Pericardial Effusion and Tamponade in Infants With Central Catheters
Todd T. Nowlen, MD*; Geoffrey L. Rosenthal, MD, PhD‡; Gregory L. Johnson, MD*; Deborah J. Tom, MD§; and Thomas A. Vargo, MD*
ABSTRACT. Objective. To describe the clinical pre-sentation, cause, and outcome of central venous catheter (CVC)-related pericardial effusions (PCE) in infants.
Methods. A retrospective case review was conducted of CVC-related PCE at university and private neonatal intensive care units. Data from our cases were combined with published case reports and included clinical presen-tation and outcome; biochemical evaluation of pericar-dial fluid; days until diagnosis; cardiothoracic ratios; and CVC characteristics, insertion site, and tip placement site. Results. In our cases, 6 different neonatology groups cared for 14 patients at 6 different hospitals in 2 cities. These data were combined with 47 cases reviewed from the literature. Pericardial fluid was obtained in 54 cases from the combined group and was described qualita-tively as consistent with the infusate in 53 of 54 cases (98%). Biochemical analysis was performed in 37 cases, and in 36 of 37 cases (97%), the pericardial fluid was consistent with the infusate. The median gestational age at birth was 30.0 weeks (range: 23.5– 42). The median time from CVC insertion to diagnosis was 3.0 days (range: 0.2–37;nⴝ59). Sudden cardiac collapse was reported in 37 cases (61%), and unexplained cardiorespiratory insta-bility was reported in 22 cases (36%). The CVC tip was last reported within the pericardial reflections on chest radiograph in 56 cases (92%) at the time of PCE diagnosis. The mean cardiothoracic ratio increased 17% (nⴝ14). No patients died among our cases. Among the reviewed cases, 45% mortality was reported. For the combined group, mortality was 34%. For the combined group, mor-tality was 8% (3 of 37) in the patients who underwent pericardiocentesis versus 75% (18 of 24) for the patients who did not . In 21 patients, the catheter was withdrawn and remained in use. Survivors and nonsurvivors had comparable gestational age at birth, birth weight, days to PCE diagnosis, and day of life of PCE symptoms/diagno-sis. Access site, catheter type, and catheter size were not associated with mortality. An association between larger catheters and shorter time to PCE may be present. Access site and catheter type were not associated with time to PCE. Autopsy specimens reported 6 cases of myocardial necrosis/thrombus formation, 9 cases of perforation with-out myocardial necrosis/thrombus formation, and 2 cases in which both were reported.
Conclusions. The pericardial fluid found in CVC-as-sociated PCE is consistent with the infusate. We specu-late that there are several mechanisms, ranging from
frank perforation that seals spontaneously to CVC tip adhesion to the myocardium with diffusion into the peri-cardial space. Routine radiography should be performed, and the CVC tip should be readily identifiable. The CVC tip should remain outside the cardiac silhouette but still within the vena cavae (approximately 1 cm outside the cardiac silhouette in premature infants and 2 cm in term infants). A change in cardiothoracic ratio may be diag-nostic of a PCE, and pericardiocentesis is associated with significantly reduced mortality. Increased awareness of this complication may decrease the mortality associated with CVC-related PCE.Pediatrics2002;110:137–142; peri-cardial effusion, cardiac tamponade, catheters, indwelling, infant.
ABBREVIATIONS. PCE, pericardial effusion; CVC, central venous catheter.
P
ericardial effusion (PCE) and fatal tamponade are complications of central venous catheter (CVC) use in infants. Although the estimated incidence is low,1 many case reports describe PCEand tamponade associated with CVC placement and infusion of parenteral nutrition.2–37 Questions
re-main regarding the optimal placement of the CVC tip, the safest access route, optimal CVC type, and the cause of the CVC-associated PCE effusion. We present the largest series of infants (n⫽14) who had PCE associated with CVC use and review previously reported cases (n ⫽ 47). We describe the clinical presentation, associated laboratory findings, cause, and outcomes encountered with this complication of CVC use to improve prevention, recognition, and outcome for neonates and young infants who require central venous access.
