Cardiac tamponade with chylopericardium in a 6-year-old boy with central venous catheter: a case report

Article information

Pediatr Emerg Med J. 2024;11(2):75-81
Publication date (electronic) : 2024 January 9
doi :
1Department of Pediatrics, Seoul National University Hospital, Seoul, Republic of Korea
2Department of Integrated Care Center, Seoul National University Hospital, Seoul, Republic of Korea
3Department of Emergency Medicine, Seoul National University Hospital, Seoul, Republic of Korea
Corresponding author: Bongjin Lee Department of Pediatrics, Seoul National University Hospital, 101 Daehak-ro, Jongno-gu, Seoul 03080, Republic of Korea Tel: +82-2-2072-3682; E-mail:
*Current affiliation: Department of Pediatrics, The Catholic University of Korea, Seoul St. Mary’s Hospital, Seoul, Republic of Korea
†Current affiliation: Department of Pediatrics, Chung-Ang University Hospital, Seoul, Republic of Korea
Received 2023 November 10; Revised 2024 January 2; Accepted 2024 January 3.

Trans Abstract

Cardiac tamponade (CT) is a rare but potentially lethal complication associated with central venous catheters (CVCs). We present a 6-year-old boy who developed CT after CVC insertion in the right internal jugular vein, with its tip in the inferior vena cava. Initially, he was hospitalized to a tertiary hospital with presumptive diagnoses of pneumonia and left ankle cellulitis. Three days after CVC placement, he developed CT, manifesting as recurrent episodes of hypotension and bradycardia. Once a bedside echocardiography showed CT, pericardiocentesis was performed, resulting in successful resuscitation. Pericardiocentesis revealed a milk-appearing pericardial fluid, indicating chylopericardium. The boy also underwent debridement and joint irrigation of the left ankle, which turned out to be osteomyelitis. Although CVC tips in most reported CVC-related CTs have been commonly located in the right atrium, our case featured a tip located in the inferior vena cava. Additionally, chylopericardium was likely due to the extravasation of total parenteral nutrition fluid, rather than the usual causes, such as recent thoracic surgery. Understanding the mechanisms behind chylopericardium associated with CVCs and timely pericardiocentesis is crucial for improving the outcomes.


Cardiac tamponade (CT) is an infrequent yet life-threatening complication associated with central venous catheters (CVCs), caused by various factors such as catheter tip position, catheter drift, and chemical injury (1-3). Most CVC-related CTs have been reported in neonates or adults (4-6). According to a review article involving patients of all ages undergoing CVC placement, 1.7% (110 of 6,449) developed iatrogenic injuries, of whom 47.3% (52 of 110) died (7). In the study, 14.5% (16 of 110) had CTs with an 81.3% (13 of 16) case fatality rate (7). Timely recognition and management of CT are crucial for improving the outcomes, necessitating a high index of suspicion and the use of diagnostic tools like echocardiography (8,9).

The exact etiology of CVC-related CT remains uncertain. However, clinical and autopsy findings suggest that mechanical injury or chemical damage caused by hypertonic saline might contribute to its development (4,10,11). The myocardium in neonates, which is incompletely muscularized, may possess areas of weakness that render it susceptible to injury (12). Hou and Fu (4) reviewed 24 neonatal cases of CT associated with peripherally inserted CVCs. Among these cases, 19 exhibited the catheter tip located in the right atrium, suggesting that myocardial damage and microperforation may contribute to the development of CT.

This article presents a case of CVC-related CT with chylopericardium in a 6-year-old boy who was hospitalized in the pediatric intensive care unit (PICU) following CVC placement, with its tip placed in the inferior vena cava. The study was approved by the institutional review boards of the hospital’s ethics committee and the guardian’s consent for publication has been obtained (IRB no. 2309-091-1466).


A 6-year-old boy visited the emergency department of a tertiary hospital. He had been experiencing a fever for 3 days, and his dyspnea worsened on the day of hospitalization. He had underlying L1 cell adhesion molecule protein mutation-related malformation of the cerebral cortex.

