CASE REPORT
Celiac Artery Compression After a Gastric Bypass Nathan G. Richards, MD, Richard F. Neville, MD, Anton N. Sidawy, MD, MPH, and Fredrick J. Brody, MD, MBA
Abstract: Median arcuate ligament (MAL) syndrome or celiac artery compression occurs secondary to diaphragmatic compression of the celiac artery and the corresponding neural structures of the celiac plexus. Typically, patients present with postprandial abdominal pain, nausea, vomiting, and weight loss. Diagnostically, various radiologic studies are used to document impingement of the celiac artery including ultrasound, computed tomography, aortograms, and magnetic resonance imaging. Historically, open approaches to the aorta and the celiac artery are performed to release the MAL and relieve compression of the celiac artery and the plexus. Laparoscopic approaches are now utilized to divide the MAL. This study describes a patient who underwent a successful laparoscopic Roux-en-Y gastric bypass and lost 100 lbs over a 2-year postoperative period. Subsequently, the patient developed postprandial abdominal pain associated with nausea. She underwent a computed tomogram that diagnosed celiac compression and then a dynamic ultrasound that showed elevated velocities with deep expiration. Ultimately, a laparoscopic MAL release with division of the celiac plexus was performed. At 10 months postoperatively, the patient remains asymptomatic. To our knowledge, this report documents a rare case of CAC after Rouxen-Y gastric bypass. On the basis of this report, CAC should be considered in the differential diagnosis of postprandial abdominal pain in patients after bariatric surgery.
CASE REPORT A 36-year-old woman with a weight of 147.2 kg and a body mass index of 55.4 underwent an uneventful laparoscopic RYGB in January 2009. Intraoperatively, a 30 mL gastric pouch and a 150 cm Roux limb were created. Subsequently, she was discharged to home on postoperative day 2 tolerating a clear liquid diet. Three months postoperatively, she weighed 112 kg and she had returned to all of her normal activities. Two years postoperatively, she was asymptomatic and weighed 83.6 kg. She was tolerating a regular diet and she continued to take a multivitamin, protein supplements, calcium, and vitamin D daily. At 2 years postoperatively, a full panel of nutritional lab values discerned only a low vitamin D level of 16.8 ng/mL and a hemoglobin level of 9.6 g/dL. One month after her 2-year follow-up visit, she developed acute left upper quadrant abdominal pain after eating several caramel candies. The pain resolved spontaneously and she did not seek medical attention. However, the left upper quadrant pain recurred 8 months later and persisted for 3 days. The pain was associated with nausea and vomiting and was worse after meals.
Key Words: median arcuate ligament syndrome, celiac artery compression syndrome, Roux-en-Y gastric bypass
(Surg Laparosc Endosc Percutan Tech 2014;24:e66–e69)
H
istorically, celiac artery compression (CAC) has been an elusive diagnosis. The diagnostic accuracy of this disease has increased with recent radiologic refinements in ultrasound, computed tomography (CT), and magnetic resonance arteriography. Once CAC is diagnosed, several case reports and small series document the efficacy of a laparoscopic median arcuate ligament (MAL) release. The initial open operation was described by Harjola1 in 1963 and subsequently, Dunbar et al2 reported a series of 15 patients with CAC in 1965. Classically, the MAL is divided to resolve compression of the celiac artery and usually the celiac plexus is divided as well. To date, there are only a few studies that document long-term follow-up in the literature. This study describes a rare case of CAC after a laparoscopic Roux-en-Y gastric bypass (RYGB).
Received for publication August 28, 2012; accepted November 27, 2012. From the Department of Surgery, The George Washington University Medical Center, Washington, DC. The authors declare no conflicts of interest. Reprints: Frederick J. Brody, MD, MBA, 2150 Pennsylvania Ave, NW, Suite 6B, Washington, DC 20037 (e-mail: [email protected]). Copyright r 2014 by Lippincott Williams & Wilkins
e66 | www.surgical-laparoscopy.com
FIGURE 1. 3-dimensional reconstruction of computed tomogram of the aorta. The tip of the yellow arrow indicates the angulated celiac artery approximately 2 cm from its origin at the aorta.
