Hyponatraemia (Na <135)
Corrected Na = measured Na + BSL – 5
3
Epidemiology
1-2.5% hospitalised patients (most common electrolyte imbalance seen in hospital population)
Assoc with 60x mortality compared to normal Na inpatients
Normal Saline 154
Interstitial 144
Plasma
142
Normal
Concentrations
Ringer’s Lactate
Intracellular
130
10
Na comprises 90% of osmotically active particles in extracellular fluid and plasma
Physiology
In proximal convoluted tubule: 60% H20, 70% Na reabsorbed; angiotensin II   Na reabsorption
In loop of Henle: 20% H20, 20% Na is reabsorbed
In distal convoluted tubule: 5% Na reabsorbed; aldosterone   Na reabsorption,  K and H excretion)
In collecting ducts: 2-15% H20, 3% Na reabsorbed; ADH   H20 reabsorption controlled by
osmoreceptors in hypothalamus
Serum Na
>125
Symptoms
Symptoms
Mild GI symptoms (eg. Anorexia, nausea, vomiting); can be managed as
outpatient
115-125
Lethargy, confusion, muscle weakness; if asymptomatic, need close follow up
and repeat Na in 72 hours; if symptomatic, admit
<115
Decreased LOC, seziures; can cause brainstem herniation  cerebral oedema,
osmotic demyelination; requires emergent admission
Symptoms more likely if: fast decrease (>0.5mmol/hr) or large decrease (<120 in <24 hours) or osmolality
<240; worse in women and children
Investigations
Clinical picture; ?on diuretics; urine and blood Na and osmolality; BSL
Increased urine osmolality: SIADH, renal / hepatic / cardiac failure, hypoV, hypothyroid
Decreased urine osmolality: ADH working fine
Urine chloride <20: hypovolaemia
See below for specifics of management
General
Principles of
Management
Indications for hypertonic saline: coma, seizure, new onset profound  LOC; not indicated if
asymptomatic
Dose: give 25-100ml/hr (1-2ml/kg/hr) 3% saline via CVL
Or 100ml 3% saline (= 50mmol)
Can give more rapidly (eg. 500ml or 4-6ml/kg bolus over 10mins) if seizing; can give more rapidly if
hyponatraemia developed quickly (ie. <12-24hrs)
Endpoint: symptoms resolved / Na  by 8-20mmol/L / Na >125
Aim for correction of 1 mmol/L/hr (max 10-14mmol/L/day; Never correct faster than 25mmol/L/day;
1mmol/hr achieved by 100ml/hr)
Side effects: central pontine myelinosis (osmotic demyelination syndrome) if too rapid correction of
chronic (>48hr) hyponatraemia  develops over 3-5/7  symmetrical lesions around pons, occurs in
25% severe cases  altered LOC, seizures, brain stem signs, pseudobulbar palsy, quadriparesis,
dysarthria, dysphagia, tremor, ataxia, Parkinsonism, dystonia, catatonia, mutism, lethargy; may be
permanent; risk factors = alcoholic, malnourished,  K, burns, elderly
Aetiology
Investigations
Renal
Osmotic diuresis: glucose, urea, mannitol
Diuretics
 Mineralocorticoid: hypoaldosteronism
Na losing nephropathy: renal tubular acidosis,
chronic renal failure, interstitial nephritis,
cerebal salt wasting syndrome)
ExtraRenal
Gastrointesinal loss: diarrhoea, vomiting, NG tube
Third space loss: burns, pancreatitis, peritonitis
Sweating, blood loss
Hypovolaemic
Loss of Na > H20
Urinary Na >20
Urinary Na >20
 urinary osmolality
Kidneys reabsorb
Na to make up
for their losses
Na deficit (mmol/L) = (0.6 x kg) x (desired Na – actual Na)
Management: give normal saline
correct at <0.5mmol/hr or <12mmol/day; aim to get Na >125
Aetiology
Hypotonic
= serum
osmolality <275
Renal
Euvolaemic
ExtraRenal
Investigations
SIADH: ADH holds on to H20  concentrated
urine; accounts for 50% of all hyponatraemia;
multiple causes as below:
CNS: cancer, trauma, infection, CVA, Guillian-Barre
syndrome, delirium tremens, multiple sclerosis,
SLE, SAH, AIDS
RS: cancer (oat cell, bronchogenic), Infection,
COPD, cystic fibrosis, abscess, TB
Drugs: SSRI, TCA, MAOI, ecstasy, oxytocin,
carbamazepine, haloperidol, barbiturates,
NSAID’s, tramadol, omeprazole
Endocrine: hypothyroidism, hypocortisolism
Iatrogenic H20 overdose: bladder irrigation, IV
fluids
Polydipsia
Endocrine: hypothyroidism, hypocortisolism
Minimal increase in body water
Urinary Na >20
 urinary osmolality
Urinary Cl >40
Urinary Na <20
Large amounts
H20 in urine
No change in body Na
Management: fluid restrict to 500-1500ml/day; consider ADH antagonist if SIADH
Hypervolaemic
Aetiology
Investigations
Renal
Acute renal failure: can’t excrete water
Urinary Na >20
ExtraRenal
Cardiac failure, cirrhosis, nephrotic syndrome
 H20 but functionally underfilled  
aldosterone  Na retention
Urinary Na <20
Management: fluid and salt restrict; loop diuretics; dialysis
Isotonic
= serum
osmolality
275-295
Hypertonic
= serum
osmolality >295
No change to total body water or Na (ie. Pseudohyponatraemia)
Factitious:  protein,  lipids  artifically low Na
Therefore requires no treatment
Management: fluid restrict to 500-1500ml/day; consider ADH antagonist if SIADH
No change to total body water or Na
Extracellular solute load  water moves into extracellular fluid, diluting Na
(eg. Hyperglycaemia, mannitol, glycerol)
Management: treat cause (this may cause osmotic diuresis  genuine  Na)
IV fluids may help as often hypovolaemic