METHODS
We retrospectively reviewed the records of 14 infants (our cases) identified as having CVC-related PCE between 1995 and 1998 from 6 institutions. Our cases were obtained both by a review of our echocardiographic database and from personal experience/ recollection from multiple institutions. We also reviewed case reports (1970 –1999) of infants who had this complication and were ⱕ11 weeks postterm. From both our cases and the reviewed cases (combined cases), we abstracted the following data: gestational age (patients whose gestational age was reported as full term or were not reported were assumed to have a gestational age of 39 weeks), birth weight, day of life at CVC insertion, days to symp-toms/diagnosis of PCE, infusate glucose and lipid concentration, fluid administration rate, physical examination findings (rub, murmur, jugular venous distention, or pulsus paradoxus), cardiac rhythm at presentation, mode of presentation (unexplained car-diorespiratory instability or sudden cardiac decompensation), CVC type and insertion site, and last known CVC tip site. All cases were also evaluated for associated pleural effusion, previous tho-racic surgery, pericardiocentesis, withdrawal versus removal of
From the *Lillie Frank Abercrombie Section of Pediatric Cardiology, Texas Children’s Hospital, Baylor College of Medicine, Houston, Texas; ‡Chil-dren’s Hospital and Regional Medical Center, Seattle, Washington; and §Neonatology Associates Ltd, Phoenix, Arizona.
Received for publication May 12, 2000; accepted Mar 4, 2002
the CVC, and mortality. Biochemical evaluation of the pericardial fluid at the time of pericardiocentesis, surgery, or autopsy in-cluded glucose, triglycerides, total protein, white cell count, red cell count, and Gram stain and culture results. Patients were considered to have the CVC inserted in the right or left upper extremity when the CVC was reported in the respective brachial, cephalic, axillary, or subclavian vein. Patients were considered to have the CVC inserted in the right neck when the CVC was reported in the right internal or external jugular vein. Cardiotho-racic ratios before or at the time of CVC insertion and at the time of diagnosis were determined from 13 of our cases and available from 1 additional reviewed case. Data were not complete for all cases.
Statistical analysis was performed on the data from the com-bined group (our cases and the reviewed cases). A pairedttest was used to assess change in cardiothoracic ratios. Fisher’s exact test was used to assess the statistical significance of observed differences in mortality between patients who underwent pericar-diocentesis and those who did not. Simple logistic regression was used to test for associations between mortality and several possi-ble risk factors, including days to symptoms/diagnosis, age at diagnosis of PCE, birth weight, and gestational age. Simple un-balanced analysis of variance was used to determine differences in days to PCE across access sites and CVC types. Simple linear regression was used to assess the association between days to PCE diagnosis and catheter size as well as the association between CVC size and mortality. Contingency table analysis with Fisher’s exact testing was used to assess the associations between mortality and access sites and between CVC types and mortality.P⬍.05 was considered significant.
RESULTS
In our 14 cases, 6 different neonatology groups at 6 different hospitals in 2 cities administered care. All were receiving parenteral nutrition through the CVC. The median rate of infusion was 121 mL/kg/d (range: 70 –214). The clinical presentation in 8 cases was an acute cardiorespiratory change. In 6 of these cases, there was documented bradycardia, and in 5 cases, cardiopulmonary resuscitation was initiated. In 6 cases, the PCE was detected echocardiographi-cally during evaluation for an unexplained ventila-tor/inotropic requirement or for ductus arteriosus patency. In only 9 cases was an increase in cardio-thoracic ratio noted. Pericardiocentesis was per-formed in all 8 patients who presented acutely and in 1 of the remaining 6 cases. Five cases had smaller effusion without significant cardiac symptoms. The catheter was pulled back in 3 of these cases and removed in 2 cases with gradual resolution of the effusion. No patients died of complications related to the pericardial effusion.
In addition to the 14 cases in our study, 47 cases were identified through an exhaustive review of the literature. For the combined group, the median ges-tational age at birth was 30.0 weeks (range: 23.5– 42;
n⫽61) with a median birth weight of 1.0 kg (range: 0.38 – 6.3; n ⫽ 55). The median day of life of CVC insertion was 3.5 (range: 1–112;n⫽54). The median days from catheter insertion to symptoms/diagnosis of the PCE was 3.0 (range: 0.2–37; n ⫽ 59). The infusate glucose concentration ranged from 5 to 20
g/dL (median: 12.5;n⫽22). Reported intravenous lipid concentration (n⫽13) ranged from 10% to 20%. No patients were reported to present with a rub or jugular venous distention, and only 2 patients were noted to have pulsus paradoxus. Three patients pre-sented with a new murmur or abnormal cardiac sounds. Bradycardia was reported in 28 cases (46%),
and tachycardia was reported in 9 cases (15%). Sud-den cardiac collapse requiring cardiopulmonary re-suscitation was reported in 37 cases (61%), whereas unexplained cardiorespiratory instability was re-ported in 22 cases (36%). An associated pleural effu-sion was reported only in 4 cases (7%). In addition, only 7 patients reportedly had previous thoracic sur-gery: patent ductus arteriosus ligation in 3 patients, chest tube placement for pneumothorax/effusion in 3 patients, and esophageal repair in 1 patient. Mor-tality was 0% in our group, 45% (21 of 47) for the reviewed cases, and 34% (21 of 61) for the combined group. At last follow-up, none of the survivors had signs/symptoms of a PCE or constrictive pericardi-tis; median follow-up was 77 days (range: 7–540;n⫽
23).
