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Guiding Resuscitation in the Emergency Department

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References

A constellation of findings from the physical examination may include altered mentation, hypotension, tachycardia, and decreased urinary output by 30% to 40% intravascular volume loss.8,9Findings from the physical examination to assess fluid status should be used with caution as interobserver reliability has proven to be poor and the prognostic value is limited.

Limitations

The literature shows the limited prognostic value of the physical examination in determining a patient’s volume status and whether fluid resuscitation is indicated. For example, in one meta-analysis,10 supine hypotension and tachycardia were frequently absent on examination—even in patients who underwent large volume phlebotomy.8 This study also showed postural dizziness to be of no prognostic value.

Another study by Saugel et al7 that compared the physical examination (skin assessment, lung auscultation, and percussion) to transpulmonary thermodilution measurements of the cardiac index, global end-diastolic volume index, and extravascular lung water index, found poor interobserver correlation and agreement among physicians.

The physical examination is also associated with weak predictive capabilities for the estimation of volume status compared to the device measurements. Another contemporary study by Saugel et al9 evaluated the predictive value of the physical examination to accurately identify volume responsiveness replicated these results, and reported poor interobserver correlation (κ coefficient 0.01; 95% caval index [CI] -0.39-0.42) among physical examination findings, with a sensitivity of only 71%, specificity of 23.5%, positive predictive value of 27.8%, and negative predictive value of 66.7%.9

Serum Lactate Levels

Background

In the 1843 book titled, Investigations of Pathological Substances Obtained During the Epidemic of Puerperal Fever, Johann Joseph Scherer described the cases of seven young peripartum female patients who died from a clinical picture of what is now understood to be septic shock.11 In his study of these cases, Scherer demonstrated the presence of lactic acid in patients with pathological conditions. Prior to this discovery, lactic acid had never been isolated in a healthy individual. These results were recreated in 1851 by Scherer and Virchow,11 who demonstrated the presence of lactic acid in the blood of a patient who died from leukemia. The inference based on Scherer and Virchow’s work correlated the presence of excessive lactic acid with bodily deterioration and severe disease. Since this finding, there has been a great deal of interest in measuring serum lactic acid as a means to identify and manage critical illness.

In a 2001 groundbreaking study of EGDT for severe sepsis and septic shock, Rivers et al2 studied lactic acid levels as a marker for severe disease. Likewise, years later, the 2014 Protocol-Based Care for Early Septic Shock (PROCESS), Prospective Multicenter Imaging Study for Evaluation of Chest Pain (PROMISE), and Australasian Resuscitation in Sepsis Evaluation (ARISE) trials used lactate levels in a similar manner to identify patients appropriate for randomization.12-14 While the purpose of measuring lactic acid was only employed in these studies to identify patients at risk for critical illness, the 2012 Surviving Sepsis Campaign Guidelines recommended serial measurement of lactate, based on the assumption that improved lactate levels signified better tissue perfusion.15

Although much of the studies on lactate levels appear to be based on the treatment and management of septic patients, findings can be applied to any etiology of shock. For example, a serum lactate level greater than 2 mmol/L is considered abnormal, and a serum lactate greater than 4 mmol/L indicates a significantly increased risk for in-hospital mortality.16

Benefits

It is now a widely accepted belief that the rapid identification, triage, and treatment of critically ill patients has a dramatic effect on morbidity and mortality.4 As previously noted, lactate has been extensively studied and identified as a marker of severe illness.17,18 A serum lactate level, which can be rapidly processed in the ED, can be easily obtained from a minimally invasive venous, arterial, or capillary blood draw.18 The only risk associated with serum lactate testing is that of any routine venipuncture; the test causes minimal, if any, patient discomfort.

Thanks to advances in point-of-care (POC) technology, the result of serum lactate assessment can be available within 10 minutes from blood draw. This technology is inexpensive and can be easily deployed in the prehospital setting or during the initial triage assessment of patients arriving at the ED.19 These POC instruments have been well correlated with whole blood measurements and permit for the rapid identification and treatment of at risk patients.

Limitations

The presence of elevated serum lactate levels is believed to represent the presence of cellular anaerobic metabolism due to impaired O2 delivery in the shock state. Abnormal measurements therefore prompt aggressive interventions aimed at maximizing O2 delivery to the tissues, such as intravenous fluid boluses, vasopressor therapy, or even blood product administration.

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