Initial vital signs were as follows: blood pressure, 136/91 mmHg; heart rate, 154 beats/minute; respiratory rate, 60 breaths/minute; temperature, 39.1 °C; oxygen saturation, 85% on room air; and alert mentality. His weight and height were 22 kg (25th-50th percentile) and 122 cm (90th-95th percentile), respectively. The boy exhibited subcostal retraction and coarse breath sounds. Subsequently, he received oxygen at 1 L/min via nasal prong. Meanwhile, he exhibited edema, heat, and tenderness in the left ankle, which had lasted for 3 days, without a trauma history. A chest radiograph showed ground-glass opacities in both lungs. Laboratory findings showed a high concentration of C-reactive protein (Table 1). With presumptive diagnoses of pneumonia and left ankle cellulitis, and intravenous infusion of cefazolin, the boy was hospitalized to the general ward.

Initial laboratory findings

On day 2, an ankle sonography revealed diffuse soft tissue swelling at the left ankle and foot, without evidence of joint effusion. Given that the boy’s oxygen saturation remained at around 90% on oxygen at 1 L/minute via nasal prong, the oxygen delivery method was changed to a simple face mask at 4 L/minute. The antibiotics were escalated to vancomycin and piperacillin-tazobactam. A follow-up chest radiograph showed no interval change. Given the desaturation, a chest computed tomography was performed (Appendix 1,, confirming the ground-glass opacities in both lungs shown by the initial radiograph.

On day 4, due to the worsening respiratory distress, the boy was transferred to the PICU and underwent endotracheal intubation. On the same day, sonography-guided central venous catheterization was conducted by a pediatric intensivist at the first attempt on the right internal jugular vein (Fig. 1A). The depth of insertion was 12 cm from the skin, and a 5.5-French catheter was used. Immediately after CVC insertion, sonography confirmed that the catheter tip was located in the inferior vena cava. Antibiotics were changed to vancomycin and meropenem. On day 6, 2 days after PICU transfer, total parenteral nutrition (TPN) was initiated for nutritional support during mechanical ventilation. At this time, increases were noted in the concentrations of C-reactive protein (32.64 mg/dL) and B-type natriuretic peptide (312 pg/mL) while creatine kinase-MB and troponin I remained within the normal limits.

Fig. 1.

Serial chest radiographs. At transfer to the pediatric intensive care unit (day 4), it shows the tip of central venous catheter located in the inferior vena cava (arrowheads). An endotracheal (asterisks) and nasogastric tubes (arrows) are inserted (A). The tip position remains unchanged when sudden hypotension and bradycardia develop, before pericardiocentesis (day 7) (B), and after the pericardiocentesis (day 8) (C).

On day 7, the boy suddenly showed a blood pressure of 47/36 mmHg and a heart rate of 30 beats/minute (Fig. 1B). Cardiopulmonary resuscitation was initiated immediately. After administering an epinephrine bolus, the vital signs rapidly recovered. However, the sudden change in vital signs repeated 5 times. Bedside echocardiography revealed a significant amount of pericardial effusion, along with systolic right atrial collapse and diastolic right ventricular collapse. Approximately 90 minutes after the occurrence of hypotension and bradycardia, pericardiocentesis was performed by a pediatric intensivist via subxiphoid approach, successfully resuscitating the boy at the first attempt. A total of 7.5 mL of milky pericardial fluid was aspirated (Appendix 2, The fluid was featured by a high triglyceride level (309 mg/dL), a cholesterol/triglyceride ratio of 0.03 (Table 2), and negative fluid bacterial culture. These features indicated a chylopericardium according to a scoring system (13).

