Penatalaksanaan Stroke dan

Thrombosis Sinus Venosus

Oleh :
Dr Sugianto SpS Mkes PhD
Stroke
Stroke is the third leading cause of death in the United
States and a leading cause of long-term disability.
It affects about 795,000 people per year.
On average, someone has a stroke every 40 seconds, and
someone dies of a stroke every 4 minutes.
Stroke patients have an in-hospital mortality rate of 5 to 10%
for ischemic stroke and 40 to 60% for intracerebral
hemorrhage (ICH).
Only 10% of stroke survivors will recover completely. The
remaining survivors will be left with an impairment that will
often necessitate rehabilitation
Estimated Number per Year of First-Ever Strokes and
Transient Ischemic Attacks (TIAs) in the United States

STROKE SUBTYPE ESTIMATED

NUMBER
 Large vessel 69,000 (16%)
 Small vessel/lacunae 76,000 (17.5%)
 Cardioembolic 113,000 (26%)
 Stroke of uncommon mechanisms 15,000 (3.5%)
 Infarction of unknown cause 157,000 (36.5%)
 Total strokes and TIAs 430,000 (100%)
Most Common Sites for Hypertensive
Intracranial Hemorrhage

Affected Area Frequency

 Putamen 44%
 Thalamus 13%
 Cerebellum 9%
 Pons 9%
 Other cortical areas 25%
Deferential consideration

 Extra-axial collections of blood secondary to trauma can

mimic stroke. An epidural or subdural hematoma can
cause an altered mental status, focal neurologic signs,
and rapid progression to coma.
 Other structural lesions that may cause focal neurologic
signs include brain tumors and abscesses.
 Metabolic abnormalities also can mimic stroke syndromes.
Hypoglycemia often is responsible for an altered mental
status and is a well-known cause of sustained focal
neurologic symptoms that can persist for several days.
Stroke management

Ischemic Stroke
 MANAGEMENT COMPONENT TARGET TIME FRAME

 Door to doctor 10 min

 Door to CT completion 25 min
 Door to CT scan reading 45 min
 Door to treatment 60 min
 Access to neurologic expertise* 15 min
 Access to neurosurgical expertise* 2 hr
Stroke management

 In the prehospital setting, the focus should be on maintenance

of the ABCs (airway, breathing, and circulation), rapid
identification, early hospital notification, and rapid transport
 Overhydration should be avoided to prevent cerebral edema. By
contrast, dehydration may lead to decreased cerebral
perfusion, and saline infusion should be given if dehydration is
suspected
 Dextrose-containing solutions should be avoided in
normoglycemic patients suspected of having had a stroke
because elevated blood glucose levels may worsen an ischemic
deficit.
Antihypertensive Therapy for Acute
Ischemic Stroke
 Indication that patient is eligible for treatment with
intravenous rtPA or other acute reperfusion intervention
 Blood pressure level
 Systolic >185 mm Hg or diastolic >110 mm Hg
 Labetalol 10-20 mg IV over 1-2 min, may repeat × 1 or
 Nicardipine infusion, 5 mg/hr, titrate up by 2.5 mg/hr at 5- to 15-min intervals, maximum
dose 15 mg/hr; when desired blood pressure attained, reduce to 3 mg/hr

