Rapid overview of the initial evaluation and treatment of moderate to severe diabetic ketoacidosis in children and adolescents

Clinical suspicion

DKA is the first presentation of diabetes in approximately one-third of children. Presenting symptoms:

Initial – Polyuria, polydipsia, weight loss, nocturia, enuresis (due to hyperglycemia), fatigue.
Subsequent – Nausea/vomiting, abdominal pain, fruity breath odor, Kussmaul breathing, sometimes altered consciousness.

Definition of DKA

DKA is defined by the presence of all of the following in a patient with diabetes:

Hyperglycemia – Blood glucose ≥200 mg/dL (11 mmol/L).
Metabolic acidosis – Venous pH <7.30 and/or serum bicarbonate <18 mEq/L.
Ketosis – Elevated levels of ketones in urine or blood*.

Note: Patients with marked hyperglycemia but with mild or minimal ketosis and acidosis may have HHS^¶, which is a metabolic emergency (refer to UpToDate content on HHS).

Laboratory assessment

Immediate (point-of-care) testing:

Blood glucose.
Urine ketones and/or blood BOHB* (if available).

Laboratory tests:

Serum glucose.
Serum electrolytes, bicarbonate, creatinine, urea nitrogen.
Venous (or arterial) pH and pCO₂.
Calcium, phosphorus, magnesium.
Hemoglobin A1c^Δ.
Blood BOHB*.
Urinalysis.

Severity of DKA:

Mild – pH 7.2 to 7.3, bicarbonate 10 to 18 mEq/L.
Moderate – pH 7.1 to 7.2, bicarbonate 5 to 10 mEq/L.
Severe – pH <7.1, bicarbonate <5 mEq/L.

Degree of dehydration: Patients with DKA are usually more dehydrated than suggested by the clinical examination. Initial fluid management should be based on:

If pH <7.1 (suggesting severe DKA), BUN >20 mg/dL, or new onset of diabetes – Assume approximately 8% dehydration.
All others – Assume approximately 6% dehydration.

Neurologic status: Patients with abnormal mental status may have cerebral injury (refer to complications below). Monitor mental status closely, and treat promptly if it fails to improve or worsens during initial treatment.

Management

Fluids:

Give 10 to 20 mL/kg of 0.9% NaCl (normal saline), or other isotonic solution, administered as an IV bolus over 20 to 30 minutes:

Mild DKA – 10 mL/kg bolus.
Moderate or severe DKA – 20 mL/kg bolus.

Give additional boluses if necessary, based on cardiovascular status. Larger fluid volumes are usually needed for patients presenting with mixed features of DKA and HHS (hyperosmolar DKA), regardless of the level of acidosis.

Hypovolemic shock is a rare occurrence in DKA; continued shock after initial fluid resuscitation should prompt evaluation for other causes, such as sepsis.

Following initial fluid resuscitation, replace the estimated fluid deficit over 24 to 48 hours, in addition to maintenance fluids. IV fluids with sodium content between 0.45 and 0.9% NaCl should be used as the replacement fluid.

Electrolytes:

Sodium: Serum sodium levels are generally low (due to dilutional effect of hyperglycemia) but may be normal or even high (due to water loss). If serum sodium is low, it should rise as hyperglycemia is corrected.

Potassium: The timing of potassium replacement depends on the initial serum potassium concentration^◊:

Low potassium (<3.5 mEq/L) – Add 40 mEq/L of potassium to IV fluids as soon as possible, and delay insulin therapy until serum potassium is in the normal range.
Normal potassium (3.5 to 4.5 mEq/L) – Add 40 mEq/L of potassium to IV fluids when insulin therapy is started.
High potassium (>4.5 mEq/L) – Monitor every hour and begin potassium replacement when serum potassium decreases to the normal range and when urine production or adequate kidney function is documented.
Provide potassium as a 1:1 mixture of potassium phosphate plus either potassium chloride or potassium acetate.

