When a patient walks into the operating theater, their body enters a state of high alert. Surgical trauma and general anaesthesia disrupt the body's delicate internal chemistry, setting off a chain reaction in the neuroendocrine system—most notably waking up the sympathetic nervous system, the renin-angiotensin-aldosterone axis (RAAS), and stress-driven vasopressin release. For decades, fluid management was treated with a one-size-fits-all formula. Unfortunately, that often meant giving too much fluid (leading to swollen tissues and sluggish bowels) or too little (starving the kidneys of blood flow). Modern perioperative medicine calls for a smarter, biochemistry-guided approach. We conducted this study at PMP Medical College and Hospital, Talcher, to capture the real-world biochemical story of how surgical patients handle fluids and electrolytes, with the ultimate goal of refining our clinical protocols

• Study Design: Prospective observational study. • Study Setting: Department of Surgery and Anesthesiology, PMP Medical College and Hospital, Talcher. • Study Duration: April 2025 to June 2026 (18 months). • Sample Size: 122 adult patients (ASA physical status I to III) undergoing major abdominal, orthopedic, or oncological procedures. Inclusion Criteria: • Adults aged 18 to 70 years. • Scheduled for major elective or emergency surgeries expected to last longer than two hours. Exclusion Criteria • Pre-existing advanced kidney disease (eGFR below 30 mL/min/1.73m²). • Known primary endocrine disorders that naturally mess with fluid balance. • Patients or legal guardians who declined consent. Data Collection and Biochemical Analysis We collected blood samples at four distinct checkpoints: baseline right before surgery (T_0), midway through the procedure (T_1), immediately after the surgery wrapped up (T_2), and 48 hours down the line (T_3). The lab work looked closely at serum electrolytes (Na^+,K^+,Cl^-), blood urea nitrogen (BUN), serum creatinine, serum lactate, and arterial blood gas metrics like pH and bicarbonate levels

Out of the 122 patients enrolled, 108 successfully made it through the entire monitoring timeline and were included in the final analysis (accounting for 14 dropouts due to cancelled procedures or protocol deviations). Table 1: Baseline Demographics and Clinical Characteristics (n=108) Parameter Value Age (Mean ± SD, years) 48.6±12.4 Gender (Male / Female) 68 / 40 ASA Physical Status (I / II / III) 32 / 54 / 22 Mean Duration of Surgery (Minutes) 185.4±42.1 Total Intraoperative Fluid Administered (mL) 2150±480 Table 1 outlines the baseline profile of the 108 analyzed patients. The average age hovered around middle age (48.6 years), with a male predominance reflecting regional hospital admission trends. Most patients fell into the ASA II category, representing mild-to-moderate systemic disease managed well before surgery. The average surgical duration of roughly three hours and an average intraoperative fluid volume of 2,150 mL reflect standard major surgical workloads at our tertiary care center. Table 2: Perioperative Trends in Serum Electrolytes Electrolyte Parameter Baseline (T0) Intraoperative (T1) Immediate Post-op (T2) 48 Hours Post-op (T3) Normal Range Sodium (Na^+) (mEq/L) 138.4±3.2 136.9±4.1 133.5±4.8 135.2±3.9 135–145 Potassium (K^+) (mEq/L) 4.2±0.4 3.9±0.5 3.6±0.6 4.0±0.4 3.5–5.0 Chloride (Cl^-) (mEq/L) 103.1±3.5 105.4±4.2 107.8±5.1 104.2±3.8 96–106 Table 2 tracks the sliding scale of core electrolytes through the surgical journey. Serum sodium experienced a progressive drop, hitting its lowest point (133.5 mEq/L) right after surgery, heavily influenced by stress-induced water retention. Potassium values dipped concurrently due to internal shifts and renal losses, before climbing back toward baseline by the 48-hour mark. Chloride levels crept upward, particularly in patients receiving heavy normal saline loads, reflecting a mild hyperchloremic tendency. Table 3: Incidence of Perioperative Electrolyte Disturbances Biochemical Abnormality Number of Patients (n=108) Percentage (%) Hyponatremia (Na^+<133 mEq/L) 31 28.7% Hypokalemia (K^+<3.5 mEq/L) 24 22.2% Hyperchloremic Metabolic Acidosis 19 17.6% Hyperkalemia (K^+>5.1 mEq/L) 7 6.5% Table 3 breaks down how frequently specific chemical imbalances showed up in our cohort. Hyponatremia took the lead, affecting nearly 29% of patients, largely driven by non-osmotic vasopressin release during tissue trauma. Hypokalemia followed closely at 22.2%. Hyperchloremic metabolic acidosis also made a notable appearance in 17.6% of cases, underlining the biochemical toll of chloride-heavy IV fluids. Table 4: Renal Function and Acid-Base Status Variations Parameter Baseline (T0) Post-operative (T2/T3) p-value Serum Creatinine (mg/dL) 0.91±0.18 1.08±0.32 <0.05 Blood Urea Nitrogen (mg/dL) 14.2±3.6 18.6±5.4 <0.01 Blood pH 7.41±0.03 7.33±0.06 <0.05 Serum Lactate (mmol/L) 1.1±0.3 1.9±0.7 <0.01 Table 4 highlights the shifts in kidney function markers and blood acidity. Both serum creatinine and blood urea nitrogen showed statistically significant bumps (p<0.05 and p<0.01) following surgery, pointing toward mild, transient renal strain. A corresponding drop in blood pH and a rise in serum lactate signaled mild metabolic stress and temporary tissue hypoperfusion during major surgical stress. Table 5: Correlation Between Fluid Volume Strategy and Clinical Outcomes Fluid Strategy Category Incidence of Post-op AKI (%) Mean Hospital Stay (Days) Bowel Recovery Time (Hours) Restrictive / Balanced (n=58) 5.1% 5.2±1.4 48.2±10.5 Liberal / Saline-heavy (n=50) 18.0% 8.1±2.3 76.6±15.2 Table 5 compares patient recovery outcomes based on the fluid philosophy applied. Patients managed with a restrictive, balanced fluid protocol experienced a much lower rate of acute kidney injury (5.1% vs 18.0%), enjoyed shorter hospital stays, and saw their bowel function return much faster than those who received liberal, saline-heavy fluid loads.

The biochemical footprint we observed in our patients at PMP Medical College mirrors classic evolutionary survival responses. When tissue is cut, the body triggers a release of cortisol and vasopressin to hold onto water and salt. This natural survival mechanism explains why almost 29% of our cohort slipped into mild dilutional hyponatremia post-surgery. Our data also flags an important clinical warning regarding standard normal saline. Pumping high volumes of chloride-rich fluids into patients consistently tipped them toward hyperchloremic metabolic acidosis and forced unnecessary strain on the kidneys. By shifting toward a more balanced, individualized fluid strategy, we can protect kidney tissue, keep electrolytes closer to normal ranges, and help patients clear out of the hospital safely and quickly.

Perioperative fluid and electrolyte management should never be treated as an autopilot task. Recognizing the body's internal, stress-driven hormonal shifts allows clinicians to dodge common pitfalls like dilutional hyponatremia and acid-base imbalances. Tailoring fluid choices to individual lab biochemistry protects organ systems and elevates surgical recovery standards in busy tertiary care environments

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