Cardiac tamponade in a woman with preeclampsia

Introduction

Preeclampsia, a pregnancy-specific syndrome characterized by hypertension and proteinuria, is associated with increased maternal vascular resistance and vascular dysfunction [3]. Alterations in vascular permeability cause a redistribution of bodily fluids, with intravascular volume depletion and extravascular fluid accumulation [7]. This phenomenon may manifest as peripheral edema or noncardiogenic pulmonary edema. It is plausible that the pericardium could be similarly affected by pathologic fluid accumulation, although this has not been described in the English language medical literature. We present a rare case of otherwise-unexplained cardiac tamponade in the setting of preeclampsia and recommendations for management.

Case presentation

A 30-year-old gravida 1 female with a monochorionic, diamniotic twin gestation was admitted at 31 weeks 4 days’ gestation with mildly elevated blood pressures. She was found to have proteinuria of 2331mg in 24h and was diagnosed with mild preeclampsia. Laboratory evaluation was significant only for mild anemia; admission laboratory values included a hematocrit rate of 30.1%; platelet count of 315×10⁹/L; serum creatinine level of 0.5; aspartate transaminase and alanine transaminase levels of 19 and 16 IU/L, respectively; and lactate dehydrogenase level of 196 IU/L. Serial laboratory test results throughout the antepartum course remained stable. Unexpectedly, the patient had persistent tachycardia with a resting pulse of 100–130 beats per minute. Her tachycardia worsened with movement, and desaturations occurred with ambulation. She had been in excellent physical condition pre-pregnancy, but described recent palpitations and dyspnea. Her past medical history was significant only for beta-thalassemia trait.

An electrocardiogram demonstrated sinus tachycardia, and a chest film mild cardiomegaly. Echocardiogram revealed a small atrial septal defect, ejection fraction of 75%, and a small pericardial effusion thought to be secondary to generalized edema. Thyroid function test, lower extremity Doppler ultrasonography, and computed tomography chest angiography results were unremarkable. Repeat chest film and echocardiogram 1 week later demonstrated small pleural effusions and a slightly increased pericardial effusion. A trial of diuresis yielded minimal symptom improvement. Daily fetal non-stress tests were reactive throughout the hospital course.

At 35 weeks 1 days’ gestation, echocardiogram demonstrated a large circumferential pericardial effusion consistent with early cardiac tamponade (Figures 1 and 2). The patient was hypertensive but hemodynamically stable and was taken to the operating room for pericardiotomy and cesarean delivery.

Figure 1

Longitudinal echocardiographic image demonstrating right atrial collapse during diastole.

Figure 2

Echocardiographic image demonstrating large pericardial effusion.

Cardiothoracic surgery, obstetrics, and neonatology teams were present, and a portable ultrasound was available for intraoperative fetal monitoring. Labetalol and magnesium sulfate infusions were started for hypertension control and seizure prophylaxis, respectively. General anesthesia was induced with propofol, rocuronium, and sevofluorane. Transesophageal echocardiogram confirmed right atrial collapse during diastole. The pericardium was opened via a subxiphoid approach, and 200 mL of straw-colored fluid was drained. The patient rapidly became hypotensive, and bedside ultrasound demonstrated bradycardia of twin A. Urgent cesarean delivery of twin girls was performed; APGAR scores at 1 and 5 min of life were 2 and 7 for twin A, and 3 and 8 for twin B, respectively. The patient’s blood pressure stabilized, and the pericardiotomy was completed. Drains were left in the pericardium and the left chest. The uterine and abdominal incisions were closed without complication.

The patient was awakened, extubated, and transferred to the intensive care unit. The labetalol infusion was continued until postoperative day 1 and magnesium sulfate until postoperative day 2. The postoperative course was complicated by low-grade fevers, a transient transamninitis, and anemia requiring transfusion. The output from the pericardial and pleural drains progressively diminished, and they were removed on postoperative day 4. Pericardial fluid cultures and cytology result were negative. An autoimmune workup was unremarkable.

The patient was discharged on postoperative day 6 on oral labetalol; however, she required readmission 2 days later for hypertension and continued dyspnea. Extended-release nifedipine and furosemide were added. Echocardiogram revealed a persistent large pericardial effusion without tamponade. She was discharged in stable condition on postoperative day 11.

