NEURO-OPHTHALMIC MANIFESTATIONS OF
CEREBRAL VENOUS THROMBOSIS A CLINICAL
PROFILE
Dissertation submitted for M.S Degree (Branch III) Ophthalmology April 2015
THE TAMIL NADU DR. M.G.R MEDICAL UNIVERSITY CHENNAI
CERTIFICATE
This is to certify that this dissertation entitled “NEURO-OPHTHALMIC
MANIFESTATIONS OF CEREBRAL VENOUS THROMBOSIS-A
CLINICAL PROFILE” is a bonafide work done by Dr. M.LAVANYA under our guidance and supervision in the Neuro-ophthalmology Department of Aravind Eye Hospital and Post Graduate Institute of Ophthalmology,
Madurai during the period of her post graduate training in Ophthalmology for
May 2012-April 2015.
DR.S.MAHESH KUMAR DR. S. ARAVIND Guide Head of the Department, Consultant, Aravind Eye Hospital, Neuro-ophthalmology Madurai. Aravind Eye Hospital, Madurai.
Dr. M.SRINIVASAN Director, Aravind Eye Hospital, Madurai.
DECLARATION
I, Dr.M.Lavanya, hereby declare that this dissertation entitled,
NEURO-OPHTHALMOLOGICAL MANIFESTATIONS OF
CEREBRAL VENOUS THROMBOSIS.
Is being submitted in partial fulfilment for the award of M.S.in
Ophthalmology Degree by the Tamil Nadu DR.MGR Medical University in the examination to be held in April 2015.
I declare that this dissertation is my original work and has not formed the basis for the award of any other degree or diploma awarded to me previously.
Dr.M.Lavanya Aravind Eye Hospital, Madurai.
ACKNOWLEDGEMENT
First and foremost I am thankful to Almighty for always being with me and guiding me throughout my life.
I would like to express my heartfelt gratitude to my beloved parents for the dreams they have dreamt me and the hardships they have been through to make me stand where I am today. I also thank my friends who had been supporting me throughout my tougher times.
I take this opportunity to pay respect and homage to
Dr.G.Venkatasamy, our founder.
I am privileged to have on my side Dr.P.Namperumalsamy,
Chairman emeritus and Director of Research, Dr.G.Natchiar, Director emeritus and chief of Department of Neuro ophthalmology,
Dr.M.Srinivasan, Director emeritus and other scholars at Aravind Eye Care
System who had been a great source of inspiration to us.
I am very grateful to Dr. R.D .Ravindran, Chairman of Aravind Eye
Care System for having created an environment enriched with all the facilities for learning and gaining knowledge. Word cannot express my deep sense of gratitude and heartfelt thanks to my mentor and guide Dr.S.Mahesh Kumar, Professor Department of Neuro ophthalmology who with his able guidance , optimistic attitude and constant encouragement gave me all the confidence and determination to complete my dissertation.
My sincers thanks to Dr.N.Venkatesh Prajna, Director of Academics, who offered his guidance and support throughout my residency period.
I take the privilege to express my gratitude and humble regards to
Dr.Kowsalya, consulatant in Neuro ophthalmology for her valuable guidance, timely suggestions during my study.
My sincere thanks to Mrs.Kumaragurupari, Senior Librarian for her immediate responses in providing all the articles and the academic support required in the completion of this thesis.
I would like to thank the paramedical staffs of Neuro ophthalmology department for their support.
I would thank the countless patients who have been the learning ground for my study and my residency. CONTENTS
PART-I
S.NO TITLE PAGE NO
1 Introduction 1
2 Cerebral Venous System Anatomy 3
Etiology of Thrombosis 3 29
4 Pathogenesis of Venous Thrombosis 33
5 Investigations 40
6 Management 50
7 Review of Literature 70
PART-II
S.NO TITLE PAGE NO
8 Aims & Objective 74
9 Materials & Methods 75
10 Analysis & Results 80
11 Discussion 96
12 Conclusions 101
13 Limitations 103
Bibliography
Proforma
Master Chart
INTRODUCTION
Cerebral venous sinus thrombosis mostly affects children and young adults. Cerebral venous thrombosis is a chronic pathologic state that involves cortical veins, deep cerebral veins and dural sinuses. Since cerebral venous thrombosis is rare determining its prevalence and incidence is difficult.Incidence of cerebral venous thrombosis in children is 0.67 percent. cerebral venous thrombosis is a common sequalae of infection, coagulopathies ,trauma and dehydration in pediatric age group. Nonfocal neurologic signs and symptoms are presenting features in neonates. Deep venous system thrombosis is rare in adults and is associated with poor prognosis. In deep vein thrombosis thalami are bilaterally involved showing edema, infarction and hemorrhage right more than the left. The other differential diagnosis of bilateral thalamic infarction are glioma, metastasis, top of the basilar syndrome and encephalitis.
Cerebral venous thrombosis are serious and life threatening because of its raised intracranial tension and thrombosis of venous system. Cerebral venous thrombosis is one of the major reasons for seeking neurological consultations worldwide. The clinical features and management option depends upon the site, extent of obstruction, rate of occlusion, etiology and health of patient. Neuro – ophthalmic signs and symptoms of cerebral venous thrombosis are headache, vomiting, giddiness, double vision, papilloedema , optic atrophy etc. Visual signs and symptoms form major presentation in cerebral venous thrombosis and may be of great help in early diagnosis when initial signs are unspecific. [1]
CEREBRAL VENOUS SYSTEM ANATOMY
Cerebral Venous sinuses. Large low pressure veins within the folds of dura between fibrous dura and endosteum except for the inferior sagittal and the straight sinus which lies between two layers of fibrous dura”Cerebral venous system consists of superficial and deep veins all of which drains into the major dural venous sinuses and inturn into the internal jugular veins.The superficial veins drain the outer 2cm of cerebral cortex,the deep veins drain blood from deep white matter, basal ganglia and diencephalon. The superficial veins are thin walled, lacking a muscular wall and valves, lack well defined vascular territories and are not readily visualised with neuroimaging. By contrast the deep cerebral veins are larger, constant and identifiable on imaging.[1]
Classification
Superficial Deep
sup.sagital sinus lateral sinus
sup.cortical veins straight sinus
deep cortical veins DURAL VENOUS SINUSES
S.No Unpaired Paired
1. Superior Sagittal Transverse
2. Inferior Sagittal Sigmoid
3. Straight Cavernous
4. Occipital Superior Petrosal
5. Anterior Intercavernous Inferior Petrosal
6. Posterior Intercavernous Sphenoparietal
7. Basilar venous plexus Petrosquamous
8. Middle meningeal
CIRCULATION OF CEREBROSPINAL FLUID
BLOOD FLOW IN DURAL VENOUS SINUS
Superior sagittal sinus
Formed by the reflection of the inner layer of duramater to form the falx cerebri. Runs backwards infront of crista galli and forms a grove in frontal bone, parietal bone and occipital bone. Superior sagittal sinus ends at the internal occipital protuberance and continues with right transverse sinus.
Inferior sagittal sinus
Located within the falx cerebri at lower margin.It begins anteriorly and ends posteriorly by joining the straight sinus.
Straight sinus
Lies in the triangular interval of falx cerebri joins the tentorium cerebella. Anteriorly it receives the inferior sagittal sinus and great cerebral vein. Posteriorly the straight sinus ends by continuous with the transverse sinus of the opposite side. Sinuses that meet at the internal occipital protuberance are superior sagittal sinus, straight sinus, right and left transverse sinuses-‘Confluence of sinuses’.
Transverse sinus
It lies at the internal occipital protuberance, right transverse sinus is usually the continuation of superior sagittal sinus and the left transvers sinus is the continuation of the straight sinus.
Sigmoid sinus
The right and left sigmoid sinuses are continuations of the corresponding transverse sinuses, sigmoid sinus is S shaped.It runs downwards and medially finally forwards to reach the jugular foramen where it ends with internal jugular vein. The upper part of the sinus is related to mastoid antrum which is separated by a thin plate of bone so infaction can easily spread from mastoid antrum into the sigmoid sinus.[2]
Superficial Venous System
Dural venous sinuses have duramater in wall and are located on the surface of the cerebrum. Superior sagittal sinus flows inferiorly to the trocula and posteriorly in sagittal plane forming the confluence of sinuses the site were superficial drainage joins the deep venous system. Transervse sinuses bifurcate and travel laterally and inferiorly to form sigmoid sinuses which join to form jugular veins. [3]
Arachnoid granulations of Pacchioni are most commonly found in superior sagittal sinus and play a major role in resorption of cerebrospinal fluid. These granulations are isoattenuating or hypoattenuating relative to brain parenchyma.
