How can I tell if a patient is in diabetic ketoacidosis?

How to Diagnose Diabetic Ketoacidosis (DKA)

The Diagnostic Triad

DKA is diagnosed when all three of the following criteria are simultaneously present: hyperglycemia (blood glucose >250 mg/dL), metabolic acidosis (pH <7.3 AND serum bicarbonate <18 mEq/L), and elevated ketones in blood or urine. 1, 2, 3

You must confirm all three components—missing even one means the diagnosis cannot be made. The key is that these findings must coexist at the same time. 3

Essential Laboratory Tests to Order Immediately

When you suspect DKA, obtain the following tests without delay: 1, 2, 3

• Plasma glucose – confirms hyperglycemia (>250 mg/dL in classic DKA) 1, 2
• Arterial or venous blood gas – documents pH <7.3 (venous pH is 0.03 units lower than arterial and is sufficient for monitoring) 2
• Serum bicarbonate – must be <18 mEq/L 1, 2
• Serum electrolytes with calculated anion gap – anion gap >10-12 mEq/L supports the diagnosis 1, 2
• Blood β-hydroxybutyrate (β-OHB) – this is the preferred ketone measurement 4, 1, 2, 3
• Blood urea nitrogen and creatinine – assesses renal function and hydration status 1, 2
• Complete blood count with differential – identifies infection or other precipitants 1, 2
• Urinalysis – checks for infection and urine ketones (though blood ketones are preferred) 1, 2
• Electrocardiogram – evaluates for cardiac complications and monitors potassium effects 1, 2

Critical Point: Use β-Hydroxybutyrate, Not Urine Ketones

Blood β-hydroxybutyrate measurement is the gold standard for diagnosing and monitoring DKA—do not rely on nitroprusside-based urine or serum ketone tests. 4, 1, 2, 3

Here's why this matters clinically: 4, 1, 2

• β-OHB is the predominant ketone body in DKA and the strongest acid 4, 1, 2
• Nitroprusside tests (urine dipsticks, serum tablets) only detect acetoacetate and acetone—they completely miss β-OHB 4, 1, 2, 3
• During treatment, β-OHB converts to acetoacetate, making nitroprusside tests falsely suggest worsening ketosis even as your patient improves 4, 1, 2
• This can mislead you into thinking treatment is failing when it's actually working 1, 2

Severity Classification

Once you've confirmed DKA, stratify severity to guide monitoring intensity: 1, 2, 3

Mild DKA:

• pH 7.25–7.30
• Bicarbonate 15–18 mEq/L
• Anion gap >10 mEq/L
• Patient is alert 1, 2, 3

Moderate DKA:

• pH 7.00–7.24
• Bicarbonate 10 to <15 mEq/L
• Anion gap >12 mEq/L
• Patient is alert to drowsy 1, 2, 3

Severe DKA:

• pH <7.00
• Bicarbonate <10 mEq/L
• Anion gap >12 mEq/L
• Patient is stuporous or comatose 1, 2, 3

Severe DKA requires intensive monitoring, potentially including central venous and intra-arterial pressure monitoring. 2

Clinical Presentation: What to Look For

Physical examination findings that point toward DKA include: 1

• Kussmaul respirations (deep, labored breathing pattern indicating metabolic acidosis) 1
• Poor skin turgor (dehydration) 1
• Tachycardia and hypotension (volume depletion) 1
• Altered mental status ranging from full alertness to profound lethargy or coma 1
• Normothermia or hypothermia even with underlying infection (hypothermia is a poor prognostic sign) 1

Symptoms typically include: 1, 5

• Polyuria, polydipsia, polyphagia with weight loss 1
• Nausea, vomiting, abdominal pain (up to 25% may have coffee-ground emesis) 1
• Weakness and malaise 1
• Severe fatigue and dyspnea 5

DKA typically evolves rapidly, usually within 24 hours. 1

The Critical Exception: Euglycemic DKA

Approximately 10% of DKA cases present with blood glucose <200-250 mg/dL—this is called euglycemic DKA and can be easily missed if you rely solely on glucose levels. 3, 6, 7

For euglycemic DKA, you still need: 3

• Metabolic acidosis (pH <7.3, bicarbonate <18 mEq/L)
• Elevated β-hydroxybutyrate
• Either documented hyperglycemia at any point OR a known history of diabetes 3

Common precipitating factors for euglycemic DKA: 1, 3, 6

• SGLT2 inhibitor use (most common modern cause) 1, 3, 6, 7
• Pregnancy 1, 3, 6
• Reduced caloric intake or prolonged fasting 1, 3, 6
• Heavy alcohol consumption 1, 3, 6
• Chronic liver disease 1, 3, 6
• Recent insulin administration without adequate carbohydrate intake 6, 8

If your patient is on an SGLT2 inhibitor and presents with nausea, vomiting, or malaise, check ketones even if glucose is normal—this is a high-risk scenario. 1, 3

Differential Diagnosis: What Else Could This Be?

Other causes of high anion gap metabolic acidosis to consider: 1, 2, 3

• Alcoholic ketoacidosis – distinguished by clinical history of alcohol use; glucose is typically normal to mildly elevated (rarely >250 mg/dL) or even hypoglycemic 1, 3
• Starvation ketosis – serum bicarbonate typically ≥18 mEq/L (less severe acidosis than DKA) with prolonged fasting history 1, 2, 3
• Lactic acidosis – check lactate level 1, 2
• Toxic ingestions – salicylates, methanol, ethylene glycol 1, 2
• Chronic renal failure – though this more commonly causes hyperchloremic acidosis 2

Common Precipitating Factors to Investigate

Once you've diagnosed DKA, identify the trigger: 1

• Infection (most common) – obtain bacterial cultures of urine, blood, and throat if suspected 1, 2
• New-onset type 1 diabetes 1
• Insulin omission or inadequate insulin 1
• Myocardial infarction – check troponin 1
• Cerebrovascular accident 1
• Medications – corticosteroids, thiazides, sympathomimetic agents, SGLT2 inhibitors 1
• Pancreatitis – check amylase and lipase 1, 2
• Alcohol or drug abuse 1

Resolution Criteria: When Has DKA Resolved?

DKA is considered resolved only when ALL of the following are met: 1, 2

• Glucose <200 mg/dL 1, 2
• Serum bicarbonate ≥18 mEq/L 1, 2
• Venous pH >7.3 1, 2
• Anion gap ≤12 mEq/L 2

Critical pitfall: Ketonemia takes longer to clear than hyperglycemia, so do not stop treatment when glucose normalizes—continue monitoring β-hydroxybutyrate until it falls below 0.5 mmol/L. 1, 2

Key Pitfalls to Avoid

• Never rely on urine ketones or nitroprusside tests for diagnosis or monitoring – they miss β-OHB and can be misleading 4, 1, 2, 3
• Don't dismiss DKA because glucose is <250 mg/dL – euglycemic DKA is real and increasingly common with SGLT2 inhibitors 1, 3, 6, 7
• Don't stop checking labs when glucose normalizes – acidosis and ketosis resolve more slowly than hyperglycemia 1, 2
• Don't forget to look for the precipitating cause – failing to identify and treat the underlying trigger leads to recurrence 1, 2
• Venous pH is sufficient for monitoring after initial diagnosis – you don't need repeated arterial sticks (venous pH is 0.03 units lower than arterial) 2