Development and first application testing of a new protocol for CT-based stability evaluation of the injured upper cervical spine.

PURPOSE: For trauma surgeons, the evaluation of the stability of the upper cervical spine may be demanding. The aim of this study was to develop a protocol for decision-making on upper cervical spine stability in trauma patients based on established parameters obtained by CT imaging as well as testing the protocol by having it applied by trauma surgeons. METHODS: A structured literature search on upper cervical spine stability was performed. The best evaluated instability criteria in CT imaging were determined. Based on these parameters a protocol for stability evaluation of the injured upper cervical spine was developed. A first application testing was performed. In addition to the assessment of instability, the time required for the assessment was analyzed. RESULTS: A protocol for CT-based stability evaluation of the injured upper cervical spine based on the current literature was developed and displayed in a flow chart. Testing of the protocol found the stability of the cervical spine was correctly assessed in 55 of 56 evaluations (98.2%). In one test run, a stable upper cervical spine was judged to be unstable. Further analysis showed that this case was based on a measurement error. The assessment time of CT-images decreased significantly during repeat application of the protocol (p < 0.0001), from 336 ± 108 s (first case) to 180 ± 30 s (fourth case). CONCLUSION: The protocol can be applied quickly and safely by non-specialized trauma surgeons. Thus, the protocol can support the decision-making process in CT-based evaluation of the stability of the injured upper cervical spine.

Analysis of diagnostics, therapy and outcome of patients with traumatic atlanto-occipital dislocation.

BACKGROUND CONTEXT: Patients' outcome following traumatic atlanto-occipital dislocation (AOD) has been poor. In recent years, an increasing number of patients surviving the initial trauma are admitted to hospital. In order to further improve the management of these patients, the knowledge of diagnostics and therapy as well as possible complications should be increased. PURRPOSE: The aim of this study was to evaluate diagnostic parameters, therapy, early complications and outcome of patients with traumatic AOD. STUDY DESIGN: Monocentric retrospective cohort study. PATIENT SAMPLE: A total of 12 patients were included in this study. OUTCOME MEASURES: The main outcome measure was functional patient outcome. Furthermore, radiographic and treatment data were analyzed. METHODS: All patients suffering from traumatic AOD within an 8-year time period were included. Demographic data, radiological diagnostic parameters (condylar sum, basion dens interval, basion axis interval, power´s ratio, x-line method), as well as treatment data and complications of every patient were analyzed. Radiological parameters were compared with each other. Outcome was analyzed by a follow up examination. RESULTS: The accident mechanisms were motor vehicle accidents (MVA), fall from high and low height. Basion dens interval, basion axis interval, power's ratio and x-line method were not reliable in identifying traumatic AOD (only up to 33% of the patients were identified). Twelve patients could be reviewed. Three patients were treated with surgery, five patients were treated nonsurgically. Four patients died before surgical therapy. All seven surviving patients (survival rate: 58.3%) were re-examined (mean follow-up time: 6.7 months). All patients had a GCS of 15. Three surviving patients suffered from persisting neurological deficits. CONCLUSIONS: The most reliable way to diagnose AOD in Computer Topography is using the condylar sum. Surgical and nonsurgical measures can be employed with reasonable outcomes. Patient specific injury burden and clinical presentation should be taken into account when making treatment decisions for AOD.

Rapamycin-induced phosphaturia.

BACKGROUND: The mammalian target of rapamycin (mTOR) is known to stimulate a variety of transport mechanisms including the intestinal phosphate transporter NaPi-IIb. The present study was performed to elucidate whether mTOR similarly regulates the major renal tubular phosphate transporter NaPi-IIa. METHODS: To this end, NaPi-IIa was expressed in Xenopus oocytes with or without mTOR and phosphate transport estimated from phosphate-induced (1 mM) current (I(pi)). RESULTS: As a result, I(pi) was observed in NaPi-IIa-expressing but not in H(2)O-injected Xenopus oocytes. Co-expression of mTOR significantly enhanced I(pi) in NaPi-IIa-expressing Xenopus oocytes, an effect abrogated by treatment with rapamycin (50 nM for the last 24 h of incubation). In a second series of experiments, the effect of rapamycin was analysed in mice. The in vivo administration of rapamycin (3 microg/g body weight/day) for 3 days resulted in phosphaturia in mice despite a tendency of plasma phosphate concentration to decrease. CONCLUSIONS: mTOR contributes to the regulation of renal phosphate transport, and rapamycin thus influences phosphate balance.

Regulation of renal tubular glucose reabsorption by Akt2/PKBß.

Akt/PKB is known to regulate the facilitative glucose carrier GLUT4. Nothing is known, however, of the role of Akt/PKB in the regulation of renal epithelial transport. To explore whether Akt2/PKBß influences the Na(+)-coupled glucose cotransporter SGLT1, human SGLT1 was expressed in Xenopus laevis oocytes with or without Akt/PKB, and electrogenic glucose transport was determined by dual-electrode voltage clamp. The coexpression of Akt/PKB in SGLT1-expressing oocytes was followed by an increase in glucose-induced currents. To study the functional significance of Akt/PKB-sensitive renal glucose transport, further experiments were performed in gene-targeted mice lacking functional Akt2/PKBß (akt2(-/-)) and in their wild-type littermates (akt2(+/+)). Plasma glucose concentration was significantly higher in akt2(-/-) mice than in akt2(+/+) mice but was virtually identical to the plasma glucose concentration in fructose-treated akt2(+/+) mice. Urinary glucose excretion was significantly higher in akt2(-/-) mice compared with akt2(+/+) mice with or without fructose treatment. Moreover, the glucose-induced depolarization of proximal tubular cells was significantly smaller in isolated, perfused renal tubules from akt2(-/-) mice than in those from akt2(+/+) mice. In conclusion, Akt2/PKBß plays a role in the regulation of renal glucose transport.