Superior Mesenteric Artery Syndrome

1. Overview
2. Anatomy — The Aortomesenteric Angle
3. Predisposing Causes and Risk Factors
4. Clinical Presentation
5. Diagnosis — Upper GI Series and CT
6. Differential Diagnosis
7. Treatment — Nutritional Rehabilitation First
8. Surgical Options
9. Cast Syndrome — SMA Syndrome After Spinal Surgery
10. Prognosis and Recovery
11. Research Papers
12. Connections
13. Featured Videos

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Overview

Superior mesenteric artery (SMA) syndrome — also called Wilkie's syndrome, cast syndrome, or duodenal ileus — is a rare but real cause of upper gastrointestinal obstruction in which the third (horizontal) portion of the duodenum is compressed between two great vessels: the superior mesenteric artery (SMA) anteriorly and the aorta posteriorly. The duodenum normally passes safely between these two structures because a cushion of fat and lymph tissue maintains an adequate angle and distance between them. When that fat pad disappears — from extreme weight loss, prolonged immobility, or other causes — the vascular angle closes and the duodenum is caught in a vascular vice.

The result is a mechanical obstruction that causes postprandial pain, bilious vomiting, early satiety, and weight loss. The vicious cycle is self-perpetuating: obstruction causes nausea and poor oral intake, which worsens weight loss, which further reduces the fat pad, which tightens the obstruction. Breaking this cycle is the core of treatment.

SMA syndrome was first described systematically by the Australian surgeon D. J. Wilkie in 1927, who reported 75 cases and proposed the vascular compression mechanism. It remains controversial among some clinicians because the symptoms are non-specific and imaging findings can be subtle, leading to both underdiagnosis (in patients with genuine disease) and overdiagnosis (in patients whose narrow aortomesenteric angle is an incidental finding without functional obstruction). Contemporary imaging with CT angiography and three-dimensional vascular reconstruction has improved diagnostic precision.

SMA syndrome predominantly affects young, thin individuals — particularly adolescent girls and young women with eating disorders, patients who have recently undergone major surgery or trauma, and people with extreme rapid weight loss from any cause. Its recognition matters because the treatment — nutritional rehabilitation — is dramatically effective when applied early, but diagnostic delays lead to severe malnutrition and avoidable surgery.

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Anatomy — The Aortomesenteric Angle

Understanding SMA syndrome requires a precise mental map of the anatomical relationships in the upper abdomen. The duodenum is a C-shaped structure that wraps around the head of the pancreas. Its four portions are:

1. First portion (D1, bulb) — exits the pylorus, runs horizontally to the right of the spine.
2. Second portion (D2, descending) — runs vertically downward, receives the common bile duct and pancreatic duct at the ampulla of Vater.
3. Third portion (D3, horizontal) — crosses the spine at the level of L3, passing anterior to the aorta and inferior vena cava and directly posterior to the superior mesenteric artery as it descends from its aortic origin.
4. Fourth portion (D4, ascending) — ascends to the left, curving upward to the ligament of Treitz (the duodenojejunal flexure), where the small bowel begins.

The third portion of the duodenum (D3) is the site of compression in SMA syndrome. It is fixed in this retroperitoneal location and cannot move out of the way when the aortomesenteric space narrows.

Normal aortomesenteric relationships:

• Aortomesenteric angle (AMA): The angle between the aorta and the SMA at their point of origin from the aorta, measured on lateral CT or vascular reconstruction. Normal range: 25–60°.
• Aortomesenteric distance (AMD): The distance between the aorta and SMA at the point of maximum compression of D3, measured on axial CT. Normal range: 10–34 mm.

In SMA syndrome:

• AMA narrows to <25° (most series use <22–25° as the diagnostic threshold).
• AMD narrows to <10 mm (the "danger zone" for duodenal compression).

The fat and lymph tissue that normally occupies this space — the retroperitoneal fat pad — is what keeps the angle open. When body fat is depleted, this cushion disappears, the SMA descends toward the aorta, and the duodenum is caught between them. The angle is like a scissors blade: when it closes, it cuts off duodenal flow.

The ligament of Treitz also plays a role. This suspensory ligament anchors the duodenojejunal junction to the right crus of the diaphragm, holding the fourth duodenal portion in a fixed position. Surgical release of this ligament (Strong's procedure) can shift the duodenum out of the compression zone, though this approach is rarely used today.

