Superior Mesenteric Artery Syndrome in the Modern Trauma Patient
By Adams, John B Hawkins, Michael L; Ferdinand, Coville H; Medeiros, Regina S
In 1861, von Rokitansky described obstruction of the third part of the duodenum by external compression of the duodenum by the superior mesenteric artery (SMA). In 1926, this entity was furthermore described by Wilke in his presentation of 75 patients with "chronic duodenal compression". In 1968, Mansberger used angiography to define anatomical measurements as the diagnostic criteria for this condition. Current modalities of diagnosis of SMA syndrome include esophagogastroduodenoscopy, computerized tomography angiogram, fluoroscopy, transabdominal ultrasound, and endoscopic ultrasound. The SMA syndrome has been associated with prolonged confinement in the supine position, loss of weight, loss of abdominal wall muscle tone, application of a body cast, and severe burns. With current surgical techniques allowing early ambulation, patients are able to avoid prolonged bed rest. The use of parenteral and enteral nutritional support has limited the loss of weight associated with trauma and burn patients, making this syndrome uncommon in this patient population. Recent reports of SMA syndrome focus on the association with corrective surgical procedures for scoliosis and obesity. INTERMITTENT OBSTRUCTION OF THE third portion of the duodenum by the overlying superior mesenteric artery is a rare cause of proximal bowel obstruction. The symptoms of this condition are common to multiple upper gastrointestinal disease processes delaying its diagnosis. We present three cases of superior mesenteric artery syndrome diagnosed in the last three years at our institution to bring attention to this uncommon cause proximal small bowel obstruction. We report three recent trauma patients who developed SMA syndrome to illustrate that this uncommon cause of bowel obstruction must still be considered.Case Reports
An 18-year-old female was hypotensive with a left pneumothorax, left pubic rami fractures, and a severe closed head injury after a motor vehicle collision. She underwent splenectomy, packing of the liver laceration, left tube thoracostomy, and temporary abdominal closure. Her course was complicated by intra-abdominal sepsis, renal failure requiring dialysis, additional abdominal operations, placement of a percutaneous endoscopie gastrostomy tube, skin grafting to the abdominal wall defect, ventilator-associated pneumonia, tracheostomy, and subsequent gastrocutaneous fistula.
Enteric feeds were started on Day 4 and advanced to meet her nutritional needs by Day 7. She developed intolerance to enterai feeds with bilious gastric drainage of greater than one liter/day, and she was started on total parenteral nutrition on Day 27. To rule out an intestinal obstruction, a barium upper gastrointestinal series with small bowel follow through was obtained. It demonstrated a mass effect on the third portion of the duodenum caused by the overlying superior mesenteric artery, with dilation of the first and second portion of the duodenum, as well as reverse peristalsis in the proximal duodenum (Fig. 1). This obstruction was incomplete as barium passed into the distal duodenum and proximal jejunum. These findings were consistent with the diagnosis of superior mesenteric artery (SMA) syndrome. She was instructed to maintain an upright position in a chair for the majority of the day and to assume the left lateral decubitus position while in bed. Her nasogastric tube output decreased to less than 500 mL/day, and it was removed on Day 65. She tolerated clear liquids and a regular diet. She was discharged to a rehabilitation hospital on Day 70. She subsequently had her ventral hernia and gastrocutaneous fistula repaired and is doing well.
A 28-year-old man sustained a right pulmonary contusion, left temporal nondepressed skull fracture, a left epidural and subdural hematoma, an anoxic brain injury, a right acetabular fracture, and a liver laceration. Hepatorrhaphy and a temporary abdominal closure were required. His hospital course was complicated by respiratory failure requiring prolonged ventilator support and ventilator- associated pneumonia. Enteric feeds were provided via a nasoenteric feeding tube beginning on Day 7 with nasogastric tube output volumes of 1600 to 2700 mL/day. Total patenterai nutrition was started for nutritional support and a clear liquid diet initiated. Due to postprandial nausea and vomiting, an upper gastrointestinal series with small bowel follow-through was obtained on Day 24 and the results of the test were suggestive of SMA syndrome (Fig. 2). He was managed in the left lateral decubitos position after meals and by increasing his activity during the day with physical therapy. By Day 28, he was advanced to a regular diet and discharged on Day 29.
A thin 24-year-old male suffered a pelvic crush injury with a second lumbar vertebral body fracture, a third lumbar right pedicle fracture, bilateral kidney lacerations, a right renal artery injury, bilateral superior and inferior pubic rami fractures, and a left acetabular fracture. He underwent reimplantation of the right renal artery to the aorta, repair of a right colon perforation, and closure of a mesenteric defect. Enteric feeds were provided via a nasoenteric tube beginning on Day 3. He developed lumbar osteomyelitis requiring bed rest in the supine position for four additional weeks while receiving antibiotics. Intermittent intolerance to enteral feeding developed with nasogastric tube output of 750 to 2000 mL/day.
