How to manage metabolic acidosis intraoperatively (intraoperative period)?

Management of Intraoperative Metabolic Acidosis

Immediately address the underlying cause while simultaneously correcting severe acidosis (pH <7.2) with sodium bicarbonate, optimizing fluid resuscitation with balanced crystalloids rather than normal saline, and ensuring adequate tissue perfusion through hemodynamic monitoring. 1, 2

Identify and Treat the Underlying Cause

The first priority is determining the etiology of metabolic acidosis, as treatment must target the root cause:

• Tissue hypoperfusion/shock: Restore intravascular volume and cardiac output immediately, as inadequate resuscitation leads to ongoing lactic acidosis and organ dysfunction 1
• Mesenteric ischemia: Suspect in abdominal surgery with unexplained acidosis, rising lactate, and increasing vasopressor requirements—this requires immediate surgical exploration if peritonitis is present 1
• Hemorrhagic shock: Time-critical—every 3-minute delay to laparotomy in unstable patients with intraabdominal bleeding increases mortality by 1% 1
• Hyperkalemia and electrolyte abnormalities: Correct immediately, particularly in patients with bowel ischemia where severe hyperkalemia may accompany acidosis due to tissue necrosis 1

Fluid Resuscitation Strategy

Use balanced crystalloids (lactated Ringer's or Plasma-Lyte) rather than normal saline to avoid worsening hyperchloremic metabolic acidosis. 1, 3

• Normal saline contains supraphysiological chloride concentrations (154 mmol/L) that cause hyperchloremic acidosis, decreased renal blood flow, reduced gastric mucosal perfusion, and impaired gastric motility 1
• In a study of 172 patients undergoing major abdominal surgery, total saline infusion was an independent predictor of post-operative metabolic acidosis, with the saline group showing significantly lower base excess and higher corrected chloride 3
• Balanced solutions prevent the additional acid-base derangement from iatrogenic hyperchloremia while maintaining adequate volume resuscitation 1

Hemodynamic Optimization

Implement early hemodynamic monitoring with goal-directed fluid therapy, targeting physiologic oxygen delivery and monitoring lactate clearance as the endpoint. 1

• Avoid supraphysiologic oxygen delivery targets—current evidence does not support this approach 1
• Use vasopressors judiciously: dobutamine, low-dose dopamine, and milrinone have less impact on mesenteric blood flow compared to high-dose norepinephrine or epinephrine 1
• Maintain mean arterial pressure adequate for end-organ perfusion (kidneys, brain, gastrointestinal tract) while avoiding excessive vasopressor use that worsens splanchnic hypoperfusion 1
• Monitor for abdominal compartment syndrome in patients receiving large-volume resuscitation, as increased intraabdominal pressure reduces portal venous flow by 35% and hepatic arterial flow by 55% at pressures of 20 mmHg 1

Sodium Bicarbonate Administration

Administer sodium bicarbonate for severe metabolic acidosis (pH <7.2) in cardiac arrest, circulatory insufficiency, or severe lactic acidosis. 2, 4

Indications for bicarbonate therapy:

• Cardiac arrest: 1-2 vials (44.6-100 mEq) rapid IV bolus initially, then 50 mL (44.6-50 mEq) every 5-10 minutes guided by arterial blood gas monitoring 2
• Severe metabolic acidosis with hemodynamic instability: 2-5 mEq/kg over 4-8 hours, with stepwise titration based on clinical response 2, 4
• Hyperkalemia with acidosis: bicarbonate facilitates intracellular potassium shift 2

Critical caveats:

• Bicarbonate solutions are hypertonic and may cause undesirable hypernatremia, but in cardiac arrest the risks of acidosis exceed those of hypernatremia 2
• Avoid full correction of acidosis in the first 24 hours—target total CO2 of approximately 20 mEq/L, as overly aggressive correction causes rebound alkalosis due to delayed ventilatory readjustment 2
• Monitor plasma osmolarity, blood gases, and lactate levels during therapy 2
• Do not attempt to correct chronic metabolic acidosis rapidly, as this leads to paradoxical CNS acidosis 4

Ventilatory Management

Maintain adequate minute ventilation to allow respiratory compensation, but avoid excessive hyperventilation that causes cerebral vasoconstriction. 4

• The respiratory system compensates for metabolic acidosis through hyperventilation, reducing PaCO2 by approximately 1.2 mmHg for every 1 mEq/L decrease in bicarbonate 4
• In mechanically ventilated patients, ensure ventilator settings permit this compensatory response
• Avoid neuromuscular blockade that prevents assessment of spontaneous respiratory compensation

Monitoring and Endpoints

Serial arterial blood gas analysis, lactate levels, base excess, and hemodynamic parameters guide ongoing resuscitation. 1, 2

• Lactate clearance is a key endpoint—persistent or rising lactate despite resuscitation suggests ongoing tissue hypoperfusion or unrecognized pathology (e.g., mesenteric ischemia) 1
• Calculate the anion gap to differentiate lactic acidosis from hyperchloremic acidosis: Anion Gap = Na - (Cl + HCO3) 4, 5
• Normal anion gap acidosis (8-12 mEq/L) suggests hyperchloremic acidosis from excessive saline administration or bicarbonate loss 5, 3
• Elevated anion gap (>12 mEq/L) indicates lactic acidosis, ketoacidosis, or toxin ingestion 5

Special Considerations

Damage Control Surgery Context:

When metabolic acidosis occurs with hypothermia (temperature <34°C) and coagulopathy, this represents the "lethal triad" requiring damage control surgery—abbreviated laparotomy with temporary abdominal closure and ICU resuscitation before definitive repair 1

Avoid Common Pitfalls:

• 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
• Do not use excessive crystalloid to chase blood pressure in patients with ongoing hemorrhage—this worsens acidosis, coagulopathy, and abdominal compartment syndrome 1
• Do not ignore hyperchloremic acidosis as "benign"—it impairs gastric blood flow, decreases gastric intramucosal pH, and may contribute to anastomotic complications 1, 3