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DR SALMAN AHMAD
PG Trainee Ophthalmology
SERVICES HOSPITAL LAHORE
CHEMICAL INJURIES TO EYES &
MANAGEMENT
Background & Introduction
 True ocular emergency
 Potentially blinding ocular injuries
 Chemical burns
 Alkaline agents
 Acidic agents
 Thermal burns
 Firework explosions
 Steam
 Boiling water
 Molten metal
ALKALINE BURNS
 Alkali dissociates into a hydroxyl ion and a cation
in the ocular surface
 Hydroxyl ion saponifies cell membrane fatty acids
 Cation interacts with stromal collagen and
glycosaminoglycans leads to deeper penetration
into cornea & AC.
 Hydration of glycosaminoglycans….. Stromal
haze
 Collagen hydration…. Fibril distortion &
shortening….. Trabecular meshwork
alterations…. Increased IOP
 Inflammatory mediators cause release of
prostaglandins…… further increase IOP
Common alkali substances at home
ACIDIC BURNS
 Acid dissociates into hydrogen ion & anions
 Hydrogen ions damage ocular surface by altering
the pH
 Anions cause protein denaturation, precipitation
and coagulation
 Protein coagulation prevents deeper penetration
& responsible for ground glass appearance of
corneal stroma.
Common acidic substances at home
Severity of burn
 Severity of burn depends on
 Surface area of contact
 Depth of penetration, concentration, time of contact, time
of interference.
 Degree of stem cell injury
 Common area of damage in eye
 Anterior segment
 Cornea
 Conjuctiva
 Lens
 Deeper than cornea
 Cataract
 glaucoma
Pathophysiology of ocular injury
 Necrosis of corneal & conjuctival epithelium
 Loss of limbal stem cells
 Conjuctivalization and vascularization of the corneal
surface
 Persistent corneal epithelial defects with sterile corneal
ulceration & perforation
 Ocular surface wetting disorder
 Symblepharon formation
 Cicatricial entropion
 Corneal opacification
 Ciliary epithelial damage… ascorbate production
 Hypotony & phthisis bulbi
Pathophysiology of ocular injury
 Healing
 Epithelium
 Migration of cells from limbal stem cells
 Stroma
 Damaged stromal collagen is phagocytosed by keratocytes
& new collagen synthesized
Diagnosis
 Diagnosis is made from the history
 The staging is guided by the clinical picture.
 Intraocular structures in the anterior segment of
the eye can also be involved and can be
associated with lens opacities and secondary
glaucoma.
Severe chemical injury
Severe acid burn
Acute alkali burn
Severe alkali burn
Corneal opacity of lime burn
Alkali injury
 ‘cooked fish eye’
 Cornea white as chalk
and opaque
 Superficial and deep
vascularization
Alkali injury
 Heavily vascularized
cornea with
symblepharon
 Poor prognosis
expected for
penetrating
keratoplasty
Chemical injury
Total destructive effect
of lye burn Superglue injury
Clinical picture
Symptoms Signs
 Pain
 Lacrimation
 Photophobia
 Blepharospasm
 Blurring of vision
 Eyelid edema
 Chemosis
 Conjuctival injection
 Corneal abrasion
Effects of ocular surface burn
structure Immediate effect Delayed effect
Lid Oedema
Dermatitis
Ulcer
Cicatricial entropion
Cicatricial ectropion
Conjuctiva Conjuctival injection
Ulcer
Chemosis
Symblepharon
Xerosis
Pseudopterygium
Cornea Oedema
Ulcer
Perforation
Vascularized opacities
Xerosis
Uvea Anterior uveitis Iridocyclitis
IOP May be increased Increased (conjuctival
fibrosis)
Roper-Hall classification system
Grade Prognosis Limbal ischemia Corneal
involvement
I Good None Epithelial damage
II Good < 1/3 Haze, but iris
details visible
III Guarded 1/3 to 1/2 Total epithelial
loss with haze
that obscures iris
details
IV Poor > 1/2 Cornea opaque
with iris and pupil
obscured
A new classification of ocular burns
Grade Prognosis Clinical
findings
Conjuctival
involvement
I Very good 0 clock hours
of limbal
ischemia
0 %
II Good 3 clock hours
of limbal
ischemia
30%
III Good >3-6 clock
hours of
limbal
ischemia
> 30-50%
IV Good to
guarded
> 6-9 clock
hours of
limbal
ischemia
> 50-75%
V Guarded to
poor
>9-<12 clock
hours of
limbal
> 75 - <100%
Complications
 Primary complications
 Conjuctival inflammation
 Corneal abrasions
 Corneal haze and edema
 Acute rise in IOP
 Corneal melting & perforation
 Secondary complications
 Secondary glaucoma
 Secondary cataract
 Conjuctival scarring
 Corneal thinning & perforation
 Complete ocular surface disruption
 Corneal ulceration (sterile or infectious)
 Phthisis bulbi
 Complete cicatrization of corneal surface
Laboratory study
 The pH of ocular surface should be periodically
tested. Irrigation should be continued until the pH
reaches neutrality.
