bubble_chart Overview

The term "pterygium" is derived from foreign languages, emphasizing its wing-like shape. Traditional Chinese medicine, however, places particular emphasis on its location and developmental state, naming it "pterygium." This seems more precise than merely describing its appearance in foreign terminology. Regarding the etiology and pathogenesis of pterygium, opinions vary, and further in-depth explanations are needed. Currently, there are roughly two theories: degeneration and inflammation. Careful observation and analysis of the clinical manifestations of pterygium can aid in exploring its causes and pathogenesis.

bubble_chart Pathological Changes

The stromal connective tissue changes in pterygium are similar to those in pinguecula, manifesting as senile elastotic degeneration and hypertrophy of collagen fibers, with dense and hyaline degeneration, and even the formation of granular basophilic material due to degeneration. The stroma also contains abundant neovascularization and macrophage aggregation.

Microscopically, the epithelial changes are minimal, with subepithelial tissue showing basophilic degeneration and the dissolution or sieve-like loss of the anterior elastic membrane. Nerve fibers in this region grow upward through the gaps in the disrupted membrane, lifting the overlying corneal epithelium.

In progressive pterygium, the thickened epithelium exhibits significant goblet cell hyperplasia and subepithelial cysts, which form due to inflammatory obstruction of the subepithelial connective tissue (Vannini Angelo, 1954).

Gerondo classified the condition into three types based on the disease progression and pathological features:

1. **Papillomatous proliferative type**: Similar to the progressive pterygium described here. The papilloma structure is characterized by thickening of the conjunctival membrane and marked proliferation of subepithelial connective tissue, accompanied by edema. The connective tissue contains abundant neovascularization and extensive round cell infiltration. The epithelium exhibits long, deep folds resembling tubular glands. The nuclei of the edematous epithelial cells are deeply and finely stained, with clear cytoplasm resembling goblet cells.

2. **Fibrous type**: Corresponds to early-stage pterygium, presenting as loose epithelium, edema, densely stained nuclei, flattened cells, sparse and non-distended blood vessels. Compared to the proliferative type, the tissue cells are fewer.

3. **Atrophic sclerotic type**: Equivalent to the post-surgical cessation of pterygium growth (clinically, spontaneous atrophy of pterygium is rare). The epithelium shows significant atrophy, with subepithelial connective tissue becoming dense and sclerotic, progressing to hyaline degeneration. The epithelium may also degenerate into hyaline material or occasionally disappear. Calcification may be observed within the hyaline material. Blood vessels in the degenerated connective tissue become partially empty and atrophic. Macroscopically, the pterygium appears pale and flattened.

This demonstrates that the formation of pterygium primarily involves a shared inflammatory process between the conjunctival and corneal membranes. Isolated inflammation of either the conjunctival or corneal membrane alone is unlikely to initiate pterygium. The notion that pterygium arises solely from pinguecula lacks pathological evidence.

Despite the varying appearances due to differences in connective tissue proliferation and vascularization, the pathological changes in pterygium are fundamentally consistent across the three clinical types.

Initially, epithelial infiltration and subepithelial tissue degeneration occur in the bulbar conjunctiva at the palpebral fissure. Subsequently, in response to external pathogenic stimuli, reactive vascular proliferation, tissue thickening, and sclerotic elevation develop. The lesion may remain confined to the conjunctiva (conjunctival-type pterygium) for an extended period. However, as the disease progresses, extensive neovascularization extends into the chronically infected or inflamed caruncle tissue, potentially promoting hyperplasia and thickening of the underlying Tenon's capsule and muscle sheath. If the corneal limbus undergoes epithelial shedding due to inflammatory infiltration, the existing vascular network proliferates and merges with the pterygium's vessels, invading the Fuchs' islet region of the cornea. Depending on the extent of invasion, this results in either early-stage or late-stage (third-stage) pterygium. Most believe that corneal or limbal lesions are the basis for pterygium progression rather than its origin.

Thus, without chronic infection of the corneoconjunctival membrane, pterygium may remain static at the conjunctival stage for a long time (e.g., in indoor workers). Extensive case studies and pathological examinations confirm that outdoor laborers (e.g., farmers, fishermen, herders) exposed to prolonged solar radiation, dust, snowflakes, ice particles, etc., along with chronic conjunctival inflammation—especially trachoma-like keratitis—are highly susceptible to rapid pterygium progression. In regions with high trachoma prevalence (e.g., Guangdong 71%, Yunnan 74%), pterygium incidence is high and progresses rapidly.

