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Diabetic Ketoacidosis (DKA) - Complete EMT Guide

Based on Rosen's Emergency Medicine, Goldman-Cecil Medicine, NJ EMS Clinical Practice Protocols (2025), and the 2024 ADA Consensus Report on Hyperglycemic Crises

1. DEFINITION

DKA is a life-threatening metabolic emergency defined by a triad of:
FeatureThreshold
HyperglycemiaBlood glucose > 250 mg/dL (may be lower in euglycemic DKA)
Ketonemia/KetonuriaUrine ketones 2+ or serum β-hydroxybutyrate ≥ 3.0 mmol/L
Metabolic acidosisArterial/venous pH < 7.30; bicarbonate < 15 mmol/L
It occurs when insulin deficiency and excess counter-regulatory hormones (glucagon, cortisol, catecholamines) combine to produce a hyperglycemic, dehydrated, acidotic patient with profound electrolyte imbalances. DKA is most common in Type 1 diabetes but occurs in Type 2 as well - approximately 25% of episodes happen in patients with previously undiagnosed diabetes.
ADA 2024 Update: The updated June 2024 ADA Consensus Report introduced revised diagnostic and resolution criteria for DKA and HHS, as well as new recommendations for assessment and management. [PMID 40032308]

2. PATHOPHYSIOLOGY (Why It Happens)

Pathophysiology of Diabetic Ketoacidosis - flowchart showing three pathways: increased lipolysis leading to ketogenesis and acidosis; decreased glucose uptake leading to hyperglycemia, osmotic diuresis, and volume depletion; and increased proteolysis leading to gluconeogenesis
Three simultaneous processes drive DKA:
  1. Lipolysis pathway: Insulin deficiency activates hormone-sensitive lipase → increased free fatty acids (FFA) → FFA enter the liver → converted to ketone bodies (β-hydroxybutyrate, acetoacetate, acetone) → ketoacidosis
  2. Hyperglycemia pathway: Cells cannot uptake glucose → blood glucose rises → exceeds renal threshold → glycosuria → osmotic diuresis → loss of water, sodium, potassium, magnesium, phosphorus, chloride → profound dehydration and electrolyte depletion
  3. Proteolysis pathway: Muscle breaks down amino acids → liver uses them for gluconeogenesis → worsens hyperglycemia → worsens osmotic diuresis
The acidosis triggers Kussmaul respirations (deep, rapid breathing) as the body tries to blow off CO2 to compensate. Hyperosmolarity and acidosis together directly depress mental status.
  • Rosen's Emergency Medicine, 9th Ed.

3. CAUSES / PRECIPITANTS

The "6 I's" mnemonic covers most triggers:
CategoryExamples
InfectionUTI, pneumonia, sepsis (most common overall trigger)
Inadequate insulinMissed doses, pump failure, non-compliance, medication cost barriers
Initial diagnosisNew-onset Type 1 diabetes (25% of DKA cases)
Ischemia/InfarctionAcute MI, stroke, PE, mesenteric ischemia
IntoxicationAlcohol, cocaine
Inflammatory/Intercurrent illnessAcute pancreatitis, burns, hyperthermia, trauma
Drugs that can precipitate DKA:
  • Corticosteroids
  • SGLT-2 inhibitors (e.g., empagliflozin, dapagliflozin) - can cause euglycemic DKA (glucose may be < 250!)
  • Antipsychotics (clozapine, olanzapine)
  • Thiazide diuretics
  • Sympathomimetics
  • Goldman-Cecil Medicine, Table 210-11

4. SIGNS & SYMPTOMS

Onset (typically gradual over 12-24 hours)

Symptoms reported by the patient:
  • Polyuria - excessive urination (from osmotic diuresis)
  • Polydipsia - excessive thirst
  • Polyphagia - increased hunger (early)
  • Nausea and vomiting
  • Abdominal pain - seen in ~50% of patients, especially children; in adults, consider this as a sign of an underlying precipitant
  • Weakness and fatigue
  • Visual blurring
  • Weight loss
Physical examination findings (what you will observe):
FindingCause
Tachypnea with Kussmaul breathing (deep, labored breathing)Respiratory compensation for metabolic acidosis
Fruity/acetone odor on breathExhaled acetone (a ketone body)
TachycardiaDehydration, hypovolemia
Hypotension / orthostatic changesSevere volume depletion (average deficit 3-5 L in adults)
Dry mucous membranes, poor skin turgor, sunken eyesDehydration
Altered mental status (drowsiness → stupor → coma)Hyperosmolarity + acidosis
Warm, flushed skinPeripheral vasodilation from acidosis
Elevated temperatureRarely from DKA itself - suggests underlying infection

