Dear Editor,
Osmotic agents like intravenous mannitol have been used in the emergency management of glaucoma to decrease the intraocular pressure (IOP). They act by increasing the osmolality of plasma and drawing water from the vitreous into circulation, thereby reducing the IOP.[1,2] Mannitol also acts centrally via the osmoreceptors in the hypothalamus and decreases aqueous production.[3,4] Studies have shown similar IOP reduction with the use of mannitol in both vitrectomized and non-vitrectomized eyes.[5] Mannitol has been shown to decrease vitreous cavity depth (VCD) and increase anterior chamber depth (ACD) in non-vitrectomized eyes and hence support vitreous dehydration as the main mechanism of IOP reduction in these eyes. There is no study in the literature that has evaluated changes in the ocular biometry associated with mannitol in vitrectomized eyes. The main aim of our study was to ascertain the mechanism of IOP reduction in vitrectomized eyes.
A prospective comparative study was conducted at a tertiary eye care center in south India. The study was approved by the institutional ethics committee and adhered to the tenants of the Declaration of Helsinki. Phakic eyes of patients with IOP measuring ≥40 mmHg and open angles on gonioscopy were included. Eyes with elevated IOP after vitrectomy and silicone oil injection were classified as Group 1, and non-vitrectomized eyes with open-angle glaucoma were classified as Group 2. Eyes with overfilled silicone oil and poor quality ocular biometry scan due to corneal edema and patients with systemic contraindications for mannitol were excluded.
The IOL master measures the corneal thickness (CT), axial length (AL), ACD, and lens thickness (LT). Vitreous cavity depth was calculated by deducting the CT, ACD, and LT from AL. Intravenous mannitol (20%) was administered at a dosage of 1 g/kg body weight for over 30 minutes. IOP and ocular biometry were measured before and two hours after mannitol administration. Patients were not prescribed other antiglaucoma medication during the study period of two hours.
Twenty-five patients (eyes) were included in each group. Table 1 shows the baseline demographic characteristics. Table 2 shows the comparison of IOP and ocular biometry parameters before and after mannitol administration. Intraocular pressure was significantly reduced with mannitol in both the groups. Mean IOP reduction in vitrectomized eyes was 33% (range: 6%–62%) and in non-vitrectomized eyes was 41% (range: 7%–70%). AL and VCD decreased significantly in both vitrectomized and non-vitrectomized eyes. ACD decreased in vitrectomized eyes and increased in non-vitrectomized eyes, but the change was not statistically significant in both the groups.
Table 1.
Baseline characteristics of the study population
| Characteristics | Group 1 (Vitrectomized eyes) | Group 2 (Non-vitrectomized eyes) | P* |
|---|---|---|---|
| No. of eyes (patients) | 25 | 25 | |
| Age (in years) Mean±SD | 47±13 | 54±15 | 0.099 |
| BCVA Median (IQR) | 2/60 (5/60 to 1/60) | 6/12 (6/9 to 6/60) | <0.001 |
| IOP (mmHg) Mean±SD | 45.36±6 | 49±7.8 | 0.071 |
| CCT (mm) | 0.55±0.04 | 0.53±0.04 | 0.121 |
| ACD (mm) | 3.34±0.3 | 3.34±0.4 | 0.959 |
| LT (mm) | 4.07±0.4 | 4.03±0.5 | 0.758 |
| AL (mm) | 24.92±3.4 | 23.59±1.1 | 0.070 |
| VCD (mm) | 16.96±3.3 | 15.69±1.2 | 0.081 |
| Diagnosis | PDR (15 eyes) RRD (10 eyes) |
PXG (12 eyes) POAG (10 eyes) Steroid-induced glaucoma (3 eyes) |
*Unpaired t test. BCVA: Best-corrected visual acuity, IOP: Intraocular pressure, CCT: Central corneal thickness, ACD: Anterior chamber depth, LT: Lens thickness, AL: Axial length, VCD: Vitreous cavity depth, PDR: Proliferative diabetic retinopathy, RRD: Rhegmatogenous retinal detachment, PXG: Pseudoexfoliation glaucoma, POAG: Primary open angle glaucoma
Table 2.
Comparison of IOP and ocular biometry parameters between vitrectomized (Group 1) and non-vitrectomized (Group 2) eyes before and after mannitol administration
| Group 1 (vitrectomized eyes) | Group 2 (non-vitrectomized eyes) | |||||
|---|---|---|---|---|---|---|
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| Pre mannitol (mean±SD) | Post mannitol (mean±SD) | P* | Pre mannitol (mean±SD) | Post mannitol (mean±SD) | P* | |
| IOP (mmHg) | 45.36±6.0 | 30.24±6.5 | <0.001 | 49.00±7.8 | 28.68±9.6 | <0.001 |
| CCT (mm) | 0.55±0.04 | 0.55±0.04 | 0.424 | 0.53±0.04 | 0.52±0.04 | 0.005 |
| ACD (mm) | 3.34±0.3 | 3.33±0.3 | 0.570 | 3.34±0.4 | 3.36±0.4 | 0.104 |
| LT (mm) | 4.07±0.4 | 4.10±0.3 | 0.184 | 4.03±0.5 | 4.04±0.5 | 0.585 |
| AL (mm) | 24.92±3.4 | 24.83±3.4 | 0.002 | 23.59±1.1 | 23.53±1.1 | <0.001 |
| VCD (mm) | 16.96±3.3 | 16.85±3.3 | 0.004 | 15.69±1.2 | 15.60±1.2 | 0.001 |
*Paired t test. IOP: Intraocular pressure, CCT: Central corneal thickness, ACD: Anterior chamber depth, LT: Lens thickness, AL: Axial length, VCD: Vitreous cavity depth
Our study results did not support the hypothesis of vitreous dehydration in non-vitrectomized eyes as the predominant mechanism of IOP reduction because there was significant decrease in VCD in vitrectomized eyes as well. Similarly, our study did not support the hypothesis of decreased aqueous production in vitrectomized eyes as the predominant mechanism of IOP reduction because there was no significant change in ACD in both the groups. To conclude, both direct osmotic and central mechanism play a role in IOP reduction, as reported by Ramachandra et al.[5]
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Conflicts of interest
There are no conflicts of interest.
References
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