ERAS Protocol in Anaesthesia

Introduction

Pathophysiology Targeted by ERAS

• Insulin resistance and hyperglycemia
• Protein catabolism and muscle wasting
• Immunosuppression
• Fluid retention and third-spacing
• Ileus and impaired gut motility
• Pain sensitization

ERAS Pathway Components

A. PREOPERATIVE PHASE

B. INTRAOPERATIVE PHASE

• Prefer regional/neuraxial anaesthesia (or combined regional-general) over pure general anaesthesia when feasible - reduces opioid requirement, PONV, stress response, and facilitates early mobilization
• Short-acting anaesthetic agents: Propofol (TIVA preferred), desflurane/sevoflurane, remifentanil - allow rapid wake-up
• Avoid nitrous oxide - increases PONV, bowel distension
• BIS monitoring to avoid unnecessarily deep anaesthesia (target BIS 40-60) - reduces volatile agent use and delayed emergence

• Paracetamol (1g IV) - routine preoperative/intraoperative dose
• NSAIDs / COX-2 inhibitors (e.g., celecoxib, ketorolac) - caution with anastomotic surgery (COX-2 may increase leak risk)
• Ketamine (0.1-0.5 mg/kg) - NMDA antagonist, prevents central sensitization
• Dexmedetomidine - alpha-2 agonist, opioid-sparing, reduces emergence agitation
• Lidocaine infusion (1.5 mg/kg/hr IV) - reduces pain, ileus, and opioid consumption
• Gabapentinoids (pregabalin/gabapentin) - pre-emptive analgesia
• Magnesium sulfate - NMDA antagonism
• Epidural analgesia - gold standard for open abdominal/thoracic surgery; reduces pulmonary complications, ileus, opioid use
• Paravertebral blocks, TAP blocks, erector spinae plane blocks, quadratus lumborum blocks - procedure-specific

• Avoid both hypovolemia (organ ischemia) and hypervolemia (anastomotic leak, pulmonary edema, ileus, delayed wound healing)
• Targets normovolemia with zero fluid balance
• Uses dynamic parameters: Stroke Volume Variation (SVV), Pulse Pressure Variation (PPV), Pleth Variability Index rather than static CVP/PCWP
• Monitoring devices: FloTrac/Vigileo, LiDCO, esophageal Doppler
• Avoid normal saline in large volumes - hyperchloremic metabolic acidosis associated with increased mortality; prefer balanced crystalloids (Plasmalyte, Hartmann's)
• Colloids (albumin) used selectively for volume replacement

• Maintain core temperature >36°C
• Use: Forced-air warming blankets (Bair Hugger), fluid warmers, increased theatre temperature
• Hypothermia causes: coagulopathy, immunosuppression, cardiac arrhythmias, delayed drug metabolism, prolonged neuromuscular blockade, increased infection risk
• Temperature monitoring is a strong recommendation (evidence: High)

• Tidal volume 6-8 mL/kg ideal body weight
• PEEP 5-8 cmH2O
• FiO2 titrated to SpO2 94-98% (avoid hyperoxia)
• Periodic recruitment manoeuvres
• Reduces postoperative pulmonary complications (PPCs)

• Laparoscopic/robotic approach preferred - less surgical stress response, reduced pain, early mobilization
• VATS (Video-Assisted Thoracoscopic Surgery) for lung cancer - strong recommendation

• Routine nasogastric decompression delays GI recovery and increases pulmonary complications - not recommended
• Surgical drains removed early when used

• 0-1 risk factors: single agent (ondansetron OR dexamethasone)
• 2 risk factors: two agents (ondansetron + dexamethasone)
• 3-4 risk factors: three or more agents + TIVA (avoid volatile agents)
• Agents: ondansetron (4 mg IV), dexamethasone (4-8 mg at induction), scopolamine patch, droperidol, aprepitant (NK-1 antagonist)

C. POSTOPERATIVE PHASE

Outcomes and Evidence

• Length of stay reduced by 2-3 days across specialties
• Complication rates reduced 30-50% (respiratory, infectious, GI)
• Readmission rates comparable to or lower than conventional care
• Opioid consumption significantly reduced
• Cost savings substantial - lower hospitalization costs
• Ambulatory surgery facilitated: ERAS in ambulatory oncologic surgery centers showed same-day discharge rates increased from 7.2% to 58.6% (Miller's Anesthesia, 10e)
• For appendectomy (RCT, n=108): ERAS group discharged at mean 9.7 hrs vs 23.2 hrs with conventional care (Miller's Anesthesia, 10e)

