□
CASE REPORT
□
Suspicion of Superior Mesenteric Artery Syndrome in a Patient with Severe Gastric Dilatation after Catheter Ablation Hidehiro Kamezaki 1,2, Ryosaku Azemoto 1, Osamu Yokosuka 2, Tatsuya Fujimoto 1, Masamichi Obu 1, Masahiko Saito 3, Yu Yoshida 1, Yoshihiro Koma 1, Hitoshi Maruyama 2 and Mototsugu Fujimori 1
Abstract Catheter ablation is a widely used treatment for atrial fibrillation. Gastric hypomotility due to periesophageal vagal plexus injury is a consequence of the extracardiac penetration of ablative energy. Some affected patients develop severe gastric dilatation requiring hospitalization. However, most previous reports have stated the cause of the subject’s condition to be “unknown” or described the symptoms using obscure terms, such as “paralytic” or “gastroparesis.” For example, one report stated that a few sites of severe gastric dilatation were secondary to “pyloric spasms;” however, no illustrations were provided in the paper. “Superior mesenteric artery syndrome” is a suspected cause of such dilatation. Key words: superior mesenteric artery syndrome, catheter ablation, gastric hypomotility, gastric dilatation, periesophageal vagal plexus injury, atrial fibrillation (Intern Med 54: 605-609, 2015) (DOI: 10.2169/internalmedicine.54.3276)
to be the cause of the dilatation in this case.
Introduction Case Report Catheter ablation is a widely used treatment for atrial fibrillation. As the use of this treatment has increased, a variety of adverse effects have been reported. Atrioesophageal fistula formation was reported to be a consequence of the extracardiac penetration of ablative energy for the first time in 2004 (1). Gastric hypomotility due to periesophageal vagal plexus injury is another extracardiac adverse event (2-4), the frequency of which varies from 0.3% to 17.0% (3, 4). Most affected patients recover with symptomatic treatment, although some develop severe gastric dilatation requiring hospitalization. The causes of such cases of severe dilatation remain unidentified. We herein report a case involving a patient who exhibited severe gastric dilatation after undergoing catheter ablation. Superior mesenteric artery (SMA) syndrome was suspected
The patient was a 62-year-old man with a height of 167 cm, weight of 54 kg and body mass index of 19.4 kg/m2, all of which had remained unchanged for a long period. He underwent catheter ablation for chronic atrial fibrillation at the Department of Cardiology at Kimitsu Chuo Hospital. The radiofrequency energy was 25-30 W, and the radiofrequency delivery was stopped if the esophageal temperature reached 42℃. Even if the esophageal temperature did not reach 42℃, the radiofrequency delivery time was limited to 30 seconds at each site. The pulmonary veins were circumferentially ablated, and the endpoint of pulmonary vein isolation was the elimination of all pulmonary vein potentials. Additional substrate ablation was also performed, including the left atrial roof line and left atrial bottom line, with supe-
１
Department of Gastroenterology, Kimitsu Chuo Hospital, Japan, ２Department of Gastroenterology and Nephrology, Chiba University Graduate School of Medicine, Japan and ３Department of Internal Medicine, Kumagaya General Hospital, Japan Received for publication May 13, 2014; Accepted for publication August 11, 2014 Correspondence to Dr. Hidehiro Kamezaki, [email protected]
605
Intern Med 54: 605-609, 2015
DOI: 10.2169/internalmedicine.54.3276
SMA
st
du ao du IVC
Figure 1. An abdominal X-ray shows the double-bubble sign, indicating gastric and duodenal air bubbles with niveaus. This finding suggests the presence of obstruction on the proximal side of the duodenal bulb.
