Abdominal Pain - Case 7-3: 11-Year-Old Girl
I. History of Present Illness
The patient, an 11-year-old girl, was well until 1 year before presentation,
when she was diagnosed with streptococcal pharyngitis. At that time, she had
severe abdominal pain that caused her to double over in pain. Appendicitis was
considered, and an abdominal radiograph showed an enlarged loop of bowel. The
patient was observed, but neither the clinical picture nor the laboratory
results suggested appendicitis, and no surgery was performed. Throat culture
revealed a group A
Streptococcus infection, which was treated. Since that illness, the patient had had multiple
illnesses and missed 42 days of school with episodes of headache and abdominal
pain. The pain was described as noncrampy but sharp. It consisted of
generalized lower abdominal discomfort without radiation. During this time, the
patient was diagnosed with three UTIs secondary to pyuria on urinalysis, but
all cultures were negative. Her symptoms had been particularly bad since she
was diagnosed with mononucleosis 3 months before presentation. She had had a
poor appetite and had lost 10 pounds with the mononucleosis and 8 more pounds
since then. At presentation, she had decreased intake secondary to a sore
throat and difficulty swallowing secondary to pain. She had just completed a
full course of antibiotics for pharyngitis, which was diagnosed clinically 3
weeks earlier (cultures were negative). The patient had been missing half-days
of school for 2 months and had been sleeping in the afternoons. During the week
of presentation, she had had low-grade fevers (37.4 to 37.8
°C), neck pain, diffuse abdominal pain, and frontal headache. On the day of
admission, the patient was noted to have heme-positive stool at the primary
care provider
's office after 3 days of diarrhea and loose stools. The primary care provider's workup to date had included a CT scan of the head and sinuses, which was
negative; stool for culture, which was also negative; CBC, urinalysis, ESR,
Lyme antibody testing, immunoglobulins, ANA, chest radiography, electrolytes,
liver function tests, and thyroid testing, all of which were normal.
II. Past Medical History
The patient had had reactive airways disease as a toddler, but it was no longer
active. She had had a UTI at 5 years of age, with a negative ultrasound and a
vesicoureterogram that could not be completed because of her discomfort. She
had sustained a concussion at day camp 2 years earlier. She had no surgical
history and was taking no medications except for occasional albuterol with
colds. Family history was significant for a maternal grandmother with
diverticulitis, a maternal grandfather with ulcers, and a paternal grandmother
with irritable bowel syndrome. There was no history of inflammatory bowel
disease or childhood illnesses. The patient was in fifth grade and had done
very well in school and been very involved in sports before this illness. The
patient reported that she missed school and her friends.
III. Physical Examination
T, 38.1°C; RR, 24/min; HR, 124 bpm; BP, 105/71 mm Hg
Weight, 37 kg (75th percentile); height, 155 cm (90th percentile)
Physical examination revealed a thin Caucasian girl who appeared tired and
anxious. There was erythema of the pharynx with enlarged tonsils and
cobblestoning. There was no exudate and no asymmetry of the tonsillar crypts or
soft palate. She had good dentition, halitosis, and cracked red lips. Her neck
was supple with no adenopathy. Lungs were clear to auscultation. Cardiac
examination revealed no murmurs, rubs, or gallops. Abdominal examination
revealed good bowel sounds in all four quadrants. There was diffuse tenderness
but no guarding, no rebound, and no hepatosplenomegaly. Rectal examination
revealed no excoriation, skin tags, fissures, or hemorrhoids. She had good
rectal tone without any palpable masses. She was a Tanner II female, and there
were no obvious vaginal lesions. The neurologic examination was normal.
IV. Diagnostic Studies
The CBC revealed a 5,800 WBCs/mm3. Hemoglobin and platelets were normal. ESR was also normal at 14 mm/hour.
Electrolytes were as follows: sodium, 144 mEq/L; potassium, 4.2mEq/L; chloride,
101 mEq/L; bicarbonate, 31 mEq/L; blood urea nitrogen, 7 mg/dL, and creatinine,
0.6 mg/dL. Urinalysis showed a high specific gravity of 1.036 as well as 1+
protein, small bacteria, and large mucus. A rapid strep test was positive for
group A streptococcal antigen. Amylase was 40 U/L, and lipase was 53 U/L. Stool
cultures grew normal flora, and
Clostridium difficile testing was negative. Abdominal radiographs were normal except for scoliosis of
the lumbar spine. There was no obstruction.
V. Course of Illness
An abdominal CT revealed the diagnosis (Fig. 7-3).
Discussion: Case 7-3
I. Differential Diagnosis
Weight loss in children is a concerning symptom that requires careful thought,
especially if it is associated with abdominal pain. Oncologic processes should
be considered and are frequently the biggest concern for parents. Acute and
chronic infections are probably the most common cause of weight loss in
children. With acute infections such as mononucleosis or pharyngitis, the child
should regain the weight once the infection clears. The continuing weight loss
in this patient is one of the most concerning elements of the history. In such
cases, more chronic, insidious infections, such as an abdominal abscess,
chronic hepatitis, intestinal parasites, tuberculosis, UTI, or HIV infection,
must be considered.
With associated abdominal pain, GI disorders such as chronic constipation,
gastroesophageal reflux disease, inflammatory bowel disease (examination of
trends in growth parameters is key), pancreatitis, malabsorptive disorders such
as celiac disease, and superior mesenteric artery syndrome must be considered.
