This document provides guidelines for the management of diabetic ketoacidosis (DKA). It defines DKA and classifies its severity. The main goals of treatment are rehydration, electrolyte replacement, and insulin administration to lower blood glucose levels slowly. Treatment involves initial fluid resuscitation followed by intravenous fluids and insulin. Potassium levels must be closely monitored and replaced as needed. Fluids are given over 48 hours and patients transition to subcutaneous insulin before discharge. Complications like cerebral edema are risks that require careful monitoring of fluid, electrolyte and glucose levels during treatment.

1. MANAGEMENT OF
DKA
DR ANKIT KUMAR
PG RESIDENT
DEPT OF PAEDIATRICS
GOVT MEDICAL COLLEGE, HALDWANI

2. DEFINITION AND CLASSIFICATION
• Diabetic Ketoacidosis is defined as –
1) Hyperglycemia (Serum glucose concentration >200mg/dl)
2) Metabolic Acidosis (Blood pH <7.3 with serum bicarbonate level <15 mmol/L)
3) Ketonemia >3mmol/L (or Ketonuria, if blood ketone assays is not readily
available)

3. • Urine ketones are typically ≥2+ (moderate or large) positive.
• Blood beta-hydroxybutyrate(BOHB) concentration level is ≥3 mmol/L

4. • Infrequently adolescents with type 2 diabetes mellitus may present with
Hyperglycemic Hyperosmolar State(HHS) defined as-
1)Blood Sugar >600mg/dl
2)Increased serum osmolality >320mOsm/kg
3)In the absence of significant acidosis or ketonemia/ketonuria.
4)Arterial pH >7.3 ; venous pH>7.25
5)Serum bicarbonate >15 mmol/L
6) Obtundation, combativeness, or seizures

5. CLASSIFICATION OF DIABETIC
KETOACIDOSIS
CATEGORY VENOUS pH Plasma Bicarbonate
(mEq/L)
Clinical
Mild DKA 7.20-7.29 <15 Oriented, alert but fatigued
Moderate DKA 7.10-7.19 <10 Kussmaul respirations;
oriented but sleepy;
arousable
SEVERE DKA <7.10 <5 Kussmaul or depressed
respirations ; sleepy to
depressed sensorium to
coma

6. RISK FACTORS FOR DKA
In Newly Diagnosed Cases In Patients With Known Diabetes
• Younger Age
• Delayed Diagnosis
• Lower Socioeconomic Status
• Countries with low prevalence of type 1
DM
• Insulin omission
• Poor Metabolic Control
• Previous episodes of DKA
• Gastroenteritis with persistent vomiting
• Psychiatric disorders(including eating)
• Challenging social and family
circumstances
• Prepubertal and adolescent girls
• Limited access to medical services
• Failures in insulin pump therapy
• Stressful situations like surgery

7. PATHOPHYSIOLOGY
• Relative or Absolute deficiency of insulin(due to declining insulin production or
peripheral resistance to insulin action, in Type 1 and 2 diabetes respectively)
With or without elevation of counter-regulatory hormones in response to stress of an
infection , trauma or surgery tilts this balance.
Producing a Catabolic state in DKA

8. • Severe insulinopenia (or lack of effective insulin action) result in physiologic cascade of
events in 3 general pathway-
1) Excessive glucose production with reduced glucose utilization
raises serum glucose
produces an osmotic diuresis
with loss of fluid and electrolytes, dehydration
activation of renin-angiotensin-aldosterone axis with accelerated
potassium loss.

9. 2) Increased catabolic process result in cellular losses of sodium,
potassium and phosphate.
3) Increased release of free fatty acids from peripheral fat stores
supplies substrate for hepatic ketoacid production
ketoacids accumulate, buffer systems are depleted and metabolic
acidosis ensues.
Therapy in DKA must address both the initiating event in this cascade (insulinopenia) and
subsequent physiologic disruptions.

