Diabetic Ketoacidosis
A life-threatening complication of diabetes causing high blood sugars, dehydration, and a toxic buildup of acids (ketones) in the blood.
Emergency Management: Cardiac arrest secondary to severe hyperkalemia or hypokalemia. Herniation from cerebral edema (treat with IV Mannitol 1g/kg or 3% hypertonic saline).
Diabetic Ketoacidosis (DKA) is a severe, life-threatening metabolic complication of diabetes mellitus characterized by the biochemical triad of hyperglycemia, ketonemia (or ketonuria), and a high anion gap metabolic acidosis. It predominantly occurs in type 1 diabetes but can happen in type 2 diabetes under extreme stress.
Detailed Overview
DKA results from an absolute or relative deficiency of insulin combined with an excess of counterregulatory hormones (glucagon, catecholamines, cortisol, growth hormone). This hormonal imbalance shifts metabolism from glucose utilization to uncontrolled lipolysis and fatty acid oxidation, generating massive amounts of ketone bodies (acetoacetate and beta-hydroxybutyrate). The resulting osmotic diuresis causes profound volume depletion and electrolyte derangement.
Epidemiology & Demographics
Annual incidence in patients with type 1 diabetes is 4-8 episodes per 1000 patients. Most common in young adults (<30 years old). Mortality is <1% in specialized centers but higher in the elderly or those with severe comorbidities.
Etiological Mechanism
Precipitated by events that increase insulin requirements or interrupt insulin delivery. Non-adherence to insulin therapy is the most common cause in younger patients. Infection is the most common physiological trigger.
Primary Causes
Infection (pneumonia, UTI), omission or inadequate administration of insulin, myocardial infarction, acute pancreatitis, medications (SGLT2 inhibitors, corticosteroids, atypical antipsychotics).
Insulin deficiency allows unchecked glucagon action, activating hepatic gluconeogenesis and glycogenolysis, driving serum glucose >250 mg/dL. Simultaneously, hormone-sensitive lipase in adipose tissue is disinhibited, causing massive release of free fatty acids (FFAs). In the liver, FFAs are beta-oxidized into acetyl-CoA. Without insulin, acetyl-CoA is shunted into ketogenesis, producing beta-hydroxybutyrate and acetoacetate. These acidic ketone bodies consume bicarbonate buffering capacity, generating a high anion gap metabolic acidosis. Hyperglycemia induces an osmotic diuresis, leading to the loss of water (up to 5-8 liters), sodium, potassium, and phosphorus.
Diagnostic Criteria & Guidelines
Blood glucose > 250 mg/dL (except in euglycemic DKA), positive serum/urine ketones (specifically beta-hydroxybutyrate), arterial pH < 7.30, serum bicarbonate < 18 mEq/L, and high anion gap (> 10-12 mEq/L).
1. Fluid resuscitation: Normal saline (0.9% NaCl) at 15-20 mL/kg/hr for the first hour to restore volume. 2. Insulin therapy: Regular insulin IV bolus of 0.1 units/kg followed by continuous infusion at 0.1 units/kg/hr. 3. Potassium repletion: Add 20-30 mEq K+ to each liter of IV fluid once serum K+ is < 5.3 mEq/L (do not start insulin if K+ < 3.3 mEq/L).
Second-Line & Adjunctive Therapy
Transition to subcutaneous basal-bolus insulin once DKA is resolved (anion gap < 12, bicarb > 15, patient able to eat). Overlap IV insulin and SQ insulin by 1-2 hours to prevent rebound ketosis.
Surgical & Procedural Management
N/A for DKA itself. Surgical management applies only to triggering causes (e.g., debridement of necrotizing fasciitis, cholecystectomy).
Patient Counseling & Advice
Educate on Sick Day Management rules: never stop taking insulin even if vomiting; increase fluid intake; monitor glucose every 2-4 hours; contact provider if vomiting persists or ketones are moderate/large.
Follow-Up & Monitoring Schedule
In hospital: hourly blood glucose; basic metabolic panel every 2-4 hours until anion gap closes. Outpatient: follow-up with endocrinologist within 1-2 weeks of discharge to adjust insulin regimen.
Preventive Strategies
Diabetes education regarding insulin adherence and use of continuous glucose monitors (CGM). Prompt management of acute infections.
Overall mortality is <1% with proper management, primarily driven by underlying precipitating illness (like MI or sepsis) or complications like cerebral edema.