661331
research-article2016
CPJXXX10.1177/0009922816661331Clinical PediatricsShapiro et al
Resident Round
A Toddler With Central Venous Catheter Develops Tachycardia
Clinical Pediatrics 2017, Vol. 56(5) 496–499 © The Author(s) 2016 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/0009922816661331 journals.sagepub.com/home/cpj
Douglas Ryan Shapiro, MD1, Christopher J. Dudek, MD1, and Jason G. Ho, MD2
Case Report Our patient was a 23-month-old male with total parenteral nutrition dependence due to a neonatal history of short-gut syndrome secondary to necrotizing enterocolitis. He was hospitalized for a central line–associated infection with Candida albicans. Transthoracic echocardiography showed no evidence of vegetations or valve dysfunction; however, a borderline dilated left ventricle with normal systolic function and a very small pericardial effusion were noted.
Hospital Course Following initiation of antimicrobial therapy and repeat negative blood cultures, the patient underwent central line replacement. In the operating room under general anesthesia, pediatric surgery service inserted a 6.5-French Cook catheter into the child’s left internal jugular vein. The position of the line was confirmed to be in the right atrium by both intraoperative fluoroscopy and postoperative portable chest radiograph. Of note, the child’s vital signs prior to leaving recovery were within normal limits. After returning to the floor from the recovery area, he was noted to be in a narrow-complex tachycardia with heart rates of 230 to 240 beats per minute. Despite this, the patient was without symptoms, sitting comfortably, and eating. An electrocardiogram confirmed the rhythm as supraventricular tachycardia (SVT). The patient remained hemodynamically stable. Following repeat chest radiograph, the pediatric electrophysiology service was consulted and reviewed the electrocardiogram and chest radiograph. The recommendations were for the central line to be adjusted. The pediatric surgeon brought the patient back to the operating room where the line was pulled back 2 to 3 cm using fluoroscopy for confirmation. Vagal maneuvers were not successful in terminating the SVT. The patient was then converted to normal sinus rhythm following administration of adenosine (0.15 mg/kg/dose). Pediatric electrophysiology service recommended starting oral maintenance digoxin, and there were no further cardiac
events for the remainder of his hospitalization and through his clinic follow-up.
Final Diagnosis Supraventricular tachycardia triggered by central venous catheter placement.
Discussion Central venous catheters (CVCs) are useful for children requiring regular administration of medications and total parenteral nutrition.1 Proper positioning of CVC has been discussed in the literature; however, standard guidelines for optimal position and methods for confirming CVC position are lacking in the literature.2 Despite Food and Drug Administration recommendations to avoid CVC placement within heart chambers and traditionally safe practice for CVC tips to terminate in the superior vena cava–right atrial (SVC-A) junction,3-5 some argue in favor of right atrial placement for young patients with potential to grow.6 While the debate continues over the proper location of the distal CVC tip, accurately identifying anatomical landmarks pose its own challenge.2 Fluoroscopic placement of CVC with postplacement confirmatory chest radiograph have been the historical standard of care. However, recent pediatric literature has recommended omitting the chest radiograph in uncomplicated cases.7 The complications of CVC include infection, pneumothorax, chylothorax, arterial injury, arrhythmia, hematoma, thrombosis, air embolism, pericardial effusion, and tamponade.8-13 In the pediatric literature, arrhythmias have been categorized epidemiologically as 1
Department of Pediatrics, University of Florida College of Medicine, Jacksonville 2 Pediatric Cardiology, Department of Pediatrics, University of Florida College of Medicine, Jacksonville Corresponding Author: Douglas Ryan Shapiro, University of Florida College of Medicine, 841 Prudential Drive, Suite 1130, Jacksonville, FL 32209-6511, USA. Emails:
[email protected]
