Acute and chronic pulmonary thromboembolism: current perspectives part viii: summaRy and references

Despite considerable strides which have been made both in diagnosis and in management of PTE, both acute and chronic, it remains a significant challenging problem even to the most astute clinician. In approximately 50% of patients who suffer from acute fatal PTE the disease is not diagnosed as such during life. Accurate diagnosis of PTE requires a high index of suspicion, particularly in patients who have one or more predisposing factors (e.g., prolonged immobilization, obesity, trauma, postoperative state, advanced age, congestive heart failure, malignancy, pregnancy, postpartum state, and coagulation disorders such as antithrombin III deficiency and protein C deficiency). Despite the wide array of nonspecific and protean manifestations of acute PTE, the history and physical examination still constitute the first basis for suspecting the diagnosis. Dyspnea occurs in over 90% of the patients and the triad of dyspnea, tachypnea, and pleuritic pain is present in 70%. The combination of dyspnea, tachypnea, and DVT occurs in 99% of the patients. Conversely, in the absence of these symptoms and signs, the diagnosis of PTE is unlikely. Certain atypical manifestations which have recently been emphasized in acute PTE are high fever, abdominal pain, disseminated intravascular coagulation, and acute bronchospasm simulating bronchial asthma. Syncope, cardiovascular collapse, cyanosis, right ventricular S3 or S4, and loud P 2 suggest probability of acute massive PTE. Following the history and physical examination, chest roentgenogram, electrocardiogram, and arterial blood gas analysis should be performed to exclude other diagnoses which can mimic acute PTE (e.g., pneumonia, coronary insufficiency, and myocardial infarction). The use of VPS can identify some cases and exclude others but the procedure is usually worthless if significant parenchymal or pleural abnormalities already exist. PA and AV are often needed in many patients in order to establish definitive diagnosis of PTE and DVT, respectively. These studies can be carried out with reasonable safety and have proven to be cost effective when used on proper indications. It should be emphasized that the accurate diagnosis of acute and chronic PTE is necessary not only to insure proper management of patients but also to prevent inappropriate anticoagulation or surgery along with their inherent risks. Primary prophylaxis of DVT in certain high‐risk patients referred to above should always be preferred to the treatment of acute PTE. In this respect early ambulation and low‐dose heparin have proven very effective. Both are currently used widely in clinical practice with admitted success. The management of acute PTE is directed toward the correction of hemodynamic consequences as well as the prevention of further recurrences. The basic program consists of administering heparin intravenously, either by bolus or by continuous infusion, preferably the latter, for 7–10 days, followed by long‐term anticoagulation for 4 months following an acute episode in a patient with no existing risk factors and for 6–12 months in those patients with recurrent PTE or in the presence of significant risk factors for recurrence. Subcutaneous low‐dose heparin can be an alternative to oral anticoagulants but a significant drawback of this particular method of secondary prophylaxis is its increased cost. Not all episodes in every patient with acute PTE must be or can be treated with heparin. In case of acute massive PTE with or without shock, particularly in the latter, thrombolytic therapy utilizing either streptokinase or urokinase is the initial treatment of choice. The latter is preferred because of its greater effectiveness and lack of antigenicity. The resolution of pathologic process and hemodynamic abnormalities is accelerated, the patient thereby returning to normal cardiopulmonary status rather quickly.