Fluid, Electrolyte and Acid–Base Balance in Surgery
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Direct answer
Total body water is about 60 per cent of body weight in an adult male (roughly 50 per cent in females), distributed two-thirds intracellular and one-third extracellular; plasma is only a quarter of the extracellular compartment. Daily maintenance for a stable surgical patient is commonly estimated at 25–35 mL/kg/day of water with about 1–2 mmol/kg/day of sodium and 0.5–1 mmol/kg/day of potassium. Most postoperative derangements the exam asks about follow a predictable pattern: sodium moves with water, potassium moves with acid–base status, and uncorrected losses produce a high-anion-gap metabolic acidosis. Balanced crystalloids such as Hartmann's are generally preferred over large volumes of normal saline, which causes a hyperchloraemic acidosis.
What you must remember
- The 60–40–20 rule: 60 per cent water, 40 per cent intracellular and 20 per cent extracellular fluid by body weight; extracellular fluid splits three-quarters interstitial, one-quarter plasma.
- Normal serum sodium is 135–145 mmol/L and potassium 3.5–5.0 mmol/L; serum sodium reflects water balance, not total body sodium.
- Correct hyponatraemia slowly, no faster than about 8–10 mmol/L in 24 hours, to avoid osmotic demyelination; correct hypernatraemia by no more than about 0.5 mmol/L per hour.
- Hypokalaemia produces weakness, ileus and electrocardiographic changes of ST depression, T-wave flattening and U waves; give intravenous potassium no faster than 10–20 mmol/hour with cardiac monitoring.
- Metabolic acidosis is the commonest surgical acid–base disorder (lactate, ketones, renal failure); the anion gap is calculated as sodium minus (chloride plus bicarbonate), normally 8–12 mmol/L.
- 5 per cent dextrose distributes across total body water, normal saline stays extracellular, and colloid is no longer preferred for routine resuscitation per current guidance.
- Third-space losses into the gut wall and interstitium after laparotomy explain postoperative oliguria despite a normal haemoglobin.
Common confusion
Students repeatedly equate a low serum sodium with sodium depletion and reach for normal saline. In the postoperative patient, hyponatraemia is far more often dilutional, driven by the syndrome of inappropriate antidiuretic hormone secretion and excess hypotonic fluid, so the treatment is fluid restriction rather than salt loading. The other classic error is chasing the serum potassium without looking at the pH: acidosis shifts potassium out of cells, so a 'normal' potassium in a severely acidotic patient can crash after correction.
Exam-focused takeaway
NEET-PG frames this topic as calculation-free, principle-heavy one-liners: compartment percentages, the composition and distribution of Hartmann's versus saline versus dextrose, the maximum safe potassium infusion rate, and the anion-gap formula in plain text. They also like the clinical application — a patient with pain out of proportion, lactate of 6 and a compounding metabolic acidosis is heading towards mesenteric ischaemia, and postoperative confusion with sodium of 118 points to overzealous hypotonic infusions. Learn the numbers cold, since they appear as direct matches in stems.
Frequently asked questions
Why is Hartmann's preferred over normal saline in surgical patients?
Hartmann's is a balanced solution whose electrolyte profile approximates plasma, whereas large volumes of 0.9 per cent saline deliver a supraphysiological chloride load that produces a hyperchloraemic metabolic acidosis and may worsen renal outcomes.
How fast can hyponatraemia be corrected?
No faster than roughly 8–10 mmol/L in 24 hours in symptomatic chronic hyponatraemia, because rapid correction risks osmotic demyelination (central pontine myelinolysis); overt seizures justify careful hypertonic saline boluses.
What is the anion gap and when is it raised?
It is sodium minus (chloride plus bicarbonate), normally 8–12 mmol/L; it rises when acids such as lactate accumulate, as in shock, sepsis, mesenteric ischaemia and diabetic ketoacidosis.
What are third-space losses?
They are physiological shifts of fluid out of the functioning extracellular compartment into the bowel wall, peritoneum and interstitium after surgery or inflammation, producing intravascular depletion without external loss.