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Query: UMLS:C0019087 (hemorrhagic diathesis)
 678 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Assessment of animals with a suspected hemorrhagic diathesis of unknown cause(s) should be methodical. Most acquired coagulopathies result from thrombocytopenia. A platelet estimate (from a blood smear) and/or a platelet count on a fresh blood sample therefore are useful first steps in case evaluation. If thrombocytopenia is present, the most likely causes are immune-mediated destruction of platelets, DIC, or megakaryocytic hypoplasia. These diagnoses can be pursued by further test, including antiplatelet antibody assays (for example, the platelet factor 3 tests or an ELISA test), measurement of FDP, and bone marrow biopsy, respectively. If the platelet count is normal, a buccal mucosa bleeding time test is a useful second step. If this is prolonged, most likely causes are vWD or a thrombocytopathy (functional platelet defect). von Willebrand's disease can be diagnosed by measurement of vWf concentration or activity. A normal bleeding time does not exclude a diagnosis of vWD, but suggests that the functional activity of vWf is not compromised markedly. If the bleeding time is normal, APTT and PT should be measured. A prolonged APTT with normal PT, in the clinical setting, implies a deficiency of factor XI, IX, or VIII. A prolonged PT with normal APTT indicates factor VII deficiency. Prolongation of both APTT and PT usually is caused by a deficiency of several factors and is seen most often in cases with vitamin K deficiency or antagonism. Obviously, if a particular cause is suspected from the case history or for other reasons, appropriate tests should be evaluated at the beginning. If these do not confirm the provisional diagnosis, the just-described protocol might be a useful one to follow.
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PMID:Laboratory evaluation of hemorrhagic coagulopathies in small animal practice. 267 37

The treatment of disseminated intravascular coagulation (DIC) in infants with sepsis should be instituted after multimodality therapy of pyo-inflammatory diseases taking into account the degree of hemostatic disorders. In stage I DIC (hypercoagulation one), it is necessary to reach an adequate level of the inhibitors of the thrombin and plasmin systems. In this case it is quite sufficient to use donor's cryoplasma without heparin administration. In stage II DIC (transitory one) and stage III (hypocoagulation one), it is required that the drugs possessing antithrombin and antiplasmin activity, substitution therapy with blood preparations and components as well as measures to control hemorrhagic diathesis may be used.
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PMID:[Disseminated intravascular coagulation in newborn infants with infection]. 276 53

A female patient what M3 was seen to incur marked hemorrhagic diathesis during therapy. Heparin infusion was performed to inhibit disseminated intravascular coagulation (DIC). However, oozing from the puncture site of the r-subclavian vein was observed. Her data on coagulation were as follows: AT-3 greater than 100%, fibrinogen 69.0 mg, XIII less than 40%, FPA 2.9 ng/ml and FDP-D dimer 256 ng/ml. The alpha-2-plasmin inhibitor (alpha 2-PI) was 44% and FDP 160 microgram/ml. These results suggested DIC with activated fibrinolysis. Thus, epsilon aminocaproic acid in conjunction with heparin, fibrinogen, and concentrated XIII was administered. The abnormal bleeding improved with an increase of alpha 2-PI and XIII. This clinical response indicated that an activated fibrinolysis and a decreased XIII might have been responsible for provoking the bleeding of the patient.
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PMID:[Antiplasmin drugs and factor XIII concentrates in the treatment of a patient with acute promyelocytic leukemia (M3)]. 281 Jul 83

White-tailed deer (Odocoileus virginianus) were inoculated with bluetongue virus serotype 17 and sequentially euthanatized during infection. Ultrastructural changes in the microvasculature of tongue, buccal mucosa, heart, and pulmonary artery, platelets, and bone marrow were evaluated. Bluetongue virus was found in endothelial cells of the microvasculature by postinoculation day 4. Viral replication was associated with the development of viral matrices, viral-associated macrotubules, and aggregates of mature viral particles in the cytoplasm of infected cells. Viral infection of pericytes and vascular smooth muscle cells developed subsequent to endothelial cell infection. Viral infection was associated with striking changes in the endothelial lining of the microvasculature by postinoculation day 4. Endothelial cell degeneration and necrosis, which resulted in denudation of the endothelial lining, and endothelial cell hypertrophy frequently were observed. Thrombosis, hemorrhage, and vessel rupture developed subsequent to endothelial damage. Bluetongue virus neither infected nor directly damaged platelets or bone marrow cells. It was concluded that viral-induced endothelial damage is the primary triggering mechanism for disseminated intravascular coagulation in bluetongue virus infection. Vascular damage coupled with the development of disseminated intravascular coagulation is responsible for the hemorrhagic diathesis, which is characteristic of bluetongue virus infection in white-tailed deer.
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PMID:Experimentally induced bluetongue virus infection in white-tailed deer: ultrastructural findings. 285 10

We reported three patients who developed disseminated intravascular coagulation (DIC) accompanying thoracic and abdominal aortic aneurysm. The first case, a 26-year-old man with dissecting aortic aneurysm developed DIC with clinical bleeding after operating on glaucoma. The administration of fibrinogen concentrates and antifibrinolytic agent made his DIC improve. The second case, a 70-year-old man with abdominal aortic aneurysm developed DIC showing large ecchymosis after angiography. His DIC disappeared after operation on aneurysm. The third case, a 73-year-old woman with thoracic and abdominal aneurysm developed laboratory-DIC without severe hemorrhagic diathesis. During antifibrinolytic therapy, platelet count, fibrinogen and fibrinogen degradation product (FDP) level improved. Since the treatment of the coagulopathy might be varied in the situation of the cause and clinical course, it is noted that anti-fibrinolytic therapy was effective in our two cases.
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PMID:Disseminated intravascular coagulation accompanying thoracic and abdominal aortic aneurysm; report of three cases. 336 44

A 71-year-old male with disseminated intravascular coagulation (DIC) caused by abdominal aortic aneurysm was successfully treated surgically. He had aortic regurgitation, an old myocardial infarction, and nephrotic syndrome. The infrarenal part of the inferior vena cava, which was on the left side of the aneurysm, was temporarily transected during the surgical procedure. Preoperative heparin therapy was insufficient, but infusion of blood components during the operation and minimal dissection of the aneurysm were effective in controlling intraoperative hemorrhage. Hypofibrinogenemia and thrombocytopenia were normalized immediately after operation, and hemorrhagic diathesis was completely cured. In this case, the definitive treatment of DIC caused by an abdominal aortic aneurysm war removal of the lesion and the infusion of coagulation factors during the operation was effective in minimizing blood loss.
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PMID:Disseminated intravascular coagulation caused by abdominal aortic aneurysm. 341 54

A 19 year-old female, complaining of gigantic tumor on each breast and hemorrhagic diathesis, was admitted to our hospital. Laboratory data and clinical findings suggested the presence of DIC. Bilateral mastectomies reduced the bleeding tendency within a week. In conclusion, removal of the tumors was effective to avoid fatal hemorrhage.
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PMID:[A case of angiosarcoma of both breasts]. 357 82

Pulmonary embolus as a cause of disseminated intravascular coagulation has only recently been recognized. The hemorrhagic disorder reported in the past was associated with little or no bleeding. We report a case of pulmonary embolus associated with life-threatening disseminated intravascular coagulation.
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PMID:Pulmonary embolus-induced disseminated intravascular coagulation. 365 15

Necropsy findings in adult salmon with subclinical "Hitra disease" (hemorrhagic syndrome) varied from negligible to hemorrhagic diathesis with generalized edema. By light microscopy, minute vessels were dilated, arterioles had mural necrosis, and thrombi were present. Occlusions consisted of fused erythrocytes and fibrin. Ultrastructurally, endothelial nuclei were pyknotic with condensed chromatin. The cytoplasm contained numerous laminar structures and electron-dense particles. Damaged erythrocytes adhered to the degenerated endothelium, and coalesced erythrocytes had formed mural thrombi or filled the vascular lumen. Microthrombi were frequently seen. There were no thrombocytes in the thrombi, which consisted of erythrocytes or reticulocytes. Clinically healthy farmed salmon parr showed the same disorders as did adults, but to a far lesser degree. Wild salmon parr had normal microvasculature. Results indicate that disseminated intravascular coagulation (DIC) occurs in "Hitra disease" in farmed Atlantic salmon.
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PMID:Disseminated intravascular coagulation in "Hitra disease" (hemorrhagic syndrome) in farmed Atlantic salmon. 367 3

Septicemia is frequently accompanied by changes in the plasmatic as well as cellular coagulation systems and by microclot formation. The occurrence of a hemorrhagic diathesis and microthrombosis is best explained by the syndrome disseminated intravascular coagulation (= consumption coagulopathy). Disseminated intravascular coagulation can be initiated by different agents and by different pathways. The activation of coagulation by endotoxin is well studied; it is mediated by synthesis of tissue factor by monocytes and endothelial cells. The formation of microthrombi is caused by the precipitation of circulating soluble fibrin under the influence of localizing factors, and it is observed under conditions of reduced fibrinolysis activation. Furthermore, thrombocytopenia, thrombocytopathy and endothelial cell damage caused by a direct effect of the toxic agent contribute to the bleeding diathesis.
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PMID:[Sepsis and blood coagulation]. 371 2


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