The chest radiograph at the time of PCE diagnosis was reported as qualitatively enlarged in 25 cases (41%). The CVC was last reported within the cardiac silhouette by radiography or at autopsy in 50 cases (82%), at a right atrial/vena cavae junction in 6 cases (10%), in the superior vena cava in 4 cases, and in the left subclavian vein in 1 case. The mean cardiotho-racic ratio at the time of CVC placement was 0.48⫾ 0.07 standard deviation and at PCE diagnosis was significantly increased to 0.56⫾ 0.07 standard devi-ation (n⫽ 14;P ⬍.001).
In 5 cases, attempts to aspirate the PCE through the CVC were made without success. Pericardiocen-tesis was performed in 37 cases (61%). Mortality was 8% (3 of 37) in the patients who underwent pericar-diocentesis versus 75% (18 of 24) in the patients who did not (P⬍.001). In 21 patients (34%), the CVC was pulled back with continued use (13 of these patients also underwent pericardiocentesis). In only 2 cases did the PCE recur shortly after pericardiocentesis. Pericardial fluid was obtained in 54 cases and was described qualitatively as consistent with the infu-sate in 53 of 54 cases (98%). Biochemical analysis was performed in 37 cases, and in 36 of 37 cases (97%), at least 1 biochemical test was consistent with the infu-sate. Fluid analysis findings are summarized in Table 1. The Gram stain revealed no organisms (n ⫽ 7). Bacterial (n ⫽ 10), viral (n ⫽2), and fungal (n ⫽ 2) cultures were negative.
Data regarding mortality differences relative to gestational age, birth weight, days to symptoms/ diagnosis, and day of life at PCE are presented in Table 2. None of these variables was associated with mortality. Data regarding the CVC access site, mean days until PCE detection, and access site-specific mortality are presented in Table 3. The access site was not associated with days to PCE or mortality rate. Data regarding the CVC type, CVC size, mean days until PCE, and CVC-specific mortality are pre-sented in Table 4. There were no associations be-tween CVC types in mean days to PCE or mortality rate. The CVC size was not associated with mortality but may be inversely related to the mean days to PCE (P⫽ .051) such that with every 1 French increase in CVC size, the time to PCE decreases by 2.1 days.
Autopsy (n⫽ 18) or surgical findings (n⫽ 1) are reported in 19 cases.2– 6,12–21,36In 8 of 19 cases (42%),
tip was reported.5,12,13,15,17,18,20In these 8 cases,
silas-tic CVCs were used in 5, 1 was polyethylene, 1 was polyurethane, and the CVC type was not reported in 1 case. In 2 of these 8 cases, perforation was also detected (both associated with a silastic CVC). In 9 of 19 cases (47%), perforation without myocardial ne-crosis and/or thrombosis was detected3,4,6,12,14,19,36;
however, in 1 of these cases, a myocardial hematoma was noted.16In these 9 cases, the CVC type was not
reported in 3 cases, and there were 2 cases each with
silastic, polyethylene, and polyurethane CVCs. In 1 case, death was associated with a silastic CVC ob-structing the coronary sinus.2 In another case, no
perforation was detected and no microscopic de-scription was available.21 Myocardial necrosis,
thrombosis, or perforation was reported in the fol-lowing locations: right atrium (9); left atrium (3); right ventricle (2); and superior vena cava, superior vena cava/right atrial junction, or left subclavian vein (1).
