|Year : 2012 | Volume
| Issue : 2 | Page : 105-107
Superior mesenteric artery syndrome misdiagnosed as acute gastric dilatation
Akhlak Hussain, Kuldip Singh, Mohinder Singh, Malwinder Singh
Department of Surgery, Rajindra Hospital, Patiala, Punjab, India
|Date of Web Publication||3-Apr-2013|
Department of Surgery, Rajindra Hospital, Patiala, Punjab
Source of Support: None, Conflict of Interest: None
Acute gastric dilatation is commonly due to abdominal surgery, anorexia and bulimia nervosa, psychogenic polyphagia, trauma, diabetes mellitus, pneumonia, staphylococci. It is very rarely associated with typhoid or superior mesenteric artery syndrome and much rarely associated with both. A young thin female had been operated for signs of sub-acute intestinal obstruction and found to have very hugely dilated stomach reaching up to the pelvis along with dilated 1st and 2nd part of duodenum. But lumen was patent and no sign of obstruction was found. Later, she found to be typhoid positive. But she did not improved. CT scan revealed signs of superior mesenteric artery syndrome. Division of ligament of trietz with duodenojejunostomy done, after which she improved. It is be concluded that superior mesenteric artery compression may present as acute gastric dilatation. Typhoid may be associated with superior mesenteric artery syndrome.
Keywords: Abdominal pain, salmonella, surgical complication
|How to cite this article:|
Hussain A, Singh K, Singh M, Singh M. Superior mesenteric artery syndrome misdiagnosed as acute gastric dilatation. Arch Int Surg 2012;2:105-7
| Introduction|| |
Vascular compression of the 3rd part of duodenum between superior mesenteric artery (SMA) and aorta, so-called superior mesenteric artery syndrome (SMAS), is a rare cause of duodenal obstruction. It usually presents with nausea, vomiting, postprandial epigastric region pain, and weight loss. Occasionally, it presents with sub-acute intestinal obstruction. Very rarely, it presents as acute dilatation of stomach. Both acute gastric dilatation and SMAS are common in young thin individual and both can be associated with abnormal psychogenic eating habitat.
In our case, we misdiagnosed it as acute gastric dilatation without considering SMAS and managed accordingly. But after treatment failure and further investigation, diagnosis of SMAS was made and the patient responded well on treatment accordingly.
The purpose of this case report is to highlight the possibility of acute gastric dilatation resulting from SMAS presenting as sub-acute intestinal obstruction.
| Case Report|| |
A 15-year-old female presented to the emergency department with a 3-day history complains of sudden onset of severe colicky pain in upper abdomen, which progressed to the whole abdomen, associated with distension of whole abdomen, bilious vomiting, and obstipation. There was history of fever 10 day ago. Vital signs were stable. Examination revealed distended, tense and tender whole abdomen with involuntary muscle rigidity, and absent bowel sounds. Abdominal roentgenogram revealed only gastric fluid level of height about 2.5 cm and few radiolucencies in the right iliac region. Rest of view was radioopaque. Ultrasound showed distended gut loops with sluggish to and fro motion of echogenic material inside loops. Rest of the ultrasound was normal. The patient was resuscitated with i.v. fluids and gastric decompression. She had exploratory laparotomy and found huge dilatation of the stomach with 1st and 2nd parts of the duodenum. We suspected the possibility of acute gastric dilatation due to unknown reason because rest of the intestine and other structures were normal with normal patency of the intestine. Decompression was done through the nasogastric tube. But post-operatively, the stomach aspirates remained 500-600 ml. The Widal test for the typhoid indicated S. typhi infection (TO = 1:160 and TH = 1:160). We planned for contrast enhanced computed tomography (CECT) abdomen which revealed findings suggestive of SMAS with gross dilatation of the stomach and the duodenum up to proximal portion of its 3 rd part. Distal third of the duodenum appeared to be compressed between aorta and SMA. The aortomesenteric distance at the level of third part of the duodenum was about 4.0 mm (normal = 10-20 mm). The aortomesenteric angle was about 5° (normal = 38-65°). Thus, relaparotomy was done and division of the ligament of Treitz with duodenojejunostomy was done. Post-operatively, the patient showed marked improvement. During the follow up of 2 months, the patient did well except fever which was treated as typhoid fever.
| Discussion|| |
The aortomesenteric angle contains the left renal vein, uncinate process of the pancreas, 3 rd part of the duodenum, and the retroperitoneal fat pad. Narrowed aortomesenteric angle (6-40°) may cause vascular compression of the duodenum, which is suspended by the ligament of Treitz. SMAS is the result of compression of the third part of the duodenum between the SMA anteriorly and the aorta and vertebral column posteriorly.  In this condition, distance from the origin of the superior mesenteric artery to the mid-point of the duodenum, the aortomesenteric distance, reduced to an average of 3.3 mm. It is a secondary event, which is the result of weight loss, correction of scoliosis, obesity, enforced bed rest in the supine position, and the presence of a body cast. Some anatomical causes have also been proposed like congenitally short mesentery, aberrant SMAS, excessive mobility of right colon, malrotation, and a short suspensory ligament. It may be caused by neoplasm in the area of the mid-portion of the pancreas as the SMA arises and passes over the duodenum. Patients are typically young females with asthenic body habitus. The predominant clinical features are nausea, vomiting, and postprandial abdominal pain centered at the epigastrium.  Rarely, in acute cases, presentation is that of sub-acute intestinal obstruction. The symptoms may be relieved in lying prone, in the left lateral decubitus, or in the knee-chest position, and may aggravate when the patient is lying in the supine position.
