About OJO | Search | Ahead of print | Current Issue | Archives | Author Instructions | Reviewer Guidelines | Online submissionLogin 
Oman Journal of Ophthalmology Oman Journal of Ophthalmology
  Editorial Board | Subscribe | Advertise | Contact
https://www.omanophthalmicsociety.org/ Users Online: 475  Wide layoutNarrow layoutFull screen layout Home Print this page  Email this page Small font size Default font size Increase font size

 Table of Contents    
Year : 2013  |  Volume : 6  |  Issue : 2  |  Page : 83-86  

Ocular chemical injuries and their management

Department of Ophthalmology, V. C. S. G. Government Medical Sciences and Research Institute, Srinagar, Garhwal, Uttarakhand, India

Date of Web Publication19-Aug-2013

Correspondence Address:
Parul Singh
Department of Ophthalmology, V. C. S. G. Government Medical Sciences and Research Institute, Srinagar, Garhwal, Uttarakhand
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0974-620X.116624

Rights and Permissions

Chemical burns represent potentially blinding ocular injuries and constitute a true ocular emergency requiring immediate assessment and initiation of treatment. The majority of victims are young and exposure occurs at home, work place and in association with criminal assaults. Alkali injuries occur more frequently than acid injuries. Chemical injuries of the eye produce extensive damage to the ocular surface epithelium, cornea, anterior segment and limbal stem cells resulting in permanent unilateral or bilateral visual impairment. Emergency management if appropriate may be single most important factor in determining visual outcome. This article reviews the emergency management and newer techniques to improve the prognosis of patients with chemical injuries.

Keywords: Acid, alkali, chemical burns, eye, injury, ocular, treatment

How to cite this article:
Singh P, Tyagi M, Kumar Y, Gupta K K, Sharma P D. Ocular chemical injuries and their management. Oman J Ophthalmol 2013;6:83-6

How to cite this URL:
Singh P, Tyagi M, Kumar Y, Gupta K K, Sharma P D. Ocular chemical injuries and their management. Oman J Ophthalmol [serial online] 2013 [cited 2021 Nov 30];6:83-6. Available from: https://www.ojoonline.org/text.asp?2013/6/2/83/116624

   Introduction Top

Ocular chemical injuries are a true ocular emergency and require immediate and intensive evaluation and treatment. The sequelae of an ocular burn can be severe and particularly challenging to manage. Improvements in the understanding of the pathophysiology of chemical injuries, as well as advancements in ocular surface reconstruction have provided hope for patients who would otherwise have a dismal visual prognosis. After chemical injury, the goal of therapy is to restore a normal ocular surface and corneal clarity. If extensive corneal scarring is present, limbal stem cell grafting, amniotic membrane transplantation and possibly keratoprosthesis can be employed to help restore vision. This article will review the literature available and discuss newer techniques available to improve the prognosis of patients with chemical injuries.

   Epidemiology Top

Ocular chemical injuries can occur under diverse circumstances and in such varied locations as the home, the workplace, and school [Table 1]. These injuries are common in industrial chemical laboratories, in machine factories, in agriculture, and among laborers and construction workers. They also are frequently reported from fabric mills, automotive repair facilities, and cleaning and sanitizing crews. Chemical burns of the eyes occur most often among the age group from 20 to 40 years, with young men at greatest risk. In a retrospective study on the incidence and prevalence of ocular chemical burns, 171 consecutive patients were studied during an interval of 1 year. Industrial accidents caused 61% of these burns; 37% occurred in the home. The remainder were of unknown origin. [1] Automotive battery acid burns have become increasingly more common. During recharging of a lead acid storage battery, which contains up to 25% sulfuric acid, hydrogen and oxygen produced by electrolysis form a highly explosive gaseous mixture. [2]
Table 1: Etiological factors commonly encountered in ocular chemical injuries

Click here to view

   Etiological Factors (Commonly Encountered) Top

Recent studies put the incidence of ocular burns of the eye at 7.7-18% of all ocular traumas. The majorly of victims are young and exposure occurs at home, work and in association with criminal assaults. Alkali injuries occur more frequently than acidic injuries.

