Discussion
IE is a serious condition requiring prompt treatment [2]. IV antibiotics are the preferred initial treatment, followed by surgical evaluation. Indications for early surgery include heart failure, recurrent septic emboli, and evidence of worsening infection despite appropriate antibiotic therapy.
Native valve endocarditis is most often left-sided. Isolated right-sided IE accounts for approximately 10% of cases [5]. While these infections may result from intravascular devices or underlying cardiac anomalies, 90% are related to IVDU [6]. Endocarditis during pregnancy is a rare and serious condition with poor prognosis for the mother and fetus. If surgery is needed, the timing and sequence should account for maternal and fetal clinical status, including neonatal resuscitative capacity for a given gestational age.
Valve surgery for pregnant patients should be a last resort, reserved for cases refractory to medical therapy or those with serious complications, such as our patient with a PFO and evidence of systemic embolization. While the maternal mortality risk is like that of nonpregnant women, fetal mortality may be as high as 33 percent [7], attributable to the physiologic changes on CPB. Vasoactive substances, hypotension, hypothermia, and non-pulsatile blood flow reduce uteroplacental perfusion, causing fetal hypoxia, bradycardia, and demise [8]. Fetal stress response and catecholamine surge can also increase fetal systemic vascular resistance (SVR), which can reduce fetal cardiac output and produce severe fetal respiratory acidosis [9]. Additionally, uterine contractions and subsequent preterm labor can occur during the period of rewarming [10]. Therefore, if feasible, cardiac surgery should be delayed to avoid the risks of severe prematurity for the neonate. In cases where CPB cannot be delayed until after delivery due to maternal instability, mild hypothermia with gradual rewarming is preferred.
A combined procedure of cesarean delivery followed by cardiac surgery has also been described [11]. High-dose heparinization for CPB immediately postpartum can cause severe uterine hemorrhage. Therefore, precautions must be taken including intra-abdominal wound packing, intrauterine balloon tamponade, and use of uterotonic agents.
The physiologic changes of pregnancy pose additional challenges. Maternal SVR decreases, nadiring by the end of the second trimester followed by a slight increase thereafter. Cardiac output increases throughout pregnancy, particularly immediately post-delivery, in part due to autotransfusion of approximately 500mL to 750mL of uterine blood after placental delivery. Uterine involution after delivery decompresses the inferior vena cava, further increasing preload [11]. Although our patient was asymptomatic from severe TR, sudden hemodynamic changes following delivery may have led to rapid decompensation or sudden embolization of her massive vegetation. As such, ECLS was immediately available if she were to experience cardiovascular collapse.
In our case, the patient presented at the end of the second trimester with evidence of septic embolization to both pulmonary and systemic circulation and a large vegetation that further increased in size despite appropriate antibiotic therapy. Despite clear indications for TVR, her extremely premature gestational age was a complicating factor; surgical delay would have optimized fetal maturation. However, vegetation growth, worsening TR, and trans-PFO systemic emboli justified delivery at 28 weeks 6 days gestation followed by prompt TVR. Fortunately, both the patient and neonate survived this potentially life-threatening condition without serious complication.