 No other tests are generally necessary unless
other systemic injuries are concurrent.
Goals of Medical care
 Removing of offending agents
 Promoting ocular surface healing
 Controlling inflammation
 Preventing infection
 Controlling IOP
Immediate management of
chemical burns
Removal of inciting chemical
 Immediate copious irrigation
 Normal saline solution
 Ringer’s lactate solution
 Normal saline with bicarbonate
 Balanced salt solution (BSS)
 Irrigation continued until pH is neutralized
 Evert the upper eyelid and irrigate, and irrigate
the lower eyelid
 Check pH with litmus paper
 If litmus paper not available then continue
irrigation for 20 minutes
 Contraindications for water… burns with
chemicals of heavy metals
Eye irrigation
Transfer
 After completing initial irrigation and treatment,
patient should be transferred to facilities that have
ophthalmologists available to assume care for
them.
Acute management of chemical
burns
Acute management
 Eye speculum
 Topical anesthesia
 Eversion of eyelids
 Continue irrigation till
pH is normalized
Promote ocular surface healing
1. Remove inciting chemical
2. Debridement
3. Paracentesis
4. Early assessment followed by
1. Artificial tear supplement…
2. Ascorbate --- > improvement in corneal healing
3. Therapeutic bandage contact lens
4. Amniotic membrane transplant
Mid term management of
chemical burn
Control of inflammation
 Topical steroids
 Citrate
 Acetylcysteine 10%
 Ascorbate and citrate
Control of infection & cicatrization
 Topical antibiotic,
aggressive lubrication
with eye ointments
(steroid-antibiotic
combination)
 Prophylactic
antibiotics
Control of IOP
 Oral acetazolamide or topical beta-blockers or
aqueous suppressant are advocated to reduce
IOP.
Control of pain
 Cycloplegics for ciliary
spasm
 Oral pain medications
Improves healing
 Steroids reduce inflammation and neutrophil
infiltration
 Ascorbic acid synthesis of mature collagen
 Citric acid inhibitor of neutrophil activity
 Tetracycline inhibitor of collagenase
Delayed management of
chemical burns
1. Correction of lid deformity
2. Conjuctival or mucous membrane graft
3. Amniotic membrane transplantation
4. Limbal stem cell transplantation
5. Penetrating keratoplasty
6. Keratoprosthesis
1. Correction of lid deformity
 Cicatricial entropion or ectropion correction
surgery
2. Conjuctival or mucous membrane
graft
3. Amniotic membrane
transplantation
4. Limbal stem cell
transplantation
A. Removal of pannus
& superficial
keratectomy
B. Cicatrix removed
C. 3 to 5 mm superior
& inferior conjuctival
stem cells
D. Keratectomy 1 mm
within the limbus
with 5mm conjuctiva
5. Penetrating keratoplasty
Summary of suggested action during
the late periods
 Tear film should be augmented
 Lysis of symblephra and reconstruction of
fornices
 Correction of cicatricial entropion and trichiasis if
keratoplasty is anticipated
 Penetrating keratoplasty
Inpatient & outpatient
medications
 Prednisolone acetate 1% (qid)
 Erythromycin ophthalmic ointment (4-8 times/
day)
 Homatropine 5% or Scopolamine 0.25% (tid)
 Ascorbate 500 mg P/O qid
 Levobunolol 0.5% bd or acetazolamide 250 mg
tid if IOP > 30 mmHg
 Excessive lubricants
Prevention
 Education and training
 Safety goggles at chemical workplace
Prognosis
 Directly related to severity of insult
 Grading according to prognosis as in Roper Hall
classification
Differential diagnosis
 Conjuctivitis, acute hemorrhagic/ allergic
 Corneal abrasion
 Corneal erosion, recurrent
 Corneal foreign body
 Keratoconjuctivits sicca
 Corneal ulcer
 Chemical injuries are actually the true ocular
emergencies and don't waste time & defer the
detailed history and examination till the
appropriate irrigation has been achieved.
