TRAUMA

2.  Ocular trauma is a major cause of worldwide
visual impairment
 Of an approximately 2.4 million ocular
injuries annually :
 MALES are affected 9 times more than
females and
 Most victims are BELOW 40YRS

3. NON
MECHANICAL
CHEMICAL
THERMAL
ELECTRICAL
RADIATIONAL
MECHANICAL
OPEN GLOBE
INJURY
CLOSED
GLOBE
INJURY

6.  The four phases of blunt injury are
compression, decompression, overshooting
and oscillations.
 Anterior – posterior compression of the
globe at the cornea results in equatorial
expansion.The anterior- posterior diameter
of the globe decreases by as much as 41%
and the equatorial diameter increases up to
128% of normal.

7. The driving mechanism
for
pathological changes in
this area is the
equatorial elongation,
creating shearing forces
between the extensible
ocular wall
and the much less
extensible vitreous

8. 1. Central iris: Sphincter tear
2. Peripheral iris: Iridodialysis
3 Anterior ciliary body: Angle recession
4. Separation of ciliary body from the scleral spur:
Cyclodialysis
5.Trabecular meshwork:Trabecular meshwork
tear
6. Zonules/lens: Zonular tears with possible lens
subluxation
7. Separation of the retina from the ora serrata:
Retinal dialysis

9.  POSTERIOR SEGMENT MANIFESTATIONS

10.  Direct rupture of sclera is uncommon and
occurs at the site of impact.
 Indirect rupture occurs remote from site of
impact in an area of scleral weakness
 Phakic eye – Insertion of extraocular muscles
 Pseudophakic eye - Limbus

12.  Scleral rupture is often occult mainly because
ophthalmic examination may be limited by
ocular media opacities, including hyphema,
cataract and vitreous hemorrhage.

13.  Signs of occult rupture are
 Visual acuity of perception of light or no PL
 Markedly reduced ductions
 ocular hypotony
 hyphema
 severe chemosis
 abnormally deep or shallow anterior chamber
 afferent pupillary defect
 vitreous hemorrhage and
 a large bullous subconjunctival hemorrhage

14.  The only definitive way to rule out scleral
rupture is careful controlled exploration of
the globe. Eyes with scleral rupture have a
high incidence of microbial contamination
and are often severely injured internally.
 Early primary repair becomes the most
important step in management.

15.  Due to damage to blood vessels of the iris,
ciliary body, retina, or choroid and can also be
caused by retinal tears
 If the posterior segment cannot be seen
through a vitreous hemorrhage, ultrasound
examination is indicated. Retinal or choroidal
detachment, most retinal tears, and posterior
vitreous detachment can be detected by
ultrasound techniques.

16.  Pigment cells ('tobacco dust’) may be seen
floating in the anterior vitreous, and though
not necessarily associated with a retinal
break, should always prompt a careful retinal
assessment.

17.  Disinsertion occurs at the vitreous base, optic
nerve, retinal vessels, lattice degeneration or
scars
 Commonest changes are avulsion of the vitreous
base with associated retinal dialysis, posterior
vitreous detachment with retinal tear and
vitreous hemorrhage
 The avulsed vitreous base has the appearance of
a hammock or ribbon suspended loosely
through the vitreous cavity

20.  The term commotio retinae describes the
damage to the outer retinal layers caused by
shock waves that traverse the eye from the
site of impact following blunt trauma
 Ophthalmoscopically, a sheen like retinal
whitening appears some hours following
injury

22.  The term commotio retinae was first
introduced by Berlin in 1873.
 It is sometimes referred to as Berlin’s edema,
as Berlin believed that the whitish
appearance of the retina was due to
extracellular edema

23.  It is most commonly seen in the posterior
pole ( Berlins edema ) but may occur
peripherally as well.
 Commotio most frequently affects the
temporal fundus
 Several mechanisms for the retinal opacifi
cation have been proposed, including
extracellular edema, glial swelling, and
photoreceptor outer segment disruption

24.  Histopathologic studies of animal models
have shown that it is characterized by
disruption of the photoreceptor outer
segments with associated retinal pigment
epithelium (RPE) damage

25.  With foveal involvement, a cherry-red spot
may appear, because the cells involved in the
whitening are not present in the fovea.
 Condition clears in 3- 4 weeks
 In some cases, however, visual recovery is
limited by associated macular pigment
epitheliopathy, choroidal rupture, or macular
hole formation.There is no acute treatment.

26.  The severity of commotio retinae may be
rated as being in one of two categories: a
milder condition or retinal concussion, and a
more severe condition or retinal contusion.

