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Objectives: To investigate whether patients who develop ICU-acquired weakness have a different pattern of systemic inflammatory markers compared with critically ill patients who do not develop ICU-acquired weakness.Design: Prospective observational cohort study.Setting: Mixed medical-surgical ICU of a tertiary care hospital in the Netherlands.Patients: Newly admitted critically ill patients, greater than or equal to 48 hours on mechanical ventilation with a nonneurologic ICU admission diagnosis, were included.Interventions: A panel of systemic inflammatory markers and soluble vascular adhesion molecules were measured in plasma samples of day 0, 2, and 4 after ICU admission. ICU-acquired weakness was diagnosed by manual muscle strength testing as soon as patients were awake and attentive.Measurements and Main Results: Ninety-nine of 204 included patients developed ICU-acquired weakness. Principal component regression analysis, adjusted for confounders, showed that principal component 1, mainly loaded with interleukin-6, interleukin-8, interleukin-10, and fractalkine, was significantly higher in patients who developed ICU-acquired weakness (odds ratio, 1.35 [95% CI, 1.18-1.55]). Partial least squares-discriminant analysis also showed that these markers were the most important discriminative markers. Mixed-effects models of these markers showed that ICU-acquired weakness was associated with an independent 1.5- to two-fold increase in these markers.Conclusions: Systemic inflammation is increased in patients who develop ICU-acquired weakness compared with patients who do not develop ICU-acquired weakness in the first 4 days after ICU admission. This finding is consistent when adjusted for confounders, like disease severity. A group consisting of interleukin-6, interleukin-8, interleukin-10, and fractalkine was identified to be the most important. [ABSTRACT FROM AUTHOR]

Objective: The aim of this work was to compare the patient-reported functional health status with regard to physical, psychological, and social functioning of intensive care unit (ICU) survivors with and without ICU-acquired weakness (ICU-AW). Design: Single-center prospective study in ICU patients who were mechanically ventilated for more than 2 days and who survived to ICU discharge. Functional health status was assessed at 3, 6, and 12 months after ICU discharge, using the Sickness Impact Profile 68 (SIP68). The independent effect of ICU-AW on impaired functional status (SIP68 scores > 20) was analyzed using a multivariable logistic regression model. Results: A total of 133 patients were included, 60 with ICU-AW. Intensive care unit-acquired weakness was an independent predictor for impaired functional health status at 3 months after ICU discharge (odds ratio, 0.27; 95% confidence interval, 0.08-0.94; P = 0.04) but not at 6 and 12 months. Physical functioning was significantly more impaired in patients with ICU-AW at 3 and 12 months. Psychological functioning and social functioning were comparable between the groups, with little restrictions in psychological functioning, and severe long-lasting restrictions in social functioning. Conclusions: The findings of this study urge the need to develop interdisciplinary rehabilitation interventions for ICU survivors, which should be continued after hospital discharge. [ABSTRACT FROM AUTHOR]

Abstract: Traumatic peripheral nerve injuries are at high risk of neuropathic pain for which novel effective therapies are urgently needed. Preclinical models of neuropathic pain typically involve irreversible ligation and/or nerve transection (neurotmesis). However, translation of findings to the clinic has so far been unsuccessful, raising questions on injury model validity and clinically relevance. Traumatic nerve injuries seen in the clinic commonly result in axonotmesis (ie, crush), yet the neuropathic phenotype of "painful" nerve crush injuries remains poorly understood. We report the neuropathology and sensory symptoms of a focal nerve crush injury using custom-modified hemostats resulting in either complete ("full") or incomplete ("partial") axonotmesis in adult mice. Assays of thermal and mechanically evoked pain-like behavior were paralleled by transmission electron microscopy, immunohistochemistry, and anatomical tracing of the peripheral nerve. In both crush models, motor function was equally affected early after injury; by contrast, partial crush of the nerve resulted in the early return of pinprick sensitivity, followed by a transient thermal and chronic tactile hypersensitivity of the affected hind paw, which was not observed after a full crush injury. The partially crushed nerve was characterized by the sparing of small-diameter myelinated axons and intraepidermal nerve fibers, fewer dorsal root ganglia expressing the injury marker activating transcription factor 3, and lower serum levels of neurofilament light chain. By day 30, axons showed signs of reduced myelin thickness. In summary, the escape of small-diameter axons from Wallerian degeneration is likely a determinant of chronic pain pathophysiology distinct from the general response to complete nerve injury., (Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the International Association for the Study of Pain.)