Authors: Zografidou P1*, Papagiannopoulou O1, Grigoriou I1, Spanopoulos K2, Koraki E2
1MD, MSc, Anesthesiology
2MD, MSc, PhD, Anesthesiology
Department of Anesthesiology, General Hospital “Papageorgiou”, Thessaloniki, Greece
*Correspondance: General Hospital of Thessaloniki “Papageorgiou”, Municipality of Pavlos Melas, N. Efkarpia, 56403, email: , tel.: 00306940915003.
ABSTRACT
Peripartum cardiomyopathy is referred to as unanticipated heart failure with no determinable cause between the last trimester of pregnancy and six months post-delivery. The perioperative management of pregnant women with heart failure is challenging. We report the perioperative management of a case of peripartum cardiomyopathy with left ventricular ejection fraction less than 15%, who had reported to us at 27 weeks of gestation with a twin pregnancy for emergency caesarean section. Peripartum cardiomyopathy is a form of dilated cadiomyopathy with left ventricular systolic dysfunction, leading to signs and symptoms of heart failure.
INTRODUCTION
Peripartum cardiomyopathy (PPCM) affects 1 out of every 3000 to 4000 live births, with death rates ranging from 30 to 60%. The definition of PPCM consists of four criteria: 1) Development of cardiac failure in the last month of pregnancy or within five months of delivery, 2) Absence of an identifiable cause for the cardiac failure, 3) Absence of recognizable heart disease prior to the last month of pregnancy and 4) Left ventricular (LV) dysfunction (ejection fraction of less than 45% or decreased shortening fraction).
Risk factors of PPCM include multiparity, black race, older maternal age, preeclampsia, and gestational hypertension. PPCM symptoms, such as weariness, edema, and dyspnea, are comparable to those seen in the typical spectrum of peripartum states and pregnancy complications such pulmonary emboli and eclampsia. As a result, diagnosis is frequently delayed and the illness is under-recognized, with fatal effects.
The etiology of PPCM is not fully understood and is likely multifactorial. Suggested, but not proven, mechanisms for the development of PPCM included nutritional deficiencies, viral myocarditis, and autoimmune processes. Hemodynamic stress of pregnancy has been postulated as a potential etiology. However, the maximal cardiovascular changes occur in the second trimester, when most women with pre-existing cardiac disease develop symptomatic HF. In contrast, the majority of women with PPCM develop symptoms during late pregnancy or after the delivery1,2.
Peripartum cardiomyopathy can present in a variety of forms. In some women, the clinical and echocardiographic status improves and occasionally returns to normal, while in others, the condition progresses to severe cardiac failure and even death. In this report, we describe a case of PPCM during the 27th week of gestation in twin fetuses acquired by in vitro fertilization.
Case report
A 42 years old, nulliparous, female patient, with body mass index (BMI) value of 29.4, in the 27th week of gestation with twins, was referred to the emergency department (ED) of our hospital. She has been complaining of tachycardia, fluttering, and fatigue during the previous ten days. Upon her arrival to the ED, an echocardiography revealed that left ventricular ejection fraction (LVEF) was very low, approximately 20%. She was swiftly transferred to the cardiac intensive care unit for further testing.
According to her medical history, the pregnancy was conceived by in vitro fertilization (IVF), and she had gestational diabetes, that was managed following balanced diet. According to her surgical history, she had a left salpingectomy, two years prior, with no complications. She had no history of smoking or known allergies. She also stated she was bedridden the last 2 months, due to complications in the pregnancy, such as hemorrhage.
Throughout her hospitalization in the Cardiac Intensive Care Unit (CICU), the diagnosis of Peripartum myocardiopathy (PPCM) was established. Echocardiography revealed generalized hypokinesia, moderate left ventricular dysfunction with LVEF=20% (Image 1) and huge cardiomegaly. During the first three days of her admission, the patient was introduced to anti heart failure therapy including bed rest, propped up position, oxygen supplementation and diuretics. She was, initially, hemodynamically stable, with the same low ejection fraction (EF=20%) and no presenting edema. Despite the administration of diuretics and appropriate therapy intended at conservative improvement, she deteriorated on the fourth day of admission, with the presence of an EF less than 15%, and then she was immediately transferred to the operating room for an emergency cesarean delivery, due to severe heart failure.
