SeriesSodium
Section snippets
Control of serum sodium
The renal countercurrent mechanism, in concert with osmoreceptors in the hypothalamus that control secretion of antidiuretic hormone (ADH, vasopressin), maintains a very finely tuned balance of water that keeps the serum sodium concentration or [Na+] in the very narrow range of 138–142 mmol/L despite great variation in water intake. A defect in the urinary diluting capacity, when coupled with excess of water intake, causes hyponatraemia. A defect in urinary concentration, when not accompanied
Hypoosmolar hyponatraemia
Once preliminary evaluation reveals that the hyponatraemia is truly hypoosmolar, assessment of ECF volume allows patients to be classed as hypovolaemic, euvolaemic or hypervolaemic hyponatraemia (figure 2).
Underlying all hyponatraemic states is a limitation in urinary dilution. This is most commonly due to secretion of ADH despite serum hypoosmolality, the secretion being stimulated by non-osmotic mechanisms. Less commonly, diminished delivery of fluid to the distal nephron, due to reduced
Hyponatraemia with increased TBNa+ (hypervolaemic)
Here TBNa+ is increased but TBW is increased even more, causing hyponatraemia. Clinical settings where this is seen are heart, liver, and kidney failure and nephrotic syndrome.
In congestive heart failure the fall in cardiac output, and frequently mean arterial pressure too, lead to non- osmotic release of ADH.4 The enhanced renal effect of ADH is also reflected by the recent finding of up- regulation of AQP2, the vasopressin-regulated water channel in collecting ducts in rats with heart failure.
Hyponatraemia with normal TBNa+ (euvolaemic)
Euvolaemic hyponatraemia is the most commonly encountered dysnatraemia in hospital patients. No physical signs of increased TBNa+ are detected; they may have slight excess of volume but they are not oedematous. Likely clinical causes here include the following.
Glucocorticoid deficiency causes the impaired water excretion of primary and secondary adrenal insufficiency. Raised levels of ADH have been demonstrated even in the absence of volume contraction. ADH-independent factors are also involved
Management of hyponatraemia
Symptoms depend on the level of hyponatraemia (figure 3) and the rate at which it develops. Above 125 mmol/L symptoms are rare; in the range 125-130 mmol/L, the predominant symptoms are gastrointestinal; neuropsychiatric symptoms dominate once the serum sodium falls below 125 mmol/L. The case fatality rate in untreated severe symptomatic hyponatraemia is high and neurological symptoms in any hyponatraemic patient call for immediate treatment. Signs and symptoms of hyponatraemia are: nausea and
Hypernatraemia
The renal-concentrating mechanism is the first defence against water depletion and hyperosmolality. If the urine is inadequately concentrated or if inordinate amounts of hypotonic fluid are lost and/or not replenished, hypernatraemia results (figure 1). Thirst is an important back-up defence. Patients fall into three broad categories, depending on the TBNa+ (figure 4).
Central diabetes insipidus
In both central (CDI) and nephrogenic (NDI) diabetes insipidus the patient presents with polyuria and polydipsia. The two entities can be differentiated by measurement of vasopressin and the response to water deprivation followed by vasopressin (Panel 4). Separation of primary polydipsia (compulsive water drinking) from CDI is on clinical features. CDI usually has an abrupt onset whereas the compulsive water drinker tends to give a vague history of onset. Patients with CDI have a constant need
Signs and symptoms of hypernatraemia
Hypernatramia (Panel 6) is far less common than hyponatraemia. It always reflects a hyperosmolar state so CNS symptoms are prominent. The signs and symptoms are: altered mental status, lethargy, irritability, restlessness, seizures (usually seen in children), muscle twitching, hyperreflexia, and spasticity; fever; nausea or vomiting; laboured respiration; and intense thirst. Morbidity and mortality of patients with acute hypernatraemia are high in children and two-thirds of survivors have
Management of hypernatraemia
The primary goal in the management of hypernatraemia is restoration of serum tonicity (Panel 7). The treatment regimen depends upon the volume status. The following guidelines should be helpful.
Hypovolaemic hypernatraemia
Here there is a low TBNa+ and orthostatic hypertension, and isotonic saline should be given until systemic haemodynamics are stabilised. Thereafter, fluid management generally involves 0·45% NaCl or 5% dextrose solution to correct the water deficit.
Hypervolaemic hypernatraemia
The goal for these patients is to remove the excess Na+ which is achieved with diuretics along with 5% dextrose. If there is renal impairment, dialysis may be needed.
Euvoiaemic hypernatraemia
In this group of patients water losses far exceed solute losses, and the mainstay of therapy is 5% dextrose. To correct the hypernatraemia appropriately the TBW deficit must be estimated. This is calculated on the basis of the serum [Na+] and on the assumption that 60% of the body weight is water.
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