Complications of Orbital Decompression and Management

Complications of Orbital Decompression and Management


Jordan T. Glicksman, James N. Palmer, and Nithin D. Adappa



Abstract


• Complications of endoscopic orbital decompression are rare, but can be life or vision threatening.


• Complications of orbital decompression may be irreversible, and therefore prevention is the best form of treatment.


• A solid grasp of patient anatomy, including risk factors for complications, is essential to prevent complications.


• Intraoperative complications include corneal abrasion, optic nerve injury, extraocular muscle injury, infraorbital nerve injury, nasolacrimal duct injury, arrhythmias, skull base injuries, and vascular injuries.


• Postoperative complications include diplopia, postsurgical sinus obstruction, subcutaneous emphysema, epistaxis, and inadequate decompression or asymmetry.


• A team approach with ophthalmology is critical for management of ocular complications.


Keywords: orbital decompression, complications, endoscopic, management, anatomy


8.1 Introduction


Since described by Kennedy et al 1 in 1990, endoscopic orbital decompression has largely replaced open decompressive procedures due to the decreased morbidity associated with an incisionless approach. While in most cases endoscopic orbital decompression is performed successfully, potential complications are important to consider, both by the surgeon and by the patient. While most complications of endoscopic decompression are minor and self-limiting, the complications of the procedure can lead to severe consequences, which can be life- or vision-threatening. The complications outlined in this chapter focus on those specific to the procedure, and not those related to a general anesthetic.


8.2 Patient Selection and Indications


Complications of orbital decompression can be broken down into intraoperative or postoperative complications.


8.2.1 Intraoperative Complications


The best method of treating complications is prevention. Therefore, it is critical for the surgeon to be aware of impending complications and for the surgeon to take steps to mitigate risk of them occurring. Intraoperative complications may include corneal abrasion, optic nerve injury, extraocular muscle injury, infraorbital nerve injury, nasolacrimal duct injury, bradycardia and asystole, skull base injuries/cerebrospinal fluid (CSF) leak, and vascular injuries ( ▶ Table 8.1).














Table 8.1 Classification of complications

Intraoperative complications


Postoperative complications


Corneal abrasion


Optic nerve injury


Extraocular muscle injury


Infraorbital nerve injury


Nasolacrimal duct injury


Bradycardia and asystole


Skull base injuries/cerebrospinal fluid leak


Major vascular injuries


Retro-orbital hematoma


Diplopia


Sinus obstruction


Subcutaneous emphysema


Epistaxis


Inadequate decompression


Asymmetry


Retro-orbital hematoma



 Corneal Abrasion


Corneal abrasion is typically prevented by the use of eye protection and lubrication during surgery. Corneal shields can be used to cover the eye, or the eyelids can be taped shut during the procedure. It is preferable not to place a tarsorrhaphy stitch for endoscopic sinus surgery, as this can make monitoring of the eye more challenging during the case. If a corneal abrasion occurs despite this, topical antibiotic ointments such as erythromycin or eye drops such as ciprofloxacin or ofloxacin may be prescribed. The ideal duration of treatment has not been studied, but it would be reasonable to continue treatment until the patient is symptom free for 24 hours. Topical anesthetic agents should be avoided as they can cause further trauma to the eye to go undetected by the patient. Evaluation by an ophthalmologist using slit-lamp biomicroscopy is recommended to ensure that corneal infection does not occur during the healing phase and that the corneal epithelial defect resolves completely.


 Optic Nerve Injury


Depending on the etiology of injury, this optic nerve injury may be suspected intraoperatively and confirmed postoperatively or may only be recognized postoperatively. In either case, an ophthalmology consultation is indicated, which should include a full examination and formal visual field testing. We would recommend discussing the use of steroids with the consulting ophthalmologist to address any potential swelling around the nerve.


A computed tomography (CT) scan may elucidate if swelling or a hematoma at the orbital apex is implicated, and could reveal a bony spicule impinging on the optic nerve. If the nerve is compressed by a bone fragment, then returning to the operating room for exploration and decompression would be indicated immediately.


A retrobulbar hematoma typically presents with bruising, pain, proptosis, mydriasis, chemosis, elevated intraocular pressure, and eventually visual loss ( ▶ Fig. 8.1). Typically color vision is impaired first as nerve fibers encoding color are located at the periphery of the nerve. To help prevent this complication, dissection should be performed meticulously and vessels at risk of retracting into the orbit should be identified and coagulated prior to division, if division is required.



Photograph of a patient with a retro-orbital hematoma secondary to anterior ethmoid artery injury. Chemosis, bruising, and mydriasis are demonstrated, which are all signs of this complication. A later


Fig. 8.1 Photograph of a patient with a retro-orbital hematoma secondary to anterior ethmoid artery injury. Chemosis, bruising, and mydriasis are demonstrated, which are all signs of this complication. A lateral canthotomy and cantholysis were required to decompress the orbit.


(This image is provided courtesy of Dr. Raymond Sacks, MBBCH, FCS (SA) ORL, FRACS, MMed (ORL), University of Sydney, Sydney, Australia.)



