This document provides guidance on the diagnosis, treatment, and management of type 1 diabetes mellitus. It discusses diagnostic criteria including A1C levels and oral glucose tolerance tests. The goals of treatment are outlined as maintaining tight glucose control while avoiding hypoglycemia. Insulin therapy is described as the primary treatment involving multiple daily injections or continuous infusion. Target blood glucose ranges and total daily insulin doses are provided for different age groups. Guidance is also given on managing diabetic ketoacidosis, including precipitating factors, treatment approach involving fluid resuscitation and insulin therapy, and electrolyte monitoring and replacement.

1. Dr. Surabhi Yadav (DCH,DNB)

2.  Diagnosis
 Treatment of type 1 DM
 Diabetic ketoacidosis

3. 1) A1C >6.5%.
 A1C % plasma glucose level
 6 126 (7.0)
 7 154 (8.6)
 8 183 (10.2)
 9 212 (11.8)
 10 240 (13.4)
 11 269 (14.9)
 12 298 (16.5)
OR

4.  OR FPG >126 mg/dL (7.0 mmol/L)
 OR 2-h plasma glucose>200mg/dL
(11.1mmol/L) during an OGTT.
 OR In a patient with classic symptoms of
hyperglycemia or hyperglycemic crisis,a
random plasma glucose >200 mg/dL(11.1
mmol/L).

5.  C Peptide levels
 Serum B12 and red cell folate
 Urea and electrolytes
 Liver function tests
 Bone profile
 Fasting or random glucose
 9am or random cortisol
 Thyroid stimulating hormone, free thyroxine
 Thyroid auto-antibody screen
 Coeliac auto-antibody screen
 ECG
 Fasting lipids
 Fructosamine levels

6. To maintain a balance b/w tight glucose
control and avoiding hypoglycemia
To eliminate polyuria and nocturia
To prevent diabetic ketoacidosis
To permit normal growth and development
with minimal effect on lifestyle

7.  INSULIN THERAPY
 BASIC AND ADVANCED DIABETES EDUCATION
 NUTRIONAL MANAGEMENT
 MANAGEMENT OF DIABETIC KETOACIDOSIS

8.  Most people with type 1 diabetes should
be treated with MDI injections (three
to four injections per day of basal and
prandial insulin) or continuous subcutaneous
insulin infusion.
 Most people with type 1 diabetes
should be educated in how to match
prandial insulin dose to carbohydrate
intake, premeal blood glucose, and
anticipated activity.

9. AGE
(YRS)
TARGET
GLUCOSE
(mg/dl)
TOTAL DAILY
INSULIN
(U/kg/day)
BASAL
INSULIN,% OF
TOTAL DAILY
DOSE
BOLUS INSULIN
,UNITS ADDED
per 100mg/dl
ABOVE TARGET
100_200 0.6_0.7 25_30 0.50
80_150 0.7_1.0 40_50 0.75
80_130 1.0_1.2 40_50 1.0_2.0

10. *

11.  If fasting glucose is high – evening dose of
long acting insulin should be inc. by 10-15%
and/or additional short acting insulin should
be given at bed time.
 If noon glucose is high – morning S.A.insulin
should be increased.
 If pre supper one is high – noon dose should
be increased.

12.  HONEYMOON PERIOD
 DOSING CHANGES ACCORNDING TO
PUBERTY, HIGHER INITIAL CALORIC CAPACITY
 NO 1ST PASS METABOLISM
 HYPOGLYCEMIC REACTIONS

13. Diabetes
 Insulin (basal , prandial awa correction bolus )
 Recognition of Hypoglycemia & DKA
 Monitoring
 Meal plan
 exercise
 Sick-day management

14. Mild
hypoglycemia
Moderate
hyoglycemia
Severe
hypoglycemia
Pallor,sweating,h
unger,irritability,
aggression
Cerebral
glucopenia l/t
drowsiness,ment
al,confusion,imp
aired judgement
Inability to seek
help,seizures,co
ma

15.  5_10 gm glucose
 Check BG after 15 to 20 mins
 Not to give much glucose
 If pt. nt responding,Ready with i.m. injection
of glucagon
 0.5mg(if wt <20 kg) or 1 mg(if wt >20 kg)
 s/c dosing _ 10microgm/yr of age

16. AGE
(YRS)
TARGET PREMEAL
BG RANGE
30-DAY
AVERAGE BG
RANGE
TARGET
HBA1C(%)
<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

