Cornea Transplantation-Induced Glaucoma: A Review of Glaucoma Secondary to PKP, DMEK, and DSAEK Procedures: Difference between revisions

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{{Article
{{Article
|Authors=Abanoob Tadrosse,Albert.S.Khouri
|Authors=Abanoob Tadrosse, BA and Albert S Khouri, MD
|Category=Cornea/External Disease, Glaucoma
|Category=Cornea/External Disease, Glaucoma
|Date reviewed=February 12, 2020
|Date reviewed=February 12, 2020

Revision as of 01:05, February 13, 2020

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Article initiated by:
Abanoob Tadrosse, BA, BA and Albert S Khouri, MD
All contributors:
Vatinee Y. Bunya, MD, MSCE, Albert S Khouri, MD, Colleen Halfpenny, M.D., Zeba A. Syed, MD, Ohoud A Owaidhah, MD
Assigned editor:
Review:
Assigned status Update Pending
.


Introduction

Glaucoma is a serious complication that follows keratoplasty procedures, causing significant morbidity[1]. Cornea transplantation usually induces increased intraocular pressure (IOP), which can accelerate the rate of corneal endothelial cell loss and graft failure[2]. In fact, two leading causes of graft failure post-keratoplasty procedures are graft rejection and secondary glaucoma development[3]. Patients with pre-operative glaucoma were observed to experience approximately twice to triple as many graft rejections as those without pre-existing glaucoma[4]. History of pre-existing glaucoma predisposes eyes to risk of IOP spikes post-keratoplasty. High IOP may also have far-reaching consequences leading to optic nerve damage and irreversible vision loss. This review aims at highlighting the incidence, mechanisms, and management of glaucoma following different corneal transplant procedures. We will focus mainly on the commonly performed procedures like penetrating keratoplasty (PKP), Descemet's Membrane Endothelial Keratoplasty (DMEK), and Descemet's Stripping Automated Endothelial Keratoplasty (DSAEK).

Background

PKP involves resecting the host cornea and replacing it with a full-thickness donor graft[5]. As it involves replacement of all corneal layers, patients with conditions such as considerable stromal scarring, keratoconus, and bullous keratopathy benefit the most from the procedure. The incidence of glaucoma following PKP is roughly 9 to 50%, and ranges from 10 to 31% in the early post-operative period and from 18 to 35% in the late post-operative period [1]. Further, herpes virus infection, trauma, and repeated corneal transplantation were shown to carry an increased risk for secondary glaucoma development post-PKP[2].

DMEK has been widely adopted, since it involves the replacement of only the endothelium and Descemet’s membrane[1]. It is a well recognizable alternative to PKP for diseases that involve corneal endothelial dysfunction. An advantage of DMEK is that it avoids creating stroma-to-stroma interface[5]. Such an interface can often be irregular, which potentially limits vision post-operatively. Common indications for DMEK include Fuch’s dystrophy, bullous keratopathy and graft failure. According to Maier et al., 15.4% of post-DMEK patients develop ocular hypertension within 24 hours after the procedure. Patients undergoing DMEK procedure in combination to cataract surgery and IOL implantation tend to have even higher incidence of IOP spikes post-operatively[6].

4Similar to DMEK, DSAEK procedures have been continuously increasing, replacing many of the PKP surgeries in cases that can be managed with selective replacement of diseased layers. From 2005 to 2008, the number of endothelial transplants increased from 1, 429 to 17, 468 cases [7]. PKP cases dwindled from 45, 821 to 32, 524 cases during the same time period. DSAEK involves transplanting the donor’s endothelium, Descemet’s membrane, and stroma. Being a lamellar endothelial keratoplasty procedure like DMEK, DSAEK has similar indications. In comparison to PKP, DSAEK offers faster recovery, less astigmatism development, and suture-related complications[5]. Yet, similar to PKP and DMEK, DSAEK shows considerable rates of glaucoma development post-operatively. According to one study, the incidence rates of IOP spikes post-DSAEK are 35% if the patient has no history of glaucoma, 45% with prior history, and 43% with pre-existing glaucoma-related surgery .

