Fluid balance and acid–base for surgeons: compartments, NICE CG174 and blood gas interpretation

Where the water is

Total body water is about 60% of body weight in a young adult man — less in women, the obese and the elderly, because fat holds little water — which is roughly 42 L at 70 kg. Two-thirds of that is intracellular fluid and one-third extracellular. The extracellular compartment is itself split about 3:1 between interstitial fluid and plasma, with a small transcellular fraction (cerebrospinal, joint, pleural and gut-lumen fluid) of around 1 L that becomes clinically important when it expands, as it does in bowel obstruction and ileus.

Water crosses cell membranes freely, so osmolality is the same in every compartment — about 285–295 mOsm/kg — and the distribution of water is decided by where the solute is. Sodium and its anions are kept extracellular by the Na⁺/K⁺-ATPase, so total body sodium sets extracellular volume; potassium, phosphate and protein hold water inside cells. Between plasma and interstitium the capillary wall is freely permeable to small ions, and what keeps fluid in the vessels is the Starling balance of hydrostatic pressure against the oncotic pull of albumin. That is why a litre of 0.9% saline spreads through the whole extracellular space and only about a quarter remains intravascular after an hour, while a litre of 5% glucose, once its sugar has been metabolised, is water distributed across all 42 L with under a tenth left in the circulation: glucose solutions give water, not volume.

Daily requirements: the NICE CG174 numbers

For an adult who cannot drink and has no abnormal losses, NICE CG174 gives a maintenance prescription of 25–30 mL/kg/day of water, approximately 1 mmol/kg/day each of sodium, potassium and chloride, and 50–100 g/day of glucose to limit starvation ketosis (not to feed the patient). For a 70 kg adult that is roughly 2 L of water and about 70 mmol of each ion — which a single litre of 0.9% saline already exceeds for sodium and chloride. Use the lower end, 20–25 mL/kg/day, in the elderly and frail, in renal impairment and cardiac failure, and in the malnourished at risk of refeeding. The guideline organises every prescription around the ‘five Rs’:

• Resuscitation — for hypovolaemia (systolic pressure under 100 mmHg, heart rate over 90, capillary refill over 2 s, respiratory rate over 20, NEWS of 5 or more): a 500 mL bolus of crystalloid containing 130–154 mmol/L of sodium over less than 15 minutes, reassessed and repeated as needed, with expert help sought once 2,000 mL has gone in without the expected response.
• Routine maintenance — the numbers above, reviewed daily and stopped as soon as the patient can drink enough.
• Replacement — ongoing losses (vomit, nasogastric aspirate, stoma, fistula, drains, diarrhoea, polyuria) replaced like for like in volume and composition.
• Redistribution — oedema, sepsis, ileus and hypernatraemia change where fluid sits, and the prescription must allow for it.
• Reassessment — daily weight where possible, a fluid-balance chart, and urea and electrolytes at least daily while intravenous fluids continue.

What is in the bag

Three practical consequences follow. Hartmann's and Plasma-Lyte approximate plasma and are the default for resuscitation and most maintenance. 0.9% saline is kept for specific jobs: replacing chloride-rich gastric losses (the hypochloraemic, hypokalaemic alkalosis of gastric outlet obstruction), treating hyponatraemia, and situations where the potassium or calcium in a balanced solution is unwanted — hyperkalaemia, or the line through which blood is given, because the calcium in Hartmann's can in theory clot citrated blood in the tubing. Hypotonic fluids such as 5% glucose and 0.18%/4% have no role in resuscitation and are dangerous as routine maintenance in anyone with raised ADH, which includes almost every postoperative patient.

The metabolic response to surgery, and why patients become hyponatraemic

Tissue injury, pain, hypovolaemia, anxiety, nausea and opioids all trigger a neuroendocrine response that is adaptive for a day and a nuisance for a week. Hypothalamic release of antidiuretic hormone (ADH, vasopressin) rises for two to three days or more, driving water retention and a concentrated urine regardless of serum sodium. Reduced renal perfusion and sympathetic activation stimulate renin, angiotensin II and aldosterone, which retain sodium and excrete potassium and hydrogen ions. ACTH raises cortisol, and together with catecholamines and glucagon this produces insulin resistance, hyperglycaemia, protein catabolism and lipolysis — Cuthbertson's hypermetabolic ‘flow’ phase, after the brief hypometabolic ‘ebb’ of the first hours. Potassium released from damaged cells is excreted under aldosterone, so total body potassium falls even if the serum level is initially high.

The upshot is that the postoperative patient is programmed to hold salt and water and to pass little urine for a day or two, even when normovolaemic, so a modest oliguria in that window is not automatically a reason for more fluid: look at the whole patient. Postoperative hyponatraemia is almost always dilutional. The kidney cannot excrete free water in the face of ADH, so hypotonic maintenance fluid (5% glucose, 0.18%/4%) or large volumes of oral water are retained and the sodium falls. The danger is cerebral oedema, worst in young women and children, whose brains have least room to adapt. Prevention is to use isotonic fluid and to prescribe by weight; treatment depends on severity and speed of onset, with hypertonic saline reserved for symptomatic patients under senior supervision and the rate of correction limited to avoid osmotic demyelination.