TABLE 1. Biochemical Analysis of Pericardial Fluid
14 New Cases Case Reports All Cases
Median glucose (mg/dL) 1203 1960 1619
(range,n) (276–3150,n⫽8) (3–3020,n⫽18) (3–3150,n⫽26)
Median triglyceride (mg/dL) 137 1385 376
(range,n) (72–930,n⫽5) (600–2169,n⫽2) (72–2169,n⫽7)
Median total protein (g/dL) 0.4 0.4 0.4
(range,n) (0.2–1.0,n⫽3) (Too low to calculate–2.0,n⫽10) (Too low to calculate–2.0,n⫽13)
Median red blood cells/mm3 1538 1400 1538
(range,n) (244–26,750,n⫽7) (33–120,000,n⫽4) (33–120,000,n⫽11)
Median white blood cells/mm3 87 126 94
(range,n) (50–840,n⫽7) (2–18,700,n⫽7) (2–18,700,n⫽14)
TABLE 2. Mortality Data
Nonsurvivors (n) Survivors (n)
Case Reports/ All Cases⫾SD
14 New Cases⫾SD Case Reports⫾SD All Cases⫾SD
Mean gestational age at birth (wk) 33.6⫾6.3 (21) 30.6⫾6.8 (14) 31.3⫾5.3 (26) 31.0⫾5.8 (40)
Mean birth weight (kg) 1.8⫾1.4 (19) 1.8⫾1.5 (14) 1.4⫾0.8 (22) 1.6⫾1.1 (36)
Mean days to symptoms/diagnosis 4.3⫾4.7 (19) 5.9⫾4.0 (14) 5.2⫾8.9 (26) 5.4⫾7.5 (40)
Mean day of life at PCE 26.2⫾30.7 (16) 11.1⫾11.2 (14) 16.8⫾18.9 (24) 14.7⫾16.5 (38)
SD indicates standard deviation.
TABLE 3. Catheter Access Site, Days to PCE, and Mortality Rate
Total Mean Days to PCE⫾SD (n) Mortality Rate
14 New Cases
Case Reports
All Cases
14 New Cases
Case Reports
All Cases
14 New Cases
Case Reports
All Cases
Right neck 1 13 14 16 (1) 7.7⫾11.2 (11) 8.4⫾10.9 (12) 0/1 (0%) 6/13 (46%) 6/14 (43%)
Right upper extremity
1 12 13 12 (1) 4.8⫾9.3 (11) 5.4⫾9.1 (12) 0/1 (0%) 5/12 (42%) 5/13 (38%)
Left upper extremity
3 5 8 4.3⫾2.1 (3) 5.8⫾3.8 (5) 5.2⫾3.2 (8) 0/3 (0%) 3/5 (60%) 3/8 (38%)
Umbilical venous
9 12 21 4.6⫾2.1 (9) 2.6⫾1.5 (12) 3.4⫾2.0 (21) 0/9 (0%) 4/12 (33%) 4/21 (19%)
Lower extremity
0 3 3 1.2⫾0.7 (3) 1.2⫾0.7 (3) 1/3 (33%) 1/3 (33%)
Not reported 0 2 2 4.5⫾2.1 (2) 4.5⫾2.1 (2) 2/2 (100%) 2/2 (100%)
SD indicates standard deviation. Not all data available for all sites.
TABLE 4. Catheter Type, Size, Days to PCE, and Mortality Rate
Mean French Size (⫾SD) Mean Days to PCE (⫾SD) Mortality Rate Total
14 New Cases
Case Reports
All Cases
14 New Cases
Case Reports
All Cases
14 New Cases
Case Reports
All Cases
Silastic 3.5⫾1.2 (7) 2.2⫾1.0 (12) 2.7⫾1.2 (19) 6.9⫾4.6 (7) 6.8⫾9.6 (21) 6.8⫾8.6 (28) 0/7 (0%) 11/24 (46%) 11/31 (35%) Polyurethane 3.1⫾1.4 (7) 3.1⫾1.4 (5) 3.1⫾1.3 (12) 4.9⫾3.3 (7) 2.4⫾1.8 (8) 3.6⫾2.8 (15) 0/7 (0%) 3/8 (38%) 3/15 (20%)
Polyethylene (0) 3.7⫾1.2 (3) 3.7⫾1.2 (3) (0) 0.8⫾0.4 (4) 0.8⫾0.4 (4) 3/4 (75%) 3/4 (75%)
Polyvinyl (0) 5 (1) 5 (1) (0) 4 (1) 4 (1) 0/1 (0%) 0/1 (0%)
Not reported (0) 5 (1) 5 (1) (0) 2.6⫾2.1 (10) 2.6⫾2.1 (10) 4/10 (40%) 4/10 (40%)
SD indicates standard deviation.
DISCUSSION
PCE and fatal tamponade are complications of intracardiac CVCs. With the increased use of long-term CVCs in neonatal intensive care units, there have been many case reports of PCE associated with total parenteral nutrition. The thin wall of a prema-ture/neonatal heart probably is easier to damage than that of an older heart, with the myocardium normally absent in some sections of the atrial wall (covered only by epicardium and endocardium). Our cases were obtained both by a review of our echo-cardiographic database and from personal experi-ence/recollection from multiple institutions. The re-viewed cases were primarily individual case reports; therefore, both our cases and the reviewed cases were subject to selection and reporting bias with likely only the most severe cases either detected or reported. Nonetheless, because of the severity of the possible outcome and the potential for improvement with early recognition, we report data and analysis of 61 cases of CVC-related PCE.
