a case presentation of patient with blunt ocular trauma

1. Blunt Ocular
Trauma
Dr Abdul Munim Khan
Associate Professor and HOD
Eye Department
Mohtarma Benazir Bhutto Shaheed Medical College
Mirpur AJK

2.  In persons under 25 years of age, ocular
trauma is the number one cause of visual loss.
 In the United States in 2001, an estimated
2 million ( approx 1% of population)
individuals experienced an eye injury
requiring treatment
(McGwinG, Xie A, Owsley C. Rate of Eye Injury in the United States .
Arch Ophthalmol. 2005;123:970-976.)

3. DEMOGRAPHIC PROFILE
NAME: ABC
AGE/SEX: 10yrs/male
ADDRESS: Rawalpindi
OCCUPATION: Student
D.O.A: 15-01-09
M.O.A: ER

4. PRESENTING COMPLAINTS
 Trauma to the right eye with a tennis ball
---------- an hour back

5. HISTORY OF PRESENT ILLNESS
The patient was alright an hour back when
while playing cricket, he was hit on his right
eye with a tennis ball & presented to the ER
with the c/o
pain,
swelling and
decreased vision right eye

6. Pain was moderate to severe in
intensity, sharp pricking in character and
associated with nausea but with no
episode of vomiting.
No h/o bleeding from the eye, diplopia,
ENT bleed, loss of consciousness, fits,
numbness in the face or eyelid.
No h/o trauma to any other parts of the
body.

7. PAST Hx:
Insignificant
PERSONAL Hx:
Student of class 2.
SOCIOECONOMIC Hx:
Lower middle class.

8. EXAMINATION
GPE:
A young boy lying in bed well oriented in time,
place and person.
Pulse- 90/min
BP- 130/90mm Hg
Temp- 98.6°F
R.R- 16/min

9. EXAMINATION
CHEST:
B/L Clear
ABDOMEN:
soft, non-tender
CVS:
S1+S2+0
CNS:
intact, GCS- 15/15

10. OCULAR EXAMINATION
RT. EYE LT. EYE
VISUAL ACUITY HM +ve 6/6
ADENEXA - -
EYE LIDS Moderate swelling
& ecchymosis
-
LASHES NAD -
LID MARGINS NAD -
HEAD POSTURE: normal
FACIAL EXPRESSION: normal

11. RT. EYE LT. EYE
CONJUNCTIVA Mild chemosis &
congestion
-
SCLERA - -
CORNEA Clear -
A.C Mild hyphaema,
1mm
-
IRIS NAD -
PUPIL Mid-dilated, oval,
sluggish in reaction
to light
R, R, R
LENS Transparent Transparent
VITREOUS Clear Clear

12. RT. EYE LT. EYE
FUNDI ill defined whitish
lesion with abnormal
reflexes
and sub retinal
hemorrhage at
macula
NAD
EOM Normal Normal
NLD Patent Patent
IOP 14 14

15. INVESTIGATIONS
 Blood CP
° Hgb – 14.5gm/dL
° WBC – 8800/uL
° PLT –219000/uL
 X-ray
° skull – AP view, lateral view
° orbit – water’s view, lateral view
 CT scan brain without contrast
 OCT

16. X-RAYS
Normal bony outlines, normal orbital wall structures. Maxillary
sinuses are normal, no soft tissue density appreciated.

17. X-RAYS

19. Sub retinal hemorrhage and exudate deposits between RPE
& photoreceptor layer.
Photoreceptor layer pushed towards inner retina by sub
retinal hemorrhage.

20. VISUAL
FIELD
Shows a
central
field
defect

21. Diagnosis
 Commotio Retinae or Berlin’s Odema
 Hyphema
TREATMENT
Strict bed rest
Tobramycin + dexamethasone e/d ---- 1 drop
xTDS in to effected eye
Tab Paracetamol ----------------------1xTDS

22. FOLLOW -UP
AFTER ONE
MONTH:
 Swelling of the lids
– resolved
 Visual Acuity- 6/18
TRAUMATIC
MYDRIASIS

23. After One Month
Sub-retinal
hemorrhage &
retinal edema in
resolving stage.

24. Blunt OcularTrauma

25. Incidence of Eye Injury
 In the United States in 2001, an estimated
2 million individuals experienced an eye
injury requiring treatment
(McGwinG, XieA, Owsley C. Rate of Eye Injury in the United States .
Arch Ophthalmol. 2005;123:970-976.)
 In persons under 25 years of age, ocular
trauma is the number one cause of visual loss.

26. The most common causes of blunt trauma are:
 Sports related injuries such as cricket,
basketball, water sports and racquet sports.
 Elastic luggage straps.
 Aggression.
 Automobile accidents

27. Mechanism of Injury
 The eye is a relatively incompressible fluid-filled
globe.
 kinetic energy transfer from the moving object
to the globe.
 The energy alters the shape of the globe

28. This alteration in shape has four components:
compression,
decompression,
overshoot,
and oscillations
With each oscillation more and more energy is lost
There is progressive reduction in oscillatory extent and
eventual termination.

29.  As the eye oscillates, each ocular layer
moves at a different rate due to different
elasticity .
 This results in generation of shear forces at
the interfaces of tissues with different
elasticities.
 These shear forces causes tissue damage.

