Ocular injuries types, clinical features and management

1. COMPETENCY BASED UNDERGRADUATE
CURRICULUM (COMPETENCY NO – PA 36.1 )
OCULAR INJURIES II
Dr. Sandeep Shivran
J.S., Department of Ophthalmology,
SK Govt. Medical College and Hospital,
Sikar
1

2. OPEN-GLOBE INJURIES
Full thickness wound of the eyewall (sclera or/and
cornea)
1. Globe rupture -
Full thickness wound of the eye- wall caused by blunt
trauma
2. Globe laceration
Full-thickness wound of eyewall caused by sharp
objects
i. Penetrating injury
ii. Perforating injury
iii. Intraocular foreign bodies 2

3. PENETRATING AND PERFORATING INJURIES
 Penetrating injury - Single full-thickness wound of
the eyewall caused by a sharp object
 Perforating injury - Two full-thickness wounds (one
entry and one exit) of the eyewall caused by a
sharp object or missile
Cause severe damage to the eye and so should be
treated as serious emergencies
3

4. Modes of injury
1. Trauma by sharp and pointed instruments -
Needles, knives, nails, arrows, screw-drivers, pens,
pencils, compasses, glass pieces
2. Trauma by foreign bodies travelling at very high
speed such as bullet injuries and iron foreign bodies
in lathe workers
4

5. Mechanisms of damage
1. Mechanical effects of the trauma or physical changes
2. Introduction of infection
 Pyogenic organisms enter the eye during open globe
injuries
 Multiply there - cause varying degree of infection
depending upon the virulence & host defence
mechanism
 Ring abscess of the cornea
 Sloughing of the cornea
 Purulent iridocyclitis
 Endophthalmitis or panophthalmitis
 Rare - tetanus and infection by gas-forming organisms
(Clostridium welchii) 5

6. 3. Post-traumatic iridocyclitis
 Frequent occurrence
 If not treated properly → can cause devastating
damage
 Rare but most dangerous complication of a
perforating injury
6

7. Traumatic lesions & management
1. Wounds of the conjunctiva
 Common - associated with subconjunctival
haemorrhage
 Wound of more than 3 mm should be sutured
2. Wounds of the cornea
i. Uncomplicated corneal wounds
 Not associated with prolapse of intraocular contents
 Margins of wounds swell up - lead to automatic
sealing and restoration of the anterior chamber
Treatment
 Small central wound does not need stitching
 Pad and bandage with atropine and antibiotic
ointments
7

8.  A large corneal wound (more than 2 mm) should
always be sutured
ii. Complicated corneal wounds
 Associated with prolapse of iris, sometimes lens
matter and even vitreous
Treatment
 Sutured meticulously after abscising the iris
 Prolapsed iris should never be reposited - may
cause infection
 Lens injury and vitreous loss - lensectomy and
anterior vitrectomy may be performed along with
repair of the corneal wound
8

9. 3. Wounds of the sclera
Associated with corneal wounds
corneo-scleral tear - first suture should be applied at the
limbus
4. Wounds of the lens
Extensive lens ruptures with vitreous loss should be
managed as above
Small wounds in the anterior capsule may seal and lead
on to traumatic cataract
5. Severely wounded eye
 Extensive corneo-scleral tears associated with prolapse
of the uveal tissue, lens rupture, vitreous loss and injury
to the retina and choroid
 No chance of getting useful vision in such cases
 Preferably such eyes should be excised
9

10. Penetrating scleral wounds
10

11. Penetrating corneal wounds
(A) With iris prolapse
(B) with lens damage, showing linear cut in the lens
(arrow) and prolapsed contents
11

12. INTRAOCULAR FOREIGN BODIES
Common foreign bodies :
 Chips of iron and steel
 Particles of glass, stone, lead pellets, copper
percussion caps, aluminium, plastic and wood
 During chopping a stone with an iron chisel, it is
commonly a chip of the chisel and not of the stone
which enters the eye
12

13.  Intraocular foreign
bodies
13

14. Modes of damage and Lesions
Penetrating/perforating injury with retained foreign
body may damage the ocular structures by the
following modes:
A. Mechanical effects
B. Introduction of infection
C. Reaction of foreign bodies
D. Post-traumatic iridocyclitis
E. Sympathetic ophthalmitis
14

