This excellent resource has the clinical lab values in SI units rather than in the conventional units used in the United States. U.S. clinicians can use the Conventional and SI unit Converter for common lab values from Global RPH.
Today, I review, link to, and excerpt from The Canadian Paediatric Society’s Current recommendations for management of paediatric diabetic ketoacidosis. [PubMed Abstract] [Full-Text HTML] [Full-Text PDF]. Paediatr Child Health. 2023 May 4;28(2):128-138. doi: 10.1093/pch/pxac119. eCollection 2023 May.
All that follows is from the above resource.
Abstract
Treatment of paediatric diabetic ketoacidosis (DKA) includes careful attention to fluids and electrolytes to minimize the risk of complications such as cerebral injury (CI), which is associated with high morbidity and mortality. The incidence of cerebral edema in paediatric DKA has not decreased despite the use of fluid-limiting protocols based on restricting early fluid resuscitation. New evidence suggests that early isotonic fluid therapy does not confer additional risk and may improve outcomes in some patients. Protocols and clinical practice guidelines are being adjusted, with a particular focus on recommendations for initial and ongoing fluids and electrolyte monitoring and replacement. Initial isotonic fluid resuscitation is now recommended for all patients in the first 20 to 30 minutes after presentation, followed by repletion of volume deficit over 36 hours in association with an insulin infusion, electrolyte supplementation, and careful monitoring for and management of potential CI.
Keywords: Cerebral edema; Cerebral injury; Diabetes mellitus; Diabetic ketoacidosis; Paediatric.
© Canadian Paediatric Society 2023. Published by Oxford University Press on behalf of the Canadian Paediatric Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
BACKGROUND
Diabetic ketoacidosis (DKA) is defined by the presence of
hyperglycemia, ketosis, and acidosis as measured by serum
pH or bicarbonate (Table 1) (1,2). DKA can occur in any
patient with an absolute or relative insulin deficiency. Risk
factors for DKA include younger age, lower socioeconomic
status, and delayed diagnosis in new patients. For children
and youth with known diabetes, additional risk factors include previous DKA, poor glycemic control, unrecognized
insulin pump malfunction, infection, some medications
(e.g., long-acting insulin analogues, atypical antipsychotics,
glucocorticoids), ethnicity, limited access to care, coexisting
mental health or social and family issues, peripubertal stage,
and adolescence (1,3).
CL I N I C A L P R E S E N TAT I O N A N D D I A G N O S I S
In DKA, hyperglycemia leads to urinary losses of both water
and electrolytes, resulting in volume depletion and metabolic
disturbances. Low insulin levels reduce glucose utilization, and
subsequent cellular glycopenia triggers increased glucagon release, lipolysis, and oxidation of free fatty acids, with ensuing ketoacidosis(4,5). Serum potassium may be normal or elevated due to extracellular shifts, but total body potassium is invariably low due to osmotic diuresis and active urinary excretion. DKA should be differentiated from hyperosmolar hyperglycemic state, which is characterized by more severe volume depletion and extreme electrolyte imbalances in the absence of significant ketosis and acidosis.Presenting symptoms of DKA may include polyuria, polydipsia, polyphagia, weakness, nausea, vomiting, abdominal pain,
decreased level of consciousness, Kussmaul breathing, and acetone breath.Initial clinical assessment should include ABCDs and evaluation of tachypnea and altered breathing patterns, perfusion, fluid balance, and level of consciousness. Further evaluation should solicit history of precipitating factors (e.g., infection,
intoxication) and medication adherence for individuals with
known diabetes. Assessing volume depletion can be difficult, with substantial inter-rater variability (6–8). For fluid
calculations, it is suggested to use a minimum of 5% depletion
for a patient with mild DKA, or 7% to 10% for more severe
DKA (1).
From StatPearls article on pediatric DKA:
CEREBRAL INJURY IN DKA
Cerebral injury (CI) occurs more commonly in children than
adults (3,4,9–12) (Table 3).