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Shapiro et al an insertion-related complication of CVC.14,15 The most common types of arrhythmias we found in the literature were atrial flutter16,17 and SVT.18-21 Central venous lines are thought to trigger arrhythmias through irritation of endocardium.22 In some cases, delayed-onset arrhythmias were caused by migrating CVC tips23 or patient positional changes.24,25 Here we report a case of pediatric postoperative SVT within hours of CVC placement. SVT is an accelerated, nonsinus rhythm originating above the level of the atrioventricular (AV) junction that usually can be classified based on electrophysiologic characteristics.26,27 This rhythm bypasses the innate delay in the AV node, which in turn creates a rapid ventricular rate. For narrow-complex SVT, there are 3 mechanisms that can produce this effect: atrioventricular reentrant tachycardia (AVRT), atrioventricular nodal reentrant tachycardia (AVNRT), and atrial ectopic tachycardia.28 AVRT involves a reentrant circuit that directly connects the atria and ventricles and tends to predominate in infants and younger children. This type of SVT includes Wolff-Parkinson White syndrome (WPW). In WPW, there are 2 ways to precipitate SVT. The most common is called orthodromic reciprocating tachycardia (ORT), which involves antegrade conduction of a sinus impulse normally through the AV node with retrograde conduction via the accessory pathway at a certain interval. The less frequent type is called antidromic reciprocating tachycardia (ART), which involves a circuit conducting in the opposite direction, with antegrade conduction of a sinus impulse through the accessory pathway with retrograde conduction through the His-Purkinje system.27 AVNRT typically is seen in older children and adolescents and involves dual AV nodal pathways, including a normal fast and abnormal slow pathway. This type of SVT represents a reentrant circuit within the AV node itself that can rapidly activate the ventricles via the normal His-Purkinje system.27,29 Certain conditions and drugs are thought to precipitate episodes of SVT, including alcohol, caffeine, central line placement, and hyperthyroidism.19,30,31 However, there is some recent evidence that the role of caffeine in SVT induction is overstated.32 Once SVT is diagnosed via a rhythm strip or standard electrocardiography, the management of acute SVT depends on the hemodynamic stability of the patient. If the patient is stable, initial attempts to terminate SVT can be with vagal maneuvers. These include the Valsalva maneuver and placing a slurry of bagged ice over the nasal bridge and forehead for 30-second intervals.33,34 Carotid massage, ocular pressure, and gag reflex via nasogastric tube are not currently recommended.27 If
vagal maneuvers are unsuccessful, a rapid intravenous push of adenosine via the most central access point is then recommended with evidence pointing to 0.2 mg/kg as a starting optimal dose and 0.3 mg/kg as a second dose up to a maximum of 12 mg.27,35 This is immediately followed by a saline flush using a 3-way stopcock connector. If there is no response or the SVT terminates then reinitiates, expert consultation should be obtained. In an unstable patient, vagal maneuvers and adenosine should be bypassed and treatment should occur with synchronized cardioversion.36(pp90-91) After conversion to sinus rhythm, patients should receive an echocardiogram to assess for cardiac function and rule out congenital heart disease. In the older child, there are many options for antiarrhythmic therapy, including beta-blockers, calciumchannel blockers, or sodium-channel blockers. However, in the infant, calcium-channel blockers should be avoided due to an infant’s immature sarcoplasmic reticulum and the risk of electromechanical dissociation. Also in patients with WPW, digoxin should be avoided due to an increased risk of causing sudden cardiac death.27,36 Patients who are refractory to treatment or who want to avoid taking oral medication can choose to have curative radiofrequency ablation.28
Conclusion Central venous catheters often terminate in the right atrium/superior vena cava region, as was the case in our patient. We hypothesize temporary patient positional changes in the postoperative period caused catheter tip contact with the endometrium, allowing for SVT to be induced. Of note, after the CVC was retracted, normal sinus rhythm in this case was achieved with administration of adenosine. Iatrogenic catheter-related SVT is typically considered to be atrial flutter, which does not respond to adenosine administration. Accordingly, while our patient had no prior history of cardiac arrhythmias, his response to adenosine suggests that he likely had an arrhythmogenic substrate present that was induced due to mechanical stimulation from the CVC tip. Given the high frequency of CVC use in the pediatric population even in non–intensive care patients, the general pediatrician caring for chronically ill and hospitalized children should be aware of the complications and treatments that come with them. Author Contributions All authors influenced the case report concept, wrote and revised the manuscript and approved of the final version.
498 Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.
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