Anaesthetic Management of a Patient in DKA for Emergency Below-Knee Amputation

1. Preoperative Assessment & Resuscitation

Understand the Clinical Context

Establish the DKA Severity

Resuscitation (Run Concurrently with Surgical Prep)

• 0.9% NaCl at 2–4 L in the first 2–4 hours. Even with high osmolality, normal saline is still relatively hypotonic and the fluid of choice initially
• Once glucose falls to <250 mg/dL (13.9 mmol/L), add 10% dextrose alongside 0.9% NaCl — the saline acts as resuscitation fluid while the dextrose provides substrate for ongoing insulin infusion

• Fixed-rate IV insulin infusion at 0.1 units/kg/hour commenced as soon as DKA is diagnosed
• Do NOT give IV bolus insulin (avoid rapid glucose drop and cerebral oedema risk)
• Once glucose <250 mg/dL AND ketones <1.0 mmol/L, reduce to 0.05 units/kg/hour
• Continue background long-acting subcutaneous insulin if already prescribed, alongside IV infusion
• Blood glucose will fall ~10% per hour; acidosis resolves more slowly

• Despite apparent hyperkalemia at presentation (due to transcellular shift from acidosis), total body K⁺ is depleted
• After insulin starts, K⁺ falls rapidly
• Add K⁺ 40 mEq/L to 0.9% NaCl if serum K⁺ <5.5 mEq/L and the patient is passing urine
• Hold potassium if K⁺ >5.5 mEq/L; review urgently if K⁺ <3.5 mEq/L
• Do not start insulin if K⁺ <3.0 mEq/L — correct first

• Not routinely indicated; may paradoxically worsen CNS pH
• Consider only if pH <7.0 and not responding to fluids/insulin
• Monitor serum phosphate and magnesium; replace only if profound hypoalbuminaemia (<1.0 mg/dL phosphate) with muscle weakness

Investigations

• ABG (pH, pCO₂, HCO₃⁻, lactate)
• Blood glucose, bedside ketones (β-hydroxybutyrate preferred over urine dipstick — nitroprusside reagent does NOT detect β-hydroxybutyrate)
• U&E, creatinine, eGFR (renal impairment is common)
• FBC (WBC typically elevated in DKA even without infection — interpret cautiously)
• ECG (ischaemia; potassium-related changes — peaked T waves with hyperkalaemia, flattening/U waves with hypokalaemia)
• CXR (aspiration, pneumonia, fluid status)
• Serum amylase (may be elevated in DKA without pancreatitis — non-specific)
• Blood cultures, wound cultures
• Coagulation screen (sepsis-associated coagulopathy)
• HbA1c — gives context on baseline glycaemic control

Consider the Diabetic Complications

• Cardiovascular: IHD, HF, autonomic neuropathy → postural hypotension, blunted response to laryngoscopy/vasopressors
• Renal: Nephropathy/CKD → drug dose modification, fluid balance harder to manage
• Neuropathy: Peripheral neuropathy (relevant to regional anaesthesia documentation), autonomic neuropathy → gastroparesis = full stomach risk
• Airways: Reduced joint mobility including cervical spine — anticipate a potentially difficult airway
• Retinopathy: Avoid extremes of blood pressure (hypotension risks retinal ischaemia)

2. Risk Stratification

• Metabolic: Active DKA — acidosis, electrolyte instability, volume depletion
• Cardiovascular: Likely IHD ± autonomic neuropathy
• Renal: Likely CKD (diabetic nephropathy)
• Sepsis/systemic infection: Triggers DKA and causes further haemodynamic instability
• Aspiration: Gastroparesis from autonomic neuropathy + DKA-related ileus
• Airway: Possible cervical spine stiffness, obesity

3. Timing of Surgery

• Do not delay indefinitely: Source control (amputation) is essential to resolve the precipitating infection/ischaemia driving DKA
• Targeted resuscitation of 2–4 hours is appropriate if the patient is haemodynamically salvageable — correct fluid deficit, hyperkalaemia, severe acidosis
• If pH <7.1 and the patient is cardiovascularly unstable, liaise closely with the surgical team about the minimum acceptable metabolic status for safe anaesthesia
• Surgery should not wait for full DKA resolution (which takes 12–24+ hours)

4. Choice of Anaesthetic Technique

Regional Anaesthesia — Preferred if feasible

• Avoids general anaesthesia and the associated aspiration risk (critical in gastroparesis/full stomach)
• No requirement for airway instrumentation
• Preserves respiratory function in a patient who may already have compensatory hyperventilation (Kussmaul breathing) critical to maintaining pH
• Excellent surgical analgesia
• Reduces stress response and catecholamine surge (which worsens hyperglycaemia)
• Avoids volatile anaesthetic-related glucose dysregulation

