A message of hope to those in painful expectation of death.
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Biomedical subjects
Publications and source records attributed to P Egermayer.
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AIMS: To identify the actual duration of warfarin therapy received by patients being treated for venous thromboembolism (VTE) compared to that initially intended. To determine the incidence of major haemorrhage during therapy. METHODS: The subjects were 505 consecutive medical inpatients who were referred for a lung scan because of suspected pulmonary embolism. Three years following the discharge of the last patient, hospital notes, local and national computer databases were searched for subsequent relevant events. Surviving subjects were also contacted by telephone or letter. RESULTS: 115/505 (23%) received warfarin therapy for VTE. Direct personal contact was made with 314/352 (89%) surviving patients, including 79/82 (98%) surviving patients who were on warfarin. The intended duration of therapy was specified initially in 60/115 treated cases (52%), and these patients were less likely to be still receiving warfarin 3-4 years later (p<0.001). Indefinite therapy was initially recommended in 11/115 cases (10%), but 26/79 surviving subjects (32%) were known to be still receiving warfarin 3-4 years later. Seven treated subjects had a diagnosed recurrence of VTE. There were no clear indications for prolonged therapy in the remainder. Major haemorrhage occurred eighteen times among 115 treated patients (16%), and in two of these warfarin associated bleeding was considered to be the cause of death. None of these events was reported to the Centre for Adverse Reactions Monitoring. CONCLUSIONS: The intended duration of therapy was often unclear and warfarin was generally continued for much longer than is currently considered necessary. Haemorrhagic events were relatively common and were not reported.
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With emphasis on the pulmonary circulation, three general types of vascular disease are discussed: fibroproliferative (atherosclerosis), cellular proliferative (endothelial neoplasms) and inflammatory (granulomatous vasculitis). The causes of these phenotypic responses are invariably multifactorial, but infectious agents including viruses, Chlamydia, Helicobacter, Rickettsia, mycobacteria and other infectious agents have been increasingly implicated in the pathophysiology. The classifications of vascular diseases are complicated and confusing and many eponymous diseases are specific variations of more general disease processes. The pivotal role of the monocyte/macrophage and T-cells is discussed, particularly with regard to intracellular infections. In addition to antimicrobial therapy, modifications of macrophage function by IFN-gamma and blockade of TNF are attractive areas for therapeutic research. Diseases with many synergistic causes will probably also require multifaceted therapeutic interventions.
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The hypothesis that chronic thromboembolic pulmonary hypertension results from unresolved pulmonary embolism has strongly influenced the diagnosis and management of this disease since the 1960s. However, it is nearly impossible to induce chronic pulmonary hypertension in any animal species by means of repeated embolization of thrombotic material. The haemodynamic effects of thrombotic pulmonary embolism of different degrees of magnitude have also been studied in humans and there is little to suggest that chronic pulmonary hypertension is a likely long term outcome. Furthermore many conditions which predispose to venous thromboembolism do not appear to cause thromboembolic pulmonary hypertension. Other arteriopathic and atherosclerotic risk factors, are found in patients with chronic thromboembolic pulmonary hypertension, but not in those with venous thrombosis, suggesting that these may be unrelated conditions. Thrombosis in situ of the pulmonary arteries is common in severe pulmonary hypertension of any cause. Such thrombosis cannot usually be distinguished from pulmonary embolism. It is hypothesized that in situ thrombosis and pulmonary arteriopathy are common causes of vascular occlusion which is usually diagnosed as "chronic thromboembolic pulmonary hypertension" and that venous thromboembolism is unlikely to be a common cause of chronic pulmonary hypertension. It is further hypothesized that pulmonary embolism is seldom the sole cause of "chronic thromboembolic pulmonary hypertension".
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Epidemics of vascular disease caused by toxins and infectious agents affecting both humans and animals have been common in history. Examples of agents implicated include anorexients, ergotamine, mercury, arsenic, vinyl chloride, thorotrast, plant alkaloids, nitrites, toxic oil, tryptophan and bacterial, viral and parasitic infections. A major characteristic of these disorders is endothelial dysfunction, which may manifest itself in vasospastic disorders, sclerodermiform skin lesions, fibrosis, osteolytic lesions, polyneuropathy and portal and pulmonary hypertension. Angiosarcoma may also be a late outcome. These diseases are more common than is generally appreciated. The aetiology is usually multifactorial. This and other factors contribute to delayed recognition.
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AIM: To determine the level of utilisation of thromboprophylaxis in relation to risk factors for medical patients at Christchurch Hospital. METHODS: All medical wards were surveyed three times over a 12-week period from January 1998. Patients currently under investigation for venous thromboembolism were excluded, as were those currently receiving anticoagulant treatment for unrelated disorders. Primary prophylaxis was defined as the use of low-dose heparins or elastic stockings in asymptomatic patients. Patients with two or more risk factors were defined as being at high risk. RESULTS: Three hundred and eighty-seven patients were interviewed, of whom 80% were considered to be potentially eligible for primary prophylaxis. One hundred and one patients (33%) were at high risk, of whom 20 (20%) were given primary prophylaxis. Cancer, confinement to bed, recent surgery and heart failure were the most common risk factors. Elastic stockings and low-dose heparin were employed in the same proportion of high risk cases but no patient received both. Patients with cancer were less likely to receive thromboprophylaxis than those with the other risk factors. Overall, only about 7% of high-risk patients received thromboprophylaxis for more than 75% of the duration of their stay in hospital. CONCLUSION: Thromboprophylaxis is underutilised at Christchurch Hospital. Guidelines are required and audits of compliance are indicated.