Upon her arrival at the operating room, the patient had a pulse rate of 135/min, systolic/diastolic blood pressure (BP) 85/45 mmHg and oxygen saturation (SpO2) 95% with face mask. She had two peripheral intravenous catheters and an arterial blood pressure catheter for invasive blood pressure assessment. Defibrillator patch electrodes were stated and a cardiologist was on standby. A femoral central venous catheter was inserted, followed by a cautious volume infusion of Ringer’s lactate and Plasma-Lyte. Continuous intravenous (CIV) infusions of 8 mg Noradrenaline and 2 mg Adrenaline were administered, before anesthesia induction. When the whole team of obstetrics and neonatologists were ready, a rapid sequence of induction (RSI) was induced after the administration of 18 mg Etomidate, 50 mg Thiopental, 100 mg Rocuronium and CIV Remifentanil. Tracheal intubation was uneventful, using the McGrath video laryngoscope. Then, CIV Noradrenaline and Adrenaline were titrated in order to maintain her hemodynamics and CIV Propofol and Remifentanil for anesthesia maintenance. The neonates were delivered within 3 minutes. Apgar scores were 2 and 5 at 1 and 5 minutes post-delivery, respectively. The neonates were immediately intubated and resuscitated by a trained neonatologist. An arterial blood gas (ABG) test revealed: Ph 7,37, PaCO2 30,2 mmHg, BE=-6,8, Lac=2,54 mmol/L and PaO2= 130 mmHg with fraction of inspired oxygen (FiO2) 1%. The operation was completed and patient was hemodynamically stable. Finally, she was transferred to the Intensive Care Unit (ICU). She was extubated a few hours later, and the vasoconstriction support was progressively de-escalated. The patient transferred from the intensive care unit to the CICU on the second postoperative day. Patient was discharged from our hospital at the 10th postoperative day.
DISCUSSION
Although PPCM occurs worldwide, most epidemiologic data come from the United States, South Africa, Nigeria, and Haiti. In the US, its incidence has been estimated at between one in 900 and one in 4000 live births. A recent study, using the US Nationwide Inpatient Sample, found that its incidence increased from 1 in 1181 live births in 2004 to 1 in 849 live births in 2011. Proposed reasons for this increase include rising rates of advanced maternal age, pre-eclampsia, and multiple gestation (driven partly by the use of assisted reproductive technologies), which are risk factors for PPCM; increasing prevalence of cardiovascular risk factors such as hypertension, diabetes, and obesity among women of reproductive age and the growing recognition of PPCM as a disease entity1. Clinical features of PPCM include symptoms of congestive heart failure and chest pain. Signs can include tachycardia, tachypnea, pulmonary rales, an enlarged heart, and an S3 heart sound. Such signs and symptoms overlap with those of many other conditions, ranging from normal pregnancy to pulmonary emboli and upper respiratory infection2.
Diagnosis of PPCM includes the four criteria that were described above. There are no specific laboratory abnormalities for PPCM2.
The treatment for PPCM is the same as for other forms of congestive heart failure (fluid and salt restriction, β-blocker, diuretic, and digoxin), except for angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers, which are contraindicated in pregnancy. Hydralazine can be used during pregnancy to reduce afterload. Diuretics can be used cautiously during pregnancy to prevent dehydration and placental insufficiency. Patients with PPCM are also at high risk for thrombus formation; thus, anticoagulation should be considered especially for high-risk patients with severe LV dysfunction2.
In our case, despite being treated for heart failure, the patient’s condition deteriorated and required an emergency cesarean section.
The anesthetic care of patients with heart failure following cesarean section is challenging, and whether general or regional anesthesia is preferable remains unknown. Because regional anesthesia has been performed successfully in certain cases with PPCM, it is not necessarily contraindicated. However, the reported patients handled with regional anesthesia had relatively stable respiratory and cardiac function, whereas several of the reported PPCM cases experienced cardiac arrest following anesthesia induction. For patients who have severe cardiac and respiratory failure, only general anesthesia is encouraged3-5.
The most critical consideration during general anesthetic induction, in cases of severe cardiac failure, is the maintenance of stable hemodynamic profile. Any anesthetic agent can cause a reduction in afterload, which may result in hemodynamic collapse3. All of the agents both anesthetic and vasoactive that we chose at this case report were used in order to maintain maternal stable hemodynamic profile6.
Conclusion
PPCM has been associated with an increased likelihood of recovery than other forms of HF with reduced LVEF. Recovery is frequently seen within the first 3 to 6 months. Treatment of HF during pregnancy necessitates specific modifications to ensure fetal safety. Following delivery, most HF medications are compatible with breastfeeding. There is no established anesthetic treatment protocol, so the decision between the neuraxial block and general anesthesia must be individualized7.
Addittional materials: No
Acknowledgements: Not applicable
Authors’ contributions: ZP: data collection, planning, literature review, manuscript preparation, final draft, is the lead author, PO: literature review, manuscript preparation, critical review, GI: literature review, manuscript preparation, critical review, SK: conception, planning, supervision, critical review, KE: supervision, critical review. All authors read and approved the final manuscript.
Funding: Not applicable
Availability of supporting data: Not applicable.
Consent for publication: Patient’s consent was obtained
Ethical approval and consent to participate:
No IRB approval required.
Competing interests: The authors declare that they have no competing interests.
Received: May 2024, Accepted: May 2024, Published: July 2024.
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Citation: Zografidou P, Papagiannopoulou O, Grigoriou I, Spanopoulos K, Koraki E. Perioperative management of emergent cesarean section in a patient with peripartum cardiomyopathy: A case report. Greek e j Perioper Med. 2024;23(b):16-21. |
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