Diabetic Ketoacidosis (DKA)

🔍 Definition:

DKA is a life-threatening acute metabolic complication of diabetes mellitus (most often type 1), characterized by:

  • Hyperglycemia
  • High anion gap metabolic acidosis
  • Ketonemia / ketonuria


🧬 Pathophysiology:

Pathway Affected

Mechanism

Insulin deficiency

Absolute or relative insulin ↓ prevents glucose uptake

Counter-regulatory hormones ↑

↑ Glucagon, cortisol, catecholamines → gluconeogenesis, lipolysis

Lipolysis

FFA → liver → ketogenesis → β-hydroxybutyrate, acetoacetate

Ketone accumulation

Metabolic acidosis (high anion gap)

Hyperglycemia

Osmotic diuresis → dehydration, electrolyte loss



⚠️ Precipitating Factors:

Type

Examples

Infection

Pneumonia, UTI (most common)

Missed insulin

Poor compliance or pump failure

New-onset diabetes

Especially type 1

Stressors

MI, surgery, trauma

Drugs

Steroids, thiazides, SGLT2 inhibitors, sympathomimetics



🧪 Diagnostic Criteria (ADA/ISPAD):

Parameter

DKA Diagnosis

Plasma glucose

>250 mg/dL (can be normal in SGLT2-induced DKA)

Arterial pH

<7.3

Serum bicarbonate

<18 mmol/L

Anion gap

>12 mmol/L

Serum/urine ketones

Positive (prefer serum β-hydroxybutyrate >3 mmol/L)



🩺 Clinical Features:

System

Symptoms/Signs

General

Polyuria, polydipsia, weight loss

CNS

Lethargy, confusion, coma (severe)

CVS

Tachycardia, hypotension, dehydration

Respiratory

Kussmaul breathing, fruity breath

GI

Nausea, vomiting, abdominal pain

Eyes

Sunken eyes (dehydration)



📉 Key Labs:

Test

Expected Result

Blood glucose

↑↑ (typically >250–600)

ABG

Metabolic acidosis

Serum ketones

β-hydroxybutyrate ↑

Na⁺ (corrected)

↓ (pseudo-hyponatremia)

K⁺

Normal or ↑ initially, but total K⁺ is depleted

BUN/Creatinine

↑ (dehydration)

Osmolality

May be mildly ↑


Corrected Na⁺ = Measured Na⁺ + 1.6 × [(Glucose – 100) / 100]


🧠 Differential Diagnosis of High Anion Gap Acidosis:

“MUDPILES”:

  • M – Methanol
  • U – Uremia
  • D – DKA
  • P – Propylene glycol
  • I – Isoniazid/Iron
  • L – Lactic acidosis
  • E – Ethylene glycol
  • S – Salicylates


🛌 DKA Management: ABC + Fluids + Insulin + Electrolytes


✅ 1. Fluid Resuscitation

  • Initial: NS 15–20 mL/kg (~1 L) over 1 hour
  • Then:
    • NS 250–500 mL/hr × few hrs
    • Add 5% dextrose when glucose <200–250 mg/dL to prevent hypoglycemia and cerebral edema


✅ 2. Insulin Therapy (IV Regular Insulin)

  • Start after 1st hour of fluids
  • Bolus: 0.1 units/kg IV (optional)
  • Infusion: 0.1 units/kg/hr
  • Goal: ↓ glucose by 50–75 mg/dL per hour
  • Transition to SC insulin when:
    • Ketosis resolved
    • Patient eating
    • Overlap IV and SC for 1–2 hours


✅ 3. Potassium Replacement

Serum K⁺ Level

Management

>5.2 mEq/L

No K⁺, monitor closely

3.3–5.2 mEq/L

Add 20–30 mEq K⁺ per liter of fluids

<3.3 mEq/L

Hold insulin, replace K⁺ aggressively


Insulin will drive K⁺ into cells, worsening hypokalemia.


