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Clinical Diagnosis and Management of Ocular Trauma

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Posterior Segment

Ocular Trauma

C H A P T E R

24Management of Traumatic

Hemorrhages to the

Posterior Segment

Javier A Montero, Jose M Ruiz-Moreno (Spain)

Introduction

Ocular trauma is a significant cause of visual impairment in the United States and the leading cause of unilateral blindness worldwide. Ocular trauma is more frequent among adult males mainly due to occupational reasons, though females and children may also present ocular damage secondary to trauma. Isolated damage to the anterior segment occurs in more than half of the cases and isolated damage to the posterior segment is uncommon.1

Approximately 2.5 million injuries occur annually, 40,000 of which cause serious visual loss. Vision is lost because of primary mechanical damage of vital ocular structures and secondary complications, such as infectious endophthalmitis and retinal detachment due to intraocular fibrous proliferation and contraction.1

The presence of marked vitreous hemorrhage is associated with poor visual prognosis in ocular trauma involving the posterior segment. Poor prognostic factors include presenting visual acuity of light perception or lower, hyphema, and traumatic cataract. Severe vitreous hemorrhages after closed-globe injury are frequently associated with various anterior and posterior segment pathologies, and early vitrectomy is considered to improve early visual rehabilitation and management of any potentially treatable posterior pathology.2

Ocular hemorrhage associated with trauma may occur after blunt and penetrating injuries. A careful and complete ophthalmic examination is required in every case since injuries causing minimal signs of damage to one part of the eye may cause a significant injury in another part of the eye with severe consequences for the patient and occasionally to the ophthalmologist who has misdiagnosed the trauma.

Blunt injuries are more common and cause more cases of visual impairment than penetrating injuries, although the frequency of severe damage, blindness, and loss of the globe itself is greater with ocular

penetration or rupture. Two types of injuries may disrupt the continuity of the sclera: penetration by relatively sharp objects, and rupture caused by massive blunt trauma.

The visual prognosis is more favorable when the primary mechanical damage caused by sharp penetration is limited to the anterior segment of the eye. Modern microsurgical techniques permit better wound closure and reconstruction of the anterior ocular structures. Penetrating injuries involving the posterior segment carry a less favorable prognosis. The primary mechanical damage of vital structures by such injuries may be so great that useful vision is instantly destroyed. However, the application of appropriate vitreoretinal surgery to prevent or treat secondary complications may result in the preservation of eyes that would otherwise be lost.

Both eyes should always be examined. Visual acuity determination should be performed in the first place; if standardized charts are not available we should at least be able to determine finger counting and reading abilities and the distance of these exams should be recorded. If none of these abilities can be reached, the light perception and projection abilities should be recorded. The evaluation of the direct and consensual pupillary reflexes is of great prognostic value. Decreased visual acuity is usually a sign of severity. Over 40% of the cases report marked visual acuity loss (lower than 20/200) associated with severe ocular trauma.

Anterior segment examination may disclose corneal lacerations, traumatic iritis, hyphema, damage to lens and vitreous opacities among others, which may limit the examination of the posterior segment (Fig. 24.1). Ocular examination should be extremely careful until the absence of ocular perforation has been established, avoiding pressure on the eye ball and administration of drops or ointments (Fig. 24.2).

In the presence of hyphema posterior segment examination should be gently performed in order to prevent further bleeding and scleral indentation should be avoided for 2-3 weeks.

140

 

Clinical Diagnosis and Management of Ocular Trauma

 

 

The size, location and characteristics of hemorrhages

 

 

 

 

 

 

should be recorded. Vitreous hemorrhages may vary

 

 

 

in size, location and density. Initially they are usually

 

 

 

close to the damaged area, though they may later

 

 

 

spread and occupy the whole vitreous cavity precluding

 

 

 

examination of posterior segment structures. If

 

 

 

posterior segment examination is not satisfactory due

 

 

 

to the presence of anterior segment or vitreous hemor-

 

 

 

 

 

 

rhages contact A-scan and B-scan ultrasonography are

 

 

 

helpful for detecting posterior vitreous detachment and

 

 

 

differentiating it from retinal detachment (Fig. 24.3).

