Diabetic Ketoacidosis in Children

1
Diabetic Ketoacidosis in Children

• July 18, 2006
• Jennifer M. Barker MD
• Philippe Walravens MD
• Barbara Davis Center for Childhood Diabetes

2
Overview

• Definition and Pathophysiology of DKA
• Evaluation
• Treatment
• When is DKA life threatening?
• Caveats
• Cases

3
Overview

• Definition and Pathophysiology of DKA
• Evaluation
• Treatment
• When is DKA life threatening?
• Caveats
• Cases

4
Diabetic Ketoacidosis (DKA)

• Hyperglycemia (glucose gt 300 mg/dl)
• Evidence of significant ketosis
• (urine acetoacetate, blood beta-hydroxybutyrate)
• Acidosis (pH lt 7.30 or HCO3 lt 15)

5
Classification of DKA

• Mild pH 7.2-7.3
• Moderate pH 7.1-7.2
• Severe pH lt7.1

6
Risk factors for DKA

• 25-30 of new onsets present in DKA
• lt 5 years
• Poor access to medical care
• Lower income and parental education
• Lack of insurance

7
Risk factors for DKA

• In children with diabetes
• Risk 1-10/100 person years
• Poor metabolic control/history of DKA
• Psychiatric disorders
• Peripubertal and adolescent girls
• Unstable family situation
• Pump therapy

8
DKA

• DKA can be life threatening
• Mortality rate in U.S. is 0.15-0.3
• Causes of mortality
• Failure to make the diagnosis
• Cerebral Edema (60-90 of DKA mortality)
• Hypokalemia/ Hyperkalemia
• Hypoglycemia
• Hypovolemia

9

Diabetes Care 2006 291150-1159
10
Overview

• Definition and Pathophysiology of DKA
• Evaluation
• Treatment
• When is DKA life threatening?
• Caveats
• Cases

11
What are the presenting complaints of DKA?

• Gastro-enteritis
• Vomiting -
• but no diarrhea
• Dehydration --
• But excessive urine output !
• Respiratory distress
• But no lung findings

12
What are the presenting complaints?
History and PE 95 of diagnosis Take the
history Listen to the history

• Gastro-enteritis
• Vomiting -
• but no diarrhea
• Dehydration --
• But excessive urine output !
• Respiratory distress
• But no lung findings

13
Physical Exam

• Perfusion
• Vital Signs - including weight
• Hydration
• Mental Status
• Evidence for insulin resistance

14
Initial Laboratory Evaluation

• Venous pH
• BUN
• Serum Osmolality
• Phosphorus
• Calcium

• Glucose
• Ketones
• Sodium
• Potassium
• Chloride
• HCO3

Always perform in an ill child
15
Precision Blood Ketone Testing ß-hydroxybuterate

• lt 0.6
• normal
• 0.6 1.5
• call a healthcare provider will likely require
  subcutaneous insulin
• gt 1.5
• serious and call healthcare provider and state
  the call is urgent
• gt 3.0
• Go directly to the Emergency Room. Have someone
  take you!

16
Calculations

• Serum Osmolality
• 2NaK (glucose/18) BUN/2.8
• Serum Na
• Corrected Na
• measured Na (1.6)(glucose - 100)/100

17
Overview

• Definition and Pathophysiology of DKA
• Evaluation
• Treatment
• When is DKA life threatening?
• Caveats
• Cases

18
Treatment

• Volume depletion and cerebral edema are major
  causes of mortality and morbidity
• CVP and arterial pressure monitoring are required
  to guide fluid management in very ill patients
• Measurement of changes of osmolality can guide
  management to determine if more invasive
  measurements are required

19
Treatment

• Monitoring
• Management requires close attention to detail
• Use a flowsheet to track vital signs labs, rates
  of insulin, fluids, dextrose
• Neurological status
• consider neuro checks q 1 hr
• How does the patient look TO YOU?
• Assess, reassess and then assess again

20
Treatment

• Monitoring (contd)
• Consider ICU admission for closer monitoring if
• Severe DKA (pH lt 7.1 or lt 7.2 in young child)
• Altered level of consciousness
• Under age of 5 years
• Increased risk for cerebral edema
• Caution with meds that may alter mental status

21
(No Transcript)
22
(No Transcript)
23
Treatment

• Hydration
• Start with 10-20 cc/kg NS bolus
• Do not give more than 40 cc/kg as bolus
• Goal is to replace deficits over 48 hours
• Continually re-evaluate status of hydration

24
Treatment

• Hydration (contd)
• Replacement therapy
• Will need 3,000 mL/m2/ 24 hrs
• (usually 1.5 x Maintenance)
• Add dextrose when BG lt 250 -300 mg/dl OR decrease
  in glucose is too rapid
• Goal decrease BG by 50-100 mg/dl/ hour
• Continually re-evaluate status of hydration

25
Treatment

• Insulin
• Do NOT give initial bolus of insulin
• IV insulin drip at 0.1 units/ kg/ hour
• May decrease to 0.05 u/kg/hr if BG decreasing too
  quickly
• To get control of balance with IV fluids
• Prevent hypoglycemia
• Monitor BG at least q 1 hr

26
Sodium

• Initial hydration with NS
• May decrease to ½ to ¾ NS depending upon the
  clinical status after initial hydration
• When adding glucose decrease to ½ NS

27
Potassium

• Add potassium when Klt 5 and with urination
• K gt5.5 no potassium in IVF
• K 4.5 5.5 20 meq/L K
• K lt4.5 40 meq/L K

28
Phosphate the controversy

• Prevent depletion of RBC 2,3 DPG which will
  improve tissue oxygenation as acidosis is
  resolving
• May be useful in patients with anemia, CHF,
  pneumonia, hypoxia