   Pathogenesis Top

Acid burns

Acids have lower than normal pH values of the human eye (7.4) they precipitate tissue protein, creating a barrier to further ocular penetration. Due to this fact acid injuries tend to be less severe than alkali injuries. One exception to this is hydrofluoric acid, which may rapidly pass through cell membranes and enter anterior chamber of the eye.

It reacts with collagen resulting in shortening of collagen fibers which cause a rapid increase in intraocular pressure (IOP). After severe acid burns with ciliary body damage, decrease in levels of aqueous ascorbate has been demonstrated.

Alkali burns

Alkali burns cause corneal damage by pH change, ulceration, proteolyzes and collagen synthesis defects. Alkali substances are liphophilic and penetrate the eye more rapidly than acids. The basic substance can quickly deposit within the tissues of the ocular surface causing saponification reaction within those cells. The damaged tissue secrete proteolytic enzymes as part of an inflammatory response which leads to further damage. Alkali substances can penetrate into the anterior chamber causing cataract formation, damage to the ciliary body and damage to the trabecular meshwork.

The damage to the corneal and conjunctival epithelium from an ocular burn may be so severe as to damage the pluripotent limbal stem cell causing a limbal stem cell deficiency. This may lead to opacification and neo-vascularization of the cornea. An acute IOP rise occurrence due to shrinkage and contraction of the cornea and sclera is possible. [3] Long-term IOP rises can occur from the accumulation of inflammatory debris within the trabecular meshwork, as well as due to damage to the trabecular meshwork itself. Damage to the conjunctiva can cause extensive scarring, perilimbal ischemia, and contracture of fornices. Loss of goblet cells and conjunctival inflammation can leave the ocular surface prone to dryness. Lid malposition may be present due to symblepharon formation leading to cicatricial entropion or ectropion.

   Classification Top

Classification schemes regarding the extent of the initial injury were initially developed in the mid 1960's first by Ballen [4] and then modified by Roper-Hall. [5] The Roper-Hall classification system was largely based on the degree of corneal haze and the amount of perilimbal blanching/ischemia [Table 2].
Table 2: Roper-Hall (Ballen) classification of ocular chemical injuries

Click here to view

Pfister subsequently made a classification system varying from mild, mild-moderate, moderate severe, severe and very severe based upon pictures and photographs demonstrating corneal haze and perilimbal ischemia. [6]

Dua et al. proposed a classification scheme based upon clock hour limbal involvement as well as a percentage of bulbar conjunctival involvement [Table 3]. [7]
Table 3: New classification of ocular surface burn

Click here to view

The important thing in the clinical setting is to note the amount of limbal, corneal and conjunctival involvement at the time of the initial injury and to document changes in the examination as the patient is followed. Grading of the severity may provide the patient with a general idea of the prognosis.

   Clinical Course of Chemical Ocular Injury Top

According to McCulley the clinical course of ocular chemical injury can be divided into the following four phases: Immediate, acute, early reparative, and late reparative. [8]

Immediate phase

The immediate phase begins the moment a chemical agent comes in contact with the ocular surface. The key elements for determining the extent of chemical ocular injury and prognosis are:

  • The total area of the corneal epithelial defect
  • The area of the conjunctival epithelial defect
  • The number of clock hours or degrees of limbal blanching
  • The area and density of corneal opacification
  • Evidence of increase IOP on presentation
  • Loss of lens clarity.

Acute phase

The first 7 days after chemical eye injury constitute the acute phase of recovery. During this time, the tissues rid themselves of contaminants while re-establishing the superficial protective layer of corneal epithelium.

The epithelium serves as a protective barrier against the enzymes in tears that lead to corneal thinning and progression to perforation. It also modulates stromal regeneration and repair. Significant inflammatory mechanisms begin to evolve on the ocular surface and inside the eye. In this stage, there is the rise in IOP in a bimodal manner. [3]

Early reparative phase (8-20 days)

This is the transition period of ocular healing, in which the immediate regeneration of ocular surface epithelium and acute inflammatory events give way to chronic inflammation, stromal repair and scarring. It is during this stage, corneal ulceration tends to occur. Stromal ulceration thus resulting has been attributed to action of digestive enzymes such as collagenase, metalloproteinase and other proteases released from regenerating corneal epithelium and polymorphonuclear leukocytes.

