The increase of IOP in supine position has been previously described in several reports.16,17 De Bernardo et al.16 measured the IOP with a rebound tonometer, the Icare PRO (Icare Finland Oy, Finland version 1.1) in 120 eyes of 60 normal weight individuals in sitting, supine, standing positions and again 5 min after standing. They found IOP in supine and standing positions, to be higher than in the sitting (mean ΔIOP = + 1.16mmHg, P < 0.001) and in the standing ones (mean ΔIOP = + 1.55mmHg, P < 0.001). This latter difference was reduced over time, (mean ΔIOP between supine and standing position 5’ = +0.68mmHg, P < 0.001).16 An IOP increase in supine position was also reported in patients affected by multiple system atrophy (MSA) and Parkinson’s disease (PD).17 De Bernardo et al. demonstrated how both healthy subjects and patients with MSA or PD showed IOP increase in supine position, this increase was higher in patients with MSA.17 In addition, an IOP increase in obese patients in the supine positions compared to the sitting and the standing was firstly reported in 2015 by Geloneck et al. in which, similarly to the present study, authors measured the IOP of obese patients in 3 different positions.18 The results of the present study not only confirm that ΔIOPs between supine and other positions were statistically significant (P < 0.05) in both overweight subject and normal weight controls but, in addition to previous studies, they show that ΔIOP in supine and 5’standing positions was higher in overweight subject than in normal weight controls (P < 0.05).
Several hypotheses have been formulated to explain these findings: the IOP increase in supine position in normal weight subjects may occur because of choroidal vascular engorgement caused by the redistribution of body fluids in the supine position,19 or an increase in episcleral venous pressure.20 Higher increase in patients affected by MSA are probably due to direct pressure and volume changes in the vascular compartments within and around the eye, including the periorbital tissues and the intraocular blood volume, most of which lies in the choroid.21 IOP increase in obese patients could be explained by the fat mass compression on abdomen and thorax in supine positions, causing an increase in intra-abdominal and intrathoracic pressure thus elevating the central venous pressure (CVP).22 Since the episcleral venous system is a valves free system, the increase of the CVP is transmitted to the episcleral venous system reducing the passive outflow of the aqueous humor through the Schlemm's channel causing an increase in IOP.20
In 2017 Lam et al. reconfirmed the Geloneck et al. study, and first extended IOP measurements to obese patients with a significant reduction in BMI after bariatric surgery.23 The study showed a not significant difference in the postural change of IOP between overweight patients and normal size controls, concluding that obesity was associated just with the increase in IOP in obese patients, but not with the postural changes. The new measurements after the weight loss showed a reduction in IOP not statistically significant compared to the values obtained in the same patients in the pre-operative period, showing a weak correlation between the loss of body weight and the reduction of IOP.
Starting from these assumptions, we wanted to compare IOP changes, based on postural changes, with the two factors from which the BMI is derived: height and weight. Also in these cases, Figs. 1–3 and Table 2 showed how both factors are weakly related to variations in IOP with postural changes. Therefore, we cannot consider height and weight as factors directly responsible for the variation IOP in postural changes. Similarly, to Lam et al., our study also shows that the relationship between BMI and changes in IOP with the postural changes is weak, as showed in Fig. 1–3 and in Table 2. Among these, the only measurement that differs from the others with an ρ = 0.432 is the one that relates BMI with the IOP in supine position 5’. In this case the positive correlation between the two parameters is a little more evident than the others. On the other hand, contrary to Lam et al., our study found statistically significant differences in the postural change of IOP between overweight patients and normal weight controls, as will be discussed below.