Etiology and Pathophysiology

There are different mechanisms that contribute to keratoplasty-induced glaucoma. It is important to consider such etiologies with respect to the time period they tend to present at, early or late post-operatively, for proper treatment. Early presentation tends to present within the first week(s) after surgery while late manifestation tends to occur in several weeks or months[8]. Pre-existing glaucoma predisposes to increased IOP post-keratoplasty, and can become the culprit early or late following surgery[9].

a. Penetrating Keratoplasty:

Early-Onset Glaucoma:

1) Viscoelastic Agent:

Viscoelastic material is applied in PKP procedures in order to ensure maintaining a physical depth between the posterior transplanted cornea and underlying structures including the iris and the lens[10]. This prevents corneal endothelial damage that can arise from mechanical injury. As much as it is essential to maintain corneal graft’s survival, viscoelastic substance is associated with increased incidence of post-PKP glaucoma[3]. Viscoelastics are generally divided into ones with high cohesiveness and others with high dispersiveness; highly cohesive materials are synthesized from a larger number of molecular chains, thus acquire a higher molecular weight and tend to be more readily removed after surgery [11]. Two of the widely used ophthalmic viscoelastic devices (OVD) are Healon 5 and Healon GV. Healon 5 has a molecular weight (MW) of 4, 000 kDa while Healon GV’s is 5, 000 kDa. Although they have been shown to cause less mean endothelial cell loss than other OVDs available, they have been associated with significant IOP increases, especially during the immediate postoperative period. This is likely due to their relatively high viscosities, promoting trabecular meshwork (TM) obstruction and hindering aqueous humor outflow from the anterior chamber (AC)[12].

2) Suturing Technique and Transplant Size:

In a study by Zimmerman et al., researchers speculated the phenomenon of disproportionate early glaucoma development post-PKP between phakic and aphakic patient populations[13]. The iridocorneal angle is demarcated anteriorly by the and Schwalbe’s line (termination of Descemet’s membrane) and posteriorly by the ciliary body (where zonules attach). The aphakic eye lacks adequate posterior support as it lacks the lens-zonule attachment. Moreover, deep or midstromal corneal sutures involved in keratoplasty can produce a posterior wound gape[14]. The Descemet’s membrane, in turn, is weakened and may retract posteriorly towards the iridocorneal angle, undermining the anterior support. Altering support areas might lead to TM collapse, impeding outflow. Whereas phakic eyes suffer the weakening of only the anterior support, aphakic eyes are vulnerable to weakening anteriorly and posteriorly. This accounts for the observation that aphakic eyes more readily develop post-PKP glaucoma.

3) Inflammation:

PKP, and surgeries in general, induce tissue deformation, which promotes a state of inflammation. This leads to disruption of the blood-aqueous barrier (BAB)[15]. As a result, Inflammatory cells and normal serum components flow into the aqueous humor in large amounts. They can clump up and become entrapped, impeding the outflow system. Further, fibrin-rich exudates can form adhesions connecting the iris to the trabecular meshwork (peripheral anterior synechiae, [PAS]) blocking the meshwork, and/or the lens (posterior synechiae). This can rapidly develop into pupillary block, causing secondary angle-closure glaucoma[9].

Late-Onset Glaucoma:

1) Corticosteroid-Induced Glaucoma:

Post-PKP use of corticosteroid is essential to prevent endothelial rejection and to maintain graft survival. However, steroids are postulated to inhibit phagocytic properties in the TM. This promotes the accumulation of cellular debris and obstructs outflow, which induces glaucoma[16]. Another potential mechanism through which steroids administration can induce glaucoma is through water retention [17][18]. Corticosteroids can stabilize lysosomal membranes, thus reducing lysosomal hyaluronidase. The subsequent accumulation of mucopolysaccharides leads to edema and narrowing of the TM.

