Skip to main content


We’d like to understand how you use our websites in order to improve them. Register your interest.

Management of intra-operative acute pulmonary embolism during general anesthesia: a case report



Acute pulmonary embolism (APE) can be life-threatening. Early detection is even more difficult for patients under general anesthesia as common symptoms are not available and the pathophysiological course of intra-operative APE is influenced by procedures of surgery and anesthesia, which makes patients under general anesthesia a distinctive group.

Case presentation

We report a case of APE during orthopedic surgery under general anesthesia. A 64-year-old female with atrial fibrillation and surgical history of varicosity underwent total right hip replacement surgery under general anesthesia. No arterial or deep vein thrombosis (DVT) was found prior to the surgery, but APE still occurred intraoperatively. The sudden decrease in PETCO2 and increase in PaCO2 combined other clues raised the suspect of APE, which is further evidenced by transesophageal echocardiogram (TEE). Multidisciplinary consultation was started immediately. After discussion with the consultation team and communication with patient’s family members, anticoagulation therapy was started and IVC filter was placed to prevent PE recurrence. The patient went through the operation and discharged uneventfully 30 days later.


Pulmonary embolism is a rare and potentially high-risk perioperative situation, with a difficult diagnosis when occurs under anesthesia. The separation phenomenon of decrease in PETCO2 and increase in PaCO2 might be a useful and suggestive sign, enabling prompt management and therefore improving the prognosis.

Peer Review reports


Acute pulmonary embolism (APE) remains a significant medical problem, relating to more than 300,000 deaths per year in Europe [1]. Early detection and treatment are vital for a better prognosis [2]. Signs and symptoms such as dyspnea, chest pain, hemoptysis and syncope could be clues for APE detection [3, 4]. But they are not available for patients under general anesthesia, which increases the difficulty for early diagnosis and stresses the need for other indications. Moreover, the pathophysiologic course of intraoperative APE is affected by procedures of operation and anesthesia, which might be different from conscious patients with spontaneous respiration. The following report describes a case of APE during hip replacement surgery, that provides us with a meaningful phenomenon—an opposite trend in increased PaCO2 and decreased PETCO2—as an early sign of potential APE for patients undergoing general anesthesia and mechanical ventilation.

Case presentation

A 64-year-old, BMI 32.7 kg/m2, American Society of Anesesthesiolgists (ASA) physical status III, female was scheduled for right hip replacement because of bone fracture. She received a surgery for bilateral lower extremity varicose veins 8 years ago and recovered well. There is no past medical history of hypertension, diabetes mellitus or cerebrovascular diseases. Patient had no drug or food allergies, never smoked cigarettes or consumed alcohol.

Chest X-ray showed heart shadow enlargement (cardiothoracic ratio: 0.65) and slight pleural effusion left side. Echocardiogram showed bilateral atrial dilatation, atrial fibrillation, slight bicuspid and tricuspid regurgitation, right pulmonary mild hypertension (pulmonary arterial systolic pressure: 51 mmHg) and a decreased systolic function of left ventricular. ECG showed acceleration of ventricular rate, atrial fibrillation and T wave non specific changes. D-dimer was 2.517 μg/ml (normal: 0–0.3 μg/ml). Other laboratory assessments were within normal limits. Despite abnormal findings in pre-procedure tests, no uncomfortable symptoms were reported. She emphasized to be in good condition before the fracture that she could do Dama square dance for 2 h every day after supper. There were no complaints except for the pain due to bone fracture. She denied further examination or treatment and insisted on an operation for the fracture as soon as possible, as it reduced her life quality severely.

Therefore she was scheduled for surgery and transferred to the operating room 3 days after admission. Preoxygen and monitoring were performed, which showed BP 110/80 mmHg, HR 140 bpm and SpO2 98%. Considering her anxiety and tachycardia, 10 mg esmolol and 60 μg dexmedetomidine were given intravenously in 10 min. Soon the heart rate slowed down and stabled at 110 bpm. Arterio radialis puncture was performed for invasive blood pressure monitoring under 1% lidocaine local anesthesia. For anesthesia induction, midazolam (0.03 mg/kg), fentanyl (4 μg/kg), etomidate (0.25 mg/kg) and cisatracurium (0.2 mg/kg) were administered. After intubation, mechanical ventilation started with volume control model (RR:12 breaths per minute, tidal volume:6-8 ml/kg, PETCO2:35-45 mmHg). General anesthesia was maintained with sevoflurane (1%), propofol (4-10 mg/kg/h), remifentanil (0.1–0.2 μg/kg/min), cisatracurium (0.1 mg/kg/h) and dexmedetomidine (0.5 μg/kg/h). A central venous catheter was placed in the right internal jugular vein under ultrasonic guidance in case of mass transfusion and vasoactive drugs application intraoperatively. Patient was then placed in left lateral decubitus position and the operation began.