Surg Laparosc Endosc Percutan Tech
Volume 24, Number 2, April 2014
Surg Laparosc Endosc Percutan Tech
Volume 24, Number 2, April 2014
She ingested multiple antacids and various proton pump inhibitors without resolution of the pain. She continued to pass flatus daily and she denied radiation of her pain or changes in her bowel movements. Ultimately, she was evaluated in the emergency department. At that time, she weighed 79.6 kg with a body mass index of 29.6. On examination, her abdomen was flat with well-healed incisions. She was soft without guarding, abnormal masses, or hernia defects. Her blood work did not show any evidence of pancreatitis, biliary disease, or occult bleeding. A contrast CT scan (Fig. 1) was then obtained and showed narrowing of the celiac artery approximately 2 cm beyond its origin from the aorta. There was no evidence of an internal hernia. A Doppler study of her celiac artery showed velocities of 516 cm/s at rest, 194 cm/s at deep inspiration, and 352 cm/s with deep expiration. There was no evidence of an arterial stricture. She was diagnosed with CAC and was scheduled for a laparoscopic MAL release. The laparoscopic MAL release was completed utilizing a standard 5-port foregut approach. A pneumoperitoneum was established utilizing a Veress needle in the left upper quadrant. A Visiport trocar (Covidien Inc., Norwalk, CT) was then inserted 18 cm from the xiphoid followed by four 5-mm ports. The lateral segment of the liver was retracted anteriorly and several adhesions were lysed to expose the medial border of the gastric pouch and Roux limb. The lesser omentum had been divided previously and the caudate lobe was visualized along with the inferior vena cava. The peritoneum was divided overlying the common hepatic, left gastric, and splenic arteries utilizing the hook cautery. The 3 vessels were traced proximally to their respective origins at the celiac artery. The hook cautery was utilized to incise the peritoneum overlying the MAL, right crus, and suspensory ligament to the fourth portion of the duodenum. All of these fibers were divided with the hook cautery. Once these structures were divided, the aorta was dissected and exposed for approximately 5 cm cephalad to the origin of the celiac artery. The dissection was extended laterally to identify the lateral borders of the aorta. The neural structures along the lateral borders of the aorta were divided with cautery. The left gastric, common hepatic, and splenic arteries were then reexamined and carefully exposed for approximately 4 cm from the trifurcation of the celiac artery. Any muscular, neural, or ligamentous bands were divided along the anterior course of the celiac artery and its trifurcation. After dividing the overlying structures of the aorta and skeletonizing the celiac artery and its trifurcation, hemostasis was verified and all ports were removed. Postoperatively, the patient was started on a liquid diet and progressed quickly to a regular diet. She was discharged on postoperative day 1. At 10 months postoperatively, she is completely asymptomatic. Her postoperative ultrasound studies at 6 months showed a celiac artery velocity of 469 cm/s at rest, 206 cm/s with deep inspiration, and 378 cm/s with deep expiration.
DISCUSSION Lipshutz3 in 1917 first described compression of the celiac artery from the crus of the diaphragm, MAL, or thickened fibrous para-aortic ganglionic tissue. In 1963, Harjola1 performed the initial MAL release. In 1965, Dunbar et al2 replicated Harjola’s success in a large series of patients. However, in 1972, Szilagyi et al4 questioned the veracity of CAC syndrome. Through 157 lateral aortograms, Szilagyi and colleagues demonstrated that 49.7% of patients had some degree of incidental celiac stenosis without evidence of corresponding symptoms. More recently, Agnes et al5 showed that at the time of orthotopic liver transplant, approximately 3% to 10% of patients have asymptomatic CAC. Clearly, the diagnosis of CAC remains controversial. CAC syndrome includes symptoms that mimic those found in superior mesenteric artery (SMA) syndrome that arise when the third portion of the duodenum is compressed between the SMA and the aorta. Normally, a fairly r
2014 Lippincott Williams & Wilkins
Median Arcuate Ligament Syndrome After RYGB
prominent fat pad exists between these 2 anatomic structures. Typically, rapid weight loss or nutritional compromise leads to a loss of the aortomesenteric fat pad that preserves the near 45-degree angle that the SMA usually follows as it emerges from the aorta. As the SMA angle decreases, patients typically present with postprandial pain or intestinal angina. From a purely vascular standpoint, there are isolated cases of SMA stenosis reported throughout the literature despite the presence of significant visceral collaterals from the celiac and inferior mesenteric artery. From a pathophysiological standpoint, SMA syndrome and SMA stenosis make inherent sense, especially as the SMA provides almost the entire arterial blood supply of the small bowel and proximal colon. Attributing symptoms to CAC is less intuitive because of the significant collaterals that exist to perfuse the vital foregut organs in the event of celiac stenosis, compression, or even occlusion. These collaterals include the network of vessels from the SMA and an extensive array of vessels that communicate with the gastric and splenic vasculature. The mere presence of these collaterals continues to fuel the