252 lines
No EOL
59 KiB
XML
252 lines
No EOL
59 KiB
XML
<?xml version="1.0" encoding="utf-8"?>
|
||
<!DOCTYPE html PUBLIC "-//W3C//DTD XHTML 1.0 Transitional//EN" "http://www.w3.org/TR/xhtml1/DTD/xhtml1-transitional.dtd">
|
||
<html xmlns="http://www.w3.org/1999/xhtml" xml:lang="en" lang="en">
|
||
|
||
<head><meta http-equiv="Content-Type" content="text/html; charset=utf-8" />
|
||
<!-- AppResources meta begin -->
|
||
<meta name="paf-app-resources" content="" />
|
||
<script type="text/javascript">var ncbi_startTime = new Date();</script>
|
||
|
||
<!-- AppResources meta end -->
|
||
|
||
<!-- TemplateResources meta begin -->
|
||
<meta name="paf_template" content="" />
|
||
|
||
<!-- TemplateResources meta end -->
|
||
|
||
<!-- Logger begin -->
|
||
<meta name="ncbi_db" content="books" /><meta name="ncbi_pdid" content="book-part" /><meta name="ncbi_acc" content="NBK459315" /><meta name="ncbi_domain" content="statpearls" /><meta name="ncbi_report" content="printable" /><meta name="ncbi_type" content="fulltext" /><meta name="ncbi_objectid" content="" /><meta name="ncbi_pcid" content="/NBK459315/?report=printable" /><meta name="ncbi_app" content="bookshelf" />
|
||
<!-- Logger end -->
|
||
|
||
<title>Cerebral Venous Thrombosis - StatPearls - NCBI Bookshelf</title>
|
||
|
||
<!-- AppResources external_resources begin -->
|
||
<link rel="stylesheet" href="/core/jig/1.15.2/css/jig.min.css" /><script type="text/javascript" src="/core/jig/1.15.2/js/jig.min.js"></script>
|
||
|
||
<!-- AppResources external_resources end -->
|
||
|
||
<!-- Page meta begin -->
|
||
<meta name="robots" content="INDEX,FOLLOW,NOARCHIVE" /><meta name="citation_inbook_title" content="StatPearls [Internet]" /><meta name="citation_title" content="Cerebral Venous Thrombosis" /><meta name="citation_publisher" content="StatPearls Publishing" /><meta name="citation_date" content="2023/06/12" /><meta name="citation_author" content="Prasanna Tadi" /><meta name="citation_author" content="Babak Behgam" /><meta name="citation_author" content="Seth Baruffi" /><meta name="citation_pmid" content="29083599" /><meta name="citation_fulltext_html_url" content="https://www.ncbi.nlm.nih.gov/books/NBK459315/" /><link rel="schema.DC" href="http://purl.org/DC/elements/1.0/" /><meta name="DC.Title" content="Cerebral Venous Thrombosis" /><meta name="DC.Type" content="Text" /><meta name="DC.Publisher" content="StatPearls Publishing" /><meta name="DC.Contributor" content="Prasanna Tadi" /><meta name="DC.Contributor" content="Babak Behgam" /><meta name="DC.Contributor" content="Seth Baruffi" /><meta name="DC.Date" content="2023/06/12" /><meta name="DC.Identifier" content="https://www.ncbi.nlm.nih.gov/books/NBK459315/" /><meta name="description" content="Cerebral venous thrombosis (CVT), which includes thrombosis of the cerebral veins and the dural sinuses, is a rare disorder that can lead to significant morbidity and mortality. Cerebral venous thrombosis can present with variable signs and symptoms that include a headache, benign intracranial hypertension, subarachnoid hemorrhage, focal neurological deficit, seizures, unexplained altered sensorium, and meningoencephalitis.[1][2]" /><meta name="og:title" content="Cerebral Venous Thrombosis" /><meta name="og:type" content="book" /><meta name="og:description" content="Cerebral venous thrombosis (CVT), which includes thrombosis of the cerebral veins and the dural sinuses, is a rare disorder that can lead to significant morbidity and mortality. Cerebral venous thrombosis can present with variable signs and symptoms that include a headache, benign intracranial hypertension, subarachnoid hemorrhage, focal neurological deficit, seizures, unexplained altered sensorium, and meningoencephalitis.[1][2]" /><meta name="og:url" content="https://www.ncbi.nlm.nih.gov/books/NBK459315/" /><meta name="og:site_name" content="NCBI Bookshelf" /><meta name="og:image" content="https://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcgifs/bookshelf/thumbs/th-statpearls-lrg.png" /><meta name="twitter:card" content="summary" /><meta name="twitter:site" content="@ncbibooks" /><meta name="bk-non-canon-loc" content="/books/n/statpearls/article-19194/" /><link rel="canonical" href="https://www.ncbi.nlm.nih.gov/books/NBK459315/" /><link rel="stylesheet" href="/corehtml/pmc/css/figpopup.css" type="text/css" media="screen" /><link rel="stylesheet" href="/corehtml/pmc/css/bookshelf/2.26/css/books.min.css" type="text/css" /><link rel="stylesheet" href="/corehtml/pmc/css/bookshelf/2.26/css/books_print.min.css" type="text/css" /><style type="text/css">p a.figpopup{display:inline !important} .bk_tt {font-family: monospace} .first-line-outdent .bk_ref {display: inline} </style><script type="text/javascript" src="/corehtml/pmc/js/jquery.hoverIntent.min.js"> </script><script type="text/javascript" src="/corehtml/pmc/js/common.min.js?_=3.18"> </script><script type="text/javascript">window.name="mainwindow";</script><script type="text/javascript" src="/corehtml/pmc/js/bookshelf/2.26/book-toc.min.js"> </script><script type="text/javascript" src="/corehtml/pmc/js/bookshelf/2.26/books.min.js"> </script>
|
||
|
||
<!-- Page meta end -->
|
||
<link rel="shortcut icon" href="//www.ncbi.nlm.nih.gov/favicon.ico" /><meta name="ncbi_phid" content="CE8D0B837D8A10510000000000AB0099.m_5" />
|
||
<meta name='referrer' content='origin-when-cross-origin'/><link type="text/css" rel="stylesheet" href="//static.pubmed.gov/portal/portal3rc.fcgi/4216699/css/3852956/3985586/3808861/4121862/3974050/3917732/251717/4216701/14534/45193/4113719/3849091/3984811/3751656/4033350/3840896/3577051/3852958/3984801/12930/3964959.css" /><link type="text/css" rel="stylesheet" href="//static.pubmed.gov/portal/portal3rc.fcgi/4216699/css/3411343/3882866.css" media="print" /></head>
|
||
<body class="book-part">
|
||
<div class="grid no_max_width">
|
||
<div class="col twelve_col nomargin shadow">
|
||
<!-- System messages like service outage or JS required; this is handled by the TemplateResources portlet -->
|
||
<div class="sysmessages">
|
||
<noscript>
|
||
<p class="nojs">
|
||
<strong>Warning:</strong>
|
||
The NCBI web site requires JavaScript to function.
