PEDIATRICS Vol. 122 No. 4 October 2008, pp. e945-e947 (doi:10.1542/peds.2008-0725)
EXPERIENCE & REASON |
Severe Cardiovascular and Thromboembolic Consequences of Pneumococcal Infection in a Child
a Pediatric Intensive Care Unit, Addenbrookes Hospital, Cambridge, United Kingdom
b Pediatric Department, West Suffolk Hospital NHS Trust, Bury St Edmunds, Suffolk, United Kingdom
ABSTRACT
We present an unusually severe case of pneumococcal infection in an immunocompetent child who progressed from pneumonia to empyema, pericarditis with cardiac tamponade, and severe venous thromboembolism leading to life-threatening pulmonary embolus.
Key Words: pericarditis • pneumococcal infection • pericardial effusion • infant vaccination program • pulmonary embolus
Abbreviations: CT—computed tomography
Infant vaccination programs against pneumococcus will reduce the disease burden but currently cover a limited range of pneumococcal serotypes. Evidence from the United States suggests that complicated pneumococcal pulmonary disease may be increasing, despite widespread vaccine uptake, because of an increase in carriage of nonvaccine serotypes.1 This case illustrates the potential severity of this disease and serves to reinforce the need for early recognition and treatment.
CASE REPORT
A previously well 6-year-old girl presented to the hospital with a 10-day history of pyrexia, profuse diarrhea, vomiting, and cough. During those 10 days, she had 5 contacts with her family doctors before referral to hospital. She did not receive any antibiotic treatment before presentation to hospital. On admission, she was dehydrated and tachypneic, with bilateral basal crackles. Initial investigations revealed hyponatremia and dehydration (sodium: 125 mmol/L; urea: 10.0 mmol/L) with mild hepatic impairment (bilirubin: 39 µmol/L; alanine aminotransferase: 171 IU/L), a marked thrombocythemia of 1145 109/L with a total white cell count of 41.5 109/L, a neutrophil count of 36.6 109/L, and C-reactive protein level of 104 mg/L. A chest radiograph (Fig 1) showed bilateral consolidation with possible cavitation in the right mid zone, a right-sided pleural effusion, and an enlarged cardiac shadow. A chest computed tomography (CT) scan confirmed the presence of bilateral consolidation with bilateral pleural effusions and a 15-mm pericardial effusion.
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She was started on intravenous ceftriaxone, metronidazole, and oral clarithromycin. Intravenous fluids with oxygen therapy were commenced, but she remained tachypneic and tachycardic. On the third day of admission, she acutely deteriorated with desaturation, hypotension, and increase in work of breathing. She was intubated and ventilated. An echocardiogram showed an enlarged pericardial effusion causing cardiac tamponade. A total of 300 mL of pus was emergently drained by ultrasound-guided insertion of a sub-xiphoid pericardial catheter. Gram-stain and subsequent culture of the pericardial fluid revealed Streptococcus pneumoniae serotype 1. The same organism was also identified in the patient's nasopharyngeal aspirate, and it was sensitive to penicillin and erythromycin.
After transfer to the PICU, she remained ventilated and the pleural effusions were drained. Appropriate antibiotic therapy was continued. Although the electrocardiogram continued to show evidence of pericarditis, an additional echocardiogram showed successful drainage of the pericardial effusion with adequate biventricular function.
Swelling of the neck and upper chest developed, and ultrasound assessment of the great vessels revealed thrombosis of the left brachiocephalic, internal jugular, and subclavian veins. Heparin anticoagulation was commenced. Subsequently, 2 episodes of profound bradycardia and hypotension occurred associated with mild pulmonary hemorrhage. In view of the venous thromboembolism and associated hypoxemia, pulmonary embolism was suspected. Several coagulation studies were performed in the acute stage, which showed a prolonged prothrombin time of 23.9 seconds (11–14) and an activated partial thrmboplastin time of 45.7 seconds (22.5–34.5). Antithrombin III 43 (79–131) and protein C 38 (70–140) levels were both low, and protein S and factor V Leiden were within their normal reference range. Transfer to an extracorporeal membrane oxygenation center was arranged to allow safe administration of thrombolytic therapy. Heparinization with antithrombin III supplementation was continued during the acute phase. An additional CT scan (Fig 2) demonstrated the presence of a large right pulmonary artery thrombus. This failed to resolve radiologically, despite administration of 2 courses of recombinant tissue plasminogen activator. No additional thromboembolic events occurred. Formation of a pericardial window and bilateral pleural decortication was undertaken. She was eventually extubated on day 18 of admission.
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Heparinization was continued to 4 weeks after presentation by using subcutaneous dalteparin. Transition to warfarin therapy was undertaken on week 4. Full clinical recovery has ensued. Follow-up investigations have revealed no evidence of any underlying immunodeficiency evident by normal immunoglobulin and T-cell subsets and no prothrombotic tendency. All her coagulation tests normalized in the convalescent period.