Ideally the signs and symptoms of a retrobulbar hematoma would be recognized clinically and would obviate the need for imaging ( ▶ Fig. 8.2). In the case of a hematoma following endoscopic orbital decompression, these signs may be masked by the decompressive nature of the procedure. If the orbit has not been decompressed to the orbital apex, then emergent decompression may be warranted given the small window before vision loss. Adjunctive medical therapy such as mannitol or acetazolamide could also be considered. If packing was placed intraoperatively, it should be removed to decrease pressure on the orbital contents.



Axial CT (computed tomography) scan image demonstrating retro-orbital hemorrhage. This case occurred secondary to trauma, but this complication can also occur following orbital decompression.


Fig. 8.2 Axial CT (computed tomography) scan image demonstrating retro-orbital hemorrhage. This case occurred secondary to trauma, but this complication can also occur following orbital decompression.


(This image is provided courtesy of Dr. Raymond Sacks, MBBCH, FCS [SA] ORL, FRACS, MMed [ORL], University of Sydney, Sydney, Australia.)



 Extraocular Muscle Injury


The medial rectus muscle is at risk whenever the periorbita is violated. Whereas in most endoscopic sinus procedures it is undesirable to penetrate the lamina papyracea, removal of this structure is required for endoscopic orbital decompression. Care should be taken when dividing the periorbita to avoid penetrating the orbital contents deeply and lacerating the extraocular muscles. Although a variety of incisions have been described, the key point is the incisions through periorbita should be done in a controlled fashion and any form of debrider should never be used to resect periorbita. Injury to the medial rectus will result in diplopia and may require future strabismus surgery. Unfortunately, diplopia may persist in some fields of gaze even after successful strabismus surgery and therefore prevention is the best treatment.


 Infraorbital Nerve Injury


The infraorbital canal is the lateral limit of orbital floor decompression. It is important to recognize the position of the nerve prior to decompressing the orbital floor. If bleeding occurs in the vicinity of the nerve, care should be taken in achieving hemostasis to avoid thermal injury. Damage to the infraorbital nerve results in midfacial numbness and/or paresthesia. Ference et al 2 demonstrated the nerve traverses within the maxillary sinus in 8% of patients without an infraorbital ethmoid air cell and in 28% of patients in whom this variation exists. Care must be taken to avoid infraorbital nerve injury, as it is often irreversible. Management is typically conservative.


 Nasolacrimal Duct Injury


The nasolacrimal duct is vulnerable to injury when a maxillary antrostomy is carried too far anteriorly. In general, angled scopes are recommended to identify the true maxillary antrostomy and removal of the entire uncinate process. An angled view also allows visualization of the harder lacrimal bone that protects the nasolacrimal duct. If image guidance is available, navigation can demonstrate the border of the nasolacrimal duct. In most cases, even if an injury occurs, patients are typically asymptomatic. If complications occur, it typically is in the form of epiphora and a dacryocystorhinostomy can be performed to correct this issue.


 Bradycardia and Asystole


Bradycardia and asystole are possible complications of ocular manipulation due to the oculocardiac reflex. This reflex is mediated by the ophthalmic branch of the trigeminal nerve. The afferent pathway involves the ciliary ganglion, gasserian ganglion, and trigeminal sensory nucleus. Vagal efferents lead to parasympathetic stimulation of the heart, which can result in bradycardia and asystole.


Factors known to perpetuate this reflex include hypercarbia, hypoxemia, light anesthesia, young age, and strength and duration of the stimulus. 3 It is important to ensure the anesthesiologist you are working with is aware of this potential complication and potential exacerbating factors to minimize the risk. Communication with the anesthesiologist during the case is probably the most important aspect of care to prevent or minimize these issues. Should a patient develop bradycardia or asystole, medical management such as atropine can be administered. Persistent or recurrent bradycardia or periods of asystole may warrant external pacing and aborting the case.


 Skull Base Injuries/Cerebrospinal Fluid Leak


Skull base injuries are rarely encountered during endoscopic sinus surgical procedures. Preoperative CT imaging allows the surgeon to identify risk factors for skull base injury, such as a low-lying cribriform plate. If recognized intraoperatively, a variety of patching materials (e.g., mucosa, fascia, fat, or commercially available dural analogs) can be used to repair the leak.


It is important to recognize that an injury to the brain or its vasculature can occur when the skull base is violated. Postoperative imaging and serial clinical examination can lead to the diagnosis, and if present would warrant neurosurgical consultation ( ▶ Fig. 8.3).



Coronal CT (computed tomography) scan image demonstrating a left-sided injury to the skull base at planum sphenoidale from aggressive manipulation during an orbital decompression.


Fig. 8.3 Coronal CT (computed tomography) scan image demonstrating a left-sided injury to the skull base at planum sphenoidale from aggressive manipulation during an orbital decompression.


(This image is provided courtesy of courtesy of Dr. Raymond Sacks, MBBCH, FCS [SA] ORL, FRACS, MMed [ORL], University of Sydney, Sydney, Australia.)

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Feb 25, 2020 | Posted by in OTOLARYNGOLOGY | Comments Off on Complications of Orbital Decompression and Management
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