324 OPTIC FORAMEN FRACTURES

324FracturesCHAPTERForamen Optic •

Orbit • 29 SECTION

Abscess325 CHAPTERand Cellulitis Orbital •

Orbit • 29 SECTION

●Physical examination:

●Fever;

●Constitutional symptoms (nausea and vomiting, lethargy). More common in children.

●Laboratory:

●Leukocytosis;

●Positive blood cultures (more common in children).

●Computed tomography of orbits:

●Subperiosteal abscess (direct coronal views often delineate best);

●Adjacent sinus disease, particularly ethmoidal.

●Fungal cellulites:

●May require tissue biopsy to confirm diagnosis (cultures often are negative).

Differential diagnosis

●Neoplasms:

●Rhabdomyosarcoma;

●Lymphoma;

●Leukemia;

●Metastastic;

●Retinoblastoma.

●Thyroid-related ophthalmopathy.

●Orbital inflammation:

●Orbital pseudotumor;

●Orbital myositis;

●Wegener’s granulomatosis.

●Arteriovenous malformation.

●Carotid-cavernous sinus fistula.

TREATMENT

●Cultures:

●Blood;

●Conjunctiva;

●Discharge.

●Hospitalization:

●Intravenous antibiotics for 7 to 10 days;

●Outpatient oral antibiotics for 5 to 7 days; if concomitant chronic sinusitis or osteomyelitis, may require 3 or more weeks of antibiotics and infectious disease or otolaryngology consultation.

●Infants:

●Ceftriaxone 50 mg/kg IV every 12 to 24 hours (no more than 4 g/day).

●Children:

●Nafcillin or oxacillin 12.5 mg/kg IV every 6 hours and cefuroxime 25 to 33 mg/kg IV every 8 hours (no more than 4.5 g/day);

●Penicillin or cephalosporin allergy alternatives: chloramphenicol 12.5 to 25 mg/kg IV every 6 hours (hematologic monitoring).

●Adults:

●One of the following: ampicillin/sulbactam IV 1.5 g every 6 hours; cefuroxime 1.5 g IV every 8 hours; cefoxitin 2.0 g IV every 8 hours; cefotetan 2.0 g IV every 12 hours;

●Alternative antibiotics: ticarcillin/clavulanate 3.1 g IV every 4–6 hours; piperacillin tazobactam 3.375 g IV every 6 hours; cefotaxime 2.0 g IV every 4 hours; ceftriaxone 2.0 g IV every 24 hours.

●Sinusitis or dental abscess (upper second molar most common):

●Oral surgery consultation;

●May require surgical drainage.

●Fungal cellulites:

●Aggressive surgical debridement;

●Infectious disease and otolaryngology consultation;

●Amphotericin B 0.8 to 1.5 mg/kg/day IV;

●Correction of predisposing factors (e.g. metabolic acidosis, hyperglycemia).

●Orbital abscess:

●Children younger than 9 years: often sterile or single organism; if no optic nerve compromise, may observe because these may resolve with antibiotic treatment.

●Adults:

●Often multiple organisms;

●Surgical drainage.

●Other treatment considerations:

●Corneal exposure: lubricants;

●Ocular hypertension: topical medications; systemic carbonic anhydrase inhibitors.

●Sinus disease:

●Nasal decongestants: Children: 0.125% phenylephrine; Adults: 0.05% ocymetazoline hydrochloride;

●Systemic antihistamines.

COMPLICATIONS

●Subperiosteal abscess (7%).

●Meningitis (2%).

●Cavernous sinus thrombosis (1%):

●Nausea and vomiting;

●Headache;

●Disorientation;

●Contralateral eyelid edema/proptosis;

●Trigeminal nerve division I and II dysfunction;

●Episcleral and retinal venous engorgement.

●Visual loss (1%):

●Corneal exposure;

●Inflammatory and neovascular glaucoma;

●Exudative retinal detachment;

●Optic neuritis;

●Central retinal vein and artery occlusions.

●Intracranial abscess (1%).

●Osteomyelitis of orbital bones (1%).

