Thrombectomy for pulmonary embolism under general anesthesia and cardiopulmonary bypass: a case report

doi:10.21203/rs.3.rs-2601540/v1

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Case Report

Thrombectomy for pulmonary embolism under general anesthesia and cardiopulmonary bypass: a case report

https://doi.org/10.21203/rs.3.rs-2601540/v1

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Background

Pulmonary embolism (PE) is a kind of pulmonary circulatory failure caused by endogenous or exogenous emboli blocking the pulmonary artery or its branches. Giant embolic pulmonary embolism can cause acute right heart failure, acute respiratory failure, and even sudden death. For patients with a large number of PE and hemodynamic instability, thrombolytic therapy, inferior vena cava filter placement, or thrombectomy are usually considered. This paper reports a case of pulmonary artery thrombectomy under cardiopulmonary bypass. The patient had pulmonary thrombosis caused by deep venous thrombosis of the lower extremities and underwent pulmonary artery thrombectomy under general anesthesia and cardiopulmonary bypass.

Case presentation:

A 59-year-old man was admitted to the hospital due to chest tightness and shortness of breath for half a month, which worsened for 3 days.Pulmonary hypertension (moderate). Color Doppler ultrasound of both lower extremities demonstrated deep venous thrombosis in the left lower limb (the percentage diameter stenosis was about 100%), and no thrombosis was found in the right lower limb. Physical examination revealed swelling of the left lower limb, skin temperature and color, and dorsalis pedis artery. The patient was treated with inferior vena cava filter implantation and heparin anticoagulant before operation. After definite surgical indications, pulmonary artery thrombectomy was performed under general anesthesia and cardiopulmonary bypass. After median thoracotomy induced by general anesthesia, the innominate vein ruptured and bled, followed by circulatory failure and cardiac arrest, and emergency cardiopulmonary bypass was established under intracardiac compression. Pulmonary embolectomy and tricuspid valvuloplasty were performed under cardiopulmonary bypass. After the operation, the patient’s blood coagulation function was poor; 11 pieces of developing gauze were filled in the pericardium to stop bleeding, and chest closure was delayed. The patient died of disseminated intravascular coagulation, hemorrhagic shock, and non-infectious multiple organ dysfunction syndrome early in the morning of the next day.

Learning purpose:

The etiology and treatment of patients with this kind of pulmonary embolism need to be further discussed.

Pulmonary embolism (PE) is a kind of pulmonary circulatory failure caused by endogenous or exogenous emboli blocking the pulmonary artery or its branches. Giant embolic pulmonary embolism can cause acute right heart failure, acute respiratory failure, and even sudden death. It is reported that the mortality rate of venous thromboembolism is 12% Mui 18% ^[1–3]. For patients with a large number of PE and hemodynamic instability, thrombolytic therapy, inferior vena cava filter placement, or thrombectomy are usually considered. This paper reports a case of pulmonary artery thrombectomy under cardiopulmonary bypass. The patient had pulmonary thrombosis caused by deep venous thrombosis of the lower extremities and underwent pulmonary artery thrombectomy under general anesthesia and cardiopulmonary bypass.