Taylor examined pterygium in white and indigenous populations in the less windy and sandy western Australia, finding that whites had shorter outdoor working hours, mostly without prickly-ash-like sore (trachoma) or very mild cases, while indigenous people had longer outdoor working hours and more severe prickly-ash-like sore (trachoma). The chronic conjunctival inflammation they suffered further promoted the eye's absorption of ultraviolet radiation in the taiyang spectrum. As a result, the pterygium in indigenous patients was more hypertrophic and progressed rapidly. Kame emphasized that pterygium is not a primary degeneration but is purely caused by inflammation, believing that fibrous tissue hyperplasia is a consequence of long-term inflammation, though he did not deny that prickly-ash-like sore (trachoma) could worsen pterygium. There is naturally a causal relationship here. To quote Sedan (1968): pterygium can arise from inflamed pinguecula, but it is nurtured and enlarged by prickly-ash-like sore (trachoma).

bubble_chart Clinical Manifestations

Clinically, there are roughly three categories: initial pterygium (further divided into the conjunctival membrane stage and the pre-corneal membrane stage), progressive pterygium (corneal membrane late stage [third stage]), and postoperative pterygium (further divided into cured pterygium and recurrent pterygium).

1. Initial Pterygium: Under the slit lamp, the conjunctival membrane in the palpebral fissure appears thickened, congested, and edematous, with dilated blood vessels. Its tail adheres to the semilunar fold, and moving the bulbar conjunctiva creates a transverse band. After staining with rose bengal or fluorescein and observing under cobalt blue light, punctate epithelial shedding of the conjunctival membrane can be seen, while the adjacent conjunctival membrane covered by the eyelids does not stain. This is the conjunctival membrane stage of pterygium.

The thickened conjunctival membrane forms a triangular, congested fold. Its head crosses the corneal limbus, and its base fans out, extending over the semilunar fold toward both sides of the caruncle. In the pre-corneal limbal region, this forms the neck of the pterygium. The head of the pterygium is raised on the corneal limbus, extending inward about 2 mm, with fine blood vessels on its surface. At the tip of the head, a small island of grayish-white granular particles accumulates and invades the superficial layer of the cornea, known as Fuchs' island. The island and the surrounding corneal area exhibit a turbidity barely discernible to the naked eye. On the body side, there are also grayish-white streaks composed of particles, distributed along the dilated blood vessels at the corneal limbus. The head and neck adhere to the corneoscleral membrane within this infiltrated and congested area. Fluorescein staining reveals punctate epithelial shedding.

2. Progressive Pterygium: The head appears as a grayish-white gelatinous elevation, with its tip forming a vertical serrated white edge. The neck is filled with blood vessels, and the tissue is thickened. Due to the traction of the pterygium on the cornea, corneal astigmatism may occur, leading to a sharp decline in vision. The serrated advancing edge of the pterygium head has crossed the center of the pupil, with a slightly raised surface and scattered calcification points nearby. The advancing edge penetrates deep into the anterior elastic membrane of the cornea, with the emetic therapy epithelium raised and significantly turbid.

3. Postoperative Pterygium

⑴ Successful Surgery: Two years after pterygium excision and autologous pedicled conjunctival transplantation. At the base of the relatively clean and transparent conjunctival graft, 2 to 3 thick blood vessels from the semilunar fold enter the graft, forming loose vascular loops near the corneal limbus, barely visible to the naked eye. In avascular areas, the graft is flat, but the stromal layer still shows patchy or cloud-like turbidity. Medial to the turbid area, a white band formed by clusters of white dots can be seen.

⑵ Postoperative Recurrent Pterygium (One month after the third pterygium excision surgery): Externally, the distance from the caruncle to the corneal limbus is noticeably shortened. The pterygium area resembles a hemangioma, appearing as a mound-like elevation with its base adhering deeply to the caruncle, forming a single mass. The upper and lower conjunctiva of the "tumor" are extremely congested, extending to the lower fornix, and symblepharon has formed in the inner canthus of the lower eyelid. Upon everting the upper eyelid, the adhesion is seen starting from the caruncle, extending through the bulbar conjunctiva to the upper fornix, resembling a stalk.

bubble_chart Treatment Measures

The treatment methods include medication, radiation, and surgery. The first two are often used as supplements to the latter, serving as measures to prevent recurrence. When conservative treatment is applied alone, the efficacy is limited.

