Download I. Case History Demographics 59-year

I.
Case History
Demographics
59-year-old white male
Chief complaint
Metamorphopsia OS following a fall from a 6ft ladder resulting in coma,
multiple skull fractures, and a subarachnoid hemorrhage.
Ocular history
1. Non-visually significant cataract OD, pseudophakia OS
2. Acute posterior vitreous detachment OS two years prior
Medical history
Recent head trauma from falling off a 6ft ladder, occurred two months prior to
the eye exam, and resulted in coma, subdural hematoma, subarachnoid
hemorrhage, and multiple skull bone fractures
Hypertension
Hyperlipidemia
Sleep Apnea
Coronary Artery Disease
Aortic valve stenosis
Medications
Hydrochlorothiazide/Lisinopril
Clonidine HCL
Levetiracetam
Aspirin
II.
Pertinent findings
Clinical
Best corrected acuity: OD: 20/25; OS: 20/150, PHNI
Preliminary Testing: Amsler grid OD: normal
OS: metamorphopsia nasal and temporal
Pupils, extraocular muscles, and confrontation visual fields
were all normal
Anterior Segment Exam: unremarkable OU
Tonometry (GAT mmHg): 12 OD, 13 OS
Dilated Fundus Exam:
OD: mild sectoral optic nerve edema with small splinter hemorrhages
on nerve margin. Few scattered nerve fiber layer and intraretinal
hemorrhages throughout posterior pole.
OS: sectoral optic nerve edema. Dense intraretinal hemorrhage adjacent
to macula. Scattered large sub-retinal hemorrhages along vascular
arcades.
Imaging studies:
-CT scan of brain without contrast showing:
 Multiple skull fractures including
o Left occipital fracture with extension to the
temporal bone
o Right zygomatic process fracture
o Right lateral orbit wall fracture
 Multiple hemorrhages including:
o Subdural hematoma
o Right periorbital hematoma
o Right lateral extracranial hematoma
o Subarachnoid hemorrhage
o Hemorrhage into right lateral rectus muscle
 Pneumocephalus
-Longitudinal studies over three months with optical coherence
tomography (OCT) of retina and optic nerve with accompanying fundus
photos
-Initial and follow-up threshold visual fields
III.
IV.
Differential diagnosis
Leading
Terson’s Syndrome
Purtscher’s retinopathy
Others
Valsalva retinopathy
Commotio retinae
Hypertensive retinopathy
Diagnosis & Discussion
Terson’s syndrome (TS) refers to any form of intraocular hemorrhage, either retinal or vitreal,
following a subarachnoid hemorrhage (SAH), traumatic brain injury (TBI) or intracerebral
hemorrhage.1 Its incidence is difficult to determine due to the high mortality rate associated
with intracranial hemorrhage, though it has been reported to occur in 8-46% of patients with
SAH.2 It is an important diagnosis to make because it is associated with a low Glasgow coma
scale, high Hunt and Hess grade, high Fisher scale, and a high mortality rate of up to 90%.1, 3, 4
Historically, it was believed that TS occurred due to an aneurysmal rupture that transmitted
through the optic nerve sheath and deposited into the retina.3 Recent studies have disproved
this mechanism, though, as TS has been reported in cases in which no SAH has occurred. It is
now thought to occur due to a rapid increase in intracranial pressure (ICP) transmitted along the
optic nerve sheath resulting in venous hypertension and the rupture of retinal vessels.3
Common visual complaints from TS include blurred vision and floaters. A vitreous hemorrhage is
the most common presentation, but the macula and various layers of the retina are frequently
involved as well. Considering the accepted mechanism of TS is increased intracranial pressure,
one would expect papilledema to be a more common finding. However, given the severity of
SAH, most studies examined post-mortem eyes or eyes that had the initial intracranial
hemorrhage several months prior to the fundus exam and were unable to be examined sooner
due to coma or prolonged hospitalization. Therefore, although few studies report papilledema,
the true incidence is likely underreported. Presentation is often bilateral, though asymmetric,
and signs typically appear within hours to days of the precipitating event. An intraocular
hemorrhage may be apparent on CT scan, though definitive diagnosis should be made with
fundoscopy. TS has a good visual prognosis with most cases showing spontaneous resolution
over a course of weeks, although vitreous hemorrhages may take up to 10-12 months to
resolve.4 Close monitoring for the first three to six months is indicated as complications can
occur that may require surgical intervention including epiretinal membrane, retinal folds,
proliferative vitreoretinopathy, retinal detachment and macular holes. In these events early
vitrectomy may improve visual prognosis, especially in cases of non-clearing vitreous
hemorrhages.4,5
V.
