Early mortality and morbidity following a type II odontoid fracture in the elderly.

BACKGROUND: We aimed to analyse the rates of early and causes of death in patients aged over 65 years with a type II odontoid fracture. METHODS: A consecutive series of 93 patients with a type II fracture of the odontoid process was retrospectively identified. Data collected included patient demographics, co-morbidities, associated injuries, neurological injury, date of death and cause of death. Mean patient age was 81. Five patients (5%) were treated operatively while the rest were treated in a hard cervical collar. Five patients (5%) had an incomplete cervical cord injury secondary to the fracture. RESULTS: The rate of mortality at 30 days was 10% (9 patients) and at 90 days it was 16% (15 patients). Following multivariate analysis, the factors found to significantly increase the risk of 30-day mortality included increasing age, increasing injury severity score and leukaemia. Following univariate analysis the only factor found to increase the risk of 90-day mortality was advancing age. The commonest causes of death were pneumonia and ischaemic coronary disease. CONCLUSION: Our results suggest that this patient cohort is frail and at risk of early mortality. We suggest that their inpatient care be provided in close conjunction with elderly care physicians.

Phenotypic diversity and correlation with the genotypes of pseudohypoaldosteronism type 1.

Background Type I pseudohypoaldosteronism (PHA1) is a rare condition characterised by profound salt wasting, hyperkalaemia and metabolic acidosis due to renal tubular resistance to aldosterone (PHA1a) or defective sodium epithelial channels (PHA1b or systemic PHA). Our aim was to review the clinical presentation related to the genotype in patients with PHA1. Methods A questionnaire-based cross-sectional survey was undertaken through the British Society of Paediatric Endocrinology and Diabetes (BSPED) examining the clinical presentation and management of patients with genetically confirmed PHA1. We also reviewed previously reported patients where genotypic and phenotypic information were reported. Results Genetic confirmation was made in 12 patients with PHA1; four had PHA1a, including one novel mutation in NR3C2; eight had PHA1b, including three with novel mutations in SCNN1A and one novel mutation in SCNN1B. It was impossible to differentiate between types of PHA1 from early clinical presentation or the biochemical and hormonal profile. Patients presenting with missense mutations of SCNN1A and SCNN1B had a less marked rise in serum aldosterone suggesting preservation in sodium epithelial channel function. Conclusions We advocate early genetic testing in patients with presumed PHA1, given the challenges in differentiating between patients with PHA1a and PHA1b. Clinical course differs between patients with NR3C2 and SCNN1A mutations with a poorer prognosis in those with multisystem PHA. There were no obvious genotype-phenotype correlations between mutations on the same gene in our cohort and others, although a lower serum aldosterone may suggest a missense mutation in SCNN1 in patients with PHA1b.