DKA is a life-threatening acute complication of diabetes resulting from absolute or relative insulin deficiency, characterized by the triad of hyperglycemia, metabolic acidosis, and ketosis. [1] It can occur in both type 1 and type 2 diabetes, affects all ages, and can be the initial presentation of diabetes in approximately one-third of cases. [2] Inpatient mortality ranges from 0.2% in type 1 diabetes to 1.0% in type 2 diabetes, with 1-year post-discharge mortality 13 times higher than the general population. [3]
1. History
- Key HPI questions: Onset and duration of polyuria, polydipsia, nausea/vomiting, abdominal pain, weight loss, fatigue, dyspnea, and febrile illness [1]
- Symptom frequency: Polyuria/polydipsia (98%), weight loss (81%), fatigue (62%), dyspnea (57%), vomiting (46%), preceding febrile illness (40%), abdominal pain (32%) [2]
- Ask about insulin adherence — missed doses, pump malfunction, insulin supply issues (most common precipitant) [1]
- Recent illness, surgery, trauma, or physiologic stressor
- Medication history: SGLT2 inhibitors, corticosteroids, antipsychotics, immune checkpoint inhibitors [1][4]
- Substance use: alcohol, cocaine, cannabis [1]
- Pregnancy status — pregnant patients may present with euglycemic DKA (glucose <200 mg/dL) [4]
- Prior DKA episodes — 71% of patients with known T1DM experience recurrent DKA [5]
- Important negatives: chest pain, focal neurologic deficits, recent dietary changes (very-low-carb/fasting)
2. Alarm Features
- Altered mental status (drowsiness → stupor → coma) — correlates with severity [1]
- Kussmaul respirations (deep, labored breathing) — sign of severe acidosis
- Hemodynamic instability: hypotension, tachycardia, signs of shock
- pH <7.0 or bicarbonate <10 mEq/L (severe DKA) [1]
- Cerebral edema (especially children): new headache during treatment, vomiting, altered consciousness, bradycardia, hypertension, incontinence [1]
- Signs of precipitating emergency: MI, stroke, sepsis [3]
- Severe hypokalemia (K⁺ <3.3 mEq/L) — risk of cardiac arrhythmia; hold insulin until corrected [1][6]
3. Medications
Precipitating medications
- SGLT2 inhibitors (canagliflozin, dapagliflozin, empagliflozin, ertugliflozin) — increase DKA risk 2.5-fold in T2DM; 5–17× in T1DM; can cause euglycemic DKA [4][7]
- Corticosteroids, antipsychotics (clozapine, olanzapine, quetiapine, risperidone), immune checkpoint inhibitors, sympathomimetics, thiazides [1]
Treatment medications
- Regular insulin IV infusion: 0.1 units/kg/hr (adults); 0.05–0.1 units/kg/hr (children) [1]
- Subcutaneous rapid-acting insulin (lispro, aspart): 0.3 units/kg bolus then 0.1 units/kg hourly — acceptable for mild/uncomplicated DKA [1][3]
- Subcutaneous glargine early in treatment may speed DKA resolution and ease transition [1]
- Potassium replacement in IV fluids when K⁺ < upper limit of normal and urine output established [1]
- Bicarbonate is generally NOT recommended; consider only if pH <6.9–7.0 or severe hyperkalemia with hemodynamic instability [1][6]
Contraindicated/cautions
- Do NOT start insulin if K⁺ <3.3 mEq/L — correct potassium first [1][8]
- Hold SGLT2 inhibitors during acute illness/DKA
4. Diet
- NPO initially during active DKA management
- Very-low-carbohydrate diets and prolonged fasting are risk factors for DKA, especially with SGLT2 inhibitor use [4]
- Excessive alcohol intake precipitates DKA and can cause euglycemic DKA [1]
- Sick-day rules: maintain hydration with noncaloric fluids, do not skip basal insulin even if not eating [4]
- Resume oral intake when tolerating fluids, nausea resolved, and DKA resolving
- Long-term: consistent carbohydrate intake, carb counting education, avoidance of prolonged fasting
5. Review of Systems
- Constitutional: fever, weight loss, fatigue, malaise