27.  The initial vision is better (usually better than
20/200)
 the gray–white change is less dramatic
 the clinical changes are reversible, with vision
generally recovering fully with minimal sequelae
 On fluorescein angiography (FA) the areas of
opaque retina block background choroidal
fluorescence.
 Leakage from the retinal vessels is not observed

28.  In retinal contusion, the retinal whitening is
more intense and may be associated with
hemorrhages and more persistent visual loss
 Visual acuity may be variably affected, from mild
to severe, in a fashion that does not correlate
with the degree of retinal whitening seen
clinically.
 If the macula is affected, acuity is usually
permanently damaged.
 More intense staining or leakage is noted at the
level of the RPE on FA

29.  Traumatic macular holes (TMH) were first
described by Knapp in 1869 and by Noyes in
1875
 Mechanisms include - contusion necrosis and
vitreous traction
 Holes may be noted immediately or soon after
blunt trauma that causes severe Berlin edema,
after a sub retinal hemorrhage caused by a
choroidal rupture , following severe cystoid
macular edema, or after a whiplash separation
of the vitreous from the retina.

31.  Macular holes do not always form
immediately after trauma, but may appear
after several days.
 In some cases macular edema and cysts
develop, and eventually the roof of the cysts
erode leading to the formation of a macular
hole.

32.  There is no consensus on surgical
management for this disease, because some
cases demonstrate spontaneous closure of
the macular hole and improved visual acuity
by 6 months after injury
 Cases that close spontaneously tend to be in
younger patients and in patients with smaller
holes (less than 1/3 disc diameter) and
without a fluid cuff

33.  Choroidal rupture is a tear of the inner choroid
and overlying Bruch’s membrane and RPE
caused by mechanical disruption when the globe
is acutely deformed by blunt trauma causing
anterior posterior compression, and subsequent
horizontal expansion of the eye
 During the blunt trauma, the fortified
collagenous sclera and the naturally flexible
retina are less likely to rupture. However, the
relatively inelastic RPE, Bruch’s membrane, and
choriocapillaris, do rupture

36.  Direct choroidal ruptures are relatively
uncommon; they tend to be parallel to the ora
serrata and are found at the direct site of
impact, which is usually anterior to the equator
 Indirect choroidal ruptures resulting from
compressive injury to the posterior pole of the
eye22 are more common (about 80%) , with the
crescent-shaped tears occurring concentric to
the disc because of the tethering or stabilizing
effect of the optic nerve.The majority of indirect
ruptures occur temporal to the disc and involve
the fovea

37.  Choroidal rupture is often associated with
intrachoroidal, subretinal, and intraretinal
hemorrhage.The associated hemorrhage and
accompanying commotio retinae may conceal
the presence of the rupture, which may become
visible only after the blood clears in 2–3 months.
 ICGA appears to have an advantage in diagnosis
of choroidal rupture as it often highlights
broader areas of pathology and disturbance
compared to FA. Choroidal ruptures appear as
hypofluorescent streaks on ICGA.

38.  Occasionally, (10%) choroidal
neovascularization (CNV) develops as a late
complication in response to the damage to
Bruch's membrane
 The development of CNV was most strongly
associated with older age, macular location
of the choroidal rupture, and a greater length
of the choroidal rupture

39.  If subfoveal CNV is present, it is generally
treated with an anti-VEGF agent, although
photodynamic therapy can be used in
selected patients.Thermal laser
photocoagulation is rarely employed for
nonsubfoveal lesions. Sub foveal surgery for
CNV in patients with choroidal rupture
complicated byCNV is less commonly done
given the effectiveness of anti -VEGF agents

40.  AkaTraumatic chorioretinal rupture
 It refers to a simultaneous break in the retina
 and choroid resulting from a high-velocity
missile passing adjacent to and coming into
contact with the globe, entering the orbit
without causing a scleral rupture.This injury
causes a fullthickness chorioretinal defect
and visual loss

42.  Two mechanisms have been considered:
damage adjacent to the pathway of the high-
velocity object is responsible for the direct
injury, and the indirect injury is caused by the
shock waves transmitted to the globe

43.  TCR is a rare clinical presentation. Fundus
examination may show the chorioretinal
defect, bare sclera, pigment proliferation,
marked fibrovascular proliferation and scar
formation
 If the foreign body has come to rest deep in
the orbit, theTCR is typically oriented
radially.
 The visual prognosis depends on the extent
and location of intraocular injury

44.  Despite severe retinal and choroidal injuries
inTCR, the patients have a low chance of
retinal detachment, as marked proliferation
of fibrous tissue causes firm adherence of
retina and choroid to the sclera
 In addition, the intact posterior hyaloid that is
typically present in young patients further
mitigates the risk for retinal detachment