Deep Venous System
Drains the veins in the deep structures of the brain joining behind the midbrain to form the vein of Galen. It fuses with the inferior sagittal sinus and forms the straight sinus. At the confluence of sinuses it then joins superficial venous system.
Draining Sites:
1. Superior Sagittal sinus becomes right transverse sinus or confluenc of
sinus
2. Inferior Sagittal sinus drains into Straight sinus
3. Straight sinus typically becomes left transverse sinus or confluence of
sinus
4. Occipital sinus drains to confluence of sinus 5. Confluence of sinus drains right and left transverse sinus
6. Sphenoparietal sinus drains into cavernous sinus
7. Cavernous sinus draina into superior and inferior petrosal sinus
8. Superior petrosal sinus drains into transverse sinus which inturn drains
into sigmoid sinus.
9. Inferior petrosal and sigmoid sinuses drains into internal jugular veins.
Dural Venous Sinus
1. Posterosuperior group consisting of sagittal, straight, lateral
(transverse), sigmoid, tentorial and occipital sinuses.
2. Anteroinferior group consists of cavernous, intercavernous, basilar,
sphenoparietal and petrosal sinuses.
Situated between the two layers of the dura mater, the dural sinuses are devoid of valves and are lined by endothelial cells and connective tissue. system. The superior sagittal sinus drains most of the cerebral cortex, lateral sinus drains the posterior fossa, posterior cerebral hemispheres, cerebellum and the cavernous sinus receives the ophthalmic veins. Anatomic variations of the lateral sinuses are common. Blood flow in the lateral sinuse may decrease secondary to increased intracranial pressure. Thrombosis most commonly affects the superior sagittal and lateral sinuses. These sinuses contains most of the arachnoid granulations into which cerebrospinal fluid absorption occurs.
Pathology depends on the location, degree of clot and extent of collateral venous drainage. Venous infarction is characterised by pallor with multiple petechial haemorrhages. [3]
Specific Anatomic Features of Cerebral Venous System:
. Cerebral veins and sinus have no valves or tunica muscularis
. Blood flows in different directions
. Cortical veins have numerous anastamosis thereby developing
collateral circulation
. CSF absorption takes place in arachnoid villi and granulations more in
superior sagittal sinus so thrombosis leads to intracranial hypertension
and papilloedema. [4]
VARIANT ANATOMY OF THE SINUS
Normal structures in the dural sinus lumen or lateral lacunae are arachnoid granulation protrusions if prominent resembles sinus thrombosis.
Transverse sinus hypoplasia and atresia occurs frequently. Right hypoplasia more common, atresia or hypoplasia of medial part is more common than lateral.
Hypoplastic transverse sinus
Hypoplasia and aplasia of the right transverse sinus is a common finding and can be mistaken for sinus thrombosis. Look for the size of the jugular foramen in this condition. [5]
Predisposing factors
Oral contraceptive pill (OCP) use
Prothrombotic conditions
Adjacent infection / inflammation
Dehydration
Location of Cerebral venous thrombosis in descending order
Superior sagittal sinus, transverse, straight and sigmoid sinuses.
Cortical veins:
Vein of Labbe, which drains the temporal lobe.
Vein of Torlard, which is the largest cortical vein that drains into
the superior sagittal sinus. [6]
Deep veins:
Internal cerebral and thalamostriate veins.
Cavernous sinus.
Clinical Features Depends on
1. Site of obstruction
2. Extent
3. Rate of occlusion
4. Etiology
5. Health of patient
Acute onset lessthan 48 hrs in 1/3rd cases
Subacute onset 48-30 days found in 40% cases
Chronic onset >30 days in ¼-1/3rd cases
Symptoms and Signs:
Headache
Vomiting
Giddiness
Focal Neurologic deficits
Diplopia
Transient Obscuration of vision
Papilloedema
Sensory, motordeficits
Aphasia, homonymous hemianopia
Seizures
Pulsatile tinnitus, sixth nerve palsy
Subacute encephalopathy[7]
Fundus Picture showing chronic papilloedema of disc
Right Eye Left Eye
Features of Secondary Optic Atrophy – Marked degeneration of optic
nerve fibres with excessive proliferation of glial tissue.[8] Venous System in Neonates and Children
Venous vertebral plexus, extracranial emissary veins are collateral venous pathways.
Internal jugular vein is the major venous outflow tract when the neonates is in supine position and Venous vertebral plexus is the main outflow tract in standing position in adults. Congenital chronic venous outflow obstruction, is seen in craniosynostosis. Cavernous sinus is not connected to the cerebral veins, resulting in less reserve and increased vulnerability within the venous drainage system. [9,10]
Clinical Features of CVST in children
Seizures
coma
Lethargy
Nausea
Vomiting
Impairment of vision
Hemiparesis
Papiloedema Ataxia
Mutism
Psychiatric symptoms
Respiratory problem
Jittery movements
Thrombosis of Superficial Cerebral Veins
Occurrence of focal or generalised seizures, focal neurologic deficits are common. Occlusion of superficial cerebral veins does not usually produce visual symptoms unless occipital veins become occluded. Unilateral infarction produce homonymous visual field defect. Bilateral infarction produce cortical blindness.[11]
Thrombosis of Deep Cerebral Veins
It is often fatal and typically present with acute coma, decerebrate posturing and extra pyramidal hypertonia. Women are more commonly affected than men. Mortality is high outcome is worse than dural venous thrombosis. .[12]
Thrombosis of Lateral Sinuses
Infection spreads from mastoid air cells, scalp, par pharyngeal or retropharyngeal abscess. Unilateral Abducens nerve paresis, migraine and increased intracranial pressures. .[13]
Thrombosis of Superior Sagittal Sinus
Aseptic thrombosis affects superior sagittal sinus because of its high position, low pressure and slow flow. When anterior part is involved symptoms and signs may be minimal or absent. Involvement of posterior portion, the neurologic consequences can be devasting. Thrombosis of superior sagittal sinus is often associated with Lateral sinus thrombosis.
Meningitis, paranasal infection ,epidural abscess often involves superior sagittal sinus. .[12]
Superior sagittal sinus thrombosis
Arachnoid granulations of Pacchioni are most commonly found in superior sagittal sinus and play a major role in resorption of cerebrospinal fluid. These granulations are isoattenuating or hypoattenuating relative to brain parenchyma.
Cavernous Sinus Thrombosis
Cavernous sinus thrombosis may be due to infectious or aseptic cause.
It may be acute, subacute and chronic. Orbital signs include ptosis, chemosis and ophthalmoparesis. Thrombosis of venous sinuses are often associated with involvement of cranial nerves. Extension of thrombosis into the jugular vein, th involve cranial nerves IX, X, XI, and XII (jugular foramen syndrome). Ophthalmic vein obstruction may be associated with proptosis and ipsilateral periorbital oedema. Retinal haemorrhages and papilloedema may be present. Paralysis of extraocular movements, ptosis, and decreased sensation in the first division of the trigeminal nerve involvement.Cavernous sinus extends anteriorly upto superior orbital fissure and posteriorly upto the apex of the petrous temporal bone.Communications of cavernous sinus are valveless and the blood can flow in either direction,so infections can easily spread into cavernous sinuses. .[13]
Clinical Features
Superior sagittal sinus thrombosis
Predisposing factors – Meningitis
Features are headache, vomiting, confusion, seizure, weakness
Cavernous sinus thrombosis
Predisposing factors – Infections from face , sphenoid and ethmoid
sinuses.
Involvement of cranial nerves-III,IV,V Sigmoid sinus thrombosis cause neck pain
Transverse sinus thrombosis
Predisposing factors – mastoiditis producing Gradinego’s syndrome.
Manifestations of Cavernous sinus Thrombosis
. Central retinal artery/ vein occlusion cause vision loss or blindness
. Involvement of sympathetic plexus, oculomotor nerve and edema of
lids cause ptosis
. Thrombosis of superior and inferior ophthalmic veins causes chemosis
. Venous engorgement cause proptosis
. Sensory loss / periorbital pain is due to trigeminal nerve involvement
. Lateral rectus palsy due to abducent nerve involvement
. Involvement of II,IV,VI cranial nerves cause complete
ophthalmoplegia.[14]
Differential Diagnosis
Thyroid related ophthalmopathy
Internal carotid artery aneurysm
Orbital cellulitis
Trauma
Mucormycosis
Thrombosis of Inferior Sagittal and Straight Sinus
Lesions in the Subarachnoid space
Oculomotor nerve rest on the tentorium cerebellar edge, the portion of uncal edge overlies tentorium edge and because of this course raised intracranial tension can herniate causing displacement of midbrain compressing ipsilateral third nerve palsy. This causes ipsilateral
[14] ophthalmoplegia and mydriasis. .
