Guide — Endocrine
Diabetic Ketoacidosis (DKA)
DKA is a life-threatening emergency resulting from absolute insulin deficiency — pathophysiology, precipitating causes, clinical manifestations, laboratory findings, treatment principles, and nursing priorities.
11 min read · Endocrine
Educational use only. DKA treatment — fluid resuscitation, insulin infusion, and electrolyte replacement — is provider-directed and protocol-driven. This material supports nursing education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional policy, or medical direction. Always follow facility protocols and current provider orders.
DKA is a medical emergency with mortality risk. Treatment must be initiated rapidly and monitored closely in an ICU or step-down setting. This guide is for educational purposes.
Pathophysiology
DKA results from absolute or near-absolute insulin deficiency combined with elevated counter-regulatory hormones (glucagon, cortisol, catecholamines, growth hormone). This creates a catabolic crisis:
- No insulin → cells cannot use glucose → blood glucose rises (hyperglycemia)
- Glucagon unopposed → liver releases stored glucose (glycogenolysis) and makes new glucose (gluconeogenesis) → further hyperglycemia
- Fat breakdown (lipolysis) → free fatty acids released → liver converts to ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone)
- Ketone accumulation → metabolic acidosis (anion gap type) → pH falls
- Osmotic diuresis → dehydration, electrolyte loss (Na, K, Mg, phosphate) → volume depletion
Kussmaul respirations (deep, rapid, labored breathing) represent the respiratory compensation for metabolic acidosis — CO₂ is blown off to raise pH. Fruity breath odor = exhaled acetone.
Precipitating Causes — The 6 Is
| Cause | Mechanism | Clinical Note |
|---|---|---|
| Infection (most common) | Illness raises counter-regulatory hormones → ↑ glucose → overwhelms insulin reserves | UTI, pneumonia, cellulitis — always look for infection in DKA |
| Insulin omission | Patients forget, run out, cannot afford insulin, or intentionally omit | Most common precipitant in known Type 1 DM; assess adherence barriers |
| Initial presentation | DKA may be the FIRST presentation of new-onset Type 1 DM | Young patient, no prior diagnosis — consider DM screening |
| Infarction/Ischemia | MI, stroke → massive counter-regulatory hormone release | DKA may mask or complicate ACS — always screen for cardiac events |
| Iatrogenic | Steroids, thiazides, SGLT2 inhibitors (euglycemic DKA), antipsychotics | Euglycemic DKA: SGLT2 inhibitors can cause DKA with near-normal glucose |
| Intoxication | Alcohol, cocaine, sympathomimetics | Alcohol-induced DKA can present with lactic acidosis concurrently |
Clinical Manifestations
From Hyperglycemia
- ✦Polyuria, polydipsia
- ✦Polyphagia (early) → nausea/anorexia (acidosis)
- ✦Blurred vision
- ✦Weakness, fatigue
From Dehydration
- ✦Dry mucous membranes, poor skin turgor
- ✦Tachycardia, hypotension, orthostatic changes
- ✦Sunken eyes
- ✦Decreased urine output (late — oliguria)
From Acidosis
- ✦Kussmaul respirations (deep, rapid, labored)
- ✦Fruity breath (acetone)
- ✦Nausea, vomiting, abdominal pain
- ✦Altered mental status → coma (severe)
From Electrolyte Loss
- ✦Muscle cramps, weakness
- ✦Cardiac dysrhythmias (K⁺ changes)
- ✦Paresthesias
- ✦Ileus (low phosphate/Mg)
Laboratory Findings
| Lab | DKA Finding | Why |
|---|---|---|
| Glucose | >250 mg/dL (usually 300–600) | Absolute insulin deficiency + counter-regulatory hormone excess |
| pH (arterial) | <7.3 (mild: 7.25–7.30; mod: 7.00–7.24; severe: <7.00) | Ketoacid accumulation → metabolic acidosis |
| Bicarbonate | <18 mEq/L | Consumed buffering ketoacids |
| Anion gap | >12 mEq/L (typically 20–30+) | Unmeasured ketoacid anions (acetoacetate, BHB) |
| Ketones (serum/urine) | Positive — often 3+ or 4+ | Beta-hydroxybutyrate and acetoacetate accumulation |
| Potassium (serum) | Normal or HIGH initially — despite total body K⁺ DEFICIT | Acidosis shifts K⁺ out of cells; total body deficit from diuresis |
| Sodium | May be low, normal, or high — use corrected Na⁺ | Osmotic dilution from hyperglycemia; Na⁺ rises as glucose falls with treatment |
| BUN/Creatinine | Elevated | Prerenal azotemia from dehydration |
| WBC | Elevated (even without infection) | Stress demargination — not reliable for infection diagnosis in DKA |
Critical potassium rule: Do NOT start insulin until K⁺ ≥3.5 mEq/L. Insulin drives K⁺ into cells — if already hypokalemic, giving insulin can cause fatal cardiac dysrhythmias.
