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 Table of Contents  
INTERESTING CASE REPORT
Year : 2022  |  Volume : 6  |  Issue : 2  |  Page : 138-141

Intracardiac Thrombus in Community-Acquired Klebsiella pneumonia – An Unprecedented Complication


1 Department of Cardiology, Dayanand Medical College, Ludhiana, India
2 Department of Medicine, Dayanand Medical College, Ludhiana, Punjab, India

Date of Submission01-Aug-2021
Date of Acceptance12-Sep-2021
Date of Web Publication09-Dec-2021

Correspondence Address:
Dr. Ashish Kumar
Hero DMC Heart Institute, Ludhiana, Punjab
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jiae.jiae_46_21

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  Abstract 

Left ventricular thrombi commonly occur in the presence of left ventricular systolic dysfunction. Their occurrence in the presence of preserved left ventricular systolic function is extremely rare. Here we present a case of a diabetic lady with community acquired Klebsiella pneumonia who also had large intraventricular thrombi which were managed conservatively.

Keywords: Klebsiella pneumonia, left ventricular thrombus, left ventricular masses, intracardiac thrombi


How to cite this article:
Kumar A, Tandon R, Mohan B, Jain NP. Intracardiac Thrombus in Community-Acquired Klebsiella pneumonia – An Unprecedented Complication. J Indian Acad Echocardiogr Cardiovasc Imaging 2022;6:138-41

How to cite this URL:
Kumar A, Tandon R, Mohan B, Jain NP. Intracardiac Thrombus in Community-Acquired Klebsiella pneumonia – An Unprecedented Complication. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2022 [cited 2022 Oct 3];6:138-41. Available from: https://jiaecho.org/text.asp?2022/6/2/138/332115


  Introduction Top


The spectrum of disease caused by community acquired Klebsiella pneumonia has shown geographical differences in the past decade including preponderance of severe invasive disease like liver abscess, meningitis or endopthalmitis especially in patients with diabetes mellitus.[1] Intracardiac left ventricular (LV) thrombus formation in the absence of LV systolic dysfunction or regional wall motion abnormalities has never been reported in these subsets of patients.[2] We present one such case here.


  Case Report Top


A 55-year-old lady with diabetes mellitus presented to our hospital with acute febrile illness of 10 days duration and dyspnea for 3 days. On general physical examination, the patient was febrile (temperature 100.3°F) with pulse rate of 108 beats/min and blood pressure 120/70 mmHg. Cardiac examination revealed normal heart sounds, no murmur. Respiratory system examination revealed dull percussion note, and reduced intensity of breath sounds with crepitations at the right scapular region. Laboratory investigations showed hemoglobin: 9.5 g/dL, hematocrit: 30%, raised white blood cell count (15,000 cells/mm3), normal absolute eosinophil count (100 cells/mm3) and platelet count (233,000 cells/mm3), raised erythrocyte sedimentation rate (80 mm at 1 h), and markedly elevated random blood sugar: 503 mg/dL. Chest X-ray posteroanterior view [Figure 1] revealed a well-circumscribed cavitary homogenous opacity in the right upper and mid-zone. The patient was started on empirical antibiotic therapy. On the third day of hospital stay, she complained of worsening breathlessness. Possibility of acute pulmonary edema or pulmonary embolism was considered. Electrocardiogram revealed sinus tachycardia with no significant ST-T wave changes. Repeat chest X-ray didn't show any worsening of pneumonia or its related complication. Urgent transthoracic echocardiogram [Figure 2] and [Video 1] and [Video 2] revealed mild LV systolic dysfunction (ejection fraction of 48%) with two large mobile masses (4–5 cm in size) in the LV, one spindle-shaped attached to the apex and the other polypoidal shaped attached to the anterior septum with echogenicity comparable to endocardium (suggestive of thrombus). For further evaluation of LV masses, transesophageal echocardiography was done which again showed mildly impaired LV systolic function and two large intraventricular masses suggestive of thrombi [Figure 3] and [Video 3] and [Video 4]. The patient was started on low molecular weight heparin. In view of documented LV thrombi, the possibility of concurrent right ventricular thrombi leading to pulmonary embolism could not be ruled out. Therefore, in order to evaluate the disproportionate dyspnea, contrast-enhanced computed tomography [Figure 4] of the thorax was done that revealed cavitary pneumonia in the posterior segment of the right upper lobe (“bulging fissure sign”) with left pulmonary artery lobar segment thrombus [Figure 5], and small localized splenic infarct [Figure 6]. The typical radiological appearance of this lobar consolidation suggested the possible etiology as Klebsiella pneumoniae, Streptococcus pneumoniae, Staphylococcus aureus, Pseudomonas aeruginosa, or less likely, Legionella pneumophila, or bronchoalveolar carcinoma. Fine-needle aspiration cytology of the lung lesion was inconclusive (only hemorrhagic cells seen no evidence of malignancy). Mantoux test was negative at 72 h. Meanwhile, three sets of blood cultures came positive for K. pneumoniae. Antibiotics were changed according to sensitivity results. After reviewing the clinical presentation and investigations, the diagnosis of Klebsiella septicemia secondary to pneumonia with multiple LV thrombi and pulmonary embolism was made. The patient received 4 days of conventional heparin followed by oral anticoagulants. After 6 days of treatment, a repeat echocardiogram showed normal biventricular systolic function, but the LV thrombi were present. Overall, the patient stabilized after 3rd week of therapy. Radiological resolution [Figure 7] of consolidation was achieved at 6 weeks, while intraventricular thrombi [Figure 8] and [Video 5] and [Video 6] resolved after 12 weeks of oral anticoagulant treatment. The patient is planned to be continued for at least 6 months on oral anticoagulants.
Figure 1: Chest X-ray posteroanterior view showing well-defined homogenous opacity in the right upper zone consistent with consolidation

