Treating Large Pulmonary Emboli
Treating Large Pulmonary Emboli
The mainstay of VTE treatment is systemic anticoagulation. Management of pulmonary embolism, however, varies often based on patient presentation. Acute large or multiple pulmonary emboli may result in hemodynamic consequences of hypoxia, right ventricular dysfunction, left ventricular dysfunction and eventually hemodynamic collapse. Although compensatory mechanisms may result in early stabilization, further decompensation may occur within 24–48 h. Small, peripheral pulmonary emboli commonly do not result in systemic manifestations. The severity of pulmonary emboli should be viewed through a lens of early mortality risk rather than embolus burden or the pattern of pulmonary emboli. Accordingly, as an entity, pulmonary embolism-related mortality has been reported by various registries to be 1.65–20%. Pulmonary embolism has been divided into three categories according to patient outcome: low-risk, submassive and massive. Massive pulmonary embolism is defined as causing hypotension (defined as systolic blood pressure <90 mmHg) or a significant reduction in blood pressure in hypertensive patients for at least 15 min, and results in short-term mortality rates of ~15%, most commonly within the first hour after presentation. The identification and stratification of patients in the submassive category is often more complex and relies on the assessment of hemodynamic and right ventricular effects and hypoxia by combining clinical characteristics, biomarkers and imaging ( Table 1 ).
It is noteworthy that although each component has been validated separately, data are lacking regarding the added prognostic value that may be gained from various combinations. By using right ventricular dysfunction obtained using transthoracic echocardiography as a diagnostic criterion, submassive pulmonary embolism accounts for ~35% of all pulmonary emboli. Finally, low-risk patients with pulmonary embolism have a mortality rate of less than 1%.
Several scoring systems have been devised to predict clinical outcomes. The Pulmonary Embolism Severity Index (PESI) contains 11 readily available clinical factors whereas the simplified PESI score contains six factors. The Geneva prognostic score was also derived to identify patients with a pulmonary embolism who are at a low risk of death, a recurrent VTE or major bleeding at 3 months. All have been found to correlate with short-term all-cause mortality and adverse events and may not necessarily reflect the direct consequence of the pulmonary embolism itself, but rather the patient's underlying condition. Although these scoring systems can identify patients at low risk who can potentially be treated outside of the hospital, they have not been tested with respect to suggesting the need for aggressive intervention.
Stratification of Pulmonary Embolism Outcomes
The mainstay of VTE treatment is systemic anticoagulation. Management of pulmonary embolism, however, varies often based on patient presentation. Acute large or multiple pulmonary emboli may result in hemodynamic consequences of hypoxia, right ventricular dysfunction, left ventricular dysfunction and eventually hemodynamic collapse. Although compensatory mechanisms may result in early stabilization, further decompensation may occur within 24–48 h. Small, peripheral pulmonary emboli commonly do not result in systemic manifestations. The severity of pulmonary emboli should be viewed through a lens of early mortality risk rather than embolus burden or the pattern of pulmonary emboli. Accordingly, as an entity, pulmonary embolism-related mortality has been reported by various registries to be 1.65–20%. Pulmonary embolism has been divided into three categories according to patient outcome: low-risk, submassive and massive. Massive pulmonary embolism is defined as causing hypotension (defined as systolic blood pressure <90 mmHg) or a significant reduction in blood pressure in hypertensive patients for at least 15 min, and results in short-term mortality rates of ~15%, most commonly within the first hour after presentation. The identification and stratification of patients in the submassive category is often more complex and relies on the assessment of hemodynamic and right ventricular effects and hypoxia by combining clinical characteristics, biomarkers and imaging ( Table 1 ).
It is noteworthy that although each component has been validated separately, data are lacking regarding the added prognostic value that may be gained from various combinations. By using right ventricular dysfunction obtained using transthoracic echocardiography as a diagnostic criterion, submassive pulmonary embolism accounts for ~35% of all pulmonary emboli. Finally, low-risk patients with pulmonary embolism have a mortality rate of less than 1%.
Several scoring systems have been devised to predict clinical outcomes. The Pulmonary Embolism Severity Index (PESI) contains 11 readily available clinical factors whereas the simplified PESI score contains six factors. The Geneva prognostic score was also derived to identify patients with a pulmonary embolism who are at a low risk of death, a recurrent VTE or major bleeding at 3 months. All have been found to correlate with short-term all-cause mortality and adverse events and may not necessarily reflect the direct consequence of the pulmonary embolism itself, but rather the patient's underlying condition. Although these scoring systems can identify patients at low risk who can potentially be treated outside of the hospital, they have not been tested with respect to suggesting the need for aggressive intervention.
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