Fig. 23.1
Corneal edema after cataract surgery. A 5-year-old child develops diffuse corneal edema on postoperative day one. Slit-lamp image shows marked corneal haze
23.1.1.1 Etiology
- 1.
Surgical trauma
Intraoperative mechanical damage is the leading cause of postoperative corneal edema. Considering the restricted operating space due to the small eyeball and shallow anterior chamber of children, corneal endothelial injury tends to occur when surgical instruments are introduced in and out of the anterior chamber or an IOL is implanted. In addition, Descemet membrane detachment (DMD) caused by improper manipulation and excessive anterior chamber irrigation may also cause damage to the corneal endothelium. The rate of postoperative corneal endothelial cell loss is estimated to be between 5.1 and 9.2 %. Corneal edema may occur in severe cases [1, 2].
- 2.
Postoperative inflammation
Postoperative inflammatory response can lead to corneal endothelial pump dysfunction and a certain degree of endothelial cell apoptosis.
- 3.
Ocular hypertension
Ocular hypertension can occur in the early or late stages after cataract surgery. It can directly damage the corneal endothelial pump function and result in diffuse corneal edema, whereas sometimes in young children, the cornea remains clear even when the intraocular pressure (IOP) reaches 40 mmHg or above and therefore goes undetected.
- 4.
Others
A dislocated IOL haptic may give rise to repeated chafing of the corneal endothelium, causing progressive corneal endothelial damage and then corneal edema. The residual lens materials or vitreous strands in the anterior chamber may adhere to the corneal endothelium and disrupt its metabolism, which results in focal corneal edema. If irritation to the corneal endothelium continues, intractable corneal edema may occur. Patients with a history of corneal endothelial dystrophy, iridocorneal endothelial syndrome, and previous intraocular surgery are prone to develop postoperative corneal edema.
23.1.1.2 Clinical Manifestations
- 1.
Local edema
Local edema, manifesting as localized swelling and thickening of the cornea, is usually caused by surgical trauma. Residual lens matter in the anterior chamber should be considered if inferior focal corneal edema is observed.
- 2.
Diffuse edema
Diffuse edema usually results from postoperative inflammation, toxic anterior segment syndrome (TASS), ocular hypertension, and wide range DMD, which manifests as Descemet membrane folds, diffuse thickening, and decreased transparency of the cornea.
- 3.
Descemet membrane curled inward
Rupture of Descemet membrane may give rise to corneal edema. The curled Descemet membrane floating in the anterior chamber can be observed through the cornea or confirmed if necessary by anterior segment optical coherence tomography (OCT).
23.1.1.3 Management
- 1.
Local edema
The vast majority of focal edema after pediatric cataract surgery is caused by temporary endothelial dysfunction and may disappear within a few days without special treatment. Xiao and colleagues retrospectively analyzed postoperative complications in 186 congenital cataract eyes (105 patients), reporting that the incidence of corneal edema in early stages after surgery is 35 % (65 eyes). The cornea edema disappeared in all cases within 3–5 days without special treatment [3]. However, anterior chamber irrigation or vitrectomy is recommended when extra amounts of lens matter or prolapsed vitreous are retained in the anterior chamber, causing persistent focal edema.
- 2.
Diffuse edema
Diffuse or persistent cornea edema, being one of the most severe postoperative complications, should be treated promptly according to the causes. For inflammation-induced corneal edema, enhanced anti-inflammation medication should be administrated by using topical corticosteroids and nonsteroidal anti-inflammatory drugs (NSAIDs), such as prednisone acetate 1 % or dexamethasone 0.1 %. Simon JW et al. reviewed five eyes (four children) with corneal edema after cataract surgery, reporting that the edema disappeared in 5–14 days after administration of topical corticosteroids [4]. For diffuse corneal edema induced by intense anterior segment inflammation (for example, TASS), systemic corticosteroids should be added. For corneal edema resulting from DMD, urgent reattachment of the Descemet membrane is necessary for restoration of cornea clarity. Small ruptures may be cured by intracameral injection of air or inert gas, whereas wide range DMD should be reattached by suturing full-thickness cornea. If elevated IOP is detected after surgery, topical or systemic anti-glaucoma medications can be administrated (for details, see Sect. 23.5). Generally, corneal clarity will be restored after IOP returns to normal.
