Hypernatraemia

• Hypernatraemia is a serum sodium concentration above 145 mmol/L. It always means there is too little free water for the amount of sodium in the body: a water deficit, often with a normal or even increased total body sodium. ^[1][3]
• The most common cause is not sodium excess but failure to drink enough water, whether through inability (infants, older adults, bedbound or confused patients), impaired thirst, or water loss that outpaces intake.
• Diabetes insipidus (central or nephrogenic) is the classic internal cause of large urine losses with a good thirst response, and causes hypernatraemia when thirst or access to water is impaired.
• The main symptoms come from brain cells shrinking as water leaves them: thirst, confusion, weakness, and, in severe cases, seizures, bleeding in or around the brain, and coma.
• Treatment is free water, by mouth if possible and by vein if necessary. Replace volume first in shocked patients, correct severe depletion with isotonic saline, then replace the free water deficit gradually; over-rapid correction can cause cerebral oedema.
• Chronic or long-standing hypernatraemia should be corrected over about 48 hours, never dropping serum osmolality faster than about 0.5 mOsm/L per hour (roughly 10 to 12 mmol/L in 24 hours), because the brain adapts and can swell. ^[1]

By the end of this page you should be able to:

1. Explain why a serum sodium above 145 mmol/L represents a water deficit, not necessarily sodium excess, and classify hypernatraemia by extracellular fluid (ECF) volume.
2. List the major causes under hypovolaemic, euvolaemic, and hypervolaemic headings, and distinguish central from nephrogenic diabetes insipidus (DI) from the urine osmolality and the water deprivation test.
3. Describe the brain changes behind thirst, confusion, seizures, and intracranial bleeding in hypernatraemia.
4. Assess volume status and interpret urine volume, urine osmolality, and the response to desmopressin.
5. Manage hypovolaemic, euvolaemic, and hypervolaemic hypernatraemia with the right fluids, in the right order, at the right rate.
6. Estimate the free water deficit and monitor correction safely in a patient with chronic hypernatraemia.
7. Describe how hypernatraemia is prevented and managed when tests, intravenous (IV) fluids, and drugs are limited.

Normal plasma sodium in adults is roughly 135 to 145 mmol/L. ^[4] Because sodium and its accompanying anions are the main solutes of extracellular fluid (ECF), the sodium concentration is best understood as a ratio: total body sodium divided, roughly, by total body water. Hypernatraemia therefore tells you about water, not about sodium alone. A patient can have low total body sodium and still have hypernatraemia if water has been lost in even greater proportion. ^[1]

Hypernatraemia is always accompanied by increased serum osmolality (hypertonicity). ^[4] It is not the opposite of hyponatraemia in any simple sense: hyponatraemia usually means excess water relative to sodium, whereas hypernatraemia means insufficient free water for the sodium present.

Total body sodium content determines ECF (plasma and interstitial) volume, because sodium and chloride are the dominant osmoles of the ECF. So the first question in assessment is not "how much sodium?" but "is the patient hypovolaemic, euvolaemic, or hypervolaemic?" Each pattern points to a different cause and a different treatment. ^[1]

• Hypovolaemic hypernatraemia: total body water and total body sodium are both reduced, but water has fallen more than sodium. This is the common combined "water and salt loss" picture. ^{[1] [4]}
• Euvolaemic hypernatraemia: total body water is reduced while total body sodium is roughly normal. This is essentially a pure water deficit. ^[1]
• Hypervolaemic hypernatraemia: total body sodium is increased, sometimes with normal or increased total body water. This is sodium gain with restricted access to free water. ^[1]

Note that ECF volume is not the same as "effective" plasma volume (the perfusion seen by baroreceptors). In heart failure, hypoalbuminaemia, or capillary leak, effective plasma volume can be low even when ECF is increased. ^[1]

Hypernatraemia is much less common than hyponatraemia. ^[4] It most often occurs in infants, older adults, and anyone with impaired mental status who cannot act on thirst. ^[1] Severe hypernatraemia is uncommon in conscious, mobile, and well-cared-for patients, because thirst is a powerful defence. When it does occur, it is usually because something else went wrong: dependence on others for water, confusion, a tube feed, an impaired thirst mechanism, or a concentrating defect. ^[1]

In older adults, hypernatraemia is common after surgery and in those receiving tube feedings or parenteral nutrition. Contributing factors include dependence on others to obtain water, impaired thirst, impaired renal concentrating capacity from age, diuretics or nephron loss, and impaired angiotensin II production, which may contribute directly to an impaired thirst mechanism. ^[1]

A plain classification keeps the causes organised. The percentages and relative frequencies below are typical clinical impressions rather than precise population figures; not all have recent population data behind them.