Myocardial perforation and early effusion can oc-cur at the time of cannulation, secondary to wire use or direct CVC perforation.17,18,38In this study,
how-ever, for the combined group, the median time from catheter insertion to PCE detection was 3 days, sug-gesting that most effusions are not caused at the time of CVC insertion. The PCE was biochemically con-sistent with the infusate in 97% of cases tested (36 of 37). The exact cause of the relatively bloodless PCE remains in question. It may be secondary to a direct perforation that self-seals. Several authors, however, speculate that perforation is secondary to endocar-dial damage from repeated contact of the CVC tip with the myocardial wall, resulting in thrombus for-mation and adherence of the CVC to the myocardi-um.12,13,15,36,38 Hyperosmolar fluid in direct contact
with the endocardium then causes osmotic injury. Fluid transmurally diffuses across the myocardium, or the CVC erodes into the pericardial space, result-ing in a PCE that predominantly does not contain cellular elements. It has also been speculated that rapid injection of contrast or hyperosmolar agents at high pressure may increase the risk of perfora-tion.16,23,36 In our 14 cases, however, the median
glucose and lipid concentration and rate of infusion were within a range standard for supplying total parenteral nutrition. Thoracic surgery is known to be associated with a PCE; however, only 7 patients in the combined group underwent a thoracic proce-dure, and it did not seem to be the cause of the PCE. Review of the literature demonstrated 6 cases in which myocardial necrosis or thrombus formation was found with no evidence of perforation, 9 cases of perforation without myocardial necrosis/thrombus formation, and 2 cases in which both were detected. These data suggest that both perforation and osmotic causes are present. We speculate that a spectrum likely may exist between them, in which transmural diffusion of the infusate precedes actual perforation of the myocardium.
For the combined group, there was no significant association between CVC types or size and mortality
rate. With the small sample sizes, however, equality between groups has not been proved. In addition, within each CVC group, there were different brands; therefore, CVC stiffness within groups was not nec-essarily the same. Three studies in infants, adults, and in vivo have suggested that effusions are more common with polyethylene CVCs.12,39,40 Our data
suggest a possible inverse relationship between CVC size and mean days to PCE (P ⫽ .051), suggesting that for every 1 French increase in CVC size, the time to PCE decreases by 2.1 days. Caution in interpreting these data must be used, however, secondary to the small numbers of catheters in our report.
The autopsy observation that myocardial necro-sis/thrombus formation occurred predominantly with silastic CVCs (5 of 8 [63%]) suggests that silastic CVCs may be associated with a transmural cause for pericardial effusion formation. This data, however, may be attributable to an increased relative fre-quency of use of the silastic CVC and not to an increased incidence of myocardial necrosis/throm-bus formation or perforations. Previous studies, however, have suggested that the thin, flexible, silas-tic CVC may actually be less likely to perforate di-rectly.39No firm conclusions can or should be drawn
from these data. Controlled trials would be necessary to establish firmly whether there are any differences between CVC types.
There is considerable debate regarding the correct tip placement of a CVC. Studies in vitro and in adults suggest that an increased angle of incidence between the CVC tip and the cardiac/vessel wall increases the likelihood of perforation.39,41 For the combined
group, 82% of the CVC tips were last reported within the cardiac silhouette. An additional 10% were at a vena cavae junction with the right atrium, and there-fore 92% were documented within the pericardial reflections. We conclude that routine radiography should be performed on patients with CVC tips near the heart to ensure that the tip has not migrated. The CVC tip should remain outside the cardiac silhouette but still within the vena cavae (approximately 1 cm outside the cardiac silhouette in premature infants and 2 cm in term infants). In addition, in many patients, it can be difficult/impossible to determine accurately the CVC tip placement. Use of a more radio-opaque CVC or a marker on the tip would facilitate CVC tip monitoring. A position in the high superior vena cavae or below the inferior vena cavae/right atrial junction should keep the CVC out-side the pericardial reflections. There have been re-ports of intrathoracic or retroperitoneal/intra-ab-dominal extravasation from CVCs, and extracardiac placement may result in a higher incidence of those complications.12,19,42 Cardiac tamponade, because of
studies are necessary to define the safest CVC tip site.