Pericardial fluid analysis on day 7

Following the pericardiocentesis (Fig. 1C), echocardiography showed a moderate amount of pericardial effusion, primarily localized to the apex (Fig. 2). The CVC was removed, and subsequent echocardiography conducted after 7 hours of the removal revealed a trivial amount of pericardial effusion (Appendix 3, An electrocardiogram performed after the pericardiocentesis showed normal sinus rhythm without ST segment elevation though we did not obtain an electrocardiogram taken during the episodes of bradycardia. The pericardial fluid culture showed no growth.

Fig. 2.

After pericardiocentesis (day 7), a follow-up echocardiogram demonstrates a moderate amount of pericardial effusion. The fluid depths were 5.7 and 4.4 mm in the posterior of left ventricle on a parasternal long-axis view (A) and in the posterior of left ventricle on a parasternal short-axis view (B), respectively.

On day 9, the boy’s left foot swelling continued to worsen, accompanied by elevated values of inflammatory markers. To further investigate the cause of swelling, magnetic resonance imaging was conducted. The imaging revealed osteomyelitis and septic arthritis in the left ankle, which required debridement and joint irrigation by orthopedic surgeons under general anesthesia. The joint fluid culture proved methicillin-sensitive Staphylococcus aureus, while the blood culture showed no growth.

On day 17, follow-up echocardiography showed no pericardial effusion and good left ventricular contractility. The boy was extubated on day 18 and was started on high-flow nasal cannula therapy. On day 21, nasal bi-level positive airway pressure was initiated, and he was transferred to the ward on day 24. Finally, he was discharged uneventfully on day 56.


This current case presents a pediatric patient who developed CT with chylopericardium following CVC placement. This infrequent yet life-threatening complication adds to our understanding of potential risks in children undergoing the procedures. Additionally, the presence of chylopericardium highlights the need for investigation of the underlying mechanisms.

The exact etiology of CVC-related CT remains unclear. However, potential causes include mechanical injury during insertion, catheter migration, mechanical erosion, or chemical damage by hypertonic saline (14). Several risk factors have been associated with CVC-related CT, such as peripherally inserted CVC, improper adhesion and suturing of the catheter, catheter tip placement at a 90° angle to the endocardial wall, non-curved metallic guidewire, and flexible catheters (15). None of such factors were present in this current case.

Most reported cases of CVC-related CT have been associated with the catheter tip located either in the right atrium or in direct proximity to the pericardium (4). In contrast, in the current case, the tip was located in the inferior vena cava, and did not change during hospitalization (Fig. 1). This atypical location of the CVC tip suggests the presence of different mechanisms or contributing factors in the development of CT in this case.

Although the etiology of the case patient’s chylopericardium remains unknown, extravasation of TPN may be the most plausible cause. Secondary chylopericardium can occur due to cardiothoracic surgery, trauma, thrombus in the jugular vein, radiation therapy, lymphoma, or other malignancies. However, in the current case, there was neither a history of trauma nor a clinical manifestation of underlying malignancy. Chylopericardium or chylothorax associated with CVCs has been reported across a broad range of ages, and some cases suggest a connection with venous thrombosis (16-20). In the cited cases, catheter occlusions were clinically apparent and confirmed through imaging studies or autopsy. In our case, uncertainty of the cause of chylopericardium was attributed to the lack of signs of catheter occlusion and of imaging studies for venous thrombosis before the CVC removal. Despite another possibility of direct injury of the lymphatics during the CVC insertion, this possibility seems unlikely since the catheter was inserted at the first attempt and there was no swelling in the supraclavicular fossa before the cardiopulmonary resuscitation (21). An additional hypothesis is the extravasation of TPN solution because the pericardial fluid had a high glucose level (947 mg/dL), similar to currently available TPN solutions (22,23). According to the aforementioned scoring system (13), the boy scored 2 points, with a total cholesterol/triglyceride ratio of less than 1 and negative fluid bacterial culture. The 2 points strongly suggested the chylopericardium.

