10.3 — Water and Electrolyte Balance

Your blood sodium is held between 135 and 145 mmol/L. That is a range of about 7 percent, and moving outside it in either direction by more than a little causes confusion, seizures and death. Your potassium is held between 3.5 and 5.0 mmol/L — a range of about 40 percent, which sounds generous until you notice that the total amount of potassium in your entire bloodstream is about 15 millimoles, roughly the amount in half a banana.

The margins are that tight, and the systems holding them are worth understanding, because almost every hospital admission involves them.

Where the water is

Total body water is about 60 percent of body weight in an adult man, 50 to 55 percent in a woman. For a 70 kg man that is 42 litres.

The difference between the sexes is fat. Fat tissue contains little water; muscle contains a lot. The same reasoning explains why infants are about 75 percent water and the elderly around 50 percent, and why children dehydrate faster — they have proportionally more water to lose and a larger surface area relative to their volume.

Three compartments:

Intracellular (about 28 litres, two thirds) — inside cells. Interstitial (about 10.5 litres) — between cells. Plasma (about 3.5 litres) — in the blood vessels.

The last two together are the extracellular fluid, about 14 litres.

And the composition of the two main compartments is startlingly different.

	Inside cells	Outside cells
Sodium	10–15 mmol/L	140 mmol/L
Potassium	140 mmol/L	4 mmol/L
Chloride	4 mmol/L	100 mmol/L
Calcium (free)	very low	2.4 mmol/L

The difference is maintained entirely by the sodium–potassium pump (Chapter 1.4), running continuously in every cell and consuming a fifth of your resting energy.

Two consequences that explain a great deal of clinical medicine.

Sodium is essentially an extracellular ion and potassium an intracellular one. So blood sodium tells you about water balance, and blood potassium tells you almost nothing about total body potassium — 98 percent of it is inside cells, and the blood level reflects the shift between compartments as much as the total.

And when cells die, potassium pours out. This is why crush injury, burns, tumour breakdown and massive haemolysis all cause hyperkalaemia (Chapter 6.7).

Water balance

In: about 2,500 ml a day — 1,500 from drinking, 700 from food, 300 from metabolism itself. That last one is real: oxidising glucose and fat produces water (Chapter 1.6), and it is how a camel manages, and why a fasting person still produces urine.

Out: about 2,500 ml — 1,500 as urine, 500 through the skin, 400 from the lungs, 100 in stool.

The 900 ml lost through skin and lungs is "insensible loss" — you cannot see it and cannot control it. It rises sharply with fever (about 10 percent per degree above normal), with fast breathing, and in hot dry conditions, and forgetting it is a common cause of underestimating a patient's fluid needs.

Only urine is adjustable. The obligatory minimum is about 500 ml a day — the volume needed to excrete the day's solute load at maximum concentration.

Osmolality and thirst

Plasma osmolality is normally 275 to 295 mOsm/kg, and it is defended more tightly than almost anything else in the body.

A rough calculation that is used constantly at the bedside:

\text{Osmolality} \approx 2 \times [\mathrm{Na^+}] + \text{glucose} + \text{urea}

Sodium is doubled because each sodium is accompanied by an anion. And sodium dominates the total, which is why sodium concentration and osmolality move together and why a sodium result is read as a statement about water.

Two sensors, and they measure different things.

Osmoreceptors in the hypothalamus detect concentration. They are extraordinarily sensitive — a 1 percent rise in osmolality triggers ADH release and thirst.

Baroreceptors and volume receptors detect volume. They are much less sensitive — needing a fall of 5 to 10 percent — but when they do fire they override the osmoreceptors completely.

That override is the key to understanding several confusing clinical pictures. In severe volume depletion, the body will retain water even at the cost of diluting the blood, because circulating volume is more immediately life-threatening than concentration. This is why a shocked patient can become hyponatraemic while being obviously dehydrated.

Thirst is a genuine physiological drive with a threshold, at about 295 mOsm/kg — slightly above the ADH threshold, so the body tries to fix the problem with hormone before bothering you about it.

And thirst becomes less reliable with age. Older people have a raised thirst threshold and a reduced ability to concentrate urine, which is why dehydration in the elderly is common, easily missed, and a frequent trigger for confusion, falls and kidney injury. In an older person, thirst is not a reliable guide to fluid needs — a schedule is better.