11. FEATURES
• Polyuria, Polydipsia
• Weight loss
• Nausea, Vomiting, Abdominal Pain
• Headache
• Restlessness, irritability
• Lethargy, altered sensorium, loss of consciousness
• Fever(indicates infection)
• Recent Surgery, Psychosocial stress
• Concomitant infection
• Eating disorders

12. PAST HISTORY
• Known case of DM
• Recent changes in insulin dosage or regimen
• Poor compliance to insulin therapy
• Past history of DKA
• Inadequate blood sugar control in past
• Insulin discontinuation

13. IMPORTANT CLINICAL FEATURES OF DKA AND THEIR
UNDERLYING MECHANISM

14. MANAGEMENT
Goals of therapy in DKA include-
• Correction of dehydration and acidosis
• Slow correction of Hyperosmolality and restoration of blood glucose to near
normal
• Avoiding complications of therapy, particularly cerebral edema.
• Identification and treatment of the precipitating event
• Prevention of recurrent episodes

15. EMERGENCY ASSESSMENT
• Assess severity of dehydration-signs include-
-Prolong CFT
-Abnormal Skin Turgor
-Dry mucous membrane
-sunken eyes absent tears
-weak pulses, cool extremities
>10% dehydration is assessed by- Presence of weak or impalpable
peripheral pulses

16. • Assess level of consciousness by Glasgow Coma Scale/AVPU
• In unconscious or severely obtunded patient without normal airway protective reflexes,
secure airway
• Give 100% oxygen to patient with circulatory impairment or shock
• A second iv catheter should be placed for convenient and painless repetitive sampling.
• Give antibiotics to febrile patients after obtaining appropriate cultures of blood fluid.

17. INITIAL ASSESSMENT AND RESUSCITATION
• Mild DKA- 5% dehydration
• Moderate DKA- 5% dehydration
• Severe DKA-10% dehydration
• Hypotension or low volume/impalpable pulses and oliguria indicate severe
dehydration(weight loss ≥10%)

18. BIOCHEMICAL ASSESSMENT
Investigations sent are-
• Serum Glucose
• Electrolytes
• Albumin, calcium, phosphate and magnesium concentration
• Venous Blood Gas
• Blood Urea, Creatinine
• Hemoglobin/Hematocrit , TLC, DLC
• Serum Osmolality
• Urine for ketones by dipstick(If blood ketones not routinely measured.)
• If measurement of serum K is unavailable or delayed, a baseline ECG is obtained.

19. • Leukocytosis with leftward shift is common in DKA due to release of cytokines
and catecholamines.
• HbA1C level –
1) help in confirmation of diagnosis of DKA in patients with newly diagnosed
diabetes.
2) Assessment of glycemic control in those with established disease

20. • Serum sodium is unreliable indicator of the degree of extracellular fluid contraction
Because Glucose in the ECF leads to osmotic movement of water
causing dilutional hyponatremia

21. CALCULATION OF CORRECTED SODIUM, ANION GAP AND
OSMOLALITY
• Corrected Sodium-Measured [Na⁺]+ [Glucose(mg/dl)-5.6]/3.5
• Anion Gap=Na⁺ -(Cl⁻ + HCO3⁻)
• Effective osmolality=2[Na⁺]+[Glucose(mg/dl)]

22. 1) FLUID REPLACEMENT
• Fluid Replacement should always begin before starting insulin therapy
A. Calculation of Fluid Deficit
Mild to Moderate DKA- 50 ml/kg deficit
Severe DKA- 100ml/kg

23. B. Fluid Bolus
If Patient presents in shock, 10ml/kg of 0.9% saline or RL
administered over 15 mins.
(If Patient presents in shock, 10ml/kg of 0.9% saline or RL
administered over 30 mins.)
Repeat bolus of 10 ml/kg (upto 40ml/kg)NS
administer inotropes to restore
circulatory volume

24. C. Subsequent fluid management
• 0.9% NS or Ringer lactate used in the initial 4-6 h of management.
• Subsequent fluid replacement consists of 0.45%-0.9% NaCl
• 5%(D5) Dextrose concentration for RBS below 300mg/dl
• 10% (D10) for RBS below 200mg/dl
• If RBS falls below 100mg/dl despite D10 containing iv fluids, insulin rate can then be
decreased from 0.1 units/kg/hr

25. D. MONITORING
• Overzealous fluid resuscitation, indicated by rapid change in corrected sodium (>1-2
meq/L/hr) and effective osmolality, is associated with development of cerebral edema.
• Persistent decrease in serum glucose of >100 mg/dl/hr may increase risk of cerebral
edema
Therefore careful monitoring of serum glucose and adjustment of dextrose concentration
of iv fluids is essential

