Data Source

This is a retrospective review of the PHIS database, an administrative database operated by the Children's Hospital Association (CHA), a business alliance of international children's hospitals, from January 1, 2004, to March 31, 2022.²¹ Forty-six, tertiary pediatric hospitals affiliated with the CHA submit data to PHIS containing inpatient, emergency department, observation status, and ambulatory surgery data.²² Data quality and reliability are assured through joint effort and agreements between participating hospitals and CHA. Data are de-identified at the time of data submission, and data are subjected to several reliability and validity checks before being included in the database. Individual patients are given a unique identifier at a hospital that carries over to multiple episodes of care at that facility, but it does not carry over to partner hospitals in the CHA. Therefore, a patient can be followed longitudinally for multiple episodes of care, provided they go to the same facility. PHIS provides an admitting diagnosis, principal diagnosis, and up to 41 additional diagnoses, in addition to a principal procedure and up to 41 additional procedures for each episode of care. From 2004 through the third quarter of 2015, diagnoses and procedures were coded using the standard ICD, Ninth Revision (ICD-9). Records from the fourth quarter of 2015 through the present were coded using the Tenth Revision (ICD-10).

Study Population

Patients were identified by the presence of a diagnosis of d-TGA via ICD codes (745.10, 745.19, and Q20.3). Identification of ASO was additionally determined by ICD code using previously published parameters (Table S1).¹⁹ Demographics collected included age, sex, race, ethnicity, gestational age, and insurance status. Insurance was grouped into Private, Government (Medicare, Medicaid, Tricare, etc), and Other (eg, charity, self-pay, unknown). Clinical outcomes provided by PHIS included survival to discharge and length of stay (LOS).

PCE was defined in our cohort as those with a diagnosis code for pericardial effusion (423.9, I31.3), hemopericardium (423.0, I31.2), cardiac tamponade (423.3, I31.4), and/or those with a procedure code for pericardiocentesis or percutaneous drainage of the pericardium/mediastinum (37.0, 0W9C30Z, 0W9C3ZX, 0W9C3ZZ, 0W9C40Z, 0W9C4ZX, W9C4ZZ, 0W9D00Z, 0W9D30Z, 0W9D3ZX, 0W9D3ZZ, 0W9D40Z, 0W9D4ZX, 0W9D4ZZ) during the index hospitalization as the ASO. Further diagnoses, procedures, and outcomes were identified using ICD codes (Table S1).

Follow-up through PHIS included in the analysis was 2-fold: (1) the number of inpatient readmissions at the same index hospital and (2) the total number of hospital encounters (which encompassed all inpatient readmissions, emergency department visits, ambulatory surgery encounters, and observation status admissions) at the same hospital as the index operation throughout the study period.

Demographics

There were no associations between patient demographics or insurance status with pericardial effusions on univariate analysis (Table 1). Preoperative clinical characteristics were similar between those with and without PCE, including median gestational age at birth (39 [IQR: 38-39] vs 39 [IQR: 38-39] weeks, P=.475), diagnoses of low birth weight (N=14, 4.7% vs N=254, 5.5%, P=.526), and prematurity (N=31, 10.3% vs N=436, 9.5%, P=.629). After adjustment for potentially confounding factors with multivariable logistic regression, no demographic factors were associated with the development of PCE (Table 3).

Table 3.

Multivariable Logistic Regression for Development of Pericardial Effusion.^a

Factor	Odds ratio	95% confidence interval	P value
Preoperative factors
Female	0.83	(0.63-1.07)	.154
White	1.16	(0.88-1.54)	.3
Ethnicity
Hispanic	Referenceb	Referenceb	–
Non-Hispanic	0.95	(0.67-1.35)	.787
Unknown	1.31	(0.82-2.11)	.259
Low birth weight	0.83	(0.47-1.45)	.512
Procedural factors
Balloon atrial septostomy	0.94	(0.73-1.2)	.613
Atrial septal defect repair	0.98	(0.71-1.37)	.916
Ventricular septal defect repair	0.98	(0.74-1.3)	.895
Postoperative complications
Acute renal failure	1.4	(0.99-1.97)	.058
Pleural effusion	1.7	(1.2-2.4)	.003
Blood transfusion exposure	1.02	(0.77-1.34)	.914
Mechanical circulatory support	1.81	(1.15-2.85)	.011

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^a Additionally adjusted for Operating Hospital and Year of operation.