|
||
<a href="/guide/browsers/#enablejs" title="Learn how to enable JavaScript" target="_blank">more...</a>
|
||
</p>
|
||
</noscript>
|
||
</div>
|
||
<!--/.sysmessage-->
|
||
<div class="wrap">
|
||
<div class="page">
|
||
<div class="top">
|
||
|
||
<div class="header">
|
||
|
||
|
||
</div>
|
||
|
||
|
||
|
||
<!--<component id="Page" label="headcontent"/>-->
|
||
|
||
</div>
|
||
<div class="content">
|
||
<!-- site messages -->
|
||
<div class="container content">
|
||
<div class="document">
|
||
<div class="pre-content"><div><div class="bk_prnt"><p class="small">NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.</p><p>StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. </p></div></div></div>
|
||
<div class="main-content lit-style" itemscope="itemscope" itemtype="http://schema.org/CreativeWork"><div class="meta-content fm-sec"><h1 id="_NBK459315_"><span class="title" itemprop="name">Cerebral Venous Thrombosis</span></h1><p class="contrib-group"><h4>Authors</h4><span itemprop="author">Prasanna Tadi</span><sup>1</sup>; <span itemprop="author">Babak Behgam</span>; <span itemprop="author">Seth Baruffi</span><sup>2</sup>.</p><h4>Affiliations</h4><div class="affiliation"><sup>1</sup> Asram Medical College, Eluru, India</div><div class="affiliation"><sup>2</sup> Inspira Medical Center</div><p class="small">Last Update: <span itemprop="dateModified">June 12, 2023</span>.</p></div><div class="body-content whole_rhythm" itemprop="text"><div id="article-19194.s1"><h2 id="_article-19194_s1_">Continuing Education Activity</h2><p>Cerebral venous thrombosis (CVT), which includes thrombosis of the cerebral veins and the dural sinuses, is a rare disorder that can lead to significant morbidity and mortality. Cerebral venous thrombosis can present with variable signs and symptoms that include a headache, benign intracranial hypertension, subarachnoid hemorrhage, focal neurological deficit, seizures, unexplained altered sensorium, and meningoencephalitis. This activity reviews the cause of cerebral venous thrombosis and highlights the role of the interprofessional team in its management.</p><p>
|
||
<b>Objectives:</b>
|
||
<ul><li class="half_rhythm"><div>Review the cause of cerebral venous thrombosis.</div></li><li class="half_rhythm"><div>Describe the presentation of cerebral venous thrombosis.</div></li><li class="half_rhythm"><div>Summarize the treatment of cerebral venous thrombosis.</div></li><li class="half_rhythm"><div>Outline the importance of improving care coordination among interprofessional team members to improve outcomes for patients affected by cerebral venous thrombosis.</div></li></ul>
|
||
<a href="https://www.statpearls.com/account/trialuserreg/?articleid=19194&utm_source=pubmed&utm_campaign=reviews&utm_content=19194" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">Access free multiple choice questions on this topic.</a>
|
||
</p></div><div id="article-19194.s2"><h2 id="_article-19194_s2_">Introduction</h2><p>Cerebral venous thrombosis (CVT), which includes thrombosis of the cerebral veins and the dural sinuses, is a rare disorder that can lead to significant morbidity and mortality. Cerebral venous thrombosis can present with variable signs and symptoms that include a headache, benign intracranial hypertension, subarachnoid hemorrhage, focal neurological deficit, seizures, unexplained altered sensorium, and meningoencephalitis.<a class="bk_pop" href="#article-19194.r1">[1]</a><a class="bk_pop" href="#article-19194.r2">[2]</a></p><p>The diversity of risk factors and variable presentation present challenges in diagnosing cerebral vein thrombosis. Delay in diagnosis is common, as the median delay from symptom onset to hospital admission is four days and from symptom onset to diagnosis is seven days. Thus, having a high index of suspicion for this disorder is crucial to ensure timely diagnosis and treatment.<a class="bk_pop" href="#article-19194.r3">[3]</a><a class="bk_pop" href="#article-19194.r4">[4]</a></p></div><div id="article-19194.s3"><h2 id="_article-19194_s3_">Etiology</h2><p>Many risk factors contribute to the development of cerebral venous thrombosis. At least one risk factor was identified in more than 85% of patients with cerebral venous thrombosis, and multiple risk factors are found in more than 50% of patients with cerebral venous thrombosis.<a class="bk_pop" href="#article-19194.r5">[5]</a> In general, cerebral venous thrombosis is common in any condition that leads to a prothrombotic state, including pregnancy, the post-partum state, or those on oral contraceptives. In the International Study on Cerebral Vein and Dural Sinus Thrombosis (ICSVT), genetic and acquired thrombophilia were present in 34% of patients with cerebral venous thrombosis. Inherited thrombophilia includes protein C and protein S deficiencies, antithrombin deficiency, factor V Leiden mutation, prothrombin gene mutation <i>20210</i>, as well as hyperhomocysteinemia.<a class="bk_pop" href="#article-19194.r6">[6]</a><a class="bk_pop" href="#article-19194.r7">[7]</a></p><p>Acquired thrombophilia should be suspected in patients with a history of nephrotic syndrome (due to loss of antithrombin) or antiphospholipid antibodies. Additional causes and risk factors associated with cerebral venous thrombosis include chronic inflammatory disease states such as systemic lupus erythematosus, inflammatory bowel disease, malignancy, and vasculitides such as Wegener's granulomatosis. Local infections such as otitis and mastoiditis, which can lead to thrombosis of the adjacent sigmoid and transverse sinuses, have also been implicated in developing cerebral venous thrombosis. Cerebral venous thrombosis may also be seen in a patient with a head injury, after certain neurosurgical procedures, direct injury to the sinuses or jugular veins, such as jugular vein catheterization, and even after a lumbar puncture.<a class="bk_pop" href="#article-19194.r8">[8]</a><a class="bk_pop" href="#article-19194.r9">[9]</a></p></div><div id="article-19194.s4"><h2 id="_article-19194_s4_">Epidemiology</h2><p>Cerebral venous thrombosis is a rare disorder with an annual incidence estimated to be three to four cases per million. The frequency of peripartum and post-partum cerebral venous thrombosis is about 12 cases per 100,000 deliveries in pregnant women, which is only slightly lower than that of peripartum and post-partum arterial stroke. Cerebral venous thrombosis occurs three times more frequently in women than in men. This is thought to be due to gender-specific risk factors, for example, oral contraceptive use and, less frequently, pregnancy, puerperium, and hormone replacement therapy. More recently, there has been a significant female predominance among young adults, with the majority of cases (70% to 80%) being in women of childbearing age, but not among children or elderly persons.