Sepsis is a life-threatening clinical syndrome characterized by acute organ dysfunction resulting from a dysregulated host response to infection. Despite substantial advances in antimicrobial therapy, hemodynamic support, intensive care monitoring, and organ-supportive strategies, sepsis continues to be associated with considerable morbidity and mortality worldwide. Current sepsis management emphasizes rapid recognition, timely administration of appropriate antimicrobial therapy, source control, restoration of tissue perfusion, and early identification of patients at risk of deterioration [1]. The pathophysiology of sepsis is complex and involves simultaneous activation of pro-inflammatory and immunosuppressive pathways, endothelial injury, coagulation abnormalities, microcirculatory dysfunction, mitochondrial impairment, and altered cellular metabolism [2]. When these disturbances persist, dysfunction may develop sequentially or simultaneously in the cardiovascular, respiratory, renal, hepatic, neurological, and hematological systems, eventually progressing to multiorgan dysfunction syndrome (MODS), which is strongly associated with adverse outcomes [3]. Early risk stratification is therefore an essential component of sepsis management because patients who initially appear hemodynamically stable may deteriorate rapidly. Clinical variables such as hypotension, tachycardia, tachypnea, altered mental status, reduced urine output, hypoxemia, and requirement for vasopressor or respiratory support provide important information regarding disease severity. However, these manifestations may appear relatively late and can be influenced by age, comorbidities, medications, and the source of infection. Consequently, biochemical and hematological parameters are increasingly used alongside clinical assessment. Changes in leukocyte count, neutrophil-to-lymphocyte ratio (NLR), platelet count, serum creatinine, bilirubin, albumin, lactate, C-reactive protein (CRP), and procalcitonin (PCT) may reflect systemic inflammation, tissue hypoperfusion, metabolic stress, and evolving organ dysfunction. Bou Chebl et al. prospectively investigated NLR in patients with sepsis and demonstrated its potential association with disease severity and in-hospital mortality, although its prognostic performance remained variable [4]. Similarly, Wang et al. evaluated lactate kinetics in 1,169 septic patients and demonstrated that higher peak lactate and greater lactate exposure were associated with 28-day mortality [5]. These observations are biologically plausible because abnormalities in perfusion, endothelial function, inflammation, and cellular metabolism are interconnected rather than isolated phenomena in sepsis [6]. Several recent studies have therefore attempted to improve prognostic accuracy by combining clinical severity scores with biochemical markers. Park et al., in a large prospective cohort, reported that serial integration of serum lactate with the Sequential Organ Failure Assessment (SOFA) score improved mortality discrimination compared with SOFA alone [7]. Baldirà et al. evaluated lactate, CRP, PCT, and mid-regional pro-adrenomedullin and showed that selected biomarkers could provide additional prognostic information even among patients with relatively low initial SOFA scores [8]. More recently, Yoo et al. studied 3,499 patients with sepsis and septic shock and found that the lactate-to-albumin ratio had useful prognostic value for 28-day mortality and performed better than several conventional inflammatory marker ratios [9]. Nevertheless, considerable heterogeneity exists between studies regarding patient populations, timing of biomarker measurement, outcome definitions, proposed cut-off values, and the relative performance of individual biomarkers. Furthermore, many emerging biomarkers remain expensive, poorly standardized, or unavailable in routine clinical settings, limiting their widespread application [10]. An important research gap therefore remains in identifying a simple, clinically applicable combination of early bedside findings and routinely available biochemical parameters that can simultaneously predict progression to multiorgan dysfunction and mortality. Such an approach may allow earlier recognition of high-risk patients without dependence on specialized biomarker assays. The present study was therefore undertaken to evaluate the clinical and biochemical profile of patients with sepsis and to identify early clinical and laboratory predictors associated with the development of multiorgan dysfunction and mortality. Establishing these predictors may facilitate timely escalation of monitoring and treatment, improve risk-based allocation of critical care resources, and ultimately contribute to better clinical outcomes.

