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Show Resolution of Oculorrhea After Skull Base Fracture We recently read the interesting case of "Cerebrospinal fluid (CSF) leak presenting as oculorrhea after blunt orbitocranial trauma" by Apkarian et al (1). We report a similar case of posttraumatic oculorrhea. A 33-year-old previously healthy man was brought to our trauma center 2 hours after being involved in a motor vehicle accident. He had loss of consciousness for a few moments after the accident and suffered from anterograde amnesia. On examination, his Glasgow Coma Score (GCS) was 12 (6/5/1). He was conscious and oriented with a 5- to 6-cm laceration on his forehead, extending from the mid-portion of his left eyebrow in an oblique line toward his hairline. Visual acuity was 20/25 in each eye and pupils reacted normally. On gentle palpation, there were multiple bone fragments of frontal skull bone under the laceration. Computed tomography revealed a depressed fracture of the left frontal bone involving the frontal sinuses and left frontal lobe contusion with pneumo-cephalus. After administration of loading dosage of phenyt-oin, the patient was transferred to the operating room. The left frontal depressed skull fracture was elevated, and pieces of bone and foreign body were removed. A 2-cm dural laceration was repaired with pericranial fascia and exenteration of both frontal sinuses was perforated using abdominal wall fat tissue. Cranioplasty was done with titanium mesh, and the sub-cutaneous tissue and skin incision were sutured. The patient was transferred to the intensive care unit and extubated 2 hours later. He had a GCS of 15, the day after surgery. On the second postoperative day, he developed oculorrhea through the left medial canthus. He was afebrile and did not have meningeal signs. An external lumbar drain was placed, and 1 hour later, the oculorrhea stopped. After 4 days, his lumbar drain was clamped for 24 hours, and the patient did not develop any signs of CSF leakage. The lumbar drain was removed, and the patient was discharged the next day. Although rare, CSF oculorrhea after head trauma must be recognized promptly to prevent meningitis, seizures, in-tracranial hypotension, and encephalocele formation. Most CSF leaks tend to cease without treatment (1,2), particularly those due to minor dural defects. If the leak is persistent, options include placement of a lumbar drain or surgical ex-ploration for repair of the leakage site. We treated outpatient with lumbar drainage for 4 days resulting in successful reso-lution of CSF leakage without complications. Our experience supports the treatment plan outlined in the report by Apkar-ian et al (1). Hosseinali Khalili, MD Nima Derakhshan, MD Fahim Baghban, MD Fariborz Ghaffarpasand, MD Department of Neurosurgery, Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran ghafarf@sums.ac.ir The authors report no conflicts of interest. REFERENCES 1. Apkarian AO, Hervey-Jumper SL, Trobe JD. Cerebrospinal fluid leak presenting as oculorrhea after blunt orbitocranial trauma. J Neuroopthalmol. [published online ahead of print March 11, 2014] doi:10.1097/WNO.0000000000000099. 2. Friedman JA, Ebersold MJ, Quast LM. Post-traumatic cerebrospinal fluid leakage. World J Surg. 2001;25:1062-1066. Localizing the Lesion in Foster Kennedy Syndrome From Hemiretinal Atrophy at the Macula We read with great interest the excellent summary and historical perspective regarding Foster Kennedy syn-drome by Lai et al (1). We recently saw another fascinating case of Foster Kennedy syndrome secondary to a suprasellar pilocytic astrocytoma, which showed a characteristic fundus pattern of hemiretinal atrophy respecting the vertical meridian in association with optic disc edema in the right eye and optic atrophy in the fellow eye, which localized the site of the lesion to the chiasm, left optic nerve, and third ventricle. A 13-year-old girl with an unremarkable medical history complained of headaches accompanied by nausea and vomiting over 4 weeks. She also had been experienc-ing intermittent crossing of the eyes for 1 week with associated diplopia. Visual acuity was 20/40 in right eye and 20/60 in left eye. There was a 1.2-log unit left relative afferent pupillary defect. Ocular motility showed normal versions and ductions. She had a 20-25 prism diopter comitant esotropia. The anterior segment exam-ination was normal. Funduscopy revealed right optic disc edema and left optic disc pallor (Fig. 1). There was visible dropout of the retinal nerve fiber layer (RNFL) in the nasal macula of the right eye, which respected the vertical meridian and edema of the RNFL temporal to the vertical meridian. Optical coherence tomography (OCT) revealed RNFL edema in the right eye and RNFL thinning in the left eye (Fig. 2). There was nasal hemiretinal thinning of the macular ganglion cell-inner plexiform layer complex in the right eye and diffuse thinning of the macular gan-glion cell layer in the left eye (Fig. 3). Results of kinetic perimetry are shown in Figure 4. Magnetic resonance im-aging demonstrated a suprasellar mass and obstructive 422 Letters to the Editor: J Neuro-Ophthalmol 2014; 34: 422-428 Letters to the Editor Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. FIG. 1. In the right eye, there is optic disc edema of the superior, inferior and nasal sectors but no temporal edema. The left optic disc is pale. There is thinning of the retinal