 

 

 

The symptoms associated with posterior hemor-

 

 

Fig. 24.1: Subconjunctival hemorrhage after severe blunt

rhages will depend on the locations and size of the

 

 

hemorrhage. Peripheral retinal hemorrhages may be

 

 

trauma masking scleral rupture. The patient presented

asymptomatic; retinal, choroidal or retrohyaloidal

 

 

vitreous hemorrhage with choroidal rupture

 

 

hemorrhages affecting the posterior pole will present

 

 

 

 

 

 

as central scotomata (Fig. 24.4); and patients with

 

 

 

vitreous hemorrhages will complain of floaters, blurred

 

 

 

vision or even light perception vision, depending on

 

 

 

the amount of blood present.

Fig. 24.2: Retroequatorial intraocular foreign body which penetrated through the lower lid

A careful examination of the vitreous, posterior pole and peripheral retina under pharmacologic mydriasis is mandatory, since anterior or posterior hemorrhage may later mask damage to the posterior segment. Indirect ophthalmoscopy is a useful tool to evaluate damage to the posterior segment allowing a fast binocular examination of the vitreous and the retina and verification of the presence of intraocular foreign bodies (IOFB). Posterior pole biomicroscopy using contact and non contact lenses will improve the detailed examination of the macula, though non contact lenses are more useful reducing the risk of squeezing an injured eye. Scleral depression may increase the risk of intraocular bleeding and should only be performed once ocular rupture has been discarded.

Anterior, central and posterior vitreous examination should be performed and the presence of any hemorrhage or vitreous opacity recorded. The location and size of the opacities should be recorded, as well as the presence of posterior vitreous detachment. Pigment clusters may appear floating in the peripheral or anterior vitreous following detachment of the vitreous base from the pars plana.

Fig. 24.3: Ultrasonography A and B scan reveals a marked choroidal hemorrhage with vitreous blood

Fig. 24.4: Grade I vitreous hemorrhage

Management of Traumatic Hemorrhages to the Posterior Segment

 

141

Pathogenesis

 

penetration may cause visual impairment. They include

 

the toxic effects of IOFB, such as copper and iron,

 

Blunt trauma may cause damage to the eye by three

 

and the introduction of bacteria and fungi with

 

different mechanisms: coup, contrecoup and ocular

consequent infectious endophthalmitis. Retained lens

 

compression. Coup refers to local damage at the site

material and blood and the incarceration of vitreous

 

of impact, whereas contrecoup refers to injuries at the

and uvea causes chronic inflammation that may play

 

opposite side of the eye caused by shock waves that

an important role in the stimulation of intraocular

 

traverse the eyeball with foci of tissue damage along

fibrocellular proliferation. At a later stage, blood and

 

 

the path of the shock waves, especially at interfaces

lens material in the presence of large scleral wounds

 

of tissues of different density.

may induce formation of fibrocellular proliferation

 

The ocular compression mechanism is determined

which, upon contraction may cause traction retinal

 

by the inextensibility of the eyeball and the

detachment, retinal breaks, rhegmatogenous retinal

 

incompressibility of intraocular fluids so that when the

 

detachments, proliferative vitreoretinopathy, cyclitic

 

eye is compressed along its anterior-posterior axis, it

 

membranes, ciliary body detachments, hypotony, and

 

expands in its equatorial plane causing severe traction

 

phthisis bulbi.

