Blow Out
Orbital fractures
A blowout fracture of the orbit is
typically caused by a sudden increase in the orbital pressure by a striking
object which is greater than 5cm in diameters, such as a fist or tennis ball. It
is of two types
a)Pure:- does not involve the orbital rim
b)Impure:- involves orbital rim.
Since the bones of the lateral wall
and roof are usually able to withstand
such trauma, the fracture most frequently involves the floor of the orbit along
the thin bone covering the infraorbital canal(Orbital floor fracture). Occasionally,
the medial orbital wall may also be fractured. Clinical features vary with the
severity of trauma and the time interval between injury and examination.
Floor fracture:-
Signs:-
1)Periocular Signs:-
Include variable ecchymosis, Oedema
and subcutaneous emphysema
2)Infraorbital nerve anaesthesia:-
Involves the lower lid, cheek, side of the nose, upper lip, upper teeth and gums is very common because a blow –out fracture
frequently involves the infraorbital canal.
3)Diplopia:-Caused by the following
mechanisms.
a)Haemorrhage and oedema involve
orbital septa which connect the inferior
rectus and inferior oblique muscles to the periorbita. So they become taut and
restrict muscle movement. Ocular motility usually improves as haemorrhage and
oedema resolve.
b)Mechanical entrapment:-
within
the fracture inferior rectus or inferior oblique muscle or adjacent connective
tissue and fat are entrapped. Diplopia typically occurs in both upgaze and
downgaze(double diplopia). Diplopia may subsequently improve if mainly due to
entrapment of connective tissue and fat but usually persists if there is
significant involvement of muscles.
C) Direct injury to the muscles.
Forced
duction test to be done to confirm muscle entrapment
4)Enophthalmos:-
May be present if the fracture is
severe.It
tends to manifest after a few days as initial oedema resolves. In the absence of
surgical intervention, enophthalmos may continue to increase for about 6months
as post-traumatic orbital degeneration and fibrosis develop.
5) Ocular damage:-(e.g-hyphaema,angle
recession, retinal dialysis although uncommon, should be excluded by careful slit
lamp and fundus examination.
Investigation:-
1) CT Scan:- useful for evaluation of the extent of the fracture and also to evaluate
the entrapped muscle, fat in maxillary antrum.
2) Hess test:-useful to assess and
monitor the progression of diplopia.
3) Field test
Treatment:-
1)Initial treatment:-conservative
with antibiotics
The patient should also be instructed
not to blow the nose.
2)Subsequent treatment:-
Aimed to prevent permanent vertical
diplopia and/or cosmetically unacceptable enophthalmos.
Late complications depend upon fracture
size.herniation of orbital contents into the maxillary sinus and muscle entrapment.
Small cracks unassociated with
herniation:- Does not require treatment
Fractures involving less than half
the orbital floor with little or no herniation and improving diplopia:- Do not
require treatment unless more than 2mm of enophthalmos develops.
Fractures involving half or more of
the orbital floor with entrapment of orbital contents and persistent diplopia
in the primary position should be repaired within 2weeks. If the surgery is
delayed, the results are less satisfactory because of secondary fibrotic changes
develop in the orbit.
Surgical Technique:-
A) A transconjunctival or subciliary incision is made
B) The periosteum is elevated from the floor of the orbit and
all entrapped orbital contents are removed from the antrum
C) The defect in the floor is repaired by using synthetic
material such as supra mid, silicone or Teflon.
D) The periosteum is sutured
Medial wall fracture:-
Usually associated with floor
fracture. Isolated fractures are less common.
signs:-
a) Periorbital subcutaneous emphysema typically develops when
the patient blows the nose
b) Defective ocular motility involving adduction and abduction
Treatment:-
Involves release of the
entrapped tissue and repair of the bony defect.
Roof and Lateral wall
fractures rarely encountered by
ophthalmologist.
Blunt Trauma
The most common cause of blunt trauma
are squash balls, elastic luggage straps and champagne corks.
Severe blunt trauma results in
anteroposterior compression with simultaneous expansion in the equatorial plane, associated with a transient but severe increase in intraocular pressure.The
injury occurring during blunt trauma can be Coup(direct) or
Contrecoup(indirect) injury.
