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Biomedical subjects

R L Bick

Publications and source records attributed to R L Bick.

At least 73 records · Page 4Linked to original sources
PubMed1992

Diagnostic efficacy of the D-dimer assay in disseminated intravascular coagulation (DIC).

The D-Dimer (D-D) assay for measuring cross-linked fibrin degradation products is now available for the clinical laboratory. We combined this assay with other tests to assess patients with diagnosed or suspected DIC. Also, a small group of patients (20) with deep venous thrombosis (DVT) were studied. The D-D test, antithrombin-III assay, FDP titer, fibrinopeptide-A level, protamine sulfate test, fibrinogen, prothrombin time, and activated partial thromboplastin time were used. The D-D test was abnormal in 93.7%, the AT-III level was abnormal in 87.5%, the fibrinopeptide-A level was abnormal in 89.5%, and the FDP titer was elevated in 83.7% of patients with DIC. When assessing patients found not to have confirmed DIC the D-D assay was abnormal in 20%, the AT-III level was abnormal in 6%, and the fibrinopeptide-A level was elevated in 13%. We conclude the D-Dimer assay to be a useful molecular marker of hemostasis in diagnosing DIC and this test will often discriminate between those patients with or without DIC, especially when used with the AT-III and fibrinopeptide-A assays. Of the battery of tests used in this study, the most useful, in descending order of efficacy, appear to be the D-dimer assay (93.7% abnormal), the fibrinopeptide-A titer (89.5% abnormal), the AT-III level (87.5% abnormal), and the FDP titer (83.7% abnormal). Of the global tests, the diagnostic efficacy of the prothrombin time activated partial thromboplastin time, and protamine sulfate test were no greater than chance and appear to be of little use in aiding in a diagnosis of DIC. Also, the D-Dimer assay is similar in cost to the FDP titer and is cost effective for the routine clinical laboratory.

Disseminated Intravascular Coagulation↗
PubMed1992

Platelet function defects: a clinical review.

Platelet dysfunction, especially acquired forms, are common causes of hemorrhage, especially in association with trauma and surgery. Although the hereditary platelet function defects are generally quite rare, hereditary storage pool disease is common enough to be suspected in an individual, usually a child, with characteristic historical and clinical findings. The acquired platelet function defects, especially those resulting from drugs, are very common and should promptly be suspected in patients developing easy and spontaneous bruising, mild to moderate mucosal membrane hemorrhage, or unexplained bleeding associated with trauma or surgery. The template bleeding time is generally useful as a screening test of platelet function, but a normal template bleeding time, in the presence of a suggestive history, suggestive clinical findings, or in the patient frankly bleeding, is not reliable and platelet aggregation or lumi-aggregation should be done in appropriate clinical situations. The mainstay of therapy for essentially all these defects, if bleeding is significant, is the liberal infusion of appropriate numbers of platelet concentrates. The acquired platelet function defects, of course, should also be managed by attempts to treat or control the underlying disease, if possible, and offending drugs or potentially offending drugs should promptly be discontinued.

Blood Platelets↗
PubMed1992

Coagulation abnormalities in malignancy: a review.

As outlined in this review, patients with cancer may harbor many alterations of hemostasis. These are multifaceted and must be taken into account when trying to control hemorrhage or thrombosis in cancer patients. Often, hemorrhage or thrombosis is the final fatal event in many patients with metastatic solid tumor or hematologic malignancies. Patients with malignancy present a major clinical challenge in this new era of oncologic awareness and more aggressive care, which has led to prolonged survival for patients and a longer time frame during which these complications may develop. Therefore, these complications are occurring more commonly. It is important to realize that these alterations of hemostasis exist and must be approached in a sequential and logical manner with respect to diagnosis; only in this way can responsible, efficacious, and rational therapy be delivered to patients. By far the most common alteration of hemostasis in malignancy is that of hemorrhage associated with thrombocytopenia, either drug-induced, radiation-induced, or from bone marrow invasion. However, hemorrhage resulting from DIC is also quite common and may present as hemorrhage, thrombosis, thromboembolus, or any combination thereof. Many antineoplastic drugs and radiation therapy may lead to or significantly enhance hemorrhage in patients with malignancy. Thrombosis, also commonly seen in patients with malignancy, is often a manifestation of low-grade DIC, conspicuous as an intravascular thrombotic or thromboembolic event instead of an intravascular proteolytic (hemorrhagic) event. When suspecting this, confirmatory laboratory evidence must be sought and the patient treated appropriately. When approaching the patient with malignancy and either hemorrhage or thrombosis, all the potential defects in hemostasis must be taken into account, defined from the laboratory standpoint, and treated in as precise and logical manner as possible.