 

at the vitreous base. Ocular compression may cause

 

 

 

 

 

scleral rupture even in eyes which have not undergone

 

 

 

 

previous surgery. In these cases the two most common

Classification

 

 

locations for scleral rupture are at the limbus and

 

 

parallel to the muscle insertions between the insertion

Even though these lesions seldom appear isolated,

 

and the equator. The hallmarks of scleral rupture are

hemorrhages to the posterior segment may be classi-

 

severe reduction in visual acuity, an afferent pupillary

fied for a didactic purpose as:

 

defect, hypotony, abnormally deep anterior chamber,

Vitreous hemorrhages

 

decreased ocular ductions, severe subconjunctival

Retrohyaloidal hemorrhages

 

edema, hyphema, and vitreous hemorrhage. Scleral

Retinal hemorrhages

 

rupture can rarely be confirmed by ophthalmoscopy

Choroidal hemorrhages

 

because severe vitreous hemorrhage and/or hyphema

Papillary and peripapillary hemorrhages

 

nearly always accompany scleral rupture. Ultrasono-

Hemorrhages associated with indirect trauma

 

graphy and computed tomographic scanning may

 

 

 

 

show a shrunken globe, retinal detachment, partial or

VITREOUS HEMORRHAGES

 

complete posterior vitreous detachment and

 

The presence of vitreous hemorrhage has been

 

vitreoretinal adherences. The visual prognosis of

 

associated with retinal detachment and surgical removal

 

ruptured globes is usually very poor.

 

of the blood seems to reduce the frequency of retinal

 

The aetiologies and the mechanisms of damage of

 

detachment.3 The role of the presence and manage-

 

penetrating injuries are highly variable and cause a

 

ment of vitreous hemorrhage has been reported by

 

wide spectrum of acute structural alterations and

 

several series,4, 5 as well as the role of the quantification

 

secondary complications.

 

Penetration of the eye by relatively blunt objects

of the hemorrhage. Brinton et al reported functional

 

causes compression of the globe resulting in

recovery in 48% of the eyes presenting moderate to

 

iridodialysis, subluxation and dislocation of the lens,

severe vitreous hemorrhage vs 67% of the eyes with

 

traumatic cataract, choroidal rupture, retinal breaks

mild or no vitreous hemorrhage.6

 

at the vitreous base borders and vitreous detachment.

 

Blood proteins may be involved in vitreous proli-

 

Ruptures of the uvea produce anterior chamber,

feration mediated by hemorrhages. Fibronectin is a

 

choroidal, subretinal, and vitreous hemorrhage.

high molecular weight glycoprotein with a chemotactic

 

Massive blunt trauma causes corneal and scleral

action on retinal pigment epithelium (RPE), fibroblasts

 

ruptures and may avulse the optic nerve.

and giant cells and mediates in the interaction between

 

Penetrating objects cause lacerations of the cornea,

collagen and the RPE. Fibronectin has been detected

 

iris, lens, sclera, ciliary body, choroid, retina, and optic

in epiretinal membranes in human eyes following

 

nerve, usually combined with anterior chamber,

retinal detachment repair after ocular trauma.7, 8 Platelet

 

choroidal, subretinal, and vitreous hemorrhages and

derived growth factor (PDGF), complement and

 

occasional prolapse and incarceration of the lens, uvea,

interleukins also induce intravitreal fibrosis.

 

retina, and vitreous. Cleary and Ryan reported on the

 

It is necessary to quantify the amount of vitreous

 

increased frequency of retinal detachment following

hemorrhage. One accepted classification for this

 

penetrating ocular trauma associated with vitreous

quantification was proposed at the Vitrase for Vitreous

 

hemorrhage.3 The secondary complications of ocular

Hemorrhage study9 as Grade I when retinal detail is

 

 

 

 

 

 

 

142

 

Clinical Diagnosis and Management of Ocular Trauma

 

 

 

 

 

Fig. 24.5: Grade 3 vitreous hemorrhage

visible with some hemorrhage present and laser photocoagulations is possible; Grade 2 with large retinal vessels visible but central retinal is not visible enough to perform adequate posterior laser treatment; Grade 3 with red reflex and no retinal vessels are seen behind the equator; and Grade 4 with no red reflex.

The symptoms of vitreous hemorrhage are visual acuity loss, perception of mobile dark spots in the visual field. Associated signs are visualization of erythrocytes floating in the anterior vitreous behind the lens with dilated pupil. Intense vitreous hemorrhage may lead to loss of pupillary reflex and blurring of retinal details (Fig. 24.5). Retinal tear and detachment should be disclosed in all cases of traumatic vitreous hemorrhage. B scan ultrasonography is a useful tool to perform examination of vitreoretinal adherences.