FALSE LOCALISING SIGNS
Abducent nerve palsy
Raised intracranial pressure (supratentorial or infratentorial space occupying lesion, idiopathic intracranial hypertension, cerebral venous sinus thrombosis) are the causes. More susptibility to damage is due to its sharp bend over the superior border of the petrous temporal bone and the downward shift of the brainstem(towards the foramen magnum) produced by raised intracranial pressure. The involvement of petrous bone from otitis media cause Gradenigo syndrome characterised by [15]
Ipsilateral abducent nerve palsy
Deafness
Neuralgia in the first division of trigeminal nerve
Facial Weakness
Differential Diagnosis of Sixth cranial nerve palsy:
Duane’s retraction syndrome
Congenital esotropia with crossed fixation – pseudoabducens paralysis
Nystagmus Blockage syndrome.
HESS CHART
ETIOLOGY OF CEREBRAL VENOUS THROMBOSIS
Abnormalities of Blood Flow
Factor V Leiden mutation
Homocystinemia
Protein C & S deficiency
Sickle cell disease.[16]
Acquired Coagulopathies
Hematologic
Leukemia
Lymphoma
Polycythemia
Anticardiolipin antibodies
Paroxysmal Nocturnal Hemoglobulinuria
Sickle cell disease
Gynaecologic
Pregnancy
Postpartum
Oral Contraceptives
Ovarian Hyperstimulation syndrome Metabolic
Nephrotic syndrome
Thyrotoxicosis
High altitude.[17]
Drugs
Danazol
Tamoxifen
Androgens
Heparin Induced Thrombocytopenia
Thalidomide
Erythropoietin
Lasparginase
Epsilon aminocaproic acid
Infections
Otitis media
Mastoiditis
Sinusitis
Meningitis.[18]
Mechanical causes
Trauma
Head injury
Injury to jugular vein- jugular catheterization
Neurosurgical procedures
Lumbar puncture
Systemic Disease
Crohns disease
Ulcerative colitis
Hepatic cirrhosis
Collagen vascular disease
Systemic lupus erythematosus
Wegeners granulomatosis
Bechets disease
Sarcoidosis
Abnormalities of Blood flow Compression Meningioma
Glomus Tumor
Lymphoma
Metastasis
Dural Arteriovenous Thrombosis
Abnormalities of Vessel wall
Local Infection
Trauma
Surgical- Neck dissection, Ligation, AVM embolisation.
Vasculitis.
PATHOGENESIS OF THROMBOSIS
Factors predisposing to thrombosis are-Virchows triad
Endothelial injury
Abnormal blood flow
Hypercoagulability
A. VASOCONSTRICTION
B. THROMBUS AND ANTITHRAOMBOTIC EVENTS
C. PRIMARY HEMOSTASIS
D. SECONDARY HEMOSTASIS
Pathogenesis of cerebral venous thrombosis:
Superior sagittal sinus, Lateral sinus (Transverse sinus and Sigmoid sinus) and Cavernous sinus are more commonly involved.Straight sinus and
Vein of Galen are least commonly involved.
Local effects caused caused by venous obstruction, ischemia,
infarction, hemorrhage and neuronal dysfunction
Intracranial space occupying lesion
Edema and ischemia
Cytotoxic edema is caused by ischemia which damages the energy-
dependent cellular membrane pumps, leading to intracellular swelling.. Vasogenic edema is caused by breakdown of blood brain barrier and
leakage of blood plasma into the interstitial space. It is reversible.
Occlusion cerebral venous sinuses leads to increased intracranial
hypertension, impaired absorption of cerebrospinal fluid.CSF
obstruction occurs at its terminal pathway. Between the subarachnoid
spaces at the surface of the brain and the ventricles gradient develop.
Hence, the ventricles do not dilate, and hydrocephalous do not
normally complicate sinus thrombosis formation of a thrombosis clot in
the dural sinuses, the venous pressure increases, thus leading to a
decreased cerebral blood flow in related anatomic areas that results in
territorial cerebral ischemia. Following this, the intracranial pressure
(ICP) will increase to a low to high-grade level, which may be followed
by hemorrhage and infarction in the pertinent brain area.[19,20]
Thrombosis of cerebral veins
Elevated venous and capillary pressure causes obstruction of veins,both
cytotoxic and vasogenic edema of brain and infarction.
Thrombosis of Major sinuses
Leads to impairment of cerebrospinal fluid absorption thereby raised
intracranial tension.
Venous Infarction:
High venous pressure in venous thrombosis leads to vasogenic edema of the brain followed by cytotoxic edema.Hemorrhage is more frequently seen in venous thrombosis due to high venous pressure.In arterial infarction cytotoxic edema only develop not vasogenic edema.[22,23]
Polycythemia vera and essential thrombocythemia are typically complicated by thrombosis which accounts for about 50%.The major thrombotic events were ischemic stroke, transient ischemic attacks, acute myocardial infarction, unstable angina pectoris, peripheral arterial thrombosis, retinal artery or vein occlusion, deep venous thrombosis and pulmonary embolism. Neurological signs include.
1. Isolated Intracranial Hypertension
2. Focal Cerebral Signs
3. Cavernous Sinus Thrombosis
4. Subacute Encephalopathy
5. Unusal Presentations
An isolated manifestation of cerebral venous sinus thrombosis is
Cranial nerve palsy due to raised intracranial tension, extension thrombus to venous channels or direct pressure from the clot. Due to transient neuropraxia in intracranial segment facial palsy occurs. Because of reversible compromised oxygen or glucose consumption within the nerve tissue due to edema or backpressure cranial nerve palsy will develop.[24]
Features Arterial Thrombi Venous Thrombi
Blood Flow Rapidly flowing vessels Slow moving veins
Sites Coronary, Cerebral, Femoral Superficial, deep veins of arteries lower limbs Thrombogenesis Due to turbulence Due to stasis
Propagation Retrograde direction Antegrade direction
Macroscopy Grey white Red blue
Microscopy Lines of Zahn Lines of Zahn not distinct
Emboli Less common More common
INVESTIGATIONS
Laboratory Evaluation in Hypercoagulable State
Complete Blood Counts with Platelets
Prothrombin Time
Partial Thromboplastin Time
Fibrinogen
Serum Protein Electrophoresis
Renal function Test
Antithrombin III
Protein C & S
Homocysteine
Antiphospholipid Antibodies
Factor V
CT Angiography
Non Enhanced CT
Suspicious findings include cerebral edema, findings suggestive of bilateral infarction or infarction in a non-arterial distribution, lobar intracerebral or subarachnoid hemorrhage. Hyperdense thrombosed cortical veins or hyperdensities within the venous sinuses can be seen Hyperdense
Dural Sinus – Cord Sign.[25,26]
Cortical Vein Thrombosis- cord sign Contrast Enhanced CT
Empty Delta Sign –Triangle of low density surrounded by a border of high density.Seen in Superior sagittal sinus ,Transverse and Straight sinus thrombosis.
False Empty Delta Sign – Subdural Hematoma
Subdural Emphysema
Direct visualisation of clot in NECT – Dense clot sign
MR /CT VENOGRAPHY
Venographic techniques can directly visualise venous thrombi.
Nonenhanced time of flight magnetic resonance venography, contrast- enhanced magnetic resonance venography, and CT venographyare the most available venographic techniques. Phase-contrast magnetic resonace venography is less often used.
Time of flight magnetic resonance venography is commonly used, since their excellent sensitivity to slow flow and their diminished sensitivity to signal loss from saturation effects. Flow is perpendicular to the plane of acquisition, the coronal plane, axial and coronal planes, or an oblique plane are often used for image acquisition so 2 dimensional techniques are most sensitive.[27]
LEFT SIGMOID SINUS THROMBOSIS
CT Venography
CT venography with multiplanar reformatting has a sensitivity of 95% when compared with digital subtraction angiography (3). CT venography is advantageous because it is widely available and can be performed quickly. It is less expensive than MRI and less invasive that conventional angiography. It provides good visualization of the major venous sinuses though it is suboptimal for detection of thrombosis in the deep venous structures and cortical veins.
Disadvantages include radiation exposure and administration of intravenous contrast.[28]
straight sinus and vein of Galen Thrombosis
MR Angiography:
MR Angiography reveals abnormalities in the veins,sinuses as well as in brain parenchyma.
Acute Thrombosis Isointense in T1
40% have hyperintense clot in occluded vessel
Absence of flow in occluded sinus in 2DTOF MRV
MRI/MRV
MRI in combination with time-of-flight or contrast enhanced MR venography (MRV) is highly sensitive. Abnormal T1 and/T2 signal within the venous sinus in conjunction with absence of normal flow through the venous sinus on MRV confirms the diagnosis of venous thrombosis. The age of the thrombus determines the T1 and T2 signal characteristics.[29,30]
Signal from thrombus depending on their age
Age of the thrombus T1 T2 Reason
Less than 5 days Iso Hypo Deoxyhemoglobin
5-15 days Hyper Hyper Methhemoglobin
>15 days Low Low Recanalisation
MRV of venous sinus thrombosis
MRV can be performed using two dimensional time of flight 2D TOF digital subtraction three dimensional post gadolinium or phase contrast MR
Venography techniques. Two dimensional TOF is performed by the acquisition of 1.5-2mm thick sections. Oblique planes are selected because they are perpendicular to venous flow thereby reducing plane saturation effects.
