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Year : 2018  |  Volume : 4  |  Issue : 2  |  Page : 112-115

A case of successful management of perioperative pulmonary embolism

Department of Anaesthesiology and Critical Care, Pondicherry Institute of Medical Sciences, Puducherry, India

Date of Submission12-May-2018
Date of Acceptance02-Oct-2018
Date of Web Publication13-Dec-2018

Correspondence Address:
Sivakumar Segaran
Department of Anaesthesiology and Critical Care, Pondicherry Institute of Medical Sciences, Kalapet, Puducherry
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jcrsm.jcrsm_17_18

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Acute pulmonary embolism (PE) is a relatively common complication after major orthopedic surgeries with a high mortality rate. We present a case of L4–L5 disc prolapse with radiculopathy posted for spinal instrumentation and fusion surgery who developed PE perioperatively. It was diagnosed initially with point-of-care echocardiography and confirmed with computed tomography pulmonary angiography. The patient was thrombolyzed with streptokinase, following which she developed bleeding from the surgical site which was managed conservatively with blood transfusions. The patient recovered well and discharged after a week. The management of PE tests the skills of the anesthetist with respect to detection and rapid hemodynamic management.

Keywords: Echocardiography, pulmonary embolism, right ventricular dysfunction

How to cite this article:
Segaran S, Arish B T, Mohan A, Jayaraman V, Ramachandran A. A case of successful management of perioperative pulmonary embolism. J Curr Res Sci Med 2018;4:112-5

How to cite this URL:
Segaran S, Arish B T, Mohan A, Jayaraman V, Ramachandran A. A case of successful management of perioperative pulmonary embolism. J Curr Res Sci Med [serial online] 2018 [cited 2022 Oct 6];4:112-5. Available from: https://www.jcrsmed.org/text.asp?2018/4/2/112/247487

  Introduction Top

Pulmonary embolism (PE), a life-threatening complication, represents a major postoperative complication.[1] Surgery increases the risk of PE by five folds.[2] The incidence of PE ranges from 0.7% to 30% after all orthopedic surgical procedures.[3] The pathogenesis involves the interplay of an acute inflammatory reaction triggered by vascular endothelial injury,[4] hypercoagulability,[5] and venous stasis. Anesthesiologists may find themselves responsible for the diagnosis and management of this sometimes fatal disorder. The diagnosis is often one of the exclusion and may be obscured in the perioperative setting given the circumstances that surround this pathology. During surgery, PE often first presents with hemodynamic instability and follows a rapid course, leading to death within several hours. Prompt diagnosis and management may reduce the morbidity and mortality.

  Case Report Top

A 47-year-old female patient who was ambulatory presented with L4–L5 intervertebral disc prolapse with bilateral (B/L) radiculopathy posted for spinal fusion surgery. She is a menstruating female with regular cycles of 5/28 cycles and was not on any hormonal pills. Her preoperative investigations such as complete blood count, renal function test, electrocardiogram (ECG), and echocardiography (Echo) were within normal limits, except she is hypertensive for 6 years on regular medications. She weighed 65 kg with a height of 165 cm with body mass index of 23.9 kg/m2. On the day of surgery in the operating room, intravenous (iv) access was secured with 16G Venflon™ in the left hand, and standard anesthesia monitors such as ECG, noninvasive blood pressure, pulse oximetry, and capnography were connected. Standard anesthesia protocol for general anesthesia with endotracheal intubation was provided. The patient was positioned prone and pressure points were padded adequately. Before the end of the surgery, injection paracetamol 1 g iv was given. The entire intraoperative period was uneventful. The total duration of surgery was 150 min. At the end of the surgery, the patient was positioned supine for extubation; at that time, the patient developed ventricular bigeminy progressing to nonsustainable monomorphic ventricular tachycardia which was treated with injection amiodarone 150 mg bolus over 15 min. During that time, there were transient desaturation and hypotension which were improved with 100% oxygen and inotropes (injection dopamine 5 mcg/kg/min), respectively. Once the patient became hemodynamically stable and awake, the patient was extubated after reversing neuromuscular blockade with injection neostigmine and glycopyrrolate. It took almost 1 h to stabilize the patient hemodynamically before planning for extubation. After extubation, the patient complained of substernal chest pain but remained hemodynamically stable. On high suspicion of perioperative myocardial infarction, cardiac enzymes were sent and emergency cardiologist opinion was obtained. Echo showed right atrial and right ventricular (RV) dilatation with hypokinesia and pulmonary artery (PA) pressure of 50 mmHg, although the preoperative echo was normal. ECG was not available as we did not take a copy of it. On high suspicion of PE, injection heparin 5000 units iv was given after discussion with the surgeon. To confirm the diagnosis of PE, computed tomography (CT) pulmonary angiography was taken which showed filling defect in both the right and left PAs which confirmed the diagnosis [Figure 1] and [Figure 2]. B/L venography was also done to know the source of emboli, but there was no evidence of any deep-vein thrombosis. Now, the choice of systemic thrombolysis versus systemic anticoagulation with unfractionated heparin (UFH) as the treatment of choice has been largely debated by surgeons, cardiologists, and intensivists. Because of the acute onset with RV dysfunction and a high risk for developing recurrent PE due to postoperative state, after weighing the risks and benefits, we decided to go with systemic thrombolysis with low-dose injection streptokinase 1.5 million units over 2 h. The thrombolysis was started within 3 hrs of the onset of symptoms. After thrombolysis, the patient developed mild bleeding through the drains (~500 ml) which was conservatively managed with blood transfusions (2 units of packed cell volume), but there were no signs of spinal/epidural hematoma formation. The patient recovered well and discharged after a week with oral anticoagulants (tablet warfarin 5 mg od) to maintain international normalized ratio (INR) around 2.0. Follow-up echo was not done as the patient recovered well, but if we would have done the echo, we would have known whether thrombolysis has reversed the RV dysfunction. The patient was also evaluated for thrombotic disorders during her hospital stay and the reports were negative for antinuclear antibody, antineutrophil cytoplasmic antibody, and lupus anticoagulant. Homocysteine levels were also within normal limits. Activated partial thromboplastin time was decreased when compared to control, and prothrombin time and INR were normal. D-Dimer was positive. She was followed up regularly for monitoring coagulation parameters and for any possible complications.
Figure 1: Computed tomography pulmonary angiography showing thrombus in the pulmonary artery