45.  Management includes observation, and rarely
requires surgical intervention to repair a retinal
detachment or to remove a non-clearing
vitreous hemorrhage.
 TCR is typically caused by gun injuries resulting
in retained intraorbital metallic foreign bodies,
which are well tolerated and typically have
minimal adverse effect on visual prognosis, and
as such can be followed up without surgical
intervention

46.  The force must be sufficiently large so as to
cause an RPE tear, but not so large as to
cause both the RPE and Bruch’s membrane to
tear, as in a choroidal rupture.
 As the elastic torn edge of RPE tends to
retract over the adjacent intact RPE, RPE
tears are usually prevented from healing, and
visual recovery is generally poor

47.  Patients with traumatic RPE tears involving
the fovea usually have a poor visual
prognosis.
 Fok et al.reported spontaneous resolution of
traumatic RPE tears in a patient who
subsequently had good visual recovery.
 The mechanisms of resolution in this case
included a layer of hypopigmented RPE cells,
atrophy of the choriocapillaris, and/ or
deposition of fibrous tissue.

48.  Ocular contusion may result in numerous
types of retinal tears, such as horseshoe
tears, operculated holes, macular holes, and
retinal dialyses
 Dialysis is the most common type of retinal
break in the setting of trauma

49.  Traumatic retinal tears are predominantly
located within the vitreous base region
 Cox et al.reported that retinal tears were
limited to the ora serrata in 59% of cases with
traumatic retinal detachments (RD).
 Only 8% of the traumatic tears were in the
equatorial area
 Johnston reported that 84.4% of the patients
with traumatic retinal tears developed
rhegmatogenous RD.

51.  The presence of RD immediately following
injury is extremely rare, and in general RD
progress slowly, occurring weeks to months
following the trauma.
 The reason for the slower rate of progression
from retinal defect (tear, dialysis) to frank
detachment relates to the fact that the
vitreous is formed and may be attached in
these young patients

52.  For patients developing giant retinal tears
following trauma, the progression to
detachment is much more rapid, and these
types of tears appear to be more common in
myopic male patients

53.  This refers to a break occurring at the ora
serrata, whose anterior edge is at the ora
serrata and posterior edge is attached to th e
vitreous base.
 Dialyses account for 8–14% of RD
 Mechanical disruption of the retina by force
transmitted via the vitreous base

56.  The most common symptoms are visual field
loss or vague blurring of vision. Other
complaints include photopsias, vitreous
floaters, or both. Some patients may not
have any symptoms at the time of diagnosis.
 The dialysis-associated RD may develop at
the time of injury or months or even years
later..
 Signs of chronicity, such as demarcation lines
and intraretinal cysts, are common.

57.  A defining feature of spontaneous dialysis is
its selective localization/involvement of the
inferotemporal quadrant because of
developmental asymmetry.
 However, traumatic dialyses may involve all
quadrants. A higher frequency in the
superonasal and inferotemporal quadrants
has been reported

58.  Weidenthal and Schepenspostulated that the
nasal peripheral retina has a greater
susceptibility to traumatic dialysis secondary
to its relatively narrower vitreous base.
 The inferotemporal quadrant, being the area
least protected based on orbital anatomy,
remains susceptible to dialysis with
temporally directed trauma

59.  Patients typically describe a sudden loss of
vision at the time of the trauma.
 It is usually associated with a decelerating
injury of significant momentum

61.  A complete avulsion implies that the optic
nerve fibers are disinserted from the retina,
choroid, and vitreous and that the lamina
cribrosa is retracted from the scleral rim,
resulting in a blind eye with a fixed and
dilated pupil.

62.  Sudden extreme rotation of the globe may be
the major mechanism in some cases. Other
postulated mechanisms include a sudden
marked rise of intraocular pressure that
forces the nerve out of the scleral canal or a
sudden anterior displacement of the globe.

63.  A posterior ocular wall defect in the region of
the optic disc characterized by a hypoechoic
defect may be apparent on B scan
 A-scan ultrasonography may show a marked
widening of the optic nerve suggesting
hemorrhage and edema within the nerve
sheath

64.  There is no known effective medical or
surgical treatment for this condition. Final
visual outcome is generally poor and
dependent on initial post-injury visual acuity

65.  Purtscher’s retinopathy
 Terson’s syndrome
 Shaken-baby syndrome
 Valsalva retinopathy

66.  Purtscher in 1910 noted multiple areas of retinal
whitening and hemorrhage in the posterior poles of
both eyes.in a pt with head trauma
 The term ‘‘Purtscher-like retinopathy’’ is sometimes
used to describe the retinopathy seen in conditions
other than trauma, such as acute pancreatitis, fat
embolism syndrome, childbirth, connective tissue
disorders, and renal failure.
 Suggested pathophysiological mechanisms have
included fat embolization leading to arterial occlusion,
angiospasm, or lymphatic extravasation

68.  Acute fundus abnormalities in Purtscher’s
retinopathy include Purtscher flecken, cotton-
wool spots, retinal hemorrhage, and optic disc
swelling
 Purtscher flecken consists of multiple, discrete
areas of retinal whitening in the superficial
aspect of the inner retina, between the arterioles
and venules.
 Retinal hemorrhages are often minimal and are
typically flame-shaped, but dot and blot
hemorrhage may occur.

