First trimester superior sagittal sinus venous thrombosis and antithrombin deficiency

2005 ◽  
Vol 25 (8) ◽  
pp. 808-810 ◽  
Author(s):  
W. J. MCAuley ◽  
B. J. Hunt ◽  
H. N. Ahmad ◽  
K. Harding ◽  
C. Nelson-Piercy
Keyword(s):  
Venous Thrombosis ◽  
Superior Sagittal Sinus ◽  
First Trimester ◽  
Antithrombin Deficiency ◽  
Sagittal Sinus ◽  
Sinus Venous Thrombosis

Antithrombin Deficiency in Pregnancy.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 1879-1879
Author(s):  
Retter J. Andrew ◽  
Hunt J. Beverley
Keyword(s):  
Caesarean Section ◽  
Post Partum ◽  
Case Series ◽  
Fold Increase ◽  
First Trimester ◽  
Antithrombin Deficiency ◽  
Sagittal Sinus ◽  
Asymptomatic Patients ◽  
Estimated Blood Loss ◽  
In Pregnancy

Abstract Background: During pregnancy untreated antithrombin deficiency is associated with up to a 50% risk of venous thromboembolism (VTE) and a relative risk of pregnancy loss of 2.1 with a 5-fold increase in stillbirths. Thus thromboprophylaxis is widely used, but little data is available to select type, dose & duration of anticoagulation. Method: We performed a retrospective, single centre observational study of our antithrombin deficient pregnancies since 1996. Results: There were 9 pregnancies in 8 women; median age at conception 33 (age-range 19–37). They separated into 3 groups (1) 4 asymptomatic patients diagnosed on family screening. They received unmonitored enoxaparin 40mg until 16 weeks then 40mg BD. (2) 2 with previous VTE, received intermediate dose enoxaparin (1mg/kg), increased to BD at 16 weeks. Monitoring was done to maintain an anti-Xa trough of <0.12 iu/ml and peak <0.8iu.ml. (3) 2 referred after presenting with VTE in pregnancy. They received enoxaparin 1mg/kg BD and the same monitoring These included a known antithrombin deficient woman, referred in her second pregnancy at 26weeks gestation with premature rupture of the membranes and an iliofemoral deep vein thrombosis which developed on enoxaparin 60mg OD. Enoxaparin was increased to 1mg/kg BD and an IVC filter inserted. Despite the filter however she had a pulmonary embolism. The filter was removed after Caesarean section at 31 weeks. Two had sagittal sinus thromboses in the first trimester associated with severe hyperemesis requiring IV fluids. One was our only thromboprophylaxis failure, receiving enoxaparin 40mg OD, she weighed 80Kg. The second presented at 11weeks gestation. She was intolerant of self injecting and so switched to warfarin at 15 weeks until 35 weeks as did one other mother. All mothers had close feto-maternal monitoring with uterine artery Doppler at 24 weeks if possible and then monthly growth scans thereafter. Delivery: Thromboprophylaxis was stopped at labour initiation or 12hrs prior to Caesarean section (3 women) and 50iu/kg of antithrombin concentrate was given. Anticoagulation was restarted 24hrs after delivery. Six weeks enoxaparin post-partum thromboprophylaxis was given or the women converted back to warfarin. Estimated blood loss at delivery was a median of 200ml (range 200–500ml), no transfusions were required. There were no post partum VTEs. Nine births occurred at a median gestation of 38weeks (range 31–41), median birth weight 3045g (range 1420–4120g). One child has West’s syndrome. Conclusion: This is the largest case series on the management of antithrombin deficiency in pregnancy. The combined use of enoxaparin in pregnancy and post partum combined with antithrombin concentrate during labour appears to improve pregnancy outcome and reduce the rate of VTE. Larger studies are required to confirm this finding.

Superior sagittal sinus thrombosis as a focal point of pulmonary embolism

2021 ◽  
Vol 26 (1) ◽  
pp. 39-44
Author(s):  
G. R. Ramazanov ◽  
A. E. Talypov ◽  
A. A. Kanibolotskiy ◽  
Kh. V. Korigova ◽  
V. N. Stepanov ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Cerebrovascular Disease ◽  
Venous Thrombosis ◽  
Cerebral Venous Thrombosis ◽  
Superior Sagittal Sinus ◽  
Focal Point ◽  
Sinus Thrombosis ◽  
Sagittal Sinus ◽  
Sagittal Sinus Thrombosis ◽  
Superior Sagittal Sinus Thrombosis

