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Gastroparesis is a condition of impaired emptying of intraluminal gastric contents of the stomach into the duodenum in the absence of a mechanical obstruction. The syndrome may be caused by diabetes, occur after gastric surgery, or be idiopathic.

Gastroparesis is defined as abnormal gastric motility characterized by delayed emptying in the absence of mechanical outlet obstruction from the stomach.

The causes of gastroparesis are multifactorial. The most common causes are diabetes and postoperative complication of surgery on the stomach or vagus nerve. DiabetesOpens in new window is one of the major causes of gastroparesis—about 18% of long-term standing diabetes with poorly controlled blood sugar may have symptoms of gastroparesis which may be secondary to autonomic neuropathy.

The postoperative cause may be considered following surgery (e.g., gastric bypass, vagotomy, gastric resection) on the upper GI tract, which may involve damage to the vagus nerve. In some cases, the etiology may be unidentified (idiopathic causes).

Certain medications can cause gastroparesis. Central and peripheral diseases, including autonomic dysfunctions, enteric neuropathy, dysfunctions of ICCs, and psychosomatic disorders can result to abnormal gastric motility. Specific diseases that cause gastroparesis include:

  • intestinal pseudoobstruction accident,
  • collagen vascular diseases,
  • infectious diseases (e.g., varicella zoster,
  • Epstein-Barr virus,
  • Chagas disease,
  • clostridium botulinum,
  • thyroid disease, and
  • chronic renal failure.

Any systemic disease or condition that leads to neuromuscular dysfunction of the gastrointestinal tract may lead to gastroparesis. The most common causes in infants and children include prematurity, viral infections, drugs such as opioids and anticholinergics, metabolic disturbances such as hypokalemia, acidosis, and hypothyroidism, eosinophilic gastroenteropathy, cerebral palsy, diabetes mellitus, vagotomy, pseudo-obstruction, and muscular dystrophy.

Many patients have no apparent etiology and are diagnosed to have idiopathic gastroparesis. Postviral gastroparesis is a recently described entity in children, accounting for many forms of acquired gastroparesis. It follows a short viral illness, often rotavirus, and is associated with postprandial antral hypomotility.

In diagnostic studies conducted by Goswami and colleagues (1997), patients with idiopathic gastroparesis were more likely to note difficulty emptying (70%), whereas those with diabetic gastroparesis were more likely to have urinary frequency (71%).

The authors postulated an association between idiopathic gastroparesis and bladder dysfunction and proposed a common autonomic neuropathic syndrome may account for the bladder dysfunction in both the idiopathic and the diabetic forms of this syndrome.

Clinical Signs & Symptoms

The symptoms of gastroparesis are non-specific and include pain in the abdomen or epigastrium, vomiting, nausea, bloating, and early signs of satiety or postprandial fullness.

Some children with prolonged symptoms may have weight loss. The emesis characteristically occurs hours after eating, a differentiating feature from both GERD and rumination.


Diagnostic procedures for gastroparesis include gastric scintigraphy, 13C-octanoate breath testing, and the use of a wireless mobility capsule. Solid meal gastric scintigraphy is the gold standard.

A normal gastric emptying of a solid meal by definition rules out gastroparesis. Emptying of barium or liquid meals should not be relied upon for this diagnosis. In postviral gastroparesis, antroduodenal manometry demonstrates postprandial antral hypomotility with normal antral contractions during fasting.

Ultrasonography has been used to evaluate gastric emptying in young infants. The 13Coctanoic acid breath test is a newer, safe, nonradiologic test that has been used to measure liquid and solid gastric emptying.

It should be noted that clinical conditions such as mechanical outlet obstruction, gastric or peptic ulcer disease, gastric cancer, or other malignancies must be excluded to make the diagnosis of gastroparesis. A severity grading scale for gastroparesis is also available.

Medical Management

Management of gastroparesis is based on the etiology. Management includes relief of symptoms, normalization of nutritional state, glycemic control, and improvement of gastric emptying.

The first-line therapy involves the use of prokinetics. Patients with nausea and vomiting will benefit from the use of antiemetic medications. Selected patients will benefit from electrical stimulation of the stomach wall and surgery.

Various prokinetic medications such as cisapride, erythromycin, metoclopramide, and domperidone have been used to improve the gastric emptying. Erythromycin has proved to be the most effective gastrokinetic.

In patients with neurological impairment such as cerebral palsy, surgical pyloroplasty or pyloromyotomy remains a therapeutic option. Transpyloric feeding can be considered for a short period of time before pursuing surgery.

Complications of gastroparesis include malnutrition, weight loss, esophagitis, Mallory-Weiss tear (resulting from chronic vomiting), acute renal failure secondary to fluid volume depletion, electrolyte dysbalance, and bezoar formation.

See also:
    Adapted from: The Gastroesophageal Reflux in Infants and Children: Diagnosis, Medical .... Authored By Ciro Esposito, Philippe Montupet, Steven Rothenberg.