Figure Hypernatraemia is a water deficit — the brain shrinks and the bridging veins tear. The diabetes insipidus (the central from the brain injury, the nephrogenic from the lithium) is the free-water loss; correct the central with the desmopressin, and lower the sodium no faster than 0.5 mmol/L/hour to spare the brain the cerebral oedema. [6]
Hypernatraemia (Na >145) = water deficit relative to Na → brain cell SHRINKAGE → confusion/seizures/coma. Causes : free water loss (diabetes insipidus, diarrhoea, burns), inadequate water intake (coma/intubated), hypertonic solutions (3% saline for ICP, NaHCO3). Correction : SLOW — ≤8-10 mmol/L in 24h (rapid → cerebral oedema from water rushing back into shrunken brain). Free water deficit = TBW × (Na/140 − 1) — replace over 48-72h with 5% dextrose or 0.45% NaCl. Diabetes insipidus : central → desmopressin; nephrogenic → water + treat cause.
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SAQ — Rising sodium in DKA with evolving diabetes insipidus 10 minutes · 10 marks
Reveal all A 58-year-old man with new-onset type 1 diabetes is intubated and sedated in the ICU for severe diabetic ketoacidosis. At presentation his glucose was 48 mmol/L and sodium 128 mmol/L. After 8 hours of an insulin infusion and 0.9% saline his glucose is 18 mmol/L but his sodium has climbed to 154 mmol/L; he is passing 600 mL/h of urine with a urine osmolality of 280 mOsm/kg.
a Explain why the sodium is rising and calculate the corrected sodium at presentation. (5 marks)
b How would you confirm and manage diabetes insipidus in this intubated patient? (3 marks)
c State your target correction rate and your fluid choice for the hypernatraemia. (2 marks)
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Clinical pearls
Figure Exam overview — key physiology, red flags and first-hour management. Figure Core mechanisms examiners expect in CICM/FFICM/EDIC answers. Figure Stepwise ICU management: immediate priorities, disease-specific therapy, escalation. High-yield hypernatraemia points for CICM/FFICM exam
Brain cell SHRINKAGE — the pathophysiology. (1) NORMAL: serum osmolality 285-295 mOsm/kg. Na is the MAIN determinant of serum osmolality (Na × 2 + glucose + urea ≈ osmolality). (2) HYPERNATRAEMIA: high Na → HIGH serum osmolality (>295). (3) OSMOTIC GRADIENT: blood (high osmolality) > brain cell (normal osmolality). (4) WATER SHIFTS: from brain cell (lower osmolality) to blood (higher osmolality) → by osmosis → to equalise. (5) RESULT: brain cell SHRINKS (loses water → reduced volume). (6) CONSEQUENCES: (a) Confusion → seizures → coma (neurological dysfunction from brain shrinkage). (b) BRIDGING VEIN TEARING (brain pulls away from skull → bridging veins stretch → tear → SUBDURAL HAEMORRHAGE — especially in elderly). (c) INTRACRANIAL HAEMORRHAGE (rare — from vessel tearing). (7) KEY: hypernatraemia → brain cell shrinkage (water out) → neurological symptoms + risk of haemorrhage. CONTRAST with hyponatraemia → brain cell SWELLING (water in) → cerebral oedema.[1] }Correction rate — ≤8-10 mmol/L in 24h. (1) WHY SLOW: (a) Chronic hypernatraemia → brain ADAPTS → brain cells accumulate IDIOGENIC OSMOLES (organic solutes — myo-inositol, taurine, glutamate — to raise intracellular osmolality → match the high serum osmolality → brain cell volume returns toward normal despite high Na). (b) This adaptation takes 24-48 HOURS (osmole accumulation is gradual). (c) If corrected RAPIDLY (water given too fast → serum osmolality drops quickly) → brain cells still have HIGH osmoles (haven't had time to clear them) → water RUSHES INTO brain (from low-serum to high-brain osmolality) → brain SWELLS → CEREBRAL OEDEMA → herniation → death. (d) This is the REVERSE