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Symptoms » Lower abdominal pain » Book Sections
 

Abdominal Pain - Case 7-5: 8-Year-Old Boy

I. History of Present Illness

The patient, an 8-year-old boy, was well until 4 hours before presentation. At that time, he developed crampy periumbilical pain and bilious emesis. His family denied fever, diarrhea, or ill contacts. The pain was described as crampy and intermittent. He had six episodes of emesis before admission. His last bowel movement was 1 day before admission. His mother gave him an enema before presentation, with no relief of symptoms.

II. Past Medical History

The patient was a full-term infant without complications. His first episode of abdominal pain and bilious vomiting occurred about 3 years ago. Over the past few years, the pain and vomiting had been occurring about once every 4 months. The patient would have 2 to 3 days of emesis that was usually bilious and associated with abdominal pain. He had recently been treated with phenobarbital and atropine, without good results. He also had a history of chronic constipation that responded to mineral oil. Three months before presentation, he was admitted with similar symptoms and had a normal abdominal CT. The pain was never associated with eating, and he never missed school. There was no family history of celiac disease, cystic fibrosis, or any GI disorder.

III. Physical Examination

T 36.5°C; RR, 24/min; HR, 110 bpm; BP, 135/85 mm Hg
Weight, 26 kg
Physical examination revealed an alert child who was lying in bed and crying in pain. There were no oral lesions. The neck was supple with no lymphadenopathy. The lungs were clear to auscultation, and the cardiac examination revealed no murmurs, rubs, or gallops. On abdominal examination, there were diminished bowel sounds. Although the abdomen was soft, there was intermittent guarding and a question of a mass in the left upper quadrant, with no focal tenderness. There was no hepatosplenomegaly. Rectal examination revealed no fissures or skin tags; hard stool was palpable in the rectal vault on digital examination. He was a Tanner I male. The neurologic examination was normal.

IV. Diagnostic Studies

A CBC showed 14,500 WBCs/mm3, with 80% segmented neutrophils, 3% band forms, 7% lymphocytes, and 2% eosinophils. The hemoglobin was 12 g/dL, hematocrit 39.4%, and platelet count 314,000/mm 3. Serum bicarbonate was 18 mEq/L, but the electrolytes, blood urea nitrogen, and creatinine were otherwise normal. Liver function tests, amylase, and lipase were also normal. Urinalysis was negative except for the presence of ketones.

V. Course of Illness

The patient had an abdominal radiograph that showed a paucity of bowel gas, stool in the rectum, and no free air. An upper GI series revealed the cause of the patient 's cyclic vomiting (Fig. 7-5).
Discussion: Case 7-5

I. Differential Diagnosis

Although the differential diagnosis of abdominal pain and vomiting is important, the key to the diagnosis in this patient was the cyclic nature of the vomiting. Cyclic vomiting syndrome is an idiopathic disorder characterized by severe episodic vomiting interspersed with periods of normal health. In a study of patients with cyclic vomiting syndrome, 12% were found to have potentially life-threatening disorders such as malrotation with volvulus, obstructive uropathy, or brain tumor. The most common cause of cyclic vomiting, accounting for as many as 50% of cases, is abdominal migraine. The family history is usually significant for migraines. The second most common cause is chronic sinusitis.
Apart from malrotation with intermittent volvulus, other GI causes of cyclic vomiting include chronic idiopathic pseudo-obstruction, intestinal duplication, pancreatitis or pancreatic pseudocyst, peptic ulcer disease, and superior mesenteric artery syndrome. Urinary tract conditions include renal stones and intermittent ureteropelvic junction obstruction. There are also several endocrinologic and metabolic causes for cyclic vomiting, including Addison 's disease, porphyria, ornithine transcarbamylase deficiency, methyl malonic acidemia, and hereditary fructose intolerance.

II. Diagnosis

On the upper GI barium study, the ligament of Treitz was located at the midline, in an abnormal position compatible with a midgut malrotation (Fig. 7-5). The intraluminal contrast tapered in the proximal jejunum, in an appearance compatible with the presence of a midgut volvulus. The diagnosis is malrotation. The patient underwent a Ladd procedure with appendectomy.