</p></div><div id="article-19194.s5"><h2 id="_article-19194_s5_">Pathophysiology</h2><p>There are two pathophysiologic mechanisms thought to contribute to the clinical manifestations of cerebral venous thrombosis. First, thrombosis of the cerebral veins leads to increased venous and capillary pressure, which leads to a decrease in cerebral perfusion. Decreased cerebral perfusion results in ischemic injury, manifested by cytotoxic edema, which damages the energy-dependent cellular membrane pumps and leads to intracellular swelling. Disrupting the blood-brain barrier leads to vasogenic edema and leakage into the interstitial space. The increased pressure in the venous system can lead to an intraparenchymal hemorrhage.</p><p>The second pathophysiologic mechanism resulting in cerebral venous thrombosis is obstruction of the cerebral sinuses, particularly when the thrombus does not resolve. Normally, the cerebrospinal fluid found in the cerebral ventricles is transported through the subarachnoid space to the arachnoid granulations and absorbed into the venous sinuses. Thrombosis of the venous sinuses results in impaired cerebrospinal fluid absorption, ultimately leading to increased intracranial pressure. Increased intracranial pressure leads to cytotoxic and vasogenic edema and may result in parenchymal hemorrhage. </p></div><div id="article-19194.s6"><h2 id="_article-19194_s6_">History and Physical</h2><p>Physicians should highly suspect cerebral venous thrombosis given the variable presentation and low annual incidence. Signs and symptoms may be acute, subacute, or chronic, with the most common symptom in cerebral venous thrombosis being a headache. A subacute pattern of the clinical presentation was observed in almost 60% of cases compared to acute (<48 hours in 37%) and chronic (>30 days in 7%).<a class="bk_pop" href="#article-19194.r5">[5]</a> A headache presents in up to 90% of patients.<a class="bk_pop" href="#article-19194.r5">[5]</a></p><p>Headaches may be generalized or diffuse and tend to mimic migraines but may increase in severity slowly over days and weeks and are not relieved with sleep. In some instances, the headache may be thunderclap in nature, starting suddenly and maximal in intensity at onset, thereby mimicking the presentation of subarachnoid hemorrhage. A headache is often worsened with Valsalva or coughing, indicative of increased intracranial pressure. Papilledema and visual symptoms, such as diplopia caused by a sixth cranial nerve palsy when the intracranial pressure is too high, may accompany a headache. The funduscopic examination will reveal papilledema, which, depending on the severity, can cause visual impairment and even permanent blindness if left untreated. However, an isolated headache without any other focal neurologic deficits or papilledema has been reported in up to a fourth of patients with cerebral venous thrombosis and further complicates the diagnostic picture.</p><p>Focal neurologic signs are common and are seen in up to 44% of patients. Motor weakness, including hemiparesis, is the most common focal finding. However, unlike arterial thrombosis in the setting of cerebrovascular accidents, localization to one vascular territory is often absent. Hemispheric symptoms, such as aphasia and hemiparesis, are a characteristic but rare finding. Seizures are seen in about 40% of patients with cerebral venous thrombosis, the most common of which are focal seizures. Focal seizures account for 50% of those who experience a seizure in the setting of cerebral venous thrombosis but have the potential to generalize to a status epilepticus. Thus, cerebral venous thrombosis should be considered in any patient who presents with a headache and some combination of either focal neurologic deficit or new-onset seizures. Thrombosis of the straight sinus, or in severe cases of venous infarction with hemorrhagic transformation, can lead to compression of the diencephalon and brainstem, resulting in coma or death due to cerebral herniation.<a class="bk_pop" href="#article-19194.r10">[10]</a></p></div><div id="article-19194.s7"><h2 id="_article-19194_s7_">Evaluation</h2><p>Diagnosis of cerebral venous thrombosis is clinical and confirmed with neuroimaging. Given its varied presentation and myriad of symptoms, one must have a high index of suspicion to identify and diagnose this rare and potentially life-threatening condition correctly. It should be suspected in young and middle-aged patients, especially those with cerebral venous thrombosis risk factors, such as postpartum women, those with genetic or acquired thrombophilia, and patients with focal neurological findings. It should also be suspected in the following: </p><ul><li class="half_rhythm"><div>Under the age of 50</div></li><li class="half_rhythm"><div>Who present with atypical headaches or those having multiple repeat evaluations for an unrelenting headaches</div></li><li class="half_rhythm"><div>Focal neurological deficit</div></li><li class="half_rhythm"><div>Stroke-like symptoms, especially in the absence of vascular risk factors that would predispose to cerebral vascular accidents (carotid atherosclerosis)</div></li><li class="half_rhythm"><div>Seizures (focal, generalized, or status-epilepticus)</div></li><li class="half_rhythm"><div>Intracranial hypertension or evidence of papilledema on funduscopic exam</div></li><li class="half_rhythm"><div>Patients with CT evidence of hemorrhagic infarcts, particularly in the setting of multiple infarcts not confined to a single vascular territory</div></li></ul><p>Some important clinical clues to the diagnosis include slow progression, bilateral involvement, and concurrent seizures.<a class="bk_pop" href="#article-19194.r5">[5]</a></p><p>Laboratory evaluation should include a complete blood count, coagulation panel, chemistry panel, as well as inflammatory markers such as a sedimentation rate and C-reactive protein to evaluate for proinflammatory states. Ideally, a screening test that could effectively rule out the diagnosis without subjecting patients to neuroimaging when it is not necessary would be ideal and prove helpful to clinical practice. The D-dimer assay has been evaluated in this regard, and unfortunately, it has been shown to have an unacceptable false-negative rate of up to 26% in one study. This low sensitivity of the D-dimer assay is in contrast to the utility of the D-dimer in ruling out deep venous thrombosis, which may be due to the lower thrombotic burden of cerebral venous thrombosis compared to DVT.<a class="bk_pop" href="#article-19194.r11">[11]</a><a class="bk_pop" href="#article-19194.r12">[12]</a></p><p>Based on recent American Heart Association/American Stroke Association guidelines, a negative D-dimer does not effectively rule out<b> </b>cerebral venous thrombosis<b> </b>and should not preclude neuroimaging if there is clinical suspicion for cerebral venous thrombosis.<a class="bk_pop" href="#article-19194.r13">[13]</a><a class="bk_pop" href="#article-19194.r14">[14]</a> However, adding D-dimer (≥500 μg/L) to the clinical CVT score (comprising of variables such as seizure, known thrombophilia, oral contraceptive use, duration of symptoms for >6 days, worst headache ever, and focal neurologic deficits) has shown to improve its predictive value.<a class="bk_pop" href="#article-19194.r15">[15]</a></p><p>
|
||
<b>Neuroimaging</b>
|
||
