Retrobulbar Haemorrhage

Dr Rudraprasad Chakraborty1st Year PG Student

Department of Oral & Maxillofacial SurgeryRama Dental College Hospital And Research Centre

Kanpur, UP15/04/15

Inclusions

• Introduction

• Etiology

• Relevant Anatomy

• Clinical Features

• Treatment

Introduction

Massive retrobulbar hemorrhage in the posteriorregion of the muscle cone, triggered by vesseldisruption, leads to progressive exophthalmus withconcurrent pupil dilatation, reduced vision andincreased intraocular pressure.

(Ord 1981; Ord and El Altar 1982)

Retrobulbar hemorrhage may occur spontaneouslyor as a result of trauma, peribulbar or retrobulbarinjections, or surgery.

A Retrobulbar hemorrhage is a space-occupyinglesion of the orbit leading to forward displacementof these structures as intraorbital volume andpressure increases.

Neurological damage is caused by direct compression,by bony fragments or by an indirect compression ofthe nerves caused by hemorrhage

(Rowe and Williams 1985)

Etiology

Spontaneous :Orbital vascular abnormalityUncontrolled hypertensionCoagulopathySepticemiaVigorous activity

Post Traumatic :Orbital FracturesHigh Level Midfacial FractureLe Fort III Fracture

Post Anaesthesia :Retrobulbar injectionPeribulbar injectionSub-Tenon’s injection(episcleral )

Post Operative :

Facial /Orbital Fracture, RepairBlepheroplastyEndoscopic Sinus Surgery

Other surgeries: Strabismus surgery, Glaucoma valve implant,

Dacryocystectomy, Coil embolization of Dural Sinus Fistula, ICA Aneurysm Repair, Third Molar Extraction

Etiology

Spontaneous Retrobulbar Hemorrhage

Rare; Largest Report Describes 115 cases over 24 years of Period

Orbital Vascular Anomaly : Orbital varix, LymphangiomaArterio-venous malformation

Underlying Systemic Abnormality :CoagulopathyUncontrolled hypertensionSepticemia

Weightlifting,Scuba Diving,

SneezingOther maneuvers that increase venous pressure

Occasionally in sickle cell patients due to orbital bone marrow infarctions

May Lead to Subperiosteal Haemorrhage

Post Anaesthetic

Retrobulbar Injection

Retrobulbar local anesthetic administration can cause bleeding into the buccal fat if the needle extends through the inferior orbital fissure.

Peribulbar Injection

Sub-Tenon ( Episcleral )Injection

Post-Traumatic

A common presumed etiology of post-traumatic vision loss

Usually associated with orbital fractures but may occur without a fracture

According to two large retrospective series, the incidence of retrobulbar hemorrhage in patients with orbital fractures is 0.45 -0.6%.

R

( A ) A periorbital hematoma. ( B ) Proptosis

( C ) A coronal CT scan demonstrating an orbital floor fracture and an inferior orbital hematoma.

( D ) A sagittal CT scan demonstrating proptosis, an orbital floor fracture and a subperiosteal hematoma extending to the orbital apex

Anatomy of Orbit

Volume of around 30cc

Except for numerous small foramina, the bony orbit is a continuous structure, open only anteriorly.

Bones contributing to make Orbital Cavity : Frontal, Lacrimal, Ethmoid, Sphenoid Lesser and Greater Wings, Maxilla, Zygoma.

Nerves and Muscles in Orbit

Right Orbit Left Orbit

Structures Passing Through The SOF

The Blood Supply

The Major Blood Supply of Orbit

The ophthalmic artery contributes maximum

The central retinal artery

Penetrates the ventral dura to enter the opticnerve approximately 18.6 mm from the opticforamen and 8 mm posterior to the globe.

The optic nerve head is supplied by the

posterior ciliary arteries.

Anterior and posterior ethmoidal foramina transmit the ethmoidal branches of the ophthalmic artery.

The anterior and posterior ethmoidal foramina are located 24 and 36 mm posterior to the anterior lacrimal crest, respectively, along the frontoethmoidalsutureThe posterior ethmoidal foramen is approximately 6 mm anterior to the optic foramen

A. Opthalmic ArteryB. Lacrimal ArteryC. Medial Division of Opthalmic arteryE. Recurrent Tentorial BranchF. Recurrent Meningeal BranchG. Anterior Ethmoidal arteryH. Posterior Ethmoidal arteryI. Antero medial branchJ. Opthalmic branch of middle mengial arteryK. Anterior Deep Temporal Branches of IMAX L. Muscular M. TransosseousN. Inferior Branch of Opthalmic arteryO. Distal Inferior Br of IMAXP. Angular br facial art

The Venous Drainage

Superior Orbital VeinInferior Orbital VeinCentral Retinal Vein

Soft Tissue Considerations

The orbit is lined by periosteum thatattaches firmly at the arcus marginalis,foramina, fissures, suture lines and theposterior lacrimal crest. Between thesefirm attachments the periosteum isloosely adherent, creating a potentialspace for accumulation of blood

The characteristic CT appearance of anacute subperiosteal hematoma is abroad-based extraconal mass that abutsthe bony orbit and displaces orbitalcontents centrally. Radiographically, themass is high-density, sharply defined,homogeneous and nonenhancing

All mechanisms relate to increased intraorbital pressure and volume:

Ischemic optic neuropathy from compression or stretching of the small nutrient vessels

Direct compressive optic neuropathy

Central retinal artery occlusion

Retinal vascular ischemia

Resulting In :

The source of bleeding depends upon the inciting event.