III. Incidence and Epidemiology

It is important to understand the underlying embryology that leads to malrotation. At approximately 10 weeks ' gestation, the intestines undergo counterclockwise rotation around the mesenteric artery and finally attach themselves to the posterior abdominal wall. The midgut then rotates 270 degrees around the superior mesenteric artery, with the duodenal-jejunal loop moving posterior to the artery while the cecal-colic loop rotates anterior to it. The duodenum and ascending colon can then attach to the posterior abdominal wall. This process of rotation and attachment helps to support normal GI tract motility and balanced gut-to-mesentery vascular supply.
With malrotation, the normal process is impeded and the cecum is in the right upper quadrant, near the duodenum, while the duodenal-jejunal loop remains to the right of midline. Because there is no mesenteric attachment, volvulus of the midgut is likely to occur with malrotation. The incidence of volvulus in association with malrotation is 44% in all age groups, but in neonates it is more likely to require bowel resection because of more significant damage to the bowel.

IV. Clinical Presentation

The clinical presentation of malrotation can vary widely. Malrotation is commonly associated with other GI anomalies, namely esophageal atresia, diaphragmatic hernia, jejunal atresia, duodenal atresia, omphalocele, gastroschisis, intussusception, prune-belly syndrome, and Hirschsprung 's disease. It can also been in association with heterotaxy and congenital heart disease.
Malrotation with midgut volvulus can occur at any age but is most commonly seen in infancy. Acute volvulus manifests with bilious emesis, abdominal distention, pain (constant, not crampy), and bright red blood per rectum (suggesting ischemia). It is a surgical emergency, and untreated ischemic bowel can lead to shock and sepsis with cardiovascular collapse.
A less commonly seen entity is malrotation with intermittent volvulus. It usually manifests with recurrent abdominal pain and vomiting and signs of failure to thrive.

V. Diagnostic Approach

Upper gastrointestinal series. Although both the barium enema and the upper GI series can be used, the upper GI series is now preferred because of the possibility of cecal mobility on barium enema and its inability to show volvulus. Findings that are suggestive of malrotation in upper GI series include corkscrew-like deformity of the duodenum, displacement of the duodenum and jejunum in the right upper quadrant, and chronic obstruction of the duodenum.

VI. Treatment

In neonates, any suggestion of volvulus indicates the possibility of ischemic gut and necessitates immediate surgical intervention. In older patients with rotational abnormalities, definitive surgery is also performed. Timing depends on the presentation. If possible, patients should be prepared for surgery with nasogastric suction, fluid resuscitation, and prophylactic antibiotics to cover the possibility of bowel resection. The Ladd procedure allows definitive treatment with counterclockwise derotation of the midgut volvulus, lysis of bands, appendectomy, and placement of the duodenum in the right side of the abdomen and of the cecum in the left lower quadrant.

VII. References

 1. Tunnessen WW. Cyclic vomiting. In: Tunnessen WW, ed. Signs and symptoms in pediatrics, 3rd ed. Philadelphia: Lippincott William & Wilkins, 1999:503–507.
2. Olson AD, Li BU. The diagnostic evaluation of children with cyclic vomiting: a cost-effectiveness assessment. J Pediatr 2002;141:724–728.
3. Groff D. Malrotation. In: Ashcraft KW, Holder TM, eds. Pediatric surgery, 2nd ed. Philadelphia: WB Saunders, 1993:320–330.
4. Liu PCF, Stringer DA. Radiography: contrast studies. In: Walker WA, Durie PR, Hamilton JR, et al. eds. Pediatric gastrointestinal disease, 3rd ed. Hamilton, Ontario: BC Decker, 2000:1555–1591.
5. Shuckett B. Cross-sectional imaging: ultrasonography, computed tomography, magnetic resonance imaging. In: Walker WA, Durie PR, Hamilton JR, et al., eds. Pediatric gastrointestinal disease, 3rd ed. Hamilton, Ontario: BC Decker, 2000:1591–1633.

Pictures

Abdominal Pain - Case 7-5: 8-Year-Old Boy - 6023.1.png

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




More About This Book:
Title: Pediatric Complaints and Diagnostic Dilemmas
Authors: Samir S Shah MD; Stephen Ludwig MD
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 0-7817-4188-2

 » Next page: Abdominal Pain - Case 7-6: 2-Year-Old Girl (Pediatric Complaints and Diagnostic Dilemmas)

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