|Year : 2019 | Volume
| Issue : 1 | Page : 14-18
Pericardial effusion and outcome in children at a Tertiary Hospital in North-Western Nigeria: A 2-year retrospective review
Igoche David Peter1, Mustafa Ohikhena Asani2, Ibrahim Aliyu2
1 Paediatric Cardiology Division, The Limi Children's Hospital, Abuja, Nigeria
2 Department of Paediatrics, Aminu Kano Teaching Hospital, Bayero University, Kano, Nigeria
|Date of Web Publication||23-Apr-2019|
Dr. Igoche David Peter
Paediatric Cardiology Division, The Limi Children's Hospital, Abuja
Source of Support: None, Conflict of Interest: None
Background: Pericardial effusion may culminate in cardiac tamponade which could be fatal. This study aims to describe the prevalence of cardiac tamponade, with the etiology, and outcome of childhood pericardial effusion at Aminu Kano Teaching Hospital, Kano, Nigeria. Materials and Methods: Hospital records of children with pericardial effusion were retrospectively analyzed from June 2016 to May 2018. Data were described via percentages, tables, and bar and pie charts. Results: Of the 5876 pediatric admissions during the study duration, 10 (0.2%) children presented with cardiac tamponade (9 boys and 1 girl) and had emergency echocardiography-guided percutaneous pericardiocentesis; 5 (50%) of them had purulent, 4 (40%) had serous, and 1 (10%) had hemorrhagic pericardial effusion. Seventeen children, aged 8 months to 13 years with a male: female ratio of 2.4:1, had pericardial effusion during the study period. Pericardial effusion of infectious origin (58.8%) was the most common followed by uremic (17.4%), rheumatic (11.8%), and trauma and idiopathic (5.9%). Tuberculosis (TB) was the most implicated cause of infectious pericardial effusion (70%), and also the most common cause of cardiac tamponade (50%). Mortality was recorded in two children (11.8%) with end-stage renal disease and decompensated rheumatic heart disease, both complicated by pericardial effusion. None of them were in tamponade and hence did not have pericardiocentesis. Emergency echocardiography-guided percutaneous pericardiocentesis was safe and successful in all those who had this procedure. Conclusion: Cardiac tamponade is common in children with pericardial effusion in Kano. TB is the leading cause of childhood pericardial effusion and cardiac tamponade. Mortality was reported in two children, with pericardial effusion of uremic and rheumatic etiology each.
Keywords: Cardiac tamponade, pericardial effusion, tuberculosis
|How to cite this article:|
Peter ID, Asani MO, Aliyu I. Pericardial effusion and outcome in children at a Tertiary Hospital in North-Western Nigeria: A 2-year retrospective review. Res Cardiovasc Med 2019;8:14-8
|How to cite this URL:|
Peter ID, Asani MO, Aliyu I. Pericardial effusion and outcome in children at a Tertiary Hospital in North-Western Nigeria: A 2-year retrospective review. Res Cardiovasc Med [serial online] 2019 [cited 2019 Oct 18];8:14-8. Available from: http://www.rcvmonline.com/text.asp?2019/8/1/14/256880
| Introduction|| |
Rapid or excessive pericardial fluid accumulation results in cardiac tamponade which could be fatal., Accumulation of fluid in the pericardial space is usually secondary to infections, metabolic disorders, neoplasms, trauma, or connective tissue diseases.,,, Apart from emergency pericardial drainage, identification of the etiology of the pericardial effusion is integral to proper patient management. Jaiyesimi et al. studied infective pericarditis in Ibadan, Nigeria, and identified Mycobacterium tuberculosis as the most implicated, while Okeniyi in Ilesha, Nigeria, 29 years later, reported that Staphylococcus aureus was the most common in their series. Tabansi and Otaigbe have reported a case of trauma-related pericardial effusion in a child, but to the best of the authors' knowledge, there is no study exploring both infective and noninfective etiologies of pericardial effusion in Nigerian children.
The current study aims to determine the prevalence of cardiac tamponade, etiology, and outcome of children with pericardial effusion in Aminu Kano Teaching Hospital, Kano, Nigeria.
| Materials and Methods|| |
Hospital records of children seen at echocardiography laboratory of Aminu Kano Teaching Hospital, Kano, with pericardial effusion from June 2016 to April 2018, were retrospectively analyzed. Background clinical history, microbiology laboratory results, chest radiograph, electrocardiography (ECG), and echocardiography findings were obtained from their hospital records.