ERAS vs Fast-Track Anaesthesia

Barriers to ERAS Implementation

• Resistance from surgeons/nurses to change from traditional practices
• Conflicting team recommendations
• Poor patient compliance (especially early feeding/mobilization)
• Resource limitations in low/middle-income countries
• Need for dedicated ERAS coordinators, audit infrastructure

Setting Up an ERAS Program

1. Multidisciplinary team formation (anaesthesiologist, surgeon, nurse coordinator, dietitian, physiotherapist)
2. Baseline audit of current practice
3. Identification of evidence-based protocol elements for specialty
4. Staff education and training
5. Patient education materials
6. Prospective data collection and compliance monitoring
7. Regular feedback and iterative protocol refinement

Key Points for AIIMS Exam

1. Founder: Henrik Kehlet, 1995; ERAS Society founded 2001
2. Preoperative carbohydrate loading: 12.5% maltodextrin, 400 mL night before + 200 mL 2 hours before
3. Fasting: Solids 6 hours, clear fluids 2 hours
4. Intraoperative anaesthetic: TIVA (propofol), short-acting agents, BIS monitoring
5. Opioid-sparing multimodal analgesia: Paracetamol + NSAID + ketamine + regional block + lignocaine infusion
6. GDFT: SVV/PPV targets, balanced crystalloids, normovolemia
7. PONV: Apfel score-based multimodal prophylaxis; avoid N2O and volatile agents
8. Normothermia: Forced-air warming; strong evidence
9. Lung-protective ventilation: 6-8 mL/kg TV, PEEP 5-8
10. Postoperative: Early feeding within 6-24 hours, early mobilization within 24 hours, early removal of Foley/lines

Oxygen Flux (Oxygen Delivery - DO₂) in Anaesthesia

Definition

"Oxygen delivery, the rate at which oxygen is transported to the microcirculation, is the product of cardiac output and CaO₂ and is normally about 1,000 mL/min." - Mulholland & Greenfield's Surgery, 7e

Derivation of the DO₂ Formula

Step 1: Arterial Oxygen Content (CaO₂)

1. Bound to haemoglobin (Hb) - the dominant form
2. Dissolved in plasma - minor but important at high PaO₂

• 1.34 mL/g = Hüfner's constant (oxygen-carrying capacity of 1 g of Hb; some texts use 1.36 or 1.39)
• Hb = haemoglobin concentration (g/dL)
• SaO₂ = arterial oxygen saturation (fraction)
• 0.003 = solubility coefficient of O₂ in plasma (mL/dL/mmHg)
• PaO₂ = partial pressure of O₂ in arterial blood (mmHg)

Step 2: Oxygen Delivery (DO₂ / Oxygen Flux)

• CO = cardiac output (L/min) = HR × SV
• ×10 = unit conversion factor (dL to mL)

Normal Values Table

Oxygen Consumption (VO₂) - The Demand Side

• This is the Fick principle - the amount of O₂ consumed equals the difference between O₂ delivered and O₂ returned in venous blood
• Normal VO₂ ≈ 200-250 mL/min at rest
• In children: VO₂ ≈ 175 mL/min/m² (Miller's Anesthesia, 10e)
• Normal arteriovenous O₂ difference (a-vDO₂) = 4-6 mL/100 mL blood

Oxygen Extraction Ratio (OER / O₂ER)

• Normal OER = 22-30% (body normally extracts only ~25% of delivered O₂)
• Myocardium has the highest extraction ratio at ~75% - hence the heart is most vulnerable to reductions in DO₂
• Organs with high supply-to-demand ratios (kidney, skin, intestine) can increase extraction when DO₂ falls

DO₂-VO₂ Relationship: The Biphasic Curve (Critical Concept)

1. Flow-Independent Zone (Physiological Range)

• VO₂ remains constant over a wide range of DO₂
• As DO₂ falls, compensatory increase in OER maintains VO₂
• Body uses compensatory mechanisms: increased HR, increased stroke volume, redistribution of blood flow

2. Critical DO₂ (DO₂ crit) - The Inflection Point

• The threshold below which VO₂ becomes dependent on DO₂
• In euvolemic adults with normal cardiac function: Critical DO₂ requires Hb ≥ 3-3.5 g/dL (Barash's Clinical Anaesthesia, 9e)
• Below this point: anaerobic metabolism begins, lactic acidosis develops
• "The level of oxygen delivery at which oxygen consumption begins to decrease is called critical oxygen delivery. At the critical oxygen delivery level, tissues begin to use anaerobic glycolysis, with resultant lactate production and metabolic acidosis." (Creasy & Resnik's Maternal-Fetal Medicine)

