Pediatric Surgery

Gastroparesis

Gastroparesis is a neuromuscular stomach disorder in which food empties from the stomach more slowly than normal. In most people, undigested food moves from the stomach into the duodenum and small intestine within 2 to 4 hours after eating. In contrast, patients who have gastroparesis will retain significant amounts of food in the stomach hours after eating or longer.

Patients with gastroparesis experience a variety of upper gastrointestinal symptoms including chronic nausea, frequent vomiting, early satiety, abdominal bloating and abdominal pain. These symptoms prevent the patient from eating normally and may lead to dehydration, weight loss and eventual life-threatening electrolyte imbalances and malnutrition.

Moreover, delayed stomach emptying interferes with oral drug absorption and, in patients with diabetes mellitus, can prevent effective control of blood glucose levels.

Normal Stomach Emptying

Gastric emptying involves storage, the mixing of food with stomach secretions, the grinding of food into small particles and the movement of ground particles into the small intestine at a rate that optimizes digestion. Solids and liquids empty at different rates, and emptying is controlled by muscle contractions in different regions of the stomach.

Liquid emptying is rapid and is controlled by the upper portion of the stomach (fundus). Emptying of digestible solids is characterized by a lag during which stored food moves from the upper to the lower stomach (antrum), where it is ground into small particles by powerful circular contractions. The lag phase is followed by an emptying phase during which the ground particles move from the lower stomach into the duodenum and small intestine.

Stomach muscle contractions are controlled by electrical signals generated at the junction of the upper one-third and lower two-thirds of the stomach. The major factor controlling this electrical activity is feedback from neural receptors in the small intestine. Studies have shown that even when there is no apparent neurological damage, many cases of gastroparesis result from a deficiency in neural feedback.1

Impact of Gastroparesis on Patients

Gastroparesis is a debilitating condition because of chronic nausea and vomiting and the severity of abdominal discomfort. If vomiting episodes cannot be controlled through dietary modification or medication, then dehydration, significant weight loss and poor nutrition are inevitable.

In chronic cases, patients are forced to withdraw from school, work and social activity because they lack the physical energy needed to perform normal daily activities. Patients may become too weak to get out of bed and may require hospitalization to restore fluids and provide nutritional support.

Nutritional support via a surgically inserted feeding tube or indwelling intravenous catheter may be necessary if sufficient caloric intake cannot be maintained. These methods of nourishment carry the risk of infection in an already compromised individual.

Etiology of Gastroparesis

In a study of 146 patients with documented chronic gastroparesis, it was found that approximately:2

36% had idiopathic gastroparesis 29% had diabetic gastroparesis 13% had postsurgical gastroparesis* 22% had gastroparesis of other origins

The true prevalence of gastroparesis is not known; however, it has been estimated that up to four percent of the US population may suffer from this condition.3

*Enterra Therapy is not indicated for postsurgical gastroparesis. Please see indications statement.

References

  1. Forster J, Sarosiek I, Lin Z et al. Further experience with gastric stimulation to treat drug refractory gastroparesis. Am J Surg. 2003 Dec; 186(6):690–5.
  2. Soykan I, Sivri B, Sarosiek I, Kiernan B, McCallum RW. Demography, clinical characteristics, psychological and abuse profiles, treatment, and long-term follow-up of patients with gastroparesis. Dig Dis Sci. 1998; 43:2398–2404.
  3. Abell TL, Bernstein RK, Cutts T, et al. Treatment of gastroparesis: a multidisciplinary clinical review. Neurogastroenterol Motil. 2006 Apr; 18(4):263–283.