Approximately 1 h later, when the surgery was almost finished and the incision was closing, a sudden pronounced decrease in oxygen saturation (100%–66%) was noticed, along with gradually increased airway pressure(22-33cmH2O) and decrease in blood pressure (lowest to 89/60 mmHg). PETCO2 decreased from 34 mmHg to 22 mmHg. ECG showed rapid atrial fibrillation (heart rate 140-160 bpm). Auscultation revealed bilateral breath sounds. Central venous pressure (CVP) was assessed immediately with a value of 30cmH2O. Instant arterial blood gas analysis showed hypercapnia (Table 1). The opposite trend of PaCO2 and PETCO2, combined with other signs and medical history, indicated the possibility of APE. Transesophageal echocardiogram (TEE) was arranged at once, which showed enlargement of the right atrial, abnormal echoic area in pulmonary artery (considering thrombus) and pulmonary hypertension (pulmonary arterial systolic pressure: 77 mmHg) (Additional file 1: Movie S1).

Table 1 The arterial blood gas analysis of the patient

Additional file 1: Movie S1. A real-time TEE image revealed a mobile embolus in the PA. PA, pulmonary artery; Ao, aorta. (WMV 1mb)

Multidisciplinary consultation started simultaneously. Mechanical and manual ventilation were controlled alternately. Cedilanid (0.2 mg), phenylephrine (0.03–0.06 mg/kg/min), 5% NaHCO3 liquid (100 ml) and methylprednisolone (500 mg) were administered intravenously to maintain hemodynamic stability and improve internal environment. All fluids were limited to reduce the cardiac load. 11 min later, SpO2 increased to 95% and BP rose to 120/80 mmHg. A following systematic ultrasound examination revealed deep venous thrombosis, which was not found before the surgery and might be the source of pulmonary embolism. After discussion with surgical and respiratory consultation team and communication with the patient’s family members, low molecular weight heparin calcium(LMWHC) (6000 IU) was given and inferior vena cava (IVC) filter was implanted in DSA operating room. After surgery, the patient was transferred to ICU intubated. Patient recovered her consciousness 3 h later and extubated the next morning. Further treatment including anticoagulation, alleviation of pulmonary hypertension and atrial fibrillation therapy was continued. IVC filter was removed 20 days later. Her condition was improved and all vital signs maintained stable. The patient was discharged from hospital uneventfully one month later.


Here we described a case of intra-operative APE and reported a meaningful sign --“separation phenomenon” during general anesthesia, which means a decrease trend in PETCO2 and increase in PaCO2. This is different from conscious patients with incomplete obstruction of pulmonary artery, whose physiological dead space increases and total minute ventilation increases correspondingly. In these patients, PaCO2 is mostly lower than normal because of the compensatory mechanism. However, this mechanism does not work under general anesthesia and mechanical ventilation. Thus when APE occurred in patients with mechanical ventilation, PETCO2 does not actually reflect PaCO2 anymore. In fact, the difference of PaCO2 and PETCO2 could be a representative of dead space, which has been studied as a tool to monitor the effect of thrombolysis [5]. Beside dead space increase, low cardiac output and ventilation-perfusion mismatch also contribute to the hypoxemia and hypercapnia [6]. Though not pathognomonic, the separation phenomenon is still valuable. Just like chest pain and dyspnea, these symptoms are not specific, but in a similar context to our case, could be highly suggestive. PETCO2 is a routine monitoring under general anesthesia and arterial blood analysis is a quick bedside test. Thus we suggest strict monitoring of PETCO2 and arterial blood analysis especially when PETCO2 decreases without other reasons during general anesthesia. When the separation phenomenon occurred, PE should be taken into consideration.

We suspected venous thrombus that led to APE in this patient. First, she had a surgical history of varicosity. Although no thrombus was found before the surgery, it was a risk factor of pulmonary thromboembolism. Second, intraoperative TEE showed abnormal echoic area in pulmonary artery (considering thrombus) and the following systematic ultrasound examination revealed deep venous thrombosis. The most common cause of PE remains deep vein thrombosis [7]. Finally, anti-coagulation therapy was useful to improve the condition.