- GI: nausea, vomiting, abdominal pain (can mimic acute abdomen), anorexia
- Respiratory: dyspnea, Kussmaul breathing, cough (pneumonia as precipitant)
- GU: polyuria, polydipsia, dysuria (UTI as precipitant)
- Neuro: headache, confusion, altered consciousness, focal deficits (stroke as precipitant)
- CV: chest pain, palpitations (MI as precipitant; arrhythmia from electrolyte derangement)
- Skin: signs of infection, injection site issues, poor wound healing
- Psych: depression, eating disorders, substance use — all associated with insulin omission [9]
6. Collateral History and Family History
- Collateral: Confirm insulin adherence, last insulin dose, pump function, recent illness, oral intake, substance use
- Caregiver/family input critical in pediatric patients and those with altered mental status
- Family history: Type 1 diabetes, autoimmune conditions, type 2 diabetes
- Social context: insurance status, access to insulin and supplies, financial barriers to medication adherence, mental health, eating disorders [9]
- A family history of T1DM is actually protective against DKA at diagnosis (increased awareness leads to earlier recognition) [10]
7. Risk Factors
- Type 1 diabetes (highest risk; rates up to 44.5–82.6 per 1,000 person-years) [3]
- Insulin nonadherence/omission — most common precipitant [1][5][11]
- Prior DKA episode (strongest predictor of recurrence) [9]
- High HbA1c / poor glycemic control
- Insulin pump use (loss of basal insulin depot if interrupted) [9]
- SGLT2 inhibitor therapy [4]
- Infections (pneumonia, UTI, gastroenteritis, dental, skin/soft tissue) [1]
- Younger age, female sex, low socioeconomic status, ethnic minorities [9]
- Psychiatric disorders, eating disorders, substance use [9]
- Pregnancy (up to 2% of pregnancies with pregestational diabetes) [4]
- New-onset diabetes (especially in young children) [1]
- COVID-19 infection [4]
8. Differential Diagnosis
- Hyperosmolar hyperglycemic state (HHS): glucose >600 mg/dL, minimal/no acidosis, low/absent ketones, more severe dehydration, altered mental status; can overlap with DKA [1]
- Alcoholic ketoacidosis: history of heavy alcohol use, low/normal glucose, elevated ketones, anion gap acidosis
- Starvation ketosis: mild ketosis, minimal acidosis, low/normal glucose
- Other causes of high anion gap metabolic acidosis (MUDPILES): methanol, uremia, lactic acidosis, ethylene glycol, salicylates [1]
- Acute abdomen mimics: DKA abdominal pain can mimic appendicitis, pancreatitis, bowel obstruction — reassess after DKA treatment
- Sepsis: can be both a precipitant and a mimic; may present without fever [1]
- Euglycemic DKA: glucose <200 mg/dL — consider in patients on SGLT2 inhibitors, pregnant patients, those with reduced oral intake, alcohol use, or liver failure [1][3]
9. Past Medical History
- Type 1 vs. type 2 diabetes; duration; baseline HbA1c
- Prior DKA episodes (number, severity, precipitants)
- Insulin regimen: MDI vs. pump; type and dose of insulin
- Use of CGM or insulin pump/AID system
- Comorbidities: CKD, CHF, CAD, COPD, cirrhosis (affect treatment approach and prognosis) [12]
- Autoimmune conditions (thyroid disease, celiac, adrenal insufficiency)
- Psychiatric history, eating disorders
- Surgical history (pancreatectomy → pancreatogenic diabetes)
10. Physical Exam
- Vitals: Tachycardia, hypotension/orthostatic hypotension, tachypnea (Kussmaul respirations), fever (suggests infection), hypothermia (poor prognostic sign)
- General: Ill-appearing, signs of dehydration (dry mucous membranes, poor skin turgor, sunken eyes)
- HEENT: Fruity/acetone breath odor, dry mucous membranes, dental infection
- Cardiovascular: Tachycardia, weak pulses, delayed capillary refill