Axial plane also required to confirm venous thrombosis in posterior superior sagittal sinus and sigmoid sinus, jugular veins using oblique planes because of artifactual signal dropout. Incomplete recanalization of the chronic sinus thrombosis is a diagnostic challenge. 15% diagnosed by MR imaging may have a chronic (15- day-old) thrombus. Isointense or hyperintense on T2- weighted images and isointense on T1-weighted images are indicative of chronicity.[31,32]
Right Transverse and Sigmoid Sinus Thrombosis
Marked contrast enhancement may be observed after gadolinium administration .It may be due to secondary organized thrombus with intrinsic vascularisation. Patency is not indicated by contrast enhancement and for definitive diagnosis venography is necessary. Important diagnostic aid in acute-stage thrombosis is Gradient
Enhanced T2 imaging when the signal intensities are subtle on T1- and weighted images.
Drawbacks in CT:
Arachnoid granulations measure 2-9mm in diameter, it forms focal filling defect in venous system. They are isoattenuating 1/3 or hypoattenuating 2/3 in relative to brain parenchyma.
Drawbacks in MRI:
Variants of venous anatomy resembles venous thrombosis like hypoplasia, atresia.Arachnoid granulations and intrasinus septa are normal filling defect.[33]
MANAGEMENT
Anticoagulant Therapy
Endovascular Thrombolysis
Optic nerve sheath decompression
Lumbar puncture.
TREATMENT
Intensive Care
Prevention of Pressure sores & UTI
Anti Cerebral Edema therapy
Anti Convulsants
Heparin- Loading dose 80 units/kg bolus then IV infusion 10
units/kg/hr (aPTT) to be monitored. Heparin increases the action of
antithrombin III, leading to inactivation of coagulation enzymes
thrombin, factor Xa.[34]
Oral Anticoagulants
Heparin is replaced by oral anticoagulants after acute stage of
thrombosis. Prolonged oral administration is required in congenital
or acquired prothrombotic disorders.
Dose – 5 mg / qid
(INR to be monitored)
Thrombolytic & Fibrinolytic agents
Urokinase- 2,50,000 units/hr
Alteplase – 1 mg/cm
Streptokinase
COAGULATION PATHWAY
Anticoagulants
Oral
Parenteral
Oral Anticoagulants:
Vitamin K Inhibitors
Warfarin
Dicumarol
Direct Thrombin Inhibitors
Ximelagatron
Dabigatron
Parenteral Anticoagulants
Indirect Thrombin Inhibitors
Unfractionated Heparin
LMW Heparin
Enoxaparin
Dalteparin Tinzaparin
Fondaparinx
Idraparinx
Direct Thrombin Inhibitors
Hirudin
Lepirudin
Bivalirudin
Features Heparin OralAnticoagulants
Route Parenteral- iv, sc Oral
Onset of Action Rapid Delayed
Mechanism Activates Antithrombin III
Monitoring aPTT PT
Antagonist Protamine sulphate Vit K1
Placental Barrier Does not cross Fetal warfarin syndrome
Use To initiate therapy For Maintainence
Goals of Heparin Therapy :
. To prevent thrombus extension
. To treat underlying prothrombotic state
. To prevent recurrence of cerebral venous thrombosis
. To prevent thrombus formation in other sites.
Advantage of LMWH over Heparin
Better Bioavailability, longer t ½ after sc injection
Dose dependent clearance
Predictable response
Low risk of Osteoporosis
Low risk of Heparin induced Thrombocytopenia
Uses of Anticoagulants
Treatment and prophylaxis of venous thrombosis
Disseminated Intravascular Coagulation
Chronic Atrial Fibrillation, Stroke
Contraindications of Anticoagulants
Bleeding disorders
Peptic ulcers
Hemorrhoids
Severe Hypertension
Subacute bacterial endocarditis
Tuberculosis
Along with Aspirin and antiplatelet drugs
Anticoagulants Efficacy can be reduced by following drugs
. Oral contraceptives
. Griseofulvin
. Rifampicin
. Estrogens
. Phenytoin
Anticoagulants Efficacy can be increased by following drugs
. Salicylates
. Miconazole
. Naldixic acid
. Metronidazole
. Clofibrate
Oral Anticoagulants –Warfarin
Mechanism of Action – Inhibiting the activation of Vitamin K dependent clotting factors.Warfarin is well absorbed from Gastrointestinal tract and it is highly plasma protein bound.
Adverse Effects
Bleeding
Crosses the Placenta –Fetal Warfarin syndrome which includes growth
retardation,hypoplasia of nose and hand bones.
Prothrombin Time
This assay tests the Extrinsic and Common Coagulation pathway.So prolonged Prothrombin time can result from deficiency of Factor V, VII, X,
Prothrombin or fibrinogen.
Prothrombin time is used to adjust the dose of warfarin.Better test for monitoring the effect of oral anticoagulants is Internalised Normalised Ratio
(INR).[35]
INR = ( PT of Patient / PT of Reference )
Management of Warfarin Overdose
INR < 5 – discontinue warfarin and restart at low dose
INR 5-9 – Vitamin K1 (1-2.5mg oral)
INR >9 but no bleeding – Vitamin K1(3 -5mg oral)
INR >20 or bleeding – Fresh Frozen Plasma
INR should be 2,2.2 if INR is more than 2.5 stop anticoagulants.
Endovascular Thrombolysis :
Thrombolysis is done with administration of Urokinase into the sinus or in combination with thromboaspiration .Endovascular thrombolysis is done higher centres who have experienced interventional radiologist. Open thrombectomy and local thrombolytic therapy may be beneficial in patients with severe neurological detoriation. Treatment consists of a guiding 6F catheter to the jugular bulb or sigmoid sinus over the guidewire. Insertion of microcatheter via the internal jugular vein a superior sagittal sinus or straight sinus.[36,37]
The catheter was left in situ, and urokinase (42,000 U/h, total
1,000,000 U/day) was infused into the superior sagittal sinus or straight sinus.
Patency of the superior sagittal sinus was identified on the repeated angiogram and then infusion was stopped.Heparin was continued during thrombolytic therapy. To assess the outcome MRI was performed 2 weeks after thrombolysis. Longterm oral anticoagulation (warfarin therapy) was started after thrombolysis. Heparin dose was adjusted according to Partial
Thromboplastin time.
In our study patients of cerebral venous thrombosis were managed with Unfractioned Heparin 5000 IU qid / 7500 IU tds for 7-10 days.Maximum of 24,000 -27,000 IU of heparin.
Followed by Tab Acitrom 3mg od or Tab Warfarin 5mg od in evening time. Check Prothrombin time every month.
Optic Nerve Sheath Decompression:
Loss of vision is a serious complication of cerebral venous thrombosis
(CVT) and idiopathic intracranial hypertension (IIH). Outcomes are to improve or stabilize visual function. Optic nerve sheath decompression is an effective and safe procedure to improve or stabilize vision in patients with visual loss.[38,39]
Optic nerve sheath decompression helps in relieving headache and improving visual acuity. Medial transconjunctival orbitotomy and lateral orbitotomy and a lateral canthotomy are different approaches to optic nerve.
But both approaches have results.[40,41,42]
Optic Nerve Sheath Decompression Indications:
Progressive loss of vision despite maximal medical therapy
Severe or rapid loss of vision at the onset, relative afferent papillary
defect or signs of advanced optic nerve dysfunction
Severe papilloedema causing macular oedema or exudates
Procedures
In Optic nerve sheath decompression a window or multiple slits are made in the dural sheath of the optic nerve immediately behind the globe.The procedure immediately reduces pressure on the nerve by creating a filtration apparatus that controls the intravaginal pressure surrounding the orbital segment of the optic nerve.
Mechanism
The filtering effect with local cerebrospinal fluid pressure reduction
improving the peripapillary circulation.
Generalised decrease in the intracranial pressure after optic nerve
sheath decompression.
