871

Superior Mesenteric Artery Syndrome in Traumatic Brain Injury: Two Cases

Michael J. Pedoto, MD, Michael W. O'Dell, MD, Mark Thrun, MD, David Hollifield, MD

ABSTRACT. Pedoto M J, O'Dell MW, Thrun M, Hollifield D. Superior mesenteric artery syndrome in traumatic brain injury: two cases. Arch Phys Med Rehabil 1995;76:871-5. • One of the many causes of enteral feeding (EF) intolerance after traumatic brain injury (TBI) is superior mesenteric artery syndrome (SMAS). Although it is reported in pediatric brain injury, few cases are noted in adults. To increase awareness of this medically treatable condition, we present two patients who developed SMAS after sustaining severe brain injury. SMAS results from compression of the duodenum by the SMA against the aorta and risk factors include acute weight loss, prolonged recumbency, and spasticity--all frequently encoun- tered in severe TBI. After gastric decompression, symptoms often resolve with weight gain achieved by conserva- tive treatment; including feeding in the left lateral or prone position, hyperalimentation, or extension of a feeding tube beyond the obstruction. SMAS should be considered in the presence of EF intolerance in severe adult TBI because multiple risk factors may be present. © 1995 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation

Superior mesenteric artery syndrome (SMAS) is a rare cause of proximal intestinal obstruction resulting from com- pression of the duodenum by the SMA against the aorta] Risk factors include acute weight loss, prolonged recum- bency, and spas t i c i t y - - a l l frequently encountered in severe traumatic brain injury (TBI). 1.2

Although SMAS is reported in up to 1.5% of children after TBI, there are few adult cases noted in the literature. 2"3 To increase awareness of this medical ly treatable cause of feeding intolerance in TBI, we present two patients from our inpatient unit who developed SMAS after brain injury.

C A S E REPORTS

C a s e 1

A previously healthy 19-year-old woman weighing 50kg and measuring 173cm in height was an unrestrained driver involved in a motor vehicle accident November 1992. She was unconscious, hypotensive, and decorticate at the scene, with fixed and dilated pupils and an initial Glasgow Coma Score of 4. Magnetic resonance imaging of the brain showed shear injury and basal ganglia hemor- rhage. Increased intracranial pressure was managed with cerebro- spinal fluid drainage, mannitol, and hyperventilation. Tracheos- tomy and gastric tube (GT) were placed on the day of injury, and open reduction and internal fixation of multiple facial fractures was performed.

Persistent difficulty tolerating GT feedings was noted in the acute care setting with high gastric residuals despite flow rates as

From the Department of Physical Medicine and Rehabilitation, University of Cin- cinnati College of Medicine, Brain Injury Rehabilitation Program, The Drake Center, Inc., Cincinnati, OH.

Submitted for publication November 29, 1994. Accepted in revised form March 29, 1995.

Presented in part at the American Academy of Physical Medicine and Rehabilitation 56th Annual Assembly, Anaheim, CA, October 1994.

No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the authors or upon any organization with which the authors are associated.

Reprint requests to Micheal J. Pedoto, MD, Department of Physical Medicine and Rehabilitation, 5161 Medical Sciences Building, 231 Bethesda Avenue, Cincinnati, OH 45267-0524.

© 1995 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation

0003-9993/95/7609-332553.00/0

low as 20cc per hour. On postinjury day 8, a jejunal tube (JT) was placed through the GT and placement was confirmed with hypaque sodium (50g/120mL). a JT feedings were advanced and tolerated at a rate of 90cc per hour; howeverl gastric residuals remained ele- vated up to 700cc per day. On postinjury day 18, the JT dislodged and a trial of GT feeding resumed.

