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Address reprint requests and correspondence: William C. Yao, MD, Department of Otorhinolaryngology—Head and Neck Surgery, McGovern Medical School, University of Texas Health Science Center at Houston, 6431 Fannin St, MSB 5.036, Houston, TX 77030.
Retrobulbar hemorrhage is regarded as one of the most feared conditions in otolaryngology—its onset can be rapid and can result in irreversible blindness. While a rare occurrence, the otolaryngologist should be compulsive about recognizing this entity, as he or she may be faced with managing this condition either as a consultant, or as one of his or her personal surgical complications. Regardless, prompt recognition and swift action can prevent catastrophic visual loss. This article presents a stepwise discussion of the surgical management of retrobulbar hematoma. Specifically, we discuss lateral canthotomy, cantholysis, and endoscopic orbital decompression.
Retrobulbar hematoma (RBH) can be spontaneous, traumatic, or iatrogenic. Spontaneous RBH often is the result of blood dyscrasia, coagulopathy, or thrombocytopenia. The incidence of RBH is rare, occurring in up to 3.6% of blunt ocular trauma,
The retrobulbar compartment is the cone-shaped space posterior aspect of the orbit, with the globe itself in the anterior space of the orbit. The periorbita lines the bony orbit and continues anteriorly as the orbital septum, that helps maintain the orbit in a fixed position. Together with the bony orbit, the orbital periosteum and septum are relatively stiff structures that are not compliant in the setting of increases in orbital pressure due to increases in the volume of the orbital contents. The mechanisms leading to vision loss in RBH are poorly understood. It is theorized that excessive bleeding in this confined space leads to an “orbital compartment syndrome,” resulting in optic nerve compression, reduced retinal and optic nerve arterial blood flow, ischemic injury, and vision loss.
Retrobulbar bleeding is clinically suspected with the presence of orbital pain that is disproportionate to the injury or surgery, proptosis, periorbital ecchymosis, conjunctival hemorrhage, ophthalmoplegia, and a tense globe that resists movement with finger palpation. Due to the increased intraocular pressure (IOP), the globe will feel “rock-solid” and will not be easily “retro-pulsed.” During ESS, RBH may be suspected when an injured ethmoidal artery retracts into the orbit, or when herniation of orbital fat into the ethmoid cavity indicates breach of lamina papyracea and periorbita. Loss of red color discrimination (which often precedes loss of visual acuity), relative afferent pupillary defect (RAPD), and visual field deficits all herald threatened loss of vision.
Tonometric pressures above 20 mm Hg are abnormal and those within 20 mm Hg of mean arterial pressure may trigger irreversible vision loss. Fundoscopic exam may reveal pulsatile or intermittent retinal arterial flow. Computed tomographic evidence of raised IOP include globe “tenting”
and some investigators have shown that a decrease in “stretch angle” (measured using a line drawn from the midpoint of the optic nerve’s insertion in the posterior globe to the medial rectus’s attachment on the medial globe (Figure 1) in addition to the stretching of the optic nerve relative to the unaffected eye predicts worse vision outcomes.
Once RBH is suspected, a quick and decisive action is needed. In an experimental model of RBH conducted in cynomogulus monkeys, researchers have demonstrated that irreversible loss of vision can occur as early as 30 minutes once visual acuity is compromised.
Emergent ophthalmologic consultation is mandatory. Early, nonsurgical maneuvers, include head elevation and removal of intranasal packing (when related to ESS), and orbital massage. Traditionally, orbital massage has been recommended as a way to distribute the hematoma more evenly in the orbital space; however, the application of pressure will only apply additional pressure in a closed space. Moreover, this maneuver may cause additional trauma. Medical management includes systemic steroids (dexamethasone 0.2 mg/kg up to a maximum of 12 mg), IV mannitol (1-2 g/kg), IV acetazolamide (10-15 mg/kg), and topical beta adrenergic blockade (timolol drops). Surgical decompression of RBH should be strongly considered in the setting of rapidly expanding RBH, RAPD, persistently elevated IOPs with vision changes and when conservative efforts fail to adequately reduce IOP and/or reverse vision changes. There should be a low threshold for surgical decompression as these procedures are quick, vision-saving, and possess limited morbidity.
