Persistent Corneal Defect in Chronic Progressive External Ophthalmoplegia

Persistent Corneal Defect in Chronic Progressive External Ophthalmoplegia
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doi: 10.62055/dnjfbmdfqzjx



To present a case study and review of chronic progressive external ophthalmoplegia (CPEO) with the challenging complications of exposure keratopathy and persistent corneal defect.


A 36-year-old male presented with the complaint of redness, burning, and swelling of the left eye for the previous two weeks. He had been diagnosed with chronic progressive external ophthalmoplegia (CPEO) over 25 years prior and had undergone multiple eyelid and strabismus surgeries. After examination, he was diagnosed with exposure keratopathy with an inferior corneal defect of the left eye. Additionally, marked anterior blepharitis with suspicion of Demodex infestation was present. With topical treatment consisting of mainly corticosteroids and antibiotics, the corneal defect healed. Consistent use of preservative-free artificial tear lubricants and moisture goggles helped with chronic exposure of the ocular surface. Management of the blepharitis with eyelid hygiene, including tea tree oil, eyelid margin debridement, and warm compresses stabilized his ocular surface.


 This case highlights the challenges in the long-term management of CPEO and the associated ocular morbidities, such as exposure keratitis and persistent corneal epithelial defect.

Keywords chronic progressive external ophthalmoplegia, Demodex, blepharitis, exposure keratopathy



Chronic progressive external ophthalmoplegia (CPEO) was first described in 1868 by von Graefe and was further summarized as part of a larger syndrome in 1958 by Kearns and Sayre, with the most common ocular findings being ptosis, strabismus, cataracts and pigmentary retinal degeneration.1 Now known as Kearns-Sayre Syndrome, this rare mitochondrial disorder has multisystem involvement including neurologic, cardiac, renal, and endocrine complications. Kearns Sayre Syndrome occurs because of large-scale spontaneous mutations of mitochondrial DNA (mtDNA) early in fetal development. About fifty percent of cases are spontaneous and it typically presents before the age of twenty years. There is no current remedy and management is directed to treating the varied organ involvement.2

Complications of the ocular surface are possible, including exposure keratitis from an inability to close the eyelids, chronic anterior blepharitis and meibomian gland dysfunction from reduced blink reflex. Corneal ulceration, neurotrophic keratopathy, and corneal perforation are significant vision-threatening complications from progressive ocular surface disease. Co-management with oculoplastic and external ocular disease specialists is essential to address the treatment of chronic ptosis and the increased risk of exposure.


A 36-year-old male was referred for the chief complaint of symptoms of reduced vision, burning, swelling, and mucous discharge of the left eye. The symptoms began two weeks prior and were treated with topical gentamycin drops by his primary care provider with no effect. His ocular history was significant for chronic progressive external ophthalmoplegia that was confirmed by genetic testing at four years of age. Past non-surgical treatments included the use of preservative-free artificial tear lubricants and moisture goggles, which he used inconsistently. Previous clinical notes from other providers showed documentation of anterior blepharitis and lagophthalmos.

The patient had undergone multiple eyelid surgeries, including a left upper lid levator resection at the age of 10 to help with his decreased field of view. The remaining ptosis was not repaired at that time because of concomitant facial weakness and concern for corneal exposure. The patient also had strabismus surgery eight years prior to this visit for an exotropia of theright eye and a hypertropia of the left eye. Because of increasing eyelid dysfunction the following year, he underwent bilateral ptosis repair with a frontalis sling with bilateral lower lid retraction repair. Additional surgeries included two augmentations of the left upper eyelid, done one and two years thereafter.

Examination revealed the best-corrected distance visual acuity of 20/40 right eye and 20/30 left eye. Extraocular motilities showed a right exotropia, greater than ten prism diopters, and a right hypertropia of three prism diopters. There was 2+ ptosis of the upper lids bilaterally and a 2 mm lagophthalmos right eye and 4 mm left eye (Figure 1). There was an over action of the frontalis muscle, causing a reduction in the blink response. He had a Bell’s reflex that positioned the eyes up and out, but still had inferior corneal exposure. There was decreased corneal sensitivity in both eyes.

figure 1 cpeo (1)

Figure 1: (A) eyelid position in primary gaze. Note exotropia and hypertropia of the right eye. Also furrowing of the brow as a compensatory action to the ptosis. (B) lagophthalmos on downgaze with exposure of the inferior ocular surface.