2) Persistent Inflammation:

In case post-PKP inflammation persists for long periods, adhesions may form from the periphery of the iris to the TM—peripheral anterior synechiae (PAS)[9]. This occurrence is theorized to occur more often with an atrophic iris. PAS may lead to iridocorneal angle compression and induce IOP rise.

b. Descemet's Membrane Endothelial Keratoplasty:

Early-Onset Glaucoma:

An important mechanism for early glaucoma development in the immediate post-DMEK period is air bubble-induced angle closure. Melles et al. established a method to fixate the donor tissue to the host’s bed without sutures; he suggested introducing an air bubble in the AC to aid in holding the graft tightly to the host’s posterior stroma[19]. IOP rise almost always occurs until 2 hours following DMEK; however, persistently high IOP is estimated to take place in 12.5% of patients [20]. Larger air bubbles minimize the risk of graft detachment post-DMEK. Peripheral iridectomy should permeate flow of the aqueous humor when pupillary pathway is blocked in case the iris presses strongly against the lens. However, when the air bubble completely occupies the AC’s volume, there remains no volume for the aqueous flow into the AC through the patent peripheral iridectomy; thus, pressure builds up in the posterior chamber, as trapped fluid pushes against the iris, creating a posterior pupillary block.

Patients sitting in an upright position immediately post-DMEK may develop simultaneous anterior and posterior pupillary blocks. Peripheral iridectomy is traditionally performed in the 12-o’clock position. If an air bubble is injected such that it only partially fills up the AC, and the patient sits in the upright position, air will float upwards being less dense. This can render the iridectomy site dysfunctional as the air bubble takes space over it, and aqueous fluid may potentially overwhelm the inferior iris, displacing it forward. Both of these effects push the iris posteriorly (superiorly) and anteriorly (inferiorly), leading to angle closure.

Injected air bubble may also spread to the posterior chamber, pushing the iris anteriorly. This compresses the iridocorneal angle and obstructs aqueous flow.

Patients undergoing simultaneous DMEK and cataract surgery with IOL implantation show a greater likelihood of developing post-operative ocular hypertension or glaucoma than those receiving only DMEK. This could possibly be explained by multiple mechanisms including increased inflammation, altered angle anatomy, and the fact that the pseudophakic eyes exhibit a flexible IOL-iris diaphragm, which allows for more air to be injected into the AC. Greater air volume pumped, in turn, is more conducive to pupillary block development.

Similar to PKP-induced glaucoma, the cause of IOP spike in the early post-DMEK period can be from left-over viscoelastic material [21]. Viscoelastic material can be injected between the iris and the graft to prevent air bubble escape from the AC. Retained viscoelastic substance can induce IOP spike, as explained beforehand in post-PKP glaucoma.

Late-Onset Glaucoma:

The etiologies of observed increased IOP in the late post-operative period are not different from those seen in late-onset glaucoma for post-PKP patients. Blockage by inflammatory cells, PAS formation, and steroid use are common causes[21]. However, it is noteworthy to mention that steroid-induced glaucoma post-DMEK is not as common as that post-PKP or post-DSAEK. This is likely due to the short steroid regime post-DMEK that is usually sufficient to control inflammation and prevent IOP elevation.

c. Descemet's Stripping Automated Endothelial Keratoplasty:

The etiologies of early or late glaucoma development post-DASEK are not very different from those encountered post-PKP or post-DMEK 42. Similar to the DMEK procedure, DSAEK procedure involves the injection of an air bubble into the AC to adhere the graft to the host tissue. As such, the most common cause of early post-operative glaucoma development is pupillary block, similar to the mechanism of early IOP spike presentation in DMEK. Air in the AC can lead to pupillary block, while air that has intruded posterior to the iris may cause forward iris rotation and angle closure. In one study, pupillary block post-DSAEK was estimated to occur at a rate of 13%.

Prolonged Steroid use is a major cause of late-onset glaucoma in post-DSAEK patients. According to one study, 18.6% of post-DSAEK patients developed glaucoma secondary to steroid administration. Inflammatory glaucoma is still a possible etiology in post-DSAEK patients, but it tends to occur much less frequently than in post-PKP patients.