Most causes are the same ones that produce volume depletion generally: burns, fever with sweating, vomiting, severe diarrhoea, and osmotic diuresis. ^[1] Either hypernatraemia or hyponatraemia can follow severe volume loss depending on the relative amounts of sodium and water lost and the amount of water ingested before presentation, and these patients can be hyponatraemic, eunatraemic, or hypernatraemic. ^[1]

Renal causes include loop diuretics, which impair both sodium and water reabsorption, and intrinsic renal disease, in which concentrating ability is lost. Hyperglycaemia is the commonest osmotic diuresis, because glucose does not enter cells without insulin and worsens intracellular dehydration; the resulting "translational hyponatraemia" can also lower the measured serum sodium at first. ^[1]

Extrarenal losses, such as excessive sweating in a hot environment, cause some sodium loss but more water loss, because sweat is hypotonic, so hypernatraemia can develop before significant hypovolaemia. ^[1]

The two great internal causes are arginine vasopressin deficiency (central DI) and arginine vasopressin resistance (nephrogenic DI). In these the kidney cannot reabsorb free water in the collecting duct, producing large volumes of dilute urine (3 to 20 L/day). Thirst is normally intact, so conscious patients with water available usually remain eunatraemic; hypernatraemia appears when thirst is impaired or water cannot be obtained. ^[2][3]

Primary hypodipsia (essential hypernatraemia) is an impaired thirst mechanism, sometimes from structural or acquired midline brain disease, and is the mirror image of DI: the urine can be concentrated, but water is not sought. Altered osmotic triggering of vasopressin release can also occur. ^[1]

These are uncommon. Grossly elevated sodium intake with limited free water includes excessive hypertonic sodium bicarbonate (for example in lactic acidosis), hypertonic saline, and incorrectly formulated parenteral nutrition or tube feeds. ^[1] Salt poisoning from deliberate or accidental ingestion of concentrated salt, and forced ingestion such as seawater or soy sauce, has produced extreme hypernatraemia in case reports. ^[4] A mild elevation, typically around 147 mmol/L, can accompany mineralocorticoid excess and is usually not clinically important unless free water intake is restricted. ^[4]

• Impaired thirst or communication: infants, older adults, dementia, post-stroke or sedated patients, and anyone intubated or ventilated. ^[1]
• Dependence on others for water: post-operative patients, frail residents of institutions, prisoners, and infants. ^[1]
• Tube feeding or parenteral nutrition without adequate free water. ^[1]
• Renal concentrating defects: older adults, chronic kidney disease, diuretics, and the nephrotoxic drugs associated with nephrogenic DI. ^[1][3]
• Uncontrolled diabetes mellitus with osmotic diuresis. ^[1]
• Brain injury or surgery affecting hypothalamic thirst or vasopressin release. ^[2]

Everything about hypernatraemia follows from one relationship: the sodium concentration rises when free water falls relative to sodium. Vasopressin (antidiuretic hormone) normally prevents this by increasing collecting-duct water permeability via aquaporin-2, so water is reabsorbed and the urine concentrated. ^[4] When vasopressin is absent, ineffective, or overwhelmed, water is lost as dilute urine; if thirst and access to water are intact, polydipsia replaces the water and plasma sodium stays near normal. ^[2][3]

When serum osmolality rises, water moves from inside cells, including brain cells, into the hypertonic ECF. Brain cells shrink. ^[1] In acute hypernatraemia this shrinkage is abrupt and is the source of most serious neurological signs. If hypernatraemia develops more slowly, brain cells generate "idiogenic osmoles" (osmotically active solutes) inside themselves to pull water back and reduce shrinkage; consequently neurological symptoms are less severe in chronic than in acute hypernatraemia. ^[1] Chronic adaptation is also the reason that correcting a long-standing problem too quickly floods brain cells with water and can cause cerebral oedema. ^[1][4]

Acute brain shrinkage stretches and tears small bridging vessels, producing subcortical or subarachnoid haemorrhage and venous thromboses. These have been described particularly in children dying of severe hypernatraemia. ^[1][4]

