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Hypernatraemia

1. GENERAL INFORMATION

1.1 Definition, incidence, pathophysiology and causes

Hypernatraemia is defined as a serum sodium level >145 mEq/L. In oncology, it may be a consequence of insufficient water intake due to chemotherapy-induced nausea or vomiting or decreased conscience; due to a general poor condition; secondary renal pathology (e.g. renal diabetes insipidus due to vinblastine); or loss of free water by central diabetes insipidus due to suprasellar or intrasellar tumours.Hypernatraemia results from disequilibrium of water homeostasis. Water homeostasis is related to water intake and loss from the kidney, the lungs, the skin and the gastrointestinal tract. Salt homeostasis is regulated by the kidneys that adjust salt urine concentration to match salt intake and loss. Hypernatraemia is the result of a relative free water loss or salt loading.

Hypernatraemia causes cellular dehydration by direct extraction of water by the osmotic load of sodium or by the body’s free water deficit. The result is that cells shrink and transport electrolytes across the cell membrane to compensate for the osmotic force. Intracellular organic solutes are generated in an effort to restore cell volume and avoid structural damage.

2. DIAGNOSIS

2.1 Clinical presentation

Symptoms of hypernatraemia are non-specific and patients may complain of anorexia, restlessness, nausea, and vomiting, followed by altered mental status, lethargy or irritability, and stupor or coma.
Patients may show muscle twitching, hyper-reflexia, ataxia or tremor; non-focal neurological symptoms (e.g. mental status changes, ataxia, seizure), although focal deficits (e.g. hemiparesis) may occur.
Physical examination is non-specific but the patient might show signs of dehydration (mucous membranes, skin turgor, orthostatic vital signs, neck veins).

2.2 Diagnosis

The diagnosis depends on the patient’s volume status
•    Hypovolaemic hypernatraemia (water deficit >sodium deficit) due to extrarenal losses (e.g. diarrhoea, vomiting, fistulas, significant burns); renal losses (e.g. osmotic diuretics, diuretics, postobstructive diuresis, intrinsic renal disease) or decreased thirst.
•    Hypervolaemic hypernatraemia (sodium gain >water gain) due to hypertonic saline; sodium bicarbonate; accidental salt ingestion; mineralo-corticoid excess (Cushing syndrome).
•    Euvolaemic hypernatraemia due to extrarenal (increased insensible loss (e.g.  hyperventilation) or renal losses  (central or nephrogenic diabetes insipidus).

Diagnosis is made by serum sodium level: levels more than 190 mEq/L indicate long-term salt ingestion; more than 170 mEq/L diabetes insipidus and levels between 150-170 mEq/L dehydration.
Urine osmolarity and sodium levels should be determined
•    Hypertonic urine
o    Extrarenal hypotonic fluid losses (e.g. vomiting, low sodium diarrhoea, sweat, evaporation from burns, low sodium ostomy output).
o    Salt overload
•    Isotonic urine
o    Diuretics, osmotic diuresis (e.g. mannitol, glucose, urea)
o    Salt wasting
•    Hypotonic urine: diabetes insipidus

A water deprivation test is indicated if diabetes insipidus is suspected: water deprivation induces serum hyperosmolality and hypernatreamia, but urine osmolality does not increase appropriately.
ADH stimulation differentiates between nephrogenic and central diabetes insipidus: with nephrogenic diabetes insipidus urine osmolality does not increase after ADH or desmopressin acetate administration.
Imaging of the head by CT scan or MRI is suggested in all patients with severe hypernatraemia.

3. PROGNOSIS

The mortality rate due to hypernatraemia is high, especially among elderly patients and rates of 42-75% have been reported for acute and 10-60% for chronic hypernatraemia. Morbidity in survivors is high with many patients experiencing permanent neurological deficits.

4. TREATMENT

Hypernatraemia should not be corrected at a rate greater than 1 mEq/L per hour since cerebral oedema can occur if water replacement does not allow cellular adaptation. This is a standard option,on a type C basis.
Hypovolaemic patients with unstable vital signs should be treated with isotonic sodium chloride solutions before correcting free water deficits since hypotonic fluids leave the intravascular space and might cause more pronounced oedema. Once stabilization has occurred, free water deficits can be replaced orally or intravenously as a standard option, on a type C basis.
The standard treatment option, on a type C basis for euvolaemic patients is hypotonic fluids, either orally or intravenously (e.g. dextrose 5% in water solution, quarter or half isotonic sodium chloride solution).
Hypervolaemic patients require removal of excess sodium by a combination of diuretics and dextrose 5% in water infusion. Patients with acute renal failure may require dialysis.
The free water deficit is calculated by: body weight (kg) X TBW X ([serum Na/140] – 1), in which the TBW is 0.6% in young men; 0.5% in young women and elderly men and 0.4% in elderly women. This is a standard option, on a type C basis.

INDEX

Berk L, Rana S. Hypovolemia and dehydration in the oncology patient. J Support Oncol. 2006; 4: 447-54 [Medline]

Sedlacek M, Schoolwerth AC, Remillard BD. Electrolyte disturbances in the intensive care unit. Semin Dial 2006; 19: 496-501 [Medline]

Dr. Dirk Schrijvers (Reviewer)
University Hospital Antwerp – Antwerp, Belgium
mail: Dirk.Schrijvers@zna.be

Dr. Silvia Spinazzé (Associate Editor)
START Programme
mail: silvia.spinazze@poste.it