Metabolic acidosis is a common acid–base disorder characterized by a primary reduction in serum bicarbonate concentration, resulting in a decrease in arterial blood pH or a compensatory fall in partial pressure of carbon dioxide. It develops when there is excessive production of acids, inadequate renal excretion of hydrogen ions, excessive loss of bicarbonate, or a combination of these mechanisms (1,2). Metabolic acidosis is frequently encountered in emergency departments, medical wards, and intensive care units, where it often reflects the presence of serious underlying disease. Early recognition and prompt identification of its etiology are essential because persistent metabolic acidosis is associated with significant morbidity, prolonged hospitalization, and increased mortality (3,4). The etiological spectrum of metabolic acidosis is broad and varies according to the patient population and healthcare setting. High anion gap metabolic acidosis commonly results from conditions such as diabetic ketoacidosis, lactic acidosis, chronic kidney disease, sepsis, poisoning, and drug toxicity, whereas normal anion gap metabolic acidosis is typically caused by gastrointestinal bicarbonate loss, renal tubular acidosis, or excessive chloride administration (5). In many hospitalized patients, multiple etiological factors may coexist, making diagnosis and management more challenging. Therefore, systematic evaluation of the underlying cause is fundamental for initiating appropriate therapy and improving clinical outcomes (6). The clinical manifestations of metabolic acidosis are highly variable and depend on the severity, rate of onset, and underlying etiology. Patients may present with nonspecific symptoms such as weakness, nausea, vomiting, altered sensorium, dyspnea, and fatigue, while severe acidosis may lead to hypotension, cardiac arrhythmias, respiratory distress, shock, and multiorgan dysfunction (7). Clinical assessment alone is often insufficient to determine the exact nature of the acid–base disturbance, highlighting the importance of integrating laboratory investigations with clinical findings. A comprehensive clinico-biochemical evaluation enables clinicians to identify the primary disorder, recognize mixed acid–base abnormalities, and guide targeted management (8). Biochemical assessment plays a central role in the diagnosis and characterization of metabolic acidosis. Arterial blood gas analysis provides essential information regarding pH, bicarbonate concentration, partial pressure of carbon dioxide, and oxygenation status. Measurement of serum electrolytes allows calculation of the anion gap, which is a valuable diagnostic tool for differentiating various types of metabolic acidosis (9). Additional investigations, including serum lactate, renal function tests, blood glucose, and other disease-specific laboratory parameters, help establish the underlying cause and assess disease severity. Together, these biochemical parameters facilitate accurate diagnosis, prognostication, and monitoring of therapeutic response (10). The outcome of patients with metabolic acidosis largely depends on timely diagnosis, appropriate correction of the underlying disorder, and effective supportive management. While some patients recover completely following treatment of the precipitating cause, others experience complications requiring prolonged hospitalization or may succumb to the underlying illness (11,12). Evaluating treatment outcomes in relation to etiological and clinico-biochemical characteristics provides valuable information regarding prognostic factors and helps optimize patient care. Despite the frequent occurrence of metabolic acidosis in tertiary care hospitals, comprehensive studies evaluating its etiological profile, clinical presentation, biochemical characteristics, and outcomes remain limited (13). Therefore, the present study was undertaken to assess the etiological, clinico-biochemical profile, and treatment outcome of patients with metabolic acidosis admitted to a tertiary care centre, thereby providing evidence that may assist clinicians in early diagnosis, appropriate management, and improvement of patient outcomes. AIMS AND OBJECTIVES • To assess the etiological profile in patients with metabolic acidosis • To assess the clinical profile in patients with metabolic acidosis. • To estimate the biochemical parameters in patients with metabolic acidosis • To assess the treatment outcome in patients with metabolic acidosis.