REFERENCES

Ambati BK, Ambati J, Azar N, et al: Periorbital and orbital cellulitis before and after the advent of Haemophilus influenzae type B vaccination. Ophthalmology 107(8):1450–1453, 2000.

Jain A, Rubin PA: Orbital cellulitis in children. Internat Ophthalmol Clin 41(4):71–86, 2001.

Uehara F, Ohba N: Diagnostic imaging in patients with orbital cellulitis and inflammatory pseudotumor. Internat Ophthalmol Clin 42(1):133– 142, 2002.

326 ORBITAL GRAVES’ DISEASE 376.2

(Dysthyroid Orbitopathy, Endocrine

Ophthalmopathy, Thyroid-Associated

Eye Disease)

Kristi Bailey, MD

Portland, Oregon

Roger A. Dailey MD, FACS

Portland, Oregon

Thyroid-associated eye disease is the most prevalent cause of proptosis and compressive optic neuropathy in adults. Though typically a chronic form of orbital inflammation, it may have acute or subacute presentations. Associated systemic thyroid disease may or may not be present.

ETIOLOGY/INCIDENCE

Graves’ disease is an autoimmune disease that affects women three or four times as often as it affects men. Typically, the patient is a woman between the ages of 25 and 50, although Graves’ orbitopathy can occur at any age. A history of smoking is highly correlated with development of thyroid eye disease.

COURSE/PROGNOSIS

The spectrum of disease in Graves’ orbitopathy is broad, ranging from mild symptoms to severe disfigurement and blindness.

Clinical signs and symptoms

●Dry eyes, foreign body sensation.

●Pain.

●Photophobia.

●Diplopia.

●Eyelid edema.

●Conjunctival hyperemia and chemosis.

●Decreased vision in one or both eyes.

●Eyelid retraction.

●Eyelid lag on downgaze.

●Motility disorders.

●Hyperemia over the rectus muscle insertions.

●Proptosis and exposure keratitis.

●Optic neuropathy.

Patients may present with any combination of symptoms and signs. The active phase of disease usually stabilizes within 6 months.

DIAGNOSIS

The diagnosis is made on clinical grounds that may be supported by laboratory and other noninvasive testing. The key to diagnosis is the ophthalmologic examination, including the following:

●Visual acuity, color vision;

●Pupil examination;

●Extraocular movements and motility measurements;

●Lid evaluation;

●Exophthalmometry;

●Slit-lamp examination (chemosis, keratitis, conjunctival injection);

●Intraocular pressure (looking for significant increase in upgaze relative to primary gaze);

●Fundoscopy (looking for evidence of nerve compression).

Laboratory findings

●Visual field testing.

●Forced duction testing (for restrictive myopathy).

●Computed tomography (CT) scanning or magnetic resonance imaging (MRI).

●Thyroid function testing (T4 and thyroid-stimulating hormone).

●Thyroid-stimulating immunoglobulins.

●Endocrinology consultation.

Differential diagnosis

●Orbital myositis or pseudotumor.

●Dural or carotid cavernous fistula.

●Orbital tumors.

●Orbital vasculitis (such as Wegener’s granulomatois or polyarteritis nodosa).

●Orbital cellulites.

Risk factors

There is no specific prophylactic treatment for Graves’ disease to prevent the orbital sequelae. However, smoking has also been implicated as a risk factor for the development and worsening of thyroid eye disease. Patients should be counseled to stop tobacco use.

TREATMENT

Patients with Graves’ orbitopathy are managed on an individualized basis according to the predominant clinical findings. Management then is directed at the specific problem or problems.

Ocular

●Ocular lubricants for burning, irritation and keratitis.

●Moisture chambers, swimmer’s goggles, or humidifiers for exposure keratitis.

●Sunglasses for photophobia or tearing.

●Taping eyelids at night for lagophthalmos.

●Elevation of the head of bed at night for congestion and lid edema.

●Prisms for diplopia.

●No role for topical steroids; retrobulbar steroids of unproved effectiveness.

Systemic

●The treatment of hyperthyroidism should be performed by an internist or endocrinologist.

●Systemic corticosteroids are utilized for the treatment for congestive signs and symptoms.

