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Post cesarean delivery decompensation in a parturient with scleroderma, severe pulmonary hypertension, and right ventricular failure
Abstract Number: F-62
Abstract Type: Case Report/Case Series
A 43 year old G3 P0111 presented at 29 weeks gestation with worsening shortness of breath. Her past medical history was significant for scleroderma with interstitial lung disease, mega-esophagus, and Raynaud’s syndrome. She also had a chronic, markedly elevated left hemidiaphragm of unknown etiology, leading to stomach and bowel in the left thorax and a right mediastinal shift. Echo showed EF >55% with right ventricular systolic pressure (RVSP) of 46-50 mmHg. At 32 weeks gestation, she was scheduled for a repeat cesarean delivery due to worsening RVSP to 60-70 mmHg and inability to optimize her on intravenous (IV) prostaglandins due to her inability to lie flat for a right heart catheterization.
Anesthetic management involved cardiothoracic anesthesiologists, and the plan was for general anesthesia following awake fiberoptic intubation due to the high risk of aspiration. Nitric oxide (NO) was available and extracorporeal membrane oxygenation (ECMO) was on standby in case she decompensated. Prior to intubation and induction, the right brachial artery was cannulated for invasive blood pressure (BP) monitoring. After uneventful awake fiberoptic intubation and induction, a 9 French introducer was placed in the right internal jugular vein. A pulmonary artery (PA) catheter was placed, and initial pulmonary artery pressures (PAP) were 70/30 mmHg. The right femoral artery and left femoral vein were accessed in preparation for possible cardiac bypass or ECMO. Defibrillator pads were placed. PAP remained unchanged at incision and throughout the procedure, ranging from 60s-80s/20s mmHg without NO. A low-dose epinephrine infusion was started after delivery to improve right ventricular (RV) contractility and was continued throughout surgery. Intermittent evaluation of RV function was assessed by transthoracic echocardiography.
Although she remained stable intraoperatively, she was transferred to the ICU on low-dose vasopressors and remained intubated postoperatively in case she decompensated postpartum. She arrived to the ICU with PAP 75/30 mmHg and BP 110/70 mmHg. Within hours, after inadvertent disconnection from the ventilator, she became agitated, hypotensive, and her PAP increased to 111/41 mmHg. Resuscitation required increasing vasopressors and starting inhaled NO and IV epoprostenol. Her PAP slowly stabilized into the 60s/30s mmHg, but she still required vasopressors for BP support. She was extubated to CPAP when her respiratory status improved.
Discussion: Pulmonary hypertension is associated with maternal mortality as high as 30-50%, and may occur a few hours to several days after delivery. In scleroderma, the constricted PAs may not accommodate autotransfusion, resulting in increasing PAP and RV failure. In our case, the patient could not benefit from preoperative epoprostenol and sildenafil, which may have helped to prevent postpartum decompensation.
Moaveni et al. Int J Obstet Anesth. 2015; 24:375-82.
Goland et al. Cardiology. 2010; 115:205-8.