2. Principles of management In Childhood DKA
1. Supportive measures
2. Perform emergency assessment
3. Fluid replacement
4. Correction of hyperglycemia -insulin
5. Electrolyte replacement, especially, K.
6. Rx of precipitating causes & Complication
7. Diabetic Education
8. Prevention of recurrence.
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3. Supportive measures
1. Secure the patency of the Airway,suction oral
secretion & intubation if deep comatus
2. NGT decompression to prevent pulmonary
aspiration
3. Oxygen 100%
4. Open wide iv cannula
5. Catheterize bladder -uop
6. Changing body position & elevate the head
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4. Perform Emergency Assessment
• Confirm diagnosis
• Evaluate for evidence of infection
• Estimate for severity of Dehydration
• Bloodglucose, urine ketone, blood PH& gas
analysis
• Cardiac monitoring-ECG
• Follow with flow sheet
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6. REHAYDRATION : will decrease
Hyperglycemia by increasing renal perfusion
which improves GFR ultimately enhances
clearance of organic acids( excretion)
• Stops Osmotic Diuresis (threshold=18omg/dl)
• Will repair acidosis by helping the renal
tubules to regenerate bicarbonate
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7. • Initial iv bolus(10-20ml/kg/hr)0.9%NS/RL
isotonic fluid will quickly expand the volume
of intravascular space
• May be repeated if Dhd is still not recovered
• Subsequent fluids should be hypotonic which
allow intracellular hydration, repair free water
deficit & replace ongoing hypotonic urine loss
• Have mannitol at abed side(.5-1gm) iv push
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8. • During the second hour & subsequentlly until
patient is out of DKA half strength(.45% NS) is
used at IV rate =85ml/kg+ maintenance-bolus
over the next 23hr
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10. • Calculation of fluid deficit in DKA is a difficult
task b/c intra vascular volume is better
tolerated in hyperosmolar state at the
expense of IC fluid,i.e
• DKA Child will be more dehaydrated than
other normotonic DHD deficit
• The protocol corrects fluid deficits=
85ml/kg(8.5%Dhd) for 1st 24hr
• Mild DKA rehydrate earlier(10-20hr)
• Sever DKA with greater deficit takes up 30
to36hr
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11. INSULIN THERAPY :
• Goal of infusion:
controlling DKA with out causing hypoglycemia
& hypokalemia
accelerates glucose uptake
Reduce hyperosmolarity & Ascidosis
Decreasing gluconeogenesis & halts
mobilization of FFA to liver for ketogenesis
Will correct the anion gap which is >20-
30mmol/l in DKA. normal anion gap =Na+ -(Cl
+HCO3) which is about 10-14mmol/l 11
14. • Dose of Insulin Drip: 0.05-0.1U/kg/hr
approximates the maximum insulin out put of
a normal person during OGTT
• After commencement of insulin infusion the
desired decrement in serum glucose is
approximately (2-5mmol/L/hr)
• Insulin infusion has an inherent risk of
1. Hypoglycemia
2. Hypokalemia
3. Cerebral edema
• Adjustment &sound Medical judgument is
mandatory
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15. • Add 5% glucose solution when serum glucose
reached 300mg/dl ;if it <200mg/dl add 10%
glucose solution
• Reduce insulin infusion from its maximum
initial rate if the child is very sensitive to
insulin(=0.05u/kg/hr) or when there is a rapid
decline in serum glucose >5mmol/L/hr
• Low insulin infusion(0.02-0.05)unit/kg/hr are
sufficient to stop peripheral release of Free
fatty acid which are substrate for Ketogenesis
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16. • There for the initial infusion rate may be
decreased if blood glucose level go below
150mg/dl despite the addition of glucose to
the infusion
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18. Repair of Fluid Deficits
• Conscious effort to avoid cerebral edema
• Effective serum Osmolarity is corrected as:
• Eosm=2*[Na+uncorrected]+glucose
• It’s the accurate index of tonicity for body
fluids.
• Eosm is normaly in the range of 300-
350mmol/kg
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19. • It reflects intracellular & extracellular
hydration better than measured osmolarity.it
elevates at the beginning of a therapy but
normalizes later
• Slow/rapid decline Eosm reflects excess water
entering to vascular space posing risk of
Cerebral edema
• Monitoring input/put is crucial & NPO
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20. Na+ deficit
• Corrected deficit =[Na+]+1.6meq/L Na+ for
every 100mg/dl glucose in excess of 100
• Meaning-sodium must increase by 1.6mmol/l
for each reduction of 100mg/dl glucose
• Na+ >150mmol/l =sever DKA DHD necessitates
slow fluid replacement
• Na+<135mmol/l predispose to cerebral edema
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21. K+ defficit
Causes includes:
Catabolic loss
Metabolic acidosis-buffering effect
Osmotic diuresis
Activation of RAAS(hyperaldosteronism)
resulting in Renal loss
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22. Na+ loss can approach as high as 10-
13meq/kg (However it improves with in 24hrs
of therapy) where as a loss of K+:5-6meq/kg
And Phosphate4-5meq/kg takes several days to
repair
• Sever hypokalemia causes myocardial
dysfunction .ECG depicts flattening of T-waves
and prolonged QRS complex
• Hypokalemia also causes skeletal muscle
weakness & illeus
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23. • To correct the deficit in K+ it is better to use
potassium phosphate than KCL which can
aggravates Acidosis(Hyperchloremic ascidosis)
• Potassium acetate is beneficial which can give
additional buffer
• If k+ <3meq/L, give 0.5-0.1meq/kg as oral K+
soln or increase IV k+ to 80meq/L during 2nd
hr infusion
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24. • No Bicarbonate buffer therapy at all because
when the DHD & Hyperglycemia repair the
Distal Renal Tubules will regenerate
bicarbonate
• Bicarbonate therapy causes hypokalemia
predisposing to cerebral edema
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25. Predictor risks for Cerebral edema
Early bolus administration of insulin
High volumes of fluid
Baseline Ascidosis
Abnormality of serum electrolyte &BUN
Sever DKA
Bicarbonate thearpy
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26. Treatment of cerebral edema
• Initiate the treatment as soon as the condition is
suspected.
• Reduce rate of fluid administration by 1/3rd
• Mannitol should be given at 0.5 to1.0 g/kg IV over 20’.
• The dose may be repeated with in 30min- 2 hrs, if there is
no initial response.
• 3% saline (5 to 10 mL/kg over 30 minutes), has been
used as an alternative t o mannitol hypertonic agent???
• Intubation and mechanical ventilation may be required
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27. Cont…
• Elevate the head of the bed throughout treatment
• After treatment for cerebral edema has been started, a
cranial CT scan should be obtained to rule out other
possible causes
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29. Therapy progress
There should be a steady increase in
PH(>7.30) ,(Co2>15meq/l)& arise in
bicarbonate
Na+(135-145meq/L)
Serum glucose normalizes
Abscent kussmaul breathing
Abdominal pain should abate
Consciousness regained
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30. Flow sheet is mandatory for accurate
monitoring of:
• PH& Glucose
• Urine output
• Electrolyte &fluid balance
Persistent Ketonuria (Acetoacetate dipstick)
may not accurately reflect clinical
improvement ;also don’t reflect therapy
failure
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31. Life style Modification
Dietary modification
• Carbohydrate-55%,fat-30% &protein-15%
• Avoiding refined glucose &soft sweet drink
• Advocate high fiber diet
Regular aerobic exercise
Weight reduction
Routine blood glucose monitoring
Regular medical follow up for complication
Storage of insulin
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32. Educate about how to inject insulin
Educate about symptoms of hypoglycemia
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