26. E. RATE OF FLUID ADMINISTRATION
• Total fluid deficit should be corrected over 48hrs at infusion rate not exceeding 1.5-2
times the daily maintenance requirement.
• Resuscitation fluid – fluid boluses given for resuscitation in children with shock
should NOT be subtracted from the estimated fluid deficit.
• The initial bolus given to all non-shocked patients requiring IV fluids SHOULD be
subtracted from total calculated fluid deficit

27. • A 20 kg 6 year old boy who has a pH of 7.15 (Moderate DKA => 5% Dehydrated) will
receive a 10ml/kg bolus (200mls fluid) over 30 minutes as part of his initial management.
His ongoing fluids will comprise:
Deficit 5 % x 20 kg = 1000 ml
Subtract initial bolus 1000-200 bolus = 800ml to be replaced over 48 hours
=17 ml/hr
Maintenance 10 x 100 = 1000 ml per day for 1st 10 kg
10 x 50 = 500ml per day for next 10 kg (weighs 20kg)
=1500 ml per day total (over 24 hours)
= 62 ml/hour
Total fluid = 17ml/hour (Deficit of 5 % (minus bolus) over 48 hours)
+ 62 ml/hr (Maintenance fluids)
= 79 ml/hour

28. • If RBS> 300 mg/dl - N/2
• RBS 200-300mg/dl - N/2 D5
• RBS 100-200 mg/dl - N/2 D10
• RBS <100 mg/dl - D12.5

29. 2) INSULIN THERAPY
• Insulin therapy is essential to reverse metabolic derangements like lipolysis and
ketogenesis, and to normalise blood glucose.
• Repair of hyperglycemia occurs before correction of acidosis
Therefore, insulin therapy is still needed to control fatty acid release and ketosis after
normal glucose levels are reached.
• Timing- Therapy with insulin is started after the initial volume expansion i.e. 1-2 h after
fluid replacement.

30. • Type- Only IV regular insulin is used for treatment of DKA.
• Dose- Low dose IV insulin therapy at 0.05-0.1unit per kg per hr is the standard of care
with dose titrated to achieve a decrease in serum glucose concentration of 3-4
mmol/L(50-75mg/dl) per hour
Higher doses are associated with increased risk of hypokalemia,
hypoglycemia and too rapid a decline in serum osmolality.
• Preparation- 1ml regular insulin-40 units
Add 1ml insulin in 39ml NS to make 1unit/ml solution
• Priming of tubing- performed by flushing insulin solution through the tubing prior to
infusing the patient, because insulin binds to glass bottles, plastic iv bags, syringes and
tubings.

31. • Duration of Therapy- Dose of insulin should usually remain at 0.05-0.1 unit/kg/hr at least
until resolution of DKA.
• Dose adjustment-Following start of insulin therapy, blood glucose is expected to fall at
the rate of 36-90 mg/dl/h.
• Blood glucose normalisation occurs before resolution of ketoacidosis
Concentration of dextrose in replacement fluid should be increased as required to maintain
glucose between 150-200mg/dl.
If hypoglycaemia occurs despite increase of strength of dextrose solution up to 12.5%(15%
dextrose if central line is placed), dose of insulin may be reduced in decrements of 0.01-
0.02units/kg/hr up to 0.03-0.05 units/kg/hr

32. • Insulin resistance is suspected if rate of fall of blood glucose is <70mg/dl/h or acidosis is
not improving even though blood glucose is falling.

33. 3) Potassium Replacement
Patients with DKA have a total body potassium deficit, the initial serum level is often normal or elevated.
Because of movement of K+ from intracellular space to serum as part of ketoacid buffering process and
as part of catabolic shift
These effects are reversed with therapy and potassium returns to cell.
Also improved hydration increases renal blood flow, allowing for increased excretion of potassium in the
elevated aldosterone state.

34. The net effect is often a dramatic decline in potassium levels, especially in Severe DKA.
This precipitates changes in cardiac conductivity:
• Flattening of T wave
• Prolongation of QRS Complex
Can cause skeletal muscle weakness or ileus
1) Potassium should be added to iv fluids once serum potassium declines below
5.5mEq/L.
2) K⁺ is added to fluid at the rate of 40 mEq/L once child has voided and normal serum
level documented.

35. • During administration of potassium, adequate UO is ensured and potassium and ECG are
monitored to avoid both hyperkalemia and hypokalemia.
• The maximum recommended rate of intravenous potassium replacement is 0.5 mEq/kg/h
(or 80mEq/L intravenous fluid)
• Recheck K⁺ every 1-2h if values are outside normal range.