17.  Insulin dose
 Unusual physical activity
 Dietary changes
 Hypoglycemia
 Intercurrent illnesses
 Fructosamine and HbA1C levels

18.  At least 4 times daily ,plus at 12:am n 3;am in
night when insulin therapy initiated
 Even otherwise minimum 4 are required
 CGMS continuous glucose monitoring system

19. URINE KETONE
STATUS
GLUCOSE
TESTING
INSULIN
CORRECTION
DOSES
Negative or
small
q2 hr q2 hr for
>250mg/dl
Check ketones
every other void
Moderate to
large
q1 hr q1 hr for
>250mg/dl
Check ketones at
each void. go to
hospital if emesis

20.  CHILDREN Kcal REQUIRED/kg body
weight
0-12 months 120
1-10 years 100-75
YOUNG GIRLS
11-15 years 35
>16 years 30
YOUNG BOYS
11-15 years 80-55
>16 years 50-30

21. Carbohyates- 55% (70% of which should be
derived from complex ones.) y?
 Fats -30%(<10% saturated;=10%
polyunsaturated;remaining monounsaturated
 Proteins -15%(high proteins may contribute
to nephropathy)
 Fibers - >20gms
One carbohydrate exachange =15 gms (??)

22. 20% at breakfast
20% at lunch
30% at dinner
10% each for midmorning ,midafternoon and
evening snacks
Emphasis on regularity of food intake and
constancy of carbohydrate intake
 Adjustment constantly be made to meet
individual requirements

23.  DKA is the end result of metabolic
abnormalities due to severe deficiency of
insulin or insulin effectiveness.
 Characterised by Hyperglycemia , Acidosis
and ketosis.
 Occurs in 20-40 % of children with new onset
diabetes or who omit insulin .

24. *Precipitating factors of DKA
*Pathophysiology
*Clinical features
*Treatment
*Complications

25.  Failure to take insulin
 Failure to increase insulin
-acute illnesses
 Medical stress – counter regulatory hrmns
 Hypovolemia - increased glucagon and
catecholamines

26. Insulin Deficiency
Glucose uptake
Proteolysis
Lipolysis
Amino Acids
Glycerol
Gluconeogenesis
Glycogenolysis
Hyperglycemia Ketogenesis
Osmotic diuresis Dehydration Acidosis

27. 1. ↑↑ glucose production with ↓↓ glucose
utilisation raises serum glucose → osmotic
diuresis +activation of RAAS→ loss of fluid
electrolyte & dehydration
2. ↑ catabolic process→ cellular loss of sodium,
potassium & phosphate
3. ↑ release of FFA from peripheral fat stores→
hepatic keto acid production → buffer system
depleted → metabolic acidosis

28. CONTD….
• Electrolyte derangements
Metabolic acidosis and osmotic diuresis lead to
total body
– hypokalemia
– Hypophosphatemia
– Pseudohyponatremia
– (Naactual = [Nameasured + glucose – 100*1.6]/100
•(Each 100 mg/dl elevation in blood sugar
lowers serum sodium by 1.6 meq/dl)**

29. With prolonged illness & severe DKA :
-Total body loss of sodium can be 10-13 mEq/L
- of potassium can be 5-6 mEq/L
- of phosphate can be 4-5 mEq/L

30. Pathophysiology
(What’s wrong)
Clinical features
(What do you see)
 Elevated blood
glucose
 High lab blood glucose, glucose
meter reading or urine glucose,
polyuria, polydypsia
 Dehydration  Sunken eyes, dry mouth,
decreased skin turgor, decreased
perfusion
 Altered
electrolytes
 Irritability, change in level of
consciousness,muscle
weakness,ileus
 Metabolic acidosis
(ketosis)
 Acidotic breathing, nausea,
vomiting, abdominal pain, altered
level of consciousness

31. Normal Mild Moderate Severe
co2
(Meq/l
,venous )
20-28 16-20 10-15 ≤ 10
pH
(venous)
7.35- 7.45 7.25- 7.35 7.15- 7.25 ≤ 7.15
Clinical No change Oriented
alert but
fatigued
Kussmaul
respiration,
oriented
but sleepy,
arousable
Kussmaul
or
depressed
respirations
, sleepy to
depressed
sensorium
to coma
*Corrected Na>150meq/l = severe DKA

32.  History:
Symptoms of hyperglycemia, precipitating factors ,
diet and insulin dose.
 Examination:
Look for signs of dehydration, acidosis, and
electrolytes imbalance, including shock,
hypotension, acidotic breathing, CNS status-glassgow
coma scale.
Look for signs of hidden infections (Fever
strongly suggests infection) and If possible, obtain
accurate weight before starting treatment.

