Patent ductus arteriosus, defined as the failure in closing of the ductus arteriosus, is among the most common congenital heart diseases. Reference Baruteau, Hascoët and Baruteau1 Treatment options include fluid restriction, diuretic agents, transcatheter closure, and surgical repair. Today, the first therapeutic option is transcatheter closure, which has been widely used since 1939 with high success. Reference Kenny, Morgan and Bentham2 This procedure is often performed under general anaesthesia outside the operating theatre, called non-operating room anaesthesia. With the increasing use of transcatheter closure procedures in recent years, the incidence of intraoperative complications has increased. Herein, we aimed to report our anaesthetic management of a rare complication of this procedure – embolisation of the ductus closure device to the pulmonary artery – in a child.
Case presentation
A 4-year-old girl, 12 kg in weight (10–25 percentile) and 96 cm in length (50 percentile), underwent transcatheter closure for patent ductus arteriosus at paediatric interventional laboratuar under non-operating room anaesthesia. She was stable haemodynamically (tension arterial, 90/60 mmHg; respiratory rate, 28 per minute; hearth pulse, 104 beats/minute). Blood tests were normal. No abnormality was observed in her physical examination. She had not any syndrome associated with patent ductus arteriosus. Her Mallampati score was consistent with American Society of Anesthesiologists score 2. She was given 50 mg/kg ampicillin/sulbactam before the procedure.
Following standard monitoring, induction was slowly performed with propofol (3 mg/kg), remifentanil (0.2 mcg/kg), and rocuronium (0.4 mg/kg). The patient was then intubated with using 5 mm cuffed endotracheal tube. Anaesthesia was maintained with using 50%/50% (air/O2) and 2–3% sevoflurane without any problem. Pulmonary artery pressure was measured as 26 mmHg. Vasoreactivity test with ilioprost was accepted as positive. Then, patent ductus arteriosus closure was successfully performed with amplatzer duct occluder II device. After providing extubation criteria, the patient was successfully extubated without using a muscular relaxant antagonist.
Control transthoracic echocardiography was performed before the patient was removed from the operating table, and it was revealed that the device was dislocated and embolised to the left pulmonary artery. Thereupon, the patient was re-intubated with the administration of propofol (3 mg/kg), remifentanil (0.1 mcg/kg), and rocuronium (0.4 mg/kg). Thanks to extubation without reverse agent, no problem was observed during the second induction. However, instant hypoxia, hypo/hypercarbia, hypotension, and arrhythmias developed due to the multiple manipulations. Norepinephrine infusion (0.05–0.10 mcg/kg per minute) was started for persistent hypotension. Metabolic acidosis was treated by the administration of bicarbonate (16.8 mEq intravenous and 8.4 mEq infusion for 6 hours). Despite all manipulations lasting 4 hours, the device could not be replaced into the correct position (Fig 1a and b). Subsequently, paediatric cardiologists decided to terminate the procedure and referred the patient to surgery. She was successfully extubated with using 4 mg/kg sugammadex, and was taken to the intensive care unit. The patient was referred to the external medical centre the next day. Patent ductus arteriosus repair and removal of the device were performed surgically there.
Figure 1. (a) The closure device embolised to the right pulmonary artery (arrow). (b) The closure device embolised to the left pulmonary artery (arrow).
Discussion
Increased positive expiratory pressure (>5 mbar) and short inspiration time (0.35 second) are recommended as the ventilation strategy in order to correct impaired gas exchange, reduce left-to-right shunt, and keep systemic blood flow high. The presence of a left-to-right shunt causes an increased risk of pulmonary hypertension, which is a higher risk for perioperative cardiovascular complications, including cardiac arrest, pulmonary hypertensive crisis, and death compared with normal population. Reference Taylor, Derrick, McEwan, Haworth and Sury3 , Reference Carmosino, Friesen, Doran and Ivy4 This risk is considered to be independent of patient’s age, anaesthetic or airway technique, but to be related to the duration of anaesthesia. In anaesthesia management, hypoxia, hypercarbia, and acidosis should be prevented, and pain management should be optimal. Hypovolemia may result in a decrease in cardiac output and pulmonary blood flow. Systemic hypotension or reduction in systemic vascular resistance together with a decrease in coronary artery blood flow may lead to biventricular ischaemia. We did not see any clinical pulmonary hypertension in our patient, but it should be always kept in mind.
Balanced anaesthesia should be preferred. In the premedication, benzodiazepines are appropriate because of their less haemodynamic side effects. Inhalation agents may impair the perfusion compliance by reducing hypoxic pulmonary vasoconstriction and are also known to decrease pulmonary vascular resistance by pulmonary vasodilatation. Reference Friesen and Williams5 Although volatile anaesthetics cause prolongation of the QT interval, it was not considered clinically significant. Reference Hayman, Forrest and Kam6 Etomidat and fentanyl can be preferred, whereas thiopentalin is considered as a non-suitable agent due to its systemic hypotension effect and myocardial depression. The general opinion is that slow use of propofol in low doses should be preferred due to its impact on reducing systemic vascular resistance and contractility. Reference Türktan and Hatipoğlu7
Pulmonary gas exchange abnormalities firstly occur after embolism of pulmonary device. Increase in dead space, formation of right-to-left shunt, and ventilation/perfusion incompatibility cause this situation. Reference Hayman, Forrest and Kam6 Blood flow is directed to the remaining lung tissue instead of a clogged pulmonary artery, and pulmonary edema, alveolar haemorrhage, and surfactant loss may develop due to this increased flow. Reference Desciak and Martin8 In case of persistent embolism, left ventricular preload and subsequently left ventricular output decrease, which cause a systemic hypotension. Supportive therapies are in the forefront of anaesthesia management, and blood pressure should be increased with right ventricular stroke volume and systemic vasoconstriction, and coronary perfusion pressure should be preserved. Norepinephrine is recommended as a first inotropic agent. Reference Wood9 It provides an increase in venous return, blood pressure, and coronary perfusion pressure by increasing the systemic vasoconstriction via α-1 receptors. In addition, norepinephrine increases both right ventricle and cardiac output through the stimulation of β-1 receptor. As an alternative to norepinephrine, dopamine, epinephrine, and dobutamine can also be used. Reference Wood9 Additionally, it is unreliable to check the ventilation of patients by end-tidal carbon dioxide, because these patients have a higher physiological dead space that may cause incorrect readings. The blood sample taken from the arterial catheter inserted during the procedure can be used to determine partial carbon dioxide pressure values and be helpful for ventilation strategies.
Conclusion
Device embolisation to the pulmonary artery is a very rare complication of transcatheter closure of patent ductus arteriosus, which carries additional risks in the anaesthetic management of such patients. Therefore, we consider that this case report may be helpful and informative for all anaesthesiologists.
Financial Support
This research received no specific grant from any funding agency or from commercial or not-for-profit sectors.
Conflicts of Interest
None.
Ethical Standards
The authors assert that all procedures contributing to this work comply with the ethical standards of the relevant national guidelines on human medical regulations and with the Helsinki Declaration of 1975, as revised in 2008.