The tip of the CVC is not fixed, and lateral neck flexion or arm movement may cause perforation, with arm movement causing greater CVC tip move-ment than neck movemove-ment.12,22,43This has led to the
suggestion that more proximal placement of a CVC may result in fewer PCEs.43,44 At least 1 study of
adults suggested that access from the left venous system increases the risk of perforation, presumably secondary to the increased angle of incidence of the CVC tip and the superior vena cavae.41The absence
of any significant difference between access routes in the time of detection of a PCE after CVC insertion, or mortality rate, suggests that no access route is more likely to cause a PCE earlier or with higher mortality rate. Equality between groups secondary to the small sample size, however, has not been proved and could be firmly established only with controlled tri-als.
The diagnosis of a PCE in these cases was primar-ily by suspicion of an increased cardiac silhouette, pericardiocentesis, or echocardiogram. That 61% pre-sented with sudden cardiac decompensation and 36% presented with unexplained cardiorespiratory instability demonstrates that clinical suspicion for a PCE must be high in any patient with a CVC. This is further emphasized by the observation that for the combined group, only 3 cases reported a new mur-mur, only 2 cases had pulsus paradoxus, and no cases had a rub or jugular venous distention. The cardiothoracic ratio was significantly increased (17%;
P⬍.001) at the time of PCE diagnosis. Therefore, an increased cardiothoracic ratio must also raise the suspicion of a PCE, although a normal cardiac sil-houette does not rule out a PCE and tamponade. Although echocardiography ordinarily should be used to confirm rapidly the diagnosis, its use should not delay emergency treatment in the infant who has manifestations of cardiac tamponade and whose heart size has suddenly increased.
Mortality from PCE has been estimated at 45% to 67%, which is secondary to the lack of warning signs and sudden decompensation.12,27 Mortality was 0%
in our cases, 45% in the reviewed cases, and 34% for the combined group. The high mortality of the re-viewed cases is at least partially attributable to late diagnosis (including autopsy diagnosis). Heightened awareness and education regarding the potential complications of CVCs likely helped to reduce the overall mortality for our cases. There was no signif-icant difference between survivors and nonsurvivors relative to gestational age at birth, birth weight, days to PCE diagnosis, or day of life of PCE symptoms/ diagnosis. Mortality was significantly less (8%; P ⬍
.001) in the patients who underwent pericardiocen-tesis versus those who did not (75%). Therefore, emergent drainage of a PCE must be considered in any patient with an intracardiac CVC with sudden cardiorespiratory instability. Although direct aspira-tion from the CVC was unsuccessful in these cases, it has been reported in adults and may be attempted but should not delay pericardiocentesis or echocar-diography.38Failure of direct aspiration may be
sec-ondary to thrombus formation around the tip of the CVC. If direct CVC aspiration fails, then emergent pericardiocentesis should be performed. The obser-vation that 21 cases were able to continue use of the CVC after the tip was withdrawn suggests that com-plete removal of the CVC may not be necessary. Close follow-up is necessary to ensure that the PCE does not reaccumulate.
CONCLUSION
CVC-associated PCE is a multi-institutional/mul-tigroup/multicity phenomenon. We report the larg-est series of cases (n⫽14) from 6 different hospitals and 6 different neonatology groups, along with 47 cases reported in the literature. Our experience and the large number of reviewed cases suggest that the frequency of CVC-induced PCE is more common than generally realized. Routine radiography should be performed and the CVC tip should be readily identifiable. The CVC tip should remain outside the cardiac silhouette but still within the vena cavae (approximately 1 cm outside the cardiac silhouette in premature infants and 2 cm in term infants). A change in cardiothoracic ratio may be diagnostic of a PCE. Pericardiocentesis was associated with signifi-cantly reduced mortality and must be considered in any patient who has sudden cardiovascular or respi-ratory decompensation and has a CVC. Withdrawal of the catheter outside the cardiac silhouette may allow continued use of the catheter. The pericardial fluid found in CVC-related PCE is consistent with that infusing through the CVC. The cause is likely a spectrum between frank perforation that self-seals and adhesion of the CVC to the myocardium with diffusion into the pericardial space. No CVC type was associated with a shorter interval to PCE diag-nosis. An association between larger catheters and shorter time to PCE may be present. There was no difference in mortality between access sites or CVC types and no significant difference between survi-vors and nonsurvisurvi-vors relative to gestational age at birth, birth weight, days to PCE diagnosis, or day of life of PCE symptoms/diagnosis. Equality between groups, however, has not been proved.