Treatment & Management
The patient was initially managed for the intracranial hemorrhages and coma at the ER. He did
not need surgical intervention to relieve intracranial pressure or repair the skull bone fractures.
He is currently co-managed by his primary care physician and neurologist. The patient will
continue to be monitored in the eye clinic monthly for at least six months. As of his five month
follow-up, the patient has shown a three-line improvement in visual acuity and improvement of
retinal hemorrhages and optic nerve edema.
VI.
Conclusion
Terson’s Syndrome is a rare and likely underreported condition, yet its diagnosis is significant as
it is associated with high rate of coma and mortality. Intraocular hemorrhages often resolve
spontaneously, but they may progress to further complications. Therefore close monitoring with
fundus exams is indicated so that prompt surgical intervention can be performed if necessary to
improve visual outcome.
VII.
Bibliography
1. Czorlich, Patrick, Christos Skevas, Volker Knospe, Eik Vettorazzi, Gisbert Richard, Lars Wagenfeld,
Manfred Westphal, and Jan Regelsberger. "Terson Syndrome in Subarachnoid Hemorrhage,
Intracerebral Hemorrhage, and Traumatic Brain Injury." Neurosurgical Review Neurosurg
Rev 38.1 (2014): 129-36. Web.
2. Hassan, Anhar; Lanzino, Giuseppe; Wijdicks, Eelco; Rabinstein, Alejandro; Flemming, Kelly.
“Terson’s Syndrome.” Neurocritical Care Soceity (2011) 15:554-558.
3. Czorlich, Patrick, Christos Skevas, Volker Knospe, Eik Vettorazzi, Manfred Westphal, and Jan
Regelsberger. "Terson’s Syndrome – Pathophysiologic Considerations of an Underestimated
Concomitant Disease in Aneurysmal Subarachnoid Hemorrhage." Journal of Clinical
Neuroscience (2016): n. pag. Web.
4. Skevas, Christos, Patrick Czorlich, Volker Knospe, Birthe Stemplewitz, Gisbert Richard, Manfred
Westphal, Jan Regelsberger, and Lars Wagenfeld. "Terson's Syndrome—Rate and Surgical
Approach in Patients with Subarachnoid Hemorrhage." Ophthalmology 121.8 (2014): 1628-633.
Web
5. Ko, Fang; Knox, David. “The Ocular Pathology of Tersons’ Syndrome.” Ophthalmology (2010)
117:1423-1429.
6. Lee, Gun-Ill, Kyu-Sun Choi, Myung-Hoon Han, Hyoung-Soo Byoun, Hyeong-Joong Yi, and ByungRo Lee. "Practical Incidence and Risk Factors of Terson's Syndrome: A Retrospective Analysis in
322 Consecutive Patients with Aneurysmal Subarachnoid Hemorrhage." Journal of
Cerebrovascular and Endovascular Neurosurgery J Cerebrovasc Endovasc Neurosurg 17.3 (2015):
203.
7. Sung, Watanabe, Bordon Arnaldo, Cavalheiro Sergio, Sallum Juliana, and Farah Michel. "Terson’s
Syndrome as a Prognostic Factor for Mortality of Spontaneous Subarachnoid Haemorrhage."
Acta Ophthalmologica 89.6 (2009): 544-47.