Pterygium

From EyeWiki
Original article contributed by: Matthew Caldwell
All contributors: Matthew Caldwell, Lawrie Hirst and Maria A. Woodward, MD
Assigned editor:
Review: Assigned status Up to Date by Maria A. Woodward, MD on March 11, 2015.
{| cellspacing="5"

|-!align="right" |Lead Editors: |add |- !align="right" |Contributing Editors: |add |-

|}


Disease Entity
Pterygium.jpg
[edit | edit source]

Pterygium, from the Greek pterygos meaning “wing”, is a common ocular surface lesion originating in the limbal conjunctiva within the palpebral fissure with progressive involvement of the cornea. The lesion occurs more frequently at the nasal limbus than the temporal with a characteristic wing-like appearance.

Disease[edit | edit source]

Add text here

Etiology[edit | edit source]

The etiology is unknown. An increased incidence is noted in latitudes nearer the equator and in individuals with a history of increased UV exposure. Some studies have shown a slightly higher incidence in males than females, which may only reflect a higher rate of UV radiation.

Risk Factors[edit | edit source]

UV radiation, proximity to the equator, dry climates, outdoor lifestyle.

General Pathology[edit | edit source]

Histologically, pterygia are an accumulation of degenerated subepithelial tissue which is basophilic with a characteristic slate gray appearance on H&E staining. Vermiform or elastotic degeneration refers to the wavy worm-like appearance of the degenerate fibers. Destruction of Bowman’s layer by fibrovascular ingrowth is typical. The overlying epithelium is usually normal, but may be acanthotic, hyperkeratotic, or even dysplastic and often exhibits areas of goblet cell hyperplasia.

The American Academy of Ophthalmology's Pathology Atlas contains two virtual microscopy images of tissue samples with Pterygium:

Pterygium histopathology. H&E stain exhibiting elastotic degeneration.

Pathophysiology[edit | edit source]

The large number of theories that exist to explain the pathogenesis of pterygium growth underscores the uncertainty of the etiology. The increased prevalence in hot dry climates and regions nearer to the equator suggest a role of environmental factors such as UV radiation and dryness. Actinic changes seen on histopathology similar to actinic keratoses on the skin also supports the role of UV radiation. It has been suggested that radiation activated fibroblasts may result in excessive production of material resulting in pterygia. Other proposed theories include choline deficiency, an inflammatory disorder, disregulation of angiogenesis, immune system abnormalities, tear film abnormalities, as well as the possible role of a viral stimulus.

Recurrent pterygia appear to be more related to surgical trauma than UV radiation as avoidance of UV radiation has not been shown to affect the incidence of recurrence. The actinic damage noted histologically on primary pterygia is characteristically absent from recurrent pterygia, supporting this theory.

Primary prevention[edit | edit source]

As UV radiation is believed to play an important role in the pathophysiology, avoidance of UV exposure is probably important to primary prevention. Ocular surface lubrication may also help.

Diagnosis[edit | edit source]

The diagnosis is made by slit-lamp examination of the typical limbal growth at the characteristic location within the palpebral fissure. The diagnosis is most often clear clinically, but histopathologic confirmation is performed routinely.

History[edit | edit source]

Add text here

Physical examination[edit | edit source]

A complete eye exam should be performed on all patients with apparent pterygia focusing on assessment of visual and refractive impact as well as the exclusion of less common alternate diagnoses.

  • Visual acuity with current correction and manifest refraction
  • External examination (lids, lashes, lacrimal apparatus)
  • Examination of bulbar and palpebral conjunctiva as well as fornices
  • Slit lamp biomicroscopy of the ocular surface and anterior segment
  • Keratometry
  • Corneal Topography
  • Motility Exam
  • The remainder of a comprehensive eye exam to include pupil exam, visual fields, intraocular pressure, and dilated funduscopic exam

Signs[edit | edit source]

The diagnosis of pterygium is based on the clinical appearance of the lesion. Typical findings include

  • Fibrovascular conjunctival growth within the palpebral fissure extending onto the corneal surface
  • triangular shape with the apex, or head, extending onto the cornea
  • vascular straightening in the direction of the advancing head of the pterygium on the corneal surface.
  • May be a thin translucent membrane or significantly thickened with an elevated mound of gelatinous material.
  • It may affect the nasal and temporal limbus of both eyes or only a single location.
  • raised lesion, white to pink in color depending on vascularity
  • ranges from a fine transparent area with very mild elevation, few vessels, and minimal corneal involvement in the early stages to a thick opaque vascular growth extending to the visual axis in later stages
  • Pinguecula are often present in the ipsilateral or contralateral eye
  • A pigmented epithelial iron line (Stocker’s line) adjacent to a pterygium is evidence of chronicity.


It is unusual for pterygia to deviate from the characteristic locations of three and nine o’clock within the palpebral fissure. Pterygioid lesions in other locations should elevate suspicion for alternate diagnoses.

