Diabetic ketoacidosis

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:

Restores perfusion and renal function:

Severe volume depletion → AKI, impaired insulin metabolism
Fluids restore circulation, enabling safer insulin use

Avoids rapid osmolar shifts:

Insulin drops glucose → ↓ plasma osmolality
If fluid is not corrected first → rapid osmotic shift → cerebral edema

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