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Diabetic Ketoacidosis (DKA) — Clinical Overview

Definition / Diagnostic Criteria

The three fundamental biochemical features of DKA are:

Hyperglycemia (or known diabetes) — "D"
Ketonuria ≥2+ or serum ketones ≥3.0 mmol/L — "K"
pH <7.3 (arterial or venous) — "A"

DKA severity by pH: mild 7.20–7.30; severe <7.00.

Pathophysiology

DKA results from insulin deficiency + glucagon excess, which drives:

Hyperglycemia → osmotic diuresis → profound dehydration and electrolyte loss
Lipolysis → elevated free fatty acids → hepatic ketogenesis (β-hydroxybutyrate, acetoacetate, acetone)
Proteolysis → amino acid release → gluconeogenesis → worsening hyperglycemia
Acidosis → Kussmaul breathing (respiratory compensation), depressed mental status, hyper-kalaemia (K⁺ shifts out of cells)

In 95% of patients, total sodium is normal or low, but serum K⁺ is often falsely elevated due to acidosis — true total-body K⁺ is always depleted.

Common Precipitants

Most Common	Other
Infection	CVA, PE, pancreatitis
Missed/inadequate insulin	Alcohol intoxication
New-onset T1DM (~25% of cases)	Corticosteroids, clozapine, SGLT2 inhibitors
Acute coronary syndrome	Cocaine, sympathomimetics, thiazides

Clinical Features

Symptoms: Polyuria, polydipsia, polyphagia, blurred vision, weakness, weight loss, nausea/vomiting, abdominal pain (~50%, especially in children)
Signs: Kussmaul breathing, tachycardia, hypotension/orthostasis, acetone breath, dehydration, ± altered sensorium
Fever is not caused by DKA itself — suggests infection

Labs (DKA vs HHS)

Parameter	DKA	HHS
Glucose	>350 mg/dL	>700 mg/dL
Sodium	Low 130s mEq/L	140s mEq/L
Potassium	~4.5–6.0 mEq/L	~5 mEq/L
Bicarbonate	<10 mEq/L	>15 mEq/L
BUN	25–50 mg/dL	>50 mg/dL
Serum ketones	Present	Absent

Average fluid/electrolyte deficits in severe DKA:

Water: 70–120 mL/kg (weight-dependent)
Sodium: 8–10 mEq/kg
Potassium: 5–7 mEq/kg
Phosphorus: ~3 mEq/kg

Pitfall: Standard nitroprusside ketone tests detect acetoacetate only — β-hydroxybutyrate (often predominant) is not detected, so ketosis may be underestimated. As insulin therapy begins, β-hydroxybutyrate converts to acetoacetate, falsely suggesting worsening ketosis. Point-of-care capillary ketone monitors are preferred.

WBC is often elevated in DKA even without infection. Elevated amylase is usually non-pancreatic.

Treatment

1. Fluids (First Priority)

Fluid losses of 5–10 L, sodium losses 5–10 mmol/kg, potassium losses up to 7 mmol/kg
Restore circulating volume first — this is paramount
Caution: Large volumes of 0.9% NaCl can cause hyperchloraemic (non-anion-gap) metabolic acidosis

2. Insulin

Insulin inhibits lipolysis and gluconeogenesis, and stimulates glucose uptake
IV infusion is standard; subcutaneous rapid-acting analogues are also effective
Do not start insulin until K⁺ is ≥3.5 mEq/L — insulin drives K⁺ into cells and can cause fatal hypokalaemia

3. Potassium Replacement

Even when serum K⁺ is initially elevated, it falls rapidly after insulin is started
Replace K⁺ once it drops; monitor continuously
In DKA on insulin pumps: assume pump failure, disconnect, and start IV insulin

4. Monitoring

Continuous cardiac monitoring (ICU or intermediate care)
Capillary ketone monitoring to guide resolution
Bicarbonate use is not routinely recommended

DKA vs Alcoholic Ketoacidosis

Feature	DKA	AKA
Glucose	High (>350)	Normal or low
pH	Acidaemic	Often alkalaemic
Context	Diabetes	Recent alcohol abstinence
Main ketone	β-hydroxybutyrate	β-hydroxybutyrate

Sources: ROSEN's Emergency Medicine, pp. 2542–2546; Goldman-Cecil Medicine, pp. 2483–2484

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