• Most symptoms track how high the sodium is and how fast it rose.
• Non-specific symptoms (thirst, anorexia, muscle weakness, restlessness, nausea and vomiting) tend to occur early. ^[4]
• Serious signs appear when plasma sodium rises acutely to above about 158 to 160 mmol/L, with altered mental status, lethargy, irritability, stupor, or coma. ^[4]
• Extreme hypernatraemia can occur with salt poisoning, but such cases are reported and usually involve severe accompanying illness. ^[4]

Thirst is triggered by osmoreceptors in the hypothalamus; volume depletion is also sensed by baroreceptors. Together these make one drink, but a person who cannot drink loses both defences at once. Severe volume loss therefore often presents not with thirst but with the consequences of hypovolaemia: postural hypotension, tachycardia, dry mucous membranes, oliguria. ^[1][4]

In most cases the cause becomes clear from the history: sweating, vomiting, diarrhoea, new drugs, a recent tube feed, or a non-drinking dependent patient. ^[4] Record:

• Water intake and access (can the patient reach, request, or afford water?).
• Urine volume (polyuria points to diabetes insipidus or osmotic diuresis).
• Drugs (thiazide/loop diuretics, lithium, demeclocycline, amphotericin, dopamine).
• Co-morbidities (diabetes mellitus, heart or liver disease, psychiatric illness).
• Recent bicarbonate or hypertonic saline, operations, brain injury or surgery.
• Night-time thirst and nocturia (patients with primary polydipsia usually have no nocturia). ^[2]

• Thirst is the major symptom. In a conscious patient with normal mentation, its absence suggests an impaired thirst mechanism rather than a lack of water; such patients may present with hypernatraemia despite no complaint. ^[1]
• Patients with difficulty communicating may express thirst by becoming agitated rather than by asking for water. ^[1]
• Non-specific early symptoms: anorexia, muscle weakness, restlessness, nausea and vomiting. ^[4]
• Advanced: confusion, lethargy, irritability, stupor, coma. ^[4]
• Seizures and tetany from hypernatraemia itself or from overly rapid correction. ^[1][4]

• Confusion, neuromuscular excitability, hyperreflexia, seizures, or coma from brain cell shrinkage. ^[1]
• Intracranial bleeding, subarachnoid haemorrhage, and venous thrombosis may result from acute shrinkage tearing vessels, especially in children. ^[1][4]
• In chronic cases these neurological signs are less pronounced, because the brain has adapted with idiogenic osmoles. ^[1]

• Hypovolaemia: tachycardia, postural hypotension, reduced skin turgor, dry mucous membranes, low urine output, and, if available, low central venous pressure. ^[4]
• Hypervolaemia: raised jugular venous pressure, oedema, pulmonary congestion.
• Euvolaemia: normal perfusion and no overload; the only clue may be polyuria and dilute urine.

• Renal concentrating defects usually produce a large volume of hypotonic urine. ^[1]
• When losses are extrarenal (vomiting, diarrhoea, sweating), the route of water loss is usually evident and the urinary sodium concentration is low. ^[1]
• In diabetes insipidus, urine is very dilute: specific gravity commonly under 1.005, urine osmolality under 200 mOsm/kg (200 mmol/kg). ^{[2] [3]}

Hyperglycaemia in uncontrolled diabetes draws water out of cells and lowers the serum sodium by a dilution effect, so some patients show "translational hyponatraemia" at first despite a severe ongoing free-water deficit. Diagnosis and management must allow for glucose correction. ^[1]

The main challenge is not telling hypernatraemia from other conditions but working out why sodium is high.

• Diabetes mellitus (including osmotic diuresis from glucose) is the commonest cause of polyuria; serum glucose testing is mandatory. ^[2]
• Loop or thiazide diuretics, which produce a solute diuresis or alter concentrating ability.
• Arginine vasopressin deficiency and resistance, distinguished by the water deprivation test. ^[2][3]
• Primary polydipsia, distinguished by history, absence of nocturia, and failure to respond to vasopressin. ^[2]
• Gestational diabetes insipidus (vasopressinase in late pregnancy). ^[4]

• Serum sodium and osmolality: the defining finding.
• Urea, creatinine, glucose, lipids/protein to detect renal impairment, pseudo-hypernatraemia, and hyperglycaemia.
• Potassium and acid-base status: levels change during correction and accompanying illnesses (severe acidosis, pH below 7.10, needs specific handling). ^[1]
• Serum or plasma osmolality interpretation alongside urine osmolality.

