First case of melanoma-associated retinopathy with conjunctival melanoma
François Evoy, Jeanne Lafortune
Read MoreAcute orbital myositis preceding vesicular rash eruption in herpes zoster ophthalmicus
Austin Pereira, Angela Zhang, Pejman Jabehdar Maralani, Arun NE Sundaram
Read MoreHerpes zoster ophthalmicus (HZO) is a common ocular emergency caused by reactivation of the varicella zoster virus (VZV), leading to vesicular rash eruption in the ophthalmic division of the trigeminal nerve (V1). Clinical diagnosis is obtained with V1-distributed dermatomal rashes after a prodromal period of ocular pain, chemosis, visual impairment, diplopia, and ptosis.
Early recognition of this condition is important for timely medical management to prevent complications such as postherpetic neuralgia (PHN) and blindness. A less-documented, rare presentation of HZO is orbital myositis, which may be an early indicator of future vesicular rash eruption. We present a case of acute orbital myositis preceding vesicular rash eruption in HZO.
An 89-year-old female presented with a 4-day history of left periorbital edema, pain, and binocular diplopia. Her left eye (OS) demonstrated incomplete ophthalmoplegia, tonic pupil (fixed 5 mm), mild ptosis, proptosis, and conjunctival injection. The patient’s medical and surgical history was unremarkable except for 3+ nuclear sclerotic cataracts bilaterally. Retinal examination was unremarkable.
Two days after the initial presentation, the patient developed a vesicular rash in the left V1 distribution, with a positive Hutchinson sign. Slit-lamp examination demonstrated anterior chamber cells OS, and there was diffuse chemosis and complete ophthalmoplegia. Visual acuity OS declined from 20/200 to counting fingers, and her intraocular pressure increased from 19–22 mm Hg over these 2 days.
Axial computed tomography of the orbit (Fig. 1) and magnetic resonance imaging (MRI) brain (Fig. 2) demonstrated enlarged lateral, inferior, and medial recti muscles and proptosis OS. Immunologic and serologic analysis excluded autoimmune disorders and thyroid disease. The patient was started on intravenous acyclovir 450 mg TID and oral prednisone 60 mg. Repeat MRI done 2 weeks after initiation of treatment revealed improvement in the extraocular muscle (EOM) inflammation (Fig. 3). The patient reported localized ocular pain at initial presentation; however, this pain progressed to left facial discomfort in the V1 distribution over the following 2 months. PHN was diagnosed, and gabapentin 100 mg PO TID was started. By 4 months, her eye movements normalized in the left eye, coinciding with further improvement of the EOM thickening on MRI (Fig. 4). Visual acuity improved back to 20/200 and intraocular pressure normalized to 10 mm Hg. Symptoms of PHN resolved by the 11-month mark; MRI brain demonstrated resolution of proptosis and normal EOMs at this time (Fig. 5).
Ocular myositis is a rare inflammatory disorder of the EOMs. There are 2 major forms of ocular myositis, limited oligosymptomatic ocular myositis with conjunctival injection and severe exophthalmic ocular myositis with accompanying ptosis, diplopia, chemosis, and proptosis.
Our patient’s initial symptoms and imaging findings correlated well with severe exophthalmic ocular myositis. When the patient’s vesicular lesions erupted 2 days later, a diagnosis of HZO after reactivation of VZV was concluded. The reduction of visual acuity from 20/200 to counting fingers OS was most likely owing to uveitis secondary to HZO as demonstrated by the anterior chamber cells and the positive Hutchinson sign.
To our knowledge, only 7 previous cases of orbital myositis preceding vesicular rash eruption in patients with VZV reactivation have been published in literature. The first case published on this presentation by Volpe et al in 1991 described a 45-year-old male with unilateral periorbital edema, sharp pain, ptosis, chemosis, and diplopia owing to limited upgaze and adduction in his left eye.
Six other case reports with similar presentations of orbital myositis preceding vesicular rash eruption have since been noted in literature.
