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CASE REPORT Table of Contents   
Year : 2005  |  Volume : 39  |  Issue : 1  |  Page : 59-61
Superior mesentric artery syndrome after correction of scoliosis - A case report


Department of Paediatric Orthopaedics, Institute Calot, Berck sur mer cedex, France

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How to cite this article:
Reddy R R, Morin C, Jadav R L, Faustin K K. Superior mesentric artery syndrome after correction of scoliosis - A case report. Indian J Orthop 2005;39:59-61

How to cite this URL:
Reddy R R, Morin C, Jadav R L, Faustin K K. Superior mesentric artery syndrome after correction of scoliosis - A case report. Indian J Orthop [serial online] 2005 [cited 2019 Nov 22];39:59-61. Available from: http://www.ijoonline.com/text.asp?2005/39/1/59/36901

   Introduction Top


Superior mesenteric artery (SMA) syndrome is an unusual but well recognised clinical entity characterized by compression of the third or transverse portion of the duodenum against the aorta or vertebral body by the SMA resulting in acute, intermittent or chronic duodenal obstruction. This syndrome is also known as mesentric root syndrome, cast syndrome, Wilkie's syndrome, chronic duodenal ileus and intermittent arterio-mesentric occlusion. When the syndrome has occurred after spinal surgery, the cause has been attributed either to spinal distraction or to increased lordosis [1],[2].

We are reporting two cases that had SMA syndrome following spinal surgery for kypho-scoliosis. One patient was successfully treated by conservative means with total parental nutrition while the other required an emergency release of tension on the spinal instrumentation.


   Case Reports Top


Case 1:

A 14 year 8 month old girl admitted with severe progressive kypho-scoliosis, underwent a three stage spinal correction. Earlier to admission she was diagnosed to be associated with syringomyelia, for which the neurosurgeons opined with conservative management. Incidentally in the past she had developed chronic pain abdomen 6 months prior to admission which was evaluated and diagnosed to have chronic constipation. She was successfully treated with laxatives. Apart from the absence of superficial abdominal reflexes on the left side she had no other neurological involvement.

The first stage involved application of a Halo traction with progressive spinal distraction. Second stage was performed 3 weeks after the initial halo traction with thoracotomy and anterior release with interbody bony fusion between D7 - D12. One week later, posterior fusion with CD - Horizon instrumentation between D 3 -L 4 was performed. All the surgical procedures were unevenful. The post-operative X-rays shows Cobb's angle correction of 38° (101°), dorsal kyphosis correction of 38° (60°), and the lumber lordosis was decreased to 47° (56°) [Figure - 1],[Figure - 2]. She gained a total length of 11 cms in vertebral height (4 cms between the first and second stage, 7 cms with instrumentation). The weight loss during the course of treatment (halo traction to spinal instrumentation) was 6 kgs.

The first 8 days of post-instrumentation period was uneventful. She complained of pain abdomen on the 9th post­operative day, nausea and vomiting on the 10 th day. The initial diagnosis was morphine induced gastritis. She was started on infusion therapy with intermittent gastric aspiration through a nasogastric tube. Barium meal abdominal X-rays suggested of SMA syndrome with external construction in the 3rd part of duodenum with gastric and proximal duodenal dilation [Figure - 3]a,b. The diagnosis was confirmed by endoscopy, performed on the 13th post-operative day. Nasogastric tube was passed successfully into the jejunum under endoscopic control on the 16th post-operative day, following which nasogastric feeding (parental) was started along with infusion therapy. In the meantime gait training was started with an aid of a physiotherapist. By the 20 th post­operative day she was walking independently. Nasogastric tube was removed and oral feeds were started on the 26 th day when gastric aspiration was less than 350 ml. Since then she is asymptomatic of SMA syndrome.

Case 2:

A 19 year 6 months old male patient underwent a one stage posterior spinal instrumentation with bony fusion for severe kypho-scoliosis secondary to Scheurmann's disease. Pre-operative treatment included cast and spinal brace treatment. Dorsal kyphosis measured 75° while scoliosis measured 36°. No neurological complications were noted pre­operatively. CD spinal instrumentation was used between D2 to L2 . Surgical procedure was uneventful. Post-operative correction measured a decrease in the kyphosis by 30°. Severe pain in abdomen with distention and hyperthermia was noted on the first post-operative day. On arteriography, barium meal studies and endoscopic examination, patient was diagnosed to have superior mesentric artery syndrome. Emergency secondary procedure for the release of tension on the spinal instrumentation was performed on the third post-operative day. Patient recovered well after the second procedure. Total vertebral length gained by the surgery was 5 cms. Repeat spinal instrumentation was performed 2 months later with unevenful post-operative period.


   Discussion Top


The superior mesenteric artery syndrome is a recognized cause of upper gastrointestinal obstruction. Rokitansky described it for the first time in 1842. Since then numerous reports highlighting the causes and management of SMA syndrome has been described [1],[2],[3],[4],[5],[6],[7],[8],[9] . Various anatomical factors have been implicated in the pathogenesis of the condition. These include loss of fatty tissue around the SMA as it crosses the duodenum and hyperacute aortomesenteric angle with upward displacement of the duodenum by an abnormally high ligament of Treitz [2],[4],[7],[9] . The third part (transverse portion) of the duodenum crosses the midline anterior to the spine and aorta but posterior to the SMA [Figure - 4]. The normal aortomesentric angle averages about 45° (Range 38° to 65°) with the SMA-aorta distance of 10 to 28 mm where the third part of the duodenum crosses the aorta [6],[7] .

