To the Editor,
Hydroelectrolytic disorders are frequently associated with severe neurological problems, being involved in their pathogenesis or being a consequence of it. Hyponatraemia is the most prevalent hydroelectrolytic disorder in clinical practice and is triggered by several causes. One of them is the syndrome of inappropriate antidiuretic hormone hypersecretion (SIADH) which can also be triggered by several types of neurological diseases.
We present the case of a 63-year-old man who told us that he had fever and diarrhoea, which stopped spontaneously, for two weeks. Later, he started with paraesthesia in his hands and feet, alterations in mobility and instability when walking. He therefore came to the emergency department where his gait instability became worse and stopped him from being able to walk at all. He also presented with paresis in his four limbs and facial muscles. He is hypertensive but is not treated or monitored and drinks 20g of alcohol daily. The neurological examination showed: facial diplegia with hypophonia, absence of patellar and Achilles reflex and decreased biceps and triceps reflex with no loss of strength, absence of the vibration sensitivity and bilateral reduction in tactile and pain sensitivity with ataxic gait.
Complementary tests showed: 10 100 leukocytes with normal formula; haemoglobin: 16g/dl; creatinine: 0.6mg/dl; uric acid: 2.8mg/dl; sodium: 120mmol/l; potassium: 4.3mmol/l; chlorine: 87mmol/l; bicarbonate: 16mEq/l; total cholesterol: 232mg/dl, glucose: 110 mg/dl; and serum osmolarity: 259mOsm/kg. Sodium urine test: 144mmol/l and osmolarity in urine: 719mOsm/kg. Urinary sediment was within normal levels. The cranial tomography did not show any alterations. The cerebrospinal fluid test showed red blood cells: 1/µl; leukocytes: 1/µl; proteins: 141mg/dl; and glucose: 78mg/dl. Lastly, the electromyogram showed a diffuse peripheral and distal demyelinating neuropathy, mainly involving sensitivity. The clinical symptoms and results from the analyses and electromyogram suggested that the patient had Guillain-Barré syndrome (GBS) with SIADH.
Hyponatraemia is often associated with SIADH or salt wasting syndrome in patients with central nervous system disorders. These two conditions are the most important causes of non-iatrogenic hyponatraemia.1 GBS is a neurological disease in which the immunological system attacks the peripheral nervous system causing focal and segmental demyelinating foci that provoke an increasing paralysis, which can consequently cause respiratory failure and death. The relationship between GBS and SIADH is not very common and is described through clinical cases. The cause of GBS-related SIADH is not known, but seems to be due to independent vasopressin mechanisms, such as a long-lasting hypo-osmolarity or antidiuretic substances. It could also be caused by the renal tubule becoming more sensitive to vasopressin’s action.2 A recent study has shown a worse GBS prognosis in those patients that develop SIADH.3 It was already known that the peak of hyponatraemia often corresponds to respiratory failure and the need for mechanical ventilation, given that hyponatraemia favours depression of the respiratory centre.4 This hyponatraemia must be differentiated from pseudohyponatraemia produced by polyclonal immunoglobulin treatment at high doses, which is used for GBS.
These two processes can be differentiated from one another because there is a difference between the osmolarity calculated by an osmometre and using mathematical formulae in pseudohyponatraemia. In GBS, hydroelectrolytic disorders, especially hyponatraemia, are processes that mark the prognosis and severity of the disease and must be identified early.