The scarring of the arachnoid that may protect the optic nerve head
from elevated cerebrospinal fluid pressure.[45,46]
Complications of ONSD
. Extraocular motility dysfunction – usually involves lateral rectus
. Pupillary dysfunction
. Loss of vision from vascular occlusion-Central retinal artery
occlusion,Branch retinal artery occlusion,Choroidal ischemia/infarction . Visual field defect
. Orbital hemorrhage
. Transient or protracted blindness
. Globe perforation
Poor Outcome Predictors
Coma
Intracranial Hemorrhage
Posterior fossa lesions
Deep venous system involvement[47]
Lumbar Puncture/ Spinal Tap
Indications
Diagnostic
Infectious
Inflammatory
Neoplastic
Meningitis
Subarachnoid hemorrhage
Therapeutic
Hydrocephalous
Idiopathic intracranial hemorrhage
Spinal anaesthesia
Chemotherapy
Contraindications
Uncal herniation
Skin infection at puncture site
Sepsis
Causes and Risk Factors:
Factors favouring the fluidity of blood in the vessels are
Intact endothelium
Prostacyclin
Antithrombin III
Heparan sulphate
Thrombomodulin
Protein C & S
Fibrinolytic system Normal blood flow
Absence of prethrombotic / hypercoagulable state
Predisposing Factors :
Dehydration
Postures during sleep and travel
Prolonged Immobilisation (due to surgery/trauma)
Infection, Inflammation
Pregnancy /postpartum
Hyperhomocystienemia, polycythemia, thrombocytosis
Oral contraceptives, Hormone Replacement therapy
Liver disease, Bechets disease
Diagnostic Steps in Cerebral Venous Thrombosis:
A high index of suspicion with good clinical knowledge
CT, MRI, MR venogram helps to rule out other possible diagnosis
Evaluation of other risk factors of thrombosis by clinical, physical and
laboratory examination
WHEN TO SUSPECT THROMBOSIS
Clinically –Headache
Seizures
Loss of consciousness
Direct sign of Thrombus – Dense Clot Sign
Cord Sign
Empty delta sign
Loss of normal flow void on MR
Venous Infarction – Temporal lobe infarction
Cortical edema or hemorrhage
Peripheral lobar hemorrhage
Differential Diagnosis
Acute stroke
Blood dyscrasias
Cavernous Sinus Syndromes
Cerebral Venous Thrombosis
HIV-1 Associated Oppurtunistic Infections: Cytomegalovirus
Encephalitis Head Injury
Intracranial Epidural Abscess
Pseudotumour Cerebri
Sarcoidosis and Neuropathy
Staphylococcal Meningitis
Status Epilepticus
Subdural Empyema
SLE
PROGNOSTIC SIGN
GOOD WORST
• Early clinical diagnosis Early onset of seizures
• MRI study Impairment of consciousne
• Early intervention with Heparin Hemorrhagic infarcts on CT
& Thrombolytics
Complication of cerebral venous thrombosis
Parenchymal edema with venous infarction and hemorrhage
Pulmonary embolism
Hypopituitarism
AV malformation
Transtentorial herniation
Focal seizures
Isolated cortical venous thrombosis can present as unilateral, localized
Causes of Death in cerebral venous sinus thrombosis
Early cause
Transtentorial herniation
Diffuse edema
Focal mass effect
Late cause
Cardiopulmonary arrest
Pulmonary embolism
Sepsis
REVIEW OF LITERATURE
Prateek Agarwal, Mahesh Kumar, Vipul Arora described the rate of cerebral venous thrombosis in patients with idiopathic intracranial hypertension and importance of neuroimaging.To rule out cerebral venous thrombosis MRI combined with MRV is indicated.
Ashok Menon described a thalamic infarction due to cerebral venous thrombosis in a patient presenting as dorsal midbrain syndrome / Parinauds syndrome with blurred vision and papilloedema.
YU CHIEH described acute reversible visual loss an unusual presentation of cerebral venous thrombosis
Albert Lin reported 9.4% of patients with presumed Idiopathic intracranial hypertension have cerebral venous thrombosis.
Sasidharan described cerebral venous thrombosis should be considered in the differential diagnosis of unexplained CNS disorder of acute onset.
Goksel, Uluc, Mustafa reported obstructive hydrocephalous in children a rare complication of cerebral venous thrombosis. MTHFR 1298 polymorphism is an important risk factor Ratan Bhardwaj described the usefulness of anticoagulation therapy in the treatment of acute of posttraumatic cerebral venous thrombosis in pediatric Patients.
James, Leech reported role of neuroimaging in cerebral venous thrombosis Magnetic resonance imaging, unenhanced computed tomography, unenhanced time of flight MR Venography, MR Venography, CT
Venography.
Zafar Sajjad described MRI with MRV is the best diagnostic modality in cerebral venous thrombosis.Hyperintense T1 and T2 signal from sinus with a defect seen on MR venogram are diagnostic of cerebral venous thrombosis.
Einhaupl, M G Bousser reported Guidelines for management of
CVST in adults.
Stam J described treatment with anticoagulant and endovascular thrombolysis for cerebral venous thrombosis.
Yakovlev described endovascular treatment for acute thrombosis of cerebral veins and sinuses
Asakura described the pathophysiology and classification of thrombosis Puccinelli reported cerebral venous thrombosis after embolisation of
Pediatric AVM with jugular venous stenosis.
Bozolla reported meningococcal meningitis presenting as multiple cerebral sinus thrombosis
AI Rumayyan reported cerebral venous sinus thrombosis in a child with Nephrotic syndrome
Coutinho described Isolated Cortical vein thrombosis in which papilloedema was not a clinical features
Gulati decribed diagnosis and management of cerebral venous thrombosis
Gupta RK reported Prognostic indices of cerebral venous thrombosis on CT Perfusion
Raza reported Decompressive surgery for malignant cerebral venous thrombosis
Sahin N, Solak A described cerebral venous thrombosis a rare cause of subarachnoid hemorrhage.
Ghanderi, Riasi reported safety assessment of anticoagulation therapy in patients with hemorrhagic cerebral venous thrombosis. Takkar, Kesav reported Terson syndrome with cortical venous sinus thrombosis a rare presentation.
Lebas, Chaberier described anticoagulant treatment guidelines for cerebral venous thrombosis in neonates and children.
Leech described current imaging techniques and diagnostic pitfalls for cerebral venous thrombosis.
Chen, Yao reported lateral sinus thrombosis in patients with hypothyroidism presenting as intracranial hypertension.
Southwick, Richardson reported septic thrombosis of the dural venous sinuses.
AIMS AND OBJECTIVES
To study the clinical profile of patients with cerebral venous
thrombosis.
To correlate the ocular manifestations and site of the venous
thrombosis.
To study the behaviour and the natural course of the venous
thrombosis.
To study the improvement in ophthalmic and clinical features of
venous thrombosis after treatment.
MATERIALS AND METHODS
Study Design
Hospital Based Prospective study
Source of Data
Neuro ophthalmic Services, Aravind Eye Hospitals
Study Subjects
Patients with cerebral venous thrombosis diagnosed by neuroimaging from November 2012 to April 2014(18 months) were enrolled for study
Sample Size
31 patients who were proven to have cerebral venous thrombosis clinically and radiologically from a period of November 2012 to April 2014 for a period of 18 months who presented to the Department of Neuro ophthalmology, Aravind eye hospital, Madurai.
Study Period
November 2012 to April 2014(18 months)
DATA ANALYSIS
Statistical methods
Continuous and Categorical variables will be expressed as Mean (SD) and Frequency (Percentage) respectively. Chi-square test or Fisher’s exact test were used to assess the association between the two variables. Mann- whitney U test was used to assess association between preoperative pattern amount and Surgical outcome. Non-parametric Wilcoxon signed rank sum test was used to compare pre and post operative values. P-value less than
0.05 was considered as statistically significant. All statistical analysis was done by Statistical software STATA version 11.0
INCLUSION CRITERIA:
It includes all patients with any of the following symptoms and signs with Radiologically proven cerebral venous thrombosis
Headache
Defective vision
Double vision
Trasient Obscuration of vision
Cervical pain Vomiting, giddiness ,fever injury, tinnitus fits, vertigo
Defective colour vision
Central field abnormalities
Fundus changes – Papilloedema, optic atrophy
Extraocular movements restriction
EXCLUSION CRITERIA:
Patients with intracranial inflammatory or infective conditions proved radiologically with the same symptoms.
CLINICAL EVALUATION:
A series of 31 patients who presented to our Neuro ophthalmology department with clinically and radiologically proven diagnosis of cerebral venous thrombosis were included in our study, all these patients underwent a thorough ophthalmological and neurological evaluation.
The patients particulars like name, age, sex, address were documented in a proforma specially designed for the study, and was filled by the examining doctor. A detailed history of each and every symptom of the patient was taken, such as the onset, duration, progression, associated factors, aggravating and relieving factors were documented.
The patients were also enquired about the history of any prior visual loss, history of trauma, systemic illness, surgical or medical intervention, family history of cerebral venous thrombosis as which could influence the diagnosis.