</p><ol><li class="half_rhythm"><div><b>Non-contrast computed tomography (CT): </b> The speed and accessibility with which this test can be obtained make it the first test that should be obtained in any patient presenting with an atypical headache, focal neurologic deficit, seizures, altered mental status, or coma. A direct sign of cerebral venous thrombosis is the <b><i>cord sign</i></b>, a curvilinear hyperdensity within a cortical vein in the presence of thrombosis that can be seen for up two weeks following thrombus formation. Other direct signs include hyperdensity with a triangular shape in the superior sagittal sinus, also known as the <b><i>dense triangle sign</i></b>. Intraparenchymal hemorrhages or infarcts may be seen on non-contrast head CT and may cross vascular boundaries. In a multicentric study, brain infarction was observed in 36.4%, hemorrhagic transformation in 17.3%, and intraparenchymal hemorrhage in 3.8% of cohorts.<a class="bk_pop" href="#article-19194.r5">[5]</a> Hyperdensity within a cortical vein or dural sinus in plain CT is observed in only one-third of the cases. <a class="bk_pop" href="#article-19194.r5">[5]</a></div></li><li class="half_rhythm"><div><b>CT Venography (CTV): </b> While MRI does have a better sensitivity and specificity when compared to computed tomography, diagnostic and confirmatory venography is required to exclude cerebral venous thrombosis. The presence of new, helical CT scanners has led to evidence that CT venography is superior in the identification of cerebral veins when compared to MR venography and that the two methods are equivocal in the identification and diagnosis of cerebral venous thrombosis. The fact that CT venography can rapidly be performed following a non-contrast head CT while the patient is still in the CT scanner makes CT venography a viable option in the emergency setting when access to MRI imaging and venography may otherwise be limited or unavailable. Contrast-enhanced computed tomography illustrates the <b><i>empty delta sign</i></b>, representing contrast enhancement flowing around the comparatively hypodense region of the thrombosed superior sagittal sinus.</div></li><li class="half_rhythm"><div><b>Magnetic resonance imaging (MRI) and magnetic resonance venography (MRV) </b>are considered the gold standard in diagnosing cerebral venous thrombosis as they have a higher sensitivity than computed tomography. MRI is superior to CT when evaluating for parenchymal edema as a result of cerebral venous thrombosis. MRI findings are dependent on the age of the thrombus, as signal intensities change depending on thrombus age. Thus, MRI interpretation requires a detailed understanding of the evolutionary changes seen radiographically. An acutely formed thrombus (0 to 7 days) is harder to detect, but by week 2, abnormalities are easier to detect, with both T1 and T2-weighted images showing a hyperdense signal. The combination of an abnormal signal in a venous sinus combined with the absence of flow on MRV confirms the diagnosis of cerebral venous thrombosis. 2-dimensional lumen-based TOF showing the absence of a flow void in the dural sinus is the most sensitive imaging modality. Multiscale entropy (MSE) of hemoglobin products within the thrombus is of high diagnostic value.<a class="bk_pop" href="#article-19194.r16">[16]</a> The presence of DWI abnormality within the involved veins or sinus indicates low chances of recanalization. The differentials include arachnoid granulations and fenestrations.<a class="bk_pop" href="#article-19194.r17">[17]</a></div></li><li class="half_rhythm"><div><b>Cerebral angiography: </b>If the diagnosis is still in question after using MRI and MRV, then intra-arterial angiography is indicated. Angiography allows for superior visualization of the cerebral veins and helps identify anatomical variants of normal venous anatomy that mimic cerebral venous thrombosis. It is useful in rare cases of isolated cortical vein thrombosis without sinus thrombosis and may show indirect signs such as dilated and tortuous "corkscrew" collateral veins, evidence that there may be thrombosis further downstream of the sinuses.</div></li></ol><p>Superior sagittal sinus is most frequently involved, followed by transverse sinus.<a class="bk_pop" href="#article-19194.r5">[5]</a></p></div><div id="article-19194.s8"><h2 id="_article-19194_s8_">Treatment / Management</h2><p>Management initially focuses on identifying and addressing life-threatening complications of cerebral venous thrombosis, including increased intracranial pressure (ICP), seizures, and coma. If a patient seizes and has a lesion such as a hemorrhage or infarction on neuroimaging, then specific anticonvulsant therapy, as well as seizure prophylaxis, should be initiated. If a seizure does not occur, then seizure prophylaxis is not indicated. In the case of increased ICP, the head of the bed should be elevated, and administration of dexamethasone and mannitol should be done promptly to reduce increased ICP. This is followed by admission to the intensive care unit or stroke unit for close ICP monitoring, with a neurosurgical consultation if the patient decompensates and requires surgical decompression. Next, attention should be shifted to specific therapy, including anticoagulation and, in certain cases, catheter-directed fibrinolysis and surgical thrombectomy.</p><p>
|
||
<b>Anticoagulation</b>
|
||
</p><p>Anticoagulation has been a controversial topic due to the potential for hemorrhagic transformation of cerebral infarcts before administering anticoagulation. The goal of anticoagulation is to prevent thrombus propagation, help recanalize the lumen of occluded cerebral veins, and to prevent the complications of deep venous thrombosis and pulmonary embolism in patients who already have thrombus burden and are predisposed to forming additional thrombi. The results of two randomized controlled trials, which compared anticoagulation with placebo, although statistically insignificant, showed that anticoagulation had a favorable outcome more often than controls. They also showed that anticoagulation was safe and not contraindicated, even in patients with cerebral hemorrhage.</p><p>Based on these randomized controlled trials and other observational studies, anticoagulation is recommended as a safe and effective treatment of cerebral venous thrombosis. It should be initiated immediately upon diagnosis of cerebral venous thrombosis. Anticoagulation with intravenous unfractionated heparin or subcutaneously administered low-molecular-weight heparin is recommended as a bridge to oral anticoagulation with a vitamin K antagonist. There are no outcome differences while comparing unfractionated heparin (UFH) or low molecular weight heparin (LMWH). The European stroke organization (ESO) guidelines advocate unfractionated heparin in patients with renal insufficiency or the probability of requiring emergent reversal.<a class="bk_pop" href="#article-19194.r5">[5]</a></p><p>The target goal of treatment is an international normalized ratio of 2.0 to 3.0 cerebral venous thrombosis 3 to 6 months in patients with provoked cerebral venous thrombosis and 6 to 12 months in patients with unprovoked cerebral venous thrombosis.<a class="bk_pop" href="#article-19194.r5">[5]</a> Indefinite anticoagulation should be considered in patients with recurrent cerebral venous thrombosis, those who develop deep vein thrombosis and pulmonary embolism in addition to cerebral venous thrombosis, or those with first-time cerebral venous thrombosis in the setting of severe thrombophilia.</p><p>
