Hypernatraemia

Hypernatraemia is an increase in the serum sodium concentration above the reference interval of 133–146 mmol/ L. Just as hyponatraemia develops because of sodium loss or water retention, so hypernatraemia develops either because of water loss or sodium gain

Water loss

Pure water loss may arise from decreased intake or excessive loss. Severe hypernatraemia due to poor intake is most often seen in elderly patients, either because they have stopped eating and drinking voluntarily, or because they are unable to get something to drink, e.g. the unconscious patient after a stroke. The failure of intake to match the ongoing insensible water loss is the cause of the hypernatraemia. Less commonly there is failure of AVP secretion or action, resulting in water loss and hypernatraemia. This is called diabetes insipidus; it is described as central if it results from failure of AVP secretion, or nephrogenic if the renal tubules do not respond to AVP. Water and sodium loss can result in hypernatraemia if the water loss exceeds the sodium loss. This can happen in osmotic diuresis, as seen in the patient with poorly controlled diabetes mellitus, or due to excessive sweating or diarrhoea, especially in children. However, loss of body fluids because of vomiting or diarrhoea usually results in hyponatraemia.

Sodium gain

Hypernatraemia due to sodium gain (often referred to generically as ‘salt poisoning’ even where there is no suggestion of malicious or self-induced harm) is much less common than water loss. It is easily missed precisely because it may not be suspected. It can occur in several clinical contexts, each very different. Firstly, sodium bicarbonate is sometimes given to correct lifethreatening acidosis. However, it is not always appreciated that the sodium concentration in 8.4% sodium bicarbonate is 1000 mmol/ L. A less concentrated solution (1.26%) is available and is preferred. Secondly, near-drowning in saltwater may result in the ingestion of significant amounts of brine, the sodium concentration of which is once again vastly in excess of physiological. Thirdly, infants are susceptible to hypernatraemia if given high-sodium feeds either accidentally or on purpose. For example, the administration of one tablespoon of NaCl to a newborn can raise the plasma sodium by as much as 70 mmol/ L. 

The pathophysiological parallel to the administration of sodium is the rare condition of primary hyperaldosteronism (Conn’s syndrome), where there is excessive aldosterone secretion and consequent sodium retention by the renal tubules. Similar findings may be made in the patient with Cushing’s syndrome, where there is excess cortisol production. Cortisol has weak mineralocorticoid activity. However, in both these conditions the serum sodium concentration rarely rises above 150 mmol/ L. The mechanisms of hypernatraemia are summarized in Figure 10.1.

Fig 10.1 The causes of hypernatraemia

Clinical features 

Hypernatraemia may be associated with a decreased, normal or expanded ECF volume (Fig 10.2). The clinical context is all-important. With mild hypernatrae- mia (sodium <150 mmol/ L), if the patient has obvious clinical features of dehydration (Fig 10.3), it is likely that the ECF volume is reduced and that one is dealing with loss of both water and sodium. With more severe hypernatrae- mia (sodium 150 to 170 mmol/ L), pure water loss is likely if the clinical signs of

Fig 10.2 Hypernatraemia is commonly associated with a contracted  ECF volume, and less commonly with an expanded compartment. (a) Volumes of ECF and ICF are reduced. (b) ECF volume is shown here to be slightly expanded; ICF volume is normal.

Fig 10.3 Decreased  skin turgor. This sign is frequently unreliable in the elderly, who have reduced skin elasticity. In the young it is a sign of severe dehydration with fluid loss from the ECF.

dehydration are mild in relation to the severity of the hypernatraemia. This is because pure water loss is distributed evenly throughout all body compart- ments (ECF and ICF). (The sodium content of the ECF is unchanged in pure water loss.) With gross hypernatraemia (sodium >180 mmol/ L), one should suspect salt poisoning if there is little or no clinical evidence of dehydration; the amount of water that would need to be lost to elevate the sodium to this degree should be clinically obvious, irrespective of whether there has been concomitant sodium loss. Salt gain may present with clinical evidence of overload, such as raised jugular venous pressure or pul- monary oedema. 

Treatment

Patients with hypernatraemia due to pure water loss should be given water; this may be given orally, or intrave- nously as 5% dextrose. If there is clinical evidence of dehydration indicating prob- able loss of sodium as well, sodium should also be administered. Salt poisoning is a difficult clinical problem to manage. The sodium overload can be treated with diuretics and the natriure- sis replaced with water. Caution must be exercised with the use of intravenous dextrose in salt-poisoned patients – they are volume-expanded already and sus- ceptible to pulmonary oedema. 

Other osmolality disorders

A high plasma osmolality may sometimes be encountered for reasons other than hypernatraemia. Causes include:

- increased urea in renal disease

- hyperglycaemia in diabetes mellitus

- the presence of ethanol or some other ingested substance.

Any difference between measured osmolality and calculated osmolality is called the osmolal gap. If the gap is large, this suggests the presence of a significant contributor to the meas- ured osmolality, unaccounted for in the calculated osmolality. In practice, this is almost always due to the presence of ethanol in the blood. Very occasionally, however, it may be due to other sub- stances such as methanol or ethylene glycol from the ingestion of antifreeze. The calculation of the osmolal gap can be clinically very useful in the assess- ment of comatose patients.

The consequences of disordered osmolality are due to the changes in volume that arise as water moves in or out of cells to maintain osmotic balance. Note that of the three examples above, only glucose causes significant fluid movement. Glucose cannot freely enter cells, and an increasing ECF concentration causes water to move out of cells and leads to intracellular dehydration. Urea and ethanol permeate cells and do not cause such fluid shifts, as long as concentration changes occur slowly.

Clinical note 

Patients often become hypernatraemic because they are unable to complain of being thirsty. The comatose patient is a good example. He or she will be unable to communicate his/her needs, yet insensible losses of water will continue from lungs/skin and need to be replaced.

Hypernatraemia

- Hypernatraemia is most commonly due to water loss (e.g. because of continuing insensible losses in the patient who is unable to drink). 

- Failure to retain water as a result of impaired AVP secretion or action may cause hypernatraemia. 

- Hypernatraemia may be the result of a loss of both sodium and water as a consequence of an osmotic diuresis, e.g. in diabetic ketoacidosis. 

- Excessive sodium intake, particularly from the use of intravenous solutions, may cause hypernatraemia. Rarely, primary hyperaldosteronism (Conn’s syndrome) may be the cause. 

- A high plasma osmolality may be due to the presence of glucose, urea or ethanol, rather than sodium.