• Document pre-existing peripheral neuropathy before performing neuraxial/peripheral blocks
• Avoid neuraxial block if coagulopathy is present (sepsis, disseminated intravascular coagulation)
• Spinal anaesthesia in a dehydrated, vasodilated patient can cause profound hypotension — have vasopressors (phenylephrine, ephedrine, noradrenaline infusion) ready
• Sedation may still be required (use carefully — airway protection)

General Anaesthesia — if regional is contraindicated or insufficient

• Gastroparesis from autonomic neuropathy
• DKA-associated ileus
• Delayed gastric emptying in sepsis
• Emergency (not fasted) presentation

• Preoxygenation (3–5 min 100% O₂ or 8 vital capacity breaths)
• IV induction: Ketamine (1–2 mg/kg) — preferred in haemodynamic instability (maintains SVR and cardiac output); alternatively etomidate (0.3 mg/kg) if adrenal function is not a concern; avoid thiopentone and propofol in haemodynamic instability
• Cricoid pressure
• Neuromuscular blockade: Suxamethonium 1.5 mg/kg (check serum K⁺ first — suxamethonium raises K⁺ by ~0.5 mEq/L; if K⁺ already ≥5.5, use high-dose rocuronium 1.2 mg/kg with sugammadex reversal available)
• Cuffed ETT, confirm placement
• Consider awake fibreoptic intubation if difficult airway is anticipated

• Volatile or TIVA — both acceptable; TIVA may offer more control over haemodynamics
• Target moderate depth; multimodal analgesia (local anaesthetic infiltration, paracetamol, avoid NSAIDs in renal impairment)
• Avoid nitrous oxide (increases PONV, bowel distension in ileus)

5. Intraoperative Glucose Management

• Continue IV insulin infusion intraoperatively; do NOT stop it because of surgical stimulation
• Monitor glucose every 30–60 minutes intraoperatively (no less than hourly)
• If glucose drops toward <140 mg/dL, reduce insulin rate and increase dextrose infusion rate
• Avoid hypoglycaemia — more dangerous than moderate hyperglycaemia intraoperatively (masked by anaesthesia)
• Avoid glucose-containing fluids as primary resuscitation fluid until DKA is under control

6. Haemodynamic Management

• Volume status: These patients are typically 5–10 L fluid-depleted. Judicious fluid replacement guided by clinical response (urine output >0.5 mL/kg/hour, MAP >65 mmHg)
• Vasopressors: Noradrenaline is first-line if hypotension persists despite adequate filling. Vasopressin as second-line
• Invasive monitoring: Arterial line (A-line) is essential — continuous BP monitoring, serial ABG, glucose, electrolyte sampling; central venous access for vasoactive drugs and fluid management
• Tourniquet: Often used for BKA; inflation causes additional potassium release and metabolic load on release — be prepared for acidosis and electrolyte shift on tourniquet deflation

7. Ventilation

• If intubated: Do NOT over-correct the compensatory respiratory alkalosis (Kussmaul breathing)
• Target PaCO₂ to match the patient's pre-intubation level (estimated from pH and HCO₃⁻ using Winter's formula: expected PaCO₂ = 1.5 × HCO₃⁻ + 8 ± 2)
• Ventilating to a normal PaCO₂ of 40 mmHg in a patient with metabolic acidosis and HCO₃⁻ of 10 mEq/L will cause severe acidosis worsening — maintain hyperventilation (PaCO₂ ~20–25 mmHg if pre-intubation was that)
• Respiratory compensation is critical — do not blunt it with muscle relaxants without appropriate ventilatory targets

8. Postoperative Care

• ICU/HDU admission is mandatory
• Continue IV insulin infusion until patient can eat and drink; overlap subcutaneous insulin by 1–2 hours before stopping IV infusion to prevent rebound ketosis
• Monitor glucose 1–2 hourly, electrolytes 4-hourly
• DKA resolution criteria: pH >7.3, HCO₃⁻ >18 mEq/L, glucose <250 mg/dL, ketones <0.6 mmol/L, anion gap normalised
• Adequate analgesia (post-op regional if not done intraoperatively; PCA morphine with caution in renal impairment; avoid NSAIDs)
• PONV prophylaxis (critical in DM1 — to allow resumption of oral intake and baseline insulin regimen)
• Treat the precipitating cause — antibiotics, sepsis bundle
• DVT prophylaxis (high risk — immobility, sepsis, vasculopathy)
• Wound care and stump monitoring

Summary: Key Priorities at a Glance

• Miller's Anesthesia, 10e — Diabetes Mellitus, Perioperative Management (pp. 3964–3968)
• Goldman-Cecil Medicine — DKA Treatment (p. 2484–2485)
• Current Surgical Therapy, 14e — Perioperative Euglycemia (p. 1510–1511)
• Sabiston Textbook of Surgery — Below-Knee Amputation (p. 1516–1518)
• Barash Clinical Anesthesia, 9e — Diabetes Mellitus