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 Table of Contents  
Year : 2022  |  Volume : 2  |  Issue : 1  |  Page : 227-228

Lateral and superior orbital wall autodecompression in a patient with thyroid eye disease

Department of Ophthalmology, Shiraz University of Medical Sciences, Shiraz, Iran

Date of Submission25-Nov-2020
Date of Acceptance17-Jun-2021
Date of Web Publication07-Jan-2022

Correspondence Address:
Dr. Elham Sadeghi
Poostchi Ophthalmology Research Center, Shiraz University of Medical Sciences, Shiraz
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijo.IJO_3540_20

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Orbital autodecompression was reported previously in thyroid eye disease (TED). The reports principally focused on spontaneous orbital wall fractures or medial and inferior orbital wall expansion. This report introduces a 66-year-old man, a known case of TED with distinctive signs of lateral and superior orbital wall autodecompression on preoperative imaging.

Keywords: Orbital auto decompression, proptosis, TED

How to cite this article:
Khademi B, Sadeghi E. Lateral and superior orbital wall autodecompression in a patient with thyroid eye disease. Indian J Ophthalmol Case Rep 2022;2:227-8

How to cite this URL:
Khademi B, Sadeghi E. Lateral and superior orbital wall autodecompression in a patient with thyroid eye disease. Indian J Ophthalmol Case Rep [serial online] 2022 [cited 2022 Jan 19];2:227-8. Available from: https://www.ijoreports.in/text.asp?2022/2/1/227/334944

Auto-decompression occurs in the tight orbits of patients with thyroid eye disease (TED) to relieve high intraorbital pressure. Based on the literature review, this phenomenon happens in two ways. The most convenient form ensues from the lax orbital septum and lets the orbital content protrude anteriorly and cause proptosis. The second infrequent route for this miracle supervenes through the bony orbit.[1] Reported bony autodecompression includes medial and inferior orbital walls spontaneous fractures or remodeling.[2],[3],[4]

We report a patient with TED who had asymptomatic autodecompression of lateral and superior orbital walls found on preoperative imaging for orbital decompression. This is the first report on the lateral and superior orbital wall autodecompression in a patient with TED, to the best of our knowledge.

The report adhered to the tenants of the Declaration of Helsinki. Consent to publish the patient's photographs was taken by the senior author.

  Case Report Top

A 66-year-old nonsmoker man, a known case of hyperthyroidism for 6 years with no other history of a medical disorder, referred to the thyroid eye clinic due to proptosis, ocular pain, red-eye, and decreased vision. Thyrotoxicosis was diagnosed 6 years ago and treated with radioactive iodine several months later. At the first ophthalmologic examination, the patient was biochemically euthyroid by receiving 125 μg of levothyroxine sodium. The patient was not taking any other medication.

The best-corrected visual acuity was 20/50 on the right and 20/30 on the left eye. Marcus-Gunn was positive in the right eye. The patient's color vision was impaired by using the Ishihara plate. Intraocular pressure was 28 and 30 mmHg on the right and left eyes, respectively. Optic disc examination revealed a 0.7 cup/disc ratio on the right side and 0.5 on the left side with bilateral optic disc rim pallor.

External eye exam showed marked eyelid puffiness, dilated episcleral vessels, swollen caruncle, and severe movement restriction in all gazes. The protrusion of the eyes was measured 28 mm on the right side and 30 mm on the left side, using the Hertel ophthalmometer (base = 103) [Figure 1].
Figure 1: Clinical photography reveals bilateral proptosis, lid edema, left upper eyelid retraction, right upper eyelid ptosis, and enlarge episcleral vein

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For evaluation of thyroid optic neuropathy, Humphrey visual field testing was performed, and bilateral inferior scotoma was detected.

Multislice computed tomography (CT) scan of the orbits revealed marked bilateral enlargement of extraocular muscle bellies in all rectus muscles, leading to apical crowding. Medial orbital walls bow toward the nasal septum bilaterally. Lateral orbital walls and the lateral part of the superior orbital walls were significantly thinned [Figure 2]. The patient did not have an old CT scan to compare with the new imaging. The patient refused any previous surgery, trauma, and inflammatory signs within the orbit. He consulted with an oncologist for any malignant process within the orbital walls and other organ systems, which was negative. Bone densitometry vector image showed no evidence in favor of osteoporosis. Due to refractory optic neuropathy, he underwent trans-lid orbital decompression. On dissection of the lateral orbital wall, thinning of the greater wing of the sphenoid was confirmed.
Figure 2: a. Coronal orbital CT scan reveals resorption and autodecompression of orbital roof (arrow). b. Axial, soft tissue window orbital CT scan shows lateral wall autodepression (arrowhead). c. Axial, bone window orbital CT scan demonstrates lateral wall thinning (arrowhead)