argument against the existence of CAC syndrome. However, it seems plausible to postulate that if isolated SMA stenosis is truly a clinical diagnosis, then isolated celiac artery stenosis may be clinically possible. Unfortunately, a detailed understanding of the pathophysiology remains elusive surrounding the ebb and flow of the celiac artery and its adjacent neurovascular bundles. As detailed later, our own bias leans toward a neurologic deficiency secondary to compression of the sympathetic fibers versus a vascular entity. We feel that, impingement of the celiac artery and changes in vascular velocities with deep expiration represent a marker for neurological compression. Regardless, the patient detailed in this study presented with a prodrome similar to SMA compression or stenosis. However, her radiologic findings were consistent with CAC syndrome. Hypothetically, the rapid and significant weight loss incurred from the RYGB resulted in a drastic reduction of the aortomesenteric fat pad surrounding the celiac artery. Once the fat pad was essentially eradicated, the MAL and its associated muscular fibers compressed the celiac artery and the corresponding plexus. This resulted in abdominal pain exacerbated by ingesting food. Ultimately, the laparoscopic MAL release resolved this patient’s symptoms by relieving the compression on the celiac plexus. In 1985, Reilly et al6 studied CAC syndrome prospectively in 51 patients after celiac artery decompression with or without subsequent revascularization. At a mean of 9 years postoperatively, 81% of patients benefited from some type of surgical intervention. Although these data may confirm the existence of CAC syndrome, Reilly also demonstrated that there was no correlation between the degree of celiac stenosis and symptom relief. Their results showed that operative technique correlated with outcome. If the celiac artery was decompressed with accompanying revascularization, 76% (22/29) of patients improved. If decompression was performed without revascularization, only 53% (8/15) of the patients improved. Over the past 30 years, radiologic techniques and physiological testing have improved the ability to both define and treat this disease. For example, Faries et al7 utilized gastric exercise tonometry (GET) to assess the patients with suspected CAC. Their data demonstrated that intraluminal gastric CO2 was highly associated with symptoms secondary to CAC. Furthermore, this group www.surgical-laparoscopy.com |
e67
Richards et al
Surg Laparosc Endosc Percutan Tech
from the Netherlands8 showed that if gastric ischemia was confirmed preoperatively, improvements in GET postoperatively correlated with 100% long-term symptom relief. If the postoperative GET did not improve, surgical intervention was successful in only 25% of the patients. Interestingly, gross evidence of ischemic changes on endoscopy is usually absent despite any findings on GET that may reflect vascular involvement. Therefore, some of the associated benefit from a MAL release in terms of pain, nausea, and vomiting may be mitigated through the disruption of the sympathetic fibers of the celiac plexus. An interesting article from McCallum et al9 in 1997 describes a patient diagnosed with idiopathic gastroparesis and tachygastria. This patient underwent a gastric electrical stimulator and, subsequently, the patient was diagnosed with CAC. The patient then underwent a MAL release and, postoperatively, the gastroparesis resolved with normal gastric cycles of 3 to 3.5 cpm. Furthermore, the patient’s pain was completely resolved. The authors theorized that division of the sympathetic nerve fibers resolved the patient’s pain and restored the normal myoelectrical conduction of the stomach. McCallum and colleagues did not support a vascular etiology as several endoscopies failed to document mucosal changes consistent with ischemia. Given these data, it is important to understand how CAC presents clinically to truly understand the syndrome. Patients may present with postprandial abdominal pain, weight loss, diarrhea, and nausea with or without vomiting. Leaning forward or changing positions of the abdomen may occasionally mitigate the symptoms. Young athletes may present with exercise-induced abdominal pain. Occasionally, patients may even present with renovascular hypertension that arises from a poststenotic dilatation that affects the renal arteries.10 In addition to renovascular anatomic aberrancies, Calkins et al11 showed that pancreaticoduodenal artery aneurysms may result from CAC and lead to further symptoms. Diagnostically, CAC is usually confirmed with at least 1, if not 2, radiologic studies. These tests include mesenteric duplex of the celiac artery, SMA, and inferior mesenteric artery and perhaps the renal arteries, if there is a possibility of renovascular hypertension. This dynamic modality allows real time assessment of flow and identification of anatomic variations. CT with angiography and/or magnetic resonance arteriography are helpful but are limited by their static nature. When performed with both inspiration and expiration, biplane contrast aortography may yield a diagnosis of CAC, but this study is more invasive and is used less frequently. As mentioned previously, GET is a recently used adjunct that may demonstrate the physiological outcome of CAC in terms of gastric mucosal ischemia in patients with MAL syndrome.7,8,10 The patient detailed in this study underwent a CT scan of the abdomen that suggested stenosis at the origin of the celiac artery. Subsequently, she underwent a duplex ultrasound that confirmed the diagnosis as her celiac artery velocity was exceedingly high on expiration. Overall, our preference is to obtain at least 1 dynamic study (ultrasound or aortogram) and 1 study (magnetic resonance imaging or CT) that details the surrounding anatomy for any patient with suspected CAC. Interestingly, the patient’s follow-up ultrasound documented a decrease in the celiac artery velocity at rest and, essentially, unchanged velocities at deep inspiration and deep expiration. Again, we feel that the velocities are not indicative of a vascular etiology. Instead, these
