Utilization of base deficit and reliability of base deficit as a surrogate for serum lactate in the peri-operative setting
© Chawla et al; licensee BioMed Central Ltd. 2010
Received: 16 November 2009
Accepted: 9 September 2010
Published: 9 September 2010
Base deficit (BD) is commonly used in the operating room (OR) as an endpoint of resuscitation. BD is used as a surrogate marker for the accumulation of lactic acid(Lac). However, the BD can be affected by large amounts of saline.
We conducted a survey of anesthesiologists regarding the use of BD. We also studied the reliability of BD to determine the presence of hyperlactatemia (HL). Patients undergoing general anesthesia were eligible for enrollment if they were receiving an arterial line as part of their routine care. If an arterial blood gas was drawn by the operative team as part of the routine care, the remainder of the unused blood was also used to measure Lac.
Survey: 73 staff anesthesiologists were surveyed. Over 70% of respondents used BD as an endpoint of resuscitation.
Base Deficit Study: 35 patients were enrolled resulting in 88 arterial blood gases with corresponding Lac. Mean age was 61.4 ± 14.3 years, 43% were male. Mean pH was 7.39 ± 0.05, the mean bicarbonate was 23.0 ± 2.3 meq/L, the mean BD 1.34 ± 2.3, and the mean Lac was 1.58 ± 0.71 mmol/L. Mean ASA risk score was 3.16 ± 0.71. ROC area under the curve for base deficit to detect HL was 0.58.
BD can often mislead the clinician as to the actual Lac. Lac can now be measured in the OR in real time. Therefore, if clinicians in the operative setting want to know the Lac, it should be measured directly.
Base deficit is the amount of base (in mmol) required to titrate a liter of whole arterial blood to a pH of 7.40. Base deficit as a measure of metabolic acidosis was first proposed by Anderson and Engel in 1960. Over time, this assessment of metabolic acidosis has been incorporated into the standard information that is reported on a routine blood gas analysis. Base deficit has been advocated as a marker of resuscitation adequacy[2–6]. These recommendations are based on animal and human data that show that the base deficit is correlated with severity of injury and degree of hemorrhage[2, 5–8]. As a consequence, base deficit is commonly used in the operating room (OR) as an endpoint of resuscitation. Because base deficit accounts for the buffering effects of hemoglobin and CO2, both of which may fluctuate significantly in long complex operative procedures, base deficit is used by anesthesiologists as a surrogate marker for metabolic acidosis. The rationale for base deficit as a marker of severity of illness is based on the fact that as patients suffer from hemorrhage and hypotension, oxygen delivery becomes inadequate forcing the onset of anaerobic metabolism. Anaerobic metabolism results in accumulation of lactic acid, and base deficit has been shown to correlate with serum lactate in models of shock. However, the base deficit can be affected if large amounts of saline are administered which is common in peri-operative patients, and the base deficit does not always correlate with the serum lactate in trauma patients and patients who are critically ill[10–12]. In addition, base deficit as a surrogate for serum lactate can be confounded by renal dysfunction and ketoacidosis. We have previously studied the accuracy of base deficit as a surrogate for lactate in patients who are critically ill. However, we were unable to find any studies involving intra-operative patients that tested whether this relationship is maintained during surgery. Furthermore, the commonly held belief that the absence of base deficit rules out the presence of hyperlactatemia persists despite previous studies showing that base deficit is not effective at discriminating the presence or absence of hyperlactatemia[13–17]. Formal quantitative studies on frequency of use of base deficit in the OR and thresholds have not been conducted. We sought to better understand the utilization of base deficit as a clinical tool in the intra-operative setting.
Base Deficit Study
This part of the study was conducted from September 2007 to August 2008 in the GW hospital operating rooms. The study was approved by the Institutional Review Board (IRB) of the George Washington University Medical Center and the privacy officer of the hospital.
Those patients undergoing general anesthesia were eligible for enrollment if they were receiving an arterial line as part of their routine care. Demographic, clinical, and operative information were collected.
If an arterial blood gas was drawn by the operative team as part of the routine care, the remainder of the unused blood was also used to measure serum lactate. Blood was immediately placed on ice and evaluated for pH, partial pressure or carbon dioxide/oxygen, oxygen saturation and lactate levels using standard blood gas analysis (ABL 700; Radiometer Americ Inc; Westlake, OH). All costs for this extra analysis were paid for the Department of Anesthesiology and Critical Care Medicine.
