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|Year : 2009
: 12 | Issue : 1 | Page
|Surgical retrieval of embolised atrial septal occluder device from pulmonary artery: Pathophysiology and role of the intraoperative transoesophageal echocardiography
Shrinivas Gadhinglajkar1, KP Unnikrishnan1, Rupa Sreedhar1, Mukul Chandra Kapoor2, Praveen Kumar Neema1
1 Department of Anaesthesia, Sree Chitra Tirunal Institute For Medical Sciences and Technology, Trivandrum, Kerala, India
2 Army Hospital, New Delhi, India
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|Date of Submission||13-Mar-2008|
|Date of Acceptance||10-Nov-2008|
| Abstract|| |
Atrial septal defect is usually closed in the cardiac catheterisation laboratory using atrial septal occluder (ASO) device. One of the complications associated with the procedure is embolisation of the device into the pulmonary artery. We are reporting two cases wherein the pulmonary embolisation of ASO device occurred during the procedure in one patient and in the early post-procedure period in another; both were retrieved surgically. We are also describing the haemodynamic consequences of this complication and the role of intraoperative transoesophageal echocardiography during surgical retrieval of the device.
Keywords: Amplatzer septal occluder, atrial septal defects, blockaid, transoesophageal echocardiography
|How to cite this article:|
Gadhinglajkar S, Unnikrishnan K P, Sreedhar R, Kapoor MC, Neema PK. Surgical retrieval of embolised atrial septal occluder device from pulmonary artery: Pathophysiology and role of the intraoperative transoesophageal echocardiography. Ann Card Anaesth 2009;12:40-8
|How to cite this URL:|
Gadhinglajkar S, Unnikrishnan K P, Sreedhar R, Kapoor MC, Neema PK. Surgical retrieval of embolised atrial septal occluder device from pulmonary artery: Pathophysiology and role of the intraoperative transoesophageal echocardiography. Ann Card Anaesth [serial online] 2009 [cited 2020 May 29];12:40-8. Available from: http://www.annals.in/text.asp?2009/12/1/40/45012
| Author's Report|| |
A 27-year-old female patient, weighing 60 kg, underwent device closure of ASD in a cardiac catheterisation laboratory. Preoperatively, she was detected by transthoracic echocardiography (TTE) to have a 20 mm ostium secundum ASD with left to right shunt. On the day of procedure, standard anaesthetic induction was performed. The TOE examination revealed 18 mm size of ASD. A margin of 7 mm was observed on all sides around the ASD. A 2:1 left to right shunt was present across the ASD and the estimated pulmonary artery (PA) pressure was 30/10 mmHg. The balloon stretched ASD size was estimated to be about 20 mm. A 22 mm ASO, Blockaid device (Shanghai shape memory, Alloy Company Ltd., China) was selected for deployment. While attempting to position the left atrial disc, the device could be seen on fluoroscopy, getting embolised to right ventricle (RV) and then to main pulmonary artery (MPA). The haemodynamic parameters remained stable with BP of 120/86 mmHg, heart rate 96/min and oxygen saturation of 100%. An arterial blood gas (ABG) study on fractional inspired oxygen concentration (FiO 2 ) of 1 revealed a pH of 7.41, arterial oxygen tension (PaO 2 ) of 142 mmHg and arterial carbon dioxide tension (PaCO 2 ) of 29.4 mmHg. It was decided to transfer the patient to operation theatre (OT) for surgical retrieval of the device and ASD closure. A triple lumen cannula was inserted in the left femoral vein. Heparin (12000 units) was injected to prevent clot formation in the pulmonary circulation.
Inside the OT, we inserted a TOE probe (multiplane 4 to 6 MHz) and performed imaging using Philips EnVisor HD ultrasound system, USA. The device was found lying in the MPA and blood could flow from MPA to right pulmonary artery (RPA) [Figure 1]. There was mild distention of MPA [Figure 2] and the ME 4 chamber view revealed diastolic flattening of the interventricular septum. The RV was distending in systole, with its dimensions exceeding that of left ventricle. Short axis views at the aortic valve level revealed left to right flow across the ASD. The RV systolic pressure (RVSP) measured by TR jet method was 45 mmHg. After heparinisation, when the surgeon started cannulating the ascending aorta, the ASO device slipped back into the MPA. Within 2-3 min, severe systemic desaturation (SpO 2 65%) and hypotension (systolic blood pressure 80 mmHg) were observed, probably because of partial obstruction of the pulmonary artery. CPB was quickly established and antegrade cold blood cardioplegia was delivered into the aortic root after cross-clamping of aorta. When the right atrium (RA) was opened, the rim of IAS near inferior vena cava (IVC) was found torn. The device was palpable externally at pulmonary bifurcation. It was grasped with a long clamp passed into the pulmonary artery via the tricuspid and pulmonary valves under external digital control and was gradually withdrawn out of the right atrium. Pericardial patch was used to close the ASD. Epinephrine infusion 0.05 µg/kg/min was commenced electively while weaning the patient from CPB. The post-CPB TOE revealed normal blood flow across the left pulmonary artery (LPA). Trachea was extubated after 6 h of ventilation and epinephrine was discontinued. The postoperative course was uneventful.
