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Unexplained Fever In Hematologic Disorders Section 1. Benign Hematologic Disorders
Published in Benedict Isaac, Serge Kernbaum, Michael Burke, Unexplained Fever, 2019
The laboratory tests will show a low thrombocyte count, low plasmatic fibrinogen, prolonged prothrombin time and partial thromboplastin time, low plasmatic factors, especially VIII and V, and an elevation in fibrinogen degradation products. Fragmented erythrocytes (schistocytes) can be seen in peripheral blood smears.
Observations on the Fibrinolytic Response in Two Models of the Baboon in Response to E.Coli: Consumptive and Thrombotic Coagulopathies
Published in Pia Glas-Greenwalt, Fibrinolysis in Disease Molecular and Hemovascular Aspects of Fibrinolysis, 2019
The host, therefore, survives beyond the first 24 h, long enough to enter stage V. It is at this point that the C4b-binding protein (C4bBP) levels begin to rise and the level of free protein S is seen to decrease even further. At the same time the platelet count is driven to an extreme low while the fibrinogen concentration returns toward normal! It is also at this point that schistocytes begin to appear in the circulation and the hematocrit also decreases to an extreme low. The arterial pressure (MSAP), however, remains in the normal range while the blood urea nitrogen (BUN) and creatinine rise steadily, approaching 200 to 300 and 6 to 8 mg/dl, respectively, by 48 h. The renal tissues show the picture of cortical thrombosis, infarction, hemorrhage, and tubular necrosis associated with microvascular thrombosis.30
Hemolytic Anemias: General Considerations
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
Peripheral blood smear revealed nucleated red blood cells (not noted earlier), but no schistocytes. RPR was nonreactive. PT/PTT, plasma fibrinogen and fibrin split products were normal. Urinalysis revealed pink urine with 4+ blood detected on dipstick. Rare red blood cells were seen on microscopic examination.
Cobalamin and folic acid deficiencies presenting with features of a thrombotic microangiopathy: a case series
Published in Acta Clinica Belgica, 2022
Britt Ceuleers, Sofie Stappers, Jan Lemmens, Lynn Rutsaert
Our initial physical examination revealed a very pale, tachypneic but euvolemic woman appearing older than her stated age. There were no abnormal neurological or gastrointestinal findings. Vital signs were as follows: oxygen saturation 98%, heart rate 133/min, a blood pressure of 154/81 mmHg and a temperature of 37.3°C. A complete blood count (Table 1) revealed a severe macrocytic anemia with thrombocytopenia. Reticulocyte count was normal. An additional hemolytic workup showed elevated LDH, decreased haptoglobin, hyperkalemia, indirect hyperbilirubinemia and a negative Direct Coombs test. Laboratory findings also showed normal kidney function (creatinine 1.02 mg/dl), hypovitaminosis B12 (<148 ng/L) with hyperhomocysteinemia and normal folic acid levels (9.4 µg/L). By means of an arterial blood gas analysis, we established a high anion gap metabolic acidosis with partial respiratory compensation, assumedly as a consequence of high lactate levels in the blood. A peripheral blood smear revealed schistocytes.
Recurrent nonbacterial thrombotic endocarditis and stroke on anticoagulation
Published in Journal of Community Hospital Internal Medicine Perspectives, 2020
Sijan Basnet, Thomas Stauffer, Amar Jayswal, Biswaraj Tharu
Anticardiolipin IgG or IgM, anti-B2 glycoprotein IgG or IgM and lupus anticoagulant associated with history of thrombosis or pregnancy morbidity are required for a diagnosis of definite APS [7,9]. Patients may also have hemolytic anemia and thrombocytopenia. Schistocytes may also be present [10]. Positive antiphospholipid antibodies, negative blood cultures, and absence of systemic symptoms help differentiate NBTE from infective endocarditis [2]. Mitral valve followed by aortic valve are commonly affected valves. It can affect both normal valves and valves affected by rheumatic fever or endocarditis, chordae tendineae or the endocardium [2,3]. Valvular lesions are characterized by localized to generalized thickening with or without vegetations [3]. Vegetations are often rounded, sessile, and heterogenous and are characteristically seen along the coaptation edge of the leaflets [2,11]. There may be associated valvular regurgitation or stenosis. All these findings can be detected on TTE or TEE [3]. Definitive diagnosis can be done by biopsy of the affected valve or postmortem. Histologic examination shows fibrinoplatelet deposition with mononuclear cell infiltration [2,11].
An update on pathogenesis and diagnosis of thrombotic thrombocytopenic purpura
Published in Expert Review of Hematology, 2019
Bérangère S. Joly, Paul Coppo, Agnès Veyradier
Standard hematological and biochemical analysis are required for TMA diagnosis (Table 1) [4]. In TTP, patients present a microangiopathic hemolytic anemia with a high reticulocyte count, undetectable serum haptoglobin concentration and elevated LDH levels (hemolysis parameters), together with a consumption thrombocytopenia. Schistocytes on the blood smear represent the morphologic hallmark of TTP but their absence should not exclude TTP diagnosis and this investigation should be repeated. Erythrocyte Coombs’ test is usually negative, except in autoimmune contexts as SLE. Renal function may be altered, showing proteinuria, hematuria and sometimes acute kidney injury with elevated plasma urea and creatinine levels. Cardiac troponin has a prognosis value (>0.1 microg/L) and underlines cardiac involvement [50]. Clinical and biological TTP scores have been validated to predict acquired ADAMTS13 deficiency, including platelet count, serum creatinine level, antinuclear antibodies, D-dimer, reticulocytes count and indirect bilirubin level [64,65].