Kristine Tolentino Parra, MD1, Theodore Pratt1, and Matthew J. Martin, MD2 1 Naval Medical Center, San Diego, CA, USA 2 Trauma and Acute Care Surgery Service, Scripps Mercy Hospital, San Diego, CA, USA Orthopedic surgery carries a significant risk for pulmonary emboli (PE). The patient is demonstrating signs of an acute pulmonary embolism with shortness of breath, hypoxia, and hypotension. Pulmonary embolism leads to increased pulmonary resistance and increased right ventricular (RV) afterload and wall stress. The distribution of wall stress in the RV is not uniform, which can lead to localized free wall ischemia and dysfunction. The associated decreased RV cardiac output produces decreased left ventricular (LV) preload. Decreased LV output results in hypotension. The combination of regional RV dysfunction (RV free wall akinesis or bulging), normal RV apex, and hyperkinetic left ventricle is referred to as McConnell’s sign. Although the patient is at risk of a postoperative myocardial infarction, which can cause cardiogenic shock, this is unlikely given the patient’s preserved left ventricular function. Fat embolism would present in the operating room or shortly after surgery and typically features a syndrome including kidney injury, neurologic changes, and petechial rash. Tension pneumothorax can cause hypotension and hypoxia, but unlikely to have spontaneously developed in this patient 2 days after surgery. Sepsis is a very unlikely cause in this case. The purpose of performing an EKG is to exclude myocardial infarction, not necessarily aid in the diagnosis of pulmonary embolism. The most common EKG finding in pulmonary embolism is sinus tachycardia. McGinn‐White Sign (S1Q3T3), demonstrating cor pulmonale, is a classic finding that is not common. The mainstay of treatment for stable patients with acute pulmonary embolism is systemic anticoagulation with intravenous heparin drip or subcutaneous low‐molecular‐weight‐heparin. The patient described has a massive PE causing hemodynamic instability and hypotension. In addition to anticoagulation, this patient should be immediately considered for a surgical or transvenous pulmonary embolectomy. Patients with massive PE can also be treated with intravenous thrombolytic therapy; however, this patient has an increased risk of bleeding from her orthopedic surgery 2 days ago. The patient is unlikely to have an acute MI given her preserved LV function, therefore heart catheterization would be inappropriate. The patient is not in septic shock and therefore does not require IV antibiotics. Tube thoracostomy would be the treatment for a pneumothorax/hemothorax, which the patient does not have. Milrinone, a phosphodiesterase inhibitor, is an inotrope that improves right ventricular contractility and is a potent pulmonary artery dilator, which would decrease pulmonary pressures. This would be the best next therapeutic to administer among the choices, as it would act to reduce afterload on the right heart and improve right‐sided cardiac output. Caution should be taken when using milrinone in hypotensive patients, as it can also produce a significant decrease in systemic vascular resistance and worsen a patient’s hypotension. Veno‐venous ECMO would be inappropriate as this would only unload the right heart and improve oxygenation but would not address the patient’s hypotension. A patient with significant cardiac dysfunction and hypotension would require veno‐arterial ECMO, which can be used effectively to stabilize patients with massive pulmonary embolism as a bridge to surgical or percutaneous treatment or to aide in RV recovery after treatment. In the event that maximal medical management and milrinone was not effective, veno‐arterial ECMO would be a salvage option. Ventricular assist devices (such as the Impella) are now available but would not be a first‐line option in this patient. The patient’s elevated CVP and low UOP is due to her right heart failure, not fluid overload making diuresis inappropriate. Answers: 1) C 2) D 3) A 4) A Kearon C, Akl EA, Ornelas J, et al. Antithrombotic therapy for VTE disease: CHEST guideline and expert panel report. Chest. 2016; 149(2):315–352. doi:https://doi.org/10.1016/j.chest.2015.11.026. Lualdi JC, Goldhaber SZ. Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications. Am Heart J. 1995; 130(6):1276–1282. doi:https://doi.org/10.1016/0002‐8703(95)90155‐8. Bryce YC, Perez‐Johnston R, Bryce EB, Homayoon B, Santos‐Martin EG. Pathophysiology of right ventricular failure in acute pulmonary embolism and chronic thromboembolic pulmonary hypertension: a pictorial essay for the interventional radiologist. Insights Imaging. 