Diagnostic Workup

Pre-operative corneal disease presents a challenge to accurately assess IOP and visual field to determine a baseline for comparison in the post-operative period[22]. It is also difficult to measure IOP post-keratoplasty given changes in corneal thickness and the development of irregular astigmatism[23]. Additionally, epithelial edema and scar tissue can result in falsely reduced and elevated readings, respectively. As such, Goldmann Applanation Tonometer (GAT) readings can be imprecise as GAT is sensitive to corneal biomechanical variations. The Dynamic Contour Tonometer (DCT) serves as an alternate tool to measure IOP since it functions more independently from some mechanical factors that affect applanation tonometry[22].

It is important to mention that the gold standard for IOP measurements in post-DSAEK patients remains GAT, as increased corneal thickness is relatively minimal, thus not affecting the reading[3]. Other means of tonometry like Tono-Pen, pneumotonometer, and iCARE tonometry are other devices to measure IOP [24][25]. Moreover, disc evaluation that may include Optical Coherence Tomography or photographs should be taken on the first examination post-keratoplasty to serve as a baseline; imaging should be repeated as necessary or annually in case of glaucoma to detect any development or progression of glaucomatous optic neuropathy[26]. Diagnosis of post-keratoplasty ocular hypertension or glaucoma is established by IOP measurements early post-operatively, and by IOP measurement, visual field analysis, and optic disc changes late post-operatively.

PAS formation causing secondary angle closure is an important etiology of raised IOP post-keratoplasty in patients with totally opaque grafts[27]. Hence, ultrasound biomicroscopy (UBM) can be an important tool for determining appropriate sites for GDD placement and glaucoma filtering surgeries for this patient population. UBM is also especially useful after corneal transplantation as it can assess iridocorneal adhesions, AC depth, angle width, and corneal thickness[26].


Management

Since PKP has been the leading means of cornea transplantation before the relatively recent advent of DMEK and DSAEK, the bulk of scientific literature on post-keratoplasty glaucoma management has been studied on PKP patients. Nevertheless, the medical and surgical options available for managing IOP spikes in all three procedure types tend to be similar.

Pre-Operatively:

Operating on an eye with uncontrolled IOP can risk rapid decompensation post-keratoplasty. Hence, pre-existent glaucoma needs to be managed prior to surgery[22]. If high IOP is not adequately controlled with medical treatment, surgical intervention should be sought prior to corneal transplantation.

Intra-Operatively:

The suturing technique implemented in PKP is of critical importance. It has been shown that short and equal sutures bring forth favorable consequences due to less distortions of tissues and derangement of angle archtecture[22]. This is likely due to relatively minimal crowding of graft and host tissues, which decreases the tendency of iridocorneal angle collapse. Further, tight graft sutures prevent incarceration of the iris at the host-graft junction.

Immediately after corneal transplantation, topical steroid administration is essential to control inflammation[22]. This reduces the risk of posterior and peripheral anterior synechiae formation, which can potentially develop pupil block and PAS with IOP elevation. If given for long periods, it is imperative to monitor corticosteroid dosage given in order to reduce the risk of developing secondary steroid induced glaucoma. It is also common practice to use mydriatics in the early post-keratoplasty period to prevent pupillary block.

Moreover, leftover viscoelastic material increases the risk of TM blockage. Hence, it is crucial to remove the material as completely as possible at the conclusion of the transplantation procedure[22].

To prevent pupillary block secondary to total air filling in DMEK and DSAEK, it is recommended to fill the AC incompletely with 80% or less volume fill with air [20]. This circumvents pupillary block by disallowing air to push against the pupil, obstructing aqueous flow; air injected will rest on top of a 360-degree meniscus of aqueous fluid, which permeates aqueous fluid’s passage through the site of the peripheral iridectomy. Further, IOP may spike from pupil block when sitting in an upright position post-DMEK or DSAEK as discussed previously. This can be prevented by creating an inferior peripheral iridectomy, rather than one in the 12-o’clock position. That way aqueous flow is less likely to be hindered by the injected air bubble that will float superiorly as the patient assumes an upright position.