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Volume 24, Number 2, April 2014
velocities are indicative of the neural compression that was ultimately treated. Treatment of CAC syndrome has been performed traditionally by open techniques but several case reports and small series document successful outcomes after a laparoscopic release of the MAL. Regardless of the technique, each approach requires division of the MAL at the diaphragmatic crus just proximal to the celiac trunk. Our technique entails division of the entire diameter of tissue overlying the aorta to ensure that any obstructing fibers are divided fully. These structures include the crural mechanism, the MAL, and the suspensory ligament extending to the fourth portion of the duodenum. We also believe that the aorta should be cleared for approximately 5 cm proximal to the celiac artery origin as the patient is supine for the procedure. This length should accommodate for an erect position with full expiration. In addition, any neurovascular structures overlying the celiac artery are divided. This operative technique was certainly successful in this patient as she remains asymptomatic at 10 months. Once the MAL has been decompressed, significant debate exists over the need to revascularize the celiac artery. Reilly et al6 argued for the necessity of revascularization. Dordoni et al12 and Roayaie et al13 have both shown that laparoscopic release of the MAL with laparoscopic ultrasound and endovascular stenting of the celiac artery provide similar results. Our present technique entails an isolated decompression of the MAL as a first step for CAC. If symptoms persist, an endovascular treatment may be considered to restore the luminal diameter of the celiac artery. In conclusion, this paper presents a rare case of a morbidly obese patient who developed CAC syndrome after undergoing a successful laparoscopic RYGB. On the basis of this patient’s clinical outcome, CAC should be considered in the differential diagnosis of abdominal pain after significant weight loss after a bariatric procedure. A duplex ultrasound of the mesenteric vessels should be included in the diagnostic work-up to exclude this specific diagnosis. As demonstrated in this report, dramatic changes may be obtained in patient care with a successful laparoscopic MAL release. Finally, this patient requires a longterm follow-up with annual assessments to ensure that her pain remains resolved. A repeat duplex scan is scheduled in another 6 months to assess the celiac artery. Regardless of its anatomic structure and velocities, the patient’s symptoms will dictate the need for any further intervention. REFERENCES 1. Harjola PT. A rare obstruction of the coeliac artery; report of a case. Ann Chir Gynecolo Fenn. 1963;52:547–550. 2. Dunbar DJ, Molnar W, Berman FF, et al. Compression of the celiac trunk and abdominal angina. Am J Roentgenol Radium Ther Nucl Med. 1965;95:731–744. 3. Lipshutz B. A composite study of the celiac axis artery. Ann Surg. 1917;65:159–169. 4. Szilagyi DE, Rian RL, Elliott JP, et al. The celiac artery compression syndrome (does it exist?). Surgery. 1972;6:849–863. 5. Agnes S, Avolio AW, Magalini SC, et al. Celiac axis compression syndrome in liver transplantation. Transplant Proc. 2001;33:1438–1439. 6. Reilly LM, Ammar AD, Stoney RJ, et al. Late results following operative repair for celiac artery compression syndrome. J Vasc Surg. 1985;120:1072–1076. 7. Faries PL, Narula A, Veith FJ, et al. The use of gastric tonometry in the assessment of celiac artery compression syndrome. Ann Vasc Surg. 2000;14:20–23. r
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8. Mensink PBS, van Petersen AS, Kolkman JJ, et al. Gastric exercise tonometry: the key investigation in patients with suspected celiac artery compression syndrome. J Vasc Surg. 2006;44:277. 9. Balaban DH, Chen J, Lin Z, et al. Median arcuate ligament syndrome: a possible cause of idiopathic gastroparesis. Am J Gastroenterol. 1998;92:519–523. 10. Gloviczki P, Duncan AA. Treatment of celiac artery compression syndrome: does it really exist? Perspect Vasc Surg Endovasc Ther. 2007;19:259–263.
r
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Median Arcuate Ligament Syndrome After RYGB
11. Calkins CM, Moore EE, Turner J, et al. Combined modality treatment of ruptured pancreaticoduodenal artery aneurysms due to celiac artery compression. Surgery. 2004;136:1088–1089. 12. Dordoni L, Tshomba Y, Turner J, et al. Celiac artery compression syndrome: successful laparoscopic treatment—a case report. Vasc Endovascular Surg. 2002;36:317–321. 13. Roayaie S, Jossart G, Gitlitz D, et al. Laparoscopic release of celiac artery compression syndrome facilitated by laparoscopic ultrasound scanning to confirm restoration of flow. J Vasc Surg. 2000;32:814.