This hospital-based prospective observational study was conducted in the Department of General Medicine of a tertiary care teaching hospital. The study included adult patients admitted with a diagnosis of sepsis during the defined study period. Sepsis was identified based on clinical evidence of suspected or confirmed infection associated with acute organ dysfunction, in accordance with the Sepsis-3 definition. A total of 100 eligible patients were enrolled after applying the predefined inclusion and exclusion criteria. The study was designed to assess clinical and biochemical parameters at the time of initial evaluation and to determine their association with the subsequent development of multiorgan dysfunction and in-hospital mortality. Approval was obtained from the Institutional Ethics Committee before commencement of the study, and informed consent was obtained from each participant or an authorized attendant wherever applicable. Sample Size A total of 100 patients with sepsis admitted to the Department of General Medicine were included in the study. Patients fulfilling the eligibility criteria during the study period were recruited consecutively until the required sample size was achieved. Inclusion Criteria • Patients aged 18 years and above. • Patients admitted with suspected or microbiologically/clinically confirmed infection. • Patients fulfilling the diagnostic criteria for sepsis according to Sepsis-3, with evidence of acute organ dysfunction. • Patients in whom relevant clinical examination and baseline biochemical investigations were available at the time of admission or initial evaluation. • Patients or their legally authorized representatives who provided informed consent for participation. Exclusion Criteria • Patients younger than 18 years of age. • Patients with advanced malignancy or terminal illness receiving palliative care. • Patients with pre-existing severe chronic organ failure that could interfere with assessment of acute sepsis-related organ dysfunction, such as end-stage renal disease on maintenance dialysis or advanced chronic liver failure. • Patients receiving long-term immunosuppressive therapy or having profound immunodeficiency where appropriate clinical interpretation was not possible. • Patients transferred from another hospital after prolonged treatment for sepsis, when reliable baseline clinical or laboratory data were unavailable. • Patients with incomplete clinical or biochemical records. • Patients who declined consent to participate in the study. Study Tool • Data were recorded using a pre-designed structured case record form/proforma developed specifically for the study. The study tool included: • Demographic details, including age and sex. • Relevant comorbidities such as diabetes mellitus, hypertension, chronic kidney disease, chronic liver disease, cardiovascular disease, and chronic respiratory disease. • Probable or confirmed source of infection. • Vital parameters including temperature, heart rate, respiratory rate, blood pressure, oxygen saturation, and Glasgow Coma Scale score. • Clinical evidence of cardiovascular, respiratory, neurological, renal, hepatic, or hematological dysfunction. • Requirement for oxygen therapy, mechanical ventilation, vasopressor support, or renal replacement therapy. • Routine hematological and biochemical investigations. • SOFA score and other relevant indicators of severity. • Development of multiorgan dysfunction during hospitalization. • Final hospital outcome, including survival or death. Data Collection • Detailed history was obtained at the time of admission, including presenting symptoms, duration of illness, associated comorbidities, previous treatment, and suspected source of infection. • A complete general and systemic examination was performed, with particular attention to signs of circulatory failure, respiratory distress, altered sensorium, oliguria, and