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Disorders of water and sodium homeostasis 

Disorders of water and sodium homeostasis

Disorders of water and sodium homeostasis

Michael L. Moritz

and Juan Carlos Ayus



Prevention of hospital-acquired hyponatraemias—recommendation that use of hypotonic intravenous fluids should be restricted to patients with hypernatraemia (Na >145 mmol/L) or those with ongoing urinary or extrarenal free water losses.

Treatment of suspected hyponatraemic encephalopathy—recommendation of a 2 ml/kg intravenous bolus of 3% sodium chloride to maximum of 100 ml to produce a controlled and immediate rise in serum sodium with little or no risk of inadvertent over-correction. Discussion of management guidelines to prevent overcorrection of hyponatraemia.

Chronic hyponatraemia—increased recognition that this is associated with significant morbidity, particularly falls and bone fractures in the elderly. Use of vasopressin receptor antagonists discussed.

Updated on 25 May 2011. The previous version of this content can be found here.
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date: 24 April 2017

Regulation of water balance and sodium disorders

Water intake and the excretion of water are tightly regulated processes that are able to maintain a near-constant serum osmolality. Sodium disorders (dysnatraemias—hyponatraemia or hypernatraemia) are almost always due to an imbalance between water intake and water excretion.

Understanding the aetiology of sodium disorders depends on understanding the concept of electrolyte-free water clearance—this is a conceptual amount of water that represents the volume that would need to be subtracted (if electrolyte-free water clearance is positive) or added (if negative) to the measured urinary volume to make the electrolytes contained within the urine have the same tonicity as the plasma electrolytes. It is the concentration of the electrolytes in the urine, not the osmolality of the urine, which ultimately determines the net excretion of water.


Hyponatraemia, defined as serum sodium concentration of less than 135 mmol/litre, is a common electrolyte disorder. It is almost invariably due to impaired water excretion, often in states where ADH release is: (1) a normal response to a physiological stimulus such as pain, nausea, volume depletion, postoperative state, or congestive heart failure; or (2) a pathophysiological response as occurs with thiazide diuretics, other types of medications, or in the syndrome of inappropriate diuresis; with both often exacerbated in hospital by (3) inappropriate iatrogenic administration of water (or 5% dextrose).

Clinical features—these can range from the patient who is entirely asymptomatic at one end of the spectrum to hyponatraemic encephalopathy—most commonly manifesting with nausea, vomiting, and headache—at the other. Cerebral demyelination is a serious complication associated with hyponatraemia and its treatment, at its worst manifesting as pseudocoma with a ‘locked in’ state. Children and premenopausal women are at particular risk of poor outcomes, as are those who are hypoxic at presentation.

Management approach—the first priority is to exclude a hyperosmolar state and verify whether the patient is hypotonic, by (when possible) measuring the serum osmolality. The diagnostic approach is further based on the history, clinical assessment of the patient’s volume status, and estimation of urinary electrolytes. Key issues are to recognize that: (1) hyponatraemic encephalopathy is a medical emergency that should be diagnosed and treated promptly with hypertonic saline to prevent death or devastating neurological complications; but also (2) that patients who are asymptomatic do not require treatment with hypertonic saline, whatever their level of serum sodium. Precipitating causes (e.g. thiazide diuretics) should be withdrawn when possible.

Practical management—algorithms, even if complex, cannot accurately predict a patient’s response to treatment of hyponatraemia: close monitoring of serum sodium is essential. Patients with suspected hyponatremic encephalopathy, with either mild or advanced symptoms, children or adult, should receive a 2 ml/kg bolus of 3% NaCl with a maximum volume of 100 ml. A single bolus would result in at most a 2 mmol/L acute rise in serum sodium, which would quickly reduce brain edema. The bolus could be repeated 1 - 2 times if symptoms persist. The advantage of this approach over a continuous infusion of 3% NaCl is that there is a controlled and immediate rise in serum sodium and there is little or no risk of inadvertent overcorrection, as can occur if a 3% NaCl infusion runs at an excessive rate or for too long.

Cerebral demyelination—this is a serious complication that has been associated with the correction of hyponatraemia, hence all patients receiving an infusion of 3% saline should have their serum sodium measured at least every 2 h until they are clinically stable and the serum sodium values are stable, with appropriate modification of treatment in response to the measurements. Failure to do so, and reliance on a calculated infusion rate, can lead to significant patient injury.

Prevention—hyponatraemia is usually iatrogenic and can be avoided or detected as follows: (1) hypotonic fluids should never be administered following surgery unless used to correct a free-water deficit—0.9% (normal) saline (NaCl) should be given postoperatively if parenteral fluids are indicated; (2) all hospitalized patients should be considered at risk for the development of hyponatraemia and should not be given hypotonic fluids unless a free-water deficit is present or if ongoing free-water losses are being replaced; (3) patients taking thiazide diuretics, especially older people, should be weighed before and after starting therapy and serum electrolytes monitored to detect water retention and the development of hyponatraemia.


Hypernatraemia, defined as serum sodium concentration greater than 145 mmol/litre, is a common electrolyte disorder that occurs when water intake is inadequate to keep up with water losses. Since the thirst mechanism is such a powerful stimulus, the almost invariable context is illness and care that restrict the patient’s access to water.

Clinical features—these are mainly related to central nervous system dysfunction caused by cerebral dehydration and cell shrinkage.

Management approach—the first step in evaluation is to take a detailed history focusing on fluid intake and losses. To assess urinary water losses, it is necessary to measure the urinary cationic electrolytes (sodium and potassium) and the urinary osmolality, remembering that the urinary osmolality alone cannot always determine the presence or absence of electrolyte-free water losses in the urine, the reason being that water can be excreted with nonelectrolyte osmoles or with electrolyte osmoles.

Practical management—needs to be guided by the following principles: (1) correction of underlying deficits in circulatory blood volume by infusion of 0.9% saline; (2) correction of chronic hypernatraemia at a pace that avoids therapy-induced cerebral oedema, which requires an understanding of both the initial water deficit and of ongoing water losses if the patient is polyuric; (3) administration of water by drinking or feeding tube is preferable to treatment with intravenous fluids if possible; (4) glucose-containing solutions should be avoided if possible; (5) as for the treatment of hyponatraemia, algorithms cannot accurately predict the response to treatment of hypernatraemia, hence regular monitoring of serum sodium with appropriate adjustment of treatment in response to the values obtained is mandatory.

Prevention—(1) patients with impaired access to water (e.g. infants, elderly, and hospitalized patients) should be considered at risk for the development of hypernatraemia, and their serum sodium should be monitored; (2) urinary electrolytes should be measured in conjunction with urinary osmolality in patients with polyuria to assess water losses in the urine and urinary concentrating ability.

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