Blood Coagulation Disorders↗
PubMed1992

Acquired platelet function defects.

Platelet dysfunctions, especially acquired forms, are common causes of hemorrhage, especially when associated with trauma or surgery. Although the hereditary platelet function defects are generally quite rare, hereditary storage-pool disease is common enough to be suspected in an individual, usually a child, with characteristic historical and clinical findings. The acquired platelet function defects, especially those resulting from drugs, are very common and should promptly be suspected in patients developing easy and spontaneous bruising, mild to moderate mucosal membrane hemorrhage, or unexplained bleeding associated with trauma or surgery. The template bleeding time is generally useful as a screening test of platelet function, but a normal template bleeding time, in the face of a suggestive history, suggestive clinical findings, or in the patient frankly bleeding, is not reliable, and platelet aggregation or lumi-aggregation should be done in appropriate clinical situations. Also, prolongation of the template bleeding time is an unreliable predictor of clinical bleeding propensity. The mainstay of therapy for essentially all these defects, if bleeding is significant, is the liberal infusion of appropriate numbers of platelet concentrates. The acquired platelet function defects should also be managed by attempts to treat or control the underlying disease, if possible, and offending drugs or potentially offending drugs should immediately be stopped.

Blood Platelet Disorders↗
PubMed1992

Drug-induced alterations of hemostasis and fibrinolysis.

The hemostatic and fibrinolytic systems contribute significantly to the overall pathophysiologic status of a patient in a given clinical setting. Drug modulation of these systems plays a crucial role in the facilitation of the therapeutic effects but may also produce bleeding or thrombotic disorders. Many drugs appear inert; they can, however, modulate both the hemostatic and fibrinolytic systems. Such effects depend on several factors, however, but are significant enough to be recognized for the optimal care of patients. Therefore, it is recommended that the hemostatic and fibrinolytic systems should be routinely monitored during drug delivery.

Anticoagulants↗
PubMed1992

Disseminated intravascular coagulation.

Current concepts of the etiology, pathophysiology, clinical and laboratory diagnosis, and management of fulminant and low-grade DIC have been presented. Considerable attention has been devoted to interrelationships within the hemostasis system. Only by clearly understanding these pathophysiologic interrelationships can the clinician and laboratory scientist appreciate the divergent and wide spectrum of often confusing clinical and laboratory findings in patients with DIC. Many therapeutic decisions to be made are controversial and will remain so until more is published about specific therapeutic modalities and survival patterns. Also, therapy must be highly individualized depending on the nature of DIC, age, etiology of DIC, site and severity of hemorrhage or thrombosis, and hemodynamic and other clinical parameters. Many syndromes that are organ-specific share common pathophysiology with DIC but are typically identified as an independent disease entity, such as hemolytic uremic syndrome, adult shock-lung syndrome, eclampsia, and many other isolated "organ-specific" disorders.

Disseminated Intravascular Coagulation↗
PubMed1992

Anticardiolipin antibodies and thrombosis.

Anticardiolipin antibodies (ACLAs) are strongly associated with thrombosis and appear to be the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanism(s) whereby ACLAs alter hemostasis to induce a hypercoagulable state remain unclear, several theories, as previously discussed, have been advanced. The most common thrombotic events associated with ACLAs are deep vein thrombosis and pulmonary embolus (type I syndrome), coronary or peripheral artery thrombosis (type II syndrome), or cerebrovascular/retinal vessel thrombosis (type III syndrome), and occasionally patients present with mixtures (type IV syndrome). The relative frequency of ACLAs in association with arterial and venous thrombosis strongly suggests that these should be looked for in any individual with unexplained thrombosis; all three idiotypes (IgG, IgA, and IgM) should be assessed. Also, the type of syndrome (I through IV) should be defined if possible, because this may dictate both type and duration of both immediate and long-term anticoagulant therapy.

Adult↗
PubMed1992

Hypercoagulability and thrombosis.

