DKA: A Nurse's Guide to Diabetic Ketoacidosis

William Kelly, MSN, FNP-C

Updated June 2026 · Medically reviewed for nurses

16 min read

Diabetic Ketoacidosis (DKA) is a severe complication of diabetes that occurs when high blood sugar combines with a severe lack of insulin, forcing the body to break down fat for energy and burn ketone bodies as fuel. The result is severe acidosis — and a very sick patient.

Patients with DKA are usually admitted to the ICU. This guide walks through the pathophysiology, assessment, workup, and the step-by-step treatment you'll be managing at the bedside.

What Is DKA?

Because there's a complete or severe lack of insulin, glucose can't get into the cells — they use insulin to transport glucose across the membrane. With the cells starving, the body breaks down fat to make ketone bodies, which can passively cross the cell membrane without insulin and feed the starving cells.

The ketones created — acetoacetic acid, beta-hydroxybutyrate, and acetone — are acidic, and their rapid buildup drives a high anion gap metabolic acidosis.

Acid-Base Balance & Why DKA Happens

To understand DKA you need a working grasp of acid-base balance. The pH scale runs from 0 (most acidic) to 14 (most basic), with 7 neutral. Normal blood pH is 7.35–7.45, with 7.40 the sweet spot — slightly basic.

Two organ systems maintain pH: the respiratory system and the renal ("metabolic") system. The number of hydrogen ions determines acidity — more H⁺ means more acidic. The kidneys release buffers and excrete H⁺ in the urine; the lungs adjust the respiratory rate, blowing off more CO₂ to lower acidity.

O₂ → CO₂

Cells use oxygen to make energy via the Krebs cycle; CO₂ is a byproduct that's breathed out.

Metabolic vs Respiratory

Low bicarb causing acidity is metabolic acidosis; CO₂ buildup is respiratory acidosis. DKA is a classic metabolic acidosis.

DKA is one of the most common metabolic acidoses — multifactorial, but characterized by a rapid rise in circulating ketone bodies. For a deeper dive, see the ABG interpretation guide.

What Is the Anion Gap?

You'll hear a lot about the anion gap (AGAP) in DKA. It measures the difference between positively charged electrolytes (cations) and negatively charged ones (anions): essentially sodium minus (chloride + bicarbonate).

DKA vs Hyperglycemic Hyperosmolar State (HHS)

Many type 2 diabetics with uncontrolled sugars don't develop DKA, likely because they still produce some insulin. HHS is a different complication of high blood sugar, more common in older patients with uncontrolled diabetes.

When glucose is high, patients dehydrate quickly through osmotic diuresis — sugar pulls water into the urine. This causes hyperosmolality of the blood, drawing water out of cells (cellular dehydration). Because these patients have some insulin, the massive fat breakdown and ketone formation doesn't occur on the same scale, so severe acidosis doesn't happen. HHS is usually managed with IV fluids and subcutaneous insulin, though an IV drip is sometimes used.

Nursing Assessment

Patients in DKA are often obviously sick — vomiting, abdominal pain, dehydrated, and weak, sometimes with altered mental status. About 70–90% of DKA occurs in type 1 diabetics, usually from an identifiable trigger.

New-Onset Type 1 DM

Patients who don't yet know they're type 1 diabetic.

Insulin Noncompliance

Not taking insulin as prescribed.

Infection

Most commonly pneumonia or UTI.

Medications

Steroids, high-dose thiazides, dobutamine, terbutaline, atypical antipsychotics, or SGLT2 inhibitors.

Drugs

Cocaine use is associated with recurrent DKA.

DKA symptoms evolve rapidly over ~24 hours, whereas HHS is a slower worsening.

Nausea & Vomiting

Often from delayed gastric emptying and ileus.

Abdominal Pain

Common in DKA, but almost never in HHS.

Polyuria & Polydipsia

Excess urination from osmotic diuresis; thirst from blood hyperosmolality.

Weight Loss

From water losses plus fat losses from massive lipolysis.

Altered Mental Status

Lethargy, confusion, or obtundation. Tends to be worse in HHS due to higher hyperosmolarity.

Inspection

Kussmaul respirations (deep, fast breathing to blow off CO₂) and very dry mucous membranes — these patients are "dry as a bone."

Your Other Senses

A fruity odor on the breath is exhaled acetone — a classic DKA finding.

Vital Signs

Temp often normal (high if infection); HR tachycardic from dehydration; BP may be low with severe hypovolemia; SpO₂ usually normal; RR often >20 (Kussmaul).

Auscultation & Palpation

Heart fast and regular; lungs usually clear but deep. Peripheral pulses weak/thready; abdomen may be mildly tender without rebound or guarding.