A 22-year-old male patient, weighing 62 kg, diagnosed to have ostium secundum ASD, was scheduled for catheter intervention for the deployment of ASO device. Preoperative TTE revealed a 20 mm ASD with left to right shunt. On the morning of intervention, standard anaesthetic induction was performed. TOE examination confirmed the findings on the TTE. Catheter studies revealed the PA pressure of 32/10 mmHg. A 24-mm Amplatzer ASO device (AGA Medical Corporation, Golden Valley, Minnesota, USA) was positioned across the ASD. As the TOE and the fluoroscopy showed satisfactory positioning of the device, the neuromuscular blockade was reversed and trachea was extubated. Immediately after tracheal extubation, pulse oximetry revealed saturation of 100%, which however decreased to 60%, within 5 min, despite oxygen supplementation by face mask. Tachycardia (heart rate 110/min) and blood pressure of 90/65 mmHg were observed on the monitor. Within a couple of minutes, the SpO 2 improved to 90-95% and again decreased to 60%. The TTE and Fluoroscopy showed that the ASO device was embolised inside the MPA, with its tip projecting toward the LPA. It exhibited bobbing movements, being pushed distally during each systole and returned back to its original position during diastole. Thus, the device was embolised after completion of deployment, unlike in first patient, in whom the embolisation occurred during deployment. The patient was immediately anaesthetised and trachea was re-intubated. Heparin (12500 units) was administered to achieve anticoagulation and the patient was transferred to the OT. On arrival in the OT, the ABG analysis revealed PaO 2 of 85 mmHg on FiO2 1, PaCO 2 45 mmHg, and base deficit of 5 mmol/l. TOE showed that the ASO device was in the MPA, partially occluding the forward flow. The RV was distended and the left ventricle (LV) underfilled. RVSP calculated by TR jet method was elevated to 65-85 mmHg at the corresponding systolic BP of about 75-80 mmHg. The direction of flow across ASD was changing between left to right and right to left, with corresponding variations in the SpO 2 from 98% to 60%. After systemic heparinisation, the aorta and right atrium were cannulated and CPB established. The ASO device was removed using a long forceps introduced through the tricuspid and pulmonary valve as in the first patient. The ASD was closed with a pericardial patch. Patient was weaned off CPB with epinephrine infusion 0.1 µg/kg/min. TOE examination showed normal blood flow in the MPA and reduction in the size of RA. Artificial ventilation was discontinued 12 h after surgery, and epinephrine infusion was subsequently tapered off. TTE examination revealed that the RVSP has decreased to 30 mmHg.
| Discussion|| |
Embolisation of the device into PA has been reported to occur 10 min after deployment,  one day after deployment  and 1 week after the procedure.  In a report from University of California,  out of 450 atrial septal occlusion devices, 7 devices were embolised to the right side of heart or pulmonary circulation and all either in the catheterisation laboratory or within 12 h after the procedure. In spite of right-sided device embolisation, all these patients were haemodynamically stable. In our second patient, the clinical suspicion of embolisation aroused because of the fluctuating values of SpO 2. These swings in the oxygen saturation could be attributed to the frequent variations in the device position and the degree of pulmonary obstruction, accompanied by the right to left shunting across the ASD.
