Somatosensory profiling of patients undergoing alcohol withdrawal: Do neuropathic pain and sensory loss represent a problem?

INTRODUCTION: Chronic heavy alcohol use is known to cause neurological complications such as peripheral neuropathy. Concerning the pathophysiology, few sural nerve and skin biopsy studies showed that small fibers might be selectively vulnerable to degeneration in alcohol-related peripheral neuropathy. Pain has rarely been properly evaluated in this pathology. The present study aims at assessing pain intensity, potential neuropathic characteristics as well as the functionality of both small and large nerve sensitive fibers. METHODS: In this observational study, 27 consecutive adult patients, hospitalized for alcohol withdrawal and 13 healthy controls were recruited. All the participants underwent a quantitative sensory testing (QST) according to the standardized protocol of the German Research Network Neuropathic Pain, a neurological examination and filled standardized questionnaires assessing alcohol consumption and dependence as well as pain characteristics and psychological comorbidities. RESULTS: Nearly half of the patients (13/27) reported pain. Yet, pain intensity was weak, leading to a low interference with daily life, and its characteristics did not support a neuropathic component. A functional impairment of small nerve fibers was frequently described, with thermal hypoesthesia observed in 52% of patients. Patients with a higher alcohol consumption over the last 2 years showed a greater impairment of small fiber function. DISCUSSION: Patients report pain but it is however unlikely to be caused by peripheral neuropathy given the non-length-dependent distribution and the absence of neuropathic pain features. Chronic pain in AUD deserves to be better evaluated and managed as it represents an opportunity to improve long-term clinical outcomes, potentially participating to relapse prevention.

[Mitral valve prolapse: beyond mitral regurgitation, the arrhythmic risk]. / Prolapsus mitral : une étiologie méconnue d'arythmie ventriculaire et de mort subite.

Mitral prolapse is a common condition, defined by the systolic bulging of at least one mitral leaflet into the left atrium, which is often accompanied by various degree of mitral insufficiency. While for most of the patients the prognosis is linked to the severity of the valve regurgitation and its repercussions on the left ventricle (dilation and/or dysfunction), a minority of patients present with severe ventricular arrhythmia and an increased risk of sudden cardiac death, irrespective of the severity of the mitral regurgitation. To describe this particular condition, the terms arrhythmic or malignant mitral valve prolapse have been coined. The aim of this article is to describe the clinical, electrocardiographic and morphologic characteristics, which have been associated with an increased risk of arrhythmia in patients with mitral prolapse.

Le prolapsus mitral est une pathologie fréquente, définie par le bombement en systole d'au moins un feuillet mitral dans l'oreillette gauche, qui s'accompagne fréquemment d'un degré variable d'insuffisance mitrale. Dans la majorité des cas, le pronostic est lié à la sévérité de l'insuffisance valvulaire et ses répercussions sur le ventricule gauche (dilatation et/ou dysfonction). Toutefois, dans certaines formes, le prolapsus mitral se manifeste par une susceptibilité aux arythmies ventriculaires et s'associe à un risque accru de mort subite, indépendamment de la présence ou de la sévérité de l'insuffisance valvulaire. On parle alors de syndrome du prolapsus mitral arythmique ou prolapsus mitral malin. Cet article décrit les caractéristiques cliniques, électrocardiographiques et morphologiques associées au risque arythmique chez les patients atteints d'un prolapsus mitral.

The short-term prognosis of cardiogenic shock can be determined using hemodynamic variables: a retrospective cohort study*.

OBJECTIVES: Few reports address the relationship between hemodynamic variables and the cardiogenic shock outcome in critically ill patients. The present study aimed to investigate the association between hemodynamic variables and early cardiogenic shock mortality in critically ill patients. DESIGN: Retrospective, single-center cohort study. SETTING: Tertiary academic hospital's 36-bed multidisciplinary intensive care. PATIENTS: Initial presentation with cardiogenic shock. MEASUREMENTS AND MAIN RESULTS: The authors retrospectively analyzed medical information and the hemodynamic variables (recorded during the first 24 hr following admission to the ICU) of patients with cardiogenic shock. For all the patients, the Simplified Acute Physiology Score II, cardiac index, cardiac power index, and continuous hemodynamic values following the first 24 hours of admission were reviewed. Mortality within 28 days was the primary endpoint. All the variables were then compared with survival and nonsurvival status and those variables with a significant association in the univariate analysis were entered into a multivariate logistic regression model. Seventy-one patients were included. Among them, 26 (37%) died within 28 days after ICU admission and were classified as "nonsurvivors." The minimum value for diastolic arterial blood pressure during the first 24 hours was independently associated with the 28-day mortality in the univariate and multivariate analyses model. This model performed better than the model using the Simplified Acute Physiology Score II, even when assessing the effect of inotrope and vasoactive treatments at 24, 48, and 72 hours. CONCLUSIONS: In the first 24 hours of an ICU admission, the minimum diastolic arterial blood pressure was a hemodynamic variable that was independently associated with 28-day mortality in cardiogenic shock patients.