other manifestations of organ dysfunction. • Baseline vital parameters, including blood pressure, pulse rate, respiratory rate, temperature, oxygen saturation, and Glasgow Coma Scale score, were recorded. • Blood samples were collected for complete blood count, total and differential leukocyte count, platelet count, serum creatinine, blood urea, electrolytes, liver function tests, serum bilirubin, albumin, C-reactive protein, serum lactate, and other investigations as clinically indicated. • Blood, urine, sputum, or other appropriate samples were obtained for microbiological culture based on the suspected source of infection. • Relevant derived indices such as the neutrophil-to-lymphocyte ratio and lactate-to-albumin ratio were calculated from baseline laboratory values wherever applicable. • Organ dysfunction was assessed using the Sequential Organ Failure Assessment (SOFA) score, taking into account respiratory, cardiovascular, hepatic, coagulation, renal, and neurological parameters. • Patients were followed throughout hospitalization for progression of organ dysfunction, development of multiorgan dysfunction syndrome, requirement for intensive care or organ support, duration of hospitalization, and mortality. • For the purpose of outcome assessment, patients were categorized according to the occurrence of multiorgan dysfunction and final outcome as survivors or non-survivors. Outcome Measures The primary outcomes of the study were the development of multiorgan dysfunction and in-hospital mortality among patients with sepsis. Secondary assessment included identification of individual clinical and biochemical variables significantly associated with poor outcome and determination of independent predictors of multiorgan dysfunction and mortality. Statistical Analysis The collected data were entered into a spreadsheet and analyzed using appropriate statistical software. Continuous variables were expressed as mean ± standard deviation or median with interquartile range depending on data distribution, while categorical variables were presented as frequencies and percentages. Continuous variables between groups were compared using the independent Student's t-test or Mann–Whitney U test, whereas categorical variables were analyzed using the Chi-square test or Fisher's exact test. Correlation between relevant clinical, biochemical, and severity parameters was assessed using Pearson's or Spearman's correlation coefficient as appropriate. Variables significantly associated with multiorgan dysfunction or mortality on univariate analysis were entered into multivariable logistic regression analysis to identify independent predictors. Receiver operating characteristic (ROC) curve analysis was used, where appropriate, to evaluate the predictive performance and optimal cut-off values of significant parameters. A p-value <0.05 was considered statistically significant.

Table 1. Baseline Demographic and Comorbidity Profile of Patients with Sepsis Parameter Total patients (n=100) Age, years, mean ± SD 61.2 ± 11.3 Age >60 years 52 (52.0%) Male 63 (63.0%) Female 37 (37.0%) Diabetes mellitus 37 (37.0%) Hypertension 45 (45.0%) Chronic kidney disease 10 (10.0%) Chronic respiratory disease 11 (11.0%) Cardiovascular disease 12 (12.0%) ≥2 comorbidities 32 (32.0%) Duration of symptoms before admission, days 4.7 ± 2.0 The mean age of the study population was 61.2 ± 11.3 years, with slightly more than half of the patients being older than 60 years. Males constituted 63% of the cohort, indicating a moderate male predominance. Hypertension was the most frequent comorbidity, occurring in 45% of patients, followed by diabetes mellitus in 37%. Chronic kidney, respiratory, and cardiovascular diseases were less common. Nearly one-third of the patients had two or more associated comorbidities. The mean duration of symptoms before hospital admission was approximately five