Management of Children with Diabetic Ketoacidosis

Disclaimer: The information on this page is not intended for use by patients. Professionals must still exercise their own professional judgment in determining the course of treatment for any individual patient.

Appropriate treatment for all children with Diabetic Ketoacidosis (DKA) CANNOT be summarized in a single set of guidelines.  There is no substitute for repeated clinical and laboratory evaluations to ensure that problems are promptly recognized and therapeutic measures are administered appropriately. Deviation from this protocol may, at times be appropriate.

These guidelines are applicable to children with type 1 diabetes and true DKA. The treatment of hyperosmolar coma with mild or no ketosis is similar during the initial resuscitation, but may be different than stated here as treatment progresses.

Outline

Phase I – Initial Assessment and Resuscitation

1. Assessment
2. Diagnosis of DKA
3. Mandatory Initial Orders
4. Optional Initial Orders

Phase II – Correct Acidosis and Identify Cause

1. Ongoing Care
2. Monitoring and Adjusting Therapy
3. Complications

Phase III – Post Resolution Management

1. Transition to Subcutaneous Insulin
2. Before Discharge

Phase I – Initial Assessment and Resuscitation

A.  Assessment

• Airway and Breathing – rarely a concern
• Circulation – Usually 7-10% dehydrated
• Neurological state – Rapid assessment – expect improved level of consciousness with initial resuscitative measures

B. Diagnosis of DKA

• Biochemical Criteria
  • Moderate - pH<7.20-7.30 AND large ketonuria OR elevated serum ketones
  • Severe - pH<7.11-7.20 AND large ketonuria OR elevated serum ketones
  • Critical - pH<7.11 AND large ketonuria OR elevated serum ketones
• Severity of DKA may be increased beyond that indicated by biochemical criteria by co-existing conditions (e.g. infection, renal failure, insulin resistance)

C.  Mandatory Initial Orders for Critical DKA

• Prepare for admission to PICU (unless instructed otherwise by attending physician)
• NPO
• EKG monitor
• Accurate fluid in and out totals
• Vital Signs q1h
• Neuro check q1h
• Bedside glucose check immediately and q1h
• Urinalysis (primarily for ketonuria and evidence of acute tubular necrosis)
• STAT electrolytes, creatinine, BUN, glucose, venous (or arterial) blood gas
• Isotonic crystalloid (e.g. 0.9% saline) – 10 mL/kg over 30-60 minutes (May repeat 10 mL/kg if required to improve perfusion)
• Insulin R - 0.1 U/kg/hr IV
  • Order right away, but do not start infusion until IV fluid bolus therapy is complete
  • MUST use infusion pump.
  • Flush tubing thoroughly with insulin solution before starting IV.
  • Rarely, hourly IM insulin R injections (0.1 U/kg) are preferred to IV infusion

Insulin Drip Choice A (Good choice for children over 20 kg)
Patients weight (in kg) = number of insulin units into a 100 mL bag of normal saline. Run at 10 mL/hour

Insulin Drip Choice B (Good choice for children under 20 kg)
Put 100 Units insulin in 100 mL normal saline. Run at [0.1 X Patient Weight(kg)] mL/hour

• EVEN IF pH<7.00, DO NOT INFUSE SODIUM BICARBONATE UNLESS INSTRUCTED BY ATTENDING PHYSICIAN

C.  Optional Initial Orders

• Insert n-g tube for vomiting or abdominal distension related to Kussmaul breathing
• 12-lead EKG to check for peak T waves at start of therapy from hyperkalemia
• STAT plasma osmolality, serum beta hydroxybutyrate, CBC with diff (expect high total wbc, neutrophilia, left shift, hemoconcentration)
• Studies to look for cause of DKA (e.g. infection, surgical problem) may be indicated

Phase II – Correct Acidosis and Identify Cause

A.  Ongoing Care

• Obtain more detailed history and complete full physical exam

Focus on recent history of insulin injection
Signs and symptoms of infection, injury, surgical problem
DKA can mimic surgical abdomen with high serum amylase/lipase

• Fluid Management
  As soon as peripheral perfusion is acceptable, reduce IV crystalloid rate to EITHER:

Choice A
-6 mL/kg/hour for the first 10 kg (3-10 kg)
-5 mL/kg/hour for the second 10 kg (11-20 kg)
-4 mL/kg/hour for the third 10 kg (21-30kg)
-2 mL/kg/hour for every kg over 30 kg

OR

Choice B

-3 liters/m2/day    Note:  body surface area

• When serum K+ concentration is available, patient has voided, and bolus fluid complete
  -Add K+ to IV as follows:

 If initial serum K+ >5.5             0 mEq

            If initial serum K+ 5.0-5.5         20 mEq Kphosphate/L

            If initial serum K+ 4.0-5.0         20 mEq Kphosphate/L AND 20 mEq KAcetate/L

            If initial serum K+ <4.0 30 mEq KPhosphate/L AND 30 mEq KAcetate/L

Notes: a) KCl can be substituted for KAcetate

            b) Never add more than 30 mEq Kphosphate/L (can precipitate hypocalcemia)

●When serum glucose <300 mg/dL

            Add glucose and reduce sodium chloride in IV as follows:

                        Hang 1 bag with D10/0.45% saline/appropriate K+

                        Hang a second bag with 0.45% saline/appropriate K+

                        Divide hourly fluid rate evenly between bags to yield 5% dextrose

B.  Monitoring and Adjusting Therapy

• Continue nursing monitoring as outlined above
• Check STAT electrolytes, creatinine, BUN, glucose, venous blood gas q2h (±plasma osmolality) until tCO2>10 and fluid infusion rates and serum electrolytes concentrations are stable. Then check blood q4h until patient eating.
• Specify notification orders using guidelines immediately below:

