Anaesthetic Management of a Patient with DKA for Emergency Below Knee Amputation

1. Preoperative Assessment & Optimisation

Recognise the Urgency Spectrum

• Surgery should not proceed until DKA is at least partially corrected — but delay must be weighed against the surgical indication (sepsis, limb ischaemia).
• Aim to correct the most dangerous abnormalities: severe acidosis (pH < 7.1), hypokalaemia, and severe hypovolaemia — before or simultaneously with induction.

Establish the Diagnosis of DKA

Investigations (STAT)

• ABG — pH, PaCO₂, HCO₃⁻, base excess; assess Kussmaul respiration compensation
• Electrolytes — Na⁺, K⁺, Cl⁻, HCO₃⁻ (corrected Na for hyperglycaemia: add 1.6 mEq/L per 100 mg/dL glucose >100)
• Glucose, serum ketones (β-hydroxybutyrate)
• Urea/Creatinine — assess AKI (common in DKA due to volume depletion)
• FBC — WCC >25,000 suggests concurrent infection
• ECG — hypokalaemia changes (flat T waves, U waves, prolonged QT); silent MI (autonomic neuropathy masks ischaemia)
• Phosphate, Mg²⁺
• CXR, blood cultures if septic
• Chest auscultation — assess fluid status; be cautious with aggressive fluids in those with cardiac dysfunction

End-Organ Assessment (DM Complications)

• Cardiovascular: accelerated atherosclerosis, silent CAD (diabetic autonomic neuropathy masks ischaemia), cardiomyopathy, orthostatic hypotension
• Renal: diabetic nephropathy — check GFR; affects drug dosing and fluid handling
• Autonomic neuropathy: cardiovascular lability, gastroparesis (full stomach risk), impaired hypoxic ventilatory drive, loss of baroreceptor sensitivity
• Airway: cervical spine stiffness, limited atlanto-occipital extension; "prayer sign" (stiff hand joints) previously correlated with difficult airway — now largely refuted, but assess carefully regardless

2. Simultaneous Resuscitation While Preparing for Theatre

A. Fluid Resuscitation

• Normal saline (0.9%) — standard initial fluid; balanced crystalloids (Hartmann's/Plasmalyte) may restore volume faster in DKA
• Volume deficit in DKA: 2–4 litres
• Rate: 50–1000 mL/h depending on cardiac function
• Target: replete one-third of deficit in first 6–8 hours; adjust thereafter
• In patients with cardiac dysfunction, use less aggressive rates with invasive monitoring

B. Insulin Therapy

• Do NOT start insulin if K⁺ < 3.3 mEq/L — risk of fatal hypokalaemia and arrhythmia
• Replace potassium first, then initiate insulin
• Standard regimen: 0.1 units/kg IV bolus → 0.1 units/kg/h infusion
• Target glucose reduction: 75–100 mg/dL/hour (maximum rate regardless of dose — limited by receptor binding)
• Add dextrose (5% or 10%) to fluids when glucose falls to 200–250 mg/dL to continue insulin without hypoglycaemia
• Monitor glucose hourly

C. Potassium Replacement

• Most critical electrolyte abnormality in DKA
• Total body deficit: 3–10 mEq/kg despite normal or high initial serum K⁺
• Serum K⁺ falls rapidly within 2–4 hours of insulin initiation (intracellular shift)
• Protocol:
  • K⁺ < 3.3 → give 40 mEq/h; hold insulin
  • K⁺ 3.3–5.3 with urine output >0.5 mL/kg/h → add 20–40 mEq to each litre of crystalloid; target K⁺ 4–5 mEq/L
  • K⁺ > 5.3 → withhold potassium, monitor hourly
• Continuous cardiac monitoring mandatory

D. Bicarbonate

• Controversial; generally not indicated until pH < 7.1
• Below pH 7.1: risk of haemodynamic instability from myocardial depression and hypoventilation
• Caution: rapid bicarbonate → CO₂ diffuses across BBB faster than bicarbonate → paradoxical CSF acidosis, altered cerebral blood flow, CNS dysfunction

E. Phosphate

• Deficit ~1 mmol/kg; replace if:
  • Plasma phosphate < 1.0 mg/dL, OR
  • Cardiac dysfunction, ventilatory depression, or anaemia present

3. Choice of Anaesthetic Technique

Regional vs General Anaesthesia

• Avoids airway manipulation in a high-risk aspiration patient
• Better haemodynamic control in a vasculopathic patient
• Maintains spontaneous ventilation
• Superior perioperative analgesia
• Avoids polypharmacy in renally/hepatically compromised patient

• Acidosis and coagulopathy (if AKI or DIC present) may contraindicate spinal/neuraxial
• Patient cooperation may be impaired (altered sensorium, Kussmaul breathing)
• Sympathetic block from spinal can worsen hypotension in an already hypovolaemic patient
• Local anaesthetic toxicity risk if peripheral nerve blocks chosen (reduced clearance with renal impairment)

