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Biomedical subjects

R L Bick

Publications and source records attributed to R L Bick.

At least 109 records · Page 6Linked to original sources
PubMed1978

Disseminated intravascular coagulation and related syndromes: etiology, pathophysiology, diagnosis, and management.

Disseminated intravascular coagulation (DIC) is being recognized with increased frequency and not only are newer diagnostic modalities becoming available for this syndrome, but newer, some controversial, methods of management are also being recognized and may prove to increase survival in DIC. In addition, several syndromes classically considered separate, definitive disease entities, may actually share similar or identical pathophysiology to DIC. This review summarized current, as well as controversial aspects of etiology, pathophysiology, clinical and laboratory diagnosis, and management of DIC. In addition, a brief discussion of syndromes which may share similar or identical pathophysiology to DIC is included.

Anemia, Hemolytic↗
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↗
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↗
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↗
PubMed1976

Bleeding times, platelet adhesion, and aspirin.

The effects of aspirin on well-standardized commercially produced platelet adhesiveness devices and template bleeding times were simultaneously studied in 19 normal volunteers. As expected, there was significant prolongation of the bleeding time after aspirin, but there was no change in platelet adhesion. Reason for the different effects of aspirin on the two tests are discussed. In addition, the normal range of platelet adhesion was further defined utilizing commercially prepared glass-bead columns.

Adult↗
PubMed1975

Prothrombin complex concentrate: use in controlling the hemorrhagic diathesis of chronic liver disease.

A prothrombin complex concentrate was used in attempts to control life-threatening hemorrhage in 4 patients with chronic liver disease. The population manifested profuse bleeding from varices and/or hemorrhagic gastritis; 3 had Laennec's cirrhosis and 1 had postnecrotic cirrhosis from childhood hepatitis. In all patients the complex was given in amounts needed to raise the prothrombin (factor II) level to approximately 100% of normal. In all 4 cases the prothrombin time and prothrombin complex factors approached normal within 1-2 hr after beginning the infusion. In all patients bleeding ceased with correction of the clotting status. One patient rebled several hours after completing the infusion. In several patients, increases in factors V and VIII were noted following infusion of the concentrate. A further unexpected finding was a spontaneous increase in factors II and IX at 3 days postinfusion. Prothrombin complex concentrate appears to be useful in controlling the hemorrhage of chronic liver disease when used alone or in combination with other modalities to correct specific hemostatic defects; however, patients may be expected to rebleed when the effect of the concentrate wears off. Its use, therefore, should probably be restricted to those patients who are to undergo corrective surgery of the bleeding point once hemostasis is achieved.

Adult↗