Cerebral venous thrombosis simulating cerebral arterial thrombosis: Late complication of COVID-19?

Context: Brain venous thrombosis (BVT) is uncommon and usually has a different clinic and treatment from cerebral arterial thrombosis. In this context, COVID-19 correlates with thrombogenesis with varied clinical repercussions. This report describes an unusual BVT case as a possible late complication of COVID-19. Case report: Male, 68 years old, athlete and healthy. April/2020: COVID-19 mild symptoms. February/2021: in road-running, he fell due to sudden left hemiparesis. Upon hospital admission: contacting, persistent headache. A week after, low level of consciousness and coma, when underwent right hemicraniectomy. Remains hospitalized. On examination: weak gestural communication, tracheostomy, enteral tube feeding, voluntary blinking. Maintains neutral cervical posture, masticatory automatisms, photoreactive isocoria, generalized rigidity, decorticated right hemiparesis, left hemiplegia. On imaging: hemorrhagic infarction on the right and mass effect due to obstruction of the Basal Rosenthal and Labbé veins and transverse sinus on the right, with venous blood flow in the rest of the hemisphere diverted to the ipsilateral internal jugular vein, by anastomotic veins of the occipital foramen and suboccipital venous plexus. Obstructed left internal jugular vein, with venous collateral flow from the left hemisphere via posterior intercavernous sinus and basilar plexus to the right internal jugular vein. Conclusions: To diagnose the venous etiology that resembled segmental occlusion of the right middle cerebral artery, CT angiography was required. Late evolution of COVID-19 has been identified by the persistence of symptoms for months. Although physical activity and possible dehydration may have contributed to BVT, a prothrombotic state correlated to COVID-19 cannot be discarded.

Thyroid Disorders and Hemostasis

Lower levels of free thyroxine (whether this is endogenous or exogenous) lead to a hypocoagulable state, and higher levels of free thyroxine lead to a hypercoagulable state. In this narrative review, the effects of different levels of thyroid hormones on clinical end points are described. Hypothyroidism is associated with an increased bleeding risk, whereas hyperthyroidism leads to an increased risk of venous thrombosis. Besides, effects of thyroid hormone on the heart may indirectly influence hemostasis. Hyperthyroidism leads to a higher incidence of atrial fibrillation and atrial flutter, and, at least partly by that mechanism, a higher risk of cerebral arterial thrombosis. In addition, compression effects of goiter on developing venous thrombosis are described. This is caused by local stasis of blood due to tumor expansion.

Cerebral stroke in a teenage girl with paroxysmal nocturnal hemoglobinuria

We report a case of paroxysmal nocturnal hemoglobinuria (PNH) in a 14 year-old girl presenting a cerebral arterial thrombosis. The initial diagnosis was carential anemia due to menarche following identification of slight macrocytic anemia, leucopenia and mild thrombocytopenia at routine blood analysis. The child was eventually referred to a children’s hospital after the onset of progressive fatigue, anorexia and paleness. Severe anemia (hemoglobin 6 g/dL) with negative Coombs test, mild leucopenia (white blood cells 4.9×109/L) and thrombocytopenia (platelets 97×109/L) and high values of lactate dehydrogenase (2855 U/L) were identified; a packed red cells transfusion was administered. Her condition worsened and she subsequently presented complete right hemiplegia, aphasia and coma; magnetic resonance imaging revealed a massive ischemic lesion. A diagnosis of PNH was eventually made following high sensitivity flow cytometry, which identified a PNH clone (CD66b negative equal to 93.7% of granulocytes). Fast recovery from neurologic and hematological problems occurred in response to anticoagulant therapy and intravenous therapy with eculizumab. We are convinced that PNH should be included in the differential diagnosis of children presenting with cytopenia.

Cerebral Arterial Thrombosis in Ulcerative Colitis

Thrombosis, mainly venous, is a rare and well-recognized extraintestinal manifestation of inflammatory bowel disease (IBD). We describe a 25-year-old Caucasian man affected by ulcerative colitis and sclerosing cholangitis with an episode of right middle cerebral arterial thrombosis resolved by intraarterial thrombolysis. We perform a brief review of the International Literature.

Phospholipid inhibitors

SummaryThe antiphospholipid syndrome (APS) is defined by the association of arterial and/or venous thrombosis and/or pregnancy complications with the presence of at least one among the main antiphospholipid antibodies (aPL) (i. e., Lupus anticoagulants, LA, IgG and/ or IgM anticardiolipin antibodies, aCL, IgG and/or IgM antiβ2-glycoprotein I antibodies, aβ2-GPI). Several clinical studies have consistently reported that LA is a stronger risk factor for both arterial and venous thrombosis compared to aCL and aβ2-GPI. In particular, LA activity dependent on the first domain of β2-GPI and triple aPL positivity are associated with the risk of thrombosis and obstetrical complications.Asymptomatic aPL-positive subjects do not require primary thromboprophylaxis. Venous thromboembolism is the most common initial clinical manifestation of APS. To prevent its recurrence indefinite anticoagulation is recommended. Long duration treatment with warfarin or aspirin is used after a first cerebral arterial thrombosis. Low molecular weight heparin (LMWH) with or without aspirin is recommended to reduce the rate of obstetrical complications of APS pregnant women.