PEDBASE.org - The Pediatric Database - Detailed information of DIABETIC KETOACIDOSIS (DKA)

DIABETIC KETOACIDOSIS (DKA)

DEFINITION:

A complication of insulin-dependent diabetes mellitus characterized by hyperglycemia, metabolic acidosis, and ketouria.

EPIDEMIOLOGY:

incidence: ?
age of onset:
- any with peak in adolescence
risk factors:
- poorly controlled insulin-dependent diabetes mellitus (IDDM)

PATHOGENESIS:

1. Background

basic cause of DKA is an absolute or relative insulin deficiency:

1. Absolute

new onset IDDM
non-compliance with insulin

2. Relative

elevated levels of counterregulatory (stress) hormones (glucagon, cortisol, growth hormone, catecholamines) which antagonize insulin

these abnormalities produce a hyperglycemic state (with increased glucose production and decreased utilization) -> osmotic diuresis -> dehydration + lipolysis -> increased fatty acid oxidation -> ketone production (acetoacetate and beta-hydroxybutyrate) -> metabolic acidosis -> electrolyte disturbances (hypercalcemia)
the degree of acidosis may not correlate with the degree of hyperglycemia

CLINICAL FEATURES:

1. Classical Features of IDDM

polyuria
polydipsia
weight loss

2. Features of DKA

1. Neurological

altered level of consciousness (alert -> coma)
headache

2. Respiratory

fruity breath
hyperventilation

3. Gastrointestinal

anorexia
abdominal pain
diarrhea
nausea/vomiting

4. Genitourinary

dehydration (usually 5-10%)

3. Complications

1. Cerebral Edema

usually occurs when biochemical abnormalities are improving
cerebral edema -> raised intracranial pressure -> neuro-logical signs/symptoms -> respiratory arrest
risk factors:
- age <5 years
- new onset IDDM
factors implicated:
- too rapid a drop in glucose or hypoglycemia
- excessive fluid administration
- bicarbonate theray
- persistent hyponatremia (due to excessive free water administration)

INVESTIGATIONS:

1. Serum

metabolic acidosis with wide anion gap
hyperglycemia with high serum osmolality
dehydration (with elevated urea and creatinine)
hyperkalemia, hyponatremia

2. Urine

ketonuria
glucosuria

MANAGEMENT:

1. Supportive

moniter electrolytes, gas, serum osmolality, & glucose q1h
moniter BUN, creatinine, calcium, & phosphate q4h
moniter urinary ketones with each void
neurovitals q1h if altered level of consciousness

2. Fluid Resuscitation

1. Initial

use Normal Saline or Ringer Lactate
bolus 10-20 cc/kg over 1 hour and repeat if still unstable
rehydration acts to perfuse the kidneys and increase urinary glucose loss thus lowering serum glucose levels

2. Maintenance

switch to 0.45% NaCl and correct 50% of deficit over 8 hours and the remaining 50% over the next 16 hours
add glucose to the infusion when the serum glucose levels approach normal
add 20 mEqu KCl/500 cc fluid if potassium levels are normal or low and patient is urinating; if hyperkalemic add KCl when the potassium level start to fall

3. Insulin

dose: 0.1 U/kg/hr IV of Regular Insulin
run 30-50 cc of infusate through the tubing to saturate all in-sulin-binding sites in the tubing before initiating drip - if the acidosis has not improved within 2 hours, increase the insulin dosage to 0.15-0.2 U/kg/hr
continue IV insulin until the glucose and acidosis have corrected then switch to subcutaneous insulin (see below)

4. Potassium

total body potassium depletion with low to high K+ levels (to buffer the acidosis, H+ is driven into the cells and thus K+ is released from these cells and in the presence of an osmotic diuresis, K+ is lost through the kidneys)
as the acidosis is correcting, the serum K+ levels fall (as H+ is driven out of the cells, K+ is driven into the cells) and thus hypokalemia may become a problem

5. Phosphate

phosphate depletion due to a catabolic state, urinary losses, and insulin driving phosphate intracellular
replacement with potassium phosphate is indicated if the phos-phate level drops to less than 2 mEqu/L
moniter calcium levels as phosphate administration may cause hypocalcemia

6. Bicarbonate

indicated if severe metabolic acidosis (pH <7.1; HCO3 <5)
1-2 mEqu/L HCO3/kg over 10 minutes

7. Cerebral Edema

1. Neuroresuscitation Protocol

intubate and hyperventilate (PaCO2 25-30)
80% fluid maintenance
mannitol +/- lasix
head of bed elevation to 30 degrees
lidocaine with suctioning

8. Converting to Subcutaneous Insulin

indicated with the patient is clinically stable with normal sensorium and vital signs, the acidosis and hyperglycemia have cleared, and the patient is able to take fluids and liquids without vomiting
if known IDDM, start back on pre-DKA insulin regime
if new onset IDDM, then add up the total dosage of Regular Insulin give and then give 2/3rds in am and 1/3rd in pm with 2/3rds of NPH and 1/3rd of Regular given at each time - continue IV insulin for 30-60 minutes after the first subcutan-eous dose then discontinue the infusion
switch in the daytime
adjust dosage based upon regular serum glucose and urine ketone checks

INTERNET LINKS:

1996 DKA Treatment Guidelines

Pediatric Database - DIABETIC KETOACIDOSIS (DKA)

Pediatric Organization - Pedbase [at] Gmail.com