Medical Record Data

The patient, a 59-year-old male, was admitted to hospital at 10:12 on April 11, 2022, because he had been experiencing chest tightness and shortness of breath. The above symptoms worsened three days before admission, and chest tightness and shortness of breath also appeared at rest, so the patient could not lie flat at night, sit and breathe. Cardiac color Doppler ultrasound depicted pericardial effusion (large), normal left ventricular systolic function, pulmonary hypertension (moderate), and no abnormal color blood flow in all parts of the heart (Fig. 1). Local hospital pericardiocentesis hemorrhagic pericardial effusion. Specialist examination demonstrated that the patient had a symmetrical chest without deformity, consistent bilateral respiratory mobility, no increase or decrease of tactile speech tremor, clear sound on lung percussion, auscultation of lung breath sound clear, and no dry or wet rales. There was no abnormal eminence of the precordial region, no diffusion of apical pulsation, no palpable tremor, a small cardiac boundary, heart rate of 126/min, homogeneous rhythm, distant heart sound, no pathological murmur in each valvular region, no friction sound from the pericardium, negative for a peripheral vascular sign, and mild edema of both lower limbs. He was admitted to hospital with pericardial effusion. The patient denied hypertension, diabetes, and other medical history. The admission laboratory examination gave the following results: glucose 10.94 mmol/L, urea 10.92 mmol/L emagle, K 2.83 mmol/L emagle Lmagley 97.6 mmollemagle, Ca 2.03 mmol/L emagenl, gamma-GT83U/L, TP61.4g/L, ALB34.1/L, CK37U/L, WBC 13.06*109/L, neutrophil count 11.69mmol 109xL, lymphocyte count 0.43mmol 109xL, monocyte number 0.88mm 109L, BNP638pg, mL, PT16.7s. INR1.54, antithrombin III 79% Magi D-dimer 8.46ugqqml FDP21.46ugUniqmL Magneto TSH0.137uIUqml. To determine the source of pulmonary thrombosis, a color Doppler ultrasound examination of the lower extremities was performed, which suggested that deep venous thrombosis of the left lower extremities (the percentage diameter stenosis was about 100%), blood flow of the deep vein trunk of the right lower extremities was unobstructed, no thrombosis was found, valvular function was good, arterial blood flow of both lower extremities was smooth, no stenosis and occlusion were found, and the bilateral great saphenous veins were not dilated. Then the inferior vena cava filter was implanted and treated with 0.4 mL Q12h of enoxaparin, and the D-dimer value was monitored. After perfect preoperative preparation, pulmonary thrombus extraction was performed under general anesthesia and cardiopulmonary bypass.

Surgical Procedure

After entering the operating room, the patient was connected to ECG monitoring, SPO₂ 88%, ABP 125/71 mmHg, HR 100 times/min, oxygen inhalation, and arterial puncture was successful. Induction of anesthesia: midazolam 3 mg, etomidate 10 mg, sufentanil 100 µg, cisatracurium 20 mg, and norepinephrine 0.050.1 µg/kg/min were continuously pumped to maintain systemic blood pressure. Tracheal intubation and right internal jugular venipuncture were successful, and transesophageal ultrasound was continuously monitored. The operation started smoothly; ABP 90/50 mm/Hg in the nameless vein was ruptured and bleeding after the median incision into the chest, the heart rate decreased rapidly, the blood pressure decreased, the oxygen saturation decreased, the pericardium was opened, and a large amount of bloody pericardial effusion was seen. Epinephrine (4 mg) was given four times, and the TEE demonstrated poor myocardial contractile force. After ACT > 480 s, the aorta and superior and inferior vena cava were intubated to establish cardiopulmonary bypass. After satisfactory cardiac arrest, the right atrium, main pulmonary artery, and left and right pulmonary arteries were dissected, the pulmonary artery thrombus was removed, and the pulmonary artery incision was sutured continuously. Left atrial exhaust, aortic root exhaust. Rewarming, open circulation, automatic heart rebeating, sinus rhythm. The right atrial incision was sutured. Mechanical ventilation, free from cardiopulmonary bypass, protamine and heparin. Human fibrinogen 3 g, human prothrombin complex 1200 IU, plasma 1350 mL, red blood cell 3.5 U. The patient had difficulty in hemostasis and delayed chest closure and was transferred to the cardiac surgery ICU with tracheal intubation. Dopamine, dobutamine, epinephrine, norepinephrine, pituitrin, and another continuous pumping, giving cardiac diuresis symptomatic treatment. The patient’s blood pressure and heart rhythm could not be detected in the early morning of the same day, so he was immediately given cardiopulmonary resuscitation. After active symptomatic treatment, the patient's blood pressure and heart rhythm could not be recovered, so his family gave up treatment automatically.

