Cardiac involvement in children with community-acquired pneumonia and respiratory failure

A total of 139 patients were included in this study. After investigations, four patients were excluded. An acute asthmatic patient had no evidence of pulmonary infiltrates on CXR. Three CHD patients in this admission were diagnosed by echocardiographic examination. The cardiac defects were double aortic arch with ventricular septal defect, patent ductus arteriosus, and perimembranous type-ventricular septal defect. Of the remaining 135 patients, the mean age was 13.58 ± 9.81 months with slightly male predominant. Total duration of fever, intubation period, and length of hospital stay were 7.99 ± 4.28, 5.29 ± 4.67, and 12.47 ± 12.83 days, respectively. Viruses were more frequent causative-organisms than bacterias. Most of the mean values in basic laboratory findings as hematocrit, renal function, liver enzyme, and albumin were within a normal range. White blood cell counts revealed leukocytosis at mean 15516.56 ± 6649.06 cells/cu mm as shown in Table 1.

The admission date was 3.64 ± 1.80 days after the onset of fever. The first echocardiographic date was 9.46 ± 3.92 days after the onset of fever. The second round of laboratory investigations and echocardiography was performed 19.56 ± 5.67 days after admission. Of the 135 patients, ST/T changes occurred in 66 (49%), cardiac arrhythmia occurred in seven (5%), and myocardial injury occurred in 80 (59%). ST/T changes were a common finding from the ECGs. ST depression and ST elevation were observed in two patients. The remaining patients exhibited non-specific T-wave changes. Three cardiac arrhythmia patients exhibited premature ventricular contraction, premature atrial contraction, and first-degree atrioventricular block, and these conditions were resolved before discharge. Four patients exhibited right bundle branch blocks that persisted throughout the followed-up period. No hemodynamic instability was observed in the arrhythmic group. The incidences of all of these conditions were significantly reduced by the second investigation, as shown in Table 2.

Valvular regurgitation occurred in 30 patients (22%) and pericardial effusion occurred in 80 patients (59%). The pericardial effusions were small to medium. Among all of the pericardial-effusion patients, 35 (44%) patients had small effusions and 45 (56%) patients had medium pericardial effusions with maximal thicknesses of 3.6 mm. Mitral and tricuspid valve regurgitations were observed in approximately 80 and 20% of the patients with valvular regurgitation, respectively. Echocardiogram revealed significant improvements of RVIMP, LVIMP, and LVEF at the second investigation date. Decreasing of pericardial effusion and right ventricular systolic pressure (RVSP) was also demonstrated. No significant changes of interventricular septum, left ventricular posterior wall thickening, and left ventricular diastolic dimension was demonstrated, as shown in Table 3. There were three mortality cases in this study, and all patients exhibited evidence of myocardial injury and CHF. Ventilator-associated pneumonia, acute respiratory distress syndrome, sepsis, septic shock, and death were developed after persisted clinical signs and symptoms of CHF.

Length of hospital stays was compared between presented cardiac-involvement patients (i.e., ST/T changes, arrhythmia, pericardial effusion, valvular regurgitation, and myocardial injury), and absent cardiac-involvement patients, as shown in Table 4.

This study revealed that cardiac involvement occurred in up to 62% of the healthy children with CAP and RF. The effects possibly associated with infection, systemic inflammatory response, and cardiopulmonary interaction. Pericardial effusion, valvular regurgitation, ST/T changes, and non-fatal arrhythmia were rather common, but these conditions were mild and without severe hemodynamic effects. Myocardial injury was the most common finding but was typically asymptomatic, except for the patients who developed CHF.

Pericardial effusion and valvular regurgitation were possibly associated with an inflammation of the pericardium and valvular tissue. In agreement with the pericardial effusion results from our study, a previous study revealed evidence of pericardial effusion by computed tomography scan and echocardiography in approximately 50% of parapneumonic effusion patients [14]. This finding indicates the relationship between pulmonary and pericardial infectious processes [5]. The causative organism spreads to the pericardium via several routes that include pulmonary foci, the pleura, lymphatic channels of the hemithorax, and bacteremia [19]. However, the pericardial effusion cases with pulmonary infection included in our study typically exhibited mild to moderate pericardial effusion that resolved after treatment of the infection.

Abnormal ECG in this study was premature ventricular contraction, premature atrial contraction and first-degree atrioventricular block, ST segment elevation, and depression with non-specific T-wave changes. These were transient and disappeared after clinical improvement. The abnormal ECG findings possibly related to pericarditis and myocarditis because the causative organisms of pneumonia also cause both pericarditis and myocarditis [20]. In these conditions, non-specific ST/T-wave changes are common. However, ventricular conduction delays, supraventricular arrhythmia, and atrioventricular block are occasionally present [21, 22].

Incidences of myocardial injury approximately 60% were detected in our patients. Non-ischemic myocardial injury which reflected by increases in serum troponin levels was observed in critically ill patients without acute coronary syndrome [23, 24]. These findings were possibly due to myocarditis, systemic inflammatory responses and changes in circulatory volume [7, 25]. Viral-induced myocarditis results from various mechanisms, either direct infection of cardiac myocytes or emerging immune response. Although virus is the most common causative organism of pneumonia and myocarditis in this age group, bacteria also can cause both conditions [26,27,28]. Apart from direct infection of cardiac myocyte in bacterial infection, inflammatory cytokine, such as TNF-a and interleukin-6, were produced, causing myocardial inflammation and depression [24, 25].

The Tei index for myocardial performance revealed impairment of systolic and diastolic function in both ventricles upon admission that improved over the follow-up period. Although the initial LVEF values were within the normal range, significant improvements were observed on the second echocardiograms. In addition to myocardial depression related to infection and systemic inflammatory response which usually impact on LV dysfunction [25], the cardiopulmonary interaction and positive pressure ventilation have a potential effect on these findings. Positive pressure ventilation in RF patients causes compressive effects on both RV and LV. RV is compressed in cardiac fossa, decreased preload, and contractility with increased afterload due to increasing of pulmonary vascular resistance. LV is compressed in cardiac fossa, decreased LV preload, afterload, and compliance [29, 30]. Positive ventilation also affected intrathoracic and pulmonary pressure changes reflected by an increased RVSP on admission. Finally, it might impair cardiac function and develop low cardiac-output state.

Although the majority of cardiac involvement were mild and recovered spontaneously following pneumonia treatment, in case with progression to CHF, there were effects on hemodynamic compromise and multiorgan dysfunction. Risks of infection, such as ventilator associated pneumonia, ARDS and sepsis and prolong ventilatory support were increased. All complications have an impact on prolong hospitalization with increasing mortality.

CAP with RF is associated with cardiac involvements in as many as 62% of patients, even among healthy children without any cardiac risks. The majority of the complications, including myocardial injury, pericardial effusion, valvular regurgitation, ST/T changes, and arrhythmia, were transient and mild in this group. Significant hemodynamic changes and increased mortality risks were observed in the patients who developed CHF. Future research should examine to identify characteristics and CHF with the aim of early recognition and prompt therapeutic strategy implementation.