DKA Severity Classification (ADA 2024)

SeverityGlucose (mg/dL)pHBicarbonateMental Status
Mild> 2507.25 - 7.3015-18 mmol/LAlert
Moderate> 2507.00 - 7.2410-15 mmol/LAlert/Drowsy
Severe> 250< 7.00< 10 mmol/LStupor/Coma
  • Goldman-Cecil Medicine, Table 210-12

5. CLINICAL ASSESSMENT FOR EMTs

Scene Size-Up & Primary Survey

  • Scene safety - ensure safe environment; note any insulin/medication bottles, glucometer
  • General impression - patient may appear ill, diaphoretic, or confused
  • Airway - assess; unconscious patients at risk for aspiration (especially if vomiting)
  • Breathing - note rate, depth; Kussmaul breathing is a key finding
  • Circulation - assess skin color/moisture/temperature; radial pulse quality; signs of shock

History (SAMPLE)

  • S - Symptoms: nausea, vomiting, abdominal pain, polyuria, polydipsia, weakness
  • A - Allergies to medications (especially insulin)
  • M - Medications: insulin type/dose, any recent changes; SGLT-2 inhibitors; steroids
  • P - Past history of diabetes (Type 1 or 2), previous DKA episodes
  • L - Last oral intake; last insulin dose taken
  • E - Events: recent illness, infection, stress, trauma, medication non-compliance

Physical Assessment (Focused)

Vital Signs:
  • BP: look for hypotension or orthostatic drop
  • HR: tachycardia is expected
  • RR: Kussmaul breathing (deep and rapid)
  • SpO2: usually normal unless pulmonary complication
  • Temperature: fever suggests infection as precipitant
Blood Glucose (glucometer):
  • The cornerstone EMT assessment tool
  • DKA: typically > 250 mg/dL (but can be lower with SGLT-2 inhibitors or partial treatment)
  • Document the exact reading
Mental Status (AVPU or GCS):
  • Alert? Responsive to voice? Pain? Unresponsive?
  • Altered mental status = higher severity, faster transport
Skin: Warm, dry, flushed; poor turgor = significant dehydration
Breath odor: Fruity/ketone smell is a strong clinical clue

6. MANAGEMENT - EMT Scope of Practice

EMT-Basic (BLS) Actions

  1. Ensure scene safety and BSI (Standard Precautions - wear gloves)
  2. Primary survey and stabilize ABCs
  3. Administer oxygen to maintain SpO2 ≥ 94%
    • Do NOT suppress Kussmaul breathing with high-flow oxygen unless hypoxic - this breathing is compensatory
  4. Obtain blood glucose level via glucometer (if approved by agency Medical Director)
    • If BG < 60 mg/dL with AMS → treat as hypoglycemia instead
  5. Position the patient: semi-Fowler's if alert; recovery position if unconscious/vomiting
  6. Do NOT delay transport - DKA requires hospital-level treatment (IV fluids, insulin, electrolyte monitoring)
  7. Call for ALS intercept if the patient has:
    • Unstable vital signs
    • Altered mental status
    • Positive sepsis screen (lactate ≥ 2, suspected infection)
  8. Provide oral hydration (water only) IF: patient is alert, can swallow, and is not vomiting
  9. Monitor closely during transport - mental status, breathing, vitals

ALS / Paramedic Actions (scope for reference)

