KETOACIDOSIS
IN CHILDREN
Jose RL Batubara
Pediatric Endocrinology
Faculty of Medicine Universitas Indonesia, Jakarta
Introduction
DKA is the a leading cause of morbidity and
mortality in T1DM
Most deaths in DKA occur as a result of
cerebral edema
Incidence :
25-40% in newly diagnose type 1DM
In type 2 DM incidence varied 0-50%
Early diagnosis and adequate treatment are
important
ADA. Diabetes 2012;(6):139-49
Annual Incidence of DMT1 1991 -2013
base on National Registry
DKA from 1997 2013
base on National registry
Definition
DKA consist of biochemical triad
Hyperglycemia
Ketonemia
Acidemia
Biochemical criteria :
Hyperglycemia: BG > 200 mg/dL (>11
mmol/L)
Acidosis: pH <7,3 and/or HCO3- <15
mEq/L
Ketonemia and ketonuria
Salvodelliet al 2010. Diab Metab Syndrome 2010;2:1-9
Rosenbloom AL Diab Ther 2010;1:103-120
Walsdorf et al. 2011. Pediatr Diab.2011 10s. 118-33
Etiology
Inadequate insulin
Accidental or intentional omission
Inappropriate intervention when stressed
Newly diagnosed
Infection
Epidemiology
Frequency of DKA at onset : 15-67% in Europe
and North America
Higher in developing country
The risk of DKA : 1-10% per patient per year in
established T1DM
Usher Smith. Diabetologia 2012;55:2878-94
Rosenbloom AL Diab Ther 2010;1:103-120
Walsdorf et al. 2011. Pediatr Diab.2011 10s. 118-33
epidemiology
Risk of DKA increased in:
Poor metabolic control
Previous episode of DKA
Peripubertal and adolescent girls
Children with eating disorders
Low socioeconomic / lack of health insurance
Alvi et al:
Asian children <5 years had an eightfold
increased risk of DKA compared to non
Asian children
Rosenbloom AL Diab Ther 2010;1:103-120
Walsdorf et al. 2011. Pediatr Diab.2011 10s. 118-33
Alvi NS, dkk. Arch Dis Child 2001;85: 60-1
Morbidity and Mortality
Mortality:
USA 0,15%
UK 0,31%
Canada 0,18%
Cerebral edema is responsible for 57-87% death
in DKA
Incidence of cerebral edema :
USA 0,87%
UK 0,68%
Canada 0,46%
Rosenbloom AL Diab Ther 2010;1:103-120
Walsdorf et al. 2011. Pediatr Diab.2011 10s. 118-33
Classification
HCO3
Severity pH
(mEq/L)
Mild <7.3 <15
Severity of dehydration
severity estimation (%)
infant children
Mild 5 3
Moderate 10 6
Severe 15 9
Pathophysiology
Insulin deficiency counter regulatory hormone
Glycogenolysis Lipolysis
Gluconeogenesis Ketogenesis
Hyperglycemia Ketosis
Dehydration
Kibachi et al:
low dose insulin (0,1 U/kg/hr) is as save
and useful as high dose insulin
insulin
Decrease BG by 50-100 mg/dl/hr
If BG < 300: add D5NS ( = 1/2 D10NS +
maintenance bag)
If BG < 200: change to D10NS
May decrease insulin rate
Continue insulin until acidosis corrected
Adjust insulin and fluid BG level
between 150 250 mg/dl during ivfd
No insulin stat needed
insulin
Change to insulin sc
HCO3 > 15
At breakfast or lunch
Give insulin sc 30 minutes before meal and stop
insulin iv 1 hr later
Ketonemia typically takes longer to clear
than hyperglycemia.
During therapy, -OHB is converted to
acetoacetic acid, which may lead the clinician to
believe that ketosis has worsened.
.
Monitoring
Vital sign every 30 60 minutes
Fluid balance every hour
Neurological status every 30-60 minutes
ECG monitoring (certain indication)
Lab monitoring initially:
electrolyte, blood gas analysis BG every
hour
Clinically better, checked every 4 hr
Monitor the sign of cerebral edema
Complication
Hypoglycemia
Hypokalemia
Secondary Hyperglycemia
Cerebral edema, rare but fatal
Cerebral Edema
Potential devastating complication occurs in the first
day of treatment
Too rapid changes in intracellular and extracellular
osmolality
Should be suspected when there is unexpected
deterioration in neurological status
cerebral edema
Risk factors for cerebral edema:
serum natrium cons during treatment
Severe asidosis
Low pCO2
serum urea
Durr et al:
cerebral edema often occur before treatment
.
cerebral edema
Glaser et al (2001):
Bicarbonate is the only treatment that has an
association with the occurrence of cerebral edema
Therapy:
manitol 0,25-1,0 g/kgBW IV in 30 minutes
Prevention
Before diagnosis
Early diagnosis of DM with genetic and
immunological screening of high risk children
Increased public awareness of sign and
symptoms of DM
prevention
Beyond diagnosis
Better diabetes education to family members and
patients
Availability of 24 hour hotlines to the diabetic
center and multidisciplinary health care teams
Conclusion
DKA is an emergency and life threatening condition
Early detection and prompt treatment is mandatory
Clinical manifestation is vary, sometimes mimicking other
conditions
Diagnosis of DKA base on Hyperglycemia, acidosis and
Ketonemia
Principalof treatment consist of rehydration, insulin,
correction of aciidosis and electrolyte imbalance and
monitoring
Cerebral edema is the most common complication of DKA
Thankyou