^b Reference Category.

Bold values denote statistical significance.

Perioperative Considerations

There was no significant difference in perioperative factors between those who developed PCE and those who did not, including the median preoperative LOS (5 [IQR:2-8] vs 5 [IQR:2-7] days, P=.401) and those who underwent a balloon atrial septostomy (BAS) prior to ASO (N=137, 45.7% vs N=2150, 46.8%, P=.708). Similarly, concomitant intraoperative procedures such as ASD repair (N=247, 82.3% vs N=3785, 82.4%, P=.993) or ventricular septal defect (VSD) repair (N=78, 26% vs N=1203, 26.2%, P=.947) displayed no association with the development of PCE. After adjustment, procedural factors had no associations with the development of PCE (Table 3). The percent incidence of PCE among all undergoing ASO by year is depicted in Figure 1 with a gradual increase in PCE incidence over the duration of the study period.

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Figure 1.

Percent incidence of pericardial effusions of all arterial switch operation by year.

Clinical Associations

There were multiple clinical diagnoses associated with PCE (Table 1). These included a higher prevalence of acute renal failure (ARF) (N=56, 18.7% vs N=602, 13.1%), P=.006) and pleural effusions (N=46, 15.3% vs N=441, 9.6%, P=.001) compared to those without PCE. There was a significant association between those with PCE who had mechanical circulatory support (MCS) (N=26, 8.7% vs N=199, 4.3%, P<.001) compared to those without PCE during their hospitalization. After adjustment, pleural effusions had 1.7 odds (95% CI: 1.2-2.4, P=.003), and MCS had 1.81 odds (95% CI: 1.15-2.85, P=.011) of PCE (Table 3), while ARF no longer displayed an association with PCE.

In-Hospital Mortality and Length of Stay

There were 87 (1.8%) in-hospital mortalities during the index admission. Those with a PCE had a higher rate of in-hospital mortality (N=10, 3.3% vs N=77, 1.7%, P=.035) and had a longer median postoperative LOS (15 [IQR: 11-24.5] days vs 13 [9-20] days, P<.001) compared to those without PCE. After adjustment, patients had a 13.34% (95% CI: 6.27%-20.88%) longer postoperative LOS if a patient had PCE (Table 4); however, PCE no longer displayed an association with in-hospital mortality (odds ratio 0.85 (95% CI: 0.33-2.14), P=.723) (Table 5).

Table 4.

Multivariable Linear Regression of Postoperative Length of Stay.^a

Factor	Percent difference	95% CI	P value
Preoperative factors
Female	−3.04	(−6.2-0.22)	.068
White	−10.16	(−13.35- −6.86)	<.001
Ethnicity
Hispanic	Referenceb	Referenceb
Non-Hispanic	−3.79	(−8.02-0.64)	.092
Unknown	−9.41	(−14.71- −3.79)	.001
Low birth weight	59.34	(48.92-70.5)	<.001
Procedural factors
Balloon atrial septostomy	4.46	(1.15-7.88)	.008
Atrial septal defect repair	−1.65	(−5.7-2.58)	.44
Ventricular septal defect repair	11.76	(7.84-15.83)	<.001
Perioperative factors
Pericardial effusion	13.34	(6.27-20.88)	<.001
Acute renal failure	40.75	(33.82-48.04)	<.001
Pleural effusion	32.39	(25.63-39.53)	<.001
Mechanical circulatory support	104.97	(88.65-122.69)	<.001

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^a Additionally adjusted for operating hospital, year of operation, and in-hospital mortalities.

^b Reference Category.

Bold values denote statistical significance.

Table 5.

