What are the possible causes of decreasing base excess in a patient under anesthesia despite receiving fluids?

Decreasing Base Excess Despite Fluid Administration Under Anesthesia

When base excess continues to decline despite fluid resuscitation in an anesthetized patient, immediately suspect hyperchloremic metabolic acidosis from excessive normal saline administration, ongoing hemorrhage, tissue hypoperfusion, or inadequate ventilation causing respiratory acidosis. 1, 2

Primary Causes to Investigate

1. Iatrogenic Hyperchloremic Acidosis (Most Common)

• Administration of 0.9% normal saline or unbalanced colloid solutions is the leading cause of worsening base excess during anesthesia. 1, 2
• Normal saline contains supraphysiologic chloride concentrations (154 mEq/L vs. physiologic 100-106 mEq/L), which directly decreases the strong ion difference and lowers pH 1, 2
• This mechanism causes dilution of bicarbonate and direct chloride loading, progressively worsening metabolic acidosis despite volume replacement 1
• Immediate action: Switch to balanced crystalloid solutions (Ringer's Lactate or Plasmalyte) containing physiologic chloride concentrations 1, 2

2. Ongoing Hemorrhage or Inadequate Resuscitation

• Occult bleeding may not manifest with tachycardia in elderly patients or those on beta-blockers, making hypovolemia difficult to detect 3
• Tissue hypoperfusion from inadequate cardiac output generates lactic acidosis, progressively decreasing base excess 1
• Check for surgical bleeding, reassess hemodynamic parameters, and consider invasive monitoring (arterial line, central venous pressure) to guide resuscitation 3

3. Tissue Hypoperfusion and Lactic Acidosis

• Excessive anesthetic depth depresses cardiovascular function, reducing tissue perfusion and oxygen delivery 3, 4
• Epidural or spinal anesthesia causes vasodilation and functional hypovolemia without actual volume loss 5
• Hypothermia impairs tissue perfusion and oxygen delivery, contributing to metabolic acidosis 3
• Maintain mean arterial pressure with vasopressors once normovolemia is established, rather than excessive fluid administration 3

4. Respiratory Contribution

• Atelectasis develops in 90% of anesthetized patients, impairing gas exchange and potentially causing respiratory acidosis 6
• Inadequate minute ventilation allows CO₂ accumulation, which compounds metabolic acidosis 6
• Perform recruitment maneuvers (sustained inflation to 40 cmH₂O for 7-8 seconds) and use moderate FiO₂ (0.3-0.4) with PEEP to prevent atelectasis 6

5. Fluid Overload Complications

• Paradoxically, excessive fluid administration (>2.5L positive balance) causes tissue edema, impairing oxygen delivery and worsening acidosis 7
• Fluid overload reduces renal blood flow and glomerular filtration rate, impairing acid excretion 1, 2
• Splanchnic edema from chloride-rich fluids decreases gastric blood flow and intramucosal pH 1

Diagnostic Algorithm

Step 1: Obtain arterial blood gas immediately

• Calculate anion gap to differentiate high anion gap acidosis (lactic acidosis, ketoacidosis) from hyperchloremic acidosis 2
• Check serum chloride, sodium, and lactate levels 2

Step 2: Assess adequacy of resuscitation

• Evaluate hemodynamic parameters: blood pressure, heart rate, urine output, central venous pressure if available 3
• Consider cardiac output monitoring (esophageal Doppler) to guide fluid therapy 3
• Measure core temperature and actively warm to 37°C if hypothermic 3

Step 3: Identify and stop chloride-rich fluid administration

• Review total volume and type of fluids administered 1, 2
• Discontinue normal saline immediately and switch to balanced crystalloids 1, 2

Step 4: Optimize ventilation

• Verify adequate minute ventilation and check end-tidal CO₂ 6
• Perform recruitment maneuvers if atelectasis suspected 6

Management Strategy

Immediate Interventions

• Stop all chloride-rich fluids (0.9% saline, unbalanced colloids) and switch to balanced crystalloids (Ringer's Lactate or Plasmalyte) 1, 2
• Maintain mean arterial pressure with vasopressors (ephedrine 0.2 mg/kg or phenylephrine) rather than excessive fluid boluses 3, 5
• Target near-zero fluid balance (0-5% body weight change) to avoid complications from fluid overload 7
• Ensure adequate ventilation and perform recruitment maneuvers if needed 6
• Actively warm hypothermic patients to 37°C 3

Ongoing Monitoring

• Serial arterial blood gases every 30-60 minutes to track base excess trend 2
• Monitor serum chloride and lactate levels 2
• Assess urine output (adequate renal perfusion associated with faster resolution of acidosis) 1
• Continuous hemodynamic monitoring with invasive blood pressure monitoring 3

Critical Pitfalls to Avoid

Do not continue normal saline administration - This will progressively worsen hyperchloremic acidosis and is associated with increased 30-day mortality, acute kidney injury, and increased vasopressor requirements 1, 2

Do not assume fluid responsiveness without assessment - Epidural anesthesia causes functional hypovolemia through vasodilation, not actual volume loss; vasopressors may be more appropriate than additional fluids 5

Do not overlook occult hemorrhage - Elderly patients and those on beta-blockers may not mount tachycardic response to bleeding 3

Do not administer excessive fluids - Positive fluid balance >2.5L increases complications by 59% and prolongs hospital stay by 3.4 days 7

Do not use switching to 0.45% saline as a solution - This still contains supraphysiologic chloride (77 mEq/L) and does not address the fundamental problem 2