DISCUSSION
Pneumococcus is the most common bacterial cause of community-acquired pneumonia and is estimated to cause 26% of pneumonias in England and Wales.2 Purulent pericarditis secondary to pneumococcal disease is exceptionally rare in children. Cardiac tamponade secondary to this condition has been very rarely reported. In this case, we believe that the development of pericarditis and cardiac tamponade may have been the result of late recognition of pneumococcal infection. Earlier assessment by the general practitioner may have been compromised by the predominance of gastrointestinal symptoms.
Pulmonary embolism in children is also a very rare but potentially life-threatening event. The incidence in children is reported as 0.14 per 100 000,3 but is likely to be higher as the condition is often initially missed.4 In this case, venous thromboembolism almost certainly developed secondary to a number of risk factors, which included dehydration, thrombocythemia, uremia, impaired venous return secondary to tamponade, local inflammation, and immobility.
The recent introduction of the 7-valent conjugate pneumococcal vaccine into the United Kingdom childhood vaccination schedule in 2006 is expected to lead to a significant decrease in the incidence of invasive pneumococcal disease.
The vaccine induces long-standing immunity against the 7 pneumococcal serotypes whose capsular polysaccharides it contains. It has been estimated that the 7-valent vaccine provides serotype coverage of around 76% in the United Kingdom.5 The vaccine is also able to reduce carriage of pneumococci in healthy individuals and may lead to herd immunity in the wider population. This patient had not received either the 7-valent conjugate vaccine or the 23-valent plain polysaccharide pneumococcal vaccine before this illness.
There is evidence emerging from the United States that as the serotypes covered by the vaccine are reduced in the population, they may be replaced by other nonvaccine serotypes in both vaccinated and unvaccinated individuals.6,7 These serotypes may include those that most commonly cause empyema and invasive lung disease in childhood,1,8 including the Serotype 1, which was the causative organism in this case. There is early evidence that there may be an increase in incidence of complicated pneumonia in children in a vaccinated population.1
CONCLUSIONS
This case illustrates the severe consequences that may develop secondary to pneumococcal pneumonia. We would recommend that clinicians are increasingly vigilant in the assessment of febrile children for signs of complicated pulmonary pneumococcal infection and that they should not be entirely reassured by the introduction of the 7-valent pneumococcal vaccine.
FOOTNOTES
Accepted Jul 1, 2008.
Address correspondence to A. Al-Sabbagh, MB, ChB, MRCPCH, Addenbrooke's Hospital, Paediatric Intensive Care Unit, Hill's Road, Cambridge CB2 2QQ, United Kingdom. E-mail: afraata{at}yahoo.co.uk
The authors have indicated they have no financial relationships relevant to this article to disclose.
REFERENCES
- Byington CL, Korgenski K, Daly J, Ampofo K, Pavia A, Mason EO. Impact of the pneumococcal conjugate vaccine on pneumococcal parapneumonic empyema. Pediatr Infect Dis J. 2006;25 (3):250 –254[CrossRef][Web of Science][Medline]
- Melegaro A, Edmunds WJ, Pebody R, Miller E, George R. The current burden of pneumococcal disease in England and Wales. J Infect. 2006;52 (1):37 –48[CrossRef][Web of Science][Medline]
- Van Ommen CH, Peters M. Acute pulmonary embolism in childhood. Thromb Res. 2006;118 (1):13 –25[CrossRef][Web of Science][Medline]
- Rajpurkar M, Warrier I, Chitlur M, et al. Pulmonary embolism-experience at a single children's hospital. Thromb Res. 2007;119 (6):699 –703[CrossRef][Web of Science][Medline]
- Clarke SC, Jefferies JM, Smith AJ, McMenamin J, Mitchell TJ, Edwards GF. Pneumococci causing invasive disease in children prior to the introduction of pneumococcal conjugate vaccine in Scotland.
J Med Microbiol. 2006;55
(Pt 8):1079
–1084
[Abstract/Free Full Text] - Hicks LA, Harrison LH, Flannery B, et al. Incidence of pneumococcal disease due to non-pneumococcal conjugate vaccine (PCV7) serotypes in the United States during the era of widespread PCV7 vaccination, 1998–2004. J Infect Dis. 2007;196 (9):1346 –1354[CrossRef][Web of Science][Medline]
- Singleton RJ, Hennessy TW, Bulkow LR, et al. Invasive pneumococcal disease caused by nonvaccine serotypes among Alaska native children with high levels of 7-valent pneumococcal conjugate vaccine coverage. Invasive pneumococcal disease caused by nonvaccine serotypes among Alaska native children with high levels of 7-valent pneumococcal conjugate vaccine coverage.
JAMA. 2007;297
(16):1784
–1792
[Abstract/Free Full Text] - Byington CL, Samore MH, Stoddard GJ, et al. Temporal trends of invasive disease due to Streptococcus pneumoniae among children in the intermountain west: emergence of nonvaccine serogroups. Clin Infect Dis. 2005;41 (1)21 –29[CrossRef][Web of Science][Medline]
PEDIATRICS (ISSN 1098-4275). ©2008 by the American Academy of Pediatrics
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