Sodium

Blood sodium is a measure of water, not of salt. This is the single most important idea in this chapter and it is consistently misunderstood.

A low sodium usually means too much water, not too little salt. A high sodium usually means too little water.

Hyponatraemia (low sodium)

The commonest electrolyte abnormality in hospital.

Symptoms are neurological, and the reason is osmosis. Low sodium outside cells means water moves into cells, and brain cells swell inside a rigid skull. Nausea, headache, confusion, and at severe or rapidly developing levels, seizures and coma.

The rate of change matters more than the level. A sodium of 120 developing over months may cause few symptoms, because brain cells have had time to extrude solutes and adapt. The same level developing over hours can be fatal.

Causes are grouped by whether the person is dry, normal or overloaded, and that assessment is done clinically before any calculation.

Volume-depleted — vomiting, diarrhoea, diuretics, adrenal insufficiency. Salt and water both lost, water replaced by drinking.

Normal volume — SIADH, in which ADH is secreted inappropriately, so water is retained. Caused by lung disease, brain disease, several cancers (particularly small cell lung cancer), and many drugs. Also hypothyroidism and severe hypocortisolism.

Volume-overloaded — heart failure, liver failure, kidney failure. The body senses low effective circulating volume despite excess total fluid, so it retains water.

Exercise-associated hyponatraemia deserves a specific mention because it kills healthy people and is entirely preventable. Endurance athletes who drink large volumes of plain water during prolonged exercise dilute their sodium, and deaths have occurred in marathon runners. The advice changed as a result: drink to thirst rather than on a schedule, and use drinks containing sodium for events over a few hours.

Correction must be slow, and this is a rule with a serious reason. Correcting chronic hyponatraemia faster than about 8 to 10 mmol/L per day can cause osmotic demyelination syndrome — destruction of the myelin in the brainstem, causing severe permanent neurological damage or death, appearing days after the sodium has been "successfully" corrected. The treatment causes the catastrophe, not the disease.

Hypernatraemia (high sodium)

Almost always a water deficit.

Causes: inadequate intake — which in practice means the very old, the very young, and anyone who cannot access water or express thirst; excess loss through diabetes insipidus (Chapter 10.2), osmotic diuresis, sweating or burns.

Symptoms are again neurological, from brain cells shrinking: thirst, lethargy, irritability, weakness, seizures.

And correction is again slow, for the mirror-image reason. Correcting too fast causes cerebral oedema, because brain cells that have accumulated solutes to survive the high sodium now draw water in when the outside becomes dilute.

The general principle is worth stating plainly: however the body got there slowly, it must be brought back slowly.

Potassium

The most immediately dangerous electrolyte, because it sets the resting membrane potential of every excitable cell, and the heart is the most sensitive.

Hyperkalaemia (high potassium)

Causes: kidney failure (the commonest); drugs — ACE inhibitors, ARBs, spironolactone, NSAIDs, trimethoprim, and potassium supplements, particularly in combination; cell breakdown — crush injury, burns, rhabdomyolysis, tumour lysis; acidosis, which drives potassium out of cells; and adrenal insufficiency.

A false result is common and worth knowing about. Haemolysis in the sample tube — from a difficult blood draw or a tight tourniquet — releases potassium from red cells and gives a spuriously high reading. A surprising high potassium in a well patient is repeated before acting on it.

Symptoms are minimal until it is dangerous, which is what makes it lethal. Muscle weakness, and then cardiac arrest.

The ECG changes progress in a recognised sequence: tall peaked T waves, then a flattening P wave and widening QRS, then a sine-wave pattern, then arrest.

Emergency treatment has three steps and the order matters.

1. Protect the heart — intravenous calcium. This does not lower the potassium at all. It stabilises the cardiac membrane against the potassium's effect, and it works within minutes. It buys time.

2. Shift potassium into cells — insulin with glucose, and salbutamol. Insulin drives potassium into cells as a side effect of its normal action. Glucose is given with it to prevent hypoglycaemia, and this is a step that has caused harm when omitted.

3. Remove it from the body — diuretics, binding resins, or dialysis.

Steps 1 and 2 buy hours; only step 3 solves it. Understanding that distinction prevents the common error of treating the number and then relaxing.