1) Serum sodium should rise with time

OR Corrected serum sodium should stay stable or rise slightly

Corrected ser Na+ = Measured sodium + 2[serum glucose(mg/dL)–100]
                                                                               100

If sodium does not track as expected, consider decreasing fluid rate or increasing sodium chloride content of IV

2)If accurate total CO2 concentration available with electrolytes, blood gas not necessary (often required if tCO2<10)

3) Rate of glucose decline is hard to control and NOT critically important

4) Maintain serum/blood glucose concentration 100-250 mg/dL

5) If serum/blood glucose approaching 100 mg/dL, increase IV glucose infusion rate to 7.5% dextrose by increasing rate of D10 bag and reciprocally decreasing bag with no dextrose.  Try to avoid decreasing insulin infusion rate.

6) Even subtle changes in neurological state could indicate cerebral edema. Apart from obvious signs of coma, specifically advise nurse to watch for:

• Sudden, persistent decrease in heart rate by >20 bpm from baseline that cannot be accounted for by sleep
• age-inappropriate incontinence
• fluctuating level of consciousness or altered mentation (e.g. confusion, combativeness, hallucinations, disorientation, etc.)
• new onset headache
• new onset vomiting
• temperature instability
• lethargy (not easily roused from sleep)
• new onset diastolic BP>90 mmHg

7) Expect tCO2 to remain stable or rise slowly for first 6 hours of therapy

If severe anion gap metabolic acidosis is not resolving by 6 hours, consider:

• inadequate insulin infusion (check calculations, consider hanging new infusion and check insulin level in old bag)
• occult infection
• unsuspected cause of acidosis (e.g. toxin)

C.  Complications

• Hypoglycemia
  • Blood glucose <40 mg/dL OR symptoms of low glucose with blood glucose <60 mg/dL
  • If patient NPO, give 0.25 g/kg IV glucose bolus and increase glucose infusion rate
  • If patient tolerating po fluids, treat with 15 g oral glucose (e.g. 4 oz orange juice)
  • Monitor response to treatment q20 minutes until blood glucose concentration is stable
• Hyperkalemia
  • Serum K+>6.0 mmol/L
  • Usually resolves with DKA treatment
  • Additional treatment only required if arrhythmia present
  • Rectal kayexelate solution
  • Resist use of sodium bicarbonate
• Hypokalemia
  • Serum K+<3.0 mmol/L
  • Can be prevented with aggressive K+ replacement
  • May require central venous line if requirement exceeds 60 mEq/L in replacement fluid
• Persistent Acidemia
  • If anion gap – see Monitoring and Adjusting Therapy – Number 7.”
  • If non-anion gap – commonly develops in second 12 hours of therapy
    In absence of renal disease, is usually related to infusion of high amounts of choride
    Is clinically insignificant and requires no special treatment
• Cerebral Edema
  • For signs and symptoms, see “Monitoring and Adjusting Therapy - Number 6.”
  • Can progress rapidly to herniation and brain death
  • If you suspect cerebral edema, order mannitol infusion to bedside and call attending physician STAT
  • In view of hyperosmolar state, low doses of mannitol do not change much. Recommended dose is therefore 1 g/kg infused IV over 20 minutes. Note mannitol will not be in solution unless bottle has been warmed to 37ºC.
  • Even if you are unsure of diagnosis, GIVE MANNITOL BEFORE sending patient for CT Scan!!!
• Mucormycosis
  • Usually fatal infection starting in respiratory tract or skin
  • Consider bronchoscopy in severely ill patient with pneumonia, despite mild abnormalities on CXR
  • Aggressive surgical management required for survival
• Pulmonary Edema
  • Usually asymptomatic
  • Does not usually require diuretics (risks of accelerated electrolyte loss)
  • ARDS is rare in children with DKA
• Rhabodmyolysis
  • possibly related to hypokalemia and hyperosmolarity
  • uncommon
  • treat with saline diuresis and urine alkalinization only if required

Phase III – Post Resolution Management

A.  Transition to Subcutaneous Insulin

• Time to start oral fluids and transfer out of PICU are CLINICAL decisions, not determined by lab results
• Patient’s first request for meal often precedes their ability to actually eat it by 1 mealtime (e.g. asks for lunch, but does not eat it; then eats dinner well)
• Do not give subcutaneous insulin until meal has actually been eaten
• Consult attending physician for initial subcutaneous insulin dose
  Principle is to use one time dose to cover interval from first meal until time for next routine injection (e.g. Injection with breakfast can be usual morning insulin dose. If first injection is right after lunch, may give mixture of rapid acting and short acting insulins to cover afternoon followed by usual dose given before supper)
• In uncomplicated cases, do NOT continue blood tests (other than routine blood glucose checks) once the patient has started eating.

B.  Before Discharge

• Ensure cause of DKA has been found and addressed
• If patient is newly diagnosed, ensure family has learned skills for home management
• Most frequent cause of DKA in patients with treated diabetes is BY FAR, omitted insulin injections
• Recurrent DKA may require intensive psychotherapy/referral for medical neglect
• Ensure discharge insulin dose is appropriate
• Ensure patient has all necessary supplies and follow-up appointment with diabetes team

Copyright 2002
Medical College of Georgia
All rights reserved.

Pediatric Endocrinology
Department of Pediatrics | Medical College of Georgia
Please email comments, suggestions or questions to:
Andrew Muir, M.D., amuir@mcg.edu

February 27, 2004