Internal Carotid Artery Injury

Injury to the internal carotid artery (ICA) is perhaps the most feared complication in ESS, with a significant potential for mortality. The ICA is separated from the sphenoid sinus mucosa only by thin bone, often less than 0.5 mm, and dura. In 8% of specimens in 1 anatomic study, the bone was entirely dehiscent leaving only mucosa and dura over the ICA. Others have suggested a dehiscence rate as high as 22%. Injury to the carotid can be from a laceration with immediate massive hemorrhage, pseudoaneurysm formation with delayed hemorrhage, or present with neurologic changes from spasm or thrombosis. A review of ICA injury found only 28 case reports of ICA injury in the ESS literature.

Experience with management of this drastic although rare complication comes from the endoscopic skull base literature, where extended skull base approaches can have rates of ICA injury of around 5%. First and foremost, it is critical to adequately and thoroughly review all imaging and specifically check for carotid dehiscence before performing surgery near the sphenoid. Appropriate informed consent with risk of vascular injury when approaching the sphenoid or skull base region should always be obtained. A clear plan of action is essential in managing this emergency. Bleeding should be controlled with nasal and pharyngeal packing, and compression of the carotid in the neck while the anesthesiologist resuscitates the patient. The patient should be transferred immediately for neurointerventional angiography for coiling or possible stenting of the injured vessel. Some authors have reported success repairing an injured carotid with muscle patches.

Sphenopalatine Pseudoaneurysm

The delayed presentation of massive bleeding suggests the possibility of a ruptured pseudoaneurysm. A pseudoaneurysm is a contained arterial rupture that arises after disruption of all 3 layers of the vessel wall. Hematoma and the perivascular tissues form a wall around the pulsatile blood that tracks into the perivascular space. The pseudoaneurysm sac is at risk for delayed rupture and resultant massive bleeding. The SPA exits the sphenopalatine foramen just behind the lacrimal crest as the terminal branch of the maxillary artery. The sphenopalatine foramen is located at the posterior superior corner of the maxillary sinus where it is at risk for injury. Care should especially be taken during revision sinus surgeries or anytime a wide antrostomy is made.

Two cases of SPA pseudo aneurysm after ESS have been reported in the literature. Iatrogenic SPA pseudoaneurysms have also been encountered after maxillofacial procedures with LeFort osteotomies and transnasal or transseptal approaches to the pituitary gland. A pseudoaneurysm should be suspected when faced with delayed and recurrent epistaxis, often days after the initial arterial injury. The initial management of a pseudoaneurysm is the same as any large volume epistaxis: control with nasal packing and hemodynamic support as needed. Diagnosis is obtained by imaging with CT angiography or a formal angiogram. Definitive management requires either endoscopic ligation of the proximal SPA or maxillary artery or endovascular embolization. In the majority of reported cases of SPA pseudoaneurysm, embolization was the treatment of choice, although endoscopic ligation of the SPA proximal to the pseudoaneurysm has been reported. Often in the case of intractable epistaxis, angiography can be diagnostic and allows simultaneous intervention via embolization.

Sclerosing Lipogranuloma

Penetration through the periorbita can lead to multiple morbidities such as orbital hematoma or direct injury to the medial rectus or globe, as discussed elsewhere in this issue. A less known possibility is the development of a lipogranuloma in the violated orbital fat. The development of lipogranuloma has been attributed to surgical trauma with violation of orbital fat or the use of intranasal topical ointment. A lipogranuloma presents as a mass or swelling in the eyelid or orbit. Rarely proptosis, diplopia, or gaze restriction are present.

One series reported 10 cases of eyelid and anterior orbit lipogranuloma after ESS that presented to an ophthalmology clinic over a 5-year period. All ESS cases in this series had been complicated by an intraoperative orbital hematoma. These patients then developed slowly growing tumors of the eyelid over weeks to months. Excision of these tumors revealed infiltrative granulomas. The authors suggest a foreign body reaction to a paraffin-containing ointment used in the nasal packing as the cause.

Rosner and colleagues reported 2 cases of orbital lipogranuloma after ESS that presented to their ophthalmology clinic within days of ESS. Both patients presented with proptosis, gaze restriction, diplopia, and a mass within the orbit and eyelids. Surgical debulking was required in both cases. These authors propose that the hematoma and pressure within the orbit caused fat necrosis with a lipogranulomatous reaction occurring to exposed necrotic orbital fat and hemorrhage. Likely the cause of an orbital lipogranuloma is multifactorial, with orbital trauma, fat necrosis, ointment use, and host factors all playing a role.

Rare Causes of Blindness

Loss of vision is a feared and debilitating complication of ESS. This is most commonly caused by intraorbital hematoma. We review the uncommon causes of partial or complete vision loss.

Vanden Abeele and colleagues reported a case of blindness thought to be caused by aggressive monopolar electrocautery. This patient developed complete vision loss in 1 eye and a partial loss in the contralateral eye after electrocautery was used to control postoperative hemorrhage. Imaging was without retrobulbar hematoma or optic nerve injury, but a lamina papyracea defect was noted. This case suggests that monopolar cautery should be avoided along the orbit and course of optic nerve, especially with a defect in the lamina papyracea.

Infiltration of local anesthetic with epinephrine is thought to have caused blindness during endonasal injection. In a series of 4 patients who presented to a neuroophthalmology clinic with acute visual loss after nasal surgery, submucosal injection of anesthetic with epinephrine under pressure was deemed to be causative. The likely mechanism for an intranasal injection to affect the optic nerve is via the anterior and posterior ethmoid arteries. These anastomose with the ophthalmic artery, which is the main blood supply to the optic nerve via the posterior ciliary arteries. Vasospasm from the epinephrine is believed to have caused ischemia and a permanent deficit. Injection into the greater palatine foramen before or during ESS can result in arterial spasm and, ultimately, blindness. Care should be taken to never inject more than 2 mL of fluid or penetrate the needle further than 25 mm into the foramen. In addition, injection of steroid into nasal polyps has resulted in blindness owing to large particle size, ultimately leading to orbital vascular spasm. The dental literature has multiple reports of local anesthetic causing blindness, with the vast majority being a transient amaurosis rather than permanent blindness. Optic nerve damage leading to blindness after the direct application of adrenaline-soaked pads has also been reported in cases with an exposed optic nerve.

Rare cortical blindness, indirectly related to ESS, has been reported in the literature. One case was related to meningitis and increased intracranial pressure. The other case was related to cardiac shock from anesthesia. Ultimately, both patients had herniated cerebellar tonsils leading to traction on the central optic nerve and, ultimately, blindness.

Avoidance of orbital blindness includes excellent preoperative preparation with review of the imaging and specific evaluation of lamina dehiscence or thinning, location of the anterior ethmoid artery, or a hypoplastic maxillary sinus with plastering of the uncinate. Intraoperatively, care should always be taken to identify clearly the lamina and have a clear visualization of the operative field. The Stankiewicz maneuver, also known as the “bulb press test,” should be used to check for orbital fat herniation.