Post-Operatively:

Medical Treatment:

The initial post-operative management of keratoplasty-induced glaucoma is through topical medications[26]. Beta adrenergic blocking agents, adrenergic agonist, and topical carbonic anhydrase inhibitors lower IOP by decreasing aqueous humor production. Generally topical agents have a rapid onset, and are appropriate medications for long-term effect. While adverse effects are largely tolerable, topical agents have been associated with punctate epithelial keratopathy and corneal anesthesia that may affect the graft’s epithelium[22]. On the other hand, allergic reactions to alpha-agonists are known to occur. Brimonidine tartarate (0.15% or 0.2%) is typically used three times daily if prescribed as a monotherapy, or twice if in combination with other agents[26].

Oral carbonic anhydrase inhibitors use is typically only implemented early post-operatively, but if later usage is needed, topical CAIs are more preferred. Topical CAIs do not carry the same significant side effects of the systemic version (metabolic acidosis, paresthesia, gastrointestinal upset, kidney stones, among others)[22]. CAIs have been shown to interfere with carbonic anhydrase function in the corneal epithelium and endothelium causing irritative symptoms and risking edema and graft decompensation although very rare[28]. Therefore, patients on CAIs should be monitored for those adverse effects.

As opposed to beta-blockers and alpha-agonists, prostaglandin analogs’ effects tend to be slower, and thus are a more adequate choice for chronic post-cornea transplantation glaucoma. These agents are given once daily and are associated with fewer systemic effects. Careful and regular monitoring for side effects is important including the development of cystoid macular edema[29]. Further, some studies have shown recurrence of herpetic keratitis in patients with a history of the disease, and so prostaglandin analogs should be prescribed with caution for this patient population[30].

Laser Treatment:

Patients with keratoplasty-induced glaucoma that is not controlled with medications can be treated with Selective laser trabeculoplasty (SLT) has been largely implemented due to its relatively few complications, and comparable efficacy, relative to ALT. Since it is able to confine applied thermal radiation, SLT can operate while avoiding collateral damage to nearby tissue[31]. It is targeted to the pigmented cells in the TM, and typically functions at a power setting of 0.4-1.2 mJ. The device delivers 0 μm laser spots in 3 ns. Adding to the regional selectivity potential of SLT, it is proposed that SLT can often be used to induce more pressure lowering after a prior ALT procedure. This repeatability aspect can be as a result of SLT not causing TM scarring. Adding to the advantages of SLT implementation, it is not associated with PAS formation and causes minimal pain and flare in the AC [32]. It is important to note that although SLT has been shown to control elevated IOP secondary to keratoplasty procedure, pressure tends to rise again after approximately six months.

Nd:YAG laser iridotomy can be utilized in post-keratoplasty patients with pupillary blockage. However, the peripheral cornea is usually not transparent enough, presenting a challenge to performing the procedure 5.

Surgical Treatment:

Trabeculectomy:

Trabeculectomy is one of the surgical interventions to consider for post-keratoplasty glaucoma treatment that is progressive and refractory to medical therapy. However, challenges of subconjunctival filtering surgery in eyes with prior surgery include scar formation and the need for additional surgical interventions. This is likely due to the severe subconjunctival fibrosis secondary to prior interventions, and PAS formation[33]. Both factors can affect the long term a=outcomes after trabeculectomy. In one study, 92% of PKP-induced glaucoma patients treated with trabeculectomy still need medications, while 53% required another surgical intervention.