Diagnosis of SMAS combines an appropriate degree of clinical suspicion with radiographic confirmation. Plain abdominal radiograph may delineate a dilated stomach and proximal duodenum with abrupt vertical or oblique cut off and the absence of air distally. Among upper gastrointestinal tract series, hypotonic contrast is more specific and sensitive than barium. They reveal gastroduodenal dilatation and the characteristic linear defect (abrupt sharp cut off) indicative of extrinsic compression on the third part of the duodenum. Inability of contrast to traverse the point of duodenal obstruction is a reliable diagnostic finding. Fluoroscopy obtained during the swallow study will frequently demonstrate a "to and fro" appearance to the peristaltic waves in the proximal duodenum. A subsequent passage of contrast beyond the obstruction and simultaneous relief of attendant symptoms following positional changes during fluoroscopy is also highly suggestive of the correct diagnosis. Combining aortic and selective SMA with contrast imaging of the intestine has been used as a further confirmatory modality.  Recently, the use of contrast-enhanced spiral computed tomography can confirm the diagnosis by evaluating the aortomesenteric angle. It can also assess the amount of retroperitoneal and mesenteric fat. 
Treatment of SMA syndrome is either nonoperative or surgical management. Conservative treatment involves reversing or removing the precipitating factor. Interventions like removal of body casts and intermittent ambulation have been advocated. A patient tolerant of oral intake should have a modified diet of small meals administered more frequently. If adequate nutrition cannot be obtained by oral means, enteral nutrition via nasojejunal tube advanced endoscopically and radiographically past the point of duodenal obstruction is recommended.  For the minority of patient, total parenteral nutrition may be required A nasogastric tube should be inserted for gastroduodenal decompression. Fluid and electrolyte abnormalities should be monitored and corrected aggressively. The prone or left lateral decubitus position is useful in symptom relief in the acute state. Surgical options include duodenojejunostomy, gastrojejunostomy, and Strong's operation, which consists of division of the ligament of Treitz and derotation of the small bowel and right colon.  The most frequently used procedure is duodenojejunostomy. The patient who underwent a duodenojejunostomy concurrently with division of ligament of Treitz had a near universal 99% rate of success. 
Severe complications of SMA syndrome include acute gastric dilatation, gastric pneumatosis, gastric rupture, and cardiovascular collapse. ,, Our patient presented with massive gastric dilatation which is a life-threatening condition that may be complicated by gastric necrosis, gangrene, perforation, rupture, shock, and death. ,, But we misdiagnosed and did laparotomy with gastroduodenal decompression. When patient failed to improve, we did CT scan which finally revealed the actual cause, i.e., SMAS. The patient improved after duodenojejunostomy with division of ligament of treitz. The titer of typhoid fever when done post-operatively remained the same. Whether this finding is related to SMAS or not is unknown.
| Conclusion|| |
It is inferred that possibility of acute gastric dilation should be kept in mind in every case of sub acute intestinal obstruction and superior mesenteric artery syndrome can be the cause of acute gastric dilatation. Correlation between typhoid and SMAS is unclear. Although it is a single case, we advised that SMAS should be kept in the differential diagnosis of upper gastrointestinal obstruction.
| References|| |
|1.||Unal B, Aktaþ A, Kemal G, Bilgili Y, Güliter S, Daphan C, et al . Superior mesenteric artery syndrome: CT and ultrasonography findings. DiagnIntervRadiol 2005;11:90-5. |
|2.||Ashley SW and Menard MT. Vascular Compression of the Duodenum. Fischer's Mastery of Sugery. Vol. 1. 6 th ed. India: Wolters Kluver; 2012. p. 1089-96. |
|3.||Lippel F, Hanning C, Weiss W, Allescher HD, Classen M, Kurjak M. Superior mesenteric artery syndrome: Diagnosisand treatment from the gastro enterologist's view. J Gastroenterol 2002;37:640-3. |
|4.||Lim JE, Duke GL, Eachempati SR. Superior mesentericcartery syndrome presenting with acute massive gastric dilatation, gastric wall pneumatosis, and portal venous gas. Surgery 2003;134:840-3. |
|5.||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 1997;21:103-14. |
|6.||Sakamoto Y, Mashiko K, Matsumoto H, Hara Y, Kutsukata N, Yamamoto Y. Gastric pneumatosis and portal venous gas in superior mesenteric artery syndrome. Indian J Gastroenterol 2006;25:265-6. |
|7.||Abdu RA, Garritano D, Culver O. Acute gastric necrosis in anorexia nervosa and bulimia. Two case reports. Arch Surg 1987;122:830-2. |
|8.||Patocskai EJ, Thomas JM. Gastric necrosis in a patient with bulimia. Eur J Surg 2002;168:302-4. |
|9.||Saul SH, Dekker A, Watson CG. Acute gastric dilatation with infarction and perforation. Report of fatal outcome in patient with anorexia nervosa. Gut 1981;22:978-83. |