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American Journal of Ophthalmology Case Reports 24 (2021) 101214
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Case report
Traumatic central retinal vein occlusion following a hawk attack to the
posterior cranium
Jake E. Tenewitz
a
,
*
, Andrew A. Girard
a
, Mont J. Cartwright
a
,
b
a
University of Central Florida College of Medicine, 6850 Lake Nona Blvd, Orlando, FL, 32827, USA
b
Medical Eye Associates, 921 North Main Street, Kissimmee, FL, 34744, USA
ARTICLE INFO
Keywords:
Traumatic central retinal vein oculsion
Trauma
Acute vision loss
Bird attack
Retinal vein thrombosis
ABSTRACT
Purpose: We describe a patient who developed a central retinal vein oculsion following a diving hawk attack to
her posterior cranium.
Observations: A 50-year-old female presented with decreased visual acuity and color perception in the left eye
following a diving hawk attack to her right-posterior parietal cranium. Medical history was signicant for well-
controlled type 2 diabetes, hyperlipidemia, and obesity. Fundoscopy of the left eye revealed pre, intra and
subretinal hemorrhages in all 4 quadrants consistent with the “blood and thunder” appearance. Additional
ndings included optic disk edema, venous dilation and tortuosity. Optical Coherence Tomography of the left eye
demonstrated pronounced macular edema with intra and subretinal uid accumulation. Pattern electroreti-
nography of the left eye was attened.
Conclusions and Importance: There are few documented cases of central retinal vein occlusion following blunt
trauma to the cranium in the literature. To the best of our knowledge, this is the rst case of central retinal vein
occlusion associated with posterior cranial trauma. Also unique to the case is the mechanism of injury whereby
the patient was attacked by a hawk at a high-diving velocity.
1. Introduction
Central retinal vein occlusion (CRVO) is the second most common
retinal vascular disorder after diabetic retinopathy.
1
Currently, there is
no consensus as to the exact pathogenesis of this condition. The most
commonly held belief is that Virchow’s triad - endothelial dysfunction,
hypercoagulability, and abnormal blood ow - contributes to thrombus
formation in the central retinal vein thus leading to occlusion. Histo-
pathologic studies conducted by Green et al. supports the theory of
thrombus formation as the precipitating event for CRVO development.
In this study, a fresh or recanalized thrombus was noted in 29 eyes from
28 patients with CRVO.
2
Thrombus formation typically occurs at or
anterior to the lamina cribosa. This observation is explained by the
narrowing of the central retinal vein at the level of the lamina cribrosa,
thus promoting turbulent blood ow and thrombus formation.
3
We present a patient who developed a central retinal vein oculsion in
her left eye following a high-velocity diving attack from a hawk to her
right-posterior parietal cranium. The patient was lost to follow-up prior
to anti-VEGF therapy. While her long-term visual outcome is unknown,
her prognosis is poor.
2. Case presentation
A 50-year-old Caucasian female was walking through a Central
Florida forest preserve when a hawk ew into her right-posterior pari-
etal cranium at a high diving velocity. Upon impact, the patient expe-
rienced a brief loss of consciousness. The event was observed by another
individual who accompanied the patient. The patient presented to the
local emergency department complaining of mild pain at the impact site
and decreased visual acuity and color perception in the left eye. The
wounds appeared supercial and insignicant and were treated appro-
priately. Head and neck MRI and CT imaging were unremarkable.
The patient was seen within 12 hours post-injury by an ophthal-
mologist (MJC). Her BCVA was 20/20 OD and 20/HM OS. All exam
ndings on the right eye were within normal limits. Slit lamp exam of
the left eye and vitreous was unremarkable. Fundoscopy of the left eye
revealed pre, intra and subretinal hemorrhages in all 4 quadrants
consistent with the “blood and thunder” appearance. Additional ndings
included optic disk edema, venous dilation and tortuosity. These nd-
ings were consistent with a diagnosis of central retinal vein occlusion.
Eight days after the injury the patient presented for outpatient follow
* Corresponding author.
E-mail address: jaketenewitz@gmail.com (J.E. Tenewitz).
Contents lists available at ScienceDirect
American Journal of Ophthalmology Case Reports
journal homepage: www.ajocasereports.com/
https://doi.org/10.1016/j.ajoc.2021.101214
Received 30 October 2020; Received in revised form 7 June 2021; Accepted 20 September 2021
American Journal of Ophthalmology Case Reports 24 (2021) 101214
2
up. Visual function in the left eye had not improved. Pupils were equal,
round, and reactive to light. A relative afferent pupillary defect was not
observed. Funduscopic examination and IVFA studies of the left eye
revealed similar ndings from the initial presentation (Figs. 1 and 2).
Importantly, IVFA demonstrated delayed ow through the venous sys-
tem thus providing further evidence in favor of CRVO. Vitreous hem-
orrhage was now present and precluded an adequate view of the retina
to assess for ischemia. Optical Coherence Tomography of the left eye
demonstrated pronounced macular edema with intra and subretinal
uid accumulation. Macular thickness was increased at 441
μ
m. Pattern
electroretinography of the left eye was attened (Fig. 3).
The patient was to be re-evaluated 8 weeks status post injury for
possible anti-VEGF therapy. However, the patient had to reschedule this
appointment to 12 weeks status post injury. At this visit, the vitreous
hemorrhages had resolved, but the pronounced macular edema with
intra and subretinal uid accumulation remained unchanged. The pa-
tient’s visual acuity had not improved (20/HM OS). Intravitreal Eylea
(Aibercept) was attempted but was unsuccessful due to patient coop-
erativity. The injection was rescheduled for the following week under
anesthesia but the patient was lost to follow up.