Biomicroscopy of the right eye revealed 2+ marginal blepharitis with collarettes. The bulbar conjunctiva had mild chemosis and injection. There was 1+ inferior corneal punctate staining with sodium fluorescein along with epithelial hypertrophy. The left eyelids had a similar clinical picture however, withmore extensive blepharitis: 3+ marginal blepharitis and increased collarettes. There was pronounced bulbar conjunctival injection and chemosis. The cornea showed 3+ inferior corneal staining, filaments, mucous discharge, and a 6×2 mm inferior defect with infiltrate (Figures 2, 3 and 4).

figure 2 cpeo (1)

Figure 2: (A) marginal anterior blepharitis with collarettes right eye. (B)anterior blepharitis with margin inflammation and collarettes left eye.

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Figure 3: Left eye: anterior blepharitis and mucoid discharge; filaments and inspissated meibomian glands.

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Figure 4: Left eye: mucoid discharge; showing inferior corneal defect

Tonometry was deferred due to the condition of the ocular surface. Previous exams had shown normal intraocular pressure. An undilated view of the posterior segment demonstrated a normal appearing macula and optic disc in both eyes, without retinal pigmentation.

A diagnosis of inferior corneal defect in the left eye with bilateral exposure keratopathy was made, with secondary concerns of anterior blepharitis and suspected Demodex infestation, left eye greater than the right. A culture of the cornea and of the lid margins was obtained and sent to a laboratory for identification of any bacteria and/or fungus present and subsequent sensitivity testing.

Treatment was initiated with 0.5% moxifloxacin every 2 hours and 0.3% tobramycin every 2 hours in alternate fashion while awake and erythromycin ophthalmic ointment at bedtime in the left eye. When the initial culture results returned limited bacterial results and the clinical appearance was not indicative of a fungal infection, the management plan was amended to address the inflammatory response by substituting dexamethasone/tobramycin 0.1%/0.3% drops in place of the 0.3% tobramycin drops. Consistent use of preservative-free artificial tears every 4 hours or ointment was stressed. The patient was instructed to begin Bruder mask compresses and lid hygiene three times daily with lid scrubs three times daily in each eye to address the anterior blepharitis. The patient was also advised to be compliant with evaporation control by including consistent use of moisture goggles. It was noted that the minimal discomfort reported was inconsistent with the clinical appearance, therefore the presence of a neurotrophic process was considered. The patient was scheduled for a three-day follow-up appointment.

The patient did not return for a follow-up examination as planned but was seen six days after the initial visit. The patient reported compliance with his treatment plan. The symptoms of redness and irritation had moderately improved. The patient reported that the vision was clearer in the left eye as well.

The examination revealed stable distance visual acuities of 20/40 right eye and 20/30 left eye. Other entrance testing had not changed since the initial visit. Biomicroscopy of the right eye revealed 1+ marginal blepharitis with 1+ collarettes. The bulbar conjunctiva had 1+ chemosis and injection. There was 1+ inferior corneal punctate staining with sodium fluorescein along with epithelial hypertrophy. The left lids continued to show marked marginal blepharitis and collarettes. The bulbar conjunctival showed 2+ injection and chemosis, an improvement. There was persistent 2+ inferior corneal staining and central filaments. The mucous discharge had lessened, and the epithelial defect had decreased to 4×2 mm. The infiltrate appeared less dense.

The extended culture results showed isolated colonies of Staphylococcus aureus and Corynebacterium. The bacteria were sensitive to aminoglycosides; therefore, moxifloxacin was discontinued and dexamethasone/tobramycin 0.1%/0.3% drops three times daily in the left eye was continued. Epilation of lashes from all four eyelids and microscopic evaluation confirmed the presence of multiple Demodex mites. (Figure 5).

figure 5 cpeo (1)

Figure 5: Left upper lid lash with Demodex mite encased in congealed meibum.

