Stomach contents thus exit more slowly into the duodenum of the digestive tract, a medical sign called delayed gastric emptying.

Symptoms of delayed gastric emptying tend to be exacerbated by eating, particularly after fatty foods and indigestible solids like salads and leafy vegetables.

Physical examination in patients with gastroparesis may be completely normal or, in its more severe forms, dehydration and malnutrition, as well as a succussion splash, can be present.

[13] Gastroparesis can lead to difficult glycemic control (which exacerbates gastric dysmotility), aspiration, bezoar formation, abnormalities in fluid and electrolyte balance, and inadequate nutrition intake resulting in weight loss.

[15] Some patients may experience severe nausea and vomiting, which can lead to dehydration, as evidenced by orthostatic hypotension as well as acute renal insufficiency.

Some patients with severe gastroparesis lose a significant amount of weight and suffer from nutritional deficiencies, necessitating small bowel feeding access to bypass the stomach.

Poor gastrointestinal motility (see enteric nervous system) and gastric acid production are believed to allow bacteria to colonize the small intestine.

[23] In cases of post-infectious gastroparesis, patients have symptoms and go undiagnosed for an average of 3 weeks to 6 months before their illness is identified correctly and treatment begins.

[4] In fact, diabetes mellitus has been named as the most common known cause of gastroparesis, as high levels of blood glucose may effect chemical changes in the nerves.

[27] Transient gastroparesis may arise in acute illness of any kind, as a consequence of certain cancer treatments or other drugs which affect digestive action, or due to abnormal eating patterns.

The controlled rate of chyme released is regulated by feedback mechanisms from the stomach and small intestines, which activate the vagus nerve and other hormones.

Once an upper endoscopy has been performed to exclude peptic ulcer disease or gastric outlet obstruction as the root of their symptoms, those patients should be tested for gastroparesis.

[32] Alternatives include stable isotope breath tests with carbon-13, which is unreliable in the setting of many diseases; wireless motility capsules, which may permit a more thorough examination; and antroduodenal manometry, which is invasive but may provide some information as to the etiopathogenesis.

[36] Following ingestion, the patient undergoes standard imaging of the gastric area while standing, and the percentage of radioactivity left in the stomach is recorded using computerized software and normalized to the baseline value at 1, 2, and 4 hours postprandially.

Once ingested, the WMC continuously records measurements of the three variables as it moves through the gastrointestinal tract, and the information is wirelessly and in real-time transmitted to a receiver that the patient wears on their waist for the duration of the study.

The colon transit period (normal is 59 hours or less) is calculated from the time the WMC enters the cecum till it is expelled from the body, as indicated by a sudden drop in temperature or signal loss.

[43] Recent studies have also shown that luminal pressure measurements can be used to differentiate diabetic gastroparesis, which is characterized by a reduced amount of contractions and motility indices when compared to healthy individuals.

Assessing the rest of the gastrointestinal tract in addition to gastric emptying provides information about motility in various segments of the gut, which can change management and improve symptoms.

[47] Antroduodenal manometry aids in differentiating between myopathic (scleroderma, amyloidosis) and neuropathic (diabetes mellitus) causes of impaired motility.

[49] Although transabdominal ultrasonography and magnetic resonance imaging (MRI) have been proposed as noninvasive diagnostic tools for gastroparesis, their use is currently restricted to research.

While ultrasound appears to be an appealing safe technique, its use in the clinical setting is limited due to the significant expertise required and inadequate outcomes in obese patients.

[54] Metoclopramide has more CNS adverse effects than domperidone and carries a US FDA boxed warning for tardive dyskinesia, a potentially irreversible condition.

[59] A variety of other central neuromodulators, including (but not limited to) other antidepressants, may be tried for symptoms like bloating and distention (and not only in the setting of gastroparesis, but also for disorders of gut–brain interaction, or DGBI).

[32] Sildenafil, which increases blood flow to the genital area in men, is being used by some practitioners to stimulate the gastrointestinal tract in cases of diabetic gastroparesis.

[53] Medically refractory gastroparesis may also be treated with a pyloromyotomy, which widens the gastric outlet by cutting the circular pylorus muscle.

Vertical sleeve gastrectomy, a procedure in which a part or all of the affected portion of the stomach is removed, has been shown to have some success in the treatment of gastroparesis in obese patients, even curing it in some instances.

[63][64] Long-term studies in gastroparesis patients show that it is not a benign disease and has significant morbidity and a poor prognosis due to the limited options for treatment.

The 10 patients who died succumbed to metabolic issues, cardiac complications, renal failure, suicide, and bowel ischemia caused by adhesions.

[9] They looked at patients from 1996 to 2006 who were seeking medical attention instead of a random population sample and found that the prevalence of delayed gastric emptying was fourfold higher in women.

It is difficult for medical professionals and researchers to collect enough data and provide accurate numbers since studying gastroparesis requires specialized laboratories and equipment.