In all 6 previous cases, mean time to vesicular eruption after initial symptoms of orbital myositis was 4.8 days (range, 2–7 days); our patient presented with a V1 rash 6 days after initial symptoms. In concordance with our patient, all previous 6 cases demonstrated resolution of orbital symptoms after intravenous or oral antiviral and corticosteroid therapy. Our case further adds to the relative paucity of literature regarding the clinical course of orbital myositis preceding HZO rash presentation.
Of note, the case reported by Kim et al in 2012 was the only patient to develop PHN after initial presentation; this is a similar disease course as our patient, who experienced neurogenic left-sided facial pain.
PHN is a chronic, painful sequela of acute VZV reactivation that is the most common neurological complication of HZO and is associated with reduced quality of life.
Early and aggressive treatment of HZO with antiviral therapy could possibly reduce the risk for developing this neurological complication.
With over 90% of the world population currently hosting latent VZV, and with an estimated 25% recurrence of VZV infections, HZO is not an uncommon ocular emergency.
Common ocular involvement such as iritis, scleritis, and keratoconjunctivitis are seen in about 50% of patients with HZO,
and some of these patients may develop PHN, which can persist.
Acute orbital myositis as the initial presentation of HZO is very rare. Early recognition and prompt treatment of ocular myositis caused by HZO can possibly reduce the risk for blindness and PHN.
https://www.canadianjournalofophthalmology.ca/article/S0008-4182(19)30863-4/fulltext
Journal : CJO
Ref : HZO Orbit Orbital myositis
Primary intraocular mesenchymal chondrosarcoma: a histopathological surprise in an enucleated eye
Ratnesh Ranjan, Parag K. Shah, Sarang Giratkar, Santhi Ramachandran, Narendran Venkatapathy
Read MoreThe incidence of clinical and histopathological discordance in eyes enucleated for retinoblastoma, though not rare, has reduced significantly over a period of years.
Benign ocular lesions such as coats’ disease and persistent hyperplastic primary vitreous in end-stage conditions simulate retinoblastoma.
Nonmalignant ocular tumours such as ocular teratoma, astrocytic hamartoma, and retinal astrocytoma can also mimic retinoblastoma, clinically as well as on imaging, resulting in potentially avoidable enucleation.
Mesenchymal chondrosarcoma (MCS), a rare cartilage-forming tumour with potential aggressive course, is usually found in the skeleton. However, about one-third of the cases are also found in extra-skeletal sites, including orbit.
Although primary intraocular chondrosarcomas have been reported in fish and other mammals such as cats and dogs, there is no report of intraocular MCS in human eye. We are reporting the first case of presumed primary intraocular MCS confirmed on histopathological examination in an eye enucleated for retinoblastoma.
A 9-year-old girl was brought to our outpatient department with complaints of redness and pain in the right eye (RE) of 3 days’ duration. There was history of squinting and white reflex in the same eye for the past 3 years, but no prior ophthalmic consultation was taken. On examination, there was no perception of light in RE, and the best-corrected visual acuity in the left eye (LE) was 6/6. Anterior segment examination of RE revealed circumcorneal congestion, microcystic corneal oedema, shallow anterior chamber depth with 3+ cells, mid-dilated pupil, neovascularisation iris, and clear lens with retrolental white reflex (Fig. 1A). Findings of anterior segment and fundus examinations of LE were within normal limits. During examination under anaesthesia, same findings were noted in anterior segment of RE. Fundus examination showed exudative retinal detachment with white intraocular mass lesion. Intraocular pressure measured was 50 mm Hg in RE and 15 mm Hg in LE. Ultrasound B-scan showed well-defined mass lesion with intralesional calcification in the vitreous cavity with exudative retinal detachment suggestive of endophytic retinoblastoma (Fig. 1B). Magnetic resonance imaging (MRI) showed well-defined endophytic lesion in the temporal half of the right globe having features suggestive of retinoblastoma with scleral involvement in RE as detailed in Figure 2.
