Transscleral Cyclophotocoagulation: Laser Steps and Histology

Transscleral cyclophotocoagulation (TSCPC) is a laser treatment used to lower intraocular pressure in patients with refractory glaucoma. By targeting the ciliary body, which produces aqueous humor, this procedure helps manage cases where conventional treatments have failed or are not viable. It is often considered for patients at risk of vision loss due to uncontrolled eye pressure.

This technique involves precise laser application through the sclera, leading to structural changes that reduce aqueous humor production. Understanding the procedural steps, tissue response, and post-treatment effects is essential for optimizing outcomes and minimizing complications.

Mechanism Of Laser Tissue Interaction

The interaction between laser energy and ocular tissues in TSCPC is governed by photothermal coagulation. The diode laser, typically operating at 810 nm, is absorbed by melanin in the pigmented epithelium of the ciliary body. This absorption leads to localized heating, causing protein denaturation and coagulative necrosis. The extent of thermal damage depends on laser power, exposure duration, and tissue pigmentation. Higher melanin concentration enhances energy absorption, necessitating careful parameter selection to balance efficacy and safety.

As the laser energy penetrates the sclera, heat conduction determines the depth and spread of tissue alteration. The sclera has low absorption at this wavelength, allowing energy to reach the ciliary body with minimal collateral damage. However, thermal diffusion can extend beyond the target, affecting adjacent structures like the ciliary processes and vasculature. Research in the American Journal of Ophthalmology has shown that excessive thermal spread can lead to complications such as inflammation and prolonged hypotony. To mitigate these risks, controlled pulse durations and spacing between applications allow heat dissipation, preventing excessive cumulative damage.

Laser-induced coagulation triggers immediate structural changes, followed by delayed remodeling. The treated ciliary epithelium shrinks and loses function, reducing aqueous humor production. This effect results not only from direct tissue ablation but also from secondary vascular alterations. Coagulation can cause thrombosis in the ciliary body’s microvasculature, further impairing its secretory function. A study in Ophthalmology found that vascular occlusion significantly contributes to intraocular pressure reduction, highlighting the importance of precise energy delivery.

Procedural Steps And Equipment

Performing TSCPC requires meticulous planning to ensure effective treatment while minimizing adverse effects. The procedure begins with patient positioning and anesthesia. Peribulbar or retrobulbar anesthesia is typically preferred for ocular immobilization and pain control, though some clinicians opt for a subconjunctival injection when a less invasive approach is warranted. The choice depends on patient tolerance and the need for precise laser application.

Coupling the laser probe to the scleral surface is critical. The G-Probe, designed for controlled diode laser delivery at 810 nm, is commonly used. Its footplate ensures consistent spacing from the limbus, typically 1.2 to 1.5 mm posteriorly, to target the ciliary body without excessive energy dispersion. Proper probe orientation is necessary to maintain perpendicular contact with the sclera, preventing suboptimal energy delivery or unintended damage.

Laser settings are adjusted based on patient characteristics, with power levels generally ranging from 1,250 to 2,500 mW per pulse. Duration per application is commonly set between 1.5 and 2.5 seconds, though shorter durations may be preferred in eyes with increased pigmentation. The number of treatment spots varies depending on intraocular pressure levels and prior response, with most protocols recommending 18 to 24 applications over 270 to 360 degrees of the limbus. The 3 and 9 o’clock meridians are avoided to prevent damage to the long posterior ciliary nerves and arteries, reducing postoperative discomfort and vascular complications.

During the procedure, real-time assessment of tissue response guides laser adjustments. Audible “pops” indicate rapid vaporization of intraocular fluids and potential overtreatment. While mild popping sounds are generally acceptable, frequent or loud occurrences suggest excessive thermal buildup, warranting a reduction in power or duration. Some surgeons prefer a titration approach, starting with lower energy settings and increasing incrementally to balance efficacy and safety, reducing the likelihood of postoperative hypotony or inflammation.

Histological Alterations After Treatment

Following TSCPC, the ciliary body undergoes distinct histological changes reflecting laser-induced thermal damage. Immediate effects include coagulative necrosis of the pigmented and non-pigmented ciliary epithelium, leading to cellular shrinkage and architectural disruption. Protein denaturation causes affected cells to lose function. The surrounding stromal tissue also exhibits thermal coagulation, characterized by cytoplasmic condensation and nuclear pyknosis in fibroblasts and vascular endothelial cells. These changes contribute to reduced aqueous humor production.

The extent of structural damage varies with laser parameters and tissue pigmentation. Eyes with higher melanin content absorb more energy, leading to deeper penetration and more pronounced coagulation. Less pigmented tissues may require adjusted parameters for consistent therapeutic outcomes. Excessive energy delivery can cause extensive stromal necrosis, affecting adjacent scleral and choroidal structures. This collateral damage has been linked to increased postoperative complications, such as scleral thinning and delayed wound healing, emphasizing the importance of controlled energy application.

Over time, fibrosis develops in the treated ciliary body, modulating aqueous humor dynamics. Fibroblastic proliferation within the damaged stroma leads to extracellular matrix deposition, replacing necrotic tissue with dense connective fibers. This scarring reinforces aqueous suppression and alters the vascular supply to the ciliary processes. Electron microscopy studies show endothelial cell loss and capillary lumen narrowing in post-treatment specimens, indicating ischemic changes that contribute to long-term efficacy. The degree of fibrosis varies, with some patients developing extensive scarring that enhances pressure-lowering effects, while others exhibit partial regeneration of ciliary epithelial function.

Role Of The Ciliary Body

The ciliary body regulates intraocular pressure by controlling aqueous humor production and outflow. Composed of the pars plicata and pars plana, it houses the ciliary epithelium, which secretes aqueous humor into the posterior chamber. This fluid circulates through the pupil into the anterior chamber, exiting via the trabecular meshwork and Schlemm’s canal, with a smaller portion draining through the uveoscleral pathway. The balance between production and drainage determines intraocular pressure, making the ciliary body a primary target for glaucoma treatment.

Beyond secretion, the ciliary body plays a role in accommodation, adjusting lens curvature through ciliary muscle contraction and relaxation. This muscle, composed of longitudinal, radial, and circular fibers, modulates zonular tension to shift the focal point of incoming light. While TSCPC primarily impairs aqueous humor production, excessive collateral damage to the ciliary muscle can lead to accommodative dysfunction, particularly in younger patients. Precise laser application is crucial to preserving residual function while achieving therapeutic pressure reduction.

Post Procedure Observations

After TSCPC, close monitoring is required to assess intraocular pressure trends, tissue response, and potential complications. Patients are typically evaluated within the first week to determine treatment efficacy and identify early adverse effects. Transient ocular discomfort, mild conjunctival injection, and anterior segment inflammation are common due to thermal effects on the ciliary body and adjacent structures. Topical corticosteroids and nonsteroidal anti-inflammatory drugs are commonly prescribed to manage inflammation. Cycloplegic agents may also be used to reduce ciliary spasm and associated pain.

The pressure-lowering effect evolves over several weeks as tissue remodeling progresses. Some patients experience a delayed response, requiring additional follow-up to assess long-term efficacy. While most achieve significant intraocular pressure reduction, responses vary due to differences in ocular anatomy, ciliary body ablation, and preexisting conditions. Persistent hypotony, defined as intraocular pressure below 5 mmHg, is a rare but serious complication that can lead to visual impairment from choroidal effusion or phthisis bulbi. To mitigate this risk, clinicians often begin with lower energy settings and adjust treatment based on response. Repeat TSCPC sessions may be necessary in cases of inadequate pressure control, with careful consideration of cumulative tissue effects.