- Respiratory: Kussmaul respirations (deep, sighing), crackles (aspiration, pulmonary edema)
- Abdomen: Diffuse tenderness (common in DKA; reassess after treatment — if persistent, investigate further) [1]
- Neuro: Mental status assessment (GCS), level of consciousness, focal deficits; in children, monitor for signs of cerebral edema every 30 minutes [1]
- Skin: Injection sites, signs of infection, acanthosis nigricans
11. Lab Studies
Required for all patients: [1]
- Point-of-care glucose and serum glucose
- BMP/CMP: electrolytes (Na⁺, K⁺, Cl⁻, CO₂), BUN, creatinine, calcium, magnesium, phosphate
- Venous or arterial blood gas (pH, pCO₂) — venous pH is acceptable [1]
- Serum beta-hydroxybutyrate (preferred over urine ketones) [1][13]
- Anion gap calculation: Na⁺ − (Cl⁻ + HCO₃⁻); elevated >10–12 mEq/L
- Corrected sodium: measured Na⁺ + 1.6 × [(glucose − 100) / 100]
- CBC with differential
- Urinalysis
- HbA1c (assesses baseline control; new-onset vs. known diabetes)
Consider based on clinical presentation: [1]
- Amylase, lipase (pancreatitis)
- Hepatic transaminases
- Troponin, CK (MI, rhabdomyolysis)
- Blood and urine cultures (infection)
- Lactate (sepsis, tissue hypoperfusion)
- Serum osmolality (HHS overlap)
- Pregnancy test
Expected abnormalities
- Hyperglycemia (>250 mg/dL, though can be <200 in euglycemic DKA)
- Elevated anion gap metabolic acidosis
- Elevated beta-hydroxybutyrate (>3.0 mmol/L)
- Pseudohyponatremia (correct for glucose)
- Potassium: may be high, normal, or low despite total body depletion
- Elevated BUN/creatinine (prerenal AKI from dehydration)
- Leukocytosis (stress response; does not necessarily indicate infection)
12. Imaging
- Chest X-ray: Consider if fever, cough, dyspnea, or concern for pneumonia/aspiration [1]
- CT head: If altered mental status out of proportion to metabolic derangement, concern for cerebral edema (especially in children), or focal neurologic deficits [1]
- CT abdomen: If persistent abdominal pain after DKA treatment (rule out surgical abdomen)
- Imaging is not routinely required for uncomplicated DKA — guided by clinical suspicion for precipitating cause
13. Special Tests
Diagnostic scoring/severity classification: [1]
- Point-of-care beta-hydroxybutyrate — preferred for diagnosis and monitoring; more accurate than urine ketones [1][13]
- Calculated serum osmolality: 2(Na⁺) + glucose/18 + BUN/2.8
- DKA Mortality Prediction Model (DKA MPM Score) — can estimate in-hospital mortality risk based on comorbidities, pH, insulin requirements, glucose response, mental status, and fever at 12–24 hours
14. ECG
- ECG is required for all patients with DKA [1]
- Hyperkalemia findings: peaked T waves, widened QRS, sine wave pattern, bradycardia — life-threatening; treat emergently
- Hypokalemia findings: flattened T waves, U waves, ST depression, prolonged QT — common during treatment as insulin drives K⁺ intracellularly
- QT prolongation — a recognized complication of DKA; monitor closely [1]
- Evaluate for acute MI as precipitant (ST changes, new Q waves)
- Continuous telemetry should be considered for all patients during DKA treatment [1]
15. Assessment
DKA is a medical emergency requiring immediate recognition and protocolized management. Key assessment points:
- Classify severity (mild/moderate/severe) based on pH, bicarbonate, anion gap, and mental status [1]
- Identify and treat the precipitating cause — insulin omission is most common; infection can present without fever [1]
- ~10% of DKA presents as euglycemic DKA (glucose <200 mg/dL) — maintain high suspicion in patients on SGLT2 inhibitors, pregnant patients, and those with reduced oral intake [3]
- DKA and HHS can present concurrently (mixed DKA-HHS), which carries higher mortality than either alone [3]