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Predisposing Causes and Risk Factors

The common denominator in SMA syndrome is loss of the retroperitoneal fat pad that normally separates the SMA from the aorta. Any condition that causes rapid or severe depletion of this fat pad can precipitate SMA syndrome. The causes are diverse:

Extreme weight loss and cachexia (most common):

• Anorexia nervosa and restrictive eating disorders — one of the most frequent associations; SMA syndrome may actually worsen the eating disorder by causing severe postprandial pain and vomiting, reinforcing food avoidance. The relationship is bidirectional and clinically treacherous.
• Malignancy — cancer-associated cachexia rapidly depletes retroperitoneal fat; SMA syndrome can be a complication of chemotherapy-related anorexia.
• Burns — massive catabolic fat depletion post-burn injury.
• Postoperative malnutrition — particularly after abdominal surgery that impairs oral intake for an extended period.
• HIV/AIDS wasting, severe inflammatory disease, or prolonged critical illness.
• Psychiatric illness with severe food restriction (depression, psychotic illness).

Postural and anatomical factors:

• Prolonged bed rest or supine positioning — gravity causes posterior displacement of viscera, reducing the aortomesenteric angle. SMA syndrome is well-recognized in immobilized patients (ICU, burns, spinal cord injury).
• Scoliosis — spinal curvature rotates the aorta relative to the SMA, narrowing the angle. SMA syndrome is a recognized (though rare) complication of untreated severe scoliosis and is also precipitated by scoliosis surgery.
• Hyperlordosis — excessive lumbar curvature (sometimes in athletes or dancers) can increase lumbar extension and narrow the aortomesenteric space.

Cast syndrome (spinal casting and bracing):

• Body casts or hyperextension spinal braces applied after scoliosis surgery force the lumbar spine into hyperextension, mechanically accentuating the aortomesenteric angle narrowing. This "cast syndrome" has been recognized since the era of plaster body casts for scoliosis correction. It is a specific subset of SMA syndrome with a clear mechanical cause and is discussed further below.

Anatomical variants: A minority of SMA syndrome cases occur in individuals with a constitutionally narrow aortomesenteric angle — the SMA originates at a more acute angle from the aorta than usual — who are therefore more vulnerable to symptomatic compression with modest weight loss or postural changes.

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Clinical Presentation

The clinical picture of SMA syndrome is dominated by intermittent or chronic upper gastrointestinal obstruction. Symptoms are often postprandial (worsened by eating) and are characteristically relieved by positional changes — a distinctive feature that should raise immediate suspicion.

Cardinal symptoms:

• Postprandial abdominal pain — epigastric or periumbilical, cramping or pressure-like, beginning 30–90 minutes after meals. Patients quickly learn to eat smaller amounts to minimize pain, which perpetuates malnutrition.
• Nausea and vomiting — characteristically bilious (yellow-green) because the obstruction is distal to the ampulla of Vater, so bile-stained duodenal contents back up into the stomach and are vomited. Bilious vomiting in any context should prompt consideration of duodenal obstruction.
• Early satiety and bloating — the obstructed stomach and proximal duodenum distend with a small meal; patients feel full after just a few bites.
• Weight loss — from inadequate intake due to pain and early satiety; this worsens the underlying cause of SMA syndrome (fat pad depletion), creating a vicious cycle.
• Abdominal distension — particularly epigastric; gastric distension may be visible or palpable on examination.

The pathognomonic positional relief:

Perhaps the most distinctive feature of SMA syndrome is that symptoms are dramatically relieved by specific body positions:

• Left lateral decubitus position (lying on the left side) — shifts the SMA to the left, away from the duodenum, and reduces compression. Patients instinctively discover this maneuver.
• Prone position (lying face-down) — allows the SMA to fall anteriorly away from the aorta and duodenum.
• Knee-chest position (kneeling with chest toward knees) — a variation that also relieves compression.

A patient who reflexively assumes the left lateral decubitus or prone position after meals — or who has discovered that pain disappears when they lie on their left side — has a classic symptom of SMA syndrome until proven otherwise.

Severe or complete obstruction: When the obstruction becomes complete or near-complete, the clinical picture escalates: projectile bilious vomiting, massive gastric dilation visible on imaging, severe dehydration, and dangerous electrolyte disturbances (metabolic alkalosis from loss of hydrochloric acid in vomit; hypokalemia; hyponatremia). This presentation can be life-threatening and requires urgent decompression (nasogastric tube) and intravenous fluid and electrolyte replacement.

