Nd:YAG Capsulotomy
Jason Ellen
Sophia Leung
The use of a quick-pulsed neodymium-doped yttrium aluminum garnet (Nd:YAG) laser (1064 nm) for capsulotomy dates back to the early 1980s. A plasma microexplosion is created by the Nd:YAG laser and the resulting shockwave allows for photodisruption of ocular tissue.1 A directional offset is often used to aim the shockwave volume away from adjacent structures to avoid unwanted damage. Nd:YAG laser capsulotomy (Nd:YAG capsulotomy) is the standard treatment for posterior capsular opacification (PCO), replacing manual discission and its associated risks of endophthalmitis and vitreous loss.2
Development of PCO is mainly caused by remaining residual lens epithelial cells (LECs), which migrate and spread along the inner face and surface of the capsular bag after cataract removal. LECs transdifferentiate into myofibroblasts, which proliferate and cause fibrosis, resulting in capsular opacification. The innate immune system has also been implicated in the fibrosis process.3
Multiple forms of PCO exist. Fibrotic PCO occurs when LECs undergo fibrous metaplasia appearing as folds and wrinkles. The presence of posterior subcapsular cataracts can lead to plaque-like PCO, which appears hard, white, and dense. Elschnig pearls or Soemmering rings occur when LECs undergo crystalline-expressing lenticular fiber regeneration or when residual cortical cells proliferate.4,5 This appears as clear “droplets” and is best seen in retroillumination. Posterior capsular distension syndrome occurs when residual lens remnants are trapped and absorb fluid. The resulting appearance is focally thick and dense at the posterior capsule. Mechanical PCO results from intraoperative folds and tears that lead to posterior capsular irregularities and can have variable presentations.4 While specific classification of PCO types does not necessarily change the treatment, certain types may require higher-energy settings and specific treatment considerations, which will be discussed later (Fig. 17.1).
At five years from cataract surgery, PCO occurs in up to 29% of patients.2 Factors associated with increased PCO development include the following:
Cataract Severity at the Time of Surgery
Higher chances for residual LECs that lead to PCO formation are associated with advanced posterior subcapsular cataracts, nuclear sclerotic cataracts, and mature cataracts.5 For example, a dense posterior subcapsular cataract (PSC) may be partially
embedded into the posterior capsule risking posterior capsular rupture during extraction. Less posterior capsule polishing during surgery may be performed to mitigate the risk of posterior capsular rupture. This often leads to increased PCO. In certain cases, conversion from phacoemulsification to extracapsular cataract extraction (ECCE) may be necessary, which also increases the risk of PCO development.6
embedded into the posterior capsule risking posterior capsular rupture during extraction. Less posterior capsule polishing during surgery may be performed to mitigate the risk of posterior capsular rupture. This often leads to increased PCO. In certain cases, conversion from phacoemulsification to extracapsular cataract extraction (ECCE) may be necessary, which also increases the risk of PCO development.6
Surgical Technique
Intraocular Lens Implant Design
Intraocular lenses (IOL) that have blunt edges will have a higher rate of PCO formation, whereas IOL designs that have sharper edges are thought to disrupt LEC migration thereby reducing PCO formation.3 Hydrophilic acrylic lens materials (such as in Akreos) are more prone to posterior capsular pearl formation. Single-piece intraocular lens (IOL) designs have been observed to allow more PCO development than three-piece IOL designs.
Younger Age
This is likely due to more rapid cellular restructuring and healing in younger patients.4
Inactive or Active Uveitis
Twenty percent of patients with a history of uveitis develop PCO within the first year after cataract surgery.3
Anterior capsular opacification or anterior phimosis occurs with similar pathophysiology to PCO, but at the anterior capsulorhexis edge instead. Anterior capsular contraction syndrome occurs more often in patients with pseudoexfoliation syndrome, retinitis pigmentosa, primary angle closure, and diabetic retinopathy.8 Such contraction from anterior phimosis can result in visual disturbance, IOL decentration, and/or flexion. This can occur with or without the use of capsular tension rings (Fig. 17.2).9
INDICATIONS
Key Indications
Decreased vision, subjective visual complaints, and increased glare complaints caused by capsular opacification
Capsular contraction syndromes
Refractive shifts in plate haptic or pseudo-accommodating IOLs
Prior to refractive enhancements in pseudophakic patients
For insurance qualifications, decreased vision must be confirmed by decreased visual acuity of two lines or more, in normal lighting or by Brightness Acuity Testing (BAT). However, it is important to note that a subjective visual decrease may not involve the loss of visual acuity and, nonetheless, be visually significant to the patient. The decision to treat may be independent of whether the procedure will be reimbursed by insurance or not. Monocular diplopia and impaired contrast sensitivity are often reported symptoms as well.10 Visual acuity with multifocal IOL technology is more likely to be affected, reported, and visually symptomatic in earlier stages of capsular opacification.