1. **Medication Therapy** Strictly speaking, eye drops are not significantly effective. For pterygium in the conjunctival stage, if symptoms such as dryness or foreign body sensation occur, anti-inflammatory and corticosteroid eye drops (e.g., cortisone acetate) can be used to control chronic inflammation and irritation, preventing progression. However, they do not help eliminate the pterygium.

**Thiotepa solution (1:2000–1:1000)**: When applied starting from the second day post-surgery and continued for 6–8 weeks during the day, it is quite effective. Using thiotepa and prednisolone eye drops post-surgery can prevent pterygium recurrence in 94% of cases. However, it has no effect on eliminating pterygium in patients who have not undergone surgery.

Japanese researchers have used **mitomycin C eye drops** post-surgery with satisfactory results in preventing recurrence. It is considered superior to thiotepa due to its lower dosage, minimal irritation, ease of application, and the formation of thinner scars post-surgery. It can replace ⁹⁰ **strontium-90** for prevention. However, possible side effects include allergic conjunctivitis, scleral softening, iritis, and glaucoma.

**Prescription and Preparation**: - Mitomycin C: 2 mg/vial - Sodium chloride: 48 mg - Distilled water: added to 5 mL (final concentration: 0.4 mg/mL mitomycin C). This solution is stable at pH 6–9 and can be stored for one week under refrigeration and light protection. At pH 7–9 and 5°C, the potency remains above 90% after five days and above 80% after twenty days. At pH 5, the potency drops to about 10% after two days. The following buffer solution (pH 8) provides the most stable conditions:

- Boric acid: 0.866 g

- Borax: 0.572 g

- Sodium chloride: 0.250 g

- Distilled water: added to 10,000 mL.

**Usage**: Starting the day after surgery, apply three times daily for 5–7 days, depending on the progression of the pterygium. Concurrent use of cortisone acetate ointment can reduce congestion, drug irritation, and conjunctivitis. The transplanted conjunctiva typically flattens and aligns with the normal conjunctiva within 3–4 weeks post-surgery. According to Murakami et al., the recurrence rate was only 13% in 89 cases.

**Bleomycin (Zhengguangmycin)**: For early-stage pterygium (conjunctival or pre-corneal stage), 3–6 injections (3 injections per course, with 5–7 days between courses) can lead to varying degrees of regression, with some cases showing "dissolution" and tissue pallor. For corneal-stage pterygium, surgery is still required before injections. Care must be taken to avoid severe scleral injury.

**Injection Method**: - Bleomycin powder (5 mg/vial = 15,000 units) is diluted with 2 mL of 2% procaine to a concentration of 7,500 units/mL. - Each injection: 0.2–0.4 mL (1,500–3,000 units). For conjunctival-stage pterygium, 1,500 units per injection is usually sufficient. The solution should be injected into the degenerated tissue. - For pre-corneal pterygium, higher doses and more injections are needed. The method is as follows: 1. Draw 0.4 mL of bleomycin and inject 0.2 mL deeply into the pterygium body, ensuring uniform tissue infiltration without damaging the medial/lateral rectus sheaths. 2. Advance the needle toward the corneal limbus and inject 0.05 mL. 3. Divide the remaining 0.15 mL into three portions and inject into the areas below the caruncle and the upper/lower fornices. - To reduce reactions, 0.3 mL of prednisolone can be injected subconjunctivally on the opposite side, followed by tetracycline-cortisone ointment and bandaging. The dressing is changed the next day. - Depending on the local reaction and regression, a second injection may be given, adjusting the dose as needed. Typically, injections are given weekly for 3–6 sessions (total 10,000–80,000 units). The pterygium thins, the affected area flattens, and adhesions form with the subconjunctival atrophic tissue, limiting mobility without impairing vision.