Under normal circumstances, retroperitoneal fat and lymphatic tissues serve as a cushion and protects the duodenum from compression by the SMA [5] . Any condition that narrows the aorta-mesentric angle can produce entrapment of the duodenum as it passes under the SMA. Asthenic body build, rapid weight loss with special emphasis on the loss of fatty tissues around the SMA, prolonged bed rest in supine position and the systemic effects of trauma have all or in combination been associated with SMA syndrome [2],[7],[9] . Mechanical factors that have been specifically associated with this syndrome include diminished compliance of the abdominal wall, lumbar hyperextension, primary lumbar hyperlordosis and traction on or distraction of the spine [1],[7],[8] . The age of the paediatric patient ranges from 12 to 18 years corresponding to the adolescent growth spurt in which the bones and consequently the height are enlarged at a faster rate than the viscera, causing a temporary decrease in the SMA angle [3] .

The diagnosis is suspected when symptoms of upper gastrointestinal obstruction including post prandal discomfort, nausea, vomiting, abdominal pain and distension are observed. Symptoms can be acute or chronic with intermittent exacerbations [1],[4],[9] . The symptoms are often relieved when the patient is in the left lateral decubitus, prone or knee-chest position [6],[7] . The differential diagnosis of the SMA syndrome includes anorexia nervosa and bulimia. SMA syndrome should also be differentiated from other causes of megaduodenum, such as diabetes mellitus, collagen vascular conditions and chronic idiopathic intestinal pseudo­obstruction. Delay in the diagnosis of SMA syndrome can result in malnutrition, electrolyte imbalance, dehydration and death [7] .

In our first patient considering the past history of pain abdomen, it is likely that spinal correction may have aggravated the situation. There was no significant electrolyte imbalance seen during the total treatment period, all suggesting that, when diagnosed early and treated appropriately, favourable results can be expected. In contrast, our second patient had more severe symptoms with toxemia, demanding an immediate release of the spinal instrumentation tension. This patient was lucky enough to recover well thereafter. Gastrojejunostomy is another alternative surgical procedure when conservative methods fail [2] .

To conclude from our experience, early recognision of the SMA syndrome directly reflects on the end results and to start the parenteral nutrition at the earliest in conjunction with fluids and electrolyte therapy for better prognosis. If this fails, consideration of a secondary procedure on the spine to decrease the implant tension can be another alternative.

 
   References Top

1.Evarts CM, Winter RB, Hall JE. Vascular Compression of the Duode­num associated with the treatment of scoliosis; Review of the literature and report of eighteen cases. J Bone Joint Surg (Am). 1971; 53 (3): 431­444.  Back to cited text no. 1    
2.Munns SW, Morrissy RT, Golladay SE, McKenzie CN. Hyperalimentation for superior mesenteric-artery (cast) syndrome fol­lowing Correction of spinal deformity. J Bone Joint Surg (Am). 1984; 66(8):1175-1177.  Back to cited text no. 2    
3.Hutchinson DT, Bassett GS. Superior mesenteric artery syndrome in pediatric orthopedic patients. Clin Orthop. 1990; 250 : 250-257.  Back to cited text no. 3    
4.Gustafsson L, Falk A, Lukest PJ, Gamklou R. Diagnosis and treat­ment of superior mesentric artery syndrome. Br J Surg. 1984; 71: 499­501.  Back to cited text no. 4    
5.Laffont I, Bensmail D, Rech C, Prigent G, Loubert G, Dizien O. Late superior mesentric artery syndrome in paraplegia: a case report and review. J Spinal Cord. 2002; 40: 88-91.  Back to cited text no. 5    
6.Loeb T, Loubert G, Morsly R, Gabillet JM, Pasteyer J. Syndrome de l'artere mesenterique superieure. Ann Fr Anesth Reanim. 1999; 18: 1000-1004.  Back to cited text no. 6    
7.Shetty AK, Sommerfield ES, Haymon M, Udall JN. Radiological case of the month. Arch Pediatr Adolesc Med. 1999; 153: 303-304.  Back to cited text no. 7    
8.Warner TFCS, Shorter RG, McIlrath DC, Dupree ELJr. The cast syndrome; an unusually severe case. J Bone Joint Surg (Am). 1974; 56(6):1263-1266.  Back to cited text no. 8    
9.Veysi VT, Humphrey G, Stringer MD. Superior mesentric artery syn­drome presenting with acute massive gastric dilatation. J Paediatr Surg. 1997; 32: 1801-1803.  Back to cited text no. 9    

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Correspondence Address:
R R Reddy
#15, 29th main, Old Madiwala road, BTM 1st phase, Bangalore 560068, India

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Source of Support: None, Conflict of Interest: None


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    Figures

  [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4]



 

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