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e69
Celiac Artery Compression After a Gastric Bypass Nathan G. Richards, MD, Richard F. Neville, MD, Anton N. Sidawy, MD, MPH, and Fredrick J. Brody, MD, MBA
Abstract: Median arcuate ligament (MAL) syndrome or celiac artery compression occurs secondary to diaphragmatic compression of the celiac artery and the corresponding neural structures of the celiac plexus. Typically, patients present with postprandial abdominal pain, nausea, vomiting, and weight loss. Diagnostically, various radiologic studies are used to document impingement of the celiac artery including ultrasound, computed tomography, aortograms, and magnetic resonance imaging. Historically, open approaches to the aorta and the celiac artery are performed to release the MAL and relieve compression of the celiac artery and the plexus. Laparoscopic approaches are now utilized to divide the MAL. This study describes a patient who underwent a successful laparoscopic Roux-en-Y gastric bypass and lost 100 lbs over a 2-year postoperative period. Subsequently, the patient developed postprandial abdominal pain associated with nausea. She underwent a computed tomogram that diagnosed celiac compression and then a dynamic ultrasound that showed elevated velocities with deep expiration. Ultimately, a laparoscopic MAL release with division of the celiac plexus was performed. At 10 months postoperatively, the patient remains asymptomatic. To our knowledge, this report documents a rare case of CAC after Rouxen-Y gastric bypass. On the basis of this report, CAC should be considered in the differential diagnosis of postprandial abdominal pain in patients after bariatric surgery.
CASE REPORT A 36-year-old woman with a weight of 147.2 kg and a body mass index of 55.4 underwent an uneventful laparoscopic RYGB in January 2009. Intraoperatively, a 30 mL gastric pouch and a 150 cm Roux limb were created. Subsequently, she was discharged to home on postoperative day 2 tolerating a clear liquid diet. Three months postoperatively, she weighed 112 kg and she had returned to all of her normal activities. Two years postoperatively, she was asymptomatic and weighed 83.6 kg. She was tolerating a regular diet and she continued to take a multivitamin, protein supplements, calcium, and vitamin D daily. At 2 years postoperatively, a full panel of nutritional lab values discerned only a low vitamin D level of 16.8 ng/mL and a hemoglobin level of 9.6 g/dL. One month after her 2-year follow-up visit, she developed acute left upper quadrant abdominal pain after eating several caramel candies. The pain resolved spontaneously and she did not seek medical attention. However, the left upper quadrant pain recurred 8 months later and persisted for 3 days. The pain was associated with nausea and vomiting and was worse after meals.
Key Words: median arcuate ligament syndrome, celiac artery compression syndrome, Roux-en-Y gastric bypass
(Surg Laparosc Endosc Percutan Tech 2014;24:e66–e69)
H
istorically, celiac artery compression (CAC) has been an elusive diagnosis. The diagnostic accuracy of this disease has increased with recent radiologic refinements in ultrasound, computed tomography (CT), and magnetic resonance arteriography. Once CAC is diagnosed, several case reports and small series document the efficacy of a laparoscopic median arcuate ligament (MAL) release. The initial open operation was described by Harjola1 in 1963 and subsequently, Dunbar et al2 reported a series of 15 patients with CAC in 1965. Classically, the MAL is divided to resolve compression of the celiac artery and usually the celiac plexus is divided as well. To date, there are only a few studies that document long-term follow-up in the literature. This study describes a rare case of CAC after a laparoscopic Roux-en-Y gastric bypass (RYGB).
Received for publication August 28, 2012; accepted November 27, 2012. From the Department of Surgery, The George Washington University Medical Center, Washington, DC. The authors declare no conflicts of interest. Reprints: Frederick J. Brody, MD, MBA, 2150 Pennsylvania Ave, NW, Suite 6B, Washington, DC 20037 (e-mail: [email protected]). Copyright r 2014 by Lippincott Williams & Wilkins
e66 | www.surgical-laparoscopy.com
FIGURE 1. 3-dimensional reconstruction of computed tomogram of the aorta. The tip of the yellow arrow indicates the angulated celiac artery approximately 2 cm from its origin at the aorta.
