Spontaneous Hemorrhage of the Distal Segment of the Left Pulmonary Artery After Cardiopulmonary Bypass

A 73-year-old female patient (85 kg, 187 cm, body mass index 24), with a past medical history of hypertension, severe chronic obstructive pulmonary disease (COPD), nicotine use, multivessel coronary artery disease, gastroesophageal reflux, and diverticulosis, was admitted with shortness of breath and chest pain. A computed tomography (CT) scan of the chest performed due to an elevated D-dimer on admission was negative for pulmonary embolism, pneumothorax, and pleural effusion. Previous investigations had shown severe multivessel coronary artery disease, and the patient was scheduled for a 3-vessel coronary artery bypass graft (CABG). Of note, the day prior to her surgery, she experienced hemoptysis (blood-tinged sputum) that was not further investigated.

On the day of surgery, the patient was brought into the operating room and standard American Society of Anesthesiologists monitors with a preinduction arterial line were placed. After uneventful induction, a 7.0-mm endotracheal tube (ETT) was placed. Cerebral oximeters and bispectral index were used throughout the procedure. Prior to cardiopulmonary bypass (CPB), a 9Fr sheath was placed in the right internal jugular vein, and a pulmonary artery catheter (PAC) was inserted into the pulmonary artery under direct visualization with transesophageal echocardiography (TEE) and waveform guidance on the first attempt. The balloon was deflated, and the PAC tip was visualized on TEE to be in the main pulmonary artery trunk. Preoperative TEE indicated preserved left and right ventricular function, no significant valvular abnormalities, and no patent foramen ovale. The opening pulmonary artery pressure was 32/20 mmHg. After 88 minutes on CPB and completion of the triple grafts, the patient was successfully weaned with minimal inotropic and pressor support. Standard cerebral protection was employed throughout, with adequate perfusion pressures during CPB. Cerebral oximeters were monitored for deviations from baseline and were managed as per the authors’ institutional protocols.

Several minutes after successful weaning with minimal inotropic support and after the reversal of heparin by protamine, the patient suddenly began profusely hemorrhaging from the ETT. Rapid severe hypotension ensued, with 1.5 L of frank blood suctioned from the ETT over several minutes. A massive transfusion protocol was activated, and the patient was transfused with 4 units of packed red blood cells while maintaining hemodynamics. Despite the heparin reversal, the patient continued to have brisk bleeding from the ETT. The tidal volumes decreased to <50 mL. The tip of the PAC was confirmed by TEE to be in the main pulmonary artery. It had not been manipulated at any point during the procedure. The PAC remained locked at the depth at which it was placed. Emergent diagnostic bronchoscopy with lavage was attempted; however, it was limited by difficult visualization due to airway hemorrhage. The patient maintained oxygen saturation throughout the event, with minimal desaturation events recorded. With continued bleeding and an inability to visualize the segment of the involved lungs, the decision was made to reheparinize and go back on CPB, with the goal of decompressing the pulmonary vasculature. An additional pulmonary artery vent was placed to decompress the pulmonary vasculature. Thereafter, a repeat diagnostic bronchoscopy was performed, which localized the bleeding source to the superior segment of the left lower lobe. A 37Fr left double-lumen tube (DLT) was exchanged in place of the ETT for lung isolation.

A second attempt at weaning from CPB with left lung isolation resulted in continued hemorrhagic output from the DLT totaling another 1 L. Given this, the patient was transitioned from CPB to central venoarterial extracorporeal membrane oxygenation (VA ECMO), and interventional radiology was consulted. The patient was transported on central VA ECMO to a hybrid operating room suite, with the chest open and packed.

Interventional radiology confirmed the location of the bleed to be the distal portion of the superior segment of the left pulmonary artery (Fig 1). An attempt was made to coil embolize the vessel. After embolization, the severity of bleeding from the lungs decreased, but the patient continued to bleed from the ETT (Fig 2). Lobectomy and or pneumonectomy with surgical ligation of the feeding vessel were discussed with the surgical team; however, due to the poor prognosis, further surgical intervention was deferred. The decision was made to reverse the anticoagulation and convert from VA ECMO to central venovenous ECMO (VV ECMO), as it needs a lower degree of anticoagulation. The TEE imaging demonstrated normal biventricular function. Mixed venous oxygen saturation and cardiac output were normal, so the authors converted from VA ECMO to VV ECMO, with the right atrial and/or inferior vena cava cannula used as the inflow, and the pulmonary artery chosen as the outflow to reduce the degree of heparinization. Throughout the case, the patient was given a total of 26 units of packed red blood cells, 6 units of fresh frozen plasma, 6 units of platelets, and 20 units of cryoprecipitate. Resuscitation was managed with the guidance of a thromboelastogram. Due to severe edema of the lungs, the chest was left open, and the patient was transported to the cardiovascular intensive care unit for further management. The DLT was left in place, and the patient continued to have profuse bloody output in the first 24 hours despite lung isolation. Due to the open chest and high levels of hemodynamic support, a neurologic examination was deferred by the intensive care unit (ICU) team until hemodynamic stability could be achieved. A lung-protective ventilation strategy was used in the ICU during postoperative days (POD) 0- to-2 while on ECMO. On POD 3, DLT output decreased and was replaced by pink, frothy sputum. The DLT was replaced with a single-lumen ETT, and therapeutic bronchoscopy revealed minimal clots in the left lung. Chest radiographs throughout this time revealed improved aeration (Fig 3). From PODs 4-to-8, the patient underwent a waxing and waning ICU course, with the development of acute renal failure requiring continuous renal replacement therapy and ECMO support. The patient underwent multiple chest washouts during this time and was decannulated from ECMO on POD 10. However, her clinical status worsened on POD 11 with increasing evidence of renal failure, sepsis, and coagulopathy. Her code status was changed to comfort care (Do Not Resuscitate) as per the wishes of the family.