Echocardiography was performed using SONOSCAPE® SSI-8000 cardiac ultrasound system. Pericardial effusion was visualized as echo-free space inside the pericardium from multiple echo windows and quantified using M-mode measurement posterior to the left ventricle in diastole as shown in [Figure 1]. Cardiac tamponade was confirmed in the presence of diastolic collapse of right atrium or ventricle as shown in [Figure 2]. For those with cardiac tamponade, echo-guided pericardiocentesis and pericardiostomy tube was inserted through the subxiphoid approach after anaesthetizing the skin over the subxiphoid area with 1% lidocaine infiltration. Cardiac surgeons intervened for thick or loculated/organized pus not amenable to tube drainage. Pericardial aspirates were sent immediately to the microbiology laboratory and centrifuged at 3000 rpm for 10 min, the deposits being used for Gram staining and inoculation onto an array of culture media; nonselective enriched growth media such as blood agar for nonfastidious organisms and chocolate agar for fastidious organisms; and a selective medium-MacConkey agar for Gram-negative organisms. Blood and MacConkey agar plates were aerobically incubated, whereas chocolate plates were incubated at 5% CO2, all at 35°C for 18 h. Ziehl–Neelsen (ZN) staining and GeneXpert® test were also carried out on pericardial aspirates. Blood samples were also sent for culture using BACTEC blood culture system. Duration of hospital stay and mortality were noted. Data were described through percentages, tables, and bar and pie charts.
|Figure 1: Echocardiogram (parasternal long-axis view) showing pericardial effusion quantified using M-mode measurement posterior to the left ventricle in diastole|
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|Figure 2: Echocardiogram (apical four-chamber view) showing cardiac tamponade confirmed by diastolic collapse of the right atrium|
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| Results|| |
During the study period, they were 5876 pediatric cases hospitalized, of whom a total of 15 children (11 boys and 4 girls), with age range of 8 months to 13 years, had echo-diagnosed pericardial effusion. An additional two children (a male and a female) who were stable outpatients (not in tamponade) were also seen at our echo laboratory. [Table 1] displays a clinical summary of all the 17 cases of pericardial effusion.
Enlarged cardiac shadow on chest radiograph and sinus tachycardia with low-voltage QRS complexes were present on ECG of the cases.
Ten of all the hospitalized children evaluated for pericardial effusion (0.2%) presented in tamponade (9 boys and 1 girl); 5 were purulent, 4 were serous, and 1 had idiopathic recurrent hemopericardium. They all had emergency echocardiography-guided percutaneous pericardiocentesis with insertion of pericardiostomy tube, and the procedure was successful in all of them. Further surgical drainage was required in a patient who had loculated abscesses. Pericardiocentesis was not done in seven children as they were not in tamponade and had medical conditions which could be addressed.
Pericardial effusions were mostly of infectious origin (ten cases), of which M. tuberculosis was the most common culprit for both pericardial effusion and cardiac tamponade [Figure 3], [Figure 4], [Figure 5]. Three children had effusions of bacterial origin for which Klebsiella pneumoniae was cultured from pericardial aspirate of one, and the other two were from contiguous spread in children with bronchopneumonia (one of which additionally had parapneumonic pleural effusion) although no organisms could be isolated. These children responded to antibiotic treatment.
|Figure 4: Pie chart depicting the infectious causes of pericardial effusion|
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Uremia from end-stage renal failure accounted for pericardial effusion in three children, and they did not present in tamponade. They had salvage hemodialysis. There were two children with effusion following acute rheumatic fever with a background of rheumatic heart disease and one child with pericardial effusion following blunt chest trauma from a fall. A child with a background of sickle cell disease had recurrent hemopericardium which was labeled idiopathic after excluding other causes.
Two children (11.8% of those with pericardial effusion; cases of end-stage renal disease and decompensated rheumatic heart disease) died most likely from complications/decompensation from their primary disease. They did not have tamponade clinically, or from echo, and hence pericardiocentesis was not performed in them.
| Discussion|| |
Similar to the reports by Okeniyi in Ilesa, Nigeria, and Nessa et al. in Noakhali, Bangladesh, cardiac tamponade, a fatal complication of pericardial effusion, occurred in 0.2% of children hospitalized in the present cohort, reiterating its rarity in the pediatric population.