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Diagnosis — Upper GI Series and CT

There is no single pathognomonic test for SMA syndrome, and the diagnosis requires both anatomical confirmation of the narrow aortomesenteric space and evidence of functional duodenal obstruction. Clinical suspicion, radiological findings, and exclusion of other causes of upper GI obstruction together establish the diagnosis.

1. Upper gastrointestinal contrast study (upper GI series) — gold standard for functional obstruction

Fluoroscopic examination with barium or water-soluble contrast (gastrografin) is the most important diagnostic test. Key findings:

• Abrupt vertical or oblique compression of D3 at the L3 level, with a straight-line "cutoff" of contrast flow at the point where the SMA crosses the duodenum.
• "To-and-fro" peristalsis — duodenal contractions try to push contrast past the obstruction, fail, and propel it back toward the stomach. This is a highly characteristic fluoroscopic sign.
• Proximal duodenal dilation — the first and second portions of the duodenum dilate markedly upstream from the compression.
• Delayed gastric emptying — gastric contents accumulate because outflow into the duodenum is impaired.
• Relief with position change — if contrast flows freely through the compression point when the patient is turned to the left lateral decubitus position during the fluoroscopic study, this is strong additional confirmation of SMA syndrome.

2. CT abdomen with intravenous contrast and 3D vascular reconstruction

CT provides anatomical confirmation and rules out other causes of obstruction. It is complementary to the upper GI series rather than a replacement. Key CT findings:

• Measurement of the aortomesenteric angle on CT angiography with multiplanar reconstruction: <25° supports the diagnosis.
• Measurement of the aortomesenteric distance on axial CT at the point of duodenal compression: <10 mm supports the diagnosis.
• Duodenal distension proximal to the compression point.
• Scant retroperitoneal fat visible between the aorta and SMA — the key predisposing anatomy.
• Exclusion of extrinsic masses, adhesions, or malignancy causing obstruction.

3. Upper endoscopy (EGD)

Endoscopy is important to exclude intraluminal causes of obstruction — peptic strictures, malignancy, ingested foreign bodies. In SMA syndrome, the endoscope passes easily to the level of the duodenal compression but then meets a pulsatile extrinsic compression with the appearance of a smooth, peristaltic narrowing. The finding helps confirm an extrinsic cause but does not replace cross-sectional imaging. Endoscopy is also essential for placing a nasojejunal (NJ) tube past the obstruction for enteral nutrition — the tube can be advanced under direct vision through the compression zone into the jejunum.

4. Plain abdominal X-ray

Plain film may show the classic "double bubble" sign — a dilated stomach and dilated proximal duodenum separated by a constriction, analogous to duodenal atresia in neonates. It is non-specific but suggests proximal duodenal obstruction and is usually the first imaging obtained in an acutely ill patient.

Diagnostic pitfalls:

• A narrow aortomesenteric angle or short AMA distance on CT is common in thin individuals and does not by itself indicate SMA syndrome. The diagnosis requires clinical symptoms + functional obstruction on contrast study, not anatomy alone.
• Conversely, a normal-appearing AMA on CT does not exclude SMA syndrome if functional obstruction is clearly documented on upper GI series and other causes are excluded.
• In anorexia nervosa, gastric motility abnormalities and gastroparesis co-exist with SMA syndrome, complicating the clinical picture.

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Differential Diagnosis

The symptoms of SMA syndrome — postprandial pain, nausea, bilious vomiting, and weight loss — overlap with a wide range of upper GI conditions. Before diagnosing SMA syndrome, the following must be considered and excluded:

• Peptic ulcer disease — epigastric pain relieved by antacids/food; diagnosed by endoscopy; H. pylori testing essential.
• Gastric outlet obstruction — from peptic stricture, pyloric stenosis, or malignancy (gastric cancer, pancreatic head cancer); CT + endoscopy distinguish; non-bilious vomiting if obstruction is pre-pyloric.
• Gastroparesis — delayed gastric emptying without mechanical obstruction; associated with diabetes, post-viral, post-surgical; nuclear medicine gastric emptying scan distinguishes; the upper GI series in gastroparesis shows retention but no cut-off at D3.
• Functional dyspepsia — symptoms overlap closely (early satiety, nausea, postprandial distress); no imaging abnormality; diagnosis of exclusion.
• Small bowel obstruction from adhesions — typically presents more acutely with diffuse abdominal pain and distension; CT shows dilated small bowel loops with transition point; history of prior surgery.
• Duodenal malignancy — rare; presents with obstructive jaundice if ampullary region involved; CT and endoscopy identify mass.
• Annular pancreas — congenital duodenal encirclement by pancreatic tissue; visible on CT as tissue completely encircling D2; typically presents in infancy but can be incidentally found in adults.
• Duodenal web or atresia — congenital; typically diagnosed in neonates; occasional adult presentation of incomplete web.
• Pancreatitis — can cause duodenal obstruction by peripancreatic inflammation or pseudocyst; elevated amylase/lipase; CT shows pancreatic changes.
• Ladd's bands — congenital peritoneal bands crossing the duodenum in malrotation; CT shows right-sided small bowel, left-sided colon.
• Eating disorders with behavioral food restriction — in anorexia nervosa, the fear of eating may be behavioral even when SMA syndrome has resolved; multidisciplinary psychiatric and nutritional evaluation is essential.