Surg Laparosc Endosc Percutan Tech
Volume 24, Number 2, April 2014
Surg Laparosc Endosc Percutan Tech
Volume 24, Number 2, April 2014
She ingested multiple antacids and various proton pump inhibitors without resolution of the pain. She continued to pass flatus daily and she denied radiation of her pain or changes in her bowel movements. Ultimately, she was evaluated in the emergency department. At that time, she weighed 79.6 kg with a body mass index of 29.6. On examination, her abdomen was flat with well-healed incisions. She was soft without guarding, abnormal masses, or hernia defects. Her blood work did not show any evidence of pancreatitis, biliary disease, or occult bleeding. A contrast CT scan (Fig. 1) was then obtained and showed narrowing of the celiac artery approximately 2 cm beyond its origin from the aorta. There was no evidence of an internal hernia. A Doppler study of her celiac artery showed velocities of 516 cm/s at rest, 194 cm/s at deep inspiration, and 352 cm/s with deep expiration. There was no evidence of an arterial stricture. She was diagnosed with CAC and was scheduled for a laparoscopic MAL release. The laparoscopic MAL release was completed utilizing a standard 5-port foregut approach. A pneumoperitoneum was established utilizing a Veress needle in the left upper quadrant. A Visiport trocar (Covidien Inc., Norwalk, CT) was then inserted 18 cm from the xiphoid followed by four 5-mm ports. The lateral segment of the liver was retracted anteriorly and several adhesions were lysed to expose the medial border of the gastric pouch and Roux limb. The lesser omentum had been divided previously and the caudate lobe was visualized along with the inferior vena cava. The peritoneum was divided overlying the common hepatic, left gastric, and splenic arteries utilizing the hook cautery. The 3 vessels were traced proximally to their respective origins at the celiac artery. The hook cautery was utilized to incise the peritoneum overlying the MAL, right crus, and suspensory ligament to the fourth portion of the duodenum. All of these fibers were divided with the hook cautery. Once these structures were divided, the aorta was dissected and exposed for approximately 5 cm cephalad to the origin of the celiac artery. The dissection was extended laterally to identify the lateral borders of the aorta. The neural structures along the lateral borders of the aorta were divided with cautery. The left gastric, common hepatic, and splenic arteries were then reexamined and carefully exposed for approximately 4 cm from the trifurcation of the celiac artery. Any muscular, neural, or ligamentous bands were divided along the anterior course of the celiac artery and its trifurcation. After dividing the overlying structures of the aorta and skeletonizing the celiac artery and its trifurcation, hemostasis was verified and all ports were removed. Postoperatively, the patient was started on a liquid diet and progressed quickly to a regular diet. She was discharged on postoperative day 1. At 10 months postoperatively, she is completely asymptomatic. Her postoperative ultrasound studies at 6 months showed a celiac artery velocity of 469 cm/s at rest, 206 cm/s with deep inspiration, and 378 cm/s with deep expiration.
DISCUSSION Lipshutz3 in 1917 first described compression of the celiac artery from the crus of the diaphragm, MAL, or thickened fibrous para-aortic ganglionic tissue. In 1963, Harjola1 performed the initial MAL release. In 1965, Dunbar et al2 replicated Harjola’s success in a large series of patients. However, in 1972, Szilagyi et al4 questioned the veracity of CAC syndrome. Through 157 lateral aortograms, Szilagyi and colleagues demonstrated that 49.7% of patients had some degree of incidental celiac stenosis without evidence of corresponding symptoms. More recently, Agnes et al5 showed that at the time of orthotopic liver transplant, approximately 3% to 10% of patients have asymptomatic CAC. Clearly, the diagnosis of CAC remains controversial. CAC syndrome includes symptoms that mimic those found in superior mesenteric artery (SMA) syndrome that arise when the third portion of the duodenum is compressed between the SMA and the aorta. Normally, a fairly r
2014 Lippincott Williams & Wilkins
Median Arcuate Ligament Syndrome After RYGB
prominent fat pad exists between these 2 anatomic structures. Typically, rapid weight loss or nutritional compromise leads to a loss of the aortomesenteric fat pad that preserves the near 45-degree angle that the SMA usually follows as it emerges from the aorta. As the SMA angle decreases, patients typically present with postprandial pain or intestinal angina. From a purely vascular standpoint, there are isolated cases of SMA stenosis reported throughout the literature despite the presence of significant visceral collaterals from the celiac and inferior mesenteric artery. From a pathophysiological standpoint, SMA syndrome and SMA stenosis make inherent sense, especially as the SMA provides almost the entire arterial blood supply of the small bowel and proximal colon. Attributing symptoms to CAC is less intuitive because of the significant collaterals that exist to perfuse the vital foregut organs in the event of celiac stenosis, compression, or even occlusion. These collaterals include the network of vessels from the SMA and an extensive array of vessels that communicate with the gastric and splenic vasculature. The mere presence of these collaterals continues to fuel the argument