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We present a case of dural cerebral venous thrombosis with coexisting left frontal hemorrhage that was successfully treated with 13.79 million units of urokinase over a period of 165 hours.
Cerebral venous thrombosis is quite rare in newborn infants, but probably its incidence is not well evaluated because clinical signs and cerebral echocardiography are not specific. We report the case of an newborn infant with massive cerebral venous thrombosis associated with heart malformation: supramitral ring and partial anomalous pulmonary venous connection in the superior vena cava.
A case of orbital abscess complicated by unilateral blindness and CST as a result of an odontogenic infection is reported. The patient eventually recovered her sight. This case illustrates how appropriate consultations and prompt interventions are beneficial in giving total care to a critically ill patient.
Cerebral venous thrombosis (CVT) can be difficult to diagnose because of its wide spectrum of clinical manifestations. Its diagnosis may be further complicated when patients initially present with acute subarachnoid hemorrhage (SAH). We report on four patients with SAH revealing a CVT and discuss the role of imaging for diagnostic and pretherapeutic workup. In three women and one man presenting with severe headaches, images initially suggested SAH with no associated parenchymal bleeding. In all patients, SAH involved the sulci of the convexity and spared the basal cisterns. Digital subtracted angiography showed occlusion of intracranial venous sinuses but did not reveal any other cause of SAH. All patients improved with anticoagulant therapy. Risk factors for CVT and SAH, namely, head trauma and oral contraception, were identified in two patients. These cases highlight the fact SAH may reveal a CVT, which should be considered in the diagnostic workup of SAH, especially when the basal cisterns are not involved.
A case of parenchymal and intraventricular hemorrhage in a full-term neonate is reported. The underlying cause in our patient is thought to be related to cerebral sinovenous occlusive disease secondary to Protein C deficiency, a rare coagulopathy.
Literature reviews have indicated that thrombotic complications in leukemic patients are rare that prompt diagnosis is very difficult, and that morbidity and mortality are extremely high. We describe the successful treatment of a 36-year-old housewife suffering from chronic myelogenous leukemia with secondary myelofibrosis.
The authors report a 39-year-old woman who presented with intermittent, excruciating nuchal and occipital headache. Magnetic resonance imaging and magnetic resonance angiography scans showed bilateral subdural haematomas with veno-occlusive disease of the superficial and deep venous systems. There were bridging collaterals with scalp veins, bleeds from which could explain the subdural haematoma. There was acute on chronic veno-occlusive disease with an acute rise in intracranial pressure and a bleed from the vein of Galen.
Hereditary thrombophilias are a heterogenous group of genetic coagulation disorders which, particularly in combination with acquired prothrombotic factors, induce a predisposition to thrombosis. After characterization of frequent thrombophilic syndromes like factor V-Leiden or the prothrombin 20210GA mutation, a number of case-control studies screened for the prevalence of these mutations in ischemic stroke and cerebral venous thrombosis (CVT). Our meta-analysis shows that factor V-Leiden and prothrombin are frequent and significantly associated with CVT (16.4% vs. 4.9% or 4.3, P < 0.001, and 12.1% vs. 1.9% or 5.8, P < 0.001). In ischemic stroke, only factor V-Leiden and not prothrombin is a weak but significant risk factor (5.9% vs. 2.6% or 1.6, P < 0.001, and 4.1% vs. 3.3% or 1.4, P = 0.1). The C677T homozygous point mutation in the MTHFR, a homocysteine-degrading enzyme, was also associated with arterial stroke (16% vs. 15% or 1.5, P < 0.001). For CVT, sufficient data are lacking. We therefore recommend screening for thrombophilia in CVT. In ischemic stroke, atrial premature complex (APC) resistance should be considered. As long as controlled studies are lacking, individual anticoagulant therapy must take hereditary and precipitating factors into account to assess potential thrombotic risk.
We report herein the case of 32-year-old woman with situs inversus, thrombophilia, antiphospholipid syndrome and severe premenstrual syndrome (PMS) with cerebral edema and epileptic seizures prior to menstruation. Seven days prior to regular menstruation she developed severe PMS, including headache, blurred vision, epileptic seizures, urinary incontinence, craving for food, depression and irritability. Papilledema was detected. Daily hormone analyses prior to and during menstruation confirmed an ovulatory cycle with extremely high progesterone, prolactin and insulin levels in the late luteal phase. From day 29 to day 31, progesterone and insulin decreased sharply and the estradiol/progesterone ratio changed, leading to epileptic seizures and the peak of her symptoms. Diuretic treatment was administered. All symptoms disappeared during the first few days of menstruation. A novel oral contraceptive, containing ethinyl estradiol and drospirenone, an antimineralocorticoid progestogen, was given during the next cycle and hormone analyses were repeated. All symptoms were reduced significantly and no cerebral edema and epileptic seizures occurred. This is the first report of a woman with severe PMS and cerebral edema being treated successfully with an oral contraceptive containing drospirenone.
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Reversible posterior leucoencephalopathy and cerebral venous thrombosis share many symptoms. Both of them may lead to coma, and cause epilepsy or focal neurological signs. Moreover, diffuse leucoencephalopathy can be observed in both cases. Cerebral venous thrombosis needs anticoagulation which is not a riskless treatment. We describe a case of reversible posterior leucoencephalopathy in an hypertensed, seventy-year old man, presenting with a left lateral sinus hypoplasia whose clinical history and paramedical results first suggested a cerebral veinous thrombosis. Our case shows the misleadings a congenital vascular asymmetry can induce when confronted with a subacute coma.