●Prednisone 60 to 100 mg/day is indicated as initial, immediate treatment for vision loss from congestive optic neuropathy. If vision continues to decline or does not improve within 2–7 days, orbital decompression surgery is recommended.

●Mild diuretics such as 25 to 50 mg/day hydrochlorothiazide may reduce orbital edema.

●Systemic immunosuppressives (cyclophosphamide, azathioprine, and cyclosporine) and plasmapheresis may have benefit in carefully selected cases.

326 DiseaseCHAPTERGraves’ Orbital •

Orbit • 29 SECTION

Radiation

Radiation as a steroid-sparing treatment has a controversial role in the management of the patient with Graves’ disease. The primary indication is that the patient has disabling congestive symptoms, including conjunctival chemosis, prolapse, and injection, as well as rapidly progressive proptosis or optic neuropathy. External beam radiation in doses of 2000 cGy are delivered to the orbit in 10 fractions over 2 weeks. Improvement may be seen as early as 2 weeks post radiation, but may take several months for maximum benefit. Therefore, steroid therapy may be best continued for 4 to 6 weeks after completion of the radiation. An exacerbation of inflammatory and congestive symptoms lasting 2–3 weeks is not uncommon following radiation. It is sometimes necessary to increase the steroid dose temporarily during the radiation treatments. As a rule, patients who do not respond to steroids or who are in the fibrotic, noncongestive stage of the disease process will not respond to radiation. Patients at risk of retinopathy, such as diabetics, should probably not be irradiated.

Surgical

●Approximately 10% of patients with clinical Graves’ disease will require surgery for myopathy, lid retraction, proptosis, or optic neuropathy.

●Orbital decompression may be performed for compressive optic neuropathy as well as for the less proptotic patient with exposure problems, orbital pain, or pressure. Coronal CT scanning and MRI can be used to identify the underlying pathology and help direct the oculofacial plastic surgeon in planning the surgical strategy.

Numerous surgical techniques for decompression of one to all four of the orbital walls have been described. The amount of proptosis reduction correlates to the number and extent of walls decompressed, as well as to the specific walls chosen.

The transantral Caldwell–Luc medial and inferior wall decompression, was the procedure of choice until the early 1980s. The use of a balanced lateral and medial decompression technique to decrease the incidence of postoperative strabismus and infraorbital parasthesias has become more prominent. The orbital floor may be added to the balanced medial and lateral wall technique for a three-wall decompression yielding further proptosis reduction. Endoscopic techniques may also be employed. The orbital roof is rarely used.

●When the restrictive myopathy of Graves’ orbitopathy induces a tropia that has been stable by prism measurement for 6 months or longer (off steroids), eye muscle surgery can help restore ocular alignment. The goal is to create fusion in the primary and reading positions. Adjustable suture techniques are preferable in these patients to ensure a favorable postoperative alignment. Recessions are preferred over resections because of muscle restriction and the tendency for scar formation in the orbit of patients with Graves’ disease. Overcorrection is preferred because postoperative adjustment is easier when tightening the sutures (i.e. reducing the recession).

●For patients with primarily eyelid manifestations, several eyelid surgery techniques are available. For upper eyelid retraction of up to 2 mm, excision of Müller’s muscle is adequate to correct the problem. For larger amounts of upper eyelid retraction, levator surgery becomes necessary. A variety of procedures have been described, including levator stripping, levator marginal myotomy, recession of the levator aponeurosis, or placement of a spacer (e.g. sclera,

dura) between the aponeurosis and the upper tarsal border. Lower eyelid retraction is approached in a similar fashion. Disinsertion or extirpation of the lower lid retractors has been used with varying success. Placement of a spacer between the disinserted capsulopalpebral fascia and the lower border of the tarsus may also be used. Sclera, cartilage, fascia, or a tarsal transplant from the upper lid have all been used successfully as spacers.

●The pathologic process of dysthyroid orbitopathy frequently leads to presenile prolapse of orbital fat in the upper and lower eyelid. This prolapse is caused by a combination of factors, including orbital congestion and inflammation, weakening of the orbital septum, and an increase in the volume of orbital fat. Cosmetic blepharoplasty should be approached with this in mind, concentrating on a more aggressive approach to fat removal while being conservative with skin excision.