The present study was a prospective observational study conducted in the Department of Internal Medicine at hospitals attached to Bangalore Medical College and Research Institute (BMCRI), Bangalore, India, over a period from August 2022 to January 2024. A total of 150 adult patients with clinically suspected metabolic acidosis were enrolled after obtaining approval from the Institutional Ethics Committee and written informed consent. Patients aged more than 18 years with low serum bicarbonate associated with low or normal arterial pH, as well as those with high anion gap metabolic acidosis and normal pH, were included in the study. Patients younger than 18 years and those unwilling to provide informed consent were excluded. Following enrollment, detailed demographic and clinical information was recorded using a predesigned proforma. All patients underwent comprehensive clinical evaluation along with laboratory investigations, including arterial blood gas (ABG) analysis and serum electrolyte estimation. The initial ABG obtained at the time of hospital presentation was considered for analysis after performing a Modified Allen’s test and following standard aseptic precautions. Additional investigations relevant to identifying the underlying etiology of metabolic acidosis were performed as clinically indicated. The etiological factors, clinical manifestations, biochemical parameters, and acid–base characteristics were systematically documented for each patient. Patients were followed throughout their hospital stay to assess treatment outcomes, which were categorized as recovery or in-hospital mortality. Recovery was defined by clinical improvement, resolution of symptoms, stabilization of vital signs, normal systemic examination findings, and normalization of arterial blood gas parameters. Data were entered into Microsoft Excel and analyzed using SPSS version 26.0. Continuous variables were expressed as mean ± standard deviation, while categorical variables were presented as frequencies and percentages. Associations between categorical variables were evaluated using the Chi-square test or Fisher’s exact test as appropriate, with a p-value of <0.05 considered statistically significant. Results were presented using appropriate tables, figures, and graphs.

Table 1. Demographic characteristics of the study participants Variable Category n % Age group (years) 18–20 9 6.0 21–30 20 13.3 31–40 35 23.3 41–50 29 19.3 51–60 30 20.0 61–70 22 14.7 71–80 5 3.3 Sex Male 100 66.7 Female 50 33.3 Total 150 100.0 Graph 1. Demographic characteristics of the study participants In the present study, a total of 150 participants were included. The highest proportion of participants belonged to the 31–40 years age group, comprising 35 (23.3%) participants, followed by the 51–60 years age group with 30 (20.0%) participants, the 41–50 years age group with 29 (19.3%) participants, the 61–70 years age group with 22 (14.7%) participants, the 21–30 years age group with 20 (13.3%) participants, the 18–20 years age group with 9 (6.0%) participants, and the 71–80 years age group with 5 (3.3%) participants. Among the study participants, 100 (66.7%) were males and 50 (33.3%) were females. Thus, the study population comprised a total of 150 participants, with males constituting the majority. Table 2. Age Characteristics of the Study Participants Age characteristic Value Mean age ± SD 45.01 ± 15.39 years Age range 18–77 years Mean age of males 43.84 ± 15.43 years Mean age of females 47.34 ± 15.19 years In the present study, the mean age of the study participants was 45.01 ± 15.39 years, with an age range of 