SMA
Figure 2. Abdominal computed tomography shows that the dilated stomach is causing dorsal deviation of the superior mesenteric artery (SMA) and that the SMA and abdominal aorta are pressing upon the third portion of the duodenum. ao; aorta, du: duodenum, IVC: inferior vena cava, SMA: superior mesenteric artery, st: stomach
SMA st
st IVC
du ao du IVC
Figure 3. A repeat abdominal computed tomography scan shows that the pressure of the third portion of the duodenum has been alleviated and that the superior mesenteric arteryaorta distance increased from 6 to 9 mm immediately after the gastric drainage procedure. ao: aorta, du: duodenum, IVC: inferior vena cava, SMA: superior mesenteric artery, st: stomach
rior vena cava isolation. Finally, the patient achieved a sinus rhythm. No complications were detected during or immediately after the procedure, and he was subsequently discharged from the hospital. However, epigastric discomfort and vomiting occurred 24 hours after the operation, and these symptoms unfortunately gradually worsened. Seven days after undergoing catheter ablation, the patient received a medical examination in our department. The blood test results were normal; however, an abdominal X-ray image showed a double bubble sign (Fig. 1), which usually develops when gastric and duodenal air bubbles form niveaus, indicating the presence of obstruction in the distal duodenum. Abdominal computed tomography showed no neoplastic lesions, although the stomach was dilated, causing dorsal de-
du ao du
Figure 4. Abdominal computed tomography shows good contrast imaging of the SMA. ao: aorta, du: duodenum, IVC: inferior vena cava, SMA: superior mesenteric artery, st: stomach
viation of the SMA, and the SMA and abdominal aorta were pressing upon the third portion of the duodenum (Fig. 2). Based on the patient’s clinical course, we suspected a diagnosis of SMA syndrome and thus placed a nasogastric tube, draining approximately 2,000 mL of stomach contents. Thereafter, the patient’s symptoms significantly improved, and a repeat abdominal computed tomography examination showed that the pressure of the third portion of the duodenum had decreased, while the SMA-aorta distance at the level at which the SMA crossed the duodenum had increased from 6 to 9 mm, immediately after the drainage procedure (Fig. 3). The possibility of SMA obstruction was excluded due to the findings of good contrast imaging of the SMA (Fig. 4). A subsequent upper gastrointestinal series showed no obstructive lesions. Although esophagogastroduodenography also revealed no tumorous masses in the duodenum, a gastric ulcer was detected at the cardia, despite the use of proton pump inhibitors prior to catheter ablation. We
606
Intern Med 54: 605-609, 2015
DOI: 10.2169/internalmedicine.54.3276
assumed that this finding was due to the extracardiac penetration of ablative energy, which also induced the development of gastric hypomotility due to periesophageal vagal plexus injury. The dilated stomach then pressed upon the third portion of the duodenum as well as the SMA and abdominal aorta, which caused the contents to remain in the stomach and the stomach to further dilate in a vicious circle. The patient was treated with food restriction and given 500 mg of erythromycin intravenously twice a day for five days, after which he was able to restart oral intake. A total of 5 mg of mosapride citrate per os three times a day was subsequently administered for two months.
Discussion The esophagus and posterior left atrial wall are in close contact with each other over a large area that often lies within the zone of atrial fibrillation ablation. The layer of adipose tissue may serve to insulate the esophagus from thermal injury, explaining why atrioesophageal fistulas are rare. Once this complication develops, however, the mortality rate is approximately 50% (5). Periesophageal vagal plexus injury is another extracardiac complication of catheter ablation for the treatment of atrial fibrillation. Lo et al (6). examined the gastrointestinal myoelectrical activity using electrogastrography by placing electrodes on the abdominal skin and observed the attenuation of normal gastric slow waves with an increasing bradygastria component in patients exhibiting a pain/vagal response to isolation of the posterior wall of the left pulmonary vein during the treatment of atrial fibrillation, but not paroxysmal supraventricular tachycardia. These findings indicate the development of periesophageal vagal plexus injury following catheter ablation for atrial fibrillation. Kuwahara et al. (3) reported the frequency of periesophageal vagal plexus injury after catheter ablation in the treatment of atrial fibrillation to be 0.3% (11 of 3,695 patients), with symptoms including nausea, vomiting, bloating, constipation and gastric pain, all of which occurred within 72 hours after the procedure. The acute onset of delayed gastric emptying is also a feature of this complication. Meanwhile, Knopp et al. (4) reported that the frequency of gastroparesis after catheter ablation for atrial fibrillation is 17% (70 of 425 patients); they performed esophagogastroduodenography in all patients regardless of symptoms. We therefore assume that the incidence of asymptomatic periesophageal vagal plexus injury after catheter ablation may be high. Prokinetic medications enhance the contractility of the gastrointestinal tract and promote the movement of luminal contents in an antegrade direction. Sturm et al. (7) performed a systematic analysis and found the motilin agonist erythromycin to be superior with respect to accelerating the rate of gastric emptying, while both erythromycin and the dopamine antagonist domperidone appear to be the most effective in improving symptoms. In addition, Janssens et
