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Crit Care Med. 1999 Oct;27(10):2142-6.

Cause of metabolic acidosis in prolonged surgery.

Author information

  • 1Department of General Anesthesiology, Cleveland Clinic Foundation, OH 44195, USA. watersj@cesmtp.ccf.org

Abstract

OBJECTIVE:

The intraoperative development of metabolic acidosis is frequently attributed to hypovolemia, tissue hypoperfusion, and lactic acidosis. In this study, dilutional acidosis was evaluated as a possible mechanism for the routine development of intraoperative acidosis in noncardiac, nonvascular surgery patients.

DESIGN:

Prospective, observational study.

SETTING:

University-affiliated Veteran's Affairs Medical Center and a staff model, health maintenance organization hospital.

PATIENTS:

Twelve patients undergoing prolonged surgical procedures expected to last > or = 4 hrs were enrolled in the study.

INTERVENTIONS:

Perioperative management was based on the judgment of the attending anesthesiologist and surgeon without knowledge of the study's intent.

MEASUREMENTS AND MAIN RESULTS:

Arterial blood gas parameters, serum electrolytes, and urine electrolytes were measured pre- and postoperatively. Pulmonary artery catheters were placed for hemodynamic measurement and oxygen delivery calculations. Plasma volume was measured both pre- and postoperatively, using the Evans blue dye dilution technique. Although significant changes in lactate level (1.1 +/- 0.6-1.8 +/- 1.0) occurred, the change was not large enough to explain the degree of change in base excess (0.8 +/- 2.3 to -2.7 +/- 2.9). Chloride levels significantly increased (106 +/- 3-110 +/- 5) with a correlation (r2 = .92; p < .0001) between the degree of change in chloride and the degree of change in base excess. Plasma volume did not change. Furthermore, a correlation between the volume of normal saline administered and the change in base excess was found (r2 = .86; p < .0001), although no correlation was found with Ringer's lactate solution. An even stronger correlation was noted when the total chloride amount administered was compared with the change in base excess (r2 = .93; p < .0001).

CONCLUSIONS:

In this patient population, a common source of increasing base deficit is related to chloride administration. The largest source of chloride is usually normal saline. Classically, dilutional acidosis would explain the predominance of this acidotic change; however, no increase in plasma volume occurred. The absence of plasma volume change would suggest that the mechanism postulated to result in dilutional acidosis is incomplete. The common treatment of administering more fluid for intraoperative acidosis may be inappropriate, may have caused the acidosis, and may further exacerbate the acidosis. Chloride levels should be assessed whenever a metabolic acidosis is seen perioperatively.

Comment in

PMID:
10548196
[PubMed - indexed for MEDLINE]
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