The most common cause of pulmonary embolism is thrombosis, and deep venous thrombosis of the lower extremities is the main cause of pulmonary embolism. Studies have depicted that the causes of venous thrombosis can be divided into three categories ^[4]: venous blood stasis, venous intimal injury, and changes in the coagulation–fibrinolysis system. Venous blood stasis is related to deep venous thrombosis (DVT) of the lower extremities and thrombosis of atrial fibrillation during bed rest. Intermittent compression socks promote venous reflux, reducing the risk of DVT [3–5], but without illness or trauma, such as the risk of blood stasis while flying [6], trauma and major orthopedic surgery damaging the venous wall are the most likely mechanisms for lower extremity DVT ^[7–9]. Coagulation disorders that occur alone or in conjunction with other conditions can promote clinical venous thrombosis. Hypercoagulable states can be acquired or hereditary. In terms of hereditary diseases, the mutations expressed can be roughly divided into enhanced procoagulant factor function or loss of anticoagulant factor function. The most common hereditary hypercoagulable states include factor V Leiden mutations, prothrombin gene mutations, factor C and S deficiency, and antithrombin deficiency ^[10]. Other related studies have demonstrated that 5-methylene tetrahydrofolate reductase (MTHFR) is the key enzyme in the homocysteine metabolism pathway. MTHFR gene mutation may lead to the imbalance of vasomotor factor and DVT. MTHFR677TT mutation may be related to the occurrence of DVT, and the TT type may be a genetic risk factor for DVT ^[11]. Thrombosis is a naturally occurring process that is essential for dynamic balance after injury to prevent massive blood loss. Thrombosis can be activated by both internal and external pathways. However, these two pathways initiate the blood clotting cascade in the body, resulting in a thrombus rich in fibrin. Inflammation is closely related to the activation of the coagulation system because both processes involve a variety of cellular and plasma-related factors. In fact, monocytes are the main source of proinflammatory cytokines. Platelets contain polyphosphates and can be used as proinflammatory mediators and contact system activators ^[12]. Some studies have shown that polymorphonuclear neutrophils can produce extracellular neutrophil traps (NETs), which are highly thrombogenic ^[13]. This patient had no history of trauma and surgery and denied having hypertension, diabetes, and other chronic history, so deep venous thrombosis of the lower extremities caused by external injuries can be excluded. Reviewing the laboratory examination of this patient, we found that the numbers of neutrophils and monocytes were significantly higher than normal, so the possibility of inflammation activating the blood coagulation system could not be ruled out. At the same time, thrombus-related gene detection was not performed in this patient, so the possibility of thrombosis caused by hereditary disease or gene mutation could not be ruled out.

There are many ways to treat venous thrombosis. Anticoagulation therapy is the main treatment for venous thromboembolism, which is divided into three classic stages: the acute stage in the first 5–10 days after the diagnosis of venous thromboembolism, the maintenance period of 3–6 months, and the extended period ^[14]. Treatment options in the acute phase include subcutaneous injection of low-molecular-weight heparin or fondaparin, intravenous injection of unfractionated heparin, or direct oral administration of factor Xa inhibitors rivasaban and apexaban ^[15–16].

Patients with pulmonary embolism with unstable hemodynamics have a high risk of early death. Immediate thrombolytic therapy is needed to quickly restore pulmonary perfusion ^[17–18]. However, some researchers have questioned the risk-benefit ratio of thrombolytic therapy in patients with pulmonary embolism with right ventricular dysfunction. A trial depicted that thrombolysis did not reduce mortality compared with placebo and was absolutely associated with a significant 9% increase in massive bleeding, including a 2% increase in the risk of hemorrhagic stroke ^[19]. Based on these findings, thrombolysis should be stopped in patients with pulmonary embolism with normal blood pressure with right ventricular dysfunction.

Patients with absolute contraindications to anticoagulation should be implanted with inferior vena cava filters. If there is active bleeding or diagnosed recurrent PE, it is still necessary to place inferior vena cava filters despite adequate anticoagulant therapy. After admission, the patient was given anticoagulation therapy, and an inferior vena cava filter was placed. However, for patients with poor cardiopulmonary reserve or a high risk of pulmonary embolism, filters should not be routinely placed in anticoagulant therapy, as this does not reduce the risk of recurrence of pulmonary embolism ^[20].

