Acute pulmonary embolism

Acute Pulmonary Embolism

PULMONARY EMBOLISM, MOST COMMONLY ORIGINATING FROM DEEP VEnous thrombosis ofthe legs, ranges from asymptomatic, incidentalIy discovered emboli to massive embolism causingimmediate death. Chronic sequelae of venous thromboembolism (deep venous thrambosis and pulmonary embolism) incIude the post-thrombotic syndrorne and chronic thromboembolic pulmonary hypertension.Acute pulmonary embolism may occur rapidly and unpredictably and may be difficult to diagnose. Treatment can reduce the risk of death, and appropriate primary prophylaxis is usually effective. Patients treated for acute pulmonary embolism appear to be almost four times as likely todie ofrecurrent thromboembolism in the next year as patients treated for deep venous thrombosis (rate of death, 1.5% vs.0.4%). The primary focus of this review is acute pulmonary embolism of thrombotic origin.

EPIDEMIOLOGY AND PATHOPHYSIOLOGY

Pulmonary embolism and deep venous thrombosis represent the spectrum of one disease. Thrambi commonly form in deep veins in the calf and then propagate into the proximal veins, incIuding and above the popliteal veins, from which they are more likely to embolize. About 79%of patients who present with pulmonary embolism have evidence of deep venous thrombosis in their legs, if deep venous thrombosis is not detected in such patients, it is likely that the whole thrombus has already detached and ernbolized. Deep venous thrombosis with resultant pulmonary embolism is shown in Figure 1. Conversely, pulmonary embolism occurs in up to 50% of patients with proximal deepvenous thrombosis. Because ofthe dual pulmonary circulation arising from the pulmonary and bronchial arteries, pulmonary infarction is not usualIy presento In acute pulmonary embolism, anatornical obstruction is undoubtedly the most important cause of compromised physiology, but the release of vasoactive and branchoactive agents such as serotonin from platelets may lead to deleteriousventilation-perfusion matching. As right ventricular afterload increases, tension in the right ventricular walI rises and may lead to dilatation, dysfunction, and ischemia of the right ventriele. Death results from right ventricular failure.
Although less common in certain regions, such as Asia, venous thramboembolism is a worldwide problem, particularly in people with known risk factors. A study using aninception cohort of patients in Olmsted County, Minnesota, estimated that the average annual incidence in the United States was 1 episode per 1000 registered patients. AnnuaIly, as many as 300,000 people in the United States die from acute pulmonary embolism. and the diagnosis is often not made until autopsy+? Hospitalized patients are at particularly high risk, although thramboembolism often is notrnanifested until after discharge.

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Figure 1. Pathophysiology ofPulmonary Embolism.
Pulmonary embolism usually originates from the deep veins of the legs, most commonly the calf veins. These venous thrombi originate predominantly in venous valve pockets and at other sites of presumed venous stasis (inset, bottom). If a dot propagates to the knee vein or above, or if it originates abovethe knee, the risk of embolism increases. Thromboemboli travel thtough the right side of the heart to reach the lungs. LA denotes left atrium, LV left ventride, RA right atrium, and RV right ventride.

RISK FACTORS
ACQUIRED RISK FACTORS

Certain risk factors increase the likelihood of acute deep venous thrombosis and thus pulmonary ernbolism." Total hip and knee replacement, surgery for hipfracture, and surgery for cancer impart particularly high risks, as do trauma and spinal cord ínjury, overall, acute medical illness may be the most common setting in which thromboembolism occurs.w Markedly reduced mobility also confers an increased risk, though the degree and duration of reduced mobility that trigger the increase in risk remain unclear, often depending on concomitant risk...