The patient’s blood pressure gradually normalized and her antihypertensive regimen was weaned. Outpatient transesophageal echocardiogram 1 month postpartum demonstrated normal cardiac function, a small patent foramen ovale, and a small pericardial effusion.

Discussion

A search of PubMed/MEDLINE for “preeclampsia pericardial effusion”, “preeclampsia cardiac tamponade”, and “pregnancy cardiac tamponade” revealed three cases of preeclampsia-associated pericardial effusion in abstracts of foreign-language journals. In the Korean Journal of Anesthesiology, Seo et al. [5] reported the case of a 29-year-old gravida 1 female admitted at 31 weeks’ gestation with preeclampsia; she subsequently developed cardiac tamponade, underwent emergent pericardial drainage and cesarean delivery, and was later diagnosed with hypothyroidism. In Ginecología y Obstetricia de México, Quiroz et al. [4] reported two cases of gravida 1 females with severe preeclampsia who developed pericardial effusions, neither with cardiac tamponade. Cases of cardiac tamponade in pregnancy not associated with preeclampsia have been published, including cases associated with coexistent malignancies, autoimmune or cardiac disease, trauma, or iatrogenic causes. To my knowledge, there are no accounts of preeclampsia-associated cardiac tamponade published to date in the English medical literature.

This case demonstrates that the pericardium may pathologically accumulate fluid in preeclampsia. Dyspnea in the setting of preeclampsia frequently triggers an evaluation for pulmonary edema; however, such symptoms may also be explained by a pericardial effusion or cardiac tamponade. Although mild-moderate asymptomatic pericardial effusions are common in pregnancy [2], an effusion noted in the setting of significant cardiopulmonary symptoms may warrant serial echocardiography to monitor for gradual development of cardiac tamponade, as occurred in this case. One reasonable approach would be to repeat weekly echocardiograms to document the stability or evolution of the pericardial effusion, and to repeat the study at any time an acute change in symptoms or vital signs is noted. If the effusion decreases or stabilizes, less frequent monitoring would be reasonable. If cardiac tamponade develops, a multidisciplinary approach involving cardiothoracic surgery, obstetrics, neonatology, anesthesiology, and critical care teams is advisable in planning the perioperative management. Outright delivery should be considered beyond 32–34 weeks’ gestation, when the maternal risk would likely outweigh any fetal benefit of pregnancy continuation. Either outright delivery or expectant management could be considered at earlier gestational ages, depending on the patient’s clinical stability and the ability of cardiothoracic surgeons to conservatively treat the cardiac tamponade. If medical therapy is not indicated or not successful, either pericardiocentesis or pericardiotomy would be an acceptable treatment, depending on the clinical situation and cardiothoracic surgeon preference.

Cardiac tamponade causes impaired ventricular diastolic filling and makes cardiac output dependent upon maintenance of filling pressures and heart rate [8]. A compensatory increase in endogenous catecholamines leads to increases in heart rate, contractility, and systemic vascular resistance [6]. Preservation of these compensatory mechanisms is critical to avoid cardiovascular collapse. Most general anesthetic agents cause myocardial depression and systemic vasodilation, so the use of local anesthesia or ketamine, which better supports heart rate, contractility, and systemic vascular tone compared with other anesthetic agents [8], may be preferred. In this case, intraoperative hypotension likely resulted from anesthesia-induced vasodilation and inhibition of the compensatory adrenergic mechanism by the labetalol infusion.

Additional surgical concerns in pregnancy include prevention of aspiration [1], avoidance of aortocaval compression from the gravid uterus [1], and the ability to monitor the fetus(es) and urgently respond to intraoperative fetal distress. In our case, the rapid identification of fetal bradycardia and immediate delivery ensured the best possible neonatal outcomes.

The case presented demonstrates that cardiac tamponade may be a rare manifestation of preeclampsia. Evaluation of otherwise-unexplained cardiopulmonary symptoms in a patient with preeclampsia should include echocardiography to evaluate for pericardial effusion. Management of preeclampsia-associated cardiac tamponade should involve a multidisciplinary team to optimize maternal and neonatal outcomes.