18–77 years. The mean age of male participants was 43.84 ± 15.43 years, while the mean age of female participants was 47.34 ± 15.19 years, indicating that the mean age of female participants was higher than that of male participants. Table 3. Distribution according to the type of acid–base disorder Acid–base disorder n % Primary metabolic acidosis 100 66.7 Mixed acid–base disorder 50 33.3 Total 150 100.0 n the present study, out of a total of 150 patients, 100 (66.7%) had primary metabolic acidosis, while 50 (33.3%) had mixed acid–base disorder. Thus, primary metabolic acidosis constituted the majority of cases, accounting for 66.7%, whereas mixed acid–base disorders accounted for 33.3% of the study population. Table 4. Distribution of Primary Metabolic Acidosis Among the Study Participants Primary disorder Frequency (n) Percentage among primary cases (%) Percentage of total (%) High anion gap metabolic acidosis 74 74.0 49.3 Normal anion gap metabolic acidosis 26 26.0 17.3 Total 100 100.0 66.7 In the present study, among the 100 patients with primary metabolic acidosis, 74 (74.0%) had high anion gap metabolic acidosis, accounting for 49.3% of the total study population, while 26 (26.0%) had normal anion gap metabolic acidosis, accounting for 17.3% of the total study population. Thus, all 100 (100.0%) patients with primary metabolic acidosis constituted 66.7% of the total 150 study participants. Table 5. Distribution of Mixed Acid–Base Disorders Among the Study Participants Mixed acid–base disorder Frequency (n) Percentage among mixed cases (%) Percentage of total (%) Metabolic acidosis with respiratory acidosis 28 56.0 18.7 Metabolic acidosis with respiratory alkalosis 10 20.0 6.7 HAGMA with NAGMA 3 6.0 2.0 Metabolic acidosis with metabolic alkalosis 7 14.0 4.7 Triple acid–base disorder 2 4.0 1.3 Total 50 100.0 33.3 In the present study, among the 50 patients with mixed acid–base disorders, 28 (56.0%) had metabolic acidosis with respiratory acidosis, accounting for 18.7% of the total study population. Metabolic acidosis with respiratory alkalosis was observed in 10 (20.0%) patients, accounting for 6.7% of the total study population. Metabolic acidosis with metabolic alkalosis was present in 7 (14.0%) patients, representing 4.7% of the total study population. High anion gap metabolic acidosis (HAGMA) with normal anion gap metabolic acidosis (NAGMA) was observed in 3 (6.0%) patients, accounting for 2.0% of the total study population, while triple acid–base disorder was present in 2 (4.0%) patients, accounting for 1.3% of the total study population. Thus, all 50 (100.0%) patients with mixed acid–base disorders constituted 33.3% of the total 150 study participants. Table 6. Etiological profile of metabolic acidosis Etiology n % Chronic kidney disease 47 31.3 Lactic acidosis 42 28.0 Ketoacidosis 35 23.3 Acute gastroenteritis 20 13.3 Toxin-induced metabolic acidosis 5 3.3 Renal tubular acidosis 1 0.7 Total 150 100.0 In the present study, chronic kidney disease was the most common etiology of metabolic acidosis, observed in 47 (31.3%) patients. This was followed by lactic acidosis in 42 (28.0%) patients and ketoacidosis in 35 (23.3%) patients. Acute gastroenteritis was identified as the cause in 20 (13.3%) patients, while toxin-induced metabolic acidosis was observed in 5 (3.3%) patients. Renal tubular acidosis was the least common etiology, occurring in 1 (0.7%) patient. Thus, the etiological profile comprised a total of 150 (100.0%) patients with metabolic acidosis. Table 7. Etiology of Normal Anion Gap Metabolic Acidosis Among the Study Participants Etiology n % Acute