Vitreous hemorrhages may appear secondary to blunt trauma following scleral rupture, vitreous detachment, tears in the iris, ciliary body, choroid, or retina. We should assume that a retinal break is present until proved otherwise. Blood from choroidal ruptures accumulates beneath the neurosensory retina passing through the retina into the vitreous cavity.

Vitrectomy is indicated for vitreous hemorrhage caused by ocular contusion when a retinal detachment is suspected because of sudden additional loss of vision, when a retinal detachment is detected through a window in the hemorrhage, when a large retinal break or retinal detachment is diagnosed by ultrasound, or when there is no improvement after a reasonable period of observation.10-13

RETROHYALOIDAL HEMORRHAGES

Retrohyaloidal hemorrhages usually appear following incomplete posterior vitreous detachment as a result

Fig. 24.6: Retrohyaloidal hemorrhage

of vitreoretinal traction or transit of subretinal blood (Fig. 24.6). Retrohyaloidal or preretinal hemorrhages are usually thick, masking retinal vessels and may show a characteristic boat-shape with a superior horizontal level. Even though retrohyaloidal blood tends to disappear spontaneously, treatment has been proposed in order to reduce the contact of blood with the retina and decrease its toxic effect.14-16

INTRARETINAL HEMORRHAGES

Intraretinal hemorrhages may appear under different circumstances associated with ocular or distant trauma. The location of the blood will determine the presence of symptoms. Extrafoveal blood is usually asymptomatic. Juxtafoveal and subfoveal blood may present as paracentral or central scotomata.

Subretinal blood is toxic for the retina and the RPE17 and thick hemorrhages worsen visual prognosis. Additionally, it is considered that the presence of hemorrhage limits the closure of the retinal or choroidal tear.

The image of retinal hemorrhages may vary depending on how deep the retina is affected. Blood affecting the retinal nerve fibre layer appears as flame shaped hemorrhages, whereas hemorrhages affecting the nuclear layers appear as irregular shaped spots (Figs 24.7 to 24.9). Retinal hemorrhages usually do not mask retinal vessels.

CHOROIDAL HEMORRHAGES

Posterior choroidal ruptures are probably caused by anterior-posterior compression and equatorial expansion. Blunt trauma may produce hemorrhage into the choroid secondary to Bruch’s membrane rupture and tear of the overlying RPE and underlying choriocapillaris. Patients with angioid streaks and other conditions known to be associated with an inelastic and fragile Bruch’s membrane are especially vulnerable to choroidal rupture.

Management of Traumatic Hemorrhages to the Posterior Segment

 

143

 

Choroidal hemorrhages may vary in intensity from

 

 

small subretinal hemorrhages associated with Bruch’s

 

 

membrane ruptures to huge suprachoroidal

 

 

hemorrhages that may complicate corneal or scleral

 

 

lacerations leading to expulsive hemorrhages.

 

 

Choroidal hemorrhages may be massive leading

 

 

to ocular hypotony and choroidal detachment, usually

 

 

associated with vitreous hemorrhage or mask subretinal

 

 

 

 

hemorrhages.18

 

 

Direct choroidal ruptures are uncommon and

 

 

usually anterior and oriented parallel to the ora. Indirect

 

 

ruptures are more common and tend to occur away

 

 

from the site of impact. A choroidal rupture may be

 

 

initially obscured by a subretinal hemorrhage caused

 

Fig. 24.7: Submacular hemorrhage

by tearing of the choriocapillaris. Later, after the blood

 

has resorbed, a white curvilinear streak concentric to

 

causing central scotoma

the optic disc is seen. Only rarely is a rupture oriented

 

 

radially with respect to the optic disc. Most are temporal

 

 

to the disc and single, although nasal and multiple

 

 

ruptures can also occur (Fig. 24.10). Typical small

 

 

choroidal hemorrhages are rounded, dark red-blue

 

 

and frequently take many weeks to resorb and may

 

 

leave areas of pigment alteration.