Treatment Overview
Fluid resuscitation (FIRST priority)
Normal saline (0.9% NaCl) 1–2 L over first 1–2 hours IV bolus. Then 250–500 mL/hr ongoing. Switch to 0.45% NaCl when Na⁺ normalizes. Add dextrose (D5) when glucose reaches 200–250 mg/dL to prevent hypoglycemia while continuing insulin.
Insulin therapy (after K⁺ ≥3.5)
Regular insulin IV infusion — continuous drip. Typical starting rate: 0.1 units/kg/hr. Goal: decrease glucose 50–75 mg/dL per hour. Transition to subcutaneous insulin when: anion gap closed, patient eating, glucose <200, tolerating oral intake. Continue IV insulin 1–2 hours after first SQ dose.
Potassium replacement
Even if K⁺ appears normal initially — total body deficit exists. Add KCl to IV fluids once urine output confirmed and K⁺ <5.0. HOLD insulin if K⁺ <3.5 — replace K⁺ first. Target K⁺: 4.0–5.0 mEq/L throughout treatment.
Identify and treat precipitant
Blood/urine cultures, CXR, UA, ECG. Antibiotics if infection suspected. Do not wait for culture results if clinically ill.
Monitor and reassess
Glucose every 1 hour. BMP every 2–4 hours. Strict I&Os. Vital signs. Anion gap trending closed is the resolution endpoint — NOT just glucose normalization. Transition to SQ insulin only when anion gap has fully closed.
NCLEX Pearls
- ✦DKA = Type 1 DM primarily (can occur in Type 2 under severe stress). HHS = Type 2 DM primarily.
- ✦Classic triad: glucose >250 + pH <7.3 + serum/urine ketones positive.
- ✦Kussmaul respirations = respiratory compensation for metabolic acidosis (blowing off CO₂ to raise pH).
- ✦Fruity breath = exhaled acetone — classic DKA finding.
- ✦K⁺ appears HIGH early because acidosis shifts K⁺ out of cells — but total body K⁺ is DEPLETED from osmotic diuresis.
- ✦CRITICAL RULE: Do NOT give insulin until K⁺ ≥3.5 mEq/L — insulin drives K⁺ into cells and can cause fatal hypokalemia.
- ✦Anion gap closing = resolution criterion, NOT glucose normalization alone.
- ✦Add D5 to IV fluids when glucose reaches 200–250 to prevent hypoglycemia while continuing insulin drip.
- ✦Most common precipitant: INFECTION (UTI, pneumonia, cellulitis). Always look for a source.
- ✦Euglycemic DKA: SGLT2 inhibitors (dapagliflozin, empagliflozin) can cause DKA with glucose <250 — easy to miss.
Related Resources
Standards & sources
Fact-checked Jun 20, 2026This page is written to align with American Diabetes Association (ADA) Standards of Care · American Association of Clinical Endocrinology (AACE). It is an educational summary, not a citation of any single document — always verify specific doses, values, and protocols against current guidelines and your facility policy. How we source content →