DKA in children

Diabetic Ketoacidosis   in Children
 
                                       Presented By:
                     Dr.Md.  Maniruzzaman
                             
 Definition :

It is a Clinical Condition in children Having-
Hyperglycemia (BG >11mmol/L) , Heavy glycosuria & Dehydration (5% or more)
Acidosis: pH <7.3 and/or Bicarbonate <15mmol/L
Kitosis: Ketonemia and Ketonuria
With or without Vomiting  & Drowsiness
 Classification of DKA

Normal
      MILD
 MODERATE
    SEVERE
pH
7.35-7.45
  7.25-7.35
   7.15-7.25
        <7.15
CO2 (meq/l)
    20-28
     16-20
      10-15
          <10
Clinical
No change
Oriented, alert but fatigued.
Kussmaul respirations; oriented but sleepy; arousable.
Kussmaul or depressed respirations; sleepy to depressed sensorium to coma.
Normal
      MILD
 MODERATE
    SEVERE
pH
7.35-7.45
  7.25-7.35
   7.15-7.25
        <7.15
CO2 (meq/l)
    20-28
     16-20
      10-15
          <10
Clinical
No change
Oriented, alert but fatigued.
Kussmaul respirations; oriented but sleepy; arousable.
Kussmaul or depressed respirations; sleepy to depressed sensorium to coma.
Causes of DKA

§Insulin deficiency, either relative or absolute.
  Failing to take insulin, particularly in           adolescents.
     Too little insulin is given because of fear of            hypoglycemia.
     Insulin is omitted altogether by an           emotionally disturbed adolescent or with      menstruation or severe emotional upset.
       Risk factors of DKA

Children with poor metabolic control or previous episode of DKA.
Female gender (peripubertal or adolescent).
Psychiatric & behavioral disorders.
Children with limited access to medical service .
Insulin pump therapy.
Acute stress, like trauma, infections with elevated counter regulatory hormones.
Management of DKA:
Emergency Assessment

Characteristic history-polydipsia, polyuria.
Nausea, vomiting and abdominal pain.
Followed by unconsciousness.
Severity of dehydration.
Evidence of acidosis.
Assessment of conscious level-GCS.
Weight.
Blood glucose.
Urine for sugar and ketones.
Resuscitation:

In shock with poor peripheral pulses or coma
Oxygen 100% by mask.
20ml/kg (0.9% Nacl) boluses infused quickly
Normal saline 10ml/kg/hr, repeated if peripheral pulses remain poor (Max. 3times).
Nasogastric tube to drain stomach.
Urinary catheter.
Antibiotics to febrile pt. after obtaining culture.
Key Findings : Clinical 

Polyuria, Polydipsia , Polyphagia.
Nausea, Vomiting and Abdominal pain.
Dehydration.
Weakness, Weight loss.
Progressive loss of consciousness, convulsion.
Rapid,deep,sighing (Kussmaul) respiration.
Fruity odour of ketones on the breath. 
Key Findings : Biochemical

Always present:
Hyperglycemia, Glycosuria.
Ketonemia, Ketonuria.
Metabolic acidosis/acidemia
Hypocarbia (compensatory)
Sometimes present:  
  Apparent or actual hyponatremia  
  Hypernatremia   
  Hyperkalemia or hypokalemia
  Hypophosphatemia  
  Increased blood urea nitrogen   
  Increased serum creatinine
  Hyper triglyceridemia   
  Increased serum amylase
Acidosis and bicarbonate :

Why not use bicarbonate?
ØDecrease in tissue perfusion.
ØIncreased risk of hypokalemia.
ØDoes not hasten resolution of acidosis (other  
than very short term).
ØMay result in increased hepatic ketone production.
ØMay result in CNS acidosis.
ØIncreased risk of cerebral edema.
Complications of DKA

ØClinically-evident cerebral edema: ~ 0.5-1%
ØHypoglycemia
ØHypokalemia or Hyperkalemia
ØHyperchloremic acidosis
ØHypophosphatemia
ØCNS complication-DIC, thrombosis.
ØSepsis
ØAspiration pneumonia
ØPulmonary edema
ØAcute renal failure
Cerebral edema

ØApproximately 0.5-1.5% children presenting with DKA develop cerebral edema with a high mortality and morbidity.

ØThose who developed CE in DKA
    64%-died, 13%-severe disability, 9%-minor disability and 14% survived without disability.
Ø CE most commonly occurs in the first 24 hrs. and is present both at presentation and during DKA treatment.
Warning signs / symtoms of CE

ØHeadache & slowing of heart rate.
Ø
ØChange in neurological status(restlessness, irritability, increased drowsiness, incontinence).
Ø
ØRising BP, decreased O2 saturation
Ø
ØConvulsions, papilloedema, respiratory arrest are late sings




 


 





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