Once the corneal defect improved and the inflammation was controlled, in-office debridement of the lashes and a hypochlorous spray was added to the lid hygiene regimen twice daily. The patient was instructed to continue to use other previous lubrication treatment and preventative measures to reduce exposure and was scheduled for a one-week follow-up examination.

At subsequent follow up, the patient then reported that the symptoms were “quite a bit better” with less injection and improved vision. He reported compliance with his ocular medication. The examination revealed stable distance visual acuities of 20/40 right eye and an improvement to 20/25 left eye. Biomicroscopy of the right eye revealed persistent 1+ marginal blepharitis with 1+ collarettes. The bulbar conjunctiva had minimal chemosis and injection. Scant inferior punctate erosions were still present. The left lids continued to show moderate marginal blepharitis and collarettes. The bulbar conjunctiva showed mainly focal injection near the epithelial defect, improved from previous exams. . The 2+ inferior corneal staining was persistent and unchanged. The central filaments were resolved, and the inferior epithelial defect had epithelialized but now stromal thinning was noted. The infiltrate appeared less dense (Figure 6).

figure 6 cpeo (1)

Figure 6: Improved blepharitis and less collarettes right eye; improved blepharitis and collarettes with epithelialized defect left eye.

Repeated culture results continued to show no significant additional bacteria growth or fungus species. The collarettes and lid debris were again debrided. The patient was instructed to continue with the 0.02% hypochlorous spray, and  terpinen-4-ol wipes BID. The dexamethasone/tobramycin 0.1%/0.3% was reduced to twice daily left eye. The patient was encouraged to continue previously recommended lubrication and preventative measures to reduce exposure and was scheduled for a two-week follow-up examination.

The patient returned one month later and reported improvement in symptoms and no fluctuation in vision. He was compliant with the medication regimen and lid hygiene and compresses. He continued to use preservative-free artificial tears during the day and ointment at night. He had purchased some wrap-around moisture glasses for daytime and standard goggles to use during sleep.

The examination showed stable visual acuities in both eyes, 20/50 OD and 20/25 OS. Biomicroscopy findings demonstrated mild persistent blepharitis and scant collarettes. There was less focal injection and the corneal defect had closed with resolution of the infiltrate, although the cornea was thinned about 25% in this area (Figure 7). Intraocular pressures were 15 mmHg in each eye.

figure 7 cpeo (1)

Figure 7: Minimal collarettes with persistent marginal blepharitis right eye; resolution of inferior corneal defect and infiltrate left eye.

The final culture results did not reveal any significant growth of bacteria or fungal species. The patient was to continue with the 0.02% hypochlorous spray, discontinue the terpinen-4-olwipes and replaced with lid scrubs BID OU. The dexamethasone/tobramycin 0.1%/0.3% was reduced to once daily left eye for two weeks and then discontinued. Aggressive lubrication was re-emphasized to reduce exposure risks. An oculoplastics consultation was scheduled to address the lagophthalmos and a 6-month follow-up examination.

Over the next six months the patient was seen several times. He maintained good visual acuity, there was no change in extraocular motilities or lid position. The biomicroscopy appearance fluctuated, and continued patient education was dispensed regarding the chronic nature of the condition and the risk of visually significant complications.

Alternative non-surgical therapies considered included a bandage contact lens or amniotic membrane if the epithelial defect had persisted. Punctal occlusion was not considered since there was already reduced tear clearance due to poor blink reflex function.

Although this patient’s ocular surface is currently stable, the prognosis for corneal compromise including perforation is a concern. Discussions regarding surgical intervention continued and a plan for raising the lower lid was being developed. The patient declined temporary lateral tarsorrhaphy. A bandage contact lens could have been useful to prevent desiccation of the exposed cornea, but with the narrowed palpebral aperture, insertion and removal were a concern for the patient. Chronic anterior blepharitis also increased the risk of infectious keratitis with the use of a long-term bandage contact lens. A scleral lens was also a possible alternative but with the patient’s apprehension with insertion and removal, a fitting was deferred. Likewise, an amniotic membrane was not used since the defect had healed with standard therapy and the patient was unlikely to tolerate a membrane. Temporary external lid weights were considered, but the superior visual field was already affected by the ptosis and would not improve the lagophthalmos due to the overall malposition of the lower eyelid.

