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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
Thank You