Port Catheter Fracture: A Silent Intrusion into the Right Ventricle

Abstract

Central venous port-a-catheters play a pivotal role in various medical procedures, yet they are associated with a spectrum of complications. Catheter fracture with cardiac migration is a rare complication, occurring in less than 1% of patients. Although not very common, it can cause severe issues, necessitating fragment removal. We present a case of spontaneous mediport fracture and migration in a patient with a history of Hodgkin’s lymphoma and prior chemotherapy. He presented with nausea, vomiting, and tachycardia. Further evaluation revealed elevated total leukocyte count and labs consistent with diabetic ketoacidosis. He was diagnosed with new-onset diabetes mellitus. Imaging studies confirmed the presence of the fragmented catheter within the right ventricle. Although telemetry monitoring and electrocardiogram (EKG) did not detect arrhythmias, interventional radiology successfully removed the critical fragment from the right ventricle while leaving two smaller non-intravascular fragments in the neck. This case underscores the importance of early identification and interdisciplinary collaboration in managing port catheter fractures and migrations, even in the absence of typical symptoms.

1. Background

Amediport or a port-a-cath is a type of central venous catheter that is placed subcutaneously and terminates at the junction of the superior vena cava and right atrium. It is used for venous blood sampling and medication administration like chemotherapy. Catheter breakage with cardiac migration is a rare complication that occurs in less than 1% of patients.1,2 The fractured mediport can migrate and dislodge in the superior vena cava, right atrium and ventricle, inferior vena cava, or pulmonary artery. It may cause thrombosis, embolism, cardiac perforation, cardiac arrest, and arrhythmias, necessitating the removal of the fragment either surgically or endovascular removal. Herein we describe a case of spontaneous fracture and migration of a fragment of the mediport in a patient who did not have any symptoms pertaining to catheter migration and later had it removed successfully by interventional radiology (IR).

Our case report highlights the importance of maintaining a high level of vigilance and conducting patient education for patients with indwelling mediports.

2. Case presentation

A 47-year-old male with a medical history significant for Hodgkin’s lymphoma status post doxorubicin, bleomycin, vinblastine, and dacarbazine therapy four years prior, in remission, presented to the emergency department with nausea and vomiting for three days. On admission, vitals were significant for tachycardia with a heart rate of 123/min. His blood work was remarkable for total leukocyte count (TLC) of 33.86 × 10³/mm³ with a left shift with 81% neutrophils and 4% lymphocytes, suggesting reactive etiology, glucose 469 mg/dL, bicarbonate 12 mEq/L, and an anion gap of 26 mEq/ L. He was found to have new-onset diabetes mellitus and was admitted for an insulin drip for the management of diabetic ketoacidosis. Due to elevated TLC, a chest x-ray (CXR) was done (Fig. 1A), which showed a disrupted mediport with a portion of it within the right ventricle. He also got a computed tomography (CT) of the chest (Fig. 1B) demonstrating the same.

Fig. 1.

(A) Chest X-ray showing a disrupted mediport with fractured segments and their dimensions. (B) CT Chest displaying a dislodged mediport.

However, chest imaging did not reveal any signs of infection. Similarly, urinalysis did not indicate any evidence of infection. Flow cytometry was negative. The leukocytosis observed resolved the next day. It was likely attributable to non-infectious systemic inflammation associated with diabetic ketoacidosis and broken port-a-cath. Telemetry monitoring and electrocardiogram (EKG) did not show any arrhythmias. Interventional radiology was consulted. They successfully retrieved the broken fragment of the mediport from the right ventricle. Two smaller fragments in the soft tissues of the neck were left in place, given their depth and the fact that they were not intravascular. The patient remained asymptomatic throughout and was discharged with a follow-up scheduled with his primary care physician. Additionally, it was explained to him that in the future, should he develop sepsis or bacteremia, consideration should be given to the removal of the small fragments, as they may serve as a potential source for infection. Although the suspicion of malignancy recurrence was low, given the resolution of leukocytosis, he was also advised to follow up with hematology/oncology outpatient.

3. Discussion

Complications of port catheters can emerge during the implantation procedure or maintenance period. Early complications occur within 30 days of implantation and include pneumothorax, hemothorax, and malposition. In contrast, delayed complications that occur in the maintenance period occur after 30 days and include thrombosis, infection, and catheter fracture with migration. Catheter fracture with migration is infrequent, occurring in less than 1% of the patients.1

There are three primary causes of port catheter fracture or dissection. First, there is pinch-off syndrome (POS), a mechanical complication that occurs when the catheter gets compressed between the clavicle and the first rib.3,4 Second, external contact forces, such as the use of seatbelts, can contribute to fracture. Finally, flushing the catheter with a small syringe can generate excessive pressure inside the catheter, leading to weakening and eventual fracture over time.3 Other documented risk factors include manufacturing defects, material fatigue, improper fixation of the port to local tissue, causing movement at the port-catheter junction, and infection. Certain catheter materials, especially polyurethane, have also been associated with a higher risk of fracture.5,6 No definitive association has been established between the type of chemotherapy received and the incidence of port fractures.

The most prevalent sites of migration are within the right heart chambers.7 The site of migration depends on a number of factors, including the route of entry, catheter materials, flow patterns in the vessel or heart chambers, and the patient’s position during fracture. The most common locations include the superior vena cava-right atrium (23.9%), right atrium-inferior vena cava (20.6%), right atrium-hepatic vein (11.9%), and right atrium-right ventricle (10.8%).8

The clinical manifestations of port catheter fracture encompass a range of symptoms, including asymptomatic cases, resistance to irrigation, mild pain or swelling in the clavicular region, shoulder pain, chest discomfort, and potentially lethal arrhythmias.7,8 In most instances, patients experience minimal or no symptoms. The migration of a fractured port catheter fragment can lead to severe complications. Some notable complications are pseudoaneurysm, ventricular rupture, cardiac tamponade, thrombosis, dysrhythmia, endocarditis, or sepsis.

To prevent such fractures, it is advisable to insert the catheter more laterally to the mid-clavicular line, where the angle between the clavicle and the first rib is wider. Other methods to reduce the complication of POS include repeating chest x rays (CXRs) every 2–3 months to look for catheter indentation at the thoracic inlet, removing the catheter if the imaging is suggestive of catheter indentation, and instructing the patient to avoid aggressive shoulder movements.3,4,9 Central venous port-a-catheters need regular heparinization, accomplished by employing a 10 mL syringe right after each utilization or on a monthly basis when not in active use.10

Prompt extraction of the fragmented catheter is recommended to prevent these complications, which can be achieved through either endovascular intervention or a surgical approach. Endovascular intervention is the preferred method due to its effectiveness and lower complication rate compared to surgery.4,11 Prior to non-surgical or surgical interventions, a thorough evaluation of the foreign body’s exact position and size should be conducted.

Our patient did not exhibit any symptoms or signs related to catheter fracture and migration. Following the completion of chemotherapy for Hodgkin’s lymphoma, he did not maintain regular follow-ups with his primary care physician or oncologist, leading to a missed opportunity for repeat chest X-rays and potential mediport removal. His hospitalization for diabetic ketoacidosis incidentally unveiled a port-a-cath fracture with fragment migration into the right ventricle. Our case highlights the significance of routine surveillance through chest X-rays to detect potential complications such as fractures, the timely retrieval of fragmented catheters in case of fracture occurrence, and the removal of catheters if not in use as a precautionary measure.