|
||
<b>Thrombolysis</b>
|
||
</p><p>Although most patients see clinical improvement with anticoagulation therapy, a small subset of patients do not, and these individuals clinically deteriorate despite anticoagulation. In these cases, where the prognosis is poor, systemic and catheter-directed thrombolysis is indicated in patients with large and extensive cerebral venous thrombi who clinically deteriorate despite treatment with anticoagulation. As is the case, whenever fibrinolytics are used, there is an increased risk of intracranial hemorrhage. Based on a systemic review conducted in 2003, which looked at 72 studies and 169 patients with cerebral venous thrombosis, there seems to be a possible clinical benefit due to the use of fibrinolytics in patients with a severe presentation. Intracranial hemorrhage occurred in 17% of patients treated with fibrinolytics and was associated with clinical deterioration in 5% of cases. Overall, endovascular thrombolytics should be used at centers with staff experienced in interventional radiology and should be reserved for patients who are clinically deteriorating and despite treatment with anticoagulation. A systematic has shown local thrombolysis to be beneficial only in patients with severe CVT, whereas the results are anecdotal for mechanical thrombectomy.<a class="bk_pop" href="#article-19194.r5">[5]</a> </p><p>
|
||
<b>Surgical Intervention</b>
|
||
</p><p>Surgical thrombectomy is reserved for cases of severe neurological deterioration despite maximal medical therapy. In the case of large venous infarcts and hemorrhages causing a mass effect with risk of herniation, decompressive surgery has been thought to improve clinical outcomes, especially if done early, although this is level C evidence. Decompressive surgery is life-saving, with favorable outcomes observed in more than 50% of patients, with a mortality rate of approximately 20%.<a class="bk_pop" href="#article-19194.r5">[5]</a></p><p>
|
||
<b>Supportive Care</b>
|
||
</p><p>It is important to elucidate the underlying contributory factors of cerebral venous thrombosis and devise a treatment strategy to correct them. Women on hormonal contraceptive therapy should seek non-estrogen-based methods of contraception such as levonorgestrel and copper intrauterine devices or progestin-only pills. Further testing to identify the etiology of all acquired and reversible thrombophilic states should be conducted and, when possible, corrected. In addition to clinical follow-up, the American Heart Association and American Stroke Association recommend follow-up imaging 3 to 6 months after diagnosis to assess for recanalization.</p><p>The risks for ICH following anticoagulation therapy ranged from zero to 5.4%. A systematic review has shown that the overall mortality was 9.4%, and dependency of 9.4% and 9.7%, respectively.<a class="bk_pop" href="#article-19194.r18">[18]</a><a class="bk_pop" href="#article-19194.r19">[19]</a></p><p>
|
||
<b>The quality of evidence and the strength of recommendations of the European Stroke Organization guideline for the diagnosis and treatment of cerebral venous thrombosis (2017) can be summarized as follows:</b>
|
||
</p></div><div id="article-19194.s9"><h2 id="_article-19194_s9_">Differential Diagnosis</h2><ul><li class="half_rhythm"><div>Abducens nerve palsy</div></li></ul><ul><li class="half_rhythm"><div>Blood dyscrasias</div></li></ul><ul><li class="half_rhythm"><div>Cavernous sinus syndrome</div></li></ul><ul><li class="half_rhythm"><div>Head injury</div></li></ul><ul><li class="half_rhythm"><div>Intracranial abscess</div></li></ul><ul><li class="half_rhythm"><div>Neurosarcoidosis</div></li></ul><ul><li class="half_rhythm"><div>Pediatric status epilepticus</div></li></ul><ul><li class="half_rhythm"><div>Pseudotumor cerebri</div></li></ul><ul><li class="half_rhythm"><div>Staphylococcal meningitis</div></li></ul><ul><li class="half_rhythm"><div>Subdural empyema</div></li></ul></div><div id="article-19194.s10"><h2 id="_article-19194_s10_">Enhancing Healthcare Team Outcomes </h2><p>The diagnosis and management of cerebral venous thrombosis are challenging and best managed by an interprofessional team that includes a neurologist, neurosurgeon, radiologist, hematologist, anesthesiologist, ICU nurses, and intensivist. Other members of the interprofessional team include nursing staff, mid-level practitioners (NPs and PAs), and pharmacists. Management is initially focused on identifying and addressing life-threatening complications of cerebral venous thrombosis, including increased intracranial pressure (ICP), seizures, and coma. Next, attention should be shifted to specific therapy, including anticoagulation and, in certain cases, catheter-directed fibrinolysis and surgical thrombectomy. The prognosis of these patients is guarded. Even those who survive are often left with permanent neurological deficits.<a class="bk_pop" href="#article-19194.r20">[20]</a><a class="bk_pop" href="#article-19194.r21">[21]</a></p></div><div id="article-19194.s11"><h2 id="_article-19194_s11_">Review Questions</h2><ul><li class="half_rhythm"><div>
|
||
<a href="https://www.statpearls.com/account/trialuserreg/?articleid=19194&utm_source=pubmed&utm_campaign=reviews&utm_content=19194" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">Access free multiple choice questions on this topic.</a>
|
||
</div></li><li class="half_rhythm"><div>
|
||
<a href="https://mdsearchlight.com/neurology/cerebral-venous-thrombosis/?utm_source=pubmedlink&utm_campaign=MDS&utm_content=19194" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">Click here for a simplified version.</a>
|
||
</div></li><li class="half_rhythm"><div>
|
||
<a href="https://www.statpearls.com/articlelibrary/commentarticle/19194/?utm_source=pubmed&utm_campaign=comments&utm_content=19194" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">Comment on this article.</a>
|
||