Anterior capsular contraction syndrome results when anterior phimosis results in lens flexing. Treatment to reduce tension is necessary. Anterior phimosis also warrants treatment if opacification is observable within the pupil margin, which affects visual acuity or causes subjective visual complaints. In posterior capsular contraction syndrome, early signs of Z formation of an IOL (as seen with Crystalens) warrant Nd:YAG capsulotomy. Z formation presents as an asymmetric vaulting where one plate haptic is bent forward while the other is bent backward, resulting in astigmatic and myopic shifts. It is now standard to perform early Nd:YAG capsulotomy in all Crystalens patients as soon as fibrosis or lenticular astigmatism is observed.11 If Nd:YAG capsulotomy is insufficient, surgical correction may be required (Fig. 17.3).
A “pre-refractive” Nd:YAG capsulotomy may be warranted prior to corneal refractive surgery enhancement for pseudophakic patients so that future lens flexion and refractive error changes from capsular contraction syndromes are prevented. This is more commonly considered in “refractive cataract surgery” patients.
CONTRAINDICATIONS
Key Relative Contraindications
If visual complaints are due to other treatable ocular pathology
Corneal scars and opacities that prevent capsular opacifications to be clearly visible
If the patient is unable to fixate stably or sit stably for the procedure
Active intraocular inflammation (uveitis, cystoid macular edema) or high risk of intraocular inflammation (history of cystoid macular edema, diabetes, epiretinal membrane)
Patients with high risk of retinal detachment
Despite the presence of capsular opacification, other treatable ocular pathology that is more responsible for patient complaints ought to be addressed first and expectations set appropriately.
Use caution if performing Nd:YAG capsulotomy in an eye where visibility is hindered by corneal pathology (previous radial keratotomy, epithelial basement membrane dystrophy (EBMD), Fuchs dystrophy, corneal edema, and scars). Using a
contact capsulotomy laser lens helps to improve visualization through corneal opacities. It also provides better focusing and concentration of the Nd:YAG laser beams.12 However, in patients who have advanced EBMD, a laser lens may not be appropriate due to a higher risk of unintentional corneal debridement from suction upon laser lens removal. Corneal opacities may also necessitate an increase in overall energy level, which may increase the risk of inflammation, intraocular pressure (IOP) spike, cystoid macular edema (CME), and potentially retinal detachments.14
contact capsulotomy laser lens helps to improve visualization through corneal opacities. It also provides better focusing and concentration of the Nd:YAG laser beams.12 However, in patients who have advanced EBMD, a laser lens may not be appropriate due to a higher risk of unintentional corneal debridement from suction upon laser lens removal. Corneal opacities may also necessitate an increase in overall energy level, which may increase the risk of inflammation, intraocular pressure (IOP) spike, cystoid macular edema (CME), and potentially retinal detachments.14
For patients who have trouble with stable fixation, a contact laser lens is extremely helpful. A laser lens provides 1.8× magnification, which is especially helpful in the presence of anterior segment opacities. As previously mentioned, it also helps concentrate the laser energy through corneal opacities.12 A laser lens also provides stabilization of the patient’s eye during treatment by negating the blink reflex. In addition, a contact laser lens is useful with heavy breathers as it helps maintain the IOL on a single plane as the patient breathes (Fig. 17.4).
For patients who are unable to sit still for the procedure, utilization of head straps or having an assistant help stabilize a patient’s head position at the laser can be effective. This increases accuracy and ease during the procedure. In certain situations, an oral sedative may be helpful to decrease uncontrollable movement and tremors, and a pinhole capsulotomy may be sufficient enough to improve functional vision. If stability is not possible, Nd:YAG capsulotomy should not be performed. Surgical discission under general anesthesia performed by a retina or cataract surgeon may be required in such cases. This may be warranted in patients with nystagmus, for example.
Active intraocular inflammation should be treated and managed prior to performing Nd:YAG capsulotomy. This includes postoperative inflammation from cataract surgery. Generally, one should wait at least three months after cataract surgery before doing a Nd:YAG capsulotomy. Although limited evidence is found for this recommendation, general consensus for the three-month postoperative period is to conservatively allow for IOL exchange if necessary. Some recommendations also include waiting at least one month after intraocular inflammation has resolved.10
The presence of CME is also a relative contraindication and CME should be treated, stable, or resolved prior to the procedure. In patients who are at higher risk of developing
CME (i.e., diabetic, presence of epiretinal membrane, previous vitrectomy),15 pretreatment with a topical nonsteroidal anti-inflammatory agent (NSAID) or topical corticosteroid the week prior to the procedure may be warranted, per doctor’s discretion.2
CME (i.e., diabetic, presence of epiretinal membrane, previous vitrectomy),15 pretreatment with a topical nonsteroidal anti-inflammatory agent (NSAID) or topical corticosteroid the week prior to the procedure may be warranted, per doctor’s discretion.2
Patients with a high risk of retinal detachment must be monitored carefully during the postoperative period. These include patients who have a history of retinal detachments, lattice degeneration, axial length greater than 24 mm, vitreoretinal pathology, and intraoperative complications.2