blunt ocular trauma

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a case presentation of patient with blunt ocular trauma

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Blunt Ocular

Trauma

Dr Abdul Munim KhanAssociate Professor and HOD

Eye Department

Mohtarma Benazir Bhutto Shaheed Medical College

Mirpur AJK

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 (McGwin G, Xie A, Owsley C. Rate of Eye Injury in the United States . Arch Ophthalmol. 2005;123:970-976.)

DEMOGRAPHIC PROFILE

NAME: ABC

AGE/SEX: 10yrs/male

ADDRESS: Rawalpindi

OCCUPATION: Student

D.O.A: 15-01-09

M.O.A: ER

PRESENTING COMPLAINTS

Trauma to the right eye with a tennis ball

---------- an hour back

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

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.

PAST Hx:

Insignificant

PERSONAL Hx:

Student of class 2.

SOCIOECONOMIC Hx:

Lower middle class.

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

EXAMINATIONCHEST:

B/L Clear

ABDOMEN:

soft, non-tender

CVS:

S1+S2+0

CNS:

intact, GCS- 15/15

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

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

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

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

X-RAYS

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

X-RAYS

Sub retinal hemorrhage and exudate deposits between RPE & photoreceptor layer.

Photoreceptor layer pushed towards inner retina by sub retinal hemorrhage.

VISUAL

FIELD

Shows a

central

field

defect

Diagnosis

Commotio Retinae or Berlin’s Odema

Hyphema

TREATMENT

Strict bed rest

Tobramycin + dexamethasone e/d ---- 1 drop

x TDS in to effected eye

Tab Paracetamol ----------------------1x TDS

FOLLOW -UP

AFTER ONE

MONTH:

Swelling of the lids

– resolved

Visual Acuity- 6/18

TRAUMATIC

MYDRIASIS

After One Month

Sub-retinal

hemorrhage &

retinal edema in

resolving stage.

Blunt Ocular Trauma

Incidence of Eye Injury

In the United States in 2001, an estimated 2 million individuals experienced an eye injury requiring treatment (McGwin G, Xie A, 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.

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

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

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.

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.

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

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

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

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.

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 %).

Effects of blunt trauma on various ocular tissues

CONJUNCTIVASUB-CONJUNCTIVAL HAEMORRHAGE

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

CORNEAL EDEMA

due to dysfunction of corneal endothelium.

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

ANTERIOR UVEA

IRIDODIALYSISdehiscence of the iris from the ciliary body at its root.

The pupil is typically “D” shaped

dark biconvex area near the limbus.

PUPIL

pigment imprinting on the anterior capsule (Vossiusring).

traumatic mydriasis.

Radial tears in pupillarymargin.

CILIARY BODY

may react to severe blunt trauma by temporary

cessation of aqueous secretion (ciliary shock)

resulting in ocular hypotony.

.

LENS

damage to the lens fibers & minute ruptures in lens capsule

cataract forms along posterior sutures resulting in a flower-shaped “rossette” opacity.

LENS

SUBLUXATION

tearing of suspensory ligament

iris may tremble on ocular movement

(iridodonesis).

DISLOCATION

due to 360° rupture of the zonule

VITREOUS

Posterior vitreous detachment which may be

associated with vitreous hemorrhage

RETINAL BREAKS & RETINAL DETACHMENT

RETINAL BREAKS & RETINAL DETACHMENT

COMMOTIO RETINAE

CHOROID

CHOROIDAL RUPTURE involves the choroid, Burch membrane and RPE

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).

GLOBE RUPTUREin the vicinity of schlemm canal, with prolapse of intraocular structures such as lens, iris, ciliary body

and vitreous.

Commotio Retinae

Commotio Retinae

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

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

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

PathologyThe 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

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.

Subsequent course

Over a course of weeks the retinal opacificationdiminishs with sequelae variable from no signs to a dramatic pigment epitheliopathy.

In mild injury cases the opacity will clear completely without clinically observable signs

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

Overview of effects of

blunt Ocular trauma

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

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.

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

THANK

YOU

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