REFERENCES
1. Schiff DE, Stonestreet BS. Central venous catheters in low birth weight infants: incidence of related complications.J Perinatol.1993;13:153–158 2. Altman RP, Randolph JG. Application and hazards of total parenteral
nutrition in infants.Ann Surg.1971;174:85–90
3. Collier PE, Goodman GB. Cardiac tamponade caused by central venous catheter perforation of the heart: a preventable complication.J Am Coll Surg.1995;181:459 – 463
4. van Engelenburg KC, Festen C. Cardiac tamponade: a rare but life-threatening complication of central venous catheters in children.J Pe-diatr Surg.1998;33:1822–1824
5. Pesce C, Mercurella A, Musi L, Campobasso P, Negri M. Fatal cardiac tamponade as a late complication of central venous catheterization: a case report.Eur J Pediatr Surg.1999;9:113–115
6. Torres MA, Lima RV, Hernandez SF, los Santos LF, Arenas Leon JL, Falcon ER. [Cardiac tamponade in newborn infants with central venous catheter receiving parenteral nutrition].Arch Inst Cardiol Mex.1998;68: 64 – 68
7. Van Niekerk M, Kalis NN, Van der Merwe PL. Cardiac tamponade following umbilical vein catheterisation in a neonate. S Afr Med J.
8. Sutcliffe AG. Total parenteral nutrition tamponade.J R Soc Med.1995; 88:173P–174P
9. Fioravanti J, Buzzard CJ, Harris JP. Pericardial effusion and tamponade as a result of percutaneous silastic catheter use.Neonatal Netw.1998;17: 39 – 42
10. van Ditzhuyzen O, Ronayette D. [Cardiac tamponade after central venous catheterization in a newborn infant]. Arch Pediatr. 1996;3: 463– 465
11. Chang LY, Horng YC, Chou YH, Tsou KI. Umbilical venous line related pericardial effusion in a premature neonate: report of a case.J Formos Med Assoc.1995;94:355–357
12. Keeney SE, Richardson CJ. Extravascular extravasation of fluid as a complication of central venous lines in the neonate.J Perinatol.1995;15: 284 –288
13. Giacoia GP. Cardiac tamponade and hydrothorax as complications of central venous parenteral nutrition in infants.JPEN J Parenter Enteral Nutr.1991;15:110 –113
14. Johns AW, Kitchen WH, Leslie DW. Complications of umbilical vessel catheters.Med J Aust.1972;2:810 – 815
15. Rogers BB, Berns SD, Maynard EC, Hansen TW. Pericardial tamponade secondary to central venous catheterization and hyperalimentation in a very low birthweight infant.Pediatr Pathol.1990;10:819 – 823
16. Purohit DM, Levkoff AM. Pericardial effusion complicating umbilical venous catheterization.Arch Dis Child.1977;52:520
17. Byard RW, Bourne AJ, Moore L, Little KE. Sudden death in early infancy due to delayed cardiac tamponade complicating central venous line insertion and cardiac catheterization.Arch Pathol Lab Med.1992;116: 654 – 656
18. Bar-Joseph G, Galvis AG. Perforation of the heart by central venous catheters in infants: guidelines to diagnosis and management.J Pediatr Surg.1983;18:284 –287
19. Mupanemunda RH, Mackanjee HR. A life-threatening complication of percutaneous central venous catheters in neonates.Am J Dis Child.
1992;146:1414 –1415
20. Garg M, Chang CC, Merritt RJ. An unusual case presentation: pericar-dial tamponade complicating central venous catheter.J Perinatol.1989; 9:456 – 457
21. Sullivan CA, Konefal SH Jr. Cardiac tamponade in a newborn: a com-plication of hyperalimentation.JPEN J Parenter Enteral Nutr.1987;11: 319 –321
22. Fischer GW, Scherz RG. Neck vein catheters and pericardial tampon-ade.Pediatrics.1973;52:868 – 871
23. Cherng YG, Cheng YJ, Chen TG, Wang CM, Liu CC. Cardiac tampon-ade in an infant. A rare complication of central venous catheterisation.
Anaesthesia.1994;49:1052–1054
24. Kulkarni PB, Dorand RD, Simmons EM Jr. Pericardial tamponade: complication of total parenteral nutrition.J Pediatr Surg.1981;16:735–736 25. Beattie PG, Kuschel CA, Harding JE. Pericardial effusion complicating a percutaneous central venous line in a neonate.Acta Paediatr.1993;82: 105–107
26. Khilnani P, Toce S, Reddy R. Mechanical complications from very small percutaneous central venous silastic catheters.Crit Care Med.1990;18: 1477–1478
27. Wirrell EC, Pelausa EO, Allen AC, Stinson DA, Hanna BD. Massive pericardial effusion as a cause for sudden deterioration of a very low birthweight infant.Am J Perinatol.1993;10:419 – 423
28. Walker D, Pellett JR. Pericardial tamponade secondary to umbilical vein catheters.J Pediatr Surg.1972;7:79 – 80
29. Neubauer AP. [250 central venous silastic catheters in premature infants less than 1.500 g. A clinical study of technique and complications].
