Dr. Surabhi Yadav (DCH,DNB)

*

Diagnosis

Treatment of type 1 DM

Diabetic ketoacidosis

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

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).

*

OTHER INVESTIGATIONS 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

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

INSULIN THERAPY

BASIC AND ADVANCED DIABETES EDUCATION

NUTRIONAL MANAGEMENT

MANAGEMENT OF DIABETIC KETOACIDOSIS

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.

SUBCUTANEOUS INSULIN DOSING

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

*

*

ADJUSTMENTS IN DOSING 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.

PITFALLS OF INSULIN THERAPY HONEYMOON PERIOD

DOSING CHANGES ACCORNDING TO PUBERTY, HIGHER INITIAL CALORIC CAPACITY

NO 1ST PASS METABOLISM

HYPOGLYCEMIC REACTIONS

Diabetes

Insulin (basal , prandial awa correction bolus )

Recognition of Hypoglycemia & DKA

Monitoring

Meal plan

exercise

Sick-day management

Symptoms of hypoglycemiaMild hypoglycemia

Moderate hyoglycemia

Severe hypoglycemia

Pallor,sweating,hunger,irritability,aggression

Cerebral glucopenia l/tdrowsiness,mental,confusion,impaired judgement

Inability to seek help,seizures,coma

Treatment of hypoglycemia

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

MONITORINGAGE(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

*What else to monitor Insulin dose

Unusual physical activity

Dietary changes

Hypoglycemia

Intercurrent illnesses

Fructosamine and HbA1C levels

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

GUIDELINES FOR SICK DAY MANAGEMENT

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

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

COMPOSITION OF CALORIC MIXTURE

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 (??)

DIVISION OF DAILY DIET

20% at breakfast20% at lunch30% at dinner10% each for midmorning ,midafternoon

and evening snacksEmphasis on regularity of food intake and

constancy of carbohydrate intakeAdjustment constantly be made to meet

individual requirements

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 .

* *Precipitating factors of DKA

*Pathophysiology

*Clinical features

*Treatment *Complications

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

catecholamines

Insulin Deficiency

Glucose uptakeProteolysis

Lipolysis

Amino Acids

Glycerol

GluconeogenesisGlycogenolysisHyperglycemia Ketogenesis

AcidosisOsmotic diuresis Dehydration

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

• Electrolyte derangementsMetabolic acidosis and osmotic diuresis lead to

total body – hypokalemia – Hypophosphatemia – Pseudohyponatremia – (Naactual = [Nameasured + glucose – 100*1.6]/100

CONTD….

• (Each 100 mg/dl elevation in blood sugar lowers serum sodium by 1.6 meq/dl)**

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

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

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

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.

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.

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.

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.

1. Correction of shock2. Correction of dehydration3. Correction of hyperglycaemia4. Correction of deficits in electrolytes5. Correction of acidosis6. Treatment of infection7. Treatment of complications

Slide no 36

Ensure appropriate life support (Airway, Breathing, Circulation, etc.)

Give oxygen to children with impaired circulation and/or shock

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

Slide no 37

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

The Milwaukee protocol for DKA treatment

1.Calculate fluids based on 8.5 % dehydration.

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.

IV rate = 85 ml/kg + maintenance – bolus 23 hr

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

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

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

C. CORRECTION OF ELECTROLYTES

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

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 .

4. If blood glucose drop to ≤ 150 mg/dl , reduce insulin drip in decrements of 0.02 u/kg/hr

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

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.

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

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

• 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 .

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

• 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

Starting insulin from the first hr.

Changing type of fluid from 2nd hr.

Not good fr managing dka with severe hypernatremia.

Remember child can die of DKA from:

CREBRAL EDEMA HYPOKALEMIA ASPIRATION PNEMONIA

Most dangerous complication of DKA is

Cerebral Oedema

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.

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.

deterioration of level of consciousness. lethargy & decrease in arousal. headache & pupillary changes. seizures & incontinence. bradycardia. & respiratory arrest when

brain stem herniation takes place.

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.

• acute gastric dilatation or erosive gastritis

• Vascular thrombosis

• Respiratory distress syndrome

• Pancreatitis occasionally seen

• Acute tubular necrosis

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

Type of fluids…………….how to prepare