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Diagnosis and Management of Superior Ophthalmic Vein Thrombosis

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Diagnosis and Management of Superior Ophthalmic Vein Thrombosis Ophthalmic Pearls OCULOPLASTICS Diagnosis and Management of Superior Ophthalmic Vein Thrombosis by jaya badhwar kumar, md, betsy colón-acevedo, md, and jason liss, md edited by sharon fekrat, md, and ingrid u. scott, md, mph lthough rare, superior oph- 1 thalmic vein thrombosis (SOVT) can lead to devas- tating complications if it is not detected and managed Apromptly and appropriately.1,2 While the exact pathogenesis of SOVT is un- clear, certain factors are known to pre- dispose individuals to this condition (which is not to be confused with su- perior branch retinal vein occlusion). A high level of suspicion is required to make the diagnosis. Etiology and Risk Factors Congestion of the superior ophthalmic vein (SOV) may occur as a result of infection, trauma, inflammation, hy- percoagulable states, neoplasm, and ANATOMY. The superior ophthalmic vein originates in the superomedial orbit, orbital crowding.3 In patients with or- passes through the superior orbital fissure, and ends in the cavernous sinus. bital infection, the concurrent orbital congestion can incite an inflammatory ptosis. The optic nerve may be affected if there is suspicion of SOVT or CST.1,4 cascade that culminates in thrombo- by compression, with clinical signs of MRI may demonstrate a dilated SOV phlebitis with thrombus formation; al- optic neuropathy such as reduced vi- and extraocular muscle enlargement. ternatively, thrombosis may be caused sual acuity, abnormal color vision, and Doppler imaging with ultrasound can by direct vascular invasion by the relative afferent pupillary defect.1,4,5 also be used to confirm the lack of pathogen. Offending bacteria may be SOVT may progress to cavernous si- flow in the SOV.6 aerobic or anaerobic, with Staphylococ- nus thrombosis (CST), and the patient Systemic associations. Patients cus aureus and anaerobic streptococci may have both conditions at the time with SOVT should be evaluated, in being the most common causative of presentation. consultation with an internist, for un- organisms.1,4 derlying systemic illness. Laboratory Diagnosis and Workup investigation should include a com- Presentation In the early stages, a mildly enlarged plete blood count looking for leukocy- Patients with SOVT may complain of SOVT may be missed on CT scans, tosis or left shift, an increase in the ra- orbital or facial pain and swelling, and decreased blood flow through the tio of immature to mature leukocytes. double vision, or decreased vision. SOV and cavernous sinus may not be Inflammatory and autoimmune Clinical findings generally indicate an apparent. Magnetic resonance imaging workup may be indicated, including orbital process and, depending on the (MRI) and magnetic resonance venog- laboratory tests for serum angiotensin- specific etiology, may include propto- raphy are more sensitive early in the converting enzyme, rheumatoid factor, bcsc section 5, 2013-2014 sis, chemosis, ophthalmoplegia, and disease process and are recommended antineutrophil cytoplasmic antibody, eyenet 35 Ophthalmic Pearls antimicrosomal antibody, and thyroid 2A 2B function.1,7 Chest x-ray may also be in- dicated to evaluate for sarcoidosis. If there are no signs of infection or inflammation, evaluation for a hypercoagulable condition may be warranted, including factor V Leiden, prothrombin gene mutation, lupus an- ticoagulant, and antithrombin III.1 SOVT SECONDARY TO SEPSIS. (2A) A 50-year-old diabetic man was admitted with methicillin-resistant S. aureus bacteremia, endocarditis, and new-onset left scalp Management phlebitis with associated left eye pain. Visual acuity was 20/50 in the left eye; The appropriate management of SOVT and ptosis, proptosis, chemosis, and incomplete ophthalmoplegia were present. depends on the