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Department of Pediatrics : Academic Divisions : Emergency Medicine : Resident Manual : Pediatric ED Treatment Guidelines : Diabetic Ketoacidosis in Children

Definition:

Blood bicarbonate < 15 mmol/l
   and/or
pH < 7.25 (< 7.3 if arterial or capillary)

Pathophysiology of DKA

Pathophysiology of DKA

Clinical manifestations:

Polyuria, polydipsia, signs of dehydration, deep sighing respirations to reduce pCO2 and buffer acidosis, and progressive obtundation leading to coma.

Severity of DKA:

Table 1:

DegreeVenous pH% dehydration
Mild7.2 to 7.24< 5 %
Moderate7.1 to < 7.25 to < 10 %
Severe< 7.110 % or greater


Note: Increased serum urea nitrogen and hematocrit may be useful markers of the severity of extracellar fluid loss.

Management of DKA

See standing order form.
Note:
Document fundoscopic examine to rule out papilledema.
Normal to increased temperature may indicate infectious cause to DKA.

Calculations:

  • Anion gap = Na - (Cl + HCO3); normal is 12 ± 2 mmol/l
  • Corrected sodium = measured Na + 1.6 × [(measured glucose mg/dl - 100) ÷ 100]
  • Body Surface Area (m²) = square root of {[Height (cm) × Weight (kg)] divided by 3600}
  • Maintenance fluids (ml/hr) = (0-10kg) × 4 + (11-20kg) × 2 + (21-measured wt kg) × 1

Fluid and electrolyte losses in DKA

Table 2 - Usual losses of fluids and electrolytes in DKA and normal maintenance requirements

 Average losses per kg (range)Maintenance requirements
Water70 (30-100) ml1,500 ml/m²
Sodium~6 (5-13) mmol45 mmol/m²
Potassium~5 (3-6) mmol35 mmol/m²
Chloride~4 (3-9) mmol30 mmol/m²
Phosphate~0.5-2.5 mmol0.5-1.5 mmol/kg*


Table 3 - Fluid and electrolyte losses based on assumed 10% dehydration in a child (weight 30 kg, surface area 1 m²) with DKA

Fluid and electrolyteApproximate accumulated losses with 10% dehydrationApproximate requirements for maintenance
(48 h)
Working total (48 h)
Water (ml)3,0003,0006,000
Sodium (mEq)18090270
Potassium (mEq)15070220
Chloride (mEq)12060180
Phosphate (mmol)752095


Fluid therapy

First hour:

Uncompensated shock [hypotension per age: < 1yr = < 70 mmHg, 1 -10 yrs = < (70 mmHg + 2 x age in years), > 10 yrs = < 90 mmHg] administer NS 20ml/kg rapid bolus. If hypotension not corrected after three 20ml/kg rapid infusions, consider other non-hypovolemia causes for hypotension; septic shock, heart failure or obstructive causes (tension pneumothorax or pericardial tamponade).

Compensated shock (tachycardia, tachypnea, narrow pulse pressure, altered mental status, capillary refill > 3 seconds, cool extremities, normal systolic BP) administer NS 20ml/kg over 30 to 60 minutes. If no improvement in clinical signs of compensated shock after three 20ml/kg fluid boluses, consider non-hypovolemia causes of shock as above.

No signs of shock administer NS 10ml/kg over 1 hour. Monitor output (urine and emesis). If output approaches or exceeds input in the 1st hour, repeat NS bolus over the second hour at the appropriate rate.

Second Hour:

Administer NS + 20mEq potassium acetate per liter + 20mEq potassium phosphate per liter at 2 x maintenance rate. Write order for this fluid at the beginning of the first hour. Note: regular insulin drip 0.1 units/kg/hr is started at the second hour.

After the second hour:

Continue NS + 20mEq potassium acetate per liter + 20 mEq potassium phosphate per liter at 2 x maintenance rate until serum glucose decreases to 300 mg/dl. At this time change to D5 0.45 NaCl + 20mEq potassium acetate per liter + 20 mEq potassium phosphate per liter at 2 x maintenance rate. Write order for this fluid at the beginning of the second hour.