 If blood pressure does not decline and remains >185/110

mm Hg, do not administer rtPA
ISCHEMIC CEREBROVASCULAR DISEASE

 Treatment of ischemic stroke has improved significantly in

the past few years, and mortality and disability rates due
to this condition have decreased.
 Control of vascular risk factors has decreased the number
and severity of events.
 Improved management has included high-quality
rehabilitation, which is started as soon as possible to
improve the recovery (i.e., functional independence) of
stroke survivors.
 The multidisciplinary management of stroke can be
improved with specific educational programs aimed at
increasing awareness of stroke in the general population
and among professionals
 The concept of time is brain has a great value in
emphasizing that stroke is an emergency.
 Because the window for the available time-dependent
treatments is very narrow, avoiding delay is the major
goal in the prehospital phase of acute stroke care.
 All stroke patients must be transported as soon as possible
to the closest hospital with a stroke unit.
prevention
 Lifestyle modification can be a major contributor to
reducing the risk of ischemic stroke.
 Strategies to achieve this protection include avoiding
smoking and excessive alcohol consumption
 keeping a low–normal body mass index
 practicing regular exercise
 and having a diet low in salt and saturated fat, high in
fruit and vegetables, and rich in fiber.
 There is no need to add vitamin supplements to the diet
because they have not been found to affect stroke
prevention.
 Regular assessment of vascular risk factors (e.g.,
hypertension,diabetes, hypercholesterolemia) is important
because their control can reduce significantly the incidence of
vascular events.
 Blood pressure should be managed with diet and pharmacologic
therapy, aiming at normal levels of 120/80 mm Hg.
 Diabetes should be manage with lifestyle modification and
pharmacologic therapy as required.
 The best antihypertensive treatments for diabetics are
angiotensin-converting enzyme (ACE) inhibitors or angiotensin
receptor antagonists.
 Hypercholesterolemia should be managed with lifestyle
modification and a statin. After a noncardioembolic ischemic
stroke, statins are beneficial in all patients for secondary
prevention.
 Postmenopausal hormone replacement therapy should be
avoided for the primary or secondary prevention of stroke
because it can increase the risk of new vascular events.
 Other strategies to prevent stroke include the treatment
of obstructive sleep apnea with continuous positive airway
pressure (CPAP) breathing.
THREE STROKE TYPES
Focal Brain Dysfunction

Ischemic Intracerebral Subarachnoid

Stroke Hemorrhage Hemorrhage

85% 10% 5%

Clot occluding Bleeding Bleeding

artery into brain around brain

Diffuse Brain Dysfunction

ACUTE ISCHEMIC STROKE (AIS) & TIA
LOW BLOOD FLOW TO FOCAL AREA OF BRAIN

 Pathophysiology:
INFARCT
 Usually thromboembolism (blood
clot forms in vascular system,
travels downstream, plugs
cerebral artery)
 Acute therapy:
 Thrombolysis (or thrombectomy)
 Do NOT lower BP
CLOT  Avoid aspiration / IV glucose
 2 prevention:
Ischemic stroke =
Infarction with sequelae  Antithrombotic therapy
 Vascular risk factor therapy
Transient ischemic attack =
 Possible carotid endarterectomy
No infarction and no sequelae
(CEA) or angioplasty (CAS)
ISCHEMIC STROKE PATHOPHYSIOLOGY
The First Few Hours
“TIME IS BRAIN: Penumbra
SAVE THE PENUMBRA”
Penumbra is zone of Core
reversible ischemia around
core of irreversible
infarction—salvageable in
first few hours after
ischemic stroke onset

Penumbra damaged by:

• Hypoperfusion
• Hyperglycemia Clot in
Artery
• Fever
• Seizure
 Penumbra
ISCHEMIC PENUMBRA: PATHOPHYSIOLOGY
OF THERAPEUTIC WINDOW
Core

CEREBRAL Normal
BLOOD 20 function
FLOW
(ml/100g/min) 15
Neuronal CBF
PENUMBRA dysfunction 8-18
10

5 Neuronal CBF
CORE death <8

1 2 3
TIME (hours)

Identification of penumbra through MRI perfusion-diffusion

mismatch or perfusion CT may replace time as the major
indication for emergency acute ischemic stroke therapies.
ORGANIZED CARE OF STROKE PATIENTS:
PERFORMANCE IMPROVEMENT / UTILIZATION REVIEW

 Acute stroke team Supportive medical care

Treatment of acute stroke
 Stroke multidisciplinary team Rehabilitation
Outpatient planning
 Stroke unit Keep away future strokes
Etiologic evaluation
 Prewritten stroke orders
 Address each aspect of care each day
An organized approach enables
emergency treatment, a thorough evaluation,
and improved patient outcome at decreased cost.

Stroke unit care results in decreased rate of aspiration pneumonia,

decubiti, stroke progression or recurrence, and death.
STROKE EMERGENCY BRAIN IMAGING:
NONCONTRAST CT SCAN
Acute (4 hours) Subacute (4 days)
Infarction Infarction
R L R L

Subtle blurring of gray- Obvious dark changes

white junction & sulcal & “mass effect” (e.g.,
effacement ventricle compression)
STROKE EMERGENCY BRAIN IMAGING:
NONCONTRAST CT SCAN
Intracerebral Hemorrhage Subarachnoid Hemorrhage

