Severe Hyponatraemia

Introduction

 

Severe Hyponatraemia is plasma Na <110-120 .

Etiology

1. Decreased extracellular volume (hypovolaemia)
1. Renal loss
1. Diuretic therapy (especially thiazides)
2. cal failure (Addison’s, Hypopituitarism)
2. Gastrointestinal loss
1. Vomiting
2. Diarrhoea
3. Skin loss

• Burns
1. Normal extracellular volume (euvolaemia)
1. Primary polydipsia (psychogenic)
2. Excessive sodium free water infusion (eg. 5% DA)
3. SIADH

0. CNS disorders: Tumours, Stroke, Trauma, Infection, Psychosis.
1. Pulmonary disorders: pneumonia, TB, COPD
2. Drugs: anticonvulsants, psychotropics, antidepressants,
3. Cytotoxics, oral hypoglycaemic agents, opiates
4. Idiopathic
3. Hypothyroidism
2. Increased extracellular volume (hypervolaemia)
1. Heart failure
2. Liver failure
3. Hypoalbuminaemia
4. Nephrotic syndrome
5. Oliguric kidney injury

Artefactual causes of hyponatraemia:

6. Severe hyperlipidaemia
7. Hyperproteinaemia

Transient hyponatraemia:

8. Acute hyperglycaemia
9. Mannitol infusion.

Clinical Features 

Symptomatic hyponatremia is usually seen in patients with serum sodium levels less than 120 mEq/L. But clinical manifestations are more related to the speed of onset rather than their severity.

1. often asymptomatic
2. anorexia, nausea, vomiting,
3. confusion, lethargy,
4. seizures and coma.

[when hyponatraemia develops gradually, cerebral neurons have time to respond by reducing intracellular osmolality, through excreting potassium and reducing synthesis of intracellular organic osmolytes ]

Investigations 

This is particularly needed when there is euvolaemic hyponatraemia.

To identify SIADH.

1. Serum electrolytes - ↓Na⁺ (typically   <130 mmol/L)
2. Plasma osmolality (< 270 mmol/kg)
3. Urinary electrolytes - ↑Na⁺ (typically > 30 mmol/L) i.e., not minimally low
4. Urinary osmolalities- ↑(typically >150 mmol/kg) i.e., not minimally low
5. ↓Plasma urea, ↓creatinine, ↓uric acid.

To exclude other causes like ^Addison’s disease, hypothyroidism

Management 

The treatment for hyponatraemia is dependent on

• the rate of development
• severity
• on the underlying cause.

1. Mild asymptomatic hyponatremia: generally of little clinical significance and requires no treatment.
2. If there are central nervous system symptoms, hyponatremia should be rapidly treated at any level of serum sodium concentration.

Choice of fluid:

In general, if hyponatraemia has developed rapidly (over hours to days), it is generally safe to correct the plasma sodium relatively rapidly. This can include infusion of hypertonic (3%) sodium chloride solutions, especially when the patient is drowsy or convulsing.

Caution:

hypertonic (3%) sodium chloride solutions can be very hazerdaous if not judiciously used.

• Hazard of rapid correction: Rapid correction of hyponatraemia which has developed slowly (over weeks to months) can itself be hazardous to the brain - Central pontine myelinolysis or osmotic demyelination syndrome (ODS).

The rate of correction:

• In chronic asymptomatic hyponatraemia correction should not exceed 10 mmol/l/day, and an even slower rate would generally be safer.
• If hyponatraemia has developed rapidly (over hours to days), it is generally safe to correct the plasma sodium relatively rapidly.

A reasonable approach is to increase the serum sodium concentration by no more than 1–2 mEq/L/h and not more than 25–30 mEq/L in the first 2 days; the rate should be reduced to 0.5–1 mEq/L/h as soon as neurologic symptoms improve.

Under normal conditions, total body water is 50 or 60% of lean body weight in women or men, respectively. Therefore, to raise the plasma Na⁺ concentration from 105 to 115 mmol/L in a 70-kg man requires 420 mmol [(115 – 105) x 70 x 0.6] of Na⁺]

[1 L of NS contain 154 mEq of Na⁺ ]

Specific treatment measures- Should be related to the underlying cause.

1. Hypovolaemic patients:
1. Controlling the source of sodium loss
2. Administering intravenous saline (isotonic or half-normal (0.45%) saline) if clinically warranted.
2. Dilutional hyponatraemia:
1. Fluid restriction in the range 600-1000 ml/day
2. Withdrawal of the precipitating stimulus (e.g. a drug causing SIADH).
3. Demeclocycline 600-900 mg/day may enhance water excretion, by interfering   with collecting duct responsiveness to ADH.
4. oral urea^ therapy (30-45 g/day), which provides a solute load to promote water excretion.

Hypervolaemic patients:

1. Treatment of the underlying condition
2. Cautious use of diuretics- potassium sparing diuretics( eg. ) may be particularly useful in this context where there is significant secondary hyperaldosteronism.
3. Strict fluid restriction.