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Emergency and Acute Medicine - Diabetic Ketoacidosis
Basics
Description Diabetic ketoacidosis (DKA) results from absolute or relative insulin deficiency with excess counterregulatory hormones (catecholamines, glucagon, growth hormone, cortisol). This leads to dehydration from osmotic hyperglycemic diuresis and reduced oral intake, anion gap metabolic acidosis, ketone formation from unrestrained lipolysis and ketogenesis, hyperglycemia from increased gluconeogenesis and glycogenolysis, and significant electrolyte disturbances including hypokalemia, hypo- or hypernatremia, and hypophosphatemia.
Etiology
Medication noncompliance is the most common cause. New-onset diabetes mellitus (type 1 or type 2) is a frequent presentation. Underlying medical illness increases counterregulatory hormones and insulin resistance, including infection, myocardial infarction, gastrointestinal bleeding, and central nervous system events. Pregnancy contributes through relative insulin deficiency. Medications such as protease inhibitors and atypical antipsychotics (e.g., olanzapine, clozapine) and alcohol abuse are additional contributors.
Diagnosis
Signs and symptoms Patients often report polyuria, polydipsia, weakness, abdominal pain, nausea, vomiting, chest pain, febrile illness, and medication noncompliance. Altered mental status may be present. Physical examination commonly reveals tachycardia, hypotension from dehydration or sepsis, tachypnea with hyperpnea, Kussmaul respirations, dehydration with poor skin turgor and dry mucous membranes, ketone odor on the breath, and diffuse abdominal tenderness. Temperature abnormalities may reflect infection.
Essential workup
Diagnostic criteria include venous pH <7.3, serum bicarbonate <15 meq />, hyperglycemia >250 mg/dL, and ketonemia or ketonuria. Initial evaluation requires bedside glucose testing, venous blood gas, serum electrolytes, BUN and creatinine, urine dipstick for ketones, and assessment for a precipitating cause.
Diagnosis tests & interpretation
Lab Serum glucose confirms hyperglycemia. Electrolytes show an increased anion gap metabolic acidosis [Na − (Cl + HCO₃)] >12. Serum sodium may be falsely low due to hyperglycemia and should be corrected by adding 1.6 mEq/L for every 100 mg/dL glucose above 100 mg/dL. Potassium is often normal or elevated initially due to extracellular shift, despite a total body deficit of 3-5 mEq/kg; levels fall rapidly with insulin and fluids. Bicarbonate is typically markedly reduced. BUN and creatinine reflect prerenal azotemia from dehydration. Serum ketones must be present; β-hydroxybutyrate predominates and may be underestimated by nitroprusside testing. Urine ketone dip testing is highly sensitive, and point-of-care β-hydroxybutyrate testing can aid early diagnosis. CBC often shows stress leukocytosis. Serum osmolality may be elevated (>320 mOsm/L). Imaging includes chest radiography for suspected pneumonia, ECG to assess ischemia or potassium abnormalities, and head CT if altered mental status is unexplained.
Differential diagnosis
Other causes of anion gap metabolic acidosis include alcoholic ketoacidosis, lactic acidosis, toxic ingestions (salicylates, methanol, ethylene glycol), uremia, starvation or sepsis, and hyperglycemic hyperosmolar nonketotic syndrome.
Treatment
Pre hospital Early fluid resuscitation is often initiated; total prehospital volume should be documented to guide ongoing therapy.
Initial stabilization/therapy Address airway, breathing, and circulation, particularly in patients with altered mental status. Administer supplemental oxygen as needed and give an initial bolus of 0.9% normal saline for hypotension or tachycardia.
Ed treatment/procedures Continuous cardiac monitoring and pulse oximetry are required for unstable patients. Fluid therapy assumes a total deficit of approximately 100 mL/kg. Administer 1–2 L of 0.9% normal saline in the first hour. Continue isotonic saline if corrected sodium is low, or switch to 0.45% saline if corrected sodium is normal or high. Replace the remaining deficit gradually over 24–36 hours to avoid rapid osmolar shifts. Insulin therapy is initiated with continuous IV regular insulin at 0.1 U/kg/h after confirmation of DKA and adequate potassium levels, titrated to close the anion gap rather than normalize glucose alone. Add dextrose-containing fluids when serum glucose falls below 250–300 mg/dL. Potassium replacement is essential once urine output is established and serum potassium is <5.5 meq />; insulin should be delayed if potassium is <3.5 meq />. Bicarbonate therapy is generally avoided and reserved only for severe acidosis (pH <6.9) with cardiovascular compromise. phosphate and magnesium replacement are not routine but may be required in severe deficiencies. the underlying precipitating cause must identified treated.< />pan>
Medication
Regular insulin infusion at 0.1 U/kg/h IV. Potassium chloride supplementation as indicated. Dextrose-containing IV fluids once glucose levels decline. Magnesium sulfate or phosphate replacement when clinically necessary.
Follow-up disposition
Admission criteria ICU admission is required for severe DKA with pH <7.0, altered mental status, hemodynamic instability, serious comorbid illness, or extremes of age. moderate dka may be managed in a monitored unit, while mild cases without complications observed.< />pan>
Discharge criteria Resolution of anion gap acidosis, tolerance of oral intake, stable vital signs, no ongoing precipitating illness, and reliable follow-up with clear insulin instructions.
Pearls and pitfalls
Insulin infusion should not be reduced or stopped solely because glucose normalizes; it must continue until acidosis and anion gap resolve. Failure to aggressively monitor and replace potassium is a common and dangerous error.