One month after injury, the patient was admitted to the rehabili- tation unit. Physical examination was remarkable for a thin woman who weighed 43kg and had decorticate posturing, severe lower- extremity spasticity, and functioned at Ranchos level II. Persistent difficulties tolerating GT feedings with high gastric residuals, bil- ious emesis, and weight loss recurred. Hyperactive bowel sounds were intermittently noted, particularly in the fight upper quadrant. Abdominal radiograph on day 31 showed gastric and duodenal distension up to the third portion of the duodenum. Two days later, an upper gastrointestinal series (UGIS) showed obstruction to contrast flow past the third portion of the duodenum relieved in the left lateral position, consistent with SMAS (fig 1).

A JT was replaced through the GT past the point of obstruction and the existing GT was used for gastric aspiration as needed. Over the next 5 weeks, the patient tolerated jejunal feeding with an increase in weight from 4t to 44kg and a concurrent decrease in gastric residuals. After 8 weeks, although essentially unchanged in neurological status, she was able to resume feeding via GT without recurrence of symptoms.

Case 2

A 23-year-old 67kg man involved in a motor vehicle accident sustained a severe TBI with bifrontal contusions and diffuse axonal injury. He was transferred to rehabilitation at Ranchos level II for sensory stimulation 39 days postinjury. Persistent decorticate posturing made positioning difficult, and he remained in a recum- bent or side lying posture. By day 67 postinjury, he had a slowly progressive weight loss of 9kg from baseline. On day 72 postinjury, he experienced a large emesis and aspiration, which required trans- fer to acute care hospital for respiratory distress.

He returned to rehabilitation 2 weeks later, and by day 120 postinjury, his weight was decreased to 50kg despite tolerating tube feedings at 90mL per hour with low residual volumes. On day 121 postinjury, he had another large bilious emesis and required intermittent gastric suction and intravenous fluids. Bowel sounds remained normal. An UGIS obtained to rule out obstruction was consistent with SMAS (fig 2). A gastrojejunostomy tube was placed

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Fig 1 re(A) Film from UGIS of case 1 showing marked proximal duodenal dilatation with abrupt vertical termination of contrast in the third portion of the duodenum. (B) Early resolution of obstruction to contrast flow with patient in the left lateral position.

endoscopically the following day. Tube feeding was tolerated at 110cc per hour without further emesis. Increase in weight as well as decrease in posturing and diaphoresis were subsequently noted.

DISCUSSION

SMAS is known by a variety of pseudonyms including vascular compression of the duodenum, arteriomesenteric duodenal obstruction, chronic duodenal ileus, cast syndrome, and Wilkie's syndrome. 2'4 This condition was first described by Rokitansky in 1842, with Wilkie reporting the first com- prehensive series in 1927. Subsequent studies refute the syn- drome or consider it an overdiagnosed entity. However, modern radiographic techniques would appear to confirm its existence. 2

SMAS is a rare cause of duodenal obstruction proximal to the ligament of Treitz. It is caused by compression at the third part of the duodenum by the SMA against the aorta. 4 Over 400 cases are reported among all age groups, but 75% range from 10 to 39 years of age, with a higher incidence in women, s'6

Precipitating factors include prolonged supine position, visceroptosis, exaggerated lumbar lordosis, abnormally high fixation of the duodenal fixture of the ligament of Treitz, and marked acute weight loss resulting in loss of mesenteric and retroperitoneal fat. ~'2 Notably, 80% of patients with SMAS are underweight. 4

Two distinct presentations are recognized. An acute form presents in previously healthy patients who suffer weight loss through severe illness or dieting. A chronic form that typically occurs in tall slender women is also recognized. 5

The associated conditions that predispose to SMAS have been divided into five categories2"3:

1. severe wasting diseases such as cancer and burns;

2. severe injuries such as head trauma and spinal cord injury;

3. disease, deformity, or trauma to the spine, including application of a body cast or spinal instrumentation;

4. disorders resulting in malnutrition such as anorexia nervosa or malabsorption;

5. the postoperative state. The mechanism of the obstruction that occurs at the third

part of the duodenum is not entirely clear and is likely multi- factorial. 5'7 Symptoms of this syndrome have a proposed anatomic basis. 4 The third, or transverse, portion of the duo- denum is retroperitoneal, crossing the aorta at approximately the level of the L3 vertebra. It is relatively immobile because of its fixation at the duodenojejunal flexure by the ligament of Treitz. The SMA arises from the aorta at the level of the L1 vertebra and runs in the root of the mesentery ventrally and caudally over the third portion of the duodenum. This places the transverse segment of the duodenum between the vertically oriented SMA and the aorta s (fig 3).