●When indicated, orbital decompression should be undertaken before strabismus or eyelid surgery because the decompression may alter the ocular alignment and eyelid position. Similarly, eye muscle surgery, especially inferior rectus recession, will affect the position of the eyelids. Accordingly, when eye muscle surgery is indicated, it is usually done before any contemplated eyelid surgery. Cosmetic blepharoplasty is best reserved for last when patients with Graves’ disease require more than one ophthalmic surgical procedure.

COMPLICATIONS

The side effects and complications of corticosteroid therapy are well known. Chronic steroid therapy should be managed with the assistance of an internist or endocrinologist.

Orbital radiation should be performed by a radiation specialist who is experienced with irradiation of the orbit. The retrobulbar area is treated while the globe itself is shielded. Every patient should be informed of the risk, albeit very slight, of radiation-induced cataract or retinopathy.

Complications of orbital decompression include diplopia and strabismus, globe dystopia, periorbital paresthesia and dysesthesia, CSF leak, intraparynchemal injury, lacrimal gland injury, temporalis muscle atrophy, hematoma, globe or optic nerve injury, inadequate decompression, infection, ptosis, or vision loss.

Complications of surgery for lid retraction include ptosis (usually more prominent nasally), persistent retraction (usually more prominent temporally), contour abnormalities, ocular irritation or lid thickening induced by spacers (e.g. sclera), and damage to the lacrimal gland and its ducts.

Eye muscle surgery for restrictive myopathy has the same risks as standard strabismus surgery; however, exposure is usually more difficult because of the tethering effect of the muscles. Adhesions and scarring are more of a problem because of the orbital inflammation, especially in reoperations.

REFERENCES

Bailey KL, Tower RN, Dailey RA: Customized, single-incision, three-wall orbital decompression. Ophthal Plast Reconstruct Surg 21(1):1–9; discussion 9–10, 2005.

Baldeschi L, et al: Early versus late orbital decompression in Graves’ orbitopathy: a retrospective study in 125 patients. Ophthalmology. 113(5):874–878, 2006.

Bartalena L, et al: An update on medical management of Graves’ ophthalmopathy. J Endocrinolog Invest 28(5):469–478, 2005.

Hatton MP, Rubin PAD: Controversies in thyroid related orbitopathy: radiation and decompression. Internat Ophthalmol Clin 45(4):1–14, 2005.

Kennerdell JS, Maroon JC, Buerger GF: Comprehensive surgical management of proptosis in dysthyroid orbitopathy. Orbit 6:153–179, 1987.

Mizen TR: Thyroid eye disease. Sem Ophthalmol 18(4):243–247, 2003.

Putterman AM: Surgical treatment of thyroid-related upper eyelid retraction. Ophthalmology 88:507–512, 1981.

Rootman J: Graves’ orbitopathy. In: Rootman J, ed: Diseases of the orbit. Philadelphia, JB Lippincott, 1988:241–280.

327 ORBITAL HEMORRHAGES 376.32

Klaus D. Teichmann, MD, FRCSC, FRACO, DiplABO

Riyadh, Saudi Arabia

Orbital hemorrhage often occurs acutely. Because there is little room for expansion, any substantial hemorrhage behind the orbital septum will raise intraorbital and intraocular pressure (IOP) and may cause orbital compression or compartment syndrome. The globe is pushed forward until it reaches the limits of anatomic constraint. If bleeding continues, rising intraorbital pressure will compromise blood circulation of the optic nerve and possibly of the globe. Central retinal artery occlusion (CRAO), high IOP, choroidal ischemia, anterior or posterior ischemic optic neuropathy, and direct compressive optic neuropathy are mechanisms by which vision can be lost.

In milder cases, where there is no significant or progressive visual loss, imaging studies, laboratory tests, and a complete work-up may be performed. In severe cases with rapid or progressive visual loss, immediate orbital decompression should be considered to save visual function. Imaging can be undertaken once vision has improved (or at least stabilized). Vision-threatening acute orbital hemorrhage constitutes one of the few true ophthalmologic emergencies, and every ophthalmologist should be prepared to provide prompt and effective treatment.

