The use of delayed computerized tomography in the evaluation of blunt abdominal trauma: a preliminary report

This purpose of this study was to analyze the use of abdominal computed tomography (CT) imaging in patients with possible blunt abdominal trauma. A retrospective analysis of all trauma patients over a 1-year period (1993-1994) was conducted, with prospective study protocol in 52 patients using serial abdominal exam and hematocrits (Hcts) instead of abdominal CT for evaluation of blunt abdominal trauma. Urgent abdominal CT was used as the initial diagnostic test for evaluation of blunt abdominal trauma in 813 patients over this 1-year period. CT was obtained in 379 (46.6%) of these patients who arrived hemodynamically stable (admission systolic blood pressure > or = 90), had a Glasgow Coma Scale > 13, and had admission Hct > or = 35 because of distracting injuries, possible traumatic brain injury, or alcohol/drug use, which might render the abdominal physical exam unreliable. Only 47 CT scans (12.4%) were positive, and three patients (0.8%) required laparotomy. In an effort to more efficiently use abdominal CT, we performed a prospective study in 52 patients with possible blunt abdominal trauma, admission systolic blood pressure > or = 90, Hct > or = 35, Glasgow Coma Scale > 13, and a normal abdominal exam on admission. These patients were followed with serial abdominal examinations and Hcts every 6 hours for 24 hours, and delayed CT, when applicable. CT was obtained in seven patients (13.5%) for evaluation of fall in Hct or abnormal abdominal examination; all were negative for abdominal injury. A protocol using serial abdominal exams, Hcts, and delayed abdominal CT imaging may be useful in select patients to decrease the high number of negative routine abdominal CTs that are obtained in the evaluation of blunt abdominal trauma.     

Neuroprotective effects of modulators of P2 receptors in primary culture of CNS neurones.

In previous studies (Volonté and Merlo, 1996. J. Neurosci. Res. 45, 183-193) basilen blue was shown to be a P2 receptor antagonist which abrogated glutamate-mediated cytotoxicity in cerebellar neurones in primary culture. Our work has now been extended to evaluate the neuroprotective action of the compound in additional neuronal systems, as well as in a different paradigm of cell death. We show that basilen blue prevents L-glutamate-mediated neurotoxicity in rat cerebellar (90-100% inhibition), cortical (60-70%) and hippocampal (50%) neurones. Similarly, glutamate-dependent progressive darkening of cell bodies, loss of phase-brightness and rapid cellular swelling are inhibited. Basilen blue is significantly less toxic and more effective at blocking L-glutamate toxicity in mixed cortical/glial cultures, compared to its structural analogue cibacron blue. Moreover, its neuroprotective effect is correlated with the time of incubation with granule neurones. Other purinoceptor ligands, including 2,2'-pyridylisatogen, but not pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid 4-sodium, are also effective in preventing glutamate toxicity. Furthermore, basilen blue prevents serum deprivation- and low potassium-induced apoptotic cell death in cerebellar granule neurones. In summary, our data extend and reinforce the possibility of a potential therapeutic use of P2 receptor modulators as neuroprotective agents for the central nervous system.     

Evaluation and management of mechanical dysfunction in continent colonic urinary reservoirs

