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Year : 2020  |  Volume : 58  |  Issue : 4  |  Page : 313-315

Late-onset limbal ischemia in alkali burns

Department of Ophthalmology, Mahatma Gandhi Medical College and Research Institute, Sri Balaji Vidyapeeth University, India

Date of Submission24-Jun-2020
Date of Decision04-Aug-2020
Date of Acceptance07-Aug-2020
Date of Web Publication16-Dec-2020

Correspondence Address:
Dr. Krishnagopal Srikanth
Department of Ophthalmology, Mahatma Gandhi Medical College and Research Institute, Pillaiyarkuppam, Puducherry - 607 402
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/tjosr.tjosr_78_20

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Chemical injury is one of the common ocular emergencies in ophthalmology practice. Ocular burns, especially with alkaline solution, can lead to hazardous effects on eye structures. Limbal ischemia resulting from such injury carries a grave prognosis. Lack of standard criterion results in difficult assessment of limbal ischemia. Diagnosis of limbal ischemia is purely dependent on subjective assessment. A 40-year-old female presented to our emergency department with alkali injury. Alkali injury was promptly diagnosed and treated. There was no sign of limbal ischemia during initial evaluation. On follow-up, the patient developed late-onset limbal ischemia.

Keywords: Alkali burns, late onset, limbal ischemia

How to cite this article:
Shaikh ZM, Srikanth K, Muthukrishnan V. Late-onset limbal ischemia in alkali burns. TNOA J Ophthalmic Sci Res 2020;58:313-5

How to cite this URL:
Shaikh ZM, Srikanth K, Muthukrishnan V. Late-onset limbal ischemia in alkali burns. TNOA J Ophthalmic Sci Res [serial online] 2020 [cited 2021 Apr 23];58:313-5. Available from: https://www.tnoajosr.com/text.asp?2020/58/4/313/303660

  Introduction Top

Chemical injuries account for 11.5%–22.1% of all ocular traumas.[1] Exposure to chemical causes widespread damage to ocular surface, extending to deeper structures of the eye. Alkali burn tends to be more severe than acid burn. Cation released from alkaline solution combines with carboxyl group of stromal collagen leading to stromal edema and loss of transparency and thus invading deeper layers of the cornea.[2] Evaluation of the limbus plays a crucial role in management. Diagnosing limbal ischemia is an arduous task because of confounding factors such as chemosis and congestion. No definite criterion exists to diagnose limbal ischemia; hence, its diagnosis is subjective and unreliable.[3]

  Case Report Top

A 40-year-old female presented to the emergency department with an alleged history of exposure to cleaning solution (Lysol) to both the eyes, the content of which was highly basic potassium hydroxide (3%–4%). She complained of burning, stinging sensation, pain, and blurring of vision along with superficial burns all over the face [Figure 1]a.
Figure 1: Day 1 of alkali burn. (a) Superficial burns and periorbital edema. (b) Right eye mild chemosis and epithelial defect. (c) Severe chemosis. (d) Left eye

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She was admitted and evaluated further. On the day of presentation, vision in the right eye (RE) was 6/24p. On examination, an irregular epithelial defect of 10 mm × 10 mm with positive fluorescein staining was observed [Figure 1]b. Anterior chamber flare of 1 + was appreciated. Visual acuity of the left eye (LE) was 6/36p. There was a ground-glass appearance of the cornea with a 10.5 mm × 10 mm epithelial defect on fluorescein stain [Figure 1]d. Stromal edema was appreciated at 4–7'o clock at the inferior paracentral area [Figure 2]. Both eyes showed periorbital edema, chemosis, and diffuse conjunctival congestion with greater severity in LE [Figure 1]c.
Figure 2: Left eye stromal edema with chemosis

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RE examination showed no limbal ischemia. LE limbal ischemia could not be evaluated due to severe chemosis. Based on Roper-Hall grading, the patient was diagnosed with Grade II chemical (alkali) injury (left > right).

Thorough eyewash was given with Ringer lactate solution as per standard protocol.

Treatment was initiated with antibiotic-steroid combination eyedrops, carboxymethylcellulose eye ointment and eyedrops, carboxymethylcellulose eyedrops, oral Vitamin C 500 mg, silver sulfadiazine gel topical application over facial burns, systemic steroids, and antibiotics.