The Blockaid ASO device is an exact morphological replica of the Amplatzer ASO device,  having approval from Chinese authorities, it is widely used in Asian countries. Although, the embolised ASO device is pushed to the level of pulmonary arterial confluence, the peripheral portions of disks may get moulded into either RPA or LPA, thus permitting blood to flow through the other branch artery. For an Amplatzer device larger than 11 mm and up to 34 mm in size, the LA disk is 14 mm and RA disk is 10 mm larger than the connecting waist.  This means that a 22 mm Amplatzer device should have 36 mm LA disk and 32 mm RA disk. Considering that the size of MPA in an average size adult patient is about 20 mm, an ASD device having 36 mm LA disk impacted in MPA is capable of producing significant obstruction to the blood flow. Haemodynamic consequences of pulmonary embolisation of an ASO device depend upon the site of its impaction in the pulmonary circulation, its position with respect to the MPA lumen, the extent to which it obstructs the pulmonary blood flow and also the right ventricular function. If the ASD device is located primarily in the MPA and the peripheral portions of disks in either RPA or LPA, as in our first patient, the pulmonary obstruction remains minimal [Figure 3]. During surgical manipulation, the device position inside the PA can change and may produce variable degree of PA obstruction and shunt across the ASD and changes in SpO 2 . Changes in the position of the device, corresponding alterations in the pulmonary circulation and distention of the MPA were well-visualised on the TOE.
Pulmonary embolism of an ASD device should be treated on an urgent basis. ,, If the pulmonary obstruction is mild, no aggressive treatment is required to stabilise haemodynamics. Vital parameters should be strictly monitored and serial blood gas measurements should be performed to assess any metabolic acidosis and a decrease in PaO 2 . In the presence of moderate pulmonary obstruction, shunting may occur across the ASD in right-to-left direction, which offers two-fold benefits. It maintains preload and cardiac output and also effectively decompresses the right ventricle. Inotropes act as a bridge to the CPB to some extent. If the device is firmly impacted inside the RPA or LPA, the aorta and MPA should be handled gently to prevent its dislodgement.
It is important to locate the exact site of impaction of an ASD device in pulmonary circulation. The Amplatzer device has optimal echogenicity because of its Nitinol mesh structure.  TOE is used not only as a diagnostic tool but also as a monitoring adjunct for the operative and percutaneous cardiac procedures including the ASD device closure. We found it useful in the intraoperative period for inspecting the device, assessing the pulmonary blood flow and monitoring the RV function. The extent of the RV pressure overload is indicated by the direction of flow across the ASD and increase in the RVSP. When the right atrial pressure exceeds that of the left atrium, the flow reversal occurs cross the ASD. The embolised ASD device is retrieved via pulmonary and tricuspid valves using a forceps. Pulmonary arteriotomy is rarely indicated for that purpose. The Nitinol mesh of the device may be covered with a thrombus, which forms as a result of stagnation of blood beyond the site of impaction. Retrieving the device should resume the distal pulmonary circulation after weaning the patient from bypass. Rarely, the ASO device may be embolised into the left heart or aorta. The haemodynamic consequences may be catastrophic requiring urgent surgical intervention.
In summary, pulmonary embolisation of an ASO device induces varying degree of obstruction depending upon the location and lie of the device within the MPA. Fluctuating levels of the SpO 2 after the procedure warrants a high index of suspicion of this complication. Even in the presence of moderate MPA obstruction, the haemodynamic condition may remain stable. Right-to-left shunting of blood across the ASD works as a buffering mechanism that preserves the RV function in the presence of an acute pressure overload. The TOE plays a very important role in the intraoperative monitoring of the device position and pulmonary blood flow; extent of the RV dysfunction; and direction of the shunt across the ASD during pre-CPB period. It is also helps to assess the pulmonary circulation after retrieval the ASO device.
| Expert's Comments 1 (Mukul Chandra Kapoor )|| |
Cardiac catheterisation has changed its role from a diagnostic to a therapeutic procedure. Interventional catheterisation now plays a significant role in the treatment of congenital heart diseases with development of percutaneous treatment of various cardiac malformations. Despite improvement of technical skills and miniaturisation of interventional tools, catheterisation is still burdened by substantial risk. ,
Surgical closure of the defect is, until date, the standard therapy for the secundum atrial septal defect (ASD). However, this entity is slowly slipping out of the surgeon's hands. Percutaneous device usage, for occlusion of secundum ASD, has gone up significantly and with satisfactory results reported with the use of a number of such devices. Device closure of an ASD offers the advantages of a short learning curve, cosmetic benefits, safety and avoidance of major surgery on cardiopulmonary bypass, with potential reduction in blood product utilisation, perioperative morbidity, and length of hospital stay. , In most centres in the developed world, device closure has become the treatment of choice for secundum ASDs. 
