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 Table of Contents  
CASE REPORT
Year : 2016  |  Volume : 4  |  Issue : 2  |  Page : 67-69

Thrombolysis for postoperative Submassive pulmonary Embolism


Department of Cardiology, Sree Uthram Thirunal Royal Hospital, Ulloor, Medical College (PO), Tiruvananthapuram, Kerala, India

Date of Web Publication6-Jun-2016

Correspondence Address:
Biji Soman
Department of Cardiology, Sree Uthram Thirunal Royal Hospital, Ulloor, Medical College (PO), Tiruvananthapuram - 695 011, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2321-449X.183524

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  Abstract 

Pulmonary embolism (PE) is the most preventable cause of inhospital death. Although safe and effective, thrombolytic therapy is relatively contraindicated within 10 days of major surgery due to the risk of bleeding. Our patient developed submassive PE, within 48 h of surgery and had catheter-directed thrombolysis with Streptokinase (STK) injection successfully, without any bleeding complications. This case demonstrates that thrombolysis may be safely and effectively done in postoperative patients. In such scenarios, where the therapy is relatively contraindicated, the decision whether to thrombolyse or not, must be multidisciplinary, giving utmost importance to the patient's best interest and to ensure that no single individual is denied potentially life-saving therapy.

Keywords: Catheter-directed thrombolysis, postoperative, complication, submassive pulmonary embolism (PE)


How to cite this article:
Soman B. Thrombolysis for postoperative Submassive pulmonary Embolism. Heart India 2016;4:67-9

How to cite this URL:
Soman B. Thrombolysis for postoperative Submassive pulmonary Embolism. Heart India [serial online] 2016 [cited 2021 Jan 18];4:67-9. Available from: https://www.heartindia.net/text.asp?2016/4/2/67/183524


  Introduction Top


Pulmonary embolism (PE) and deep vein thrombosis (DVT) constitute one of the big three cardiovascular killers along with myocardial infarction and stroke. The case fatality for PE, approximately 15%, exceeds the mortality rate for acute myocardial infarction. PE has been known as a great masquerader because it mimics other illnesses such as pneumonia and congestive heart failure. Once the diagnosis of acute PE is established, rapid and precise risk stratification is of paramount importance.

Normotensive patients with acute PE and evidence of right ventricular (RV) dysfunction are classified as having submassive PE. [1] Although advanced therapy with fibrinolysis is considered a life-saving intervention in massive PE, it remains controversial in patients with submassive PE. [2]


  Case report Top


We report a case of 70-year-old lady, with high body mass index (BMI), history of hypothyroidism on regular treatment. She underwent laparoscopic cholecystectomy under general anesthesia. After 2 days, while in the ward, she developed sudden onset dyspnea, tachypnea, and tachycardia. The patient was hemodynamically stable and O 2 saturation in room air was 85%. Investigation revealed elevated cardiac troponin 480 ng/mL [normal responders (NR) 0-60 ng/mL], D dimer: 500 ng/mL (NR <500 ng/mL), N-terminal of the prohormone brain natriuretic peptide (pro NT BNP): 15,600 pg/mL (NR <500 pg/mL). A 12-lead electrocardiogram (ECG) revealed: S1 Q3 T3, T inversion in precordial chest leads.

Bedside screening of two-dimensional (2D) transthoracic echocardiogram showed enlarged right atrium (RA), right ventricle (RV), hypokinesia of RV free wall, interventricular septal flattening, and paradoxical motion toward the left ventricle (LV), moderate tricuspid regurgitation (TR), estimated pulmonary artery systolic pressure (PASP) of 70 mmHg, inferior vena cava (IVC) >2 cm, with loss of inspiratory collapse. Acute PE was suspected, as the patient was hemodynamically stable and the risk of surgical site bleeding was high. Heparin injection as continuous intravenous infusion at a low dose of 500 U/h was started, while waiting for computed tomography pulmonary angiography (CTPA).

CTPA showed filling defects in both right and left distal main pulmonary artery with the evidence of RV strain, suggestive of acute submassive PE [Figure 1] and [Figure 2]. Catheter-directed intrapulmonary thrombolysis was planned. Pulmonary artery catheterization revealed high pulmonary artery pressure (PAP): 65/30 mmHg. Streptokinase (STK) injection was started at the rate of 1 lakh U/h. Clinically, there was not much improvement after 24 h, hence, STK injection infusion rate was increased to 1.5 lakh U/h. STK injection was stopped after 48 h, as the patient was symptomatically better and her O 2 saturation in room air had returned to an acceptable level. Heparin injection continued at 5,000U Q8H s/c and oral anticoagulants were started.

Follow-up CTPA on the 10th day showed only residual partial thrombus in the segmental arteries,[Figure 3] with no evidence of RV strain. The patient was discharged with advice to continue with oral anticoagulants and have regular outpatient follow-up.
Figure 1: Axial thin contrast-enhanced computed tomography (CECT) sections of the pulmonary arteries showing thrombus in the right and left distal main pulmonary arteries, bilateral lobar, and segmental arteries

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Figure 2: Computed tomography of the chest with contrast-enhancement showing right ventricular strain with RV: LV ratio of >1, bowing of interventricular septum (IVS) to LV

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Figure 3: Follow-up contrast-enhanced computed tomography (CECT) sections of the pulmonary arteries showing resolution of clots from the right and left main pulmonary arteries, with residual partial thrombus in the lobar and segmental arteries

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  Discussion Top


Acute PE represents a spectrum of clinical syndromes with a variety of prognostic implications. Patients with acute PE who have normal systemic arterial pressure and preserved RV function have an excellent prognosis with therapeutic anticoagulation alone. In contrast, patients with massive PE present with syncope, systemic arterial hypotension, cardiogenic shock, or cardiac arrest and have an increased risk of adverse outcomes, including death. [3]

Our patient, even though hemodynamically stable, showed evidence of RV dysfunction as cardiac biomarkers; both cardiac troponin I and pro NT BNP were elevated. ECG showed T inversion in precordial chest leads and combination of an S wave in lead I, Q wave in lead III, and T-wave inversion in lead III (S1Q3T3) signify RV strain. Transthoracic echocardiogram showed characteristic echocardiographic findings seen in patients with submassive PE.