Insulin: After the initial fluid bolus is complete, begin a continuous insulin infusion at 0.1 units/kg per hour^§. Mix 50 units of regular insulin in 50 mL of saline (0.45 or 0.9% NaCl), such that 1 mL of the infusion provides 1 unit of insulin.

Glucose: Add dextrose to the IV fluids when the blood glucose falls below approximately 300 mg/dL (17 mmol/L) to prevent hypoglycemia during treatment^¥.

Monitoring

Monitor and record hourly:

Vital signs.
Neurologic status.
Fluid intake (IV and oral) and losses.

Laboratory monitoring:

Blood glucose hourly.
Electrolytes, venous pH and pCO₂ every 2 to 4 hours.
Calcium, phosphorous, and magnesium every 4 to 6 hours.

More frequent monitoring may be necessary for patients with severe electrolyte derangements or rapid changes in these laboratory values.

Complications

Cerebral injury:

Risk factors – Greater degrees of acidosis, hypocapnia, dehydration, and younger age.
Symptoms and signs – Monitor neurologic status carefully during the first 12 to 24 hours of DKA treatment. Suspicious symptoms include changes in mental status, new or worsening headache, recurrence of vomiting, and age-inappropriate incontinence^‡.
Initiate treatment promptly with 0.5 to 1 g/kg of mannitol if cerebral injury is suspected based on signs and symptoms. Do not rely on cerebral imaging to make or exclude the diagnosis.

Venous thrombosis: Avoid central venous catheters, if possible, because of increased risk for venous thrombosis in these patients.

Mild pancreatic enzyme elevations are common in patients with DKA; no specific therapy is needed other than correction of DKA unless other symptoms of pancreatitis are present.

This table outlines a typical protocol for management of DKA in an urgent care setting. Somewhat different approaches to fluid volumes and composition may be used, according to patient characteristics and clinician preference.

BOHB: beta-hydroxybutyrate; BUN: blood urea nitrogen; DKA: diabetic ketoacidosis; HHS: hyperglycemic hyperosmolar state; IV: intravenous; NaCl: sodium chloride; pCO₂: partial pressure of carbon dioxide.

* Ketosis is ideally determined by measuring serum BOHB in the laboratory or by a point-of-care device. BOHB concentrations ≥3 mmol/L (31 mg/dL) are consistent with DKA.

¶ HHS is defined by plasma glucose concentration >33.3 mmol/L (600 mg/dL), venous pH >7.25 (arterial pH >7.30), serum bicarbonate >15 mmol/L, minimal ketosis, and effective serum osmolality >320 mOsm/kg.

Δ Hemoglobin A1c is useful in patients with known diabetes to evaluate the degree of metabolic control or in rare cases in which the diagnosis of diabetes/DKA is uncertain.

◊ Regardless of the initial measured serum potassium concentration, patients with DKA have a total body potassium deficit and therapy with insulin and fluids will lower serum potassium concentration. Use of a mixture of potassium salts (potassium phosphate plus either potassium chloride or potassium acetate) is recommended to decrease chloride administration and replace phosphorus losses.

§ For mild DKA treated in the emergency department or in unusual circumstances where facilities to administer IV insulin are not readily available, subcutaneous insulin can be used.

¥ A "2-bag system" is a method to maintain the patient's blood glucose in an acceptable range. In this technique, 2 bags of the selected IV fluid solution are infused concurrently, one containing 10% dextrose and the other containing no dextrose. By adjusting the relative rates of fluid administration from each bag, the rate of fluid and electrolyte administration can be maintained constant, while varying the rate of dextrose infusion to respond to changes in the patient's blood glucose concentrations.

‡ Altered mental status in DKA can be caused by a variety of factors other than cerebral injury, including acidosis, other metabolic derangements, and sleep deprivation. Nonetheless, clinicians should maintain a high level of suspicion for evidence of cerebral injury and intervene promptly if the diagnosis is suspected. Refer to UpToDate content on signs and symptoms cerebral injury in DKA.

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Rapid overview of the initial evaluation and treatment of moderate to severe diabetic ketoacidosis in children and adolescents