A diagnosis of stage 0 group E retinoblastoma was made, and the patient underwent enucleation with implant in RE. Enucleated globe was sent for histopathological analysis. Gross appearance of the cut open eye globe showed an intraocular multilobular greyish white well-defined tumour, measuring 1.2 cm × 1.4 cm, with interspersed tiny hemorrhagic foci arising from the posterior pole and extending anteriorly. The tumour appeared to be originating from choroid pushing retinal pigment epithelium, and causing retinal detachment (Fig. 3). Anterior chamber, sclera, and optic nerve were found uninvolved. Microscopic analysis of hematoxylin and eosin–stained sections from the eye ball showed intraocular tumour tissue involving choroid and vitreous, and closely intricated with retina. Tumour tissue showed sheets of undifferentiated round, oval, and spindle cells with abrupt transition. Small well-defined nodules of well-differentiated hyaline cartilage with central calcification and ossification were also seen. Areas of cartilaginous foci blending in hemangiopericytomatous pattern with undifferentiated cell tumour, haemorrhage, and necrosis were present. Immunohistochemical analysis confirmed the presence of cartilage by positive staining for S100 (Fig. 4). The histopathological features were suggestive of intraocular MCS.
Postenucleation computed tomography (CT) scan of the right orbit showed no residual lesion, whereas CT scan of the left orbit was normal. The child was referred to paediatric oncologist for systemic evaluation, but no other tumours or skeletal lesions were identified, ruling out the possibility of ocular metastasis.
Extraskeletal MCS is a very rare tumour, with orbit being the third most common site following meninges and lower extremities.
Since the first case reported by Cardenas-Ramirez et al in 1971, approximately 40 cases of primary orbital MCS are reported in literature till now, highlighting the rarity of primary intraocular MCS.
No case of intraocular MCS, primary or metastatic, in human being has been previously reported in literature.
Naturally occurring cartilage in fish eyes could be the source of origin for primary intraocular MCS in fish.
Mammals do not have cartilage or bone within their globes, and hence the source of origin of intraocular MCS is not clear in mammals. In mammals, the multipotent mesenchymal stem cells derived from the trabecular meshwork or from pericytes of bovine retina are found to have potential to differentiate into osteoblasts and chondrocytes, and hence could be the possible origin for the tumour in our case.
Extraskeletal MCS is usually seen in younger age group compared with conventional chondrosarcoma. Although orbital MCS commonly presents in second or third decades of life, paediatric cases, including congenital orbital MCS, are also reported.
Orbital MCS tends to present like benign orbital tumours with globe compression resulting in progressive proptosis, diplopia, reduction in visual acuity, and pain of variable severity.
In our case, due to its highly unusual location and late presentation, tumour mimicked as end-stage retinoblastoma and presented with pain and redness.
Imaging features of orbital MCS on CT and MRI scan are well described. CT scan shows well-defined, heterogeneously enhancing mass with calcification seen as high-intensity signal.
It usually causes widening of bony orbit without bone erosion.
MRI shows hypo- or isointense signal in T1-weighted scans, isointense signal in T2-weighted scans, and moderate to marked heterogenous enhancement of the soft-tissue component. Intralesional calcifications are seen as low-signal-intensity spots.
As an orbital tumour, ultrasonographic feature of MCS is very rarely reported in literature appearing as well-demarcated hypoechoic mass lesion with heterogenous echogenicity.
In our case, intraocular MCS appeared as large, well-defined, moderately echoic mass lesion with intralesional calcification causing high echogenicity and back-shadowing.
Macroscopic and microscopic features of tumour in our case were consistent with histological features of orbital MCS. Macroscopically, MCS appears as lobulated, soft-to-firm, grey-white mass with focal calcification or cartilaginous component
Microscopically, bimorphic appearance is the pathognomonic feature of MCS characterized by the presence of undifferentiated, round, or spindle-shaped mesenchymal cells arranged in sheets or small clusters, and islands of mature hyaline cartilaginous tissue. This cartilaginous differentiation is crucial for diagnostic confirmation, which often shows central calcification and even ossification.
Some tumours may show arrangement of mesenchymal cell surrounding vascular space resembling hemangiopericytoma.
