Post on 30-May-2015
description
Dr. Surabhi Yadav (DCH,DNB)
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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).
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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
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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