Intraoperative Pulmonary Embolism During General Anesthesia Diagnosed with Transesophageal Echocardiography: A Case Report

doi:10.21203/rs.3.rs-4864666/v1

Download PDF

Case Report

Intraoperative Pulmonary Embolism During General Anesthesia Diagnosed with Transesophageal Echocardiography: A Case Report

https://doi.org/10.21203/rs.3.rs-4864666/v1

This work is licensed under a CC BY 4.0 License

Version 1

posted

You are reading this latest preprint version

Acute pulmonary embolism (APE) can be a life-threatening event with significant morbidity and mortality, particularly in the perioperative period. While early detection and intervention are essential, the common signs and symptoms are not overtly detectable under general anesthesia. Here, we present a case of an otherwise healthy 43-year-old female who presented with an intraoperative pulmonary embolism during general anesthesia for left patella tendon repair following a ground-level fall. Rescue transesophageal echocardiography (TEE) revealed a thrombus in the right main pulmonary artery and signs of right heart strain, including tricuspid regurgitation and right ventricular dilation. The patient was emergently taken to the interventional radiology suite and treated with catheter thrombectomy. The patient’s condition stabilized post-procedure, and she was subsequently discharged with anticoagulation therapy. The current case study elucidates the clinical challenges of diagnosing intraoperative APE, particularly in anesthetized patients where typical symptoms are masked. Intraoperative TEE played a pivotal role in early embolism detection and facilitated prompt, life-saving intervention. This case recapitulates the vital importance of utilizing advanced diagnostic tools in managing intraoperative emergencies. Future studies on developing pathophysiologic models and flowcharts specifically for intraoperative APE could significantly reduce adverse outcomes in diagnostically challenging cases.

Anesthesiology & Pain Medicine

Cardiac & Cardiovascular Systems

Pulmonology

Acute pulmonary embolism (APE)

transesophageal echocardiography (TEE)

Intraoperative diagnosis

Catheter thrombectomy

Interventional radiology (IR)

Venous thromboembolism

Despite contemporary advances in diagnostic tools and treatment strategies, Pulmonary Embolism (PE) persists as a clinical entity with substantial life-threatening outcomes. Perioperative acute pulmonary embolism (APE), in particular, is associated with a high level of morbidity and mortality [1, 2]. The common signs and symptoms include chest pain, dyspnea, anxiety, and tachypnea, which are not present in the anesthetized patient [1]. Vigilance is required to recognize the intraoperative signs of pulmonary embolism, which may include a sudden drop in end-tidal carbon dioxide (EtCO2), hypoxia, hypotension, shock, or cardiac arrest [3, 4]. Here, we present a young, healthy patient who experienced an intraoperative pulmonary embolism during general anesthesia. Furthermore, we discuss the immediate echocardiographic findings, subsequent management, and broader implications.

A 75-kg 43-year-old female patient with a previous medical history of obesity was scheduled for left patella tendon repair after a ground-level fall. She was physically active, had a body mass index (BMI) of 32 kg/m2, and did not smoke or consume recreational drugs or alcohol.

Preoperatively, the patient was notably anxious and was given 2 mg of midazolam intravenously, and an ultrasound-guided left femoral nerve block was performed for postoperative pain control. The patient was induced with 200mg of propofol intravenously, and a laryngeal mask airway (LMA) was placed, with the patient breathing spontaneously. Prior to the incision, a tourniquet was inflated to 300 mmHg over the thigh of the operative side with a total tourniquet time of 60 minutes. Upon deflation of the tourniquet, the patient had a sudden onset of hypoxia from 100–85%, EtCO2 dropped precipitously from 42 to 6 mmHg, and heart rate increased from 73 to 120 beats per minute. The patient was intubated and placed on a 100% fraction of inspired oxygen (FiO2), with an improvement in hypoxia of 97% and an improvement in EtCO2 of 25. Intraoperative arterial blood gas (ABG) showed an arterial pH of 7.33, O2 partial pressure of 141 mmHg, carbon dioxide (CO2) partial pressure of 44.1 mmHg, and hemoglobin concentration of 12.2 g/dL.