33.  Known diabetic children _confirm D hyperglycemia,
K ketonuria & A acidosis.
 Newly diagnosed diabetic children_ don’t miss _
because it may mimic serious infections like
meningitis.
 Both Hyperglycemia (using glucometer) glycosuria, &
ketonuria (with strips) must be done in the ER and
treatment started, without waiting for Lab results
which may be delayed.

34. The initial Lab evaluation includes:
 Plasma & urine levels of glucose & ketones.
V/ ABG, U&E (including Na, K, Ca, Mg, Cl, PO4,
HCO3), & arterial pH .
 Venous pH is as accurate as arterial (an error of
0.025 less than arterial pH)
 Complete Blood Count with differential.
Further tests e.g., cultures, X-rays…etc , are done
when needed.

35.  High WBC: may be seen in the absence of infections.
 BUN: may be elevated with prerenal azotemia
secondary to dehydration.
 Creatinine: some assays may cross-react with ketone
bodies, so it may not reflect true renal function.
 Serum Amylase: is often raised, & when there is
abdominal pain, a diagnosis of pancreatitis may
mistakenly be made.

36. 1. Correction of shock
2. Correction of dehydration
3. Correction of hyperglycaemia
4. Correction of deficits in electrolytes
5. Correction of acidosis
6. Treatment of infection
7. Treatment of complications
Slide no 36

37.  Ensure appropriate life support (Airway,
Breathing, Circulation, etc.)
 Give oxygen to children with impaired
circulation and/or shock
Slide no 37
 Set up a large IV cannula/intra-osseous access.
 Give fluid (saline or Ringers Lactate) at
10ml/kg over 30 minutes if in shock,
otherwise over 60 min. Repeat boluses of 10
ml/kg until perfusion improves

38. The Milwaukee protocol for DKA treatment
Time Therapy
1st hour 10-20 ml/kg i.v.
bolus 0.9 % NaCl
or RL .
Insulin drip at 0.05 to
0.10 u/kg/hr
2nd hour until DKA
resolution
0.45 % NaCl ; plus
continue insulin drip
20 meq /l Kphos and
20 meq/l KAc

39. 1.Calculate fluids based on 8.5 % dehydration.
IV rate = 85 ml/kg + maintenance – bolus
23 hr
2.Give 0.9% NS in the 1st hr of correction then change it to
0.45% NS.**
3.Total fluids must not exceed 4000 ml/msq /day , unless
patient is in hypovolemic shock.
4.Correct DKA in 20-30 hrs if milder or in 30-36 hrs if severe.

40. 5.If there is severe diuresis, replace it by
0.45%NS + KCl.

41.  POTASSIUM
 Potassium (20-40 mEq/l ; ½ KAc and ½ KPO4 ) is added
in fluids after urine flow is established and serum
potassium is ≤ 5.5 meq /l .
 If k ˂ 3 meq/l , give 0.5 to 1.0 meq/kg as oral K
solution OR increase IV K to 80 meq/l.
 KPO4 is used rather than KCl because pt will receive an
excess of chloride , which may aggravate acidosis.
Slide no 41

42. SODIUM
 Sodium should rise gradually with decrease in
glucose levels ,if not , donot change 0.9% to 0.45%
NS.(declining Na may indicate excessive free water
accumulation & the risk of cerebral edema)
PHOSPHATE
 No clinical benefit of correcting it

43. 1.Start insulin drip at 0.1 u/kg/hr . If patient is a known
diabetic & has received insulin subcutaneously start
lower insulin dose 0.05 u/kg/hr
2.When blood glucose ≤ 300 mg/dl , change IV fluids to
5% dextrose with 0.45 saline.
3. If blood glucose drops to ≤ 180 mg/dl , inspite of D5 in
IV fluids , change IV fluids to 10% dextrose in 0.45
saline

44. 4. If blood glucose drop to ≤ 150 mg/dl , reduce
insulin drip in decrements of 0.02 u/kg/hr
5. The rate of fall of plasma glucose should be 80-100
mg/hr or 40 mg/hr in the presence of severe
infection .if there is no change in plasma glucose in
2×3 hr , increase the insulin infusion ( 0.15 u/kg/hr)
6.Never give insulin bolus .