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Figure 2: Transthoracic echocardiography shows well-defined masses in the the left ventricular cavity consistent with thrombi (arrows)

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Figure 3: Transesophageal echocardiography shows two large intraventricular masses

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Figure 4: Contrast-enhanced computed tomography of the thorax shows well-defined cavitary lesion (red arrow)

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Figure 5: Contrast-enhanced computed tomography of the thorax showing round-shaped clot in a branch of left pulmonary artery (red arrow)

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Figure 6: Contrast-enhanced computed tomography of the abdomen showing splenic infarct (red arrow)

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Figure 7: Chest X-ray posteroanterior view (follow -up) showing complete resolution of consolidation

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Figure 8: Follow-up transthoracic echocardiography shows complete resolution of thrombi after treatment

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[Additional file 1]

Video 1: Transthoracic echocardiography in the apical four-chamber view showing well-defined masses in the left ventricle consistent with mobile thrombi.

[Additional file 2]

Video 2: Transthoracic echocardiography in the parasternal long-axis view showing well-defined masses in the left ventricle consistent with mobile thrombus.

[Additional file 3]

Video 3: Transesophageal echocardiography in the mid-esophageal four-chamber view shows mildly impaired left ventricular systolic function and two large intraventricular thrombi.

[Additional file 4]

Video 4: Transesophageal echocardiography in the mid-esophageal two-chamber view showing two large intraventricular thrombi.

[Additional file 5]

Video 5: Follow-up transthoracic echocardiography in the apical four-chamber view shows complete resolution of left ventricular thrombi after treatment

[Additional file 6]

Video 6: Follow-up transthoracic echocardiography in the parasternal long-axis view shows complete resolution of left ventricular thrombi after treatment


  Discussion Top


Gram-negative septicemia is a dramatic example of a link between inflammation and thrombosis. When Gram-negative bacteria release their endotoxin into the bloodstream, the lipopolysaccharide can change the endothelial lining of blood vessels from an anticoagulant profibrinolytic surface into one that promotes thrombosis.[3] LV thrombus formation is common in the setting of LV systolic dysfunction as in myocardial infarction and dilated cardiomyopathy. There are anecdotal case reports of LV thrombus formation with normal LV systolic function, but a similar occurrence in the setting of K. pneumonia has never been described in the literature.[4],[5] Our patient had transient but mild LV systolic dysfunction which might have predisposed to the formation of thrombi in the LV. Septicemia and metabolic acidosis might have triggered LV systolic dysfunction in our patient. Few case reports have hypothesized that the hypercoagulable state could be an important causative mechanism of LV thrombus formation in normally functioning ventricles. Schmaier et al. described a patient with LV mural thrombus that was ascribed to giant, hyperaggregable platelets with polycystic disease.[4] Toto et al. described an apical LV thrombus in a patient with myeloproliferative disorder.[5] Chin et al. reported LV thrombus with systemic emboli in a patient with ulcerative colitis and cocaine abuse.[6] The resolution of intraventricular thrombi and lung consolidation after antibiotics, unfractionated heparin, and vitamin K antagonist favored the plausible relation between Klebsiella septicemia and intraventricular thrombi in our case.


  Conclusion Top


In addition to other invasive complications, the increased thrombogenicity leading to a hypercoagulable state should also be considered as one of the serious complications in association with K. pneumonia. Intracardiac thrombi should be suspected as a complication especially in the background of K. pneumoniae infection when clinical signs of acute respiratory distress are present. We propose a syndromic and multimodality approach by the physicians treating these patients, especially diabetics of Asian origin.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Saccente M. Klebsiella pneumoniae liver abscess, endophthalmitis, and meningitis in a man with newly recognized diabetes mellitus. Clin Infect Dis 1999;29:1570-1.  Back to cited text no. 1
    
2.
Ko WC, Paterson DL, Sagnimeni AJ, Hansen DS, Von Gottberg A, Mohapatra S, et al. Community-acquired Klebsiella pneumoniae bacteremia: Global differences in clinical patterns. Emerg Infect Dis 2002;8:160-6.  Back to cited text no. 2
    
3.
Jadhav S, Misra R, Gandham N, Ujagare M, Ghosh P, Angadi K, et al. Increasing incidence of multidrug resistance Klebsiella pneumoniae infections in hospital and community settings. Int J Microbiol Res 2012;4:253-7.  Back to cited text no. 3
    
4.
Schmaier AH, Denenberg B. Left ventricular thrombus with normal left ventricular function and hyperaggregable platelets in a patient with polycystic disease of multiple organs. Am J Med Sci 1984;288:223-7.  Back to cited text no. 4
    
5.
Toto AS, Parameswaran R, Kotler MN, Parry W. Rapid development of left ventricular thrombus in a patient with myeloproliferative disorder. Am Heart J 1987;114:436-7.  Back to cited text no. 5
    
6.
Chin WW, Van Tosh A, Hecht SR, Berger M. Left ventricular thrombus with normal left ventricular function in ulcerative colitis. Am Heart J 1988;116:562-3.  Back to cited text no. 6
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]



 

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