As for any volume disorder: pulse, postural blood pressure, jugular venous pressure, skin turgor, mucous membranes, and review of fluid balance and weights. ^[4] Examination for causes such as heart failure, cirrhosis, edema, or nephrotic syndrome. ^[4]

• Urine volume and osmolality (preferably) or specific gravity.
• Urinary sodium concentration: low (under 30 mmol/L) in extrarenal loss or hypovolaemia; high when the kidney is the source or in euvolaemic/hypervolaemic states. ^[4]
• Glucose and ketones on urine dipstick to detect osmotic diuresis.
• 24-hour urine collection for volume and osmolality when DI is suspected. ^[3]

• Brain imaging when central DI or an impaired thirst mechanism is suspected, or after head injury or surgery. ^[2]
• If urine osmolality is very low with a history of DI: the water deprivation test and desmopressin response.
• Plasma vasopressin or copeptin: the most direct measure, but difficult to assay and not routinely available. ^[2]
• In children or families suspected of inherited DI, specialist genetic assessment may be arranged; routine genetic testing is not required for most adults. ^[3]

There is no single diagnostic score for hypernatraemia: the diagnosis is the laboratory value, and the assessment is clinical-plus-urinalysis. A practical assessment order is:

1. Confirm serum sodium above 145 mmol/L and estimate duration (acute vs chronic, often from history, baseline labs, and admission weight).
2. Decide volume status (hypovolaemic, euvolaemic, hypervolaemic) from examination and bedside observations.
3. Interpret urine volume and osmolality:
   • Hypernatraemia with a concentrating kidney (normal or high urine osmolality) points to non-renal water loss, access problems, or primary hypodipsia.
   • Hypernatraemia with dilute, high-volume urine points to DI, osmotic diuresis, or drugs.
4. If urine osmolality is under 300 mOsm/kg (300 mmol/L), distinguish DI from other causes with a water deprivation test and desmopressin. ^[2][3]
5. Look for the cause of volume excess or the triggering drug, nephrotoxin, or brain lesion.

This test must be started in the morning, with continuous supervision in hospital, because serious dehydration can occur. In a frightened or confused patient it is not appropriate; treat first. ^[2][3]

Why the test works: increasing plasma osmolality by dehydration normally leads to concentrated, low-volume urine; vasopressin or desmopressin concentrates the urine only if the renal tubule can respond. In central DI the ducts have never "seen" vasopressin and respond to replacement; in nephrogenic DI they cannot respond. ^[2][3]

The overall goal is to replace both intravascular volume and the free water deficit, at the right speed, while tracking other electrolytes. ^[1]

• Oral hydration works when the patient is conscious and has no significant gastrointestinal dysfunction; it is the safest route. ^[1]
• IV hydration is preferred in severe hypernatraemia or when the patient cannot drink (continued vomiting, altered mental status). ^[1]
• Under 24 hours acuity: hypernatraemia developing in less than 24 hours should be corrected over the next 24 hours. ^[1]
• Chronic or unknown duration: correct over about 48 hours, and do not lower serum osmolality faster than about 0.5 mOsm/L per hour (roughly 10 to 12 mmol/L in 24 hours), to avoid cerebral oedema from excess brain solute. ^[1]
• Acute severe hypernatraemia (hours): where the process developed over a period of hours, rapid correction (falling about 1 mmol/L per hour) may improve prognosis without causing convulsions or cerebral oedema. ^[4]
• These two statements reflect genuine guideline differences about how quickly "acute" can be corrected; in practice both agree that speed must follow how fast the abnormality developed, that shocked patients need volume first, and that chronic problems must be corrected slowly. If the acuity is unclear, behave as if it were chronic.

• Shocked or severely depleted patients need ECF volume first. Intravenous normal saline restores perfusion; calculating the free water deficit then determines how much 5% dextrose to give. ^[4]
• Once perfusion is adequate (or when sodium and water depletion are modest), the free water deficit can be replaced with hypotonic fluid, often 0.45% saline. ^[1]
• In diabetic non-ketotic hyperglycaemic coma, 0.45% saline can be given as an alternative to a combination of 0.9% normal saline and 5% dextrose in water to replenish both sodium and free water. ^[1]
• Alternatively, replace ECF volume and free water separately, using the free water deficit estimate. ^[1]
• When severe acidosis is present (pH under 7.10), sodium bicarbonate can be added to 5% dextrose or 0.45% saline, provided the final solution remains hypotonic. ^[1]