 

 

Visual prognosis is generally good unless the

 

 

choroidal rupture is under the foveola, or an associated

 

 

subretinal hemorrhage extends under the foveola).

 

 

The overlying nerve fiber layer is almost never torn.

 

 

Therefore, a rupture can be located between the disc

 

 

and the macula and yet not affect the visual acuity.

 

 

Choroidal ruptures can, months to years later, be

 

 

complicated by the development of a choroidal

 

 

neovascular membrane, with serous or hemorrhagic

 

 

retinal detachment and loss of central vision.19 In these

 

Fig. 24.8: Spontaneous resorption of

cases photodynamic therapy20 and more recently

 

intravitreal antiangiogenic therapy may be useful.

 

submacular hemorrhage

 

 

 

 

PAPILLARYAND PERIPAPILLARY

 

 

HEMORRHAGES

 

 

Papillary and peripapillary hemorrhages may appear

 

 

following optic nerve damage by blunt trauma. Possible

 

Fig. 24.9: Complete spontaneous resorption of macular

 

hemorrhage. Visual acuity was 20/20

Fig. 24.10: Choroidal ruptures

144

 

Clinical Diagnosis and Management of Ocular Trauma

 

mechanisms include compression by intrasheath

and venules. The aetiology of the white retinal

 

 

 

 

hemorrhage and oedema and direct shock-wave

lesions resulted is controversial. Extravasated lymph

 

 

trauma to the nerve fibers. The management involves

from retinal vessels, reflux venous shock waves,

 

 

high-dose intravenous steroids, especially if they can

arteriolar and fat emboli and blood product emboli

 

 

be started within 8 hours, surgical decompression of

formed after complement activation have been

 

 

optic nerve sheath hematoma and neurosurgical

proposed. Clinically, the retinal lesions resolve over

 

 

decompression of the optic canal. Avulsion of the optic

a period of weeks to a few months followed

 

 

nerve may be accompanied by severe damage to other

occasionally by pigment migration and optic

 

 

 

ocular tissues or be the sole manifestation of apparently

atrophy. Visual acuity may return to normal or near

 

 

minor direct trauma.

normal.

 

 

 

• Valsalva retinopathy is characterized by preretinal

 

 

HEMORRHAGE ASSOCIATED WITH

(retrohyaloidal) hemorrhages in the macular area,

 

 

INDIRECT TRAUMA

and is secondary to Valsalva manoeuvres associated

 

 

• Shaken baby syndrome may be associated in one

with vomiting, coughing. Visual function usually

 

 

returns to normal spontaneously. Hemorrhages

 

 

third of the cases with ocular manifestations, above

 

 

located on the macula may present as decreased

 

 

all subconjunctival and retinal hemorrhages.

 

 

visual acuity, but the syndrome is usually

 

 

Intraocular hemorrhages are considered to be a

 

 

asymptomatic.

 

 

predictive of intracranial bleeding and the severity

 

 

• Retinitis sclopetaria is defined by the rupture of the

 

 

of the latter is related to that of the neurological

 

 

choroid or retina caused by shock waves generated

 

 

lesion. Funduscopic examination usually reveals

 

 

by passage of a high-velocity missile through the

 

 

retinal hemorrhages, perimacular folds, cotton

 

 

orbit without directly striking the eye. Initial clinical

 

 

wool spots, optic disk edema, and venous stasis.

 

 

manifestations may be a subretinal or vitreous

 

 

Less frequently, vitreous hemorrhages, retinal

 

 

hemorrhage with decreased visual acuity. As the

 

 

detachment, retinoschisis and chorioretinal atrophy

 

 

blood clears, breaks in the Bruch’s membrane and

 

 

are seen.

 

 

in the choriocapillaris are frequently seen as well

 

 

• Terson syndrome is characterised by a preretinal

 

 

as fibrous tissue proliferation into the eye. Retinal

 

 

hemorrhage associated with subarachnoidal

 

 

detachment rarely occurs because of fibrous tissue

 

 

hemorrhage. The intraocular hemorrhage has been

 

 

proliferation binding the retina to the choroid.

