Erratum: Author Correction: Spaceflight associated neuro-ocular syndrome (SANS) and the neuro-ophthalmologic effects of microgravity: a review and an update.

[This corrects the article DOI: 10.1038/s41526-020-0097-9.].

Spaceflight associated neuro-ocular syndrome (SANS) and the neuro-ophthalmologic effects of microgravity: a review and an update.

Prolonged microgravity exposure during long-duration spaceflight (LDSF) produces unusual physiologic and pathologic neuro-ophthalmic findings in astronauts. These microgravity associated findings collectively define the "Spaceflight Associated Neuro-ocular Syndrome" (SANS). We compare and contrast prior published work on SANS by the National Aeronautics and Space Administration's (NASA) Space Medicine Operations Division with retrospective and prospective studies from other research groups. In this manuscript, we update and review the clinical manifestations of SANS including: unilateral and bilateral optic disc edema, globe flattening, choroidal and retinal folds, hyperopic refractive error shifts, and focal areas of ischemic retina (i.e., cotton wool spots). We also discuss the knowledge gaps for in-flight and terrestrial human research including potential countermeasures for future study. We recommend that NASA and its research partners continue to study SANS in preparation for future longer duration manned space missions.

Origins of Cerebral Edema: Implications for Spaceflight-Associated Neuro-Ocular Syndrome.

BACKGROUND: Spaceflight-associated neuro-ocular syndrome (SANS) was first described in 2011 and is associated with structural ocular changes found to occur in astronauts after long-duration missions. Despite multiple insufficient potential terrestrial models, an understanding of the etiology has yet to be described. EVIDENCE ACQUISITION: A systematic review was conducted on literature published about the pathophysiology of cerebral edema. Databases searched include PubMed, Scopus, and the Texas Medical Center Online Library. This information was then applied to create theories on mechanisms on SANS etiology. RESULTS: Cerebral edema occurs through 2 general mechanisms: redistribution of ions and water intracellularly and displacement of ions and water from the vascular compartment to the brain parenchyma. These processes occur through interconnected endocrine and inflammatory pathways and involve mediators such as cytokines, matrix metalloproteases, nitric oxide, and free radicals. The pathways ultimately lead to a violation of cellular membrane ionic gradients and blood-brain barrier degradation. By applying the principles of cerebral edema pathophysiology to the optic disc edema (ODE) see in SANS, several theories regarding its etiology can be formed. Venous stasis may lead to ODE through venous and capillary distension and leak, as well as relative hypoxia and insufficient ATP substrate delivery causing axoplasmic flow stasis and local oxidative stress. CONCLUSIONS: Using the pathophysiology of cerebral edema as a model, hypotheses can be inferred as to the etiology of ODE in SANS. Further studies are needed to determine the presence and contribution of local vascular stasis and resulting inflammation and oxidative stress to the pathophysiology of SANS.

Spaceflight associated neuro-ocular syndrome.

PURPOSE OF REVIEW: Several decades of long duration space flight missions by the National Aeronautics and Space Administration has revealed an interesting and unique constellation of neuro-ophthalmic findings now called spaceflight associated neuro-ocular syndrome (SANS). The unique space environment of microgravity produces novel physiological changes and derangements that present a challenge to astronauts in current and future long duration space missions. Although the precise mechanism of SANS is not fully understood, in this review, we examine recent developments that may to help explain possible causes and potential countermeasures. RECENT FINDINGS: The cause of SANS is still largely unknown. A growing body of evidence implicates multiple factors that contribute to the development of SANS including cephalad fluid shifts, increased intracranial pressure, venous/lymphatic stasis, inflammation, metabolism, axoplasmic stasis and radiation exposure. SUMMARY: The pathologic mechanism behind SANS may be multifactorial and may be amenable to different countermeasures for prevention and management of SANS.

Point-of-Care Ultrasound Utility and Potential for High Altitude Crew Recovery Missions.

INTRODUCTION: Flights to high altitude can lead to exposure and unique pathology not seen in normal commercial aviation. METHODS: This paper assesses the potential for point-of-care ultrasound to aid in management and disposition of injured crewmembers from a high altitude incident. This was accomplished through a systematic literature review regarding current diagnostic and therapeutic uses of ultrasound for injuries expected in high altitude free fall and parachuting. RESULTS: While current research supports its utility in diagnostics, therapeutic procedures, and triage decisions, little research has been done regarding its utility in high altitude specific pathology, but its potential has been demonstrated. DISCUSSION: An algorithm was created for use in high altitude missions, in the event of an emergency descent and traumatic landing for an unconscious and hypotensive pilot, to rule out most life threatening causes. Each endpoint includes disposition, allowing concise decision-making.Galdamez LA, Clark JB, Antonsen EL. Point-of-care ultrasound utility and potential for high altitude crew recovery missions. Aerosp Med Hum Perform. 2017; 88(2):128-136.