What Causes Negative Base Excess in Anesthetized Patients
Excessive administration of 0.9% normal saline is the dominant cause of negative base excess (metabolic acidosis) in anesthetized patients, producing hyperchloremic acidosis that worsens progressively with the volume of chloride-rich fluid infused. 1, 2, 3
Primary Mechanisms of Negative Base Excess Under Anesthesia
Hyperchloremic Acidosis from Fluid Resuscitation
The infusion of normal saline at approximately 30 mL/kg/hour during anesthesia inevitably produces metabolic acidosis with negative base excess, which does not occur with balanced crystalloid solutions like lactated Ringer's. 3
- Base excess decreases by approximately -0.4 to -0.07 mmol/L for each millimole per kilogram of chloride administered during surgery 4, 5
- The supraphysiologic chloride concentration (154 mEq/L) in normal saline causes hyperchloremia, which directly decreases the strong ion difference and produces acidosis 3, 6
- This hyperchloremic acidosis becomes the dominant cause of negative base excess by 8-12 hours post-resuscitation, even when lactic acidosis was initially present 4
- The acidosis persists as long as the elevated chloride load remains, and resolves faster with higher urine output or diuretic administration 4
Tissue Hypoperfusion and Lactic Acidosis
Inadequate tissue perfusion from hypovolemia, hemorrhage, or reduced cardiac output generates lactic acidosis with progressively negative base excess. 2, 7
- Hypotension may result from multiple mechanisms: intravascular volume depletion from surgical losses, vomiting, or excessive secretions; trauma-induced internal bleeding; or reduced cardiac output from negative inotropic effects 1
- Lactate levels and total infused saline are independent factors associated with post-operative metabolic acidosis 7
- Rising lactate despite adequate fluid resuscitation indicates ongoing tissue hypoperfusion or unrecognized surgical pathology requiring immediate intervention 8
Fluid Overload and Splanchnic Edema
Excessive fluid administration beyond 2.5 liters causes splanchnic edema, reduced mesenteric blood flow, and gastrointestinal mucosal acidosis, further worsening base excess. 1
- Fluid overload impairs gastric blood flow and decreases gastric intramucosal pH, particularly in elderly surgical patients 1
- Both hyperchloremic acidosis from saline and metabolic acidosis from any cause impair gastric motility and tissue perfusion 1
Inadequate Fluid Resuscitation
Conversely, fluid restriction causing hypovolemia decreases venous return, cardiac output, and tissue oxygen delivery, producing negative base excess from hypoperfusion. 1
- Induction of anesthesia in fluid-depleted patients further reduces effective circulatory volume by decreasing sympathetic tone 1
- Inadequate resuscitation leads to gastrointestinal mucosal acidosis and worse outcomes 1
Critical Diagnostic Algorithm
When encountering negative base excess intraoperatively or postoperatively:
Immediately obtain arterial blood gas to calculate anion gap and differentiate high anion gap acidosis (lactic acidosis, ketoacidosis) from normal anion gap hyperchloremic acidosis 2, 9
Check serum chloride and calculate corrected chloride (accounting for sodium changes) to identify hyperchloremic component 7
Review total chloride administered during resuscitation, as this directly correlates with degree of hyperchloremic acidosis 4, 5
Assess hemodynamic parameters with consideration for invasive monitoring if hemorrhage or inadequate resuscitation suspected 2
Management Priorities
Stop all chloride-rich fluids immediately and switch to balanced crystalloids (lactated Ringer's or Plasma-Lyte) to prevent further worsening of base excess. 2, 8
- Balanced crystalloids do not produce the hyperchloremic acidosis seen with normal saline 3, 7
- Target near-zero fluid balance once normovolemia achieved to avoid complications from fluid overload 2
- Maintain mean arterial pressure with vasopressors rather than excessive fluid boluses, particularly in patients receiving epidural analgesia 1, 2
Common Pitfalls to Avoid
Do not continue normal saline administration once hyperchloremic acidosis is identified, as this worsens outcomes including increased 30-day mortality, acute kidney injury, and vasopressor requirements. 2
Do not assume all negative base excess represents inadequate resuscitation requiring more fluid—hyperchloremic acidosis from prior saline administration creates a persistent base deficit that should not trigger additional volume loading. 6
Do not overlook occult hemorrhage as the cause, particularly in elderly patients or those on beta-blockers who may not mount a tachycardic response to bleeding. 2