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Treatment — Nutritional Rehabilitation First

The guiding principle of SMA syndrome management is straightforward: restore the fat pad by restoring body weight and nutritional status, and the obstruction resolves on its own. For most patients, particularly those with a clear precipitating cause of weight loss, this approach is highly effective and avoids surgery entirely. The critical question is how to deliver nutrition when the GI tract is partially or fully obstructed.

Step 1: Acute stabilization

In patients presenting with severe symptoms or acute complete obstruction:

• Nasogastric tube decompression — to relieve gastric distension, reduce vomiting, and allow the obstructed stomach to decompress. This is the first step when the patient is in distress.
• Intravenous fluid and electrolyte replacement — bilious vomiting causes dehydration, metabolic alkalosis (loss of hydrochloric acid), and hypokalemia. Vigorous IV resuscitation with normal saline and potassium replacement is essential before advancing to nutritional rehabilitation.
• Positional therapy — nursing and keeping the patient in the left lateral decubitus, prone, or knee-chest position during and after meals to reduce compression. Even partial relief of obstruction while nutrition is established is valuable.

Step 2: Enteral nutrition past the obstruction — the cornerstone of treatment

The obstruction is in the third portion of the duodenum. If a feeding tube can be placed past the compression point — into the proximal jejunum — the bowel distal to the obstruction is normal and can absorb nutrition. This allows nutritional rehabilitation while bypassing the obstruction:

• Nasojejunal (NJ) tube placement — the tube is passed through the nose into the stomach and then advanced through the duodenum, past the compression, into the jejunum. Placement requires endoscopic guidance (the endoscopist advances the tube under direct vision through the compressed D3 using a wire) or fluoroscopic guidance. Once in place, continuous jejunal feeds of a polymeric or semi-elemental enteral formula provide high-calorie nutrition without requiring the obstructed duodenum to function.
• Small frequent meals + left lateral decubitus positioning — as weight is gained and the obstruction partially improves, carefully graded oral intake (small, frequent, low-fat, semi-liquid meals) can be added to NJ feeds. Patients should eat in the left lateral decubitus or prone position and remain in that position for at least 30–45 minutes after meals.
• Caloric targets — sufficient to restore weight (typically 30–40 kcal/kg/day); dietitian-guided caloric titration is essential, especially in patients with anorexia nervosa where aggressive refeeding risks refeeding syndrome (hypophosphatemia, cardiac complications).

Step 3: Parenteral nutrition (TPN) — when enteral is not feasible

If endoscopic NJ tube placement is not possible (severe obstruction preventing tube passage, patient refusal, anatomical challenges) or if enteral feeds are not tolerated, total parenteral nutrition (TPN) via a central venous catheter can sustain nutritional rehabilitation until the obstruction resolves sufficiently to allow enteral access. TPN is a bridge, not the preferred long-term strategy, because of catheter-related infection risk and hepatic complications with prolonged use.

Timeframe for response: Most patients gain meaningful relief as they gain weight. The fat pad begins to restore within 2–6 weeks of sustained positive caloric balance. Full resolution of obstruction may take 4–12 weeks. Repeat upper GI series or CT demonstrates increasing aortomesenteric distance and resolution of duodenal compression as weight is restored.

Concurrent treatment of the underlying cause: Nutritional rehabilitation must proceed hand-in-hand with treatment of the underlying condition that caused the weight loss:

• Anorexia nervosa — psychiatric and psychological treatment, often requiring inpatient or day-hospital eating disorder program.
• Malignancy — oncological treatment directed at the cancer; SMA syndrome management is supportive.
• Post-surgical malnutrition — optimization of post-operative care; early dietitian involvement in high-risk patients (bariatric surgery, major abdominal operations).
• Burns — aggressive burn nutritional protocols.

