Admission Serum Lactate Levels Do Not Predict Mortality in the Acutely Injured Patient

Pal, Jay D.; Victorino, Gregory P.; Twomey, Patrick; Liu, Terrence H.; Bullard, M. Kelley; Harken, Alden H.

doi:10.1097/01.ta.0000205858.82575.55

Cited by 70 publications

(50 citation statements)

References 28 publications

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“…Although lactate and base deficit (BD) are resuscitation markers that act as independent variables (50 -52), there is a low correlation between urinary output, mean arterial pressure, serum lactate, and base deficit (51). Serum lactate trends provide greater information regarding the homeostatic status (53,54). Determinations of BD do not demonstrate the same predictive power; the effect of specific correction of the BD during fluid resuscitation is unknown (13,50,52).…”

Section: First-line Monitoringmentioning

confidence: 97%

Critical care of the burn patient: The first 48 hours

Latenser

2009

Critical Care Medicine

185

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The critically burned patient differs from other critically ill patients in many ways, the most important being the necessity of a team approach to patient care. The burn patient is best cared for in a dedicated burn center where resuscitation and monitoring concentrate on the pathophysiology of burns, inhalation injury, and edema formation. Early operative intervention and wound closure, metabolic interventions, early enteral nutrition, and intensive glucose control have led to continued improvements in outcome. Prevention of complications such as hypothermia and compartment syndromes is part of burn critical care. The myriad areas where standards and guidelines are currently determined only by expert opinion will become driven by level 1 data only by continued research into the critical care of the burn patient.

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Section: First-line Monitoringmentioning

confidence: 97%

Critical care of the burn patient: The first 48 hours

Latenser

2009

Critical Care Medicine

185

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“…In addition to ischemia and hypoxia, lactate may be elevated due to other etiologies, including circumstances that may either increase lactate production (such as white blood cells or certain medications) or decrease its clearance (such as liver or kidney failure) [1]. Lactate's inability to correlate with other indicators of injury severity and to predict poor clinical outcome has also been reported [2]. Furthermore, since neurons exposed to lactate concentrations of 20 mmol/L for 6 h at normal pH are not damaged [3], it is unclear whether lactate itself is dangerous to cells.…”

Section: Introductionmentioning

confidence: 99%

A Different View of Lactate in Trauma Patients: Protecting the Injured Brain

Cureton

Kwan

Dozier

et al. 2010

Journal of Surgical Research

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“…Serum lactate is an ideal biomarker because the technology is inexpensive 23 , the test is fast 24 , and there are multiple ways to obtain equivalent samples 25–28 . Many studies that examined the utility of lactate clearance have used in-hospital mortality as the endpoint 29–34 , yet death in the hospital can be caused by many events unrelated to the adequacy of resuscitation. Lactate has a half-life of 15–30 minutes in healthy subjects 35 , suggesting lactate levels may change rapidly in response to resuscitative efforts.…”

Section: Introductionmentioning

confidence: 99%

Failure to clear elevated lactate predicts 24-hour mortality in trauma patients

Dezman

Comer

Smith

et al. 2015

Journal of Trauma and Acute Care Surgery

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Background Lactate clearance is a standard resuscitation goal in patients in non-traumatic shock but has not been investigated adequately as a tool to identify trauma patients at risk of dying. Our objective was to determine if trauma patients with impaired lactate clearance have a higher 24-hour mortality rate than patients whose lactate concentration normalizes. Methods A retrospective chart review identified patients who were admitted directly from the scene of injury to an urban trauma center between 2010 and 2013 and who had at least one lactate concentration measurement within 24 hours. Transfers, patients without lactate measurement, and those who were dead on arrival were excluded. Of the 26,545 screened patients, 18,304 constituted the initial lactate measurement population and 3,887 were the lactate clearance cohorts. Results Initial lactate had an area-under-the-receiver operating curve of 0.86 and 0.73 for mortality at 24 hours and in-hospital, respectively. An initial concentration ≥3 mmol/L had sensitivity of 0.86 and specificity of 0.73 for mortality at 24 hours. The mortality rate among patients with elevated lactate concentrations (n=2381, 5.6±2.8 mmol/L) that did not decline to <2.0 mmol/L in response to resuscitative efforts (mean second measurement, 3.7±1.9 mmol/L) was nearly seven times higher (4.1% vs 0.6% [p<0.001]) than among those with an elevated concentration (n=1506, 5.3±2.7 mmol/L) that normalized (1.4±0.4 mmol/L). Logistic regression analysis showed that failure to clear lactate was associated with death more than any other feature (OR=7.4; CI, 1.5–35.5), except having an Injury Severity Score >25 (OR=8.2; CI, 2.7–25.2). Conclusions Failure to clear lactate is a strong negative prognostic marker after injury. An initial lactate measurement combined with a second measurement for high-risk individuals might constitute a useful method of risk-stratifying injured patients.

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Admission Serum Lactate Levels Do Not Predict Mortality in the Acutely Injured Patient

Cited by 70 publications

References 28 publications

Critical care of the burn patient: The first 48 hours

Critical care of the burn patient: The first 48 hours

A Different View of Lactate in Trauma Patients: Protecting the Injured Brain

Failure to clear elevated lactate predicts 24-hour mortality in trauma patients

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