ETIOLOGY/INCIDENCE

Blunt or penetrating orbital trauma frequently is associated with orbital hemorrhage. Its incidence after retrobulbar injection is reported at 1% or higher but can be significantly reduced with proper technique. Less commonly, periocular or sinus surgery is responsible: orbital hemorrhage was associated with 0.055% of cosmetic lid surgeries (1 in 2000 cases), wITH permanent visual loss in 0.0045% (1 in 20000 cases). Values are higher for orbital surgery.

Violation of the orbital fat is a common cause for postoperative orbital hemorrhage, as traction on orbital fat can tear deep orbital vessels. Local vascular disease (e.g. venous anomalies, advanced atherosclerosis, aneurysms of the ophthalmic artery, arteriovenous malformations, carotid cavernous sinus fistula, lymphangioma, hemangioma) predisposes to orbital hemorrhages, as do some systemic disorders including hypertension, anemia, leukemia, hemophilia and other clotting disorders, uremia, scurvy, sickle cell disease, and malaria. Orbital hemorrhage may occur spontaneously or be precipitated by an increase

in venous pressure (e.g. Valsalva maneuvers such as coughing, straining, labor, and weight-lifting and prolonged head-down positioning).

COURSE/PROGNOSIS

Orbital hemorrhage usually takes a benign course, with spontaneous resolution or hematic cyst formation and without any visual loss. Temporary or permanent loss of vision may occur, however, due to retinal or optic nerve damage (particularly with arterial hemorrhages and optic nerve sheath hematomas). Survival time of retinal tissue after a CRAO may be less than 2 hours, whereas permanent optic nerve damage can occur in less than 3 hours. In certain cases, however, all (or some) vision may be regained even when treatment is delayed for several hours or days. Vision regained after the institution of therapeutic measures can be lost again if bleeding continues. Therefore, frequent monitoring over 24 to 48 hours is mandatory. Orbital hemorrhages tend to develop during the first 24 hours after surgery, particularly in the first 3 hours, but may occur as late as several days postoperatively.

DIAGNOSIS

Clinical signs and symptoms

The diagnosis is usually based on history (trauma, surgery, local or systemic predisposing disease) and the typical clinical findings, as follows:

●Symptoms include:

●Ocular, orbital, and/or periorbital pain;

●Sensation of pressure;

●Nausea, vomiting;

●Diplopia;

●Dimming of vision up to total unilateral (or bilateral) loss of vision.

●Signs include:

●Tight or swollen eyelids with or without ecchymoses, ptosis, or lid retraction;

●Tense orbit with or without proptosis;

●Immobile globe;

●Hemorrhagic chemosis of the conjunctiva;

●High IOP;

●Cloudy cornea;

●Afferent pupillary defect or motor anomalies of the pupil;

●Disk pallor or hyperemia;

●Disk edema;

●Pulsating or collapsed retinal arteries;

●Choroidal folds.

A cherry-red spot and cloudy swelling of the retina are rare. Features suggestive of central retinal vein occlusion indicate possible optic nerve sheath hemorrhage.

Differential diagnosis

This includes orbital compression syndromes without hemorrhage:

●Orbital cellulites;

●Emphysema of the orbit;

●Fluid exudation after thermal burns (particularly where there is facial involvement);

●Carotis-cavernous sinus fistula;

327 CHAPTERHemorrhages Orbital •

Orbit • 29 SECTION

●Granulocytic sarcoma (acute myelogenous leukemia);

●Rhabdomyosarcoma;

●Metastatic neuroblastoma (in children).

PROPHYLAXIS

●Before any ocular and orbital surgery, systemic hypertension, renal disease, Graves’ disease, and glaucoma should be noted as factors predisposing to orbital hemorrhage, as should the use of platelet inhibitors (aspirin, dipyridamole, ticlopidine), nonsteroidal antiinflammatory drugs or warfarin. Suspected bleeding disorders should be elucidated based on prothrombin time (PT), partial thromboplastin time (PTT), platelet count, and bleeding and clotting times.

