A revision of the Trauma Score

The Trauma Score (TS) has been revised. The revision includes Glasgow Coma Scale (GCS), systolic blood pressure (SBP), and respiratory rate (RR) and excludes capillary refill and respiratory expansion, which were difficult to assess in the field. Two versions of the revised score have been developed, one for triage (T-RTS) and another for use in outcome evaluations and to control for injury severity (RTS). T-RTS, the sum of coded values of GCS, SBP, and RR, demonstrated increased sensitivity and some loss in specificity when compared with a triage criterion based on TS and GCS values. T-RTS correctly identified more than 97% of nonsurvivors as requiring trauma center care. The T-RTS triage criterion does not require summing of the coded values and is more easily implemented than the TS criterion. RTS is a weighted sum of coded variable values. The RTS demonstrated substantially improved reliability in outcome predictions compared to the TS. The RTS also yielded more accurate outcome predictions for patients with serious head injuries than the TS.     

Effects of cigarette smoking on spatial working memory and attentional deficits in schizophrenia: involvement of nicotinic receptor mechanisms

BACKGROUND: Cigarette smoking rates in schizophrenia are higher than in the general population. OBJECTIVES: To determine whether cigarette smoking modifies cognitive deficits in schizophrenia and to establish the role of nicotinic acetylcholine receptors (nAChRs) in mediating cigarette smoking-related cognitive enhancement. DESIGN: Neuropsychological assessments were performed at smoking baseline, after overnight abstinence, and after smoking reinstatement across 3 separate test weeks during which subjects were pretreated in a counterbalanced manner with the nonselective nAChR antagonist mecamylamine hydrochloride (0, 5, or 10 mg/d). PARTICIPANTS: Twenty-five smokers with schizophrenia and 25 control smokers. SETTING: Outpatient mental health center. MAIN OUTCOME MEASURES: Visuospatial working memory (VSWM) and Continuous Performance Test (CPT) scores. RESULTS: In smokers with schizophrenia and control smokers, overnight abstinence led to undetectable plasma nicotine levels and an increase in tobacco craving. While abstinence reduced CPT hit rate in both groups, VSWM was only impaired in smokers with schizophrenia. Smoking reinstatement reversed abstinence-induced cognitive impairment. Enhancement of VSWM and CPT performance by smoking reinstatement in smokers with schizophrenia, but not the subjective effects of smoking, was blocked by mecamylamine treatment. CONCLUSIONS: Cigarette smoking may selectively enhance VSWM and attentional deficits in smokers with schizophrenia, which may depend on nAChR stimulation. These findings may have implications for understanding the high rates of smoking in schizophrenia and for developing pharmacotherapies for cognitive deficits and nicotine dependence in schizophrenia.     

Partial protection against muscle damage by eccentric actions at short muscle lengths

PURPOSE: This study investigated the hypothesis that maximal eccentric actions at a short muscle length would fail to confer a protective effect against muscle damage induced by maximal eccentric exercise at a long muscle length. METHODS: Eleven males performed 24 maximal eccentric actions of the nondominant elbow flexors over a short extension range from an elbow joint angle of 0.87-1.74 rad (S-ECC) followed 4 wk later by eccentric actions at a long range of 2.27-3.14 rad (L-ECC). A second group of 11 males performed L-ECC on two occasions using the nondominant arm separated by 4 wk. Changes in maximal isometric strength, range of motion, upper arm circumference, muscle soreness, plasma creatine kinase and aspartate aminotransferase activities, and B-mode ultrasound images were compared between bouts and between groups by two-way repeated measures ANOVA. RESULTS: All measures changed significantly (P < 0.01) after the first bout; however, the effects were significantly (P < 0.01) smaller after S-ECC compared with L-ECC. The second bout resulted in significantly (P < 0.01) reduced changes in all measures compared with the first bout in the subjects who performed L-ECC on both occasions. The subjects who performed S-ECC in the first bout displayed significantly smaller changes after L-ECC than those seen after L-ECC alone, with the degree of attenuation being around 50-70%. CONCLUSION: Contrary to the hypothesis, S-ECC provided partial but effective protection against L-ECC. This result suggests adaptations associated with the repeated bout effect were also produced after S-ECC, but the degree of adaptations was not as strong as that by L-ECC. Eccentric exercise at a short extension range can be used as a strategy to present severe muscle damage.     

