Botulinum toxin complications and management
Michael Parker, Charlie James in Fundamentals for Cosmetic Practice, 2022
Orbital cellulitis will present with localised oedema and erythema in the soft tissues surrounding the eye similar to periorbital cellulitis. Key discriminating factors which should make you consider orbital cellulitis as a likely diagnosis is proptosis, ophthalmoplegia, decreased visual acuity (and colour vision) and painful eye movements. In severe cases, patients may have a relative afferent pupillary defect or present with symptoms of stroke or encephalitis. Should a patient present with any of these symptoms, also take the time to take a full set of observations including their neurological status. Please note, following botulinum toxin therapy, should a patient present with an isolated ophthalmoplegia, then this may be due to misadministration of toxin as opposed to an underlying infection.
Radiological Interpretation in Neuro-Ophthalmology
Vivek Lal in A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Inflammatory pathologies may be in the form of sarcoidosis, inflammatory pseudotumor, thyroid ophthalmopathy, granulomatous polyangiitis, etc. Imaging shows orbital soft tissue with fat heterogeneity giving it a dirty appearance. Muscle thickening may involve single/multiple extraocular muscles with involvement of their tendinous insertions (cf, thyroid orbitopathy, which involves multiple muscle bellies sparing their tendinous insertions; Figure 22.10). Thyroid profile is also frequently deranged. Orbital cellulitis may be secondary to spread of infection from the paranasal sinuses. Although the imaging may not be different from other inflammations earlier on in the disease process, presence of sinus disease and systemic signs of fever favor it. During the latter part of the infection, there may be formation of abscess which manifests as a peripherally enhancing centrally diffusion restricting lesion (Figure 22.11). Restriction of selective ocular movements may at times be secondary to individual muscle involvement by a cysticercus cyst (Figure 22.12) or bony entrapment of its belly due to bony injury (consequence of fracture leading to muscle impingement, commonly of the inferior rectus).
Accident and Emergency
Nagi Giumma Barakat in Get Through, 2006
A 3-year-old is brought to A&E with a swollen left eye. Orbital cellulitis is diagnosed. A baby girl presents with a history of oral thrush for the last 3 weeks. She is treated with nystatin orally, but without improvement.A 15-year-old girl presents with a history of vaginal discharge, and Trichomonas is isolated from the vaginal swab.An 8-year-old girl presents with a history of a productive cough, weight loss and a mild temperature. The chest X-ray shows right upper lobe consolidation with hilar lymphadenopathy and a strongly positive Heaf test.
Microbiological profile and antibiotic susceptibility trends in orbital cellulitis in India: an analysis over 15 years
Published in Orbit, 2022
Joveeta Joseph, Roshni Karolia, Savitri Sharma, Harithaa Choudhary, Milind N. Naik
Orbital cellulitis is an acute infection involving the postseptal orbital tissues, with paranasal sinuses being the most common source of organisms.1The infection may also spread from the eyelids, face, or lacrimal sac, directly lodged via penetrating injuries and retained orbital foreign bodies, or via hematogenous spread from distant sources. Less-common causes include acute dacryocystitis, dental infection, panophthalmitis, secondary infection in an orbital tumor, and mucormycosis.2,3 Presenting ocular signs include eyelid swelling, redness, pain, proptosis, and vision changes. Most patients are initially treated with empirical antibiotic therapy based on the suspected source of organisms. Surgical drainage is indicated if there is lack of improvement, worsening of symptoms, or compressive optic neuropathy.4 Since serious adverse outcomes can occur rapidly, and since the first line of management is empirical antibiotics, it is important to know the microbiologic trends related to this sight threatening eye infection. Microbiological susceptibility to antibiotics may also change over the years, warranting change in treatment practices.5,6 These pathogens can be isolated from various sites, such as the drained orbital pus, conjunctival/nasal swabs, blood culture, or even cerebrospinal fluid in rare cases of intracranial extension.
Superior ophthalmic vein thrombosis: A rare complication of Graves’ orbitopathy
Published in Orbit, 2018
Dante Sorrentino, Kenneth J Taubenslag, Lance M Bodily, Katherine Duncan, Tonya Stefko, Jenny Y Yu
Optimal treatment for SOVT remains subject to debate. However, intervention should depend, at least partially, on etiology. Orbital cellulitis necessitates antibiotic therapy. If an orbital inflammatory syndrome is diagnosed, corticosteroids should be considered. In the setting of hypercoagulable state, anticoagulation is logical option in the absence of contraindication.2 Because of the rarity of SOVT, the utility of anticoagulation has not been established by large-scale study or randomized trial and discussion of anticoagulation in the literature applies primarily to cases with extension of thrombosis to the cavernous sinus. Still, anticoagulation is almost always a reasonable therapeutic option, though it was not pursued in the present case beyond basic venous thromboembolism prophylaxis. We elected for definitive surgical decompression in this case for several reasons. As a current smoker with a known history of non-adherence to follow-up, as well as SOVT and exposure keratopathy, her prognosis without aggressive multimodal therapy was poor. Simultaneous total thyroidectomy was performed to reduce her risk of recurrent eye disease.
Bilateral periorbital leukemia cutis presenting as suspected cellulitis
Published in Orbit, 2022
Lalita Gupta, Melissa A. Levoska, Timmie Sharma, Kord Honda, Mark A. Prendes
A 79-year-old female with relapsed monoblastic AML presented from an outside hospital for management of bilateral eyelid edema unresponsive to empiric antibiotics and acyclovir. Eight years prior, she had been diagnosed with AML with normal cytogenetics, and received standard induction and consolidation chemotherapy with complete remission. Three months prior to presentation, she was found to have relapsed AML, with nucleophosmin 1 (NPM1), isocitrate dehydrogenase-2 (IDH2), and FMS-like tyrosine kinase 3 (FLT3) mutations, which was refractory to treatment with decitabine and venetoclax. She was to start azacitidine and enasidenib, but before she could begin these therapies, she was admitted for neutropenic fever to an outside hospital where she was found to have neutropenic enterocolitis and treated with intravenous antibiotics. Blood and urine cultures were negative. One week into her admission, she developed left periorbital edema, erythema and pain which rapidly progressed to bilateral involvement. CT orbits did not show findings of orbital cellulitis. Herpes zoster ophthalmicus was suspected and intravenous acyclovir was started.