Hyponatraemia: assessment and management

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9

Hyponatraemia

assessment and management

Severity

In assessing the risk of serious morbidity or mortality in the patient with hyponatraemia, several pieces of information should be used:

The serum sodium concentration itself gives some indication of dangerous or life-threatening hyponatraemia. Many experienced clinicians use a concentration of 120 mmol/L as a threshold in trying to assess risk (the risk declines at concentrations significantly greater than 120 mmol/L, and rises steeply at concentrations less than 120 mmol/L). However, this arbitrary cut-off should be applied with caution, particularly if it is not known how quickly the sodium concentration has fallen from normal to its current level. A patient whose serum sodium falls from 145 to 125 mmol/L in 24 hours may be at great risk.

Often, the clinician must rely exclusively on history and, especially, clinical examination to assess the risk to the patient. Symptoms due to hyponatraemia reflect neurological dysfunction resulting from cerebral overhydration induced by hypo-osmolality. They are non-specific and include nausea, malaise, headache, lethargy and a reduced level of consciousness. Seizures, coma and focal neurological signs are not usually seen until the sodium concentration is less than about 115 mmol/L.

If there is clinical evidence of sodium depletion (see below), there is a high risk of mortality if treatment is not instituted quickly.

Mechanism

Clinical examination

The clinical signs characteristic of ECF and blood volume depletion are shown in Figure 9.1. These signs should always be looked for; in hyponatraemic patients they are diagnostic of sodium depletion. If they are present in the recumbent state, severe life-threatening sodium depletion is present and urgent treatment is needed. In the early phases of sodium depletion postural hypotension may be the only sign. By contrast, even when water retention is strongly suspected, there may be no clinical evidence of water overload. There are two good reasons for this. Firstly, water retention due to the SIAD (the most frequent explanation) occurs gradually, often over weeks or even months. Secondly, the retained water is distributed evenly over all body compartments; thus the increase in the ECF volume is minimized.

Biochemistry

Sodium depletion is diagnosed largely on clinical grounds, whereas in patients with suspected water retention, history and examination may be unremarkable. However, both sodium depletion and SIAD produce a similar biochemical picture (Table 9.1) with reduced serum osmolality reflecting hyponatraemia, and a high urine osmolality reflecting AVP secretion. In sodium depletion, AVP secretion is appropriate to the hypovolaemia resulting from sodium and water loss; in SIAD it is inappropriate (non-osmotic). Urinary sodium excretion is often increased in SIAD (a hypervolaemic state). It may be low or high in sodium depletion depending on whether the pathological loss is from gut or kidney.

Table 9.1

Clinical and biochemical features of sodium depletion and SIAD

  Sodium depletion Water retention
Symptoms* Often present, e.g. dizziness, light-headedness, collapse Usually absent
Signs* Often present. Signs of volume depletion, e.g. hypotension (see Fig 9.1) Usually absent
Oedema
Clinical value of signs Diagnostic of sodium depletion if present Oedema narrows differential diagnosis
Clinical course Rapid Slow
Serum osmolality Low Low
Urine osmolality High High
Urinary sodium excretion Low if gut/skin loss of sodium
Variable if kidney loss		 Variable but usually increased
Water balance Too little Too much
Sodium balance Too little Normal
Too much if oedema
Treatment aim Replace sodium Restrict water
Natriuresis if oedema

*Relating specifically to the mechanism. There may well be symptoms/signs relating to the underlying cause.

Oedema

Oedema is an accumulation of fluid in the interstitial compartment. It is readily elicited by looking for pitting in the lower extremities of ambulant patients (Fig 9.2), or in the sacral area of recumbent patients. It arises from a reduced effective circulating blood volume, due either to heart failure or hypoalbuminaemia.

The response to this is secondary hyperaldosteronism. Aldosterone causes sodium (and water) retention, thus expanding the ECF volume. Patients with oedema become hyponatraemic despite sodium retention because the effective hypovolaemia also stimulates AVP secretion, resulting in additional water retention (Fig 9.3).

Treatment

Hypovolaemic patients are sodium-depleted and should be given sodium. Normovolaemic patients are likely to be retaining water and should be fluid restricted. Oedematous patients have an excess of both total body sodium and water; they should be given a diuretic to induce natriuresis, and be fluid restricted. More aggressive treatment (usually requiring hypertonic saline) may be indicated if symptoms attributable to hyponatraemia are present, or the sodium concentration is less than 110 mmol/L.

image Clinical note

The use of oral glucose and salt solutions to correct sodium depletion in infective diarrhoea is one of the major therapeutic advances of the last century and is life-saving, particularly in developing countries.

Family practitioners, nurses and even parents are able to treat sodium depletion using these oral salt solutions, without making biochemical measurements.

Case history 5

A 42-year-old man was admitted with a 2-day history of severe diarrhoea with some nausea and vomiting. During this period his only intake was water. He was weak, unable to stand and when recumbent his pulse was 104/minute and blood pressure was 100/55 mmHg. On admission, his biochemistry results were:

image

Comment on page 164.

Hyponatraemia

clinical assessment and management

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