The frequency of clinically significant CI may be as high as 1%, and those individuals experience a morbidity between 21% and 25% and a mortality between 21% and 24% (3,13). Clinical CI is more frequent in severe DKA (9–11) and may be present before treatment is initiated (10,14,15) (Table 4).
Although patients with DKA present with volume depletion, intravenous (IV) fluids have traditionally been restricted
in paediatric patients out of concern for potentiating CI (16).
As an alternative to the traditional osmotic hypothesis of CI,
cerebral hypoperfusion and reperfusion likely play a significant
role in DKA-related CI. Several levels of evidence, including
computed tomography (CT), magnetic resonance imaging, and
cerebral blood flow studies, have shown changes in biochemical
markers and progression from cytotoxic to vasogenic edema
(17–19).MANAGEMENT RECOMMENDATIONS
Treatment of DKA includes progressive volume expansion and
a careful reduction in plasma glucose. The diagnosis of DKA should be confirmed (Table 1) before initiating anyvinterventions.
From Pediatric Diabetic Ketoacidosis from StatPearls:
According to the International Society for Pediatric and Adolescent Diabetes, DKA is defined by the presence of all of the following in a patient with diabetes:
It is important to remember that DKA in children is managed differently than in adults. The differences to consider in paediatric patients include (3,4):
• Extra caution when administering IV fluids
• Initiating insulin only after IV fluids
• Replacing potassium earlier and more aggressively
• Avoiding insulin boluses and sodium bicarbonateGoals for management are to:
• Correct volume depletion
• Correct acidosis
• Stop ketogenesis
• Correct electrolyte imbalances
• Restore normal blood glucose
• Monitor for and prevent complications (CI, hypoglycemia, symptomatic electrolyte deficiencies, hyperchloremic acidosis)
• Manage coexistent illness or precipitating factorsFluids
All patients with DKA require careful monitoring and attention
to fluid administration, particularly children and youth at higher risk for CI. In paediatric patients without clinical symptoms of CI, no harm has been demonstrated by using more liberal initial fluid resuscitation, with the primary goal of improving tissue perfusion (13,20,21).Both saline and balanced crystalloids are appropriate for use
as IV fluids in DKA. Balanced crystalloids (e.g., Ringer’s lactate,
Plasmalyte) are recognized as safe alternatives to saline for both
bolus and ongoing infusions and may minimize hyperchloremic
metabolic acidosis, as well as potentially reduce CI and renal
injury (22–25). While ongoing therapy with 0.45% NaCl with
dextrose and added potassium can be safe for most patients with
DKA and a normal neurologic status, hypotonic fluids should be
avoided in all patients with symptoms of CI.Specific fluid recommendations for DKA include the following:
• Administer 10 mL/kg to 20 mL/kg (to a maximum 1,000
mL) of isotonic fluid with 0.9% NaCl or a balanced crystalloid for all patients over 20-30 minutes, regardless of hemodynamic status.
• In settings of hypotension or compensated shock, give a
fluid bolus within 10 to 15 minutes and administer additional isotonic fluid rapidly, in 10 mL/kg increments to a maximum of 40 mL/kg, in consultation with a paediatric intensivist.
• After the initial isotonic fluid bolus(es), calculate a starting hourly fluid rate to incorporate both maintenance and deficit fluids, based on replacing an assumed 10% deficitover 36 hours (26) (Table 5). Administering twice the usual rate of maintenance fluids is generally safe until
the detailed fluid calculation is completed. Changes in
the hourly rate may be considered for patients with less
severe volume depletion, and many can transition safely
from IV to oral rehydration when ketoacidosis has resolved.