23.1.2 Corneal Epithelial Abrasion
Corneal epithelial abrasion often occurs in the early postoperative period and may be caused by intraoperative trauma or rubbing eyes due to the discomfort caused to the patient. Additionally, for children in need of contact lens to correct aphakic refractive error without IOL implantation, caution should be consideration given to the corneal epithelium defects that may be induced by disinfectant solutions or the daily action of wearing and removing the contact lens.
Clinical manifestations of corneal epithelial abrasion include mixed hyperemia, punctuate or flake-shaped epithelial defects, positive fluorescein staining, redness of the eye, tearing, and pain.
For mild corneal epithelial abrasion, topical medications, such as recombinant bovine basic fibroblast growth factor and preservative-free artificial tears, can be used to promote corneal epithelial healing, whereas a bandage is recommended in severe cases to reduce blinking, relieve pain, and promote corneal epithelial healing.
23.2 Complications Associated with the Uvea
23.2.1 Uveitis
Uveitis is the most common complication after pediatric cataract surgery. Other complications, such as corneal edema, ocular hypertension, IOL-related complications, and even secondary blindness, may be induced or aggravated without timely treatment.
23.2.1.1 Etiology
- 1.
Immature blood-ocular barrier
Due to the immature blood-ocular barrier in pediatric eyes, surgical trauma is likely to give rise to nonspecific inflammatory response by the release of inflammatory substances such as cytokines, prostaglandins, and arachidonic acid and the bringing about of large amounts of cellulose inflammatory exudates.
- 2.
Improper incision construction
Since young children’s eyes have thin walls, iris prolapse may occur when the incision is not properly constructed. Repeated restoration of the prolapsed iris may exacerbate postoperative inflammation.
- 3.
Failure of in-the-bag IOL implantation
Despite the favorable biocompatibility of currently used IOLs, it is still regarded as a foreign body by nature. IOL implantation in the eye can therefore induce a series of cellular immune responses, especially when the IOL is not placed in the bag (such as in ciliary sulcus fixation and asymmetric implantation, say one haptic in the bag and the other in the sulcus). In these cases, the IOL haptics may rub the uvea and induce a significant inflammatory response.
- 4.
Residual lens matter
Residual lens matter in the aqueous humor can give rise to the autoimmune response and lead to phacoanaphylactic uveitis.
23.2.1.2 Clinical Manifestations
In mild cases, they show signs of aqueous flare and cells in the anterior chamber (Fig. 23.2a). In severe cases, fibrinous exudates, anterior and posterior iris synechiae, pupil deformation, and inflammatory membrane formation (Fig. 23.2b, c), as well as occlusion of the pupil, iris bombe, and secondary glaucoma, can be detected. Generally, the inflammatory response is more pronounced in pseudophakic eyes than in aphakic eyes.
Fig. 23.2
Clinical manifestations of uveitis after pediatric cataract surgeries. (a) Cells in the anterior chamber; (b) formation of inflammatory membrane on the anterior surface of IOL; (c) formation of inflammatory membrane on the posterior surface of IOL
23.2.1.3 Prevention and Management
- 1.
Preoperative
The pupil should be dilated adequately and NSAIDs should be applied if necessary.
- 2.
Intraoperative
- 1.
Be aware of the incision construction, to prevent irritation to the iris induced by iris prolapse.
- 2.
Reduce the frequency of the instruments moving in and out of the anterior chamber.
- 3.
Clear lens matter as thoroughly as possible.
- 4.
Achieve in-the-bag IOL implantation in order to reduce the contact and abrasion between IOL and the surrounding tissues. This helps to release postoperative uveal complications.
- 5.