36. 4)CORRECTION OF METABOLIC ACIDOSIS AND
BICARBONATE THERAPY
• Acidosis in DKA responds to insulin and fluid therapy.
• Bicarbonate administration is considered in children with:
- cardiac dysfunction secondary to profound acidosis(pH<6.9)
-Life threatening Hyperkalemia
• Given at 1-2meq/kg over 60min diluted in 0.45% saline.

38. MONITORING
Clinical signs to be monitored every hour initially
GENERAL SIGNS NEUROLOGIC SIGNS
Heart Rate
Respiratory Rate
Blood Pressure
Hydration tatus
Fluid Intake
Urine Output
Sensorium(GCS)
Restlessness or irritability
Headache
Recurrence of vomiting
Increased drowsiness
Incontinence
Cranial Nerve Examination(for new
onset palsies,Abnormal pupillary
response)

39. TRANSITION TO SUBCUTANEOUS INSULIN THERAPY
• Oral fluids introduced when:
- clinical improvement occurs
-metabolic acidosis corrected
-Patient indicates a desire to eat
• When oral fluid is tolerated, iv fluid reduced accordingly so that sum does not exceed the
calculated iv rate.

40. TIMING TO SWITCH TO SUBCUTANEOUS ROUTE
• The ideal time to begin administration of subcutaneous insulin is just before meal.
• To avoid rebound hyperglycemia, rapid acting insulins(Lispro and aspart) are administered
subcutaneously 15-30 min prior and regular insulin 1-2h prior, to stopping insulin
infusion.
• For example, for patients on basal bolus insulin regimen, the first dose of basal insulin
may be administered in the evening and insulin infusion is stopped the next morning.

41. STARTING DOSE OF SUBCUTANEOUS INSULIN(UNITS/KG/DAY)
NO DIABETIC DIABETIC KETOACIDOSIS
Prepubertal 0.25-0.5 0.75-1.0
Pubertal 0.5-0.75 1.0-1.2
Postpubertal 0.25-0.5 0.8-1.0

42. PREVENTION OF COMPLICATIONS OF THERAPY
Complications of Therapy
Hypoglycemia
Hypokalemia
Hyperchloremic Acidosis
Infections eg-Mucormycosis
Renal Failure
Cerebral Edema
Rhabdomyolysis
Arrythmia
Pulmonary Edema

43. CEREBRAL EDEMA
• Risk Factors for Cerebral Edema in patients with DKA
Intrinsic or Disease related risk factors
Age<5yr
New Onset Diabetes
Long duration of DKA symptoms before presenting to health facility
Severe acidosis or severe hypocapnia after adjusting for degree of acidosis
Treatment related risk factors
Use of bicarbonate
Rapid decline in serum osmolality
Attenuated rise in sodium during therapy
Higher volumes of fluid infused in first 4h
Early administration of insulin within the 1st hour of treatment

44. MANAGEMENT OF CEREBRAL EDEMA
1. The head end of bed is elevated
2. The fluid administration rate is reduced to1/2
3. The airway is secured, if warranted by deterioration in sensorium, the patient should be
intubated and mechanically ventilated
4. During ventilation, aggressive hyperventilation(PCO2<22mmHg) is avoided
5. Intravenous 3% saline is given as 5-10 ml/kg over 30 min, alternatively mannitol is
administered at 5mI/kg over 20 mins.
6. The dose is repeated if no response is perceived within 30 min to 2 hr
7. Following institution of therapy, a cranial CT is ordered to rule out other treatable
causes of neurological deterioration like thrombosi or hemorrhage.

45. CASE HISTORY
• An 11-year old female child, known case of Type 1 Diabetes Mellitus diagnosed at
7 years of age and taking regular insulin since then presented with complaints of
15- 20 episodes of vomiting for 2 days, pain abdomen and altered consciousness
since 4 hours.
• History of skipping morning dose of insulin
• On examination the patient was in altered sensorium GCS 11, sunken eyes with
vitals
HR=138/minute, RR=28/ minute, BP= 132/72 mm Hg.

46. INVESTIGATIONS
• RBS= 373mg/dl, s. calcium= 1.44 mmol/l
pH = 7.085 s. sodium= 140 mmol/l
pO2=138.7 mm Hg s. potassium =5.0 mmol/l
pCO2 =21.45 mm Hg
HCO3= 6.49
WBC = 30,620/ mm3
Hb = 12.2 mg/dl

47. THANK YOU