DISCUSSION

Current study was conducted in order to find out the role of arterial serum lactate as a predictor
of undifferentiated shock on admission and its outcome. We tried to establish correlation of
arterial serum lactate level & duration of ICU stay & mortality. We also assessed correlation of
arterial serum lactate and acid base status with ionotropic support required for patient. We
concluded that patients with raised serum lactate levels at admission needed longer ICU stay,
inotropic support and had higher incidence of mortality.

Lactate levels in clinical practice are often used as a surrogate for illness severity and to gauge
response to therapeutic interventions. The use of lactate as a clinical prognostic tool was first
suggested in 1964 by Broder and Weil 1 when they observed that a lactate excess of > 4 mmol/L
was associated with poor outcomes in patients with undifferentiated shock.Since that time, much
has been published on the utilization of lactate in a variety of patient populations. Moreover,
causes of elevated lactate apart from tissue hypoperfusion have been recognized and should be
considered in the appropriate clinical context 2.

This prospective study was carried out in Intensive care units of Poona Hospital and Research
Centre (PHRC), Pune, over a period of two years on 168 patients admitted with systolic blood
pressure <90 mmHg, Heart rate more than 100/min & Respiratory rate more than 20/min in
Poona Hospital & Research Center, Pune.

In our study, the maximum percentage of patients was in the age range of 50 to 59 years (39.9%)
with average age 52.6 years. Minimum to maximum age range was 30-74 years. There were only
5 cases with >70 years of age. The male to female ratio was 1.95: 1.00.

Majority patients were presented with septic shock constituting 70.2% of cases followed by
hypovolemic shock in 17.3% of cases. Patients with neurogenic shock were least.

In a study conducted by Karen Beke3on lactate clearance in shock patients and 30 day mortality
in these patients, mean age was 57.4 years and male to female was 1.51: 1. The occurrence of
septic shock was observed in majority of cases with 51% of patients. Hypovolemic shock was
present in 34% cases.
In another study conducted by Vitek V et al4 on serum lactate levels in different types of shock,
majority of cases were presented with septic shock followed by cardiogenic shock. Least number
of the patients were observed in hemorrhagic and combination group.

Serum lactate levels were monitored on admission, at 12 hours and at 24 hours. Cases were
divided in three groups as follows:

 Group I: serum lactate 0 – 18 (<2 mmol/L)

 Group II: serum lactate 18 – 36 (2 – 4 mmol/L)
 Group III: serum lactate >36 (>4 mmol/L)

Group I was used as a control group and Group II and III were compared against it.

In present study, on admission, majority cases had serum lactate levels more than 4 mmols/L.
41.1% had serum lactate levels between 2-4 mmol/L and only 11 cases had less than 2 mmol/L.

On 12 hours, serum lactate levels were measured again. In this reading, 20 patients had their
serum lactate level below 2 mmol/L and 90 cases had more than 4mmol/L.

The samples drawn at 24 hours showed that 30 patients had their serum lactate levels less than 2
mmol/L and 55cases had 2-4 mmol/L. 83 (49.4%) had serum lactate levels above 4 mmol/L in
the study group.

the median serum sample level at admission and at 12 hours was 38.50 and at 24 hours it was
36.Distribution of median serum lactate levels at admission is significantly higher compared to
median serum lactate levels at 12-Hrs and 24-Hrs.

In a study of Karen Beke,3 Average lactate serum level on admission was 40.2± 35.7 mg/dl
(4.5±3.9mmol/L). The median lactate serum decrease within 6 hours was – 31% [median,
25thperc: -52% - 75thperc: -7%].

In a study conducted by Julian Villar et al5 median lactate 1.7 mmol/L (interquartile range [IQR]
1.2-2.6) was found. They also stated that a lactate level cutoff of ⩾4 mmol/L had best test
characteristics (sensitivity 52.4%, specificity 91.4%) to predict increased 3-day mortality.
Median value of serum lactate level at admission was highest in septic shock patients followed
by in neurogenic shock. The 12 hour values suggest that there was rise in serum lactate in
neurogenic shock patients and the highest median serum lactate was in septic shock. At 24 hours,
neurogenic shock patients showed highest median value. The distribution was found to be
significant in all the groups.

In a recent study conducted by Jan Bekker et al6 found initial serum lactate values as 4.7 ± 2.5
mmol/L in survivors of septic shock and 5.6 ± 3.7 mmol/L in non survivors.

A recent study by Howell et al7 suggested that serum lactate was associated with mortality
independent of blood pressure. However, the mortality in this sepsis cohort was only 5.7% and it
seemed that the association between serum lactate levels and mortality was modified in the
presence of shock.

Of total 168 cases, 46 did not require ionotropes and 122 cases were treated with ionotropes. It
was observed that, patients with higher values of serum lactate at admission require ionotropes
frequently.

Duration of ICU stay was more in patients with higher serum lactate value at admission. Patients
with serum lactate value more than 4mmol/L were stayed in the ICU for more duration with
median of 6 days and ranges from 2-12 days.

Patients with greater values of serum lactate on admission had a greater risk of mortality. It was
observed that none cases died having serum lactate below 2mmol/L while 3 cases died who were
having serum lactate value of 2-4 mmol/L and 20 cases having serum lactate value more than 4
mmol/L.