of ODS in hyponatraemia — but SAME mechanism (rapid change in osmolality → brain can't adapt → swelling/shrinkage → injury). (2) RATE: ≤8-10 mmol/L in 24h (≈0.5 mmol/L/hr). (3) MONITOR: Na every 2-4h during correction — adjust fluid rate — if falling too fast → slow. (4) ACUTE hypernatraemia (<48h — e.g., hypertonic saline bolus for ICP): brain hasn't adapted → can correct faster (1-2 mmol/L/hr) — but still monitor. (5) CHRONIC (>48h — most ICU): correct SLOWLY (≤8-10/24h). (6) KEY: same principle as hyponatraemia — correct SLOWLY (≤8-10/24h) — rapid correction → cerebral oedema.[5] }Free water deficit calculation. (1) FORMULA: Water deficit = TBW × (serum Na / 140 − 1). (2) TBW (total body water) = body weight × factor: (a) Men <65: 0.6. (b) Women <65: 0.5. (c) Men >65: 0.5. (d) Women >65: 0.45. (3) EXAMPLE: 70 kg man, Na 160 → TBW = 70 × 0.6 = 42 L → deficit = 42 × (160/140 − 1) = 42 × 0.143 = 6.0 L. (4) REPLACE over 48-72h: (a) deficit / 48h = 6.0 / 48 = 125 mL/hr (from deficit alone). (b) PLUS ongoing insensible losses (~1.5 L/day = 62 mL/hr) + any abnormal losses (DI polyuria — 5 L/day = 208 mL/hr). (c) TOTAL fluid rate: 125 + 62 + 208 = 395 mL/hr (of 5% dextrose or 0.45% NaCl). (5) MONITOR: Na every 2-4h — adjust rate (if Na falling >0.5 mmol/L/hr → reduce rate; if not falling → increase rate). (6) KEY: calculate deficit + add ongoing losses → replace over 48-72h → monitor + adjust.[3] }Diabetes insipidus — central vs nephrogenic. (1) CENTRAL DI (lack of ADH): (a) CAUSES: brain injury (TBI, SAH — especially anterior communicating artery aneurysm, neurosurgery — pituitary/hypothalamic, tumour — craniopharyngioma, metastases, meningitis, brain death). (b) PHASES after brain injury: (i) Phase 1 (0-5 days): POLYURIA (from initial ADH inhibition/inhibition — or neuronal shock — reduced ADH release). (ii) Phase 2 (5-15 days): SIADH (from ADH release from degenerating neurons — transient hyponatraemia). (iii) Phase 3 (>15 days): PERMANENT DI (from destruction of ADH-producing cells — permanent polyuria + hypernatraemia). (c) MANAGEMENT: DESMOPRESSIN (DDAVP — synthetic ADH — 1-4 mcg IV/SC q8-12h — titrate to urine output [target <2.5 L/day] + Na [target 140-145]). (2) NEPHROGENIC DI (kidney can't respond to ADH): (a) CAUSES: LITHIUM (most common — impairs aquaporin-2 insertion in collecting duct), hypercalcaemia, hypokalaemia, demeclocycline (old DI treatment for SIADH — causes DI!), foscarnet, congenital (rare). (b) MANAGEMENT: WATER (adequate — match urine output). THIAZIDE diuretics (paradoxical — mild volume depletion → increased proximal Na/water reabsorption → less delivered to collecting duct → less water loss). LOW SALT diet (reduce solute load → less osmotic diuresis). STOP causative drug (lithium — if possible). AVOID DDAVP (ineffective — kidney can't respond to ADH). (3) DISTINGUISH: give DDAVP → if urine concentrates → CENTRAL (responds). If stays dilute → NEPHROGENIC (doesn't respond). (4) KEY: DI = high Na + dilute urine + polyuria. Central → DDAVP. Nephrogenic → water + thiazide + stop cause.[4] }ICU-acquired hypernatraemia — common + preventable. (1) EPIDEMIOLOGY: 20-40% of ICU patients develop hypernatraemia (Na >145) during their ICU stay. (2) WHY SO COMMON: (a) FLUID LOSS (diuresis — frusemide; fever — insensible; diarrhoea; burns; open abdomen). (b) INADEQUATE FREE WATER (intubated/sedated patients can't drink — depend on IV fluids — which often contain Na [0.9% NaCl = 154 mmol/L Na — adding Na without proportionate water]). (c) ENTERAL NUTRITION (formula is hypertonic — concentrated solutes → osmotic diuresis → water loss → hypernatraemia — need free water supplement). (d) RRT (clears free water → if replacement fluid has high Na → hypernatraemia). (3) ASSOCIATED with WORSE outcomes: (a) Higher mortality (Lindner 2018 — ICU-acquired hypernatraemia OR ~1.5-2.0 for mortality — but it's a MARKER of illness severity — sicker patients develop it). (b) Longer ICU + hospital stay. (4) PREVENTION: (a) Give FREE WATER (5% dextrose infusion — or oral water if able) to match insensible + abnormal losses. (b) MONITOR Na daily (or more frequently if at risk). (c) FLUID PRESCRIPTION: calculate free water requirement (insensible ~10 mL/kg/day + urine output + GI losses) — don't just give 0.9% NaCl (adds Na without free water). (d) ENTERAL NUTRITION: add free water flushes (between feeds — to dilute the osmotic load). (e) AVOID prolonged 0.9% NaCl (use balanced solutions — Hartmann's — lower Na — or add 5% dextrose). (5) KEY: ICU-acquired hypernatraemia is COMMON + PREVENTABLE — give adequate free water + monitor Na.[2] }Hypertonic saline for ICP — intended hypernatraemia. (1) HYPERTONIC SALINE (3%, 5%, 23.4%) — used in neurocritical care (TBI, SAH, ALF): (a) RAISES serum Na → induces HYPERNATRAEMIA (Na 145-155) → osmotic gradient → water pulled FROM brain → reduces cerebral oedema → lowers ICP. (b) TARGET: Na 145-155 (don't exceed 160 — risk of AKI, neurological deterioration). (c) MONITOR: Na every 4-6h (adjust infusion rate — 3% at 30-50 mL/hr — titrate to Na target). (2) IF Na >160: (a) Reduce/stop hypertonic saline. (b) Give free water (5% dextrose — slow correction — but DON'T over-correct below 145 — the hypernatraemia was INTENTIONAL for ICP — maintain Na 145-150). (c) MONITOR ICP (if ICP rises after reducing hypertonic saline → may need to continue — balance Na vs ICP). (3) OSMOTIC DEMYELINATION RISK: theoretical — but from HYPOcorrection (Na falling too fast from high to normal → cerebral oedema). Maintain slow correction (≤8-10/24h) — but maintain target (145-150 for ICP). (4) KEY: hypertonic saline → intended hypernatraemia → monitor Na (target 145-155 — max 160). If >160 → reduce saline + give free water slowly.[6] }Sodium bicarbonate — iatrogenic hypernatraemia. (1) NaHCO3 (sodium bicarbonate) contains HIGH SODIUM: (a) Each 100 mL of 8.4% NaHCO3 = 100 mmol Na + 100 mmol bicarbonate. (b) Used for: metabolic acidosis (pH <7.1 — controversial — BICAR-ICU), TCA overdose (sodium load + alkalinisation), hyperkalaemia (shift K into cells). (2) MULTIPLE DOSES → HYPERNATRAEMIA: (a) If giving 200-300 mmol NaHCO3 → adds 200-300 mmol Na → raises serum Na significantly (especially in AKI — can't excrete). (b) Also: metabolic alkalosis (from bicarbonate) + hypokalaemia (bicarbonate shifts K into cells). (3) MONITOR: Na (if giving >1-2 doses of NaHCO3 — especially in AKI). (4) ALTERNATIVES: carbicarb (less Na — not widely available), Tribonat (mixed buffer). (5) KEY: NaHCO3 → high Na load → monitor Na if giving multiple doses (especially in AKI).[1] }Clinical assessment — volume status. (1) WHY VOLUME STATUS MATTERS: guides FLUID CHOICE (hypovolaemic → 0.9% NaCl first to restore volume → then hypotonic; euvolaemic → pure water replacement). (2) HYPOVOLAEMIC (most common): (a) Clinical: DRY mucous membranes, ↓skin turgor, tachycardia, hypotension (late), oliguria, ↑urea:creatinine ratio (>20:1). (b) CAUSE: extrarenal water loss (diarrhoea, burns, sweating, fever) — urine osm HIGH (>800 — kidney concentrating maximally). (c) MANAGEMENT: 0.9% NaCl FIRST (restore volume + perfusion — then switch to hypotonic once volume restored). (3) EUVOLAEMIC: (a) Clinical: NO volume depletion signs (normal BP, JVP, perfusion). (b) CAUSE: pure water loss (DI — urine osm LOW [<300 — can't concentrate]; OR inadequate intake — urine osm HIGH). (c) MANAGEMENT: 5% dextrose (pure free water) or oral water. (4) HYPERVOLAEMIC (least common): (a) Clinical: OEDEMA (peripheral, pulmonary — overload signs). (b) CAUSE: sodium gain (hypertonic saline, NaHCO3, Conn's syndrome). (c) MANAGEMENT: 5% dextrose (free water — dilute the Na) + frusemide (remove excess Na — but diuresis removes water too → need to replace free water selectively). (5) KEY: assess volume status → guides fluid choice (hypovolaemic → saline first; euvolaemic → 5% dextrose; hypervolaemic → 5% dextrose + frusemide).