al. (8) reported that the intravenous administration of 200 mg of erythromycin normalizes the prolonged duration of gastric emptying for both solids and liquids in patients with diabetic gastroparesis, and Kuwahara et al. (3) subsequently reported that, among seven patients with severe gastric dilatation after catheter ablation for atrial fibrillation, most subjects responded to treatment with intravenous erythromycin (3 mg/kg every 8 hours for 2-7 days). The latter group commented that intravenous administration may effectively restart contractions in the stomach during acute episodes of gastric stasis in which oral intake is not tolerated. However, there are currently no assessments regarding the proper dosage. In addition to erythromycin, Kuwahara et al. (3) attempted to administer oral mosapride citrate or metoclopramide in certain patients after they were able to eat. These medications are 5-HT4 receptor agonists; mosapride citrate, in particular, is a selective 5-HT4 receptor agonist that enhances gastric emptying and motility in the upper gastrointestinal tract, thus facilitating acetylcholine release from enteric cholinergic neurons. Most patients eventually recover with symptomatic treatment, although some develop severe gastric dilatation requiring hospitalization, the cause of which remains unidentified. Most previous reports have stated that the cause of their patient’s condition was “unknown” or described the symptoms using obscure terms, such as “paralytic” or “gastroparesis” (2-4, 6). Gastroparesis itself occurs in many clinical conditions, including diabetes, a post-gastric surgery state, Parkinson’s disease, collagen vascular disorders and others. However, none of these conditions were applicable in the present case. One report stated that a few sites of severe gastric dilatation had occurred secondary to “pyloric spasms” (2, 3); however, no illustrations were provided in that paper. Therefore, the validity of this speculation remains uncertain. To our knowledge, this case is the first report of severe gastric dilatation caused by periesophageal vagal plexus injury-induced SMA syndrome following catheter ablation for atrial fibrillation. The average measurements of the angiographically calculated SMA-aorta distance in patients with SMA syndrome have been reported to be 2.3 and 3.3 mm, with average control values of 14 and 18 mm, respectively (9, 10). The average measurement on computed tomography has also been reported to be 6.4 mm, with the average control value being 14.6 mm (11). The SMA-aorta distance in our patient was 6 mm at disease onset and 9 mm at the time of remission. SMA syndrome may develop when the anatomical relationships between the third portion of the duodenum, spine, aorta and SMA are distorted by weight loss, spinal traction or lumber hyperlordosis (12, 13). One main cause of SMA syndrome is significant weight loss due to an eating disorder. Once the severity of gastroparesis has progressed to the point at which hospitalization is required (i.e., SMA syndrome has become obvious), prokinetic medication alone is
607
Intern Med 54: 605-609, 2015
DOI: 10.2169/internalmedicine.54.3276
insufficient for treatment. Instead, nasogastric tube drainage should be initiated; specifically, the pressure in the third portion of the duodenum between the SMA and abdominal aorta that develops secondary to severe gastric dilatation must be released (14). The obstruction of the third portion of the duodenum observed in cases of SMA syndrome may be intermittent, partial or complete and acute or chronic. For instance, weight loss is a considered to be a risk factor for SMA syndrome because it depletes the retroperitoneal fat and lymphatic tissues, which, under normal circumstances, serve as a cushion that holds the SMA off of the aorta and protect the third portion of the duodenum from compression (15). Conservative approaches as first-line therapy for SMA syndrome are aimed at replenishing the mesenteric fat stores and decompressing the third portion of the duodenum (16). Additionally, positional changes, such as assuming the knee-chest or side-lying position after eating, tend to widen the SMAaorta distance, which partially relieves the degree of duodenal obstruction and facilitates the movement of gastric contents through the area of constriction (17). In the acute setting, as in the current case, manual decompression of the duodenum and stomach with a nasogastric tube is often preferred to treat the patient’s symptoms (14, 18). In addition, nasojejunal tubes are sometimes inserted beyond the site of obstruction, often endoscopically, in severely ill, malnourished and/or elderly patients to enable the administration of sustained nutrition while initiating parenteral feeding (15). Surgery is indicated in patients who do not improve with conservative management (15). Most surgeons prefer duodenojejunostomy as the procedure of choice in cases of SMA syndrome (19), and treatment has also recently been conducted laparoscopically (17, 20). Our patient had risk factors for SMA syndrome, since he was lean and his SMA-aorta distance was short. However, as he was not extremely skinny, only a small amount of the dilated stomach pressed on the third portion of the duodenum while eating a normal quantity of food prior to catheter ablation. Subsequently, gastric hypomotility due to periesophageal vagal plexus injury after catheter ablation induced severe gastric dilatation even when the patient ate a normal quantity of food, which increased the pressure in the third portion of the duodenum between the SMA and abdominal aorta. Importantly, we remain concerned that the SMA syndrome may again become obvious while eating large quantities of food at once, even if the gastric hypomotility has recovered. We herein presented a case involving a patient who developed severe gastric dilatation after undergoing catheter ablation for the treatment of atrial fibrillation. Most previous reports have stated the cause of this condition to be “unknown,” “paralytic” or “gastroparesis.” In addition, some reports have argued that “pyloric spasms” contributed to their patient’s condition, although no illustrations have been provided. Therefore, the validity of this speculation remains uncertain. To our knowledge, this is the first report of severe
gastric dilatation caused by periesophageal vagal plexus injury-induced SMA syndrome after catheter ablation for atrial fibrillation. The authors state that they have no Conflict of Interest (COI).