In Karen Beke3 study eighty seven out of 124 (70.2%) patients were categorized as responders to
shock treatment as their serum lactate levels dropped by more than 20% within 6 hours after
treatment initiation, 37 out of 124 (29.8%) patients were categorized as non-responders to shock
treatment within 6 hours. No significant differences were observed between the initial serum
lactate of the responders (31.2±33.8 mg/dl - 3.5±3.7 mmol/L) and non-responders (45.1± 40.8
mg/dl -5.0±4.5mmol/L). No significant differences of serum lactate change within 6 hours were
observed between types of shock (ANOVA F =1.530, p = 0.221). The 30-day mortality rate of
patients with a lactate decrease > 20% later than 6 hours, i.e. at 12 hours or at 24 hours, was
compared to the mortality rate of non-responders. No significant differences were observed
between groups.

A study conducted by Mikkelsen et al8 on association of serum lactate with mortality. They
divided patients in two groups based on whether the patient had shock or not. In the non-shock
subgroup, the initial median serum lactate level was significantly higher in non-survivors
compared with survivors at 28 days (3.4 vs. 2.6 mmol/L, p <0.001). In the shock subgroup, non-
survivors alsohad significantly higher initial median serum lactate levels compared with
survivors (5.2 vs. 3.3 mmol/L, p< 0.001).Each of the 28 patients with an initial serum lactate <1
mmol/L survived, including four in the shock subgroup. They found that initial serum lactate was
associated with mortality independent of organ dysfunction in this study of ED patients with
severe sepsis.

LIMITATIONS –

As reviewed above, the etiologies of lactate elevation are quite varied and the clinical
significance of elevated lactate also varies widely. This difference highlights the importance of
considering all potential etiologies in the initial evaluation and using the test result in context
with the overall clinical picture. In addition, multiple reasons for lactate elevation can be present
in a given patient making interpretation challenging.

Given the wide variety of etiologies of lactate and the varied clinical significance (depending on
etiology), lactate is not necessarily specific for either diagnosis or prognosis unless thoughtfully
coupled with the overall clinical picture. In addition to being a nonspecific test, lactate may not
be as sensitive a test as is commonly thought. In a study by Dugas et al9, 45% of patients in
vasopressor-dependent septic shock did not mount a lactic acid level > 2.4 mmol/L initially, but
their mortality remained high. The reason some patients express lactate more than others in these
scenarios is not well understood. Dugas et al9 found an association between elevated lactate and
both liver disease and bacteremia in their study of patients in vasopressor-dependent shock. The
association between lactate elevation and liver injury in the Dugas et al, study illustrates a
potential confounder that may occur in patients with sepsis given the high frequency of
concurrent liver involvement9.

SUMMARY

The present study was carried on 168 cases admitted to the emergency department with
undifferentiated shock. Serum lactate levels were measured at admission, at 12 hours and at 24
hours. We observed the following findings-

 In our study, majority of cases were from age group 50 to 59 years with age ranging from
30 to 74 years. Mean age was found to be 52.6 years.
 We observed male preponderance with 1.51: 1 male to female ratio.
 70.2% of cases were presented with septic shock constituting majority of cases. 29 cases
had hypovolemic shock.Only 7 cases were presented with neurogenic shock.
 Majority cases had their serum lactate levels at admission more than 4mmol/L with
52.4% cases. Only 11 cases had their serum lactate levels below 2 mmol/L at admission.
 At 12 hours, 20 cases had serum lactate below 2mmol/L and 90 cases had serum lactate
above 4mmol/L.
 On 24 hours, serum lactate values were above 4 mmol/L in 83 cases and in 55 cases had
serum lactate in between in 2-4 mmol/L.
 Distribution of median serum lactate levels at admission did not differ significantly
compared to median serum lactate levels at 12-Hrs.
 Distribution of median serum lactate levels at admission is significantly higher compared
to median serum lactate levels at 12-Hrs and 24-Hrs.
 Median serum lactate levels at admission is lowest in Hypovolemic Shock and highest in
Septic Shock group.
 Significantly higher proportion of cases with higher on admission serum lactate levels
had higher incidence of requirement of inotorpes.
  Patients with hyperlactatemia on admission needed longer stay in ICU compared to other
groups with statistically significant association.
 Significantly higher proportion of cases with higher on admission serum lactate levels
had higher incidence of mortality.

CONCLUSION –

Serum lactate levels at admission were found to be raised in patients with undifferentiated shock.
Raised serum lactate levels were found to be positively correlating with need for inotropic
support, longer hospital stay and increased incidence of mortality. Lactate level should be used to
risk-stratify patients’ disease severity, independent of disease process, with elevated lactates
indicating higher risk of mortality. This may help identify patients in need of additional scrutiny
and monitoring. Though the serum lactate levels cannot be used as a sole prognostic marker of
survival, the combination of decrease in serum lactate levels, and specific clinical and treatment
variables may provide insight into the severity of shock, the efficacy of treatment and the vital
outcome. Aiming for therapeutic decrease in serum lactate as a goal-setting could affect shock
patients’ survival. An intervention-design study would hopefully explore this question.

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