No subjects were readmitted for pleural effusions while using a regimen of no diuretics in “regular risk” or a five-day course in “high-risk” patients after discharge. Four subjects were readmitted for pericardial effusions which was an increase compared to a historical control. The number of subjects readmitted for pericardial effusion was quite low with a small fragility index which constrains the conclusions that can be drawn from this. Despite the small number of subjects affected by pericardial effusion, one presented in tamponade which highlights the importance of further exploring this finding.
Trivedi et al published a quality improvement project that reduced their post-discharge diuretic regimen from 32 to 10 days [6]. They found no change in the small number of pleural effusions discovered after discharge. Only three pleural effusions were found out of 115 patients post-protocol implementation and it was unclear if any were re-admitted. They found no change in readmission rates pre- and post-protocol implementation. Interestingly, the frequency of pericardial effusions decreased (p = 0.03) in their post-intervention group. This could be related to a protocolized practice change shortly before beginning their quality improvement project that involved the use of ibuprofen as an outpatient when pericardial inflammation was suspected. This may explain the discrepant pericardial effusion findings between these two studies.
Trivedi’s quality improvement project and this prospective study both found extremely low rates of pleural effusion and no increase in readmissions for pleural effusions. This study was halted prior to reaching a goal of 154 subjects. However, the absence of any re-admissions for pleural effusion through 61 subjects suggests that if routine diuretic therapy has any utility in preventing readmissions for pleural effusions, then the number needed to treat is likely to be high. Diuretics may not be needed once the initial fluid overload has been ameliorated as the lymphatic system may be able to increase clearance when needed, especially in the absence of the systemic venous hypertension seen in single ventricle physiology.
In contrast, the lymphatic system cannot clear pericardial effusions and we found a higher frequency of this complication while using our diuretic regimen. These results are driven by very small numbers and the fragility index shows us that a change in 1 or 2 patient outcomes would have made the results non-significant statistically. We also examined these re-presentations by symptoms since the decision to re-admit may vary between providers and found that this was also increased. Given the statistical significance of both of these outcomes combined with the plausibility that longer courses of diuretics suppress pericardial effusions suggest that diuretics may decrease the frequency of these effusions becoming clinically relevant.
The frequency of readmissions for pericardial effusion during the historical control was 0.2%, similar to the rate of 1.1% found in retrospective review of 142,633 cases reported in the pediatric health information database [7]. We suspect many of those patients in the database would have been treated with diuretics as we believe this is a widespread practice. We saw a higher rate during our study era (2.9%) which supports the hypothesis that diuretics, a treatment for pericardial effusions, may decrease the symptoms.
If diuretics suppress the incidence of symptomatic pericardial effusions, this still may not justify routine use of diuretics after all two-ventricle repairs given the very low numbers. A more targeted approach may be sufficient to prevent an increase of pericardial effusions in the absence of routine, prolonged, diuretic courses. This targeted approach could be used for patients with a rub, those with an ASD repair and those with diffuse ST segment changes, all risk factors for pericardial effusion. Non-steroidal anti-inflammatory drugs (not used routinely on the subjects in our study) may more appropriately address the cause of pericardial effusion and thus be more effective than furosemide. Further study of when or if furosemide is necessary post-discharge and how to address pericardial effusions in that context warrants further study. This could be pursued most efficiently in a quality improvement format that allows for flexibility in treatment regimen.
The limitations of this study include the unexpected increase in pericardial effusions that led to stopping the study prior to full enrollment. Additionally, we did not have standardized criteria for pericardial effusion detection, treatment or readmission in the historical or study periods. This may have led to readmissions that could have been treated outpatient, one reason ‘symptomatic’ effusions were included in the analysis as this is not provider dependent. Lastly, this is a single center experience and local diuretic or other practices may influence results.