CT detects all ICHs CT detects 90% of SAHs;

immediately if SAH suspected &
CT negative, must LP
 AIS EMERGENCY THERAPY:
IV TISSUE PLASMINOGEN ACTIVATOR (T-PA)
 Must give < 4.5 h—earlier you give it, better the outcome
 Stroke onset = last time known to be normal
 Do NOT give if glucose < 50
 Do NOT give if BP > 185/110
 Disability risk  30% despite ~5% symptomatic ICH risk
 Lawsuits for not giving >>> lawsuits for giving
< 3.0 Hours 3.0-4.5 Hours
 No upper age limit  Do NOT give if:
 No limit on stroke size  Pt > 80 yo
 Can give if taking warfarin & INR
 NIHSS > 25
< 1.7
 DM w/ previous stroke
 Taking warfarin at all
 AIS ED STROKE CARE 24/7:
1-H EVALUATION, 1-H INFUSION

I. Triage–10 min III. CT & Labs–45 min

 Review t-PA criteria  Obtain lab results
 Page acute stroke team  Read CT
 Draw pre t-PA labs*  Return pt to ED
II. Medical Care–25 min IV. Treatment–60 min
 Place O2 , 2 NS IVs  Start IV t-PA
 Obtain BP, weight, NIHSS  Monitor for ICH sxs
 Obtain 12-lead ECG  HTN, headache
 Send patient to CT  N/V,  neuro status

*CBC, platelets, PT/INR, PTT, chem 7, cardiac panel

THE AIS-BP RELATIONSHIP

In AIS, high BP is a response,

Penumbra
not a cause—don’t lower it!
 BP increase is due to arterial Core
occlusion (i.e., an effort to
perfuse penumbra)
 Failure to recanalize (w/ or w/o
thrombolytic therapy) results in
high BP and poor neuro outcomes
 Lowering BP starves penumbra,
worsens outcomes Clot in
Artery
Management of Acute Ischemic Stroke
 For the detection and early management of the medical
complications of stroke, neurologic status, pulse, blood
pressure, temperature, and oxygen saturation should be
monitored
 serum glucose levels need to be monitored and
hyperglycemia treated with insulin accordingly.
 Normal saline is recommended for fluid replacement
during the first 24 hours after stroke.
 If the patient has fever, treatment with paracetamol
 Reducing blood pressure is recommended only in patients
with extremely high blood pressure or when indicated by
other medical conditions.
Intravenous Administration of Tissue
Plasminogen Activator
 Infuse 0.9 mg/kg (maximum dose 90 mg) of tissue plasminogen
activator (tPA) over 60 minutes, with 10% of the dose given as a bolus
over 1 minute.
 Admit the patient to a stroke unit for monitoring. Perform neurologic
assessment and blood pressure measurement every 15 minutes during
the infusion, every 30 minutes thereafter for the next 6 hours, and
then hourly until 24 hours after treatment. Administer
antihypertensive medications to maintainsystolic blood pressure 180
and diastolic 105.
 If intracranial hemorrhage is suspected, discontinue the infusion and
obtain an emergency CT scan.
 Obtain a follow-up CT scan at 24 hours before starting anticoagulants
or antiplatelet agents.
Fibrinolytic therapy for acute ischemic stroke
in the 0- to 3-Hour Time Window

Inclusion Criteria
 Age 18 years or older
 Clinical diagnosis of ischemic stroke causing a measurable
neurologic deficit
 Time of symptom onset well established to be less than
180 minutes before treatment would begin
Fibrinolytic therapy for acute ischemic stroke
in the 0- to 3-Hour Time Window
Exclusion Criteria
 1. Evidence of intracranial hemorrhage on noncontrast head CT
 2. Only minor or rapidly resolving stroke symptoms
 3. High clinical suspicion of subarachnoid hemorrhage even with normal CT
findings
 4. Active internal bleeding (e.g., gastrointestinal or urinary bleeding within
last 21 days)
 5. Known bleeding diathesis, including but not limited to
 Platelet count <100,000/μL
 • Patient has received heparin within 48 hours and had an elevated
activated partial thromboplastin time (greater than upper limit of normal for
laboratory)
 • Recent use of anticoagulant (e.g., warfarin sodium) and elevated
prothrombin time >15 seconds
Fibrinolytic therapy for acute ischemic stroke
in the 0- to 3-Hour Time Window

 6. Within 3 months of intracranial surgery, serious head trauma, or previous stroke

 7. Within 14 days of major surgery or serious trauma
 8. Recent arterial puncture at noncompressible site
 9. Lumbar puncture within 7 days
 10. History of intracranial hemorrhage, arteriovenous malformation, or aneurysm
 11. Witnessed seizure at stroke onset
 12. Recent acute myocardial infarction
 13. On repeated measurements, systolic pressure >185 mm Hg or diastolic pressure
>110 mm Hg at time of treatment, requiring aggressive treatment to reduce blood
pressure to within these limits
Fibrinolytic Therapy for Acute Ischemic
Stroke in the 3- to 4.5-Hour Time Window:

Main Inclusion Criteria

 Acute ischemic stroke
 Age 18 to 80 years
 Onset of stroke symptoms 3 to 4.5 hours before initiation
of study-drug administration
 Stroke symptoms present for at least 30 minutes with no
significant improvement before treatment
Fibrinolytic Therapy for Acute Ischemic Stroke in the 3
to 4.5 Hour Time Window:

Main Exclusion Criteria

 Intracranial hemorrhage
 Time of symptom onset unknown
 Symptoms rapidly improving or only minor before start of infusion
 Severe stroke as assessed clinically (e.g., NIHSS score >25) or by
appropriate imaging techniques*
 Seizure at the onset of stroke
 Stroke or serious head trauma within the previous 3 months
 Combination of previous stroke and diabetes mellitus
 Administration of heparin within the 48 hours preceding the onset of
stroke, with an activated partial-thromboplastin time at presentation
edxceeding the upper limit of the normal range
Fibrinolytic Therapy for Acute Ischemic Stroke in the
3 to 4.5 Hour Time Window:
 Platelet count of less than 100,000/mm3
 Systolic pressure greater than 185 mm Hg or diastolic pressure greater
than 110 mm Hg, or aggressive treatment (intravenous medication)
necessary to reduce blood pressure to these limits)
 Blood glucose less than 50 mg/dL or greater than 400 mg/dL
 Symptoms suggestive of subarachnoid hemorrhage, even if CT scan
was normal
 Oral anticoagulant treatment
 Major surgery or severe trauma within the previous 3 months
 Other major disorders associated with an increased risk of bleeding
Hemorrhagic stroke
 Major therapies aimed at reducing this risk include BP
reduction, anticoagulation reversal, and hemostatic
therapy.
 BP control is commonly performed after ICH
 The majority of patients with an acute hemorrhagic stroke
should be admitted to an intensive care unit in which
specialty consultation is available.
 The two main approaches are often considered in the
treatment of intracranial hemorrhage have been (1) to
stop the source of bleeding and (2) to remove hematoma
to mitigate mass effect and toxic effects of free radicals
from blood breakdown.
Antithrombotic Drugs

 Early administration of unfractionated heparin, low-

molecular-weight heparin, or heparinoids is not indicated
in acute ischemic stroke patients.
 All patients should receive a low dose of aspirin daily, and
this should be started within 48 hours after stroke onset
Medical Complications

Complications of Immobility :
 Deep Vein Thrombosis / Pulmonary Embolism
 Falls
 Pressure sores / ulceration

Infections :
 Chest Infection
 Urinary Tract Infection
 Other Infections
Medical Complications
Malnutrition :
 Dysphagia
 Dehydration

Pain :
 Shoulder pain ( subluxation in the paretic limb )
 Miscellaneous pain ( headache, musculoskeletal )

Neuropsychiatric Disturbances :
 Depression
 Acute Confusional States ( Delirium )
Medical Complications

Miscellaneous :
 Cardiac Complications ( Arrhythmias, Myocardial
Infarction )
 Gastrointestinal Bleed
 Constipation
DVT Prophylaxis

 Early Mobilization

 Mechanical Compressive Devices :

 Antiembolic stockings
 Sequential Pneumatic Compression Devices

 Subcutaneous Unfractionated Heparin

 Low molecular weight Heparin

 Early mobilization after stroke is an effective measure to
reduce incidence of DVT

 Contraindications : hemodynamically unstable patients

patients with fluctuating symptoms
patients treated with thrombolytics
- in first 24 hrs.
 Antiembolic Stockings : Knee – high or Thigh – high : reduce venous stasis in
legs
 Sequential Pneumatic Compression Devices

 Prophylaxis in those with

contraindications for antithrombotic therapy
in first 24 hrs post thrombolysis
hemorrhagic infarcts

 Caution : patients with Peripheral arterial disease

Peripheral Neuropathy
 Subcutaneous administration of Unfractionated Heparin &
Low molecular weight Heparin

 LMWH has more favourable risk-benefit profile for

reduction of DVT & PE after ischemic stroke

 Contraindication : for 24 hours after thrombolytic therapy

 DVT : Asymptomatic / Symptomatic

 Edema of lower limbs

 Pain
 Acute onset of breathlessness : Pul embolism
 Invg : Doppler of Lower limbs
Echocardiogram
MDCT Pulmonary Angiogram
 Anticoagulants
 Falls

