Diabetic Ketoacidosis (DKA) Adults

🚑 Diabetic ketoacidosis (DKA) = medical emergency. Treat the triad: ketonaemia + acidosis + hyperglycaemia and actively find the trigger. Common killers are 🦠 sepsis, ❤️ ACS/MI, 🫀 pancreatitis, missed insulin, and (in women) 🤰 pregnancy. Remember: with SGLT2 inhibitors (e.g. dapagliflozin, empagliflozin), DKA can be euglycaemic — ketones and pH matter most.

✅ Guideline anchor (UK): This structure matches the JBDS DKA guideline (March 2023) and the JBDS single-page pathway (March 2023 update). Use local trust charts for exact infusion set-up, monitoring frequency, and escalation pathways.

🧬 DKA aetiology (precipitants)

DKA happens when insulin supply is insufficient for the body’s needs, allowing unchecked lipolysis and ketone production. In most cases the “cause” is not diabetes alone but a trigger that increases stress hormones or interrupts insulin delivery—so you must hunt it actively while treating the DKA.

• 🦠 Infection (most common): pneumonia, UTI/pyelonephritis, skin/foot infection, line infection.
• 💉 Missed insulin / pump failure: deliberate or accidental omission, blocked cannula, empty reservoir, poor access to meds.
• ❤️ MI/ACS (may be silent), 🧠 stroke.
• 🫀 Pancreatitis.
• 💊 Drugs: SGLT2 inhibitors (can cause euglycaemic DKA), steroids, atypical antipsychotics, sympathomimetics; alcohol/cocaine.
• 🤰 Pregnancy (lower threshold for ketosis; can be euglycaemic).
• 🩺 New diagnosis of type 1 diabetes / LADA, or significant intercurrent illness (trauma, surgery).
• 🧠 Psychosocial factors: eating disorder (“diabulimia”), depression, safeguarding issues, chaotic lifestyle—needs diabetes CNS input before discharge.

🩺 Clinical presentation of Diabetic Ketoacidosis (DKA)

DKA is a syndrome of absolute/relative insulin deficiency with excess counter-regulatory hormones (glucagon, adrenaline, cortisol, GH) → lipolysis and hepatic ketogenesis (β-hydroxybutyrate predominates) → metabolic acidosis. Hyperglycaemia drives osmotic diuresis, so patients are often profoundly dehydrated even if they “don’t look dry” initially. Symptoms can evolve over hours (sometimes 24–48 h), and the trigger (infection, missed insulin, MI, pancreatitis, steroids, SGLT2 inhibitors) is often the main threat.

🚩 Typical symptoms (what the patient tells you)

• Polyuria, polydipsia and nocturia (osmotic diuresis) 💧🚽
• Marked thirst, dry mouth, weight loss
• Nausea, vomiting, abdominal pain (ketones + gut hypoperfusion) 🤢
• Fatigue, weakness, reduced exercise tolerance
• Breathlessness or “air hunger” (compensatory hyperventilation)
• Altered mental state: irritability → confusion → drowsiness; coma if severe

🔎 Key signs (what you find)

• Dehydration: tachycardia, postural drop/hypotension, dry mucosae, delayed capillary refill, cool peripheries
• Kussmaul breathing: deep, rapid respirations as compensation for acidosis
• “Fruity”/acetone breath (not universal; can be subtle)
• Abdominal tenderness (can mimic an acute abdomen; improves as acidosis resolves)
• Reduced GCS in severe DKA; consider cerebral oedema (rare in adults) if headache, agitation, focal neurology
• Temperature may be normal even with sepsis (don’t be reassured)

⚠️ Presentations that catch people out

• Euglycaemic DKA (often SGLT2 inhibitor-related, pregnancy, starvation): glucose may be only mildly raised but ketones/pH are abnormal.
• Mixed DKA/HHS: very high glucose/osmolality plus ketones/acidosis—often older patients with type 2 diabetes.
• New diabetes / LADA: rapid weight loss, ketones, “type 2 phenotype” but insulin-deficient.
• Infarction-triggered DKA: chest pain may be absent (“silent MI”), especially in older adults/diabetes.

🧪 DKA investigations (what to do and why)

• Bedside (immediate):
  • Capillary glucose (severity + response to treatment).
  • Blood ketones (β-hydroxybutyrate; primary marker of resolution).
  • VBG: pH, HCO₃⁻, K⁺, lactate (acidosis severity; potassium safety; lactate for shock/sepsis).
  • ECG (hyper/hypokalaemia changes; screen for MI/arrhythmia).
  • Observations: BP, HR, RR, SpO₂, temperature, GCS; strict fluid balance and urine output.
• Blood tests:
  • U&E/creatinine/eGFR (AKI, dehydration; guides K replacement and drug decisions).
  • FBC and CRP (infection/inflammation; note WCC can rise from stress alone).
  • LFTs (baseline; hypoperfusion/cholestasis clues).
  • Serum osmolality or calculated osmolality (consider mixed DKA/HHS if very high).
  • Magnesium & phosphate if severe/prolonged DKA, arrhythmia, malnutrition, or ICU-level illness.
  • Troponin if ACS possible (diabetes + DKA can mask pain).
  • Lipase (± amylase) if pancreatitis suspected (abdominal pain/vomiting, high triglycerides).
  • Blood cultures if sepsis suspected (before antibiotics if possible, but don’t delay treatment).
• Urine:
  • Urinalysis (infection; ketones if blood ketones unavailable).
  • Urine culture if UTI suspected.
• Imaging / other tests (trigger-directed):
  • CXR if respiratory symptoms/signs or sepsis work-up.
  • Pregnancy test (β-hCG) in women of childbearing potential.
  • CT head if reduced consciousness not improving, focal neurology, or concern for cerebral oedema/stroke.