✅ 4. Bicarbonate (controversial)

  • Only if:
    • pH <6.9
    • Give 50–100 mEq NaHCO₃ in 200 mL D5W over 1 hour


🛑 When to Switch to Subcutaneous Insulin:

  • Anion gap closed
  • Glucose <200 mg/dL
  • pH >7.3, HCO₃ >18
  • Patient eating
  • Start SC insulin 2 hours before stopping IV insulin


⚠️ Complications of DKA or Its Treatment:

Complication

Risk Factor

Cerebral edema

Rapid glucose drop, children

Hypoglycemia

Excess insulin without dextrose

Hypokalemia

Insulin, urinary loss

ARDS, shock

Sepsis-induced DKA



🧠 Summary Mnemonic – “D-K-A = D-E-K-A”

  • D – Dehydration → IV Fluids
  • E – Electrolyte correction (K⁺, Na⁺)
  • K – Ketosis → Insulin
  • A – Acidosis → Monitor & sometimes bicarbonate


🔄 DKA vs HHS: Comparison Table

Feature

DKA

HHS

Underlying Diabetes

Type 1 (mostly)

Type 2 (mostly)

Onset

Rapid (hours to 1–2 days)

Insidious (several days to weeks)

Plasma Glucose

>250 mg/dL

>600 mg/dL

Serum Osmolality

Mild–moderate ↑

>320 mOsm/kg

pH

<7.30

>7.30

Serum Bicarbonate

<18 mmol/L

>18 mmol/L

Anion Gap

Elevated (>12)

Normal or mildly ↑

Ketones (urine/serum)

Present (β-hydroxybutyrate ↑)

Minimal or absent

Acidosis

High anion gap metabolic acidosis

No significant acidosis

Mental Status

Alert to comatose (depends on severity)

Altered sensorium common, seizures possible

Volume Depletion

Moderate (~6 L deficit)

Severe (~8–12 L deficit)

Typical Age Group

Younger (children, adolescents)

Older adults (often >60 years)

Mortality

~2–5%

10–20% (higher)

Treatment Priorities

Fluids → Insulin → Electrolytes

Fluids → Electrolytes → Insulin

Risk of Cerebral Edema

Higher in children

Rare, but possible if glucose ↓ too rapidly



❓ 1. Why Pseudohyponatremia in DKA/HHS?

🧠 Mechanism:

  • In DKA and HHS, very high plasma glucose levels cause hyperosmolarity.
  • This draws water out of intracellular space into the extracellular compartment.
  • The dilutional effect causes a decrease in measured serum sodium, although total body sodium is not actually low.


❓ 2. Why Hypokalemia in DKA/HHS (despite high serum K⁺ initially)?

🧠 Mechanism:

  • Insulin deficiency → K⁺ shifts out of cells (causing normal or high serum K⁺ initially).
  • Osmotic diuresis → Renal loss of K⁺ in urine
  • Vomiting, acidosis → Further K⁺ loss
  • Total body potassium is severely depleted, even if serum K⁺ is normal/high.


❓ 3. Why Give Fluids Before Insulin?

🧠 Rationale:

  1. Restores perfusion and renal function:
    • Severe volume depletion → AKI, impaired insulin metabolism
    • Fluids restore circulation, enabling safer insulin use
  1. Avoids rapid osmolar shifts:
    • Insulin drops glucose → ↓ plasma osmolality
    • If fluid is not corrected first → rapid osmotic shift → cerebral edema
  1. Enhances insulin sensitivity:
    • Dehydration and acidosis reduce insulin efficacy
    • Fluids help lower counter-regulatory hormones (e.g., cortisol, glucagon)


🚨 Summary of the Order:

Step

Action

Rationale

1

Fluids (NS)

Correct dehydration, restore perfusion

2

Potassium replacement

Prevent insulin-induced hypokalemia

3

Start insulin

After adequate volume & K⁺ correction