15. A. Mechanical effects
 Depend upon the size, velocity and type of the
foreign body
 Foreign bodies greater than 2 mm in size caus
extensive damage
 Lesions caused also depend upon the route of
entry and the site up to which a foreign body has
travelled
Traumatic lesions produced by intraocular foreign
bodies
 Corneal or/and scleral perforation, hyphaema, iris
hole,
 Rupture of the lens and traumatic cataract,
 Vitreous haemorrhage and/or degeneration,
15

16.  Choroidal perforation, haemorrhage and
inflammation
 Retinal hole, haemorrhages, oedema and
detachment
Locations of IOFB
May be retained at any of the following sites:
1. Anterior chamber
 Sinks at the bottom
 Tiny foreign body may be concealed in the angle of
anterior chamber, and visualised only on gonioscopy
2. Iris - Entangled in the stroma
16

17. 3. Posterior chamber
May sink behind the iris after entering through pupil or
after making a hole in the iris
4. Lens
Present on the anterior surface or inside the lens
Either an opaque track may be seen in the lens or the
lens may become completely cataractous
5. Vitreous cavity
May reach here through various routes
17

18. 6. Retina, choroid and sclera
Obtain access to these structures through corneal
route or directly from scleral perforation
7. Orbital cavity
Piercing the eyeball may occasionally cause double
perforation and come to rest in the orbital tissues
18

19. Common sites for retention of an intraocular foreign
body:
1. anterior chamber
2. iris
3. lens
4. vitreous;
5. retina
6. choroid
7. sclera
8. orbital cavity
19

20. Depiction of routes of access of a foreign body in the
vitreous, through:
A. cornea, pupil, lens
B. cornea, iris, lens
C. cornea, iris, zonules
D. sclera, choroid, retina
20

21.  Fundus photograph depicting intravitreal foreign
body
21

22. B. Introduction of infection
 Small flying metallic foreign bodies are usually
sterile due to the heat generated on their
commission
 Pieces of the wood and stones carry a great
chance of infection
 Once intraocular infection is established it usually
ends in endophthalmitis or even panophthalmitis
22

23. C. Reactions of the foreign body
i. Reactions of Inorganic foreign body
Depending upon its chemical nature - types of
reactions are
1. No reaction is produced by the inert substances -
glass, plastic, porcelain, gold, silver and platinum
2. Local irritative reaction - leading to encapsulation
of the foreign body occurs with lead and aluminium
particles
3. Suppurative reaction is excited by pure copper,
zinc, nickel and mercury particles
4. Specific reactions are produced by iron (Siderosis
bulbi) and copper alloys (Chalcosis)
23

24. Siderosis bulbi
 Ocular degenerative changes produced by an iron
foreign body
 Usually occurs after 2 months to 2 years of the
injury
 Earliest changes have been reported after 9 days of
trauma
Mechanism:
 Iron particle undergoes electrolytic dissociation by
the current of rest and its ions are disseminated
throughout the eye
 These ions combine with the intracellular proteins
and produce degenerative changes
 Epithelial structures of the eye are most affected 24

25. Clinical manifestations include:
1. Anterior epithelium and capsule of the lens:
Rusty deposits are arranged radially in a ring - lens
becomes cataractous
2. Iris : Stained greenish and later on turns reddish
brown (heterochromia iridis)
3. Retina: develops pigmentary degeneration which
resembles retinitis pigmentosa
Electroretinography (ERG) – progressive attenuation
of the b-wave over time
4. Secondary open angle glaucoma may occur due
to degenerative changes in the trabecular meshwork
25

26. 26

27. Chalcosis
 Specific changes produced by the alloy of copper in
the eye
Mechanism of chalcosis:
 Copper ions from the alloy are dissociated
electrolytically & deposited under the membranous
structures of the eye
 Unlike iron ions these do not enter into a chemical
combination with the proteins of the cells - produce
no degenerative changes
27