etiology. (2B) MRI shows a T2 hypointense filling defect in the left superior ophthalmic Antibiotics. Infection is one of the vein, suggesting SOVT. Edema in the superior orbit extends into the left superior most common causes of SOVT and rectus muscle. After the patient was treated with IV vancomycin and IV heparin, associated CST. For this reason, em- VA improved to 20/25, and proptosis, ptosis, and ophthalmoplegia resolved fully. piric treatment with broad-spectrum antibiotics is recommended while are typically withheld in the acute 2012;70(9):2085-2091. awaiting culture results. Vancomycin phase of the disease, and patients 3 Grassi MA et al. Surv Ophthalmol. 2003; and ceftazidime are a typical initial are managed with IV antibiotics and 48(5):555-561. regimen.8 anticoagulation. If the etiology is non- 4 Cumurcu T et al. Semin Ophthalmol. 2013; Antibiotics should be extended for infectious, high-dose steroids may be 28(2):58-60. two weeks beyond clinical resolution used in the acute phase, followed by a 5 Berenholz L et al. Arch Otolaryngol Head of the infection, as pathogens may be slow taper for several weeks. Neck Surg. 1998;124(1):95-97. sequestered within the thrombus.4 If It has been suggested that noninfec- 6 Flaharty PM et al. Arch Ophthalmol. 1991; there is no evidence of local infection, tious SOVT may be a variant of idio- 109(4):582-583. a remote nidus should be considered, pathic orbital inflammatory disease, 7 Park HS et al. J Craniofac Surg. 2014;25(4): such as bacterial endocarditis.5 which may be steroid responsive. e322-324. Anticoagulation. The role of anti- Surgery. Surgical intervention is 8 Schmitt NJ et al. Ophthal Plast Reconstr coagulation therapy in isolated SOVT indicated in the presence of an orbital Surg. 2005; 21(5):387-389. is unclear. However, SOVT that is abscess or sinus disease to drain the 9 Einhaupl A et al. Lancet. 1991;338(8767): not treated with anticoagulation may primary source of infection as soon as 597-600. progress to CST, and some evidence possible.2 supports anticoagulation in the setting If orbital crowding is causing visual Dr. Kumar is an ophthalmology resident, Dr. of CST.2 Thus, if there are no contra- loss, orbital decompression may be an Colón-Acevedo is a fellow in oculoplastic indications to anticoagulation, such as option for some patients. n and reconstructive surgery, and Dr. Liss is an risk factors for intracranial or retro- oculoplastic surgeon; all are at the Duke Eye peritoneal hemorrhage, then systemic 1 Lim LH et al. Eye. 2014;28(3):348-351. Center in Durham, N.C. The authors report anticoagulation should be initiated.4 2 Desa V, Green R. J Oral Maxillofac Surg. no related financial interests. Dose-adjusted intravenous (IV) heparin is the recommended treat- 3A SOVT IN PROTHROMBIN MUTATION. ment. One randomized controlled trial (3A, 3B) A 54-year-old woman with a suggests an IV bolus injec tion of 3,000 history of prothrombin gene mutation IU followed by 25,000 to 65,000 IU/ presented after two days of worsening day continuous IV infusion, adjusted right eye pain and headache. She had according to prothrombin time (PTT) 3B visual acuity of 20/30 in both eyes, and such that the PTT is doubled but does ptosis and proptosis were apparent on 9 not exceed 120 seconds. her right side. (3C) Contrast-enhanced Steroids. The role of corticosteroids MRI shows a tubular hyperdensity in the 2,8 in SOVT is, likewise, controversial. right superior ophthalmic vein with no Although limiting the inflammation of evidence of cavernous sinus thrombosis. thrombophlebitis within the tight con- 3C She was treated with IV heparin and fines of the orbit would be beneficial, bridged to the oral anticoagulant rivarox- the risk-to-benefit ratio of this inter- aban. She ultimately had full resolution vention has not been determined. of ptosis and proptosis. If the etiology is infectious, steroids betsy colón-acevedo, md 36 may 2015.
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