Late reparative phase and sequelae

Three weeks after a chemical injury occurs the healing process begins late reparative phase. This stage is characterized by completion of healing with good visual prognosis (Grade I and II) and complications in those with guarded visual prognosis (Grade III and IV). The late complications of chemical burns include poor vision, corneal scarring, xerophthalmia, dry eyes, symblepharon, ankyloblepharon glaucoma, uveitis, cataract, adenexal abnormalities such as lagophthalmos, entropion, ectropion and trichiasis.

   Management of Chemical Burns Top

Immediate initiation of treatment influences the final outcome favorably and one should not wait for careful assessment of the injury.

Initial evaluation and immediate treatment

Patients suffering from a chemical injury often present to the emergency. Once history of chemical exposure is obtained chemical should be identified if possible, but this should but delay treatment. Immediate treatment should include copious irrigation prior to ophthalmic evaluation irrigation with isotonic saline or lactate ringer solution should be performed and sometimes irrigating volumes up to 20 L or more is required to change pH to physiological levels (pH testing should be done). Once copious irrigation is achieved and pH is neutralized, the ocular examination should proceed with attention is being paid to fornices, visual acuity, IOP, perilimbal blanching. In pediatric cases, if the examination is not possible under topical anesthesia it should be done under general anesthesia.

Acute phase treatment

Once the emergency treatment and evaluation are completed, the challenging task of healing the chemically injured eye begins. The major treatment goals that are important throughout the healing phases are: (a) reestablishment and maintenance of an intact and healthy corneal epithelium (b) control of the balance between collagen synthesis and collagenolysis and (c) minimizing the adverse sequelae that often follow a chemical injury. Acute phase treatment includes a broad spectrum topical antibiotic, cycloplegic and antiglaucoma therapy. Apart from above mentioned medications various therapies to promote reepithelization, support repair and control inflammation are used.

Modalities to promote reepithelization are:

  1. Tear substitutes: Preservative free tear substitutes can ameliorate persistent epitheliopathy, reduce the risk of recurrent erosions and accelerate visual rehabilitation
  2. Bandage soft contact lens: Hydrophilic high oxygen permeability lenses should be preferred. They promote epithelial migration, helps in the basement membrane regeneration and enhances epithelial stromal adhesion
  3. Investigational drugs:
    1. Retinoic acid - Has shown promise in treatment of ocular surface disorders associated with goblet cell dysfunction
    2. Epidermal growth factor and fibronectin - Has a favorable effect on promoting epitheliazation.

Drugs that support repair and minimizing ulceration

  1. Ascorbate: Ascorbate is an essential water soluble vitamin that is a cofactor in rate limiting step of collagen formation. Supplementation of ascorbate by restoring depleted aqueous ascorbate levels reduces the incidence of corneal thinning and ulceration. Oral ascorbate (2 g/day) and topical 10% solution formulated in artificial tears are effective
  2. Collagenase inhibitors: Collagenase inhibitors promote wound healing by inhibiting collagenolytic activity and thus preventing stromal ulceration. Several collagenase inhibitors including cysteine, acetylcysteine, sodium ethylenediamine tetra acetic acid (EDTA), calcium EDTA, penicillamine and citrate have been reported to be efficacious. Only 10-20% acetylcysteine (mucomist) is available commercially. It is an unstable solution and has to be refrigerated and used within 1 week of its preparation.

Drugs to control inflammation

Corticosteroids reduce inflammatory cell infiltration and stabilize neutrophilic cytoplasmic and lysosomal membranes. Use of topical steroids alone can potentially lead to a further increase in corneoscleral melt. [9] Davis et al. evaluated patients with topical prednisolone 0.5% in conjunction with topical ascorbate 10% and concluded that there was not an associated increase in corneoscleral melt if topical steroids were used until reepithelization. [10]

Early reparative phase treatment

An intact epithelium should have already been achieved by this time. If it has not been, then aggressive therapy is instituted by use of lubricants, punctual plugs, punctual occlusion with cautery, bandage contact lens, tarsorrhaphy. If epithelium is not intact, corticosteroids dosage is tapered and discontinued by 14 th day after injury. Ascorbate and citrate are continued, antiglaucoma therapy is continued as required. Antibiotics are maintained and examination for the formation of symblepharon continued.