Blood Glucose Conversion Chart From Alberta Health Services
Canadian value = U.S. value divided by 18 (mg/dl / 18 = mmol/L)
• Dextrose-free isotonic fluids should be continued with a goal of decreasing blood glucose by no more than 5 mmol/L/hour [90 mg/dl] until the glucose level is between 15 mmol/L [270 mg/dl] and 17 mmol/L [306 mg/dl]. At this point, dextrose (usually 5%) should be added and adjusted to maintain a blood glucose of 7 mmol/L [126 mg/dl] to 11 mmol/L [200 mg/dl]. This range of blood glucose helps minimize glucosuria, which occurs when the glucose level exceeds 12 mmol/L [216 mg/dl].
• A two-bag protocol, with each bag containing the same amount of electrolytes but only one containing dextrose,
can be used to quickly adjust administered dextrose concentration with finesse (and some cost saving) in response to blood glucose (Table 6) (27).
The second bag should (ideally) contain 12.5% dextrose to maximize peripheral venous delivery if needed, but 10% dextrose may also be used.
• Patients with mild DKA may be treated with reduced
amounts of IV fluids or oral fluids if they are tolerating enteral intake.Insulin
Insulin should be started only after the first hour of fluid
therapy (9) AND when potassium levels are >3.0 mmol/L, and
never as an IV bolus. Replace potassium before starting insulin if potassium levels are less than or equal to 3.0 mmol/L.• An infusion of rapid-acting insulin at 0.05 unit/kg/hour to 0.1 unit/kg/hour is preferred, without a weight-based maximum. However, intermittent subcutaneous insulin can be used if IV administration is not possible or in some cases of mild DKA, with the support of expert consultation.
• If blood glucose has been decreasing at a rate greater than 5 mmol/L/hour [90mg/dl] AND administration of IV dextrose has been maximized, reduce insulin infusion to 0.05 unit/kg/hour.
• A further gradual decrease to no less than 0.025 unit/kg/
hour can be considered if blood glucose continues to fall
rapidly, or as a bridge until the next mealtime (and associated subcutaneous insulin dose) if acidosis has corrected.Electrolytes
Patients with DKA present with a relative or total body deficiency of sodium, potassium, phosphate, and magnesium.
Hyperglycemia results in factitious hyponatremia but measured
Na can be used to calculate the initial anion gap (28). Assessment and decision-making should be based on the corrected serum sodium (corrected sodium = measured sodium + [{glucose—5} × 0.3]). An elevated corrected sodium indicates more severe volume depletion. Corrected sodium levels should be carefully monitoredbecause a decrease (or increase) of more than 2 mmol/L/hour to 3 mmol/L/hour may indicate excessive (or inadequate) fluid resuscitation, with increased risk for CI or acute kidney injury (29,30).DKA treatment lowers serum potassium levels, and supplemental potassium of at least 40 mmol/L should be added to IV fluids when measured potassium is <5 mmol/L [5 mmol/L and 5 mEq/L are both units of measurement for potassium levels in the blood, and they are equivalent: Explanation: 1 millimole (mmol) is equal to 1 milliequivalent (mEq).] and after recent urine output is documented.
Serum phosphate may be normal or high despite a total body
deficit. Insulin therapy will lower serum phosphate. Consider
replacement if measured phosphate is below 0.5 mmol/L [One millimole (mmol) of phosphate is equal to two milliequivalents (mEq) of HPO3. The milliequivalent unit is used to measure the concentration of ions, and it takes into account both the ion’s concentration and its charge. For ions with a charge of one, like sodium (Na+), one milliequivalent is equal to one millimole.] , or if there are concerns of cardiac dysfunction, respiratory failure, gastrointestinal dysmotility, or metabolic encephalopathy (31,32). Follow local protocols for phosphate administration.Sodium bicarbonate should not be given as a treatment for
metabolic acidosis because it increases the risk for CI (25).
Adequate treatment with fluids and insulin is sufficient for the
correction of acidosis, unless indicated as part of active cardiopulmonary resuscitation or symptomatic hyperkalemia.Monitoring and treatment of cerebral edema
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