Fluid Resuscitation (highest priority):
  • Adults: 1,000 mL isotonic crystalloid (Normal Saline or Lactated Ringer's) IV/IO bolus; reassess and repeat if indicated
  • Pediatrics: 20 mL/kg NS bolus during first hour
  • If in hypovolemic shock: administer as rapidly as possible until SBP > 80 mmHg
  • Average fluid deficit is 3-5 liters in adults
  • ⚠️ Use 10 mL/kg bolus in pediatric patients to reduce risk of cerebral edema (NJ EMS Protocol 2025)
  • Recent meta-analysis (2024) supports balanced electrolyte solutions (e.g., LR) over 0.9% saline for faster DKA resolution [PMID 38925619]
Electrolyte Considerations:
  • Potassium is likely total-body depleted (even if serum K appears normal/high due to acidosis)
  • Do NOT give insulin until potassium ≥ 3.3 mEq/L - insulin drives K into cells and can cause life-threatening hypokalemia
  • Add 20-40 mEq KCl per liter of fluid once K < 5.5 mEq/L and renal function is adequate
Insulin (hospital/ALS):
  • 0.1 units/kg/hour regular insulin IV infusion
  • Switch IV fluid to D5W/0.45% NS when glucose ≤ 300 mg/dL (to prevent hypoglycemia while continuing insulin)
  • Reduce to 0.05 units/kg/hour when glucose ≤ 250 mg/dL AND ketones < 1.0 mmol/L
Airway:
  • Avoid intubation if at all possible - patients have tremendous respiratory drive; matching minute ventilation with a ventilator is extremely difficult
  • Intubate only if patient is comatose or vomiting with inability to protect airway
  • If intubated: maintain hyperventilation to prevent worsening acidosis
Treat the precipitant: Search for and treat underlying infection or other cause

7. KEY EMT PEARLS & RED FLAGS

  • Fruity breath + high BG + Kussmaul breathing = DKA until proven otherwise
  • Do NOT give insulin in the field - dangerous without potassium monitoring
  • Hyperglycemia worsens brain ischemia - be extra cautious in patients with concurrent stroke, cardiac arrest, or head trauma
  • SGLT-2 inhibitor patients may have euglycemic DKA (BG < 250) - don't rule out DKA on BG alone if clinical picture fits
  • Fever is NOT caused by DKA itself - always suspect infection as the trigger if temperature is elevated
  • Abdominal pain in adults = consider real abdominal pathology triggering DKA (not just a DKA symptom)
  • Bicarbonate is NOT routinely given - only considered if pH < 7.0 and not responding to fluids/insulin
  • DKA patients on hemodialysis may not have osmotic diuresis and can present atypically

8. DIFFERENTIAL DIAGNOSIS

Other conditions that can mimic DKA or co-exist with it:
ConditionKey Differentiator
Hyperosmolar Hyperglycemic State (HHS)BG > 600 mg/dL, minimal/no ketosis, profound neurologic deficits
Alcoholic ketoacidosisEuglycemic or hypoglycemic; recent alcohol use/cessation
Starvation ketosisMild, BG normal/low; no acidosis
Lactic acidosisShock state; elevated lactate; BG may be normal
SepsisMay co-exist; fever, leukocytosis, source of infection
Acute abdomenCan trigger DKA AND be an actual surgical emergency

9. DOCUMENTATION CHECKLIST FOR EMTs

  • Blood glucose reading (with time)
  • Mental status on arrival and at handoff
  • Respiratory rate and pattern (note Kussmaul breathing if present)
  • Breath odor (fruity/acetone)
  • Vital signs (BP, HR, RR, SpO2, Temp if available)
  • Skin assessment (turgor, moisture, color)
  • Last insulin dose and time
  • Last oral intake
  • Medications (especially SGLT-2 inhibitors or steroids)
  • Oral fluids given en route (if applicable)
  • ALS intercept requested/obtained (Y/N)
  • Oxygen administered (rate/delivery device)

Sources:
  • Rosen's Emergency Medicine: Concepts and Clinical Practice, 9th Ed. (Chapter 115, DKA section)
  • Goldman-Cecil Medicine International Edition (Chapter 210, Table 210-11/12)
  • NJ EMS Clinical Practice Protocols & Guidelines v1.0, August 2025 (Protocol 2.7A - Diabetic Emergencies: Hyperglycemia)
  • 2024 ADA Consensus Report on Hyperglycemic Crises - Rodriguez Alvarez et al., Cleveland Clinic Journal of Medicine, 2025 [PMID 40032308]
  • Szabó et al. (2024) - Balanced electrolyte solutions vs. 0.9% saline in DKA (Meta-Analysis) [PMID 38925619]
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