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  Discussion Top

Increased pressure in a closed bony space can lead to bone remodeling. Skull expansion can occur in the presence of an increase in intracranial pressure. This pressure effect can similarly occur in orbit.[5] Increased intraorbital pressure in patients with TED gradually propels toward bony orbital remodeling. Bone formation and resorption is a dynamic phenomenon that was regulated through mechanotransduction.[6]

Orbital autodecompression occurs as a protective measure against increased orbital pressure in patients with TED. Orbital septal laxity and consequent proptosis are the most tangible forms of this phenomenon. Autodecompression in bony orbit is, however, farfetched. The main areas of focus for bony autodecompression are the medial and inferomedial orbital walls.[7] All of the reports and investigations on orbital wall remodeling in TED report expansible changes in these two walls.[2],[3],[4],[7] Superior and lateral orbital walls, as the two thickest walls, were not reported as an object in autodecompression.

Three mechanisms can be proposed for this type of decompression in TED. Intraorbital pressure increases two times in patients with TED in comparison to healthy individuals. This rises even more in patients with dysthyroid optic neuropathy.[8] A long-standing increment in orbital pressure can lead to bone resorption, especially if the orbital septum is taut. The orbital bone expansion leads to intraorbital pressure reduction and might have a protective effect against optic neuropathy's development or progression.[4]

The second mechanism occurs through the stimulatory ability of the thyroid hormone on the bone turnover. The hyperthyroid state was demonstrated to decrease the bone mass densitometry. Although this effect was reported to be reversible, when it occurs concurrently with high intraorbital pressure it can augment the bony autodecompression.[9] The last mechanism could occur due to the osteoporotic effect of steroids. Our patient did not mention any course of steroid usage in the last 6 years.

To put it all together, we suggest that orbital autodecompression could be a systemic phenomenon. Increased bone turnover by thyroid hormone and glucocorticoids alongside the diffuse and local compressive effect of orbital contents expand the bony orbital cavity. We present a case of lateral and superior orbital bony wall expansion in TED, which was not reported previously. This finding gives a new insight into TED's autodecompressive effect, which could happen through a diffuse rise in the orbital content and hormonal imbalance.

  Conclusion Top

To the best of the authors' knowledge, this is the first report of the lateral and superior orbital wall autodecompression in TED. Although previous spontaneous autodecompression cases of the medial and inferior walls were reported, the underlying mechanism is not exactly well known, and ophthalmologists should carefully consider it before surgical decompression.

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


Conflicts of interest

There are no conflicts of interest.

  References Top

Bhermi GS, Gauba V, Brittain P. Spontaneous bony orbital auto-decompression in thyroid ophthalmopathy. Orbit (Amsterdam, Netherlands) 2006;25:123-5.  Back to cited text no. 1
Kashkouli MB, Pakdel F. Spontaneous orbital floor fracture in thyroid eye disease. Ophthalmic Plast Reconstr Surg 2010;26:301-2.  Back to cited text no. 2
Vaidya A, Lee PAL, Kitaguchi Y, Kakizaki H, Takahashi Y. Spontaneous orbital decompression in thyroid eye disease: New measurement methods and its influential factors. Graefes Arch Clin Exp Ophthalmol 2020;258:2321-9.  Back to cited text no. 3
Kang EM, Yoon JS. Clinical and radiological characteristics of Graves' orbitopathy patients showing spontaneous decompression. J Craniomaxillofac Surg 2015;43:48-52.  Back to cited text no. 4
Heifetz MD, Weiss M. Detection of skull expansion with increased intracranial pressure. J Neurosurg 1981;55:811-2.  Back to cited text no. 5
Robling AG, Castillo AB, Turner CH. Biomechanical and molecular regulation of bone remodeling. Annu Rev Biomed Eng 2006;8:455-98.  Back to cited text no. 6
Tan NYQ, Leong YY, Lang SS, Htoon ZM, Young SM, Sundar G. Radiologic parameters of orbital bone remodeling in thyroid eye disease. Invest Ophthalmol Vis Sci 2017;58:2527-33.  Back to cited text no. 7
Riemann CD, Foster JA, Kosmorsky GS. Direct orbital manometry in patients with thyroid-associated orbitopathy. Ophthalmology 1999;106:1296-302.  Back to cited text no. 8
Vestergaard P, Mosekilde L. Hyperthyroidism, bone mineral, and fracture risk--A meta-analysis. Thyroid 2003;13:585-93.  Back to cited text no. 9


  [Figure 1], [Figure 2]


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