45. 7. When patient is acidotic and ketotic never decrease
insulin infusion below 0.05 u/kg/hr & never discontinue
insulin infusion until after subcutaneous insulin has been
given.
8. Monitor blood glucose every 30 min when changing
insulin drip or if blood glucose drops ≤ 150 mg/dl
9. Insulin must be continued until pH ≥ 7.36 or serum
bicarbonate ≥ 20 meq/l

46. By correction of ketosis.low insulin infusion
(.02-.05U/kg/hr) are sufficient to stop
peripheral release of FFA and thereby to
eliminate substrate for ketogenesis.
BICARBONATE THERAPY
1.Not used routinely
2.Can precipitate cerebral edema by ↑ CNS
acidosis , ppt hypokalemia ,alter Calcium
ionization & tissue hypoxia.

47. 3.Indicated for symptomatic hyperkalemia or if blood
pH persist at ˂ 6.9 after 1st hour of rehydration with
instability
4. mL of sodium bicarb
=0.15 × base deficit × wt
5. Added to N/2 saline infusion over 2 hr , stopped
when
pH is ˃7.0

48.  Infection can precipitate the development of
DKA
 Often difficult to exclude infection in DKA, as
the white cell count is often elevated because
of stress
 If infection is suspected, treat with broad-spectrum
antibiotics
Slide no 48

49. •Once DKA has resolved
•Total CO2 ˃ 15 mEq/l
•pH ˃ 7.30
•Sodium stable between 135 and 145 mEq/l
•No emesis
•An initial dose ( 0.02-0.04 units/kg ) of
regular insulin is given, half an hr after which
the insulin infusion is stopped & child allowed
to eat .

50. Monitoring :
•Clinical parameters like vital signs, hydration ,sensorium,
Pupils, urine output, fluid infused, insulin infusion rate
Must be done every hourly
•RBS by finger prick at bedside every hour initially and
later every 2 hourly

51. •Serum sodium , potassium , bicarbonate every 4
hourly initially and later 6 hourly
•Urine ketones, serum phosphorus & calcium may
be done every 8-12 hours
•With insulin therapy unmeasured ketone ( β-
hydroxy butyrate ) is converted to acetone &
acetoacetate, So Urine ketone may seem to worsen

52.  Starting insulin from the first hr.
 Changing type of fluid from 2nd hr.
 Not good fr managing dka with severe
hypernatremia.

53.  Remember child can die of DKA from:
 CREBRAL EDEMA
 HYPOKALEMIA
 ASPIRATION PNEMONIA

54. Most dangerous complication of DKA is
Cerebral Oedema

55.  Clinically apparent Cerebral edema occurs in 1-2% of
children with DKA. It is a serious complication with a
mortality of > 70%. Only 15% recover without
permanent damage.
 Typically it takes place 6-10 hours after initiation of
treatment, often following a period of clinical
improvement.

56. The mechanism of CE is not fully understood, but many
factors have been implicated:
 rapid and/or sharp decline in serum osmolality with
treatment.**
 high initial corrected serum Na concentration. **
 high initial serum glucose concentration.
 longer duration of symptoms prior to initiation of
treatment.
 younger age.
 failure of serum Na to raise as serum glucose falls
during treatment.

57. deterioration of level of consciousness.
 lethargy & decrease in arousal.
 headache & pupillary changes.
 seizures & incontinence.
 bradycardia. & respiratory arrest when brain
stem herniation takes place.

58.  Rule out hypoglycemia
 Reduce IV fluids
 Raise head end of bed
 High flow oxygenation
 IV Mannitol .5-1gm/kg over 20 minutes or
 Hypertonic 3% N.S. 5ml/kg over 30 minutes
 Elective Ventilation
 Dialysis if associated with fluid overload or renal
failure.
 Use of IV dexamethasone is not recommended.

59. • acute gastric dilatation or erosive gastritis
•Vascular thrombosis
•Respiratory distress syndrome
•Pancreatitis occasionally seen
•Acute tubular necrosis

60.  Life threatening condition
 Requires care at the best available facility
 Morbidity and mortality reduced by early
treatment
 Adequate rehydration and treatment of shock
crucial
 Written guidelines should be available at all
levels of the healthcare system
Slide no 60

61.  Type of fluids…………….how to prepare