28.  Clinical features:
1. Kayser-Fleischer ring - golden brown ring which
occurs due to deposition of copper under peripheral
parts of the Descemet’s membrane of the cornea
2. Sunflower cataract - produced by deposition of
copper under the posterior capsule of the lens
Brilliant golden green in colour and arranged like the
petals of a sunflower
3. Retina - Show deposition of golden plaques at the
posterior pole which reflect the light with a metallic
sheen
28

29. ii. Reaction of organic foreign bodies
 Organic foreign bodies - wood and other vegetative
materials produce a proliferative reaction
characterised by the formation of giant cell
 Caterpillar hair produces ophthalmia nodosum -
characterised by a severe granulomatous
iridocyclitis with nodule formation
29

30. Management of Retained intraocular foreign
Bodies (IOFB)
Diagnosis
 Important - particularly as the patient is often
unaware that a particle has entered the eye
1. History - careful history about the mode of injury
may give a clue about the type of IOFB
2. Ocular examination - thorough ocular
examination with slit-lamp including gonioscopy
should be carried out
Signs which may give some indication about IOFB
are:
 Subconjunctival haemorrhage, corneal scar, holes
in the iris, and opaque track through the lens 30

31.  With clear media - sometimes IOFB may be seen
on ophthalmoscopy in the vitreous or on the retina
 IOFB lodged in the angle of anterior chamber may
be visualised by gonioscopy
3. Plain X-rays orbit
Anteroposterior and lateral views - recommended for
the location of IOFB ( most foreign bodies are radio
opaque)
 CT images are required for suspected IOFB, even if
PFR is negative
31

32. 4. Localization of IOFB
 Once IOFB is suspected clinically and later
confirmed, on fundus examination and/or X-rays -
its exact localization is mandatory to plan the
proper removal
Radiographic localization
 Limbal ring method- Simple method
 Metallic ring of the corneal diameter is stitched at
the limbus and X-rays are taken
 One exposure is taken in the anteroposterior view.
In the lateral view three exposures are made one
each while the patient is looking straight, upwards
and downwards, respectively
32

33. The position of the foreign body is estimated from its
relationship with the metallic ring in different positions
33

34. Ultrasonographic localization –
 Tells the position of even non-radioopaque foreign
bodies
CT scan
 With axial and coronal cuts, CT scan is presently
the best method of IOFB localization
 Provides cross-sectional images with a sensitivity
and specificity that are superior to plain radiography
and ultrasonography
34

35. Magnetic resonance imaging (MRI)
 Not recommended as a general screening tool
 Can cause further damage by producing movement
of a magnetic IO foreign body
 After the CT has excluded the presence of a
metallic IO foreign body - MRI has a special role in
localizing small plastic or wooden IO foreign bodies
35

36. Treatment
 IOFB should always be removed
 Except when it is inert and probably sterile or when
little damage has been done to the vision and the
process of removal may be risky and destroy sight
 E.g., minute FB in the retina
 Removal of magnetic IOFB is easier than the
removal of non-magnetic FB
 Usually a hand-held electromagnet is used for the
removal of magnetic foreign body
36

37. Hand-held magnet
37

38. 1. Foreign body in the anterior chamber
 Removed through a corresponding corneal incision
directed straight towards the foreign body
 Should be 3 mm internal to the limbus and in the
quadrant of the cornea lying over the foreign body
 Magnetic foreign body is removed with a hand- held
magnet
 It may come out with a gush of aqueous
 Non-magnetic foreign body is picked up with
toothless forceps
38

39. Removal of a magnetic intraocular foreign body from
the anterior chamber
 A. Wrong incision
 B. Correct incision
39

40. 40
2. Foreign body entangled in the iris tissue (magnetic
as well as non-magnetic)
 Removed by performing sector iridectomy of the
part containing foreign body
3. Foreign body in the lens
 Magnet extraction is usually difficult for
intralenticular foreign bodies
 Magnetic foreign body should also be treated as
nonmagnetic foreign body
 An extracapsular cataract extraction (ECCE) with
intraocular lens implantation should be done
 Foreign body may be evacuated itself along with
the lens matter or may be removed with the help of
forcep

