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 Table of Contents  
CASE REPORT
Year : 2021  |  Volume : 1  |  Issue : 2  |  Page : 383-385

Ophthalmic artery occlusion due to orbital compartment syndrome after a frontotemporal craniotomy


1 Department of Ophthalmology, New York University, New York, NY, USA
2 Department of Ophthalmology, New York University; Department of Ophthalmology, Manhattan Eye, Ear, and Throat Hospital, Northwell Health, New York, NY, USA
3 Department of Ophthalmology, New York University; Department of Ophthalmology, Columbia University, New York, NY, USA

Date of Submission20-Jun-2020
Date of Acceptance29-Sep-2020
Date of Web Publication01-Apr-2021

Correspondence Address:
Dr. Lauren DeMaria
New York University, 222 East 41st Street, 3rd Floor, New York, NY - 10017
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijo.IJO_1982_20

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  Abstract 


A 32-year-old female with a right frontal lobe glioma underwent an elective frontotemporal craniotomy. One hour postoperatively, the patient developed a right orbital compartment syndrome (OCS) with unilateral acute vision loss, proptosis, afferent pupillary defect, and complete ophthalmoplegia. The patient underwent emergent lateral canthotomy and inferior cantholysis. Neuroimaging revealed extensive vascular congestion along the extraocular muscles at the orbital apex. Retinal imaging demonstrated an ophthalmic artery occlusion. OCS following a frontal or frontotemporal craniotomy relates to increased orbital venous congestion from direct compression of the myocutaneous flap and subsequent intraorbital pressure elevation, vascular compromise, and ocular ischemia.

Keywords: Craniotomy, frontotemporal craniotomy, ophthalmic artery occlusion, orbital compartment syndrome


How to cite this article:
DeMaria L, Tran AQ, Tooley A, Abdelhakim A, Belinsky I, Kim E. Ophthalmic artery occlusion due to orbital compartment syndrome after a frontotemporal craniotomy. Indian J Ophthalmol Case Rep 2021;1:383-5

How to cite this URL:
DeMaria L, Tran AQ, Tooley A, Abdelhakim A, Belinsky I, Kim E. Ophthalmic artery occlusion due to orbital compartment syndrome after a frontotemporal craniotomy. Indian J Ophthalmol Case Rep [serial online] 2021 [cited 2021 Apr 11];1:383-5. Available from: https://www.ijoreports.in/text.asp?2021/1/2/383/312347



Acute vision loss after a craniotomy is an uncommon event, occurring in about 10% of cases from orbital roof defects, manipulation of the optic nerve, or manipulation of the ophthalmic artery.[1],[2] In rare cases, irreversible vision loss can occur from orbital compartment syndrome (OCS).[3],[4],[5] The etiology is related to the reflected myocutaneous flap inadvertently compressing the orbit and inducing vascular congestion. Herein, the authors present an ophthalmic artery obstruction and unilateral OCS following a frontotemporal craniotomy with a bicoronal myocutaneous flaps. This case was reported in compliance with the Health Insurance Portability and Accountability Act and adheres to the Declaration of Helsinki.


  Case Report Top


A 32-year-old female with a frontal lobe glioma underwent a right frontal craniotomy [Figure 1]a. The patient's head was tilted to the right in a supine position using a Mayfield three-pin fixation device. Bicoronal myocutaneous flaps were reflected anteriorly and secured with fishhooks over the orbit. A wedge resection involving the superior frontal gyrus, orbital gyrus, and gyrus rectus was performed. The craniotomy was closed with titanium miniplates and screws and staples to the scalp with a Jackson-Pratt drain placed. The surgery lasted 8 h without direct manipulation to the optic strut, orbital roof, or orbital apex.
Figure 1: (a) Preoperative MRI highlighting the right frontal lobe glioma without involvement of the orbit. (b) Postoperative coronal CT revealing significantly enlarged right extraocular muscles at the orbital apex. (c) Postoperative T2 coronal MRI with contrast revealing enhancement of intraorbital portion of the right optic nerve and (d) engorged extraocular muscles at the right orbital apex

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Upon awakening, the patient developed right ocular injection and mild extraocular restriction. Within an hour, the symptoms progressed to periorbital swelling, proptosis, complete ophthalmoplegia, and vision loss. The patient's visual acuity declined from hand motion to light perception. The intraocular pressure was 53 mmHg with a brisk relative afferent pupillary defect. Posterior examination demonstrated a perfused optic disc without frank edema. The patient underwent an inferior canthotomy and cantholysis and was given 1 g of intravenous acetazolamide, topical latanoprost, timolol, dorzolamide, and brimonidine [Figure 2]. Computed tomography (CT) of the orbits illustrated extensive enlargement of the extraocular muscles extending to the right orbital apex [Figure 1]b. Subsequent magnetic resonance imaging of the orbits revealed persistent swelling of the extraocular muscles and mild enhancement of the intraorbital optic nerve [Figure 1]c and [Figure 1]d.
Figure 2: External photography of the patient's right eye after canthotomy and inferior cantholysis, demonstrating periorbital swelling, proptosis, and ophthalmoplegia

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Despite 3 days of 1 g of intravenous methylprednisolone, the patient's vision deteriorated to no light perception (NLP). Repeat posterior examination 24 h later demonstrated a pale fundus with scattered dot–blot hemorrhages and blurred disc margins. Optical coherence tomography and fundus images demonstrated diffuse retinal edema that eventually progressed to retinal and choroidal atrophy over 3 months [Figure 3]a, [Figure 3]b, [Figure 3]c. The right eye remained NLP with persistent complete ophthalmoplegia 3 months later.
Figure 3: Fundus and OCT photos of the right eye at postoperative (a) week 1, (b) month 2, (c) and month 3 highlighting initial diffuse retinal swelling with eventual development of choroidal and retinal atrophy