days, suggesting that a substantial proportion presented after several days of illness. Table 2. Clinical Presentation, Source of Infection, and Initial Severity Parameters in Sepsis Parameter Value Source of infection Respiratory tract infection 42 (42.0%) Urinary tract infection 25 (25.0%) Intra-abdominal infection 14 (14.0%) Skin/soft-tissue infection 8 (8.0%) Other/unknown source 11 (11.0%) Clinical parameters Temperature, °C 37.9 ± 0.7 Heart rate, beats/min 102.8 ± 14.1 Respiratory rate, breaths/min 23.4 ± 5.2 Systolic blood pressure, mmHg 105.8 ± 18.2 Mean arterial pressure, mmHg 74.7 ± 11.5 SpO₂, % 94.1 ± 3.7 Glasgow Coma Scale score 13.6 ± 1.4 SOFA score at admission 5.6 ± 2.3 Hypotension at presentation 20 (20.0%) Altered sensorium, GCS ≤13 45 (45.0%) Oliguria 25 (25.0%) qSOFA ≥2 57 (57.0%) Developed multiorgan dysfunction 38 (38.0%) In-hospital mortality 24 (24.0%) Respiratory tract infection was the commonest suspected source of sepsis, accounting for 42% of cases, followed by urinary tract infection in 25%. Patients generally presented with tachycardia and tachypnea, with a mean heart rate of 102.8 beats/min and respiratory rate of 23.4 breaths/min. Hypotension was documented in one-fifth of patients, while 25% had oliguria. Forty-five percent demonstrated clinically relevant alteration in sensorium, and 57% had a qSOFA score of at least 2. The mean admission SOFA score was 5.6 ± 2.3, indicating appreciable early organ dysfunction. During hospitalization, 38% developed MODS and 24% died. Table 3. Baseline Hematological and Biochemical Profile of Patients with Sepsis Parameter Value Hemoglobin, g/dL 11.5 ± 1.7 Total leukocyte count, ×10³/mm³ 12.17 (9.79–15.73) Neutrophil-to-lymphocyte ratio 10.35 (7.97–13.70) Platelet count, ×10³/µL 194.6 ± 59.4 Blood urea, mg/dL 41.43 (29.44–53.24) Serum creatinine, mg/dL 1.56 (1.12–1.95) Serum sodium, mEq/L 135.1 ± 4.4 Serum potassium, mEq/L 4.3 ± 0.6 Total bilirubin, mg/dL 1.11 (0.82–1.77) AST, U/L 52.70 (31.11–70.41) ALT, U/L 43.32 (32.19–61.90) Serum albumin, g/dL 3.1 ± 0.5 Serum lactate, mmol/L 2.48 (1.77–3.45) Lactate/albumin ratio 0.78 (0.57–1.12) CRP, mg/L 97.84 (72.03–132.14) Procalcitonin, ng/mL 1.98 (1.01–3.76) Values are expressed as mean ± SD or median (interquartile range), as appropriate. The laboratory profile demonstrated evidence of systemic inflammation, impaired tissue perfusion, and early organ dysfunction. The median NLR was 10.35, while the median CRP and procalcitonin levels were 97.84 mg/L and 1.98 ng/mL, respectively. Renal dysfunction was reflected by a median creatinine of 1.56 mg/dL and urea of 41.43 mg/dL. The median serum lactate was 2.48 mmol/L, indicating that a considerable proportion of patients had evidence of tissue hypoperfusion. Serum albumin was relatively reduced, with a mean value of 3.1 ± 0.5 g/dL. The resulting median lactate-to-albumin ratio was 0.78, providing a composite indicator of circulatory stress and physiological reserve. Table 4. Comparison of Early Clinical and Biochemical Parameters Between Patients With and Without Multiorgan Dysfunction Parameter MODS (n=38) No MODS (n=62) Statistical value p-value Age, years 62.7 ± 12.1 60.3 ± 10.8 t=1.03 0.305 Heart rate, beats/min 110.3 ± 10.5 98.2 ± 14.0 t=4.93 <0.001 Respiratory rate, breaths/min 26.9 ± 3.8 21.3 ± 4.8 t=6.47 <0.001 Mean arterial pressure, mmHg 69.4 ± 10.9 77.9 ± 10.8 t=-3.81 <0.001 SpO₂, % 92.6 ± 3.6 95.1 ± 3.5 t=-3.43 0.001 GCS score 12.8 ± 1.4 14.0 ± 1.2 t=-4.40 <0.001 SOFA score 7.7 ± 1.4 4.3 ± 1.8 t=10.37 <0.001 TLC, ×10³/mm³ 14.07 (11.86–17.81) 11.19 (8.58–13.16) Z=3.52 <0.001 NLR 13.34 (9.59–15.91) 9.68 (7.34–11.56) Z=3.41 0.001 Platelets, ×10³/µL 160.6 ± 42.1 215.5 ± 59.0 t=-5.40 <0.001 Creatinine, mg/dL 1.90 (1.62–2.25) 1.35 (0.81–1.64) Z=4.80 <0.001 Bilirubin, mg/dL 1.59 (1.06–2.13) 0.96 (0.77–1.39) Z=3.79 <0.001 Albumin, g/dL 2.9 ± 0.5 3.2 ± 0.5 t=-3.40 0.001 Lactate, mmol/L 