DIABETES IN CHILDREN
INTRODUCTION
• Type 1 diabetes, previously referred to as insulin-dependent diabetes mellitus or juvenileonset diabetes
because of its earlier onset, is characterized by an abrupt and frequently complete decline in insulin
production.
• Type 2 diabetes, formerly referred to as non–insulin-dependent diabetes mellitus or adult-onset
diabetes, is marked by increasing insulin resistance and most commonly occurs in the overweight adult
or adolescent; there is a strong genetic tendency toward the disease.
• The third main form of diabetes affecting children is gestational diabetes, which can affect pregnant
teens as well as the infants of diabetic mothers
• Diabetes is the most common pediatric endocrine disorder, with an estimated prevalence of 1 in 400
CLINICAL FEATURES
• POLYURIA
• POLYDIPSIA
• POLYPHAGIA
• WEIGHT LOSS
• SECONDARY ENURESIS
• ANOREXIA
• ABDOMINAL DISCOMFORT
• VISUAL CHANGES
• GENITAL CANDIDIASIS
DIABETIC KETO ACIDOSIS (DKA)
• DKA is generally defined as a metabolic acidosis (ph <7.30 or serum bicarbonate level of <15 meq/L)
with hyperglycemia (serum glucose level of >200 milligrams/dl or 11 mmol/L) and ketonemia or
ketonuria
• DKA is much more common in patients with type 1 diabetes than in those with type 2
• The most common cause of DKA in children and adolescents with known diabetes is poor adherence to
the prescribed insulin regimen.
• Physical findings in dka are due to dehydration and metabolic acidosis.
• Children are dehydrated, tachycardic, and may be hypotensive.
• Respiratory compensation for acidosis is noted in the deep kussmaul respirations
• Acetoacetate is converted to acetone and is responsible for the classic breath odour of nail polish.
• The level of consciousness may range from alert to somnolent to comatose.
DIABETIC KETO ACIDOSIS (DKA)
• Other precipitants include intercurrent viral illness and focal infections such as urinary tract infection or
gastroenteritis.
• Patients complain of polydipsia and polyuria ,diffuse nonfocal abdominal pain often associated with
vomiting, difficulty breathing, and generalized malaise, in addition to any localizing complaints related
to a precipitating trigger.
• Kussmaul breathing may be mistaken for pulmonary pathology or even anxiety with hyperventilation
• In a child with DKA and a depressed level of consciousness, consider the development of cerebral
edema
CEREBRAL EDEMA
• Cerebral edema, which occurs in approximately
0.5% to 1% of all children presenting with DKA,
is the most dreaded complication, accounting
for 60% to 90% of all pediatric DKA-associated
deaths
• the specific risk factors associated with overt,
life-threatening cerebral edema are young age,
severe hyperosmolality, persistent
hyponatremia, and severe acidosis
CLINICAL FEATURES
• Cerebral edema typically manifests itself 6 to 12 hours after the onset of therapy
• Many children appear to be improving clinically and biochemically prior to deterioration from cerebral
edema.
• Premonitory symptoms occur in as few as 50% of patients and include severe headache, declining
mental status, seizures, and papillary edema.
• Early aggressive intervention based on the clinical evaluation, often before confirmatory CT findings, is
vital to prevent respiratory arrest, herniation, and death.
• Once respiratory arrest has occurred, meaningful recovery is unlikely
TREATMENT
• Standard treatment for cerebral edema is mannitol (0.25 to 1 gram/kg IV bolus) and endotracheal
intubation if necessary
• Limit additional fluid administration to the minimum possible to retain a functioning IV catheter
• NEW STUDIES SHOW 10 mL/kg of 3% hypertonic saline infused over 30 minutes had improved findings
on neurologic examination
LABORATORY EVALUATION IN DKA
TREATMENT OF DKA
• Direct attention to perfusion, electrolyte disturbances, mental status, hyperglycemia and ketonemia
• Concurrently identify and treat associated infections
• Cardiac monitoring of all children with DKA and a prolonged QTc interval occurs frequently during DKA
and is correlated with ketosis.
• QTc prolongation can lead to life-threatening arrhythmias such
• Intensive monitoring and meticulous care of the patient with DKA improves outcome
NEW ONSET HYPERGLYCEMIA
• Many children with new-onset diabetes present with classic symptoms of diabetes such as polydipsia,
polyuria, and malaise, and are identified before significant ketoacidosis develops
• In general, children with hyperglycemia but no DKA are only mildly dehydrated, urinary ketones may or may
not be present, and the serum pH is >7.3
• The speed at which such children descend toward actual DKA is largely a function of hydration status and
age.
• Infants and very young children progress more rapidly because of their inability to access fluids
independently and their increased metabolic rate.
• With appropriate hydration and timely insulin administration, DKA is very unlikely to develop in the hospital
• ED management should be restricted to drawing samples for baseline laboratory studies; providing fluids
PO or IV and possibly administering the first dose of insulin.
• An acceptable initial dose is 0.1 unit/kg SC of regular insulin
HYPERGLYCEMIA IN PATIENTS WITH
PREDIAGNOSED DIABETES
• Management should focus on the primary reason for the ED visit.
• An additional dose of 10% of the child’s normal daily insulin dose can be administered as regular insulin
S/C for simple hyperglycemia.
• An acceptable approach if the child has an intercurrent illness and no urinary ketones is to administer
an additional 5% of the daily insulin dose every 4 to 6 hours until the condition resolves.
• If the child has urinary ketones, administer 10% of the daily dose every 4 to 6 hours until the ketonuria
resolves, and then decrease to 5%
