LETTER
Risk Factors for Ocular Hypertension After Penetrating Keratoplasty To the Editor: Oruc¸oglu et al1 have recently published an interesting study investigating the risk factors contributing to ocular hypertension after penetrating keratoplasty (PK). The authors reported that 47.7% of the patients included in their study, manifested at least 1 consecutive episode of high intraocular pressure (IOP) (>21 mm Hg) during a mean follow-up of 24.4 months. The onset of IOP elevation was after a mean postoperative period of 70.3 ± 15.8 days and the mean duration of the observed ocular hypertension was 15.6 ± 2.0 days. Half of these patients presented a second episode of ocular hypertension occurring 212.2 ± 46.8 days after the surgery, with a mean duration of 18.1 ± 2.9 days. This study revealed that history of preexisting glaucoma, as well as additional surgical procedures combined with PK, were significant factors predicting the occurrence of ocular hypertension after PK. Nevertheless, we would like to highlight some aspects which, in our opinion, merit further consideration. It is well established that ocular hypertension may occur in the early postoperative period after PK.2,3 These episodes of IOP elevation are usually transient and resolve spontaneously without surgical intervention. However, the incidence of postkeratoplasty glaucoma, requiring surgical intervention or regular medication, is significantly lower compared to the ocular hypertension observed in the immediate postoperative period, as indicated in relevant studies.1–3 Therefore, one should distinguish between the benign, transient ocular
TO THE
EDITOR
hypertension after PK and the true postkeratoplasty glaucoma. Several mechanisms have been suggested as causative factors for ocular hypertension after PK, such as postoperative inflammation, potential steroid response, suturing technique, the diameter of the graft, etc., as also mentioned by the authors. It has also been highly assumed that anatomic changes in the anterior chamber and, predominantly, changes in the anterior chamber angle (ACA) could be associated with the occurrence of post-PK glaucoma; Olson and Kaufmann4 in their mathematical model attempted to correlate the IOP with the amount of ACA distortion. However, until today there was no evident proof of this clinical hypothesis. Our group has recently documented that ocular hypertension in the early postoperative period after PK for keratoconus is significantly correlated with changes in the anterior chamber architecture.5 Specifically, central and peripheral corneal thickness was significantly increased 2 months after PK, whereas anterior chamber depth, anterior chamber volume, and ACA in all 4 quadrants were significantly decreased,5 indicating potential significant reduction of outflow facility due to compression of the trabecular meshwork. These anatomic changes, which are probably induced by the postoperative inflammatory reaction and surgical stress (increase of corneal thickness and subsequent decrease of ACA), but also by the graft diameter and suturing/surgical technique (decrease of ACA) are partially reversible, resulting in spontaneous resolution of postkeratoplasty ocular hypertension (data under submission). However, these anatomic changes of the anterior chamber persist in some patients and together with the presence of anterior synechiae, they contribute to the occurrence of postkeratoplasty glaucoma (Mauer B, 2013, data under submission).
In conclusion, we fully agree with the authors that preexisting glaucoma is an important risk factor for the development of postkeratoplasty glaucoma, as also indicated by our study,5 but the transition of the observed postoperative ocular hypertension to true postkeratoplasty glaucoma involves much more complex mechanisms, such as the development of anterior synechiae and the permanent modification of the anterior chamber architecture, with significant decrease of the ACA. Georgios D. Panos, MD* Xuefei Song, MDw Berthold Seitz, MD, PhDw Zisis Gatzioufas, MD, PhD* *Department of Ophthalmology, Geneva University Hospitals HUG, Geneva Switzerland wDepartment of Ophthalmology, University Medical Center of Saarland UKS Homburg/Saar, Germany
REFERENCES 1. Oruc¸oglu F, Blumenthal EZ, FruchtPery J, et al. Risk factors and incidence of ocular hypertension after penetrating keratoplasty. J Glaucoma. 2013. [Epub ahead of print]. 2. Ayyala RS. Penetrating keratoplasty and glaucoma. Surv Ophthalmol. 2000; 45:91–105. 3. Karadag O, Kugu S, Erdogan G, et al. Incidence of and risk factors for increased intraocular pressure after penetrating keratoplasty. Cornea. 2010; 29:278–282. 4. Olson RJ, Kaufman HE. A mathematical description of causative factors and prevention of elevated intraocular pressure after keratoplasty. Invest Ophthalmol Vis Sci. 1977;16:1085–1092. 5. Gatzioufas Z, Labiris G, Mauer B, et al. Elevated intraocular pressure in the early postoperative period following excimer laser penetrating keratoplasty for keratoconus. Ophthalmic Surg Lasers Imaging. 2012;43:467–471.
