The rate of sodium correction in hypernatraemia is the most clinically critical parameter and the source of the most serious iatrogenic complications — the brain adapts to chronic hypernatraemia by generating idiogenic osmoles (taurine, glutamine, inositol, myoinositol) within neurons to prevent cell shrinkage. If hypernatraemia is corrected too rapidly, the intracellular osmoles cannot be cleared quickly enough, causing net influx of water into neurons — cerebral oedema, resulting in seizures, herniation, and death. The correction rate rule: for chronic hypernatraemia (duration >48 hours or unknown): maximum fall in serum sodium of 0.5 mmol/L per hour, or maximum 10-12 mmol/L per 24 hours. For acute hypernatraemia (clearly <24 hours duration): can correct at up to 1 mmol/L per hour. In practice, most community-presenting hypernatraemia has been developing over days — treat as chronic. Serial 2-4 hourly sodium monitoring during correction is mandatory.

The corrected sodium in hyperglycaemia is an essential calculation that GPs must be able to perform when reviewing a patient with both elevated glucose and elevated or apparently normal sodium — hyperglycaemia causes water to move from the intracellular to extracellular compartment (by osmotic effect), diluting the plasma sodium. As a result, the measured sodium appears lower than the true sodium that would exist if glucose were normal. The correction formula: for every 5.6 mmol/L (100 mg/dL) rise in glucose above 5.6 mmol/L: add 1.6 mmol/L to the measured sodium. Example: glucose 33.6 mmol/L (6 × 5.6 mmol/L rise above normal), measured Na 136 mmol/L → corrected Na = 136 + (6 × 1.6) = 136 + 9.6 = 145.6 mmol/L. A 'normal' sodium of 136 in a patient with glucose of 33.6 is actually a corrected hypernatraemia. This matters for HHS management — as glucose falls with treatment, the measured sodium rises (water moves back intracellularly), and if hypernatraemia is not anticipated and managed, severe hypernatraemia may emerge during treatment.

The urine osmolality in hypernatraemia is the key discriminating investigation between appropriate physiological response, diabetes insipidus, and primary polydipsia — in normal hypernatraemia from water depletion, the hypothalamus detects high plasma osmolality and releases ADH, which causes the kidney to retain water and concentrate the urine maximally. Expected urine osmolality in appropriate response to hypernatraemia: >600-800 mOsm/kg (very concentrated urine). In diabetes insipidus: the kidney cannot concentrate urine because either ADH is absent (central DI) or the kidney cannot respond to ADH (nephrogenic DI). Urine osmolality in DI: <300 mOsm/kg (inappropriately dilute for the degree of hypernatraemia). The diagnostic test: water deprivation test (inpatient) — urine osmolality is measured as fluid is withheld, then desmopressin is given. If urine concentrates after desmopressin: central DI. If urine does not concentrate: nephrogenic DI. If urine concentrates before desmopressin: not DI (appropriate response, or primary polydipsia).

Lithium-induced nephrogenic DI is one of the most common and practically important causes of polyuria encountered in primary care — approximately 40-50% of patients on long-term lithium develop some degree of nephrogenic DI, ranging from mild polyuria to severe diabetes insipidus with urine outputs of 5-10 litres per day. The mechanism: lithium enters renal collecting duct principal cells via the epithelial sodium channel (ENaC) and inhibits the adenylate cyclase pathway, reducing aquaporin-2 (AQP2) water channel expression and impairing ADH-mediated water reabsorption. In early stages, this is reversible on stopping lithium; in patients with prolonged lithium treatment and high trough levels, some tubular damage may be permanent. The clinical management in a patient who cannot stop lithium: amiloride 5-10 mg OD (blocks ENaC, reduces lithium entry into principal cells — often dramatically reduces polyuria and has become the treatment of choice for lithium-induced NDI), adequate hydration (dehydration dramatically increases lithium serum levels and toxicity risk), and lowest effective lithium dose.