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Figure 2: Computed tomography pulmonary angiography showing thrombus in the right main pulmonary artery

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  Discussion Top

PE is a common postoperative complication with a varying symptomatology spectrum. The onset of symptoms may be sudden as in this patient or gradual. The most common signs and symptoms are usually nonspecific. ECG findings include ST-segment and T-wave abnormalities, sinus tachycardia, right bundle branch block, and S1Q3T3 pattern. Atrial fibrillation/flutter, heart blocks, and ventricular dysrhythmias are present in <5%–10% of patients. The American Heart Association defines massive PE as an acute event coupled with sustained hypotension (systolic blood pressure <90 mmHg for >15 min or requiring inotropic support). Submassive PE is hemodynamically stable PE with right ventricular dysfunction. These patients are still at a heightened risk for adverse events and require emergent interventions to decrease clot burden and improve mortality.[6] Low-risk PE patients are those with normal hemodynamics and no signs of RV dysfunction.

To establish a definitive diagnosis in the perioperative setting with basic investigations such as ECG, chest radiography and arterial blood gas analysis are very unlikely. Echo is highly useful in the recognition of PE and also to assess the severity of the PE and the patient's response to therapy.[7] The echocardiographic evidence of PA obstruction (RV dysfunction, moderate-to-severe tricuspid regurgitation, and leftward bowing of the interatrial septum) may be helpful in supporting a diagnosis of PE. CT pulmonary angiography is the gold standard for PE, as it not only assesses clot burden but also helps to identify patients with RV enlargement who are at an increased risk of early death. Treatment modalities for acute massive PE include anticoagulation, thrombolysis, inferior vena cava filters, and open surgical embolectomy. As soon as massive PE is suspected, anticoagulation with high-dose UFH should be started with a bolus dose followed by infusion along with simultaneous hemodynamic support with fluid, inotropes, vasopressors, etc. Thrombolytic agents such as alteplase, although recommended as the first-line treatment for massive PE, may cause major bleeding complications. Open surgical embolectomy is indicated in patients with contraindications to thrombolytic therapy.

Our patient had the onset of symptoms at the time of extubation which made the diagnosis of PE very difficult because of hemodynamic fluctuations that coincided with the extubation response. This patient presented with ventricular dysrhythmias, which is an uncommon presentation of PE. Patients with PE should be judged unstable if they present with RV hypokinesis by echocardiogram, even in the presence of a normal systemic arterial pressure.[8] Despite adequate heparin anticoagulation, patients with RV hypokinesis are at a high risk of recurrent PE and clinical deterioration, even if they are normotensive.[9],[10],[11] Such patients therefore are prime candidates for more aggressive treatment with thrombolytic therapy or mechanical intervention. Hence, pulmonary angiography was done to confirm the diagnosis and then treated with thrombolysis. However, the choice of thrombolysis in submassive PE[12],[13],[14] should be done on a case-by-case basis depending on the patient's co-morbidities and hemodynamic status. We present this case because of the rare incidence of perioperative PE and unusual presentation of ventricular arrhythmias in the perioperative setting.

