Disseminated Intravascular Coagulation Syndrome as a Complication in Acute Spontaneous Canine Babesiosis

AbstractThe polyetiological syndrome of disseminated intravascular coagulation (DIC) is characterized by changes in patients’ hemostasis. The aim of the current research was to elucidate the main factors for the development of DIC syndrome during canine babesiosis, and to assess their correlation level. Dogs included in this study were of various breeds and sex, weighing 10-40 kg and aged 2-7 years. They were separated in two groups (n=50) according to their diagnosis to babesiosis. Oscillometry (blood pressure, pulse rate), vascular-platelet hemostasis, coagulogram, hematological, biochemical (fibrinogen, fibrin degradation product, soluble fibrin-monomer complex) and hemodynamic (circulating blood volume) assessment methods were used. The group of dogs positive on Babesia spp., had clear manifestation of DIC with 5-7% of the erythrocyte population being affected. DIC was manifested by a significant increase in soluble fibrin-monomer complex and fibrin degradation product (p<0.001), hypofibrinogenemia (p<0.001), thrombocytopenia (p<0.001), and an increase in indicators of spontaneous aggregation ability of platelets and red blood cells (p<0.001). Significant hemodynamic disorders were observed: a decrease in circulating blood volume, circulating erythrocytes volume (p<0.05), specific circulating blood volume and hematocrit value (p<0.001). The average blood pressure was reduced (p<0.001), and the Allgöwer’s shock index was increased 2 times (p<0.05). A shock of II degree (medium, subcompensated) was confirmed. Therefore, it can be concluded that acute spontaneous dogs’ babesiosis can be characterized by the occurrence of DIC in a consumption coagulopathy form, and shock of II degree. This condition renders the patients for emergency admission.

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Higher prognostic value of soluble fibrin complexes than D-dimer and fibrin degradation product for disseminated intravascular coagulation in patients with liver cirrhosis

Blood Coagulation & Fibrinolysis ◽

10.1097/mbc.0b013e32835aef6b ◽

2013 ◽

pp. 1 ◽

Cited By ~ 2

Author(s):

Seon Young Kim ◽

Ji-Eun Kim ◽

Hyun Kyung Kim ◽

Inho Kim ◽

Sung-Soo Yoon ◽

...

Keyword(s):

Liver Cirrhosis ◽

Disseminated Intravascular Coagulation ◽

Degradation Product ◽

Prognostic Value ◽

Fibrin Degradation Product ◽

Soluble Fibrin ◽

Intravascular Coagulation ◽

D Dimer

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Splenomegaly development and disseminated intravascular coagulation syndrome in acute canine babesiosis

Regulatory Mechanisms in Biosystems ◽

10.15421/022192 ◽

2021 ◽

Vol 12 (4) ◽

pp. 670-675

Author(s):

O. A. Dubova ◽

D. V. Feshchenko ◽

T. I. Bakhur ◽

A. A. Dubovyi ◽

O. A. Zghozinska ◽

...

Keyword(s):

