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Diabetic ketoacidosis in adults: Rapid overview of emergency management

Diabetic ketoacidosis in adults: Rapid overview of emergency management
Clinical features
DKA usually evolves rapidly over a 24-hour period.
The earliest symptoms of marked hyperglycemia are polyuria, polydipsia, and weight loss. Common, early signs of ketoacidosis include nausea, vomiting, abdominal pain, and hyperventilation.
As hyperglycemia worsens, neurologic symptoms appear and may progress to include lethargy, focal deficits, obtundation, seizure, and coma.
Common causes of DKA include: infection, nonadherence, inappropriate adjustment or cessation of insulin, new-onset diabetes mellitus, and myocardial ischemia.
Evaluation and laboratory findings
Assess vital signs, cardiorespiratory status, and mental status.
Assess volume status: vital signs, skin turgor, oral mucosa, urine output.
Obtain the following studies: serum glucose, urinalysis and urine ketones, serum electrolytes, BUN and creatinine, plasma osmolality, mixed venous blood gas, electrocardiogram, serum ketones (if available; may be measured initially or if urine ketones present).
DKA is characterized by hyperglycemia, an elevated anion gap* metabolic acidosis, and ketonemia. Volume contraction and potassium deficits are often severe.
Serum glucose is usually ≥200 mg/dL (11.1 mmol/L) and less than 800 mg/dL (44.4 mmol/L). In certain instances (eg, insulin given prior to emergency department arrival, SGLT2 inhibitor use), the glucose may be normal or only mildly elevated (<200 mg/dL [11.1 mmol/L]).
Additional testing is obtained based on clinical circumstances to identify potential precipitants and may include: blood or urine cultures, lipase, chest radiograph.
Management
Stabilize the patient's airway, breathing, and circulation.
Obtain large bore IV (≥16 gauge) access; monitor using a cardiac monitor, capnography, and pulse oximetry.
Monitor serum glucose hourly, and basic electrolytes, BUN, creatinine, phosphorus, serum ketones, and venous pH or bicarbonate every 2 to 4 hours until the patient is stable.
Identify and manage any underlying cause of DKA (eg, pneumonia or urinary tract infection, myocardial ischemia, intentional withholding of insulin).
Replete ECF volume and free water deficits:
  • For patients with signs of shock, administer several liters of IV isotonic fluid (0.9% saline or buffered crystalloid) as rapidly as possible.
  • For patients with hypovolemia but without shock and without signs of cardiac or kidney compromise, administer IV isotonic fluid (0.9% saline or buffered crystalloid) at a rate of 0.5 to 1 L per hour for the first few hours.
  • For patients with mild hypovolemia, individualize fluid replacement.
  • After intravascular volume is restored:
    • If corrected serum Na is normal or elevated, give one-half isotonic saline (0.45%) at 250 to 500 mL/hour.
    • If corrected serum Na is low, continue isotonic saline until hyponatremia resolves.
  • Add dextrose (5 to 10%) to the saline solution when the serum glucose reaches <250 mg/dL (13.9 mmol/L).
Replete potassium (K+) deficits:
  • Regardless of the initial measured serum K+, most patients with DKA have a large total body K+ deficit.
  • Manage replacement based on initial serum K+ value:
    • <3.5 mEq/L – Delay initiation of insulin and give potassium chloride 10 to 20 mEq per hour IV until K+ concentration is >3.5 mEq/L; rarely, additional potassium supplementation may be necessary to avoid life-threatening muscle weakness and cardiac arrhythmias.
    • 3.5 to 5.0 mEq/L – Give potassium chloride 10 to 20 mEq per liter IV fluid; maintain serum K+ between 4 to 5 mEq/L.
    • >5.0 mEq/L – Do not give potassium; check serum K+ every 2 hours; administer potassium chloride as needed to maintain serum K+ between 4 and 5 mEq/L.
Give insulin:
  • For patients with K+ <3.5 mEq/L, do not give insulin; replete K+ and fluid deficit first.
  • For patients with K+ ≥3.5 mEq/L, give regular insulin using either regimen:
    • Fixed-rate continuous IV infusion 0.1 units/kg per hour (if establishing venous access is delayed, administer an IV 0.1 unit/kg bolus prior to continuous infusion).
    • Variable-rate continuous IV infusion determined by a nurse-driven protocol.
  • For fixed-rate insulin infusion:
    • If serum glucose does not fall by at least 50 to 70 mg/dL (2.8 to 3.9 mmol/L) in the first hour, double the rate of insulin infusion.
    • When serum glucose is <250 mg/dL (13.9 mmol/L), decrease the infusion rate to 0.05 units/kg per hour. Adjust rate further as needed to maintain glucose at approximately 200 mg/dL (11.1 mmol/L).
  • Continue insulin infusion until ketoacidosis is resolved, serum glucose is below 200 mg/dL (11.1 mmol/L), and subcutaneous insulin is begun.
Bicarbonate and phosphate (rarely indicated)
  • If the arterial pH is <7.0, give 100 mEq of sodium bicarbonate in 400 mL sterile water over 2 hours; if serum potassium is <5.0 mEq/L, add 20 mEq potassium chloride. Bicarbonate administration may be repeated as needed to raise pH to >7.0.
  • If serum phosphate is <1 mg/dL, add 20 to 30 mEq potassium phosphate to IV fluids.
For monovalent ions, 1 mEq/L = 1 mmol/L.

BUN: blood urea nitrogen; DKA: diabetic ketoacidosis; ECF: extracellular fluid; IV: intravenous; K+: potassium; Na+: sodium; SGLT2: sodium-glucose cotransporter 2.

* Patients with DKA usually present with a serum anion gap greater than 20 mEq/L (normal range approximately 3 to 10 mEq/L). However, the increase in anion gap is variable and determined by several factors: the rate and duration of ketoacid production, the rate of metabolism of the ketoacids and their loss in the urine, and the volume of distribution of the ketoacid anions.

¶ Serum Na+ should be corrected for hyperglycemia; for each 100 mg/dL serum glucose exceeds 100 mg/dL (5.5 mmol/L), add 2 mEq to plasma Na+ for correction of Na+ value for hyperglycemia. A calculator to determine serum Na+ corrected for hyperglycemia is available separately in UpToDate.
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