Retroperitoneal fat and lymphatic tissue elevate the mes- enteric root away from the aorta so that the normal angle between the SMA and the aorta is 38 to 65 ° in an erect posture.~'3'8 The normal distance between the two vessels at the level of L3 averages 10 to 20mm. 9

Any condition that decreases this angle between the SMA and the aorta may result in compression of the duodenum, described as the "nutcracker" effect s (fig 3). The aortomes- enteric angle is most acute in the supine position. Sudden weight loss may decrease the protective layer of periduode- nal mesenteric adipose. Hyperextension of the spine, as a result of spinal orthosis, hip flexor muscle tightness, spas- ticity, or posturing causes increased lumbar lordosis, which pushes the duodenum anteriorly into the SMA. A flaccid

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SUPERIOR MESENTERIC ARTERY SYNDROME IN TBI, Pedoto 873

Fig 2 - - ( A ) UGIS of case 2 with obstruction to contrast flow at the third portion of the duodenum. (B) Resolution of obstruction with patient in the left lateral position.

abdominal wall with visceroptosis exerts downward traction on the mesenteric pedicle and artery. 8 A congenitally short suspensory attachment serves to wedge the duodenum within the angle of the mesentery, increasing the chance of obstruc- tion. 7 Rapid growth in height as observed in adolescents may decrease the SMA angle and predispose to SMAS.~° Others have noted that variation of the level of origin of the SMA and the level at which the duodenum crosses the vertebrae are related to the incidence of SMAS. ~ A lower duodenal position, as it crosses the spine, may not be advantageous as the spine curves forward at L4 so that the distance between the limbs of the vascular angle is not increased above that at L3. j2 Greater lumbar lordosis in women as compared with men may explain the female predominance. 5 These factors can reduce the aortomesenteric angle to 6 to 16 °8 and de- crease the distance between the two vessels to an average of 2.5mm, predisposing to obstruction. 9

The classic symptoms of SMAS are postprandial epigas- tric pain, nausea, fullness, vomiting, and weight loss with partial or complete relief when the patient assumes knee- elbow or left lateral position, thereby allowing the SMA to fall away from the duodenum.~ In the low level TBI patient it presents, as in this case, with intolerance to gastric feeding. Abdominal distension may occur with associated hyperac- tive bowel sounds. 2

Other conditions may be found in association with SMAS.

Peptic ulcer disease is most common, occurring in 25% to 45% of patients. Duodenal ulcer and pancreatitis also are noted.4,9,13. J4

Routine laboratory tests are not helpful. 9 Flat-plate ab- dominal x-rays may show nonspecific gas patterns or a "double-bubble" gas pattern caused by marked stasis and dilatation within the stomach and duodenum. 5'6

Upper gastrointestinal contrast x-ray study is the standard for making the diagnosis. Hines and associates ~ used the following roentgenographic criteria for making the diagno- sis: dilation of the first and second portions of duodenum, abrupt vertical and oblique compression of mucosal folds, antiperistaltic flow of barium proximal to the obstruction, delay in transit of 4 to 6 hours through the gastroduodenal region, and relief of obstruction when the patient is placed in the knee-elbow or left lateral position. Because the condi- tion may be intermittent, a negative study does not rule out its presence. 4 In addition, it is helpful to obtain the barium study during an active episode.