Blunt
trauma gives rise to the following injuries:-
Eyelid:-Haematoma(black eye), lid laceration
Treatment:-
Lid Haematoma-Cold
compression, systemic antibiotics,non-steroidal antibiotics, Serratiopeptidase to
be given. any associated globe injury to be ruled out.
Any lid defect should be repaired by direct
horizontal closure whenever possible, even if under tension; since this affords
the best functional and cosmetic results
Conjunctiva:-Subconjunctival haemorrhage, Conjunctival chemosis,
Subconjunctival emphysema
Treatment:-
Subconjunctival haemorrhage and chemosis as such requires no treatment;
but underlying globe rupture to be excluded
In subconjunctival
emphysema-underlying injury to the sinuses to be ruled out.
Cornea:-1)Corneal abrasion(stains with fluorescein)
Treatment:- a)topical antibiotic drops
and ointment
b)Lubricating
dros(e.g:-Carboxymethylcellulose)
c) topical cycloplegic
drops(Atropine-sulfate1% eye drop,Homatropine2%eye drop)
2)Acute corneal oedema:- may develop
secondary to focal or diffuse dysfunction of the corneal endothelium.Commonly
associated with folds in Descemet's membrane and stromal thickening
Treatment:- Usually clears
spontaneously
Anterior Chamber:-
A)Hyphaema:-Blood in the anterior chamber is a common complication.The
source of bleeding is the iris or ciliary body(mainly due to disruption of the
major arterial circle and its branches, recurrent choroidal arteries or ciliary
body veins. Approximately 15% of hyphaemas arise from ruptured iris vessels, cyclodialysis
or iridodialysis)
The
red blood cells sediment inferiorly with a resultant fluid level; the height of
which should be measured and documented during slit-lamp examination.
Grading
Scheme for traumatic hyphaema:-
Grade
|
Size of hyphaema
|
Microscopic
|
No layered
blood, circulating red blood cells only
|
1
|
<1/3rd
|
2
|
1/3rd-1/2
|
3
|
½ - near total
|
4
|
Total(eight ball)
|
Treatment:-The immediate risk is that of secondary haemorrhage, often
larger than the original hyphaema, which may occur at any time up to a week
after the original injury(most commonly within the first 24hours).
The
main aims of treatment are therefore prevention of secondary
haemorrhage, control of any elevation of intraocular pressure and management of
associated complications.
a) Bed rest with head elevation to approximately 30 degrees enhances
dependent settling of blood and may permit earlier posterior segment clinical
examination.
b) Cycloplegics:- enhance patient comfort in the setting of traumatic
iritis and due to immobilization of pupil chances of rebleeding reduces
c) Topical Steroids(1% Prednisolone Acetate, 0.1% Dexamethasone) :-helps to reduce associated traumatic uveitis.
d) Antifibrinolytic Agents:-Aminocaproic acid and tranexamic acid have been proposed to
reduce rebleeding.
The current recommended dose of aminocaproic acid is-50mg/kg
orally every 4 hours, up to 30gm/day, for a total of 5 days (contraindicated in
active intravascular clotting disorders, pregnancy, cardiac, hepatic and renal
disease).
Tranexamic acid is used orally,dose-25mg/kg t.i.d.(role
controversial)
e) Avoid drugs which prevent platelet aggregation like aspirin
Surgical intervention(Clot expression and limbal
delivery, anterior chamber wash, or automated hyphectomy by automated
cutting/aspiration instruments):-
Indications:-
1)Intraocular pressure(IOP) criteria:-If IOP is
>50mmhg for 5 days or >35mmhg for 7 days to avoid optic nerve damage.
2) Corneal blood staining:- Patients with total or near-total
hyphaemas and IOP>25mmhg for 5 days should undergo surgery to prevent corneal blood staining.
3) Prolonged clot duration:- Blood clot>10 days duration may
lead to peripheral anterior synechiae formation-So, surgical intervention is
required.
4)Total hyphaemas which are not resolving by 5 days.
Complications of
Hyphaema:-
a)Rebleeding
b)Glaucoma:- Aqueous
suppressants, both topical beta-blockers and oral carbonic anhydrase
inhibitors,are the mainstays of therapy(e.g:-topical Timolol-maleate 0.5% twice
daily, Acetazolamide 250mg 4 times a day)
Peripheral iridectomy and trabeculectomy may be required in
some cases if medically not controlled.
c) Corneal blood staining:-
It may require 2 years to resolve
B) Traumatic Uveitis:-
Requires treatment with
topical steroid and cycloplegic eye drops.