Endocrinologic disorders associated with weight loss include Addison's disease (abdominal pain and skin discoloration frequently seen), diabetes
mellitus (with associated polyphagia, polydipsia, and polyuria), and
hyperthyroidism. Cardiopulmonary disorders include asthma, chronic congestive
heart failure, cystic fibrosis, and an untreated cardiac disease. Other causes
include nutritional deficiencies (iron and zinc), neurologic diseases
(increased intracranial disorders that lead to headache and neurodegenerative
disorders), connective tissue diseases, and renal failure.
The most common causes of weight loss, particularly in adolescent girls, are
dieting, increased physical activity, depression, anorexia nervosa, and
bulimia. Although an eating disorder was a possibility in this patient due to
her age and preceding illness, it could not explain her associated abdominal
pain.
II. Diagnosis
Abdominal CT revealed abnormal dilation of the stomach and proximal duodenum,
with tapering of the second part of the duodenum to the level of the space
between the superior mesenteric artery and the aorta, consistent with superior
mesenteric artery syndrome (Fig. 7-3).
The diagnosis is superior mesenteric artery syndrome.
III. Incidence and Epidemiology
Superior mesenteric artery syndrome is an uncommon disorder that has also been
referred to as cast syndrome, Wilkie
's syndrome, duodenal ileus, and arteriomesenteric duodenal compression syndrome.
The obstruction is extrinsic and either acute, chronic, or intermittent. It is
caused by compression of the transverse portion of the duodenum by the superior
mesenteric artery anteriorly and by the aorta and vertebral column posteriorly,
which causes classic
“megaduodenum” on upper GI series. Although the syndrome was first described in 1861 by Von
Rokitansky, many have disputed its existence, believing that it has been
confused with other causes of megaduodenum, such as diabetes, collagen vascular
diseases, and other causes of chronic intestinal pseudo-obstruction.
The syndrome is most common in older children and adolescents, and it is more
common in girls and in those individuals who have risk factors for narrowing
the angle between the aorta and the superior mesenteric artery, which results
in compression of the duodenum. These risk factors include linear growth during
the growth spurt that is not accompanied by weight gain, extreme lumbar
lordosis, rapid weight loss that markedly decreases the mesenteric fat pad,
severe trauma or surgery that necessitates prolonged bed rest, use of a body
cast, and scoliosis surgery. Anatomic predisposition is present in individuals
with a short suspensory ligament of Treitz. Recently, there has been a
connection with eating disorders, in that the syndrome can appear clinically
like an eating disorder and can sometimes precipitate an eating disorder
because of the development of food avoidance to avoid pain.
IV. Clinical Presentation
Presenting symptoms can be either acute or chronic (usually with exacerbations)
and typically include epigastric and abdominal pain, bilious emesis, and pain
after eating. Infrequently, patients present with small-bowel obstruction.
Patients with severe cases that have gone undiagnosed may present with signs of
malnutrition and dehydration with prostration and electrolyte abnormalities.
V. Diagnostic Approach
Abdominal imaging. Although plain abdominal radiographs are often normal, they can show gastric
distention. The diagnosis is usually made by upper GI series, which shows
dilatation of the first two portions of the duodenum with a cutoff at the third
potion of the duodenum. Hypotonic duodenography can also display the site of
obstruction, and CT can provide more detailed information about the
aortomesenteric angle and anatomic issues that are creating the obstruction.
VI. Treatment
Treatment should begin with stabilization of the patient. To avoid gastric
perforation, nasogastric decompression should be performed and intravenous
fluids administered to correct electrolyte imbalances. The patient should be
counseled to avoid the supine position, which exacerbates the obstruction, and
to remain either upright or in the left lateral decubitus position to open up
the aortomesenteric angle. Although some patients cannot tolerate even slow
nasogastric feeds, parental nutrition is rarely warranted and nasojejunal feeds
are often successful. Metoclopramide may help the patient tolerate feeds.
Treatment is conservative until weight gain is achieved. Surgical interventions
such as the Ladd procedure or duodenojejunostomy are indicated in cases
recalcitrant to other therapies.
VII. References
1. Tunnessen WW. Weight loss. In: Tunnessen WW, ed. Signs and symptoms in pediatrics, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 1999:36–40.
2. Wesson DE, Haddock G. The surgical abdomen. In: Walker WA, Durie PR,
Hamilton JR, et al., eds.
Pediatric gastrointestinal disease, 3rd ed. Hamilton, Ontario: BC Decker, 2000:435–444.
3. Shetty AK, Schmidt-Sommerfeld E, Haymon ML, et al. Radiological case of the
month: superior mesenteric artery syndrome.
Arch Pediatr Adolesc Med 1999;153:303–304.
4. Jordaan GP, Muller A, Greeff M, et al. Eating disorder and superior
mesenteric artery syndrome.
J Am Acad Child Adolesc Psychiatry 2000;39:1211.
5. Crowther MA, Webb PJ, Eyre-Brock IA. Superior mesenteric artery syndrome
following surgery for scoliosis.
Spine 2002;27:e528–e533.
Pictures
Book Source Details
- Book Title: Pediatric Complaints and Diagnostic Dilemmas
- Author(s): Samir S Shah MD; Stephen Ludwig MD
- Year of Publication: 2003
- Copyright Details: Pediatric Complaints and Diagnostic Dilemmas, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright Details: Pediatric Complaints and Diagnostic Dilemmas, Copyright © 2008 Williams & Wilkins.
More About Causes of Lower abdominal pain
» Next page: Abdominal Pain - Case 7-4: 9-Year-Old Girl (Pediatric Complaints and Diagnostic Dilemmas)
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