Emergent Surgical Embolectomy for Massive Pulmonary Embolism Causing Intraoperative Cardiac Arrest

DISCUSSION

PEs are categorized either as submassive or massive. Patients with a submassive PE have evidence of right ventricular dysfunction but are hemodynamically stable. Patients with a massive PE have severe right ventricular dysfunction, are not hemodynamically stable, and may have cardiogenic shock.²

A massive PE resulting from a large thrombus can impede blood flow from the systemic to pulmonary vasculature, causing an acute increase in pulmonary vascular resistance that leads to pulmonary hypertension. The right ventricular myocytes, which are designed to work in a low-pressure system, are not able to sustain the mechanical strain and acute rise in metabolic demand. Cardiac output eventually decreases, and hemodynamic instability follows.⁴ A massive PE is associated with high mortality—up to 50%—within the first 6 hours, making the initial therapeutic management an important determinant in the patient's outcome.^5,6

Treatment selection depends on several factors, including the risk of bleeding, stability of the patient, resource availability, and thrombus burden.⁵ Thrombolysis is considered the first-line intervention for PE. A 2016 case report reported favorable outcomes with the use of intravenous thrombolytic therapy administered intraoperatively in a patient undergoing repair of an open left tibial fracture.⁷ Thrombolysis is a relative contraindication, however, in intraoperative patients and has been associated with an increased rate of major bleeding and intracranial hemorrhage compared to anticoagulation therapy alone.^7,8 Catheter-directed embolectomy is an alternative to thrombolysis, especially for patients who have contraindications or who have failed thrombolysis therapy; however, complications include distal thrombus embolization, right ventricular injury, arrhythmia, pulmonary hemorrhage, pericardial tamponade, and femoral venous injury.⁹

Surgical embolectomy is indicated for patients who have a PE that causes hemodynamic instability, particularly for patients who have failed or have contraindications for thrombolytic therapy or for those with a patent foramen ovale or right heart thrombus.³ Thrombus from the pulmonary arteries and the right side of the heart can be rapidly removed using open surgical embolectomy.¹⁰ Preoperative imaging is integral to planning the appropriate surgical approach.¹¹ Usually, computed tomography angiography is obtained as part of the preoperative workup to determine the thrombus location and extent. A TEE is obtained to evaluate for right ventricular strain and dysfunction and can also determine if a patent foramen ovale is present.¹¹ Surgery is typically successful when the PE is centrally located—namely in the main, left, or right pulmonary arteries—and without extensive distal thrombus load.⁶

The overall mortality rate for massive PE has been reported to be 52.4%. If a massive PE causes cardiac arrest, the mortality rate approaches 74%,^12,13 but the rate significantly decreases with surgical intervention. In a 2016 multiinstitutional study, the mortality rate for massive PE was 23.7% after surgical embolectomy.¹⁴ In our patient, TEE revealed saddle embolus in the pulmonary artery and a possible embolus in the right atrium. Consequently, both the pulmonary artery and the right atrium were opened to remove the thrombi.

Our patient sustained intraoperative cardiac arrest following an acute massive PE. He survived with surgical intervention and a 27-day postoperative hospital course. Rapid diagnosis and intervention, along with the patient's relatively preserved functional status prior to his hospitalization, increased his likelihood of survival. In healthy patients, hemodynamic instability and acute pulmonary hypertension secondary to right heart failure are reversible.¹⁵ Early and late death may also be reduced in patients without major comorbidities.⁴ However, once multiorgan dysfunction and cardiac arrest occur, the prognosis is poor.^1,16

Patients may benefit from therapy selective for the pulmonary vasculature such as inhaled nitric oxide that improves ventilation-perfusion matching by increasing perfusion to areas of the lung that are well ventilated. Also, as a selective pulmonary vasodilator, inhaled nitric oxide has been suggested as a safe and effective agent to decrease the pulmonary vascular bed in patients with pulmonary hypertension and has been shown to have an effect similar to intravenous nitric oxide in pulmonary hypertension, although no mortality difference has been shown in long-term outcomes.^17,18 In patients refractory to the above therapies, right ventricular assist device implantation should be considered. Our institution did not stock nitric oxide, but we used epoprostenol, a synthetic prostacyclin, as monotherapy to reduce the patient's pulmonary hypertension with the aim of reducing right ventricle strain caused by the massive PE. A 2017 randomized study found that prostacyclin significantly reduced pulmonary artery pressure and pulmonary vascular resistance and can be used as an alternative to nitric oxide for pulmonary hypertension therapy.¹⁹

From the time of fracture to his presentation at our hospital, the patient did not receive deep vein thrombosis (DVT) prophylaxis. He left the initial facility against medical advice because he wanted to receive care at our facility. In a case series of 115 patients undergoing surgical embolectomy, DVT was a risk factor for PE in 37% of patients.¹¹ Although an ultrasound may have revealed DVT of the deep veins of the lower extremity prior to our patient's orthopedic surgery, this test was not performed. As a result, we have implemented a DVT ultrasound screening protocol to help prevent this kind of situation from recurring.