References 1. Pappone C, Oral H, Santinelli V, et al. Atrio-esophageal fistula as a complication of percutaneous transcatheter ablation of atrial fibrillation. Circulation 109: 2724-2726, 2004. 2. Shah D, Dumonceau JM, Burri H, et al. Acute pyloric spasm and gastric hypomotility: an extracardiac adverse effect of percutaneous radiofrequency ablation for atrial fibrillation. J Am Coll Cardiol 46: 327-330, 2005. 3. Kuwahara T, Takahashi A, Takahashi Y, et al. Clinical characteristics and management of periesophageal vagal nerve injury complicating left atrial ablation of atrial fibrillation: lessons from eleven cases. J Cardiovasc Electrophysiol 24: 847-851, 2013. 4. Knopp H, Halm U, Lamberts R, et al. Incidental and ablationinduced findings during upper gastrointestinal endoscopy in patients after ablation of atrial fibrillation: a retrospective study of 425 patients. Heart Rhythm 11: 574-578, 2014. 5. Lemola K, Sneider M, Desjardins B, et al. Computed tomographic analysis of the anatomy of the left atrium and the esophagus: implications for left atrial catheter ablation. Circulation 110: 36553660, 2004. 6. Lo LW, Lu CL, Lin YJ, et al. A novel finding-impairment of gastric myoelectricity after catheter ablation of atrial fibrillation. Circ J 77: 2014-2023, 2013. 7. Sturm A, Holtmann G, Goebell H, Gerken G. Prokinetics in patients with gastroparesis: a systematic analysis. Digestion 60: 422427, 1999. 8. Janssens J, Peeters TL, Vantrappen G, et al. Improvement of gastric emptying in diabetic gastroparesis by erythromycin. Preliminary studies. N Engl J Med 322: 1028-1031, 1990. 9. Mansberger AR Jr, Hearn JB, Byers RM, Fleisig N, Buxton RW. Vascular compression of the duodenum. Emphasis on accurate diagnosis. Am J Surg 115: 89-96, 1968. 10. Lukes PJ, Rolny P, Nilson AE, Gamklou R, Darle N, Dotevall G. Diagnostic value of hypotonic duodenography in superior mesenteric artery syndrome. Acta Chir Scand 144: 39-43, 1978. 11. Applegate GR, Cohen AJ. Dynamic CT in superior mesenteric artery syndrome. J Comput Assist Tomogr 12: 976-980, 1988. 12. Adson DE, Mitchell JE, Trenkner SW. The superior mesenteric artery syndrome and acute gastric dilatation in eating disorders: a report of two cases and a review of the literature. Int J Eat Disord 21: 103-114, 1997. 13. Altiok H, Lubicky JP, DeWald CJ, Herman JE. The superior mesenteric artery syndrome in patients with spinal deformity. Spine 30: 2164-2170, 2005. 14. Mathenge N, Osiro S, Rodriguez II, Salib C, Tubbs RS, Loukas M. Superior mesenteric artery syndrome and its associated gastrointestinal implications. Clin Anat 27: 1244-1252, 2014. 15. Laffont I, Bensmail D, Rech C, Prigent G, Loubert G, Dizien O. Late superior mesenteric artery syndrome in paraplegia: case report and review. Spinal Cord 40: 88-91, 2002. 16. Shiu JR, Chao HC, Luo CC, et al. Clinical and nutritional outcomes in children with idiopathic superior mesenteric artery syndrome. J Pediatr Gastroenterol Nutr 51: 177-182, 2010. 17. Gersin KS, Heniford BT. Laparoscopic duodenojejunostomy for treatment of superior mesenteric artery syndrome. JSLS 2: 281284, 1998. 18. Welsch T, Büchler MW, Kienle P. Recalling superior mesenteric artery syndrome. Dig Surg 24: 149-156, 2007.
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Intern Med 54: 605-609, 2015
DOI: 10.2169/internalmedicine.54.3276
19. Jain R. Superior mesenteric artery syndrome. Curr Treat Options Gastroenterol 10: 24-27, 2007. 20. Fraser JD, St Peter SD, Hughes JH, Swain JM. Laparoscopic duo-
denojejunostomy for superior mesenteric artery syndrome. JSLS 13: 254-259, 2009.