[1] }Neurological complications — seizures + haemorrhage. (1) SEIZURES: (a) From brain cell shrinkage (hyperexcitability — neuronal irritability from osmotic shift). (b) More common in ACUTE hypernatraemia (brain hasn't adapted — sudden osmotic gradient → severe shrinkage → neuronal dysfunction). (c) Treat: benzodiazepines (for acute seizure) + CORRECT Na slowly (the definitive treatment — don't just suppress seizures with antiepileptics). (2) INTRACRANIAL HAEMORRHAGE: (a) From BRIDGING VEIN TEARING (brain shrinks → pulls away from skull → bridging veins [connect brain surface to dural venous sinuses] stretch → tear → SUBDURAL HAEMORRHAGE). (b) Especially in ELDERLY (brain atrophy → more space → more traction on bridging veins). (c) Also: INTRAPARENCHYMAL (rare — from osmotic vascular injury). (3) CLINICAL: (a) Any hypernatraemic patient with NEW neurological symptoms (seizure, altered consciousness, focal deficit) → CT brain (exclude haemorrhage). (b) Subdural: crescent-shaped extra-axial collection on CT — managed neurosurgically (drain if large). (4) KEY: hypernatraemia → seizures + subdural haemorrhage (from brain shrinkage → bridging vein tearing). Any new neurology → CT brain. Correct Na slowly.[1] }5% dextrose vs 0.45% NaCl — which to choose. (1) 5% DEXTROSE (pure free water — no Na — no electrolytes): (a) BEST for PURE WATER DEFICIT (euvoalemic hypernatraemia — DI, inadequate intake). (b) Each litre provides 1 L of free water (no Na → effectively dilutes serum Na). (c) MONITOR GLUCOSE (dextrose → hyperglycaemia — especially in diabetic/septic — may need insulin — or use oral water instead). (d) Rate: limited by glucose tolerance (too fast → hyperglycaemia → osmotic diuresis → worsens hypernatraemia paradoxically). (2) 0.45% NaCl (half-normal saline — 77 mmol Na/L): (a) Provides SOME Na + free water (less Na than 0.9% — more than 5% dextrose). (b) GOOD for HYPOVOLAEMIC hypernatraemia (some Na for volume + free water for deficit). (c) SAFER than 5% dextrose (less glucose — good for diabetic). (d) But: still adds Na (less effective at lowering Na than pure water — but more volume). (3) ORAL WATER (if patient can drink): (a) BEST (self-regulating — gut absorbs what's needed — no IV line — no glucose load — no Na). (b) Use whenever patient is conscious + able to swallow. (c) May need NG water if intubated (give free water via NG — between feeds). (4) CHOICE: (a) EUVOLAEMIC + can drink → ORAL WATER (best). (b) EUVOLAEMIC + can't drink → 5% dextrose (monitor glucose). (c) HYPOVOLAEMIC → 0.9% NaCl first (volume) → then 0.45% NaCl or 5% dextrose (free water). (d) HYPERVOLAEMIC → 5% dextrose + frusemide. (5) KEY: oral water (best if able); 5% dextrose (pure water — but monitor glucose); 0.45% NaCl (water + some Na — for hypovolaemic).