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Superior Mesenteric Artery (SMA) Syndrome

Superior Mesenteric Artery (SMA) Syndrome. SMA Syndrome. Compression of the 3th portion of the duodenum due to narrowing of the space between the SMA and aorta and is primarily attributed to loss of the intervening mesenteric fat pad. Prevalence ~0.013-0.3% Female > Male

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Superior Mesenteric Artery (SMA) Syndrome

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  1. Superior Mesenteric Artery (SMA) Syndrome

  2. SMA Syndrome Compression of the 3th portion of the duodenum due to narrowing of the space between the SMA and aorta and is primarily attributed to loss of the intervening mesenteric fat pad. Prevalence ~0.013-0.3% Female > Male Mostly 10-39 years old Other names: Aortomesenteric duodenal compression Duodenal vascular compression Wilkie’s syndrome Cast syndrome

  3. Controversy Symptoms do not always correlate well with abnormal anatomic findings on radiology studies. Symptoms may not resolve completely following treatment. The diagnosis may be confused with other anatomic or motility related causes of duodenal obstruction.

  4. History 1842: 1st described by the Austrian professor Carl von Rokitansky 1908: 1st operative treatment by Stavely (DJ) 1927: Wilkie published thelargest SMA syndrome study based on 75 cases. He concluded that DJ was the treatment of choice 1995: 1st laparoscopic treatment performed by Massoud, by dividing the ligament of Treitz 1998: 1st laparoscopic DJ performed by Gersin and Heniford

  5. Anatomy

  6. Anatomy L1 normal = 38-65º L3 Normal = 10-28mm

  7. In SMA syndrome The angle can be narrowed to as low as 6 degrees. The aortomesenteric distances as low as 2 mm. The left renal vein may also be compressed – nutcracker syndrome.

  8. Predisposing factors 1. Rapid weight loss 2. Following surgery 3. Rarely anatomical variants -High ligament of Treitz -Low origin of the SMA 4. Compression from an AAA or SMA aneurysm

  9. Predisposing factor:Rapid weight loss Reduction of the mesenteric fat around the SMA Causes: AIDS, malabsorption, cancer, cerebral palsy, and other conditions associated with cachexia Catabolic conditions e.g. burns Eating disorders e.g. anorexia nervosa and drug abuse Aorta

  10. Predisposing factor:Following surgery Spine surgery Scoliosis correction, due to a relative lengthening of the spine post-op (prevalence 0.5-2.4%) Surgery associated with rapid weight loss Bariatric surgery, esophagectomy, abdominal trauma

  11. Predisposing factors:Anatomical variants Anatomic variants high ligament of Treitz low origin of the SMA

  12. Symptoms Nausea Voluminous vomiting (bilious or partially digested food. Intermittent or post-prandialepigastric pain relieved by a prone or knee-chest (open up the aortomesenteric angle) Esophageal reflux Anorexia Weight loss

  13. Physical Asthenichabitus 80% Succussion splash Peptic ulcer disease 25-45% Hyperchlorhydria 50%

  14. DD Other causes of bowel obstruction Diseases associated with duodenal dysmotility (DM, scleroderma, vascular diseases) Chronic mesenteric ischemiasmokers, risk factors for atherosclerosis with weight loss and food intolerance. Not have obstructive syndroms.

  15. Diagnosis High index of suspicion Symptoms Radiological evidence of D3 compression by SMA Aorto-mesenteric angle <25º (normal 38-65º) Aorto-mesenteric distance <8mm (normal 10-28mm) Proximal duodenal dilation with cut-off at D3

  16. Radiological investigations Plain abdominal filmsgastric distension, dilation of the proximal duodenum, abrupt vertical cutoff of air in the 3D. Contrast X-ray studies Barium studies CT abdomen (with oral contrast) CT angiogram

  17. Treatment Conservative management In the absence of displacement by an abdominal mass, an aneurysm or another pathologic condition that requires immediate surgical exploration Surgical management If conservative management fails

  18. Conservative Treatment NG tube decompression Replacement of fluids and electrolytes Nutritional support with nasojejunal feeds when possible or TPN in selected patients Positioning the patient in a knee-to-chest position or prone after eating to improve symptoms

  19. Surgical Treatment Strong`s procedure Gastrojejunostomy Duodenojejunostomy with or without division of the 4th portion of the duodenum.

  20. Surgical Treatment Strong’s procedure Mobilize the DJ flexure and divide the ligament of Treitz Move D3 away from the narrow aorto-mesenteric angle

  21. An end-to-side gastrojejunostomy can be fashioned to bypass an obstructed segment of duodenum using sutures or staples.

  22. Duodenojejunostomy is accomplished without (A) or with (B) division of the 4th portion of the duodenum.

  23. Outcomes of surgery One of the largest report of long term outcomes – 16 patients, 7 years. Weight loss had been corrected in all patients. Vomiting was significantly decreased. Significant weight gain was not seen and other symptoms were essentially unchanged.

  24. Strong`s procedure • No bowel anastomosis • Maintains bowel integrity • Earlier post-op recovery • Failure occurs in up to one fourth of patients.

  25. Gastrojejunostomy Decompresses the stomach Failure to relieve the duodenal obstuction may result in recurrent symptoms requiring a second procedure. Blind loop syndrome Peptic ulceration

  26. Duodenojejunostomy Having superior results to both Strong`s procedure and gastroenterostomy. DJ with division of the 4th part of D:- bowel continuity-minimizes the issues associated with a blind loop.

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