Chest case of the day. Pulmonary edema associated with tocolytic therapy

Autor: John A. Worrell, Frank E. Carroll, D M O'Donnell, J P Brunner
Rok vydání: 1992
Předmět:
Zdroj: AJR. American journal of roentgenology. 158(6)
ISSN: 0361-803X
Popis: This i 6-year-old was a late registrant for prenatal care when she was noted on sonography to have twin fetuses of approximately 20 weeks’ gestational age. She presented at 24 weeks with uterine contractions. Physical examination at this time revealed cervical dilatation of 4 cm with bulging membranes, but no fluid leakage. Temperature was 37.8#{176}C, pulse i05 beats per minute, blood pressure i24/77. The WBC count was i i ,900/dI (i i .9 x i 0 /I) with 78% segmented neutrophils. She was treated with bed rest, and tocolytic therapy with IV magnesium sulfate was initiated. She also received betamethasone in an effort to accelerate fetal lung maturity and empiric antibiotic coverage as a precaution against subclinical amnionitis. On the third day in the hospital, she became short of breath, and decreased urine output was noted. Arterial blood gases on room air revealed a pH of 7.44, Pco2 of 33, P02 of 67, and -0.6 base excess. A positive fluid balance was discovered, and 40 mg furosemide was administered IV. The patient responded with a brisk diuresis and improved respirations, but the uterus continued to be irritable. Furosemide was administered again on the fourth day, but with poor response. An anteroposterior portable chest radiograph at this time (Fig. i A) showed diffuse bilateral alveolar edema with the heart larger than normal for the gravid state. The patient’s contractions increased in frequency with further cervical dilatation to 7 cm. At this point, the IV tocolytic therapy was discontinued. The membranes ruptured spontaneously the next day, and the cervix dilated to 9 cm. Subcutaneous terbutaline was administered twice, but the labor persisted. Live-born twin male neonates were delivered, but both died later of complications of extreme prematurity. Furosemide was again administered, and the pulmonary edema had resolved by the second day after delivery (Figs. i B and i C). The subsequent postpartum course was uneventful. The occurrence of pulmonary edema in association with tocolytic therapy has been noted in the obstetric literature for the past i 0 years [i , 2]. Agents used to inhibit uterine contractility include the beta-mimetics terbutaline, isoxsuprine, ritodrine, fenoterol, salbutamol, and the calcium antagonist magnesium sulfate [2]. In addition to suppressing uterine contractions, these medications can cause tachycardia, hyperglycemia, hypokalemia, antidiuresis, pulmonary edema, cardiac arrhythmias, and hypotension as a result of and Ifi2-receptor effect as well as other more complex and incompletely understood mechanisms [3, 4]. The infusion of large volumes of saline in the healthy young adult should not result in pulmonary edema, nor should betamimetic therapy in nongravid patients [3, 5]. This pulmonary edema, unique to the gravid state, may be due to a combination of factors. Simply assuming the supine position, for example, decreases sodium and water excretion. In addition, tocolytic agents increase the secretion of antidiuretic hormone, and the twin pregnancy may be at special risk because the physiologic increase in intravascular volume is greater than in the singleton pregnancy [i]. Neither a direct cardiac effect with left ventricular failure nor a decrease in the pulmonary lymphatic flow has been substantiated [1 , 3]. The combination of fluid overload, decreased plasma colloid oncotic pressure, and the physiologic alterations of pregnancy is sufficient to account for this predisposition to pulmonary edema. Increased capillary permeability, especially in the presence of a bacterial infection such as amnionitis, also may contribute [1-4]. Pisani and Rosenow [1] have divided the criteria for diagnosis of pulmonary edema associated with tocolysis into major and minor criteria (Table 1). Mothers at increased risk include those with hypertension, diabetes, coronary and valvular heart disease, and obstructive cardiomyopathy. Other risk factors include multiple pregnancy, amniotic fluid infection, and possibly smoking [4]. The differential diagnosis of dyspnea of acute onset in the pregnant patient includes venous thromboembolism, amniotic fluid embolization, adult respiratory distress syndrome, peripartum cardiomyopathy, and pneumomediastinum [1].
Databáze: OpenAIRE