The patient was hospitalized for 10 days and with vigilant monitoring. During discharge, vision in RE was 6/18 and LE 6/36p; periorbital edema, chemosis, and congestion were reduced. There was a resolution of epithelial defect in RE resolved, and fluorescein stain was negative. Corneal stromal edema and epithelial defect appeared to have resolved in LE with pooling of fluorescein stain. The patient was discharged with medications including oral doxycycline, antibiotic-steroid eyedrops with tapering dose, and carboxymethylcellulose eye ointment and eyedrops in BE, along with topical therapy facial burns. The patient was reviewed after 1 week. Vision in RE was 6/12 and LE 6/36. RE examination was within the normal level [Figure 3]. LE showed corneal haze, micro-bullae at the limbus, hyperpigmented frill at the limbus with early pannus formation, and infiltrates at 5'o clock [Figure 4]. Limbal ischemia was assessed by slit-amp examination which showed an area of blanching and discontinuity of vessels 360° around the limbus. The development of late limbal ischemia was noted 2 weeks after injury.
Figure 3: Right eye normal slit-lamp examination of the anterior segment

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Figure 4: Late-onset limbal ischemia with early pannus formation

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The patient was counseled to undergo amniotic membrane transplant but was lost to follow-up.

  Discussion Top

Chemical injuries commonly present in the emergency department with a wide range of clinical manifestations. Direct exposure to harmful chemical leads to grave ocular injuries. The degree of injury depends on numerous factors such as duration of exposure, surface area of exposure, and also the type and composition of chemical. The severity of chemical injury is more in alkali burn due to high degree of penetration, leading to surface damage of conjunctiva and deeper layers of the cornea. In such grievous injury, the limbus plays a crucial role in controlling repair and regeneration of corneal epithelium.[2]

Detection of extent and severity of limbal ischemia shapes the prognosis and overall course of management. The clinical assessment of limbal ischemia remains a key variable for the management of ocular burns. Strikingly, there is no standard criterion for diagnosing this most essential prognostic factor. Ophthalmologists depend on appearance of vascularity and color of the perilimbal region. Confounding factor like extensive chemosis also plays a role in masking the limbal ischemia. However, it is a highly subjective and less reliable method, which leads to false stratification of patients. This can have an adverse influence on the management protocol of ocular burns.[3],[4]

Limbal stem cells, located in deeper layers which survive the initial insult, can show 360° surface staining in superficial limbal involvement. It is clinically impossible to detect this situation during initial assessment as the level of limbal involvement is based on clock hours. Contrariwise, in some cases, a segment of the limbus that lasts the initial insult can slough off in the postinjury period. This scenario can make the diagnosis more severe.[5]

This case portrays late-onset limbal ischemia in a case of severe alkali injury. We would like to highlight the occurrence of late-onset limbal injury which was not observed during the initial insult because of severe chemosis and periorbital edema.

A study showing delayed-onset and chronic keratitis, secondary to mustard gas toxicity, postulated several theories including an autoimmune reaction to corneal antigen altered by the mustard agent, toxic by-products, and necrotic changes.[6] In early reparative phase, rejuvenation of surface epithelium and acute inflammatory response gives way to chronic inflammatory response, stromal repair, and scarring.[7] A similar pathogenesis for limbal ischemia could be explained in our case.

In our case, there was initial chemosis with severe circumcorneal congestion and periorbital edema. Severe chemosis and local loss of conjunctival melanocytes abutting the limbus with early pannus formation were noted several days later. A late-onset limbal ischemia showcasing typical changes in vasculature was noted. Evaluation of limbal ischemia was done on a purely clinical basis.

Assessment of limbal ischemia in a case of chemical injury can be fallacious due to associated conjunctival injury which can result in delayed treatment, portending a poor visual prognosis. Associated corneal and anterior chamber findings should alert the clinician about the severity. The absence of limbal ischemia at the initial presentation does not rule out its occurrence at a later stage which should be promptly diagnosed and treated in chemical injuries. A regular follow-up is hence desirable for a gratifying outcome.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Sharma N, Kaur M, Agarwal T, Sangwan VS, Vajpayee RB. Treatment of acute ocular chemical burns. Surv Ophthalmol 2018;63:214-35.  Back to cited text no. 1
Wagoner MD. Chemical injuries of the eye: Current concepts in pathophysiology and therapy. Surv Ophthalmol 1997;41:275-313.  Back to cited text no. 2
Kam KW, Patel CN, Nikpoor N, Yu M, Basu S. Limbal ischemia: Reliability of clinical assessment and implications in the management of ocular burns. Indian J Ophthalmol 2019;67:32-6.  Back to cited text no. 3
[PUBMED]  [Full text]  
Beare JD. Eye injuries from assault with chemicals. Br J Ophthalmol 1990;74:514-8.  Back to cited text no. 4
Dua HS, King AJ, Joseph A. A new classification of ocular surface burns. Br J Ophthalmol 2001;85:1379-83.  Back to cited text no. 5
Javadi MA, Yazdani S, Sajjadi H, Jadidi K, Karimian F, Einollahi B, et al. Chronic and delayed-onset mustard gas keratitis: Report of 48 patients and review of literature. Ophthalmology 2005;112:617-25.  Back to cited text no. 6
Eslani M, Baradaran-Rafii A, Movahedan A, Djalilian AR. The ocular surface chemical burns. J Ophthalmol 2014;2014:196827.  Back to cited text no. 7


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]


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