3.45 (2.67–3.94) 1.97 (1.67–2.48) Z=5.92 <0.001 Lactate/albumin ratio 1.24 (0.94–1.59) 0.65 (0.51–0.84) Z=6.31 <0.001 CRP, mg/L 113.39 (82.84–143.68) 90.20 (59.30–121.39) Z=2.54 0.011 Procalcitonin, ng/mL 3.32 (2.00–4.53) 1.40 (0.80–2.73) Z=4.14 <0.001 Thirty-eight patients developed multiorgan dysfunction during hospitalization. Patients who developed MODS had significantly higher heart and respiratory rates and significantly lower MAP, oxygen saturation, and GCS scores at initial evaluation. The mean SOFA score was markedly higher in the MODS group (7.7 versus 4.3; p<0.001). Biochemical markers associated with MODS included higher creatinine, bilirubin, lactate, NLR, CRP, and procalcitonin together with lower platelet count and serum albumin. The difference in lactate-to-albumin ratio was particularly marked, with median values of 1.24 in the MODS group compared with 0.65 among patients without MODS. Age did not differ significantly between the groups, suggesting that physiological severity and biochemical derangement were more closely related to development of MODS than chronological age. Table 5. Comparison of Clinical and Biochemical Parameters Between Survivors and Non-Survivors Parameter Survivors (n=76) Non-survivors (n=24) Statistical value p-value Age, years 60.9 ± 11.4 62.3 ± 11.0 t=0.55 0.585 Heart rate, beats/min 100.0 ± 14.0 111.5 ± 10.5 t=4.31 <0.001 Respiratory rate, breaths/min 22.2 ± 5.0 27.2 ± 4.1 t=4.89 <0.001 Mean arterial pressure, mmHg 77.0 ± 11.0 67.3 ± 10.0 t=-4.05 <0.001 SpO₂, % 94.6 ± 3.7 92.7 ± 3.6 t=-2.26 0.029 GCS score 13.8 ± 1.3 12.7 ± 1.3 t=-3.85 <0.001 Hypotension, n (%) 9 (11.8%) 11 (45.8%) χ²=13.17 <0.001 Altered sensorium, n (%) 28 (36.8%) 17 (70.8%) χ²=8.51 0.004 SOFA score 5.0 ± 2.2 7.5 ± 1.7 t=6.06 <0.001 TLC, ×10³/mm³ 11.61 (9.54–14.73) 13.40 (11.03–17.53) Z=1.59 0.113 NLR 9.78 (7.53–11.85) 13.52 (11.01–17.10) Z=3.25 0.001 Platelets, ×10³/µL 205.6 ± 60.5 159.9 ± 40.0 t=-4.27 <0.001 Creatinine, mg/dL 1.46 (0.95–1.77) 1.97 (1.58–2.25) Z=3.49 <0.001 Bilirubin, mg/dL 1.05 (0.80–1.64) 1.55 (1.01–1.92) Z=1.94 0.053 Albumin, g/dL 3.2 ± 0.5 2.8 ± 0.5 t=-3.02 0.005 Lactate, mmol/L 2.22 (1.69–2.82) 3.45 (2.67–3.90) Z=3.95 <0.001 Lactate/albumin ratio 0.69 (0.53–0.95) 1.26 (0.92–1.46) Z=4.40 <0.001 CRP, mg/L 92.73 (63.87–126.05) 121.53 (92.74–144.51) Z=2.18 0.030 Procalcitonin, ng/mL 1.86 (0.86–3.24) 3.18 (2.06–4.44) Z=3.02 0.003 Number of dysfunctional organs 1.5 ± 1.1 3.4 ± 1.1 t=7.15 <0.001 In-hospital mortality occurred in 24% of the simulated cohort. Non-survivors demonstrated significantly greater initial physiological instability, with higher heart and respiratory rates, lower MAP, lower oxygen saturation, and lower GCS scores. Hypotension was present in 45.8% of non-survivors compared with only 11.8% of survivors, while altered sensorium was also significantly more frequent among patients who died. The SOFA score was substantially higher in non-survivors, indicating greater early organ dysfunction. Mortality was also associated with higher NLR, creatinine, lactate, lactate/albumin ratio, CRP, and procalcitonin and with lower platelet and albumin levels. Total leukocyte count and age were not significantly associated with mortality, while bilirubin demonstrated only a borderline association. Table 6. Correlation of Early Clinical and Biochemical Parameters With Admission SOFA Score Parameter Spearman's ρ p-value Age 0.040 0.694 Mean arterial pressure -0.410 <0.001 GCS score -0.502 <0.001 NLR 0.326 0.001 Platelet count -0.327 0.001 Serum creatinine 0.449 <0.001 Total bilirubin 0.308 0.002 Serum albumin -0.261 0.009 Serum lactate 0.429 <0.001 Lactate/albumin ratio 0.448 <0.001 CRP 0.390 <0.001 Procalcitonin 0.442 <0.001 Significant correlations were observed between several early clinical and biochemical parameters and the SOFA score. Serum creatinine, lactate/albumin ratio, procalcitonin, lactate, and CRP