[3] }Cerebral salt wasting vs DI — distinguish (post-brain injury). (1) BOTH occur after brain injury (TBI, SAH, surgery). (2) DI (diabetes insipidus): (a) Na HIGH (>145) — from water loss (no ADH → dilute polyuria → water loss → Na rises). (b) Urine DILUTE (osm <300). (c) EUVOLAEMIC or hypovolaemic (pure water loss — volume may be maintained initially). (d) MANAGEMENT: DDAVP (central) or water (nephrogenic). (3) CEREBRAL SALT WASTING (CSW): (a) Na LOW (<135) — from SODIUM loss (brain releases natriuretic peptides → kidney wastes sodium → Na drops → hyponatraemia). (b) Urine CONCENTRATED (osm >300 — high Na in urine). (c) HYPOVOLAEMIC (true sodium + volume loss — dehydrated). (d) MANAGEMENT: SODIUM (0.9% NaCl or hypertonic — replace the lost sodium + volume) + FLUIDS. AVOID fluid restriction (worsens CSW → cerebral ischaemia in SAH). (e) FLUDROCORTISONE (mineralocorticoid — promotes sodium retention — for refractory CSW). (4) KEY DISTINCTION: DI → HIGH Na (water loss); CSW → LOW Na (sodium loss). OPPOSITE sodium direction. Management OPPOSITE: DI → DDAVP (retain water); CSW → sodium replacement. DON'T fluid-restrict CSW (would worsen hypovolaemia → cerebral vasospasm in SAH → stroke). (5) PRACTICE: post-brain injury + Na abnormal → check urine osm + Na + volume status → if Na high + dilute urine → DI → DDAVP; if Na low + concentrated urine + dehydrated → CSW → salt + fluids.[4] }Outcomes + prognosis. (1) MORTALITY: (a) Severe hypernatraemia (Na >160) → mortality 30-50% (but it's a MARKER of illness severity — sicker patients develop it — not necessarily the CAUSE of death). (b) ICU-acquired hypernatraemia → OR ~1.5-2.0 for mortality (Lindner 2018). (2) NEUROLOGICAL OUTCOMES: (a) If corrected SLOWLY → most recover fully (brain adapts + no cerebral oedema). (b) If corrected RAPIDLY → cerebral oedema → may have permanent neurological damage or death. (c) Subdural haemorrhage → neurological deficit (depending on size + location). (3) PREVENTION: (a) Give adequate FREE WATER (especially in intubated/sedated/elderly — who can't drink or have reduced thirst). (b) MONITOR Na daily in ICU (detect rising Na early — intervene before severe). (c) AVOID prolonged 0.9% NaCl without free water supplement. (d) ENTERAL NUTRITION: add free water flushes. (e) RRT: monitor Na + adjust replacement fluid composition. (f) HYPERTONIC SALINE: monitor Na (target 145-155 — don't exceed 160). (4) KEY: hypernatraemia is COMMON in ICU + associated with WORSE outcomes — PREVENT (adequate free water + monitor Na) — correct SLOWLY (≤8-10/24h).[2] } Red flags
Critical hypernatraemia red flags
Na >145 → brain cell SHRINKAGE (water out of brain) → confusion, seizures, coma.[1] }Correct SLOWLY: ≤8-10 mmol/L in 24h (rapid → cerebral oedema from water rushing back into adapted brain).[5] }Free water deficit = TBW × (Na/140 − 1) — replace over 48-72h with 5% dextrose or oral water.[3] }Diabetes insipidus : Na high + urine dilute (osm <300) + polyuria. Central → DDAVP; nephrogenic → water + thiazide.[4] }ICU-acquired hypernatraemia (20-40% of ICU) — PREVENT (adequate free water + monitor Na).[2] }Hypertonic saline for ICP : target Na 145-155 (max 160) — intended hypernatraemia.[6] }Subdural haemorrhage (from bridging vein tearing — brain shrinkage) → any new neurology → CT brain.[1] }CSW vs DI (post-brain injury): CSW → LOW Na (sodium wasting); DI → HIGH Na (water loss).[4] } Prognosis
Hypernatraemia evidence and outcomes [5]
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Causes — deep dive
Hypernatraemia causes, correction, and DI — 15 high-yield points
Adrogué–Madias formula — predict Na change per litre. (1) ΔNa = (Na_infusate + K_infusate − Na_serum) / (TBW + 1). (2) 5% dextrose (Na = 0) gives the MAXIMAL drop per litre. (3) EXAMPLE: 70 kg man, TBW 42, Na 160, giving 1 L of 5% dextrose → ΔNa = (0 − 160)/43 = −3.7 mmol/L → to correct 10 mmol/24 h needs ~2.7 L PLUS ongoing losses. (4) 0.45% NaCl (Na 77): ΔNa = (77 − 160)/43 = −1.9 mmol/L — slower, safer if overcorrection is a concern. (5) LIMITATION: closed-system estimate; ignores ongoing urine/insensible/GI losses → re-check Na every 2-4 h.Hypothalamic (adipsic) hypernatraemia — rare but exam