3. Orbital floor fracture
caused by a sudden increase in the orbital pressure from an
impacting object that is greater in diameter than the orbital
aperture (about 5 cm), such as a fist or tennis ball , so that the
eyeball itself is displaced and transmits rather than absorbs the
impact
4. Diagnosis
1.Visual function
• should be recorded and monitored as necessary,
particularly in the acute situation.
2.Periocular signs
• ecchymosis, oedema and occasionally
subcutaneous emphysema .
3.Infraorbital nerve anaesthesia
• involving the lower lid, cheek, side of nose, upper lip,
upper teeth and gums is very common as the fracture
frequently involves the infraorbital canal.
5. 4. Diplopia :
○ Haemorrhage and oedema in the orbit .
○ Mechanical entrapment within the fracture
Diplopia typically occurs in both upgaze and
downgaze.
Forced duction and the differential (IOP) test
are positive.
Improve if it is mainly due to entrapment of
oedematous connective tissue and fat.
persists if there is significant involvement of the
muscles themselves.
. ○ Direct injury to an extraocular muscle,
negative forced duction test.
The muscle fibres usually regenerate and normal
function often returns within about 2 months.
6. 5. Enophthalmos :-
if the fracture is severe,
although it tends to manifest only after a few days as initial oedema
resolves.
In the absence of surgical intervention, enophthalmos may continue to
increase for about 6 months as post-traumatic orbital tissue
degeneration and fibrosis develop.
• 6. Ocular damage
(e.g. hyphaema, angle recession, retinal dialysis) should be
excluded by careful examination of the globe, although this
is relatively uncommon in association with a blowout
fracture.
7.
8. Treatment
• Initial treatment
• observation, with the
prescription of oral antibiotics;
ice packs and nasal
decongestants .
• The patient should be instructed
not to blow his or her nose,
because of the possibility of
forcing infected sinus contents
into the orbit.
• Systemic steroids are
occasionally required for severe
orbital oedema, particularly if
this is compromising the optic
nerve.
• Subsequent treatment
○ Small cracks unassociated with herniation
do not require treatment .
○ Fractures involving up to one-half of the
orbital floor, with little or no herniation,
no significant enophthalmos and
improving diplopia, also do not require
treatment.
○ Fractures involving more than one-half of
the orbital floor will usually develop
significant enophthalmos if left
untreated.
o Fractures with entrapment of orbital
contents, enophthalmos of greater than 2
mm, and/or persistent and significant
diplopia in the primary position should
be repaired within 2 weeks. If surgery is
delayed, the results are less satisfactory
due to secondary fibrotic changes.
o Early marked enophthalmos may also be
an indication for urgent repair.
9. ‘White-eyed’ fracturea subgroup for which urgent repair
is required to avoid permanent
neuromuscular damage.
The scenario is generally seen in
patients less than 18 years of
age, typically with little visible
external soft tissue injury, and
usually affects the orbital floor.
It involves the acute incarceration
of herniated tissue in a trap-
door effect occurring due to the
greater elasticity of bone in
younger people.
Patients may experience acute
nausea, vomiting, and
headache; persistent activation
of the oculocardiac reflex can
occur.
CT features may be subtle.
Eight year old male patient with
"White eyed blowout fracture
" left. Preoperative view (A).
CT show trap door type orbital floor
fracture
Preoperative extraocular muscle
1 month postoperative view
limitation was improved (B) .
10. Surgical repair
a transconjunctival or
subciliary incision or
the maxillary sinus,
with elevation of the periosteum from the orbital floor, freeing of trapped
orbital contents and repair of the bony defect with a synthetic implant.
11.
12. Treatment
Small fractures may not require
treatment but it is important to
exclude a CSF leak, which carries a risk
of meningitis.
Sizeable bony defects with downward
displacement of fragments usually
warrant reconstructive surgery.
Roof fracture
Roof fractures are rare. Isolated fractures, caused by falling on a sharp
object or sometimes a relatively minor blow to the brow or forehead,
are most common in children and often do not require treatment.
Diagnosis
A haematoma of the upper eyelid with periocular ecchymosis.
Large fractures may be associated with pulsation of the globe due to
transmission of (CSF) pressure, best detected with applanation
tonometry.
13. Lateral wall fracture
Acute lateral wall fractures are rarely encountered by
ophthalmologists. Because the lateral wall of the orbit is more
solid than the other walls, a fracture is usually associated with
extensive facial damage.