References

  1. ↑ Jump up to: 1.0 1.1 1.2 Haddadin, Ramez I., and James Chodosh. “Corneal Transplantation and Glaucoma.” Seminars in Ophthalmology, vol. 29, no. 5-6, 2014, pp. 380–396., doi:10.3109/08820538.2014.959201.
  2. ↑ Jump up to: 2.0 2.1 Baltaziak, Monika, et al. “Glaucoma after Corneal Replacement.” Survey of Ophthalmology, vol. 63, no. 2, 2018, pp. 135–148., doi:10.1016/j.survophthal.2017.09.003    
  3. ↑ Jump up to: 3.0 3.1 3.2 Al-Mahmood, Ammar M., et al. “Glaucoma and Corneal Transplant Procedures.” Journal of Ophthalmology, vol. 2012, 2012, pp. 1–9., doi:10.1155/2012/576394    
  4. ↑ Janson, Ben J., et al. “Glaucoma-Associated Corneal Endothelial Cell Damage: A Review.” Survey of Ophthalmology, vol. 63, no. 4, 2018, pp. 500–506., doi:10.1016/j.survophthal.2017.11.002    
  5. ↑ Jump up to: 5.0 5.1 5.2 Boynton, Grace E., and Maria A. Woodward. “Evolving Techniques in Corneal Transplantation.” Current Surgery Reports, vol. 3, no. 2, 2015, doi:10.1007/s40137-014-0079-5    
  6. ↑ Maier AK, Wolf T, Gundlach E, et al. Intraocular pressure elevation and post-DMEK glaucoma following Descemet membrane endothelial keratoplasty. Graefes Arch Clin Exp Ophthalmol. 2014;252:1947–1954    
  7. ↑ Eye Banking Statistical Report. Washington, District of Columbia, USA: EyeBank Association of America; 2007    
  8. ↑ Rumelt, Shimon. “Glaucoma in Cases of Penetrating Keratoplasty, Lamellar Procedures and Keratoprosthesis.” Glaucoma - Basic and Clinical Concepts, 2011, doi:10.5772/23895.    
  9. ↑ Jump up to: 9.0 9.1 9.2 Greenlee, Emily C., and Young H. Kwon. “Graft Failure: III. Glaucoma Escalation after Penetrating Keratoplasty.” International Ophthalmology, vol. 28, no. 3, 2008, pp. 191–207., doi:10.1007/s10792-008-9223-5    
  10. ↑ Sugar, Alan, and Joel Sugar. “Techniques in Penetrating Keratoplasty.” Cornea, vol. 19, no. 5, 2000, pp. 603–610., doi:10.1097/00003226-200009000-00005    
  11. ↑ Holzer, Mike P, et al. “Effect of healon5 and 4 Other Viscoelastic Substances on Intraocular Pressure and Endothelium after Cataract Surgery.” Journal of Cataract & Refractive Surgery, vol. 27, no. 2, 2001, pp. 213–218., doi:10.1016/s0886-3350(00)00568-x    
  12. ↑ Stamper , Robert, et al. “Effect of Intraocular Aspiration of Sodium Hyaluronate on Postoperative Intraocular Pressure.” Ophthalmic Surgery, Lasers and Imaging Retina, vol. 21, no. 7, 1 July 1990, pp. 486–491., doi:10.3928/1542-8877-19900701-08    
  13. ↑ Zimmerman, Thom. “Transplant Size and Elevated Intraocular Pressure.” Archives of Ophthalmology, vol.96,no.12,1978, p.2231.,doi:10.1001/archopht.1978.03910060533012    
  14. ↑ Zimmerman, T. J., et al. “The Effect of Suture Depth on Outflow Facility in Penetrating Keratoplasty.” Archives of Ophthalmology, vol. 96, no. 3, 1978, pp. 505–506., doi:10.1001/archopht.1978.03910050273018    
  15. ↑ Bodh, Sonama, et al. “Inflammatory Glaucoma.” Oman Journal of Ophthalmology, vol. 4, no. 1, 2011, p. 3., doi:10.4103/0974-620x.77655    
  16. ↑ Kersey, J P, and D C Broadway. “Corticosteroid-Induced Glaucoma: A Review of the Literature.” Eye, vol. 20, no. 4, 2005, pp. 407–416., doi:10.1038/sj.eye.6701895    
  17. ↑ Francois J .Corticosteroidglaucoma. Ann Ophthalmol 1977; 9: 1075–1080    