Ⓒ 2015 The Japanese Society of Internal Medicine http://www.naika.or.jp/imonline/index.html
609
CASE REPORT
□
Suspicion of Superior Mesenteric Artery Syndrome in a Patient with Severe Gastric Dilatation after Catheter Ablation Hidehiro Kamezaki 1,2, Ryosaku Azemoto 1, Osamu Yokosuka 2, Tatsuya Fujimoto 1, Masamichi Obu 1, Masahiko Saito 3, Yu Yoshida 1, Yoshihiro Koma 1, Hitoshi Maruyama 2 and Mototsugu Fujimori 1
Abstract Catheter ablation is a widely used treatment for atrial fibrillation. Gastric hypomotility due to periesophageal vagal plexus injury is a consequence of the extracardiac penetration of ablative energy. Some affected patients develop severe gastric dilatation requiring hospitalization. However, most previous reports have stated the cause of the subject’s condition to be “unknown” or described the symptoms using obscure terms, such as “paralytic” or “gastroparesis.” For example, one report stated that a few sites of severe gastric dilatation were secondary to “pyloric spasms;” however, no illustrations were provided in the paper. “Superior mesenteric artery syndrome” is a suspected cause of such dilatation. Key words: superior mesenteric artery syndrome, catheter ablation, gastric hypomotility, gastric dilatation, periesophageal vagal plexus injury, atrial fibrillation (Intern Med 54: 605-609, 2015) (DOI: 10.2169/internalmedicine.54.3276)
to be the cause of the dilatation in this case.
Introduction Case Report Catheter ablation is a widely used treatment for atrial fibrillation. As the use of this treatment has increased, a variety of adverse effects have been reported. Atrioesophageal fistula formation was reported to be a consequence of the extracardiac penetration of ablative energy for the first time in 2004 (1). Gastric hypomotility due to periesophageal vagal plexus injury is another extracardiac adverse event (2-4), the frequency of which varies from 0.3% to 17.0% (3, 4). Most affected patients recover with symptomatic treatment, although some develop severe gastric dilatation requiring hospitalization. The causes of such cases of severe dilatation remain unidentified. We herein report a case involving a patient who exhibited severe gastric dilatation after undergoing catheter ablation. Superior mesenteric artery (SMA) syndrome was suspected
The patient was a 62-year-old man with a height of 167 cm, weight of 54 kg and body mass index of 19.4 kg/m2, all of which had remained unchanged for a long period. He underwent catheter ablation for chronic atrial fibrillation at the Department of Cardiology at Kimitsu Chuo Hospital. The radiofrequency energy was 25-30 W, and the radiofrequency delivery was stopped if the esophageal temperature reached 42℃. Even if the esophageal temperature did not reach 42℃, the radiofrequency delivery time was limited to 30 seconds at each site. The pulmonary veins were circumferentially ablated, and the endpoint of pulmonary vein isolation was the elimination of all pulmonary vein potentials. Additional substrate ablation was also performed, including the left atrial roof line and left atrial bottom line, with supe-
１
Department of Gastroenterology, Kimitsu Chuo Hospital, Japan, ２Department of Gastroenterology and Nephrology, Chiba University Graduate School of Medicine, Japan and ３Department of Internal Medicine, Kumagaya General Hospital, Japan Received for publication May 13, 2014; Accepted for publication August 11, 2014 Correspondence to Dr. Hidehiro Kamezaki, [email protected]
605
Intern Med 54: 605-609, 2015
DOI: 10.2169/internalmedicine.54.3276
SMA
st
du ao du IVC
Figure 1. An abdominal X-ray shows the double-bubble sign, indicating gastric and duodenal air bubbles with niveaus. This finding suggests the presence of obstruction on the proximal side of the duodenal bulb.
