Corrigendum: Iatrogenic air embolism: pathoanatomy, thromboinflammation, endotheliopathy, and therapies.

[This corrects the article DOI: 10.3389/fimmu.2023.1230049.].

Iatrogenic air embolism: pathoanatomy, thromboinflammation, endotheliopathy, and therapies.

Iatrogenic vascular air embolism is a relatively infrequent event but is associated with significant morbidity and mortality. These emboli can arise in many clinical settings such as neurosurgery, cardiac surgery, and liver transplantation, but more recently, endoscopy, hemodialysis, thoracentesis, tissue biopsy, angiography, and central and peripheral venous access and removal have overtaken surgery and trauma as significant causes of vascular air embolism. The true incidence may be greater since many of these air emboli are asymptomatic and frequently go undiagnosed or unreported. Due to the rarity of vascular air embolism and because of the many manifestations, diagnoses can be difficult and require immediate therapeutic intervention. An iatrogenic air embolism can result in both venous and arterial emboli whose anatomic locations dictate the clinical course. Most clinically significant iatrogenic air emboli are caused by arterial obstruction of small vessels because the pulmonary gas exchange filters the more frequent, smaller volume bubbles that gain access to the venous circulation. However, there is a subset of patients with venous air emboli caused by larger volumes of air who present with more protean manifestations. There have been significant gains in the understanding of the interactions of fluid dynamics, hemostasis, and inflammation caused by air emboli due to in vitro and in vivo studies on flow dynamics of bubbles in small vessels. Intensive research regarding the thromboinflammatory changes at the level of the endothelium has been described recently. The obstruction of vessels by air emboli causes immediate pathoanatomic and immunologic and thromboinflammatory responses at the level of the endothelium. In this review, we describe those immunologic and thromboinflammatory responses at the level of the endothelium as well as evaluate traditional and novel forms of therapy for this rare and often unrecognized clinical condition.

Effect of a 2-week trial of functional electrical stimulation on gait function and quality of life in people with multiple sclerosis.

BACKGROUND: Footdrop is a common gait deviation in people with multiple sclerosis (MS) leading to impaired gait and balance as well as decreased functional mobility. Functional electrical stimulation (FES) provides an alternative to the current standard of care for footdrop, an ankle-foot orthosis (AFO). FES stimulates the peroneal nerve and activates the dorsiflexor muscles, producing an active toe clearance and a more normal gait. This study was undertaken to determine the effects of a 2-week FES Home Assessment Program on gait speed, perceived walking ability, and quality of life (QOL) among people with MS-related footdrop. METHODS: Participants completed the Timed 25-Foot Walk test (T25FW) and two self-report measures: 12-item Multiple Sclerosis Walking Scale (MSWS-12) and 29-item Multiple Sclerosis Impact Scale (MSIS-29). Measures were taken without FES before and with FES after 2 weeks of full-time FES wear. RESULTS: A total of 19 participants (10 female, 9 male) completed the study; mean age and duration of disease were 51.77 ± 10.16 and 9.01 ± 7.90 years, respectively. Use of FES for 2 weeks resulted in a significant decrease in time to complete the T25FW (P < .0001), the MSWS-12 standardized score (P < .0001), and the MSIS-29 total (P < .0001), Physical subscale (P < .0001), and Psychological subscale (P = .0006) scores. CONCLUSIONS: These results suggest that use of FES can significantly improve gait speed, decrease the impact of MS on walking ability, and improve QOL in people with MS-related footdrop even over a short period of time.