Open Journal of Pediatrics, 2011, 1, 94-97 OJPed
doi:10.4236/ojped.2011.14022 Published Online December 2011 (
Published Online December 2011 in SciRes.
Superior mesenteric artery syndrome and acute pancreatitis in
a boy with eating disorder: a case report
Toru Wa tanabe 1, Motoi Fujita2, Yutaka Hirayama3, Yasushi Iinuma3
1Departments of Pediatrics, Niigata City General Hospital, Niigata, Japan;
2Department of Pediatrics, Niigata National Hospital, National Hospital Organization, Kashiwazaki, Japan;
3Pediatric Surgery, Niigata City General Hospital, Niigata, Japan.
Received 2 October 2011; revised 12 November 2011; accepted 20 November 2011.
Eating disorders are an important cause of physical
and psychosocial disturbances. Gastrointestinal com-
plications in eating disorders are common and in-
clude pancreatitis and superior mesenteric artery
syndrome (SMAS). However, only two patients who
simultaneously suffered from both SMAS and pan-
creatitis in the setting of an eating disorder have ever
been reported in the literature. We describe here a
patient with eating disorder not otherwise specified
(ED-NOS) who exhibited both SMAS and pancreati-
tis concomitantly. An 11-year-old boy with ED-NOS
had presented with the sudden onset of recurrent
bilious vomiting, abdominal distension and abdomi-
nal pain. Laboratory and imaging studies revealed
that the patient had SMAS and acute pancreatitis.
Gastric decompression and intravenous infusion of
fluids promptly improved his abdominal symptoms
and laboratory data. This is the first case report of a
patient with ED-NOS who simultaneously suffered
from SMAS and pancreatitis in the pediatric litera-
ture. Since SMAS and pancreatitis can both cause
patients to be severely ill, these diseases should be
considered in patients with eating disorders who ex-
hibit abdominal symptoms such as vomiting or ab-
dominal pa in.
Keywords: Eating Disorder Not Otherwise Specified;
Superior Mesenteric Artery Syndrome; Pancreatitis;
Gastrointestinal Complicatio ns
Eating disorders are an important cause of physical and
psychosocial disturbances, which primarily affect ado-
lescent females and can have life-threatening medical
consequences [1]. They are categorized into three disor-
ders including anorexia nervosa, bulimia nervosa and
eating disorder not otherwise specified (ED-NOS) in the
Diagnostic and Statistical Manual of Mental Disorders,
fourth edition (DSM-IV) [2]. ED-NOS includes patients
with clearly aberrant eating patterns and weight man-
agement habits who do not meet the criteria for anorexia
nervosa or bulimia nervosa [2].
The physical abnormalities in eating disorders are
secondary to the patients’ disturbed eating habits and
their compromised nutritional state, which may induce
endocrine, cardiovascular, hematological and gastroin-
testinal system dysfunctions as well as other metabolic
abnormalities [2].
Gastrointestinal complications in eating disorders are
common and include parotid enlargement with hypera-
mylasemia, dysphagia, gastric dilatation due to delayed
gastric emptying, constipation, pancreatic abnormalities
[1] and superior mesenteric artery syndrome (SMAS) [3].
However, only two patients who simultaneously suffered
from both SMAS and pancreatitis have ever been re-
ported in eating disorders [4,5]. We describe here a pa-
tient with ED-NOS who exhibited both SMAS and pan-
creatitis concomitantly, the first case report of a patient
with these diseases in the pediatric literature.
An 11-year-old boy was admitted to our hospital with a
one-day history of recurrent bilious vomiting, abdominal
distension and abdominal pain. The patient had been
diagnosed with ED-NOS 1 month before because of
3-month history of excessive exercising and restricted
intake without severe body image disturbance that led to
a 6 kg weight loss; in addition, the patient denied the
serious nature of his illness. He had a past medical his-
tory notable for Kawasaki syndrome complicated by
coronary artery aneurysms at 3 years of age, which was
treated with high-dose gamma globulin therapy and a
duodenal ulcer at 8 years of age. His older sister has also
suffered from anorexia nervosa and selective mutism
T. Watanabe et al. / Open Journal of Pediatrics 1 (2011) 94-97 95
since 10 years of age.
Physical examination on admission revealed extreme
emaciation with a weight of 27 kg (37% below normal
for age/height), height of 150 cm, body mass index
(BMI) of 12 kg/m 2, bradycardia (pulse rate was 40/bpm),
abdominal distention with hypoactive bowel sounds and
diffuse abdominal tenderness to p alpation without guard-
ing or rebound.
Laboratory studies disclosed metabolic alkalosis with
respiratory compensation (pH 7.455, HCO3 36.3 mmHg,
and PCO2 52.8 mmHg) , hypernatremia (Na 15 0 mEq/l),
elevated blood urea nitrogen (51.4 mg/dl) and serum
creatinine (1.10 mg/dl) levels, and hyperamylasenemia
(484 IU/l) with a predominant increase of pancreatic
isozymes. Serum lipase (608 U/l [normal 13 - 49 U/l]),
trypsin (900 ng/ml [normal 110 - 460 ng/ml]) and elas-
tase-1 (1400 ng/ml [no rmal 100 - 400 ng/dl]) levels wer e
also increased. Liver function tests, white blood cell
counts, blood glucose levels and concentrations of C-
reactive protein were within the normal ranges.