In the post-ESS setting in which the patient is complaining of visual changes, the ophthalmology service cannot always be reached urgently. In this acute situation, the authors recommend a bedside physical examination applying pressure to the eye to measure the degree of retropulsion. If the eye is immobile (“rock-solid”) compared to the contralateral unaffected eye, RBH should be suspected. The patient should be given the medications mentioned previously to help decrease the IOP. Simultaneously, the surgeon should prepare for a bedside canthotomy and cantholysis followed by an emergent surgical decompression in the operating room (discussed later).
The maneuvers described below act to release the resistance offered by the periorbita, orbital septum, and lamina papyracea, thereby increasing orbital volume and reducing IOP.
This procedure can be performed rapidly in the OR, or at the bedside with the patient fully awake as a bridge to decompression of the RBH (Figure 2A). In an experimental model of RBH conducted by Yung et al., normal saline was injected into the retrobulbar compartment in ruminant mammals and reduction in IOP after canthotomy was measured. This study found that canthotomy reduces IOP by an average of 14.2 mm Hg.
The lateral canthal region is anesthetized with lidocaine 1% with 1:100,000 epinephrine (if readily available). This step should not delay subsequent steps. The lower eyelid is drawn outward with toothed forceps. A hemostat is advanced around the lateral canthal skin and soft tissue until the lateral bony orbital rim is palpated with the tip of instrument tines. The skin and soft tissue are clamped with an instrument for up to 30 seconds to help with hemostasis. Sharp dissecting scissors (ie, Wescott tenotomy or curved Iris) are then used to make a horizontal incision across the lateral canthal skin and soft tissue down to the bone of the lateral orbital rim. Inferior retraction of the lower lid should reveal the superior and inferior crus of the lateral canthal tendon fibers at their attachment to the lateral orbital rim.
In general, lateral canthotomy should not be considered a standalone procedure; that is, when a surgeon performs a lateral canthotomy, the next step invariably should be cantholysis.
This maneuver further increases orbital volume by releasing inferior orbital septum’s attachment to the lateral orbital rim at Whitnall’s tubercle (Figure 2B). In the study by Yung discussed above, cantholysis produced a mean IOP reduction of 30.4 mm Hg.
Oester simulated RBH in a cadaveric model using glycerin or hydroxyethyl cellulose injections and demonstrated that cantholysis performed together with canthotomy reduces orbital compartment pressure (a correlate of IOP) an average of 56 mm Hg.
After canthotomy, inferior retraction of the lower lid allows visualization of the inferior lateral canthal tendon. Sharp dissecting scissors are oriented downward, perpendicular to the direction canthal tendon fibers, and the inferior tendon is transected. Once performed, the lower lid will demonstrate a noticeable increase in laxity with gentle traction. After complete cantholysis, it should be possible to fold the lower lid across the cheek easily; if the surgeon cannot do this easily, the additional canthal ligament fibers are still intact and must be lysed.
The incision typically heals well by secondary intention, or can be repaired in a delayed fashion. An oculoplastic consultation in the early postoperative period is recommended for management of this incision for optimal esthetic and functional outcomes over the long term.
At times, the canthotomy and cantholysis can be done simultaneously by incorporating the lower canthal tendon in the canthotomy by angling the scissors inferiorly at an angle of 15°-20°.
Endoscopic orbital decompression
Endoscopic decompression may be indicated when RBH occurs intraoperatively or as an adjunct to canthotomy or cantholysis to further decrease the IOP (Figure 3). This technique has been shown to reduce IOP an additional 10 mm Hg after canthotomy or cantholysis.