The initial clinical symptoms in this case could also suggest a pneumothorax. But there was no further evidence. Procedure of central venous of catheterization might be a cause for pneumothorax. But the process was guided by ultrasound without any abnormal sign. Also, instant intraoperative auscultation confirmed bilateral breath sounds.

Since it was a hip surgery, the intra-operative APE might also be caused by cement embolus. The known bone cement implantation syndrome (BCIS) is commonly caused by PE, which is characterized by a number of clinical features such as hypoxia, hypotension, cardiac arrhythmias and increased pulmonary vascular resistance. It usually occurs at one of these stages of surgical procedure including femoral reaming, acetabular or femoral cement implantation, insertion of the prosthesis or joint reduction [8]. However, in this case, the hemodynamic changes and hypoxia presented at none of these stages but at the end of operation, when the wound was closing. There are studies showing that cement embolic events are common and most patients tolerate well [9]. Even if BCIS occurs, there is no specific treatment at present [8]. To confirm the cause of APE might need further test, like computed tomography. It was not conducted in this case, which was a pity, considering the high cost and little effect on the treatment.

Combining all the clues, the most possible reason for the hemodynamic and respiratory changes in this case was pulmonary thromboembolism. The treatment requires rapid and accurate risk assessment. Thrombolytic treatment restores pulmonary perfusion more rapidly than anticoagulation alone, but it also carries a risk of major bleeding, including intracranial hemorrhage. And the increased age and presence of comorbidity have been associated with higher risk of hemorrhage [10]. Surgery is also a relative contraindication to thrombolysis. After discussion with the consultation team and communication with patient’s family members, anticoagulation therapy was started and IVC filter was placed to prevent PE recurrence. The patient finally discharged uneventfully.

The good clinical outcome could be predicted by the lactate value. Plasma lactate concentration is a sensitive marker of tissue hypoxia and persistent tissue hypoxia may cause irreversible cell injury which was associated with the adverse outcome in critically ill patients [11, 12]. Studies showed that plasma lactate was prognostic for short-term PE-related complications and high plasma lactate (≥2 mol/L) was associated with increased in-hospital mortality [13,14,15]. Lactate concentration in this case remained at a low level which might due to our fast detection and treatment. Thus tissue hypoperfusion was temporary and reversible.

Despite updated guidelines, PE remains an important clinical problem with a high mortality rate. Even with prophylaxis, it could still happen and sometimes appeared as an emergency [16]. A flow diagram specific to intra-operative APE might be a useful aid, especially for this infrequent and high-risk situation. Also, multidisciplinary cooperation is necessary to get the most appropriate treatment strategy.


Pulmonary embolism is a rare and potentially high-risk perioperative situation, with a difficult diagnosis when occurs under anesthesia. The separation phenomenon of decrease in PETCO2 and increase in PaCO2 might be a useful and suggestive sign, enabling prompt management and therefore improving the prognosis.



Acute pulmonary embolism


Central venous pressure


Deep vein thrombosis


Inferior vena cava


End-tidal CO2 pressure


Transesophageal echocardiogram


  1. 1.

    Cohen AT, Agnelli G, Anderson FA, Arcelus JI, Bergqvist D, Brecht JG, et al. Venous thromboembolism (VTE) in Europe. The number of VTE events and associated morbidity and mortality. Thromb Haemost. 2007;98(4):756–64.

    CAS  PubMed  Google Scholar 

  2. 2.

    He J, Cheng X, Gao M. Survey of diagnosis and treatment of acute pulmonary embolism in 21 hospitals in China. Zhonghua Yi Xue Za Zhi. 2001;81(24):1490–2.

    CAS  PubMed  Google Scholar 

  3. 3.

    Wells PS, Ginsberg JS, Anderson DR, Kearon C, Gent M, Turpie AG, et al. Use of a clinical model for safe management of patients with suspected pulmonary embolism. Ann Intern Med. 1998;129(12):997–1005.

    CAS  Article  PubMed  Google Scholar 

  4. 4.

    Prandoni P, Lensing AW, 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):1524–31.

    Article  PubMed  Google Scholar 

  5. 5.

    Wiegand UK, Kurowski V, Giannitsis E, Katus HA, Djonlagic H. Effectiveness of end-tidal carbon dioxide tension for monitoring thrombolytic therapy in acute pulmonary embolism. Crit Care Med. 2000;28(11):3588–92.