against the existence of CAC syndrome. However, it seems plausible to postulate that if isolated SMA stenosis is truly a clinical diagnosis, then isolated celiac artery stenosis may be clinically possible. Unfortunately, a detailed understanding of the pathophysiology remains elusive surrounding the ebb and flow of the celiac artery and its adjacent neurovascular bundles. As detailed later, our own bias leans toward a neurologic deficiency secondary to compression of the sympathetic fibers versus a vascular entity. We feel that, impingement of the celiac artery and changes in vascular velocities with deep expiration represent a marker for neurological compression. Regardless, the patient detailed in this study presented with a prodrome similar to SMA compression or stenosis. However, her radiologic findings were consistent with CAC syndrome. Hypothetically, the rapid and significant weight loss incurred from the RYGB resulted in a drastic reduction of the aortomesenteric fat pad surrounding the celiac artery. Once the fat pad was essentially eradicated, the MAL and its associated muscular fibers compressed the celiac artery and the corresponding plexus. This resulted in abdominal pain exacerbated by ingesting food. Ultimately, the laparoscopic MAL release resolved this patient’s symptoms by relieving the compression on the celiac plexus. In 1985, Reilly et al6 studied CAC syndrome prospectively in 51 patients after celiac artery decompression with or without subsequent revascularization. At a mean of 9 years postoperatively, 81% of patients benefited from some type of surgical intervention. Although these data may confirm the existence of CAC syndrome, Reilly also demonstrated that there was no correlation between the degree of celiac stenosis and symptom relief. Their results showed that operative technique correlated with outcome. If the celiac artery was decompressed with accompanying revascularization, 76% (22/29) of patients improved. If decompression was performed without revascularization, only 53% (8/15) of the patients improved. Over the past 30 years, radiologic techniques and physiological testing have improved the ability to both define and treat this disease. For example, Faries et al7 utilized gastric exercise tonometry (GET) to assess the patients with suspected CAC. Their data demonstrated that intraluminal gastric CO2 was highly associated with symptoms secondary to CAC. Furthermore, this group www.surgical-laparoscopy.com |
e67
Richards et al
Surg Laparosc Endosc Percutan Tech
from the Netherlands8 showed that if gastric ischemia was confirmed preoperatively, improvements in GET postoperatively correlated with 100% long-term symptom relief. If the postoperative GET did not improve, surgical intervention was successful in only 25% of the patients. Interestingly, gross evidence of ischemic changes on endoscopy is usually absent despite any findings on GET that may reflect vascular involvement. Therefore, some of the associated benefit from a MAL release in terms of pain, nausea, and vomiting may be mitigated through the disruption of the sympathetic fibers of the celiac plexus. An interesting article from McCallum et al9 in 1997 describes a patient diagnosed with idiopathic gastroparesis and tachygastria. This patient underwent a gastric electrical stimulator and, subsequently, the patient was diagnosed with CAC. The patient then underwent a MAL release and, postoperatively, the gastroparesis resolved with normal gastric cycles of 3 to 3.5 cpm. Furthermore, the patient’s pain was completely resolved. The authors theorized that division of the sympathetic nerve fibers resolved the patient’s pain and restored the normal myoelectrical conduction of the stomach. McCallum and colleagues did not support a vascular etiology as several endoscopies failed to document mucosal changes consistent with ischemia. Given these data, it is important to understand how CAC presents clinically to truly understand the syndrome. Patients may present with postprandial abdominal pain, weight loss, diarrhea, and nausea with or without vomiting. Leaning forward or changing positions of the abdomen may occasionally mitigate the symptoms. Young athletes may present with exercise-induced abdominal pain. Occasionally, patients may even present with renovascular hypertension that arises from a poststenotic dilatation that affects the renal arteries.10 In addition to renovascular anatomic aberrancies, Calkins et al11 showed that pancreaticoduodenal artery aneurysms may result from CAC and lead to further symptoms. Diagnostically, CAC is usually confirmed with at least 1, if not 2, radiologic studies. These tests include mesenteric duplex of the celiac artery, SMA, and inferior mesenteric artery and perhaps the renal arteries, if there is a possibility of renovascular hypertension. This dynamic modality allows real time assessment of flow and identification of anatomic variations. CT with angiography and/or magnetic resonance arteriography are helpful but are limited by their static nature. When performed with both inspiration and expiration, biplane contrast aortography may yield a diagnosis of CAC, but this study is more invasive and is used less frequently. As mentioned previously, GET is a recently used adjunct that may demonstrate the physiological outcome of CAC in terms of gastric mucosal ischemia in patients with MAL syndrome.7,8,10 The patient detailed in this study underwent a CT scan of the abdomen that suggested stenosis at the origin of the celiac artery. Subsequently, she underwent a duplex ultrasound that confirmed the diagnosis as her celiac artery velocity was exceedingly high on expiration. Overall, our preference is to obtain at least 1 dynamic study (ultrasound or aortogram) and 1 study (magnetic resonance imaging or CT) that details the surrounding anatomy for any patient with suspected CAC. Interestingly, the patient’s follow-up ultrasound documented a decrease in the celiac artery velocity at rest and, essentially, unchanged velocities at deep inspiration and deep expiration. Again, we feel that the velocities are not indicative of a vascular etiology. Instead, these
