Community-acquired pneumonia (CAP) is one of the leading causes of morbidity and mortality across the globe. According to the World Health Organization (WHO), among the respiratory diseases, lower respiratory tract infections and CAP are the most common causes of death worldwide, particularly in the adult population [1]. CAP is one of the major concerns in hospitalized patients, where it prolongs the duration of hospital stays, and a high rate of mortality is noticed in patients with severe disease of comorbid conditions [2]. Risk stratification early in the course of the disease is thus needed to help in guiding clinical decision-making, allocating resources, and ensuring better patient outcomes. Many different clinical score systems have been developed in an attempt to predict the prognosis in cases of CAP, including the Pneumonia Severity Index (PSI) and CURB-65, which classify the need to be hospitalized or in an intensive care unit (3,4). These scoring tools, however, are associated with limitations, with some of them being complex in calculation and dependent on several variables, and their feasibility is limited in cases of acute settings. Therefore, search for easy-to-measure and reliable biomarkers is increasingly being investigated to complement clinical prediction and provide reliable prognostic information.

In this regard, serum lactate, which is also a marker of tissue hypoxia and impaired tissue perfusion, has been studied extensively in sepsis and critical cases. Increased serum lactate levels is directly proportional to degree of anerobic metabolism and lack of oxygen delivery to tissue or decreased utilization of oxygen which are generally associated with worst outcomes across a spectrum of acute conditions [5, 6] Lactate has been established as a prognostic biomarker in sepsis where its higher concentrations have been associated with mortality as well as mortality, increased length of stay in intensive care and the requirement of vasopressor therapy [7]. This has prompted the inclusion of lactate measurement in the Surviving Sepsis Campaign guidelines as an element of the initial resuscitation bundle [8]. Serum lactate has been of interest in the context of CAP as a predictor of the severity of the disease and outcome. Increased lactate concentration in CAP patients is not only an indication of whole-body hypoperfusion as a result of an infection but can also be a sign of local tissue hypoxia in the lungs caused by gas exchange dysfunction, extensive inflammation, and microcirculatory dysfunction [9]. Various studies have indicated that baseline lactate levels on hospitalization are independent predictors of ICU admission, need for artificial breathing, and mortality in patients with CAP [10, 11]. In addition, lactate clearance in time was suggested as a dynamic measure of therapeutic response and prognostic improvement [12]. Importantly, serum lactate measurements can be performed much faster using point-of-care testing, which can play an essential role in emergency and intensive care, where targeted triage is critical. In contrast to the complex scoring system, lactate measurements, being a single biomarker, can be valuable in assisting with the identification of high-risk patients who may otherwise appear clinically stable [13]. It has been proposed that the use of lactate levels with any established severity scores could improve predictive accuracy and aid in providing early aggressive care, including changing the level of care to a higher level of care, closer hemodynamic monitoring, and early broad-spectrum antibiotics [14].  Since the burden of CAP is increasing globally in recent times, the assessment of the prognostic value of serum lactate in adult CAP has important clinical implications. With a better knowledge of its role, risk stratification models may be clarified, optimal management pathways may be optimized, and hopefully, mortality will diminish. This study was aimed at examining the correlation between serum lactate levels and community-acquired pneumonia patient outcomes in the adult population presenting to our tertiary care hospital.

This prospective observational study was conducted in the Department of Respiratory Medicine, Prathima Institute of Medical Sciences, Naganoor, Karimnagar, Telangana. Institutional Ethical approval was obtained for the study after duly following the procedure for human research based on the Helsinki declaration. No interventions beyond standard care were utilized in the study. Written consent was obtained from all the participants of the study after explaining the nature of the study in the vernacular language.

Inclusion criteria

1. Clinical and radiographic diagnosis of CAP (new infiltrate on chest radiographs or CT plus ≥1 with symptoms of cough, fever, dyspnea, pleuritic chest pain).
2. With symptom onset in the community or ≤48 h after hospital arrival.
3. Serum lactate was obtained within 2 hours of the procedure.
4. Aged > 18 years
5. Males and Females

Exclusion criteria

1. Hospital-acquired or ventilator-associated pneumonia.
2. Prior hospitalization within 14 days.
3. Primary cardiogenic pulmonary edema.
4. Active gastrointestinal or metabolic conditions.
5. Pregnancy.
6. Inability to complete follow-up.

A total of 40 consecutive adults (≥18 years) presenting with community-acquired pneumonia (CAP) were recruited based on the inclusion and exclusion criteria.  On Admission, demographic profile, comorbidities (Charlson Comorbidity Index), vital signs, laboratory values (CBC, CRP, creatinine, bilirubin), arterial or venous blood gas, and imaging findings were recorded. Pneumonia Severity Index (PSI) and CURB-65 were calculated by the study team, blinded to outcomes.

