The present case is of a year old

The present case is of a 39-year-old woman with a left temporal hemorrhagic lesion and an associated DVA. The patient underwent craniotomy and surgery for removal of the mass. Dudeck et al reported a case wherein a DAVF developed in the proximity of a preexisting DVA after resection of a brainstem cavernoma. Wilson hypothesized that restriction of venous outflow or undampened transmission of acute increases in venous intracranial pressure (ICP) through large radicles of a DVA results in transient or sustained elevation of pressure within this lesion. Such pressure overload transmitted to a capillary network because of a DVA during surgery might have induced the development of the DAVF. Wilson also speculated that an inconspicuous thrombosis of one of the radicles of the DVA could cause an increased pressure within the DVA, promoting the de novo formation of a DAVF. In conclusion, the physiopathogenesis and incidence of a postoperative developmental DAVF remains unclear. However, factors such as changes in ICP or intracranial blood flow caused by surgery and chronic local hypoperfusion, and the potential role of the DVA, may contribute to the development of a DAVF. De novo formation of a DAVF following supratentorial surgery is rare. The present case provides clear radiographic proof of an acquired postoperative developmental DAVF. Although de novo formation of a DAVF after supratentorial surgery is uncommon, surgeons should preoperatively warn their patients of this morbidity.
Introduction Pseudothrombocytopenia (PTCP) is an in vitro phenomenon of platelet aggregation that results in spurious reporting of a low platelet count by automatic cell counters, which are typically EDTA dependent. In general, EDTA, a calcium chelator, is considered a safe and reliable anticoagulant for a complete blood count test because of its Merimepodib in blood cell counting and sizing. However, platelet clumping occurs occasionally. People with malignancy, chronic liver disease, infection, pregnancy, autoimmune diseases, and cardiovascular diseases have an increased risk of EDTA-dependent PTCP. It has also been observed in disease-free patients. Platelet clumping in the presence of EDTA is caused by an autoantibody against glycoprotein IIb/IIIa located on the cell membrane of platelets. Although other anticoagulants such as heparin and sodium citrate rarely induce such a phenomena, it is possible. Misdiagnosis of PTCP leads to unnecessary diagnostic tests and treatments, such as bone marrow biopsy, holding surgery, splenectomy, steroid therapy, and platelet transfusion. Therefore, when a low platelet count is noted, PTCP must also be considered. In this study, we report two cases of EDTA-dependent PTCP.
Case reports
Discussion Thrombocytopenia is caused by increased destruction of platelets (hemolytic uremic syndrome, immune thrombocytopenia, and disseminated intravascular coagulation), decreased production of platelets (leukemia, sepsis, human immunodeficiency virus, and decreased production of thrombopoietin), hemodilution, or the use of certain drugs (valproic acid, methotrexate, pantoprazole, and heparin). PTCP caused by platelet aggregation in blood containing EDTA should also be considered when a low platelet count is noted. Since 1973, EDTA-dependent PTCP has been widely reported. The prevalence rate of EDTA-dependent PTCP is approximately 0.1–2% in hospitalized patients. The mechanism involves the binding of an antiplatelet autoantibody to the glycoprotein located on the cell membrane of platelets. A combined action of the chelating effect of EDTA on calcium ions and low temperature affects the platelet membrane glycoprotein complex IIb/IIIa and reveals the epitope of glycoprotein IIb, which normally remains hidden in the glycoprotein complex IIb/IIIa. When the autoantibody binds to the epitope of glycoprotein IIb, platelet aggregation occurs. The primary antibodies involved in this mechanism are immunoglobulin (Ig)G, IgM, and IgA, and combinations of IgG and IgM, or IgA and IgG are also observed. Most of the agglutinins react strongly at room temperature or low temperatures, but some agglutinins are temperature-independent or react most strongly at 37°C.