RETROBULBAR HEMORRHAGE

OUTLINE
● Introduction
● Anatomy
● Etiology
● Pathophysiology
● RETROBULBAR HEMORRHAGE: Clinical Features
● Diagnostics
● Management
● Journal
Retrobulbar Hemorrhage is an
ocular emergency resulting
from arterial bleeding in the
orbital cavity behind the eye.
Patel AD, Alford M, Carter KD. Persistent visual loss following retrobulbar hemorrhage. Can J
Ophthalmol. 2002;37(1):34–6. 
Retrobulbar Hemorrhage is an
ocular emergency resulting
from arterial bleeding in the
orbital cavity behind the eye.
Patel AD, Alford M, Carter KD. Persistent visual loss following retrobulbar hemorrhage. Can J
Ophthalmol. 2002;37(1):34–6. 
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Etiology
• Trauma resulting in orbital fractures
• Eyelid surgery
• Lower blepharoplasty
• Retrobulbar anesthesia
• Endoscopic surgery
• Dental surgery
• Orbital tumors – including vascular (cavernous hemangioma,
hemangiopericytomas, orbital varix, lymphangioma, or arteriovenous
malformation)
• Severe hypertension
• Spontaneous
• Following a Valsalva maneuver
• Following a sneeze
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 Increase intraorbital pressure

Exceeds CRA Venous pooling

pressure
Pressure on
CRA inclusion tissues
increases
Retinal damage
begins Arterial flow stops
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 Pathophysiology

● Venous pooling is observed due to increasing intraorbital pressure after retrobulbar

hemorrhage leading to a further increase in the orbital pressure. As the pressure on
the tissues increase, arterial flow will stop.
● If the vasa nervorum is affected, optical nerve involvement is expected as well.
● When the orbital pressure exceeds the CRA pressure, retina begins to be affected
● Basically, with an increase in the orbital pressure and decrease in perfusion, damage
starts and pathology establishes.
● Further, the optical nerve may be damaged due to compression and tension. Visual loss
generally develops as a result of the CRA occlusion, direct compression to the optical
nerve or to the blood vessels feeding the optical nerve.
● Visual loss may also develop after blunt ocular trauma due to retinal detachment,
hyphema, rupture of the globe and vitreous hemorrhage. Although the mechanism of
visual loss is not clear, recovery of vision after decompression suggests that ischemia
and reperfusion lie under the pathogenesis of this condition.
 DIAGNOSTICS Central
vein
Funduscopy occlusion
○ edema of the optic
disc or retina or
retinal venous
congestion Central
○ venous retinal
insufficiency artery
occlusion

The Retinal Atlas 13

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 DIAGNOSTICS

Ophthalmic retinal artery optic nerve atrophy, severe

occlusion with localized vascular attenuation, and diffuse
hemorrhages retinal pigment mottling
The Retinal Atlas 14
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 DIAGNOSTICS

CT scan
○ if clinical findings are inconclusive
○ determine the nature and degree of optic nerve injury.

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 MANAGEMENT

Retrobulbar Hemorrhage
● loss of vision is irreversible within 60-100 minutes
after the onset of ischemia
● IOP >40 mm Hg - risk of visual compromise and
demands immediate treatment
● Decompression is indicated

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 MANAGEMENT

● Treatment requires prompt recognition followed by

measures to decrease pressure on the globe
● Prompt control of pain & blood pressure elevation
● application of light intermittent pressure on the orbit

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 MANAGEMENT

IOP-lowering agents:

1. IV carbonic anhydrase inhibitors

○ inhibit the activity of CA in the ciliary processes of the
eye thus decreasing aqueous humor formation
○ Treatment for glaucoma
○ Ex. Acetazolamide

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 MANAGEMENT
2. Topical beta-blocker
○ Ex. Timolol, betaxolol, levobunolol, metipranolol, and
carteolol

3. Alpha agonists
○ Ex. Clonidine, Apraclonidine, Brimonidine
○ no effects on cardiopulmonary function

4. Mannitol
● 1.5-2 g/kg intravenously (IV) infused over 30-60
minutes
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 MANAGEMENT

Lateral canthotomy
○ a temporizing, vision-saving measure before definitive
decompression.

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 Fig. 61.13
A. Lateral canthotomy

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 B.
1. Preoperative view of orbit.
2. Incision for lateral
canthotomy.
3. Identification and incision
of inferior canthal tendon,
completing cantholysis.
4. View after lateral
canthotomy and inferior
cantholysis, creating
maximal immediate
decompression by allowing
eyeball and orbital contents
to move anteriorly.

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Definitive Treatment

Orbital decompression
● removes the bones and sometimes the fat in the orbit
(socket) of the eye
● prevents further vision loss.
● Goal: To create more space in the eye socket to allow the
eyes to move back to a normal position.

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Journal Presentation

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Methods

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Methods

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Transcutaneous Transseptal Orbital Decompression Technique

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Lateral cantothomy

● Procedure to release an orbital compartment syndrome caused by an increased

pressure the pushes the eye forward usually by a retrobulbar hematoma
● 40 is the intraocular pressure wherein we need to do this procedure inorder to
release the compartment syndrome.
● First step is to numb the area by injecting lidocaine and epinephrine
● Clamp for 1 min the lateral cantus inoder to devascularize the area
● Cut the lateral canthus towards the orbital rim laterally
● Cut the lateral vathal ligament which has a superior and inferior crus. Cut the inferior
crus first which may sometimes release the pressure on its won but if not cut the
superior crus
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● Recheck intraocular pressure
Results

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Results

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Conclusion

● Acute RBH can be classified into RBH classes I to III,

providing a simple tool for rapid identification and treatment
of this rare condition.
● Elderly women and severely injured patients are at a higher
risk of developing acute RBH.
● Visual acuity should be monitored for 24 hour in RBH class I,
orbital trauma, or after surgical procedures.
● RBH class II and class III with either decreasing visual acuity
or/and typical radiological features should be treated
immediately via surgical decompression.
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Conclusion

● Electrophysiological evaluation (VEP or ERG) can provide

diagnostic information for a therapeutic decision in severely
injured patients or in those with compromised clinical tests.
● Conservative therapy should be considered an absolute
exception (patient’s refusal).
● Since objective anesthesiological and surgical
contraindications exist only in cases of pulsating
exophthalmos, transcutaneous transseptal orbital
decompression in combination with the methylprednisolone
megadose regimen provides a fast and efficient approach
for treating acute RBH. 35