Immunohistochemical analysis often reveals strong positivity for the S-100 protein by the cartilaginous component, whereas the cellular component shows positivity for CD99, vimentin, and Leu7. For diagnostic confirmation, however, immunohistostaining is used only in case of doubt when tumours such as malignant lymphoma, hemangiopericytoma, Ewing sarcoma, and soft-tissue chondroma mimic MCS.
Radical surgical excision with negative margins is the most effective treatment modality for MCS. Vision and globe salvaging resection is possible in cases of extraskeletal orbital MCS.
In our case, MCS being intraocular, enucleation was the only option for complete surgical removal, though it was done for a suspected diagnosis of retinoblastoma. Role of radiotherapy or chemotherapy in the management of MCS is limited for cases with incomplete removal or histologically aggressive tumour.
To the best of our knowledge, this is the first case to report intraocular MCS in the human eye. The presentation of intraocular MCS can mimic retinoblastoma. Imaging studies are of little use in differentiating intraocular MCS from retinoblastoma due to common imaging features. Being a malignant tumour with risk of distant metastasis, enucleation is the best treatment modality for intraocular MCS. Diagnostic confirmation is possible only after histopathological study of enucleated specimen.
https://www.canadianjournalofophthalmology.ca/article/S0008-4182(19)30546-0/fulltext
Journal : CJO
Ref : Mesenchymal chondrosarcoma Ocular Oncolgy RB Retinoblastoma
Pulsating lid: a rare presentation of sinus pericranii
Swan Kang, Shirin Hamed-Azzam, Fergus Robertson, Indran Davagnanam, David H. Verity
Read MoreSinus pericranii (SP) is a rare trans-osseous communication between the intracranial and extracranial venous drainage systems, and has only rarely been reported with signs in the superior eyelid.
In this report, we present a case of SP with venous drainage outflow located in the medial aspect of the upper eyelid.
A 50-year-old Caucasian woman presented with a 5-year history of a painless gradually enlarging left-upper-lid lump. There was no history of neurological deficit or periocular or head trauma, and apart from a history of hypercholesterolemia and a stable left iris nevus for 20 years, she was otherwise entirely well.
Examination revealed a subtly pulsatile fullness to the medial upper eyelid with engorged subcutaneous venous channels in the lateral half of the eyelid (see Fig. 1 and Video 1, Supplemental Digital Content [available online], which demonstrates prominent left-upper-lid vessels with a biphasic pulsatile pattern). However, there was no associated ptosis, and the signs did not change with the Valsalva manoeuvre. Her visual acuity and colour appreciation were normal, as were her pupil reactions to light, and ocular ductions. Finally, her retinal vessels in the left eye were mildly dilated.
Ultrasonography revealed grossly dilated nasal upper lid vessels that were compressible and hypo-echoic. Magnetic resonance imaging with time-of-flight angiography revealed a subtle midline frontal transcranial deficit conducting a vascular channel (see Figs. 2 and 3). This communicates with a prominent vessel, which descends over the forehead to dilated left preseptal draining veins. Digital subtraction angiography (DSA) confirmed a sinus pericranii draining the cerebral veins of the front third of the brain and communicating with left preseptal veins and thereafter the left facial vein (see Fig. 4, Fig. 5, Fig. 6).
Therapeutic options, including monitoring and surgical occlusion of SP, were considered. Although considered to be an accessory SP, a significant drainage area was noted on DSA, and thus occlusion of the venous connection was considered potentially unsafe, with possible compromise to frontal lobe drainage with risks of cerebral hemorrhage or infarction. Thus, and in the absence of recent progression, or functional or major aesthetic compromise, a period of active monitoring was agreed.
The report adhered to the ethics principles outlined in the Declaration of Helsinki as amended in 2013. A written consent was obtained and is on file.
Discussion
SP is an unusual venous anomaly characterized by communication of scalp veins with an underlying dural sinus. The condition was first described by Stromeyer in 1850.
SP typically presents in childhood with a nonpulsatile reducible soft tissue mass that increases in size with increased venous pressure.
SP is usually asymptomatic and most commonly occurs in the midline or the frontal region, and communicates with the superior sagittal sinus.