Disclosure: The authors declare no conflict of interest. DOI: 10.1097/IJG.0000000000000176
662 | www.glaucomajournal.com
J Glaucoma
Volume 23, Number 9, December 2014
Risk Factors for Ocular Hypertension After Penetrating Keratoplasty To the Editor: Oruc¸oglu et al1 have recently published an interesting study investigating the risk factors contributing to ocular hypertension after penetrating keratoplasty (PK). The authors reported that 47.7% of the patients included in their study, manifested at least 1 consecutive episode of high intraocular pressure (IOP) (>21 mm Hg) during a mean follow-up of 24.4 months. The onset of IOP elevation was after a mean postoperative period of 70.3 ± 15.8 days and the mean duration of the observed ocular hypertension was 15.6 ± 2.0 days. Half of these patients presented a second episode of ocular hypertension occurring 212.2 ± 46.8 days after the surgery, with a mean duration of 18.1 ± 2.9 days. This study revealed that history of preexisting glaucoma, as well as additional surgical procedures combined with PK, were significant factors predicting the occurrence of ocular hypertension after PK. Nevertheless, we would like to highlight some aspects which, in our opinion, merit further consideration. It is well established that ocular hypertension may occur in the early postoperative period after PK.2,3 These episodes of IOP elevation are usually transient and resolve spontaneously without surgical intervention. However, the incidence of postkeratoplasty glaucoma, requiring surgical intervention or regular medication, is significantly lower compared to the ocular hypertension observed in the immediate postoperative period, as indicated in relevant studies.1–3 Therefore, one should distinguish between the benign, transient ocular
TO THE
EDITOR
hypertension after PK and the true postkeratoplasty glaucoma. Several mechanisms have been suggested as causative factors for ocular hypertension after PK, such as postoperative inflammation, potential steroid response, suturing technique, the diameter of the graft, etc., as also mentioned by the authors. It has also been highly assumed that anatomic changes in the anterior chamber and, predominantly, changes in the anterior chamber angle (ACA) could be associated with the occurrence of post-PK glaucoma; Olson and Kaufmann4 in their mathematical model attempted to correlate the IOP with the amount of ACA distortion. However, until today there was no evident proof of this clinical hypothesis. Our group has recently documented that ocular hypertension in the early postoperative period after PK for keratoconus is significantly correlated with changes in the anterior chamber architecture.5 Specifically, central and peripheral corneal thickness was significantly increased 2 months after PK, whereas anterior chamber depth, anterior chamber volume, and ACA in all 4 quadrants were significantly decreased,5 indicating potential significant reduction of outflow facility due to compression of the trabecular meshwork. These anatomic changes, which are probably induced by the postoperative inflammatory reaction and surgical stress (increase of corneal thickness and subsequent decrease of ACA), but also by the graft diameter and suturing/surgical technique (decrease of ACA) are partially reversible, resulting in spontaneous resolution of postkeratoplasty ocular hypertension (data under submission). However, these anatomic changes of the anterior chamber persist in some patients and together with the presence of anterior synechiae, they contribute to the occurrence of postkeratoplasty glaucoma (Mauer B, 2013, data under submission).
In conclusion, we fully agree with the authors that preexisting glaucoma is an important risk factor for the development of postkeratoplasty glaucoma, as also indicated by our study,5 but the transition of the observed postoperative ocular hypertension to true postkeratoplasty glaucoma involves much more complex mechanisms, such as the development of anterior synechiae and the permanent modification of the anterior chamber architecture, with significant decrease of the ACA. Georgios D. Panos, MD* Xuefei Song, MDw Berthold Seitz, MD, PhDw Zisis Gatzioufas, MD, PhD* *Department of Ophthalmology, Geneva University Hospitals HUG, Geneva Switzerland wDepartment of Ophthalmology, University Medical Center of Saarland UKS Homburg/Saar, Germany
REFERENCES 1. Oruc¸oglu F, Blumenthal EZ, FruchtPery J, et al. Risk factors and incidence of ocular hypertension after penetrating keratoplasty. J Glaucoma. 2013. [Epub ahead of print]. 2. Ayyala RS. Penetrating keratoplasty and glaucoma. Surv Ophthalmol. 2000; 45:91–105. 3. Karadag O, Kugu S, Erdogan G, et al. Incidence of and risk factors for increased intraocular pressure after penetrating keratoplasty. Cornea. 2010; 29:278–282. 4. Olson RJ, Kaufman HE. A mathematical description of causative factors and prevention of elevated intraocular pressure after keratoplasty. Invest Ophthalmol Vis Sci. 1977;16:1085–1092. 5. Gatzioufas Z, Labiris G, Mauer B, et al. Elevated intraocular pressure in the early postoperative period following excimer laser penetrating keratoplasty for keratoconus. Ophthalmic Surg Lasers Imaging. 2012;43:467–471.
Disclosure: The authors declare no conflict of interest. DOI: 10.1097/IJG.0000000000000176
662 | www.glaucomajournal.com
J Glaucoma
Volume 23, Number 9, December 2014
