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A complication of
insulin-dependent diabetes mellitus characterized by hyperglycemia,
metabolic acidosis, and ketonuria.
Age of onset
is any with a peak in adolescence. Risk factors are primarily poorly
controlled insulin-dependent diabetes mellitus (IDDM). The basic cause
of DKA is an absolute or relative insulin deficiency:
1.
Absolute
i. New onset IDDM
ii. Non-compliance with insulin
2.
Relative
i. Elevated levels of counterregulatory (stress)
hormones (glucagon, cortisol, growth hormone,
and catecholamines) which antagonize insulin
ii. These abnormalities produce a hyperglycemic
state (with increased glucose production and
decreased utilization) leading to osmotic
diuresis leading to dehydration + lipolysis
leading to increased fatty acid oxidation
leading to ketone production (acetoacetate and
beta-hydroxybutyrate) leading to metabolic
acidosis leading to electrolyte disturbances (hypercalcemia)
The degree of
acidosis may not correlate with the degree of hyperglycemia.
Clinically,
there is a triad of polyuria, polydipsia and weight loss. An altered
level of consciousness, headache, fruity breath, hyperventilation,
anorexia, abdominal pain, diarrhea, nausea/vomiting, and dehydration
(usually 5-10%) may be present. Complications include cerebral
edema, which usually occurs when biochemical abnormalities are
improving. Risk factors include a child < 5 years of age, new onset
IDDM, with too rapid of a drop in glucose or hypoglycemia, excessive
fluid administration, bicarbonate therapy, and/or persistent
hyponatremia (due to excessive free water administration).
Investigations
include serum samples to determine metabolic acidosis with wide anion
gap, hyperglycemia with high serum osmolality, dehydration (with
elevated urea and creatinine),hyperkalemia, and hyponatremia. Urinalysis
will reveal ketonuria and glucosuria.
Management
includes monitoring electrolytes, blood gas, serum osmolality, and
glucose q1h; BUN, creatinine, calcium, and phosphate q4h; urinary
ketones with each void, and neurovitals q1h if an altered level of
consciousness is present. Initial fluid resuscitation should include a
normal Saline or Ringer lactate bolus of 10-20 cc/kg over 1 hour, with a
repeat if still unstable.
Rehydration
acts to perfuse the kidneys and increase urinary glucose loss, thus
lowering serum glucose levels. Maintenance fluid therapy includes
changing to 0.45% NaCl, and correcting the fluid deficit over 24-48
hours. Add glucose to the infusion when the serum glucose levels
approach normal.
Add 20 mEq KCL/500
ml fluid if potassium levels are normal or low, and the patient is
urinating; if hyperkalemic add KCl when the potassium level starts to
fall. Total body potassium depletion occurs 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. Phosphate depletion
may occur due to a catabolic state, urinary losses, and insulin driving
phosphate intracellularly. Calcium levels should be monitored as
phosphate administration may cause hypocalcemia. Bicarbonate is
indicated if severe metabolic acidosis (pH <7.1; HCO3 <5) is present.
General dosing is 1-2 mEq/L HCO3/kg over 10 minutes.
Insulin dosing
is 0.1 U/kg/hr iv of regular insulin, which is continued until the
glucose and acidosis have corrected. Subcutaneous insulin (indicated
when the patient is clinically stable with normal sensorium and vital
signs, acidosis and hyperglycemia have cleared, and the patient is able
to take fluids and liquids without vomiting. If the child is a known
IDDM, start back on pre-DKA insulin regime. If new onset IDDM, then add
up the total dosage of regular insulin given, and then give 2/3rds in
the am and 1/3rd in the 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 subcutaneous dose then discontinue the infusion.
Neuroresuscitation
protocol for cerebral edema includes intubation and conventional
cerebral edema treatment (mild hyperventilation, fluid restriction,
mannitol +/- lasix, and head elevation).
This edited version is
being used with the permission of its original author, Dr.
Alan Gandy.
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