- Atypical presentations: elderly patients may present with more subtle symptoms; children are at higher risk for cerebral edema [1]
- Complications to anticipate: hypokalemia, hypoglycemia, cerebral edema (children), hyperchloremic acidosis, AKI, venous thrombosis, QT prolongation [1]
16. Treatment Plan
The following figure outlines the adult DKA management algorithm:
Initial stabilization
- ABCs; IV access × 2; cardiac monitor; continuous pulse oximetry
- Fluid resuscitation: 1 L 0.9% NS in the first hour (adults); then 250–500 mL/hr based on volume status. ADA recommends 0.45% NS if corrected Na⁺ is normal/high [1]
- Children: 10 mL/kg 0.9% NS over 30 minutes (up to 75 kg), then deficit replacement over 24–48 hours [1]
Insulin (start 1–2 hours after fluids): [1]
- IV regular insulin: 0.1 units/kg/hr (adults); 0.05–0.1 units/kg/hr (children)
- When glucose reaches 250 mg/dL, reduce insulin to 0.05 units/kg/hr AND add D5 to IV fluids to prevent hypoglycemia while continuing to clear ketoacidosis [1]
- Mild DKA alternative: SQ rapid-acting insulin (lispro/aspart) 0.3 units/kg bolus → 0.1 units/kg hourly [1][3]
- Consider early SQ glargine (continue home dose or 0.3 units/kg) alongside IV insulin for faster resolution and smoother transition [1]
Potassium: [1]
- If K⁺ <3.3 mEq/L: hold insulin, replace K⁺ aggressively (20–30 mEq/hr) until >3.3
- If K⁺ 3.3–5.3 mEq/L: add 20–30 mEq K⁺ per liter of IV fluid
- If K⁺ >5.3 mEq/L: hold K⁺, recheck every 2 hours
- Monitor K⁺ every 2 hours (hourly if abnormal)
Bicarbonate: Generally NOT recommended. Consider if pH <6.9–7.0 or severe hyperkalemia with hemodynamic compromise [1][6]
Phosphate/Magnesium: Not routine; replace if severely depleted (PO₄ <1 mg/dL, Mg <1.2 mg/dL) [1]
Monitoring during treatment: [1]
- Hourly: vitals, mental status, POC glucose, fluid balance; consider hourly POC beta-hydroxybutyrate
- Every 2–4 hours: BMP, VBG/ABG, beta-hydroxybutyrate
- Continuous telemetry recommended
Resolution criteria: Clinical improvement + pH >7.3 + bicarbonate ≥18 mEq/L + anion gap normalized + glucose <200 mg/dL + beta-hydroxybutyrate normalized [1]
Transition to subcutaneous insulin: [3]
- Administer basal insulin 2–4 hours before stopping IV insulin to prevent rebound hyperglycemia/ketoacidosis
- Overlap IV insulin for 30–60 minutes after SQ rapid-acting insulin
- Home regimen if well-controlled, or start 0.5–0.8 units/kg/day (half basal, half prandial)
17. Disposition
ICU admission criteria
- Severe DKA (pH <7.0, bicarbonate <10, altered mental status) [1][14]
- Hemodynamic instability or shock
- Need for continuous IV insulin infusion (in many institutions)
- Significant comorbidities (MI, sepsis, stroke as precipitant)
- Children <2 years or with severe DKA [1]
General medical floor/step-down
- Mild-moderate DKA managed with SQ insulin protocol may be safely managed outside the ICU [3][15]
- A hospital-wide SQ insulin DKA protocol demonstrated safe management on general medical-surgical wards with decreased ICU utilization [15]
Discharge criteria
- DKA fully resolved (pH >7.3, bicarbonate ≥18, anion gap closed, glucose <200)
- Tolerating oral intake
- Successfully transitioned to SQ insulin with stable glucose
- Precipitating cause identified and addressed
- Patient educated on DKA prevention, sick-day rules, and insulin management [3]
Specialist consultation triggers
- Endocrinology: new-onset diabetes, recurrent DKA, insulin regimen optimization
- Pediatric endocrinology/PICU: all pediatric DKA
- Nephrology: significant AKI or ESRD
- Neurosurgery: suspected cerebral edema
- Psychiatry/social work: insulin omission due to psychiatric illness, eating disorder, or social barriers
18. Follow Up / Return Precautions
Follow-up timing
- Endocrinology/PCP within 1–2 weeks of discharge