favourite. (1) ADIPSIA = absent thirst from destruction of anterior hypothalamic osmoreceptors. (2) CAUSES: craniopharyngioma (classic — especially after surgery/radiotherapy), germinoma, pineal tumour, neurosarcoidosis, Langerhans cell histiocytosis, congenital (septooptic dysplasia), rupture/clipping of an anterior communicating artery aneurysm. (3) PATIENT has hypernatraemia + NO THIRST + usually coexisting CENTRAL DI (combined osmoreceptor + ADH-neuron injury). (4) MANAGEMENT: PRESCRIBED daily free water (NOT thirst-driven — they will not drink) + DDAVP + daily Na monitoring — these patients oscillate between hyper- and hyponatraemia because the entire osmoregulatory loop is destroyed.Insensible water loss — underappreciated in the ICU. (1) NORMAL insensible loss ~10 mL/kg/day (~700 mL in a 70 kg adult) — respiratory (humidified circuit largely abolishes this) + skin (sweat + transepidermal). (2) INCREASED loss in: fever (~10% extra per °C above 37), burns (massive evaporative loss from an open wound — up to 4-5 L/day if >50% TBSA), open abdomen, tachypnoea (non-intubated), high ambient temperature, thyrotoxicosis. (3) PRESCRIPTION: add ~300-500 mL/day free water BEYOND the calculated deficit + measured ongoing losses in any febrile / burned / open-abdomen patient. (4) UNMONITORED insensible loss is the commonest OCCULT cause of ICU-acquired hypernatraemia.GI loss and hypernatraemia. (1) DIARRHOEA (secretory or osmotic — viral, Clostridioides difficile, VIPoma) loses water RELATIVE to sodium → hypernatraemia. (2) VOMITING usually produces hypokalaemic hypochloraemic metabolic ALKALOSIS; hypernatraemia only if the patient cannot replace water. (3) LACTULOSE (hepatic encephalopathy) — osmotic diarrhoea → free-water loss → hypernatraemia; common in decompensated cirrhosis where thirst (adipsia) is also impaired. (4) HIGH-OUTPUT fistula (small bowel, pancreatic) — electrolyte-rich but water-rich → hypernatraemia if not matched. (5) URINE osm HIGH (>800) in pure GI loss (kidney concentrating maximally) — distinguishes from DI.Lithium-induced nephrogenic DI — mechanism. (1) Lithium enters the principal cell through ENaC (the epithelial sodium channel) → inhibits adenylate cyclase → ↓cAMP → ↓aquaporin-2 (AQP2) synthesis and apical insertion → collecting duct becomes impermeable to water → dilute polyuria. (2) Affects ~20-40% of long-term lithium users; chronic use also causes chronic interstitial nephritis. (3) PARTIALLY REVERSIBLE early (within months of cessation) but becomes IRREVERSIBLE after years (tubular atrophy). (4) AMILORIDE is the disease-modifying drug of choice — blocks lithium entry via ENaC. (5) THIAZIDES work but increase proximal lithium reabsorption (volume depletion) → CHECK lithium levels.Thiazide for nephrogenic DI — the paradox explained. (1) Thiazides (bendroflumethiazide, hydrochlorothiazide) block the Na-Cl cotransporter in the distal tubule → mild volume depletion → increased PROXIMAL tubular reabsorption of Na + water → less water delivered to the defective collecting duct → LESS polyuria. (2) Dose: bendroflumethiazide 2.5-5 mg PO mane. (3) COMBINE with low-Na diet (Na restriction enhances proximal reabsorption) and AMILORIDE (potassium-sparing + lithium-specific). (4) MONITOR K, Na, renal function — hypokalaemia itself downregulates AQP2 and worsens NDI.DDAVP (desmopressin) dosing — central DI. (1) IV/SC: 1-4 mcg q8-12h — onset 30 min, duration 8-12 h (most reliable in critical illness). (2) INTRANASAL: 10-40 mcg daily — variable absorption (rhinitis, post-surgery). (3) ORAL: 60-120 mcg bd-tds (low bioavailability ~3%). (4) TITRATE to urine output (target 1-2 mL/kg/h) and Na (140-145). (5) RISK: water intoxication/hyponatraemia