Monatsschr Kinderheilkd.1991;139:810 – 815
30. Savani RC, Valentini RP, Mimouni F. Neonatal radiology casebook. Pericardial effusion as a complication of umbilical catheterization.J Perinatol.1990;10:443– 445
31. Scharf J, Rey M, Schmiedl N, Stehr K. [Pericardial tamponade as a complication of the use of peripheral percutaneous silastic catheters].
Klin Padiatr.1990;202:57–59
32. Donnou-Da Lage MD, Guillois B, Colin A, Alix D. [Neonatal hydroperi-cardium caused by a silicone epicutaneo-caval catheter].Pediatrie.1988; 43:23–25
33. Chatel-Meijer MP, Roques-Gineste M, Fries F, et al. [Cardiac tamponade secondary to umbilical venous catheterization accident in a premature infant].Arch Fr Pediatr.1992;49:373–376
34. Sigda M, Speights C, Thigpen J. Pericardial tamponade due to umbilical venous catheterization.Neonatal Netw.1992;11:7–9
35. Opitz JC, Toyama W. Cardiac tamponade from central venous catheterization: two cases in premature infants with survival.Pediatrics.
1982;70:139 –140
36. Agarwal KC, Khan MA, Falla A, Amato JJ. Cardiac perforation from central venous catheters: survival after cardiac tamponade in an infant.
Pediatrics.1984;73:333–338
37. Aiken G, Porteous L, Tracy M, Richardson V. Cardiac tamponade from a fine silastic central venous catheter in a premature infant.J Paediatr Child Health.1992;28:325–327
38. Defalque RJ, Campbell C. Cardiac tamponade from central venous catheters.Anesthesiology.1979;50:249 –252
39. Gravenstein N, Blackshear RH. In vitro evaluation of relative perforat-ing potential of central venous catheters: comparison of materials, se-lected models, number of lumens, and angles of incidence to simulated membrane.J Clin Monit.1991;7:1– 6
40. Bersten AD, Williams DR, Phillips GD. Central venous catheter stiffness and its relation to vascular perforation.Anaesth Intensive Care.1988;16: 342–351
41. Tocino IM, Watanabe A. Impending catheter perforation of superior vena cava: radiographic recognition.AJR Am J Roentgenol.1986;146: 487– 490
42. Spriggs DW, Brantley RE. Thoracic and abdominal extravasation: a complication of hyperalimentation in infants.AJR Am J Roentgenol.
1977;128:419 – 422
43. Maschke SP, Rogove HJ. Cardiac tamponade associated with a multi-lumen central venous catheter.Crit Care Med.1984;12:611– 613 44. Kalen V, Medige TA, Rinsky LA. Pericardial tamponade secondary to
DOI: 10.1542/peds.110.1.137
2002;110;137
Pediatrics
Thomas A. Vargo
Todd T. Nowlen, Geoffrey L. Rosenthal, Gregory L. Johnson, Deborah J. Tom and
Pericardial Effusion and Tamponade in Infants With Central Catheters
Services
Updated Information &
http://pediatrics.aappublications.org/content/110/1/137
including high resolution figures, can be found at:
References
http://pediatrics.aappublications.org/content/110/1/137#BIBL
This article cites 44 articles, 3 of which you can access for free at:
Subspecialty Collections
http://www.aappublications.org/cgi/collection/cardiology_sub Cardiology
following collection(s):
This article, along with others on similar topics, appears in the
Permissions & Licensing
http://www.aappublications.org/site/misc/Permissions.xhtml
in its entirety can be found online at:
Information about reproducing this article in parts (figures, tables) or
Reprints
http://www.aappublications.org/site/misc/reprints.xhtml
DOI: 10.1542/peds.110.1.137
2002;110;137
Pediatrics
Thomas A. Vargo
Todd T. Nowlen, Geoffrey L. Rosenthal, Gregory L. Johnson, Deborah J. Tom and
Pericardial Effusion and Tamponade in Infants With Central Catheters
http://pediatrics.aappublications.org/content/110/1/137
located on the World Wide Web at:
The online version of this article, along with updated information and services, is
by the American Academy of Pediatrics. All rights reserved. Print ISSN: 1073-0397.