Our observation of infections as the most common cause of pericardial effusion is in agreement with Akhtar et al. in Pakistan and Bagri et al. in India. Considering that sub-Saharan Africa has high tuberculosis (TB) disease burden, it is not surprising that it is also the most common implicated etiology of pericardial effusion and cardiac tamponade in our series, and this is in agreement with an earlier report by Jaiyesimi et al. in Ibadan, Nigeria. Of the seven children in our series with TB pericarditis, one was diagnosed by GeneXpert and found to have multidrug-resistant TB, another one was diagnosed by histological examination of pericardial tissue yielding typical granulomatous lesions (she also had a positive ZN stain), two had positive ZN stains (one of pericardial aspirate and the other of sputum), while three with a strong history of contact responded to TB therapeutic trial.
Other patients in our series had pericardial effusion from uremic, rheumatic, trauma, and idiopathic etiology, portraying the diverse etiology of pericardial effusion in children. The child with idiopathic effusion had recurrence of hemopericardium and presented in tamponade in both cases. Three of our patients with end-stage renal disease had pericardial effusion occurring prior to commencement of hemodialysis which defines uremic pericarditis. While the pathogenesis of uremic pericarditis remains multifactorial, it is thought that albuminuria worsening endothelial permeability in a low inflammatory state contributes to the development of pericarditis. The mainstay of therapy for these patients is scheduled salvage hemodialysis, as effusion was closely monitored. Rutsky and Rostand reported a survival rate of 89.7% among their cohort of patients with uremic pericarditis, and we recorded mortality in one of our patients who probably died from other complications of renal disease as she was neither in tamponade, nor was effusion found to increase in size. Death was also recorded in another child who had disseminated TB (pericardial and right pleural) with a background of rheumatic heart disease. We, therefore, had an overall 11.8% mortality which is considered significant among pediatric patients with pericardial effusion. Suffice it to say that these deaths did not occur among those who had cardiac tamponade, as they had emergency pericardiocentesis which was safe and successful. Therefore we infer that while TB is the most common cause of pericardial effusion and even cardiac tamponade, it is not necessarily fatal if pericardiocentesis and anti-TB medications (with steroids) are commenced early. Follow-up of all except one patient (with idiopathic recurrent pericardial effusion) showed complete resolution of effusion. None of them developed clinical or echo features of constrictive pericarditis over a median follow-up period of 3–21 months as none was found to have any complaints such as weakness, anorexia, exertional dyspnea, or elevated jugular venous pressure, neither did they have pericardial effusion or thickening of pericardium nor abnormal septal motion on echo. Mortality occurred in children with effusions of uremic and rheumatic etiology.
The present study is limited by a small sample size and retrospective design. The rarity of the disease condition accounted for this bird eye's view of pericardial effusion and cardiac tamponade in a region where these have not been reviewed. A structured prospective and multicentric study in future is hoped to be better illuminating. There is absence of facilities for BACTEC-enhanced culture of aspirates and aerobic culture at the time of this study. Viral studies were also not available at the study center; hence, the term “infectious” cause may encompass viral and/or bacterial causes. Of the three “infectious” cases, however, Klebsiella pneumonia was cultured from pericardial aspirate in one and the other two cases followed complicated bronchopneumonia. Although both responded to empirical antibiotics, aspirate and blood cultures were negative.
| Conclusion|| |
The present study reveals that cardiac tamponade is common in children with pericardial effusion in Kano. Of the various aetiologies of pericardial effusions reviewed, TB is the leading cause of childhood pericardial effusion and cardiac tamponade. Mortality was reported in two children, with pericardial effusion of uremic and rheumatic etiology each, and mortality is most likely attributable to the underlying medical condition.
There is a need for early case detection and prompt TB chemotherapy to prevent effusion and tamponade as complications. Primary prevention of acute rheumatic fever will forestall the occurrence of fatal pericardial effusions of rheumatic etiology. Early collaborations between the pediatric nephrologist and cardiologist will afford better care of children with chronic renal insufficiency who are at risk of pericardial complications.
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Conflicts of interest
There are no conflicts of interest.
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