This article represents the discussion of a clinical case of superior sagittal sinus thrombosis as a focal point of fatal pulmonary embolism. Pulmonary embolism is a life-threatening condition, with a mortality rate of up to 40%. The direct source of pulmonary embolism is deep vein thrombosis of the lower extremities and pelvis in 80–90% of all cases. The veins of the upper extremities and venous heart cause it less often. Pulmonary embolism in patients with cerebral venous thrombosis is observed in 1.4% of patients.Cerebral venous thrombosis is a cerebrovascular disease manifested by venous outflow disorders due to acute occlusion of the sinuses and veins of the brain. It requires immediate treatment in order to prevent the development of intracranial hemorrhage, venous infarction, disability and death. Cerebral venous thrombosis accounts for approximately 0.5% of all cases of cerebrovascular disease worldwide. In contrast to ischemic stroke, cerebral venous thrombosis is more common in younger patients. Currently, the diagnosis of cerebral venous thrombosis is based on neuroimaging data, and timely treatment leads to a decrease in disability and mortality.

scholarly journals Cerebral Sinus and Venous Thrombosis in Rats Induces Long-Term Deficits in Brain Function and Morphology—Evidence for a Cytotoxic Genesis

1994 ◽  
Vol 14 (2) ◽  
pp. 289-300 ◽  
Author(s):  
Kai U. Frerichs ◽  
Maria Deckert ◽  
Oliver Kempski ◽  
Ludwig Schürer ◽  
Karl Einhäupl ◽  
...  
Keyword(s):  
Locomotor Activity ◽  
Intracranial Pressure ◽  
Venous Thrombosis ◽  
Brain Function ◽  
Superior Sagittal Sinus ◽  
Spontaneous Locomotor Activity ◽  
Tissue Impedance ◽  
Sagittal Sinus ◽  
Long Term Changes

The pathophysiology of cerebral venous infarctions is poorly understood, due partially to the lack of a suitable experimental model. Therefore, we developed a model in rats to study acute and long-term changes of brain function and morphology following thrombosis of the superior sagittal sinus. The superior sagittal sinus of rats was exposed, ligated, and injected with thrombogenic material. Thrombosis of the longitudinal sinus and ascending cortical veins was monitored by intravital fluorescence angiography. Histology was studied at 24 h and 4 weeks after thrombosis and changes in intracranial pressure, electroencephalogram (EEG), and tissue impedance were noted. Spontaneous locomotor activity was followed for 4 weeks after thrombosis. The effect of heparin treatment on tissue impedance was evaluated. Thrombosis of the superior sagittal sinus could be regularly induced, although pathological sequelae developed only if ascending veins were affected. Sinus and venous thrombosis was histologically characterized by bilateral, parasagittal infarctions. Thrombosis induction was followed by an increase in intracranial pressure from 4.7 ± 1.6 to 12.8 ± 2.4 mm Hg (n = 4) at 1 h after thrombosis, associated with an exponential rise in tissue impedance to 165 ± 14% (n = 8) of the control. EEG changes were similar to those following global cerebral ischemia and remained pathological for up to 6 months after thrombosis (n = 6). As a permanent behavioral deficit spontaneous locomotor activity was reduced to 60 ± 10% (n = 6) of the control. Finally, the administration of heparin (1 IU/g body weight) after thrombosis induction was found to reverse the pathological tissue impedance response of the brain. In conclusion, involvement of ascending cortical veins following sinus thrombosis appears to be critical for the development of irreversible tissue damage, such as infarction. Changes in intracranial pressure and tissue impedance suggest that the venous thrombosis was followed by brain edema of a predominantly cytotoxic nature. Venous thrombosis led to long-term changes of brain function, as demonstrated by persistent disturbances of the EEG or of the spontaneous locomotor drive. These deficits may be amenable to treatment with heparin.

Anti-MOG Antibody Syndrome and Cerebral Sinovenous Thrombosis: A Cause–Effect Hypothesis

2020 ◽  
Author(s):  
Alessandra Fontana ◽  
Filippo Greco ◽  
Pierluigi Smilari ◽  
Andrea D. Praticò ◽  
Agata Fiumara ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Cerebral Venous Thrombosis ◽  
Superior Sagittal Sinus ◽  
Demyelinating Diseases ◽  
Sagittal Sinus ◽  
Cerebral Sinovenous Thrombosis ◽  
Sinovenous Thrombosis ◽  
Clinical Relationship ◽  
Effect Hypothesis ◽  
The Right

AbstractCerebral venous thrombosis is an uncommon event of stroke in childhood. Its origin is multifactorial and often it manifests with nonspecific symptoms that may overlap with underlying predisposing factors. Anti–myelin oligodendrocyte glycoprotein (MOG) antibody syndrome is a group of recently recognized acquired demyelinating diseases that occur more commonly in children, usually, with a favorable outcome. The association between cerebral venous thrombosis and demyelinating syndrome has been reported but their clinical relationship is matter of debate and various hypotheses have been advanced including intravenous (IV) steroid therapy and/or the consequence of a shared inflammatory-thrombotic process. Herein, we report the case of a child with anti-MOG antibody syndromes who developed a thrombosis of the superior sagittal sinus and of the right Trolard's vein.

