Copper is an essential trace element that is involved in a number of important enzymatic processes throughout the body. Recent single case reports and small studies have shown that deficiency of copper can cause reversible haematological changes and irreversible neurological injury. We chose to undertake a national study, looking at all cases of copper deficiency in Scotland over a 5-yr period using information from a national reference laboratory. From 16 identified patients, we determined that 86% had both haematological and neurological features of copper deficiency, while 18% had haematological features only at presentation. Twelve of the sixteen patients had high serum zinc concentrations (>18 lm/L) nine patients were using zinc-containing dental fixatives at time of diagnosis. 94% of patients had haematological features as an initial manifestation of copper deficiency, which included anaemia, thrombocytopenia and neutropenia. Patients who underwent later bone marrow testing had appearances in keeping with refractory cytopenia with multilineage dysplasia, refractory anaemia with excess of blasts, unclassified marrow dysplasia or probable myelodysplasia (MDS). 75% of patients had neurological symptoms or signs, including progressive walking difficulties and paraesthesia, or gait difficulties without sensory signs. Clinical examination was in keeping with spastic paraparesis (either with or without sensory neuropathy). Magnetic resonance imaging (MRI) showed multifocal T2 hyper intense foci in the subcortical white matter, and atrophy of the cerebrum and cerebellum was also seen on computerised tomography (CT). MRI of the spinal cord showed signal change in the dorsal columns in either the cervical or thoracic cord. 93% of cytopenias responded to copper replacement and addressing the original cause of the copper deficiency, but only 25% of patients had improvement in their neurological function, while 33% deteriorated and 42% remained unchanged. Our study demonstrates that copper deficiency is an underrecognised cause of several types of cytopenia, which are reversible but can progress to significant neurological injury if left untreated. We illustrate the importance of identifying these patients early to prevent irreversible neurological injury.

Background:In 2014, the WHO reported that 6% of all deaths were attributable to excess alcohol consumption. The aim of the present study was to examine the relationship between serum magnesium concentrations and mortality in patients with alcohol withdrawal syndrome (AWS). Materials and methods:A retrospective review of 700 patients with documented evidence of previous AWS indicating a requirement for benzodiazepine prophylaxis or evidence of alcohol withdrawal syndrome between November 2014 and March 2015. Results: Of 380 patients included in the sample analysis, 64 (17%) were dead at 1 year following the time of treatment for AWS. The majority of patients had been prescribed thiamine (77%) and a proton pump inhibitor (66%). In contrast, the majority of patients had low circulating magnesium concentrations (<0.75 mmol/L) (64%)and had not been prescribed magnesium (90%). The median age of death at one year was 55 years (P = 0.002). On univariate analysis, age (P < 0.05), GMAWS (P < 0.05), BDZ (P < 0.05), bilirubin (P < 0.001), alkaline phosphatase (P < 0.001), albumin (P < 0.001), CRP (P < 0.05), AST:ALT ratio >2 (P < 0.001), sodium (P < 0.05), magnesium (P < 0.001), platelets (P < 0.05) and the use of proton pump inhibitor medication (P < 0.001) were associated with death at 1 year. On multivariate binary logistic regression analysis, age > 50 years (OR 3.37, 95% CI 1.52-7.48, P < 0.01), AST:ALT ratio >2 (OR 3.10, 95% CI 1.38-6.94, P < 0.01) and magnesium < 0.75 mmol/L (OR 4.11, 95% CI 1.3-12.8, P < 0.05) remained independently associated with death at 1 year. Conclusion: Overall, 1-year mortality was significantly higher among those patients who were magnesium deficient (<0.75 mmol/L) when compared to those who were replete (≥0.75 mmol/L; P < 0.001).

We describe a young woman who presented with malignant systemic hypertension and fulminant idiopathic intracranial hypertension. This is a rare combination, but both diagnoses should be considered in patients with optic disc swelling in whom cerebral imaging does not suggest an alternative cause. In this case, malignant hypertension was identified and treated before the idiopathic intracranial hypertension was recognised. Visual failure was evident at presentation and prior to blood pressure manipulation. It is likely that a combination of both conditions increased the vulnerability of the optic nerve head to ischaemic damage. It is also possible that reducing blood pressure in such patients, without treating coexisting raised intracranial pressure, may compound an already compromised ciliary arterial perfusion pressure. We therefore recommend careful blood pressure measurement in all patients presenting with idiopathic intracranial hypertension and advise that lumbar puncture is performed in patients with malignant hypertension with optic disc oedema, particularly in overweight young females.

Purpose: Our primary objective was to determine incidence of status epilepticus in adults admitted to 5 ITU settings in Glasgow over 18 years. We wanted to investigate if there are any change in causes and outcomes of SE over last decade. We also compared outcomes of De Novo statuts Epilpeticus (DNSE) and Stauts Epilepticus in patients with previous Epilepsy (SEPE). Methods: The NHS GGC Research Ethics Committee gave permission for this study to continue without a full ethics submission. Between 2013 and 2016, coding records were searched across NHS Greater Glasgow and Clyde for adults over the age of 16 years admitted to an Intensive Care Facility in any of the hospitals in Glasgow. Results: 633 cases were included in study. Cases were separated depending on whether there had been previous epilepsy (SEPE n = 214) or De Novo Status Epilepticus (DNSE, n = 419). Causes in both groups were listed, with 52% of those with DNSE having some contribution from substance misuse. In SEPE, this was felt to play a role in 33.7%. Duration of stay in both groups was similar, but the longest in-patient stays were in the DNSE group. Admission mortality was significantly higher in DNSE than in SEPE (13.8% versus 7.5%). This mortality risk was most closely associated with substance misuse in the group with DNSE. Conclusion: DNSE has a worse prognosis than SEPE. A presentation with DNSE is sign of a system in peril, even where episodes are provoked by alcohol and or drug use. Such episodes should spark off a chain of multispecialty care in order to address this recurring and persisting public health catastrophe.