Abstract
I
A 1-year prospective study was conducted at a tertiary care institute in North Eastern India to examine the occurrence of CSCR among security personnel stationed at HA above 8,000 ft for more than 3 months after completing the acclimatization process. During the study period, a total of 68 cases with decreased vision presented, among which 16 cases were diagnosed with CSCR. The security personnel were posted at HA locations ranging from 8,000 to 19,500 ft, with a mean altitude of 12,000 ft. The average visual acuity at the time of presentation was 20/100. Among the diagnosed CSCR cases, 10 patients recovered within 3 months, while 6 patients developed chronic CSCR. All participants in the study were male and aged between 20 and 35 years. They reported experiencing decreased vision accompanied by metamorphopsia.
Although a direct causal link between HA and CSCR hasn't been established yet, observations point to some noteworthy correlations. Notably, a study described a case of an aviator who developed CSCR while receiving training in a hypobaric hypoxic chamber (Ide, 2014). This calls for additional research and also highlights the necessity of investigating the underlying mechanisms causing CSCR to arise in HA.
First, stress, both physical and psychological, is an important component that necessitates attention toward development of CSCR in HA. Since HA situations are inherently difficult, people frequently have stress. Cortisol production, which is increased during stress, has been associated with CSCR (Schellevis et al. 2019). The sensitive fluid dynamics of the subretinal space can be upset by cortisol, which could lead to fluid leakage and eventual buildup. Therefore, it is critical to take into account stress as a potential component influencing the development of CSCR in HA contexts, emphasizing the need of stress management in people exposed to HA. Second, HA may lead to hypobaric hypoxia, which may cause vasoconstriction, especially in the choroidal blood vessels. This restriction may alter the dynamics of normal blood flow, impede fluid drainage systems, and thus contribute to the subretinal fluid observed in CSCR.
Third, a number of genetic variants, including ARMS2, CFH, and TNFRSF10A, have been linked to CSCR (Chen et al. 2022). It may be possible to gain important insights into the underlying mechanisms and help identify people who may be more susceptible by determining whether there are any particular genetic variations or gene–environment interactions that predispose people to CSCR in high-altitude surroundings. Fourth, the development of CSCR may also be impacted by the sympathetic nervous system which is activated in response to low oxygen levels at HA. Activation of the sympathetic nervous system may result in elevated levels of stress hormones, which may encourage fluid leakage from choroidal blood vessels into the subretinal space.
Fifth, inflammation has been implicated in the pathogenesis of CSCR, and its association with HA environments is worth exploring (Sirakaya et al. 2020). Hypoxia and other stressors at HAs can trigger inflammatory responses in the body, which may have implications for the development of CSCR. Investigating the role of inflammatory mediators and the immune response in high-altitude-induced CSCR could provide a better understanding of the condition.
In conclusion, more research is needed to determine whether HA and the onset of CSCR are possibly related. The multifactorial nature of CSCR in HA settings points to a complicated interplay between sympathetic nervous system activity, stress, and hypoxia. For those who reside or spend extended period at HA, effective management and prevention efforts must take into account the underlying mechanisms.