from overshoot — especially if free water is prescribed on top; pair with monitored intake. (6) Selective V2 agonist → minimal pressor (V1) effect — safe even in coronary disease (unlike vasopressin).Cerebral oedema from over-rapid correction — the danger. (1) MECHANISM: brain accumulates IDIOGENIC OSMOLES (myo-inositol, taurine, glutamine, betaine) during chronic hypernatraemia → these CANNOT be cleared rapidly (transporter downregulation takes 24-48 h) → if serum osmolality drops >10 mmol/L/24 h → osmotic gradient brain→serum → water influx → astrocyte swelling → cerebral oedema → seizure, coma, herniation. (2) HIGHEST RISK: children, elderly, women, hepatic failure, post-transplant, hypoxaemia. (3) TREAT over-correction: STOP hypotonic fluid → give DDAVP 1-2 mcg IV (water retention re-raises Na) ± 3% saline bolus if actively seizing. (4) This is the MIRROR of osmotic demyelination in hyponatraemia — but here the danger is cerebral oedema, not ODS.Hypernatraemia in the brain-dead organ donor. (1) VERY common (>80%) — central DI from posterior pituitary necrosis / neurohypophyseal axonal death. (2) MUST manage to protect graft function (kidney grafts do worse with severe donor hypernatraemia): DDAVP 1-4 mcg IV bolus then as required, OR vasopressin infusion 0.5-3 units/h (supports haemodynamics AND reduces DI). (3) Replace urine output mL-for-mL with 5% dextrose or 0.45% NaCl. (4) Na target 140-150 — avoid swings >10 mmol/24 h even here.Sodium overload / salt poisoning. (1) IATROGENIC: hypertonic saline boluses for ICP; repeated NaHCO3 for TCA overdose or hyperkalaemia. (2) ACCIDENTAL: concentrated infant formula errors, salt emetics, sea-water drowning. (3) PATTERN: HYPERVOLAEMIC + HIGH Na + HIGH urine Na (>100) — kidney is excreting sodium but cannot keep up. (4) MANAGEMENT: frusemide (remove Na + water) + 5% dextrose (replace free water) = "desalination." (5) RRT (CVVHD) if AKI or refractory overload.Conn's / primary hyperaldosteronism and mild hypernatraemia. (1) MILD hypernatraemia (often 145-150) from aldosterone-driven Na retention + mild ADH suppression from volume expansion. (2) Almost always with HYPERTENSION + HYPOKALAEMIA + METABOLIC ALKALOSIS — the diagnostic clue. (3) Na rise is limited by aldosterone "escape" (ANP-mediated natriuresis). (4) DIAGNOSIS: aldosterone:renin ratio (high ARR, suppressed renin) → confirm with saline or captopril suppression test → CT adrenal / adrenal vein sampling. (5) TREAT the cause (adrenalectomy for adenoma; spironolactone/eplerenone for hyperplasia).Distinguishing solute vs water diuresis in the polyuric ICU patient. (1) POLYURIA = urine output >3 L/day. (2) WATER diuresis (low urine osm <300, low urine Na): DI (central/nephrogenic), primary polydipsia. (3) SOLUTE diuresis (HIGH urine osm >300, high urine Na/urea/glucose): osmotic diuretics (mannitol — ICU favourite), hyperglycaemia (DKA/HHS — glucose), urea (high-protein feeds, post-obstructive diuresis, recovering ATN). (4) CALCULATE daily solute excretion = urine osm × urine volume — >1500 mOsm/day = solute diuresis. (5) TREATMENT: solute diuresis → address cause (stop mannitol, insulin, reduce protein); water diuresis → DDAVP (central) or water + thiazide (nephrogenic).Hypernatraemia + hyperglycaemia — always calculate corrected Na. (1) Hyperglycaemia draws water osmotically from ICF to ECF → DILUTIONAL hyponatraemia (Na falls ~2.4 mmol per 5.5 mmol/L glucose rise). (2) So a DKA/HHS patient may have a "normal" MEASURED Na but a HIGH CORRECTED Na → once insulin starts (water shifts back into cells) the measured Na RISES → frank hypernatraemia. (3) CORRECTED Na = measured Na + 2.4 × (glucose − 5.5)/5.5 (mmol/L). (4) HHS commonly presents with corrected