14.
15. Blunt trauma
• Severe blunt trauma to the
globe results in
anteroposterior
compression with
simultaneous expansion in
the equatorial plane
associated with a transient
but severe increase in IOP.
• Although the impact is
primarily absorbed by the
lens–iris diaphragm and the
vitreous base, damage can
also occur at a distant site
such as the posterior pole.
16.
17. Cornea
• Corneal abrasion involves a breach of the epithelium, and stains well with
fluorescein . If located over the pupillary area, vision may be grossly impaired.
• Acute corneal oedema :- secondary to focal or diffuse dysfunction of the
endothelium and is sometimes seen underlying a large abrasion. It is commonly
associated with folds in Descemet membrane and stromal thickening, but usually
clears spontaneously.
• Tears in Descemet membrane are usually vertical and most commonly
arise as the result of birth trauma.
18. Hyphaema
Hyphaema is a common complication of
blunt ocular injury.
The source of bleeding is typically the
iris root or ciliary body face.
Characteristically, the blood settles
inferiorly with a resultant ‘fluid level’
except when the hyphaema is total .
Treatment is aimed at the prevention of
secondary haemorrhage and control of
any elevation of IOP , which as well as
optic neuropathy can lead to staining of
ocular tissues, particularly the cornea
19. Anterior Uvea
• Pupil :-
The iris may momentarily be compressed against the anterior surface of the
lens by severe anteroposterior force, with resultant imprinting of pigment from
the pupillary margin.
Transient miosis accompanies the compression, evidenced by the pattern of
pigment corresponding to the size of the miosed pupil (Vossius ring ).
Damage to the iris sphincter may result in traumatic mydriasis, which can be
temporary or permanent; the pupil reacts sluggishly or not at all to both light
and accommodation.
Radial tears in the pupillary margin are common
20. •Iridodialysis
• is a dehiscence of the iris from the ciliary body at its root.
•The pupil is typically D-shaped and the dialysis is seen as a dark biconvex area
near the limbus .
• An iridodialysis may be asymptomatic if covered by the upper lid; if exposed in
the palpebral aperture, uniocular diplopia and glare sometimes ensue, and may
necessitate surgical repair of the dehiscence.
•Traumatic aniridia (360° iridodialysis) is rare; in a pseudophakic eye, the
detached iris may be ejected through the cataract surgical incision
21. Lens
• Cataract formation:- is a common sequel to blunt trauma.
•A ring-shaped anterior subcapsular opacity may underlie a Vossius ring.
• Commonly opacification occurs in the posterior subcapsular cortex along the posterior
sutures, resulting in a flower-shaped (‘rosette’) opacity that may subsequently disappear,
remain stationary or progress to maturity .
• Subluxation of the lens
A subluxated lens tends to deviate towards the meridian of intact zonule;
the anterior chamber may deepen over the area of zonular dehiscence, if the lens rotates
posteriorly. trembling of the iris (iridodonesis) or lens (phakodonesis) may be seen on ocular
movement.
• Dislocation :- due to 360° rupture of the zonular fibres is rare .
an underlying predisposing condition such as pseudoexfoliation should be suspected.
22. • Globe rupture
• Rupture of the globe may result from severe blunt trauma;
the prognosis is poor if the initial visual level is light
perception or worse.
• Anterior :- The rupture is usually anterior, in the vicinity of the
Schlemm canal, with prolapse of structures such as the lens,
iris, ciliary body and vitreous ,
• may be masked by extensive subconjunctival haemorrhage .
• Rupture at the site of a surgical wound (e.g. cataract,
keratoplasty, vitrectomy) is common with substantial blunt
force.
23. • Posterior :-
• An occult posterior rupture can be associated
with little visible damage to the anterior
segment, but should be suspected if there is
asymmetry of anterior chamber depth – the
anterior chamber of an affected eye is
classically deep, with posterior rotation of the
iris– lens diaphragm – and IOP in the affected
eye is low.
• Gentle B-scan ultrasonography may
demonstrate a posterior rupture, but CT or
MR may be necessary; MR is not performed if
there is a risk of ferrous IOFB.
24.
25. Vitreous haemorrhage
• may occur, commonly in association with posterior vitreous
detachment.