- Diabetes education referral for sick-day management, insulin adjustment, ketone monitoring [3-4]
- Review and ensure access to insulin, supplies, and ketone testing at every visit [4]
Return precautions — instruct patients to seek immediate care if:
- Persistent vomiting or inability to tolerate oral fluids
- Blood glucose >300 mg/dL not responding to correction doses
- Positive ketones (blood beta-hydroxybutyrate >1.5 mmol/L or moderate/large urine ketones)
- Altered mental status, confusion, excessive drowsiness
- Rapid or labored breathing
- Severe abdominal pain
- Signs of infection with inability to manage glucose [4]
Patient counseling points
- Never stop basal insulin, even when not eating [4]
- Know sick-day rules: increase glucose monitoring, check ketones, maintain hydration, contact diabetes team early
- Blood ketone monitoring reduces hospitalization risk by ~50% compared to urine ketone monitoring [4]
- Ensure uninterrupted access to insulin and supplies — financial barriers are a common cause of recurrence
- Expected recovery: most DKA episodes resolve within 12–36 hours with appropriate treatment [11]
- 1-year post-DKA mortality is significantly elevated — emphasize the importance of follow-up and prevention [3]
References
1. Diabetic Ketoacidosis: Evaluation and Treatment. — Veauthier B, Levy-Grau B. American Family Physician. 2024.
2. Diabetic Ketoacidosis: Evaluation and Treatment. — Westerberg DP. American Family Physician. 2013.
3. 16. Diabetes Care in the Hospital: Standards of Care in Diabetes-2026. — American Diabetes Association Professional Practice Committee for Diabetes*. Diabetes Care. 2026.
4. 6. Glycemic Goals, Hypoglycemia, and Hyperglycemic Crises: Standards of Care in Diabetes-2026. — American Diabetes Association Professional Practice Committee for Diabetes*. Diabetes Care. 2026.
5. Current Clinical Features of Diabetic Ketoacidosis in Adults: A German Multicenter Study 2022-2023. — Linck JA, Michels C, Schwanstecher A, et al. Diabetes Technology & Therapeutics. 2026.
6. ACOG Practice Bulletin No. 201: Pregestational Diabetes Mellitus. — Committee on Practice Bulletins—Obstetrics Obstetrics and Gynecology. 2018.
7. FDA Orange Book. — FDA Orange Book. 2026.
8. Approach to the Treatment of Diabetic Ketoacidosis. — Kamel KS, Schreiber M, Carlotti AP, Halperin ML. American Journal of Kidney Diseases : The Official Journal of the National Kidney Foundation. 2016.
9. The Management of Type 1 Diabetes in Adults. A Consensus Report by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). — Holt RIG, DeVries JH, Hess-Fischl A, et al. Diabetes Care. 2021.
10. Factors Associated With Diabetic Ketoacidosis at Onset of Type 1 Diabetes Among Pediatric Patients: A Systematic Review. — Rugg-Gunn CEM, Dixon E, Jorgensen AL, et al. JAMA Pediatrics. 2022.
11. Precipitating Factors, Complications, and Outcomes of Diabetic Ketoacidosis (DKA) in Adults and Pediatrics: A Descriptive Study From Two Tertiary Centers in Riyadh, Saudi Arabia. — Alfayez OM, Almutairi GG, Alqudhibi SB, et al. Journal of Clinical Medicine. 2025.
12. Management of Diabetic Ketoacidosis. — Barski L, Golbets E, Jotkowitz A, Schwarzfuchs D. European Journal of Internal Medicine. 2023.
13. Guidelines and Recommendations for Laboratory Analysis in the Diagnosis and Management of Diabetes Mellitus. — Sacks DB, Arnold M, Bakris GL, et al. Diabetes Care. 2023.
14. Management of Diabetic Keto-Acidosis in Adult Patients Admitted to Intensive Care Unit: An ESICM-endorsed International Survey. — Jozwiak M, Hayes MM, Canet E, et al. Critical Care. 2024.
15. Evaluation of Outcomes Following Hospital-Wide Implementation of a Subcutaneous Insulin Protocol for Diabetic Ketoacidosis. — Rao P, Jiang SF, Kipnis P, et al. JAMA Network Open. 2022.