gastroenteritis 20 76.9 Chronic kidney disease 5 19.2 Renal tubular acidosis 1 3.8 Total 26 100.0 In the present study, among the 26 patients with normal anion gap metabolic acidosis (NAGMA), acute gastroenteritis was the most common etiology, observed in 20 (76.9%) patients. Chronic kidney disease was the etiology in 5 (19.2%) patients, while renal tubular acidosis was observed in 1 (3.8%) patient. Thus, a total of 26 (100.0%) patients with normal anion gap metabolic acidosis were included in this analysis. Table 6. Etiology of Lactic Acidosis Among the Study Participants Etiology n % Sepsis 30 71.4 Cardiogenic shock 8 19.0 Seizure 3 7.1 Malignancy 1 2.4 Total 42 100.0 In the present study, among the 42 patients with lactic acidosis, sepsis was the most common etiology, observed in 30 (71.4%) patients. Cardiogenic shock was the etiology in 8 (19.0%) patients, while seizure was observed in 3 (7.1%) patients and malignancy in 1 (2.4%) patient. Thus, a total of 42 (100.0%) patients with lactic acidosis were included in this analysis. Table 9. Etiology of Ketoacidosis Among the Study Participants Etiology n % Diabetic ketoacidosis 32 91.4 Alcoholic ketoacidosis 3 8.6 Total 35 100.0 In the present study, among the 35 patients with ketoacidosis, diabetic ketoacidosis was the most common etiology, observed in 32 (91.4%) patients, while alcoholic ketoacidosis was observed in 3 (8.6%) patients. Thus, a total of 35 (100.0%) patients with ketoacidosis were included in this analysis. Table 10. Clinical presentation of patients with metabolic acidosis Clinical feature n % Fever 93 62.0 Breathlessness 93 62.0 Vomiting 84 56.0 Abdominal pain 73 48.7 Decreased urine output 72 48.0 Easy fatigability 71 47.3 Decreased appetite 56 37.3 Cough 48 32.0 Abdominal distension 45 30.0 Pedal oedema 45 30.0 Diarrhoea 40 26.7 Altered sensorium 33 22.0 Burning micturition 15 10.0 Polyuria 6 4.0 Seizure 5 3.3 Alleged poison consumption 5 3.3 Chest pain 4 2.7 Binge alcohol consumption 3 2.0 Yellowish discoloration of eyes 3 2.0 Bilateral lower-limb weakness 1 0.7 In the present study, fever and breathlessness were the most common clinical features, each observed in 93 (62.0%) patients. Vomiting was present in 84 (56.0%) patients, followed by abdominal pain in 73 (48.7%), decreased urine output in 72 (48.0%), and easy fatigability in 71 (47.3%) patients. Decreased appetite was observed in 56 (37.3%) patients, cough in 48 (32.0%) patients, and both abdominal distension and pedal oedema in 45 (30.0%) patients each. Diarrhoea was present in 40 (26.7%) patients, while altered sensorium was observed in 33 (22.0%) patients. Burning micturition was reported by 15 (10.0%) patients, polyuria by 6 (4.0%) patients, seizure and alleged poison consumption by 5 (3.3%) patients each, chest pain by 4 (2.7%) patients, binge alcohol consumption and yellowish discoloration of eyes by 3 (2.0%) patients each, and bilateral lower-limb weakness by 1 (0.7%) patient. Table 11. Comorbidities and personal habits Comorbidity n % Diabetes mellitus 83 55.3 Hypertension 51 34.0 Cardiac illness 18 12.0 Hypothyroidism 4 2.7 Chronic liver disease 3 2.0 Hyperthyroidism 1 0.7 Obstructive sleep apnoea 1 0.7 In the present study, diabetes mellitus was the most common comorbidity, observed in 83 (55.3%) patients. This was followed by hypertension in 51 (34.0%) patients and cardiac illness in 18 (12.0%) patients. Hypothyroidism was present in 4 (2.7%) patients, while chronic liver disease was observed in 3 (2.0%) patients. Hyperthyroidism and obstructive sleep apnoea were the least common comorbidities, each observed in 1 (0.7%) patient. Table 