🧠 Management

“DKA typically presents with polyuria, polydipsia, dehydration, nausea/vomiting and abdominal pain, and Kussmaul breathing with possible acetone breath, plus tachycardia, hypotension and varying reduced consciousness. I would actively look for triggers such as infection, missed insulin, MI, pancreatitis, steroids, pregnancy or SGLT2 inhibitor use.”

📌 JBDS treatment focus: Treat to clear ketones and correct acidosis. Glucose will fall, but stopping insulin early risks ongoing ketogenesis. Also note: no IV insulin bolus is recommended if FRIII is started promptly.

1) ABCDE first (0–10 min)

• Airway/Breathing: sit up; give O₂ only if SpO₂ <94% (or 88–92% if CO₂ retainer).
• Circulation: 2 large-bore IV cannulas; continuous ECG, BP, SpO₂; strict fluid balance; consider catheter if very unwell or not passing urine.
• Disability: GCS; capillary glucose + capillary ketones; assess for headache/behaviour change.
• Exposure: examine for trigger (infection sources, pump/insulin omission, abdominal pain, chest pain).

2) Confirm DKA (diagnostic triad)

• 💉 Glucose > 11 mmol/L or known diabetes (may be lower with SGLT2-related DKA).
• ⚡ Blood ketones > 3.0 mmol/L (or urine ketones ≥2+ if blood ketones unavailable).
• 🧪 Acidosis: venous pH < 7.3 or HCO₃⁻ < 15 mmol/L.

3) Immediate tests

• Bedside: capillary glucose, capillary ketones, VBG (pH/HCO₃/K⁺/lactate), ECG.
• Bloods: FBC, U&E/creatinine, LFTs, CRP; cultures if sepsis suspected; troponin per ACS pathway; lipase (± amylase).
• Other: urine dip ± culture; CXR if respiratory features; β-hCG in women with childbearing potential.

4) Fluids (JBDS template; individualise)

• If SBP <90 mmHg: 500 mL 0.9% saline over 10–15 min, reassess, repeat as needed; involve critical care early.
• If SBP ≥90 mmHg: 1 L 0.9% saline over 60 min (no K in the first litre).
• Then:
  • 1 L 0.9% saline (+KCl as below) over 2 hours
  • 1 L 0.9% saline (+KCl) over 2 hours
  • 1 L 0.9% saline (+KCl) over 4 hours
  • 1 L 0.9% saline (+KCl) over 6 hours (then reassess at 12 hours for further fluid needs and overload)
• More cautious / consider HDU: age 18–25, elderly, pregnancy, heart failure, renal failure.

5) Potassium (start early; check frequently)

Total body potassium is depleted even if the initial serum K⁺ is normal/high. Insulin drives K⁺ into cells → dangerous hypokalaemia if you don’t replace. Add potassium only if K⁺ <5.5 mmol/L AND the patient is passing urine.

6) Insulin + glucose (clear ketones, not just glucose)

• Start FRIII: 0.1 units/kg/hour IV (e.g., 50 units soluble insulin in 50 mL 0.9% saline). No IV bolus.
• Continue basal insulin (glargine/detemir/degludec) at the usual dose and time.
• When glucose <14 mmol/L: start 10% glucose at 125 mL/hour alongside saline.
• Consider reducing FRIII to 0.05 units/kg/hour once glucose is <14 mmol/L if ketones are falling and acidosis improving.

7) Treat the trigger (parallel)

• Sepsis: Sepsis Six + IV antibiotics within 1 hour if suspected (local policy).
• ACS/MI: ECG on arrival; troponin per pathway; early cardiology if high-risk/ongoing pain.
• Pancreatitis: lipase (preferred); consider triglycerides and imaging if indicated.
• Pregnancy: urgent obstetric input; tighter fluid balance and monitoring.
• Medication-related: stop SGLT2 inhibitor during DKA; address missed insulin/pump failure and psychosocial factors.

8) Monitoring & targets

• Hourly: capillary glucose; capillary ketones if available; NEWS2; fluid balance; urine output (aim ≥0.5 mL/kg/hr).
• VBG: pH/HCO₃/K⁺ at 60 min, 2 h, then 2-hourly (more often if K abnormal).
• Targets: ketones ↓ ≥0.5 mmol/L/hr or HCO₃⁻ ↑ ≥3 mmol/L/hr; glucose ↓ ≥3 mmol/L/hr; keep K in range.
• Resolution: ketones < 0.6 mmol/L AND venous pH > 7.3 AND HCO₃⁻ > 15 mmol/L, clinically improving and able to eat/drink.

9) Step-down to subcutaneous insulin

• When resolving and eating: give rapid-acting SC insulin with first meal, then stop IV insulin 30 minutes later.
• Ensure basal insulin is continued; provide sick-day rules, hypo education, and follow-up.

10) Escalate early (HDU/ICU indicators)

• pH < 7.0 or HCO₃⁻ < 5; ketones > 6; K⁺ < 3.5 despite replacement; persistent hypotension; hypoxia; GCS < 12; severe comorbidity (pregnancy, frailty, cardiac/renal failure).

Common pitfalls

• ❌ Stopping long-acting insulin.
• ❌ Under-replacing potassium / not checking it frequently early on.
• ❌ Stopping insulin when glucose normalises (you must clear ketones).
• ❌ Missing sepsis/ACS/pancreatitis/pregnancy as the trigger.
• ❌ Over-resuscitating fluids in frail/cardiac/renal patients without senior review.

📚 Guidelines / UK references

• JBDS 02: Management of DKA in Adults (March 2023, full guideline)
• JBDS DKA single-page pathway (March 2023)
• JBDS DKA single-page pathway (updated version)
• BNF/NICE treatment summary: Diabetic hyperglycaemic emergencies