scholarly journals Pathogenetic therapy of vascular-platelet hemostasis disorders in canine acute spontaneous babesiosis

2021 ◽  
Vol 23 (103) ◽  
pp. 96-102
Author(s):  
O. A. Dubova ◽  
A. O. Rudchenko ◽  
D. V. Feshchenko ◽  
A. A. Dubovyi ◽  
I. V. Chala ◽  
...  

The article presents the results of a study of the vascular-platelet hemostasis disorders processes in complications of canine acute spontaneous babesiosis, as well as a clinical trial of plasma substitute infusion for the purpose of identified disorders pathogenetic therapy. It was found that acute spontaneous Babesiosis is accompanied by complications in the form of subcompensated shock and a thrombogenic link of disseminated intravascular coagulation syndrome (DIC). This determines the potential risk of complications with a cautious prognosis. The basis for the diagnosis of complications is the establishment of the following changes: a significant deficit in the volume of circulating blood (a decrease in the hematocrit value, the volume of circulating plasma, the volume of circulating red blood cells, the specific volume of circulating blood), as well as significant changes in the functioning of the vascular-platelet link of hemostasis – thrombocytopenia against the background of an increase in the spontaneous aggregation ability of platelets and red blood cells, an increase in the wetting index of the vascular wall, which determines the thrombogenic state, and pronounced thrombocytopenia indicates the consumption of these shaped elements in blood clots. The described changes indicate the development of subcompensated shock and the thrombogenic component of DIC syndrome. Given the prognostic danger of established complications, there is a need for pathogenetic therapy of severe conditions. Infusions of plasma substitute solutions have been proposed to eliminate shock phenomena and the thrombogenic state of disseminated intravascular coagulation syndrome. A clinical trial of intravenous administration of Rheosorbylact solution and a mixture of Rheosorbylact with Dipyridamole was conducted in a comparative aspect. It is shown that a mixture of Rheosorbylact 100 ml and Dipyridamole solution 0.5 % 4 ml in the form of infusions at a dose of 5 ml/kg of animal body weight per day for 3 days can bring hemodynamic parameters and parameters of vascular-platelet hemostasis to physiological ones within 48 hours compared to an infusion of Rheosorbylact solution in its pure form. The synergy of the crystalloid solution of Rheosorbylact and the disaggregating vasodilator Dipyridamole enhances the disaggregating effect of both drugs, and the crystalloid solution itself is able to restore the lost volume of circulating blood.

Author(s):  
A. Kulikov

Presented material reveals main links in the pathogenesis of hemostatic disorder. In particular, attention is paid to the role of the lungs, liver and other organs in the development of this process. Role of vascular wall and blood cells in regulation of the physical state of blood is described in detail. The most frequent factors leading to hypercoagulation are indicated. Difference between hypercoagulation and thrombophilia is shown. The latter is found in clinical practice quite often, but at the same time, it is poorly diagnosed. Such a terrible complication of hemostatic disorder as disseminated intravascular coagulation is described. Its classification, stages of development, clinical manifestations are offered to the readers.


Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 5141-5141
Author(s):  
Vipul R. Patel ◽  
Jatinder Khokhar ◽  
Hemant S Murthy ◽  
Albert S. Braverman

Abstract Abstract 5141 Burr red blood cells (BC) in patients with disseminated intravascular coagulation (DIC). Background: Angiopathic hemolysis with schistocytes occurs in a minority of DIC patients. Burr cells (BC), are morphologically homogeneous, with a serrated membrane resembling that of red cells (RBC) in a hypertonic medium. They are associated with acute renal insufficiency, and have been observed in DIC. Methods: Criteria for patient inclusion were sepsis, often with multi-organ failure and hypotension. Of the 39 patients studied, 20 had DIC, based on platelet counts <100,000, and an International Society of Hemostasis and Thrombosis score of ≥5, derived from D-dimer or fibrin split product levels, prothrombin time elevations, and fibrinogen levels. The percentages of BC and schistocytes were determined by 1000 RBC counts, without knowledge of data concerning DIC. Patients' [Hb]'s, serum creatinine and blood urea nitrogen (BUN), were recorded. Results: Five of the 20 DIC patients succumbed to their acute illness, while 15 recovered without developing renal insufficiency. The BC%'s of the 20 DIC patients ranged from 0–80%, with a median of 18% and a mean of 27%; in the 19 patients without DIC the range was 0–45%, the median 6.4% and the mean 11% (p=0.046). The schistocyte percentages in patients with and without DIC ranged from 0.20–17, and 0–78; the respective medians and means were 1.1% and 1.0%, and 3.0–5.8%. The median and mean [Hb]'s of the patients with and without DIC were 9.3 and 11, and 9.6 and 10.3, respectively. BC% did not correlate with the [Hb]. The median creatinine levels of patients with and without DIC were 0.92 and 0.93 mg/dl, though the DIC patients' BUN's were higher (medians 31 vs 15). The BC% correlated with neither the BUN nor the BUN/creatinine ratio. The median and mean serum sodium levels in patients with and without DIC were 137. Conclusion: BC's are significantly more frequent in septic patients with DIC than in those without it. BC% did not correlate with anemia, implying that BC do not cause significant hemolysis, though there was a trend to lower [Hb] in the DIC patients. BC% was much higher than that of schistocytes in both groups, and schistocyte percentages did not correlate with DIC or BC%. Because of the DIC patients' higher BUN's and BUN/creatinine ratio's, we cannot exclude a role for the factors, which caused pre-renal azotemia in BC formation. BC formation may prove to be a criterion for DIC. Disclosures: No relevant conflicts of interest to declare.