Each one of the patient included in our study has to undergone routine
Visual acuity by snellens chart
Refraction
Pupillary reaction for RAPD, sluggish pupil, dilated fixed pupil or
normal pupil
General ophthalmic examination by torch light and slit lamp
Intraocular pressure measurement for patients above 40 years by non
contact tonometry
Fundus examination by direct ophthalmoscope and slit lamp
biomicroscopy using +90 dioptre lens and indirect ophthalmoscopy
Extraocular movement examination using torch light Hess and diplpopia charting when needed
Colour vision evaluated by Ishiharas chart
Central fields by Bjerrums screen
A complete neurological evaluation was done to every patient including
general consciousness, cranial nerve examination, motor system
evaluation (superficial and deep tendon reflexes), sensory system,
cerebellar signs including gait, balance, Rombergism,
Dysdiadochokinesia, finger nose testing and other system examinations
were done.
Neuroimaging was done in all patients either CT, MRI/MRV with or
without contrast depending upon the need and affordability of the
individual patients
During followup visual acuity, pupillary reactions, colour vision, fields
and fundus was done at one month and three months.
ANALYSIS
Analysis of collected data was done based on the following
1. Incidence
2. Age and sex distribution
3. Various symptoms
4. Onset of symptoms –Acute/Subacute/Chronic
5. Best Corrected Visual Acuity-
a. 6/6 – 6/60 -1
b. 5/60 -1/60 -2
c. <1/60 -3
6. Anterior segment examination
7. Colour vision – Normal/Defective/Inconclusive because of poor
vision
8. Central fields
9. Nystagmus – Present/Absent
10. Fundus status - Normal/Abnormal
11. Central nervous system –Normal/Abnormal
12. Radiological Findings
13. Treatment –Medical/Surgical 14. Visual Acuity at followup – Static/Improved/Worsened
15. Fundus status at follow up
RESULTS
Table : 1 Gender
Sex Percentage
Male 58.1%
Female 41.9%
Sex
100%
80%
58.1% 60%
41.9% 40%
20%
0% Male Female Table : 2 Complaints
Complaints Percentage
Defectivevision 16.1%
Double vision 22.6%
Headache 54.8%
Drooping 3.2%
Transient Blurring of vision 3.2%
Complaints
Defectivevision Double vision Headache Drooping Transient Blurring of vision
Table : 3 Duration
Duration Percentage
<1 Month 67.7%
1 Month - 1 Year 22.6%
> 1 Year 9.7%
Duration
100%
80% 67.7%
60%
40%
22.6% 20% 9.7%
0% <1 Month 1 Month - 1 Year > 1 Year
Table :4 Pupil
Pupil Percentage
Normal 83.9%
RAPD 9.7%
Dilates & Fixed Pupil 6.4%
Pupil
100%
83.9% 80%
60%
40%
20% 9.7% 6.4%
0% Normal RAPD Dilates & Fixed Pupil
Table : 5 Extra Ocular Movements
Extra Ocular Movements Percentage
Normal 79.0%
Abducent nerve 17.7%
Oculo motor nerve 1.6%
Facial nerve 1.6%
Extra Ocular Movements
Normal Abducent nerve Oculo motor nerve Facial nerve
Table :6 Fundus
Fundus Percentage
Normal 6.9%
Early papilloedema 44.8%
Established papilloedema 17.2%
Chronic papilloedema 27.6%
Secondary optic atrophy 3.4%
Fundus
Normal Early Established Chronic Secondary optic atrophy
Table :7 Neuro Imaging
Single sinus Multiple sinus
involvement involvement
Superior sagittal sinus 25.8% -
Superior sagittal sinus, 32.3%
Transverse, Sigmoid -
Superior sagittal sinus, 6.5%
Transverse, Sigmoid, Straight sinus -
Superior sagittal sinus, Inferior 3.2% sagittal sinus -
Transverse sinus, Sigmoid sinus - 32.3%
Superior sagittal sinus S i n g l e
s i n u
Ss uperior sagittal sinus, Transverse, Sigmoid
i MRI/MRV ,CT brain n v o l v e m e n t Superior sagittal sinus, Transverse, Sigmoid, Straight sinus M u l t i p l e
s i n
Su perior sagittal sinus, Inferior sagittal sinus s
i n v o l v e m e n t Transverse sinus, Sigmoid sinus
Table : 8 Nuero Imaging
MRI-MRV/CT Percentage
MRI-MRV 87.1%
CT 12.9%
MRI/CT
100%
90% 87.1%
80%
70%
60%
50%
40%
30%
20% 12.9% 10%
0% MRI / MRV CT
Table : 9 Visual Acuity
Visual Acuity 6/6 – 6/60 <1/60
Baseline 93.6% 6.4%
Followup1 95.2% 4.8%
Followup2 94.8% 5.2%
Visual Acuity
/6 – 6/60
Baseline Followup1 Followup2 Table : 10 Colour Vision
Colour Vision Baseline Followup 1 Followup 2
Normal 87.1% 80.7% 82.8%
Abnormal 12.9% 19.3% 17.2%
Colour Vision
100%
90% 87.1% 82.8% 80.7% 80%
70%
60% Baseline
50% Followup 1 40% Followup 2 30%
19.3% 20% 17.2% 12.9% 10%
0% Normal Abnormal
Table : 11 Central Fields
Central Fields Baseline Followup 1 Followup 2
Normal 83.9% 87.1% 89.7%
Abnormal 16.1% 12.9% 10.3%
Central Fields
100%
90% 87.1% 89.7% 83.9% 80%
70%
60% Baseline 50%
40% Followup 1
30% Followup 2
20% 16.1% 12.9% 10.3% 10%
0% Normal Abnormal
Table : 12 Treatment
Treatment Baseline Followup 1 Followup 2
Medical 83.9% 93.6% 100.0%
Surgical 16.1% 6.4% 0.0%
Treatment
100% 100.0% 93.6%
83.9% 80%
60% Baseline
40% Followup 1
Followup 2
20% 16.1%
6.4% 0.0% 0% Medical Surgical
Table : 13 ONSD
ONSD Percentage
Unilateral 6.5%
Bilateral 3.2%
Optic nerve sheath decompression
Unilateral Bilateral
DISCUSSION
Cerebral venous sinus thrombosis mostly affects children and young adults. Cerebral venous thrombosis is a chronic pathologic state that involves cortical veins, deep cerebral veins and dural sinuses. Since cerebral venous thrombosis is rare determining its prevalence and incidence is difficult.
Incidence of cerebral venous thrombosis in children is 0.67 percent. cerebral venous thrombosis is a common sequalae of infection, coagulopathies ,trauma and dehydration in pediatric age group. Nonfocal neurologic signs and symptoms are presenting features in neonates. The other differential diagnosis of bilateral thalamic infarction are glioma, metastasis, top of the basilar syndrome and encephalitis.
In our prospective study we included 31 patients, the mean age of presentation is 33(11.56%) and the range is 8-70.Males 18(58.1%) are most frequently involved than females13(41.9%) Presenting complaints Headache
17(54.8%), Defective vision 5(16.1%),Transient blurring of vision 1(3.2%)
Drooping of lids1(3.2%), Double vision in 7 patients. Most of the patients presented within 1 month duration. Relative Afferent pupillary defect was found in 6(9.75%) cases Dilated and fixed pupil in 4(6.4%) Abducent nerve were involved in 10 patients, third nerve in 1 patient and facial nerve in
1patient.Fundus was normal in 4 cases, early papilloedema in 13 cases, chronic papilloedema in 9 cases and established papilloedema in
5cases.Cerebral venous thrombosis was diagnosed by CT Brain in 4 (12.9%),
MRI/MRV in87.1%.In our study Superior sagittal sinus 25.8% cases, multiple sinuses like Superior sagittal sinus, Transverse sinus, Sigmoid sinus were involved in 32.3%.
Prateek Agarwal did a retrospective study in 308 patients of Idiopathic
Intracranial Hypertension of which 35(11.4%) patients was found to have cerebral venous thrombosis. Mean age of presentation was 31.4 years, 26 males and 9 females[3] were identified which was similar to our results.
Owen Samuel described the most common presenting complaints of
Cerebral venous thrombosis Headache 90%, Vision loss 13%, seizures 40%, double vision13%, coma13%.In our study seizures was not a presenting feature.
Patil et al reported cerebral venous thrombosis in a tertiary eye care centre 26% have papilloedema. In our study papilloedema was found in
91.4% of which Early papilloedema in 13cases, Chronic papilloedema in
9cases and established papilloedema in 5 cases. Wang, Peng et al described cerebral venous thrombosis in Chinese population. He found that CT scan revealed cerebral venous thrombosis in
17.4%, MRI with MRV in 27.5% .The results were similar to our study with
CT scan 12.9%, MRI with MRV in 87.1%
AI Hashel JY reported prospective study of cerebral venous thrombosis Superior sagittal sinus thrombosis 54.5% was most commonly involved, Transverse sinus in 52%.