With continued and consistent therapy, the patient’s ocular surface status remains stable as of the most recent visit. The patient was scheduled for additional lid revision surgery in the future to elevate the lower lid.


This case demonstrates the ocular surface complications of CPEO and the challenge in managing these patients long-term. Although the patient in this case presented with an extensive history of ptosis and strabismus, the complaints of redness, irritation and blurred vision were new concerns. Careful comprehensive examination is essential to effectively manage these complex patients. All aspects of treatment must be individually tailored for optimal management of chronic, vision-threatening issues.

Initial Treatment Phase:

The initial treatment, pending culture results, should be to manage a case presenting similarly to this one as an infectious keratitis, especially given marked marginal eyelid disease and large corneal epithelial defect. The initial choice of alternating moxifloxacin and tobramycin, rather than fortified antibiotics, was based on the broad coverage for gram-positive and gram-negative organisms, and the ease and availability of procuring the medications versus fortified antibiotics. Adjunctive therapy such as a bandage contact lens or amniotic membrane may be considered for persistent epithelial defects. If initial culture results show normal flora or limited bacteria, and the clinical appearance is not indicative of a fungal infection, management may be altered to address the acute inflammatory response. Concurrent eyelid hygiene measures and aggressive lubrication are key early in the treatment regimen.

Long Term Treatment Phase:

As the ocular surface inflammation slowly subsides, the frequency of anti-inflammatory agents may be reduced and then discontinued.. The next phase of management is to address chronic exposure and anterior blepharitis. If recurrent clinical signs and symptoms reappear, additional repeat therapy is required. Punctal occlusion is an option, but success may be limited due to reduced tear clearance because of poor blink reflex function. Epiphora and increased tear lake could adversely affect vision.

Non-surgical temporary external lid weights may be considered in these cases, but the increased ptosis may worsen the visual field and ultimately, may not improve the lagophthalmos due to overall malposition of the lower eyelid.3 Other postsurgical complications include peaked upper eyelid, entropion, increased lagophthalmos and poor blink reflex.


While the weakening and decompensation of the extraocular muscles is the hallmark of CPEO, there can be serious secondary complications such as refractory exposure keratopathy, meibomian gland dysfunction, and neurotrophic ulceration.4 Corneal epithelial damage due to long-term exposure can lead to filamentary keratitis, scarring and corneal thinning/perforation in severe cases. Typical symptoms include irritation, redness, dryness, and decreased vision.

Corneal decompensation in CPEO can occur either due to eyelid dysfunction or after a surgical ptosis repair, which can cause poor tear spreading.3,5,6 A healthy tear film is critical for maintenance of corneal and conjunctival health and for good vision. Incomplete blinking causes exposure and induces epithelial damage and cell autophagy to occur.7 Autophagy is an adaptive response to tear film hyperosmolarity. Lagophthalmos with the absence of Bell’s reflex can exacerbate exposure keratopathy and increase the risk of persistent corneal defects, ulcers, and perforation. Corneal thinning and linear epithelial hypertrophy have been noted in cases of spontaneous perforation.8 In CPEO, the trauma to the cornea is mechanical from the continuous exposure to the environment and subsequent lack of a competent tear film, which depletes the epithelial stem cells.9 A neurotrophic process should be considered when the symptoms do not correlate with the clinical findings.

In addition, the poor blink reflex reduces the normal clearance of bacteria and toxins from the ocular surface. This increases the risk of developing persistent corneal epithelial defects or infectious keratitis. Without normal protective tear levels of β-lysine, lactoferrin and immunoglobulins, this may increase the risk of microbial infection.10 Additionally, the reduction of tear clearance can adversely impact the lid margins with the development of blepharitis and meibomian gland inflammation.