  18. ↑ Armaly MF . Effect of corticosteroids on intraocular pressure and fluid dynamics: I. The effect of dexamethasone in the normal eye. Arch Ophthalmol 1963; 70: 482–491    
  19. ↑ Melles GR, Lander F, Nieuwendaal CP. Sutureless, posterior lamellar keratoplasty: a case report of a modified technique. Cornea. 2002;21:325–327    
  20. ↑ Jump up to: 20.0 20.1 Röck, Daniel, et al. “Air Bubble–Induced High Intraocular Pressure After Descemet Membrane Endothelial Keratoplasty.” Cornea, vol. 35, no. 8, 2016, pp. 1035–1039., doi:10.1097/ico.0000000000000901    
  21. ↑ Jump up to: 21.0 21.1 Ang, Marcus, and Chelvin C.a. Sng. “Descemet Membrane Endothelial Keratoplasty and Glaucoma.” Current Opinion in Ophthalmology, vol. 29, no. 2, 2018, pp. 178–184., doi:10.1097/icu.0000000000000454    
  22. ↑ Jump up to: 22.0 22.1 22.2 22.3 22.4 22.5 22.6 22.7 Zemba, Mihail, and Alina-Cristina Stamate. “Glaucoma after Penetrating Keratoplasty.” Romanian Journal of Ophthalmology, vol. 61, no. 3, 2017, pp. 159–165., doi:10.22336/rjo.2017.30    
  23. ↑ Ayyala, Ramesh S. “Penetrating Keratoplasty and Glaucoma.” Survey of Ophthalmology, vol. 45, no. 2, 2000, pp. 91–105., doi:10.1016/s0039-6257(00)00141-7    
  24. ↑ West, Carol E., et al. “Measurement of Intraocular Pressure with a Pneumatic Applanation Tonometer.” American Journal of Ophthalmology, vol. 74, no. 3, 1972, pp. 505–509., doi:10.1016/0002-9394(72)90917-8    
  25. ↑ Rootman, David S. “Accuracy and Precision of the Tono-Pen in Measuring Intraocular Pressure After Keratoplasty and Epikeratophakia and in Scarred Corneas.” Archives of Ophthalmology, vol. 106, no. 12, 1988, p. 1697., doi:10.1001/archopht.1988.01060140869030    
  26. ↑ Jump up to: 26.0 26.1 26.2 26.3 Dada, Tanuj, et al. “Post-Penetrating Keratoplasty Glaucoma.” Indian Journal of Ophthalmology, vol. 56, no. 4, 2008, p. 269., doi:10.4103/0301-4738.41410.    
  27. ↑ Dada, Tanuj, et al. “Ultrasound Biomicroscopy in Opaque Grafts With Post-Penetrating Keratoplasty Glaucoma.” Cornea, vol. 27, no. 4, 2008, pp. 402–405., doi:10.1097/ico.0b013e31816373c5    
  28. ↑ Konowal, A, et al. “Irreversible Corneal Decompensation in Patients Treated with Topical Dorzolamide.” American Journal of Ophthalmology, vol. 127, no. 4, 1999, pp. 403–406., doi:10.1016/s0002-9394(98)00438-3    
  29. ↑ Kaufman, Herbert E, et al. “Latanoprost Increases the Severity and Recurrence of Herpetic Keratitis in the Rabbit.” American Journal of Ophthalmology, vol. 127, no. 5, 1999, pp. 531–536., doi:10.1016/s0002-9394(99)00089-6    
  30. ↑ Wand, Martin, et al. “Latanoprost and Herpes Simplex Keratitis.” American Journal of Ophthalmology, vol. 127, no. 5, 1999, pp. 602–604., doi:10.1016/s0002-9394(99)00050-1    
  31. ↑ Mcalinden, C. “Selective Laser Trabeculoplasty (SLT) vs Other Treatment Modalities for Glaucoma: Systematic Review.” Eye, vol. 28, no. 3, 2013, pp. 249–258., doi:10.1038/eye.2013.267    
  32. ↑ Nakakura, Shunsuke, et al. “Selective Laser Trabeculoplasty for Glaucoma After Penetrating Keratoplasty.” Optometry and Vision Science, vol. 86, no. 4, 2009, doi:10.1097/opx.0b013e318199d226    
  33. ↑ Gilvarry, A M E, et al. “The Management of Post-Keratoplasty Glaucoma by Trabeculectomy.” Eye, vol. 3, no. 6, 1989, pp. 713–718., doi:10.1038/eye.1989.110    
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