This article has summarized known congenital and acquired alterations of hemostasis leading to thrombosis. Decreases in coagulation inhibitors, including antithrombin III, heparin cofactor II, and protein C and protein S, are of major importance in assessing patients with hypercoagulable states or patients with unexplained thrombosis. Newer assays for components of the fibrinolytic system, plasminogen, t-PA and t-PA inhibitor are also now readily available and are important for defining congenital or acquired fibrinolytic defects leading to hypercoagulability and thrombosis. By judicious use of these assays, combined with clinical evaluation, many patients with thrombosis will have an underlying etiologic blood protein defect defined. Delineating reasons for a thrombotic event is of obvious importance for planning long-term prophylactic therapy and for diagnosing and counseling afflicted family members. In this manner, newly found patients can be treated prophylactically before unalterable morbidity or mortality occurs.

Antithrombin III↗
PubMed1992

Disseminated intravascular coagulation syndromes.

Current concepts of the etiology, pathophysiology, diagnosis and management of fulminant as well as low-grade disseminated intravascular coagulation have been presented. Considerable attention has been devoted to interrelationship within the hemostasis system. Only by clearly understanding these pathophysiological interrelationships can the clinician and laboratory scientists appreciate the divergent and wide spectrum of often confusing clinical and laboratory findings in patients with disseminated intravascular coagulation. Many therapeutic decisions to be made in these patients are controversial and will remain so until more series of patients are published about specific therapeutic modalities and survival patterns. Also, therapy must be highly individualized depending on the nature of DIC, age, etiology of DIC, site and severity of hemorrhage or thrombosis and hemodynamic and other clinical parameters. Many syndromes which are organ specific share common pathophysiology with disseminated intravascular coagulation but are typically identified as an independent disease entity, such as hemolytic uremic syndrome, adult shock lung syndrome, eclampsia, and many other isolated "organ-specific" disorders. Many of these similar disorders, some systemic and some organ specific or multi-organ specific are listed in Table 8.

Disseminated Intravascular Coagulation↗
PubMed1992

Disseminated intravascular coagulation syndromes.

Current concepts of the etiology, pathophysiology, diagnosis, and management of fulminant as well as low-grade disseminated intravascular coagulation have been presented. Considerable attention has been devoted to interrelationships within the hemostasis system. Only by clearly understanding these pathophysiological interrelationships can the clinician and laboratory scientists appreciate the divergent and wide spectrum of often confusing clinical and laboratory findings in patients with disseminated intravascular coagulation. Many therapeutic decisions to be made in these patients are controversial and will remain so until more series of patients are published concerning specific therapeutic modalities and survival patterns. In addition, therapy must be highly individualized depending upon the nature of DIC, age, etiology of DIC, site and severity of hemorrhage or thrombosis and hemodynamic and other clinical parameters. Many syndromes which are organ specific share common pathophysiology with disseminated intravascular coagulation but are typically identified as an independent disease entity, such as hemolytic uremic syndrome, adult shock lung syndrome, eclampsia, and many other isolated "organ-specific" disorders.

Disseminated Intravascular Coagulation↗
PubMed1988

Disseminated intravascular coagulation and related syndromes: a clinical review.

Current concepts of the cause, pathophysiologic mechanisms, diagnosis, and management of acute and chronic DIC have been discussed. Considerable attention has been devoted to interrelationships that have remained confusing. Only by clearly understanding these pathophysiologic interrelationships can the clinician and laboratorian appreciate the divergent and wide clinical spectrum of often confusing clinical and laboratory findings in patients with DIC. Many of the therapeutic decisions to be made in these patients remain controversial and will remain so until more series of patients are published with respect to specific therapeutic modalities and survival patterns. Many syndromes that remain organ specific share common pathophysiologic properties with DIC but are identified as an independent disease entity, such as HUS, adult shock lung syndrome, eclampsia, and many other isolated organ-specific disorders. Many of these similar disorders, some systemic and some organ specific or multiorgan specific, are listed in Table 36.

Disseminated Intravascular Coagulation↗
PubMed1987

Fully automated antithrombin-III assays by synthetic substrate on the Multistat III.

Antithrombin-III assays are performed to assess response to heparin therapy and efficacy of antithrombin concentrate therapy and in diagnosing hereditary thrombophilia, deep venous thrombosis, pulmonary embolus, and disseminated intravascular coagulation. Synthetic substrate assays for antithrombin-III are the methods of choice; however, most existing assay systems are semiautomated. A fully automated, antithrombin-III assay using the Kabi Chromogenic Synthetic Substrate S-2238 COATEST on the MULTISTAT III has been developed. This assay was compared with the Dade Protopath fluorometric assay. The correlation (r-sq) between the two assay systems was 0.82. Additionally, a three-way assay comparison was also performed, incorporating a new fluorometric substrate for antithrombin-III. The three-way comparative assays revealed correlation as follows: MULTISTAT III fluorometric assay and the MULTISTAT III/Kabi COATEST assay r-sq = 0.90; MULTISTAT III fluorometric assay and the Dade fluorometric assay r-sq = 0.86; and the MULTISTAT III/Kabi COATEST assay and the Dade Protopath fluorometric assay r-sq = 0.95. These automated assays were extremely cost effective and were a fraction of the cost of performing other types of antithrombin-III assays.