Nursing Interventions

When you receive a DKA patient, several things happen quickly:

DKA Workup & Diagnosis

DKA is diagnosed on lab work alone — a high anion gap PLUS a high sugar usually means DKA.

Blood Glucose

From a capillary monitor or the CMP. DKA sugars often run 350–550 mg/dL.

Anion Gap

The hallmark of DKA — usually >20, from reduced bicarb and accumulating ketones.

Plasma Osmolality

Always elevated in HHS, not always in DKA. >295 mOsm/kg is hyperosmolar; HHS often exceeds 320.

CO₂ (Bicarb)

Serum CO₂ in the CMP equals bicarb on an ABG. <18 generally indicates metabolic acidosis.

Sodium

Usually mildly low and appears lower still — high glucose dilutes it. Correct by adding 2 mEq/L per 100 mg/dL of glucose above 100.

Potassium

Total body deficit of 300–600 mEq, but lab levels look normal or high. Don't be fooled — insulin drives K⁺ back into cells.

BUN/Creatinine

May be elevated from prerenal AKI (dehydration, hypovolemia) or underlying diabetic nephropathy.

Leukocytosis

Mild and proportional to ketone load. A WBC >25 or bands >10% should raise suspicion for infection.

ABG

Rarely needed. If drawn: pH <7.35, HCO₃ <18, CO₂ <35 (respiratory compensation).

VBG

Often ordered instead of an ABG — we mainly want pH and bicarb, which are essentially equivalent.

Serum Ketones

Directly detect blood ketones (acetone or beta-hydroxybutyrate). Not needed if there's already an AGAP acidosis with hyperglycemia.

Urinalysis

Often shows decreased specific gravity (osmotic diuresis), large glucose, and ketones. See UA interpretation.

DKA Treatment

Treatment aims to reverse the acidosis and lower the glucose. Protocols vary by facility, but the core components are fluids, insulin, and potassium replacement.

IV Isotonic Fluidsfirst step

The first step is fluid replacement, usually with normal saline — it stabilizes vitals, replaces losses, improves insulin responsiveness, and reduces stress hormones. Typically 2–4 L NS over the first 3–4 hours at 1 L/hr. Slow it down with careful monitoring in CHF or advanced renal failure.

IV Insulin Driponly if K⁺ >3.3

As long as potassium is >3.3, insulin can start. Many protocols give a bolus of ~10 units (0.1 u/kg) then an infusion at 0.1 u/kg/hr. Regular and rapid-acting insulins are equally effective. Once glucose reaches 200–300 mg/dL, dextrose is added to the fluids until the acidosis resolves.

IV Potassiumgoal 4–5 mEq/L

• >5.3 mEq/L: hold potassium; recheck hourly until below 5.3.
• 3.3–5.3 mEq/L: start K⁺ if urine output >50 mL/hr — usually 20–30 mEq per liter of fluid.
• <3.3 mEq/L: give 20–40 mEq/hr until above 3.3. Don't start insulin until K⁺ >3.3.

Continued IV Fluidsguided by corrected sodium

After the first few hours, fluids continue at a slower rate selected by the corrected sodium: if still low, continue NS; if corrected sodium is normal, switch to hypotonic saline (½ NS). Usually run at 250–300 mL/hr.

IV Dextroseonce glucose 200–300

It seems counterintuitive, but dextrose is added once glucose falls to 200–300 mg/dL — insulin is still needed to close the gap, but the glucose can drop too far. Letting it fall below this range raises the risk of cerebral edema. Keep glucose ≥250–300 in HHS and ≥200 in DKA. A typical fluid is D5 ½ NS (often with potassium added). See the IV fluids guide.

Patient Monitoring

DKA patients are at high risk for complications and should be monitored closely, usually in the ICU.

Blood Glucose

Usually checked every hour on a drip. Once below 250 mg/dL, add dextrose-containing fluid until the AGAP normalizes — lowering glucose too much risks cerebral edema.

Serum Potassium

A BMP every 2–4 hours while on an insulin drip.

Cardiac Monitor / EKG

Watch for tachycardia, ectopy, or arrhythmias. Severe hypokalemia and acidosis can cause VFib, asystole, and PEA.

Blood Pressure

Acidosis and hypovolemia cause hypotension — and when acidotic, vasopressors work poorly.

Anion Gap

Once the AGAP normalizes, the gap is "closed" — the insulin drip can stop and the patient transitions to subcutaneous insulin.

Related Guides

Labs

ABGs: Blood Gas Interpretation

Critical Care

Types of IV Fluids

Cardiac

VTach & VFib: Ventricular Arrhythmias

Assessment

Blood Pressure Crash Course