Treatment Goals:

The goal of treatment in exposure keratitis is to protect visual function by minimizing trauma to the cornea and ocular surface. It is essential to maintain tear film stability and inhibit the ocular inflammatory response with the consistent use of preservative free artificial tears and ointments, taping of the eyelid, soft bandage contact lenses, or temporary or permanent tarsorrhaphy. Frequent manual lid closure is also indicated. Increasing humidity levels in common living areas is also a key supportive option. Moisture chambers and polyethylene film covers also help prevent evaporation in severe cases.11

Persistent epithelial defects should be managed quickly as any delay could result in chronic erosion and corneal scarring. Despite negative culture results, repeat corneal culture and biopsy could be considered in non-responsive cases.12 Combination therapy of β-lactam and aminoglycoside antibiotics is most often given until culture results rule out infectious etiology. Current standard management includes aggressive lubrication, punctal plugs, bandage contact lenses, and oral tetracyclines. Prophylactic antibiotics or short-term topical corticosteroids are indicated but concern for corneal melting must be considered. Refractory cases can use blood derived therapies such as autologous serum or plasma rich in growth factor drops. Albumin eye drops have also been reported to be helpful in chronic ocular surface defects.13 Dehydrated or cryopreserved amniotic membranes have shown to be effective in the healing of corneal defects, although repeated applications may be necessary in exposure cases.14

The use of scleral contact lenses has been shown to protect the corneal surface. In addition, because of the larger size of scleral lenses, they can provide improved visual acuity and cosmesis by supporting the upper lid and reducing ptosis. A modified front surface shelf protrusion scleral lens has been used as well.15 The condition of the cornea must be carefully monitored with the use of scleral lenses since oxygen transmissibility may be reduced even with the use of high oxygen permeable materials.16

When other treatment options are not possible due to patient ability or the ocular surface condition does not allow, temporary or permanent tarsorrhaphy is an effective surgery for persistent corneal defects from exposure keratitis. N-Butyl cyanoacrylate can create a temporary tarsorrhaphy. Permanent reduction in the palpebral aperture is done surgically by attaching the anterior and posterior lamella of the upper and lower eyelid. Another option is a transconjunctival flap, which can significantly improve the corneal epithelial defect in both medial and lateral defects. These flaps are optimal for medial closure because of risk of punctum or lacrimal canalicular damage with standard techniques.17

Prevention of infection with use of topical broad-spectrum antibiotics is indicated until the corneal defect is closed. Bacterial and fungal cultures can be used to identify pathogens for more specific treatment. If inflammation is present then a topical antibiotic/corticosteroid can be used, although there is ongoing debate on whether this might delay healing or increase the risk of infectious keratitis.18-20

As previously mentioned, research in autophagy regulation has had positive results in animal studies and may be a potential future therapeutic option for exposure-based keratitis.21



This unique case highlights the difficulties of managing not only CPEO but of the complications related to the ocular surface and adnexa, including exposure keratitis and persistent corneal defect. Close follow-up and consistent lid hygiene and lubrication are essential to prevent progressive ocular surface desiccation and damage. The progressive nature of this disorder leads to multiple sequential surgeries and the development of potentially sight-threatening complications. Co-management between specialists is critical to achieving an optimal outcome.Various chronic management strategies for these complications must be carefully considered and individually tailored to each patient.