</div></li></ul></div><div class="floats-group" id="article-19194.s12"></div><div id="article-19194.s13"><h2 id="_article-19194_s13_">References</h2><dl class="temp-labeled-list"><dt>1.</dt><dd><div class="bk_ref" id="article-19194.r1">Rawala MS, Noorani MM, Gulati R, Waqas S, Dave D. Elevated Factor VIII Level Associated with Transverse Cerebral Venous Sinus Thrombosis. <span><span class="ref-journal">Am J Case Rep. </span>2019 Mar 02;<span class="ref-vol">20</span>:274-277.</span> [<a href="/pmc/articles/PMC6410610/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC6410610</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/30824680" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 30824680</span></a>]</div></dd><dt>2.</dt><dd><div class="bk_ref" id="article-19194.r2">Farooq S, Testai FD. Neurologic Complications of Sickle Cell Disease. <span><span class="ref-journal">Curr Neurol Neurosci Rep. </span>2019 Feb 28;<span class="ref-vol">19</span>(4):17.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/30820687" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 30820687</span></a>]</div></dd><dt>3.</dt><dd><div class="bk_ref" id="article-19194.r3">Zhu L, Cheng J, Gu P, Liu Y, Liu J, Wang J, Shen H. Therapeutic strategies of thromboembolic events in patients with inflammatory bowel diseases: Two case reports. <span><span class="ref-journal">Medicine (Baltimore). </span>2019 Mar;<span class="ref-vol">98</span>(9):e14622.</span> [<a href="/pmc/articles/PMC6831449/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC6831449</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/30817579" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 30817579</span></a>]</div></dd><dt>4.</dt><dd><div class="bk_ref" id="article-19194.r4">Tekesin A, Tunç A. Inflammatory markers are beneficial in the early stages of cerebral venous thrombosis. <span><span class="ref-journal">Arq Neuropsiquiatr. </span>2019 Feb;<span class="ref-vol">77</span>(2):101-105.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/30810594" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 30810594</span></a>]</div></dd><dt>5.</dt><dd><div class="bk_ref" id="article-19194.r5">Ulivi L, Squitieri M, Cohen H, Cowley P, Werring DJ. Cerebral venous thrombosis: a practical guide. <span><span class="ref-journal">Pract Neurol. </span>2020 Oct;<span class="ref-vol">20</span>(5):356-367.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/32958591" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 32958591</span></a>]</div></dd><dt>6.</dt><dd><div class="bk_ref" id="article-19194.r6">Leite J, Ribeiro A, Gonçalves D, Sargento-Freitas J, Trindade L, Duque V. Cerebral Venous Thrombosis as Rare Presentation of Herpes Simplex Virus Encephalitis. <span><span class="ref-journal">Case Rep Infect Dis. </span>2019;<span class="ref-vol">2019</span>:7835420.</span> [<a href="/pmc/articles/PMC6360035/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC6360035</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/30800483" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 30800483</span></a>]</div></dd><dt>7.</dt><dd><div class="bk_ref" id="article-19194.r7">Taneda K, Adachi T, Watanabe Y, Hanajima R. Cerebral Venous Thrombosis due to Nontyphoidal Salmonella Bacteremia. <span><span class="ref-journal">Intern Med. </span>2019 Jul 01;<span class="ref-vol">58</span>(13):1943-1946.</span> [<a href="/pmc/articles/PMC6663523/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC6663523</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/30799361" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 30799361</span></a>]</div></dd><dt>8.</dt><dd><div class="bk_ref" id="article-19194.r8">Mikulenka P, Peisker T, Vasko P, Stetkarova I. Diagnosis of cerebral venous thrombosis: a single centre experience. <span><span class="ref-journal">Neuro Endocrinol Lett. </span>2019 Jan;<span class="ref-vol">39</span>(6):473-479.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/30796798" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 30796798</span></a>]</div></dd><dt>9.</dt><dd><div class="bk_ref" id="article-19194.r9">Martín-Masot R, Ortiz Pérez P, Serrano Nieto J, Martínez León M, Pascual Martínez A, Blasco-Alonso J, Navas-López VM. Central Venous Sinus Thrombosis in a Boy With Acute Severe Ulcerative Colitis. <span><span class="ref-journal">Front Pediatr. </span>2019;<span class="ref-vol">7</span>:19.</span> [<a href="/pmc/articles/PMC6367252/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC6367252</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/30775357" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 30775357</span></a>]</div></dd><dt>10.</dt><dd><div class="bk_ref" id="article-19194.r10">Aarju G, Birinder Singh P, Vipin K, Alisha S, Gunchan P. Neurological Predictors of Functional Outcome in Cortical Venous Sinus Thrombosis. <span><span class="ref-journal">J Neurosci Rural Pract. </span>2022 Apr;<span class="ref-vol">13</span>(2):290-294.</span> [<a href="/pmc/articles/PMC9187406/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC9187406</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/35694057" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 35694057</span></a>]</div></dd><dt>11.</dt><dd><div class="bk_ref" id="article-19194.r11">Weimar C, Holzhauer S, Knoflach M, Koennecke HC, Masuhr F, Mono ML, Niederstadt T, Nowak-Göttl U, Schellong SM, Kurth T. [Cerebral venous and sinus thrombosis : S2k guidelines]. <span><span class="ref-journal">Nervenarzt. </span>2019 Apr;<span class="ref-vol">90</span>(4):379-387.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/30758512" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 30758512</span></a>]</div></dd><dt>12.</dt><dd><div class="bk_ref" id="article-19194.r12">Monagle P, Newall F. Management of thrombosis in children and neonates: practical use of anticoagulants in children. <span><span class="ref-journal">Hematology Am Soc Hematol Educ Program. </span>2018 Nov 30;<span class="ref-vol">2018</span>(1):399-404.</span> [<a href="/pmc/articles/PMC6245972/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC6245972</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/30504338" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 30504338</span></a>]</div></dd><dt>13.</dt><dd><div class="bk_ref" id="article-19194.r13">Monagle P, Cuello CA, Augustine C, Bonduel M, Brandão LR, Capman T, Chan AKC, Hanson S, Male C, Meerpohl J, Newall F, O'Brien SH, Raffini L, van Ommen H, Wiernikowski J, Williams S, Bhatt M, Riva JJ, Roldan Y, Schwab N, Mustafa RA, Vesely SK. American Society of Hematology 2018 Guidelines for management of venous thromboembolism: treatment of pediatric venous thromboembolism. <span><span class="ref-journal">Blood Adv. </span>2018 Nov 27;<span class="ref-vol">2</span>(22):3292-3316.</span> [<a href="/pmc/articles/PMC6258911/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC6258911</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/30482766" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 30482766</span></a>]</div></dd><dt>14.</dt><dd><div class="bk_ref" id="article-19194.r14">Wangqin R, Laskowitz DT, Wang Y, Li Z, Wang Y, Liu L, Liang L, Matsouaka RA, Saver JL, Fonarow GC, Bhatt DL, Smith EE, Schwamm LH, Prvu Bettger J, Hernandez AF, Peterson ED, Xian Y. International Comparison of Patient Characteristics and Quality of Care for Ischemic Stroke: Analysis of the China National Stroke Registry and the American Heart Association Get With The Guidelines--Stroke Program. <span><span class="ref-journal">J Am Heart Assoc. </span>2018 Oct 16;<span class="ref-vol">7</span>(20):e010623.</span> [<a href="/pmc/articles/PMC6474951/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC6474951</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/30371291" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 30371291</span></a>]</div></dd><dt>15.</dt><dd><div class="bk_ref" id="article-19194.r15">Heldner MR, Zuurbier SM, Li B, Von Martial R, Meijers JCM, Zimmermann R, Volbers B, Jung S, El-Koussy M, Fischer U, Kohler HP, Schroeder V, Coutinho JM, Arnold M. Prediction of cerebral venous thrombosis with a new clinical score and D-dimer levels. <span><span class="ref-journal">Neurology. </span>2020 Aug 18;<span class="ref-vol">95</span>(7):e898-e909.