• Free water can be replaced with either 5% dextrose in water or 0.45% saline. ^[1]
• Then treat the underlying cause: repair a thirst or access problem, treat fever, or correct diabetes mellitus.
• Central DI: give desmopressin. Treatment of the cause (for example tumour, trauma, or surgery) is added where possible. ^[2]
• Nephrogenic DI: ensure free water, restrict dietary salt and protein to reduce solute load, correct hypercalcaemia or hypokalaemia, and stop nephrotoxins such as lithium or amphotericin if possible. Symptoms that persist can be treated with a thiazide diuretic and sometimes an NSAID or amiloride. ^[3]

• Replace the free water deficit with IV 5% dextrose in water, which can be supplemented with a loop diuretic, especially when there is sodium overload. ^[1]
• Infuse 5% dextrose in water slowly: too rapid an infusion can cause glucosuria, increasing salt-free water loss and worsening hypertonicity, especially in diabetes mellitus. ^[1]
• Monitor other electrolytes, especially potassium and bicarbonate, replacing them as needed. ^[1]

Desmopressin is a synthetic vasopressin analogue with minimal vasoconstriction and prolonged antidiuresis (12 to 24 hours in most patients). It can be given intranasally, orally, subcutaneously, or intravenously. Intranasal dosing is the commonest: a spray delivers 10 mcg of desmopressin in 0.1 mL. ^[2]

• Because individual duration of action varies greatly, the dose and timing must be established for each patient. ^[2]
• The nightly dose is the lowest dose that prevents nocturia; morning and evening doses are adjusted separately. ^[2]
• Parenteral dosing is reserved for hospitalised patients; desmopressin may be given IV when a rapid effect is needed, and aqueous vasopressin 1 to 2 mcg subcutaneously or intramuscularly lasts up to 12 hours. ^[2]
• Overdosage causes fluid retention and hyponatraemia, which in small children can lead to seizures; furosemide may be used to induce diuresis if this occurs. ^[2]
• Desmopressin is used with care in central DI to avoid water intoxication; one practical approach is to delay one dose each week to let a "breakthrough" polyuria reset the system, in patients prone to hyponatraemia on desmopressin. ^[4]

For nephrogenic DI: hydrochlorothiazide 25 mg orally once or twice daily can paradoxically reduce urine volume by reducing distal water delivery. NSAIDs (such as indomethacin) or amiloride can also help. ^[3] Thiazides may also reduce urine volume in complete or partial central DI, but desmopressin is preferred and non-hormonal measures seldom needed. ^[2]

Merck Manual gives an estimate based on total body water (TBW), where TBW in litres = weight in kilograms x 0.6 for men and x 0.5 for women, based on serum sodium. In this standard estimate the serum sodium is divided by 140 mmol/L to calculate the multiplier; the formula reads: ^[1]

Free water deficit (L) ≈ TBW (L) x (serum sodium ÷ 140 − 1) ^[1]

This is an estimate, and it assumes constant total body sodium content. If total body sodium is depleted (hypovolaemic patients), the true deficit is greater than the estimate. ^[1] It also does not account for ongoing losses, which must be added to the maintenance requirement.

Interpret the result with caution: it helps plan, but bedside perfusion, urine losses, and electrolytes decide what fluid is actually given. Re-estimate at least daily and after each new serum sodium. ^[1]

• Re-check serum sodium regularly during IV therapy (commonly every 4 to 6 hours in severe cases until stable).
• Track weight, input/output, and urine losses; ongoing losses must be replaced in addition to the deficit.
• Monitor potassium and bicarbonate in particular; add them as needed. ^[1]
• Take care not to drop sodium too fast: falling below the planned rate is also not necessarily safe if it occurs abruptly.

• Cerebral oedema from over-rapid correction of chronic hypernatraemia, which can cause seizures, permanent brain damage, or death. ^[1]
• Intracranial bleeding and venous thrombosis from acute brain shrinkage. ^[1][4]
• Seizures from hypernatraemia or its correction. ^[1][4]
• Acute renal injury or worsening chronic kidney disease from severe dehydration. ^[1]
• Volume overload and pulmonary oedema if hypotonic fluids are mismanaged.
• Desmopressin-related water intoxication and hyponatraemia, especially in small children. ^[2]
• In nephrogenic DI, intellectual disability in infants if treatment is not started early; other complications are preventable with adequate water. ^[3]

Hypernatraemia has a worse prognosis than hyponatraemia and is associated with a high mortality, largely because it marks serious underlying illness, functional impairment, or difficulty communicating thirst. ^[1][4] Prognosis is dominated by the cause (for example stroke, sepsis, dehydration, or serious brain disease) rather than by the sodium concentration alone. Better prognosis generally follows correction of the underlying cause, recovery of access to water, and slow, monitored replacement of free water. Chronic hypernatraemia with adaptation is usually less symptomatic per given sodium level than acute hypernatraemia. ^[1]

