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Year : 2019  |  Volume : 6  |  Issue : 6  |  Page : 36-38

Septic pulmonary artery thrombosis in a child with community acquired pneumonia: A case report

1 Director Pediatric Emergency, Critical care and Pulmonology, Sir Ganga Ram Hospital, Rajinder Nagar, New Delhi, India
2 Fellow Pediatric Pulmonology, Sir Ganga Ram Hospital, Rajinder Nagar, New Delhi, India
3 Pediatric Cardiologist, Sir Ganga Ram Hospital, Rajinder Nagar, New Delhi, India
4 Pediatric Intensivist, Sir Ganga Ram Hospital, Rajinder Nagar, New Delhi, India

Date of Submission16-Sep-2019
Date of Acceptance12-Nov-2019
Date of Web Publication20-Dec-2019

Correspondence Address:
Anil Sachdev
Director, Pediatric Emergency, Critical care and Pulmonology Department of Pediatrics, Sir Ganga Ram Hospital, Rajinder Nagar, New Delhi 110060
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Source of Support: None, Conflict of Interest: None

DOI: 10.21304/2019.0606.00544

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Septic pulmonary embolism is a diagnosis seldom considered in children. We present the clinical course of a 6 year-old child with septic pulmonary embolism secondary to community acquired Pseudomonas pneumonia. Chest radiograph revealed bilateral pneumonia and pleural effusion. CT pulmonary angiogram showed hypodense filling defects in pulmonary artery branches along with consolidations. Pseudomonas aeruginosa was isolated in bronchoalveolar lavage culture. Child was treated with IV antibiotics and low molecular weight heparin. Follow up clinical and investigations revealed remarkable improvement.

Keywords: Pneumonia, Pulmonary artery thromboembolism, Pseudomonas aeruginosa

How to cite this article:
Sachdev A, Ghimire A, Agarwal N, Gupta N. Septic pulmonary artery thrombosis in a child with community acquired pneumonia: A case report. J Pediatr Crit Care 2019;6:36-8

How to cite this URL:
Sachdev A, Ghimire A, Agarwal N, Gupta N. Septic pulmonary artery thrombosis in a child with community acquired pneumonia: A case report. J Pediatr Crit Care [serial online] 2019 [cited 2022 Dec 6];6:36-8. Available from: http://www.jpcc.org.in/text.asp?2019/6/6/36/279475

  Introduction Top

Septic pulmonarythromboembolism (SPE) has been defined as embolization of lung caused by a blood clot infected with any of several bacterial or fungal species.To date 27 children with SPE were reported in the English literature.[1]In the pediatric population, respiratory manifestations are not common and the symptoms are mainly related to the source of infection, like osteomyelitis, septic arthritis, cellulitis, making the diagnosis of SPE more challenging. SPE are usually associated with right sided endocarditis or other intravascular devices.[2]

We hereby discuss an unusual presentation of pulmonary artery thrombosis in an immuno-competent child with community acquired P. aeruginosa pneumonia.

  Case Report Top

A six year, previously healthy boy was admitted with complaints of fever and respiratory distress for 10 days. He had no history of recurrent infections, previous hospital admissions or repeated visits to health care facility. On examination, his weight was 16 kg(5th centile for age and gender). He was conscious, toxic looking, febrile (103°F) and tachypneic (68 breaths/min) with chest retractions. Air entry was reduced over bilateral lung fields. SpO2 at room air was 82% which increased to 91% with supplement oxygen. In view of persistent respiratory distress, child was initiated on non-invasive ventilation (NIV) support. Child tolerated NIV interface. He showed improvement in respiratory distress and was maintaining SpO2> 96%. Child used to demand for NIV mask instead of simple oxygen mask during resting time from NIV.

His hemoglobin was 13gm/dl with total leucocyte count of 9700/cu mm (neutrophil 92%), platelet 1.61 thousand/μl, C-reactive protein 106mg/dl (N <6)) and ESR 30mm 1st hr. Blood culture was sterile. Chest x-ray revealed bilateral pleural effusion with left lower zone consolidation and right mid zone patchy infiltrates. Pleural fluid aspiration revealed straw colored fluid with total count 240cells/cumm (lymphocyte 90%), glucose 83 mg/dl, protein 3.9 gm/dl (serum protein 4.55gm/dl). The fluid had no microbiological isolation and ZN stain for tuberculosis and Xpert MTB/RIF (or Gene Xpert) assay were negative. Child was started on parenteral antibiotics. Functional echocardiography showed normal chamber sizes with no valvular lesion and normal pulmonary artery pressure. There was some improvement after 60 hours of admission in work of breathing and toxemia with persistence of fever. After 72 hours of admission, child was uncomfortable and refused to accept NIV interface. In view of persistent work of breathing and chest radiograph findings, bedside flexible fiberoptic bronchoscopy was done.

Bronchoscopic examination was suggestive of cheesy material in left lower lobe segmental bronchus. Pseudomonas aeruginosa sensitive to multiple antibiotics was isolated in the bronchoalveolar lavage culture. Antibiotics were adjusted according to the sensitivity. Immunological studies were non-contributory.