41. 4. Foreign body in the vitreous and the retina is removed
by the posterior route:
i. Magnetic removal
 Technique is used to remove a magnetic foreign body
that can be well localized and removed safely with a
powerful magnet without causing much damage to the
intraocular structures
 An intravitreal foreign body is preferably removed
through a pars plana sclerotomy (5 mm from the
limbus)
41

42.  At the site chosen or incision, conjunctiva is
reflected and the incision is given in the sclera
concentric to the limbus
 A preplaced suture is passed and lips of the wound
are retracted
 A nick is given in the underlying pars plana part of
the ciliary body
 And the foreign body is removed with the help of a
powerful hand-held electromagnet
 Preplaced suture is tied to close the scleral wound
 Conjunctiva is stitched with one or two interrupted
sutures
42

43. For an intraretinal foreign body
 Site of incision should be as close to the foreign
body as possible
 A trapdoor scleral flap is created, the choroidal bed
is treated with diathermy, choroid is incised and
foreign body is removed with either forceps or
external magnet
43

44. ii. Forceps removal with pars plana vitrectomy
 Technique is used to remove all non-magnetic
foreign bodies and those magnetic foreign bodies
that cannot be safely removed with a magnet
 Foreign body is removed with vitreous forceps after
performing three-pore, par plana vitrectomy under
direct visualization using an operating microscope
44

45. SYMPATHETIC OPHTHALMITIS
 Serious bilateral granulomatous panuveitis which
follows a penetrating ocular trauma
 Injured eye is called exciting eye and the fellow eye
which also develops uveitis is called sympathizing
eye
 Rarely, sympathetic ophthalmitis can also occur
following an intraocular surgery
45

46. Incidence
 Markedly decreased in the recent years due to
meticulous repair of the injured eye utilizing
microsurgical techniques and use of the potent
steroids
Etiology
 Etiology of sympathetic ophthalmitis is still not
known exactly
Predisposing factors
1. It almost always follows a penetrating injury
2. Wounds in the ciliary region (dangerous zone) are
more prone to it
46

47. 3. Wounds with incarceration of the iris, ciliary body
or lens capsule are more vulnerable
4. It is more common in children than in adults
5. It does not occur when actual suppuration
develops in the injured eye
Pathogenesis
 Various theories have been put forward
 Most accepted one is allergic theory
 Postulates that the uveal pigment acts as a allergen
and excites plastic uveitis in the sound eye
47

48. Pathology
Characteristic of granulomatous uveitis present
 Nodular aggregation of lymphocytes, plasma cells,
epitheloid cells and giant cells scattered throughout
the uveal tract
 Dalen-Fuchs’ nodules are formed due to
proliferation of the pigment epithelium (of the iris,
ciliary body and choroid) associated with invasion
by the lymphocytes and epitheloid cells
 Sympathetic perivasculitis - Retina shows
perivascular cellular infiltration
48

49. Clinical features
i. Exciting (injured) eye
 Shows clinical features of persistent low grade
plastic uveitis
 Ciliary congestion, lacrimation and tenderness
 Keratic precipitates may be present at the back of
cornea (dangerous sign)
ll. Sympathizing (sound) eye
 Usually involved after 4-8 weeks of injury in the
other eye
 Earliest reported case is after 9 days of injury
 Most of the cases occur within the first year
49

50.  Delayed and very late cases are also reported
 Sympathetic ophthalmitis, almost always, manifests
as acute plastic iridocyclitis
 Rarely it may manifest as neuroretinitis or
choroiditis
 Clinical feature of the iridocyclitis in sympathizing
eye can be divided into two stage
1. Prodromal stage:
Symptoms
Sensitivity to light (photophobia) and transient
indistinctness of near objects (due to weakening of
accommodation) are the earliest 50

51. Signs
 First sign may be presence of retrolental flare and
cells or the presence of a few keratic precipitates
(KPs) on back of cornea
 Other signs - mild ciliary congestion, slight
tenderness of the globe, fine vitreous haze and disc
oedema which is seen occasionally
2. Fully-developed stage
 Clinically characterised by typical signs and
symptoms consistent with acute plastic iridocyclitis
51