Late reparative phase treatment

The patient whose injured eye has not achieved an intact epithelium by the 21 st day is at significant risk of permanent vision loss. Along with continued medical treatment, surgical modalities are the mainstay of treatment in this state of ocular burn. The various strategies include conjunctival/tenons advancement, tissue adhesives, therapeutic penetrating keratoplasty, amniotic membrane transplantation.

Rehabilitative phase

After the eye has stabilized, limbal stem cell transplantation has shown remarkable promise in rehabilitating ocular chemical injuries that have resisted treatment. Limbal stem cell can be donated from the patient uninjured fellow eye, a blood relative or a post mortem globe. All have shown promise in reestablishing a healthy ocular surface prior to further reconstructive surgery. Once a healthy surface is achieved, penetrating keratoplasty or keratoprosthesis may be considered. [11]

   Conclusion Top

Patient coming with chemical ocular injury need a through and immediate evaluation and intensive treatment. Advances in understanding of the pathophysiology of the injury have led to improvement in treatment such as use of topical ascorbate and citrate, as well as surgical treatment such as Amniotic membrane transplantation, stem cell transplantation, penetrating keratoplasty and ultimately keratoprosthesis placement if necessary. The goal of treatment is restoration of the normal ocular surface anatomy and lid position, control of glaucoma and restoration of corneal clarity.

   References Top

1.Kuckelkorn R, Makropoulos W, Kottek A, Reim M. Retrospective study of severe alkali burns of the eyes. Klin Monbl Augenheilkd 1993;203:397-402.  Back to cited text no. 1
2.Holekamp TL. Ocular injuries from automobile batteries. Trans Sect Ophthalmol Am Acad Ophthalmol Otolaryngol 1977;83:805-10.  Back to cited text no. 2
3.Paterson CA, Pfister RR. Intraocular pressure changes after alkali burns. Arch Ophthalmol 1974;91:211-8.  Back to cited text no. 3
4.Ballen PH. Treatment of chemical burns of the eye. Eye Ear Nose Throat Mon 1964;43:57-61.  Back to cited text no. 4
5.Roper-Hall MJ. Thermal and chemical burns. Trans Ophthalmol Soc U K 1965;85:631-53.  Back to cited text no. 5
6.Pfister RR. Chemical injuries of the eye. Ophthalmology 1983;90:1246-53.  Back to cited text no. 6
7.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. 7
8.McCulley JP. Chemical injuries. In: Smolin G, Thoft RA, editors. The Cornea: Scientific Foundation and Clinical Practice. Boston, Mass: Little, Brown and Co; 1987. p. 527-42.  Back to cited text no. 8
9.Donshik PC, Berman MB, Dohlman CH, Gage J, Rose J. Effect of topical corticosteroids on ulceration in alkali-burned corneas. Arch Ophthalmol 1978;96:2117-20.  Back to cited text no. 9
10.Davis AR, Ali QK, Aclimandos WA, Hunter PA. Topical steroid use in the treatment of ocular alkali burns. Br J Ophthalmol 1997;81:732-4.  Back to cited text no. 10
11.Dohlman CH, Schneider HA, Doane MG. Prosthokeratoplasty. Am J Ophthalmol 1974;77:694-70.  Back to cited text no. 11


  [Table 1], [Table 2], [Table 3]