In cardiac procedures that use access to the right atrium, the coronary sinus is at risk of accidental trauma and subsequent thrombosis as demonstrated by the two cases reported in this paper. The thromboses occurred in the setting of right heart failure and after procedures that involved catheterization or cannulation of the right atrium. A review of the literature revealed only rare instances of this complication, but, with the increasing use of the right atrium and coronary sinus for diagnostic and therapeutic purposes, injury to the coronary sinus must be considered.
In order to evaluate the contribution of computerized tomography (CT) to the diagnosis of cerebral thrombophlebitis, a series of 28 cases was reviewed and compared with data from the literature. In an examination carried out 4 to 5 days of its constitution the thrombus may be directly visualized as a spontaneous hyperdensity. This early but very transient sign, called "cord sign", can easily be overlooked, which explains why it was found in only 5 of our 28 cases and in 2% of the largest series of the literature. The thrombus thereafter becomes hypodense and can be intensified by peripheral contrast enhancement which produces the classical "delta sign". This sign is more frequent: 13/28 in our series and 16 to 30% in published cases. It is usually found in the superior sagittal sinus and must be distinguished from anatomical variations which are common at that level. These two direct signs acquire a greater value when associated with such indirect signs as diffuse or localized cerebral oedema (12 to 52%) and venous ischaemia (22 to 59%). Venous ischaemia is characterized by its strong bleeding potential (more than 50% of the cases) and by its usually favourable course; these two elements and its site differentiate it from arterial ischaemia. Finally, venous stasis is responsible, in 5 to 19% of the cases, for intense enhancement of the tentorium cerebelli; this sign is not specific but easy to evidence and of great value when associated with a direct sign. Dilatation of cortical veins, found in 4 of our 28 cases, also seems to be an interesting sign which, to our knowledge, has not yet been mentioned in the literature. Since in 3.6 to 26% of the cerebral thrombophlebitis the CT scan is normal, a negative CT examination does not rule out this disease, and in many cases the exploration must be rapidly completed by angiography or MRI. Because it is non-invasive and very sensitive to flows, MRI has become the key examination to assert the diagnosis. Angiography is now restricted to those cases where cases where MRI cannot be performed promptly or to certain, purely cortical thrombophlebitis which might pass unnoticed at MRI. When carried out and interpreted cautiously, angiography always shows the venous thrombosis, its exact size and its suppletive network. The results of this study show that MRI alone can diagnose cerebral thrombophlebitis in most patients, that CT well done and interpreted often provides useful but seldom sufficient indices, and that angiography should be reserved for difficult cases.
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Dural carotid cavernous fistulas (DCCF) can be associated with venous thrombosis. We report on a rare case of a patient who developed a venous infarct, which was diagnosed on CT and MRI. The DCCF predominantly drained through a frontobasal cortical vein into the superior sagittal sinus. The shunt volume was small and was therefore thought not to be sufficient to explain the massive ocular signs, such as severe exophthalmus and reduction of visual acuity. We therefore postulated a venous congestion owing to a secondary spontaneous venous thrombosis of the draining venous pathways to be responsible for the ocular signs. Under anticoagulative medication, the patient's signs and symptoms improved gradually. Control angiography after 3 months showed that the DCCF had disappeared. In the presence of DCCF, anticoagulation should always be considered when a venous thrombosis is suspected.
A 33-year-old man with a 13-year history of ulcerative colitis developed generalized clonic convulsions after transient right hemiparesis. A computed tomographic scan revealed a hemorrhagic lesion in the left frontal lobe and contrast tomography demonstrated delta-sign in the occipital area. A sagittal gadolinium-contrast magnetic resonance imaging scan demonstrated a low signal intensity area in the superior sagittal sinus. The venous phase of his carotid angiogram showed a lack of filling of the superior sagittal sinus. Coagulation studies revealed abnormal findings, elevated fibrinogen and increased aggregation of platelets. Cerebral venous or sagittal thrombosis occurring in ulcerative colitis is very rare in Japan. But thromboembolism is known as one of the extraintestinal complications of ulcerative colitis, and a hypercoagulable state may occur even in the inactive state. Ulcerative colitis should be considered as one of the etiologies of thromboembolism in addition to the results of coagulation studies for the prevention of cerebrovascular diseases.
An intravital microscopy imaging method was developed to visualize active cerebral thrombus and blood-brain barrier (BBB) disruption using Near Infrared Fluorescent (NIRF) probes. A circular craniotomy was made in CD-1 mice. Thrombi were formed by applying 10%-FeCl3 to the entire exposed superior sagittal sinus (SSS, 5 mm), or to the posterior 2.5 mm of the SSS for 5 mins. Control animals were pretreated with heparin (50 U/kg) before thrombus induction. Three hours after thrombus formation, a FXIIIa-targeted NIRF imaging probe (A15) was intravenously injected, and the SSS was imaged by intravital microscopy. This was followed by injection of indocyanine green (ICG) to assess BBB permeability. The A15 optical probe bound to thrombus, and the fluorescent signal emitted by the bound agent corresponded well with histologically confirmed thrombus. A15 initially remained intravascular, followed by excretion and subsequent decrease in all tissues except for thrombus, where it was retained. The subsequent ICG was also intravascular immediately after injection, but then began to leak into the cerebral parenchyma at 3 to 5 mins. The sites of leakage were adjacent to thrombosed areas. Heparin pretreatment prevented thrombus formation and reduced ICG leakage significantly. This demonstrates the feasibility of simultaneous in vivo monitoring of thrombus and BBB permeability in an animal model of cerebral venous thrombosis.