Atrial septal occluder devices
The first reports of transcatheter device closure of secundum ASDs in humans were published in 1976 by King and Mills. In the last two decades, a number of ASD septal occluder devices have undergone evaluation. Amongst the devices evaluated are Hooked, Clamshell, Das Angel Wing, Sideris Centering Buttoned device (1st, 2nd and 3rd generation), Centering-on-demand buttoned device (Buttoned 4 th generation), ASDOS, Amplatzer, CardioSeal/StarFLEX, and Gore Helex. Clinical trials on some of these devices have been discontinued, whilst some are still in clinical trials. The FDA has approved none, except Amplatzer and Gore Helex, for general use.
The Amplatzer septal occluder (AGA Medical Corporation, Golden Valley, MN) is a self-expandable, double-disc device made of Nitinol wire mesh. It is the most widely used, with over 1,50,000 devices delivered worldwide to date. The device consists of a short waist, corresponding to the size of the ASD, linking two discs. The manufacturers overcame a number of disadvantages of previously used devices; namely large introducer sheaths, large overall device for complete closure of the defect, difficult application procedures, inability to recapture, structural failure causing damage to neighbouring structures, dislodgment, embolisation, and high rates of residual shunts.  Its high success rate of closure (99%)  is attributed to its functional design, the self-centering mechanism stenting the potential ASD, and forcing blood through a highly thrombogenic dacron network.
The Gore Helex Septal Occluder (WL Gore and Associates, Inc, Flagstaff, AZ), which is composed of ePTFE patch material supported by a single Nitinol wire frame. The super-elastic property of Nitinol is used to form the wire frame into two equal-size opposing discs that bridges and eventually occludes the septal defect. Over the course of several weeks to months, cells begin to infiltrate and grow over the ePTFE membrane, ensuring successful closure of the defect. The device has received FDA approval recently. The immediate occlusion rate of the device, after 24 h, was 91%. The device adapts well to the anatomical structures. 
The Centering on Demand Buttoned device Fourth Generation (Pediatric Cardiology Custom Medical Devices, Athens, Greece) is composed of three components: an occluder, a counter-occluder and a delivery system. The occluder is composed of an X-shaped wire skeleton covered with polyurethane foam. In the fourth generation device, the button loop attached to the occluder was modified so that there were two radio-opaque spring buttons mounted 4 mm apart in contrast to one button in the earlier versions of the device, with an intent was to reduce unbuttoning seen with earlier generations. Successful device implantation was reported accomplished in 99.8% patients in whom the device was released or 89.2% of patients brought to the catheterisation laboratory with the intent to occlude the defect. 
The CardioSEAL (Nitinol Medical Technical Inc., Boston, Massachusetts) is a double-umbrella device developed from the Clamshell occluder. It consists of a metallic framework covered, in umbrella-like fashion, by knitted polyester fabric. The CardioSEAL/StarFLEX is the recently modified version of the device, with a flexible self-centering mechanism, inserted on a front-loading system. The Nitinol wires are woven tight into two flat buttons (disc) with a 4-mm connecting waist that dictates the device diameter. Three Dacron polyester patches are sewn securely, with polyester thread, into each disc and the connecting waist to increase the thrombogenicity of the device. The immediate occlusion rate of the device has been reported as 90%. 
In the last couple of years, cheaper replicas of the popular Amplatzer device have been introduced commercially. Most of these devices are manufactured in China and are Chinese FDA approved. The Blockaid septal occluder (ASDSO-28, Shanghai Shape Memory Alloy Company Ltd, China), used in one of the patients, in this case report, is a morphological replica of the Amplatzer device and is available at a fraction of the cost. Though literature regarding trial use of these devices is lacking, they are immensely popular in the developing world, owing primarily to their cost. There is a need for formal trials of such devices and their designs, prior to approval for their safe use. 
Recommendations for selection of patients for ASD device closure
The manufacturers recommend that a distance of 5 mm be present from the margins of the defect, to the coronary sinus, the atrio-ventricular valves, and the right upper lobe pulmonary vein, for successful implantation. This is critical to provide support and stability to the device edges and to avoid occlusion of these structures by impingement of the device. To qualify for device placement, the patient should weigh > 8 kg and should show a pulmonary-to-systemic flow ratio of 1.5:1 or greater. The device size selected is 2 mm larger than the ASD diameter measured. However, institutions have diluted these criteria over time and have accepted smaller septal rims. ,, The acceptance of smaller aortic rims, whilst deploying newer self-centering devices, may predispose to device embolisation or displacement, both early and late. 