52. Treatment
a. Prophylaxis
i. Early excision of the injured eye
Best prophylaxis when there is no chance of saving
useful vision
ii. When there is hope of saving useful vision –
1. A meticulous repair of the wound using
microsurgical technique should be carried out, taking
great care that uveal tissue is not incarcerated in the
wound
2. Immediate expectant treatment with topical as well
as systemic steroids and antibiotics along with topical
atropine should be started
52

53. 3. When the uveitis is not controlled after 2 weeks of
expectant treatment
Lacrimation, photophobia and ciliary congestion
persist and if KPs appear - injured eye should be
excised immediately
B. Treatment when sympathetic ophthalmitis has
already supervened
I. Early excision (enucleation)
Should be done when the case is seen shortly after
the onset of inflammation (i.e., during prodromal
stage) in the sympathizing eye
Injured eye has no useful vision, this useless eye
should be excised 53

54. II. Conservative treatment of sympathetic ophthalmitis
- on the lines of iridocyclitis should be started
immediately
1. Corticosteroids should be administered by all
routes, i.e., systemic, periocular injections and
frequent instillation of topical drops
2. Immunosuppressant drugs should be started in
severe cases, without delay
3. Atropine should be instilled three times a day in all
cases
Treatment should be continued for a long time
54

55. Prognosis:
 If sympathetic ophthalmitis is diagnosed early
(during prodromal stage) and immediate treatment
with steroids is started, a useful vision may be
obtained
 Advanced cases - prognosis is very poor, even
after the best treatment
55

56. CHEMICAL INJURIES
Vary in severity from a trivial and transient irritation of
little significance to complete and sudden loss of
vision
Modes of chemical injury
Usually occur due to external contact with chemicals
under following circumstances:
1. Domestic accidents, e.g., with ammonia, solvents,
detergents and cosmetics.
2. Agricultural accidents, e.g., due to fertilizers,
insecticides, toxins of vegetable and animal origin
56

57. 3. Chemical laboratory accidents, with acids and
alkalies
4. Deliberate chemical attacks, especially with acids
to disfigure the face
5. Chemical warfare injuries
6. Self-inflicted chemical injuries are seen in
malingerers and psychopath
57

58. Types of chemical injuries
 Serious chemical burns mainly comprise alkali and
acid burns
a. Alkali burns
 Most severe chemical injuries
 Common alkalies responsible for burns are:
 Lime, caustic potash or caustic soda and liquid
ammonia (most harmful)
58

59. Mechanisms of damage produced by alkalies
includes:
1. Alkalies dissociate and saponify fatty acids of the
cell membrane
Destroy the structure of cell membrane of the tissues
2. Hygroscopic - extract water from the cells, a factor
which contributes to the total necrosis
3. Combine with lipids of cells to form soluble
compounds - produce a condition of softening and
gelatinisation
59

60.  Result in an increased deep penetration of the
alkalies into the tissues
 Alkali burns - spread widely, their action continues
for some days and their effects are difficult to
circumscribe
 Prognosis in such cases must always be guarded
60

61. Clinical feature can be divided into three stages:
1. Stage of acute ischaemic necrosis
Conjunctiva shows marked oedema, congestion,
widespread necrosis and a copious purulent
discharge
Cornea develops widespread sloughing of the
epithelium, oedema and opalescence of the stroma
Iris becomes violently inflamed
Severe cases - both iris and ciliary body are replaced
by granulation tissue
61

62. 2. Stage of reparation
Conjunctival and corneal epithelium regenerate –
corneal vascularization and inflammation of the iris
subsides
3. Stage of complications
Development of symblepharon
Recurrent corneal ulceration
Development of complicated cataract and secondary
glaucoma
62

63. Acid burns
 Acid burns are less serious than alkali burns
 Common acids responsible for burns are:
 Sulphuric acid, hydrochloric acid and nitric acid
Chemical effects:
 Strong acids cause instant coagulation of all the
proteins which then act as a barrier and prevent
deeper penetration of the acids into the
 Tissues lesions become sharply demarcated
63