If not already performed, the nose is decongested with 1:1,000 epinephrine or 0.05% oxymetazoline-soaked pledgets, followed by injection with 1% lidocaine with 1:100,000 epinephrine in the axilla of the middle turbinate, the head of the middle turbinate, and at the region of the sphenopalatine foramen. The procedure is begun with an uncinectomy, after which, a large maxillary antrostomy is created, from the natural ostium to posterior maxillary sinus wall. Total endoscopic sphenoethmoidectomy is performed to widely expose the lamina papyracea from the maxillary line posteriorly to the sphenoid face (Figure 3A). In addition, the lamina should be exposed from the maxillary sinus up to the fovea ethmoidalis. If the RBH occurs in the postoperative setting following an ESS, most often a part of the dissection or the exposure of the lamina has already been performed.
Once the lamina has been exposed, the lamina papyracea is gently fractured at its softest point and subsequently elevated from the underlying periorbita with the Cottle elevator. The lamina is removed from the maxillary ostia to the sphenoid face (Figures 3B and 4). Attention should be concentrated on the posterior aspect of the lamina papyracea to prevent prolapse of the orbital contents into the frontal recess. The orbital periosteum is incised with a sharp sickle knife from a posterior to anterior direction to prevent blood and orbital contents from obscuring the surgeon’s view (Figure 3C). First, a superior incision is made at the superior aspect of the exposure followed by the inferior incision which is along the infraorbital strut. Making a superior and inferior incision will prevent inadvertent injury to the medial rectus muscle. The 2 incisions are connected posteriorly to allow for the decompression of the RBH and orbital fat (Figure 5). If excessive bleeding is noted, cauterization can be performed in the extraconal compartment (lateral to the medial rectus muscle) with a bipolar device with constant saline irrigation to prevent injury to the ophthalmic arteries and optic nerve. When using the bipolar device, the surgeon should proceed with extreme caution and should be cognizant of the relative location of the ophthalmic artery, optic nerve, and oculomotor nerve, which all lies deep to the medial rectus muscle. Medial decompression is now complete. The frontal outflow, maxillary and sphenoid ostia are checked for patency after the orbital decompression is complete to decrease the ischemic time of the nerve. The need for a speedy orbital decompression should take precedence to refining and “perfecting” the surgical sinus openings. Again, IOP and pupillary responses are checked to ensure adequate decompression. No intranasal packing material should be placed to prevent additional pressure on the globe.
The patient is admitted to the floor for observation. Ophthalmology consultation, if not already obtained intraoperatively, is mandatory. IV dexamethasone (8 mg every 8 hours for 24 hours) and topical timolol drops are administered. Intravenous acetazolamide can also be considered to decrease intraorbital pressure. Serial eye exams assessing visual acuity, tonometry, and pupillary responses are performed to ensure stable resolution of symptoms. For endoscopic decompression, the patient is started on gentle saline irrigations on postoperative day 1. As alluded earlier, canthotomy and cantholysis incisions may heal by secondary intention, or can be repaired in a delayed fashion several days later.
The decision to proceed with surgical decompression for RBH is a clinical one informed by the tempo of bleeding, concomitant raise in IOP, vision changes, and an individual’s clinical experience. In certain scenarios, RBH can be managed expectantly. Han et al found in a retrospective review of 22 patients that 77% of cases of RBH could be managed without surgery with acceptable results.
This may be feasible in patients with slow, venous bleeding, and normal IOP. Others advocate that early surgical decompression results in improved visual outcomes when compared with medical management, especially when patients present with RAPD.
While criteria for surgical decompression may vary, the importance of early recognition and intervention, medical or surgical, remains constant, as delayed intervention may result in failed visual recovery and blindness.
The importance of emergent ophthalmology consultation can also not be overstated, as their expertise is invaluable.
With the exception of traumatic cases, RBH can be prevented. With regard to ESS, careful preoperative planning should be undertaken, with special attention to location of anterior ethmoid and posterior ethmoid arteries, and lamina papyracea dehiscence. When external periorbital surgery is endeavored, meticulous hemostasis and gentle handling of periorbital soft tissues, including orbital fat, fat pads, and capsulopalpebral fascia should remain a top priority. In this manner, emergent measures and catastrophic visual loss can be avoided.
The authors reported no proprietary or commercial interest in any product mentioned or concept discussed in this article.
Incidence of retrobulbar hemorrhage in the emergency department.