Grand Rounds
Eddie Apenbrinck M.D.
University of Louisville School of Medicine
Department of Ophthalmology & Visual Sciences
5/1/2015
Subjective
CC: blurry vision and headache
HPI:47 year old white male admitted to the VA
hospital for syncope after climbing a flight of stairs
2 days prior to admission. Consulted for blurry
vision associated with headache.
POH: refractive error (lost glasses)
PMHx: seizures (not on medication),
bipolar disorder (not on medication),
GERD
left upper deep venous thrombosis (5 years ago) and
pulmonary embolus (10 years ago)
ROS: denies any flashes/floaters/ocular pain. +intermittent
dizziness
Meds: Cetirizine 10mg daily
Omeprazole 20mg daily,
Allergies: NKDA
Social:+Cocaine use
Denies cigarettes and alcohol use
Imaging: On admission

CT head:


High attenuation in the right transverse dural venous
sinus as well as the posterior descending portion of
the superior sagittal sinus. “These may be normal
intravascular blood in a patient with high hematocrit.”
MRI/MRV: pending
CT head
Superior
Superior Sagittal Sinus
Right Transverse Sinus
Inferior
Exam
OD
OS
VA(cc, near):
20/30-2
20/40-2
Pinhole
20/20
20/20
Pupils:
3
3
2
2
no RAPD
IOP:
EOM:
16
15
full
full
Exam
OD
Anterior Segment
L/L:
C/S:
Cornea:
AC:
I/L:
Vitreous:
OS
WNL OU
WNL OU
WNL OU
No cell or flare OU
WNL OU
WNL OU
DFE
Optic Nerve:
MVP:
3+ disc edema
WNL OU
Optic Nerve iPhone Photo
OD
OS
MRV showing dural venous
thrombosis
Normal
Normal
Dural venous thrombosis involving superior sagittal sinus, right transverse sinus
and right sigmoid sinus. No flow seen in the right internal jugular vein
Normal MRV
MRI T2 Axial:
Absence of Flow Void
Absence of flow void in superior sagittal sinus
Labs

CBC:
13.9
5.9
334
40.7

PT:
12.0

INR:
1.0

PTT:
25.0
(11.8-14 seconds)
(21.7-36.5 seconds)
Labs: Hypercoagulation Workup

Prothrombin Gene Mutation: not detected

Factor V Leiden Gene Mutation: not detected

Antithrombin III:

Protein C and Protein S: WNL

Cardiolipin IgG and IgM: WNL
WNL
Assessment and Plan

Assessment:


47 year old white male with bilateral disc edema secondary to
Dural Venous Thrombosis involving the right transverse
sinus and the superior sagittal sinus
Plan:




Anticoagulate with heparin
Discuss medication compliance and need to stop cocaine use
Patient was transferred to UL for Neurosurgery evaluation
Hematology consult placed once patient at UL
UL Hospital Course

Ophthalmology:


Re-consulted for bilateral papilledema, planned for
outpatient followup at the VA for HVF testing and
refraction
Neurosurgery:

Initially planned for angiography with attempt to do
a thrombectomy but deemed unrealistic as patient
had complete occlusion of the right internal jugular
UL Hospital Course

Hematology

Reviewed hypercoagulability work-up and were
unable to determine cause of patient’s clotting
disorder

Patient initially placed on heparin drip during
hospitalization then placed on Lovenox and bridged
to Coumadin, planned for life-long anticoagulation

Follow-up arranged with VA hematology/oncology
2 months Hematology Follow-up

No additional thrombotic events

Patient to remain on chronic anticoagulation due
to high risk of another thrombotic event despite
negative tests.

Plan to complete hypercoagulable work up:

flow cytometry for PNH and lupus anticoagulant
Cerebral Venous Thrombosis

Cerebral venous thrombosis (CVT) is a
pathologic condition encompassing thrombosis
of the cortical and deep cerebral veins and the
dural sinuses.

First described in the early 19th century in a 45year-old man harboring a systemic malignancy
who had thrombosis of the superior sagittal
sinus demonstrated at autopsy.
Cerebral Venous Thrombosis
Incidence

Rare disease and the incidence is unknown as
most of the estimates are derived from autopsy
studies

Autopsy studies have reported the incidence to
be as low as 0.03% and as high as 9%.
Cerebral Venous Thrombosis

Despite a long list of possible causes of CVT,
some investigators estimate that as many as 40%
of cases are idiopathic

CVT affects all age groups and both sexes, but
with a strong preponderance in women between
20 and 40 years of age
Clinical Findings

Highly variable clinical manifestations

Increased intracranial pressure is thought to be
the underlying cause of these symptoms.
Headache is the most common and often the earliest
symptoms seen in ~80% of patients
 Papilledema ~50%
 Mental status changes ~25%
 Nausea, Vomiting

Diagnosis/Treatment

Diagnosis:
MRI/MRV gold standard
 CTA/CTV


Treatment
Treatment of underlying condition
 Anticoagulation
 Thrombolytics
 Thrombectomy
 Endovascular stenting


Literature review to determine the link between
cocaine and arterial or venous thrombosis

Review of Medline, CINAHL, Embase,
Psycinfo, and Cochrane databases

2458 abstracts reviewed with 15 full-texts papers
meeting inclusion criteria
Conclusions:

Cocaine is a pro-thrombotic agent that activates the
thrombotic pathways

There is an association between cocaine and myocardial
infarction particularly among young adults

Cocaine may casually associated with cerebrovascular accident
though studies lacked sufficient power to determine a
statistically significant effect

There is a gap in the evidence pertaining to the issue of
cocaine and venous thrombosis

Case report of a 30 year patient who presented with occipital
headache and vomiting without a history of trauma but
admitted to extensive cocaine abuse

Examination revealed bilateral papilloedema and imaging
confirmed a superior sagittal and transverse sinus thrombosis.

The patient was diagnosed with cocaine-induced central
venous thrombosis

Managed with routine anticoagulation and a repeat MRV
showed re-cannulation of the vessels.
References
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Nat MJ Wright, Matthew Martin, Tom Goff, et al. Cocaine and thrombosis: a narrative
systematic review of clinical and in-vivo studies. Substance Abuse Treatment,
Prevention, and Policy 2007, 2:27
Hunt MG, Lee AG, Kardon RH, et al. Improvement in papilledema and visual loss
after endovascular stent placement in dural sinus thrombosis. Neuroophthalmology 2001
Sep;26(2):85-92.
Burns H, Rich P, An Unpleaseant hit from Cocaine: A Case of Cocaine-induced
Cerebral Venous Sinus ThrombosisJ Neurol Neurosurg Psychiatry 2012;83:A1
Carhuapoma JR, Mitsias P, Levine SR. Cerebral venous thrombosis and anticardiolipin
antibodies. Stroke. 1997;28:2363.
Erez N, Babuna C, Uner A. Low incidence of thromboembolic disease. An evaluation
of obstetric and gynecologic patients in Istanbul. Obstet Gynecol. 1966;27:833.
Towbin A. The syndrome of latent cerebral venous thrombosis: its frequency and
relation to age and congestive heart failure. Stroke. 1973;4:419.
Ribes M. Des rescherches faites sur la phlébite. Revue Médicale Française et Etrangère et
Journal de Clinique de l’Hôtel-Dieu et de la Charité de Paris. 1825;3.
Bousser MG, Chiras J, Bories J, et al. Cerebral venous thrombosis—a review of 38
cases. Stroke. 1985;16:199.