Pulmonary embolism

Abstract

Pulmonary embolism (PE) is caused by emboli, which have originated from venous thrombi, travelling to and occluding the arteries of the lung. PE is the most dangerous form of venous thromboembolism, and undiagnosed or untreated PE can be fatal. Acute PE is associated with right ventricular dysfunction, which can lead to arrhythmia, haemodynamic collapse and shock. Furthermore, individuals who survive PE can develop post-PE syndrome, which is characterized by chronic thrombotic remains in the pulmonary arteries, persistent right ventricular dysfunction, decreased quality of life and/or chronic functional limitations. Several important improvements have been made in the diagnostic and therapeutic management of acute PE in recent years, such as the introduction of a simplified diagnostic algorithm for suspected PE as well as phase III trials demonstrating the value of direct oral anticoagulants in acute and extended treatment of venous thromboembolism. Future research should aim to address novel treatment options (for example, fibrinolysis enhancers) and improved methods for predicting long-term complications and defining optimal anticoagulant therapy parameters in individual patients, and to gain a greater understanding of post-PE syndrome.

COVID‐19 associated coagulopathy and thromboembolic disease: Commentary on an interim expert guidance

“…For critical patients with severe acute respiratory distress syndrome who require prone positioning, radiological imaging for PE may not be directly possible. An option may be to consider echocardiography to assess for signs of worsening right ventricular overload, especially in patients experiencing hemodynamic collapse 14 . Nevertheless, suspicion for VTE should be high in the case of hypoxemia disproportionate to other known respiratory pathologies, acute unexplained right ventricular dysfunction, or unexplained leg swelling or pain.…”

Evaluation of the predictive value of the bleeding prediction score VTE‐BLEED for recurrent venous thromboembolism

“…One of the most debated challenges of management of patients with venous thromboembolism (VTE) is the determination of the optimal duration of anticoagulation. As the risk of recurrent VTE is low after VTE associated with a major transient risk factor (eg, major surgery), current international guidelines recommend cessation of anticoagulant treatment after a minimum of 3 months . On the other hand, patients with active cancer‐associated VTE are candidates for extended anticoagulation in light of the substantial risk for recurrence.…”

Acute Pulmonary Embolism: Contemporary Approach to Diagnosis, Risk-Stratification, and Management

“…Hypercoagulability can be either genetic (e.g., factor V Leiden mutation, prothrombin gene mutation, antithrombin III deficiency, protein C, S deficiency, and increased homocysteine levels) or an acquired disorder (e.g., antiphospholipid syndrome, infection, inflammatory conditions, cancer, nephrotic syndrome, smoking, estrogen (e.g., hormonal contraceptives, hormone replacement therapy, or pregnancy). 3,[5][6][7][8][9][10][11] Patients with severe obesity (body mass index [BMI] >35) have a six times higher risk of developing VTE compared with patients with normal BMI (<25). 8 The clinical presentations of PE are heterogeneous and range from asymptomatic in incidentally discovered small subsegmental embolus to massive saddle embolism to car-diogenic shock and/or sudden death in the context of massive saddle embolism.…”

“…Massive PE can markedly increase physiological dead space and impair CO 2 exchange. [9][10][11][12][13][14] Importantly, not all patients are hypoxemic (32% of PE cases demonstrate PaO 2 > 80 mm Hg), and that the majority of patients (81%) hyperventilate despite the increased dead space with nearly one-third of patients have normal A-a gradient. 12,13…”