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  Discussion Top


OCS after a craniotomy surgery is a rare and devastating event. The majority of cases describe bilateral OCS following a bifrontal craniotomy or unilateral OCS after an ipsilateral frontal or frontotemporal craniotomy.[3],[4],[5] Patients at risk of postoperative OCS are those with a larger degree of preoperative proptosis and those undergoing aneurysm repair.[6] In cases of OCS with aneurysm repairs, vision loss does not result from direct injury to the ophthalmic artery.[6]

Previously, “orbital infarction syndrome” was thought to occur secondary to a sudden decrease in intracranial pressure and vasoregulatory mechanisms.[7] This resulted in acute orbital hypoperfusion and vascular insult to the ophthalmic artery. Nonetheless, due to anastomoses of the ophthalmic artery with the external carotid arteries, orbital ischemia usually develops from hypoperfusion of its terminal branches.[5] Thus, posterior ischemic optic neuropathy and central retinal artery occlusion are possible consequences of this vascular compromise.[4]

Recent studies have investigated causes of increased intraorbital pressure and vascular compromise from external surgical factors. Direct compression of the globe from the myocutaneous flap can increase orbital venous congestion, compromise perfusion pressure, and eventually cause compressive optic neuropathy and related artery occlusions.[8] Specifically, venous congestion of the supraorbital vein from the coronal flap propagated to the superior ophthalmic vein leading to compression and hypoperfusion of the ophthalmic artery at the orbital apex. Additionally, the flap traction can compress orbital contents, impair venous outflow, and collapse intraorbital perfusion.[6] Propagation of pericranial edema from the resulting flap may also play a role. In the authors' presented case, tension from the fishhooks stabilizing the bilateral myocutaneous scalp resulted in elevated intraorbital pressure and impaired orbital venous outflow. The patient's right head tilt in the supine position contributed to additional gravitational effects worsening the periorbital edema to the right side, explaining the possibility of why the left eye was unaffected. This resulted in rapidly engorged extraocular muscles, increased in intraorbital pressure, and compressive effect of the optic nerve and ophthalmic artery. Although additional mechanisms contributing to ophthalmic artery occlusion were not ruled out, the clinical and radiographical evidence supports OCS as the main contributing factor for the patient's acute ocular deterioration.

Special consideration intraoperatively can help minimize the risk. Standard neurosurgical positioning precautions can decrease the tension on the orbit such as stretching the skin flap 30-45 degrees from the horizontal plane.[6],[9],[10] Minimizing surgical hooks to retract the scalp can decrease the amount of intraorbital pressure. Frequent eye checks to assess intraorbital pressure should be considered. The use of an eye shield instead of a bulky gauze between the eye and the scalp can assure more adequate ocular protection.[9]


  Conclusion Top


While unilateral or bilateral vision loss due to OCS is a rare sequela of a frontal or frontotemporal craniotomy, neurosurgeons and ophthalmologists should be aware of this possible complication. The authors present a unique case of unilateral vision loss and complete ophthalmoplegia that resulted from bicoronal myocutaneous flaps. Prevention measures should be taken to avoid direct ocular pressure from the myocutaneous scalp flap, minimize pericranial congestion from head positioning in a supine position, and ensure adequate intraoperative eye protection.

Acknowledgments

This research was supported in part by an Unrestricted Grant from Research to Prevent Blindness to NYU Langone Health Department of Ophthalmology.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Habets JGV, Haeren RHL, Lie SAN, Bauer NJC, Dings JTA. Acute monocular blindness due to orbital compression syndrome following pterional craniotomy. World Neurosurg 2018;114:72-5.  Back to cited text no. 1
    
2.
Rizzo JF III. Visual loss after neurosurgical repair of paraclinoid aneurysms. Ophthalmology 1995;102:905-10.  Back to cited text no. 2
    
3.
Takahaski Y, Kakizaki H, Selva D, Leibovitch I. Bilateral orbital compartment syndrome and blindness after cerebral aneurysm repair surgery. Ophthalmic Plas Reconstr Surg 2010;26:299-301.  Back to cited text no. 3
    
4.
Vahedi P, Meshkini A, Mohajernezhadfar Z, Tubbs RS. Post-craniotomy blindness in the supine position: Unlikely or ignored? Asian J Neurosurg 2013;8:36-41.  Back to cited text no. 4
[PUBMED]  [Full text]  
5.
Maier P, Felgen N, Lagreze WA. Bilateral orbital infarction syndrome after bifrontal craniotomy. Arch Ophthalmol 2007;125:442-3.  Back to cited text no. 5
    
6.
Pahl FH, de Oliveira MF, Dal Col Lucio JE, Souza E Castro EF. Orbital compartment syndrome after frontotemporal craniotomy: Case report and review of literature. World Neurosurg 2018;109:218-21.  Back to cited text no. 6
    
7.
Beck RW, Greenberg S. Post-decompression optic neuropathy. J Neurosurg 1985;63:196-9.  Back to cited text no. 7
    
8.
Gauden AJ, Hardy T, Mack HV, Danesh-Meyer HV, Kaye AH. Orbital compartment syndrome following aneurysm surgery. J Clin Neurosci 2012:19:1032-6.  Back to cited text no. 8
    
9.
Kim TS, Hur JW, Park DH, Kang SH, Park JY, Chung YG, et al. Extraocular pressure measurement to avoid orbital compartment syndrome in aneurysm surgery. World Neurosurg 2018;118:e601-9.  Back to cited text no. 9
    
10.
Choudhari KA, Pherwani AA. Sudden visual loss due to posterior ischemic optic neuropathy following craniotomy for a ruptured intracranial aneurysm. Neurol India 2007;55:163-5.  Back to cited text no. 10
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