see also: [[Blood gas#correct Na for glucose|corrected sodium for hyperglycaemia]], [[hypernatremia#Free water deficit / fluid deficit|Free Water deficit for ↑ Na]], [[Paediatric fluids]], [[Diabetes insipidus]] see: [Deranged physiology: Hyperosmolar hyponatremia](https://derangedphysiology.com/main/required-reading/electrolytes-and-fluids/Chapter%205.3.2/hyperosmolar-hyponatremia), [deranged physiology - hypernatremia](https://derangedphysiology.com/main/required-reading/electrolytes-and-fluids/Chapter%20541/hypernatremia), [Marinos - Hypernatremia](x-devonthink-item://E1BD9A1B-B9D6-4AEA-8B93-01670E2EAA15?page=622) > [!treatment] > - Correction with IV NaCl ok > - lethal Na+ load **<6 hours** (0.75-3g/kg) : rapid correction likely safe IF known normal \[Na] prior > - onset **<48 hours**: correction 1 mEq/L/h. In an alert patient capable of safely drinking water, the route of administration should be two-thirds free water orally and one third IV. > - onset over **>48 hours**: slower to avoid the risk of cerebral edema, at no more than *0.5* mEq/L/h or *10 to 12 mEq/24 h* (although there is little evidence that rapid correction of hypernatremia causes a higher risk of mortality, seizure, ALOC, or cerebral oedema) # Causes - spurious (eg ↓ protein or contamination of blood gas machine ports) - iatrogenic - [[HCO3 therapy|NaHCO3]] overdose (see [case report](https://www5.austlii.edu.au/au/cases/act/ACTCD/2025/1.html)) - hypertonic saline - 0.9% saline (Na <150) - salt ingestion : 0.75-3g/kg potentially fatal - one tablespoon of salt weighs ~15g - Extra renal fluid loss - [[Burns]] - sweating - GI fluid loss - enviornmental exposure - renal losses - osmotic diuretics (mannitol, glucose) - [[Hyperaldosteronism]] - associated with ↑ urinary K - primary = Conn's syndrome - secondary associated with heart failure, cirrhosis, or nephrotic syndrome - [[Diabetes insipidus]] : polyuria, serum osmol >290 mosmol/L, serum Na >145, urine osmol <150 - idiopathic - neurogenic (trauma, CNS infection, guillain barre) - nephrogenic - eg amuloid, polycystic kidneys, pyelonephritis - drug-related - ethanol - phenytoin - lithium - electrolyte abnormalities - severe [[hypokalemia|hypo-k]] - [[hypercalcaemia|hypercalcemia]] ## Tox causes - [[Valproate]] — consider valproate tox in comatose pt with access to valproate and ↑ Na # Clinical features - depends on cause of hyper-Na - vomiting - lethargy - polyuria - diabetes - [[hypercalcaemia|hypercalcemia]] - [[hypokalemia|hypo-k]] - loop diuretics - [[Diabetes insipidus]] # pathophysiology ![[Pasted image 20240208083448.png| adaptation of brain volume to hypernatremia and correction]] ↑ Na → water drawn out of cells by osmosis → cell shrinkage → treatment → cells swell and cerebral oedema → ↑ ICP → ischaemia and brain damage/death Hypernatremia increases the [[Osmolality and Osmolarity|osmolality]] of the extracellular fluid, which draws water out of cells and decreases cell volumes. This effect is most prominent in the **brain**. However, the shrunken brain cells begin to regain volume after about 9 hours, thanks to the intracellular accumulation of “idiogenic osmolytes", and the cells can return to their normal volumes after just 48 hours. Sudden shrinkage of brain cells in acute hypernatremia can lead to parenchymal or subarachnoid / subdural haemorrhages (more common in paeds and neonates than adults). [[hyponatremia#Osmotic demyelination syndrome|Osmotic demyelination]] can rarely occur, and osmotic damage to muscles can lead to hypernatraemic [[rhabdomyolysis]]. # Complications ## hypernatremic encephalopathy The most common complication of hypernatremia is an encephalopathy that varies widely in incidence and severity. It is more likely to appear when the rise in serum sodium is rapid, and can present with lethargy, cognitive impairment, delirium, [[Seizures]] and even coma. **Cell shrinkage** and **osmotic demyelination** are recognized as the culprits. ## cerebral oedema Rare, but can occur as a result of over-correction too quickly > There is little evidence that rapid correction of hypernatremia causes a higher risk of mortality, seizure, ALOC, or cerebral oedema in *adults* ([Harrison's](x-devonthink-item://D7D7DEE3-8F19-43B8-9F8B-9722C906DAB6?page=387&start=273&length=182&search=recent%20evidence%20does%20not%20indicate%20that%20rapid%20correction%20of%20hypernatremia%20is%20associated%20with%20a%20higher%20risk%20for%20mortality,%20seizure,%20alteration%20of%20con-%20sciousness,%20and%2For%20cerebral%20edema) pg 347), but is much riskier in paeds and neonates; aim to correct by < 10 mmol/day. ## Others Hypernatremia has surprisingly few adverse consequences other than the encephalopathy. - There are occasional reports of rhabdomyolysis, which often appears along with the encephalopathy. - Hypertonicity also has negative inotropic effects, but there is no evidence that this results in heart failure. - Hypotonic fluid loss **does not decrease the blood pressure unless fluid losses are severe**, because the loss of hypotonic fluids increases the osmotic pressure in plasma, which draws fluid from the interstitial space into the plasma to help maintain intravascular volume. # Free water deficit / fluid deficit > **Free water deficit** = $(TBW * P_{osm} ) - \frac{285}{P_{osml}}$ > TBW = 0.5 or 0.6 x weight (female or male) > > The degree of hypernatremia almost always equals the total body water (TBW) deficit in adults > **TBW deficit** = $TBW * \frac{(serum~Na^{+} - 140)}{140}$ Other fluid deficit calculation: 0.6 x pt Weight x (1 - \[140 / corrected Na]) example: pt weighs 160 kg, glucose 65, VBG Na is 140. calculate his fluid deficit Corrected Na = 140 + (65 - 5)/3 = 160 Deficit = 0.6 x 160 x (1 - 140/160) = 12L # Treatment - correct ↑ Na of unknown duration over 48 hours - most patients have hypovolaemia; restore intravascular volume with NaCl or Hartmann's - maintenance fluids 0.45% saline - can consider 5% dextrose and loop diuretics if hypervolaemia - [[haemodialysis|dialysis]] if renal function poor - desmopressin for central DI : give only after intravascular volume depletion is corrected Aggressive infusion of hypotonic fluids has always been discouraged because of the risk of cerebral edema, which is heightened by the accumulation of osmolytes in shrunken brain cells that helps regain the original cell volume. The optimal correction rate for hypernatremia is not known, but the traditional recommendation has been to limit the rate of correction to **≤0.5 mEq/L/hr**. However, correction rates exceeding 0.5 mEq/L/hr have been used safely, without causing cerebral edema. Another approach is to calculate the [[Osmolality and Osmolarity|effective osmolality]] (2xNa + glucose) and aim for a reduction of 3-6 mosmol/hour slowly.