Multivariable Logistic Regression for In-hospital Mortality.^a

Factor	Odds ratio	95% CI	P value
Preoperative factors
Low birth weight	5.51	(2.41-12.6)	<.001
Procedural factors
Ventricular septal defect repair	2.07	(1.15-3.72)	.015
Perioperative factors
Pericardial effusion	0.85	(0.33-2.14)	.723
Acute renal failure	7.91	(4.17-14.99)	<.001
Pleural effusion	0.95	(0.41-2.16)	.898
Mechanical circulatory support	104.15	(51.79-209.42)	<.001

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^a Additionally adjusted for operating hospital and year of operation.

Bold values denote statistical significance.

Demographics and Perioperative Characteristics

This study did not identify any association of PCE with background demographics or birth characteristics. It is known that there is a strong male preponderance for d-TGA (60%-70%),^11,17,24 but this study did not find any associations between sex and PCE. This stands in contrast to that found in Cheung and colleagues’ review of 77 PCE patients with all-encompassing CHD diagnoses in which they found female sex to significantly increase PCE with a relative risk of 2.05, although their study is limited by a small sample size and could be influenced by sex differences in underlying CHD diagnoses and surgeries performed.¹¹ Of note, the cohort included 15 ASO patients with similar male predominance (73.3%) and only 1 reported PCE.¹¹

The lack of associations with baseline patient characteristics of this relatively homogeneous patient population may suggest intraoperative or postoperative factors as reasons for the development of PCE.^16,17 When looking at procedural considerations, however, BAS, ASD repair, and VSD repair were not associated with the development of PCE. Because of the refinement in surgical technique across institutions and over time, and with the trend of increasing percent incidence of PCE over the study period, operating hospital and discharge year were incorporated into our regression models. However, our analysis was limited by the inability to look at individual intraoperative technical and procedural components such as surgical approach, anesthesia duration, cardiopulmonary bypass strategy, and mediastinal chest tube management.^9,10

Fluid Overload and Inflammatory State

The main associations identified in this study include the development of PCE in the setting of pleural effusion (~15%) and MCS (~9%), even when adjusting for preoperative and intraoperative factors, operating center, and year of procedure. MCS demonstrated the highest odds of PCE (1.81). Within the limitations of analyzing an administrative database—where we cannot elucidate the timing of each diagnosis—this suggests that fluid overload and a systemic inflammatory state may influence the development of PCE and should be a focus of future research.²⁵

Hospital Course and Survival to Discharge

This study identified an overall in-hospital mortality rate among those undergoing ASO at 1.8%—in keeping with previous reports.^17,26 The rate of in-hospital mortality was twice as high if a patient had a PCE; however, this association did not persist on multivariable analysis. The associations found likely reflected the complexity of disease. For example, the addition of a VSD repair increases a patient's Society of Thoracic Surgeons-European Association for Cardio-Thoracic Surgery mortality score for ASO, low birth weight patients can be technically more difficult, and MCS indicates a cardiac or respiratory failure with a need for increased support. For postoperative LOS, this study did identify on both univariate and multivariable analysis that PCE was associated with prolonged LOS. These together reinforce that PCE after pediatric cardiac surgery can have significant clinical consequences, demand increased resource utilization, and highlight the need to identify high-risk patients and implement effective screening and treatment when appropriate.

Long-Term Follow-up

After reviewing more than 140 000 pediatric cardiac surgical cases, Elias et al reported only a 1.1% overall readmission rate for PCE after congenital heart surgery.⁷ Interestingly, they report more complex surgeries such as ASO conferred less risk of readmission compared to isolated ASD repairs.⁷ However, they did not report the number of patients who developed PCE during their initial postoperative hospitalization. This study found a similar rate of readmission for PCE after the ASO (2%), although the presence of PCE during index hospitalization did not result in increased readmissions or overall hospital encounters compared to those without PCE.

The authors would like to acknowledge the Health Transformation and Design team who support clinical research such as this within the Texas Center for Pediatric and Congenital Heart Disease.