Letters to the Editor Resolution of Oculorrhea After Skull Base Fracture
W
e 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 pneumocephalus. After administration of loading dosage of phenytoin, 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 subcutaneous 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,
Localizing the Lesion in Foster Kennedy Syndrome From Hemiretinal Atrophy at the Macula
W
e read with great interest the excellent summary and historical perspective regarding Foster Kennedy syndrome 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 experiencing intermittent crossing of the eyes for 1 week with 422
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, intracranial 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 exploration for repair of the leakage site. We treated outpatient with lumbar drainage for 4 days resulting in successful resolution of CSF leakage without complications. Our experience supports the treatment plan outlined in the report by Apkarian 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 [email protected]
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.
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 examination 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 ganglion cell layer in the left eye (Fig. 3). Results of kinetic perimetry are shown in Figure 4. Magnetic resonance imaging demonstrated a suprasellar mass and obstructive Letters to the Editor: J Neuro-Ophthalmol 2014; 34: 422-428
Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited.
W
e 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 pneumocephalus. After administration of loading dosage of phenytoin, 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 subcutaneous 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,
Localizing the Lesion in Foster Kennedy Syndrome From Hemiretinal Atrophy at the Macula
W
e read with great interest the excellent summary and historical perspective regarding Foster Kennedy syndrome 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 experiencing intermittent crossing of the eyes for 1 week with 422
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, intracranial 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 exploration for repair of the leakage site. We treated outpatient with lumbar drainage for 4 days resulting in successful resolution of CSF leakage without complications. Our experience supports the treatment plan outlined in the report by Apkarian 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 [email protected]
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.
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 examination 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 ganglion cell layer in the left eye (Fig. 3). Results of kinetic perimetry are shown in Figure 4. Magnetic resonance imaging demonstrated a suprasellar mass and obstructive Letters to the Editor: J Neuro-Ophthalmol 2014; 34: 422-428
Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited.
