis and monitoring of
the treatment of DKA.
• urinary ketone levels-for diagnosis, not for
monitoring
• Urinary ketones of more than ketones++ on
standard dipsticks are typically equivalent to
near patient blood ketones of >3.0 mmol/l.
Urinary ketones must be read 15 seconds
after stick is dipped
DIAGNOSIS

8. Goals of therapy
• to correct dehydration, correct acidosis
• reverse ketosis, gradually restore
hyperosmolality
• blood glucose concentration to near normal,
• monitor for complications of DKA
• its treatment, and identify and treat any
precipitating event.

9. severity of DKA
• Mild DKA - pH 7.2- 7.29 or bicarbonate < 15
mmol/l.
Assume 5% dehydration
• Moderate DKA - venous pH 7.1-7.19 or
bicarbonate < 10 mmol/l.
Assume 7% dehydration
• Severe DKA - venous pH less than 7.1 or serum
bicarbonate < 5 mmol/l.
Assume 10% dehydration

10. With or without shock?
• with shock-defined as the APLS definition of
tachycardia, prolonged CRT,poor peripheral
pulses
• hypotension (though this is a late sign of
shock). It is not just poor peripheral perfusion.

11. EMERGENCY MANAGEMENT IN A & E
• GCS
• SECURE AIRWAY
• GASTRIC LAVAGE if any consumption of
sweetened beverages
• O2
• CARDIAC MONITORING
• PERIPHERAL IV CATHETER
• ANTIBIOTICS
• BLADDER CATHETHERIZATION

12. Initial fluid bolus
• NO SHOCK- 10 ml/kg 0.9% sodium chloride bolus over 60
minutes
• defined as the APLS definition of tachycardia, prolonged
CRT,poor peripheral pulses
• hypotension (though this is a late sign of shock). It is not
just poor peripheral perfusion.
• SHOCK- 20 ml/kg bolus of 0.9% saline over 15 minutes
• reassessed and further boluses of 10 ml/kg UPTO
40ml/kg-then inotropes
• w/f signs of cerebral edema

13. Initial Investigations
• Blood glucose
• Urea and electrolytes
• Blood gases (venous or capillary)
• Ketones - Near patient blood ketones (beta-
hydroxybutyrate) testing should be used.
• If able to obtain sufficient blood, send new
diagnosis investigations as well (HbA1c, TFT,
Coeliac screen)

14. only if indicated
• CXR, throat swab, blood cultures, urinalysis,
culture and sensitivity etc. (A raised white blood
cell count is common in DKA and does not
necessarily indicate sepsis).
• Suspect sepsis if there is fever or hypothermia,
hypotension, refractory acidosis or lactic
acidosis.

15. FULL CLINICAL ASSESSMENT:
Conscious Level
• hourly neurological observations with GCS
• If reduced conscious level on admission,
• urgent anaesthetic review->discuss with a
paediatric critical care specialist->senior
pediatrician
• conscious level is directly related to degree of
acidosis
• signs of raised intracranial pressure suggest
cerebral oedema

16. Full Examination
• cerebral oedema headache, irritability,
slowing pulse, rising blood pressure, reducing
conscious level ,desaturation
• papilloedema is a late sign.
• infection
• ileus (which is common in DKA)

17. Management
• all fluids given are documented
• Requirement = Deficit + Maintenance
• Fluid Deficit - based on the initial blood pH
• Deficit replaced over 48 hours alongside
maintenance fluids

18. • Assume a 5% fluid deficit in children and young
people in mild DKA (indicated by a blood pH
7.2-7.29 &/or bicarbonate <15)
• Assume a 7% fluid deficit in children and young
people in moderate DKA (indicated by a blood
pH of 7.1- 7.19 &/or bicarbonate <10)
• Assume a 10% fluid deficit in children and
young people in severe DKA (indicated by a
blood pH <5)

19. Resuscitation fluid
• fluid boluses given in children with shock
should NOT be subtracted from the estimated
fluid deficit
• initial 10ml/kg bolus given to all non-shocked
patients requiring IV fluids SHOULD be
subtracted from total calculated fluid deficit

20. Maintenance fluid
• Holliday ± Segar formula
• 100 ml/kg/day for the first 10 kg of body weight
x
• 50 ml/kg/day for the next 10 to 20 kg x
• 20 ml/kg/day for each additional kilogram
above 20 kg
• Neonatal DKA -larger volumes of fluid than
those quoted may be required, usually 100-150
ml/kg/24 hours

21. Weight for Fluid Calculation
• Wherever possible the patients actual weight
on admission
• To avoid excessive amounts of fluid in
overweight and obese children it is
recommended that consideration be given to
using a maximum weight of 80kg or 97th
centile weight for age (whichever is lower)

22. POTTASIUM REPLACEMENT
• every 500 ml bag of fluid contains 20 mmol potassium
chloride (40 mmol per litre)
• Potassium is only added to Intravenous fluids after the
patient has passed urine
• or after the Potassium has fallen to within the upper limit
of the normal range
• Potassium phosphate 20 mEq/L/ Kcl 20 mEq/L / potassium
acetate 20 mEq/L given as a combination
• Maximum recommended rate of iv K+ is 0.5 mEq/kg/h
If hypokalemia persists, rate of insulin infusion can
be reduced

23. INSULIN THERAPY
• start an intravenous insulin infusion 1-2 hours
after beginning intravenous fluid therapy
• add 50 units of soluble insulin (e.g. Actrapid) to
49.5ml 0.9% sodium chloride [1unit=1ml]
• LOW DOSE IV INSULIN – 0.05 to 0.1 units/kg/h
• 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.
• Iv bolus is not suggested and an iv infusion is
preferred

24. Other insulin management
• on continuous subcutaneous insulin infusion
(CSII) pump therapy- stop the pump when
starting intravenous insulin.
• children who are already on long-acting
insulin- to continue this at the usual dose and
time throughout the DKA treatment

25. MONITORING & ASSESSMENT
• strict fluid balance including oral fluids and
urine output
• CBG hourly
• Sr electrolytes every 2nd hrly
• Blood BOHB every 2nd hrly
• hourly level of consciousness
• half-hourly neurological observations-
children <2yr &pH < 7.1
• Measure body weight twice daily
• w/f signs of cerebral edema, hypokalemia

26. • ANION GAP CALC: in DKA, 20-30 mmol/l in a
patient with ketoacidosis. anion gap >35 mmol/l
may suggest concomitant lactic acidosis due to
sepsis or poor perfusion
• Corrected sodium = measured Na + 2 ( [plasma
glucose-100] /100) mg/dl . Hypernatremic – no
problem(protecive against cerebral edema).
Hyponatraemia occurs in DKA
• adjusting the total fluid rate using corrected
Sodium (Nacorr)
• This represents expected serum sodium
concentraion in the absence of hyperglycemia

27. Hyperchloraemic metabolic acidosis
• following the administration of large amounts of
chloride containing fluids
• preferential renal excretion of ketones instead of
chloride - result in hyperchloraemia
• acidifying effect of chloride can mask the resolution
of ketoacidosis so measuring blood BOHB is ideal
• Acidosis due to hyperchloraemia will correct
spontaneously and doesn’t require any treament
• Chloride induced base deficit = plasma Na – plasma
Cl
• Normally it will be 30-35mmol/L

28. BICARBONATE
• Do not give
• consider bicarbonate if - life threatening
hyperkalaemia ,
• severe acidosis with impaired myocardial
contractility.

29. HYPOPHOSPHATEMIA
• Depletion of intracellular phosphate – bcz of
osmotic diuresis – exacerbated by insulin therapy
• Decrease in 2-3 diphosphoglycerate level which
increases affinity of hemoglobin for oxygen &
reduced o2 release in tissues
• Metabolic encephalopathy: irritability, paresthesia,
confusion, seizure, coma
• Impaired myocardial contractility, RS failure,
proximal myopathy, dysphagia, ileus, decreased
phagocytosis, granulocyte chemotaxis, defective
clot retraction

30. FLUID AND SALT CORRECTION

31. CONTINUING MANAGEMENT
• 0.9% NS containing 20 mmol KCl in 500ml until
blood glucose levels have fallen to 14 mmol/l
• blood glucose rises out of control, or the pH
level is not improving after 4-6 hours-re-
evaluate &consider starting whole protocol
again
• blood ketone level is not falling within 6±8
hours consider increasing the insulin dosage to
0.1 units/kg/hour or greater

32. • Once the blood glucose has fallen to 14 mmol/l add glucose to
the fluid
• Change the fluid to contain 5% glucose; use 500 ml bags of
0.9% NS with 5% glucose and 20 mmol KCl in 500ml
• Reduce insulin infusion rate to 0.05 units/kg/hr from 0.1
Units/kg/hour
• Once ketones are < 1.0 mmol/l, consider switching from IV to
s.c insulin
• Do not change from intravenous insulin to subcutaneous
insulin until ketosis is resolving (for example, blood beta-
hydroxybutyrate level below 1.0 mmol/litre) and the child or
young person with DKA is alert and is tolerating fluids without
nausea or vomiting

33. S.C INSULIN IN DKA
• Initial dose of 0.3 unit/kg followed by 0.1
unit/kg every one hr or 0.2 unit/kg every 2 to
3 hrs.
• Regular insulin starting dose 0.8 to 1 unit per
kg per 24hrs. The calculated 24 hr dose is
divided by 6 to provide an insulin dose
injected every 4 hrs

34. CEREBRAL EDEMA
• PATHOGENESIS: Rapid fluid administration with
abrupt changes in serum osmolality
• RISK FACTORS: greater hypocapnia after adjusting
degree of acidosis
• Increased serum urea nitrogen
• More severe acidosis at presentation
• Bicarbonate treatment for acidosis correction
• Early decrease in serum effective osmolality
• Attenuated rise in serum Na conc or an early fall
in glucose corrected Na during therapy
• Greater volume of fluid in first 4 hrs
• Insulin before fluid therapy

35. • DIAGNOSTIC CRITERIA: abnormal motor or verbal resp to
pain
• Decorticate or decerbrate posture
• Cranial nerve palsy (3rd ,4th, 6th)
• Cheyne stoke respiration
• MAJOR CRITERIA: ALOC, fluctuating LOC
• Sustained HR decelration (decrease more than 20 bpm)
• MINOR CRITERIA: vomiting
• Headache
• Lethargy
• Diastolic bp >90 mmHg
• Age <5yrs

36. TREATMENT OF CEREBRAL EDEMA
• One diagnostic criterion, two major criteria or
one major and two minor criteria
• Mannitol 0.5 to 1 g/kg iv over 10-15 mins
• Hypertonic saline 2.5 to 5ml/kg over 10-
15mins
• Reduce iv fluids rate
• intubation and controlled ventilation
• Elevate head end by 45 dgree

38. HYPERGLYCEMIA HYPEROSMOLAR
STATE
• k/a hyperosmolar nonketotic coma – type2DM
• Plasma glucose concentration (600mg/dl)
• Arterial pH >7.3 ; venous pH >7.25
• Sr bicarb >15mmol/L
• Small ketonuria, absent ketonemia
• Obtundation, combativeness, seizures

39. TREATMENT OF HHS
• Appropriate fluid therapy that decrease sr glu 75-
100mg/dl per hr if effective in restoring renal
perfusion
• Insulin initiated <50mg/dl sr glu.. At cont infusion
0.025 to 0.05 units/kg/h and titrated later
• Potassium at 40mmol/L infusion started after
insulin infusion.
• Hypomagnesemia 25 to 50mg/kg per dose for 3-4
doses every 4-6hrs.

41. Recent studies
1. Comparison of subcutaneous insulin aspart
and intravenous regular insulin for the
treatment of mild and moderate diabetic
ketoacidosis in pediatric patients.
• CONCLUSIONS: To manage mild/moderate diabetic-
ketoacidosis in children/adolescents, subcutaneous rapid-
acting insulin aspart is an alternative to intravenous infusion
of regular insulin. Subcutaneous insulin treated moderate DKA
with faster recovery/shorter hospital stay

42. 2. 0.9% saline versus Plasma-Lyte as initial fluid
in children with diabetic ketoacidosis (SPinK
trial): a double-blind randomized controlled
trial.
• CONCLUSIONS: The incidence of new or progressive AKI and
resolution of AKI were similar in both groups. Plasma-Lyte-A
was similar to 0.9% Saline in time to resolution of DKA, need
for RRT, mortality, and lengths of PICU and hospital stay.

43. 3. Low-Dose (0.05 Unit/kg/hour) vs Standard-
Dose (0.1 Unit/kg/hour) Insulin in the
Management of Pediatric Diabetic Ketoacidosis:
A Randomized Double-Blind Controlled Trial.
• CONCLUSIONS: Time for resolution of ketoacidosis was similar
in the low-dose and standard-dose insulin with a lower rate of
therapy-related complications in the low-dose group. Hence,
low-dose insulin infusion can be a safer approach in the
management of pediatric DKA.

44. Thank you