Lactate assessment: Baseline lactate (L₀): venous whole-blood lactate measured by point-of-care analyzer or central lab enzymatic method within 2 hours of ED arrival; values recorded in mmol/L, and the assay method documented. Repeat lactate (L₆): obtained at 6±1 hours when clinically feasible for calculation of lactate clearance: Clearance (%) = Lo - L6 / Lo × 100. Normal (<2.0 mmol/L), intermediate (2.0–3.9 mmol/L), high (≥4.0 mmol/L). Lactate clearance was dichotomized at ≥10% for secondary analyses. Therapies recorded within first 6 h: antibiotic timing and spectrum, IV fluids (type/volume), vasopressors, oxygen and ventilatory support (HFNC/NIV/IMV), and disposition (ward vs ICU).

The primary outcome determined was the in-hospital composite adverse outcomes. (a) all-cause mortality, (b) need for invasive mechanical ventilation, or (c) vasopressor requirement ≥6 h after presentation. Secondary outcomes: (1) ICU admission within 24 h; (2) length of stay (LOS); (3) 30-day all-cause mortality; (4) clinical deterioration within 24 h (new organ dysfunction: ΔSOFA ≥2); (5) time to clinical stability (afebrile, HR<100, RR<24, SBP≥90 without vasopressors, SpO₂≥90% on ≤4 L/min).

Statistical analysis: All the available data were segregated, refined, and uploaded to an MS Excel spreadsheet and analyzed by SPSS version 26 in Windows format. The continuous variables were reported as mean ± SD or median (IQR). Group comparisons across lactate categories used ANOVA. Discrimination of L₀ for the primary outcome assessed by AUROC with 95% CI (DeLong method). Optimal cut-point identified by Youden index; sensitivity, specificity, and likelihood ratios reported.

The baseline characteristics of the 40 enrolled patients categorized by initial lactate levels are shown in Table 1. The mean age of the population was 68.5 years, with a tendency toward higher age in patients with lactate >4.0 mmol/L (78 years), as compared to those with lactate <2.0 mmol/L (65.1); however, the values did not reach the level of significance (p=0.08).  There was no significant difference between categories, as male sex predominated across all of them (60%). However, the lactate levels were closely related to clinical severity. The percentage of patients with severe pneumonia (PSI classes IV-V) rose sharply with increasing lactate, ranging between 45.5% of patients in the <2.0 mmol/l group, to 100% in the>4.0 mmol/l group (p=0.02). Along the same line, a CURB-65 score of 3 or greater was more common among patients with elevated lactate (66.7% vs. 13.6%, p=0.03). Hypotension was only noted in elevated lactate groups, witnessed in 50% of lactate >4.0 mmol/L (p=0.01). Median Charlson Index was significantly greater in patients with elevated lactate (5 in >4.0 mmol/L group, p=0.04). There was also more renal dysfunction as demonstrated by increasing median creatinine with increasing lactate, to 2.0mg/dL in those with lactate levels of >4.0mmol/L (p=0.02). These results indicate that increased levels of lactate correlate with a more advanced age, manifested levels of illness, low blood pressure, a high burden of comorbidities, and impaired renal function.

Table 2 depicts the outcomes by initial lactate levels in the cohort. A critical analysis of the table shows that there is a significant relation between initial lactate level and poor clinical outcomes. The total composite primary outcome was reached in 22.5% of patients; however, this varied widely depending on the range of lactate levels [4.5% in the <2.0 mmol/L range, 25.0% in 2.0-3.9 mmol/L, and an alarming 83.3% in the >4.0 mmol/L range (p <0.001)]. 50% of cases of mortality occurred only in patients with higher lactate levels (>4.0mmol/L), and p-values were found to be significant. Vasopressor requirements showed that 66.7% of cases with lactate exceeding 4.0 mmol/L were given vasopressors, and none required vasopressors in the low lactate group. The p-values were found to be significant (p=0.001). Admission in the ICU within 24 hours occurred significantly more frequently as lactate rose, with a range of 13.6% (<2.0 mmol/L) to 66.7% (>4.0 mmol/L, p=0.02). Lactate was also strongly associated with mortality at thirty days, with an increase to 50% in the highest quartile (p=0.004). Although invasive mechanical ventilation trended higher with increasing lactate (33.3% in >4.0mmol/L vs. 4.5% in <2.0 mmol/L), the difference was not significant (p=0.12). This table demonstrates the predictive importance of lactate on presentation, where higher levels are greatly associated with adverse short-term and longer-term outcomes.

Table 3 shows the discriminatory performance of lactate and clinical scores for the primary composite outcome. Analysis of the table shows that the predictive value of serum lactate is comparable to prognostic scores. Initial lactate (AUROC 0.89, 95 % CI 0.79-0.99) was shown to be a better predictor of the composite adverse outcome compared to PSI (AUROC 0.78) and CURB-65 (AUROC 0.71). A threshold value of ≥ 2.8 mmol/L, as identified with the Youden index, showed high sensitivity (88.9%) and specificity (80.6%), a positive likelihood ratio of 4.6, and a small negative likelihood ratio (0.14), which demonstrated strong rule-in and rule-out capabilities. The overall accuracy was lower with lower likelihood ratios on PSI and CURB-65. Adding lactate to PSI further enhanced the AUC (0.92), further pointing to the efficacy of including biochemical and clinical markers. These results indicate that lactate, especially when combined with PSI, has strong prognostic differentiating abilities and can be more common than traditional risk scores to identify high-risk CAP patients.