Na 150-170. (5) Use 0.9% NaCl initially (volume), then 0.45% NaCl as Na rises — AVOID 5% dextrose until glucose <14 mmol/L (dextrose worsens hyperglycaemia / osmotic diuresis).Enteral nutrition and refeeding hypernatraemia. (1) Concentrated enteral feeds (2 kcal/mL) deliver a HIGH solute load → obligate free-water excretion (solute diuresis) → hypernatraemia. (2) SOLUTION: free-water flushes (250-500 mL/day) via NG, or dilute the feed, or switch to a lower-osmolality formula. (3) Verify total prescribed fluid is adequate — feeds alone rarely supply enough free water. (4) Same principle in REFEEDING (carbohydrate-driven insulin → intracellular K/P/Mg shift + intracellular osmole generation) — monitor Na alongside K, P, Mg.Monitoring during correction — practical. (1) Na every 2-4 h until <150, then every 6-12 h. (2) Strict INPUT:OUTPUT via urinary catheter — replace urine output mL-for-mL in DI. (3) Glucose every 1-2 h on 5% dextrose (risk hyperglycaemia/osmotic diuresis). (4) NEURO OBS hourly — GCS, pupils (new seizure/coma = too fast OR new bleed → CT brain). (5) Re-calculate the free-water deficit every 12 h from the CURRENT Na — never lock the initial rate. (6) DOCUMENT the planned AND observed correction rate (safety + exam defence). [5]
Additional red flags — DI and overcorrection
Hypernatraemia red flags — DI, Adrogué–Madias, and overcorrection
Adrogué–Madias formula : ΔNa per litre = (Na_infusate + K − Na_serum) / (TBW + 1) — estimate, then re-check Na.[3] }Hypothalamic / adipsic hypernatraemia : no thirst + central DI → PRESCRIBE free water (do not rely on thirst).[1] }Central DI : DDAVP 1-4 mcg IV/SC q8-12h — risk of hyponatraemia from overshoot.[4] }Nephrogenic DI (lithium) : amiloride (blocks Li entry via ENaC) + thiazide + free water — DDAVP useless.[4] }Over-rapid correction (>10 mmol/24 h) → cerebral oedema → treat with DDAVP + 3% saline if seizing.[5] }Triple phase post-TBI : DI → SIADH → permanent DI — reassess before each DDAVP dose (avoid DDAVP in phase 2).[4] }Hyperglycaemia masks hypernatraemia — always calculate corrected Na in DKA/HHS.[1] }Organ-donor DI : DDAVP ± vasopressin infusion — protect kidney graft; Na target 140-150.[7] } Correction-rate and DI treatment evidence
Adrogué–Madias and DI treatment evidence Densification notes for fellowship revision
This leaf is densified to the ICU fellowship gate standard (CICM / FFICM / EDIC): embedded SAQ practice, multi-figure visual scaffolding, examiner map alignment, and MCQ coverage of definition, mechanism, first-hour management, evidence, and traps.
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Revision checkpoint 1: restate definition, one number examiners expect, and one absolute do-not-miss action.
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Revision checkpoint 8: restate definition, one number examiners expect, and one absolute do-not-miss action.
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[6] References [1] Adrogué HJ et al. Hypernatremia. N Engl J Med , 2000.PMID 10816188 [2] Lindner G et al. Hypernatremia in critically ill patients. J Crit Care , 2013.PMID 22762930 [3] Adrogué HJ et al. Aiding fluid prescription for the dysnatremias. Intensive Care Med , 1997.PMID 9083234 [4] Christ-Crain M et al. Diabetes insipidus. Nat Rev Dis Primers , 2019.PMID 31395885 [5] Chauhan K et al. Rate of Correction of Hypernatremia and Health Outcomes in Critically Ill Patients. Clin J Am Soc Nephrol , 2019.PMID 30948456 [6] Cook AM et al. Guidelines for the Acute Treatment of Cerebral Edema in Neurocritical Care Patients. Neurocrit Care , 2020.PMID 32227294 [7] Refardt J et al. Diabetes Insipidus: An Update. Endocrinol Metab Clin North Am , 2020.PMID 32741486 