TEE performed showed venous thromboembolism in the right main pulmonary artery (PA) and a normal left PA (Fig. 1A). Furthermore, a modified bicaval view showed tricuspid regurgitation (TR) with a peak velocity of 294 cm/s and a gradient of 35 mmHg (Fig. 1B). Interventional radiology was immediately consulted, and the decision was made to proceed to the interventional radiology (IR) suite for thrombectomy due to the patient’s unstable condition. Left patellar tendon repair was completed, and the patient was immediately transported to the IR suite for thrombectomy. A pulmonary angiogram was performed, showing a filling defect in the right main pulmonary artery extending into the right upper, middle, and lower PA segments (Fig. 2A), consistent with intraoperative TEE findings. Pre-thrombectomy ABG showed a pH of 7.16, O2 partial pressure of 129 mmHg on 95% oxygen, carbon dioxide (CO2) partial pressure of 70.4 mmHg, and hemoglobin concentration of 11.9 g/dL. Aspiration thrombectomy was performed using a Cat Penumbra thrombectomy device [5]. Thrombi were removed from the right main, right upper, right middle, and right lower PA segments (Fig. 2C). A repeat angiogram showed markedly improved perfusion to the right lung (Fig. 2B), accompanied by improvement in vital signs. Post-thrombectomy ABG showed an arterial pH of 7.37, O2 partial pressure of 278 mmHg on 40% oxygen, carbon dioxide (CO2) partial pressure of 44 mmHg, and hemoglobin concentration of 11.2 g/dL. The patient remained intubated and was transferred to the surgical intensive care unit, where she received a heparin bolus and started on a heparin infusion.

Bilateral lower extremity Doppler ultrasound on postoperative day (POD) 1 demonstrated a clot in the left common femoral, left femoral, and left popliteal veins consistent with acute deep venous thrombosis (DVT). The patient remained intubated until POD 1, at which point she was extubated to room air. Transthoracic echocardiography prior to discharge revealed improvement in right ventricular function and only a trace tricuspid regurgitant jet. The patient was discharged on POD5 with Rivaroxaban for anticoagulation.

The incidence of acute pulmonary embolism has been reported to be as high as 30% after orthopedic surgeries [1, 6]. Risk factors can be hereditary traits (protein C deficiency, etc.), acquired (malignancy, trauma, etc.), medications, such as oral contraceptives, or surgical factors (ex. Hip or knee replacement) [7, 8]. Intraoperative PE can be especially difficult to diagnose as the common signs and symptoms, such as chest pain, dyspnea, anxiety, and tachypnea, are not available while the patient is under general anesthesia [9, 10]. Hence, early diagnosis and treatment are of critical importance and can significantly aid in reducing morbidity and mortality [11, 12].

Intraoperative diagnosis of PE is a diagnosis of exclusion. Other pathologies that might present similarly include malposition or dislodgement of the endotracheal tube, pneumothorax, myocardial ischemia, and bronchospasm. Changes seen on standard intraoperative monitors can help raise suspicion and warrant further diagnostic testing. In addition, the pathophysiologic genesis and timeline of intraoperative APE are influenced by the operation procedures and general anesthesia, which follow distinct pathways from the spontaneous respiration patterns of patients in preoperative and postoperative contexts [13].

Electrocardiography (EKG) changes in APE frequently point to signs of right heart strain. The most common EKG findings reported include sinus tachycardia, T-wave inversion in lead V1-V4, III and aVF, S-wave in lead I, Q-wave in lead III, right bundle branch block, P pulmonale, and ST-segment elevation in leads V1-V2 [1, 2]. While these signs may be seen with cases of APE, they may be difficult to appreciate intraoperatively, as intraoperative tachycardia may be due to the light plane of anesthesia, pain or hypovolemia. Furthermore, echocardiography may provide direct visualization of the thrombus and or the right heart strain sequelae of APE. Modified bicaval views showing TR greater than 270 cm/s are associated with PE. Midesophageal 4-chamber views may demonstrate right ventricular (RV) dilation, increase in RV to left ventricle (LV) dimension ratio, septal shift into the LV, RV free wall hypokinesis, akinesis, or McConnell’s sign [1]. Our patient had a peak TR jet velocity of 294cm/s, RV dilation, and a large thrombus visualized in the right main pulmonary artery.

An elevated PaCO2 accompanied our patient’s precipitous drop in EtCO2, sometimes referred to as a “separation phenomenon” [14]. This is unlike a spontaneously breathing patient whose blood gas changes would commonly show respiratory alkalosis due to tachypnea [1, 14]. Pneumothorax was considered, but given peak airway pressures were not elevated and auscultation confirmed equal and bilateral breath sounds, a diagnosis of pneumothorax less likely.

Our presentation is similar to a previous case report of a 28-year-old female undergoing open reduction internal fixation of her left clavicle and left ankle after a motor vehicle collision. However, our patient did not share some of the comorbidities of the former patient, such as BMI in the morbid obesity range, multiple orthopedic traumas, or a history of smoking.