 

 

classically attributed to transit of blood through the

 

 

 

 

 

optic nerve sheaths. Presently, intraocular blood

 

 

 

is considered to be secondary to rupture of

Medical Management

 

 

peripapillary and epipapillary capillaries caused by

 

 

Intravitreal ovine hyaluronidase has been used to

 

 

increased intracranial pressure. Ophthalmoscopy

 

 

usually reveals a preretinal hemorrhage in the

promote resorption of intravitreous blood. 1125

 

 

peripapillary and macular area located exterior to

patients with vitreous hemorrhage and visual acuity

 

 

the inner limiting membrane (ILM). However, blood

worse than 20/200 during more than one month were

 

 

may go through the ILM and appear as a vitreous

randomized 55 IU or 75 IU ovine hyaluronidase or

 

 

hemorrhage. The most frequent complication of

saline. Clearance of blood was achieved at months

 

 

Terson syndrome is the appearance of epiretinal

1, 2 and 3 in 13%, 26%, and 33% of patients injected

 

 

membranes.

with 55 IU compared with 6%, 16%, and 26% of

 

 

• Purtscher retinopathy is a haemorrhagic vasculo-

saline-treated patients.9

 

 

pathy characterized by multiple retinal

Tissueplasminogen activator has been used in

 

 

hemorrhages, areas of retinal pallor around the

combination with surgery,21 with intravitreal injection

 

 

optic disk and decreased visual acuity. A serous

of gas (in patients with traumatic choroidal rupture)22

 

 

macular detachment may appear associated with

or as isolated therapy23 with favorable results,

 

 

vascular dilation and tortuosity and optic disk

improving vision and occasionally deferring the need

 

 

oedema. Purtscher retinopathy is secondary to

for vitrectomy. These procedures have been used in

 

 

blunt head trauma and thoracic compression. This

cases of subfoveal21, 22, 24 and retrohyaloidal23 thick

 

 

syndrome is usually bilateral and the symptoms

hemorrhages. After a mean follow-up of 10.5 months

 

 

usually appear 48 hours after the trauma. The

final visual acuity improved by 2 lines or greater in

 

 

peripheral retina is commonly spared. Fluorescein

10 (67%) of 15 eyes and measured 20/80 or better

 

 

angiography can reveal focal areas of arteriolar

in 6 (40%) of 15 eyes in on series with complications

 

 

obstruction, capillary nonperfusion, disc edema,

including breakthrough vitreous hemorrhage in three

 

 

and dye leakage from retinal arterioles, capillaries,

eyes and endophthalmitis in one eye.24 However the

 

 

 

 

Management of Traumatic Hemorrhages to the Posterior Segment

 

145

reported series were short and randomized clinical trials

because of the removal of nonclearing vitreous

 

are missing.

hemorrhage. Vitreoretinal surgery is also of great value

 

Krypton, Argon and Nd-YAG laser treatment have

in the repair of penetrating injuries with retained

 

been performed in patients with intraocular

nonmagnetic foreign bodies and selected cases of

 

hemorrhages to improve visual acuity by removing

magnetic IOFB that are difficult or dangerous to extract

 

preretinal blood permitting its transit to the vitreous

with an electromagnet and in the management of eyes

 

cavity. Dellaporta reported on the use of argon laser

with posttraumatic endophthalmitis. Secondary

 

retinotomies to the posterior pole of one patient with

complications, including traction and rhegmatogenous

 

 

thick submacular hemorrhage permitting escape of

retinal detachments, are minimized by the timely

 

subretinal blood into the vitreous.25 A less aggressive

removal of hemorrhage, disrupted lens, and damaged

 

approach using Nd-YAG laser was tried on patients

vitreous.