Intrapulmonary hemorrhage has been documented postcardiac bypass. Described causes in the literature include rupture of the pulmonary artery, damage to the bronchial arteries, arteriovenous malformations (AVMs), iatrogenic injuries, and protamine administration, but most notably idiopathic without a defined cause.^{,  ,  ,  ,  ,  ,} 

Perforation of the pulmonary artery by the PAC, which is estimated to have an incidence of 0.05%-to- 0.2%, is one of the causes of intraoperative lung hemorrhage during CABG.^, Although intraoperatively, some information that can be derived from a PAC may also be gathered by TEE, continuous real-time monitoring by TEE is not feasible in the postoperative period when patients are extubated. Thus, PAC placement is an institutional practice used by the critical care team for postoperative monitoring and resuscitation in selected patients.

Damage to the pulmonary artery has been successfully managed via several different methods, including lobectomy, pneumonectomy, hilar clamping of the lung and surrounding vessels, and surgical banding of the offending artery.^,, The cases involving pulmonary artery rupture occurred almost exclusively in women >50 years old with pulmonary hypertension, and wee localized to the right pulmonary artery.^, In the authors’ patient, bleeding arose from a branch of the left pulmonary artery.

One case has been documented of successful coil embolization of a bleeding pseudoaneurysm in the right pulmonary artery due to PAC insertion. Extracorporeal membrane oxygenation was used to prevent re-bleeding of the aneurysm and provide ventilatory support. Similarly, VA ECMO was used in this patient because a lower activated clotting time is needed for the ECMO circuit than for the CPB machine. Subsequently, the patient was transitioned to VV ECMO to decrease the anticoagulation needed.

One case report described pulmonary hemorrhage after bypass that was attributed to surgical damage of pulmonary structures during minimally invasive repair of an atrial septal defect with lung isolation. The literature has also described a patient in whom a massive hemorrhage occurred due to a root vent in the pulmonary vasculature, damaging a lower lobe vessel posterior to the vein. Hemorrhage was controlled in the aforementioned patient by temporary balloon occlusion of the feeding pulmonary artery under direct fluoroscopic guidance.

A ruptured AVM was considered a possible cause. This diagnosis would require a feeder artery that surpasses a capillary bed and connects directly to a draining vein. Rupture of an AVM is uncommon; however, it is more frequently seen in patients with pulmonary arterial hypertension (PAH). The alteration in flow to a high-flow state in friable tissue has been linked to the rupture of AVMs. The process of weaning from CPB creates a state of rapid high flow in the pulmonary vasculature that could lead to AVM rupture. The transthoracic echocardiogram in this patient did not provide a right ventricular systolic pressure, and she had no prior diagnosis of PAH; however, opening PA pressures were within normal limits. She did have severe COPD, a known predisposing risk factor for PAH. Furthermore, the preoperative CT angiogram did not reveal an AVM. Because there was no indication for off-pump CABG in this patient, the deviation from the institutional practice of on-pump CABG was not considered.

Protamine has been linked to intraalveolar hemorrhage; however, in this patient, the amount of bleeding and the nature of the sudden onset of bleeding did not correlate with a protamine reaction leading to alveolar hemorrhage. Interstitial hemorrhage has also been observed in rats in which protamine was given to reverse heparin. Of note, the presence of normal right heart hemodynamic parameters with normal biventricular function on TEE and via visualization of the surgical field rules out any protamine reaction.

Bronchial artery hemorrhage has also been described as a cause of massive hemoptysis postbypass. The management of bronchial artery hemorrhage differs in that it is prudent to expedite weaning from bypass and heparin reversal because the bronchial arteries anatomically arise from the aorta.

Patients with COPD commonly present with hemoptysis. Most of the cases are benign and self-limiting. Occasionally, these patients experience worsening symptoms and life-threatening pulmonary hemorrhage. Risk factors for a sentinel bleed include age >50, active nicotine use, diagnosed COPD, coronary artery disease, other conditions that predispose to cardiovascular disease, and drugs that promote bleeding. This patient had many of those risk factors, which were exacerbated by heparinization before going on CPB. Studies show that in close to 25% of patients with hemoptysis due to COPD, the exact location of the bleed cannot be localized. However, in many patients, the bleeding can be localized via bronchoscopy or angiogram and managed with intervention. Although iatrogenic injury cannot be excluded, COPD was the likely cause of hemorrhage in this patient.

In summary, massive hemorrhage after CPB can be attributed to pulmonary artery rupture, protamine administration, surgical manipulation, rupture of an AV malformation, or exacerbation of a preexisting bleed due to heparinization. It can be a catastrophic complication, and prompt intervention and multidisciplinary collaboration are essential for management.