Definitions and Analysis
For each patient, arterial serum lactate (Lac) was measured, and the standard base deficit (BD) was calculated from the arterial blood gas (ABL 700; Radiometer Americ Inc; Westlake, OH). Standard base deficit (BD) was determined using the modified Van Slyke equation.1
Proportions of patients with certain characteristics were compared using the chi-square test. We assessed the distribution of variables. Variables with normal distribution were compared using two-tailed unpaired t-tests, while data that did not conform to a normal distribution were compared using the Mann-Whitney rank sum test. BD and Lac were compared using Pearson correlations. Receiver operating characteristic (ROC) curves were determined for BD to detect the presence of hyperlactatemia. Hyperlactatemia was defined as a serum lactate greater than 2.0 mmol/L. Unless otherwise specified, all means are reported as ± S.D. All statistics were performed with SPSS 11.0 (SPSS, Chicago, IL.).
How frequently do you use base deficit as a marker of resuscitation in the Operating Room?
What level of base deficit will change your management of resuscitation?
How frequently do you use serum lactate as a marker of resuscitation in the Operating Room?
What level of serum lactate will change your management of resuscitation?
Base Deficit Study
61.4 ± 14.3 years
12.8 ± 1.7 g/dL
Serum Bicarbonate (mean,sd)
23.0 ± 2.3 meg/L
3.6 ± 1.5 g/dL
7.39 ± 0.05
1.34 ± 2.3
Serum Lactate (mmol/L)
1.58 ± 0.71
Hyperlactatemia n (%)
ASA Class n(%)
Operation n (%)
Other Cardiac Surgery
Correlations of Covariates
In this study, we showed that BD is used commonly by anesthesiologists as an endpoint of resuscitation ( > 70% of respondents use BD at least "sometimes"). The absolute value of BD used by different clinicians for assessing was variable, and many clinicians indicated that the absolute BD value was not as important as the trend. In comparison, fewer of these same respondents used serum lactate as an endpoint of resuscitation. In this study, we have demonstrated that BD is not a suitable surrogate for hyperlactatemia. These data are consistent with our previous findings in critically ill patients[11, 12]. Moreover, our data indicate that the base deficit would often mislead the clinician as to the true serum lactate. We showed that the ROC area under the curve for BD to predict hyperlactatemia was 0.58 (0.50 is a coin toss); thus demonstrating the poor performance of BD as a surrogate for serum lactate (Figure 4).
These results are not surprising given previous literature assessing the capacity of base deficit as a surrogate for resuscitation and serum lactate in the critical care and trauma setting. We have previously shown that BD is not reliable as a surrogate for serum lactate in critically ill patients[11, 12]. In addition BD has also been shown to be insensitive for detecting hyperlactatemia in surgical patients. In a study by Mikulaschek et al of trauma patients, resuscitation decisions would have been wrong 33-58% of the time if BD or anion gap had been used as the sole criterion rather than serum lactate concentration. Waters et al showed that in a study of surgical patients, elevations in BD without concomitant rise in lactate were attributed to hyperchloremia and were a manifestation of successful resuscitation rather than fluid deficit. Base deficit is useful as a surrogate for resuscitation so long as it is a result of hyperlactatemia, but if it is caused by a hyperchloremic acidosis due to saline loading this relationship becomes discongrous. In addition, base deficit as a surrogate for serum lactate can be confounded by renal dysfunction and ketoacidosis.
This study is the first to test this concept on patients undergoing general anesthesia in the operating room. These data are noteworthy because based on our survey results, clinicians routinely use BD as an endpoint of resuscitation. The assumptions underlying this physiology may be faulty in many patients because BD does not discriminate the cause of the acidosis. Since previous studies have shown that the accumulation of chloride from normal saline tends to increase the base deficit, many patients in the peri-operative setting may receive more volume and blood product transfusions than they should because the BD is increasing due to the saline loading, and the clinician may incorrectly interpret this rising BD as an indication that the patient in under resuscitated. In this study, we were unable to show that the discrepancy between BD and serum lactate worsened with the amount of volume resuscitation or the duration of the case (Figure 3). This is not surprising given the multitude of intra-operative activities that can affect acid base status ( e.g. resuscitation, saline from iv fluids, citrate from blood products, etc) However, since the level of agreement between BD and serum lactate was so poor at baseline, the effect would have had to be dramatic in order to detect it.
The study was limited by its modest size. Larger studies involving a wide variety of operative patients need to be conducted to validate these findings.
In aggregate, the use of BD as a surrogate for serum lactate is not warranted. BD can often mislead the clinician as to the actual serum lactate concentration. With the widespread availability of point of service testing for lactate, the serum lactate can now be measured in the operating room in real time. Therefore, if clinicians in the operative setting want to know the serum lactate, it should be measured directly.
