Vitamin D deficiency is prevalent in patients with chronic spinal cord injury (SCI) and has been implicated as an aetiologic factor of osteoporosis and various skeletal and extra-skeletal issues in SCI patients. Few data were available regarding vitamin D status in patients with acute SCI or immediately assessed at hospital admission. This retrospective cross-sectional study evaluated vitamin D status in SCI patients at admission to a UK SCI centre in January–December 2017. A total of 196 eligible patients with serum 25(OH)D concentration records at admission were recruited. The results found that 24 % were vitamin D deficient (serum 25(OH)D < 25 nmol/l), 57 % of the patients had serum 25(OH)D < 50 nmol/l. The male patients, patients admitted in the winter–spring time (December–May), and patients with serum sodium < 135 mmol/l or with non-traumatic causes had a significant higher prevalence of vitamin D deficiency than their counterparts (28 % males v. 11⋅8 % females, P = 0⋅02; 30⋅2 % in winter–spring v. 12⋅9 % in summer–autumn, P = 0⋅007; 32⋅1 % non-traumatic v. 17⋅6 % traumatic SCI, P = 0⋅03; 38⋅9 % low serum sodium v. 18⋅8 % normal serum sodium, P = 0⋅010). There was a significant inverse association of serum 25(OH)D concentration with body mass index (BMI) (r = −0⋅311, P = 0⋅002), serum total cholesterol (r = −0⋅168, P = 0⋅04) and creatinine concentrations (r = −0⋅162, P = 0⋅02) that were also significant predictors of serum 25(OH)D concentration. Strategies for systematic screening and efficacy of vitamin D supplementation in SCI patients need to be implemented and further investigated to prevent the vitamin D deficiency-related chronic complications.

Pseudohypoaldosteronism type I is caused by a peripheral resistance to aldosterone and can present with electrolyte abnormalities, poor growth, or dehydration. Although a rare disease, several case reports have been published regarding Pseudohypoaldosteronism type I in neonates and infants. We report a case of failure to thrive and hyponatremia in an infant with hypoplastic left heart syndrome who was subsequently found to have Pseudohypoaldosteronism type I.

Objectives: The objectives of this paper are to review the presentation of hyponatraemia and diagnose its cause in psychiatric inpatients.

Method: Episodes of significant hyponatraemia (sodium <130mmol/L) were identified from computerised biochemical data and a retrospective review of patients' notes was carried out.

Result. The diagnoses of hyponatraemia reached were different for the two groups of patients studied, adults of over 65 years and under 65 years. Carbamazepine, polydipsia and medical conditions were found as causes in the below 65 age group. Diuretics, medical conditions and lofepramine were identified as causes in the over 65 age group. Inpatients with polydipsia below the age of 65 had lower sodium (p = 0.013) and urea levels (p = 0.00059) than other groups and patients with carbamazepine induced hyponatraemia tended to have episodic hypocalcaemia (p = 0.056). These groups were compared using Fisher's exact test. This study also showed the overall frequency of serum sodium of less than 135mmol/L to be 9.5% in psychiatric inpatients.

Conclusion: Hyponatraemia is a not uncommon finding in psychiatric inpatients. Attention to drug therapy and biochemical findings are helpful in its diagnosis. Accurate diagnosis is usually possible and may vary according to age-group.

Two cases of atypical transurethral resection (TUR) syndrome occurring during the post-operative course are reported. Atypical clinical events such as confusion, drowsiness and sudden hypotension could not be explained by the amount of glycine fluid absorption, because in both cases this was less than 1000 mL. However, high serum concentrations of glycine were noted without marked hyponatraemia and with normal measured osmolalities. We suggest that the absorption of glycine is related to its high lipid solubility rather than to its direct passage through an evident prostatic effraction or periprostatic extravasation.

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) canhave multiple causes. Surgical neck dissections may have an association with this syndrome and represent the basis for this study. A retrospective review of 50 patients undergoing neck dissections was performed to evaluate for the development of hyponatraemia as a consequence of SIADH. Based on the results of this review, a prospective study of 20 consecutive patients undergoing 22 neck dissections was performed to determine the incidence ofSIADH. A control group of 25 consecutive patients undergoing major non-neck dissection surgery was also studied. SIADH developed in nine of 50 patients (18 per cent) of our retrospective group with a high incidence of development in those who had jugular vein ligation (JVL) (22 per cent), pre-operative radiation therapy (25 per cent) or squamous cell cancers (32 per cent). SIADH developed in six patients undergoing 22 neck dissections (27 per cent) in our prospective group. A high incidence was also noted for those with JVL (42 per cent), pre-operative radiation therapy (67 per cent) or squamous cell cancer (40 per cent). No patients developed symptomatic hyponatraemia. No patients in the prospective control group developed SIADH. Neck dissection surgery is associated with a significant risk for the development of SIADH. Factors such as jugular vein ligation (JVL), pre-operative radiotherapy and squamous cell cancer appear to increase this risk.