Because an abdominal X-ray demonstrated an extre-
mely dilated stomach, the patient underwent nasogastric
tube decompression with drainage of 500 ml of bilious
fluid, which improved his abdominal signs and symp-
toms promptly. A post-contrast abdominal computed
tomography after nasogastric tube insertion revealed loss
of intra-abdominal ad ipose tissue, reductio n of the aorto-
mesenteric distance (4 mm [normal 10 - 28 mm]) and the
aorto-mesenteric angle (13 [normal 38 - 65]) [6] without
any abnormal findings of the other organs including
pancreas (Figure 1). An upper gastrointestinal tract con-
trast-medium study demonstrated an abrupt vertical cut
off of the t hird portion of the du o den um (Figure 2).
The patient was diagnosed as having ED-NOS com-
plicated by SMAS and pancreatitis, and he underwent
Figure 1. Axial post-contrast computed tomography of the
abdomen demonstrating duodenal obstruction between the
superior mesenteric artery and the aorta (arrow).
Figure 2. Upper gastrointestinal tract contrast-medium study
showing an abrupt cut off the third portion of duodenum (ar-
intravenous fluid infusions and enteral feedings by naso-
jejunal tube. His serum levels of amylase and lipase de-
creased into the normal range one week following the
initiation of treatment, although his weight and nutri-
tional status did not improved. The other abnormal
laboratory tests also normalized within two weeks.
Because the patient had exhibited psychiatric symp-
toms including irritability and profound anxiety, he was
transferred to the eating disorders unit. He underwent
psychiatric care in addition to the nutritional therapy,
which improved his condition gradually. The patient
became well with body weight of 37 Kg (14% below
normal for age/height) two months after being trans-
ferred to the unit and was discharged.
SMAS and pancreatitis are well-known gastrointestinal
complications of eating disorders [1]. However, only two
patients who concurrently suffered from both SMAS and
pancreatitis similarly to our patient have been repo rted in
eating disord ers.
Keane et al. presented a 16-year-old girl with anorexia
nervosa who developed acute gastric dilation and duo-
denal ileus due to SMAS and acute pancreatitis follow-
ing rapid refeeding [4]. Gwee et al. recently described a
17-year-old girl with anorexia nervosa who exhibited
acute abdominal symptoms following rapid refeeding,
and was diagnosed with SMAS and acute pancreatitis [5].
opyright © 2011 SciRes. OJPed
T. Watanabe et al. / Open Journal of Pediatrics 1 (2011) 94-97
Unlike these two cases, our patient with ED-NOS de-
veloped SMAS and pancreatitis simultaneously without
rapid refeeding.
SMAS involves the entrap ment and obstru ction of the
third part of the duodenum between the SMA and aorta
due to the narrowing of the angle between both vessels
[6]. The cause of this narrowing is related to loss of in-
tra-abdominal adipose tissue, which may result from
eating disorders [6]. Symptoms of SMAS can be acute or
chronic, with intermittent exacerbation [6]. Our patient
developed acute-onset SMAS. Although SMAS has
commonly been reported to present as a chronic condi-
tion in adulthood, one pediatric study reported that
SMAS was more likely to present acutely, with sudden
onset of symptoms related to bowel obstruction [7]. It
may be difficult to distinguish whether gastrointestinal
symptoms of patients with eating disorders result from
the eating disorders themselves or from chronic SMAS
associated with the eating disorders [3]. SMAS can pre-
cipitate and exacerbate anorexia nervosa because of
nausea associated with a small bowel obstruction and
conversely, anorexia nervosa prevents the patient from
being willing or able to ingest adequ ate calories to allow
the SMAS to resolve [8]. Moreover, some fatal cases of
SMAS in eating disorders have been reported due to
duodenal obstruction or gastric perforation [9]. There-
fore patients with eating disorders should undergo im-
aging studies to rule out SMAS, if they exhibit abdomi-
nal symptoms such as vomiting or abdominal pain.
Pancreatitis is a potentially life-threatening illness
with significant morbidity and mortality, and can occur
in eating disorders [5]. Although the exact mechanism
underling the development of pancreatitis in eating dis-
orders remains unclear, two mechanisms have been sug-
gested: pancreatic injury caused by chronic protein en-
ergy malnutrition and pancreatic regurgitation from in-
creased duodenal pressure resulting from SMAS [4,5].
Protein energy malnutrition causes acinar cell atrophy,
epithelial metaplasia and cystic d ilatation of the ducts in
the pancreas [10]. It is also associated with a depleted
antioxidant status and subsequent susceptibility to oxi-
dative stress and damage, and with an increase in in-
flammatory mediators such as TNF-alpha, IL-1 and IL-6,
which have been proposed to play a role in pancreatitis
[10]. Meanwhile SMAS can cause duodenal ileus and
dilatation, which leads to high pancreatic duct pressure
or reflux of duodenal contents into the pancreatic duct
[5]. This process leads to pancreatic cell damage th rough
autolysis thus causing the patients to develop pancrea-
titis [5]. Because abdominal symptoms and elevated
serum amylase levels of our patient improved rapidly
following only gastric decompression, an increased
duodenal pressure resulting from SMAS was the most
likely cause of the pancreatitis in our patient.
Our patient had a past medical history of Kawasaki
syndrome complicated with coronary aneurysm and a
family history of anorexia nervosa. Long-term disease
condition of Kawasaki syndrome affected on the psy-
chological condition of the patient with a family history
of ED and might develop ED-NOS in this patient.
In summary, we reported a patient with ED-NOS who
simultaneously suffered from SMAS and pancreatitis.
Since SMAS and pancreatitis can cause patients to be-
come severely ill, these diseases should be con sidered in
patients with eating disorders who exhibit abdominal
symptoms such as vomiting or abdominal pain.
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