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/32576633" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 32576633</span></a>]</div></dd><dt>16.</dt><dd><div class="bk_ref" id="article-19194.r16">Boukobza M, Crassard I, Bousser MG, Chabriat H. MR imaging features of isolated cortical vein thrombosis: diagnosis and follow-up. <span><span class="ref-journal">AJNR Am J Neuroradiol. </span>2009 Feb;<span class="ref-vol">30</span>(2):344-8.</span> [<a href="/pmc/articles/PMC7051397/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC7051397</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/19095790" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 19095790</span></a>]</div></dd><dt>17.</dt><dd><div class="bk_ref" id="article-19194.r17">Poon CS, Chang JK, Swarnkar A, Johnson MH, Wasenko J. Radiologic diagnosis of cerebral venous thrombosis: pictorial review. <span><span class="ref-journal">AJR Am J Roentgenol. </span>2007 Dec;<span class="ref-vol">189</span>(6 Suppl):S64-75.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/18029905" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 18029905</span></a>]</div></dd><dt>18.</dt><dd><div class="bk_ref" id="article-19194.r18">Ferro JM, Canhão P, Stam J, Bousser MG, Barinagarrementeria F., ISCVT Investigators. Prognosis of cerebral vein and dural sinus thrombosis: results of the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT). <span><span class="ref-journal">Stroke. </span>2004 Mar;<span class="ref-vol">35</span>(3):664-70.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/14976332" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 14976332</span></a>]</div></dd><dt>19.</dt><dd><div class="bk_ref" id="article-19194.r19">Saposnik G, Barinagarrementeria F, Brown RD, Bushnell CD, Cucchiara B, Cushman M, deVeber G, Ferro JM, Tsai FY., American Heart Association Stroke Council and the Council on Epidemiology and Prevention. Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professionals from the American Heart Association/American Stroke Association. <span><span class="ref-journal">Stroke. </span>2011 Apr;<span class="ref-vol">42</span>(4):1158-92.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/21293023" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 21293023</span></a>]</div></dd><dt>20.</dt><dd><div class="bk_ref" id="article-19194.r20">Xu Y, Meng R, Rajah GB, Ding Y, Wu Y, Wu Y, Ji K, Wu C, Zhao W, Ji X. Long-term Outcomes of Cerebral Venous Sinus Stenosis Corrected by Stenting. <span><span class="ref-journal">Curr Neurovasc Res. </span>2019;<span class="ref-vol">16</span>(1):77-81.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/30727893" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 30727893</span></a>]</div></dd><dt>21.</dt><dd><div class="bk_ref" id="article-19194.r21">Lal D, Gujjar AR, Ramachandiran N, Obaidi A, Kumar S, El-Tigani M, Al-Azri F, Al-Asmi AR. Spectrum of Cerebral Venous Thrombosis in Oman. <span><span class="ref-journal">Sultan Qaboos Univ Med J. </span>2018 Aug;<span class="ref-vol">18</span>(3):e329-e337.</span> [<a href="/pmc/articles/PMC6307648/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC6307648</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/30607274" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 30607274</span></a>]</div></dd></dl></div><div><dl class="temp-labeled-list small"><dt></dt><dd><div><p class="no_top_margin">
|
||
<b>Disclosure: </b>Prasanna Tadi declares no relevant financial relationships with ineligible companies.</p></div></dd><dt></dt><dd><div><p class="no_top_margin">
|
||
<b>Disclosure: </b>Babak Behgam declares no relevant financial relationships with ineligible companies.</p></div></dd><dt></dt><dd><div><p class="no_top_margin">
|
||
<b>Disclosure: </b>Seth Baruffi declares no relevant financial relationships with ineligible companies.</p></div></dd></dl></div><div class="bk_prnt_sctn"><h2>Figures</h2><div class="whole_rhythm bk_prnt_obj bk_first_prnt_obj"><div id="article-19194.image.f1" class="figure bk_fig"><div class="graphic"><a href="/core/lw/2.0/html/tileshop_pmc/tileshop_pmc_inline.html?title=Illustration%20of%20cerebral%20venous%20thrombosis&p=BOOKS&id=459315_cerebral__venous__thrombosis.jpg" target="tileshopwindow" class="inline_block pmc_inline_block ts_canvas img_link" title="Click on image to zoom"><div class="ts_bar small" title="Click on image to zoom"></div><img src="/books/NBK459315/bin/cerebral__venous__thrombosis.jpg" alt="Illustration of cerebral venous thrombosis" class="tileshop" title="Click on image to zoom" /></a></div><div class="caption"><p>Illustration of cerebral venous thrombosis. Superior sagittal sinus, cortical veins, inferior sagittal sinus, Vein of Galen, internal cerebral veins, straight sinus, transverse sinus, sigmoid, jugular veins. Contributed by Chelsea Rowe</p></div></div></div></div><div class="bk_prnt_sctn"><h2>Tables</h2><div class="whole_rhythm bk_prnt_obj bk_first_prnt_obj"><div id="article-19194.table0" class="table"><p class="large-table-link" style="display:none"><span class="right"><a href="/books/NBK459315/table/article-19194.table0/?report=objectonly" target="object">View in own window</a></span></p><div class="large_tbl" id="__article-19194.table0_lrgtbl__"><table style="height: 764px;"><tbody><tr><td rowspan="1" colspan="1" style="width: 452.967px;vertical-align:top;">
|
||
<p><b>Recommendations</b></p>
|
||
</td><td rowspan="1" colspan="1" style="width: 265.5px;vertical-align:top;">
|
||
<p><b>Quality of evidence </b></p>
|
||
</td><td rowspan="1" colspan="1" style="width: 429.533px;vertical-align:top;">
|
||
<p><b>Strength of recommendations</b></p>
|
||
</td></tr><tr><td rowspan="1" colspan="1" style="width: 452.967px;vertical-align:top;">
|
||
<p>MRV and CT venography as an alternative to DSA</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 265.5px;vertical-align:top;">
|
||
<p>Very low</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 429.533px;vertical-align:top;">
|
||
<p>Weak</p>
|
||
</td></tr><tr><td rowspan="1" colspan="1" style="width: 452.967px;vertical-align:top;">
|
||
<p>CT venography as an alternative to MRV</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 265.5px;vertical-align:top;">
|
||
<p>Very low</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 429.533px;vertical-align:top;">
|
||
<p>Weak</p>
|
||
</td></tr><tr><td rowspan="1" colspan="1" style="width: 452.967px;vertical-align:top;">
|
||
<p>D-dimer before neuroimaging</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 265.5px;vertical-align:top;">
|
||
<p>Low</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 429.533px;vertical-align:top;">
|
||
<p>Weak</p>
|
||
</td></tr><tr><td rowspan="1" colspan="1" style="width: 452.967px;vertical-align:top;">
|
||
<p>Thrombophilia screening is not recommended</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 265.5px;vertical-align:top;">
|
||
<p>Very low</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 429.533px;vertical-align:top;">
|
||
<p>Weak</p>
|
||
</td></tr><tr><td rowspan="1" colspan="1" style="width: 452.967px;vertical-align:top;">