Intervention measures other than anticoagulant therapy can be taken to reduce the risk of short-term mortality in patients with a medium and high risk of PE. This is especially true for high-risk PE, as the associated mortality rate may exceed 50% ^[21]. In addition to systemic anticoagulation, there are catheter thrombolysis or embolus removal, extracorporeal membrane oxygenation (ECMO) support, and surgical embolectomy. The clinical practice guidelines of the American College of Thoracic Physicians ^[22], the American Heart Association ^[23], and the European College of Cardiology ^[17] recommend surgical pulmonary thrombectomy (SPE) for moderate- and high-risk PE patients. After induction of general anesthesia, the median sternal approach opened the pericardium. Catheterization of the superior and inferior vena cava and ascending aorta was established, and cardiopulmonary bypass (CPB) was initiated. If intracardiac thrombectomy is required, cardiac arrest and aortic clamping may be required ^[17]. Intraoperative transesophageal echocardiography can be used to evaluate right atrial or right ventricular thrombus during the operation. In this case, anticoagulant therapy and an inferior vena cava filter were implanted before operation. Surgical pulmonary thrombectomy under general anesthesia and cardiopulmonary bypass were selected, and transesophageal echocardiography monitoring was performed throughout the operation (Fig. 2). Emboli were removed from the main pulmonary artery and the left and right pulmonary arteries during the operation (Fig. 3).

Disseminated intravascular coagulation (DIC) is a serious disease in which systemic and sustained coagulation activation occurs in the presence of underlying pathology, leading to the formation of microthrombi in microvessels. Activation of fibrinolysis was observed at the same time as coagulation ^[24]. The patient had a preoperative D-dimer level of 8.46 µg/mL, PT16.7s, fibrinogen degradation products of 21.46 µg/mL, and antithrombin II of 79%. He experienced cardiac arrest and cardiac compression during the operation and had a postoperative D-dimer level of 160.36 µg/mL, PT17.5s. Fibrinogen degradation product 392.64 µg/mL, antithrombin III of 36%. Studies have shown that PE and CPR patients have three times higher D-dimer than PE patients without cardiac arrest, prothrombin time (PT) is prolonged, the platelet count is decreased, and the fibrinogen and antithrombin (AT) levels are decreased. Among PE and CPR patients, 100% had abnormal D-dimer, 44% had abnormal PT, 53% had abnormal AT, 19% had abnormal fibrinogen, and 25% had abnormal platelet ^[25]. Some authors have suggested that patients after cardiac arrest and resuscitation are associated with: 1) DIC triggers, such as DAMPs, inflammatory cytokines, and catecholamines; 2) platelet activation and failure and decreased platelet count; 3) systematic activation of the coagulation system; 4) impaired anticoagulation pathway; 5) increased fibrinolysis and DIC followed by inhibition of fibrinolysis; 6) neutrophil activation and endothelial injury, and 7) microvascular fibrin thrombosis. Severe and prolonged hypoxia/ischemia and reperfusion due to cardiac arrest and resuscitation can lead to DIC, which may affect the prognosis of patients with postcardiac arrest syndrome ^[26].

PE Pulmonary Embolism

DVT Deep Venous Thrombosis

CPB Cardiopulmonary Bypass

DIC Disseminated Intravascular Coagulation

Acknowledgements

Not applicable.

Author contributions

Jun Li conceived the investigation, reviewed and edited the paper. Jun Li and Jie Liu

analyzed the data and wrote the manuscript.All authors read and approved the final manuscript.

Funding

Not applicable.

Availability of data and materials

All data in the study are included in this published article.

Declarations

Ethics approval and consent to participate

Not applicable.

Consent for publication

Informed consent of clinical detail and image publication was obtained from

the patient.

Competing interests

The authors declare that they have no competing interests.

Author details

^*1 The Second Hospital of Lanzhou University，Department of Anesthesiology，Gan Su Lan Zhou 730030，China

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Thrombectomy for pulmonary embolism under general anesthesia and cardiopulmonary bypass: a case report

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Abstract

Background

Case presentation:

Learning purpose:

Figures

Introduction

Medical Record Data

Surgical Procedure

Discuss

Abbreviations

Declarations

References

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