The authors would like to thank the nurses, respiratory therapists, and physician assistants that make this research possible. Financial support was provided for by the Department of Anesthesiology and Critical Care Medicine at the George Washington University Medical Center
- Siggaard-Andersen O: The van Slyke equation. ScandJ ClinLab Invest Suppl. 1977, 37 (146): 15-20. 10.3109/00365517709098927.View ArticleGoogle Scholar
- Davis JW, Kaups KL, Parks SN: Base deficit is superior to pH in evaluating clearance of acidosis after traumatic shock. JTrauma. 1998, 44 (1): 114-118.Google Scholar
- Davis JW, Mackersie RC, Holbrook TL, Hoyt DB: Base deficit as an indicator of significant abdominal injury. AnnEmergMed. 1991, 20 (8): 842-844.Google Scholar
- Davis JW, Shackford SR, Holbrook TL: Base deficit as a sensitive indicator of compensated shock and tissue oxygen utilization. SurgGynecolObstet. 1991, 173 (6): 473-476.Google Scholar
- Kaups KL, Davis JW, Dominic WJ: Base deficit as an indicator or resuscitation needs in patients with burn injuries. JBurn Care Rehabil. 1998, 19 (4): 346-348. 10.1097/00004630-199807000-00013.View ArticleGoogle Scholar
- Rixen D, Raum M, Bouillon B, Lefering R, Neugebauer E: Base deficit development and its prognostic significance in posttrauma critical illness: an analysis by the trauma registry of the Deutsche Gesellschaft fur unfallchirurgie. Shock. 2001, 15 (2): 83-89. 10.1097/00024382-200115020-00001.View ArticlePubMedGoogle Scholar
- Davis JW, Parks SN, Kaups KL, Gladen HE, O'Donnell-Nicol S: Admission base deficit predicts transfusion requirements and risk of complications. JTrauma. 1996, 41 (5): 769-774.Google Scholar
- Davis JW, Shackford SR, Mackersie RC, Hoyt DB: Base deficit as a guide to volume resuscitation. JTrauma. 1988, 28 (10): 1464-1467.Google Scholar
- Davis JW: The relationship of base deficit to lactate in porcine hemorrhagic shock and resuscitation. JTrauma. 1994, 36 (2): 168-172.Google Scholar
- Brill SA, Stewart TR, Brundage SI, Schreiber MA: Base deficit does not predict mortality when secondary to hyperchloremic acidosis. Shock. 2002, 17 (6): 459-462. 10.1097/00024382-200206000-00003.View ArticlePubMedGoogle Scholar
- Chawla LS, Jagasia D, Abell LM, Seneff MG, Egan M, Danino N, Nquyen A, Ally M, Kimmel PL, Junker C: Anion Gap, Anion Gap corrected for Albumin, and Base Deficit Fail to Accurately Diagnose Clinically Significant Hyperlactatemia in Critically Ill Patients. J Intensive Care Med. 2008, 23 (2): 122-127. 10.1177/0885066607312985.View ArticlePubMedGoogle Scholar
- Chawla LS, Shih S, Davison D, Junker C, Seneff MG: Anion gap, anion gap corrected for albumin, base deficit and unmeasured anions in critically ill patients: implications on the assessment of metabolic acidosis and the diagnosis of hyperlactatemia. BMCEmergMed. 2008, 8: 18-Google Scholar
- Iberti TJ, Leibowitz AB, Papadakos PJ, Fischer EP: Low sensitivity of the anion gap as a screen to detect hyperlactatemia in critically ill patients. Crit Care Med. 1990, 18 (3): 275-277. 10.1097/00003246-199003000-00005.View ArticlePubMedGoogle Scholar
- Jeng JC, Jablonski K, Bridgeman A, Jordan MH: Serum lactate, not base deficit, rapidly predicts survival after major burns. Burns. 2002, 28 (2): 161-166. 10.1016/S0305-4179(01)00098-5.View ArticlePubMedGoogle Scholar
- Levraut J, Bounatirou T, Ichai C, Ciais JF, Jambou P, Hechema R, Grimaud D: Reliability of anion gap as an indicator of blood lactate in critically ill patients. Intensive Care Med. 1997, 23 (4): 417-422. 10.1007/s001340050350.View ArticlePubMedGoogle Scholar
- Mikulaschek A, Henry SM, Donovan R, Scalea TM: Serum lactate is not predicted by anion gap or base excess after trauma resuscitation. JTrauma. 1996, 40 (2): 218-222.Google Scholar
- Singh RN, Singh NC, Hutchison J, Moses GC: Lower anion gap increases sensitivity in predicting elevated lactate. ClinIntensive Care. 1994, 5 (5): 221-224.Google Scholar
- Husain FA, Martin MJ, Mullenix PS, Steele SR, Elliott DC: Serum lactate and base deficit as predictors of mortality and morbidity. AmJSurg. 2003, 185 (5): 485-491.Google Scholar
- Waters JH, Miller LR, Clack S, Kim JV: Cause of metabolic acidosis in prolonged surgery. Crit Care Med. 1999, 27 (10): 2142-2146. 10.1097/00003246-199910000-00011.View ArticlePubMedGoogle Scholar
- The pre-publication history for this paper can be accessed here:http://www.biomedcentral.com/1471-2253/10/16/prepub
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