Guidelines for the Early
Management of Diabetic
Ketoacidosis in Children
Michael Bressack, MD
DEFINITION
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Hyperglycemia (serum glucose >300
mg/dl) with glycosuria
Metabolic acidosis
(serum bicarbonate <15, elevated
anion gap, pH <7.30)
Ketonemia with ketonuria
CLINICAL PRESENTATION HYPERGLYCEMIA
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Polyuria
Polydipsia
Weight loss
Dehydration/shock
Decreased level of consciousness
CLINICAL PRESENTATION METABOLIC ACIDOSIS
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Kussmaul breathing
Fruity breath (acetone)
? decreased level of consciousness
? depressed cardiac function
? intestinal ileus (vomiting, pain)
LABORATORY DATA
 Hyperglycemia
 Metabolic

acidosis (anion gap)
[Na+]-([Cl-]+[HCO3-])
 OH
butyrate
 Low [Na+]
[Nac+] = [Nam+] + 1.6(blood glucose-100)
100
LABORATORY DATA
 Hyperglycemia
 Metabolic

acidosis (anion gap)
[Na+]-([Cl-]+[HCO3-])
 OH
butyrate
 Low [Na+]
 Abnormal [K+]
 Pre-renal azotemia
MONITORING
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Blood glucose q 1 h - q 4 h
Electrolytes q 1 h - q 4 h
Anion gap q 1 h - q 4 h
Renal function q 4 h – q 6 h
Cardiac monitor/EKG
CLINICAL MONITORING
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Cardiovascular
Intake/urinary output
Neurologic status (Glasgow
Coma Scale)
CARDIOVASCULAR
TREATMENT
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Treat shock immediately
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10-20 ml/kg doses of NS or LR
Slow rehydration for 5-15% deficit
over 48 hours
SLOW REHYDRATION
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Maintenance, deficit, excessive urine
(because of the risks of cerebral
edema, infuse fluid at a maximal
rate of 1.5 to 2 times maintenance)
Normal saline is usually the best
initial fluid (avoid hypotonic fluid)
Follow [Na+] closely
(keep [Na+corrected] 135meq/l)
TREATMENT FOR HYPERGLYCEMIA / KETOACIDOSIS
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Rehydration lowers blood
glucose
Low-dose continuous insulin
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(.05 - 0.1 u/kg/hr)
IV bolus of insulin is not
necessary
CONTINUOUS INSULIN DRIP
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Decrease blood glucose 50-100 mg/dl/hr
(after the initial drop due to rehydration)
Add glucose to intravenous fluid when
blood glucose <250-300 mg/dl
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add glucose to maintenance fluids only
Increases bicarbonate and decreases anion
gap (takes longer to correct ketoacidosis
than hyperglycemia)

use enough insulin to correct the anion gap
acidosis, and add enough glucose to the
intravenous fluid to tolerate the insulin
TREATMENT FOR K+
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Usually hyperkalemia on presentation
Total body K+ deficit
Monitor EKG
Initiate K+ replacement when serum level
<5.5meq/l and adequate urine output
In the rare situation of hypokalemia at
presentation, immediately treat with K+
replacement and fluid therapy, but delay
insulin treatment until K+ >3.3meq/l
INDICATION FOR
BICARBONATE
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Life-threatening hyperkalemia
Bicarbonate has no place in the
management of DKA
Cerebral edema is a
medical emergency
(major cause of death
in pediatric DKA)
Causes of Morbidity/Mortality
in DKA
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Cerebral edema/dysfunction (80-90% of
deaths)
Shock/ischemia
Hyper/hypokalemia
Hypoglycemia
Sepsis
ARDS
Thrombosis
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Central venous catheters are particularly
prone to thrombosis. If used, prophylaxis
with low-dose heparin should be considered.
Cerebral Edema/CNS Dysfunction
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Clinical cerebral edema occurs in 0.5-0.9% of all episodes of DKA
and accounts for 57-87% of all DKA deaths
A clinical, not a radiological, diagnosis (e.g. CNS dysfunction does
not correlate with CT changes)
Mortality ~25% (respiratory arrest on presentation has the worst
prognosis)
Significant morbidity in survivors (~25%)
Morbidity/mortality from herniation
Major cause of death in DKA
Occurs nearly exclusively in patients <20 years old
More common in:
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younger children
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children who have a longer duration of DKA before treatment
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children with newly diagnosed diabetes

elevated initial BUN

low initial pCO2

rapid administration of hypotonic fluids

failure of corrected serum sodium to rise during treatment

treatment with bicarbonate
Occurs within first 24 hours after starting Rx (usually 4-12hrs)
Signs and Symptoms of Cerebral
Edema
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Headache, emesis
Lethargy, incoherence, agitation, incontinence, coma
Seizures
Sudden, persistent bradycardia (decline >20bpm) not
attributable to improved intravascular volume or sleep state
Abnormal neurogenic respiratory pattern (e.g. tachypnea,
Cheyne-Stokes respiration, apneusis)
Decreasing Glasgow Coma Scale
Cranial nerve palsy (e.g. III, IV, VI)
Cushing’s reflex (e.g. hypertension)
Decorticate / decerebrate posturing
Cardiopulmonary arrest
Etiology of Cerebral
Edema
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Cerebral edema due to osmotic
shift of fluid
Primary ischemia/hypoxia with
secondary cerebral edema
Prevention and Treatment of
Cerebral Edema
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Cardioplumonary stabilization on presentation
 fluid boluses of isotonic crystalloids for shock
 intubation/ventilation for respiratory failure
After acute therapy for shock, avoid excessive
fluid or hypotonic fluid (use only 0.45%saline or
normal saline)
Avoid medications that can mask intracranial
hypertension e.g. phenergan, benzodiazepines
Promptly give intravenous mannitol (0.51.0gm/kg) or 3% saline (5-10ml/kg) for clinical
signs of elevated ICP
Consider intubation for neurologic deteriorationrisks include pCO2, which can elevate ICP, and
pCO2, which causes cerebral ischemia