Thank you

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CHEMICAL INJURIES.pptx

  • 1.
  • 2. DR SALMAN AHMAD PG Trainee Ophthalmology SERVICES HOSPITAL LAHORE CHEMICAL INJURIES TO EYES & MANAGEMENT
  • 3. Background & Introduction  True ocular emergency  Potentially blinding ocular injuries  Chemical burns  Alkaline agents  Acidic agents  Thermal burns  Firework explosions  Steam  Boiling water  Molten metal
  • 4. ALKALINE BURNS  Alkali dissociates into a hydroxyl ion and a cation in the ocular surface  Hydroxyl ion saponifies cell membrane fatty acids  Cation interacts with stromal collagen and glycosaminoglycans leads to deeper penetration into cornea & AC.  Hydration of glycosaminoglycans….. Stromal haze  Collagen hydration…. Fibril distortion & shortening….. Trabecular meshwork alterations…. Increased IOP  Inflammatory mediators cause release of prostaglandins…… further increase IOP
  • 6. ACIDIC BURNS  Acid dissociates into hydrogen ion & anions  Hydrogen ions damage ocular surface by altering the pH  Anions cause protein denaturation, precipitation and coagulation  Protein coagulation prevents deeper penetration & responsible for ground glass appearance of corneal stroma.
  • 8. Severity of burn  Severity of burn depends on  Surface area of contact  Depth of penetration, concentration, time of contact, time of interference.  Degree of stem cell injury  Common area of damage in eye  Anterior segment  Cornea  Conjuctiva  Lens  Deeper than cornea  Cataract  glaucoma
  • 9. Pathophysiology of ocular injury  Necrosis of corneal & conjuctival epithelium  Loss of limbal stem cells  Conjuctivalization and vascularization of the corneal surface  Persistent corneal epithelial defects with sterile corneal ulceration & perforation  Ocular surface wetting disorder  Symblepharon formation  Cicatricial entropion  Corneal opacification  Ciliary epithelial damage… ascorbate production  Hypotony & phthisis bulbi
  • 10. Pathophysiology of ocular injury  Healing  Epithelium  Migration of cells from limbal stem cells  Stroma  Damaged stromal collagen is phagocytosed by keratocytes & new collagen synthesized
  • 11. Diagnosis  Diagnosis is made from the history  The staging is guided by the clinical picture.  Intraocular structures in the anterior segment of the eye can also be involved and can be associated with lens opacities and secondary glaucoma.
  • 16. Corneal opacity of lime burn
  • 17. Alkali injury  ‘cooked fish eye’  Cornea white as chalk and opaque  Superficial and deep vascularization
  • 18. Alkali injury  Heavily vascularized cornea with symblepharon  Poor prognosis expected for penetrating keratoplasty
  • 19. Chemical injury Total destructive effect of lye burn Superglue injury
  • 20. Clinical picture Symptoms Signs  Pain  Lacrimation  Photophobia  Blepharospasm  Blurring of vision  Eyelid edema  Chemosis  Conjuctival injection  Corneal abrasion
  • 21. Effects of ocular surface burn structure Immediate effect Delayed effect Lid Oedema Dermatitis Ulcer Cicatricial entropion Cicatricial ectropion Conjuctiva Conjuctival injection Ulcer Chemosis Symblepharon Xerosis Pseudopterygium Cornea Oedema Ulcer Perforation Vascularized opacities Xerosis Uvea Anterior uveitis Iridocyclitis IOP May be increased Increased (conjuctival fibrosis)
  • 22. Roper-Hall classification system Grade Prognosis Limbal ischemia Corneal involvement I Good None Epithelial damage II Good < 1/3 Haze, but iris details visible III Guarded 1/3 to 1/2 Total epithelial loss with haze that obscures iris details IV Poor > 1/2 Cornea opaque with iris and pupil obscured
  • 23. A new classification of ocular burns Grade Prognosis Clinical findings Conjuctival involvement I Very good 0 clock hours of limbal ischemia 0 % II Good 3 clock hours of limbal ischemia 30% III Good >3-6 clock hours of limbal ischemia > 30-50% IV Good to guarded > 6-9 clock hours of limbal ischemia > 50-75% V Guarded to poor >9-<12 clock hours of limbal > 75 - <100%
  • 24. Complications  Primary complications  Conjuctival inflammation  Corneal abrasions  Corneal haze and edema  Acute rise in IOP  Corneal melting & perforation  Secondary complications  Secondary glaucoma  Secondary cataract  Conjuctival scarring  Corneal thinning & perforation  Complete ocular surface disruption  Corneal ulceration (sterile or infectious)  Phthisis bulbi  Complete cicatrization of corneal surface
  • 25. Laboratory study  The pH of ocular surface should be periodically tested. Irrigation should be continued until the pH reaches neutrality.  No other tests are generally necessary unless other systemic injuries are concurrent.