SMA
Figure 2. Abdominal computed tomography shows that the dilated stomach is causing dorsal deviation of the superior mesenteric artery (SMA) and that the SMA and abdominal aorta are pressing upon the third portion of the duodenum. ao; aorta, du: duodenum, IVC: inferior vena cava, SMA: superior mesenteric artery, st: stomach
SMA st
st IVC
du ao du IVC
Figure 3. A repeat abdominal computed tomography scan shows that the pressure of the third portion of the duodenum has been alleviated and that the superior mesenteric arteryaorta distance increased from 6 to 9 mm immediately after the gastric drainage procedure. ao: aorta, du: duodenum, IVC: inferior vena cava, SMA: superior mesenteric artery, st: stomach
rior vena cava isolation. Finally, the patient achieved a sinus rhythm. No complications were detected during or immediately after the procedure, and he was subsequently discharged from the hospital. However, epigastric discomfort and vomiting occurred 24 hours after the operation, and these symptoms unfortunately gradually worsened. Seven days after undergoing catheter ablation, the patient received a medical examination in our department. The blood test results were normal; however, an abdominal X-ray image showed a double bubble sign (Fig. 1), which usually develops when gastric and duodenal air bubbles form niveaus, indicating the presence of obstruction in the distal duodenum. Abdominal computed tomography showed no neoplastic lesions, although the stomach was dilated, causing dorsal de-
du ao du
Figure 4. Abdominal computed tomography shows good contrast imaging of the SMA. ao: aorta, du: duodenum, IVC: inferior vena cava, SMA: superior mesenteric artery, st: stomach
viation of the SMA, and the SMA and abdominal aorta were pressing upon the third portion of the duodenum (Fig. 2). Based on the patient’s clinical course, we suspected a diagnosis of SMA syndrome and thus placed a nasogastric tube, draining approximately 2,000 mL of stomach contents. Thereafter, the patient’s symptoms significantly improved, and a repeat abdominal computed tomography examination showed that the pressure of the third portion of the duodenum had decreased, while the SMA-aorta distance at the level at which the SMA crossed the duodenum had increased from 6 to 9 mm, immediately after the drainage procedure (Fig. 3). The possibility of SMA obstruction was excluded due to the findings of good contrast imaging of the SMA (Fig. 4). A subsequent upper gastrointestinal series showed no obstructive lesions. Although esophagogastroduodenography also revealed no tumorous masses in the duodenum, a gastric ulcer was detected at the cardia, despite the use of proton pump inhibitors prior to catheter ablation. We
606
Intern Med 54: 605-609, 2015
DOI: 10.2169/internalmedicine.54.3276
assumed that this finding was due to the extracardiac penetration of ablative energy, which also induced the development of gastric hypomotility due to periesophageal vagal plexus injury. The dilated stomach then pressed upon the third portion of the duodenum as well as the SMA and abdominal aorta, which caused the contents to remain in the stomach and the stomach to further dilate in a vicious circle. The patient was treated with food restriction and given 500 mg of erythromycin intravenously twice a day for five days, after which he was able to restart oral intake. A total of 5 mg of mosapride citrate per os three times a day was subsequently administered for two months.
Discussion The esophagus and posterior left atrial wall are in close contact with each other over a large area that often lies within the zone of atrial fibrillation ablation. The layer of adipose tissue may serve to insulate the esophagus from thermal injury, explaining why atrioesophageal fistulas are rare. Once this complication develops, however, the mortality rate is approximately 50% (5). Periesophageal vagal plexus injury is another extracardiac complication of catheter ablation for the treatment of atrial fibrillation. Lo et al (6). examined the gastrointestinal myoelectrical activity using electrogastrography by placing electrodes on the abdominal skin and observed the attenuation of normal gastric slow waves with an increasing bradygastria component in patients exhibiting a pain/vagal response to isolation of the posterior wall of the left pulmonary vein during the treatment of atrial fibrillation, but not paroxysmal supraventricular tachycardia. These findings indicate the development of periesophageal vagal plexus injury following catheter ablation for atrial fibrillation. Kuwahara et al. (3) reported the frequency of periesophageal vagal plexus injury after catheter ablation in the treatment of atrial fibrillation to be 0.3% (11 of 3,695 patients), with symptoms including nausea, vomiting, bloating, constipation and gastric pain, all of which occurred within 72 hours after the procedure. The acute onset of delayed gastric emptying is also a feature of this complication. Meanwhile, Knopp et al. (4) reported that the frequency of gastroparesis after catheter ablation for atrial fibrillation is 17% (70 of 425 patients); they performed esophagogastroduodenography in all patients regardless of symptoms. We therefore assume that the incidence of asymptomatic periesophageal vagal plexus injury after catheter ablation may be high. Prokinetic medications enhance the contractility of the gastrointestinal tract and promote the movement of luminal contents in an antegrade direction. Sturm et al. (7) performed a systematic analysis and found the motilin agonist erythromycin to be superior with respect to accelerating the rate of gastric emptying, while both erythromycin and the dopamine antagonist domperidone appear to be the most effective in improving symptoms. In addition, Janssens et