Other diagnostic tests that may be useful if the diagnosis remains in question include angiography, hypotonic duode- nography, and computed tomography (CT). 2'6'15 Angiogra- phy can measure the aortomesenteric angle and distance be- tween the SMA and aorta, which are decreased in patients with SMAS. 2'9'16-18 Hypotonic duodenography shows the site of obstruction, proximal duodenal dilatation, and antiperi-

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874 SUPERIOR MESENTERIC ARTERY SYNDROME IN TBI, Pedoto

\

t

ta

SMA Duodenum

Fig 3--Diagram showing the anatomic relationship between the duodenum, aorta, and the superior mesenteric artery in SMAS. The lateral view demonstrates "nutcracker effect" with compression of the duodenum between the vascular struc-

tures. (Reprinted with permission) ° )

staltic waves within the dilated portion. 15 CT demonstrates proximal duodenal distension and close proximity of the SMA and aorta. 6

Other conditions may mimic SMAS. Chronic idiopathic intestinal pseudo-obstruction, especially if localized to the duodenum (megaduodenum), is difficult to distinguish from SMAS. It presents with recurrent attacks of obstruction that are highly variable in frequency, severity, and duration. Bar- ium studies will not show a mechanical obstruction; how- ever, there will be a prolonged transit time of barium to the colon. 9

Other causes of compression of the distal duodenum in- clude intrinsic, pancreatic, or retroperitoneal tumor; adhe- sions; and adjacent inflammatory conditions, including scle- roderma and systemic lupus erythematosis] 9-21 Reduced duodenal peristalsis may result from diabetes, pancreatitis, myxedema, amyloidosis, and myotonic dystrophy. 2~

The complications of SMAS may be severe; delay in diag- nosis may result in dehydration, malnutrition, metabolic im- balance, aspiration, or death) Treatment by conservative measures should be initiated, followed by surgical measures if conservative treatment fails.

There are several conservative therapeutic approaches, in- cluding frequent small feedings with optimal positioning

(prone, knee-chest, or left lateral position), gastric decom- pression, feeding through a tube passed distal to the obstruc- tion, and correction of fluid and electrolyte imbalance. Total parenteral nutrition, by producing a rapid increase in weight, has been an effective adjunct if weight loss is considered a precipitating factor. In theory, weight increase results in a deposition of adipose tissue within the mesentery and around the SMA, relieving the duodenal compression] 'j6

Care should be taken to identify and correct any precipitat- ing factors. Prolonged supine position should be avoided, and measures to avoid spasticity and soft-tissue contractures at the hip should be instituted. Spinal hyperextension ortho- ses should be removed. Use of abdominal binders to support the abdominal wall may be tried. Metoclopramide, or prefer- ably, cisapride may be helpful in improving gastrointestinal transit.~'4'8 In our two cases, gastric decompression, enteral feeding beyond the obstruction, and proper positioning to avoid prolonged supine position and hip flexion contractures allowed significant weight gain and the ability to tolerate feedings without recurrence of symptoms.

If symptoms are not relieved after a prolonged period of medical therapy, or in the presence of associated diseases like peptic ulcer disease or pancreatitis, then surgical man- agement of SMAS is indicated.1'10"19 Various surgical proce- dures have been employed including duodenojejunostomy, section of the ligament of Treitz, and relocation of the duode- nojejunal junction. 1.3,4.10,18,21,22

S U M M A R Y

SMAS results from compression of the third part of the duodenum by the SMA against the aorta. Obstruction is likely caused primarily by a decrease in the aortomesenteric angle and may be related to acute weight loss, prolonged recumbency, posturing, and spasticity--all of which are common in severe TBI. Typical presentation is postprandial bilious emesis, epigastric pain, and abdominal distension. UGIS is the diagnostic standard. Conservative treatment in- cludes gastric decompression, gastric feeding in the left lat- eral or prone position, parenteral alimentation, or a feeding tube passed distal to the obstruction. Surgical correction is indicated if there is no response to conservative measures.

The cases presented demonstrate that SMAS in adult TBI patients, although rare, does occur and may be related to acute weight loss, prolonged recumbency, and spasticity. A high index of suspicion is necessary in the presence of feed- ing intolerance, particularly if concurrent weight loss and prolonged recumbency are present. Increased awareness of this condition and timely management will decrease morbid- ity and complications that may interfere with the recovery process after brain injury.

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