Glaucoma After Cataract Surgery


Key Points

  • Clear corneal phacoemulsification generally reduces intraocular pressure (IOP) in glaucoma and ocular hypertensive eyes.

  • A list of differential diagnoses should exist in the minds of all cataract surgeons when evaluating patients with elevated IOP after cataract surgery.

  • Immediate postoperative IOP spikes can be common, especially in glaucoma patients, and can be mitigated using specific medical agents.

  • Warning signs and risk factors for the development of intraoperative or postoperative malignant glaucoma should be identified.

  • The timing of and features of steroid response should be considered, especially in patients with preexisting glaucoma.

Introduction

Although modern cataract surgery has become exceedingly safe and predictable, unique challenges remain with regards to postoperative development of elevated intraocular pressure (IOP). Increasing evidence suggests that cataract surgery tends to reduce IOP in patients with glaucoma or ocular hypertension. Several causes of increased IOP shortly after cataract surgery should be considered, and they can be easily differentiated based on timing of presentation, examination findings, and response to therapy. These etiologies are as follows:

  • Retained ophthalmic viscosurgical device (OVD) in the anterior segment

  • Malignant glaucoma

  • Steroid response

  • Overfilled anterior chamber

  • Post Nd:YAG capsulotomy

An additional cause of a relatively late development of glaucoma after cataract surgery is the development of uveitis-glaucoma-hyphema (UGH) syndrome.

Rare causes of elevated IOP after cataract surgery need not be discussed in detail and include postoperative inflammation, potentially with associated pupillary seclusion and pupillary block, retained lens material, hyphema, capsular bag distension syndrome, vitreous block, tight-closure techniques, suture compression, and edema mechanically distorting the angle and compromising aqueous outflow in traditional extracapsular surgery (generally not seen in modern scleral tunnels, manual small-incision cataract surgery, and clear cornea phacoemulsification techniques).

Causes

The main causes of glaucoma or elevated IOP after cataract surgery can be broken down based on timing and examination findings.

Retained OVD

Insufficient irrigation and aspiration of OVD at the conclusion of cataract surgery can result in an elevated postoperative IOP. This typically results in an IOP elevation shortly after surgery, with peak incidence within the first 1 to 2 postoperative days. Often, these IOP elevations can be identified within hours of surgery. In a study of glaucoma patients undergoing cataract surgery, 17% of subjects experienced at least a 50% increase in IOP compared with their preoperative baseline.

Risk factors for this sort of early postoperative IOP spike include underlying glaucoma diagnosis, as evidenced by known examination findings, elevated preoperative IOP, use of antiglaucoma medications, or history of laser trabeculoplasty. Furthermore, eyes with a longer axial length were noted to be at higher risk for early postoperative IOP spike.

Examination of eyes with retained OVD can often be unremarkable. Because this is a relatively early postoperative issue, expected postoperative edema and inflammation may be evident. However, the retained OVD may result in a relatively static appearance to the anterior chamber cells caused by the greater viscosity of OVD relative to aqueous humor.

Malignant Glaucoma

Malignant glaucoma (MG) is a relatively rare cause of postoperative IOP increase. This condition is characterized by an axial shallowing of the anterior chamber in the absence of choroidal effusions.

  • This condition should be distinguished from fluid misdirection syndrome, in which intraoperative irrigation fluid crosses the zonular plane and hydrates the vitreous body, thus causing anterior chamber shallowing.

    • Although fluid misdirection is a self-limited process as the excess fluid is reabsorbed, MG can progressively worsen unless managed.

  • The pathophysiology of MG remains debated. Popularly known as aqueous misdirection , there has been no evidence of truly misdirected aqueous humor, and such a mechanism would require a one-way ball valve to exist in the eye. Instead, MG is thought to be incited by an expansion of the choroidal volume, often because of transient intraoperative hypotony of the anterior chamber. This choroidal expansion causes a relative increase in the pressure of the posterior segment and resultant compaction of the vitreous body. This compaction causes inability of this increased posterior segment pressure to be transduced across the anterior vitreous, thus resulting in an axial shallowing of the lens and iris. IOP ultimately increases when this axial shallowing results in angle closure.

  • Clinical presentation of postoperative MG can be subtle in its early stages. A myopic refractive surprise is often identified. On clinical examination, the distance between the IOL and the iris may appear smaller than usual ( Fig. 51.1 ).

    Fig. 51.1, Anterior segment ultrasound biomicroscopy (UBM) demonstrating an axial anterior shift of the intraocular lens and capsule complex, with resultant angle closure.

  • With progression of the underlying pathophysiology, further axial shallowing can occur, and gonioscopy can reveal closed angles with an elevated IOP. Importantly, IOP may not increase until angle closure develops, but the underlying process should be identified nevertheless.

  • In a series of 20 eyes developing MG after cataract surgery, presentation occurred at 5.8 ± 7.1 weeks after surgery. All eyes had narrow or closed angles preoperatively and were often hyperopes.

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