Effect of drug-induced platelet dysfunction on surgical bleeding

1982 ◽  
Vol 143 (2) ◽  
pp. 215-217 ◽  
Author(s):  
Lynn Kitchen ◽  
Robert B. Erichson ◽  
Henry Sideropoulos
Keyword(s):  
Platelet Dysfunction ◽  
Drug Induced ◽  
Surgical Bleeding

Clot Impedence As An Indicator Of Platelet Dysfunction Following Cardiopulmonary Bypass

1981 ◽  
Author(s):  
A Saleem ◽  
D H Yawn ◽  
S A Saleh ◽  
E S Crawford
Keyword(s):  
Cardiopulmonary Bypass ◽  
Blood Sample ◽  
Platelet Function ◽  
Postoperative Bleeding ◽  
Coagulation Factors ◽  
Initial Slope ◽  
Platelet Dysfunction ◽  
Number Of Patients ◽  
Precision Evaluation ◽  
Surgical Bleeding

Post-operative bleeding following cardiopulmonary bypass remains a serious problem. Recent studies have indicated platelet dysfunction may be responsible for altered hemostasis in a significant number of patients. Although evaluation of coagulation factors can usually be done with speed and precision, evaluation of platelet function is time-consuming. We have evaluated a clot impedence device (Sonoclot®, Sieneo Inc., Colorado) to measure platelet function. The device measures and records the clot impedence to a vibrating probe as the blood sample clots and retracts. In our evaluation of healthy subjects, we found the initial slope of the impedence curve and the entire retraction phase are influenced by the number of platelets. Extrapolating this information to the patients undergoing cardiovascular bypass, we found 7 out of 11 patients with postoperative bleeding had poor retraction phase in spite of an adequate platelet count. This suggested platelet dysfunction. All seven patients achieved satisfactory hemostasis after platelet transfusion. This was correlated with a normal clot impedence study. Four patients with normal clot impedence were found to have surgical bleeding. The test is easy to perform and the result is available within fifteen minutes of drawing the blood sample. In our hands, the measurement of clot impedence appears to be a reliable adjunct in the etiological diagnosis of post-operative bleeding.

Platelet Dysfunction in Major Pediatric Scoliosis Surgery: A Cause of Common Surgical Bleeding Phenotypes

2021 ◽  
Author(s):  
Lydia McKeithan ◽  
Matthew Duvernay ◽  
Vaibhav Tadepalli ◽  
Stephanie N. Moore-Lotridge ◽  
Breanne Gibson ◽  
...  
Keyword(s):  
Scoliosis Surgery ◽  
Platelet Dysfunction ◽  
Surgical Bleeding

Do patients with epistaxis have drug-induced platelet dysfunction?

1995 ◽  
Vol 20 (5) ◽  
pp. 407-410 ◽  
Author(s):  
J. R. LIVESEY ◽  
M. G. WATSON ◽  
P. J. KELLY ◽  
P. J. KESTEVEN
Keyword(s):  
Platelet Dysfunction ◽  
Drug Induced

RIBAVIRIN: STUDIES OF THE EFFECTS OF THE ANTIVIRAL DRUG ON PLATELET FUNCTION

1987 ◽  
Author(s):  
T M Cosgriff ◽  
P G Canonico ◽  
L Hodgson ◽  
D Parrish ◽  
T Chapman ◽  
...  
Keyword(s):  
Platelet Function ◽  
Influenza A ◽  
Platelet Rich Plasma ◽  
Antiviral Drug ◽  
Hemorrhagic Fever ◽  
Lassa Fever ◽  
Chinese Patients ◽  
Platelet Dysfunction ◽  
Drug Induced ◽  
Syncytial Virus

Ribavirin is a broad-spectrum antiviral drug which is presently undergoing testing in patients with AIDS-related complex. It has also been shown to have activity against respiratory syncytial virus, Sicilian sandfly fever virus, influenza A and B viruses, as well as several hemorrhagic fever viruses. It has proved effective in clinical trials in Lassa fever and shows promise as therapy for hemorrhagic fever with renal syndrome. Because platelet dysfunction may contribute significantly to hemostatic impairment in viral hemorrhagic fever, the effects of ribavirin on platelet function were measured in rhesus monkeys after daily injections of 100 mg/kg IM for 14 days. Drug administration led to a significant increase in platelet count associated with megakaryocyte hyperplasia but had no effect on aggregation of platelet-rich plasma (PRP) in response to either collagen (1.6 μg/ml) or ADP (10 μM/ml). Aggregation in whole blood was also unaffected. Addition of ribavirin to human PRP in concentrations up to 0.5 mg/ml had no effect on aggregation in response to collagen, ADP, or epinephrine (5 μg/ml). Preliminary data from Chinese patients treated with ribavirin for hemorrhagic fever with renal syndrome also reveal no evidence of drug-induced platelet dysfunction as indicated by normal aggregation and release reactions to collagen (3 μg/ml) and ADP (10 μM/ml). Bone marrow studies of megakaryocyte number and ploidy are presently underway to further characterize drug-associated thrombocytosis

Is Platelet Adhesion Assay Able To Quantify Drug-Induced Platelet Dysfunction?