●During surgery, meticulous hemostasis should be maintained with cautery, ligatures, hemostats and simple compression. Traction on the orbital fat should be minimized. Prolapsed fat is removed with unipolar cautery, and visible vessels are coagulated before resection. The distal stump of fat should be examined for bleeding before being released into the orbit. Moist absorbable gelatin sponge segments, soaked in thrombin solution and applied to sites where fat was excised, may help promote hemostasis.

●The use of epinephrine in local anesthesia is not without risk: it may provoke a marked rise in blood pressure, as well as causing a deceptively bloodless field during surgery. Diffuse oozing may then set in once pharmacological vasoconstriction has subsided.

●A rubber (Penrose) drain or a suction drain (Hemovac) is advisable for deep orbital surgery.

●In any orbital surgery, the wound should not be closed until bleeding has stopped completely.

●After completion of the surgery, tight bandages, if used at all, should not be left on for longer than 30 to 60 minutes. If pain is reported, they should be removed immediately and the surgical site should be most closely monitored.

●Gauze pads soaked in iced saline may decrease postoperative swelling and abort hemorrhage.

●After any lid or orbital surgery, the patient’s head should be elevated 30 to 40 degrees.

●Close postoperative observation is mandatory. Patients should be asked to immediately report severe or sudden pain. In case of doubt, look for proptosis or ecchymosis; check IOP, vision and pupillary action; examine the fundus for optic disk swelling or pallor and to rule out complete or partial CRAO. Postoperatively, vomiting, coughing, strenuous physical activity and bending over should be avoided for several days.

TREATMENT

Systemic

●Most orbital hemorrhages require no treatment; patients should merely be observed.

●Imaging studies (computed tomography, magnetic resonance imaging, ultrasound) may provide valuable information about extent and location of a hemorrhage (intraconal, extraconal, within optic nerve sheath, subperiosteal, subTenon, preseptal), possible associated bony injuries, intra-

cranial injury, intraocular or intraorbital foreign bodies, and underlying disease (e.g. lymphangioma).

●Imaging studies are crucial in diagnosing optic nerve compression, which may be present even when intraorbital pressure is normal.

●Preliminary orbital decompression may be required before time-consuming imaging studies are performed. These should, however, be requested wherever possible because they are likely to provide valuable diagnostic information, as well as guidance for definitive surgical management.

●Relevant laboratory tests, if not done before surgery, should be performed if a bleeding diathesis is suspected.

●Medication is used to control blood pressure and bleeding disorders.

●Analgesics (not aspirin) and antiemetics are administered as required.

●Intravenous acetazolamide or hyperosmotic agents cannot effectively decompress the orbit, but may be tried.

●Systemic steroids (e.g. 250 mg methylprednisolone IV every 6 hours for several days) may be given to reduce orbital swelling, decrease vascular permeability, and protect the optic nerve from ischemic damage.

●Megadose steroids (e.g. methylprednisolone: initial dose of 30 mg/kg IV; followed by 5.4 mg/kg/hour IV for 48 hours) may be given in the presence of optic nerve sheath hemorrhage.

●If vision recovers, taper the steroids over one week.

●If vision fails to regenerate, discontinue the steroids after 2 days.

●Other neuroprotective agents are under investigation and may be useful in the future.

Ocular

●Lubrication to prevent exposure keratopathy.

●Topical medications to lower IOP are usually ineffective but may be tried.

●Ice-cold compresses may reduce tissue swelling, stop bleeding, and prolong survival time of neural tissue.

●Direct compression applied to the orbit may help arrest bleeding, but compromises perfusion. The same is true for compression of the ipsilateral carotid artery.

Surgical

Surgical decompression is the cornerstone of therapy for orbital hemorrhage. It can be achieved in different ways: (1) through the release of orbital tension by means of canthotomy, cantholysis, or fracturing the orbital floor, or (2) through drainage of blood from the orbit.

●Lateral canthotomy and inferior cantholysis (possibly followed by superior cantholysis) effectively lower a raised intraorbital pressure. Straight scissors are used for making a horizontal cut from the lateral canthal angle to the orbital rim. The lower eyelid is stretched anteriorly and the inferior crus of the lateral canthal tendon is severed with the scissors, at which time the lower eyelid should swing away from the globe.

●If decompression is inadequate after cantholysis, the orbital septum may need to be opened across the eyelids.