Venous outflow patterns associated with SP are classified as either dominant or accessory,and although most SPs occur as solitary lesions, up to 20% of patients are reported to have associated venous malformations elsewhere.
In some cases of SP with accessory venous outflow, surgical excision or endovascular embolization have been performed to improve cosmesis, to prevent hemorrhage, or to minimize the risk of air embolism.
SP is either congenital or acquired (possibly after trauma), with the former being differentiated from the latter by the presence of an endothelial lining.
Those presenting as a congenital extradural developmental venous anomaly are thought to be formed by transient venous hypertension during embryogenesis,
whereas in traumatic cases, injury to the emissary vein or dural sinuses is thought to lead to abnormal communications between the epicranial and dural venous systems.
Most cases of congenital SP present in children or young adults with equal gender distribution, whereas in traumatic cases there is a male preponderance.
Although patients with SP are often asymptomatic, headache, vertigo, dizziness, and pulsatile tinnitus are sometimes reported.
This anomaly is rare, and its natural history is unclear. In a previously reported case series of 21 patients, only 2 cases of untreated accessory SP resolved spontaneously, and the outcomes of dominant SP—which is almost always managed conservatively—depended on the underlying clinical and comorbid neurological conditions.
Evaluation of SP requires a thorough neurovascular imaging assessment, with investigations including colour Doppler ultrasonography, computed tomography, and magnetic resonance imaging. DSA is the gold-standard imaging modality as it clearly defines the lesional anatomy and the extent of the dependent cerebral venous territory.
There is no consensus or guideline on the optimal management strategy for this condition, and the therapeutic decision is individually tailored. Dominant SP, where the anomaly forms the major outflow for intracranial venous drainage, is best managed conservatively with life-time surveillance to monitor complications such as cerebral venous hypertension or hemorrhage.
Accessory SP can be treated with surgical or endovascular interventions depending on the presence of refractory symptoms and/or psychological impact caused by disfigurement. SP can be treated with endovascular or percutaneous image-guided embolization techniques or with open surgical ligation.
There have been only 4 cases reported in the literature of the SP involving the eyelid, and few cases in adults and pulsatile. The case reported herein is both exceptionally rare and atypical in a number of ways: (i) it involved the upper eyelid; (ii) there was subtle (transmitted) pulsatility and no enlargement with Valsalva manoeuvre; (iii) the patient presented in the fifth decade of life. Although rare, physicians should consider SP in the differential diagnosis of a vascular lid anomaly. Appropriate comprehensive neuroimaging should include catheter angiogram where diagnostic uncertainty persists. Surgery carries significant potential risk of air embolus, venous hypertension with consequent cerebral venous hemorrhage or infarction.
https://www.canadianjournalofophthalmology.ca/article/S0008-4182(19)30504-6/fulltext
Journal : CJO
Anterior approach levatorpexy for correction of congenital ptosis
Suresh Sagili, Jerome Ha
Read MoreWe describe a novel modification of levator advancement for congenital upper eyelid ptosis, in a case series. Written informed consent was obtained from all patients/parents. Local institutional review board approval was granted.
All procedures were performed under general anaesthesia. A cornea protector is recommended to protect the globe. The upper eyelid is everted and local anaesthetic (bupivacaine 0.25% with 1:200 000 adrenaline) is injected subconjunctivally (0.5 mL), superior to the tarsus. Local anaesthetic is also injected subcutaneously (1 mL) along the pretarsal region. An incision is placed in the upper eyelid skin crease, and dissection through the orbicularis is aimed toward the superior tarsus. The levator aponeurosis is grasps and dissection is then continued between the posterior levator aponeurosis and Müller’s muscle/conjunctival tissue, exposing the posterior surface of levator aponeurosis, commonly visible as a “white line.” Blunt dissection is then continued in this tissue plane to expose the posterior surface of levator. A single-armed 5-0 Vicryl suture (1/4 circle, spatulated needle) is placed partial thickness through the posterior surface of levator and advanced toward the previously exposed anterior tarsus (Fig. 1). Two sutures on a temporary knot are placed 2 mm on either side of the midpupillary line. The upper eyelid margin is left at the level of the superior limbus. The eyelid height can be adjusted by placing the sutures lower or higher on the posterior surface of the levator muscle if the upper eyelid appears overcorrected or undercorrected, respectively. The sutures are then permanently tied. The skin incision is closed with dissolvable sutures.