This article has been cited by
1 Air pollution and hospital outpatient visits for conjunctivitis: a time-series analysis in Tai’an, China
Renchao Chen, Jun Yang, Di Chen, Wen-jing Liu, Chunlin Zhang, Hao Wang, Bixia Li, Peng Xiong, Boguang Wang, Yi Wang, Shanshan Li, Yuming Guo
Environmental Science and Pollution Research. 2021; 28(12): 15453
[Pubmed] | [DOI]
2 Acute management of ocular chemical injury using a combination eyelid retraction and irrigation instrument
William R. Bloom, Jay P. Mathias, Srinivas Sai A. Kondapalli
Advances in Ophthalmology Practice and Research. 2021; 1: 100003
[Pubmed] | [DOI]
3 Magnesium ocular injury – A case report
Andrea Little, Megan Dietze-Fiedler, Colton Fernstrum, Norberto Mancera, Richard Wilcox, Viet Do
Burns Open. 2021; 5(1): 6
[Pubmed] | [DOI]
4 Hydroxypropyl methacrylamide-based copolymeric nanoparticles loaded with moxifloxacin as a mucoadhesive, cornea-penetrating nanomedicine eye drop with enhanced therapeutic benefits in bacterial keratitis
Sanjay Ch, Priyasha Mishra, Himanshu Bhatt, Balaram Ghosh, Sanhita Roy, Swati Biswas
Colloids and Surfaces B: Biointerfaces. 2021; 208: 112113
[Pubmed] | [DOI]
5 A New Risk of Using Alkaline Drops in Patients With Laryngopharyngeal Reflux
Tyler Pion, Ghiath Alnouri, Robert T. Sataloff
Journal of Voice. 2021;
[Pubmed] | [DOI]
6 The two-faced effects of nerves and neuropeptides in corneal diseases
Romina Mayra Lasagni Vitar, Paolo Rama, Giulio Ferrari
Progress in Retinal and Eye Research. 2021; : 100974
[Pubmed] | [DOI]
7 Bio-polymeric hydrogels for regeneration of corneal epithelial tissue*
Bahareh Pourjabbar, Esmaeil Biazar, Saeed Heidari Keshel, Milad Ahani-Nahayati, Alireza Baradaran-Rafii, Reza Roozafzoon, Mohammad Hasan Alemzadeh-Ansari
International Journal of Polymeric Materials and Polymeric Biomaterials. 2021; : 1
[Pubmed] | [DOI]
8 The Role of Inflammatory Cytokines in Neovascularization of Chemical Ocular Injury
Alireza Shahriary, Milad Sabzevari, Khosrow Jadidi, Farshad Yazdani, Hossein Aghamollaei
Ocular Immunology and Inflammation. 2021; : 1
[Pubmed] | [DOI]
9 Determining the effect of ocular chemical injuries on topical drug delivery
Ghazala Begum, Thomas Leigh, David Stanley, Ann Logan, Richard James Blanch
Drug Delivery. 2021; 28(1): 2044
[Pubmed] | [DOI]
10 Priming human adipose-derived mesenchymal stem cells for corneal surface regeneration
Núria Nieto-Nicolau, Eva M. Martínez-Conesa, Sherezade Fuentes-Julián, Francisco Arnalich-Montiel, Ignacio García-Tuñón, María P. De Miguel, Ricardo P. Casaroli-Marano
Journal of Cellular and Molecular Medicine. 2021; 25(11): 5124
[Pubmed] | [DOI]
11 Evaluation of Clinical and Histological Outcomes of Adipose-Derived Mesenchymal Stem Cells in a Rabbit Corneal Alkali Burn Model
Diamantis Almaliotis, Angelos Thomas, Anastasia Komnenou, Eleni Gounari, Stavroula Almpanidou, Thomas Siempis, Nikolaos Papaioannou, Georgios Koliakos, Eleni Papakonstantinou, Konstadinos Sotiropulos, Vasileios Karampatakis, Valeria Sorrenti
Stem Cells International. 2021; 2021: 1
[Pubmed] | [DOI]
12 A Novel Therapeutic Approach to Corneal Alkaline Burn Model by Targeting Fidgetin-Like 2, a Microtubule Regulator
Jessie Wang, Abhinav Dey, Adam H. Kramer, Yuan Miao, Juan Liu, Lisa Baker, Joel M. Friedman, Parimala Nacharaju, Roy S. Chuck, Cheng Zhang, David J. Sharp
Translational Vision Science & Technology. 2021; 10(1): 17
[Pubmed] | [DOI]
13 Assessment of the corneal collagen organization after chemical burn using second harmonic generation microscopy
Juan M. Bueno, Francisco J. Ávila, Elvira Lorenzo-Martín, Patricia Gallego-Muñoz, M. Carmen Martínez-García
Biomedical Optics Express. 2021; 12(2): 756
[Pubmed] | [DOI]
14 Hospital Based Longitudinal Study on Artificial Snow Spray Induced Ocular Injuries and Its Correlation with the Awareness among the Study Population at Medical College Hospital, Bhubaneswar
Lipika Panda, Arun Kumar Samal, Lisa Sarangi
Journal of Evidence Based Medicine and Healthcare. 2021; 8(22): 1764
[Pubmed] | [DOI]
15 Fibrin-Plasma Rich in Growth Factors Membrane for the Treatment of a Rabbit Alkali-Burn Lesion
Ronald Sánchez-Ávila, Natalia Vázquez, Manuel Chacón, Mairobi Persinal-Medina, Agustín Brea-Pastor, Silvia Berisa-Prado, Luis Fernández-Vega-Cueto, Eduardo Anitua, Álvaro Meana, Jesús Merayo-Lloves
International Journal of Molecular Sciences. 2021; 22(11): 5564
[Pubmed] | [DOI]
Biju Gopal, I Anesha Isaac, Adithya Shankar, Hasanul Banna KM, N Rajendran
[Pubmed] | [DOI]
17 Ocular firecracker injury
RanjanK Behera, ParulC Gupta, Surbhi Khurana, Jagat Ram
Indian Journal of Ophthalmology - Case Reports. 2021; 1(2): 181
[Pubmed] | [DOI]
18 Lesson to be learned: A case of ocular trichloroacetic acid burn in an infant
Saroj Gupta, Deepak Soni
Indian Journal of Ophthalmology - Case Reports. 2021; 1(4): 634
[Pubmed] | [DOI]