Irrigate the anti-inflammatory drugs into the anterior chamber. Studies have shown that the addition of heparin in irrigating solutions reduced postoperative inflammatory responses and inflammation-related complications, including posterior iris synechiae, pupil dislocation, and IOL decentration [5]. Additionally, intracameral injection of triamcinolone acetonide could relieve anterior segment inflammation and prevent visual axis obscuration (VAO) [6]. Moreover, application of intracameral recombinant tissue plasminogen activator (r-TPA) during cataract extraction, anterior vitrectomy, and IOL implantation is effective in inhibiting the inflammatory response and preventing fibrinous membrane formation [7].
- 6.
Implant heparin-surface-modified (HSM) IOLs to control inflammation and pigment deposited on the surface of the IOL [8].
- 1.
- 3.
Postoperative
In most cases of mild postoperative inflammation, a combination of the topical short-acting mydriatics, corticosteroids, and NSAIDs can control the inflammation, while in severe cases, systemic corticosteroids or NSAIDs should be added. However, potent mydriatics are not generally recommended because of the risk of pupillary capture of the IOL. When inflammatory membranes block the visual axis or cause pupillary occlusion, Nd:YAG laser may be performed to retract the membranes. If the inflammatory membranes are too thick for laser therapy, membranectomy may be considered.
23.2.2 Toxic Anterior Segment Syndrome
TASS is an aseptic inflammation following anterior segment surgeries [9]. It is associated with substances with incorrect pH, concentration, or osmolarity, gaining access to the anterior chamber, such as irrigating solutions, antibiotics, OVDs, and residue left behind by substances used during the cleaning and sterilization of instruments and resulting in cytotoxicity and tissue injuries.
The most common manifestations of TASS include acute diffuse corneal edema, pupil dilation and fixation, ocular hypertension, and anterior chamber inflammation with or without significant pain. Since children are often too young to describe their complaints properly, detailed examinations are essential and endophthalmitis should be considered in the differentiation.
The preventive methods of TASS include following standardized procedures for cleaning and sterilizing intraocular surgical instruments, avoiding preservatives during and after surgery, and ensuring rational use of intraocular drug dosage and concentration.
The main treatment of TASS is topical and systemic application of corticosteroids to control inflammation and reduce tissue damage. Huang et al. [9] reported that though corneal edema and inflammation were controlled after aggressive treatment, cornea opacity and pupil deformation still remained, which indicates that to deal with TASS, the emphasis should be put on prevention.
23.2.3 Implantation Cyst of Iris
Cases of implantation cyst of iris after cataract surgery are rare, most of them are traumatic cataract patients. Generally, this disease has a long course and progresses very slowly. It is caused by conjunctival or corneal epithelial cells growing along the wound and slowly migrating into the iris stroma (Fig. 23.3). The cysts are most likely found to grow at the root of the iris and are filled with a white sticky fluid. They seldom cause pain but could result in various degrees of visual axis occlusion, uveitis, and corneal edema. Large cysts may even cause severe complications, including obstruction of anterior chamber angle, IOP elevation, and secondary glaucoma.
Fig. 23.3
Implantation cyst of iris. A 5-year-old boy with traumatic cataract underwent cataract extraction surgery combined with IOL implantation 1 year after surgery. (a) Iris cyst adherent to the nasal corneal wound; (b) slit-lamp examination; (c) 1 week after local iridectomy of the cyst
For small cysts, laser treatment is feasible with a certain risk of recurrence, while for large cysts, surgical excision combined with local iridectomy is necessary. In order to prevent recurrence, the cysts should be excised integrally and completely.
23.3 Complications Associated with the Lens Capsule
23.3.1 Posterior Capsular Opacification (PCO)
PCO is one of the most common complications after pediatric extracapsular cataract extraction (ECCE) surgery and can occur as early as 1 week postoperatively. The pathogenesis and prevention of PCO are described in detail in Chap. 24.