• Pigment cells (‘tobacco dust’) may be seen floating in the
anterior vitreous, and though not necessarily associated with a
retinal break, should always prompt careful retinal assessment.
26. Commotio retinae
• caused by concussion of the sensory retina resulting in
cloudy swelling that gives the involved area a grey
appearance .
• It most frequently affects the temporal fundus. If the
macula is involved, a ‘cherry-red spot’ may be seen at
the fovea.
• Severe involvement may be associated with intraretinal
haemorrhage that can involve the macula.
• The prognosis in mild cases is good, with spontaneous
resolution in around 6 weeks.
• Sequelae to more severe commotio may include
progressive pigmentary degeneration and macular hole
formation .
27. (A) Wide-field imaging showing
typical appearance;
(B) associated with retinal
haemorrhages
(C) macular hole following resolution
of commotio at the posterior pole
28. Choroidal rupture
involves the choroid, Bruch membrane and
retinal pigment epithelium; it may be direct
or indirect.
Direct ruptures are located anteriorly at the
site of impact and run parallel with the ora
serrata.
Indirect ruptures occur opposite the site of
impact.
A fresh rupture may be partially obscured
by subretinal haemorrhage , which may
break through the internal limiting
membrane with resultant subhyaloid or
vitreous haemorrhage.
Weeks to months later, on absorption of
the blood, a white crescentic vertical streak
of exposed underlying sclera concentric
with the optic disc becomes visible .
The visual prognosis is poor if the fovea is
involved. An uncommon late complication is
choroidal neovascularization.
(A) Acute foveal disruption with
subretinal and sub-RPE haemorrhage
(B) old lesions
29. Retinal breaks and detachment
• • A retinal dialysis
• is a break occurring at the ora serrata, caused by
traction from the relatively inelastic vitreous gel
along the posterior aspect of the vitreous base.
• The tear may be associated with avulsion of the
vitreous base, giving rise to an overhanging
‘bucket-handle’ appearance comprising a strip of
ciliary epithelium, ora serrata and the immediate
post-oral retina into which basal vitreous gel
remains inserted .
• Traumatic dialyses occur most frequently in the
superonasal and inferotemporal quadrants.
Although they occur at the time of injury they do
not inevitably result in RD.
• In cases that detach, subretinal fluid commonly
does not develop until several months later, and
progression is typically slow.
Trauma is responsible for about 10% of all cases of retinal detachment (RD) and is
the most common cause in children, particularly boys.
Dialysis with retinal detachment
avulsed vitreous base
30. • • Equatorial breaks
• are less frequent; they are due
to direct retinal disruption at
the point of scleral impact.
• • Macular holes :-
• may occur either at the time of
injury or following resolution
of commotio retinae.
equatorial retinal breaks
traumatic macular hole
31. Traumatic optic neuropathy
• follows ocular, orbital or head trauma as sudden
visual loss that cannot be explained by other
ocular pathology. It occurs in up to 5% of facial
fractures.
• • Classification:-
• (a) Direct, due to blunt or sharp optic nerve
damage from agents such as displaced bony
fragments, a projectile, or local haematoma;
• (b) indirect, in which force is transmitted
secondarily to the nerve without apparent direct
disruption due to impacts upon the eye, orbit or
other cranial structures.
32. Mechanisms
• contusion, deformation, compression or
transection of the nerve, intraneural
haemorrhage, shearing (acceleration of the
nerve at the optic canal where it is tethered
to the dural sheath, thought to rupture the
microvascular supply), secondary vasospasm,
oedema and transmission of a shock wave
through the orbit.
33. Presentation
• indirect neuropathy is considerably more common than direct.
• Vision is often very poor from the outset, with only perception of
light in around 50%.
• Typically, the only objective finding is an afferent pupillary defect;
the optic nerve head and fundus are initially normal, with pallor
developing over subsequent days and weeks.
• It is important to exclude potentially reversible causes of
traumatic visual loss such as compressive orbital haemorrhage;
• more controversially, some cases of compression – bony and
possibly haemorrhagic – due to fracture within the optic canal or
elsewhere may be amenable to intervention.
• Investigation.
• CT is more effective in the demonstration of bony abnormalities
such as optic canal fracture.
• MR is superior for soft tissue changes (e.g. haematoma); with
both modalities, very thin sections are recommended.