Blood ◽  
1957 ◽  
Vol 12 (9) ◽  
pp. 834-843 ◽  
Author(s):  
JULIUS R. KREVANS ◽  
DUDLEY P. JACKSON ◽  
C. LOCKARD CONLEY ◽  
ROBERT C. HARTMANN

Abstract A hemorrhagic diathesis has been observed in 2 patients who received 500 ml. of incompatible whole blood. In both, hypofibrinogenemia, hypoprothrombinemia and thrombocytopenia were observed and there was no evidence of increased fibrinolytic activity. In one, accelerin activity was reduced and there was transient evidence of a low-titered circulating anticoagulant. The most likely explanation for the observed changes is intravascular coagulation in the recipient, presumably initiated by the thromboplastin-like activity of the hemolyzed red blood cells.


Blood ◽  
2003 ◽  
Vol 102 (6) ◽  
pp. 2240-2242 ◽  
Author(s):  
Leopold Oehler ◽  
Eva Jaeger ◽  
Alexander Eser ◽  
Christian Sillaber ◽  
Heinz Gisslinger ◽  
...  

Abstract The overproduction of red blood cells in patients with polycythemia vera (PV) is reflected in vitro by the formation of erythroid burst-forming units (BFU-Es) in the absence of exogenous erythropoietin. In contrast to other myeloproliferative disorders, the molecular mechanism of PV is unknown and no specific chromosomal abnormality has been described. We speculated that imatinib mesylate may reverse the pathological overproduction of red cells by inhibition of autonomous erythropoiesis. In the present study, imatinib mesylate was found to either block or strongly inhibit autonomous BFU-E formation in vitro in all patients tested. Moreover, autonomous BFU-E growth was also markedly reduced by exposure of PV cells to imatinib mesylate prior to cultivation in semisolid medium. The profound effect of imatinib mesylate on autonomous erythropoiesis suggests the involvement of an as yet unidentified kinase in the pathogenesis of PV and should provide the rationale for a forthcoming clinical trial.


2021 ◽  
Vol 9 ◽  
Author(s):  
Viviana Clavería ◽  
Philippe Connes ◽  
Luca Lanotte ◽  
Céline Renoux ◽  
Philippe Joly ◽  
...  

Red blood cells in sickle cell anemia (sRBC) are more heterogeneous in their physical properties than healthy red blood cells, spanning adhesiveness, rigidity, density, size, and shape. sRBC with increased adhesiveness to the vascular wall would trigger vaso-occlusive like complications, a hallmark of sickle cell anemia. We investigated whether segregation occurs among sRBC flowing in micron-sized channels and tested the impact of aggregation on segregation. Two populations of sRBC of different densities were separated, labeled, and mixed again. The mixed suspension was flowed within glass capillary tubes at different pressure-drops, hematocrit, and suspending media that promoted or not cell aggregation. Observations were made at a fixed channel position. The mean flow velocity was obtained by using the cells as tracking particles, and the cell depleted layer (CDL) by measuring the distance from the cell core border to the channel wall. The labeled sRBC were identified by stopping the flow and scanning the cells within the channel section. The tube hematocrit was estimated from the number of fluorescence cells identified in the field of view. In non-aggregating media, our results showed a heterogeneous distribution of sRBC according to their density: low-density sRBC population remained closer to the center of the channel, while the densest cells segregated towards the walls. There was no impact of the mean flow velocity and little impact of hematocrit. This segregation heterogeneity could influence the ability of sRBC to adhere to the vascular wall and slow down blood flow. However, promoting aggregation inhibited segregation while CDL thickness was enhanced by aggregation, highlighting a potential protective role against vaso-occlusion in patients with sickle cell anemia.


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