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Surgical Options

Surgery is reserved for patients who fail conservative nutritional rehabilitation after a genuine 4–6 week trial, or who present with acute complete obstruction requiring urgent intervention. It is not the first-line treatment and should not be offered until nutritional rehabilitation has been fully optimized.

Duodenojejunostomy — the procedure of choice

A side-to-side anastomosis is created between the obstructed duodenum (proximal to the compression point) and a loop of proximal jejunum, bypassing the vascular obstruction entirely. This is the most effective surgical treatment for SMA syndrome — long-term success rates of 80–90% are reported in modern series. The procedure can be performed laparoscopically by experienced surgeons, with faster recovery than open surgery.

Strong's procedure (division of the ligament of Treitz)

Division of the suspensory ligament of Treitz releases the fixed attachment of the duodenojejunal junction and allows the fourth portion of the duodenum to descend, increasing the aortomesenteric distance. This is a simpler procedure than duodenojejunostomy but has a higher recurrence rate because it relies on anatomical repositioning rather than bypass. It is less commonly performed today and is mainly considered in specific anatomical situations or as an adjunct to other approaches.

Gastrojejunostomy

A connection between the stomach and the jejunum, bypassing the entire duodenum, is occasionally used when the obstructed duodenum is severely diseased or when duodenojejunostomy is technically difficult. It carries the disadvantage of bypassing the ampulla of Vater (bile and pancreatic juice enter the bypassed duodenum, reducing digestive efficiency).

Laparoscopic approach

All three procedures can be performed laparoscopically in experienced centers. Minimally invasive surgery is associated with shorter hospital stays, faster return to diet, and reduced wound complications. The choice of procedure and approach should be individualized by a surgeon experienced with duodenal surgery.

Pre-operative nutritional optimization: Even patients who ultimately require surgery benefit from pre-operative nutritional rehabilitation (via TPN or NJ feeds) to improve surgical risk, particularly wound healing and immune function in severely malnourished patients.

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Cast Syndrome — SMA Syndrome After Spinal Surgery

Cast syndrome is a specific form of SMA syndrome occurring in the context of spinal immobilization or surgery, most classically after scoliosis correction with spinal fusion and rod placement. It is called "cast syndrome" because it was first widely recognized in the era when body casts (plaster or fiberglass jackets encasing the trunk) were routinely applied after spinal surgery to maintain correction.

Mechanism: Surgical correction of scoliosis extends and rotates the spine, changing the relationship between the abdominal aorta and the SMA. The correction may straighten a curved spine but simultaneously narrows the aortomesenteric angle by stretching the duodenum across a more anteriorly positioned SMA. The combination of spinal correction-related anatomical change and the postoperative period of bed rest, pain-related poor oral intake, and catabolism rapidly depletes the retroperitoneal fat pad, triggering SMA syndrome.

Clinical presentation in cast syndrome: Bilious vomiting typically begins 3–10 days after surgery. The patient is lying in a hospital bed after spine surgery, often immobilized, with nausea and projectile bilious vomiting despite a functioning bowel. The diagnosis is frequently delayed because vomiting is attributed to post-operative ileus, opioid side effects, or routine post-surgical dysmotility. Any patient who develops bilious vomiting after spine surgery — particularly after scoliosis correction — should be evaluated for SMA syndrome.

Treatment: Identical to non-surgical SMA syndrome — nasogastric decompression, NJ tube placement, enteral or parenteral nutritional rehabilitation. Nutritional recovery is often faster because the underlying musculoskeletal anatomy has been corrected; once weight is regained, the syndrome does not recur. The cast or brace (if present) may be modified or temporarily removed to allow positional change that relieves compression.

Prevention in high-risk patients: Orthopedic surgeons operating on thin scoliosis patients (particularly low-BMI adolescent girls) now routinely consider perioperative nutritional optimization and early post-operative NJ tube feeding to prevent cast syndrome in high-risk individuals.

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Prognosis and Recovery

The prognosis of SMA syndrome is excellent when the underlying cause is reversible and nutritional rehabilitation is promptly implemented. Most patients whose weight loss is from a treatable or self-limited cause — post-surgical malnutrition, burns, acute illness — recover fully without surgery, and the obstruction does not recur once normal weight is maintained.