After a one month course, the patient complained of epigastric fullness and abdominal pain with nausea and bilious vomiting 30 minutes after meals. A barium upper gastrointestinal series was consistent with SMA syndrome. Oral nutrition and postprandial lateral decubitos position was implemented. His gastrointestinal symptoms resolved despite other issues related to his injury.
In 1861, von Rokitansky first described obstruction of the third part of the duodenum by external compression of the retroperitoneal duodenum by the superior mesenteric artery.1 The first duodenojejunostomy for SMA syndrome was performed in 1907 by Stavely.2 In 1926, this syndrome was furthermore described by Wilke in his presentation of 75 patients who suffered from "chronic duodenal compression".3 Anderson discovered radiographie evidence of SMA syndrome in 32 of 24,000 exams performed on patients with upper gastrointestinal complaints.4 The incidence of SMA syndrome in patients with gastrointestinal symptoms has been reported as 0.1 to 0.3 per cent.5
The transverse segment of the duodenum travels posterior to the SMA and anterior to the spine and aorta at approximately the level of the second lumbar vertebra. The superior mesenteric artery exits the aorta at a mean angle of 41.65 degrees.6 Conditions that decrease this angle can lead to SMA syndrome.2,5 In burns, multiple trauma, eating disorders, gastric bypass, and loss of retroperitoneal tissue that elevates the SMA can lead to SMA syndrome. Prolonged bed rest in the supine position and applications of body cast have also been described as etiologies of SMA syndrome.7-13 Spinal cord injury with loss of innervation of the abdominal wall musculature can result in visceroptosis and SMA syndrome.14 SMA syndrome has also been associated with surgical correction of scoliosis.12,15,16
In ambulatory patients, this condition is characteristically seen in young female adults with a thin body habitus.17 These patients frequently present with complaints of epigastric fullness with voluminous bilious vomiting usually occurring within one hour of a meal, eructation, and weight loss.3,7,8,17,18 These general symptoms of upper gastrointestinal distress have led to prolonged delay in diagnosis of SMA syndrome.2,4,5,18,19
Due to the nonspecific nature of presenting symptoms and lack of findings on physical exam, the diagnosis is routinely made with radiographie studies. The barium upper gastrointestinal series is the most widely used exam to evaluate for SMA syndrome. An upper gastrointestinal series is considered indicative of SMA syndrome, if it reveals dilatation of the proximal duodenum, vertical obstruction of the third portion of the duodenum, antiperistalsis, delay of passage of barium into the distal duodenum, and relief of the obstruction in the decubitus or prone position.4,7,8,10,13 Akin determined the upper gastrointestinal series to be diagnostic in 79 per cent of patients when the above criteria are fulfilled.17 However, a mild degree of compression can be observed in asymptomatic patients.2 Others have observed these diagnostic criteria in association with scleroderma, malignancy, gastroparesis, and inflammatory conditions of the retroperitoneum.20,21
The low specificity of the upper gastrointestinal series led Mansberger to perform the first in vivo study to determine the criteria for the diagnosis and the validity of the existence of this condition. Utilizing biplanar angiography, he measured a mean aortomesenteric angle of 56 (45-65) degrees and a mean aortomesenteric distance of 14 (7-20) mm in five normal patients. In comparison, the three patients affected by SMA syndrome demonstrated a mean aortomesenteric angle of 15 (12-22) degrees and a mean aortomesenteric distance of 2 (2-3) mm. By demonstrating the difference in the aortomesenteric angle and distance using angiography, he established a precedent for the diagnosis of SMA syndrome by definable anatomical criteria.18 Newer modalities have also been used to evaluate the relationship of the SMA, aorta, and duodenum. Konen used computerized tomography angiography to measure a mean aortomesenteric angle of nine degrees and a mean aortomesenteric distance of 8.1 mm in patients with SMA syndrome. The addition of three dimensional reconstructions and enhanced anatomical detail of computerized tomography angiography makes it the diagnostic modality of choice in his opinion.20 Neri used transabdominal ultrasound to measure an aortomesenteric angle of less than 25 degrees in 29 confirmed cases of SMA syndrome. Avoiding contrast, radiation, and expense are advantages of transabdominal ultrasound in the screening for SMA syndrome.5 Additionally, esophagogastroduodenoscopy and endoscopic ultrasound have been used to demonstrate compression of the duodenum by the SMA.7,8,22
