POSTERIOR SEGMENT MANIFESTATIONS OF BLUNT TRAUMA

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 40 YRS

OCULAR INJURIESNON MECHANICAL

CHEMICAL

THERMAL

ELECTRICAL

RADIATIONAL

MECHANISMS

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.

The driving mechanism forpathological changes in this area is the equatorial elongation,creating shearing forces between the extensible ocular walland the much less extensible vitreous

  SEVEN RINGS OF BLUNT TRAUMA TO EYE

1.  Central iris: Sphincter tear2.  Peripheral iris: Iridodialysis3 Anterior ciliary body: Angle recession4.  Separation of ciliary body from the

scleral spur: Cyclodialysis5. Trabecular meshwork: Trabecular

meshwork tear6.  Zonules/lens: Zonular tears with possible

lens subluxation7. Separation of the retina from the ora

serrata: Retinal dialysis

POSTERIOR SEGMENT MANIFESTATIONS

SCLERAL RUPTURE

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

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

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

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.

VITREOUS HEMORRHAGE

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.

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.

VITREOUS DISINSERTION 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

COMMOTIO RETINAE

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

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

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

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

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.

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.

RETINAL CONCUSSION 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

RETINAL CONTUSION 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

POSTTRAUMATIC MACULAR HOLE 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.

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.

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

CHOROIDAL RUPTURE 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

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

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.

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

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 by CNV is less commonly done given the effectiveness of anti -VEGF agents

RETINITIS SCLOPETARIA

Aka Traumatic 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

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

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, the TCR is typically oriented radially.

The visual prognosis depends on the extent and location of intraocular injury

Despite severe retinal and choroidal injuries in TCR, 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

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

TRAUMATIC RETINAL PIGMENT EPITHELIAL TEARS 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

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.

TRAUMATIC RETINAL TEARS AND DETACHMENTS 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

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.

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

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

RETINAL DIALYSES

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

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.

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

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

OPTIC NERVE AVULSION

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

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.

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.

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

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

CHORIORETINOPATHIES FROMINDIRECT OCULAR INJURIES Purtscher’s retinopathy Terson’s syndrome Shaken-baby syndrome Valsalva retinopathy

Purtscher’s retinopathy 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

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.

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

Terson’s syndrome

Intraocular hemorrhage secondary to either subarachnoid hemorrhage or subdural hemorrhage is named Terson syndrome after Albert Terson

The reported incidence of Terson syndrome in patients suffering from subarachnoid hemorrhage ranges from 10% to 50%

There are two plausible mechanisms for Terson 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.

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 in Terson syndrome usually results in substantial improvement in visual acuity

Shaken-baby syndrome

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.

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

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

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

Valsalva retinopathy

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

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

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 in Valsalva retinopathy include conservative management, surgery (vitrectomy), and Nd:YAG laser membranotomy