69.  Without treatment, these findings resolve
spontaneously within 1–3 months and may be
replaced by mottling of the RPE, temporal
disc pallor, or attenuation or sheathing of the
retinal vessels

70.  Intraocular hemorrhage secondary to either
subarachnoid hemorrhage or subdural
hemorrhage is namedTerson syndrome after
AlbertTerson
 The reported incidence ofTerson syndrome in
patients suffering from subarachnoid
hemorrhage ranges from 10% to 50%

71.  There are two plausible mechanisms forTerson
syndrome.
 One explanation is that the vitreous hemorrhage may
derive from ocular blood.The sudden rise in
intracranial pressure may lead to a decrease in venous
return to the cavernous sinus or obstruct the
retinochoroidal anastomoses and central retinal vein,
culminating in venous stasis and hemorrhage.
 Another explanation is that the vitreous hemorrhage
may be caused by a large amount of blood entering
the subarachnoid space around the optic nerve,
subsequently infiltrating the intraocular space
through the perivascular space around the central
retinal vessels within the optic nerve.

72.  Current recommendations in the literature
suggest 3–6 months of observation after the
acute event, followed by vitrectomy if there is
no improvement in visual acuity.
 Vitrectomy inTerson syndrome usually
results in substantial improvement in visual
acuity

73.  Shaken-baby syndrome (SBS) is a type of
child abuse especially prevalent in infants
under 3 years of age.
 The mechanism of retinal hemorrhage has
not been clarified; however, it is assumed
that the acceleration–deceleration causes
relative movements of the vitreous body on
the one hand and the retina and vessels on
the other.

75.  Ocular examination is critical because up to 90% of
babies with SBS display unusual ocular findings.
 Findings in such cases are typically bilateral but can be
asymmetrical. Dilated fundus examination may
demonstrate posterior pole retinal hemorrhages,
involving any of the layers of the retina. Heavy
vitreous hemorrhage, retinal folds, choroidal rupture,
and/or retinoschisis may be observed.There may be
disc edema secondary to elevated intracranial
pressure or indirect optic canal damage and optic
sheath hemorrhage. Horseshoe tears and retina
detachment may also be found

76.  Hospital admission of an SBS patient is indicated
not only on medical grounds but also to avoid
the risk of further abuse.
 Most intraretinal, subretinal, and preretinal
hemorrhages clear spontaneously within 4
weeks after injury.Vitreous hemorrhage may
clear or persist longer than a few months.
Schisis, choroidal rupture, retinal folds, retinal
detachment, and optic nerve trauma may be
safely observed until the patient is stabilized and
the appropriate surgical strategy is determined

77.  For nonclearing vitreous hemorrhage or
subhyaloid hemorrhage overlying the
macula, trans-pars plana vitrectomy should
be considered, as irreversible visual loss
owing to deprivation amblyopia may occur in
as little as 4 weeks.
 Retinal detachment should be repaired with
scleral buckling or vitrectomy

78.  Valsalva retinopathy was first described in
1972 byThomas Duane as a particular form of
retinopathy, preretinal and hemorrhagic in
nature, secondary to a sudden increase in
intrathoracic pressure

80.  Increasing intrathoracic pressure against a
closed glottis diminishes venous return to the
heart, decreasing stroke volume and
subsequently increasing venous system
pressure..
 This pressure rise causes a decompensation at
the level of the retinal capillary bed resulting in
either unilateral or bilateral retinal hemorrhages,
which are usually found below the internal
limiting membrane, but can occasionally break
through to become a subhyaloid or intravitreal
hemorrhage

81.  The anatomic location of the premacular
hemorrhage is described as subinternal limiting
membrane (ILM), subhyaloid, or a combination
of both. Optical coherence tomography (OCT)
can be used to distinguish clinically between a
subhyaloid and a sub-ILM hemorrhage.
 Therapeutic options inValsalva retinopathy
include conservative management, surgery
(vitrectomy), and Nd:YAG laser membranotomy