Elsevier

Journal of Critical Care

Volume 27, Issue 4, August 2012, Pages 344-350
Journal of Critical Care

Sepsis
Prevalence and characteristics of nonlactate and lactate expressors in septic shock

https://doi.org/10.1016/j.jcrc.2012.01.005Get rights and content

Abstract

Purpose

The study's objective was to determine the proportion and patient characteristics of patients in vasopressor-dependent septic shock who presented without lactatemia.

Methods

A retrospective review of patients presenting to an urban tertiary-care emergency department between December 2007 and September 2008 was conducted. Patients with a final diagnosis of septic shock requiring vasopressors were divided, based on initial lactate, to nonlactate expressors (0-2.4 mmol/L), intermediate (2.5-3.9 mmol/L), and high (>4.0 mmol/L) lactate groups.

Results

Among 123 patients with vasopressor-dependent septic shock, 55 (45%) were nonlactate expressors (lactate ≤2.4 mmol/L). Acute liver injury, history of liver disease, and presence of bacteremia were associated with elevated lactate.

Conclusion

Almost one-half of patients with vasopressor-dependent septic shock did not express lactate on presentation, although a high mortality rate remains in this population. We found a significant association between lactate expressors and liver disease and between lactate expressors and positive blood cultures. The use of lactatemia as the sole indicator of need for additional intravenous fluid or an end point of resuscitation in septic shock may be inadequate.

Introduction

Severe sepsis and septic shock cause significant morbidity and mortality worldwide. In the United States, there are estimated to be 751 000 cases of severe sepsis each year (3.0 per 1000 population), leading to some 215 000 deaths [1]. In addition, sepsis carries a remarkable financial burden averaging $44 600 for the index admission and $78 500 in the first year for each patient [2]. Given this striking morbidity and mortality, the ability to identify and risk-stratify septic patients may improve outcomes as well as reduce health care costs.

Lactate has commonly been used by investigators as a marker of severe sepsis and septic shock, and several studies have shown that lactatemia in emergency department (ED) patients with suspected infection is an indicator of poor prognosis [3], [4], [5]. However, recent literature has suggested expanding the role of lactate beyond that of a prognostic indicator. Based on this association between lactatemia and mortality, lactate has been proposed as an obligatory criterion for the diagnosis of septic shock [6]. In addition, based on the improved prognosis of patients in septic shock who clear an existing lactatemia, lactate clearance has been proposed as a goal of resuscitation [7]. Although lactatemia and lactate clearance are useful prognostic tools, lactatemia may not develop in all patients in septic shock or in those who eventually die of septic shock. The prevalence of lactatemia and the characteristics of patients who express, or do not express lactate in vasopressor-dependent septic shock, have not been reported in the literature. The identification of patient characteristics that affect the likelihood of developing lactatemia should increase our understanding of the mechanism of lactatemia in septic shock.

We hypothesized that a proportion of patients in septic shock will not express lactate despite refractory hypotension. This group is termed nonlactate expressors because of their failure to mount or “express” a lactate in response to refractory hypotension. To test this hypothesis, we evaluated patients with vasopressor-dependent septic shock to determine the prevalence of nonlactate expressors and to identify patient characteristics associated with the development of lactatemia.

Section snippets

Study design and setting

We performed a retrospective evaluation of patients with vasopressor-dependent septic shock at an urban, university-affiliated, tertiary care center with an ED volume of more than 50 000 annual patient visits between December 2007 and September 2008. The ED followed the Multiple Urgent Sepsis Treatments protocol, an aggressive screening and treatment protocol for all patients with suspected bacteremia or sepsis, including initial screening lactic acid level and blood cultures drawn before the

Results

A total of 349 ED visits from 319 distinct patients were reviewed. Of these, 141 patients received vasopressors for an infection-related diagnosis in the ED. Three of these patients did not have an initial lactate sent from the ED, 11 did not have a confirmed hospital discharge diagnosis of sepsis, and 4 had less than 2 systemic inflammatory response criteria. The remaining 123 patients who met all study inclusion criteria during the study period were included in this analysis. The median age

Discussion

We observed that almost half of all patients do not express lactate even in the setting of septic shock. In our study, 45% of the patients in vasopressor-dependent septic shock did not express lactate, yet this group of patients had a mortality of 20%. Although there is a basic understanding of the pathophysiologic mechanisms involved in the formation and clearance of lactic acid, the reason why some patients with septic shock express an elevated lactate while others do not remains unclear.

Conclusion

Almost one-half of a cohort of patients with vasopressor-dependent septic shock did not express lactatemia on presentation, despite an overall high mortality in this population. The use of lactatemia as the only indication of perfusion status or a sole end point of resuscitation in septic shock may be inadequate. Lactate expression is associated with acute liver injury, a history of liver disease, and positive blood cultures.

Funding

The project described was supported in part by Grant Number UL1 RR025758- Harvard Clinical and Translational Science Center, from the National Center for Research Resources. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of Health. Michael W. Donnino is support by the NIH- R21AT005119.

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