2019; 10(1). doi:https://doi.org/10.1186/s13244‐019‐0695‐9. A 64‐year‐old man with type 2 diabetes and hypertension presented to the emergency department with chest pain, shortness of breath, and hypotension. His electrocardiogram (EKG) shows an ST‐elevation myocardial infarction (STEMI), and his cardiac catheterization demonstrates an acute thrombotic occlusion of the mid‐left anterior descending (LAD) artery. After treatment with placement of an intra‐aortic balloon pump and inotropic medications, the patient is transferred to the ICU in guarded condition. A Swan‐Ganz catheter is placed for monitoring. He has elevated troponins, and a bedside echocardiogram demonstrates a left ventricular ejection fraction (LVEF) of 25% with a dyskinetic anterolateral wall. On hospital day 5, the patient has an acute drop in blood pressure with decreased cardiac output and elevated ventricular filling pressures. A repeat bedside echocardiogram demonstrates a new moderate‐sized effusion. The patient presented with a STEMI. Cardiac catheterization demonstrated occlusion of the left anterior descending artery and should be treated with percutaneous stent placement. Options for revascularization include percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG). Surgical revascularization in the acute setting carries a significant mortality risk and would not be indicated in this case with single vessel disease. Systemic fibrinolytic therapy can be considered for reperfusion in patients with STEMIs where PCI is not available if the patient does not have contraindications. Patients requiring systemic fibrinolytic therapy due to limitations of the facility should be transferred to a center with specialty capabilities expeditiously. The patient will likely require dual antiplatelet therapy with aspirin and clopidogrel; however, he requires an intervention to revascularize the LAD. Systemic anticoagulation with warfarin for acute treatment in this case is not indicated. Mechanical complications of an acute myocardial infarction (AMI) include ventricular septal rupture, free wall rupture, and ischemic mitral regurgitation. The incidence of these is quite low, but significantly contribute to the total mortality of AMI. Classically these complications occur 3–7 days after an acute MI. With the advent of thrombolytics and PCI, they can present as soon as 24 hours after presentation. There should be a high level of suspicion for mechanical complications in a patient after an MI who becomes acutely hypotensive. Emergent surgical repair usually will be required. Free wall rupture is the most common major mechanical complication of an acute MI and carries a high fatality rate, oftentimes resulting in immediate death. The patient above has a ventricular free wall rupture with tamponade based on the presence of a new effusion and will require emergency surgery. Papillary muscle rupture will result in severe mitral regurgitation, which will be visualized on echo. Typically, these patients present with fulminant heart failure and pulmonary edema and would not have an acute effusion. Ventricular septal rupture will cause an acute left‐to‐right shunt seen on echo and will cause pulmonary vascular congestion. Atrial septal rupture does not occur in this setting. Acute stent thrombosis would present with an EKG consistent with large MI in the distribution of the coronary artery with the stent. Answers: 5) C 6) B Manhart JD. Acute myocardial infarction. McGill Med J. 1954; 23(3):161–168. doi:https://doi.org/10.1056/NEJMra1606915. Farina P, Gaudino MFL, Taggart DP. The eternal debate with a consistent answer: CABG vs PCI. Semin Thorac Cardiovasc Surg. 2020; 32(1):14–20. A 64‐year‐old man underwent left pneumonectomy for non‐small‐cell lung carcinoma. Five weeks after surgery, he presented to the Emergency Department with tachycardia and tachypnea. CT scan of the chest demonstrates irregular pleural thickening, and air‐filled pockets throughout the left hemithorax (Figure 45.1 ). The patient has a post‐pneumonectomy empyema (Figure 45.1) likely caused by a bronchopulmonary fistula, and the space will require drainage in the short term, but will not be definitive treatment. Because of the late presentation and the complexity of the