Such patients may initially appear clinically stable. However, even if they are normotensive initially, despite adequate heparin anticoagulation, patients with RV hypokinesis are at a high risk of recurrent PE and clinical deterioration; [4],[5],[6] these patients should be treated more aggressively with thrombolytic therapy. As per the guidelines of the American College of Chest Physicians, the use of thrombolytic therapy is recommended for patients with evidence of hemodynamic compromise, unless there is major contraindication owing to bleeding risk (Grade1 B) and in selected high risk patients without hypotension who are judged to have a low risk of bleeding,(Grade 2 B). [7]

Our patient was first anticoagulated with intravenous unfractionated heparin. Intravenous unfractionated heparin offers the advantage of immediate discontinuation and rapid reversal in the event of bleeding complications. Once embolism was confirmed, catheter-directed intrapulmonary thrombolysis with STK was started. Considering the early postoperative state, STK was given into the pulmonary artery at a lower dose, hoping to reduce bleeding complications. Recurrent showers of embolism were suspected, as the patient continued to be tachypneic and had a drop in O 2 saturation; hence, the dose of STK was increased and infusion continued for a further 24 h.

Thrombolysis in high risk PE patients remains controversial. [8] The fear is that, the risk of bleeding complications, especially intracranial hemorrhage, outweighs any potential benefit. Women may not gain as much benefit from PE thrombolysis as men do.

However, once it occurs, it is difficult to diagnose, expensive to treat, and potentially lethal despite therapy. Therefore, venous thromboembolism (VTE) prevention is of paramount importance. Low-fixed-dose anticoagulant prophylaxis is effective. [9]


  Conclusion Top


To conclude, acute PE is the third most common cause of death among hospitalized patients; [10] acute PE should be suspected in postoperative patients who develop a sudden onset of shortness of breath. Catheter-directed thrombolysis with low-dose STK injection may be considered in postoperative submassive PE, on who continued intravenous heparin has not produced the desired result. In addition, we would like to emphasize, that the treatment strategy for each patient should be individualized, keeping in view the risks and benefits of each treatment option available. If not diagnosed and treated promptly and aggressively, PE could be fatal.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Sanchez O, Trinquart L, Colombet I, Durieux P, Huisman MV, Chatellier G, et al. Prognostic value of right ventricular dysfunction in patients with haemodynamically stable pulmonary embolism: A systematic review. Eur Heart J 2008;29:1569-77.  Back to cited text no. 1
    
2.
Piazza G, Goldhaber SZ. Acute pulmonary embolism: Part II: Treatment and prophylaxis. Circulation 2006;114:e42-7.  Back to cited text no. 2
    
3.
Kucher N, Goldhaber SZ. Management of massive pulmonary embolism. Circulation 2005;112:e28-32.  Back to cited text no. 3
    
4.
Goldhaber SZ, Haire WD, Feldstein ML, Miller M, Toltzis R, Smith JL, et al. Alteplase versus heparin in acute pulmonary embolism: Randomised trial assessing right ventricular function and pulmonary perfusion. Lancet 1993;341:507-11.  Back to cited text no. 4
    
5.
Konstantinides S, Geibel A, Olschewski M, Heinrich F, Grosser K, Rauber K, et al. Association between thrombolytic treatment and the prognosis of haemodynamically stable patients with major pulmonary embolism: Results of multicenter registry. Circulation 1997;96:882-8.  Back to cited text no. 5
    
6.
Goldhaber SZ, Visani L, De Rosa M. Acute pulmonary embolism: Clinical outcomes in the international cooperative pulmonary embolism registry (ICOPER). Lancet 1999;353:1386-9.  Back to cited text no. 6
    
7.
Kearon C, Kahn SR, Agnelli G, Goldhaber S, Raskob GE, Comerota AJ; American College of Chest Physicians. Antithrombotic therapy for venous thromboembolic disease: Amercan College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8 th Edition). Chest 2008;133(Suppl):454-545S.  Back to cited text no. 7
    
8.
Todd JL, Tapson VF. Thrombolytic therapy for acute pulmonary embolism: A critical appraisal. Chest 2009;135:1321-9.  Back to cited text no. 8
    
9.
Wein L, Wein S, Haas SJ, Shaw J, Krum H. Pharmacological venous thromboembolism prophylaxis in hospitalised medical patients: A meta-analysis of ramdomised controlled trials. Arch Intern Med 2007;167:1476-86.  Back to cited text no. 9
    
10.
Pulido T, Aranda A, Zevallos MA, Bautista E, Martínez-Guerra ML, Santos LE, et al. Pulmonary embolism as a cause of death in patients with heart disease: An autopsy study. Chest 2006;129:1282-7.  Back to cited text no. 10
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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