scholarly journals Cerebral Venous Thrombosis in the Superior Sagittal Sinus as a Rare Cause of a Paroxysmal Kinetic Tremor

2017 ◽  
Vol 8 (3) ◽  
pp. 276-281 ◽  
Author(s):  
Kei Murao ◽  
Shuji Arakawa ◽  
Yoshihiko Furuta ◽  
Masahiro Shijo ◽  
Tetsuro Ago ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Cerebral Venous Thrombosis ◽  
Clinical Presentation ◽  
Superior Sagittal Sinus ◽  
Epileptic Seizures ◽  
Repetitive Movement ◽  
Sagittal Sinus ◽  
Kinetic Tremor ◽  
History Of ◽  
The Common

Cerebral venous thrombosis (CVT) has a broad spectrum of clinical presentation compared to arterial etiology. Seizure is one of the common symptoms and is more frequent than in other stroke types. Hence, transient neurological symptoms in CVT patients are usually due to epileptic seizures, while transient repetitive movement disorder is extremely rare except as a complication of epilepsy. We report a case of CVT in the superior sagittal sinus with a 1-year history of paroxysmal kinetic tremor without evident epilepsy.

Perioperative and Long-term Outcomes From the Management of Parasagittal Meningiomas Invading the Superior Sagittal Sinus

Neurosurgery ◽  
2010 ◽  
Vol 67 (4) ◽  
pp. 885-893 ◽  
Author(s):  
Shaan M Raza ◽  
Gary L Gallia ◽  
Henry Brem ◽  
Jon D Weingart ◽  
Donlin M Long ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Recurrent Disease ◽  
Superior Sagittal Sinus ◽  
Pathological Examination ◽  
Karnofsky Performance Score ◽  
Long Term Outcomes ◽  
Sagittal Sinus ◽  
Operative Notes

Abstract BACKGROUND: Parasagittal meningiomas invading the superior sagittal sinus (SSS) pose formidable obstacles to surgical management. Invasion is often considered a contraindication to surgery because of associated morbidity, such as cerebral venous thrombosis. OBJECTIVE: We report our most recent experience with the resection of parasagittal meningiomas invading the SSS. METHODS: Between 1992 and 2004, 110 patients with parasagittal meningiomas underwent surgery at the Johns Hopkins Medical Institutions. Clinical charts, radiological studies, pathological features, and operative notes were retrospectively analyzed; only those patients with minimum 24 months follow-up (n = 61) were further studied. RESULTS: Tumor distribution by location along the SSS was: 21% anterior, 62% middle, and 17% posterior. All patients were managed with initial surgical resection with radiosurgery for residual/recurrent disease if indicated (19.6%). Pathological examination revealed 80% grade I meningiomas, 13% grade II meningiomas, and 7% grade III meningiomas. Simpson grade I/II resection was achieved in 81% of patients. Major complications included venous thrombosis/infarction (7%), intraoperative air embolism (1.5%), and death (1.5%); long-term outcomes assessed included recurrence (11%) and improvement in Karnofsky Performance Score (85%). CONCLUSION: On the basis of our study, the incidence of postoperative venous sinus thrombosis is 7% in the setting of a recurrence rate of 11% with a mean follow-up of 41 months. In comparison with the published literature, the data corroborate the rationale for our treatment paradigm; lesions invading the sinus can initially be resected to the greatest extent possible without excessive manipulation of vascular structures, whereas residual/recurrent disease can be observed and managed with radiosurgery.

scholarly journals Cerebral Venous Thrombosis in Two Patients with Spontaneous Intracranial Hypotension

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
M. C. Garcia-Carreira ◽  
D. Cánovas Vergé ◽  
J. Branera ◽  
M. Zauner ◽  
J. Estela Herrero ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Cerebral Venous Thrombosis ◽  
Intracranial Hypotension ◽  
Superior Sagittal Sinus ◽  
Spontaneous Intracranial Hypotension ◽  
Cerebrospinal Fluid Leak ◽  
Cerebral Veins ◽  
Cortical Vein ◽  
Sagittal Sinus ◽  
Fluid Leak

Although few patients with spontaneous intracranial hypotension develop cerebral venous thrombosis, the association between these two entities seems too common to be simply a coincidental finding. We describe two cases of spontaneous intracranial hypotension associated with cerebral venous thrombosis. In one case, extensive cerebral venous thrombosis involved the superior sagittal sinus and multiple cortical cerebral veins. In the other case, only a right frontoparietal cortical vein was involved. Several mechanisms could contribute to the development of cerebral venous thrombosis in spontaneous intracranial hypotension. When spontaneous intracranial hypotension and cerebral venous thrombosis occur together, it raises difficult practical questions about the treatment of these two conditions. In most reported cases, spontaneous intracranial hypotension was treated conservatively and cerebral venous thrombosis was treated with anticoagulation. However, we advocate aggressive treatment of the underlying cerebrospinal fluid leak.

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