Management of Intraoperative Metabolic Acidosis
Immediately address the underlying cause while simultaneously optimizing fluid resuscitation with balanced crystalloids, ensuring adequate tissue perfusion through hemodynamic monitoring, and reserving sodium bicarbonate only for severe acidosis (pH < 7.15-7.2). 1, 2
Immediate Assessment and Priorities
Identify the Underlying Cause First
The most critical step is determining whether acidosis results from:
- Tissue hypoperfusion/shock: Restore intravascular volume and cardiac output immediately, as inadequate resuscitation leads to ongoing lactic acidosis and organ dysfunction 1
- Hemorrhagic shock: Time-critical—every 3-minute delay to laparotomy in unstable patients with intraabdominal bleeding increases mortality by 1% 1
- Mesenteric ischemia: Suspect in abdominal surgery with unexplained acidosis, rising lactate, and increasing vasopressor requirements; requires immediate surgical exploration if peritonitis is present 1
- Hyperchloremic acidosis: Most commonly iatrogenic from excessive normal saline administration 3, 1, 4, 5
Critical Trigger Points for Damage Control
Consider abbreviated surgery and ICU resuscitation when metabolic acidosis occurs with:
- pH < 7.2 or base deficit > 8 2
- Hypothermia (core temperature < 35°C) 2
- Coagulopathy 2
- Signs of sepsis/septic shock 2
This "lethal triad" requires temporary abdominal closure and physiological normalization before definitive repair 1, 2
Fluid Resuscitation Strategy
Use Balanced Crystalloids, Not Normal Saline
Switch immediately to balanced crystalloids (lactated Ringer's or Plasma-Lyte) rather than normal saline to avoid worsening hyperchloremic metabolic acidosis. 3, 1
The evidence is compelling:
- Normal saline contains supraphysiological chloride (154 mmol/L) that directly causes hyperchloremic acidosis through decreased strong ion difference 3, 5
- Total infused saline volume is an independent predictor of postoperative metabolic acidosis 4
- A 1:1 ratio of saline to Ringer's solution maintains stable acid-base balance better than saline alone 6
- Normal saline is associated with renal vasoconstriction, increased acute kidney injury risk, and increased vasopressor requirements 3
Resuscitation Targets
- Administer crystalloid boluses at 20 mL/kg initially if signs of shock are present 7
- Target mean arterial pressure ≥ 65 mmHg 2
- Target central venous pressure 8-12 mmHg 2
- Target central venous oxygen saturation ≥ 70% 2
- Target urine output > 0.5 mL/kg/h 7
- Monitor lactate clearance as the key endpoint 1
Critical pitfall: Avoid excessive crystalloid overload, which can worsen bowel edema and perfusion 7. However, fluid restriction can be equally detrimental, causing decreased venous return and tissue perfusion 3
Hemodynamic Optimization
Vasopressor Management
- Noradrenaline is the first-line agent 2
- Adrenaline is the second-line agent 2
- Restrict dopamine use 2
- Use vasopressors judiciously—dobutamine, low-dose dopamine, and milrinone have less impact on mesenteric blood flow compared to high-dose norepinephrine or epinephrine 1
Monitoring Strategy
- Serial arterial blood gas analysis every 2-4 hours initially 7
- Continuous lactate monitoring—persistent or rising lactate despite resuscitation suggests ongoing tissue hypoperfusion or unrecognized pathology 1
- Base excess and chloride levels 4, 5
- Hemodynamic parameters with goal-directed fluid therapy 1
Bicarbonate Administration
When to Use Sodium Bicarbonate
Bicarbonate administration is NOT recommended for hypoperfusion-induced lactic acidosis unless pH < 7.15. 2, 1
Alkalinizing agents may be needed in:
- Severe acidosis (pH < 7.15) secondary to catecholamine receptor resistance-induced hypotension 2
- Cardiac arrest: rapid IV dose of 44.6-100 mEq (one to two 50 mL vials) initially, continued at 44.6-50 mEq every 5-10 minutes as indicated by arterial pH and blood gas monitoring 8
Critical caution: Bicarbonate solutions are hypertonic and may produce undesirable rises in plasma sodium concentration 8. In less urgent metabolic acidosis, aim for total CO2 content of approximately 20 mEq/L at the end of the first day—attempting full correction within 24 hours may cause unrecognized alkalosis 8
Ventilatory Management
- Maintain adequate minute ventilation to allow respiratory compensation 1
- Avoid excessive hyperventilation that causes cerebral vasoconstriction 1
- Ensure ventilator settings permit compensatory response in mechanically ventilated patients 1
Surgical Decision-Making
Timing of Intervention
- Achieve resuscitation goals within 6 hours from admission—survival rate drops to 0% when time to surgery exceeds 6 hours in GI perforation with septic shock 2
- Do not delay surgical intervention in patients with peritonitis or suspected bowel ischemia while attempting medical correction of acidosis—surgical source control is paramount 1
- Few hours of resuscitation are necessary before surgical intervention to prevent hemodynamic instability on induction of anesthesia 2
Damage Control Principles
For severely unstable patients:
- Obtain source control as the primary goal 2
- Defer anatomical reconstruction and abdominal closure to secondary procedures after physiological normalization 2
- Consider loop ileostomy for right-sided obstruction in severely unstable patients 2
- Consider loop transverse colostomy for left-sided obstruction in severely unstable patients 2
- Delay stoma creation if open abdomen is required 2
Special Considerations
Hyperchloremic Acidosis Prevention
- Discontinue normal saline infusions immediately 3
- Use balanced crystalloids for priming volume during cardiopulmonary bypass 3
- Maintain near-zero fluid and electrolyte balance during procedures—reduces complications by 59% 3
Renal Replacement Therapy
Consider urgent hemodialysis or continuous renal replacement therapy for severe metabolic acidosis refractory to bicarbonate therapy 7
Postoperative Fluid Management
If IV fluids are required postoperatively, administer at 25-30 mL/kg/day with no more than 70-100 mmol sodium/day 3
Clinical Outcomes
Metabolic acidosis is associated with:
- Increased 30-day mortality in surgical patients 3
- Longer ICU stay (trend toward +1.3 days) 9
- Longer hospital stay (trend toward +3.2 days) 9
- Increased tissue injury and organ dysfunction 3
Key insight: Metabolic acidosis begins before incision in most patients, with 78% developing significant acidosis postoperatively 9. The early phase (hyperchloremic) appears unavoidable or unpredictable, but the late phase (lactic) might be modified by early fluid administration with balanced solutions 9