hrombosis limited strictly to the superficial veins of the saphenous system is treated with analgesia, elastic support, heat, and rest. If it does not soon subside or if deep-vein involvement is suspected, appropriate diagnostic measures are performed. Supericial vein thrombosis raises the risk of deep-vein thrombosis four-to sixfold. Heparin is given if deep-vein involvement is conirmed (Roach, 2013). Superficial thrombophlebitis is typically seen in association with varicosities or as a sequela of an indwelling intravenous catheter.
lthough it causes approximately 10 percent of maternal deaths, pulmonary embolism is relatively uncommon during pregnancy and the puerperium. he incidence averages 1 in 7000 pregnancies. According to Marik and Plante (200S), 70 percent of gravidas presenting with a pulmonary embolism have associated clinical evidence of deep-vein thrombosis. And recall that between 30 and 60 percent of women with a deep-vein thrombosis will have a coexisting silent pulmonary embolism.
In almost 2500 nonpregnant patients with a proven pulmonary embolism, symptoms included dyspnea in S2 percent, chest pain in 49 percent, cough in 20 percent, syncope in 14 percent, and hemoptysis in 7 percent (Goldhaber, 1999). Pollack and coworkers (2011) found similar symptoms. Other predominant clinical indings typically include tachypnea, apprehension, and tachycardia. In some cases, an accentuated pulmonic closure sound, rales, and/or friction rub is heard.
ight axis deviation and T -wave inversion in the anterior chest leads may be evident on the electrocardiogram. In at least 40 percent, chest radiography results are normal. In others, nonspecific indings may include atelectasis, an iniltrate, cardiomegaly, or an efusion (Pollack, 2011). Vascular markings in the lung region supplied by the obstructed artery can be lost. Although most women are hypoxemic, a normal arterial blood gas analysis does not exclude pulmonary embolism. Approximatelyaa third of young patients have P02 values >SO mm Hg. hus, the alveolar-arterial oxygen tension diference is a more useful indicator of disease. More than S6 percent of patients with acute pulmonary embolism will have an alveolar-arterial diference >20 mm Hg (Lockwood, 2012). Even with massive pulmonary embolism, signs, symptoms, and laboratory data to support the diagnosis may be deceptively nonspecific.
his is defined as embolism causing hemodynamic instability (Tapson, 200S). Acute mechanical obstruction of the pulmonary vasculature causes increased vascular resistance and pulmonary hypertension followed by acute right ventricular dilation. In otherwise healthy patients, significant pulmonary hypertension does not develop until 60 to 75 percent of the pulmonary vascular tree is occluded (Guyton, 1954). Moreover, circulatory collapse requires 75-to SO-percent obstruction. This is depicted schematically in Figure 52-4 and emphasizes that most acutely symptomatic emboli are large and likely a saddle embolism. hese are suspected when the pulmonary artery pressure is substantively increased as estimated by echocardiography.
If there is evidence of right ventricular dysfunction, the mortality rate approaches 25 percent. This compares with a I-percent rate without such dysfunction (Kinane, 200S). It is important in these cases to infuse crystalloids carefully and to support blood pressure with vasopressors. As discussed on page lOIS, oxygen treatment, endotracheal intubation, and mechanical ventilation are completed preparatory to thrombolysis, filter placement, or embolectomy (T apson, 200S).