Contrast enhanced computerized tomography of chest showed bilateral consolidation with hypodense filling defects in bilateral pulmonary artery branches suggestive of pulmonary thromboembolism which was confirmed with CT pulmonary angiogram. [Figure 1] Ultrasound Doppler examination was done to rule out deep vein thrombosis. No evidence of pulmonary hypertension in repeat echocardiography. Ventilation/perfusion (V/Q) scan revealed multiple large matched and mismatch ventilation perfusion defects involving the bilateral lungs (left more than right)[Figure 2]. Low molecular heparin (enoxaparin 16 mg twice a day) was started. The condition of the child improved gradually. Heparin dose was adjusted to maintain Anti-factor Xa level between 0.6-1.1U/ ml.
Figure 1: Contrast computerized tomography sagittal view of pulmonary angiography reveals large parenchymal consolidation in the left lung and irregular fi lling defects in the right descending pulmonary artery

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Figure 2: Multiple large matched and mismatch ventilation perfusion defects involving the bilateral lungs (left more than right)

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Patient received 3 weeks of IV antibiotics followed by 5 weeks of oral antibiotics along with enoxaparin. On repeated follow up visits, there was fever or respiratory distress even on exertion and persistent fine crepitations were present on left lung base. Repeat CT showed marked regression of consolidation. Enoxaparin was continued for 6 months followed by oral acenocoumarol for 6 months. At 12 months follow up, there was no fever, cough and dyspnea on excertion and child was gaining weight appropriately. V/Q scan at 12 months showed multiple segmental and subsegmental perfusion defects in the left lung. There was no segmental perfusion defect in the entire right lung.

  Discussion Top

SPE is very uncommon in pediatric population probably due to low index of suspicion or low incidence of disease.To the best of our knowledge and extensive review of the literature, there are no cases reported in children with community acquired Pseudomonas pneumonia with pulmonary thrombosis. Our patient presented with bilateral pneumonia with no other foci of infection.On literature review, most of the cases had more than one focus of infection.[3] There were no risk factors in our patient to develop Pseudomonas pneumonia.[4]

The presented child accepted and tolerated NIV and showed reasonable improvement in his respiratory status initially. But later he refused to apply NIV interface since he felt breathing difficulty. Child was noted to have tachycardia and tachypnea.The physiological reason is increase in right ventricular afterload and reduction in right ventricular preload induced by positive pressure ventilation in the presence of pulmonary artery thrombosis.[5] Also there is V/Q mismatching and increase in dead space ventilation.

The diagnosis of SPE should be based on a high probability ventilation-perfusion scan or a positive spiral chest CT. Frequently, in adult patients with unstable hemodynamics, thrombolytic therapy is initiated on clinical suspicion. No such guidelines are available for pediatric patients. Eradication of infection is the cornerstone in the management of SPE along with anticoagulants.[6],[7]The role of anticoagulation in the treatment of SPE remains controversial due to risk of bleding.[8],[9] Thus, recommendations are based largely on observational studies and expert opinion. So therapy needs to be individualized for each patient. Monitoring for hemorrhagic complications is always in order.

  Conclusion Top

Community acquired pneumonia caused by Pseudomonas leading to pulmonary artery thrombosis is a rare combination in a previously healthy child. Timely and judicious investigations with high index of suspicion lead to potentially fatal diagnosis and specific treatment.

Source of Funding: Nil

Conflicts of Interest: Nil

  References Top

Thabet FC, Alhejaili AS, Alodayani AN. Septic pulmonary embolism secondary to Staphylococcus aureus septic thrombophlebitis in a pediatric patient. Saudi Med J 2013; 34: 1080-2.  Back to cited text no. 1
Celebi S, Hacmustafaoglu M, Demirkaya M. Septic pulmonary embolism in a child. Indian Pediatr 2008;45:415-7.  Back to cited text no. 2
Wong KS, Lin TY, Huang YC, Hsia SH, Yang PH, Chu SM. Clinical and radiographic spectrum of septic pulmonary Embolism. Arch Dis Child2002;87:312-5.  Back to cited text no. 3
Zhang Q, Smith JC, Zhu Q, Guo Z, MacDonald NE. A five-year review of Pseudomonas aeruginosa bacteremia in children hospitalized at a single center in southern China. International J Infectious Diseases 2012:16:628-32.  Back to cited text no. 4
Shekerdemian L, Bohn D. Cardiovascular effects of mechanical ventilation.Arch Dis Child 1999;80:475-80.  Back to cited text no. 5
Daniels LB, Parker JA, Patel SR, et al. Relation of the duration of symptoms with the response to thrombolytic therapy in pulmonary embolism. Am J Cardiol1997;80:184-8.  Back to cited text no. 6
Viola L, Langer A, Pulitano S, Chiaretti A, Piastra M, Polidori G. Serious Pseudomonas aeruginosa infection in healthy children: case report and review of the literature. Pediatr Int2006;48:330-3.  Back to cited text no. 7
Lee SJ, Oh SS, Lim DS, Hong SK, Choi RK, Park JS. Usefulness of anticoagulant therapy in the prevention of embolic complications in patients with acute infective endocarditis. BioMed Research International 2014,1-7.  Back to cited text no. 8
Hart RG, Kagan-Hallet K, Joerns SE. Mechanisms of intracranial hemorrhage in infective endocarditis. Stroke 1987;18: 1048-56.  Back to cited text no. 9


  [Figure 1], [Figure 2]


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