Prevention of postoperative deep vein thrombosis with dipyridamole and aspirin.

Renney, J. T. G.; O’Sullivan, E. F.; Burke, Paul

doi:10.1136/bmj.1.6016.992

Cited by 52 publications

(10 citation statements)

References 17 publications

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“…[209][210][211] With the current trend of using antiplatelet agents as prophylaxis for thrombotic events, modalities to assess the efficacy of antiplatelet therapy are needed; platelet indices and platelet size distributions may give a reasonable clinical indication of response to antiplatelet therapy. [212][213][214] As platelets become activated, there is release of platelet factor 4 (PF4), beta-thromboglobulin (BTG), and thromboxane A 2 and as platelets are consumed, subsequent to activation, large young platelets are anticipated in the peripheral blood. Thus, platelet activation is associated with elevated PF4, BTG, the degradation product of thromboxane A 2 , thromboxane B 2 , and an increase in MPV.…”

Section: Hyperactive Prethrombotic Plateletsmentioning

confidence: 99%

Platelet Function Defects: A Clinical Review

Bick¹

1992

Semin Thromb Hemost

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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.

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Section: Hyperactive Prethrombotic Plateletsmentioning

confidence: 99%

Platelet Function Defects: A Clinical Review

Bick¹

1992

Semin Thromb Hemost

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“…Three prospective randomized trials using aspirin for prevention of venous thromboembolism after general surgery have been published [33,42,156,159]. In addition, one prospective randomized trial using a combination of aspirin with dipyridamole has been published [209], and two other trials combining these two drugs are available in abstract form or are in press [192,283]. The British Medical Research Council [33] conducted a well designed trial, using 125 I-fibrinogen leg scanning for diagnosis.…”

Section: Effect Of Aspirin On Abnormal Platelet Behavior In Vivomentioning

confidence: 99%

“…In a randomized prospective trial [209], Renney et al gave to the group of treated patients calcium aspirin (1,000 mg) and dipyridamole (100 mg) daily, starting the evening before operation. Venous thrombosis was diagnosed by the 125 I-fibrinogen test.…”

Section: Prevention Of Venous Thromboembolism 711 General Surgery (mentioning

confidence: 99%

Acetylsalicylic Acid, Hemostasis and Human Thromboembolism

Jobin¹

2008

Semin Thromb Hemost

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“…Every year new approaches to the problem of preventing PE are being explored. Medical treatments which have proved effective include ancrod (Lowe et al 1978), dextran (Davies 1978), dihydroergotamine and heparin (Kakkar et al 1979), aspirin and dipyridamole (Renney et al 1976) and intravenous lignocaine (Cooke et al 1977).…”

Section: Prophylaxis Of Dvtmentioning

confidence: 99%

Value of Anticoagulants in the Treatment of Pulmonary Embolism: A Discussion Paper¹

Egermayer

1981

J R Soc Med

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Heparin and warfarin were first widely used to treat pulmonary embolism (PE) in the early 1940s. Early acceptance of these drugs was widespread and, in retrospect, rather uncritical. In the face of enthusiastic reports it became very difficult to mount properly controlled trials. Other treatments which evolved in a similar way, and have also been in widespread use, have proved ineffective when formally assessed. It is the purpose of this paper to ask the question: 'How do we know that anticoagulants are of benefit in the treatment of PET Review of the literature Barritt & Jordan (1960) A widely quoted paper on the treatment of PE appeared in the Lancet in 1960. Barritt and Jordan embarked on a trial of anticoagulants (heparin and nicoumalone) versus no treatment, but abandoned it when they found that 5of their original 19 untreated patients had died; none of their 16 treated patients had died. As this is the only prospective controlled trial showing benefits from treatment, it will be reviewed in detail. Patients were referred into the trial by doctors other than the authors, so that selection was not random. Furthermore, the trial was not conducted in a double-blind fashion. No information is provided regarding the comparability of the treated and untreated patients. The incidence of massive pulmonary infarction among the patients who died (40%) is unusually high. Most other studies quote a 10% incidence of this complication (Moser 1977). The criteria used to make a diagnosis of PE arouse further doubts. Symptoms thought suggestive of PE were 'central chest pain, haemoptysis and faintness'. In a larger, more recent series using angiography to establish the diagnosis, these symptoms were present in fewer than 23% of PE patients (Urokinase PE Trial 1973). Two constellations of signs were supposed to be diagnostic of PE: (l) 'right heart failure: a fall in blood pressure, rise in JVP, together with changes in the ECG'; (2) 'pulmonary infarction: haemoptysis, fever, pleural friction, loss of resonance at the lung bases, rales, and in these patients it was usual to find changes in the bedside chest radiograph'. ECG changes are now thought to be nonspecific (Bell 1977), and from the clinical signs described for pulmonary infarction, one wonders how many patients in this series were placed on anticoagulants for pneumonia. Regarding non-fatal recurrences, no information is given, other than that 5 occurred in the untreated group. Considering the 5 deaths in the untreated group, one was due to cerebral infarction. This patient also had a PE, but so do between 20% and 60% of all persons who come to postmortem (Freiman et al. 1965). Four deaths were said to be due to PE : 2 of these patients died from sepsis (pneumonia with lung cavitation), one patient died 48 hours after the lodging of the first embolus, and one died immediately after a second embolization. The high incidence of lung cavitation among the deaths attributed to PE is striking. Sevitt & Gallagher (1961) found only 5% of lung cavitation among their PE fatalit...

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Prevention of postoperative deep vein thrombosis with dipyridamole and aspirin.

Cited by 52 publications

References 17 publications

Platelet Function Defects: A Clinical Review

Platelet Function Defects: A Clinical Review

Acetylsalicylic Acid, Hemostasis and Human Thromboembolism

Value of Anticoagulants in the Treatment of Pulmonary Embolism: A Discussion Paper¹

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Prevention of postoperative deep vein thrombosis with dipyridamole and aspirin.

Cited by 52 publications

References 17 publications

Platelet Function Defects: A Clinical Review

Platelet Function Defects: A Clinical Review

Acetylsalicylic Acid, Hemostasis and Human Thromboembolism

Value of Anticoagulants in the Treatment of Pulmonary Embolism: A Discussion Paper1

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Value of Anticoagulants in the Treatment of Pulmonary Embolism: A Discussion Paper¹