|
||
<p>Screening for occult malignancy is not recommended</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 265.5px;vertical-align:top;">
|
||
<p>Very low</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 429.533px;vertical-align:top;">
|
||
<p>Weak</p>
|
||
</td></tr><tr><td rowspan="1" colspan="1" style="width: 452.967px;vertical-align:top;">
|
||
<p><b>Treatment with heparin at a therapeutic dose, including those with ICH</b></p>
|
||
</td><td rowspan="1" colspan="1" style="width: 265.5px;vertical-align:top;">
|
||
<p><b>Moderate</b></p>
|
||
</td><td rowspan="1" colspan="1" style="width: 429.533px;vertical-align:top;">
|
||
<p><b>Strong</b></p>
|
||
</td></tr><tr><td rowspan="1" colspan="1" style="width: 452.967px;vertical-align:top;">
|
||
<p>Use of LMWH instead of UFH</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 265.5px;vertical-align:top;">
|
||
<p>Low</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 429.533px;vertical-align:top;">
|
||
<p>Weak</p>
|
||
</td></tr><tr><td rowspan="1" colspan="1" style="width: 452.967px;vertical-align:top;">
|
||
<p>No recommendation on thrombolysis</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 265.5px;vertical-align:top;">
|
||
<p>Very low</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 429.533px;vertical-align:top;">
|
||
<p>Uncertain</p>
|
||
</td></tr><tr><td rowspan="1" colspan="1" style="width: 452.967px;vertical-align:top;">
|
||
<p>Oral vitamin K antagonist for 3 to 12 months</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 265.5px;vertical-align:top;">
|
||
<p>Very low</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 429.533px;vertical-align:top;">
|
||
<p>Weak</p>
|
||
</td></tr><tr><td rowspan="1" colspan="1" style="width: 452.967px;vertical-align:top;">
|
||
<p>No recommendation for using NOACs</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 265.5px;vertical-align:top;">
|
||
<p>Very low</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 429.533px;vertical-align:top;">
|
||
<p>Weak</p>
|
||
</td></tr><tr><td rowspan="1" colspan="1" style="width: 452.967px;vertical-align:top;">
|
||
<p>No recommendation on therapeutic LP</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 265.5px;vertical-align:top;">
|
||
<p>Very low</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 429.533px;vertical-align:top;">
|
||
<p>Uncertain</p>
|
||
</td></tr><tr><td rowspan="1" colspan="1" style="width: 452.967px;vertical-align:top;">
|
||
<p>Acetazolamide and steroid not recommended</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 265.5px;vertical-align:top;">
|
||
<p>Low</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 429.533px;vertical-align:top;">
|
||
<p>Weak</p>
|
||
</td></tr><tr><td rowspan="1" colspan="1" style="width: 452.967px;vertical-align:top;">
|
||
<p>Shunting alone is not recommended</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 265.5px;vertical-align:top;">
|
||
<p>Very low</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 429.533px;vertical-align:top;">
|
||
<p>Uncertain</p>
|
||
</td></tr><tr><td rowspan="1" colspan="1" style="width: 452.967px;vertical-align:top;">
|
||
<p><b>Decompressive surgery in impeding herniation</b></p>
|
||
</td><td rowspan="1" colspan="1" style="width: 265.5px;vertical-align:top;">
|
||
<p><b>Low</b></p>
|
||
</td><td rowspan="1" colspan="1" style="width: 429.533px;vertical-align:top;">
|
||
<p><b>Strong</b></p>
|
||
</td></tr><tr><td rowspan="1" colspan="1" style="width: 452.967px;vertical-align:top;">
|
||
<p>AEDs in supratentorial lesions and seizures</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 265.5px;vertical-align:top;">
|
||
<p>Very low</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 429.533px;vertical-align:top;">
|
||
<p>Uncertain</p>
|
||
</td></tr><tr><td rowspan="1" colspan="1" style="width: 452.967px;vertical-align:top;">
|
||
<p>LMWH in pregnant and puerperal patients</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 265.5px;vertical-align:top;">
|
||
<p>Low</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 429.533px;vertical-align:top;">
|
||
<p>Weak</p>
|
||
</td></tr><tr><td rowspan="1" colspan="1" style="width: 452.967px;vertical-align:top;">
|
||
<p>OCP use is not advised in women of fertile age and prior CVT</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 265.5px;vertical-align:top;">
|
||
<p>Very low</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 429.533px;vertical-align:top;">
|
||
<p>Weak</p>
|
||
</td></tr><tr><td rowspan="1" colspan="1" style="width: 452.967px;vertical-align:top;">
|
||
<p> LMWH during pregnancy/puerperium  with a previous history of CVT</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 265.5px;vertical-align:top;">
|
||
<p>Very low</p>
|
||
</td><td rowspan="1" colspan="1" style="width: 429.533px;vertical-align:top;">
|
||
<p>Weak</p>
|
||
</td></tr></tbody></table></div></div></div></div></div></div>
|
||
<div class="post-content"><div><div class="half_rhythm"><a href="/books/about/copyright/">Copyright</a> © 2025, StatPearls Publishing LLC.<p class="small">
|
||
This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)
|
||
(<a href="https://creativecommons.org/licenses/by-nc-nd/4.0/" ref="pagearea=meta&targetsite=external&targetcat=link&targettype=uri">
|
||
http://creativecommons.org/licenses/by-nc-nd/4.0/
|
||
</a>), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.
|
||
</p></div><div class="small"><span class="label">Bookshelf ID: NBK459315</span><span class="label">PMID: <a href="https://pubmed.ncbi.nlm.nih.gov/29083599" title="PubMed record of this page" ref="pagearea=meta&targetsite=entrez&targetcat=link&targettype=pubmed">29083599</a></span></div></div></div>
|
||
|
||
</div>
|
||
</div>
|
||
</div>
|
||
<div class="bottom">
|
||
|
||
<div id="NCBIFooter_dynamic">
|
||
<!--<component id="Breadcrumbs" label="breadcrumbs"/>
|
||
<component id="Breadcrumbs" label="helpdesk"/>-->
|
||
|
||
</div>
|
||
|
||
<script type="text/javascript" src="/portal/portal3rc.fcgi/rlib/js/InstrumentNCBIBaseJS/InstrumentPageStarterJS.js"> </script>
|
||
</div>
|
||
</div>
|
||
<!--/.page-->
|
||
</div>
|
||
<!--/.wrap-->
|
||
</div><!-- /.twelve_col -->
|
||
</div>
|
||
<!-- /.grid -->
|
||
|
||
<span class="PAFAppResources"></span>
|
||
|
||
<!-- BESelector tab -->
|
||
|
||
|
||
|
||
<noscript><img alt="statistics" src="/stat?jsdisabled=true&ncbi_db=books&ncbi_pdid=book-part&ncbi_acc=NBK459315&ncbi_domain=statpearls&ncbi_report=printable&ncbi_type=fulltext&ncbi_objectid=&ncbi_pcid=/NBK459315/?report=printable&ncbi_app=bookshelf" /></noscript>
|
||
|
||
|
||
<!-- usually for JS scripts at page bottom -->
|
||
<!--<component id="PageFixtures" label="styles"></component>-->
|
||
|
||
|
||
<!-- CE8B5AF87C7FFCB1_0191SID /projects/books/PBooks@9.11 portal106 v4.1.r689238 Tue, Oct 22 2024 16:10:51 -->
|
||
<span id="portal-csrf-token" style="display:none" data-token="CE8B5AF87C7FFCB1_0191SID"></span>
|
||
|
||
<script type="text/javascript" src="//static.pubmed.gov/portal/portal3rc.fcgi/4216699/js/3879255/4121861/3501987/4008961/3893018/3821238/3400083/3426610.js" snapshot="books"></script></body>
|
||
</html> |