Remember that the treatment of patients with diabetic ketoacidosis (DKA) is dependent upon theprovision of insulin
Remember that the treatment of patients with diabetic ketoacidosis (DKA) is dependent upon theprovision of insulin: Excerpt from Avoiding Common Pediatric Errors
Author:
Renée Roberts, MD
What to Do - Make a Decision
The insulin infusion should never be discontinued until the acidosis is corrected. Rather, use additional sources of dextrose containing intravenous
(IV) fluids if hypoglycemia develops.
DKA is the presenting symptom in approximately 40% of children and
teenagers at the time of diagnosis and the most frequent diabetes-related
cause of death in children, teenagers, and young adults. Most DKA-related
morbidity and mortality can be avoided via early recognition and early intervention.
The underlying pathophysiologic cause of DKA is an absolute or relative deficiency of insulin. Declining insulin production lowers the ratio of
insulin to glucagon, which leads to excess hepatic glucose production stimulating glycogenolysis and gluconeogenesis. When the serum glucose rises
above 200 mg/dL, the renal threshold for glucose reabsorption is exceeded,
causingosmoticdiuresiswithincreasedurineoutput.Physiologicstressfrom
acidosisandprogressivedehydrationstimulatesreleaseofthecounterregulatory hormones, cortisol, catecholamines (epinephrine and norepinephrine),
and growth hormone. These hormones shift the metabolism of carbohydrate, protein, and lipids; and further increase hepatic glucose production,
ketogenesis, and peripheral insulin resistance, thereby worsening acidosis
and dehydration. The acidosis and dehydration in turn accelerate the development of DKA by further stimulating increase in the counterregulatory
hormones. This cycle is responsible for the development of severe ketoacidosis.
The classic triad of DKA is hyperglycemia, ketosis, and acidosis. Presenting symptoms include polyuria polydipsia, weight loss, abdominal pain,
nausea, vomiting, tachycardia, and hypoperfusion (cool extremities, decreased capillary refill, dry mucous membranes, poor skin turgor). The following lab criteria are used to diagnose DKA: blood glucose >250 to 300
mg/dL, pH <7.3, serum bicarbonate <15mEq/L, urinary ketones >3+,
serum ketones positive. Furthermore, there is a high anion gap metabolic
acidosis due to the ketoacids. Severe DKA should be treated as a potentially
life-threatening condition, thus frequent monitoring of patient status, and
accurate intake and output, electrolytes, and blood pH is crucial.
The initial interventions should be
1. To ensure adequate ventilation and cardiovascular function and satisfactory mental status. If there is hemodynamic instability, inability to protect the airway, and obtundation, this is severely decompensated diabetes
should be managed in the intensive care unit (ICU).
2. Correctfluiddeficitsandelectrolytedisturbanceswithfluidtherapy.This
includes frequent monitoring and blood work every 1 to 2 hours.
3. Continuous low-dose insulin to interrupt ketoacidosis and minimize osmotic diuresis.
4. Correct metabolic acidosis with fluids and insulin.
5. Treat any underlying cause (infection).
6. Monitor for complications.
Volume expansion should be initiated immediately (usually 10–20
mL/kg) with isotonic saline over 30 to 60 minutes. A recent study in 2004
showed most clinician's assessment of children with DKA often underestimate the severity of dehydration. If the child is obviously in shock or very
hypotensive or has poor perfusion (cap refill <3 seconds) then an extra
10 mL/kg should be bolused. The deficit (plus maintenance) should be corrected evenly over 24 to 48 hours and include losses from diarrhea, vomiting,
and osmotic diuresis. Potassium should be added to the rehydration fluid,
usually by adding 30 to 40 mEq/L. The goal is to maintain potassium levels in the range of 4 to 5 mEq/L To prevent hypokalemia both from fluid
administration and insulin, the potassium level should be checked to prevent cardiac arrhythmias. Kidney function should also be checked before
administering any exogenous potassium.
Blood glucose will decline quickly during theearlytreatment ofDKAas
a result of volume expansion and insulin action. The same amount of glucose
in a larger extracellular volume allows the blood glucose to fall rapidly by 200
to 400 mg/dL/hr, or about 23%. This reduction is not dependent on insulin
administration or action. After the initial drop, a decline in blood glucose
level >100 mg/dL/hr should not be exceeded in the treatment of DKA
because more rapid correction of serum glucose concentration increases the
risk of cerebral edema. The optimal rate of decrease of serum glucose is 50
to 70 mg/dL/hr.