    CAS  Article  PubMed  Google Scholar 

  6. 6.

    Goldhaber SZ, Elliott CG. Acute pulmonary embolism: part I: epidemiology, pathophysiology, and diagnosis. Circulation. 2003;108(22):2726–9.

    Article  PubMed  Google Scholar 

  7. 7.

    Konstantinides SV, Torbicki A, Agnelli G, Danchin N, Fitzmaurice D, Galie N, et al. 2014 ESC guidelines on the diagnosis and management of acute pulmonary embolism. Eur Heart J. 2014;35(43):3033–69. 3069a

    CAS  Article  PubMed  Google Scholar 

  8. 8.

    Donaldson AJ, Thomson HE, Harper NJ, Kenny NW. Bone cement implantation syndrome. Br J Anaesth. 2009;102(1):12–22.

    CAS  Article  PubMed  Google Scholar 

  9. 9.

    Ereth MH, Weber JG, Abel MD, Lennon RL, Lewallen DG, Ilstrup DM, et al. Cemented versus noncemented total hip arthroplasty--embolism, hemodynamics, and intrapulmonary shunting. Mayo Clin Proc. 1992;67(11):1066–74.

    CAS  Article  PubMed  Google Scholar 

  10. 10.

    Mikkola KM, Patel SR, Parker JA, Grodstein F, Goldhaber SZ. Increasing age is a major risk factor for hemorrhagic complications after pulmonary embolism thrombolysis. Am Heart J. 1997;134(1):69–72.

    CAS  Article  PubMed  Google Scholar 

  11. 11.

    Bakker J, Nijsten MW, Jansen TC. Clinical use of lactate monitoring in critically ill patients. Ann Intensive Care. 2013;3(1):12.

    Article  PubMed  PubMed Central  Google Scholar 

  12. 12.

    Shoemaker WC, Appel PL, Kram HB. Tissue oxygen debt as a determinant of lethal and nonlethal postoperative organ failure. Crit Care Med. 1988;16(11):1117–20.

    CAS  Article  PubMed  Google Scholar 

  13. 13.

    Vanni S, Viviani G, Baioni M, Pepe G, Nazerian P, Socci F, et al. Prognostic value of plasma lactate levels among patients with acute pulmonary embolism: the thrombo-embolism lactate outcome study. Ann Emerg Med. 2013;61(3):330–8.

    Article  PubMed  Google Scholar 

  14. 14.

    Vanni S, Jimenez D, Nazerian P, Morello F, Parisi M, Daghini E, et al. Short-term clinical outcome of normotensive patients with acute PE and high plasma lactate. Thorax. 2015;70(4):333–8.

    Article  PubMed  Google Scholar 

  15. 15.

    Vanni S, Socci F, Pepe G, Nazerian P, Viviani G, Baioni M, et al. High plasma lactate levels are associated with increased risk of in-hospital mortality in patients with pulmonary embolism. Acad Emerg Med. 2011;18(8):830–5.

    Article  PubMed  Google Scholar 

  16. 16.

    Goldhaber SZ, Visani L, De Rosa M. Acute pulmonary embolism: clinical outcomes in the international cooperative pulmonary embolism registry (ICOPER). Lancet. 1999;353(9162):1386–9.

    CAS  Article  PubMed  Google Scholar 

Download references


We would like to thank Professor Yanli Ma, Bin Li, Yong Wang and Liwei Li for their help in the rescue.



Availability of data and materials

All data and materials described in the manuscript will be freely available to any scientist wishing to use them for non-commercial purposes. Raw data are not available as all are in the patient electronic medical record. Please consider the edited data in the case report.

Authors’ contributions

YM and SW contributed equally to this paper: Preparation of the manuscript. GC, WZ and YA participated in patient care. JY involved in the case and drafted the manuscript. All authors read and approved the final manuscript.

Competing interests

The authors declare that they have no competing interests.

Consent for publication

Written informed consent was obtained from the patient for publication of this case report. A copy of the written consent is available for review by the Editor of this journal.

Ethics approval and consent to participate

Not applicable.

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Author information



Corresponding author

Correspondence to Jingjing Yuan.

Rights and permissions

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (, which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Mao, Y., Wen, S., Chen, G. et al. Management of intra-operative acute pulmonary embolism during general anesthesia: a case report. BMC Anesthesiol 17, 67 (2017).

Download citation


  • Intra-operation
  • Acute pulmonary embolism
  • General anesthesia
  • Multidisciplinary consultation