12. Distribution of Type of Diabetes Mellitus Among Patients with Diabetes. Diabetes type n % Type 1 diabetes mellitus 14 16.9 Type 2 diabetes mellitus 67 80.7 Other/type 3 diabetes 2 2.4 Total 83 100.0 In the present study, among the 83 patients with diabetes mellitus, 67 (80.7%) had type 2 diabetes mellitus, 14 (16.9%) had type 1 diabetes mellitus, and 2 (2.4%) had other/type 3 diabetes. Thus, a total of 83 (100.0%) diabetic patients were included in this analysis, with type 2 diabetes mellitus being the most common type. Table 13. Distribution of Personal Habits Among the Patients with Metabolic Acidosis Personal habit n % Alcohol consumption only 28 18.7 Alcohol consumption with smoking 26 17.3 Smoking only 4 2.7 No ill habits 92 61.3 Total 150 100.0 In the present study, 92 (61.3%) patients had no ill habits, while 28 (18.7%) patients reported alcohol consumption only. Alcohol consumption with smoking was observed in 26 (17.3%) patients, and smoking only was reported by 4 (2.7%) patients. Thus, the study included a total of 150 (100.0%) patients with respect to personal habits. Table 14. Clinical examination findings at admission Parameter Category n % Pulse rate Bradycardia 3 2.0 Normal 45 30.0 Tachycardia 102 68.0 Respiratory rate Normal 40 26.7 Tachypnoea 110 73.3 Blood pressure Normal 66 44.0 Hypotension 40 26.7 Hypertension 44 29.3 Oxygen saturation Normal, 95–100% 79 52.7 Reduced, <95% 71 47.3 Glasgow Coma Scale 3–8 10 6.7 9–12 23 15.3 13–15 117 78.0 In the present study, regarding pulse rate, 102 (68.0%) patients had tachycardia, 45 (30.0%) had a normal pulse rate, and 3 (2.0%) had bradycardia. Regarding respiratory rate, 110 (73.3%) patients had tachypnoea, while 40 (26.7%) had a normal respiratory rate. With respect to blood pressure, 66 (44.0%) patients had normal blood pressure, 44 (29.3%) had hypertension, and 40 (26.7%) had hypotension. Regarding oxygen saturation, 79 (52.7%) patients had normal oxygen saturation (95–100%), whereas 71 (47.3%) had reduced oxygen saturation (<95%). Based on the Glasgow Coma Scale (GCS), 117 (78.0%) patients had a GCS score of 13–15, 23 (15.3%) had a GCS score of 9–12, and 10 (6.7%) had a GCS score of 3–8. Table 15. Biochemical and arterial blood gas parameters Parameter Mean ± SD Median Minimum Maximum pH 7.18 ± 0.16 7.24 6.60 7.43 PaCO₂ (mmHg) 26.29 ± 12.09 24.00 2.00 70.00 HCO₃⁻ (mEq/L) 10.50 ± 4.31 10.55 2.00 19.50 Serum lactate (mmol/L) 3.89 ± 3.19 3.35 0.40 20.20 Expected PaCO₂ (mmHg) 23.69 ± 6.55 23.75 11.00 38.00 Sodium (mEq/L) 136.31 ± 6.99 135.00 118.00 161.00 Potassium (mEq/L) 4.54 ± 1.41 4.22 2.20 13.80 Chloride (mEq/L) 101.42 ± 7.46 100.15 83.00 120.00 Anion gap (mEq/L) 24.54 ± 9.25 25.45 4.00 49.00 Albumin (g/dL) 3.22 ± 1.67 3.05 1.70 4.50 Corrected anion gap (mEq/L) 26.68 ± 11.30 29.30 2.00 52.30 In the present study, the mean pH was 7.18 ± 0.16 (median 7.24; range 6.60–7.43), mean PaCO₂ was 26.29 ± 12.09 mmHg (median 24.00; range 2.00–70.00), and mean HCO₃⁻ was 10.50 ± 4.31 mEq/L (median 10.55; range 2.00–19.50). The mean serum lactate was 3.89 ± 3.19 mmol/L, expected PaCO₂ was 23.69 ± 6.55 mmHg, serum sodium was 136.31 ± 6.99 mEq/L, potassium was 4.54 ± 1.41 mEq/L, chloride was 101.42 ± 7.46 mEq/L, anion gap was 24.54 ± 9.25 mEq/L, albumin was 3.22 ± 1.67 g/dL, and corrected anion gap was 26.68 ± 11.30 mEq/L, with their respective median and minimum–maximum values as shown in the table. Table 16. Biochemical profile according to the type of acid–base disorder Acid–base disorder pH PaCO₂ (mmHg) HCO₃⁻ (mEq/L) Lactate (mmol/L) Anion gap (mEq/L) Corrected anion gap (mEq/L) HAGMA (n=74) 7.20 ± 0.13 21.56 ± 