Pupil and Iris and Ciliary
body:-
Pupil:-
Severe contusion may
result in transient miosis.
Alternatively, damage to
the iris sphincter may result in traumatic mydriasis, which is often permanent:-
the pupil
reacts sluggishly or not at all to both light and accommodation.
Radial tears in the pupillary margin
are common.
Iridodialysis:- It is dehiscence of the
iris from the ciliary body at its root. The
pupil is typically D shaped and
dialysis is seen as a biconvex area near the limbus. Sometimes traumatic aniridia(360 degree iridodialysis)
may occur.
Ciliary body:-
Severe trauma results in cessation of aqueous secretion(ciliary
shock)-hypotony results.
Tears may occur in between
the longitudinal and circular muscle fibres of the ciliary muscle. It is called angle recession and it may lead to late-onset glaucoma due to associated trabecular meshwork injury.
A separation of the scleral spur from its ciliary body attachments occurs(called cyclodialysis) and it may lead to hypotony.
Treatment:- Dialysis may be asymptomatic if it is small and covered by the eyelid
requiring no treatment.
If it is large enough and
situated in the exposed palpebral aperture, it may require surgical repair of
the dehiscence(repaired with one or more mattress sutures of double-armed 10-0
polypropylene sutures tied externally under a sclera flap)
Gonioscopy and applanation tonometry to be done to rule out
angle recession and late-onset glaucoma
Lens:-
a)Vossius ring:-
A circular ring of faint
or stippled opacity is seen on the anterior surface of the lens due to
multitudes of brown amorphous granules of pigment lying on the capsule.It
usually has about the same diameter as the contracted pupil and is due to the
impression of the iris on the lens. It is produced by the force of the blow driving the
cornea and iris backwards. Minute, discrete subcapsular opacities may be seen
after resorption of the pigment.
b)Concussion cataract:-It forms due to traumatic damage to the lens fibres
themselves and minute ruptures in the lens capsule with an influx of aqueous
humour.Hydration of the lens fibres and consequent opacification.
The most typical appearance
of concussion injury to lens is rosette-shaped cataract usually in
the posterior cortex, sometimes in the anterior cortex or both.in this
condition, an accumulation of fluid marks out the architectural arrangement of
the lens. The star-shaped cortical sutures are therefore delineated and feathery
lines of opacities outlining the lens fibres radiate from them. It may
disappear, remain stationary or may progress to total cataract. a late rosette-shaped cataract may develop in the posterior cortex one to two
years after injury.
Treatment:- If rapid intumescence of the lens produces
secondary glaucoma then urgent cataract surgery is required. In other cases of visually disturbing cataract surgery should be
delayed until all signs of inflammation subside. It is wise to go for pre-operative ultrasonography in these cases to assess the posterior capsular
integrity as well as to assess the posterior segment.it may guide the
surgical procedure.
c) Subluxation:- of the lens may occur, secondary to tearing of zonules. A subluxated lens tends
to deviate towards the meridian of intact zonule. The anterior chamber may deepen
over the area of zonular dehiscence, iridodonesis may be present. The edge of the
subluxated lens may be visible under mydriasis. Subluxation of a magnitude
sufficient to render the pupil partly aphakic and may lead to uniocular
diplopia. Lenticular astigmatism may occur.
Treatment:- Depends upon the degree
of subluxation.smaller degree of subluxation, without any cataract formation and
without any associated complications and having good vision requires only
observation.
Moderate degree of
subluxation may be managed by cataract surgery+capsular tension ring
placement+/- anterior vitrectomy+posterior chamber intraocular lens
implantation.
If the subluxation is near
360 degree then anterior vitrectomy+removal of crystalline lens+anterior
chamber intraocular lens/scleral fixation lens implantation may be required.
d) Dislocation:- due to 360 degree zonular dehiscence. Dislocation may be in the vitreous or rarely it may be in the anterior
chamber or it may be expelled out subconjunctivally through the scleral
rupture.
Treatment:- If it is in vitreous cavity then pars plana vitrectomy is required.If
the dislocation is in the anterior chamber then removal of the lens through limbal
incision along with anterior vitrectomy is required. The aim is to restore the
vision with the primary implantation of the intraocular lens if there is no
contraindication.