If GA is Required — Airway & Induction

• Gastroparesis from diabetic autonomic neuropathy (delayed gastric emptying)
• Emergency setting
• Possible opioid premedication
• Metabolic acidosis → nausea/vomiting

1. Pre-oxygenate with 100% O₂ for 3–5 minutes (denitrogenation)
2. Cricoid pressure (Sellick's manoeuvre)
3. Induction agent:
   • Ketamine (1–2 mg/kg IV): preferred — maintains haemodynamics, bronchodilator; avoid if ICP raised
   • Etomidate (0.3 mg/kg IV): haemodynamically stable; single dose acceptable (adrenal suppression less critical in short-term use)
   • Avoid propofol in haemodynamically compromised patients
4. Succinylcholine 1.5 mg/kg IV (or high-dose rocuronium 1.2 mg/kg if succinylcholine contraindicated — reverse with sugammadex)
5. Intubate — have difficult airway trolley available

4. Intraoperative Management

Monitoring (Minimum)

• 5-lead ECG (detect silent ischaemia, arrhythmias from electrolyte disturbance)
• SpO₂ with waveform
• ETCO₂ — critical; Kussmaul breathing is a compensatory mechanism; avoid over-ventilating (normalising CO₂ too rapidly can worsen acidosis)
• Invasive arterial line — continuous BP monitoring + repeated ABG/glucose sampling
• Urinary catheter — hourly urine output (resuscitation target >0.5 mL/kg/h)
• Central venous access — CVP monitoring; potassium replacement
• Temperature — risk of hypothermia (peripheral vasodilation from acidosis, cool fluids)
• Neuromuscular blockade monitor if GA

Ventilation Strategy (if GA)

• Maintain the patient's compensatory hyperventilation
• Target PaCO₂ proportional to degree of metabolic acidosis — do NOT normalise PaCO₂ until acidosis corrects (sudden PaCO₂ normalisation in severe acidosis → severe drop in blood pH)
• Formula: Expected PaCO₂ = (1.5 × HCO₃⁻) + 8 ± 2 (Winter's formula)
• Tidal volume 6–8 mL/kg; PEEP 5 cmH₂O
• Avoid excessive PEEP (impairs venous return in volume-depleted patient)

Blood Glucose Monitoring

• Check every 30 minutes intraoperatively
• Target: 140–180 mg/dL intraoperatively (tight control not beneficial and risks hypoglycaemia)
• Continue insulin infusion; add dextrose-containing fluids when glucose < 200 mg/dL

Potassium — Continuous Vigilance

• Check every 1–2 hours intraoperatively
• ECG changes mandate urgent K⁺ check
• Have 40 mEq KCl readily available to add to running fluids

Haemodynamic Management

• Expect haemodynamic lability:
  • Hypovolaemia from DKA (2–4 L deficit)
  • Vasodilation from acidosis
  • Autonomic neuropathy (blunted baroreceptor response)
  • Cardiovascular comorbidities (cardiomyopathy, CAD)
• Vasopressors: Noradrenaline preferred; consider early if refractory to fluid
• Avoid excessive fluid in those with cardiac dysfunction

Analgesia

• Peripheral nerve block (sciatic + femoral) provides excellent intraoperative and postoperative analgesia — even as an adjunct if GA used
• Opioids: use cautiously; impair gastric emptying; renally-excreted metabolites accumulate in AKI (morphine-6-glucuronide)
• Consider paracetamol IV (renal/hepatic function dependent) and ketamine infusion (0.1–0.3 mg/kg/h) for opioid-sparing

Surgical Considerations

• Tourniquet application raises serum K⁺ on release → anticipate
• Blood loss is typically limited in BKA
• Consider cell salvage if anticipated blood loss significant

5. Postoperative Management

Destination

• ICU/HDU — mandatory; ongoing DKA management, haemodynamic monitoring, ventilatory support if required

Ongoing DKA Management

• Continue IV insulin infusion until anion gap normalises and bicarbonate >18 mEq/L
• Do not stop insulin when glucose normalises — add dextrose and continue insulin until ketosis clears
• Transition to subcutaneous insulin only when eating/drinking and ketosis resolved

Pain Management

• Maximise regional/peripheral nerve block analgesia
• Multimodal approach (paracetamol, low-dose opioids, ketamine infusion)
• Phantom limb pain protocols should be initiated early

Continue Monitoring

• Hourly glucose, 2-hourly electrolytes until DKA resolved
• Fluid balance charting
• Monitor for AKI progression (creatinine, urine output)
• Watch for cerebral oedema (rare in adults; more common in children)
• ECG monitoring until K⁺ stable and normalised

Identify and Treat the Precipitant

• The most common triggers are infection (sepsis), MI, poor insulin compliance
• In this case, foot/limb infection is the precipitant — surgical removal is definitive treatment
• Send wound cultures; rationalise antibiotics post-culture

Summary: Key Priorities at a Glance