EMBOLIC DISEASE



Thromboemboli directly or indirectly cause 200,000 deaths per year. Common and uncommon sources of emboli are listed in Table 21-2. Clin­ical presentation results from physiological ab­normalities caused by increases in pulmonary vascular resistance. Significant alterations occur only after more than 50 per cent of the pulmonary vascular bed has been occluded. Embolization of substances such as fat, amniotic fluid, or air, how­ever, markedly alter alveolar capillary membrane integrity and present as the adult respiratory dis­tress syndrome (ARDS) (see Chapter 22). The most frequently embolized material is blood clot, an ex­tremely common cause of hospital morbidity and mortality.

Most thromboemboli (> 85 per cent) originate in the ileofemoral deep veins. Less common sources include pelvic veins, upper extremities, and mural thrombi in the right side of the heart. Stasis and intimal injury are important factors in the development of thrombosis. The clinical di­agnosis of deep venous thrombosis is highly in­accurate, as physical examination is often mis­leading and specialized diagnostic techniques should be utilized whenever it is suspected.

The diagnosis of pulmonary embolism is often missed in sick hospitalized patients, while in the healthy outpatient population it is overdiagnosed. Predisposing situations are listed in . Clinical findings suggestive of pulmonary embo­lism are nonspecific and are often more com­monly indicative of other acute cardiopulmonary disorders. Typical symptoms include dyspnea, pleuritic chest pain, and hemoptysis (20 to 30 per cent). Physical findings include tachypnea (in­variable), obvious thrombophlebitis (unusual), acute right ventricular strain (right ventricular heave, increased P2, gallop) in less than 40 per cent of cases, and occasionally rubs, crackles, or wheezing. A normal chest examination is not un­usual. Cardiac output is decreased in severe cases. Excluding a diagnosis of pneumonia or pleurisy is difficult, as all may be associated with pyrexia and leukocytosis, although persistent high fever and marked leukocytosis are unusual in embolic disease.

Abnormal chest x-ray findings are common but nonspecific: atelectasis, infiltrates, pleural effu­sions, and an elevated diaphragm. Clear-cut hy-povascularity is difficult to detect. The electro­cardiograph (EKG) helps to exclude myocardial infarction and may show right ventricular strain, but nonspecific ST and T wave changes are more common and sinus tachycardia is usually the only abnormality. Hypoxemia and hypocapnia are typ­ical, but arterial Po2 is greater than 80 mm Hg in 13 per cent of patients. In summary, the clinical presentation and routine laboratory studies may suggest the diagnosis, but confirmation requires specific investigations.

Absence of activity on the perfusion lung scan, which visualizes the gross distribution of blood flow in the lung, may be due to anatomical block­age of the vessels or to vasoconstriction. A normal scan excludes pulmonary embolism. Lobar or multiple segmental defects that do not correspond to abnormalities on chest x-ray are considered high-probability scans consistent with pulmonary emboli. A ventilation scan helps to differentiate anatomical from functional blockage of blood flow. Inhalation of radioactive gas defines the dis­tribution of ventilation, and delayed clearance during washout of the gas suggests that airway disease may have caused the decreased perfusion secondary to hypoxic vasoconstriction. A normal ventilation scan with a high-probability perfusion scan is highly successful at diagnosing pulmonary embolism. A normal perfusion scan excludes pul­monary emboli, but anything other than a highprobability perfusion scan with a normal venti­lation scan is nondiagnostic and cannot confirm or exclude pulmonary embolism.





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