  Conclusion Top

PE is relatively a common complication after orthopedic procedures, but to diagnose perioperative PE, one should have a high index of suspicion with adequate clinical judgment. PE should be included in the differential diagnosis of perioperative hypoxemia, hypotension, tachycardia, or acute reduction in end-tidal CO2. Even in massive embolism with shock, the outcome can be favorable with timely aggressive management. Patients who appear to be deceptively hemodynamically stable after initial resuscitation are at risk of deterioration if there is evidence of RV hypokinesis by Echo and require aggressive primary therapy with thrombolysis.


The authors would like to thank:

  1. Prof. Ranjan RV DA, DNB (Anaesthesia), Professor, Department of Anaesthesiology, Pondicherry Institute of Medical Sciences (PIMS)
  2. Prof. Mark Christopher DM (Cardiology), Professor, Department of Cardiology, PIMS
  3. Prof. Jayakumar MS (Orthopaedics), Professor, Department of Orthopaedics, PIMS
  4. Dr. Yuvraj MS (Orthopaedics), Assistant Professor, Department of Orthopaedics, PIMS.


Written informed consent was obtained from the patient for publication of the case report and accompanying images.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initial will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Idiz M, Konuralp C, Ates M. Under diagnosis of pulmonary embolism: A recurrent nightmare for surgeons. Eastern J Med 2003;8:1-6.  Back to cited text no. 1
Geerts WH, Bergqvist D, Pineo GF, Heit JA, Samama CM, Lassen MR, et al. Prevention of venous thromboembolism: American college of chest physicians evidence-based clinical practice guidelines (8th edition). Chest 2008;133:381S-453S.  Back to cited text no. 2
Arcelus JI, Kudrna JC, Caprini JA. Venous thromboembolism following major orthopedic surgery: What is the risk after discharge? Orthopedics 2006;29:506-16.  Back to cited text no. 3
Desciak MC, Martin DE. Perioperative pulmonary embolism: Diagnosis and anesthetic management. J Clin Anesth 2011;23:153-65.  Back to cited text no. 4
Collins GJ Jr., Barber JA, Zajtchuk R, Vanek D, Malogne LA. The effects of operative stress on the coagulation profile. Am J Surg 1977;133:612-6.  Back to cited text no. 5
Jaff MR, McMurtry MS, Archer SL, Cushman M, Goldenberg N, Goldhaber SZ, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: A scientific statement from the American heart association. Circulation 2011;123:1788-830.  Back to cited text no. 6
McConnell MV, Solomon SD, Rayan ME, Come PC, Goldhaber SZ, Lee RT, et al. Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism. Am J Cardiol 1996;78:469-73.  Back to cited text no. 7
Nass N, McConnell MV, Goldhaber SZ, Chyu S, Solomon SD. Recovery of regional right ventricular function after thrombolysis for pulmonary embolism. Am J Cardiol 1999;83:804-6, A10.  Back to cited text no. 8
Goldhaber SZ, Haire WD, Feldstein ML, Miller M, Toltzis R, Smith JL, et al. Alteplase vs heparin in acute pulmonary embolism: Randomised trial assessing right-ventricular function and pulmonary perfusion. Lancet 1993;341:507-11.  Back to cited text no. 9
Konstantinides S, Geibel A, Olschewski M, Heinrich F, Grosser K, Rauber K, et al. Association between thrombolytic treatment and the prognosis of hemodynamically stable patients with major pulmonary embolism: Results of a multicenter registry. Circulation 1997;96:882-8.  Back to cited text no. 10
Martin C, Sobolewski K, Bridgeman P, Boutsikaris D. Systemic thrombolysis for pulmonary embolism: A Review. P T 2016;41:770-5.  Back to cited text no. 11
Konstantinides S. Should thrombolytic therapy be used in patients with pulmonary embolism? Am J Cardiovasc Drugs 2004;4:69-74.  Back to cited text no. 12
Chen H, Ren C, Chen H. Thrombolysis versus anticoagulation for the initial treatment of moderate pulmonary embolism: A meta-analysis of randomized controlled trials. Respir Care 2014;59:1880-7.  Back to cited text no. 13
Sadeghi HA, Heidarali M, Faraji F, Ghadrdoost B, Shojaeifard M. Outcome of sub-massive pulmonary thromboemboli in patients who received thrombolytic and or non-thrombolytic therapy. Res Cardiovasc Med 2016;5:e29638.  Back to cited text no. 14
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  [Figure 1], [Figure 2]


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