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Volume 24, Number 2, April 2014
velocities are indicative of the neural compression that was ultimately treated. Treatment of CAC syndrome has been performed traditionally by open techniques but several case reports and small series document successful outcomes after a laparoscopic release of the MAL. Regardless of the technique, each approach requires division of the MAL at the diaphragmatic crus just proximal to the celiac trunk. Our technique entails division of the entire diameter of tissue overlying the aorta to ensure that any obstructing fibers are divided fully. These structures include the crural mechanism, the MAL, and the suspensory ligament extending to the fourth portion of the duodenum. We also believe that the aorta should be cleared for approximately 5 cm proximal to the celiac artery origin as the patient is supine for the procedure. This length should accommodate for an erect position with full expiration. In addition, any neurovascular structures overlying the celiac artery are divided. This operative technique was certainly successful in this patient as she remains asymptomatic at 10 months. Once the MAL has been decompressed, significant debate exists over the need to revascularize the celiac artery. Reilly et al6 argued for the necessity of revascularization. Dordoni et al12 and Roayaie et al13 have both shown that laparoscopic release of the MAL with laparoscopic ultrasound and endovascular stenting of the celiac artery provide similar results. Our present technique entails an isolated decompression of the MAL as a first step for CAC. If symptoms persist, an endovascular treatment may be considered to restore the luminal diameter of the celiac artery. In conclusion, this paper presents a rare case of a morbidly obese patient who developed CAC syndrome after undergoing a successful laparoscopic RYGB. On the basis of this patient’s clinical outcome, CAC should be considered in the differential diagnosis of abdominal pain after significant weight loss after a bariatric procedure. A duplex ultrasound of the mesenteric vessels should be included in the diagnostic work-up to exclude this specific diagnosis. As demonstrated in this report, dramatic changes may be obtained in patient care with a successful laparoscopic MAL release. Finally, this patient requires a longterm follow-up with annual assessments to ensure that her pain remains resolved. A repeat duplex scan is scheduled in another 6 months to assess the celiac artery. Regardless of its anatomic structure and velocities, the patient’s symptoms will dictate the need for any further intervention. REFERENCES 1. Harjola PT. A rare obstruction of the coeliac artery; report of a case. Ann Chir Gynecolo Fenn. 1963;52:547–550. 2. Dunbar DJ, Molnar W, Berman FF, et al. Compression of the celiac trunk and abdominal angina. Am J Roentgenol Radium Ther Nucl Med. 1965;95:731–744. 3. Lipshutz B. A composite study of the celiac axis artery. Ann Surg. 1917;65:159–169. 4. Szilagyi DE, Rian RL, Elliott JP, et al. The celiac artery compression syndrome (does it exist?). Surgery. 1972;6:849–863. 5. Agnes S, Avolio AW, Magalini SC, et al. Celiac axis compression syndrome in liver transplantation. Transplant Proc. 2001;33:1438–1439. 6. Reilly LM, Ammar AD, Stoney RJ, et al. Late results following operative repair for celiac artery compression syndrome. J Vasc Surg. 1985;120:1072–1076. 7. Faries PL, Narula A, Veith FJ, et al. The use of gastric tonometry in the assessment of celiac artery compression syndrome. Ann Vasc Surg. 2000;14:20–23. r
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8. Mensink PBS, van Petersen AS, Kolkman JJ, et al. Gastric exercise tonometry: the key investigation in patients with suspected celiac artery compression syndrome. J Vasc Surg. 2006;44:277. 9. Balaban DH, Chen J, Lin Z, et al. Median arcuate ligament syndrome: a possible cause of idiopathic gastroparesis. Am J Gastroenterol. 1998;92:519–523. 10. Gloviczki P, Duncan AA. Treatment of celiac artery compression syndrome: does it really exist? Perspect Vasc Surg Endovasc Ther. 2007;19:259–263.
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11. Calkins CM, Moore EE, Turner J, et al. Combined modality treatment of ruptured pancreaticoduodenal artery aneurysms due to celiac artery compression. Surgery. 2004;136:1088–1089. 12. Dordoni L, Tshomba Y, Turner J, et al. Celiac artery compression syndrome: successful laparoscopic treatment—a case report. Vasc Endovascular Surg. 2002;36:317–321. 13. Roayaie S, Jossart G, Gitlitz D, et al. Laparoscopic release of celiac artery compression syndrome facilitated by laparoscopic ultrasound scanning to confirm restoration of flow. J Vasc Surg. 2000;32:814.
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