Basics
Description Diabetic ketoacidosis (DKA) results from absolute or relative insulin deficiency with excess counterregulatory hormones (catecholamines, glucagon, growth hormone, cortisol). This leads to dehydration from osmotic hyperglycemic diuresis and reduced oral intake, anion gap metabolic acidosis, ketone formation from unrestrained lipolysis and ketogenesis, hyperglycemia from increased gluconeogenesis and glycogenolysis, and significant electrolyte disturbances including hypokalemia, hypo- or hypernatremia, and hypophosphatemia.
Etiology
Medication noncompliance is the most common cause. New-onset diabetes mellitus (type 1 or type 2) is a frequent presentation. Underlying medical illness increases counterregulatory hormones and insulin resistance, including infection, myocardial infarction, gastrointestinal bleeding, and central nervous system events. Pregnancy contributes through relative insulin deficiency. Medications such as protease inhibitors and atypical antipsychotics (e.g., olanzapine, clozapine) and alcohol abuse are additional contributors.
Diagnosis
Signs and symptoms Patients often report polyuria, polydipsia, weakness, abdominal pain, nausea, vomiting, chest pain, febrile illness, and medication noncompliance. Altered mental status may be present. Physical examination commonly reveals tachycardia, hypotension from dehydration or sepsis, tachypnea with hyperpnea, Kussmaul respirations, dehydration with poor skin turgor and dry mucous membranes, ketone odor on the breath, and diffuse abdominal tenderness. Temperature abnormalities may reflect infection.
Essential workup
Diagnostic criteria include venous pH <7.3, serum bicarbonate <15 meq />, hyperglycemia >250 mg/dL, and ketonemia or ketonuria. Initial evaluation requires bedside glucose testing, venous blood gas, serum electrolytes, BUN and creatinine, urine dipstick for ketones, and assessment for a precipitating cause.
Diagnosis tests & interpretation
Lab Serum glucose confirms hyperglycemia. Electrolytes show an increased anion gap metabolic acidosis [Na − (Cl + HCO₃)] >12. Serum sodium may be falsely low due to hyperglycemia and should be corrected by adding 1.6 mEq/L for every 100 mg/dL glucose above 100 mg/dL. Potassium is often normal or elevated initially due to extracellular shift, despite a total body deficit of 3-5 mEq/kg; levels fall rapidly with insulin and fluids. Bicarbonate is typically markedly reduced. BUN and creatinine reflect prerenal azotemia from dehydration. Serum ketones must be present; β-hydroxybutyrate predominates and may be underestimated by nitroprusside testing. Urine ketone dip testing is highly sensitive, and point-of-care β-hydroxybutyrate testing can aid early diagnosis. CBC often shows stress leukocytosis. Serum osmolality may be elevated (>320 mOsm/L). Imaging includes chest radiography for suspected pneumonia, ECG to assess ischemia or potassium abnormalities, and head CT if altered mental status is unexplained.
Differential diagnosis
Other causes of anion gap metabolic acidosis include alcoholic ketoacidosis, lactic acidosis, toxic ingestions (salicylates, methanol, ethylene glycol), uremia, starvation or sepsis, and hyperglycemic hyperosmolar nonketotic syndrome.
Treatment
Pre hospital Early fluid resuscitation is often initiated; total prehospital volume should be documented to guide ongoing therapy.
Initial stabilization/therapy Address airway, breathing, and circulation, particularly in patients with altered mental status. Administer supplemental oxygen as needed and give an initial bolus of 0.9% normal saline for hypotension or tachycardia.
Ed treatment/procedures Continuous cardiac monitoring and pulse oximetry are required for unstable patients. Fluid therapy assumes a total deficit of approximately 100 mL/kg. Administer 1–2 L of 0.9% normal saline in the first hour. Continue isotonic saline if corrected sodium is low, or switch to 0.45% saline if corrected sodium is normal or high. Replace the remaining deficit gradually over 24–36 hours to avoid rapid osmolar shifts. Insulin therapy is initiated with continuous IV regular insulin at 0.1 U/kg/h after confirmation of DKA and adequate potassium levels, titrated to close the anion gap rather than normalize glucose alone. Add dextrose-containing fluids when serum glucose falls below 250–300 mg/dL. Potassium replacement is essential once urine output is established and serum potassium is <5.5 meq />; insulin should be delayed if potassium is <3.5 meq />. Bicarbonate therapy is generally avoided and reserved only for severe acidosis (pH <6.9) with cardiovascular compromise. phosphate and magnesium replacement are not routine but may be required in severe deficiencies. the underlying precipitating cause must identified treated.< />pan>
Medication
Regular insulin infusion at 0.1 U/kg/h IV. Potassium chloride supplementation as indicated. Dextrose-containing IV fluids once glucose levels decline. Magnesium sulfate or phosphate replacement when clinically necessary.
Follow-up disposition
Admission criteria ICU admission is required for severe DKA with pH <7.0, altered mental status, hemodynamic instability, serious comorbid illness, or extremes of age. moderate dka may be managed in a monitored unit, while mild cases without complications observed.< />pan>
Discharge criteria Resolution of anion gap acidosis, tolerance of oral intake, stable vital signs, no ongoing precipitating illness, and reliable follow-up with clear insulin instructions.
Pearls and pitfalls
Insulin infusion should not be reduced or stopped solely because glucose normalizes; it must continue until acidosis and anion gap resolve. Failure to aggressively monitor and replace potassium is a common and dangerous error.
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