Significance of markedly raised lactate at emergency room admission

Measurement of serum lactate is increasingly being used in the assessment of emergency department (ED) patients. The prognostic significance of raised lactate (hyperlactatemia) at ED admission is the subject of a recent study conducted at the ED of a secondary and tertiary referral teaching hospital located in the Netherlands. 

The stated aim of this retrospective study was to assess 28-day mortality of emergency room patients with an admission lactate concentration of >4.0 mmol/L and compare it with 28-day mortality of two reference patient groups: those whose ED admission lactate concentration is <4.0 mmol/L; and those whose condition did not, in the opinion of attending doctor, warrant lactate measurement. 

A distinction is made between type A hyperlactatemia (increased lactate caused by tissue hypoxia) and type B hyperlactatemia (increased lactate in the absence of tissue hypoxia). A secondary aim of the study was to establish if 28-day mortality of those with type A hyperlactatemia (>4.0 mmol/L) differs from those with type B hyperlactatemia (>4.0 mmol/L).

Investigators retrospectively interrogated records of all 19,822 ED patients admitted during the period of January 2011 to October 2014 to identify all patients who had lactate measured at admission. Of the 19,822 patients, 1144 (5.8 %) had lactate levels determined, of whom 207 (18.1 %) had lactate >4.0 mmol/L. 

The detailed medical records of all 207 patients were retrieved in order to determine not only outcome (death or survival 28 days after ED admission) but also detail of patient monitoring and final diagnosis. These data were used in turn to make best assessment of the cause of hyperlactatemia in each case, and determine if patient was suffering type A or type B hyperlactatemia. 

Two reference patient groups were constructed by randomly selecting 200 of the 937 patients whose lactate was <4.0 mmol/L (the lactate <4 group) and 200 of the 18,678 patients who did not have lactate measured (the no lactate group). The detailed medical records of each of these reference group patients was also interrogated to retrieve the same data retrieved from the medical records of the study group (i.e. those whose lactate was >4.0 mmol/L). 

Mortality at 28 days post ED admission was significantly higher among those with lactate >4.0 mmol/L than those in the lactate <4 group, and those in the no lactate group: 40.6 % versus 18.5 % and 9.5 %, respectively. 

Data was sufficient to make a diagnosis of type A or type B hyperlactatemia in 197 of the 207 patients with lactate >4.0 mmol/L. Of these 197, 165 (83.7 %) were judged to have suffered type A hyperlactatemia and 32 (16.2 %) to have suffered type B hyperlactatemia. Those with type A hyperlactatemia were shown to have much worse outcome overall (28-day mortality 45.8 %) than those with type B hyperlactatemia (28-day mortality just 12.5 %).

In summary, results of this study indicate that ED patients with marked increase in plasma lactate (>4.0 mmol/L) have an extremely poor prognosis; in this study close to half (40.6 %) of these patients died within 28 days of ED admission.

However, the underlying cause of the hyperlactatemia has been shown by this study to have major prognostic significance. Those whose hyperlactatemia is the result of tissue hypoxia have a much worse prognosis than those whose hyperlactatemia occurs in the context of adequate/normal tissue oxygenation. 

In discussion of their study, the authors acknowledge the selection bias inherent in the retrospective nature of their study design. Only 5.3 % of ED patients had lactate measured. They make the important point that before lactate can be reliably used to risk-stratify ED patients, prospective studies are required in which lactate is determined in all ED patients, not a selected few.