al. (8) reported that the intravenous administration of 200 mg of erythromycin normalizes the prolonged duration of gastric emptying for both solids and liquids in patients with diabetic gastroparesis, and Kuwahara et al. (3) subsequently reported that, among seven patients with severe gastric dilatation after catheter ablation for atrial fibrillation, most subjects responded to treatment with intravenous erythromycin (3 mg/kg every 8 hours for 2-7 days). The latter group commented that intravenous administration may effectively restart contractions in the stomach during acute episodes of gastric stasis in which oral intake is not tolerated. However, there are currently no assessments regarding the proper dosage. In addition to erythromycin, Kuwahara et al. (3) attempted to administer oral mosapride citrate or metoclopramide in certain patients after they were able to eat. These medications are 5-HT4 receptor agonists; mosapride citrate, in particular, is a selective 5-HT4 receptor agonist that enhances gastric emptying and motility in the upper gastrointestinal tract, thus facilitating acetylcholine release from enteric cholinergic neurons. Most patients eventually recover with symptomatic treatment, although some develop severe gastric dilatation requiring hospitalization, the cause of which remains unidentified. Most previous reports have stated that the cause of their patient’s condition was “unknown” or described the symptoms using obscure terms, such as “paralytic” or “gastroparesis” (2-4, 6). Gastroparesis itself occurs in many clinical conditions, including diabetes, a post-gastric surgery state, Parkinson’s disease, collagen vascular disorders and others. However, none of these conditions were applicable in the present case. One report stated that a few sites of severe gastric dilatation had occurred secondary to “pyloric spasms” (2, 3); however, no illustrations were provided in that paper. Therefore, the validity of this speculation remains uncertain. To our knowledge, this case is the first report of severe gastric dilatation caused by periesophageal vagal plexus injury-induced SMA syndrome following catheter ablation for atrial fibrillation. The average measurements of the angiographically calculated SMA-aorta distance in patients with SMA syndrome have been reported to be 2.3 and 3.3 mm, with average control values of 14 and 18 mm, respectively (9, 10). The average measurement on computed tomography has also been reported to be 6.4 mm, with the average control value being 14.6 mm (11). The SMA-aorta distance in our patient was 6 mm at disease onset and 9 mm at the time of remission. SMA syndrome may develop when the anatomical relationships between the third portion of the duodenum, spine, aorta and SMA are distorted by weight loss, spinal traction or lumber hyperlordosis (12, 13). One main cause of SMA syndrome is significant weight loss due to an eating disorder. Once the severity of gastroparesis has progressed to the point at which hospitalization is required (i.e., SMA syndrome has become obvious), prokinetic medication alone is
607
Intern Med 54: 605-609, 2015
DOI: 10.2169/internalmedicine.54.3276
insufficient for treatment. Instead, nasogastric tube drainage should be initiated; specifically, the pressure in the third portion of the duodenum between the SMA and abdominal aorta that develops secondary to severe gastric dilatation must be released (14). The obstruction of the third portion of the duodenum observed in cases of SMA syndrome may be intermittent, partial or complete and acute or chronic. For instance, weight loss is a considered to be a risk factor for SMA syndrome because it depletes the retroperitoneal fat and lymphatic tissues, which, under normal circumstances, serve as a cushion that holds the SMA off of the aorta and protect the third portion of the duodenum from compression (15). Conservative approaches as first-line therapy for SMA syndrome are aimed at replenishing the mesenteric fat stores and decompressing the third portion of the duodenum (16). Additionally, positional changes, such as assuming the knee-chest or side-lying position after eating, tend to widen the SMAaorta distance, which partially relieves the degree of duodenal obstruction and facilitates the movement of gastric contents through the area of constriction (17). In the acute setting, as in the current case, manual decompression of the duodenum and stomach with a nasogastric tube is often preferred to treat the patient’s symptoms (14, 18). In addition, nasojejunal tubes are sometimes inserted beyond the site of obstruction, often endoscopically, in severely ill, malnourished and/or elderly patients to enable the administration of sustained nutrition while initiating parenteral feeding (15). Surgery is indicated in patients who do not improve with conservative management (15). Most surgeons prefer duodenojejunostomy as the procedure of choice in cases of SMA syndrome (19), and treatment has also recently been conducted laparoscopically (17, 20). Our patient had risk factors for SMA syndrome, since he was lean and his SMA-aorta distance was short. However, as he was not extremely skinny, only a small amount of the dilated stomach pressed on the third portion of the duodenum while eating a normal quantity of food prior to catheter ablation. Subsequently, gastric hypomotility due to periesophageal vagal plexus injury after catheter ablation induced severe gastric dilatation even when the patient ate a normal quantity of food, which increased the pressure in the third portion of the duodenum between the SMA and abdominal aorta. Importantly, we remain concerned that the SMA syndrome may again become obvious while eating large quantities of food at once, even if the gastric hypomotility has recovered. We herein presented a case involving a patient who developed severe gastric dilatation after undergoing catheter ablation for the treatment of atrial fibrillation. Most previous reports have stated the cause of this condition to be “unknown,” “paralytic” or “gastroparesis.” In addition, some reports have argued that “pyloric spasms” contributed to their patient’s condition, although no illustrations have been provided. Therefore, the validity of this speculation remains uncertain. To our knowledge, this is the first report of severe
gastric dilatation caused by periesophageal vagal plexus injury-induced SMA syndrome after catheter ablation for atrial fibrillation. The authors state that they have no Conflict of Interest (COI).