●In the absence of a surgical wound, Steven scissors can be inserted through the conjunctiva and Tenon’s capsule in the inferior nasal quadrant, between the medial and the inferior rectus muscles. By inserting and spreading the scissors (but not cutting), or by inserting an 18-gauge needle, a retrobulbar hemorrhage can at times be drained.

●Where there is a surgical wound, it should be opened, any hematoma should be drained, and bleeding vessels should be cauterized or tied.

●Subperiosteal hemorrhages can be drained directly.

●If drainage fails, a small curved mosquito clamp can be inserted through an opening made in the inferior nasal fornix. The closed clamp is advanced posteriorly, with its convex side upwards, along the medial orbital floor for about 20 mm. Rotational pressure then is applied, breaking the orbital floor and the maxillary sinus mucosa. The defect is enlarged by spreading and rotating the blades of the clamp. This maneuver may be facilitated by a preceding lateral canthotomy and inferior cantholysis.

●Exploration of the orbit may become necessary if hemorrhage continues, in order to identify the source of the bleeding and permit meticulous cautery of bleeding points, drainage of fluid blood, and removal of clots. The most likely source of bleeding is the ophthalmic artery or its branches (including the anterior and posterior ethmoidal arteries). The latter can be approached by means of a semicircular incision medial to the nasal canthus, followed by wide opening of the periosteum and removal of ethmoidal cells including the lamina papyracea.

●In diffuse oozing, the local application of hemostatic agents (e.g. topical thrombin, absorbable gelatin sponge, microfibrillar collagen) and compression may achieve hemostasis. In some cases of diffuse bleeding, the increased volume of orbital tissues may require extensive decompression through removal of the orbital floor and the medial orbital wall.

●If optic nerve compression is localized to the orbital apex, the posterior ethmoid should be removed.

●For optic nerve sheath hematomas, fenestration of the optic nerve sheath and removal of blood clots is mandatory in cases where visual function fails to recover after orbital decompression.

●Intraoperatively, pupillary response to light, flash visual evoked potentials, or — provided the patient is awake — visual acuity can serve as guides for success of decompression. The wound should be closed only after all bleeding has ceased. Insertion of a drain is advisable.

COMPLICATIONS

Complications include permanent loss of vision, delayed wound healing, infection, hematic cyst formation, cholesterol granulomas, discoloration of the skin, fibrosis, enophthalmus, motility restriction, diplopia, lid retraction, ectropion, entropion, and infraorbital nerve anesthesia (which may be transient).

COMMENTS

Preseptal orbital hemorrhages do not require surgical intervention.

Direct compression of the optic nerve may be present in the absence of raised intraorbital pressure. It can be due to optic nerve sheath hematoma, subperiosteal hemorrhage near the orbital apex, or large intraconal blood clots. Surgical evacuation through a medial or lateral orbitotomy or via an ethmoidectomy (near the orbital apex) is often required if the optic nerve is compromised.

For non-vision-threatening subperiosteal hemorrhages, surgical drainage is recommended only if the blood has not spontaneously resorbed after a few weeks.

Anterior chamber paracentesis as an emergency measure in orbital hemorrhage may convert a hard globe with a formed anterior chamber into a hard globe with an absent anterior chamber. Because its effect is small and the procedure is fraught with complications, it is not recommended as treatment of high IOP in the presence of a high intraorbital pressure.

REFERENCES

Bains RA, Rubin PAD: Blunt orbital trauma. Int Ophthalmol Clin 35:37– 46, 1995.

Hargaden M, Goldberg SH, Cunningham D, et al: Optic neuropathy following simulation of orbital hemorrhage in the nonhuman primate. Ophthal Plast Reconstr Surg 12:264–272, 1996.

Liu D: A simplified technique of orbital decompression for severe retrobulbar hemorrhage. Am J Ophthalmol 116:34–37, 1993.

Yung CW, Moorthy RS, Lindley D, et al: Efficacy of lateral canthotomy and cantholysis in orbital hemorrhage. Ophthal Plast Reconstr Surg 10:137– 141, 1994.

327 CHAPTERHemorrhages Orbital •