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Hyponatraemia

Cancer patients frequently suffer from hyponatraemia, the physiopathology of which is not always clearly understood. Generally, it is fortuitously discovered on a systematic ionogram. However, hyponatraemia increases patient fatigue and can possibly be complicated by somnolence or seizures.

Hyponatraemia is often observed in preterminal stages of severe disease. Patients excrete the sodium excesses administered in order to correct hyponatraemia and liquid restriction leads to more severe dehydration than that already observed. Surprisingly, if patients are able to resume normal eating, a spontaneous correction of hyponatraemia is observed.

Thus, this preterminal hyponatraemia should be distinguished from an inappropriate secretion of ADH which is a genuine paraneoplastic syndrome (occurring in lung cancer for instance). Hyponatraemia leads to severe neurological disorders and to an exaggerated water excretion by the kidney (excessive urinary osmolality). In such cases, fluid restriction is useful, but more particularly the treatment of cancer, where possible, will improve the clinical situation.

Another frequent cause of hyponatraemia in cancer patients is the presence of oedema leading to a dilution syndrome. Such a clinical situation can be observed when ascitis or major pleural effusion occur. Whereas symptomatic treatment (ascitic puncture, diuretics) may be useful, only aetiological treatment will actually correct hyponatraemia for a reasonably long time.

Tumour lysis syndrome

The term tumour lysis syndrome covers the quick appearance in blood of intra-cellular products (nuclear acid metabolites) after the death of a great number of cancer cells due to efficient chemotherapy.

This syndrome is observed for cancers with very quick tumour growth, important cellular turnover, important tumour burden and great sensitivity to chemotherapy (or radiotherapy) such as leukaemia, high grade lymphoma, small cell lung carcinoma or myeloma.

Uric acid is the final degradation product of purinic nucleic acid: in urine, the acidity transforms the sodium form into uric acid which is not very soluble at this pH level. Crystals appear and provoke an obstructive nephropathy and, secondarily, renal insufficiency. In the case of massive cellular necrosis induced by chemotherapy, we can also observe hyperkaliaemia and hyperphosphataemia with hypocalcaemia, thus involving a risk of cardiac arrhythmia and sudden death.

The urological syndrome generally appears two days after chemotherapy.

Treatment includes massive hydration but more importantly prevention by systematic prophylactic administration of allopurinol a few days before the beginning of chemotherapy. This drug blocks xanthine oxydase and inhibits the formation of uric acid. Another important point is to alkalinise urines and obtain major diuresis through infusion before chemotherapy (at least three litres per day).