|Year : 2022 | Volume
| Issue : 1 | Page : 45
Superior orbital fissure syndrome secondary to ophthalmic herpes zoster: Case Report
Katia Marquez Gonzalez, Joel Isai Quetzal Herrera
Department of Ophthalmology, General Regional Hospital, Merida, Yucatan, Mexico
|Date of Submission||23-Jul-2022|
|Date of Decision||14-Aug-2022|
|Date of Acceptance||15-Aug-2022|
|Date of Web Publication||22-Sep-2022|
Joel Isai Quetzal Herrera
Avenue Miguel Hidalgo 216, Garcia Gineres, 97070 Merida, Yucatan
Katia Marquez Gonzalez
Avenue Miguel Hidalgo 216, García Ginerés, 97070 Mérida, Yucatan
Source of Support: None, Conflict of Interest: None
Objective: The objective of this study is to report a case of superior orbital fissure syndrome (SOFS), secondary to ocular herpes zoster, with a favorable evolution.
Materials and Methods: Herpes zoster ophthalmicus (HZO) usually presents with ocular manifestations, being infrequent with the ophthalmoplegia. SOFS secondary to HZO is rare. We present the case of a 72-year-old man with dermatome involvement of the first left trigeminal branch, secondary to herpes zoster infection, who also developed herpetic keratitis in the left eye. After 8 days of antiviral treatment, he developed total left eye ophthalmoplegia that required steroid treatment. The evolution of the ophthalmoplegia was favorable with resolution at 3 months of follow-up.
Conclusions: It is essential to make known one of the complications of HZO infection, although not as frequent, just as important, is to recognize this pathology when it occurs for prompt management and recovery.
Keywords: Herpes zoster, neurological manifestations, ophthalmoplegia, orbital apex syndrome, orbital fissure syndrome
|How to cite this article:|
Gonzalez KM, Quetzal Herrera JI. Superior orbital fissure syndrome secondary to ophthalmic herpes zoster: Case Report. Pan Am J Ophthalmol 2022;4:45
|How to cite this URL:|
Gonzalez KM, Quetzal Herrera JI. Superior orbital fissure syndrome secondary to ophthalmic herpes zoster: Case Report. Pan Am J Ophthalmol [serial online] 2022 [cited 2022 Oct 3];4:45. Available from: https://www.thepajo.org/text.asp?2022/4/1/45/356712
| Introduction|| |
Varicella-zoster virus (VZV) is a DNA virus that is part of the herpesviridae family, it is neurotrophic and its main reservoir is found in humans. Herpes zoster ophthalmicus (HZO) is defined as herpes zoster virus (HZV) involvement of the ophthalmic division of the trigeminal nerve (CNV1). In the literature, HZO represents 7% of all cases of herpes zoster, and can include blepharitis, conjunctivitis, keratitis, uveitis, and retinal manifestations.
Cases of superior orbital fissure syndrome (SOFS) due to HZO have been reported in the literature; however, they are rare., We present the case of a 72-year-old patient with SOFS secondary to HZO.
| Case Report|| |
A 72-year-old male patient presented to the ophthalmology department reporting a skin rash, increased volume, and redness in the upper left eyelid region. In addition, he complained of pain in the upper and lower eyelids of the left eye. In laboratory studies performed at the time of consultation, diagnosis of type 2 diabetes mellitus was made. On examination, vesicular lesions were observed in the frontal region, orbit, tip, and dorsum of the nose (Hutchinson's sign) compatible with HZO.
His best visual acuity in the right eye was 20/30, and in the left eye, it was 20/50. The intraocular pressure was 22 mmHg in both eyes. The primary gaze position was in orthoposition, without limitation in eye movement.
In addition, he presented with blepharedema and Eyelid erythema. Biomicroscopy revealed conjunctiva with mixed hyperemia, chemosis, cornea with superficial punctate keratopathy, and crystalline with slight opacity. Fundoscopy was normal. The patient was diagnosed with HZO, and treatment was started with acyclovir 800 mg every 4 h, acyclovir ointment every 4 h for 10 days, and ciprofloxacin (ophthalmic solution).