nerve fiber layer in the nasal macula of each eye with delineation along the vertical meridian of the right eye (arrows), most visible superior to the fovea. FIG. 2. OCT reveals RNFL edema in a "twin peaks" distribution in the right eye and RNFL atrophy in the left eye (see quadrant and clock hour sector probability plot, right eye) that was not as obvious in the fundus photographs of the optic nerve shown in Figure 1 (comparisons are made with the normative database for 18-year-old individuals for illustrative purposes). OCT, optical coherence tomography; RNFL, retinal nerve fiber layer. Letters to the Editor: J Neuro-Ophthalmol 2014; 34: 422-428 423 Letters to the Editor Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. hydrocephalus (Fig. 5). Biopsy of the mass showed Grade 1 pilocytic astrocytoma. In our patient, one could predict the chiasmal location of the mass based on the fundus pattern of hemi-RNFL edema and atrophy in the same eye. The OCT findings further substantiated chiasmal involvement. It is known that chiasmal compressive lesions can produce a "bow-tie" pattern of optic nerve atrophy secondary to retrograde degeneration of the ganglion cells and axons supplying the temporal visual field (2). Our patient's right optic nerve appearance showed only FIG. 3. Macular ganglion cell-inner plexiform layer analysis shows thinning of the ganglion cell layer nasal to the fovea of the right eye, corresponding to temporal field loss. The pattern of retinal ganglion cell layer thinning respects the vertical me-ridian, especially in the superior retina. The retinal ganglion cell layer is diffusely thin in the left eye (comparisons are made with the normative database for 18-year-old individuals for illustrative purposes). FIG. 4. Kinetic perimetry demonstrates generalized visual field depression in each eye with temporal loss in the right eye, respecting the vertical meridian. 424 Letters to the Editor: J Neuro-Ophthalmol 2014; 34: 422-428 Letters to the Editor Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. a "half bow-tie" with edema superiorly, inferiorly, and nasally along with atrophy of the temporal sector. A pattern of supe-rior and inferior disc edema separated by a nasal and temporal band of atrophy has been described previously as "twin peaks" papilledema (3-6). Although this was not readily visualized on funduscopic examination, the OCT plot of peripapillary RNFL in the right eye showed a twin peaks pattern of edema. Our patient's fundus pattern of hemiretinal nerve fiber atro-phy respecting the vertical meridian through the fovea helped to localize the lesion to the chiasm and constitutes a diagnostic retinal feature. Although Sanders (1) ends his historical com-mentary on Foster Kennedy syndrome with a humorous com-ment "In Gowers' day, the clinician localized the lesion. Today, the neuroradiologist does it for him." Our case dem-onstrates the ability of the ophthalmologist to localize a lesion with accuracy that rivals the best neuroimaging. Jesse M. Vislisel, MD John J. Chen, MD, PhD Randy H. Kardon, MD, PhD Department of Ophthalmology, University of Iowa, Iowa City, Iowa The authors report no conflicts of interest. REFERENCES 1. Lai AT, Chiu SL, Lin IC, Sanders M. Foster Kennedy syndrome: now and then. J Neuroophthalmol. 2014;34:92-94. 2. Hoyt WF, Kommerell G. Der fundus oculi bei homonymer hemianopsie (article in German). Klin Monbl Augenheilkd. 1973;162:456-464. 3. Czarnecki JS, Weingeist TA, Burton TC, Thompson HS. "Twin peaks" papilledema: the appearance of papilledema with optic tract atrophy. Can J Ophthalmol. 1976;11:279-281. 4. Paul TO, Hoyt WF. Funduscopic appearance of papilledema with optic tract atrophy. Arch Ophthalmol. 1976;94:467-468. 5. Ing EB, Leavitt EA, Younge BR. Papilledema following bowtie optic atrophy. Arch Ophthalmol. 1996;114:356-357. 6. Mehta JS, Plant GT, Acheson JF. Twin and triple peaks papilledema. Ophthalmology. 2005;112:1299-1301. Thyroid Eye Disease: Therapy in the Active Phase: A Comment Bhatti and Dutton (1) recently published an eloquent review entitled: "Thyroid Eye Disease: Therapy in the Active Phase." Although the review is interesting and well written, we believe important information was left out from randomized controlled trials (RCTs) and published guidelines. We wish to address 3 major topics. First, the authors state that "Few randomized controlled studies have systematically evaluated these treatment strategies. . .." However, in reviewing the literature, quite a few RCTs have been conducted on the subject. A systematic review and meta-analysis published in 2009 in the Journal of Clinical Endocrinology & Metabolism evaluated 33 RCTs comparing treatment modalities for Graves orbitopathy (GO) (2). This meta-analysis demonstrated that intravenous pulse corticosteroids therapy had a small but statistically significant advantage over oral therapy, correlating with the consensus statement by the European Group on Graves Orbitopathy (EUGOGO) published in 2008 (3) and the American Thyroid Association (ATA) and American Association of Clinical Endocrinologists (AACE) guidelines FIG. 5. Contrasted axial (A) and coronal (B) magnetic resonance imaging reveals a 3 · 5 cm suprasellar mass involving the optic chiasm and left optic nerve and causing obstructive hydrocephalus. Letters to the Editor: J Neuro-Ophthalmol 2014; 34: 422-428 425 Letters to the Editor Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |
