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At least 19 recordsLinked to original sources
PubMed1976

[Legal abortion and hemostasis. Histological examinations and comparison to post partum hemostasis (author's transl)].

30 women were examined to determine the hemostasis during the legally induced abortion. The blood coagulated in the intervillous spaces while the fetus is removed. Immediately after the termination of the curettment the nidation area is covered by filaments of fibrin and incorporated erythrocytes. More frequent as post partum platelet thrombi occur especially in the area of decidua parietalis. The intravascular findings are similar to post partum changes after the removal of the placenta. Obstruction clots of the spiral arterioles contain fibrin deposits, pletelet thrombi and erythrocytes (mixed form of thrombi). Residual decidua and trophoblast cells are seldom involved in the obturation of the vessels. The traumatic damages of the uterine wall are described (extravascular fibrin deposits, interstitial bleeding, succulent tissue a.s.o.).

Abortion, Legal↗
PubMed1976

Alterations of hemostasis associated with cardiopulmonary bypass: pathophysiology, prevention, diagnosis, and management.

This chapter has provided a review of available literature regarding alterations of hemostasis associated with CPB. The primary pathology of altered hemostasis during CPB appears to be two-fold: (1) a functional platelet defect of unclear etiology, which occurs in virtually all patients, and (2) a primary hyperfibino(geno)lytic defect which occurs in the majority of patients undergoing cardiopulmonary bypass. Significant thrombocytopenia does not appear to be a consistent problem, and is probably a function of perfusion technics; this may, however, be an important source of hemorrhage in some instances. Although hyperheparinemia, heparin rebound, and protamine excess have occasionally been incriminated as sources of hemorrhage during CPB, no well documented cases appear in the literature. Likewise, although DIC gained popularity in early reports of CPB hemorrahge, it appears that this syndrome rarely, if ever, arises as a consequence of CPB alone; it can be seen, however, in CPB patients who are provided a triggerin situation for DIC, such as shock, sepsis, or hemolytic transfusion reaction. It is likely that many reported alterations of hemostasis during CPB which were concluded to represent DIC actually were due to hyperfibino(geno)lysis. The key to prevention of CPB hemorrhage rests simply in obtaining an adequate preoperative workup. Of extreme importance is an adequate history with respect to bleeding tendencies in both patient and family; of equal importance is a careful history regarding antiplatelet drugs. A careful physical examination, searching for clues of a real or potential bleeding diathesis, also can often prevent catastrophic cases of CPB hemorrhage. Lastly, an adequate presurgical laboratory screen must be performed; in addition to the usual prothrombin time, partial thromboplastin time, and platelet count, a thrombin time and standardized template bleeding time must be added. The addition of these two simple modalities will insure against significant defects in fibrinogen, the fibrinolytic system, vascular function, and platelet function. When CPB hemorrhage occurs, simple laboratory screening will usually allow for a quick hemostasis evaluation. The parameters recommended in this review will distinguish between surgical and nonsurgical bleeding and should, therefore, allow for a quick decision regarding necessity for reexploration and the adequacy of hemostasis if reexploration is needed. In addition, this screen will distinguish between difficulties with heparin, protamine, and the fibrinolytic system. The vast majority of nonsurgical hemorrhages during CPB is due to a functional platlet defect, primary hyperfibrino(geno)lysis, or a combination of these. The quick administration of platelet concentrates, while awaiting laboratory evaluation, will control or significantly blunt most instances of CPB hemorrhage. If platelets fail to control bleeding, and reasonable laboratory evidence of primary hyperfibrino(geno)lysis is present, antifibrinolytics should then be used...

Blood Coagulation Factors↗
PubMed1992

Percutaneous vascular hemostasis device for interventional procedures.

A new 11.5F over-the-wire vascular hemostasis device was compared to conventional manual compression in normal swine femoral arteries. Using percutaneous techniques, the collagen was deposited and hemostasis achieved in 7 vessels after 1 minute total, plus 4 minutes partial compression, while control manual compression required more than 5 minutes total compression to avoid hematoma formation. One month follow-up of treated arteries (n = 4) and controls (n = 3) showed no impairment in distal pulse or differences in histology at the puncture site in the control and treated arteries. Thus, the vascular hemostasis device technique is safe and effective, achieves hemostasis with less compression time and complications, and does not interfere with arterial wall healing or compromise the lumen.

Angioplasty, Balloon↗
PubMed1976

Laboratory modalities for assessing hemostasis during cardiopulmonary bypass.

This discussion has outlined several simple and reliable test systems which have been found useful in assessing disorders of hemostasis in the hemorrhaging CPB patient. When these tests are utilized as described in the preceding article, they have been extremely helpful in studying hemostasis in the CPB patient to be reexplored; they are equally helpful to quickly render a differential diagnosis of altered hemostasis when hemorrhage occurs. In addition, several "special" procedures, the AT-III and heparin assays, have been reviewed; these have been found quite useful in special instances of CPB hemorrhage, and community cardiovascular teams may wish them to be available. This paper has not presumed to be "authoritative" with respect to the "best" tests for assessing CPB hemostasis, but rather has offered only an approach helpful to the authors. The intent has, however, been to provide guidelines for instituting simple, reliable, and workable procedures for the community hospital where CPB is now routinely performed.

Antithrombins↗
PubMed1978

Alterations of hemostasis associated with malignancy: etiology, pathophysiology, diagnosis and management.

As outlined in this paper, the patient with disseminated malignancy suffers many alterations of hemostasis; in addition, hemorrhage or less commonly thrombosis is the final clinical event in many of these patients. Patients with malignancy present a major clinical challenge in this day of new oncological awareness and more aggressive care. Thus, it is important to realize that these alterations of hemostasis do exist and they must be approached in a logical manner with respect to diagnosis as well as efficacious therapy. By far the most common alteration of hemostasis in malignancy is that of hemorrhage associated with thrombocytopenia either drug-induced or from bone marrow invasion. However, hemorrhage due to disseminated intravascular coagulation is also quite common. In addition, many antineoplastic drugs, as well as radiotherapy, may lead to hemorrhage in these patients. Thrombosis, which is also commonly seen in the patient with malignancy, is usually a manifestation of disseminated intravascular coagulation manifest as an intravascular thrombotic rather than an intravascular proteolytic event. When suspecting this, confirmatory laboratory evidence must be sought and the patient treated apropriately. When approaching the patient with malignancy and either hemorrhage or thrombosis, all of the potential defects in hemostasis must be taken into account, defined from the laboratory standpoint, and treated in as precise a manner as possible.

Blood Coagulation Disorders↗
PubMed1975

The effectiveness and mechanism of collagen-induced topical hemostasis.

Microcrystalline collagen is a recently developed material possessing remarkable topical hemostatic properties. The potential utility of this substance for cardiovascular surgery was evaluated in a canine arterial bleeding model. A hemostatic protocol allowed comparison of initial and final hemostasis rates as well as the time required to accomplish hemostasis. The results of these studies revealed that microcrystalline collagen, or MCC, achieved hemostasis more frequently and rapidly than either pressure alone or oxidized cellulose cloth. MCC also was highly effective initially after large doses of heparin and in the presence of platelets with function rendered deficient by acetyl salicylate. Only in the presence of profound thrombocytopenia was any loss of initial effectiveness observed. Some delayed hemorrhage occurred in the heparin-treated groups leading to a lessened incidence of final hemostasis, a result intimately related to MCC's probable mechanism of action. However, even under the extreme conditions imposed by this severe experimental model, MCC remained effective in greater than 70 percent of the trials. On this basis MCC seems to possess great potential as a useful adjunct during cardiovascular surgical procedures.

Administration, Topical↗
PubMed1992

Effect of thrombin-induced hemostasis on the efficacy of an absorbable adhesion barrier.

Serosal injury, bleeding and fibrin deposition are major factors in the development of surgical adhesions; meticulous hemostasis is desirable but not always achievable. The effects of thrombin on adhesion formation and the performance of Interceed Barrier were tested in separate series using a standard model and two levels of bleeding: an "oozing" model in which rabbit uterine horns were scraped to produce uncontrolled punctate bleeding and a "bleeding" model, in which four small blood vessels nicked on the ligament to each horn produced heavier bleeding. Substantial clots in the bleeding model were not removed. Adhesions, assessed after two weeks, were not worsened by the use of thrombin to control bleeding. While Interceed Barrier alone did not reduce adhesions at sites of bleeding, achieving hemostasis with thrombin and then applying Interceed Barrier significantly reduced adhesions. The effect was not achieved by applying thrombin to previously blood-soaked Interceed Barrier. The efficacy of Interceed Barrier applied after achieving hemostasis was further improved by moistening it with heparin. Achieving hemostasis at a bleeding site with thrombin facilitates the efficacy of Interceed Barrier.

Animals↗
PubMed1979

Willebrand factor in hemostasis in the in vitro bleeding time.

Heparinized porcine blood and plasma, at constant hydrostatic pressure, was allowed to flow through a 5-mm incision in a small piece of porcine skin. Changes in the exuded blood volume were measured, and the incision site was examined microscopically. When normal blood flowed through either normal or von Willebrand skin, the exuded blood volume decreased gradually and eventually stopped. Microscopic examination revealed a platelet plug in the incision site. This plug was positive for Willebrand factor when examined by immunofluorescence. In contrast, the blood from von Willebrand pigs continued to flow constantly, and a platelet plug was not seen. The delayed in vitro hemostasis in von Willebrand blood was corrected to the normal range by the addition of either normal plasma or partially purified Willebrand factor. Normal blood, in which the Willebrand factor was immunologically inhibited, showed delayed hemostasis. For this in vitro system, it appeared that plasmatic Willebrand factor played an essential role in hemostasis.

Animals↗
PubMedDate not supplied

[Disorder of the thrombocytic-vascular component of hemostasis in thyrotoxicosis].

Hemocoagulation and the platelet-vascular hemostasis mechanism were investigated in 79 patients suffering from thyrotoxicosis of different severity by clinical observations and laboratory studies. Along with hemocoagulation defects, there were revealed thrombocytopenia, reduction of the platelet adhesive-aggregation activity and of the vascular wall resistance. The extent of these disturbances depended on the severity of thyrotoxicosis. In the authors opinion, affection of the platelet-vascular hemostasis component, combined with hemocoagulation disturbances played an important role in the development mechanism of increased hemorrhagic tendency of the tissues and hemorrhagic diathesis in thyrotoxicosis. The necessity of complex treatment of patients with thyrotoxicosis with prescription of agents normalizing hemocoagulation and the platelet-vascular hemostasis mechanism is founded.

Blood Coagulation Disorders↗
PubMed1979

[Principal symptoms in hemostasis disorders].

In a retrospective study the results of laboratory investigations were correlated with actual or previous bleeding symptoms of 40 patients. In 22 patients, a defect of hemostasis was documented in the laboratory, whereas the bleeding disorder, suggested by severe hemorrhage, could not be classified in 3 additional patients. In the remaining 15 individuals, no abnormality could be detected by the available laboratory methods. In the group with a documented bleeding disorder, 13 of 22 patients had prolonged bleeding following dental extraction or other surgery of the oral cavity. Other bleeding symptoms were equally distributed among patients with and without a documented defect. 3 patients had a positive family history, i.e. relatives with a hemorrhagic tendency. In 6 patients, a correlation between bleeding and the ingestion of acetylsalicylic acid could be established, while in 4 it was probable. Hemorrhagic complications following oral surgery, particularly in combination with drugs known to interfere with platelet function and a positive family history, strongly suggest an abnormality of hemostasis. Among the 22 patients with a documented defect of hemostasis, only 6 were found who did not present at least one of these leading symptoms.

Blood Coagulation Disorders↗
PubMed2025

Historical review: more than two decades understanding the genetic architecture of hemostasis and thrombosis.

From the beginning of the millennium and the development of genome-wide analyses, the technical advances and remarkable increase in research sample sizes have led to an escalating number of discoveries revealing genetic determinants of levels of the main factors regulating hemostasis and thrombosis and demonstrating a clear polygenic complex regulation of most coagulation factors. These discoveries have been useful to understand the biology underlying hemostasis regulation and to understand risk of associated thrombotic disease, such as venous thromboembolism, coronary artery disease, and ischemic stroke. In this historical review, we outline the main discoveries in genetic studies of coagulation factors (fibrinogen and its alternatively spliced γ' isoform, D-dimer, factor [F]V, FVII, FVIII, von Willebrand factor, and FXI), the main natural anticoagulants (protein C, protein S, and antithrombin), components of fibrinolysis (tissue plasminogen activator and plasminogen activator inhibitor-1), and global coagulation tests (prothrombin time and activated partial thromboplastin time). We explore the clinical implications of these discoveries and suggest new avenues for future investigation.

Humans↗
PubMed1979

Disorders of hemostasis in malignancy.

Disorders of hemostasis are frequent in malignant disease and their cause is often multifactorial and complex. Both primary (platelets and vessel walls) and secondary (coagulation factors) hemostasis are impaired, often concurrently. Therapy is most often directed toward the underlying disease; however, a knowledge of the complications and treatment of each malignancy will often prevent a number of the problems cited in this chapter. The hypercoagulable states are still poorly understood and need better definition, but their recognition, treatment and prevention may decrease morbidity significantly.

Blood Coagulation Disorders↗
PubMed1976

Post-extraction hemostasis during coumarin anticoagulant therapy with a locally applied coagulation-active substance.

A safe and simple method for the dento-alveolar attendance of patients on coumarin derivative therapy is reported. It eliminates the need to interrupt anticoagulant administration, while a physiologic coagulation-active substance consisting of fibrin, thrombin, and the patient's venous blood is used for hemostasis. This easy-to-prepare substance was applied following 53 extractions, two alveolar corrections and one resection of the third molar, and excellent hemostasis was observed without the occurrence of a secondary hemorrhage.

Administration, Topical↗
PubMed1977

Alteration of primary hemostasis in hemophiliacs after treatment with lyophilized antihemophilic globulin.

Seven patients with classic hemophilia A had alteration of primary hemostasis after treatment with lyophilized antihemophilic globulin (LAHG). The following test results, which were normal before treatment, became abnormal after treatment: bleeding time, bleeding intensity, and platelet adhesiveness. In two patients, the fibrin-fibrinogen-degradation products increased to more than 40 microgram/ml. In three patients, the bleeding symptoms became worse with LAHG therapy although no inhibitor against Factor VIII was demonstrated. In one of these patients, the bleedings symptoms disappeared when the use of LAHG was discontinued and prednisone was given; at the same time, the altered primary hemostasis returned to normal. In the remaining two patients, prednisone did not have any effect. In these two patients, however, the bleeding stopped, and the bleeding time became normal immediately after freshly prepared blood-group compatible cryoprecipitate was given.

Adolescent↗
PubMed1977

The importance of continuous pump suction in TUR hydraulic hemostasis.

An intravesicoprostatic hydrostatic pressure below 10 mm Hg maintains normal anatomy and physiology of the muscular and vascular prostatic structures by continuous pump suction. An increase of the hydrostatic intravesicoprostatic pressure above 10 mm Hg produces a distortion in the musculature of the prostate, especially at the true capsule, opening the cut vessels, making possible the absorption of the irrigant free of electrolytes (TUR syndrome). A low hydrostatic intravesicoprostatic pressure permits the compression of cut vessels by the inflow hydraulic pressure of 90 cm H2O achieving hydraulic hemostasis during TURP reducing the bleeding and operative time by more than 50% and making hemostasis easier. In our last 400 TURs, blood transfusions have been unnecessary. Less electrocoagulation is required, resulting in a more rapid recovery.

Endoscopy↗