On the 18th day of treatment, the patient reported a left hemicranial headache, with severe intensity and inability to open the left eyelid. Ophthalmological examination revealed severe left ptosis and total limitation of all ocular movements of the left eye; to the biomicroscopy, pseudodendrites, and stromal edema [Figure 1]. In addition, corneal hypoesthesia was found. Due to the increase in volume and the total paralysis of the left eye, an orbital tomography was requested, without evidence of tumor lesions [Figure 2].
|Figure 1: (a) Clinical photo showing skin lesions on the left side of the face, as well as left ptosis. (b) Biomicroscopy of the left eye, showing conjunctival hyperemia, cornea with stromal edema|
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|Figure 2: Simple tomography of the skull and orbits, without evidence of tumor lesions|
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After 11 days of antiviral treatment, limitation of eye movements was added [Figure 3]. It was decided to start treatment with prednisone 50 mg every 24 h, pregabalin 75 mg every 24 h, and timolol-dorzolamide every 12 h. Seven days after steroid initiation, left eye exotropia and a slight improvement in eye movements were evident [Figure 4].
|Figure 3: Strabogram, in which limitation of all the ductions of the left eye is observed|
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Three months after the first symptoms and signs of HZO, the patient presented improvement in both visual acuities, with 20/25 vision in both eyes, and eye movements, showing no limitations to versions or ductions [Figure 5].
| Discussion|| |
In people with a prior history of VZV infection, the virus remains latent within a dorsal root ganglion. The virus remains inactive in immunocompetent patients; however, the virus can be reactivated in immunocompromised. Involvement of the ophthalmic nerve (V1) gives rise to HZO after being latent within the Gasserian ganglion. HZV infection can affect any of the three branches of CNV.
The lifetime risk of developing herpes zoster is estimated at 25% and for those over 85 years of age, the risk increases to 50%. Among patients diagnosed with herpes zoster, some epidemiological studies estimate that around 8% to 20% are complicated by HZO. Of HZO cases, 20% to 79% have orbital involvement. Paralysis of the extraocular muscles in patients with HZO occurs in 3.5%–10.1%. Tran et al. describe recurrence rates at 1, 3, and 5 years for recurrent eye disease or rash of 8%, 17%, and 25%, respectively.
Manifestations of HZO can be classified by anatomical area:
- Periocular region: Unilateral radicular pain and vesicular rash,
- Conjunctiva: Follicular or papillary conjunctivitis
- Anterior segment: Episcleritis, scleritis, punctate epithelial keratitis, “pseudodendritic” keratitis, neurotrophic keratopathy, and among other
- Uvea: Iritis, iris atrophy, iridocyclitis, and panuveitis
- Vitreous and retina: Exudative or rhegmatogenous retinal detachment, acute retinal necrosis, progressive external retinal necrosis, and progressive outer retinal necrosis
- Neuro-ophthalmological: Optic neuritis and ophthalmoplegia.,
Ophthalmoplegia is one of the secondary neurological manifestations of HZO reported in the literature, whose main manifestation is paralysis of the III CN. Similarly, there are complications that involve more than one cranial nerve such as SOFS, which consists of dysfunction of the III, IV, and VI CN and the ophthalmic division of the nerve trigeminal nerve (V1). Moreover, it differs from orbital apex syndrome (OAS) in that the latter, in addition to having involvement of the previously mentioned nerves, presents affection of the optic nerve (II CN). Therefore, clinically, SOFS can be distinguished from OAS by preserving visual acuity and the pupillary reflex; signs that are compromised in affections of the orbital apex.
The median time to onset of HZV ocular involvement has been reported to be 1.82 weeks after the onset of skin lesions in dermatome V1.
The pathological mechanisms of ophthalmoplegia in HZO cases are not clear. Here are some of the hypotheses that have been raised:
- Perivascular and perineural inflammation: Histopathologic studies have shown inflammation of the vasculature and neural tissue in various ocular tissues,,
- Cytopathic damage to the virus to neural tissue and direct spread of HZV
- Cranial nerve compression: Caused by edema of the orbital soft tissue,,
- Microinfarct: Garg et al., proposed that there may be microinfarct of the cranial nerves.
The available literature on HZO with SOFS reports clinical improvement with the use of steroids and systemic antiviral medications. Recovery time for HZO-related ophthalmoplegia was reported to be 4.4 months on average, with a range of 2 weeks to 1.5 years. Complete recovery rates for ophthalmoplegia and optic neuropathy have been reported as 76.5% and 75%, respectively.
The clinical presentation of our patient with a previous diagnosis of HZO, with subsequent limitation of all eye movements (paralysis of the III, IV, and VI cranial nerves) of the left eye, as well as corneal hypoesthesia, an intact pupillary reflex (absence of optic nerve involvement), was consistent with SOFS. The patient was treated with systemic steroids, presenting complete improvement of the ophthalmoplegia.
Few cases of total ophthalmoplegia due to HZO have been reported; and of these, few are the case reports of SOFS secondary to HZO in the current literature.
| Conclusions|| |
Although SOFS secondary to HZV infection is rare, ophthalmologists should be aware that complete ophthalmoplegia can follow cutaneous or ophthalmic herpes zoster infection, so its timely diagnosis and treatment are essential.
Declaration of patient consent
The authors certify that they have obtained patient consent. The patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published, and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]