2005 ◽  
Vol 31 (04) ◽  
pp. 476-481 ◽  
Author(s):  
Alrun Schumann ◽  
Elke Bucha ◽  
Götz Nowak
Keyword(s):  
Platelet Adhesion ◽  
Adhesion Assay ◽  
Platelet Dysfunction ◽  
Drug Induced

Platelet Disorders

2017 ◽  
Author(s):  
Michael Perry ◽  
John Bedolla ◽  
Truman John Milling
Keyword(s):  
Bone Marrow ◽  
Platelet Transfusion ◽  
Bleeding Time ◽  
Complete Blood Count ◽  
Systemic Disease ◽  
Coagulation Cascade ◽  
Platelet Dysfunction ◽  
Drug Induced ◽  
Platelet Disorders ◽  
Plug Formation

Hemostasis occurs in two steps: platelet plug formation followed by fibrin deposition. Platelet disorders cause incomplete or absent platelet plug formation. Platelets form in bone marrow and have an 8- to 9-day life span. A careful history and physical examination can distinguish between platelets or the coagulation cascade as the cause of deranged hemostasis. Platelet disorders are characterized by mucosal and small vessel bleeding, and petechiae are characteristic. A complete blood count and prothrombin time/international normalized ratio testing reveal most causes. Many drugs can alter platelet production, function, and longevity, but antiplatelet therapy is the most common cause. Other causes include congenital, medication side effects, sepsis, bone marrow suppression, and systemic disease. The platelet count may be low, elevated, or normal. Bleeding time is virtually always prolonged in platelet dysfunction. Therapy for platelet dysfunction depends on the etiology and severity. Platelets are short-lived, and platelet transfusion may be necessary in the unstable or actively bleeding patient. In most other cases, removing the cause or treating the systemic disease will improve hemostasis. Emergency physicians treating patients with abnormal bleeding should understand the coagulation cascade and drug-induced coagulopathy from older and newer agents. Key words: bleeding time, coagulopathy, drug induced, hemostasis, megakaryocyte, mucosal bleeding, petechiae, platelet plug, platelet transfusion, platelets, thrombocytopenia

Early Development of Drug-Induced Hepatic Necrosis

1971 ◽  
Vol 29 ◽  
pp. 576-577
Author(s):  
F. G. Zaki ◽  
E. Detzi ◽  
C. H. Keysser
Keyword(s):  
Early Development ◽  
Hepatic Necrosis ◽  
Screening Tests ◽  
Dense Matrix ◽  
Sprague Dawley ◽  
Electron Microscopic ◽  
Drug Induced ◽  
Hepatocellular Damage ◽  
Sprague Dawley Rats ◽  
Microscopic Studies

This study represents the first in a series of investigations carried out to elucidate the mechanism(s) of early hepatocellular damage induced by drugs and other related compounds. During screening tests of CNS-active compounds in rats, it has been found that daily oral administration of one of these compounds at a dose level of 40 mg. per kg. of body weight induced diffuse massive hepatic necrosis within 7 weeks in Charles River Sprague Dawley rats of both sexes. Partial hepatectomy enhanced the development of this peculiar type of necrosis (3 weeks instead of 7) while treatment with phenobarbital prior to the administration of the drug delayed the appearance of necrosis but did not reduce its severity.Electron microscopic studies revealed that early development of this liver injury (2 days after the administration of the drug) appeared in the form of small dark osmiophilic vesicles located around the bile canaliculi of all hepatocytes (Fig. 1). These structures differed from the regular microbodies or the pericanalicular multivesicular bodies. They first appeared regularly rounded with electron dense matrix bound with a single membrane. After one week on the drug, these vesicles appeared vacuolated and resembled autophagosomes which soon developed whorls of concentric lamellae or cisterns characteristic of lysosomes (Fig. 2). These lysosomes were found, later on, scattered all over the hepatocytes.

Effect of piperacillin on morphology and viability of gram-negative bacteria

1984 ◽  
Vol 42 ◽  
pp. 218-219
Author(s):  
R. H. Liss
Keyword(s):  
Inhibitory Concentration ◽  
Cytoplasmic Membrane ◽  
Drug Binding ◽  
Gram Negative Bacteria ◽  
Bacterial Cells ◽  
Drug Induced ◽  
Penicillin Binding Proteins ◽  
Lactam Antibiotic ◽  
Drug Free ◽  
Tube Dilution

Piperacillip (PIP) is b-[D(-)-α-(4-ethy1-2,3-dioxo-l-piperzinylcar-bonylamino)-α-phenylacetamido]-penicillanate. The broad spectrum semisynthetic β-lactam antibiotic is believed to effect bactericidal activity through its affinity for penicillin-binding proteins (PBPs), enzymes on the bacterial cytoplasmic membrane that control elongation and septation during cell growth and division. The purpose of this study was to correlate penetration and binding of 14C-PIP in bacterial cells with drug-induced lethal changes assessed by microscopic, microbiologic and biochemical methods.The bacteria used were clinical isolates of Escherichia coli and Pseudomonas aeruginosa (Figure 1). Sensitivity to the drug was determined by serial tube dilution in Trypticase Soy Broth (BBL) at an inoculum of 104 organisms/ml; the minimum inhibitory concentration of piperacillin for both bacteria was 1 μg/ml. To assess drug binding to PBPs, the bacteria were incubated with 14C-PIP (5 μg/0.09 μCi/ml); controls, in drug-free medium.

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