23.3.2 Capsular Shrinkage
Capsular shrinkage usually occurs 3–30 weeks after cataract surgery, manifesting as the decreasing of capsular diameter on the equator, combined with anterior capsule cystic fibrosis and diminished capsulotomy opening [10]. Factors such as surgical injuries, irritation of IOL material, inflammatory reaction, and disruption of the blood-aqueous barrier, stimulate residual lens epithelial cells to proliferate and transform into fibroblasts. These fibroblasts highly express α-smooth muscle actin and produce large amounts of collagen and other extracellular matrix which accumulates between the retained anterior capsule and IOL optic zone, leading to anterior capsule cystic fibrosis and turbidity. Additionally, α-smooth muscle actin from the fibroblasts contracts and pulls the capsulotomy opening toward the center and results in capsular shrinkage. The shrunken capsule may contribute to IOL dislocation or IOL capture, leading to postoperative diplopia, glare, and refractive errors, severely affecting the recovery of visual acuity.
The following advice may help to prevent capsular shrinkage: gentle surgical manipulation, avoidance of iris and blood-aqueous barrier damage, and the alleviation of postoperative inflammation. Furthermore, the diameter of capsulotomy openings should be controlled to around 5 mm. Small openings are prone to capsular shrinkage [11]. Moreover, IOL materials with good biocompatibility, such as acrylic IOL, can be chosen to reduce the IOL irritation to the capsule [12]. When capsular shrinkage induces IOL dislocation and affects the visual function significantly, Nd:YAG laser may be applied for anterior capsulotomy, while more severe cases will require surgical treatment.
23.4 Complications Associated with IOL
Compared with adults, inflammation responses are more severe, and the incidence of IOL-related complications is higher in children. The younger the patient, the higher the incidence of severe complications.
23.4.1 IOL Malposition
IOL malposition is associated with inflammation, incomplete openings during capsulotomy, organization and contraction of the capsule, asymmetric fixation of the IOL (a haptic in the bag, the other in the sulcus), IOL quality, residual lens matter, and lens epithelial proliferation following the cataract surgery.
Mild IOL malposition manifests as IOL decentration (Fig. 23.4a) and can only be detected after mydriasis. Generally, it requires no special treatment other than follow-up observation regarding changes in the IOL location and refractive error. Severe IOL malposition, shown as IOL dislocation (Fig. 23.4b) or IOL capture (Fig. 23.5), may contribute to monocular diplopia or high degree of astigmatism, significantly affecting the visual function. Pupillary capture of the IOL can also result in secondary increase of IOP. Surgery is often needed to reposition or remove the IOL. The indications and surgical techniques of repositioning and explantation are described in detail in Chap. 25.
Fig. 23.4
IOL malposition. (a) IOL decentration; (b) IOL dislocation
Fig. 23.5
IOL pupillary capture. (a) Partial pupillary capture of the IOL optic; (b) complete pupillary capture of the IOL optic
23.4.2 Deposits on the IOL Surface
Deposits on the IOL surface are more common in children than adults, which may be related to the immature blood-aqueous barrier and intense postoperative inflammation. It is also associated with the size, location, and quality of the IOL. If the IOL is too small, it is movable inside the eye and may rub the uvea, resulting in IOL surface deposits. Compared with sulcus-fixated IOLs, the in-the-bag fixation of IOLs has a lower occurrence of deposits, and the severity is minimal, because in-the-bag implantation reduces the chances of abrasion between the IOL optic and the surrounding tissue. The deposits can be pigmented (Fig. 23.6) or nonpigmented. No special treatment is required if the visual acuity is not affected. However, if the visual acuity is affected, it is suggested that Nd:YAG laser be employed to eliminate the deposits.
Fig. 23.6
Deposits on the surface of IOL
23.4.3 Opacification of IOL
Opacification of the IOL (Fig. 23.7) is mostly seen in silicone and hydrophilic acrylic materials [13] and is mainly associated with the biocompatibility of the IOL materials. Opaque IOL explanted from surgeries manifests calcification deposits under electron microscope examination, due to the deposition of calcium phosphate from the aqueous humor onto the surfaces or the inside of IOL. Owing to the development of IOL materials and improved production techniques over the past decades, this complication is rarely seen. Once the IOL opacification affects visual function significantly, IOL removal or exchange should be performed. Surgical techniques are detailed in Chap. 25.