Fifteen eyelids of 14 patients (8 males, 6 females) were included in this study. Median age was 17 years (range 7–42 years). Thirteen patients had unilateral congenital ptosis and one was bilateral. None had jaw-wink synkinesis and recurrent ptosis.
The mean postoperative follow-up was 14 months (range 2–48 months). Mean levator function was 8 mm (range 6–10 mm). Mean preoperative margin reflex distance (MRD1) was 0.5 mm (range 0–1 mm), and the mean postoperative MRD1 was 3.2 mm (range 2–4 mm).
Postoperative results are shown (Fig. 2). There were 2 undercorrections and no overcorrections. All patients had mild exposure keratopathy, which improved with conservative management.
Anterior approach levatorpexy surgical technique is similar to the anterior approach white-line advancement, described by Sagili, for correction of adult aponeurotic upper eyelid ptosis.
However, in levatorpexy the dissection is continued upward beyond the levator aponeurosis (white-line) to expose and advance the levator muscle. We perform anterior levatorpexy in patients with a levator function of 6 mm or better.
Posterior approach levatorpexy described by Al-Abbadi et al is a similar technique, where the posterior surface of the levator is advanced through a conjunctival incision. Posterior approach upper eyelid ptosis correction techniques are believed to provide better cosmetic results because these techniques do not disrupt the orbital septum and pre-aponeurotic fat pad.
Anterior approach levatorpexy retains this advantage of keeping the orbital septum and pre-aponeurotic fat pad intact and avoids a conjunctival incision or excision of any tissue.
https://www.canadianjournalofophthalmology.ca/article/S0008-4182(19)31077-4/fulltext
Journal : CJO
Ref : Anterior levatorpexy Congenital Ptosis Oculoplastics Ptosis
Guidelines for vismodegib in the management of periocular basal cell carcinoma
Ahsen Hussain, Nancy Tucker, Dan D. DeAngelis, Vivian T. Yin, Edsel Ing, Bryan Arthurs, Harmeet S. Gill, Isabelle Hardy, Jeff Hurwitz, Vladimir Kratky, Babak Maleki, Navdeep Nijhawan, James Oestreicher, Aftab Zafar
Read MoreObjective
The management of advanced basal cell carcinoma (BCC) in the periocular region remains a clinical challenge. Vismodegib (Erivedge TM) has been approved in 2013 by Health Canada for adult patients with “histologically confirmed metastatic BCC or locally advanced BCC inappropriate for surgery or radiation.” An expert consensus was sought to create a standardised approach in the use of this novel treatment.
Methods
Fourteen practicing oculoplastic surgeons across Canada were involved in formulating and reviewing guidelines until consensus was reached. A consultancy meeting was followed by further ratification of guidelines over email. Two voting surveys were performed of the group to objectively assess agreement over each statement within the guidelines. Ratification continued until at least two-thirds of the group agreed on every guideline statement.
Results
The guidelines summarize 21 statements in a major and minor criteria format. A multidisciplinary team review is suggested for each patient with the involvement of recommended specialists. The internal survey revealed 100% agreement over 9 statements, 91.7% agreement over 8 statements, 83.3% agreement over 4 statements, and 2 statements had 66.7% and 58.7% agreement each. All statements with less than 91.7% agreement were surveyed again, and they were kept, modified, or removed on the basis of a consensus of over 66.7%.
