Acute pulmonary edema in pregnancy

Sciscione, Anthony; Ivester, Thomas; Largoza, Marissa; Manley, James S.; Shlossman, Philip; Colmorgen, Garrett H. C.

doi:10.1016/s0029-7844(02)02733-3

Cited by 94 publications

(39 citation statements)

References 19 publications

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“…APE during pregnancy occurs in 0.08–0.5% of the cases regardless of the etiology [29]. Out of 900 patients with a tocolytic indication, nicardipine was used in 742 patients between January 2009 and December 2013 in our hospital (55 births a week).…”

Section: Discussionmentioning

confidence: 99%

Nicardipine-Induced Acute Pulmonary Edema: A Rare but Severe Complication of Tocolysis

Serena

Bégot²,

Cros

et al. 2014

Case Reports in Critical Care

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We report four cases of acute pulmonary edema that occurred during treatment by intravenous tocolysis using nicardipine in pregnancy patients with no previous heart problems. Clinical severity justified hospitalization in intensive care unit (ICU) each time. Acute dyspnea has begun at an average of 63 hours after initiation of treatment. For all patients, the first diagnosis suspected was pulmonary embolism. The patients' condition improved rapidly with appropriate diuretic treatment and by modifying the tocolysis. The use of intravenous nicardipine is widely used for tocolysis in France even if its prescription does not have a marketing authorization. The pathophysiological mechanisms of this complication remain unclear. The main reported risk factors are spontaneous preterm labor, multiple pregnancy, concomitant obstetrical disease, association with beta-agonists, and fetal lung maturation corticotherapy. A better knowledge of this rare but serious adverse event should improve the management of patients. Nifedipine or atosiban, the efficiency of which tocolysis was also studied, could be an alternative.

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Section: Discussionmentioning

confidence: 99%

Nicardipine-Induced Acute Pulmonary Edema: A Rare but Severe Complication of Tocolysis

Serena

Bégot²,

Cros

et al. 2014

Case Reports in Critical Care

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“…[1] In 1991, Dote et al [6] first described a syndrome characterized by transient wall motion abnormalities that extended beyond a single coronary distribution and involved the apical and mid-portions of the left ventricle in the absence of significant obstructive coronary disease. The syndrome was initially described in Japan as “takotsubo” due to the similarity in its shape to that of a Japanese octopus pot.…”

Section: Discussionmentioning

confidence: 99%

“…[1] Pulmonary edema development is more likely in pregnant women due to the physiological changes associated with pregnancy. Other known causes of pulmonary edema during pregnancy include simultaneous use of multiple tocolytics, infection, pre-existing cardiac disease, preeclampsia, and eclampsia.…”

Section: Introductionmentioning

confidence: 99%

“…Other known causes of pulmonary edema during pregnancy include simultaneous use of multiple tocolytics, infection, pre-existing cardiac disease, preeclampsia, and eclampsia. [1] Pulmonary edema development during pregnancy is associated with an increased risk of maternal and fetal morbidity and mortality. [2] In the present report, we describe a rare case of acute pulmonary edema that was likely caused by takotsubo cardiomyopathy in a pregnant woman.…”

Section: Introductionmentioning

confidence: 99%

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Acute pulmonary edema caused by takotsubo cardiomyopathy in a pregnant woman undergoing transvaginal cervical cerclage

et al. 2017

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Background:The physiological changes associated with pregnancy may predispose pregnant women to pulmonary edema. Other known causes of pulmonary edema during pregnancy include tocolytic drugs, preeclampsia, eclampsia, and peripartum cardiomyopathy.Methods:We describe a rare case of pulmonary edema caused by takotsubo cardiomyopathy in a pregnant woman at 14 weeks of gestation who was undergoing emergency transvaginal cervical cerclage.Results:Intraoperative chest radiography revealed severe pulmonary edema and echocardiography indicated moderate left ventricular dysfunction with akinesia of the mid to apical left ventricular wall segment, which is reflective of takotsubo cardiomyopathy.Conclusion:With early detection and appropriate management, the patient was stabilized in a relatively short period of time. Based on her clinical signs and symptoms, we suspect that the pulmonary edema was caused by takotsubo cardiomyopathy.

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“…However, PE is unusual in nonpregnant patients receiving β -adrenergic therapy, for example, antiasthmatic treatment. Several conditions may account for this complication in pregnant women such as increased blood volume, increased cardiac output, hemodilution with reduction of oncotic plasma pressure due to activation of the renin-angiotensin-aldosterone system, iatrogenic fluid overload, increased pulmonary capillary permeability, preexisting cardiovascular disease, and others [93, 98–100]. β -AR stimulation can amplify some of these factors, for example, cardiac output and activity of the renin-angiotensin-aldosterone system.…”

Section: Effects Of β-Adrenergic Stimulationmentioning

confidence: 99%

Contribution ofα- andβ-Adrenergic Mechanisms to the Development of Pulmonary Edema

Raßler

2012

Scientifica

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Endogenous or exogenous catecholamines can induce pulmonary edema (PE). This may occur in human pathologic conditions such as in pheochromocytoma or in neurogenic pulmonary edema (NPE) but can also be provoked after experimental administration of adrenergic agonists. PE can result from stimulation with different types of adrenergic stimulation. With α-adrenergic treatment, it develops more rapidly, is more severe with abundant protein-rich fluid in the alveolar space, and is accompanied by strong generalized inflammation in the lung. Similar detrimental effects of α-adrenergic stimulation have repeatedly been described and are considered to play a pivotal role in NPE or in PE in patients with pheochromocytoma. Although β-adrenergic agonists have often been reported to prevent or attenuate PE by enhancing alveolar fluid clearance, PE may also be induced by β-adrenergic treatment as can be observed in tocolysis. In experimental models, infusion of β-adrenergic agonists induces less severe PE than α-adrenergic stimulation. The present paper addresses the current understanding of the possible contribution of α- and β-adrenergic pathways to the development of PE.

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Acute pulmonary edema in pregnancy

Abstract: The most common causes of pulmonary edema are the use of tocolytic agents, underlying cardiac disease, fluid overload, and preeclampsia.

Cited by 94 publications

References 19 publications

Nicardipine-Induced Acute Pulmonary Edema: A Rare but Severe Complication of Tocolysis

Nicardipine-Induced Acute Pulmonary Edema: A Rare but Severe Complication of Tocolysis

Acute pulmonary edema caused by takotsubo cardiomyopathy in a pregnant woman undergoing transvaginal cervical cerclage

Contribution ofα- andβ-Adrenergic Mechanisms to the Development of Pulmonary Edema

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