  1. Kearns TP, Sayre GP. Retinitis pigmentosa, external ophthalmophegia, and complete heart block: unusual syndrome with histologic study in one of two cases. AMA archives of ophthalmology. 1958;60(2):280-9.
  2. Phadke M, Lokeshwar MR, Bhutada S, Tampi C, Saxena R, Kohli S, et al. Kearns Sayre Syndrome–case report with review of literature. Indian journal of pediatrics. 2012;79(5):650-4.
  3. Dollin M, Oestreicher JH. Adult-onset exposure keratitis after childhood ptosis repair with frontalis sling procedure. Canadian journal of ophthalmology Journal canadien d’ophtalmologie. 2009;44(4):412-6.
  4. Zhu CC, Traboulsi EI, Parikh S. Ophthalmological findings in 74 patients with mitochondrial disease. Ophthalmic genetics. 2017;38(1):67-9.
  5. Boonstra F, Claerhout I, Hol F, Smit G, van Collenburg J, Meire F. Corneal decompensation in a boy with Kearns-Sayre syndrome. Ophthalmic genetics. 2002;23(4):247-51.
  6. Chang TS, Johns DR, Stark WJ, Drachman DB, Green WR. Corneal decompensation in mitochondrial ophthalmoplegia plus (Kearns-Sayre) syndrome. A clinicopathologic case report. Cornea. 1994;13(3):269-73.
  7. Wang G, Xue Y, Wang Y, Dong F, Shen M, Zong R, et al. The role of autophagy in the pathogenesis of exposure keratitis. J Cell Mol Med. 2019;23(6):4217-28.
  8. Schmitz K, Lins H, Behrens-Baumann W. Bilateral spontaneous corneal perforation associated with complete external ophthalmoplegia in mitochondrial myopathy (kearns-sayre syndrome). Cornea. 2003;22(3):267-70.
  9. Vaidyanathan U, Hopping GC, Liu HY, Somani AN, Ronquillo YC, Hoopes PC, et al. Persistent Corneal Epithelial Defects: A Review Article. Med Hypothesis Discov Innov Ophthalmol. 2019;8(3):163-76.
  10. Alhoutan K, Alarfaj K. Exposure Keratopathy: An Idiopathic Lagophthalmos Case Report. Cureus. 2021;13(10):e18945.
  11. Grixti A, Sadri M, Edgar J, Datta AV. Common ocular surface disorders in patients in intensive care units. The ocular surface. 2012;10(1):26-42.
  12. Robaei D, Chan UT, Khoo P, Cherepanoff S, Li YC, Hanrahan J, et al. Corneal biopsy for diagnosis of recalcitrant microbial keratitis. Graefes Arch Clin Exp Ophthalmol. 2018;256(8):1527-33.
  13. Schargus M, Kohlhaas M, Unterlauft JD. Treatment of severe ocular surface disorders with albumin eye drops. J Ocul Pharmacol Ther. 2015;31(5):291-5.
  14. McDonald MB, Sheha H, Tighe S, Janik SB, Bowden FW, Chokshi AR, et al. Treatment outcomes in the DRy Eye Amniotic Membrane (DREAM) study. Clin Ophthalmol. 2018;12:677-81.
  15. Katsoulos K, Rallatos GL, Mavrikakis I. Scleral contact lenses for the management of complicated ptosis. Orbit (Amsterdam, Netherlands). 2018;37(3):201-7.
  16. Bergmanson JP, Ezekiel DF, van der Worp E. Scleral contact lenses and hypoxia: Theory versus practice. Contact lens & anterior eye : the journal of the British Contact Lens Association. 2015;38(3):145-7.
  17. Jang SY, Yoon JS. Treatment of refractory exposure keratitis with modified medial tarsorrhaphy using tarsoconjunctival flap. Graefes Arch Clin Exp Ophthalmol. 2013;251(5):1369-72.
  18. Srinivasan M, Mascarenhas J, Rajaraman R, Ravindran M, Lalitha P, Glidden DV, et al. Corticosteroids for bacterial keratitis: the Steroids for Corneal Ulcers Trial (SCUT). Arch Ophthalmol. 2012;130(2):143-50.
  19. Khoo P, Cabrera-Aguas M, Watson SL. Topical Steroids as Adjunctive Therapy for Bacterial Keratitis: Evidence From a Retrospective Case Series of 313 Cases. Asia Pac J Ophthalmol (Phila). 2020;9(5):398-403.
  20. Hossain P. The corneal melting point. Eye (Lond). 2012;26(8):1029-30.
Medical College of Wisconsin | Milwaukee, WI

John Conto, OD, Dipl. AAO completed his optometric training at the Pennsylvania College of Optometry and finished a residency in Primary Care Optometry at The Eye Institute, Philadelphia. Currently, He holds the faculty rank of Associate Professor at the Medical College of Wisconsin and is the Chief of Vision Services at Froedtert Hospital. Dr. Conto is a Diplomate in Anterior Segment of the American Academy of Optometry and is board certified through the American Board Certification in Medical Optometry.

Medical College of Wisconsin | Milwaukee, WI

Jane Bachman Groth, OD, FAAO completed her optometric training at The Illinois College of Optometry. and finished a residency in Primary Care Optometry at the Illinois College of Optometry. Currently, she holds the faculty rank of Associate Professor at the Medical College of Wisconsin. Dr. Bachman Groth is a Fellow of the American Academy of Optometry and is board certified through the American Board Certification in Medical Optometry.

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