Table 4 shows the adjusted calculation of predictors of the composite adverse outcome. Initial lactate was the strongest predictor after adjustment for age, PSI class, hypotension, and CRP levels. Odds of poor outcome were almost three times higher with each 1 mmol/L increment in lactate (aOR 2.85, 95% CI 1.42 to 6.12, p=0.006). None of the other variables were statistically significant, although hypotension was a source of marginal concern (aOR 4.21, p=0.19). Age and CRP were insignificant, and PSI experienced a wide standard error, possibly due to limitations related to the small sample size. The model calibrated well (Hosmer-Lemeshow p=0.62), and this shows that the findings are reliable. Those findings validate lactate as an independent predictive biomarker of CAP and extend when compared to established clinical severity scores in CAP.

Table 5 shows the prognostic value of lactate clearance at 6 hours.  In n=32 patients with serial lactate levels, clearance ≥10% was followed by significantly superior outcomes, as only 11.1% experienced the composite endpoint, in contrast to 42.9% with clearance <10% (adjusted OR 5.8, 95% CI 1.3-28.4). Similarly, when lactate normalization (<2.0 mmol/L) occurred within 6 hours, improved survival and only 6.7% had an adverse outcome. Whereas 41.2% of patients with persistently elevated lactate worsened. These results indicate that not only the baseline lactate but also its tendency to decrease or not provides crucial information. Dynamic monitoring of lactate can be used to guide clinicians on patients who are at risk, even though they have been receiving certain initial practices.

The current study aimed to evaluate the prognostic value of serum lactate in adult patients with community-acquired pneumonia (CAP) presenting to our tertiary care hospital. The results of our study showed that elevated lactate levels at admission were significantly correlated to increased disease severity, including duration of hospital stay in ICU and mortality. This shows that serum lactate can act as a simple, rapid, and inexpensive biomarker for predicting the prognosis of CAP cases. Lactate is the metabolic product of anaerobic metabolism, and its increase occurs mostly due to tissue hypoxia. However, recent studies have shown that hyperlactatemia in pneumonia and sepsis, apart from hypoxia, could be because of increased glycolysis caused by systemic inflammation and in response to catecholamine surge [15]. This underscores its diagnostic value as a composite marker for both perfusion and metabolic stress. In this study, patients with higher lactate levels were all associated with increased severity of CAP requiring ICU care in concordance with the pathophysiological mechanism. Previous studies have shown that initial lactate levels can act as a reliable predictor in cases of infection. Wang et al. [16] have shown that lactate levels ≥2 mmol/L were independently correlated with the rate of increase in mortality at the end of 28 days in CAP cases. Similarly, Kim et al. [17] found that lactate levels on admission acted as a better prognostic marker based on its accuracy as compared to the traditional scoring systems, such as CURB-65 alone, especially in critically ill patients. These findings are in agreement with the results found in our study, where the lactate levels had a significant correlation with the severity of disease and mortality.

The results of this study are in agreement with the recent concept of lactate clearance as the dynamic marker of prognosis. Our results also agree with previous research, which suggests that patients with decreasing lactate levels in 6 – 24 hours have an improved survival rate compared to those with persistently elevated or increasing lactate levels [18]. Although our study collected samples at admission Lo, and after 6 hours L6, future studies on serial lactate monitoring in CAP patients can better determine the prognostic accuracy and guide resuscitation more efficiently. Other makers of inflammation, such as procalcitonin (PCT) and C-reactive protein (CRP), have several advantages. PCT and CRP are only inflammation markers, and they reflect bacterial burden or inflammation, as the lactate levels show systemic hypoperfusion and metabolic stress, which is important for the determination of prognosis [19]. Recent studies have shown that a combination of lactate levels and clinical severity scores may improve risk stratification as compared to either method applied alone [20]. Our results support integrating lactate measurements with scoring systems such as PSI or CURB-65 to refine prognosis and guide clinical decision making, which includes ICU admissions. Importantly, serum lactate is a widely available test that is relatively inexpensive, thus useful in resource-poor contexts. Although desired imaging modalities and advanced biomarkers are not always available, lactate assessment can be done in a short time setting at the bedside, enabling early selection of high-risk patients. This has significant ramifications for triage and in the overcrowded emergency departments. The limitations of our study were a small sample of patients (n=40), which may reduce generalizability, and multicentre studies are required to confirm the above results. Moreover, the baseline levels of lactate were chosen instead of serial measurements, which may better demonstrate the outcomes of the patients. Although these limitations exist, the findings we present contribute to the emerging data regarding serum lactate level as a utility measure in determining prognosis in adult CAP patients.

In conclusion, within the limitations of our study, we found that elevated serum lactate at admission is strongly associated with adverse outcomes in community-acquired pneumonia, including higher disease severity, ICU requirement, and mortality. Routine measurement of lactate may therefore serve as a valuable biomarker in early risk stratification, guiding clinical management, and optimizing resource utilization in adult CAP patients.

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