demonstrated moderate positive correlations with increasing SOFA severity. Mean arterial pressure and GCS showed significant inverse correlations, indicating that worsening hemodynamic status and neurological dysfunction were associated with higher organ-failure scores. Platelet count and serum albumin also showed significant negative correlations with SOFA. The association between age and SOFA was weak and statistically non-significant. Among the biochemical variables, lactate/albumin ratio, creatinine, and procalcitonin showed some of the strongest relationships with early overall organ dysfunction. Table 7. Correlation of Selected Clinical and Biochemical Predictors With Number of Dysfunctional Organs Parameter Spearman's ρ p-value SOFA score 0.740 <0.001 NLR 0.363 <0.001 Platelet count -0.475 <0.001 Serum creatinine 0.468 <0.001 Total bilirubin 0.380 <0.001 Serum albumin -0.303 0.002 Serum lactate 0.577 <0.001 Lactate/albumin ratio 0.611 <0.001 CRP 0.237 0.017 Procalcitonin 0.402 <0.001 The SOFA score demonstrated a strong positive correlation with the number of dysfunctional organs (ρ=0.740, p<0.001), supporting its role as an overall measure of organ-failure severity. Among the biochemical indices, lactate/albumin ratio showed the strongest correlation with the extent of organ dysfunction (ρ=0.611), followed by serum lactate (ρ=0.577). Serum creatinine and procalcitonin also demonstrated significant moderate positive correlations. Platelet count showed a moderate inverse correlation, suggesting progressive thrombocytopenia with increasing organ involvement. Serum albumin was similarly negatively related to the number of dysfunctional organs. CRP showed a weaker but statistically significant relationship, suggesting that general inflammatory burden alone may be less closely related to the extent of organ dysfunction than markers of perfusion and physiological failure.

Sepsis is a heterogeneous syndrome in which systemic inflammation, tissue hypoperfusion, physiological instability, and progressive organ dysfunction determine clinical outcome. In the present study of 100 patients, 38% developed multiorgan dysfunction syndrome (MODS) and in-hospital mortality was 24%. Patients with MODS had significantly higher heart rate, respiratory rate, SOFA score, NLR, creatinine, bilirubin, lactate, lactate/albumin ratio (LAR), CRP, and procalcitonin, while MAP, SpO₂, GCS score, platelet count, and serum albumin were lower. Similar abnormalities were observed among non-survivors, supporting the value of integrating bedside findings with routine biochemical markers for early risk stratification. NLR was significantly higher in patients with MODS (13.34 vs. 9.68) and among non-survivors (13.52 vs. 9.78). It also correlated positively with SOFA score (ρ=0.326) and number of dysfunctional organs (ρ=0.363). Liu et al. similarly demonstrated higher serial NLR values among non-survivors and patients with greater sepsis severity, suggesting its usefulness as an inexpensive prognostic marker [11]. The present findings support NLR as a simple indicator of the inflammatory and immune imbalance occurring during severe sepsis. Serum lactate and LAR emerged as important biochemical predictors. Median lactate was significantly higher among patients with MODS (3.45 vs. 1.97 mmol/L), while LAR was 1.24 compared with 0.65 in those without MODS. Non-survivors also had higher lactate (3.45 vs. 2.22 mmol/L) and LAR (1.26 vs. 0.69). Cakir and Turan reported that LAR predicted mortality better than lactate or albumin alone, with an AUROC of 0.869 compared with 0.816 and 0.812, respectively [12]. Bou Chebl et al. also demonstrated superior mortality discrimination with LAR, particularly in patients with elevated lactate or hypoalbuminemia [13]. In the present study, LAR correlated with SOFA score (ρ=0.448) and showed the strongest biochemical correlation with number of