During blepharoplasty with removal of fat :

Bleeding may occur from direct trauma to the vessels of the anterior fat pads, tearing of deep orbital vessels from traction on orbital fat

after operations involving the orbital floor, possibly due to damage to the infraorbitalartery

The orbital perforating branch of theinfraorbital artery is rarely mentioned inanatomy texts and is especially susceptibleto damage during operations involving theorbital floor.

Rubin et al

After endoscopic sinussurgery occurs byviolation of the laminapapyracea portion of theethmoid bone duringethmoidectomy.

Sign and symptoms

Massive retrobulbar hemorrhage in the posterior region of the muscle cone, triggered by vessel disruption, leads to progressive exophthalmus with concurrent pupil dilatation, reduced vision and increased intraocular pressure.

(Ord 1981; Ord and El Altar 1982)

The following are typical signs of an intraorbital hemorrhage with or without orbital fracture (Doden and Schnaudigel 1978):

Livid (cyanotic) swollen eyelids with narrow spontaneous palpebral lid opening, which may be opened actively, though passive opening is only slight

Protrusion of the globe (up to 10 mm) with increasing active and passive immobility

Ischemia of the optic disk and retina with clearly reduced vision or amaurosis

Increased intra-ocular pressure more than 80 mmHg

The most common symptoms :pain : Severe and Steady Lancinating Qualitypressure, loss of vision, diplopia, nausea and vomiting

In addition

visual flashes, amaurosis fugax or hemianopsia

Imaging :

May be indicated in unusual cases of retrobulbar hemorrhage or in cases associated with trauma.

MRI scans provide better visualization of the soft tissues of the orbit

Even Ultra Sonography may give an instant Diagnosis

Owing to the emergent nature of retrobulbar hemorrhage, imaging studies to confirm the diagnosis are not indicated and will delay treatment

CT scans are preferred because of their fast acquisition time and better visualization of the bony anatomy

Therapeutic Options

Once the diagnosis is made, therapy should begin immediately.

Optic nerve damage was proportional to the duration of occlusion of CRA

Occlusion of 105 min or longer produced irreversible optic nerve damage

Occlusion greater that 240 min produced near total optic nerve atrophy

Treatment is aimed at lowering intraorbital or intraocular pressure and protecting the optic nerve from damage

Rapid surgical intervention remains the mainstay of treatment

Medical Treatment

The medical treatments for retrobulbar hemorrhage are controversial.

Medical treatment should not delay surgical treatment

Medical treatment options include :

Oxygen therapy………(95% O2, 5% CO2) may decrease the ischemic insult by dilating

intraocular vessels.

Mannitol 20% IV ……. The hyperosmotic agent, rapid IV infusion of 1.5 - 2 g/kg over

30 min, with the first 12.5 g over the first 3 min.

Acetazolamide …….. The carbonic anhydrase inhibitor, 500 mg IV, Also lowers

intraocular pressure

Steroids ……. Methylprednisolone, 100 mg, decrease inflammation and edema and

provide some neuroprotection to the optic nerve by stabilizing cell membranes

Topical β-blockers ……. Decrease intraocular pressure by lowering aqueous humor

secretion.

Therapies aimed primarly at reducing intraocular pressure, such asacetazolamide and topical β-blockers, do not address the elevated orbitalpressure and do not improve the blood supply to the proximal optic nerve.

Surgical Treatment

Postoperative retrobulbar hemorrhage

Dressings and sutures should be removed at bedside.

The wound opened and explored

Decompress the orbit

Locate and cauterize the offending bleeding vessel

Immediate Postoperative Period

Patient should be transported back to the operating room

Perform exploration, evacuation of the hematoma and control of hemostasis

Late Postoperative Period

Hemorrhage is not postoperative in etiology

Relieve orbital compression primarily

Can often be achieved via a lateral canthotomy and inferior cantholysis

If further decompression is needed, a lateral anterior orbitotomy may be required to break the fibrous septa of the orbital fat compartments

Pterional orbital decompression

Korinth et al. reported a series of 16 cases

A neurosurgical approach

Removal of the bony lateral and superolateralorbital walls to maximally decompress the orbit

Visualize and treat any additional abnormalities, such as focal hematomas or lymphangiomas

The patient must be closely followed with serial examinations

Pupillary light reflexesVisual acuityIntraocular pressureFundoscopy.

The head of the bed may be elevated to decrease arterial pressure.

The lateral canthotomy and cantholysis may be repaired days later to allow for further drainage in the event of additional hemorrhage or it may be allowed to heal spontaneously

Referrence Books

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