2. Beta Ray Therapy Generally, the ⁹⁰ strontium applicator is commonly used. The method involves first applying 1% dicaine for surface anesthesia, then disinfecting and drying the applicator before placing it on the center of the pterygium. Fractionated interval therapy is often employed, with each dose ranging from 300 to 1000 rads, and a total dose of 4000 to 12000 rads. For congestive and hypertrophic pterygium, this method only provides temporary suppression. After pterygium excision, beta-ray applicator therapy should be added no later than 5 days postoperatively, with the total dose reduced accordingly to around 4000 rads, and each dose ranging from 600 to 800 rads.

Post-treatment reactions: After irradiation, corneal epithelial edema, vascular invasion, and conjunctival congestion and edema may occur. If the dose is between 1500–2000 rad, no significant adverse reactions are observed; between 2000–5000 rad, photophobia, tearing, burning sensation, itching, and punctate corneal epithelial staining may appear 4–6 weeks later; doses above 6000 rad can cause equatorial and anterior/posterior subcapsular cortical opacities in the lens; doses exceeding 20000 rad may lead to severe complications such as radiation-induced cataract, iris and ciliary body atrophy, corneal ulceration, or even perforation.

3. Surgical Therapy After the failure of Hotz’s simple pterygium excision, Desmarres first introduced the transfer method, which was later improved by McReynolds and further refined by Busacca. Additionally, methods by O’Brien and Stocker, among others, have been proposed. In China, numerous innovative surgical techniques have also been developed. Despite continuous advancements, none have fully guaranteed the prevention of pterygium recurrence.

Our experience suggests the following points are key to surgical success.

(1) For conjunctival-type pterygium: Within a six-month observation period, if the pterygium head gradually approaches the corneal limbus and the vascular network shows hyperplasia or disorganization, surgery is advisable (regardless of fluorescein staining). Experience shows that long-standing, static thick plaque-like pterygia may unpredictably transition into progressive forms. Thus, early or late excision is generally recommended.

(2) For pre-corneal and corneal-stage pterygia, consider the following:

① Thoroughly excise all degenerative tissue at the corneal limbus, sclera, and cornea (including the milky-white Fuchs islets "progression zone," the neck-head junction, and adhesion sites) and expose the area to create a buffer zone preventing conjunctival fibrous tissue invasion into the cornea.

Alternatively, scrape a 1-mm-wide scleral depression lateral to the corneal limbus as a barrier against conjunctival fibrous invasion and expose it.

② The excised edges of the pterygium head and the transferred conjunctival flap (if the entire pterygium is removed) should be rolled inward toward the wound, ensuring epithelial surfaces align during suturing.

③ Carefully excise the deep tissue on both sides of the caruncle, extending to the fibrous tissue expanding into the superior and inferior fornices, avoiding residual "tentacles" (which often trigger conjunctival epithelial and fibrous tissue hyperplasia). When dissecting subpterygial connective tissue, avoid injuring the underlying medial/lateral rectus muscle sheaths. Air injection can help separate the conjunctiva from deeper tissues.

④ The prepared conjunctival flap for transfer should be fully dissected, larger than the pterygium area, with minimal sutures. After suturing, the flap ends should extend to the superior and inferior fornices without trimming.

Specific steps:

① Place a 5–7 mm trephine (selected as needed) with its edge 1 mm beyond the corneal milky-white zone. After marking with fluorescein, use the same trephine to cut, applying pressure on the corneal side to penetrate the superficial stroma (about 1/3 of its thickness).

② Starting from the corneal surface, create a gap by natural lamellar stromal dissection, then switch to a Desmarres blade to excise a strip of degenerative tissue (including limbal vascular network and superficial sclera, about 3 mm wide), exposing the sclera. The length depends on the pterygium width. Note the differing curvatures of the cornea and sclera to avoid scleral injury.

③ Grasp the pterygium head with toothed forceps, stretch it taut, and meticulously excise the subpterygial fibrous tissue along its edges, staying close to the sclera until reaching the deep caruncle sides and medial canthus fornices, ensuring no "tentacles" remain.

④ Use a curette to scrape all exposed sclera starting from the corneal limbus (scraping causes less tissue irritation than electrocautery, coagulation, or chemical corrosion, with reliable efficacy).

⑤ Sever the pterygium 1 mm anterior to the caruncle.

⑥Depending on the size, thickness, and whether it is primary or recurrent, choose to perform either a pedicle transfer or free conjunctival membrane transplantation (when suturing, ensure the cut edge is folded towards the wound surface). A small scleral groove is dissected along the lateral side of the corneal membrane.