64. Ocular lesions include:
1. Conjunctiva
 Immediate necrosis followed by sloughing
 Symblepharon is formed due to fibrosis
2. Cornea
 Also necrosed and sloughed out
 Extent of damage depends upon the concentration
of acid and the duration of contact
 In mild to moderate degree of corneal burns→ end
result is corneal opacification of varying degree
 In severe cases → whole cornea may slough out
followed by staphyloma formation
64

65. Grading of chemical burns
Depending upon the severity of damage caused to
the limbus and cornea → extent of chemical burns
may be graded in Roper-Hall classification
65

66. 66

67. Treatment of chemical burns
1. Prevent further damage by following measures:
 Immediate and thorough irrigation with the
available clean water or saline delivered through an
IV tubing
 Deliver minimum of 2 L of water in 20 - 30 minutes
or until pH is restored
 Mechanical removal of contaminant Ex:lime
Removed carefully with a swab stick
 Removal of contaminated and necrotic tissue.
 Necrosed conjunctiva should be excised
 Contaminated and necrosed corneal epithelium
should be removed with a cotton swab stick
67

68. 2. Maintenance of favourable conditions for rapid and
uncomplicated healing
 Topical antibiotic drops, e.g., moxifloxacin 4 – 6 times a
day, to prevent infection
 Steroid eye drops - reduce inflammation, neutrophil
infiltration, and address anterior uveitis
 Cautious use is recommended after 2 weeks, as
steroids may interfere with collagen synthesis
 Cycloplegics, e.g., atropine, may improve the comfort
 Ascorbic acid, in the form of 10% sodium ascorbate
eyedrops (4 - 5 times) along with systemic use (1-2 gm
orally/day) → improves wound healing and promotes
synthesis of the mature collagen by corneal fibroblasts
68

69.  Lubricant eyedrops (preservative free) - used in
abundance to promote the healing
 Autologous serum, instilled as eyedrops, provides
growth factors, collagenase inhibitors, retinoic acid,
fibrinogen activator and promotes epithelial healing
 Sodium citrate - 10% topical eyedrops stabilizes
neutrophils and reduces collagenase release
 Doxycycline, 100 mg BD - chelates zinc which is
necessary for collagenase
3. Prevention of symblepharon –
Using a glass shell or sweeping a glass rod in the
fornices twice daily
69

70. 70

71. 4. Treatment of complications
Secondary glaucoma - topical 0.5% timolol, instilled twice
a day along with oral acetazolamide 250 mg, 3 times a
day.
Poor corneal healing with limbal stem cell deficiency -
amniotic membrane transplantation with or without limbal
stem cell transplantation
Pseudopterygium - Excised together with conjunctival
autograft or amniotic membrane facilitated by antimitotic
drugs (e.g., mitomycin C)
Symblepharon - Surgical treatment
Corneal opacity - keratoplasty
Keratoprosthesis - severely damaged eyes where
keratoplasty is not possible
71

72. Keratoprosthesis - severely damaged eyes where
keratoplasty is not possible
72

73. NON-MECHANICAL INJURIES
Thermal injuries
 Caused by fire, or hot fluids
 Main brunt of such injuries lies on the lids
 Conjunctiva and cornea may be affected in severe
cases
Treatment for burns of lids is on general lines:
 Cornea is affected - Should be treated with
atropine, steroids, antibiotics and lubricants
73

74. Electrical injuries
 The passage of strong electric current from the
area of eyes may cause
1. Conjunctiva becomes congested
2. Cornea develops punctate or diffuse interstitial
opacities
3. Iris and ciliary body are inflamed
4. Lens may develop electric cataract’ after 2-4
months of accident
5. Retina may show multiple haemorrhages
6. Optic nerve may develop neuritis
74

75. Radiational injuries
1. Ultraviolet radiations
(i) photoophthalmia
(ii) May be responsible for senile cataract
2. Infrared radiations - cause solar macular burns
3. Ionizing radiational injuries
Following radiotherapy to the tumours in the vicinity of
the eyes.
Ocular lesions include:
 Radiation keratoconjunctivitis
 Radiation dermatitis of lids
 Radiation cataract
 Radiation retinopathy 75

76. 76