We have reported a case of intraoperative APE in a patient undergoing orthopedic surgery following a ground-level fall that was diagnosed by emergent intraoperative TEE. The patient developed hypoxia and a steep drop in EtCO2, prompting the provider to utilize emergent intraoperative TEE to confirm a diagnosis of APE. This led to immediate treatment via aspiration thrombectomy with improvement in vital signs. TEE or transthoracic ultrasounds are becoming more readily available and can be implemented intraoperatively while performing other tests to narrow a diagnosis.

CONFLICT OF INTEREST

Financial Disclosures: None.

Conflicts of interest: None.

AUTHOR’S CONTRIBUTIONS

Sassan Rafizadeh, M.D., Ph.D. – Substantial contribution to conception and design, acquisition of data, drafting of the article, its critical revision to ensure critically important intellectual content, responsible for ensuring the integrity and accuracy of the case report herein investigated, and final approval of the version to be published.

Matthew Abikenari, M.S – Substantial contribution to conception and design, acquisition of data, drafting of the article, manuscript preparation and submission, and final approval of the version to be published.

Clinton Kakazu, M.D., M.B.A. –Substantial contribution to conception and design, acquisition of data, Drafting of the article, its critical revision to ensure critically important intellectual content, and final approval of the version to be published.

ACKNOWLEDGEMENTS

N/A.

Consent to publish was obtained and all identifying information has been anonymized.

Desciak MC, Martin DE. Perioperative pulmonary embolism: diagnosis and anesthetic management. J Clin Anesth. 2011;23(2):153-165.
Bělohlávek J, Dytrych V, Linhart A. Pulmonary embolism, part I: Epidemiology, risk factors and risk stratification, pathophysiology, clinical presentation, diagnosis and nonthrombotic pulmonary embolism. Exp Clin Cardiol. 2013;18(2):129-138.
Ward KR, Yealy DM. End-tidal Carbon Dioxide Monitoring in Emergency Medicine, Part 2: Clinical Applications. Acad Emerg Med. 1998;5(6):637-646.
Dudaryk R, Benitez Lopez J, Louro J. Diagnosis and Thrombolytic Management of Massive Intraoperative Pulmonary Embolism Guided by Point of Care Transthoracic Echocardiography. Case Rep Anesthesiol. 2018;2018:1-5.
Penumbra Inc. Indigo® System CAT™ RX. Available from: https://www.penumbrainc.com/peripheral-device/indigo-cat-rx/
Geerts WH, Bergqvist D, Pineo GF, et al. Prevention of venous thromboembolism: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest. 2008;133(6 Suppl):381S-453S.
Ji Q, Wang M, Su C, Yang Q, Feng L, Zhao L, et al. Clinical symptoms and related risk factors in pulmonary embolism patients and cluster analysis based on these symptoms. Sci Rep. 2017;7(1).
Tapson VF. Acute Pulmonary Embolism. N Engl J Med. 2008;358(10):1037-1052.
Wells PS. Use of a Clinical Model for Safe Management of Patients with Suspected Pulmonary Embolism. Ann Intern Med. 1998;129(12):997.
Prandoni P, Lensing AWA, Prins MH, Ciammaichella M, Perlati M, Mumoli N, et al. Prevalence of Pulmonary Embolism among Patients Hospitalized for Syncope. N Engl J Med. 2016;375(16):1524-1531.
Ozsu S, Oztuna F, Bulbul Y, Topbas M, Ozlu T, Kosucu P, Ozsu A. The role of risk factors in delayed diagnosis of pulmonary embolism. Am J Emerg Med. 2011;29(1):26-32.
UHLAND H, GOLDBERG LM. Pulmonary Embolism: A Commonly Missed Clinical Entity. Dis Chest. 1964;45(5):533-536.
Goldhaber SZ. Acute Pulmonary Embolism: Part I: Epidemiology, Pathophysiology, and Diagnosis. Circulation. 2003;108(22):2726-2729.
Mao Y, Wen S, Chen G, Zhang W, Ai Y, Yuan J. Management of intra-operative acute pulmonary embolism during general anesthesia: a case report. BMC Anesthesiol. 2017;17(1).

The authors declare no competing interests.

Download PDF

Version 1

posted

You are reading this latest preprint version

Intraoperative Pulmonary Embolism During General Anesthesia Diagnosed with Transesophageal Echocardiography: A Case Report

Status:

Version 1

Abstract

Figures

INTRODUCTION

CASE REPORT

DISCUSSION

CONCLUSION

Declarations

References

Additional Declarations

Status:

Version 1