Hypokalaemia (low potassium)

Causes: diuretics (much the commonest), vomiting and diarrhoea, poor intake, alkalosis, and excess aldosterone.

Symptoms: weakness, cramps, constipation, and cardiac arrhythmias.

And there is a link that is frequently missed: low potassium is often caused by low magnesium, and will not correct until the magnesium is corrected. Magnesium is required for the pump that retains potassium in cells. Replacing potassium alone in a magnesium-depleted patient simply does not work, and this is one of the most useful practical facts in fluid and electrolyte management.

Low potassium also potentiates digoxin toxicity (Chapter 1.4) and prolongs the QT interval (Chapter 7.3).

Calcium, magnesium and phosphate

Calcium — 2.2 to 2.6 mmol/L total, but only the free ionised fraction is active. About 40 percent is bound to albumin.

So a low albumin gives a low total calcium with normal ionised calcium, and the reported value must be corrected for albumin — a calculation done automatically by most laboratories and a genuine source of confusion when it is not.

And pH shifts the binding, which is why alkalosis causes the tingling and spasms of hyperventilation (Chapter 8.5) with a completely normal total calcium.

High calcium — most often from hyperparathyroidism or cancer. "Stones, bones, groans and psychiatric moans" — kidney stones, bone pain, abdominal pain and constipation, and confusion or depression. Treated with fluids and bisphosphonates.

Low calcium — tingling around the mouth and in the fingers, muscle spasms, and at the extreme, laryngeal spasm and seizures. Two classic signs: tapping over the facial nerve causes the facial muscles to twitch, and inflating a blood pressure cuff on the arm produces a characteristic spasm of the hand within three minutes.

Magnesium — required by every enzyme using ATP, and involved in potassium and calcium handling as above. Deficiency is common and under-tested, particularly with diuretics, alcohol dependence, and proton pump inhibitors.

Phosphate — essential for ATP itself. Refeeding syndrome is the important scenario: giving carbohydrate to a severely malnourished person causes insulin release, which drives phosphate, potassium and magnesium into cells, and the resulting severe hypophosphataemia can cause heart failure, respiratory failure and death. The prevention is to feed slowly and replace electrolytes first, and it is a genuine hazard in treating anorexia nervosa, alcohol dependence and prolonged starvation.

Assessing fluid status

Done clinically first, and the signs are cumulative.

Dehydration: thirst, dry mouth and tongue, reduced skin turgor, sunken eyes, reduced urine output, and — later — low blood pressure and a fast pulse. In children, a sunken fontanelle (Chapter 5.2) and reduced tears.

Postural blood pressure is one of the most useful bedside tests: a fall of more than 20 mmHg systolic on standing suggests significant volume depletion.

Capillary refill — press a fingertip for five seconds; colour should return within two.

And weight is the most accurate measure of all. One kilogram of weight change is one litre of fluid, and daily weights are more reliable than any examination sign in monitoring fluid balance in hospital.

Overload: swollen ankles, distended neck veins, crackles in the lungs, and weight gain.

Fluids given by drip

Three main choices, and each goes somewhere different.

0.9% sodium chloride (normal saline) — 154 mmol/L of sodium. Isotonic, so it stays in the extracellular compartment. Good for volume replacement.

Balanced solutions such as Hartmann's or Ringer's lactate contain sodium, potassium, calcium and a buffer, in proportions closer to plasma. Large volumes of normal saline cause a hyperchloraemic acidosis, because 154 mmol/L of chloride is well above the plasma level of about 100 — so balanced solutions are increasingly preferred for resuscitation.

5% dextrose — glucose in water. The glucose is metabolised, so it is effectively free water and distributes throughout all compartments. Only about one twelfth of it stays in the circulation. Useful for water replacement, useless for volume resuscitation, and giving it to a shocked patient is a serious error.

And the rules of thumb worth carrying: replace what is being lost with something resembling what is being lost; think about the deficit, the maintenance requirement and the ongoing losses separately; and reassess frequently, because fluid prescribing is one of the commonest sources of avoidable harm in hospital — in both directions.

What the next page fixes

The kidney's other great regulatory job is the one operating on the tightest tolerance of all. Chapter 10.4 covers acid–base balance — why blood pH is held within 0.1 of a unit, how the lungs and kidneys divide the work, and how to read an arterial blood gas in four steps.