Therapeutic options for SMA syndrome are conservative management or surgical bypass of the obstruction. The goal of medical therapy is to induce weight gain, which would presumably result in an increase in fat at the mesenteric root. Left lateral decubitus, knee to chest, or prone positioning decrease the mesenteric pressure on the duodenum and allows temporary alleviation of the duodenal obstruction. The patient may then be able to tolerate frequent small meals to increase caloric intake. Alternatively, enterai nutrition can be provided by a nasoenteric feeding tube positioned distal to the ligament of Treitz, or total parenteral nutrition can be provided for patients with contraindications to enterai nutrition. If successful, the restoration of retroperitoneal fat accompanying weight gain widens the aortomesenteric angle and increases the aortomesenteric angle, alleviating the symptoms of SMA syndrome in 62 to 66 per cent of patients with a brief duration of symptoms.5,9,12,15
The primary indication for surgery is failure of conservative therapy. Initially, gastrojejunostomy was considered an acceptable approach; however this technique has been abandoned secondary to the risk of bile gastritis.4,22 In 1958, Strong described lysis of the ligament of Trietz and mobilization of the duodenum to caudally displace the duodenum to a location where the SMA is a greater distance anterior to the aorta.23 However, this approach may be limited by placing the duodenum at risk for ischemia.18 The most accepted method of surgical correction is the duodenojejunostomy, which provides adequate drainage of both the duodenum and stomach. Duodenojejunostomy has a success rate of 90 per cent and can be successfully performed laparoscopically.7,9,24
Due to the increased awareness of the importance of early enterai nutritional support, widespread availability of parenteral nutrition, and early mobilization with markedly decreased length of bed rest for many injured or ill patients, the incidence of SMA syndrome has decreased in recent years. The low incidence of SMA syndrome may result in delayed recognition and, thus, delayed treatment. Most patients can be managed by relatively simple and noninvasive measures once the syndrome is recognized.
9. Schroeppel TJ, Chilcote WS, Lara MD, Kothari SN. Superior mesenteric artery syndrome after laparoscopie Roux-en-Y gastric bypass. Surgery 2005;137:383-5.
10. Hines JR, Gore RM, Ballantyne GH. Superior mesenteric artery syndrome diagnostic criteria and therapeutic approaches. Am J Surg 1984;148:630-2.
11. Kepros JP. Superior mesenteric artery syndrome after multiple trauma. J Trauma 2002;53:1028.
12. Zhu Z, Qiu Y. Superior mesenteric artery syndrome following scoliosis surgery: Its risk, indicators, and treatment strategy. World J Gastroenterol 2005;1 1:3307-3310.
13. Milner EA, Cioffi WG, McManus WF, Pruit BA Jr. Superior mesenteric artery syndrome in a burn patient. Nutr Clin Pract 1993;8:264-6.
14. Laffont I, Bensmail D, Rech C, et al. Late superior mesenteric artery syndrome in paraplegia: Case report and review. Spinal Cord 2002:40:88-91.
15. Shah M, Albright M, Vogt M, Moreland M. Superior mesenteric artery syndrome in scoliosis surgery: Weight percentile for height as an indicator of risk. J Pediatr Orthop 2003;23:665-8.
16. Crowther MA, Webb PJ, Eyre-Brook IA. Superior mesenteric artery syndrome following surgery for scoliosis. Spine 2002; 27:E528- 33.
17. Akin JT, Gray SW, Skandalakis JE. Vascular compression of the duodenum: Presentation of ten cases and review of the literature. Surgery 1976;79:5 15-22.
18. Mansberger AR, Hearn JB, Byers RM, et al. Vascular compression of the duodenum. Am J Surg 1968;1 15:89-96.
19. Gustafsson L, Faulk A, Lukes PJ, Gamklou R. Diagnosis and treatment of superior mesenteric artery syndrome. Br J Surg 1984:71:499-501.
20. Konen E, Amitai M, Apter S, et al. CT angiography of superior mesenteric artery syndrome. Am J Roentgenol 1998;171: 1279-81.
21. Cimmino CV. Arteriomesenteric occlusion of the duodenum: An entity? Radiology 1961;76:828-9.
22. Lippl F, Hannig C, Weib W, et al. Superior mesenteric artery syndrome: Diagnosis and treatment from the gastroenterologist's view. J Gastroenterol 2002;37:640-3.
23. Strong EK. Mechanics of arteriomesenteric duodenal obstruction and direct surgical attack upon etiology. Ann Surg 1958; 148:725-30.
24. Richardson WS, Surowiec WJ. Laparoscopie repair of superior mesenteric artery syndrome. Am J Surg 2001;181:377-8.