Prompt pericardiocentesis successfully managed the CT in the case patient who had no underlying heart disease. This critical intervention occurred 3 days after the CVC placement, and the boy was discharged safely on day 56. After the intervention, he showed the resolution of CT and improvement in ventricular contractility. Despite his favorable outcome, it is important to acknowledge the potential challenges and complications that may arise during the management of CT, particularly in children (24).

There is a connection between osteomyelitis and endocarditis because the former entity may occur as a complication of the latter (25). However, the impact of the severe infection on endocardial vulnerability is not fully understood.

In conclusion, this case report highlights the importance of early recognition and prompt management of CVC-related CT in children. The unique feature of chylous fluid accumulation within the pericardium highlights the need for increased awareness of potential complications related to CVC placement. Understanding the mechanisms underlying chylopericardium associated with CVCs can guide the development of preventive strategies. Emergency physicians or pediatricians should maintain a high level of suspicion and adhere to best practices in CVC placement and monitoring.


Author contributions

Conceptualization, Formal analysis, and Investigation: IK Lee and B Lee

Data curation, Methodology, Project administration, Resources, Software, Supervision, Validation, and Visualization: IK Lee

Writing-original draft: IK Lee

Writing-review and editing: all authors

All authors read and approved the final manuscript.

Conflicts of interest

No potential conflicts of interest relevant to this article were reported.

Funding sources

No funding source relevant to this article was reported.

Data availability

All data generated or analyzed during this study are included in this published article.


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Appendix 1. Chest computed tomography finding (day 2). It shows multifocal patchy and nodular ground glass opacities at both lungs, suggestive of bronchopneumonia.


Appendix 2. Clinical photo graph s of the pericardial fluid (day 7). A total of 7.5 mL of milky pericardial fluid was aspirated


Appendix 3. A follow up echocardiogram (day 8), taken 7 hours after r emoval of the central venous catheter , showed a trivial amount of pericardial effusion.


Article information Continued

Fig. 1.

Serial chest radiographs. At transfer to the pediatric intensive care unit (day 4), it shows the tip of central venous catheter located in the inferior vena cava (arrowheads). An endotracheal (asterisks) and nasogastric tubes (arrows) are inserted (A). The tip position remains unchanged when sudden hypotension and bradycardia develop, before pericardiocentesis (day 7) (B), and after the pericardiocentesis (day 8) (C).

Fig. 2.

After pericardiocentesis (day 7), a follow-up echocardiogram demonstrates a moderate amount of pericardial effusion. The fluid depths were 5.7 and 4.4 mm in the posterior of left ventricle on a parasternal long-axis view (A) and in the posterior of left ventricle on a parasternal short-axis view (B), respectively.

Table 1.

Initial laboratory findings

Finding Value
Complete blood count
 White blood cells, ×103/mm3 13
 Red blood cells, ×106/mm3 3.4
 Hemoglobin, g/dL 11.1
 Hematocrit, % 31.7
 Platelets, ×103/mm3 234
 Segmented neutrophils, % 74.1
 Sodium, mmol/L 132
 Potassium, mmol/L 3.7
 Chloride, mmol/L 94
 Calcium, mg/dL 8.3
 Phosphorus, mg/dL 3.7
 Blood urea nitrogen, mg/dL 5
 Creatinine, mg/dL 0.36 (reference, 0.3-0.7)
 C-reactive protein, mg/dL 25.96
B-type natriuretic peptide, pg/mL 262 (reference, < 100)
Creatine kinase-MB, ng/mL 0.4 (reference, < 5.0)
Troponin I, pg/mL < 0.1 (reference, < 45.2)

Table 2.

Pericardial fluid analysis on day 7

Finding Value
Color White
Turbidity Turbid
Red blood cells, /mm3 0
White blood cells, /mm3 648
  Polymorphonuclear 14
  Lymphocytes 6
  Others 80
Cholesterol, mg/dL 10 (reference, 0-240)
Albumin, g/dL 1.1
Triglyceride, mg/dL 309 (reference, 0-200)
Protein, g/dL 3.6
Glucose, mg/dL 947
Chloride, mmol/L 91