Becauseallpatientsareinastateofabsoluteorrelativeinsulindeficiency,
exogenous insulin must be provided during therapy. The insulin reverses
protein breakdown and lipolysis, and suppresses ketone body and ketoacid
formation, thus interrupting the excess production of acid. Insulin will also
lower blood glucose by inhibiting glycogenolysis and gluconeogenesis and
stimulating glucose uptake. IV insulin is clearly the route of choice for initial
therapy because the absorption of subcutaneous or intramuscular insulin
may be reduced or delayed.
The most effective means of insulin replacement is a continuous infusion of "low-dose" regular insulin (0.1 U/kg) followed by a continuous
infusion of 0.1 U/kg/hr (not to exceed 5–7 U/hr). This allows a steady state
of circulating insulin concentration. The insulin should be infused separately so the rate can be maintained separate from the rehydration fluid,
which then can be changed independently. It is wise to flush the tubing with
the insulin solution as some will adhere to the infusion tubing and bag.
The rate of insulin infusion should not be reduced because of falling
blood glucose in the absence of significant correction of the ketoacidotic
state. Instead dextrose should be added to the IV solution to maintain the
desired blood glucose level. A solution of 5% dextrose is added to the IV
fluids when plasma glucose level falls to <=250 mg/dL. This addition allows
continued administration of insulin until the acidosis and ketonemia have
resolved, and prevents iatrogenic hypoglycemia. One method to allow good
glycemic control is to have two glucose concentrations (0% and 10%), then
the rate of infusion of both bags can be adjusted to administer between 0%
and 10% glucose.
The insulin infusion should not be discontinued until the acidoses and
ketonemia have improved significantly and the anion gap is normal or near
normal. Resolution of ketosis and the attainment of a serum bicarbonate
level >=18mEq/L indicate that the IV insulin may be stopped. However
when converting to subcutaneous insulin, time must be allowed for steady
state. It is vital then to continue the IV insulin (half-life of 7 minutes) to
prevent rapid onset of hyperglycemia.
Complications of DKA include hypoglycemia, fluid overload causing
congestive heart failure and aspiration of gastric contents in those with altered mental status. The most morbid complication, however, is cerebral
edema (1%–2% of children). Although subclinical cases of cerebral edema
are evident on a computed tomography scan for many children in DKA,
the progression to fulminant cerebral edema is dire. Even with accurate and
careful management, symptomatic cerebral edema occasionally occurs in
children with severe DKA within 24 hours after therapy initiation without
any apparent cause. Although many mechanisms have been proffered, the
only correlating symptoms include high blood urea nitrogen concentrations
at presentation and more profound hypocapnia. The best treatment of cerebral edema is early mannitol (0.2–1 g/kg over 30 minutes) and decrease in
fluid administration rate with an immediate neurology consult and transfer
to the ICU. The signs and symptoms include headache, deteriorating level
of consciousness, development of seizures, recurrence of vomiting, and signs
ofincreasingintracranialpressure(hypertension,bradycardia,papilledema).
About one third of children with cerebral edema die, and one third are neurologically impaired.
Suggested Readings
Glaser N. Pediatric diabetic ketoacidosis and hyperglycemic hyperosmolar state. Pediatr Clin
North Am. 2005;52(6):1611–1635.
Magee MF, Bhatt BA. Endocrine and metabolic dysfunction syndromes in the critically ill. Crit
Care Clin. 2001;17(1):75–106.
White NH. Diabetic ketoacidosis in children. Endocrinol Metab Clin North Am. 2000;29(4):657–
682.
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Book Source Details
- Book Title: Avoiding Common Pediatric Errors
- Author(s): Anthony D Slonim MD, DrPH; Lisa Marcucci MD
- Year of Publication: 2008
- Copyright Details: Avoiding Common Pediatric Errors, Copyright © 2008 Lippincott Williams & Wilkins.
More About Diabetic Ketoacidosis
More Medical Textbooks Online about Diabetic Ketoacidosis
Review other book chapters online related to Diabetic Ketoacidosis:
Medical Books Excerpts
- Diabetes Mellitus
- "The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter" (2000)
- [ read ]
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Avoiding Common Pediatric Errors
Authors: Anthony D Slonim MD, DrPH; Lisa Marcucci MD
Publisher: Lippincott Williams & Wilkins
Copyright: 2008
ISBN: 0-7817-7489-6
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