Chessa et al. have reported on a large series of 417 patients, who had catheter closure of secundum ASDs, of whom 159 received CardioSEAL/STARFlex and 258 Amplatzer septal occluder devices.  The overall incidence of complications, including those due to the learning curve for each device, was 8.6% with use of Amplatzer and CardioSeal/StarFLEX device. They classified the complications as major (events leading to one of the following: death; life-threatening haemodynamic decompensation requiring immediate therapy; need for surgical intervention; and significant permanent anatomic or functional lesion) and minor (events that were transient and resolved with specific treatment). 
Embolisation/malposition of the device is the most common complication (3.5%) accounting for almost half of major events. Both the patients, in this case report, had device embolisation to the pulmonary circulation. In case 1, the embolisation of the Blockaid device occurred during the process of positioning the left atrial disc. The event appears to have occurred due to operator error either by faulty mounting of the device on the delivery cable or due to premature opening up of the screw holding the device, as the left atrial disc placement can be adjusted only till it is attached to the delivery cable. In case 2, the embolisation of the Amplatzer device occurred, soon after device deployment. Embolisation of the device probably occurred due to improper sizing of the device, incorrect placement, inadequate atrial septal rims, oblong shape of the defect or erosion of the septal rim during balloon sizing of the defect. The inherent tendency of interventionalists to grossly oversize the device to avoid device embolisation and paradoxically perpetuate this problem, has also been reported to be a cause of embolisation. 
Arrhythmias are the next most common complication (2.6%) i.e. atrial fibrillation, supraventricular tachycardia and even AV block. Embolisation of the device has been reported on attempting electric cardioversion of arrhythmia.  Other complications reported include pericardial effusion, septal tearing, pulmonary vein dissection, atrio-ventricular valve incompetence, cardiac perforation, thrombus formation on the left atrial disc, vascular trauma, septal aneurysm formation, systemic allergic reaction to nickel and residual shunt. ,,
Late complications include peripheral embolisation of thrombus/device, sudden death, aortic arch embolisation, erosion of an Amplatzer septal occluder into the ascending aorta with associated aortic-to-right atrial fistula formation, deep vein thrombosis, cardiac perforation presenting as cardiogenic shock and infective endocarditis. ,,,
Effects of acute obstruction of pulmonary circulation
This case report documents the effects of migration of atrial septal devices into the pulmonary circulation. In one patient, the embolised device migrated proximally from the LPA to acutely occlude the main PA. The patho-physiological changes of the partial/near total occlusion of the pulmonary blood flow, in presence of an ASD, are different from those due to occlusion of the pulmonary artery by massive embolism. Systemic oxygenation is the first to suffer due to a sudden drop in pulmonary perfusion.  Dilatation of the right ventricle (RV) then occurs due to a sudden pressure load on the ventricle. The dilatation of the RV has backpressure effects leading to reversal of the inter-atrial shunt to right-to-left. The central venous pressure rise is not commensurate to the RV dilatation. Unlike in acute pulmonary embolism, the reversal of the inter-atrial shunt prevents a sudden cardiovascular collapse, by restoring the left atrial preload. However, RV dilatation leads to a leftward shift of the inter-ventricular septum adversely affecting the LV preload and haemodynamics. In case the PA occlusion is near total, the consequent reduction in systemic tissue oxygenation gradually leads to metabolic acidosis further reducing the cardiac output.
Role of echocardiography
Echocardiography is a valuable tool for correct selection, sizing, positioning and testing device stability. The role of peri-procedural TOE monitoring is invaluable to assess the cardiac performance and in addition help detect migration of the device. TOE is commonly used but has associated limitations, specifically the need for general anaesthesia and airway management.
Recently, intra-cardiac echocardiography (ICE) has been found to be a feasible and accurate alternative imaging modality for transcatheter device closure of ASD.  ICE provided accurate assessment of the atrial septum, position and size of the defects, adequacy of the rims, and drainage of the pulmonary veins in all patients. ICE provides adequate, complete imaging, which allows successful device placement with extremely few complications. ICE also provides anatomical detail of ASD and cardiac structures facilitating congenital cardiac interventional procedures. Finally, ICE gives the interventional cardiologist the ability to control all aspects of imaging without relying on additional echocardiographic support.  However, the use of ICE is presently limited to adults and bigger children, as it must be introduced through an 11F sheath. 