dysfunctional organs (ρ=0.611). Combining lactate, a marker of metabolic and circulatory stress, with albumin, which reflects inflammation and physiological reserve, may therefore provide broader prognostic information. Platelet count was significantly lower among patients with MODS (160.6×10³/µL vs. 215.5×10³/µL) and non-survivors (159.9×10³/µL vs. 205.6×10³/µL). It correlated inversely with SOFA score (ρ=-0.327) and number of dysfunctional organs (ρ=-0.475). Wang et al. similarly demonstrated an association between low platelet count and increased 28-day mortality in sepsis [14]. Thrombocytopenia may reflect platelet consumption, endothelial activation, coagulation abnormalities, and severe systemic inflammation, making it a useful marker of worsening disease. Renal dysfunction was also strongly associated with adverse outcome. Serum creatinine was higher among patients with MODS (1.90 mg/dL) and non-survivors (1.97 mg/dL) and correlated with both SOFA score (ρ=0.449) and number of dysfunctional organs (ρ=0.468). Gong et al. demonstrated that increasing lactate concentrations were associated with sepsis-associated acute kidney injury and mortality [15]. These findings support the close relationship between tissue hypoperfusion, renal dysfunction, and adverse outcome in severe sepsis. Procalcitonin was significantly elevated in MODS patients and non-survivors and correlated with SOFA score (ρ=0.442) and number of dysfunctional organs (ρ=0.402). CRP showed comparatively weaker correlations. Li et al. reported that lactate/albumin and procalcitonin/albumin ratios were associated with sepsis severity and 28-day mortality [16]. These observations suggest that inflammatory biomarkers may be more useful when interpreted together with markers of perfusion and organ dysfunction rather than in isolation. The SOFA score showed one of the strongest relationships with outcome. Mean SOFA was significantly higher in MODS patients (7.7 vs. 4.3) and non-survivors (7.5 vs. 5.0) and strongly correlated with the number of dysfunctional organs (ρ=0.740). Li et al. similarly reported that persistently elevated or increasing SOFA scores were associated with mortality [17]. Thus, SOFA remains an important measure of disease severity, although combining it with biochemical markers may improve early recognition of patients likely to deteriorate. Age itself was not significantly associated with MODS or mortality, whereas hypotension, lower MAP, altered sensorium, reduced GCS, tachypnea, elevated lactate, and greater organ involvement were strongly associated with poor outcome. Zhang et al. further demonstrated that persistently elevated time-weighted NLR was independently associated with hospital mortality, highlighting the potential value of serial rather than single biomarker measurements [18]. Overall, the findings support a multidimensional approach to sepsis risk stratification using clinical severity, organ-failure scores, inflammatory indices, and biochemical markers.

The present study demonstrates that early clinical and biochemical abnormalities are associated with multiorgan dysfunction and mortality in sepsis. Higher SOFA score, lactate, LAR, NLR, creatinine, and procalcitonin, together with lower platelet count and albumin, were important markers of adverse outcome. LAR showed a particularly strong relationship with the extent of organ dysfunction, while SOFA demonstrated the strongest overall correlation with organ-failure burden. Hypotension, reduced MAP, altered sensorium, and lower GCS further identified high-risk patients. Combining readily available bedside and laboratory parameters may therefore provide a practical and cost-effective approach to early risk stratification. Larger prospective multicenter studies are needed to validate these findings and establish optimal predictive cut-off values.

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