 

with retrohyaloidal hemorrhages.14 Visual acuity in all

Additionally, the presence of vitreous hemorrhage,

 

cases before laser treatment was hand movement.

as well as delay in IOFB removal, preoperative retinal

 

After laser treatment, the hemorrhage instantly drained

detachment and primary surgical repair combined with

 

into the vitreous cavity, resulting in rapid improvement

the IOFB removal have been significantly associated

 

of vision. After a mean follow-up of 26.3 months no

with the postoperative retinal detachment and a poorer

 

retinal damage or rebleeding occurred due to the laser

visual outcome.27

 

treatment, and vitrectomy was not required in any

The aim of vitrectomy is to remove vitreous

 

eye. However most of the reports lack long term

opacities. A standard three-port 25 or 23 G vitrectomy

 

follow-up. Ulbig et al reported on the the effects of

technique is preferred for nonclearing vitreous

 

drainage of premacular subhyaloid hemorrhage into

hemorrhage. Initially, a central core of opaque vitreous

 

the vitreous with an Nd-YAG laser in a large series of

is removed, beginning sufficiently close to the lens that

 

21 patients with a circumscribed premacular subhyaloid

the tips of the cutter and endoilluminator can be

 

hemorrhage of various causes with long-term follow-

visualized, while maintaining the cutting orifice of the

 

up. Even though in 16 eyes visual acuity improved

probe under visual control in order to be able to

 

within 1 month, four eyes had persistent, dense,

examine the aspirated material. The excision is

 

nonclearing vitreous opacity for at least 3 months and

progressively carried posteriorly until the anticipated

 

finally required vitrectomy. One case with clotted

plane of the posterior hyaloid is approached. A small

 

hemorrhage did not drain into the vitreous. Final visual

opening is made in the detached posterior hyaloid,

 

outcome was determined by the underlying diagnosis,

through which unclotted blood is aspirated by use of

 

such as Valsalva retinopathy (7 eyes), diabetic

active suction from a soft-tipped cannula. Once the

 

retinopathy (7 eyes), branch retinal vein occlusion (4

retina has been visualized, it is best to remove as much

 

eyes), and retinal macroaneurysm, Terson syndrome,

retrohyaloidal blood as possible to prevent dispersion

 

or blood dyscrasia (1 eye each). Eyes with Valsalva

into the vitreous cavity with consequent loss of visual

 

retinopathy fared the best. Complications included a

control.

 

macular hole in 1 eye and a retinal detachment from

Recently opacified vitreous may be red, yellow or

 

a retinal break in a myopic patient. The authors

mild green whereas old blood looks brown and dirty.

 

concluded that drainage of premacular subhyaloid

While removing dense haemorrhagic vitreous we may

 

hemorrhage into the vitreous with an Nd-YAG laser

find areas with old liquefied blood that may obscure

 

is a viable treatment alternative for eyes with recent

visualization of the retina. In such cases we should bring

 

bleeding, but the risks and benefits have to be weighed

the probe forward in order to be able to visualize its

 

in a randomized trial and compared with those of

tip until visualization of the vitreous cavity has become

 

deferral of treatment or primary vitrectomy.

clearer. Actively bleeding foci in the iris, ciliary body

 

Nd-YAG laser has been reported to complete

or retina are treated by raising the intraocular pressure

 

vitreous hemorrhages in order to achieve vitreolysis

and using endodiathermy if necessary. If visualization

 

and permit spontaneous resorption of the vitreous

of the bleeding foci is not possible, a fluid-air

 

blood.26

interchange can be performed to permit

 

SURGICAL MANAGEMENT

endodiathermy and the eye is refilled with liquid in

 

order to proceed with vitrectomy. Fresh blood tends

 

Vitreoretinal surgery is helpful in the management of

to clot and firmly adhere to the retina, whereas old

 

subluxation or dislocation of the lens, vitreous

blood liquefies in a few days and is more easily

 

hemorrhage, and retinal detachment caused by ocular

aspirated.

 

trauma, permitting identification and treatment of

Significant vitreous hemorrhages occurring weeks

 

retinal breaks created at the time of blunt injuries

before surgery are usually associated with sponta-