The oral rehydration strategy for mild hypernatraemia (sodium 145-150 mmol/L) in a cognitively intact adult who can drink is the preferred approach in community management — intravenous fluids introduce the risk of overcorrection and are not necessary in mild cases with adequate oral access. Free water (plain water, not sports drinks or normal saline) is the appropriate correction fluid for water-deficit hypernatraemia. Oral rehydration solution (ORS) may be used for combined isotonic + water losses (gastroenteritis). The important contraindication to oral correction: any patient with reduced consciousness, swallowing difficulty, or who cannot reliably drink adequate volumes needs IV correction in a monitored setting. The monitoring requirement even for oral correction: repeat sodium 4-6 hours after initiating rehydration to confirm the correction rate is within safe limits (<0.5-1 mmol/L per hour).

The desmopressin hyponatraemia risk is a critical prescribing safety point that must be communicated to every patient on desmopressin for central DI — desmopressin is a synthetic analogue of ADH that maximally stimulates V2 receptors in the renal collecting duct, causing maximal urinary concentration and water retention. If the patient drinks ad libitum with unrestricted fluid intake while on desmopressin, they will over-retain water and develop hyponatraemia. The safety instruction: patients on desmopressin must: (1) take the lowest effective dose; (2) not over-drink; (3) allow at least one or two dilute urinary voids per day (before the next desmopressin dose) to provide a 'safety escape' for excess water; and (4) have serum sodium checked after any dose change, illness, or change in fluid intake. Hyponatraemia from desmopressin overdose in central DI patients presents with headache, nausea, seizures, and confusion — identical to SIADH — and is treated by stopping desmopressin and fluid restriction.

The JBDS HHS management protocol represents current best practice for a condition with historically high mortality — the key departure from classical teaching is that insulin infusion should be DELAYED in HHS until adequate fluid resuscitation is underway and the corrected sodium is beginning to fall. The reason: in HHS, the high glucose is maintaining intravascular osmolality and volume — rapid insulin administration before adequate fluid replacement causes glucose (and therefore osmolality) to fall precipitously, drawing water back intracellularly and causing circulatory collapse. Equally important: the initial fluid of choice for HHS is 0.9% NaCl despite the hypernatraemia — the priority is restoring circulating volume and avoiding further osmotic instability. The switch to 0.45% NaCl occurs once haemodynamic stability is achieved and the glucose is beginning to fall. This is counterintuitive for trainees who naturally want to give hypotonic fluid for hypernatraemia — understanding the two-phase HHS protocol prevents this management error.

The dehydration assessment in elderly care home residents is one of the most common and practically impactful primary care interventions — studies consistently show that approximately 30-40% of care home residents are chronically mildly hypernatraemic (sodium 145-148 mmol/L) from inadequate daily fluid intake. The consequences: impaired cognition, increased falls risk, constipation, urinary tract infection susceptibility, pressure sore development, and acute kidney injury vulnerability. The Dehydration Recognition in its Earliest Stages (DREI) toolkit and NICE NG21 provide structured approaches for care homes. GPs conducting care home visits or reviewing care home residents should check: whether the resident has a documented daily fluid intake target, whether fluid intake is monitored, whether thickened fluids are offered where needed for dysphagia, and whether medications that increase water loss (diuretics, laxatives) are being managed in the context of adequate fluid replacement.

The central DI triphasic response after pituitary or hypothalamic surgery is a specific clinical pattern that GPs whose patients have had trans-sphenoidal pituitary surgery must know — Phase 1 (days 1-3): acute DI from surgical trauma and oedema disrupting ADH release from the neurohypophysis — polyuria + hypernatraemia requires desmopressin. Phase 2 (days 4-7): SIADH — damaged neurons release stored ADH uncontrolled — water retention + hyponatraemia. Stop desmopressin during this phase. Phase 3 (permanent): if the ADH-producing neurons are permanently damaged, permanent DI — restart desmopressin. If neurons recover, DI resolves. The risk of unrecognised Phase 2 SIADH while continuing desmopressin is severe hyponatraemia. Post-operative endocrine monitoring is specialist-led but GPs should be aware of this pattern when patients present post-operatively with sodium abnormalities.