Clinical Presentation of Diabetic Ketoacidosis (DKA)
A patient with DKA typically presents with the classic triad of polyuria, polydipsia, and polyphagia, accompanied by gastrointestinal symptoms (nausea, vomiting, abdominal pain), Kussmaul respirations, altered mental status ranging from alert to coma, and signs of dehydration—symptoms that usually evolve rapidly within 24 hours. 1, 2
Cardinal Symptoms
Metabolic Symptoms
- Polyuria, polydipsia, and polyphagia with associated weight loss are the hallmark presenting features 1, 2
- These symptoms typically evolve within 24 hours in most patients, though some may develop over several days 2
- Occasionally patients present acutely with no prior warning symptoms 2
Gastrointestinal Manifestations
- Nausea and vomiting occur in up to 25% of patients 1, 2
- Vomiting may be coffee-ground in appearance and guaiac positive due to hemorrhagic gastritis 1, 2
- Abdominal pain is a specific symptom of DKA (not seen in hyperosmolar hyperglycemic state) 2
- Weakness and malaise are frequently reported 1
Physical Examination Findings
Respiratory Signs
- Kussmaul respirations (deep and labored breathing pattern) indicate metabolic acidosis and are a characteristic finding 1, 2
Cardiovascular Signs
- Tachycardia and hypotension from volume depletion are common 1
Neurological Status
- Altered mental status ranges from full alertness to profound lethargy or coma depending on severity 1, 2
- Lethargy is particularly common when pH <7.0 2
- Mental status correlates with DKA severity: alert in mild DKA, alert/drowsy in moderate DKA, and stupor/coma in severe DKA 3
Signs of Dehydration
Temperature Abnormalities
- Normothermia or hypothermia may be present even with underlying infection 1, 2
- Hypothermia is a poor prognostic sign 1, 2
Diagnostic Laboratory Triad
The diagnosis requires simultaneous presence of all three criteria: 1, 3
- Hyperglycemia: Blood glucose >250 mg/dL (though euglycemic DKA with glucose <250 mg/dL can occur, especially with SGLT2 inhibitor use) 1, 3
- Metabolic acidosis: Arterial pH <7.3 AND serum bicarbonate <18 mEq/L 1, 3
- Ketosis: Positive ketones in serum or urine, with β-hydroxybutyrate being the preferred measurement 1, 3
Severity Stratification Based on Presentation
Mild DKA
- Arterial pH 7.25–7.30 3
- Serum bicarbonate 15–18 mEq/L 3
- Anion gap >10 mEq/L 2, 3
- Mental status: Alert 3
Moderate DKA
- Arterial pH 7.00–7.24 3
- Serum bicarbonate 10 to <15 mEq/L 3
- Anion gap >12 mEq/L 2, 3
- Mental status: Alert/drowsy 3
Severe DKA
- Arterial pH <7.00 1, 3
- Serum bicarbonate <10 mEq/L 1, 3
- Anion gap >12 mEq/L 3
- Mental status: Stupor/coma 3
Important Clinical Pitfalls
Euglycemic DKA
- SGLT2 inhibitors significantly increase DKA risk and commonly cause euglycemic DKA (glucose <250 mg/dL with ketoacidosis) 1, 3, 4
- Other causes include pregnancy, reduced food intake, alcohol use, and liver failure 1
- Clinicians must maintain high suspicion for DKA in patients with metabolic acidosis and ketosis irrespective of glucose levels, particularly in those on SGLT2 inhibitors 4, 5
Ketone Measurement
- β-hydroxybutyrate measurement in blood is the preferred method for diagnosis rather than nitroprusside-based tests 1, 3
- Nitroprusside methods (urine dipsticks, serum tablets) only detect acetoacetate and acetone, NOT β-hydroxybutyrate, which is the predominant ketone in DKA 1, 3
- During treatment, β-hydroxybutyrate converts to acetoacetate, making nitroprusside tests falsely suggest worsening ketosis when the patient is actually improving 3
Common Precipitating Factors to Identify
- Infection is the most common precipitating factor 1, 6
- Insulin omission or inadequate insulin therapy 1, 6
- New-onset type 1 diabetes 1
- Acute vascular events: myocardial infarction, cerebrovascular accident, stroke 7, 1
- Drug use: corticosteroids, thiazides, sympathomimetic agents 1
- Alcohol abuse 1
- Pancreatitis 1