Kardas, Sayin et al described the outcomes of retrospective study of cerebral venous thrombosis in Turkey population Transverse sinus 78.4% was most commonly involved.
In our study isolated thrombosis of Superior sagittal sinus was seen in
25.8% whereas multiple sinuses like superior sagittal sinus, transverse sinus, sigmoid sinus were involved in 32.3%.
Dorino reported Transverse sinus thrombosis in 2 patients of which 1 patient had died due to intracerebral bleed.No deaths were reported in our study.Isolated transverse sinus involvement was not reported in our study.
Albert Lin, Robert et al[11] reported Transverse sinus involvement in 1 patient remaining have multiple sinuses involvement in this study he classified cerebral venous thrombosis based on their Body Mass Index.Our study has not included Body Mass Index.
J Kuehen et al [33] reported cranial nerves involvement in cerebral venous thrombosis.Most commonly affected nerves were Abducent nerve,
Facial nerve, Vestibulocochlear nerve. Least involved are Oculomotor and
Trigeminal nerve.
In our study Abducent nerve was most commonly involved in
10patients of which bilateral sixth nerve palsy in 1patient others are
Oculomotor nerve and Facial nerve.
Straub reported Facial palsy in a patient with Protein C deficiency on
Oral Contraceptives.
Annie, Kenneth described a retrospective study of 578 eyes of 331 patients who underwent optic nerve sheath decompression in Idiopathic
Intracranial Hypertension, Non Arteritic Ischemic Optic Neuropathy and
Optic nerve Drusen. Visual Acuity in post operative followup remained stable or improved in 94.4% and worsened in5.6% .
Suneetha Nithyanantham, George reported “Optic nerve sheath decompression in Idiopathic Intracranial Hypertension in a tertiary eye care centre, Visual acuity and visual fields improved or stabilised in94% eyes”. In our study 3 patients (4 Eyes) underwent optic nerve sheath decompression 9.7%
CONCLUSION
1. The mean age is 33.0(11.56%) and the range is 8-70.
2. 2Males are most frequently involved than females. Males 18 (58.1%),
Females 13(41.9%)
3. Most of the patients presented with Headache 17(54.8%), Defective vision
5(16.1%),Transient blurring of vision in3.2%,Double vision in 22.6%
4. Mostly presented within 1month duration 67.7% of symptoms.
5. Relative Afferent Pupillary defect was found in 9.7%,dilated and fixed in
6.4%
6. Extraocular movements was restricted in 21%.Right Lateral Rectus was
most commonly involved than left, Bilateral involvement of Lateral
Rectus was found in 1 patient. Oculomotor and Facial nerve palsy was
found in 1 patient.
7. Papilloedema- Early papilloedema44.8% Chronic papilloedema 27.6% and
Established papilloedema in 17.2%. Secondary optic atrophy3.4%.
8. CT Brain were done in 4 patients12.9%, MRI with MRV was done in
87.1%
9. Superior Sagittal sinus, Transverse sinus, Sigmoid sinus were most
commonly involved. 10. Lumbar Puncture was done in 2 cases
11. Optic Nerve Sheath Decompression was done in 3 cases( 4Eyes).
12. Jak 2 Mutation was positive –Polycythemia Vera in 1 case,Antinuclear
Antibody was positive in 1 patient.
13. Other risk factors noted are infertility in 1 case, infections in 3 cases
14. Limb weakness was found in 2 patients, Drowsiness in 1 case, Seizures in
2 cases.
15. Visual Acuity was less than 1/60 in 3 cases
16. Follow up visit at 3 months and 6 months showed resolving symptoms,
papilloedema in most cases. Secondary optic atrophy was seen in 2
patients, Pale disc was found in 5 patients.
17. Patients were treated with Heparin, Acitrom , Diamox, Steroids were given
orally for 2 cases, Intravenous Methylprednisolone for ONSD patients .
LIMITATIONS
3 patients lost follow up so correct analysis of vision and fundus could not
be analysed.
For some patients MRIwas not done because of cost factor, patients were
not affordable and so CT was done.
Only 31 patients are included in our study and the followup of the study
was short duration.
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PROFORMA
OCULAR MANIFESTATION OF CEREBRAL VENOUS THROMBOSIS
STUDY NO.
Name……………………………………. Date…………..
Age MR NO.
Gender M-Male, F-Female
Address……………………………………………….
………………………………………………
……………………………………………….
Phone number …………………………………….
Diagnosis ……………………………………..
CHIEF COMPLAINTS /DURATION
Headache
Defective Vision 1-Present
Transient Obscuration 2-Absent
Vomiting
Giddiness 1-<1month
Fever 2-1month to 1year
Injury 3->1year
Tinnitus seizures Vertigo
Ear discharge
Sleep disturbances
Mental changes
Systemic diseases
Diabetus Mellitus
Hypertension
Ischemic Heart Disease
Bronchial Asthma
Tuberculosis
OCULAR EXAMINATION:
RE LE
BCVA 1-6/6 to 6/60
2-5/60 to 1/60
3-<1/60
LIDS 1-Normal
2-Abnormal
PUPIL: RE LE
A.Anisocoria
B.Direct
C.Indirect D.RAPD 1-Normal
2-RAPD
3-Dilated fixed pupil
4-Sluggish pupil
Red color desaturation
Brightness sensitivity
Corneal sensation
CENTRAL FIELDS:
Normal
Enlarged blind spot
Generalised constriction
FUNDUS:
Normal
Papilloedema
Pale disc
Macula
Higher functions
Cranial nerves
Gait
Rombergism INVESTIGATIONS:
1. RBS 2. Complete blood count 3. LFT 4. Lipid profile 5. CRP 6. ANA 7. PT/INR 8. APTT 9. Antithrombin III 10. Prothrombin C&S 11. CT Brain 12. MRI &MRV Brain
TREATMENT:
Medical
Surgical
FOLLOW UP:
Date
Complaints
BCVA
Pupil
CV
CF
Fundus
Male-1
Female-2 Duration of complaints:
<1 month-1
1-6months-2
>6months-3
Visual Acuity:
6/6 -6/60 -1
5/60-1/60-2
<1/60-3
Extraocular movements:
Full-1
Restricted-2
Colour Vision:
Normal-1
Abnormal-2
Complete Blood Counts:
1-Normal
2-Abnormal
Lipid Profile:
1-Normal
2-Abnormal
CRP, ANA, Protein C&S, Antithrombin III, HIV,Antiphospholipid antibody Test:
1-Positive
1-Negative
Homocysteine :
1-Elevated
2-Normal
LH, FSH, Prolactin,Sr Estradiol level:
1-Normal
2-Raised
Prothrombin time, Activated Partial Thromboplastin time:
1-Normal
2-Prolonged
ABBREVATIONS
BCVA – Best Corrected Visual Acuity
V/A – Visual Acuity
PL – Perception of Light
HM – Hand Movements
RAPD – Relative Afferent Pupillary Defect
CT – Computed Tomography
MRI – Magnetic Resonance Imaging
SOA – Secondary Optic Atrophy
CVST - Cerebral Venous Sinus Thrombosis
LFT - Liver Function Test
EOM - Extraocular movements
CRP - C Reactive Protein
ANA - Antinuclear antibody HIV - Human Immunodeficiency virus
PT - Prothrombin time
APTT - Activated Partial Thromboplastin time
LH - Leutinising Hormone
FSH - Follicle Stimulating Hormone
SSS - Superior sagittal sinus
ISS - Inferior sagittal sinus
ONSD - Optic Nerve Sheath Decompression
31 10Pothum ponnu 1Shanty 12Karuppasamy 13Ravi 14Gurusamy 15Thangapandi 16Nagarajan 17Rajapandian 18Chandra 19Satinder singh 20Biju Mathew 21Murugesan 2Meenakshi 23Rajamuniyandi 24Lakshmi 25Lekha 26Manjula 27Pragadeeswaran 28Mahalakshmi 29Nagarani 30Velpandi 1 2 3 4 5 6 7 8 9 S.No Sabareeswaran Subramanian Gurunath Subramanian Palaniyammal Sirangammal Vembu Murugan Sudha Rajkumar