Insulin

The plasma glucose concentration typically decreases at a rate of 54-90 mg/dl/hr. To prevent an unduly rapid decrease in plasma glucose concentration and hypoglycemia, 5% glucose should be added to the intravenous fluid when the plasma glucose falls to 300 mg/dl. If blood glucose falls very rapidly (> 90 mg/dl/hr) after the initial period of volume expansion, consider adding glucose even before plasma glucose has decreased to 300 mg/dl. It may be necessary to use 10% or even 12.5% dextrose to prevent hypoglycemia while continuing to infuse insulin to correct the metabolic acidosis. If the patient demonstrates marked sensitivity to insulin (e.g., some young children with DKA and patients with hyperglycemic hyperosmolar syndrome), the dose may be decreased to 0.05 units/kg/hr, or less, provided that metabolic acidosis continues to resolve. If biochemical parameters of DKA (pH, anion gap) do not improve, reassess the patient, review insulin therapy, and consider other possible causes of impaired response to insulin (e.g., infection, errors in insulin preparation). If no obvious cause is found, increase the insulin infusion rate and adjust the rate of glucose infusion as needed to maintain a glucose concentration of 300 mg/dl.

Table 4 - Insulin regimens for newly diagnosed diabetes after resolution of DKA

PrepubertalTDD 0.75-1.0 unit/kg
PubertalTDD 1.0-1.2 unit/kg
Before breakfastTwo-thirds of TDD
  • One-third rapid-acting insulin*
  • Two-thirds intermediate-acting insulin
Before dinner
  • One-third to one-half of the remainder of the TDD as rapid-acting insulin*
Before bedtime
  • One-half to two-thirds of the remainder of the TDD as intermediate-acting insulin
An alternative, basal-bolus method consists of administering
  • One-half of the TDD as basal insulin (using insulin glargine)
AND
  • One-half of the TDD as rapid-acting insulin; the dose before each meal comprises ~15Ð20% of the TDD


* In infants, toddlers, and preschool-age children, some clinicians use relatively smaller proportions of rapid-acting insulin before breakfast and dinner (e.g., one-quarter to one-third rather than one-third to one-half) and relatively larger amounts of intermediate-acting insulin. TDD, total daily dose.

Potassium

Children with DKA suffer total-body potassium deficits of the order of 3-6 mmol/kg. The major loss of potassium is from the intracellular pool. Intracellular potassium is depleted because of transcellular shifts of this ion caused by hypertonicity. Increased plasma osmolality results in osmotic water transport from cells to the ECF, thereby concentrating cellular potassium. As a result of the increased potassium gradient, potassium is drawn out of cells. Glycogenolysis and proteolysis secondary to insulin deficiency also cause potassium efflux from cells. Acidosis may play a minor role in the distribution of potassium to the ECF.

Potassium is lost from the body as a consequence of vomiting, urinary ketoanion excretion (which requires excretion of cations, particularly sodium and potassium), and osmotic diuresis. Volume depletion causes secondary hyperaldosteronism, which promotes urinary potassium excretion. Thus, total-body depletion of potassium occurs, but at presentation serum potassium levels may be normal, increased, or decreased. Renal dysfunction, by enhancing hyperglycemia and reducing potassium excretion, contributes to hyperkalemia. Administration of insulin and the correction of acidosis drive potassium back into the cells, decreasing serum levels. The serum potassium concentration may decrease abruptly, predisposing the patient to cardiac arrhythmias.

Potassium replacement therapy is required regardless of the serum potassium concentration; start replacing potassium after initial volume expansion and concurrent with starting insulin therapy. However, if the patient is hypokalemic, start potassium replacement immediately after initial volume expansion and before starting insulin therapy. If the patient is hyperkalemic, defer potassium replacement therapy until urine output is documented. The starting potassium concentration in the infusate should be 40 mmol/l; subsequent potassium replacement therapy should be based on serum potassium measurements. Potassium administration should continue throughout the period of intravenous fluid therapy. Potassium phosphate may be used together with potassium acetate (e.g., 20 mmol/liter potassium phosphate + 20 mmol/liter potassium acetate.

Acidosis

Severe acidosis is reversible by fluid and insulin replacement. Controlled trials have shown no clinical benefit from bicarbonate administration, and there are well-recognized adverse effects of bicarbonate therapy, including paradoxical CNS acidosis and hypokalemia from rapid correction of acidosis. Failure to account for the sodium being administered and appropriately reducing the NaCl concentration of the fluids can result in increasing osmolality. Nevertheless, there may be selected patients who may benefit from cautious alkali therapy. These include patients with severe acidemia (arterial pH <6.9), in whom decreased cardiac contractility and peripheral vasodilatation can further impair tissue perfusion, and patients with life-threatening hyperkalemia.