 Fall prevention should be an important part of initial mobilization

 Patients with stroke during hospitalization : high risk for falls
 Incidence of second falls is almost twice that of first falls
 Risk factors : Heart disease
Pre stroke cognitive impairment
Urinary incontinence
 Most happen during day ( 45 % )
patient’s room ( 51 % )
during visits to bath room ( 20 % )
Measures to prevent falls in hospitalized paitents with stroke :

 Use adult assistive walking devices

 Motion detectors
 Bed alarms
 Use of convex mirrors to enable nursing staff to view hallways from nursing
stations
 Continuing staff education
 Minimal use of sedative medications
Pressure sores and Ulceration

 In dependent areas ( sacrum , greater trochanter )

 Measures to reduce the incidence :

 Early mobilization of neurologically stable patients

 Those who cannot be mobilized, routine assessment of skin breakdown is to be made
 Frequent Turning
 Keep skin dry and free of moisture
 Use oscillating mattresses to minimize the pressure on susceptible areas ( sacrum ,
greater trochanter )
 Antibiotics and debridement
 Infections : Pneumonia & UTI

 Poststroke infection is common during first 5 days after admission

 Fever : Heralding sign of infection

 High risk factors : Age > 65 yrs

Patients with dysphagia
Patients with dysarthria
Failure of bedside water swallow test
 Measures to prevent pneumonia :

 Airway Suctioning
 Aggressive Pulmonary Toilet especially in patients with reduced level of
consciousness
 Incentive Spirometry : to facilitate air movement and prevent ateclectasis at lung
bases
 Mobilization and Frequent changes in position

 A study of Prophylatic antibiotics to prevent infection after stroke does not support
their routine use ( Chamorro et al 2005 )

 Prompt antibiotic therapy is warranted in patients with radiographically confirmed

chest infecion and in those where clinical suspicion is high

 Empiric coverage for both aerobic and anaerobic pathogens should be used until
cultures reports are available
 Urinary Tract Infection : a common infection in hospitalized patient with
stroke
 Associated with use of indwelling bladder catheter
 Preventive measures : Intermittent catheterization
Anticholinergic drugs
 Peform Urine analysis on routine basis
 Prompt antibiotic therapy : helps to prevent bacteremia, sepsis

 Less common infections : Cellulitis

Cholecystitis
Infective Endocarditis (s/p IV drugs)
Dysphagia

 Clinically apparent dysphagia after stroke : 51 – 55 %

 Diagnosis : clinical screening

videofluroscopy

 A diverse array of stroke localizations may result in dysphagia

 Hemispheric lesions : motor impairment of face, lips, tongue

attention deficit
 Brain stem lesions : impair normal pharyngeal swallow
laryngeal elevation
glottic closure
cricopharyngeal relaxation
 Consequences : Aspiration pneumonia
Dehydration
Malnutrition
Difficulty in administring drugs

 High risk presentations for dysphagia :

 Brain stem stroke

 Impaired consciouness
 Difficulty / Inability to sit upright
 Shortness of breath
 Slurred speech
 Facial weakness
 Wet cough
 Weak cough
 Hoarse voice
 3-oz water swallow test

 For those who fail in swallow test : to keep NPO

 Nasogastric tube / Nasoduodenal tube

 Don’t delay antiplatelet therapy as per rectal

preparations of aspirin are available
Pain
 Hemiplegic shoulder pain : a common complication in patients with
significant proximal muscle weakness

Measures :
 Functional electric stimulation
 Positioning
 External shoulder support devices
 Intraarticular steroid injections
 Therapeutic strapping of at risk hemiplegic shoulder
 Headache : in acute / subacute phase
in approximately 25 % of patients

 Discomfort involving cervical and lumbar spine, hip, knee

 Treatment
 Anti inflammatory drugs
 Use of orthotic devices
Cerebral venous thrombosis

 Thrombosis of the dural sinus and/or cerebral veins (CVT)

is an uncommon form of stroke, usually affecting young
Individuals
 CVT represents 0.5% to 1% of all strokes
 CVT is more commonly seen in young individuals
 According to the largest cohort study (the International
Study on Cerebral Venous and Dural Sinuses Thrombosis
[ISCVT]), 487 (78%) of 624 cases occurred in patients < 50
years of age
Sinus and Cerebral Vein Thrombosis

Sinus and cerebral vein clots are uncommon.