• Make water reachable and labelled (bedside, within hand span; changed every shift).
• Reassess any dependent patient's intake and output every day, especially after surgery and in heatwaves.
• Use enteral feeds and parenteral nutrition with enough free water, checking the sodium in the bag or feed, and avoid concentrating a feed to reduce volume when the patient cannot drink.
• Check serum sodium in older, acutely confused, post-operative, or ventilated patients who are not drinking, and in infants with fever.
• Diuretic review: avoid sodium-wasting regimens that precipitate depletion and reassess the need for loop or thiazide therapy.
• Disaster and transport: heat, inadequate water during journeys, and poor staffing are recurring causes of iatrogenic hypernatraemia.
• For inherited nephrogenic DI, screen at-risk infants and start water access early. ^[3]

• Infants and children: cannot communicate thirst; inherited nephrogenic DI presents with irritability, persistent fever, failure to thrive, and hypernatraemia, and delay can cause permanent intellectual disability. ^[3]
• Pregnancy: gestational DI from placental vasopressinase can occur in the latter half of pregnancy; it is usually mild and treated as central DI. ^[4]
• Older adults: impaired thirst, unassisted intake, and renal concentrating impairment make this the commonest group. ^[1]
• People with mental illness or cognitive impairment: can drink excessively (primary polydipsia) or forget to drink; both extremes matter.

• The single most useful test is a bedside or laboratory serum sodium; if unavailable, clinical volume status and urine output are the guides.
• A urine specific gravity dipstick or "feel and float" assessment can separate concentrated from dilute urine when osmolality is unavailable; specific gravity under 1.005 supports DI.
• Oral rehydration and oral water replace most deficits if the patient can swallow; teach families to help a dependent patient drink small, frequent amounts.
• 0.45% saline and 5% dextrose often are not available; if only normal saline is available, use it to restore volume first, then add oral water once perfusion is adequate.
• Desmopressin is costly or absent; nephrogenic DI can still be managed with water access, a low-salt and low-protein diet, and thiazides where they are on the essential medicines list. ^[3]
• For central DI in hospitalised patients, water can be replaced parenterally or enterally while arrangements are made; uncontrolled polyuria needs supervision because nocturnal dehydration is dangerous.
• Any infant or child with polyuria, fever, hypernatraemia, or failure to thrive should be referred promptly for urine testing and measurement of sodium.
• Both temperature and infection (for example dysentery leading to diarrhoea, or fever raising insensible loss) are common triggers where a tube or tap water must be actively provided.

• Hypernatraemia is a serum sodium above 145 mmol/L and means water is low relative to sodium, often with normal or increased total body sodium.
• Volume status (hypovolaemic, euvolaemic, hypervolaemic) is the first branch in both diagnosis and treatment.
• The cause is usually obvious from the history; the commonest cause is inadequate water intake, especially in those who cannot drink, communicate thirst, or care for themselves.
• Thirst is the major symptom; its absence in a conscious patient suggests an impaired thirst mechanism.
• Brain shrinkage explains confusion, seizures, and occasionally intracranial bleeding; chronic adaptation lowers symptoms but raises the risk of cerebral oedema during correction.
• Hypovolaemic patients need volume (isotonic saline) first, then hypotonic fluid; euvolaemic and hypervolaemic patients need free water.
• Central diabetes insipidus responds to desmopressin; nephrogenic diabetes insipidus does not, and is managed with water access, a low-sodium and low-protein diet, and thiazides.
• Chronic hypernatraemia is corrected over about 48 hours at no more than about 0.5 mOsm/L per hour (roughly 10 to 12 mmol/L in 24 hours); acute deficits that developed in hours can be corrected faster.
• The free water deficit is estimated as total body water x (serum sodium ÷ 140 − 1), with TBW as weight x 0.6 for men and x 0.5 for women; it is an underestimate when sodium is also depleted.
• Older adults, infants, post-operative, and dependent patients need active, daily water access; most cases are preventable.

• Arginine vasopressin deficiency (central diabetes insipidus)
• Arginine vasopressin resistance (nephrogenic diabetes insipidus)
• Hyponatraemia
• Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
• Hyperosmolar hyperglycaemic state
• Acute kidney injury
• Coma and disorders of consciousness
• Seizures and status epilepticus
• Paediatric fluid and electrolyte disorders
• Dialysis and renal replacement therapy