Blood Volume ◽

Disseminated Intravascular Coagulation ◽

Degradation Products ◽

Additional Parameter ◽

Moderate Degree ◽

Consumption Coagulopathy ◽

Laboratory Studies ◽

Canine Babesiosis ◽

Circulating Blood Volume ◽

Intravascular Coagulation

Disseminated intravascular coagulation (DIC) syndrome is the main defining process in the pathogenetic axis of complications in canine babesiosis. The involvement of the spleen with further irreversible changes in the organ largely determines the severity of the animal’s condition after spontaneous babesiosis. The work presented here aimed to determine the role of the DIC syndrome as a triggering factor for lesions of the spleen. Clinical and laboratory studies (haematological, biochemical, hemodynamic) have been carried out. Pathological studies of the removed spleen were carried out by histological methods using universal and specific staining. After suffering acute spontaneous babesiosis, the development of hypersplenism and splenomegaly was found in dogs. The diagnosis was confirmed haematologically by the detected cytopenia, normochromic type anaemia. An additional parameter was a significantly increased erythrocyte sedimentation rate. The biochemical profile indicated the development of bilirubinaemia due to the conjugated fraction, hyperfermentation of transaminases, hypoalbuminemia, which reflected the development of hepatitis and liver failure. Markers of DIC syndrome in laboratory studies are represented by reliable hypofibrinogenemia, increased level of fibrinogen/fibrin degradation products, including D-dimer, and soluble fibrin monomer complexes. The multidirectional indices of coagulation tests (activated partial thromboplastin and prothrombin time) made it possible to classify the stage of “consumption coagulopathy” of the DIC syndrome. The haemodynamic parameters of the sick dogs were characterized by a significant deficit in the circulating blood volume. Together with the indicators of the “consumption coagulopathy” stage of the DIC syndrome, the hemodynamic indexes indicate a moderate degree of shock stage II – the stable reversibility, but the magnitude of the circulating blood volume deficit determines the tendency towards shock irreversibility. Histological studies have established a significant proliferation of the stromal elements of the organ, the formation of specific complexes of vessels with sinuses, clogging with blood clots, and the organ's parenchyma dystrophy. Such changes characterize complete splenomegaly, which is based on the organo-pathology of the DIC syndrome. The deposition of “old” fibrin in the connective tissue structures of the spleen indicates that DIC syndrome continues throughout the entire period of hyperplastic changes in the organ. The presence of hyalinosis in blood vessel walls of the spleen parenchyma determines irreversible changes in them. Thus, DIC syndrome is the basis for splenomegaly development in dogs after acute spontaneous babesiosis. It is confirmed by laboratory blood tests and histologically by the presence of fibrin thrombi in the structures of the organ, which determine the organopathology of the syndrome. The information obtained serves to expand the concepts of the pathogenesis of blood protozoal disease, define the high risk of complications that can become fatal for the health and life of animals.

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Measurement of soluble fibrin monomer-fibrinogen complex in plasmas derived from patients with various underlying clinical situations

Thrombosis and Haemostasis ◽

10.1055/s-0037-1613469 ◽

2003 ◽

Vol 89 (05) ◽

pp. 832-836 ◽

Cited By ~ 15

Author(s):

Yumiko Kazahaya ◽

Yuichi Shintani ◽

Kensuke Yamazumi ◽

Yutaka Eguchi ◽

Shin Koga ◽

...

Keyword(s):

Molecular Markers ◽

Disseminated Intravascular Coagulation ◽

Degradation Products ◽

Research Society ◽

Distinct Entity ◽

Soluble Fibrin ◽

Intravascular Coagulation ◽

Fibrin Degradation Products ◽

Fibrin Monomer ◽

D Dimer

SummaryWe previously reported a monoclonal antibody named IF-43 that specifically recognizes thrombin-modified fibrinogen (desAA- and desAABB- fibrin monomer) bound with fibrinogen or other D1 domain-containing plasmic fragments such as fragments X, Y, and D1, but not intact fibrinogen or cross-linked fibrin degradation products (XDP). Here, we tentatively named such complexes, soluble fibrin monomer (FM) -fibrinogen complex.By utilizing IF-43, we have developed a kit to measure soluble FM-fibrinogen complex and compared the profiles with those of two established molecular markers for thrombo-embolic disorders: i.e. the thrombin-antithrombin complex (TAT) and the D-dimer in plasma of patients who underwent surgery without any thrombo-embolic complications. The result indicated that soluble FM-fibrinogen complex is a distinct entity from the two established molecular markers. We have also attempted to observe their profiles in patients with the disseminated intravascular coagulation syndrome (DIC). Although the profiles of soluble FM-fibrinogen complex in individual patients appeared to vary from one patient to the other, the plasma level of soluble FM-fibrinogen complex was found to be increased at the initial phase of disseminated intravascular coagulation syndrome. Thus, the soluble FM-fibrinogen complex may serve as an independent molecular marker for the detection of thrombin generation and the diagnosis of thrombosis. The soluble FM-fibrinogen complex may also serve as a risk factor for thrombosis, because it may precipitate as insoluble complexes beyond its threshold in plasma, or when it is modified by thrombin.Part of this paper was originally presented at the 17th International Fibrinogen Workshop of the International Fibrinogen Research Society (IFRS) held in Munich, Germany, September, 2002.

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