Reading a blood gas: a stepwise approach

1. Oxygenation first. Read the PaO₂ against the inspired oxygen; a PaO₂ of 12 kPa on 60% oxygen is not reassuring.
2. pH. Below 7.35 is acidaemia, above 7.45 alkalaemia. A normal pH with an abnormal PaCO₂ and bicarbonate means either full compensation or a mixed disorder.
3. PaCO₂ (4.7–6.0 kPa). The respiratory component. If it has moved in the direction that explains the pH — a high PaCO₂ with acidaemia — the primary disorder is respiratory.
4. Bicarbonate (22–26 mmol/L) and base excess (−2 to +2). The metabolic component. A base deficit beyond −2 means metabolic acidosis, and in trauma it tracks the depth of shock.
5. Is compensation appropriate? The lungs respond to a metabolic disorder within minutes; the kidneys take two to five days to compensate for a respiratory one. Compensation never overshoots, so a pH on the far side of normal means a second primary disorder.
6. Anion gap for every metabolic acidosis. Na⁺ − (Cl⁻ + HCO₃⁻), normally about 8–12 mmol/L (higher if potassium is included), corrected downwards by roughly 2.5 mmol/L for every 10 g/L of albumin below 40. A raised gap means an unmeasured acid has been added; a normal gap means bicarbonate has been lost or chloride gained.
7. Then the clinical question: lactate, glucose, ketones, urea and drugs — and what needs to happen in the next ten minutes.

Hyperchloraemic acidosis from saline

0.9% sodium chloride is ‘normal’ only in the historical sense: its chloride content is about half as much again as plasma. Infuse enough and the plasma chloride rises. In the traditional Henderson–Hasselbalch view this dilutes bicarbonate; in Stewart's physicochemical view the narrowing of the strong ion difference between sodium and chloride forces more water to dissociate and the hydrogen ion concentration up. Either way the result is a normal anion gap metabolic acidosis, usually mild and self-limiting but easy to misread as persistent hypoperfusion if the lactate is not checked. Hyperchloraemia also reduces renal blood flow through tubuloglomerular feedback, and large-volume saline has been associated with more acute kidney injury than balanced solutions in large trials, although the effect is modest. The working rule: balanced crystalloid by default; saline when you specifically want its chloride, or want to avoid potassium, calcium or hypotonicity.

Potassium: principles of management

About 98% of body potassium is intracellular, so the serum level (3.5–5.0 mmol/L) is a poor guide to total stores, and a shift of a few per cent between compartments produces dangerous changes. Insulin, β₂-agonists and alkalosis drive potassium into cells; acidosis, tissue breakdown, haemolysis and insulin deficiency release it. The kidney, under aldosterone, is the main regulator.

Hyperkalaemia

Causes: acute kidney injury, potassium-sparing diuretics, ACE inhibitors and angiotensin receptor blockers, tissue injury (crush, rhabdomyolysis, tumour lysis, burns), acidosis, massive transfusion and — commonly — a haemolysed sample. ECG: tall tented T waves, flattened P waves, a prolonged PR interval and widening QRS progressing to a sine wave and asystole. Principles, in order: stop the cause and any contributing drug; with ECG changes give intravenous calcium to stabilise the myocardium (it does not lower the potassium); shift potassium into cells with insulin and glucose, with nebulised salbutamol as an adjunct, and correct acidosis; then remove it with potassium binders, loop diuretics and renal replacement therapy if it is refractory or the kidneys have failed. Recheck the potassium and the glucose — the shift is temporary.

Hypokalaemia

Causes: gastrointestinal losses (vomiting, diarrhoea, high-output stoma, villous adenoma), loop and thiazide diuretics, insulin and refeeding, alkalosis, hypomagnesaemia (which makes it refractory), corticosteroids and hyperaldosteronism. ECG: flattened T waves, ST depression, U waves, prolonged PR and QT intervals and arrhythmias, especially in patients on digoxin. Principles: oral replacement if mild and the gut works; otherwise intravenous potassium chloride in ready-mixed bags, by infusion and never by bolus, within the rate and concentration limits the BNF sets for a peripheral line (faster only through central access with continuous cardiac monitoring); and correct magnesium at the same time.

Refeeding risk

Starved cells switch to fat and ketone metabolism and intracellular phosphate, potassium and magnesium are depleted even when serum levels look acceptable. Reintroducing carbohydrate — by mouth, tube or vein, and a dextrose infusion counts — provokes an insulin surge that drives these ions and water into cells, so serum phosphate collapses (the hallmark), with hypokalaemia, hypomagnesaemia, fluid retention and thiamine deficiency. The result can be arrhythmia, heart failure, respiratory muscle weakness and Wernicke's encephalopathy. NICE's nutrition support guideline (CG32) defines high risk as any one of: BMI under 16, unintentional weight loss over 15% in three to six months, little or no intake for more than 10 days, or low potassium, phosphate or magnesium before feeding; or any two of: BMI under 18.5, weight loss over 10%, little intake for more than five days, or a history of alcohol misuse or of insulin, chemotherapy, antacid or diuretic use. The principles are to start feeding at a small fraction of requirement and build up over several days, to give thiamine and B vitamins before and during the first days, to replace electrolytes before and as feeding proceeds, and to check phosphate, potassium and magnesium daily at first.