To conclude, patients should be taken up early for surgery, before haemodynamic compromise/further migration of the device. Intense peri-operative monitoring and vigilance is required to detect complications/altered haemodynamics early, to minimise the risk of serious adverse outcomes.  The increased exposure of interventional cardiologists to transcatheter techniques has resulted in cardiologists increasingly attempting to treat patients with ASDs of more complex morphology. Once equilibrium of expertise and patient selection is achieved, complications could be reduced but not completely abolished. 
| Expert's Comments 2 (Praveen Kumar Neema )|| |
The first experimental non-surgical closure of an ASD was performed in 1974 by King and Mills.  Interventional ASD closure is now widely practiced, and thousands of patients have undergone non-surgical device closure of both single and multiple atrial septal defects. ,, Improvements in design have made the devices retrievable, and reduction in the size of the introduction systems allows interventional treatment even in young patients.  Two different types of device are in widespread use, the patch type occlusion device - represented by the Cardio SEAL, or its modification, the STAR Flex occluder (NMT Medical, Boston, Massachusetts, USA) and the self centering Amplatzer septal occluder (AGA Medical Corporation, Golden Valley, Minnesota, USA). The percutaneous closure is associated with less morbidity, no surgical scar and reduced hospital stay; however, several complications have been identified with this new technology. This commentary will focus on the technique and pathophysiology of various complications of interventional ASD closure using Amplatzer Septal Occluder, and the role of anaesthesiologist during interventional ASD closure.
Device and technique
The Amplatzer Septal Occluder is a self-expanding, self-centring, and repositionable double disc device constructed of a mesh of 72 Nitinol wires. A 3-4 mm short cylindrical waist connects the two round discs. Additionally, polyester fibres are sewn into the device promoting thrombosis and complete defect occlusion. The Amplatzer Septal Occluder is designed to 'plug' the ASD with the middle waist, whereas the left and right occluders (discs) cover the defect on each side, providing the support to hold the device in position.  The Amplatzer Septal Occluder stretches and stents the ASD. Thus, the diameter of the waist has to correspond to the so-called 'stretched' diameter of the ASD, determined by a 'balloon-sizing catheter'. To 'size' the defect before implantation of the Amplatzer Septal Occluder, a compliant balloon is advanced over a wire to straddle the ASD. The balloon is inflated to low pressures until all flow across the septum ceases (assessed by Doppler colour-flow mapping).  At this point, there will be an indentation of the balloon, superiorly and inferiorly on an antero-posterior projection corresponding to the impression of the margins of the defect. Selection of the Amplatzer Septal Occluder device size is based on the stretched diameter. A device is chosen with a middle waist diameter that is equal or slightly larger (2 mm) than the balloon-stretched diameter. In this way, it can be assured that the device will be adequately supported by ASD margins. Recently, Ewert et al . described Transcatheter closure of atrial septal defects under TOE guidance without X-ray.Presently, in our institute, all the Transcatheter ASD closure is carried out under TOE guidance. Closure of an ASD is complicated by the fact that each defect is unique in its size, in its position in the septum, and in its shape. Twenty-seven different sizes with waist diameters from 4-40 mm are available. The device is delivered via the femoral vein. Once a device is selected, an appropriate-sized delivery system (6F-12F) is advanced to the LA over a wire. The Amplatzer Septal Occluder is collapsed into the sheath and pushed to the LA. The LA occluder is opened by pushing it out of the end of the delivery system. The device is then withdrawn toward the septum, the middle waist is opened within the defect, and the right atrial occluder is opened on the RA side of the septum. The tissue rims are therefore captured between the left and right atrial occluders. After implant, the stretched septum recoil toward its original dimensions, resulting in the septum firmly 'grabbing' the device to better stabilise its position.
A clear understanding of the mechanism of device closure of ASD may explain the mechanisms of complications. Briefly, on implantation of the ASD device, the stretched septum recoil toward its original dimensions resulting in firm 'grabbing' of the device and the ASD tissue rims are captured between the left and right atrial occluders for better stabilisation. Apparently, the factors that lead to successful device implantation are - matching of the size of the device and the ASD, the adequacy of ASD rim, and the size of the left and right atrial occluders. It is intuitive that closure of the defect with an undersized device or an ASD with deficient tissue rim can be associated with both residual shunts and unstable device positions and embolisation. Embolisation may also occur when the septal margins are not captured between the left and right atrial disks or the septal margins are torn due to oversized device. The operator can inadvertently pull the leading edge of the device back through the defect to the right atrial side, resulting in both disks on the RA side or the right atrial occluder can be opened with its trailing rim remaining in the LA. Complications of the procedure such as device embolisation and the need for surgical retrieval tend to occur early in the learning curve.
