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.