Cerebral edema

Symptomatic cerebral edema occurs in 0.5-1% of pediatric DKA episodes. This complication has a high mortality rate (21-24%), and a substantial percentage of survivors (15-26%) are left with permanent neurological injury.

Symptoms and signs of cerebral edema:

  • Headache
  • Recurrence of vomiting
  • Inappropriate slowing of heart rate
  • Rising blood pressure
  • Decreased oxygen saturation
  • Change in neurological status:
    • Restlessness, irritability, increased drowsiness, incontinence
    • Specific neurologic signs, e.g., cranial nerve palsies, abnormal pupillary responses, posturing

Risk factors

Children at greatest risk for symptomatic cerebral edema are those who present with high blood urea nitrogen concentrations and those with more profound acidosis and hypocapnia. A lesser rise in the measured serum sodium concentration during treatment (as the serum glucose concentration falls) has also been associated with cerebral edema. Treatment with NaHCO3 is also associated with an increased risk of cerebral edema.

Treatment of cerebral edema

Because cerebral edema occurs infrequently, data are limited regarding the effectiveness of pharmacological interventions for treatment of cerebral edema. Case reports and small case series suggest that prompt treatment with mannitol (0.25-1 g/kg) may be beneficial. Recent case reports also propose the use of hypertonic saline (3%), 5-10 ml/kg over 30 min, as an alternative to mannitol. Intubation may be necessary to protect the airway and insure adequate ventilation; however, hyperventilation (pCO2 <22 mmHg) in intubated patients with DKA-related cerebral edema has been correlated with poorer neurological outcomes. In intubated patients, therefore, hyperventilation beyond that which would normally occur in response to metabolic acidosis should likely be avoided unless absolutely necessary to treat elevated intracranial pressure.

References

  1. Wolfsdorf J, Glaser N, Sperling MA. Diabetic Ketoacidosis in Infants, Children, and Adolescents. A consensus statement from the American Diabetes Association. Diabetes Care. 2006,29:1150-1159.
  2. Dunger DB, Sperling MA, Acerini CL, et al. European Society for Paediatric Endocrinology/Lawson Wilkins Pediatric Endocrine Society Consensus Statement on Diabetic Ketoacidosis in Children and Adolescents. Pediatrics. 2004,113:e133-140.
  3. Glaser N, Barnett P, McCaslin I, et al. Risk Factors for Cerebral Edema in Children with Diabetic Ketoacidosis. NEJM. 2001,344:264-269.


Institute per Standing Order Policy (C-68)

Age ________   Weight: ________ kg   Height: ________ cm

  1. For patients with suspected diabetic ketoacidosis, follow the medical directive for suspected diabetic ketoacidosis.
    1. Initiate INT (intermittent access IV)
    2. Perform the following labs:
      • POCT: Blood glucose, VBG, sodium, potassium
      • HgbA1C
      • BMP, Mg, Phos, Ionized Ca
      • CBC with diff
      • Venous blood gas (VBG)
    3. Report POCT results to physician (blood glucose, VBG, sodium and potassium)
    4. Initiate IVF 0.9 % NaCl at rate per physician order _______ ml/hr
    5. Collect clean catch urine, perform dip urinalysis and report results to physician
    6. Insert heparin lock for phlebotomy in extremity not used for IV fluids
    7. Document time, size, site and rate for IVÕs
    8. Document Input and Output
  2. For patients with new-onset diabetes with hyperglycemia follow the medical directive for new-onset diabetes with hyperglycemia:
    1. Initiate INT (intermittent access IV)
    2. Draw the following labs:
      • POCT: Blood glucose, VBG, sodium, potassium
      • HgbA1C
      • BMP, Mg, Phos, Ionized Ca
      • CBC with diff
      • TSH, T4-Free, anti-insulin antibody, anti-GAD antibody, anti-islet cell antibody, ICA 512, C-peptide
      • Venous blood gas (VBG)
    3. Report POCT results to physician (blood glucose, VBG, sodium and potassium)
    4. Initiate IVF 0.9 % NaCl at rate per physician order _______ ml/hr
    5. Collect clean catch urine, perform dip urinalysis and report results to physician
    6. Insert heparin lock for phlebotomy in arm not used for IV fluids
    7. Document time, size, site and rate for IVÕs
    8. Document Input and Output



RN initiating orders signature __________________   Date _______   Time ______ AM/PM


Physician Signature ________________ Pager ID _______ Date _______ Time _____ AM/PM

(must be countersigned within 24 hours)
 
 
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