Fatal pulmonary embolism caused by streptokinase treatment of deep venous thrombosis of the leg?

During the last 10 years, four of 150 (2.7%) patients with deep venous thrombosis (DVT) treated with streptokinase (SK) at our department have died of pulmonary embolism (PE). A retrospective study of 1393 DVT patients treated with heparin during the period 1973-1986 showed that five (0.36%) of these patients died of PE while still on heparin. In this paper we describe the four patients treated with SK who developed fatal PE. In our opinion this increase in mortality does not warrant the use of SK in routine treatment of DVT of the leg before a proper trial has been conducted to compare the frequencies of pulmonary embolism after both treatments.     

Inadvertent embolic obstruction of abdominal aorta from left atrial thrombus after percutaneous mitral valvuloplasty

Inadvertent embolic obstruction of the distal abdominal aorta and left renal artery during a percutaneous mitral valvuloplasty procedure in a patient with mitral stenosis is reported. The embolism was from a left atrial thrombus which was detected by magnetic resonance imaging (MRI) but not by transesophageal echocardiography.     

Is sickle cell crisis a thrombotic event?

Although large vessel thrombi are occasionally reported in patients with homozygous sickle cell disease, the role of intravascular coagulation in typical pain crises is controversial. Therefore, we studied 24 sickle cell patients during and between episodes of pain crisis, using several sensitive tests of hemostasis. Fibrinogen was measured by a clotting assay, beta-thromboglobulin (beta-TG) and fibrinopeptide A (FPA) were quantitated by radioimmunoassay, and protein C was determined by absorbing the zymogen from test plasma, activating it with thrombin-thrombomodulin complex, and measuring activity with a selective synthetic substrate. Fibrinogen was elevated in asymptomatic patients (355 +/- 145 mg/dl) but was no different from the value in these same patients during crisis (333 +/- 180 mg/dl, p greater than 0.1). Similarly, beta-TG 136 +/- 52 ng/ml vs 118 +/- 56; FPA 3.7 +/- 4.8 ng/ml vs 5.2 +/- 4.5, and protein C 71 +/- 20% vs 66 +/- 19 showed no important changes during crisis. However, all these values were significantly different from those in age- and sex-matched healthy controls. beta-TG, fibrinogen, and FPA were elevated (p less than 0.001, 0.005, and 0.05, respectively), and protein C was decreased (p less than 0.003). We conclude that while chronic intravascular coagulation is common in patients with sickle cell disease, there is no evidence that the pain crisis per se is a thrombotic event.     

Late greenfield filter vena cava perforation causing a small bowel obstruction: Case report

This report describes a symptomatic case of vena caval perforation caused by a vena cava filter. Functional small bowel obstruction due to vascular compromise was caused by a prong of the filter.     

Findings of magnetic resonance imaging in cerebral venous occlusion: Difference from hemorrhagic infarction

A case of cerebral venous occlusion is reported. X -ray computed tomography showed a high-density lesion mimicking an intracerebral hemorrhage. In contrast, magnetic resonance images taken at the early clinical stage revealed a high-intensity lesion in both T₁- and T₂-weighted images. Follow-up magnetic resonance images at the chronic phase revealed that the intensity of this lesion had changed to low in the T1-weighted image, while still being high in the T₂-weighted image. These findings suggest that the lesion might be due to venous congestion produced by cerebral venous occlusion rather than hemorrhage into the cerebral parenchyma.     

An abnormal pattern of multiple platelet function abnormalities and increased thromboxane generation in patients with primary thrombocytosis and thrombotic complications.

Platelet aggregation (PA) induced by ADP, collagen and epinephrine, plasma levels of beta-thromboglobulin (beta TG) and thromboxane B2 (TXB2) and serum TXB2 generation were studied in 11 patients with primary thrombocytosis (7 with essential thrombocythaemia and 4 with polycythaemia vera) and compared with 16 healthy subjects. 5 patients suffered from peripheral vascular ischaemia and another 3 had venous thrombosis, but none had bleeding complications. The patients showed an abnormal pattern of platelet function and of thromboxane generation distinct from the healthy subjects in three aspects. a) Shape change was 5-26 times greater, the lag-time of collagen PA was 2.3-2.9 times longer and the extent of epinephrine PA was nil or very low. ADP- or collagen-induced PA was also reduced (p less than 0.02). b) Plasma TXB2 generation (corrected to a normal platelet concentration) stimulated by the three PA inducers was within the range of the healthy subjects in spite of the reduced extent of PA. c) Plasma beta TG level and serum TXB2 generation (both corrected to a normal platelet concentration) were 2.9-7.1 times higher (p less than 0.001) indicating enhanced in vivo platelet activation and possibly increased thrombin generation. These abnormalities were not detected in another 4 patients with secondary thrombocytosis. The abnormal pattern of platelet function and thromboxane generation can be a useful laboratory method in the evaluation of patients with primary thrombocytosis. It might also explain the thrombotic complications which occurred in 8 of the patients in a manner such that increased or normal TXB2 generation overcomes the reduced extent of PA. In this respect, the pronounced serum TXB2 synthesis might be a marker of intravascular thrombosis.     

彩色多普勒对下肢深静脉血栓的诊断分析

目的探讨彩色多普勒诊断下肢深静脉血栓的价值。方法回顾性分析294例临床怀疑深静脉血栓患者的超声表现。结果根据彩色多普勒诊断深静脉血栓的4个主要诊断依据及4个次要依据及下肢深静脉血栓不同阶段的特点，86例（29．4％）有深静脉血栓，急性、亚急性、慢性分别为73例（85．4％）、9例（10．4％）和4例（4．2％），累及双侧下肢17例（19．8％）。结论彩色多普勒对深静脉血栓的诊断有较大的价值，为临床提供可靠的诊疗依据。     

Review article: Coagulation cascade and therapeutics update: Relevance to nephrology. Part 1: Overview of coagulation, thrombophilias and history of anticoagulants

Coagulation involves the regulated sequence of proteolytic activation of a series of zymogens to achieve appropriate and timely haemostasis in an injured vessel, in an environment that overwhelmingly favours an anticoagulant state. In the non-pathological state, the inciting event involves exposure of circulating factor VII/VIIa to extravascularly expressed tissue factor, which brings into motion the series of steps which results in amplification of the initial stimulus, culminating in the conversion of fibrinogen to fibrin and clot formation. The precisely synchronized cascade of events is counter-balanced by a system of anticoagulant mechanisms, which serve to ensure that the haemostatic effect is regulated and does not extend inappropriately. Conversely, in pathological states, these events can escape normal control mechanisms, due to either inherited or acquired defects, which lead to thrombosis. Current anticoagulant therapy, although based on medications that have been in existence for upwards of 80 years, is moving towards targeted therapy for specific coagulation factors and events in the coagulation cascade, based on the current knowledge of the main triggers and key events within the series of reactions that culminates in haemostasis. It remains to be seen whether these newer medications will become first-line therapies for thrombosis in the coming decade. This review aims to elucidate the main events within the coagulation cascade as it is currently understood to operate in vivo , with a brief discussion focusing on hypercoagulable states, and also a short review of the history of anticoagulants as they relate to this model.