29
Phosphate - the Data

• Phosphate therapy increased 2,3 DPG in treated
  group at 48 hrs (N/S)
• Glucose and acidosis rates of correction were not
  improved
• Treated group had significantly lower plasma
  ionized calcium.
• Tetany has been reported in pediatric patients
  given all replacement as KPO4

Fisher and Kitabihi 1983
30
Overview

• Definition and Pathophysiology of DKA
• Evaluation
• Treatment
• When is DKA life threatening?
• Caveats
• Cases

31
Causes of mortality

• Failure to make the diagnosis
• Cerebral Edema
• Hypokalemia/ Hyperkalemia
• Hypoglycemia
• Hypovolemia

32
Causes of mortality

• Failure to make the diagnosis
• Cerebral Edema
• Hypokalemia/ Hyperkalemia
• Hypoglycemia
• Hypovolemia

ASK THE QUESTIONS!
33
Causes of mortality

• Failure to make the diagnosis
• Cerebral Edema
• Hypokalemia/ Hyperkalemia
• Hypoglycemia
• Hypovolemia

ASSESS REASSESS ASSESS AGAIN FLOWSHEETS CONSIDER
CVP MONITORING
34
Causes of mortality

• Failure to make the diagnosis
• Cerebral Edema
• Hypokalemia/ Hyperkalemia
• Hypoglycemia
• Hypovolemia

Is the most common cause of DKA related mortality
35
Cerebral Edema

• Major cause of death in childhood DKA
• 20 with cerebral edema die
• 20 with mild to severe neurologic outcomes
• At risk
• Initial pH lt 7.1
• Baseline mental status abnormal
• Newly diagnosed, lt 5 years old
• Rapid rehydration (gt 50cc/ kg in first 4 hrs)
• Hypernatremia/ persistent hyponatremia

36
Age distribution of affected children
37
Proposed Pathophysiology of Cerebral Edema

• Cytotoxic and Vasogenic edema
• Dehydration and acidosis
• Vasogenic due to increased BBB permiability -
  hyperosmolality
• Cytotoxic due to idiogenic osmoles and /or
  vasopressin dysregulation
• Warning sign may be falling corrected serum
  sodium

Glaser et al J Peds 2004145164-171
38
MRI changes in subjects during DKA
Glaser et al J Peds 2004145164-171
39
Excessive Free Water

• Corrected Na Na(measured)1.6 (glucose-100)/100
• Calculated sodium is low and falling in many
  cases of cerebral edema
• ADH levels rise 5-50 times in DKA and contribute
  to increase in free water and hyponatremia

40
Cerebral Edema

• Know what to look for
• Altered mental status/ severe headache
• Recurrence of vomiting
• Changes in pupil size, seizures, bradycardia
• Clinical worsening despite improving lab values
• CT/ MRI changes may not be seen in early cerebral
  edema

41
Cerebral Edema Bedside Score
Caveat note that patient needs to be
significantly affected to meet diagnostic
criteria
Muir Diab Care 2004 271541-46
42
Timing of presentation of cerebral edema
43
Treatment of cerebral edema

• Mannitol 1 gram/ kg IV over 30 minutes
• Elevate the head of the bed
• Decrease IVF rate and insulin infusion rate
• Pediatric ICU management
• Do not delay treatment until radiographic
  evidence

44
Transition off IV insulin

• pH gt 7.30 and HCO3 gt 15-18
• Patient able to eat
• Subcutaneous insulin
• Give sq injection, D/C IV insulin / IV dextrose,
  feed child
• Known diabetes patient
• Previous dosing
• May need additional rapid acting insulin to
  overcome insulin resistance after DKA
• New patient
• 0.7 1.0 units/kg/ day

45
Overview

• Definition and Pathophysiology of DKA
• Evaluation
• Treatment
• When is DKA life threatening?
• Caveats
• Cases

46
DKA Caveats

• Type 2 diabetes can present in DKA
• Type 2, and rarely type 1, can present with
  nonketotic, hyperosmolar, hyperglycemic state
• This is frequently in teens with ready access to
  quantities of high sugar oral fluids
• Cerebral edema can occur in NKHHS

47
DKA - Caveats

• Type 2 patients may be very robust appearing
  and their degree of dehydration is difficult to
  assess clinically
• Capillary refill time may be more difficult to
  assess in darker skinned children
• When in doubt, additional monitoring is better,
  i.e. CVP, arterial line

48
Overview

• Definition and Pathophysiology of DKA
• Evaluation
• Treatment
• When is DKA life threatening?
• Caveats
• Cases

49
ANYONE? ANYONE?
50
DKA Cases

• 12 year old admitted with
• pH 7.0
• Na 136, K3.8, glucose 583mg/ dl
• She is oriented and conversant on admission, you
  follow the DKA protocol,
• 2 hours later she becomes difficult to arouse and
  is responsive only to deep pain. - What do you
  do?
• Presume cerebral edema
• Decrease fluid infusion to insensible losses
• Give mannitol 1 gm/kg

51
DKA Cases

• 6 y/o boy is admitted in severe DKA. The family
  has been traveling and he has been ill for
  several days.
• Initial pH7.0, K 3.7, glucose is 350mg.
• Despite replacement, his K now is 1.9 mg/dl -
  what do you do?
• A bolus of potassium at TCH is actually an
  infusion over an hour. An actual bolus of
  potassium into a central vein may be lethal

52
DKA Cases

• 16 year old boy is admitted in moderate to severe
  DKA (pH7.23), his weight is 230 lbs, his BG is
  1400, serum osm is 360 mOsm/L, what do you do?
• Monitor! Everything you can!

53
Successful Management

• Careful attention to detail
• Careful record keeping
• A detailed flow chart is essential
• Following the data recorded is also essential
• Repeated examination of the patient