Fluid and electrolyte disturbances in older patients and their management

The ageing kidney is the substrate for every disturbance. GFR peaks at about 140 mL/min/1.73 m² in the third decade and then falls by roughly 8 mL/min/1.73 m² per decade; effective renal plasma flow falls proportionally more (10% per decade), so the filtration fraction rises. Add aglomerular circulation, medullary hypotonicity, tubular dysfunction and tubular frailty — the ageing kidney has narrowed margins in every direction.

Body water is reduced, and the loss is intracellular. Total body water is lower in older people and lower in elderly women than elderly men. Because the reduction takes place in the intracellular compartment, hypovolaemia always represents a pathological state in older adults — it is never a normal age change.

Thirst is blunted. When healthy, active older volunteers were water-restricted for 24 hours, their threshold for thirst was increased and water intake reduced compared with younger controls. Contributors: dryness of the mouth, decreased taste, altered mental capacity or cortical cerebral dysfunction, reduced sensitivity of both osmoreceptors and baroreceptors, and a lower concentration of angiotensin, a powerful generator of thirst.

Urinary concentrating ability is impaired. Maximum urinary concentration remains normal until about the third decade, then falls by about 30 mOsm/kg per decade. Mechanisms: aglomerular circulation, defective sodium reabsorption in the ascending limb of Henle, reduced distal urea reabsorption, and decreased responsiveness of the collecting tubule epithelium to antidiuretic hormone — which is why plasma vasopressin levels are higher in older adults.

Urinary diluting ability is also impaired. Minimum urine concentration is only 92 mOsm/kg in the elderly versus 52 mOsm/kg in the young, and maximum free water clearance falls from 16.2 to 5.9 mL/min. Clinical consequence: older people develop dehydration and hypernatraemia under water restriction, and volume overload and hyponatraemia under a water load.

Sodium is wasted and conserved slowly. The 24-hour urinary sodium output and fractional excretion of sodium are significantly greater in old and very old people. Clinically this produces slow adaptation to salt restriction or salt loss, orthostatic hypotension, and a tendency to hypovolaemia during illness, fasting or bowel preparation.

Potassium — depleted stores but a tendency to retain. Total body potassium is lower (reduced muscle mass, poor intake), yet renal potassium excretion is significantly lower in the aged because of reduced serum aldosterone and reduced tubular response to aldosterone, plus increased H⁺/K⁺-ATPase activity in the intercalated cells of the aged collecting duct. Result: serum potassium is usually normal, but older people develop hypokalaemia more rapidly on diuretics and are predisposed to hyperkalaemia on NSAIDs, ACE inhibitors, beta blockers and potassium-sparing diuretics.

Urea and creatinine handling changes. The fractional excretion of urea is increased — 65% in the old versus 50% in the young — contributing to osmotic diuresis and nocturia, medullary hypotonicity, and a characteristically low serum urea in the healthy older person. Healthy older people also show net creatinine tubular reabsorption, so creatinine clearance underestimates true glomerular filtration.

Calcium, phosphate and magnesium. Serum levels and fractional excretion are similar in the healthy young, old and very old. However, low dietary vitamin D, reduced sunlight exposure, decreased renal hydroxylation of vitamin D and low sex hormone levels, combined with poor intestinal calcium absorption, lead to senile secondary hyperparathyroidism. On volume overload, renal magnesium excretion increases enough to significantly lower serum magnesium.

Acid–base. The ageing kidney handles an acute acid load poorly — acidification is slower and recovery is slower — so metabolic acidosis is both commoner and more prolonged. Type 4 renal tubular acidosis (hyporeninaemic hypoaldosteronism) is common in the older diabetic and presents as a normal anion gap acidosis with hyperkalaemia.

Dehydration is the commonest disturbance. Causes: reduced intake — dementia, delirium, immobility, dysphagia, depression, fear of incontinence, restricted access to fluid, restraint; and increased losses — fever, diarrhoea, vomiting, diuretics, uncontrolled hyperglycaemia, hot weather. Physical signs are unreliable in the elderly: skin turgor and mucous membranes mislead. Use instead serial daily weight, postural blood pressure, urine output, urea:creatinine ratio and serum osmolality.