6.65 9.42 ± 3.98 3.90 ± 3.13 28.60 ± 6.35 32.10 ± 6.01 NAGMA (n=26) 7.26 ± 0.10 25.42 ± 6.01 11.93 ± 2.90 2.78 ± 1.26 8.84 ± 3.14 9.95 ± 3.67 Metabolic acidosis with respiratory acidosis (n=28) 7.05 ± 0.21 40.27 ± 15.24 10.25 ± 4.93 5.00 ± 4.14 27.56 ± 6.40 31.36 ± 6.62 Metabolic acidosis with respiratory alkalosis (n=10) 7.14 ± 0.17 13.34 ± 5.88 9.32 ± 3.69 2.35 ± 1.66 27.85 ± 5.65 31.60 ± 4.64 HAGMA with NAGMA (n=3) 7.19 ± 0.16 26.88 ± 4.97 10.90 ± 3.36 2.95 ± 0.85 17.33 ± 5.80 20.12 ± 0.84 Metabolic acidosis with metabolic alkalosis (n=7) 7.36 ± 0.05 33.70 ± 3.94 17.40 ± 1.74 3.68 ± 2.21 25.17 ± 3.11 28.54 ± 3.81 Triple acid–base disorder (n=2) 7.09 ± 0.05 54.50 ± 10.61 17.10 ± 2.12 6.49 ± 1.10 24.40 ± 6.51 29.53 ± 8.45 Inthe present study, patients with HAGMA (n=74) had a mean pH of 7.20 ± 0.13, PaCO₂ of 21.56 ± 6.65 mmHg, HCO₃⁻ of 9.42 ± 3.98 mEq/L, lactate of 3.90 ± 3.13 mmol/L, anion gap of 28.60 ± 6.35 mEq/L, and corrected anion gap of 32.10 ± 6.01 mEq/L. Patients with NAGMA (n=26) had corresponding mean values of 7.26 ± 0.10, 25.42 ± 6.01 mmHg, 11.93 ± 2.90 mEq/L, 2.78 ± 1.26 mmol/L, 8.84 ± 3.14 mEq/L, and 9.95 ± 3.67 mEq/L, respectively. Patients with metabolic acidosis with respiratory acidosis (n=28) had mean values of 7.05 ± 0.21, 40.27 ± 15.24 mmHg, 10.25 ± 4.93 mEq/L, 5.00 ± 4.14 mmol/L, 27.56 ± 6.40 mEq/L, and 31.36 ± 6.62 mEq/L, while those with metabolic acidosis with respiratory alkalosis (n=10) had mean values of 7.14 ± 0.17, 13.34 ± 5.88 mmHg, 9.32 ± 3.69 mEq/L, 2.35 ± 1.66 mmol/L, 27.85 ± 5.65 mEq/L, and 31.60 ± 4.64 mEq/L, respectively. Patients with HAGMA with NAGMA (n=3) had mean values of 7.19 ± 0.16, 26.88 ± 4.97 mmHg, 10.90 ± 3.36 mEq/L, 2.95 ± 0.85 mmol/L, 17.33 ± 5.80 mEq/L, and 20.12 ± 0.84 mEq/L. Patients with metabolic acidosis with metabolic alkalosis (n=7) had mean values of 7.36 ± 0.05, 33.70 ± 3.94 mmHg, 17.40 ± 1.74 mEq/L, 3.68 ± 2.21 mmol/L, 25.17 ± 3.11 mEq/L, and 28.54 ± 3.81 mEq/L, while those with triple acid–base disorder (n=2) had mean values of 7.09 ± 0.05, 54.50 ± 10.61 mmHg, 17.10 ± 2.12 mEq/L, 6.49 ± 1.10 mmol/L, 24.40 ± 6.51 mEq/L, and 29.53 ± 8.45 mEq/L, respectively. Table 17. Overall, in-hospital outcome Outcome n % Recovery and discharge 105 70.0 In-hospital mortality 45 30.0 Total 150 100.0 In the present study, 105 (70.0%) patients recovered and were discharged, while 45 (30.0%) patients experienced in-hospital mortality. Thus, among the total 150 (100.0%) patients with metabolic acidosis, the majority recovered and were discharged. Table 18. Outcome according to the type of acid–base disorder Acid–base disorder Total cases Death, n Recovery, n Mortality rate (%) Primary metabolic acidosis 100 25 75 25.0 Mixed acid–base disorder 50 20 30 40.0 Total 150 45 105 30.0 In the present study, among the 100 patients with primary metabolic acidosis, 25 patients died and 75 recovered, resulting in a mortality rate of 25.0%. Among the 50 patients with mixed acid–base disorders, 20 patients died and 30 recovered, with a mortality rate of 40.0%. Overall, among the 150 patients, 45 patients died and 105 recovered, resulting in an overall in-hospital mortality rate of 30.0%. Table 19. Outcome Among Individual Acid–Base Disorders in Patients with Metabolic Acidosis. Acid–base disorder Total cases Death, n Recovery n Mortality rate (%) HAGMA 74 24 50 32.4 NAGMA 26 1 25 3.8 Metabolic acidosis with respiratory acidosis 28 14 14 50.0 Metabolic acidosis with respiratory alkalosis 10 1 9 10.0 HAGMA with NAGMA 3 1 2 33.3 Metabolic acidosis with metabolic alkalosis 7 2 5 28.6 Triple acid–base disorder 2 2 0 100.0 Total 150 45 105 30.0 In