Management Strategies of Ocular Chemical Burns: Current Perspectives

Mohammad Soleimani, Morteza Naderan
Clinical Ophthalmology. 2020; Volume 14: 2687
[Pubmed] | [DOI]
20 Anti-VEGF Treatment in Corneal Diseases
Giuseppe Giannaccare, Marco Pellegrini, Cristina Bovone, Rossella Spena, Carlotta Senni, Vincenzo Scorcia, Massimo Busin
Current Drug Targets. 2020; 21(12): 1159
[Pubmed] | [DOI]
21 In vitro potential of human mesenchymal stem cells for corneal epithelial regeneration
Núria Nieto-Nicolau, Beatriz Martín-Antonio, Claudia Müller-Sánchez, Ricardo P Casaroli-Marano
Regenerative Medicine. 2020; 15(3): 1409
[Pubmed] | [DOI]
22 Health Impacts of a Traditional Illicit Brew (Kaanga) Consumed in Meru County, Kenya
Atuna Titus Gitari, Osano Aloys, Bakari Chaka, Bulitia Godrick
European Journal of Environment and Public Health. 2020; 5(1): em0065
[Pubmed] | [DOI]
23 Heparin-Modified Amniotic Membrane Combined With Growth Factors for Promoting Corneal Wound Healing After Alkali Burn
Xuan Zhao, Xin Zuo, Jing Zhong, Bowen Wang, Saiqun Li, Yichen Xiao, Jin Yuan
Frontiers in Bioengineering and Biotechnology. 2020; 8
[Pubmed] | [DOI]
24 Therapeutic Potential of Extracellular Vesicles for the Treatment of Corneal Injuries and Scars
Sophie X. Deng, Aurelie Dos Santos, Serina Gee
Translational Vision Science & Technology. 2020; 9(12): 1
[Pubmed] | [DOI]
25 A Systematic Review of Emerging Therapeutic Strategies in the Management of Chemical Injuries of the Ocular Surface
Stephanie Hiu Ling Poon, William Ho Lam Wong, Yashan Bu, Amy Cheuk Yin Lo, Vishal Jhanji, Yau Kei Chan, Kendrick Co Shih
Eye & Contact Lens: Science & Clinical Practice. 2020; 46(6): 329
[Pubmed] | [DOI]
26 Plasma fibroblast skin tightening treatment resulting in bilateral chemical eye injury secondary to EMLA cream: a case report
Sirjhun Patel, Mohith Shamdas, Caroline Cobb
BMC Ophthalmology. 2020; 20(1)
[Pubmed] | [DOI]
27 Wound Healing After Alkali Burn Injury of the Cornea Involves Nox4-Type NADPH Oxidase
Nora Y. Hakami, Gregory J. Dusting, Elsa C. Chan, Manisha H. Shah, Hitesh M. Peshavariya
Investigative Opthalmology & Visual Science. 2020; 61(12): 20
[Pubmed] | [DOI]
28 AMPK Activation by 5-Amino-4-Imidazole Carboxamide Riboside-1-ß-D-Ribofuranoside Attenuates Alkali Injury-Induced Corneal Fibrosis
Selikem Abla Nuwormegbe, Sun Woong Kim
Investigative Opthalmology & Visual Science. 2020; 61(6): 43
[Pubmed] | [DOI]
29 The Therapeutic Effects and Possible Mechanism of Pranoprofen in Mouse Model of Corneal Alkali Burns
Minting Chen, Abdirahman Abdinasir Gureeye, Yacouba Cissé, Lang Bai
Journal of Ophthalmology. 2020; 2020: 1