Conclusions
These guidelines serve to act as a framework for physicians considering vismodegib for the medical management of patients with advanced or metastatic periocular BCC. Future applications, including neoadjuvant uses of the drug, may become apparent through further research.
https://www.canadianjournalofophthalmology.ca/article/S0008-4182(19)30989-5/fulltext
Journal : CJO
Ref : Eyelid BCC Ocular Oncology Periocular Basal Cell Carcinoma Vismodegib
Sudden-onset diplopia after LeFort I advancement
Christopher R. Dermarkarian, Honey Herce, Richard C. Allen
Read MoreA LeFort I osteotomy with horizontal advancement is a commonly used procedure to correct both class II and class III malocclusions, as well as dentofacial asymmetries.1 Complications associated with this procedure are variable but can include malposition of the maxilla, abscess formation, epistaxis, unilateral third nerve palsy, and Adie’s tonic pupil.1 We report a rare case of carotid-cavernous fistula and pseudoaneurysm formation after LeFort I advancement in a 24-year-old male with a unilateral left paramedian cleft palate with class III malocclusion and maxillary hypoplasia…..
https://www.canadianjournalofophthalmology.ca/article/S0008-4182(19)30749-5/fulltext
Journal : CJO
Ref : Carotid cavernous fistula Diplopia Lefort 1 Orbit Pseudo-aneurysm
Ophthalmia nodosa secondary to caterpillar-hair-induced conjunctivitis in a child
Solin Saleh, Seymour Brownstein, Mustafa Kapasi, Michael O’Connor, Paula Blanco
Read MoreOphthalmia nodosa is an inflammatory reaction in and around the eyes to certain types of insect and plant hairs possessing unique characteristics, including mechanical and toxic attributes.1,2 We recommend that ophthalmologists and paediatricians be informed of the potential complications from direct contact with these insects…..
https://www.canadianjournalofophthalmology.ca/article/S0008-4182(19)30817-8/fulltext
Journal : CJO
Vision loss secondary to sinusitis-related subperiosteal orbital hemorrhage
Jack H. Jeanes, David S. Curragh, Dinesh Selva, Gary Davis
Read MoreWe report a case of subperiosteal orbital hemorrhage secondary to sinusitis resulting in visual loss. A 74-year-old male presented to a rural emergency department with a less than 12-hour history of right-sided peri-orbital swelling and subsequent loss of vision in the eye. He had been generally unwell for 2 days before presentation with neck pain and frontal headache. Medical history included Parkinson’s disease and his medications included Aspirin.
On examination, visual acuities (VA) were hand motions in the right eye and 6/12 in the left eye. There was right upper lid swelling and restricted eye movements in all directions. There was right-sided proptosis (Fig. 1). He was febrile, and serological testing revealed an elevated white cell count and C-reactive protein.
The patient underwent an urgent canthotomy and cantholysis. Urgent computed tomography (CT) demonstrated a subperiosteal mass in the right superior orbit and opacification of the right sphenoid and ethmoid sinuses. Magnetic resonance imaging (MRI) demonstrated a well-defined orbital lesion that was bi-convex and showed T1-weighted hypointensity and T2-weighted hyperintensity (Fig. 2).
He received antibiotics and was transferred to a tertiary centre by air transport. On arrival, the right VA was perception of light; there was 8 mm of right proptosis, near total ophthalmoplegia, and a right relative afferent pupillary defect. A right temporal disc hemorrhage was present, and the orbit was tight. The initial cantholysis was assessed as incomplete and was immediately released before transfer to theatre where drainage of the orbital collection was performed. The superior orbit was approached via a sub-brow incision, where dark blood was released. A limited functional endoscopic sinus surgery was performed with pus drained from his posterior ethmoid and sphenoid sinuses.
After 24 hours, the right VA was hand motions in the right eye and progressed to counting fingers after 48 hours. After 5 days, the VA was 6/60, only in the inferior hemifield. He received IV antibiotics for a total of 5 days and was discharged on a further 10-day course of antibiotics. No growth was cultured from swabs from the orbit or sinuses. At 3 months visual loss from presumed inferior anterior ischemic optic neuropathy was sustained.