Predictors of good outcomes:

• Clear reversible precipitating cause of weight loss.
• Early diagnosis and prompt initiation of NJ enteral nutrition.
• Absence of complete (versus partial) obstruction at presentation.
• Motivated patient (and family, in adolescents) committed to nutritional recovery.
• No concurrent gastroparesis or severe GI dysmotility.

Challenging scenarios:

• Anorexia nervosa — the most difficult context because the underlying illness prevents weight gain by design. SMA syndrome in anorexia nervosa requires multidisciplinary management (gastroenterology + psychiatry + dietetics) with careful coordination. NJ feeding may be the only way to initiate weight restoration in a patient who refuses oral intake. The relationship between SMA syndrome and anorexia nervosa is bidirectional: SMA syndrome causes real postprandial pain that reinforces food avoidance, making it impossible to separate behavioral food restriction from genuine pain-driven avoidance without treating both simultaneously. SMA syndrome is not a cause of anorexia nervosa but is a serious medical complication that must be addressed alongside psychiatric treatment.
• Malignancy-related cachexia — SMA syndrome in the context of cancer may be irreversible if the malignancy cannot be controlled. In these patients, management focuses on symptom palliation (decompression, NJ feeds or TPN for comfort and quality of life) rather than cure.

Long-term after surgery: Patients who undergo duodenojejunostomy have excellent long-term outcomes — the procedure is definitive and recurrence is uncommon. Late complications are rare and relate primarily to anastomotic issues (stricture, bleeding) rather than recurrent obstruction.

Prevention: In patients at risk — thin adolescents undergoing spine surgery, critically ill patients with progressive weight loss, bariatric surgery patients — proactive nutritional screening, early dietitian involvement, and prophylactic NJ feeding can prevent SMA syndrome from developing.

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Research Papers

1. Wilkie DPD. Chronic duodenal ileus. Br J Surg. 1921;9(34):204–214. Classic original description by Wilkie (1921)
2. Gustafsson L, Falk A, Lukes PJ, Gamklou R. Diagnosis and treatment of superior mesenteric artery syndrome. Br J Surg. 1984;71(7):499–501. PMID 6733402
3. Raissi B, Taylor BM, Trad KS. Recurrent superior mesenteric artery syndrome: a case report and review of the literature. Am Surg. 1996;62(2):141–146. PMID 8546549
4. Merrett ND, Wilson RB, Cosman P, Biankin AV. Superior mesenteric artery syndrome: diagnosis and treatment strategies. J Gastrointest Surg. 2009;13(2):287–292. PMID 18810589
5. Unal B, Aktaş A, Kemal G, et al. Superior mesenteric artery syndrome: CT and ultrasonography findings. Diagn Interv Radiol. 2005;11(2):90–95. PMID 15971114
6. Lee TH, Lee JS, Jo Y, et al. Superior mesenteric artery syndrome: where do we stand today? J Gastrointest Surg. 2012;16(12):2203–2211. PMID 22941408
7. Hines JR, Gore RM, Ballantyne GH. Superior mesenteric artery syndrome: diagnostic criteria and therapeutic approaches. Am J Surg. 1984;148(5):630–632. PMID 6496365
8. Biank V, Werlin S. Superior mesenteric artery syndrome in children: a 20-year experience. J Pediatr Gastroenterol Nutr. 2006;42(5):522–525. PMID 16707974
9. Tsirikos AI, Jeans LA. Vertebral column resection for spinal deformities — complications and related outcomes in 89 consecutive cases. Eur Spine J. 2012;21(Suppl 2):226–238. PMID 22286508
10. Ylinen P, Kinnunen J, Hockerstedt K. Superior mesenteric artery syndrome: a follow-up study of 16 operated patients. J Clin Gastroenterol. 1989;11(4):386–391. PMID 2754412
11. Gersin KS, Heniford BT. Laparoscopic duodenojejunostomy for treatment of superior mesenteric artery syndrome. JSLS. 1998;2(3):281–284. PMID 9876743
12. Lippl F, Hannig C, Weiss W, Classen M, Kurjak M. Superior mesenteric artery syndrome: diagnosis and treatment from the gastroenterologist's view. J Gastroenterol. 2002;37(8):640–643. PMID 12203086

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Connections

• Small Bowel Obstruction
• Mesenteric Ischemia
• Gastroparesis
• Functional Dyspepsia
• Short Bowel Syndrome
• Peptic Ulcer Disease
• Pancreatitis
• Whipple's Disease
• Cyclic Vomiting Syndrome
• Eosinophilic Gastroenteritis
• Gastroenterology Overview
• Diseases Overview

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