The manufacturers recommended exclusion criterion is an ASD with a rim to the atrioventricular valves of less than 5 mm. While most clinicians adhere to the criteria concerning minimum requisite margins of the Superior, Inferior, SVC and IVC rims, the small or deficient aortic rim is often ignored with newer self-centring devices. In one report, up to 40% of patients with deficient aortic rims underwent percutaneous closure of their ASDs.  Reports have indicted a deficient 'aortic rim' in the majority of cases associated with embolisation or displacement of the device. However, deficient rims in vulnerable areas could increase the chance of contact between the device and the atrial wall. ASD closure with an oversized device may result in erosion into the aorta, or into the roof of left or right atrium. This predilection for the 'aortic rim' erosion in patients with device-defect mismatch has been postulated to arise from a 'see-saw' grinding movement between the inflated left atrial segment of the device and the aortic sinus wall with each cardiac cycle. Haemopericardium and aorta-left atrial fistula has been reported after ASD device closure. Additionally, an oversized left atrial occluder can also result in compromise of opening of right superior pulmonary vein and incompetence of the mitral valve. Apparently, the key to avoid device related complications are - strict adherence to selection criteria that is at least 5 mm rim of tissue around ASD, meticulous sizing of the ASD and device selection based on ASD size, the length of the interatrial septum and size of the left and right atrium.
The other complications of interventional ASD closure are related to the procedure itself. A retroperitoneal hematoma due to rupture of a small branch of femoral artery and cardiac tamponade due to cardiac chamber perforation were reported earlier. These complications are inherent to any cardiac catheterisation procedure. The presence of an intracardiac communication and direct instrumentation of the left side of the heart add substantially to the potential for coronary and cerebral thrombo-embolisation, which would result in myocardial ischemia or stroke. Whether or not one should use general anaesthesia for specific interventional procedures may be a question of institutional logistics? However, unlike adult patients, a child will not tolerate the TOE probe without heavy sedation. Heavy sedation and continued spontaneous breathing may carry a risk of air embolism through the long sheath, owing to the negative intrathoracic pressure. Indeed, Amin et al. described occurrence of air embolism in one of their patients under propofol sedation; however, when air embolism occurred, the device was already in place and closed the communication to the left heart. These authors describe, 'while this event was without sequel, it was striking enough to result in a change of policy in our institution. In order to avoid irreversible myocardial or cerebral damage or even death after air embolism to the left heart, we now perform all interventional ASD closures under general anaesthesia with mechanical ventilation'. Apart from the risk of air embolism, the other indications for anaesthesia care are control of the airway (i.e., for Transoesophageal echocardiography), maintenance of haemodynamic stability, patient comfort, and immobilisation of paediatric patients who may be unable to cooperate during delicate procedures. It is therefore important for the anaesthesiologist to become familiar with the risks of interventional cardiology procedures so that they can appropriately manage patients during the procedure and during a complication requiring surgical intervention. Evidently, all interventional ASD closures should be performed under general anaesthesia with mechanical ventilation.
I thank the author(s) for presenting two interesting cases of ASD device embolisation, in both the cases the device embolization was diagnosed soon after its occurrence; and within few hours, the ASDs were closed surgically and the devices were retrieved during surgery without further complication. However, I respectfully disagree with some of the observations of the authors. In the first patient, the device embolised while attempting to position the left atrial disc; 1] I believe device embolization is not possible until the device is deployed and unscrewed. 2] I agree the haemodynamic consequences of pulmonary embolization of an ASO device would depend upon the extent of pulmonary blood flow obstruction; however, because of its superelastic properties, the device would migrate distally until impacted. This is why in both the cases the devices were impacted at pulmonary bifurcation with a part of it projecting in LPA.
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Department of Anaesthesia Sree Chitra Tirunal Institute For Medical Sciences and Technology, Trivandrum, Kerala
Source of Support: None, Conflict of Interest: None
Clinical trial registration None
[Figure 1], [Figure 2], [Figure 3]
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