empyema, definitive management can be achieved with a thoracotomy and Eloesser flap. An Eloesser flap is a single‐staged operation with placement of a U‐shaped incision and the resection of several adjacent posterolateral ribs, creating a permanent communication. This can be done after initial drainage and stabilization of the mediastinum. Although VATS can be considered, it is unlikely to be successful given the expected postoperative changes and diffuse nature of the disease process as described. IV antibiotics will be included in this patient’s care but will not be enough to resolve the patient’s empyema alone. Minimally invasive approaches for infected post‐pneumonectomy spaces have a high incidence of failure. Figure 45.1 Left post‐pneumonectomy infected space with multiple air‐filled pockets. Answer: 7) B Groth SS, Burt BM, Sugarbaker DJ. Management of complications after pneumonectomy. Thorac Surg Clin. 2015; 25(3):335–348. doi:https://doi.org/10.1016/j.thorsurg.2015.04.006. Clark JM, Cooke DT, Brown LM. Management of complications after lung resection: prolonged air leak and bronchopleural fistula. Thorac Surg Clin. 2020; 30(3):347–358. doi:https://doi.org/10.1016/j.thorsurg.2020.04.008. A 44‐year‐old man with longstanding hypertension presents to the emergency department with acute, severe, ripping chest pain. The patient has a heart rate of 96 beats/min with a systolic blood pressure of 110/60 mm Hg. CXR reveals a widened mediastinum. Bedsides echo shows preserved ventricular function with no wall motion abnormalities, moderate aortic valve insufficiency, and a large pericardial effusion. Accurate and timely diagnosis of acute aortic dissection is necessary. The current patient’s presentation is suspicious for a dissection complicated by a pericardial effusion and tamponade. The best imaging modality for diagnosis, if patient stability allows, would be CT angiogram of the chest. The accuracy of CT in diagnosing an aortic dissection is 98–100%. In addition, CT provides vital information for operative planning. Although transthoracic echocardiography can be a quick and adequate assessment of the aorta, it has limitations even with skilled technicians visualizing the proximal aorta. Transesophageal echocardiogram can provide clear anatomical imaging due to the proximity of the esophagus to the aorta, but the test requires sedation and expertise. In a patient with presentation suggestive of dissection, instability, and CXR showing widened mediastinum, a TEE can be performed under general anesthetic in the operating room just prior to cardiac surgery. CT PE protocol would be the diagnostic test of choice for pulmonary embolism. Diagnostic catheterization in this setting is not indicated. Initial management of the aortic dissection should be directed at immediate blood pressure control with beta blockade to decrease heart rate (and the stress on the aortic wall defined as the change in pressure over time (Dp/Dt). This patient has a proximal or type A aortic dissection as evidenced by the aortic valve pathology and pericardial effusion. Patients with type A dissection require emergent surgical consultation and operative repair for definitive management. Proximal propagation of the dissection can occur, causing rupture and cardiac tamponade, coronary compression, or aortic valve insufficiency. This is in contrast to patients with a type B dissection and stable hemodynamics, who can largely be managed nonoperatively. Answers: 8) A 9) C Hiratzka LF, Bakris GL, Beckman JA, et al. ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease: executive summary: a report of the american college of cardiology foundation/american heart association task force on practice guidelines, american association for thoracic surgery, american college of radiology, american stroke association. Circulation. 2010; 121(13):266–369. doi:https://doi.org/10.1161/CIR.0b013e3181d4739e. Stevens LM, Madsen JC, Isselbacher EM, et al. Surgical management and long‐term outcomes for acute ascending aortic dissection. J Thorac Cardiovasc Surg. 2009; 138(6):1349–1357.e1. doi:https://doi.org/10.1016/j.jtcvs.2009.01.030. Thrumurthy SG, Karthikesalingam A, Patterson BO, Holt PJE, Thompson MM. The diagnosis and management of aortic dissection. BMJ. 2012; 344(7839). doi:https://doi.org/10.1136/bmj.d8290.
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Cardiovascular and Thoracic Surgery
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