We examined 80 patients with acute obstructive anuria by ultrasound (US). Four of the 80 patients did not have dilatation of the urinary tract. In all four cases, antegrade pyelography guided by real-time US demonstrated urinary tract obstruction after the four patients had experienced 4, 5, 8, and 34 days of anuria, respectively. Diuresis occurred as a result of percutaneous nephrostomy in all four cases. Three of the patients were successfully treated by percutaneous techniques alone. Our findings demonstrate that even a complete and long-term obstruction of the urinary tract does not necessarily induce dilatation in the upper part of the tract. In such cases, only the direct opacification of the urinary tract can help confirm that the obstruction is present. Even in the absence of dilatation, antegrade pyelography guided by real-time US is a possible diagnostic method and can be the first step in the performance of percutaneous nephrostomy.
Question addressedIn contrast with pain, dyspnoea is not visible to the general public who lack the corresponding experiential baggage. We tested the hypotheses that the generalised use of face masks to fight SARS-CoV2 dissemination could change this and sensitise people to respiratory health.MethodsGeneral population polling (1012-person panel demographically representative of the adult French population –quota sampling method–; 517 women, 51%). 860 (85%) answered “no” to “treated for a chronic respiratory disease” (“respiratory healthy”, RH) and 152 “yes” (“respiratory disease”, RD). 14% of RH respondents reported having a close family member treated for a chronic respiratory disease (RH-family+ and RH-family−). Respondents described mask-related attitudes, beliefs, inconveniencies, dyspnoea, and changes in their respiratory health vision.ResultsCompliance with masks was high (94.7%). Dyspnoea ranked first among mask inconveniencies (RD 79.3%, RH 67.3%, p=0.013). “Air hunger” was the main sensory dyspnoea descriptor. Mask-related dyspnoea was independently associated with belonging to RH-family+ (Odds Ratio [OR] [95% confidence interval (CI)]: 1.85 [1.16–2.98]) and removing masks to improve breathing (OR 5.21 [3.73–7.28]). It was negatively associated with considering masks effective to protect others (OR]: 0.42 [0.25–0.75]). Half the respondents were more concerned with their respiratory health since wearing masks; 41% reported better understanding patients’ experiences.Answer to the questionWearing protective face masks leads to the mass discovery of breathing discomfort. It raises the public's awareness of what respiratory diseases involve and sensitises to the importance of breathing. These data should be used as the fulcrum of respiratory-health-oriented communication actions.
The primary pathogenetic mechanism responsible for the distinctive demyelinating lesions in the Central Nervous System (CNS) in Multiple Sclerosis (MS), first described in remarkable detail by Charcot more than 170 years ago, remains one of the most baffling conundrums in medicine. A possible role for bacterial cell molecules and transportable proteins in the pathogenesis of MS is reviewed. The ability of bacterial toxins to distort immunity and to cause distinctive toxic damage in the nervous system is discussed in the light of largely forgotten data linking bacterial nasopharyngeal infections with optic neuritis, optochiasmatic arachnoiditis and MS. While the blood-brain barrier substantially protects the CNS from hematogenous toxins, there is a route by which the barrier may be by-passed. Data is reviewed which shows that the CSF and extra-cellular fluid circulation is bi-directionally linked to the lymphatic drainage channels of the nasopharyngeal mucosa. While this provides a facility by which the CNS may mount immunological responses to antigenic challenges from within, it is also a route by which products of nasopharyngeal infection may drain into the CNS and be processed by the immune cells of the meninges and Virchow-Robin perivascular spaces. If potentially toxic bacterial products are identified in early MS tissues at these sites, this would provide an entirely new insight into the pathogenetic mechanisms of this frustratingly enigmatic disease.
Intensive care unit (ICU) patients are exposed to many sources of discomfort, among which dyspnoea is one of the more severely distressing [1]. In invasively mechanically ventilated patients, dyspnoea is frequent (47% of intubated patients report breathing discomfort when they can first communicate with caregivers) and severe (median rating of 5 on a dyspnoea visual analogue scale (D-VAS); association with anxiety and neurovegetative signs of stress) [2]. It is often linked to ventilator settings and seems to be associated with poorer clinical outcomes (e.g. delayed extubation and post-traumatic stress disorders) [2,3]. As in other settings, identifying and quantifying dyspnoea in mechanically ventilated patients is therefore a major clinical issue. This is challenging because self-report and self-assessment, prerequisites for D-VAS assessment [4], are often impossible or very difficult in this setting. Unfortunately, caregivers markedly underestimate dyspnoea in this context [5,6]. The risk of occult respiratory suffering is therefore major in the ICU setting and neglecting it would amount to medical error [7].
Highly significant clinical, epidemiological and pathogenetic similarities between multiple sclerosis (MS) and nasopharyngeal sinusitis has led to the hypothesis that MS is caused by the inadvertent incorporation of the lymphatic drainage of the nasopharynx into the extracellular fluid circulation of the CNS. It has been postulated that, in response to antigenic and toxic products generated by the mucosal nasopharygeal flora, the leptomeninges and CNS parenchyma acquire the characteristics of a persistently stimulated lymphoid organ. Using an extensive panel of bacterial antibodies, tissues from exceptionally early cases, identified and classified using multifactorial cluster analysis, were screened for bacterial antigens using immunohistological methods. Anti-staphylococcal antibodies detected antigen co-locating with IgG/C3d immune complexes in pre-demyelinating and in primary lesions. The distribution of the antigen in relation to the morphogenesis of early acute MS lesions is detailed. Evidence for the intrathecal processing of staphylococcal antigen was obtained using isoelectric focusing and antigen imprinting to identify antigen-specific oligoclonal bands. Employing a combination of isoelectric focusing, western blotting and mass spectrometric analysis, evidence for the intrathecal processing of staphylococcal β-haemolysin (sphingomyelinase) was obtained using CSF from MS cases. While a myelinolytic transportable toxin may be an important component in the pathogenesis of demyelination, in oligodendrocyte apoptosis, and in deviant immune responses within the CNS, the detection of other as yet unidentified staphylococcal-positive and negative oligoclonal bands points to the involvement of a cocktail of transportable antigens leaking in a similar manner into the CNS from the paranasal sinus mucosal tissues where these molecules are conserved by the resident flora to manipulate and subvert the normal processes of local and systemic immunity. Evidence for the access of other bacterial transportables to the CNS in MS should now be sought. The presence of 'high-output' toxigenic bacterial strains within the nasopharyngeal flora of MS patients should also be explored. The use of tracer molecules to detect and quantify nose-to-brain transport in MS patients is clearly apposite.
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