In addition, our study confirms findings demonstrated by previous studies, that there are no significant changes in IOP after a short period of time spent in a supine position. In fact, previous reports have shown how IOP can rise for 30 minutes after passing in supine position, others have found no difference between IOP at time 0 and at 15 minutes.24–26
IOP changes in our study could be due to other factors such as vascular dysfunction secondary to endothelial damage, insulin resistance or autonomic nervous system deficit,27–29 resulting overall in a difficult blood flow and in an unstable tissue perfusion. In fact, obesity increases the risk of developing hypertension and atherosclerosis underlying the ischemic hypoperfusion injury.30–33
In 2019 Panon et al.34 investigated the correlation between anterior chamber depth (ACD), IOP and BMI, finding a strong positive correlation between ACD and BMI and between IOP and BMI, with higher IOP in overweight subjects compared to normal weight control subjects, concluding that the degree of obesity was a significant factor. According to the authors, the reasons for this correlation were due to the large amount of periorbital fat, the increased blood viscosity and the reduced episcleral outflow caused by the leptin-induced oxidative damage that are typically observed in overweight subjects.34 In 2020 also Ahn et al.,2 with their study that investigated the relationship between IOP and obesity on 40.850 patients, also found ocular hypertonus in overweight subjects and traced this condition to the increased orbital adipose tissue that increases the episcleral venous pressure hindering the outflow blood, the increased secretion of cortisol characteristic of obese subjects and the dysmetabolic syndrome that typically affects such patients.2 Çekiç et al.35 investigated the correlation between IOP and the extraocular orbital vessels with ultrasound associated with eco-color doppler (CDU) and to investigate the effects of obesity on retrobulbar flow,35 starting from what was argued by Stojanov et al.,36 namely that the focal accumulation of fat in certain anatomical regions, such as in the retrobulbar region, could cause morphological and functional changes in that body district.36 Evaluating these parameters in overweight and normal size patients without vascular diseases and exclusively of white race, because retrobulbar flow is strongly influenced by ethnicity,37 they demonstrated the increase of IOP in overweight patients and the related decreases in blood flow velocity in the ophthalmic artery, concluding that the increase in IOP, along with the decrease in retrobulbar blood flow, especially in obese patients, may increase the risk of developing glaucoma. We must remember that these measurements are only a snapshot of the actual IOPs since it is shown that IOP has circadian fluctuations that can influence the progression of glaucoma,38,39 but this does not invalidate the results of our study where only the pressure differences in different positions on which circadian variations should have no influence were evaluated.
A point of strength of this study is the evaluation not only of IOP measurements of both patients and controls in different position, but also the ΔIOP differences in both populations: in this way, it was possible to detect the entity of IOP variation between overweight patients and normal size controls. In this way, the comparison between patients and controls was not affected by the baseline IOP, and it was possible to investigate more precisely the existence of a greater variability of the IOP in overweight patients than normal weight subjects. In fact, as shown in Table 2, statistically significant differences were detected in ΔIOP obtained with the two supine positions and prolonged standing position, with a significantly increase of IOP in overweight patients that was > 1.00mHg in both cases (+ 1.10mmHg ΔIOP supine/standing 5’ and + 1.02 supine 5’/standing 5’).
It could be considered that a limitation of our study was the use of the TPA instead of the Goldmann applanation tonometry (GAT), which is considered the gold standard, but the latter requires the slit lamp that does not meet the need to measure the ocular tone in various positions. Moreover, obese patients have extreme difficulty in resting chin and forehead on the chin guard of the slit lamp to be examined. This is the reason why the study was conducted with the TPA, that uses the same physical principle as GAT to measure IOP and whose reliability is guaranteed by the numerous previous studies that have shown reliable measurements when compared to the GAT in a sitting position.40
In obese patients there is a statistically significant increase in IOP in the supine positions. BMI is only weakly correlated with IOP and ΔIOP in postural changes, however further studies that do not estimate only the BMI but also evaluate the fat mass distribution with the waist-to-waist ratio or that distinguish it from the lean mass with bio-impedance analysis, could confirm or eventually deny these findings. In obese patients there is an increase in IOP in the supine position that is greater than normal weight population. ΔIOP differences were statistically significant between all supine positions and standing 5’ position.