the present study, among the 74 patients with high anion gap metabolic acidosis (HAGMA), 24 patients died and 50 recovered, resulting in a mortality rate of 32.4%. Among the 26 patients with normal anion gap metabolic acidosis (NAGMA), 1 patient died and 25 recovered, with a mortality rate of 3.8%. Among the 28 patients with metabolic acidosis and respiratory acidosis, 14 patients died and 14 recovered, resulting in a mortality rate of 50.0%. Among the 10 patients with metabolic acidosis and respiratory alkalosis, 1 patient died and 9 recovered, with a mortality rate of 10.0%. Among the 3 patients with HAGMA and NAGMA, 1 patient died and 2 recovered, resulting in a mortality rate of 33.3%. Among the 7 patients with metabolic acidosis and metabolic alkalosis, 2 patients died and 5 recovered, with a mortality rate of 28.6%. Among the 2 patients with triple acid–base disorder, both patients died, resulting in a mortality rate of 100.0%, and no patient recovered. Overall, among the 150 patients, 45 patients died and 105 recovered, resulting in an overall mortality rate of 30.0%. Table 20. Association of serum lactate with in-hospital outcome Serum lactate level Death, n Recovery, n Total Mortality within category (%) <2 mmol/L 3 36 39 7.7 2 to <4 mmol/L 13 55 68 19.1 ≥4 mmol/L 29 14 43 67.4 Total 45 105 150 30.0 In the present study, among the 39 patients with serum lactate level <2 mmol/L, 3 patients died and 36 recovered, resulting in a mortality rate of 7.7%. Among the 68 patients with serum lactate level between 2 and <4 mmol/L, 13 patients died and 55 recovered, with a mortality rate of 19.1%. Among the 43 patients with serum lactate level ≥4 mmol/L, 29 patients died and 14 recovered, resulting in a mortality rate of 67.4%. Overall, among the 150 patients, 45 patients died and 105 recovered, resulting in an overall in-hospital mortality rate of 30.0%. Table 21. Association of arterial pH with in-hospital outcome Arterial pH Death, n Recovery, n Total Mortality within category (%) ≤7.20 24 41 65 36.9 >7.20 21 64 85 24.7 Total 45 105 150 30.0 In the present study, among the 65 patients with arterial pH ≤7.20, 24 patients died and 41 recovered, resulting in a mortality rate of 36.9%. Among the 85 patients with arterial pH >7.20, 21 patients died and 64 recovered, resulting in a mortality rate of 24.7%. Overall, among the 150 patients, 45 patients

The present prospective observational study evaluated the etiological, clinico-biochemical profile and outcomes of patients with metabolic acidosis admitted to a tertiary care centre. The mean age of the study population was 45.01 ± 15.39 years, with a male predominance (66.7%). Primary metabolic acidosis was observed in 66.7% of patients, while 33.3% had mixed acid–base disorders. These findings are consistent with Kraut and Madias (2010), who described metabolic acidosis as a common acid–base disorder with diverse etiologies and varying clinical severity (2). High anion gap metabolic acidosis was the predominant primary disorder. Chronic kidney disease was the leading etiology (31.3%), followed by lactic acidosis (28.0%) and ketoacidosis (23.3%). Acute gastroenteritis was the most common cause of normal anion gap metabolic acidosis. Similarly, Kharsa et al. (2025) highlighted the importance of classifying metabolic acidosis based on the anion gap for identifying the underlying cause, while Tinawi (2021) reported that chronic kidney disease, lactic acidosis and diabetic ketoacidosis are among the most frequent causes encountered in clinical practice (1,5). Fever and breathlessness were the most common presenting symptoms, followed