P028: REPERFUSION SYNDROME AFTER PULMONARY THROMBOENDARTERECTOMY CAUSING HYPOXEMIA
George Soliman, MD, Wesley L Allen, MD; Mayo Clinic
Chronic thromboembolic pulmonary hypertension (CTEPH) is an uncommon disease of unclear etiology. Fortunately, this form is potentially treatable with surgical intervention. Pulmonary thromboendarterectomy is indicated for symptomatic relief and in asymptomatic patients who develop pulmonary hypertension while exercising.5 The following is a case of symptomatic CTEPH s/p successful thromboendarterectomy complicated by refractory hypoxemia secondary to reperfusion syndrome.
A 65-year-old Hispanic female with a history of PHTN, multiple DVTs and PEs underwent a bilateral pulmonary arterial thromboendarterectomy with CPB and DHCA. Preliminary intra-operative TEE confirmed normal RV function with hypertrophy, moderated TR with peak jet gradient 50mmHg. Post-bypass she exhibited moderate RV depression and dobutamine, vasopressin and iNO were initiated. Post-operatively the patient was transferred, intubated to the ICU.
Postoperative day 1, utilizing high flow nasal cannula with iNO, the patient was extubated. The iNO was subsequently weaned and Swan Ganz catheter removed. 48 hours postoperatively, NIPPV and iNO therapy were initiated due to hypoxemia from new-onset pulmonary edema. After a prolonged ICU course, refractory hypoxemia responded to supportive care without intubation. Her hospital course was complicated with SVT arrhythmias, UTI, Klebsiella pneumonia. On POD 26 she was discharged on 2L NC.
Pulmonary thromboendarterectomy (PTE) is the definitive treatment for chronic pulmonary hypertension as the result of thromboembolic disease with the only surgical alternative consisting of organ transplantation.4 CTEPH is characterized by intraluminal thrombus organization and fibrotic scar-tissue-like stenosis. Pulmonary thromboendarterectomy results in immediate decrease in pulmonary arterial pressures. However, in up to 33% of patients, pulmonary hypertension may persist and is associated with increased risk of in-hospital death8.
The most common immediate postoperative complication of PTE is reperfusion injury8. Ranging in severity, typical onset is within the first 24-72 hours postoperatively1. Reperfusion lung injury is characterized by pulmonary edema resulting in hypoxia8. Early management consists of diuresis, avoidance of anemia and ventilation strategies similar to ARDS utilizing PEEP. In patients exhibiting refractory hypoxemia venovenous ECMO may be required.
Preventative techniques have been studied with some preliminary evidence in support of the use of preoperative transcatheter occlusion of the bronchopulmonary collateral artery. A retrospective study by Gan HL et al. found that a significantly lower proportion of patients whom underwent preoperative occlusion of the bronchopulmonary collateral artery required ECMO for refractory hypoxemia3. Additionally, decreased intubation duration, ICU days and improved post-PTE hemodynamics were seen in comparison to the control group. According to Kerr et al. methylprednisolone had no clinical preventative impact on the incidence of reperfusion lung injury. The group also found no significant impact on the number of ventilator-free, ICU-free or hospital-free days2. Interestingly, in rat models, iNO was shown to prevent ischemic-reperfusion edema by blocking neutrophil attachment at the capillary level, attenuating the microvascular leak. However, this was ineffective at treating existent pulmonary edema.9
Postoperative management of PTE patients can be challenging. Immediate improvement in pulmonary hemodynamics may entice clinicians into de-escalating the acuity of care within the first 72 hours. Understanding of the risk and window of reperfusion injury in this patient population is imperative for optimal care.