31. The extent of ocular damage depends on:
 size of the blunt object
 hardness of the blunt object
 velocity of the blunt object
 force imparted directly to the eye

32. Direct blow to the globe from a blunt object “larger than the
orbital opening”
Energy absorbed by all of the orbital contents leading to
rise of intra-orbital pressure
Fractures of the thin bones of orbit
This "pressure-release valve" may prevent serious ocular
injury

33. Direct blow to the globe from a blunt object “smaller than
orbital opening”
Energy directly absorbed by the eye ball
Severe increase in IOP and consequently greater ocular
damage

34. Effects of blunt ocular
trauma
Although the impact of a blunt trauma is
primarily absorbed by lens-iris diaphragm &
vitreous base,
damage can also occur at a distant sites such
as the posterior pole.

35. Incidence of various ocular
injuries after trauma
85 % of the patients were male.
50% were 10 to 29 years old.
Visual impairment was rarely
induced by large objects like
soccer balls.
viestenz and kuchle 1985-95
Hyphema (73 %),
Angle recession (71 %),
Iris sphincter tears (20 %),
Iridodialysis (10 %),
Cyclodialysis (3,4 %),
Lens dislocation (15 %),
Traumatic cataract (10 %),
Choroidal rupture (7 %),
Retinal tear or detachment (7 %),
Berlin's edema (35,5 %),
Globe rupture (4,6 %),
Blow-out-fracture (8,3 %).

36.  Effects of blunt trauma on various
ocular tissues

37. CONJUNCTIVA
SUB-CONJUNCTIVAL HAEMORRHAGE

38. CORNEA
CORNEAL ABRASION
it is a breach of the epithelium.
If over the pupillary area, vision may be grossly impaired.
Corneal abrasion with
fluorescein stain

39. CORNEAL EDEMA
due to dysfunction of
corneal endothelium.

40. HYPHAEMA
Hemorrhage into the
anterior chamber.
Source of bleeding is
the iris or ciliary body.
RBCs sediment
inferiorly with a
resultant “fluid level ”
Total hyphaema

41. ANTERIOR UVEA
IRIDODIALYSIS
dehiscence of the iris from the ciliary body at its root.
The pupil is typically “D” shaped
dark biconvex area near the limbus.

43. PUPIL
 pigment imprinting on the
anterior capsule (Vossius
ring).
 traumatic mydriasis.
 Radial tears in pupillary
margin.

44. CILIARY BODY
may react to severe blunt trauma by temporary
cessation of aqueous secretion (ciliary shock)
resulting in ocular hypotony.
.

45. LENS
damage to the lens fibers & minute ruptures in lens
capsule
cataract forms along posterior sutures resulting in a
flower-shaped “rossette” opacity.

46. LENS
SUBLUXATION
tearing of suspensory ligament
iris may tremble on ocular movement
(iridodonesis).

47. DISLOCATION
due to 360° rupture of the zonule

48. VITREOUS
Posterior vitreous detachment which may be
associated with vitreous hemorrhage

49. RETINAL BREAKS & RETINAL DETACHMENT

50.  RETINAL BREAKS & RETINAL DETACHMENT

51. COMMOTIO RETINAE

52. CHOROID
 CHOROIDAL RUPTURE involves the choroid,
Burch membrane and RPE

53. OPTIC NERVE
 OPTIC NEUROPATHY
presents as sudden visual loss.
Damage to optic nerve can be:
direct (haemorrhage or compression)
Indirect shearing (acceleration of the nerve at
the optic canal where it is tethered to the dural
sheath).

54. GLOBE RUPTURE
in the vicinity of schlemm canal, with prolapse of
intraocular structures such as lens, iris, ciliary body
and vitreous.

55. Commotio Retinae

56. Commotio Retinae
It is characterized by a milky-white deep retinal
clouding with irregular margins.

57. Mechanism
 After blunt trauma the eyeball changes its shape
rapidly
 shear forces are created at the interfaces of tissues
with different elasticities.
 The retina is relatively elastic compared to the
sclera-RPE complex and significant shear forces act
across this interface causing retinal damage

58. Location
Commotio retinae presents in the retinal quadrant
opposite to the site of impact
(countercoup injury)
It may be located in any region of the retina but is
common in the posterior pole and macula
Commotio retinae involving the posterior pole has
been referred to as Berlin’s edema

60. Pathology
The classic Histopathological work of Sipperly, Quigley and
Gass (1978)
 Disruption of the photoreceptor outer segments.
 The photoreceptor cells undergo degeneration.
 RPE phagocytize degenerating photoreceptor
outer segments.
 The opacity of is due to disrupted photoreceptor
cells

61. FFA findings
 Fundus fluorescein angiography of retina
involved in commotio retinae shows blocked
choroidal fluorescence
 studies have indicated that the blood-retina
barrier remains relatively intact in this condition.

62. Subsequent course
 Over a course of weeks the retinal opacification
diminishs with sequelae variable from no signs
to a dramatic pigment epitheliopathy.
 In mild injury cases the opacity will clear
completely without clinically observable signs

63.  when the photoreceptors and RPE have been
extensively damaged, the functional deficits are
more likely to be severe and permanent

64. Overview of effects of
blunt Ocular trauma

66.  ocular injury in blunt trauma is due to direct
kinetic energy transfer to the globe and/or
orbit.
 Assessment and evaluation is difficult and
treatment is complex.
 Even with good management, functional
outcome is often compromised and vision is
impaired.
 Patients suffer from complications for many
years following the acute event

67. Prevention is better than cure
In sports pre-participation evaluation
high myopes, any intra-ocular surgery
and strong family history of retinal
detachment.
proper eye and facial protection
techniques
use of protective devices.

68. Take home message
 Never take blunt trauma to eye lightly
 Patient should always be referred to
an ophthalmologist
 Always wear protective goggles in
contact sports and when performing
chisel and hammer type of work

69. THANK
YOU