Anesth Analg 2002;94:1593-1594
© 2002 International Anesthesia Research Society
OBSTETRIC ANESTHESIA
The Treatment of Severe Pulmonary Edema Induced by Beta Adrenergic Agonist Tocolytic Therapy with Continuous Positive Airway Pressure Delivered by Face Mask
Arnaud de La Chapelle, MD*,
Stephane Benoit, MD*,
Mohamed Bouregba, MD*,
Marc Durand-Reville, MD , and
Marc Raucoules-Aimé, MD PhD*
*Département d’Anesthésie-Réanimation Ouest, Service de Gynéco-Obstétrique. CHU Archet 2, 151 route St Antoine Ginestiere, BP3079, 06202 Nice Cedex 3, France.
Address correspondence to Arnaud de La Chapelle, MD, Département d’Anesthésie-Réanimation, CHU Archet 2, 151 route St Antoine Ginestiere, BP3079, 06202 Nice Cedex 3, France. Address e-mail to anesthesiologie{at}chu-nice.fr
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Abstract
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IMPLICATIONS: We report the case of a pregnant patient who developed severe pulmonary edema secondary to beta-adrenergic agonist tocolytic therapy (salbutamol) and was successfully treated with mask-delivered continuous positive airway pressure ventilation.
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Introduction
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Beta-adrenergic agonists are the most widely used tocolytic drugs for treatment of preterm labor (1). They act by a variety of mechanisms and have numerous side effects and anesthetic interactions, some of which can be life-threatening (1). The most serious complication associated with ß-adrenergic agonists is pulmonary edema, with a reported incidence as frequent as 5% (2). Some of these patients will require admission to an intensive care unit (ICU), and 15% will require intubation and positive-pressure ventilation for persistent hypoxemia (3). In obstetric patients, intubation may be problematic (4). Continuous positive airway pressure (CPAP) delivered by mask can reduce the need for intubation and mechanical ventilation for patients with severe cardiogenic pulmonary edema (5), but it has not been previously reported for use in parturients with tocolytic-induced pulmonary edema. We report the case of a pregnant patient who was successfully treated with mask-delivered CPAP ventilation for severe pulmonary edema that occurred during ß-adrenergic agonist tocolytic therapy with salbutamol.
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Case Report
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A 35-yr-old woman was admitted to the maternity ward at 28-wk gestation for preterm labor with rupture of the membranes. She had no history of cardiovascular or pulmonary disease. Tocolytic treatment was started with salbutamol infusion in 5% dextrose solution at a rate of 900 g/h (90 mL/h) and a 12-mg betamethasone injection per day. Sixty hours after initiating the tocolytic treatment, the patient developed severe dyspnea and had a respiratory rate of 30 breaths/min, heart rate of 150 bpm, and saturation (SpO2) of 80% by pulse oximetry. Crepitations at lung auscultation and chest radiograph confirmed the diagnosis of severe pulmonary edema. The electrocardiogram was normal. Salbutamol was stopped, large concentration oxygen therapy by mask with reservoir bag was started at 10 L/min, and three injections of furosemide 40 mg were administered IV over 1 h. The electrocardiographic recordings and troponin Ic remained unchanged. On 10 L/min oxygen therapy, PaO2 was 68 mm Hg, PaCO2 was 29 mm Hg and pH was 7.48. Echocardiography showed normal size cavities, homogeneous kinetics, an absence of valvulopathy, and good left ventricular diastolic and systolic function. Fourteen hours after discontinuing salbutamol, the patient was transferred to the ICU. Despite a diuresis of 2900 mL, dyspnea did not improve, tachycardia persisted, the respiratory rate was 25 breaths/min, her Glasgow Coma Scale score (GCS) was 10–11, SpO2 was 85%, and mechanical ventilation was considered necessary. A high-flow circuit (CF 800; Dräger Medical LTD, Lübeck, Germany) was used with a full-face mask to provide constant airway pressure. The inspired oxygen concentration was 60%. A threshold resistor valve was attached to the outlet of the circuit to provide 10 cm H2O CPAP. The respiratory rate decreased below 20 breaths/min, SpO2 increased above 95%, and the GCS was 15. Just after initiation of CPAP and without further diuretic injection, we noticed a marked increased in urine output of 450 mL/h for 2 h, at which time CPAP weaning was possible. Eighteen hours after discontinuing the salbutamol, a cesarean delivery was performed because of continuation of labor and breech presentation. Spinal anesthesia was chosen. Bupivacaine 15 mg 0.5%, 2.5 mcg sufentanil, and 0.1 mg morphine were injected into the subarachnoid space. Heart rate, blood pressure, and SpO2 remained unchanged on 5 L/min nasal oxygen therapy throughout the cesarean delivery. A 950-g male infant was delivered with 1- and 5-min Apgar scores of 6 and 10. The supplemental oxygen was tapered off over 12 h in the postoperative ICU and the patient was then transferred to the maternity ward, where she recovered uneventfully.
