William L. Hasler


Curr Opin Gastroenterol. 2012;28(6):621-628. 

In This Article

Causes of Gastroparesis

Gastroparesis most often is idiopathic, diabetic, or postsurgical in nature, with other causes representing a minority of cases. Sixty-four percent of a large database was comprised of idiopathic patients, whereas 31% were diabetic.[5]

Idiopathic Gastroparesis

Idiopathic gastroparetics are young (mean 41 years), mostly women (88%), and report predominant symptoms of nausea (34%), vomiting (19%), and pain (23%).[5] Depression (18%) and anxiety (36%) are commonly experienced. The condition may develop after acute infection (gastroenteritis, food poisoning, respiratory infection) in 20%, but causative organisms are rarely found. Idiopathic gastroparesis overlaps with several Rome III diagnoses including chronic idiopathic nausea and functional vomiting. Furthermore, 86% meet Rome III criteria for the postprandial distress variant of functional dyspepsia.[5]

Several factors contribute to idiopathic gastroparesis pathophysiology. Twenty-nine percent exhibit heightened perception of gastric distention, whereas 43% show blunted fundic accommodation reflexes. Other abnormalities include vagal neuropathy and increased inflammatory markers.

Diabetic Gastroparesis

Diabetes is the disease often associated with gastroparesis. A recent questionnaire study observed that 9.8% of type 1 diabetics experienced gastroparesis symptoms that correlated with neuropathy (P < 0.001) and retinopathy (P = 0.006) with trends to correlation with nephropathy (P = 0.08).[7] Incidences for developing gastroparesis are reportedly low (5.2% over 10 years in type 1 versus 1% in type 2 diabetes) but are greater versus controls (0.2%).[8] Delayed emptying is demonstrable in 27–65% with type 1 diabetes and up to 30% with type 2 diabetes. Type 2 diabetics with gastroparesis are 13 years older than idiopathic patients and have higher body mass.[9] Obesity itself is reportedly a predictor of gastroparesis symptoms in type 2 diabetics, suggesting a possible pathogenic role.[10] Type 1 patients more often are hospitalized and use prokinetic agents versus type 2 diabetic and idiopathic patients. Symptoms most often promoting evaluation are vomiting in diabetics and pain in idiopathics.

The pathogenesis of diabetic gastroparesis is multifactorial. Regional defects are demonstrable including blunted antral contractions, spastic pyloric and small intestinal motility, hypersensitivity to fundic distention, and impaired gastric accommodation to meals. Autonomic and vagal neuropathy may be prominent. Smooth muscle contractility is impaired in some type 1 patients. Acute hyperglycemia delays gastric emptying, disrupts antropyloric motility, and blunts responsiveness to prokinetic medications.

Postsurgical Gastroparesis

Gastroparesis may complicate operations for peptic ulcer disease, esophagogastric neoplasia, and weight reduction. Vagal damage occurs in 4–40% of patients undergoing laparoscopic fundoplication that can rarely cause gastroparesis. Delayed gastric emptying after pancreaticoduodenectomy has been stratified into three severity grades and is seen most often in women and with preoperative heart failure or a complicated postoperative course.[11]

Other Causes

Other defined causes of gastroparesis include radiation therapy, radiofrequency ablation of atrial arrhythmias, gastric ischemia from celiac artery occlusion or the median arcutate ligament syndrome, paraneoplastic influences, connective tissue diseases (scleroderma, systemic lupus erythematosus, polymyositis), Chagas disease, neurologic disorders (Parkinson's disease, stroke, dysautonomia syndromes, multiple sclerosis, spinal injury, neurofibromatosis, peripheral nerve disorders), eating disorders, pregnancy, and other hormonal dysregulation (hypothyroidism, hyperparathyroidism, Addison's disease), Crohn's disease, pancreatic disease, and other functional bowel disorders, and dysmotility syndromes. Exogenous causes include prescription drugs, cancer chemotherapy, and total parenteral nutrition. A recent report characterized gastroparesis as a complication of lung transplantation, particularly in individuals who develop bronchiolitis obliterans.[12] Children may develop gastroparesis from viral infection (18%) or mitochondrial dysfunction (8%).[13] Affected infants are predominantly boys; most adolescent gastroparetics are girls.