This is a five year old male who was struck by an 
automobile four weeks ago, sustaining a right femur 
fracture.  He was placed in a spica cast and 
hospitalized for a week without complications.  He was 
discharged in the spica cast.  Over the past 10 days, he 
began vomiting everyday (without blood or bile), usually 
one hour after meals.  Although he says he "can't keep 
anything down", his urine output has been reported as 
normal.  His mother says that he has had fevers 
ranging from 39 to 40 degrees.  He continues to have 
1-2 normal formed bowel movements per day without 
diarrhea.  He has complained of intermittent leg pain 
and headache although there are no current 
complaints.  He has not complained of any abdominal 
pain.
     His past history is significant for attention deficit 
disorder and modest developmental delays.  
Medications include methylphenidate and 
acetaminophen.
     Exam:  VS T36.5, HR 86, BP 84/54, RR 20.  He is 
alert, apprehensive at first but cooperative with time, in 
no distress.  Moist mucous membranes.  Clear pharynx, 
conjunctiva, and tympanic  membranes.  Neck supple 
without significant lymphadenopathy.  Cardiac exam 
normal.  Lungs clear to auscultation.  His abdomen is 
difficult to fully examine because of the spica cast.  His 
limited abdomen is soft and non-tender without masses.  
Skin turgor good.  No rashes.  Extremities symmetric 
with good pulses and brisk capillary refill.  No 
neurological deficits are noted.
     Labs:  Na 141, K 3.9, Cl 106, bicarb 25, BUN 6, 
creatinine 0.3, amylase 39, calcium 10, albumin 4.2.  
UA: specific gravity 1.023, trace protein otherwise dip 
negative.

     An abdominal flat-plate is ordered.

View abdominal film.


Discussion
     If you diagnosed the cast syndrome, you correctly 
identified the clinical signs consistent with this 
syndrome.  This is due to an extrinsic compression of 
the third portion of the duodenum by the superior 
mesenteric artery.  This syndrome is also referred to as 
superior mesenteric artery (SMA syndrome) or acute 
gastric dilatation.  This radiograph shows a dilated 
gas-filled stomach suggesting a partial gastric outlet 
obstruction.
     Cast syndrome is common in the second decade of 
life which may be attributable to the increased flexibility 
of the spine in young adults.  Truncal casting can 
increase lumbar lordosis.  This can change the take-off 
of the superior mesenteric vessels which crosses the 
horizontal part of the duodenum.  Patients with the cast 
syndrome may have mesenteric vessels with a more 
acute angle and a shorter distance from the take-off to 
the duodenum.
     Many cases of cast syndrome are observed in 
patients with spinal disease.  Most commonly it involves 
fractures of the pelvis or femur.  Other patients with this 
syndrome may have congenital deformities or have 
experienced rapid weight loss.  Handicapped children 
may also develop this type of functional obstruction 
perhaps related to poor fat mass, hypotonicity and 
skeletal distortion as has been reported in one child 
with cerebral palsy. 
     Clinical signs include intermittent or continuous 
nausea, vomiting and abdominal distention.  Sequelae 
include dehydration, metabolic alkalosis and shock.  
Fatalities have been reported when recognition or 
treatment has been delayed.  Symptoms may begin 
immediately after casting or up to 12 weeks thereafter.  
Compression of the duodenum by the cast is one 
mechanism postulated for the cast syndrome.  Another 
contributory factor may be weight loss and associated 
loss of fat in the mesentery.  Retroperitoneal fat may 
keep the duodenum from being compressed by the 
superior mesenteric trunk or the spine.  The diagnosis 
can be confirmed by a flat plate of the abdomen which 
may reveal dilatation of the stomach and duodenum.  
The diagnosis can be confirmed by an upper 
gastrointestinal series.

View UGI series.

     This view from the UGI series shows a narrowing in 
the third portion of the duodenum due to external 
compression.  The nasojejunal tube failed to negotiate 
the duodenum and coiled on itself.
     A duodenal hematoma may result in a similar 
obstruction.  However, this would occur during the initial 
trauma, or soon after.
     Treatment includes IV replacement therapy, 
electrolyte maintenance, a nasogastric tube to 
decompress the stomach and duodenum, along with 
replacement of the cast.

References
     Bisla RS, Louis HJ.  Acute vascular compression of 
the duodenum following cast application. Surg Gynecol 
Obstet 1975;140:563-566.
     Vaisman N, Stringer DA,  Pencharz P.  Functional 
duodenal obstruction (Superior mesenteric artery or 
cast syndrome) in cerebral palsy.  Journal of Parenteral 
and Enteral Nutrition 1989;13:326-328.