Fig. 23.7
Opacification of IOL
23.5 Postoperative Ocular Hypertension and Secondary Glaucoma
Postoperative ocular hypertension and secondary glaucoma are major complications affecting visual function rehabilitation after pediatric cataract surgery. Postoperative ocular hypertension refers to a postoperative IOP higher than 21 mmHg, which is a risk factor for secondary glaucoma. But apart from high IOP, the diagnosis of glaucoma also includes optic nerve damage and visual field defect. Since these children are too young to cooperate with examinations such as IOP, optic nerve, and visual field measurement, it’s quite difficult to confirm diagnosis and evaluate the effect of treatments.
The reported incidence of ocular hypertension and glaucoma after pediatric cataract surgeries varies considerably (5–32 %) due to variance in the period of follow-up [14, 15]. From 2011, Zhongshan Ophthalmic Center (ZOC) has established a clinical database for pediatric cataract patients. Through follow-up observations of 206 pediatric cataract patients (379 eyes) under 10 years old for a period of 10–16 months, Lin reported that the incidence of postoperative ocular hypertension was 17.4 % [16]. Therefore, long-term follow-up of IOP measurement helps to prevent the occurrence of irreversible optic nerve damage in children following cataract surgery.
The types of secondary glaucoma following pediatric cataract surgery can be divided into two types: angle-closure and open-angle glaucoma, while the late-onset open-angle glaucoma is the most common. During the early and late postoperative period, angle-closure glaucoma can sometimes also occur.
23.5.1 Secondary Angle-Closure Glaucoma
Acute angle-closure glaucoma (Fig. 23.8) is a common complication after pediatric cataract surgery due to the limitations in surgical techniques and facilities during the past decades. With the development of surgical techniques, the incidence of this kind of complication decreases remarkably. The main cause is excessive lens cortex remnants inducing peripheral iris bombe and angle closure, while other causes are vitreous hernia and posterior synechiae (Fig. 23.9) and pupillary block due to pupillary occlusion. Francois and colleagues reviewed the causes of secondary angle-closure glaucoma after cataract surgery (Table 23.1) [17].
Fig. 23.8
Angle-close glaucoma after cataract surgery, showing shallow anterior chamber
Fig. 23.9
Pseudophakic eye with pupillary posterior synechia
Table 23.1
The causes of angle-closure glaucoma after congenital cataract surgery
1. Pupillary block or peripheral anterior synechia caused by uveitis |
2. Proliferative membrane and pupillary block caused by postoperative inflammation |
3. Delayed formation of the anterior chamber |
4. Vitreous prolapse into the anterior chamber |
5. Corneal epithelium grows into the anterior chamber |
6. Hyphema and intraocular hemorrhage |
7. Iris prolapse |
8. IOL-related glaucoma |
Chronic angle-closure glaucoma is quite rare, resulting mainly from intraocular chronic inflammation caused by residual lens matter, followed by occlusion of pupil, and finally elevation of IOP.
23.5.2 Secondary Open-Angle Glaucoma
Open-angle glaucoma is usually late onset and is the most common type of glaucoma after pediatric cataract surgery. Phelps and colleagues reviewed 18 cases with secondary glaucoma following congenital cataract surgeries and reported that the IOP could elevate between 2 and 45 years following the surgeries [18]. The angle in all the above cases was open and six of them had optic nerve damage. Pathogenesis of secondary open-angle glaucoma is not yet clear. Based on present studies, it is probably associated with residual viscoelastic agents, congenital glaucoma or abnormal anterior chamber angle structure that existed preoperatively [19] and surgery-induced defects in anterior chamber angle structure and trabecular meshwork [14], combined with ocular abnormalities including microcornea, microphthalmos, poorly dilated pupils, congenital rubella syndrome, Lowe’s syndrome, persistent embryonic eye vascularization, and other ocular anomalies [15]. Open-angle glaucoma is also related to surgery-induced mechanical and biochemical injuries, long-term usage of glucocorticoids, and other factors [20].
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