Hyponatraemia
Differentials
- Pseudohyponatraemia:
- Hyperlipidaemia
- Hyperglycaemia
- Hyperproteinaemia
- Fluid Overloaded – ECF increased:
- CCF
- Chronic liver disease
- CKD/ nephrotic syndrome
- Hepatorenal syndrome
- Steroids
- Euvolaemic – ECF normal:
- Water intoxication
- SIADH (multiple medications:
- Malignancy (Small cell lung, pancreas, prostate, leukaemia, cervical)
- Hypothyroidism
- “Beer potomania”
- Dehydrated – ECF decreased:
- Diarrhoea/ sweating/ vomiting
- Burns
- Fistula
- Villous adenoma of rectum
- Addison’s disease
– Diuretics (thiazides)
| ……………….. |  |
| Ur Na | < 20mmol | >20mmol | >20mmol | <20mmol/l | >20mmol/l | |
| Ur Osm | lower | higher | ||||
| Serum Osm | higher | lower |
Clinical
- Severity of symptoms associated with rapidity of loss and extent of fall
- >125 Asymptomatic
- 115-125 Lethargy, confusion, anorexia, nausea, vomiting
- <115 Muscle cramps and weakness, convulsions, coma
- History consistent with common causes for hyponatraemia
- History of fluid intake/losses
- Clinical assessment of the current hydration status
- Neurological status
- Red Flags
- Nausea and vomiting
- Irritability
- Headache
- Decreased conscious state
- Seizures
Complications
- Cerebral oedema
- Secondary to abrupt sodium losses and free water shift from vascular to interstitial space
- ECG changes
- Cause of non-ischaemic ST elevation on ECG
- Pontine demyelinosis (no clear evidence that associated with rapid correction)
- Develops 3-5 days after treatment
- Demyelination of central pons, corticobulbar and corticospinal tracts
- Altered mental state, pseudobulbar palsies
- Dysphasia and spastic quadriparesis
- More likely in chronic hyponatraemia
Correction
Depends on rapidity of onset and clinical symptoms
- Hypovolaemic hyponatraemia
- may respond to intravenous sodium chloride 0.9%, with potassium supplements if required.
- Hypervolaemic hyponatraemia
- who are oedematous due to heart, liver or kidney failure may respond to fluid restriction.
- A loop diuretic may be added as long as the effective intravascular volume is not depleted further
- Euvolaemic hyponatraemia
is based on:
- the presence of central nervous system symptoms (unconsciousness, seizure, drowsiness, headache)
- the severity
- the rate of development.
- Mild to moderate in euvolaemic or hypervolaemic patients (serum sodium concentration from 120 to 135 mmol/L, no cerebral symptoms)
- fluid restriction
- (eg restrict to 500 mL to 1 litre per 24 hours, or 500 mL less than daily urine output)
- Monitor serum electrolytes, creatinine and urine output daily or twice daily
- fluid restriction
- Severe Hyponatremia
- serum sodium concentration lower than 120 mmol/L OR
- with cerebral symptoms
- Treat with
- IV sodium chloride 3% (513 mmol/L)
- The initial target serum Na should NOT be higher than 120 mmol/L
- Correction should be:
- not more than 10 mmol/L in the first 24 hours
- not more than 18 mmol/L in the first 48 hours.
Calculations:
- Calculate Na deficit = (desired Na-current Na) x (0.6 x body weight)
Correction
- In acute severe hyponatraemia, aim for 1-2mEq/hour correction
- In chronic severe hyponatraemia aim for 0.5-1mEq/hour correction.
- Hypertonic saline replacement
- 3% saline (513mEq/L) by giving (deficit/513) to the patient at the rate of 1mEq/hour over 4 hours
- Rapid correction may lead to pontine myelinolysis
- Patients with chronic hyponatraemia (ie known duration more than 48 hours) are particularly at risk. Additional factors that increase this risk include:
- serum sodium concentration lower than or equal to 105 mmol/L
- hypokalaemia
- alcoholism
- malnutrition
- advanced liver disease
- More rapid initial correction can be considered in patients with:
- seizures or coma, regardless of whether the hyponatraemia is known to be chronic
- self-induced acute water intoxication (eg psychiatric conditions, endurance exercise)
- known hyponatraemia for less than 24 to 48 hours
- intracranial pathology or increased intracranial pressure