Table of Contents · 11 sections
In a nutshell. Acute complications of DM: DKA (pH < 7.3, HCO₃ < 18, ketonuria, glucose typically 14–33 mmol/L) and HHS (glucose > 33, osmolality > 320, minimal ketoacidosis). Management: rehydration, insulin 0.1 IU/kg/h, K⁺ and acidosis correction. Chronic complications include microvascular (retinopathy, nephropathy, neuropathy) and macrovascular (CHD, stroke, PAD). Screening and control of HbA1c, BP, LDL are the foundation of prevention.
1. DKA Criteria
- Glycemia > 14 mmol/L (euglycemic DKA may occur with SGLT-2 inhibitors).
- Arterial blood pH < 7.3; HCO₃ < 18 mmol/L.
- Urinary ketones ≥ 2+ or β-hydroxybutyrate > 3 mmol/L.
- Anion gap > 12 mmol/L.
Mild DKA: pH 7.25–7.30; moderate: 7.0–7.24; severe: < 7.0.
2. DKA Triggers
- Infections (30–40%).
- Insulin omission, improper administration.
- New-onset Type 1 Diabetes.
- Myocardial infarction, stroke.
- Medications: glucocorticoids, thiazide diuretics, SGLT-2 inhibitors (euglycemic DKA).
- Stress, surgery, pregnancy.
3. Pathogenesis
Insulin deficiency + excess counterregulatory hormones (glucagon, catecholamines, cortisol, GH) → lipolysis → free fatty acids → hepatic β-oxidation → acetoacetate and β-hydroxybutyrate → metabolic acidosis. Osmotic diuresis due to hyperglycemia → dehydration and electrolyte imbalances.
4. Clinical Presentation of DKA
- Polyuria, polydipsia, progressive fatigue.
- Nausea, vomiting, abdominal pain (mimicking an acute abdomen).
- Kussmaul breathing (deep, labored respiration).
- Fruity (acetone) breath odor.
- Dehydration, tachycardia, hypotension.
- Altered mental status ranging from somnolence to coma.
5. Hyperglycemic Hyperosmolar State (HHS)
- Glucose > 33 mmol/L.
- Effective osmolality > 320 mOsm/kg.
- pH > 7.3; HCO₃ > 18; minimal ketonuria.
- Typical for Type 2 DM in elderly patients, associated with infection, dementia.
- Dehydration of 8–10 L, frequent multi-organ failure.
- Higher mortality than DKA (up to 15%).
6. Management of DKA and HHS
1. Rehydration
- First hour: 0.9% NaCl 15–20 mL/kg (~1 L in adults).
- Subsequent: 250–500 mL/h; if Na is normal or high — 0.45% NaCl.
- When glycemia reaches 14 mmol/L — switch to 5% glucose with insulin (to prevent hypoglycemia and cerebral edema).
2. Insulin
- After potassium recovery ≥ 3.3 mmol/L — regular insulin 0.1 IU/kg IV bolus + 0.1 IU/kg/h infusion.
- Goal — reduce glucose by 3–4 mmol/L/h.
- Do not stop the infusion until acidosis resolves (HCO₃ > 18, pH > 7.3, anion gap < 12) — otherwise relapse will occur.
3. Potassium
- > 5.5 — do not administer, monitor every 2 h.
- 3.3–5.5 — infuse 20–30 mmol/L.
- < 3.3 — hold insulin, administer 20–30 mmol/h, restart insulin when K⁺ ≥ 3.3.
4. Bicarbonate
- Only if pH < 6.9: 100 mL of 8.4% (100 mmol) over 2 h.
- In HHS — not used.
5. Prevention of Complications
- Cerebral edema (children, adolescents) — slow rehydration, not > 40 mL/kg in the first 4 h.
- Hypophosphatemia — replenishment if < 0.3 mmol/L.
- Thromboembolism prophylaxis (especially in HHS) — LMWH.
7. Hypoglycemia
- Level 1: < 3.9 mmol/L.
- Level 2: < 3.0 mmol/L.
- Level 3: accompanied by altered consciousness.
- Conscious — 15 g of fast-acting carbohydrates (15/15 rule).
- Unconscious — glucagon 1 mg IM, 40% glucose 40–60 ml IV.
- In insulin-treated patients with hypo unawareness — long-term continuous glucose monitoring (CGM) is indicated.
8. Chronic complications
Microvascular
| Complication | Screening | Tactics |
|---|---|---|
| Diabetic retinopathy | Ophthalmoscopy starting from diagnosis (type 2 DM) or after 5 years (type 1 DM), then annually | Glycemic and BP control; laser photocoagulation, anti-VEGF (ranibizumab) |
| Diabetic nephropathy | Albumin-to-creatinine ratio (ACR), eGFR annually | ACE inhibitors / ARBs, SGLT-2 inhibitors (empagliflozin, dapagliflozin), finerenone |
| Diabetic neuropathy | Annually: vibration, tactile sensation, Achilles reflexes, 10 g monofilament | Glycemic control; symptomatic treatment — pregabalin, duloxetine, α-lipoic acid |
Macrovascular
- CHD — DM is a coronary heart disease risk equivalent; statins for all adults with DM.
- Stroke — risk ↑ 2-fold.
- Peripheral artery disease — ABI annually in patients > 50 years.
Diabetic foot
- Foot inspection annually, daily self-inspection by the patient.
- Ulcers: offloading, debridement, antibiotics, revascularization if necessary.
- Charcot neuroarthropathy — immobilization for 3–6 months.
9. Treatment goals
- HbA1c < 7% (individualized 6.5–8%).
- BP < 130/80 in high risk, < 140/90 otherwise.
- LDL < 1.8 mmol/L in high risk, < 1.4 in very high risk.
- Smoking cessation.
- Physical activity ≥ 150 min/week of moderate intensity.
10. Special situations
- Pregnancy and DM — HbA1c < 6%, fasting glucose < 5.3 mmol/L, 1-h postprandial < 7.8; insulin therapy.
- Perioperative period — insulin, target 6–10 mmol/L; discontinue SGLT-2 inhibitors 3 days prior to surgery.
- ICU — target 7.8–10 mmol/L, continuous IV insulin infusion.
- Elderly — avoid hypoglycemia: relaxed HbA1c goals < 8%, avoid sulfonylureas.
11. FAQ
How does "euglycemic" DKA differ from classical DKA?
Glucose < 14 mmol/L in patients taking SGLT-2 inhibitors. Clinical presentation is masked by normoglycemia; ketones and acidosis are the key diagnostic markers. Discontinue SGLT-2 inhibitors, initiate insulin + 5% glucose.
When to switch to subcutaneous insulin after DKA?
After resolution of acidosis, normalization of consciousness, and resumption of oral intake. IV insulin infusion must overlap with SC long-acting insulin injection by at least 2 hours.
Why calculate the anion gap in DKA?
An indicator of acidosis resolution: once normalized (< 12), insulin infusion can be discontinued, even if pH remains slightly low (hyperchloremic acidosis from 0.9% NaCl is possible).
Which insulin is preferred in type 1 DM?
Basal-bolus regimen with analogs: basal — glargine 300 or degludec, boluses — aspart/lispro/glulisine. Insulin pump therapy with continuous monitoring provides flexible control.
What is the "honeymoon phase" after type 1 DM onset?
A partial remission period of 3–12 months after starting insulin: residual β-cells secrete insulin, requiring lower doses. Immunosuppressive therapy (teplizumab) is being investigated as a method to prolong it.
See also: Glucose-lowering drugs · Thyroid gland · Heart failure · Stroke · Catalog