[Pubmed] | [DOI]
30 Chemical eye injury: pathophysiology, assessment and management
Harminder S. Dua, Darren Shu Jeng Ting, Ahmed Al Saadi, Dalia G. Said
Eye. 2020; 34(11): 2001
[Pubmed] | [DOI]
31 Ophthalmic Emergencies for the Clinician
Saumya M. Shah, Cheryl L. Khanna
Mayo Clinic Proceedings. 2020; 95(5): 1050
[Pubmed] | [DOI]
32 Corneal epithelial biology: Lessons stemming from old to new
Robert M. Lavker, Nihal Kaplan, Junyi Wang, Han Peng
Experimental Eye Research. 2020; 198: 108094
[Pubmed] | [DOI]
33 Clinical profile of ocular injuries in a geographically isolated Colombian municipality
Valeria Andrea D'Antone, Laudelina Cely Quiroz, Diana Cristina Palencia Florez
International Emergency Nursing. 2020; 52: 100909
[Pubmed] | [DOI]
34 Clinical characteristics of patients hospitalized for ocular chemical injuries in Shanghai from 2012 to 2017
Tao Li, Bo Jiang, Xiaodong Zhou
International Ophthalmology. 2020; 40(4): 909
[Pubmed] | [DOI]
35 An in situ hydrogel based on carboxymethyl chitosan and sodium alginate dialdehyde for corneal wound healing after alkali burn
Wenhua Xu, Kaibin Liu, Tong Li, Wenhua Zhang, Yanhan Dong, Jiayi Lv, Wenli Wang, Jingguo Sun, Mengjie Li, Meng Wang, Zihong Zhao, Ye Liang
Journal of Biomedical Materials Research Part A. 2019; 107(4): 742
[Pubmed] | [DOI]
36 Accidental Trichloroacetic Acid Burn in a Gynecology Office
Michael Sosin, Beth Lynn Sosin, Eduardo D. Rodriguez
Obstetrics & Gynecology. 2015; 126(6): 1290
[Pubmed] | [DOI]
37 Transglutaminase binding fusion protein linked to SLPI reduced corneal inflammation and neovascularization
Juan P Salica, Diego Guerrieri, Paulo Maffia, Juan O Croxatto, H Eduardo Chuluyan, Juan E Gallo
BMC Ophthalmology. 2015; 15(1)
[Pubmed] | [DOI]
38 Chitosan-modified, collagen-based biomimetic nanofibrous membranes as selective cell adhering wound dressings in the treatment of chemically burned corneas
Juan Ye,Xin Shi,Xiaoyi Chen,Jiajun Xie,Changjun Wang,Ke Yao,Changyou Gao,Zhongru Gou
Journal of Materials Chemistry B. 2014; 2(27): 4226
[Pubmed] | [DOI]
39 A review of treatment strategies for hydrofluoric acid burns: Current status and future prospects
Xingang Wang,Yuanhai Zhang,Liangfang Ni,Chuangang You,Chunjiang Ye,Ruiming Jiang,Liping Liu,Jia Liu,Chunmao Han
Burns. 2014;
[Pubmed] | [DOI]


    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

  In this article
    Etiological Fact...
    Clinical Course ...
    Management of Ch...
    Article Tables

 Article Access Statistics
    PDF Downloaded1077    
    Comments [Add]    
    Cited by others 39    

Recommend this journal