Globe
Rupture:-
Result from severe blunt trauma.The rupture is usually anterior,in the vicinity
of Schlemm canal,with prolapsed of intraocular structures such as
lens,iris,ciliary body and vitreous.Occasionally the rupture is
posterior(occult),just behind the insertion of recti muscle, with little
visible damage to the anterior segment.Clinically ,occult rupture is suspected
if there is asymmetry of anterior chamber depth and intraocular pressure in
affected eye is low.
Treatment:-Scleral wound is repaired with 6-0/8-0 polyglactin suture(Vicryl).Every attempt should be
made to reposit exposed viable uveal tissue and cut prolapsed vitreous flush
with the wound with vitreous cutter.Non viable iris tissue to be abscised as
there is increased chance of endophthalmitis if reposited.
Vitreous:-
Posterior vitreous
detachment may occur.It may be associated with vitreous haemorrhage.No fundal reflex found
with ophthalmoscope in presence of vitreous haemorrhage.Red blood cells in
vitreous cavity shows morphological changes(Khaki
cell) and they may come in anterior chamber and blocks trabecular
meshwork producing glaucoma.
Treatment:- Para plana vitrectomy may be required if the vitreous haemorrhage is
non resolving.Antiglaucoma medication if Khaki cell glaucoma develops.
Retina:-
a)Commotio
retinae(Berlin oedema):-Indicates concussion of
the sensory retina resulting in cloudy
swelling which gives the involved area a grey appearance.
Commotio most frequently involves temporal fundus and
occasionally the macula.If it involves macula aCherry red spot may be
seen at the fovea.
The prognosis in mild
cases is good with spontaneous resolution without sequelae within 6wks.Severe
involvement of the macula may be associated with intraretinal haemorrhage.
Subsequent post-traumatic
macular changes include progressive pigmentary degeneration and macular hole
formation.
b)Retinal
breaks:-
1)Retinal dialyses:-Caused by traction by the
relatively inelastic gel along the posterior aspect of the vitreous base.The vitreous base is avulsed.Dialyses may
occur in any quadrant but are most frequent
in the upper nasal.
2) Equatorial tears:- Less frequent and due to
direct retinal disruption at the point of sclera impact.
3) Macular holes:-may occur either at the time of
injury or later following resolution of commotion retinae.
Choroid:-
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
ora-serrata.Indirect one occur opposite the site of impact.Fresh rupture may be associated with subretinal haemorrhage.Weeks to
month later on absorption of blood,a white crescent shaped,vertical streak of
exposed underlying sclera,frequently involving the macula,concentric with the
optic disc becomes visible.The visual prognosis is poor if fovea is
involved.
Optic Nerve
Optic Neuropathy:-Uncommon
but devastating cause of permanent visual loss. Optic nerve head and fundus are
initially normal.The only finding is relative afferent papillary defect(RAPD).Neither systemic steroids
nor surgical decompression of the optic canal prevent the development of optic
atrophy within 3-4wks.
Optic nerve avulsion:-Rare.Typically occurs when an object intrudes between the globe
and orbital wall;displacing the eye.Fundus shows a striking cavity where the
optic nerve head has retracted from its dural sheath.No treatment.
N.B:- I have written it long to cover
all the questions. Short notes like Vossius ring, Berlin oedema, Traumatic Hyphaema, rosette
cataract, may come. if short note comes start with the mechanism of injury with diagram.
If the question is lengthy then write
down the underlined lines only. Note in blow out fracture
there is one heading that is Globe
injury;
So blow out
fracture(cricket ball injury) covers both orbital wall fracture and globe
injury also.
Other causes
Of Hyphaema:-
1)Neovascularization
Of iris(Rubeosis Iridis);-following proliferative diabetic retinopathy, Central
retinal vein occlusion,Vasculitidis
· 2) eye infection
caused by herpes virus
·
4) intraocular lens problems (artificial lens implants)
·
5)Complication
following intraocular surgery
·
6) Intraocular
malignancy:-Retinoblastoma in children,Malignant Melanoma in adults.
·
7)Trauma
·
8)Conditions or
medications that cause thinning of the blood, such as aspirin, warfarin, or drinking alcohol may also cause hyphema.
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