34. Treatment
• Spontaneous visual improvement occurs in up
to about half of indirect injury patients, but if
there is initially no light perception this carries a
very poor prognosis.
• Steroids (intravenous methylprednisolone)
might be considered for otherwise healthy
patients with severe visual loss, or in those with
delayed visual loss.
If used, these should be started within the first 8
hours, but the optimal regimen is undetermined
and their use remains controversial !!!
35. • Optic nerve decompression :-
(e.g. endonasal, transethmoidal) may be
advocated in some – poorly defined –
circumstances such as ongoing deterioration
despite steroids and bilateral visual loss.
Compression by bony fragment or haematoma
may also be an indication;
optic canal fracture is a poor prognostic indicator
and there is no evidence that surgery improves
the outlook, whilst carrying a significant risk of
complications.
• Optic nerve sheath fenestration
has been tried in some centres.
36. Optic nerve avulsion
Optic nerve avulsion is rare and
typically occurs when an object
intrudes between the globe and the
orbital wall, displacing the eye.
Postulated mechanisms include sudden
extreme rotation or anterior
displacement of the globe.
Avulsion may be isolated or occur in
association with other ocular or orbital
injuries.
Fundus examination shows a striking
cavity where the optic nerve head has
retracted from its dural sheath .
There is no treatment; the visual
prognosis depends on whether
avulsion is partial or complete.
37.
38. • Of paramount immediate importance is the risk of
infection with any penetrating injury.
Endophthalmitis or panophthalmitis, often more
severe than the initial injury, may ensue with loss of
the eye.
• Risk factors include delay in primary repair, ruptured
lens capsule and a dirty wound.
• Prophylactic intravitreal antibiotics as for
postoperative endophthalmitis should be
considered, with the agent selected dependent on
local microbiological advice; vancomycin is a
common choice.
• tetanus status should be ascertained.
• Any eye with an open injury should be covered by a
protective eye shield upon diagnosis
39. • Corneal
• Peaking of the pupil and
shallowing of the anterior
chamber are key signs,
though full-thickness corneal
penetration may be present
without these.
• The technique of primary
repair depends on
the extent of the wound
associated complications
such as iris incarceration,
flat anterior chamber
and damage to intraocular
contents.
40. Small shelving wounds
with a formed anterior chamber may not always require suturing as they can heal
spontaneously or with the aid of a soft bandage contact lens.
Medium-sized wounds
should almost always be sutured without delay, especially if the anterior chamber is
shallow or flat.
10-0 nylon is used, with shorter stitches near the visual axis opposing perpendicular
edges first and apical portions of wounds last.
A postoperative bandage contact lens may be applied subsequently for a few days to
ensure that the anterior chamber remains deep.
The corneoscleral junction should be sutured with 9-0 nylon.
41. With iris involvement :-
Abscission (excision) of the
prolapsed portion is
commonly required ,
particularly if necrotic or there
is a risk of contamination by
foreign material.
With lens damage :-
Wounds are treated by first
suturing the laceration then
removing the lens by
phacoemulsification or with a
vitreous cutter.
Primary implantation of an
intraocular lens is frequently
associated with a favourable
visual outcome and a low rate
of postoperative
complications.
42. • Scleral
• • Anterior scleral lacerations
have a better prognosis than those posterior to the ora serrata.
An anterior scleral wound may, nevertheless, be associated
with serious complications such as iridociliary prolapse and
vitreous incarceration. The latter, unless appropriately
managed, may result in subsequent fibrous proliferation along
the plane of incarcerated vitreous, with the development of
tractional retinal detachment.
• Viable uveal tissue should be reposited and prolapsed vitreous
cut flush with the wound, with subsequent vitreoretinal
assessment.
• 8-0 nylon or 7-0 absorbable material such as polyglactin should
be used for scleral suturing in this setting.
• • Posterior scleral lacerations
are frequently associated with retinal damage.
Primary repair of the sclera to restore globe integrity should be
the initial priority.
43.
44. • Retinal detachment
• Traumatic tractional retinal detachment following
a penetrating injury may result from vitreous
incarceration in the wound, with associated
fibroblastic proliferation being exacerbated by
the presence of blood in the vitreous gel.
• Contraction of the resultant epiretinal fibrosis can
progress to an anterior tractional retinal
detachment.
• A retinal break may develop several weeks later,
leading to a more rapidly progressing
rhegmatogenous detachment.