3. Flow-Dependent Zone (Pathological)

• VO₂ falls proportionally with DO₂
• Seen in: hemorrhagic shock, cardiogenic shock, severe anemia
• Lactic acidosis is the biochemical hallmark

State-Specific Changes (from Sabiston, Fig. 33.9):

Mixed Venous Oxygen Saturation (SvO₂)

• Measured from pulmonary artery via PA catheter (true mixed venous sample from SVC + IVC + coronary sinus)
• Normal SvO₂: 60-80% (pulmonary artery)
• Normal ScvO₂: 65-85% (central venous - superior vena cava; slightly higher than SvO₂)
• Monitored continuously via reflectance oximetry (fiberoptic PAC)

Four Causes of Low SvO₂ (Fick Equation Analysis):

High SvO₂ (>80%):

• Septic shock (shunting of blood past tissues - reduced extraction)
• Cyanide/carbon monoxide poisoning (inability to utilize O₂)
• Hypothermia (reduced metabolic demand)
• Cirrhosis, hyperdynamic states

Determinants of DO₂ and How to Optimize Each

"DO2 = CO × CaO₂; CO = HR × SV; CaO₂ = (Hb × 1.34 × SaO₂) + (0.003 × PaO₂). Commonly used ways of assessing both inadequate oxygen delivery and the response to treatment include SvO₂." - Scott-Brown's Otorhinolaryngology, Vol 1

Index Values (per m² Body Surface Area)

Anaesthetic Implications

Intraoperative Effects on DO₂:

1. General anaesthesia reduces CO by 10-20% (reduced preload, myocardial depression, vasodilation) → reduced DO₂
2. Positive pressure ventilation reduces venous return and CO → reduces DO₂
3. Volatile anaesthetics (halothane > isoflurane) reduce myocardial contractility → reduces CO
4. Haemorrhage / blood loss → reduces Hb and CO → critical reduction in DO₂
5. Hypothermia → reduces VO₂ (protective in cardiac/neuro surgery) but also reduces CO
6. Vasopressors (noradrenaline) → increase afterload and MAP but may reduce CO at high doses

Clinical Monitoring of DO₂ Adequacy:

• SvO₂ monitoring via PAC (target >70%) - used in goal-directed therapy protocols (ERAS)
• ScvO₂ via central venous catheter (target >70%)
• Lactate - best surrogate for anaerobic metabolism (target <2 mmol/L)
• Base deficit on ABG
• NIRS (near-infrared spectroscopy) - regional cerebral/tissue oxygenation
• Urine output (>0.5 mL/kg/hr)

Transfusion Trigger (Barash's Clinical Anaesthesia, 9e):

• Stable, non-bleeding, euvolemic patients may tolerate Hb 6.0 g/dL
• Transfusion of some benefit between Hb 6-8 g/dL
• Rarely beneficial above Hb 10 g/dL
• Critical DO₂ requires minimum Hb 3-3.5 g/dL in normal cardiac function

Oxygen Debt and Shoemaker's Supranormalization

Summary Points for AIIMS Exam

1. DO₂ = CO × CaO₂ × 10 = normal ~1000 mL/min
2. CaO₂ = (1.34 × Hb × SaO₂) + (0.003 × PaO₂) = normal ~20 mL/dL
3. VO₂ = CO × (CaO₂ - CvO₂) × 10 = normal ~250 mL/min
4. OER = VO₂/DO₂ = normal 22-30%; myocardium ~75%
5. SvO₂ = 60-80% (PA); ScvO₂ = 65-85% (SVC)
6. Critical DO₂ = threshold below which VO₂ becomes delivery-dependent; below Hb 3-3.5 g/dL in normal cardiac function
7. Biphasic DO₂-VO₂ curve: flow-independent plateau → critical point → flow-dependent zone
8. Low SvO₂ causes: ↓SaO₂, ↓Hb, ↓CO, ↑VO₂
9. High SvO₂: sepsis (shunting), cyanide poisoning, hypothermia
10. Anaesthesia reduces DO₂ via: ↓CO (myocardial depression, vasodilation), ↓preload (positive pressure ventilation), ↓Hb (blood loss)