Description

• Diabetic ketoacidosis (DKA) is the triad of hyperglycemia, ketonemia, and acidemia.
• DKA is generally associated with type 1 diabetes mellitus (DM) but can be associated with type 2 in cases of extreme stress (sepsis, trauma etc.).
• It is classified as mild, moderate, or severe based on the pH, serum bicarbonate, and mental status.
• DKA is differentiated from hyperglycemic hyperosmolar non-ketotic (HHNK) coma which usually lacks ketones and acidemia and is more common in type 2 diabetes. HHNK is often associated with a higher serum glucose concentration that may exceed 1,000 mg/dL and the serum osmolality may exceed 380 mOsm/kg.

Etiology/Risk Factors

• Most often precipitated by infection or discontinuation of insulin
• May also develop from major illness such as myocardial infarction (MI) or cerebrovascular accident (CVA)
• Ketoacidosis may also be present with starvation or acute alcohol intoxication.

Physiology/Pathophysiology

• DKA results from a relative shortage of circulating insulin in the body, resulting in impaired glucose uptake and utilization by peripheral tissues. This can be secondary to:
  • Actual deficiency (lack of insulin administration)
  • Increased demand (sepsis or other hypermetabolic state)
• Gluconeogenesis: To counter the lack of insulin, and glucose available for cells, the body responds by releasing counter-regulatory hormones (e.g., glucagon, cortisol, catecholamines, growth hormone).
• Lipolysis: The body institutes fatty acid oxidation, or lipolysis, to provide tissues with an energy substrate. The byproducts of lipolysis are called ketone bodies.
  • B-hydroxybutyrate (technically a carboxylic acid and not a ketone)
  • Acetoacetate
  • Acetone: Produced by decarboxylation of acetoacetate
• Hypovolemia and electrolyte derangements: Glycosuria leads to an osmotic diuresis that results in:
  • Dehydration: On average, patients are negative by 5–8 L.
  • Loss of electrolytes, most notably potassium and sodium. Potassium deficits range from 200–400 mEq due to osmotic diuresis and a chronic catabolic state. However hyperkalemia is often present initially due to the lack of insulin (decreaes K⁺ intake into the cell via Na⁺/K⁺ -ATPase) and metabolic acidosis. Sodium deficits range from 350–600 mEq due to osmotic diuresis. However the patient often presents initially with a hypovolemic hypernatremia derangement due to water loss in excess of sodium loss.
  • Anion gap acidosis: Ketone bodies are acids that titrate the body's buffering bases.

Anesthetic Goals/Guiding Principles

• Delay elective procedures: The goal is to correct the inciting factor, re-establish euvolemia, and electrolyte levels as much as possible before going to the operating room.
• The indication for emergency surgery may be an inciting factor for DKA; thus, preoperative correction is not always possible. In this case, initiate measures to restore euvolemia and replete electrolytes as the first priority, then correct hyperglycemia.
• If possible, in insulin-dependent diabetes, schedule elective cases early in the day to minimize preoperative fasting and lipolysis/ketosis from a lack of insulin.

Symptoms

Weakness

Treatment History

• Volume resuscitation
• Electrolyte replacement
• Acute coronary syndrome therapy if precipitating event is cardiac ischemia or infarction
• Stroke treatment if precipitating event is cerebrovascular

Medications

• Insulin
• Antibiotics if precipitating event is sepsis or infection
• Sodium bicarbonate

CONCOMITANT ORGAN DYSFUNCTION

• Neuropathy: Autonomic nervous system dysfunction may result in difficulties with regulating blood pressure and temperature.
• Cardiovascular disease: Perioperative morbidity and mortality with DM often results from cardiac causes.
• Nonenzymatic glycosylation and formation of abnormal proteins may result in decreased elastance and thus difficult intubation.
• Gastroparesis: Many consider patients with DM as a "full stomach" despite NPO status.
• Renal insufficiency

Circumstances to delay/Conditions

Delay elective procedures: The goal is to correct the inciting factor, re-establish euvolemia and electrolyte levels as much as possible before going to the operating room.

Bed Acuity

• ICU admission is usually required as patients may have altered mental status, hypovolemia, or require vasopressors or an insulin infusion.
• Telemetry or floor bed may be considered if there is resolution of DKA as demonstrated by a closing of the anion gap (<12), serum glucose <200 mg/dL, sodium bicarbonate level 18 mEq/L, and pH >7.3.

Medications/Lab Studies/Consults

• Endocrine consult may be advantageous.
• Frequent blood glucose checks
• Electrolyte monitoring: Potassium moves intracellularly as the acidosis is corrected.
• Ketonemia and ketonuria may persist for 1–2 days with proper correction of acidemia.
• Once DKA has resolved and the patient is eating, consider resuming the patient's preoperative insulin regimen or initiating new therapy with short/long-acting agents as necessary.

Complications

• Hypoglycemia may result from excess insulin therapy.
• Overly aggressive fluid resuscitation may lead to pulmonary edema and/or congestive heart failure.
• Continued shock may occur if inadequate resuscitation is performed.
• Over-repletion of electrolytes (potassium) may lead to cardiac arrhythmia.
• Central pontine myelinolysis may result from correction of hyponatremia at a rate >10–12 mEq/hr over the first 24 hours.

• Diabetes Mellitus
• Metabolic Acidosis
• Hypokalemia
• Hyperglycemic Hyperosmolar Nonketotic Coma

ICD9

• 250.10 Diabetes with ketoacidosis, type II or unspecified type, not stated as uncontrolled
• 250.11 Diabetes with ketoacidosis, type I [juvenile type], not stated as uncontrolled
• 250.13 Diabetes with ketoacidosis, type I [juvenile type], uncontrolled
• 250.12 Diabetes with ketoacidosis, type II or unspecified type, uncontrolled

ICD10

• E13.10 Oth diabetes mellitus with ketoacidosis without coma
• E10.10 Type 1 diabetes mellitus with ketoacidosis without coma

Matthew V. Satterly , MD

Ori Gottlieb , MD