Metastases from hepatocellular carcinoma in a percutaneous access site for radiofrequency treatment: a case report

Percutaneous radiofrequency ablation for hepatic tumours is a minimally invasive procedure associated with a risk of iatrogenic dissemination. Tumour seeding along the needle tract may generate neoplastic nodules and masses in the liver, peritoneum and abdominal wall. In this report we describe a case of a large metastatic lesion of the thoraco-abdominal wall after a radiofrequency ablation procedure for hepatocellular carcinoma.     

Shock induction by arterial hypoperfusion of the gut involves synergistic interactions between the peripheral enkephalin and nitric oxide systems

To determine whether critical splanchnic artery hypoperfusion can provoke systemic shock and to identify the roles of the peripheral opioid and nitric oxide (NO) systems in this process, various degrees of superior mesenteric artery hypoperfusion (SMA-H) were produced in anesthetized adult rabbits (n=40), and hemodynamic and metabolic indices were measured. Metabolic acidosis and irreversible hypodynamic shock occurred with SMA-H at levels representing 25-20% of mean baseline SMA blood flow. In 112 other rabbits subjected to SMA-H at 20% (SMA-H20%), we studied plasma NO and enkephalin (ENK) levels, cardiovascular reactivity to selected physiological agonists, effects of ENKs on plasma NO levels, and effects of peripheral opioid receptor blockade and inducible NO synthase (iNOS) inhibition. SMA-H20% progressively increased systemic blood levels of NO and ENKs. Exogenous ENK administration accentuated SMA-H20%-induced increases in plasma NO levels, and their cardiovascular depressing effects were significantly greater when they were administered during SMA-H20% (vs. administration under baseline conditions). Selective blockade of cardiovascular delta-opioid receptors improved hemodynamics, prevented shock irreversibility and reduced plasma NO levels; similar effects were obtained by selective iNOS inhibition. These findings demonstrate that critical arterial hypoperfusion of the gut can induce hypodynamic systemic shock through ENK-induced hyperactivation of cardiovascular delta-opioid receptors, which leads to increased plasma levels of NO related in part to increased iNOS activity. Since pronounced splanchnic artery hypoperfusion occurs in all advanced systemic shock states, selective delta-opioid receptor antagonists and/or iNOS inhibitors may prove to be useful in improving shock hemodynamics and metabolic derangements and/or preventing progression toward irreversibility.     

Involvement of nitric oxide in both central and peripheral haemodynamic effect of D/L-nebivolol and its enantiomers in rats

The cardiovascular profile of the racemate D/L-nebivolol and its enantiomers administered by intravenous (i.v.) or by intracerebroventricular (i.c.v.) route was investigated in anaesthetized normotensive rats. D/L-Nebivolol (0.1-0.5 mg/kg) induced a dose-related reduction in blood pressure when administered by i.c.v. route. These hypotensive effects were more marked as compared to those achieved by peripheral administration of D/L-nebivolol (0.1-1 mg/kg i.v.). Both enantiomers contributed to the hypotensive effect of D/L-nebivolol by i.c.v. route, while the effects of the drug on blood pressure by i.v. route were due to the d-enantiomer. The bradycardic effect of the racemic form given i.v. was dose-related and, at the highest dose (1 mg/kg), was more pronounced as compared to i.c.v. route. D-Nebivolol was responsible for chronotropic effects by both the i.v. and i.c.v. route, although by i.c.v. route L-nebivolol also induced a reduction in heart rate. The nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) administered at 5 mg/kg i.v. bolus + 0.1 mg/kg/min infusion or at 2.5 mg/kg i.c.v. counteracted the effects of D/L-nebivolol (either 1 mg/kg i.v. or 0.5 mg/kg i.c.v.) on blood pressure, while it did not inhibit the cardiovascular changes induced by isoprenaline (300 ng/kg i.v.) or calcitonin gene-related peptide (CGRP; 400 ng/kg i.v.). In addition, i.c.v. effects of D/L-nebivolol on blood pressure and heart rate were not affected by pre-treatment with atropine (2 mg/kg i.v.). The present findings demonstrate that D/L-nebivolol produced haemodynamic changes following both peripheral and central administration; these latter findings are mainly due to its L-enantiomer and these effects involve the L-arginine/nitric oxide pathway.