Symptoms[edit | edit source]

Though frequently asymptomatic, pterygia can become inflamed and cause ocular surface irritation. Many patients will disclose their dislike of the appearance of the pterygium when questioned directly. As the lesion progresses vision may be affected by induction of astigmatism or obscuration of the visual axis.

Clinical diagnosis[edit | edit source]

Diagnosis is based on the typical clinical appearance

Diagnostic procedures[edit | edit source]

Assessment of visual acuity, changes in manifest refraction, and corneal topography can aid in determining the visual impact of pterygia. Histopathologic confirmation is routine for excised lesions and can be important in verifying atypical cases.

Laboratory test[edit | edit source]

Add text here

Differential diagnosis[edit | edit source]

  • Pannus
  • Conjunctival Intraepithelial Neoplasia (CIN)
  • Terrien’s marginal degeneration
  • Symblepharon secondary to chemical, thermal, or mechanical injury
  • Stevens Johnson Syndrome
  • Limbal dermoid
  • Neurotrophic keratitis

Management[edit | edit source]

Add text here

General treatment[edit | edit source]

A number of potential therapeutic options exist for the management of pterygia ranging from conservative management with lubrication to surgical excision with conjunctival autografts. Due to the potential for recurrence of a more aggressive lesion, as well as other surgical risks, the surgical removal of pterygia should not be undertaken casually.

Medical therapy[edit | edit source]

Inflamed pterygia may cause irritation, foreign body sensation, and tearing which, in many cases, can be alleviated with over the counter vasoconstrictor drops, lubricating drops and ointments.

Medical follow up[edit | edit source]

Initially, the corneal extension of the pterygium should be measured and followed every 1 to 2 years to determine the rate of growth toward the visual axis.

Surgery[edit | edit source]

Excision: simple excision or simple conjunctival closure will result in a recurrence rate as high as 80% and is now considered unacceptable.

Excision together with adjunctive therapies such as radiotherapy, mitomycin and 5FU: the use of these adjunctive agents will reduce the 80% recurrence of simple excision to about 10% but bring with them some visually threatening complications. The only real advantage of these methods is the simplicity and speed of the surgery.

Conjunctival Flap/Graft : this is considered the Gold Standard of care and carries an approximate rate of recurrence of 5-10% with minimal complications. However, it is a lengthier procedure and technically slightly more complicated than those methods above. Recently a major modification of a routine autograft, known as P.E.R.F.E.C.T. for PTERYGIUM, has reduced the recurrence rate to 1/1000 and results in a cosmetic result where the appearance of the eye after this procedure is indistinguishable from that of a normal eye.

Surgical follow up[edit | edit source]

Intensive postoperative topical steroids may be required. Patients need to be followed for one year if a recurrence is to be identified. 97% of all recurrences occur in the first year after surgery.

Complications[edit | edit source]

  • Recurrence 
  • Corneal scarring
  • Corneal perforation
  • Strabismus
  • Non-healing epithelial defect (esp with mitomycin C)
  • Scleral melt (esp with mitomycin C)

Prognosis[edit | edit source]

Recurrence rate can be as low as 1/1000 with complications being very uncommon.

Additional Resources[edit | edit source]

Add text here

References[edit | edit source]

1: Hirst LW. Recurrent pterygium surgery using pterygium extended removal followed by extended conjunctival transplant: recurrence rate and cosmesis. Ophthalmology. 2009 Jul;116(7):1278-86.

2: Hirst LW, Axelsen RA, Schwab I. Pterygium and associated ocular surface squamous neoplasia. Arch Ophthalmol. 2009 Jan;127(1):31-2.

3: Hirst LW. Prospective study of primary pterygium surgery using pterygium extended removal followed by extended conjunctival transplantation. Ophthalmology. 2008 Oct;115(10):1663-72. Epub 2008 Jun 16.

4: Hirst LW. Mitomycin C in the treatment of pterygium. Clin Experiment Ophthalmol. 2006 Apr;34(3):197-8.

5: Troutbeck R, Hirst L. Trends in beta irradiation for pterygium in Queensland. Clin Experiment Ophthalmol. 2003 Dec;31(6):545.

6: Hirst LW. The treatment of pterygium. Surv Ophthalmol. 2003 Mar-Apr;48(2):145-80. Review.

7: Jaros PA, DeLuise VP. Pingeculae and pterygia. Survey of Ophthalmology 1988;33:41-49.

8. Nemesure B, Wu S, Henis A, Leske MC, Barbados Eye Studies Group. Nine-year incidence and risk factors for pterygium in the Barbados Eye Studies. Ophthalmology 2010;115:2153-2158.

9. Detorakis ET, Spandidos DA. Pathogenetic mechanisms and treatment options for opthalmic pterygium: Trends and perspectives (Review). International Journal of Molecular Medicine 2009;23:439-447.

10. The Wills Eye Manual, 5th Edition. Ehlers and Chirag. Lippincott, 2008.

11. Ocular Pathology Atlas. American Academy of Ophthalmology Web site. https://www.aao.org/resident-course/pathology-atlas. Published 2016. Accessed January 4, 2017.