References 1. Pappone C, Oral H, Santinelli V, et al. Atrio-esophageal fistula as a complication of percutaneous transcatheter ablation of atrial fibrillation. Circulation 109: 2724-2726, 2004. 2. Shah D, Dumonceau JM, Burri H, et al. Acute pyloric spasm and gastric hypomotility: an extracardiac adverse effect of percutaneous radiofrequency ablation for atrial fibrillation. J Am Coll Cardiol 46: 327-330, 2005. 3. Kuwahara T, Takahashi A, Takahashi Y, et al. Clinical characteristics and management of periesophageal vagal nerve injury complicating left atrial ablation of atrial fibrillation: lessons from eleven cases. J Cardiovasc Electrophysiol 24: 847-851, 2013. 4. Knopp H, Halm U, Lamberts R, et al. Incidental and ablationinduced findings during upper gastrointestinal endoscopy in patients after ablation of atrial fibrillation: a retrospective study of 425 patients. Heart Rhythm 11: 574-578, 2014. 5. Lemola K, Sneider M, Desjardins B, et al. Computed tomographic analysis of the anatomy of the left atrium and the esophagus: implications for left atrial catheter ablation. Circulation 110: 36553660, 2004. 6. Lo LW, Lu CL, Lin YJ, et al. A novel finding-impairment of gastric myoelectricity after catheter ablation of atrial fibrillation. Circ J 77: 2014-2023, 2013. 7. Sturm A, Holtmann G, Goebell H, Gerken G. Prokinetics in patients with gastroparesis: a systematic analysis. Digestion 60: 422427, 1999. 8. Janssens J, Peeters TL, Vantrappen G, et al. Improvement of gastric emptying in diabetic gastroparesis by erythromycin. Preliminary studies. N Engl J Med 322: 1028-1031, 1990. 9. Mansberger AR Jr, Hearn JB, Byers RM, Fleisig N, Buxton RW. Vascular compression of the duodenum. Emphasis on accurate diagnosis. Am J Surg 115: 89-96, 1968. 10. Lukes PJ, Rolny P, Nilson AE, Gamklou R, Darle N, Dotevall G. Diagnostic value of hypotonic duodenography in superior mesenteric artery syndrome. Acta Chir Scand 144: 39-43, 1978. 11. Applegate GR, Cohen AJ. Dynamic CT in superior mesenteric artery syndrome. J Comput Assist Tomogr 12: 976-980, 1988. 12. Adson DE, Mitchell JE, Trenkner SW. The superior mesenteric artery syndrome and acute gastric dilatation in eating disorders: a report of two cases and a review of the literature. Int J Eat Disord 21: 103-114, 1997. 13. Altiok H, Lubicky JP, DeWald CJ, Herman JE. The superior mesenteric artery syndrome in patients with spinal deformity. Spine 30: 2164-2170, 2005. 14. Mathenge N, Osiro S, Rodriguez II, Salib C, Tubbs RS, Loukas M. Superior mesenteric artery syndrome and its associated gastrointestinal implications. Clin Anat 27: 1244-1252, 2014. 15. Laffont I, Bensmail D, Rech C, Prigent G, Loubert G, Dizien O. Late superior mesenteric artery syndrome in paraplegia: case report and review. Spinal Cord 40: 88-91, 2002. 16. Shiu JR, Chao HC, Luo CC, et al. Clinical and nutritional outcomes in children with idiopathic superior mesenteric artery syndrome. J Pediatr Gastroenterol Nutr 51: 177-182, 2010. 17. Gersin KS, Heniford BT. Laparoscopic duodenojejunostomy for treatment of superior mesenteric artery syndrome. JSLS 2: 281284, 1998. 18. Welsch T, Büchler MW, Kienle P. Recalling superior mesenteric artery syndrome. Dig Surg 24: 149-156, 2007.
608
Intern Med 54: 605-609, 2015
DOI: 10.2169/internalmedicine.54.3276
19. Jain R. Superior mesenteric artery syndrome. Curr Treat Options Gastroenterol 10: 24-27, 2007. 20. Fraser JD, St Peter SD, Hughes JH, Swain JM. Laparoscopic duo-
denojejunostomy for superior mesenteric artery syndrome. JSLS 13: 254-259, 2009.
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