Hyponatraemia — a serious and often overlooked problem of the older patient. Three general causes: (a) decreased renal blood flow with a decreased ability to excrete a water load; (b) diuretic administration leading to water intoxication — a condition rapidly corrected by discontinuing the diuretic; and (c) excess vasopressin secretion. Older adults seem more prone to develop SIADH, and certain drugs such as chlorpropamide and barbiturates cause it more frequently in older individuals. Elderly patients may manifest cognitive impairment with even mild hyponatraemia.

Hypernatraemia — the mirror image, with higher mortality. Almost always due to water deficit rather than salt excess: the febrile, immobile, tube-fed or institutionalised patient who cannot access water. Correct the free water deficit slowly (≤10–12 mEq/L per 24 hours) to avoid cerebral oedema, preferably by the enteral route.

Principles of management common to all these disturbances. (i) Identify and treat the underlying cause. (ii) Medication review is the single highest-yield intervention — diuretics, SSRIs, carbamazepine, NSAIDs, ACE inhibitors, PPIs, laxatives. (iii) Correct slowly: rapid correction of serum sodium should not exceed a 20 mEq/L rise during the first 48 hours (1 mEq/L/h), to avoid neurological damage and central pontine myelinolysis. (iv) Give fluid cautiously — senile hypofiltration and diastolic cardiac failure predispose healthy old people to cardiac failure and lung congestion after a saline load. (v) Prefer the oral route; use subcutaneous hypodermoclysis where venous access is difficult in the frail. (vi) Monitor daily weight, input–output and electrolytes; adjust every drug dose to the estimated GFR. Age change Physiological consequence Clinical disturbance Practical guard ↓ Thirst threshold, ↓ Inadequate water intake for a given Dehydration, hypernatraemia Scheduled fluid rounds; do osmoreceptor osmolality not rely on the patient asking sensitivity ↓ Concentrating ability Obligatory water loss continues Hypernatraemia, nocturia Daily weights; early enteral (−30 mOsm/kg per despite deficit water decade) ↓ Diluting ability (free Cannot excrete a water load Hyponatraemia Avoid hypotonic IV fluids; water clearance 5.9 review thiazides and SSRIs mL/min) ↑ FENa, ↑ FEurea Salt and urea wasting Hypovolaemia, postural Do not over-interpret a hypotension, low serum urea "normal" urea or a high FENa ↓ Aldosterone and Impaired potassium excretion Hyperkalaemia on RAS blockers Check K⁺ 1–2 weeks after any tubular response and NSAIDs RASi change ↓ Muscle mass, net Serum creatinine stays "normal" Occult renal impairment, drug Dose by estimated GFR, never creatinine reabsorption toxicity by creatinine alone LATEST UPDATES (2023–PRESENT) — 3 POINTS

Correction limits have tightened, and re-lowering is now standard practice. Current guidance caps sodium correction at ≤8–10 mEq/L in the first 24 hours and ≤18 mEq/L over 48 hours, and at ≤6–8 mEq/L per 24 hours in those at high risk of osmotic demyelination — malnutrition, alcohol use, hypokalaemia, liver disease and initial sodium below 105 mEq/L, all common in frail older patients. If the limit is breached, active re-lowering with 5% dextrose ± desmopressin (the "DDAVP clamp") is recommended, and proactive desmopressin co-administration from the outset is increasingly used to make correction predictable.

SGLT2 inhibitors have entered electrolyte medicine. In a randomised, double-blind, placebo-controlled crossover trial in outpatients with chronic SIAD (JASN 2023), four weeks of empagliflozin 25 mg added to fluid restriction raised median serum sodium by 4.1 mEq/L versus placebo, with no hypoglycaemia, hypotension, overcorrection or AKI, and a small improvement in neurocognitive function. Separately, SGLT2 inhibitors raise serum magnesium — a useful incidental effect in the older patient on a diuretic or a proton-pump inhibitor.

Potassium binders have changed the hyperkalaemia doctrine. The KDIGO 2024 CKD guideline states that potassium binders may facilitate essential use of RAS inhibitors and mineralocorticoid receptor antagonists, that binders should be considered before reducing the RAS inhibitor, and that RASi discontinuation should be the last resort. Sodium zirconium cyclosilicate and patiromer are the modern agents; sodium polystyrene sulphonate has been removed from acute guidance because of weak evidence and the risk of colonic necrosis.