PURPOSE: We analyze a group of patients who presented with mechanical dysfunction of the reservoir and/or efferent limb of a continent colonic urinary diversion, and establish an evaluation and management algorithm. MATERIALS AND METHODS: A total of 16 patients with a mean age of 58 years and 1 or more symptoms related to continent colonic urinary diversion were evaluated. Presenting symptomatology included difficult catheterization in 8 cases (50%), disabling incontinence in 8 (50%) and recurrent urinary tract infections in 6 (37.5%). All patients had normal, nonobstructed, nonrefluxing upper tracts and none presented with stone disease. Urological evaluation consisted of catheterization, fluoroscopy and urography of the pouch, retrograde urography of the external limb and urodynamics (enterocystometrogram and outlet pressure profilometry). RESULTS: Of the 8 patients with difficulty with catheterization 4 had stomal stenosis, 2 had an elongated and redundant external limb, and 2 had a false passage. Diagnosis was established by the inability to catheterize, fluoroscopy of the pouch and retrograde urography. Disabling incontinence occurred in 8 patients, including 7 who presented with an incompetent outlet and 2 with high pressure intestinal contractions of the reservoir. The aforementioned abnormalities were diagnosed by a combination of retrograde urography, urography of the pouch and urodynamics. Recurrent symptomatic urinary infections were observed in 5 patients of the previous groups and in another with an hourglass reservoir, which was primarily diagnosed by urography of the pouch. Surgical correction in 15 patients included outlet reinforcement, reservoir revision, stomal or external limb revision and conversion to a urinary conduit. Surgical treatment was successful in 14 of 15 patients (93%). CONCLUSIONS: Catheterization difficulty requires retrograde urography to define possible anatomical abnormalities (false passage, conduit elongation) if catheterization and fluoroscopy of the pouch do not demonstrate stomal stenosis. Urinary incontinence benefits from enterocystometry and outlet pressure measurement to determine reservoir and external limb function. Recurrent urinary tract infections not related to ureteral obstruction or reflux requires fluoroscopy of the pouch and external limb to determine abnormalities in patients with detubularization and localization of areas of urine pooling.     

Is public health training in Canada meeting current needs? Defrosting the paradigm freeze to respond to the post-truth era

Health scholars have long been calling for a new approach to understanding and responding to public health challenges, recognizing the dynamic influence of social and ecological processes and the importance of respecting different ways of knowing. With daunting new challenges to collective health, we sought to ascertain how future generations of public health researchers and practitioners are being prepared with the knowledge, attitudes, and skills needed for the tasks ahead. We found that of the 76 graduate level programs listed by the Public Health Agency of Canada, 65% required at least one quantitative methods course, but only 26% required qualitative methods and only 16% required a course in community engagement. While 25% had at least one required course related to social theory or social determinants of health, only 3% required a course on the ecological determinants. Our examination suggests that the majority of schools of public health may still be frozen in old paradigms wherein interdisciplinary inquiry and the development of skills to work with communities to implement and evaluate interventions to promote and protect collective health are still only peripheral considerations. With the intensification of public distrust in experts in this post-truth era, greater emphasis is needed now more than ever to develop skills in understanding and engaging the public in addressing the underlying issues threatening health. We argue that as the challenges of the Anthropocene are upon us, it is urgent that we rethink the skills we are teaching and prepare ourselves to radically adjust our approach.     

Activity of CD101, a long-acting echinocandin,against clinical isolates of Candida auris

CD101 is a new echinocandin with a prolonged half-life. CD101 was tested by broth microdilution against 100 isolates of the emerging yeast Candida auris. It showed activity against most isolates, including some that were resistant to other echinocandins.     

Sera from patients with heparin-induced thrombocytopenia generate platelet-derived microparticles with procoagulant activity: an explanation for the thrombotic complications of heparin-induced thrombocytopenia

Heparin-induced thrombocytopenia is characterized by moderate thrombocytopenia and thrombotic complications, whereas quinine/quinidine-induced thrombocytopenia usually presents with severe thrombocytopenia and bleeding. Using flow cytometry and assays of procoagulant activity, we investigated whether sera from patients with these immune drug reactions could stimulate normal platelets to generate platelet-derived microparticles with procoagulant activity. Sera or purified IgG from patients with heparin-induced thrombocytopenia stimulated the formation of platelet-derived microparticles in a heparin-dependent fashion. Further studies showed that heparin-induced thrombocytopenia sera also produced a marked increase in procoagulant activity. In contrast, sera from patients with quinine- or quinidine-induced thrombocytopenia did not generate platelet-derived microparticles nor generate increased procoagulant activity. However, quinine/quinidine-induced thrombocytopenia sera produced a significant increase in the binding of IgG to platelets in a drug-dependent fashion, whereas sera from patients with heparin-induced thrombocytopenia demonstrated no drug-dependent binding of IgG to platelets. We also observed increased levels of circulating microparticles in patients with acute heparin-induced thrombocytopenia compared with control patients. Our observations indicate that the generation of procoagulant platelet-derived microparticles in vivo is a plausible explanation for the thrombotic complications observed in some patients with heparin-induced thrombocytopenia.