Antithrombin III↗
PubMed1985

Clinical use of intrapulmonary heparin.

Of 16 patients treated with intrapulmonary heparin at doses between 10,000 and 20,000 U/week for 1592 patient days, or 4.3 years, only one rethrombosed. This patient has a congenital antithrombin III deficiency. However, the use of intrapulmonary heparin, even in this particular patient, has remarkably decreased her thrombotic events as manifested by studying her history of deep vein thrombosis and pulmonary embolism prior to starting intrapulmonary heparin. This represents a failure rate of 4.2% in the total of 1592 patient days of therapy, or a rethrombosis rate of 1.4% per year. This recurrence rate is far superior to that reported for warfarin-type therapy or for platelet suppressive therapy. From this limited experience, it appears that heparin is an extremely safe and highly effective mode of outpatient prophylaxis for deep vein thrombosis and thromboembolic disease. The ultimate aim of this study is to determine the possibility of calcium heparin being placed into a hand-held aerosol nebulizer that a patient can use at home on a weekly basis. This would provide a highly convenient, safe, and apparently very efficacious mode of therapy for the long-term outpatient prophylaxis of deep vein thrombosis and thromboembolic disease.

Administration, Intranasal↗
PubMed1985

Hemostasis defects associated with cardiac surgery, prosthetic devices, and other extracorporeal circuits.

This discussion has provided a review of the available literature regarding alterations of hemostasis associated with CPB surgery, the use of prosthetic devices, and apheresis. The key to prevention of CPB hemorrhage is to obtain an adequate preoperative workup. Of extreme importance is an adequate history with respect to bleeding tendencies and thrombotic tendencies in both the patient and the family; of equal importance is a careful history regarding the use of drugs affecting hemostasis, especially drugs known to interfere with platelet function. A careful physical examination, searching for clues of a real or potential bleeding diathesis, may also prevent catastrophic cases of hemorrhage. An adequate presurgical screen must be performed in surgical patients. In addition to the usual prothrombin time, partial thromboplastin time, and platelet count, a standardized template bleeding time (and thrombin time in patients subjected to CPB) should be performed. The use of these simple testing modalities will guard against significant defects in vascular and platelet function. Most instances of nontechnical surgical and cardiovascular surgical hemorrhage are due to several well-defined defects in hemostasis that should be readily controlled if approached in a logical manner as a team effort among surgeons, pathologists, and hematologists.

Arteriovenous Shunt, Surgical↗
PubMed1985

A comparative study of the DuPont antithrombin III and fibrinogen assay systems.

Antithrombin III (AT-III) levels are useful for diagnosing thrombosis and for assessing antithrombotic therapy. Fibrinogen levels also are useful in numerous thrombohemorrhagic disorders and for noting cessation of fibrinolysis after thrombolytic therapy. With the availability of these assays on the DuPont aca, a comparative study of AT-III and fibrinogen assays was performed. DuPont assays were compared to Dade Protopath (AT-III) and Auto-Fi (fibrinogen) assays. In 38 instances a third comparative AT-III assay also was used, namely the Kabi S-2238 method (COATEST). Poor correlation existed between the DuPont AT-III and Protopath AT-III, r - sq = 0.53 to 0.61. There also was poor correlation between the DuPont and S-2238 AT-III assay, r - sq = 0.59. Excellent correlation was noted with the Protopath and Kabi AT-III assays, r - sq = 0.90. There was poor correlation between DuPont and Dade fibrinogen levels, r - sq = 0.55. When comparing AT-III values, the DuPont level was consistently higher. DuPont fibrinogen levels also were consistently higher. The DuPont AT-III and fibrinogen levels correlate poorly with existing assays, and higher results than those noted with the other methods appear common. Spuriously high values noted with the DuPont system could misguide clinicians caring for patients with thrombohemorrhagic diseases where they would expect low levels of AT-III or fibrinogen.

Antithrombin III↗