NAME 39 32 42 17 27 30 50 30 32 30 39 70 37 38 36 32 28 20 25 38 24 40 27 25 32 50 43 39 22 21
8 AGE 116.11.2012 1 110.12.2012 101.12.2012 228.12.2012 218.01.2013 231.01.2013 120.02. 2013 217.04.2013 118.04.2013 208.03.2013 231.05.2013 121.06.2013 107.03.2013 126.03.2013 125.04.2013 120.06.2013 112.08.2013 212.10.2013 130.08.2013 121.10.2013 121.10.2013 222.10.2013 105.11.2013 219.11.2013 220.12.2013 216.12.2013 106.12.2013 230.12.2013 218.01.2014 115.03.2014 SEX 4/23/2014
DOV-1 347-8980Headache 382-8339 349-2908Double vision 348-7463Double vision 350-4644RE Drooping 351-5909Headache 352-3496Headache 353-5523Defectivevision 356-6354Headache 356-7290Headache 354-4611Double vision 359-4205Defectivevision 360-7919Headache 354-4356Headache 355-4501Headache 357-1235Headache 360-7517Diplopia 363-9340Headache 367-4819Headache 365-0563Headache 368-0034Transient BV 368-0089Headache 368-0966Headache 368-7616Double vision 369-6261Headache 371-3505Headache 371-0983Defectivevision 370-6462Diplopia 370-2828Diplopia 373-0077Defectivevision 376-4971Headache
MR NO Defectivevision
COMPLAINTS 1Diplopia 2 1Headache 1Headache 1Headache 2Double vision 3Defectivevision 3NIL 1Double vision 2NIL 1Headache 2Headache 1limbweakness 1Defectivevision 1NIL 1NIL 1Headache 1Blurringofvision 3Defectivevision 1Defectivevision 1Headache 1NIL 2NIL 1NIL 2Double vision 2Tinnitus 1Headache 1LT FaceTurn 1Headache 1Headache 1Defectivevision DURATION Headache
Associated H/O NIL NIL smoker alcoh Chickenpox Bells palsy Infertility trt NIL DM,HT seizures NIL NIL Mastoiditis Fits,HT DM NIL NIL NIL NIL NIL NIL NIL PCV NIL NIL NIL NIL Trauma LE Typhoid NIL NIL
SYSTEMIC DS 1 1 1 1 1 1 1 1 1 1 1 3 1 1 1 1 1 1 3 1 1 1 1 1 1 1 1 1 1 1 1 VA-RE 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 3 3 1 1 1 1 1 1 1 1 1 1 1 VA-LE RE-2 RE-2 LE-2 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 3 1 1 1 1 1 1 3 1 1 1 1 PUPIL-BE 1 2 1 1 2 2 1 1 2 1 2 1 1 1 1 1 1 1 1 1 1 1 1 2 2 1 1 1 1 1 1 EOM-RE 1 1 2 2 1 2 1 1 1 1 1 1 1 1 1 1 2 1 1 1 1 2 1 1 1 1 1 2 1 1 1 EOM-LE SOA Esp Esp Esp Esp CP CP CP CP CP CP CP CP EP EP EP EP EP EP EP EP EP EP EP EP EP EP EP EP N N FUNDUS-BE 1 1 1 1 1 1 1 1 1 1 1 2 1 2 1 1 1 1 2 2 1 1 1 1 1 1 1 1 1 1 1 COLOR VISION 1 1 1 1 1 1 2 1 1 1 1 2 2 1 1 1 1 1 1 2 2 1 1 1 1 1 1 1 1 1 1 CENTRALFIELDS BE VINPalsy RE -LRPalsy RE-LR Palsy RE-LR Palsy RE-LR Palsy LE-LR Palsy LE-LR Palsy LE-LR Palsy LE-LR Palsy NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL N HESS CHART NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL DIPLOPIACHART SIG,Trnv SIG,Trnv SIG,Trnv SSS CT Brain SSS SSS SIG,Trnv SIG,Trnv,SSS sig,transv,SSS SSS SSS SIG, Trnv SSS SSS SIG,Trnv SSS sig,transv,SSS SIG,Trnv SIG,Trnv SIG,Trnv SSS sig,transv,SSS SSS SSS transv,SSS,Str SSS SIG,Trnv SIG,Trnv SSS SSS,Str SIG,Trnvosis
MRI / MR Venography 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 Completebloodcount 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 Lipid Profile 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 LFT 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 CRP 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 1 2 2 2 2 2 2 2 2 2 2 2 2 ANA 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 Protein C & S 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 Antithrombin III 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 HIV 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 Homocysteine 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 APLAB 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 2 1 1 1 1 1 1 1 1 1 1 1 1 PT 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 2 1 1 1 1 1 1 1 1 1 1 1 1 APTT 1 1 1 1 1 2 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 LH 1 1 1 1 1 2 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 FSH 1 1Not Done 1Not Done 1Not Done 1Not Done 2B/LPCOD 1Not Done 1Not Done 1Not Done 1Not Done 1Not Done 1Not Done 1Not Done 1Not Done 1Not Done 1Not Done 1Not Done 1Not Done 1LeftIJVthrombosis 1Not Done 1Not Done 1Not Done 1Not Done 1Not Done 1Not Done 1Not Done 1Not Done 1Not Done 1Not Done 1Not Done 1Not Done Prolactin Not Done
USGNECK/ABDOMEN LEONSD,Antibiotics BE ONSD,Steroids REOSND,Steroids LP,ACM,DMX LP,ACM,DMX ACM,MAN ACM,DMX ACM,DMX ACM,DMX ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM,HEP
Treatment JAK2 Genetic Analysis 12/31/2012 12/11/2013 12/18/2012 3/29/2014 1/18/2014 1/23/2014 3/16/2014 5/11/2014 6/16/2014 2/14/2014 9/23/2013 7/13/2013 3/15/2013 6/25/2013 9/10/2013 10/2/2013 1/21/2013 6/13/2012 5/16/2014 2/5/2014 4/3/2014 6/8/2014 9/5/2013 4/9/2014 5/8/2014 4/3/2014 4/2/2013 7/8/2013 9/4/2013 6/8/2013 2/7/2013
DOV-2 1 1 1 1 1 1 1 1 3 1 1 1 1 3 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 VA-RE 1 1 1 1 1 1 1 1 3 1 1 1 1 3 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 VA-LE LE 2 1 1 1 1 1 1 1 1 1 1 1 1 3 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 PUPIL 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 EOM SOA RPa RPa RPa RPa RPa RPa RP CP RP RP CP RP RP CP RP RP RP RP RP CP RP N N P P P P P P P FUNDUS DEF DEF 1 1 1 1 1 1 1 1 1 1 2 1 2 1 1 1 2 2 1 1 1 1 1 1 1 1 1 1 1 COLOUR VISION 1 2 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 2 2 1 1 1 1 2 1 1 1 1 1 1 CENTRALFIELDS LPACM,DMX LPACM,DMX T.Wysolone ACM,DMX ACM,DMX ACM,DMX ACM,DMX ACM,DMX ACM,DMX ACM,DMX ACM,DMX ACM,DMX ACM,DMX ACM,DMX ACM,DMX ACM,DMX ACM,DMX ACM,DMX ACM,DMX ACM,DMX ACM,DMX ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM,HEP ACM ACM ACM ACM ACM TREATMENT 12/16/2014 12/22/2013 10/23/2013 6/14/2014 6/17/2014 4/16/2014 5/20/2014 5/14/2014 8/19/2013 7/10/2014 6/28/2014 6/30/2014 6/30/2014 7/14/2014 5/24/2014 6/10/2014 6/14/2014 5/19/2014 4/10/2014 2/18/2014 6/13/2014 5/27/2014 8/14/2014 7/18/2013 6/27/2014 4/8/2014 5/6/2014 2/9/2014 4/6/2013
DOV-3 1 1 1 1 1 1 1 1 1 3 3 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 VA RE 1 1 1 1 1 1 1 1 1 3 3 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 VA LE LE 2 1 1 1 1 1 1 1 1 1 3 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 PUPIL 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 EOM SOA DP DP DP DP DP RP RP RP RP RP RP RP RP RP RP RP RP RP RP RP RP RP RP RP RP RP N N FUNDUS 2 1 1 1 1 1 1 1 1 2 1 1 2 1 1 1 2 2 1 1 1 1 1 1 1 1 1 1 1 COLOUR VISION 2 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 2 2 1 1 1 1 1 1 1 1 1 1 1 CENTRAL FIELDS ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM ACM TREATMENT KEY TO MASTER CHART
Fundus:
EP - Early Papilloedema
ESP - Established Papilloedema
CP - Chronic Papilloedema
N - Normal
SOA - Secondary Optic Atrophy
RP - Resolving Papilloedema
DP - Disc Pallor
MRI/MRV,CT:
SSS - Superior Sagittal Sinus
Sig.S - Sigmoid Sinus
Trnv.S - Transverse sinus
Str.S - Straight Sinus
Treatment:
ACM - Acitrom
DMX - Diamox
LP - Lumbar Puncture
HEP - Heparin
MAN - Mannitol
JAK2 - Jak2 Mutation