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Discussion
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Pulmonary edema is a well-known complication of ß-adrenergic agonist tocolytic therapy. The etiology of the pulmonary edema is unclear, but is likely multifactorial (1). Both cardiogenic and noncardiogenic mechanisms have been proposed. Possible cardiogenic causes include fluid overload, catecholamine-related myocardial necrosis, cardiac failure secondary to tachycardia with deterioration of ventricular relaxation, and down-regulation of ß-receptors (6–8). It is noteworthy, however, that left ventricular systolic or diastolic dysfunction was not demonstrated by echocardiography in our patient or in others reported earlier (9). Noncardiogenic pulmonary edema mechanisms include increased permeability of the pulmonary vessels and decreased colloid pressure (6,10). Beta sympathomimetics activate the renin angiotensin system, increasing sodium and water resorption (6), but the rapid resolution of the pulmonary edema with treatment in this case makes this etiology somewhat less likely. Betamethasone is probably not a major risk factor for pulmonary edema during salbutamol therapy. It has little mineralocorticoid activity and in a series of 343 women treated by ß-adrenergic agonist tocolytic no relation between glucocorticoids and pulmonary edema was found (11).
Treatment consists of discontinuing the ß-adrenergic agonist, administration of oxygen and diuretics, and fluid restriction. Patients with severe and persistent hypoxemia may require invasive hemodynamic monitoring, endotracheal intubation, and mechanical ventilation (2). As illustrated in this case, CPAP can provide alternative ventilatory support, avoiding the need for intubation and mechanical ventilation, which may lead to major complications such as aspiration, nosocomial pneumonia, barotrauma, or tracheal injury. In pregnant women, oxygen consumption increases by 60%, and functional residual capacity is reduced to 80% of the nonpregnant volume; inspiration is almost entirely attributable to diaphragmatic excursion (12). During ß-adrenergic agonist therapy, the inhibition of the hypoxic vasoconstriction may worsen the hypoxemia that accompanies pulmonary edema (13). CPAP improves oxygenation by decreasing intrapulmonary shunting and ventilation-to-perfusion mismatch induced by pulmonary edema and worsened by ß-adrenergic agonist tocolytic therapy (14). CPAP induces an improvement in lung compliance and in lung and airway resistances, a reduction in transdiaphragmatic pressure swings, a decrease in diaphragmatic activity, and so reduces the work of breathing (14,15). In addition, CPAP decreases pulmonary arterial pressures and increases right ventricular ejection fraction (15). This improved cardiac performance and work of breathing could explain the rapid improvement in clinical signs and the final outcome in our patient. A facial mask cannot be used for patients with vomiting, swallowing troubles or a GCS score <10 (14).
The rapid improvement in clinical signs in our patient after initiation of CPAP suggests that CPAP can be successfully used in parturients with severe ß-adrenergic agonist tocolytic-induced pulmonary edema, avoiding the need for tracheal intubation.
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References
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Accepted for publication December 27, 2001.
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Abstract
Introduction