  • 26. Goals of Medical care  Removing of offending agents  Promoting ocular surface healing  Controlling inflammation  Preventing infection  Controlling IOP
  • 28. Removal of inciting chemical  Immediate copious irrigation  Normal saline solution  Ringer’s lactate solution  Normal saline with bicarbonate  Balanced salt solution (BSS)  Irrigation continued until pH is neutralized
  • 29.  Evert the upper eyelid and irrigate, and irrigate the lower eyelid  Check pH with litmus paper  If litmus paper not available then continue irrigation for 20 minutes  Contraindications for water… burns with chemicals of heavy metals
  • 30.
  • 32. Transfer  After completing initial irrigation and treatment, patient should be transferred to facilities that have ophthalmologists available to assume care for them.
  • 33. Acute management of chemical burns
  • 34. Acute management  Eye speculum  Topical anesthesia  Eversion of eyelids  Continue irrigation till pH is normalized
  • 35. Promote ocular surface healing 1. Remove inciting chemical 2. Debridement 3. Paracentesis 4. Early assessment followed by 1. Artificial tear supplement… 2. Ascorbate --- > improvement in corneal healing 3. Therapeutic bandage contact lens 4. Amniotic membrane transplant
  • 36. Mid term management of chemical burn
  • 37. Control of inflammation  Topical steroids  Citrate  Acetylcysteine 10%  Ascorbate and citrate
  • 38. Control of infection & cicatrization  Topical antibiotic, aggressive lubrication with eye ointments (steroid-antibiotic combination)  Prophylactic antibiotics
  • 39. Control of IOP  Oral acetazolamide or topical beta-blockers or aqueous suppressant are advocated to reduce IOP.
  • 40. Control of pain  Cycloplegics for ciliary spasm  Oral pain medications
  • 41. Improves healing  Steroids reduce inflammation and neutrophil infiltration  Ascorbic acid synthesis of mature collagen  Citric acid inhibitor of neutrophil activity  Tetracycline inhibitor of collagenase
  • 43. 1. Correction of lid deformity 2. Conjuctival or mucous membrane graft 3. Amniotic membrane transplantation 4. Limbal stem cell transplantation 5. Penetrating keratoplasty 6. Keratoprosthesis
  • 44. 1. Correction of lid deformity  Cicatricial entropion or ectropion correction surgery
  • 45. 2. Conjuctival or mucous membrane graft
  • 47. 4. Limbal stem cell transplantation A. Removal of pannus & superficial keratectomy B. Cicatrix removed C. 3 to 5 mm superior & inferior conjuctival stem cells D. Keratectomy 1 mm within the limbus with 5mm conjuctiva
  • 49. Summary of suggested action during the late periods  Tear film should be augmented  Lysis of symblephra and reconstruction of fornices  Correction of cicatricial entropion and trichiasis if keratoplasty is anticipated  Penetrating keratoplasty
  • 50. Inpatient & outpatient medications  Prednisolone acetate 1% (qid)  Erythromycin ophthalmic ointment (4-8 times/ day)  Homatropine 5% or Scopolamine 0.25% (tid)  Ascorbate 500 mg P/O qid  Levobunolol 0.5% bd or acetazolamide 250 mg tid if IOP > 30 mmHg  Excessive lubricants
  • 51. Prevention  Education and training  Safety goggles at chemical workplace
  • 52. Prognosis  Directly related to severity of insult  Grading according to prognosis as in Roper Hall classification
  • 53. Differential diagnosis  Conjuctivitis, acute hemorrhagic/ allergic  Corneal abrasion  Corneal erosion, recurrent  Corneal foreign body  Keratoconjuctivits sicca  Corneal ulcer
  • 54.  Chemical injuries are actually the true ocular emergencies and don't waste time & defer the detailed history and examination till the appropriate irrigation has been achieved.