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Anesthetic management of two parturients with severe mitral stenosis and pulmonary hypertension for planned Cesarean delivery: Is GA with inhalational co-induction a safe option?
Abstract Number: T4D-4
Abstract Type: Case Report/Case Series
Introduction: Cardiovascular disease is the leading cause of pregnancy-related mortality in the United States. The physiologic changes of pregnancy are detrimental for the parturient with fixed valvular lesions like mitral stenosis (MS). We present two cases of parturients with severe MS and pulmonary hypertension (pHTN).
Patient A was a 36 y/o G3P2 with prior Cesarean delivery followed by VBAC in 2015. She developed heart failure one week postpartum in 2015 and was diagnosed with rheumatic heart disease. Cardiac cath at that time showed severe MS, MR and TR with severe pHTN. She declined surgery and was lost to follow-up. Due to late presentation this pregnancy, cardiac surgery recommended surgery post-partum unless deteriorating.
Patient B was a 22 yo G2P1 with a history of asymptomatic rheumatic heart disease diagnosed as a child, prior ablation for SVT, asthma, anemia and thrombocytopenia. During this pregnancy, her MS was noted to have progressed from mild to moderate/severe on surveillance echo. She was subsequently admitted with multifocal PNA. Follow-up echo had worsened with severe MS, moderate MR and severe pHTN.
In both cases, multidisciplinary meetings were held involving OB, Anesthesia, Cardiology and Cardiac surgery. Scheduled Cesarean deliveries were performed in the cardiac OR with CT surgery and bypass available in case of peri-operative decompensation. A cardiac anesthesiologist was involved in both cases and a general anesthetic was planned to reduce sympathetic stimulation in an awake patient and allow for TEE. A pre-induction arterial line and large bore peripheral access were established. With routine aspiration prophylaxis and NPO adherence, a co-induction with sevoflurane, fentanyl and etomidate (patient A) was performed. Hemodynamics were prophylactically treated with esmolol and phenylephrine during induction. TEE was performed throughout both cases. Upon delivery of baby, 3 units oxytocin were given incrementally for Patient A, and 10 units incrementally in Patient B, without significant change in hemodynamics. Intravenous fluids were administered judiciously, with about 1L given during each case. The patients were monitored in the operating room up to one hour following delivery to monitor hemodynamics in the setting of postpartum auto-transfusion. The patients were then extubated in the operating room and transferred to the cardiac ICU.
Discussion: These cases demonstrate a unique approach to maintenance of hemodynamic stability in parturients with severe MS and pHTN. Severe MS is poorly tolerated in pregnancy and even asymptomatic patients are counseled against pregnancy until intervention is performed. In pregnancy, severe MS can lead to heart failure later in pregnancy or during or after delivery. These patients require multidisciplinary care and carefully planned delivery.
Ref: CDC. Pregnancy-Related Mortality in the United States, 2011–2013.