The patient’s ocular history was positive for primary open angle
glaucoma suspicion. Prior to the trauma, her BCVA was 20/20 bilater-
ally. Past medical history was signicant for well-controlled type 2
diabetes, hyperlipidemia, and obesity. Social history was signicant for
tobacco and alcohol use. The family history was non-contributory.
3. Discussion
Three previous studies have documented the occurrence of CRVO
following cranial trauma.
4–6
Differences, however, are noted between
this case and those described previously. Kline et al. described a patient
who experienced a blow to the right anterior cranium with a crowbar
without a loss of consciousness. The patient subsequently developed an
ipsilateral CRVO 10 days later. Venograms revealed persistent luminal
narrowing in the superior ophthalmic vein bilaterally and the authors
attributed this to a congenital abnormality, due to the bilateral nature of
the variant. Given the decreased diameter of the vein, they concluded
that ow in upstream regions was likely turbulent. They speculated that
the blow to the head was the inciting event which further perturbed
hemodynamics in the region, ultimately leading to thrombosis.
Hope-Robertson et al. and Cozzoli documented similar cases, with CRVO
development occurring over four to seven days, but failed to provide
venograms or evidence of central retinal vein or ophthalmic vein
anatomic variants.
Interestingly, the CRVO in our patient differs in two ways from
previous reports. First, the visual acuity deterioration in the left eye
occurred on the scale of minutes to hours rather than days. Second, our
patient experienced a right sided, posterior blow to the parietal region of
the skull with a contralateral CRVO.
The cause of CRVO in this patient was multifactorial, with the blow
to the right posterior cranium serving as a precipitating event for
thrombosis via disruption of normal hemodynamics. The impact likely
Fig. 1. Fundus photo of the left eye eight days after the inciting trauma.
Fig. 2. Fluorescein angiography of the left eye eight days after the
inciting trauma.
Fig. 3. Pattern electroretinography of the left eye eight days after the
inciting trauma.
J.E. Tenewitz et al.
American Journal of Ophthalmology Case Reports 24 (2021) 101214
3
caused a sudden jolt in head motion which resulted in a coup-contrecoup
injury to the brain, as evidenced by the immediate loss of consciousness.
The coup-contrecoup injury provides a plausible mechanism for the
contralateral location of the CRVO with respect to the site of trauma.
Sudden rapid displacement of the brain and orbital contents within
the rigid connes of the cranium and orbit respectively may have led to
various compressive and shearing forcing acting on the intracranial and
orbital contents (including the central retinal vein) resulting in excessive
traction on myriad nerves and vessels traversing these structures. This
might have precipitated endothelial damage and turbulent blood ow,
promoting thrombosis with subsequent occlusion of the vein.
While the conditions described above can serve as a nidus for
thrombosis in the setting of a traumatic brain injury, this phenomenon is
exceedingly rare. Therefore, additional risk factors must have been
present which predisposed this patient to CRVO.
The patient had several signicant vascular risk factors that predis-
posed her to thrombosis and increased her risk of CRVO: obesity,
hyperlipidemia, type 2 diabetes mellitus, and chronic tobacco use. The
patient’s ocular history was signicant for primary open angle glaucoma
suspicion without any past or current elevation in intraocular pressure.
While glaucoma is known to carry a signicant risk for retinal vein
thrombosis, little is known about the association between glaucoma
suspicion and CRVO.
7
Congenital vascular anatomic variants can also predispose patients
to CRVO via hemodynamic alterations. In the patient described by Kline
et al. luminal narrowing of the superior ophthalmic vein contributed to
the development of CRVO. Additional examples of such anomalies
include congenital macro vessel, excessive tortuosity, AVM, anomalous
branching, and anomalous connections.
8,9
In our patient, uorescein
angiography and fundoscopy did not reveal any vascular anomalies.
Nonetheless, this does not rule out the possibility that our patient
harbored an anatomic variant as an orbital CT angiogram and/or orbital
venogram would have provided a more complete picture of the patient’s
vascular anatomy. However, these imaging studies were not ordered as
the identication of a vascular anomaly is primarily of academic interest
and would not benet the patient.
4. Conclusion
There are few documented cases of CRVO following blunt trauma to
the cranium in the literature. To the best of our knowledge, this is the
rst case of CRVO with posterior cranial trauma. Also unique to the case
is the mechanism of injury whereby the patient was attacked by a hawk
at a high-diving velocity.
Given that the overwhelming majority of individuals who suffer a
traumatic brain injury do not develop a CRVO, we speculate that the
presence of numerous vascular risk factors in our patient predisposed
her to thrombosis and subsequent CRVO under the tumultuous condi-
tions of the TBI. The presence of a congenital venous anomaly would
have further altered the venous hemodynamics thus creating conditions
even more favorable for thrombosis. While the patient did not receive a
thorough workup for congenital venous anomalies, we surmise that the
patient has an increased likelihood of harboring such a variant with
respect to the general population.
Patient consent
The patient consented to publication of the case in writing. This
report does not contain any personal information that could lead to the
identication of the patient.
Funding source
No funding or grant support.
Authorship
All authors attest that they meet the current ICMJE criteria for
Authorship.
Intellectual property
We conrm that we have given due consideration to the protection of
intellectual property associated with this work and that there are no
impediments to publication, including the timing of publication, with
respect to intellectual property. In so doing we conrm that we have
followed the regulations of our institutions concerning intellectual
property.
Declaration of competing interest
No conict of interest exists.
Acknowledgements
None.
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J.E. Tenewitz et al.