They can lead to severe headaches, confusion, and stroke-
like symptoms.
They may lead to bleeding into the surrounding brain
tissues.
The clot can be triggered by infections of the ear, face, or
neck, by estrogen use and pregnancy, and can be caused by
inherited and acquired clotting disorders.
 Normally, blood is transported through arteries into the
brain, where it delivers oxygen and nutrients.
 Once the blood has done its job, it collects into small
veins (=cerebral veins) that drain into large veins, called
sinus veins.
 The sinus veins lead to the jugular veins in the neck,
which carry the blood back to the heart
Thrombosis Terms
 Cerebral venous thrombosis
(CVT)
 Cerebral vein thrombosis
 Cerebral venous and sinus
thrombosis,
 Cerebral venous sinus
thrombosis (CVST)
 Cerebral sinovenous thrombosis
(CSVT)
 Cerebral vein and dural sinus
thrombosis
 Sinus and cerebral vein
thrombosis
Why do symptoms occur?
 The obstruction of the blood
flow from a clot in these veins
leads to a back up of blood and
increasing blood pressure in the
blood vessels just before the
obstruction
 The increased pressure leads to
swelling of part of the brain,
which results in headaches; the
pressure can damage the brain
tissue, leading to stroke-like
symptoms.
 The increased pressure can also
lead to rupture of the blood
vessel and bleeding into the
brain (see image below).
 Cause and Pathogenesis
 Predisposing causes of CVT are multiple.
 The risk factors for venous thrombosis in general are linked classically to the
Virchow triad of stasis of the blood, changes in the vessel wall, and
changes in the composition of the blood.
 Risk factors are usually divided into acquired risks (eg, surgery, trauma,
pregnancy, puerperium, antiphospholipid syndrome, cancer, exogenous
hormones) and genetic risks (inherited thrombophilia).
 pathogenesis
When thrombosis occurs in the cerebral veins and the dural sinuses, the
resulting venous hypertension causes hypoxia of the brain, similar to the
symptomology of dural arteriovenous fistulae, with resultant neuronal
ischemia
Venous thrombosis likely also causes breakdown in the blood-brain barrier,
which leads to increased venous pressure, increased intracranial blood volume,
and intracranial hypertension
The spectrum ranges from varying degrees of cerebral edema to massive
hemorrhage and bilateral cerebral infarcts
Symptoms

 Symptoms from sinus and cerebral vein clots depend on the location
and extension of the clot and vary from patient to patient.
 The most common symptom is a severe headache, often the worst
headache that a patient has ever had.
 It can be of sudden onset, develop over a few hours, or a few days.
 Nausea and vomiting may occur, as may blurred vision.
 A variety of other neurological symptoms can occur: seizures, speech
impairment, one-sided numbness and/or weakness of an arm, a leg,
or both, confusion, a decreased level of alertness.
 Symptoms
 When thrombosis is limited to the superior sagittal sinus or transverse sinus,
the most frequent pattern of presentation is isolated intracranial
hypertension
 If the thrombosis extends to the cortical veins, focal deficits and seizures can
occur
 Bilateral deficits are typically late signs of superior sagittal sinus thrombosis
 Transverse sinus CVT may be associated with otalgia, otorrhea, cervical
tenderness, and lymphadenopathy from an underlying infection, such as
mastoiditis or otitis media
 How is it diagnosed?
 Sinus and cerebral vein thrombosis is easily
missed if the correct imaging X-ray study is
not done.
 The appropriate test to do is an MRI
venogram (=MRV) or CT venogram (=CTV).
 If available, the MRV is slightly preferred
over CTV.
therapy
 Anticoagulant therapy with heparin is targeted to avoid extension of
thrombus
 Thrombolytic therapy can give faster recanalization of veins and faster
response. Recombinant tissue plasminogen activator (rtPA) were used in
clinical studies either systemic or locally
 Oral anticoagulation (OA) by vitamin K antagonist like warfarin is the
recommended treatment. The dose of warfarin should be adjusted to
maintain INR of 2.5 to 3.
treatment
 Therapy for patients with CVT should be directed at treating the underlying
causative process, symptoms secondary to elevated intracranial pressure,
and seizures or focal deficits caused by cerebral edema and infarction
 Increased intracranial pressure can be treated with temporary short-term
hyperventilation, osmotic agents (mannitol, hypertonic saline),