by vomiting, abdominal pain and decreased urine output. Diabetes mellitus was the predominant comorbidity, followed by hypertension. Tachypnoea and tachycardia were the most frequent clinical findings, reflecting the physiological response to metabolic acidosis. Balzanelli et al. (2023) emphasized that arterial blood gas analysis, interpreted together with clinical findings, is essential for the accurate diagnosis and assessment of acid–base disorders (9). Biochemical evaluation revealed a mean arterial pH of 7.18 ± 0.16, mean bicarbonate level of 10.50 ± 4.31 mEq/L and mean serum lactate level of 3.89 ± 3.19 mmol/L, indicating significant metabolic derangement. Patients with mixed acid–base disorders demonstrated more severe biochemical abnormalities than those with isolated metabolic acidosis. Deulkar et al. (2024) reported that elevated serum lactate is a valuable indicator of tissue hypoperfusion and disease severity and is associated with poor clinical outcomes in critically ill patients (10). The overall in-hospital mortality was 30%. Mortality was higher among patients with mixed acid–base disorders, particularly those with metabolic acidosis associated with respiratory acidosis and triple acid–base disorders. Patients with serum lactate ≥4 mmol/L and arterial pH ≤7.20 had markedly higher mortality than those with lower lactate levels and higher pH values. Yagi and Fujii (2021) reported that severe metabolic acidosis is associated with increased mortality, particularly among critically ill patients, while Jung et al. (2019) recommended systematic assessment of pH, bicarbonate, lactate and anion gap for early diagnosis and management (3,4). Rebolledo-Maldonado et al. (2026) similarly demonstrated that severe metabolic acidosis is associated with acute kidney injury, multiorgan dysfunction and adverse outcomes (7). Overall, the present study demonstrates that chronic kidney disease, lactic acidosis and ketoacidosis are the predominant causes of metabolic acidosis. Severe acidemia, elevated serum lactate and mixed acid–base disorders were associated with poor prognosis and increased in-hospital mortality. Early recognition of the underlying etiology, prompt arterial blood gas analysis and timely management are essential to improve clinical outcomes in patients with metabolic acidosis.

The present study demonstrated that metabolic acidosis is a common and clinically significant acid–base disorder associated with diverse etiologies and considerable in-hospital mortality. Chronic kidney disease emerged as the leading cause, followed by lactic acidosis and ketoacidosis, with high anion gap metabolic acidosis being the predominant acid–base abnormality. Fever, breathlessness, vomiting, and abdominal pain were the most frequent clinical manifestations, while arterial blood gas analysis and biochemical investigations played a pivotal role in diagnosis and characterization of acid–base disturbances. Mixed acid–base disorders, particularly metabolic acidosis with respiratory acidosis and triple acid–base disorders, were associated with poorer outcomes. Elevated serum lactate levels, severe acidemia, altered biochemical parameters, and lower Glasgow Coma Scale scores were important predictors of mortality. Early recognition of the underlying etiology, prompt biochemical evaluation, and timely institution of appropriate management are essential to improve patient outcomes. Comprehensive assessment of metabolic acidosis can facilitate risk stratification and optimize clinical decision-making in hospitalized patients.

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