Reports of nontraumatic subperiosteal hematoma are uncommon and are typically associated with sudden events of raised cranial venous pressure.1 Harris et al postulated that orbital hemorrhage secondary to sinusitis may be caused by the transmission of phlebitis from the sinus mucosa to periorbital veins, resulting in subsequent rupture of the vessels due to vessel erosion or congestion.2
It is not common for spontaneous subperiosteal orbital hemorrhage to result in permanent loss of vision1; several mechanisms have been proposed. Direct nerve compression may occur as the superior mass exerts pressure and moves the eye downward.3 Loss of vision may also occur due to inferior optic nerve ischemia as a result of stretching or compression.3 This may explain the superior visual field defect seen in our patient. Optic nerve compromise and degree of stretch due to proptosis do not correlate with visual loss; however, acute stretching may result in permanent deficits.3
The differential diagnosis included a subperiosteal abscess. The coronal CT appearance of acute subperiosteal orbital hemorrhage is described as, “A well-defined, biconvex, non-enhancing extraconal mass with a homogeneous, high-density and a broad base abutting the bony orbit displacing peripheral fat toward the centre of the orbit.” MRI features are described as “a well-defined mass of varied signal intensity depending on the age of the haematoma.”4 Hyper-acute hemorrhages (less than 1 day) will show hypo-intensity on T1-weighted images and hyper-intensity on T2. Acute hemorrhages (1–7 days) show a low signal on both T1- and T2-weighted images.4
In contrast, subperiosteal abscesses are described as a “biconvex, well-defined mass of relatively homogenous density lower than extraocular muscle and higher than aqueous humour with a small amount of high density cotton like shadow with walls of moderate density” on coronal CT.5 CT images usually reveal association with an opacified sinus.4 MRI features were described as a “biconvex, well-defined, lesion showing T1 weighted hypo-intensity and T2 weighted hyper-intensity with arch shaped hypo-intensity on T1 and T2 weighted images displayed at the abscess wall.”5
Although conservative management may be an option in some patients, surgical drainage of subperiosteal orbital hemorrhage and subperiosteal abscesses are both indicated by optic nerve compromise.1, 4 Prompt drainage may result in early decompression and prevent sustained visual deficits.4 We report a case of subperiosteal hemorrhage secondary to sinusitis resulting in visual loss.
https://www.canadianjournalofophthalmology.ca/article/S0008-4182(19)30760-4/fulltext
Journal : CJO
Ref : Cantholysis Canthotomy Orbit Sinusitis Subperiosteal abscess Subperiosteal hemorrhage
Orbital and periorbital dermoid/epidermoid cyst: a series of 280 cases and a brief review
Neelam Pushker, Rachna Meel, Anand Kumar, Seema Kashyap, Seema Sen, Mandeep S. Bajaj
Read MoreObjective
To report one of the largest case series on periorbital and orbital dermoid/epidermoid cyst and to highlight some important and unusual findings.
Methods
Retrospective analysis of 280 cases with orbital or periorbital dermoid/epidermoid cyst that presented over a period of 14 years.
Results
Periorbital cyst was more than twice as common as orbital cyst. Majority of patients had bony changes with some unusual findings seen in cases with orbital cysts, that is, presence of fluid-fluid level, calcification in the wall, and coexistent double cysts in 19 (6.8%), 5 (1.8%), and 4 (1.5%) cases, respectively. Dumbbell dermoid cyst with connection in temporal fossa was seen in 16 (5.7%) cases. Subperiosteal location of orbital dermoid cyst was most destructive because of extensive bony invasion. Most of the periorbital cysts were removed in toto, whereas orbital cysts required decompression before removal. The histopathological diagnosis was dermoid cyst in 250 (89%) cases and epidermoid cyst in 30 (11%) cases. In 69 (25%) cases, there was a chronic inflammatory response.
Conclusions
We recommend imaging in all patients with orbital dermoid to rule out dumbbell or subperiosteal extension. Also, we advocate early removal of all dermoid cysts in view of bone changes seen in majority of our cases and presence of inflammatory cells in 25% of cases.
https://www.canadianjournalofophthalmology.ca/article/S0008-4182(19)30650-7/fulltext
Journal : CJO
Ref : Dermoid cyst Epidermoid cyst Orbit Orbital cyst Periorbital cyst