Delayed gastric emptying is also referred to as gastroparesis and describes the condition of a retarded passage of food from the stomach to the duodenum.
The most frequently experienced symptoms are nausea, vomitus and stomach pain . Patients report a heightened perception of stomach distention and prolonged or continuous feelings of satiety or even fullness. Bloating is also common.
These symptoms not only interfere with nutrition but also with the patients' overall quality of life. Many DGE patients suffer from diabetes mellitus and are overweight, but daily caloric intakes are often lower than 60% of the recommended amounts. Nutrient deficiencies, particularly deficits regarding vitamin A, B6, C and K as well as potassium, zinc, and iron, can frequently be detected. Continuity and severity of symptoms cause anxiety and depression, but also prompt affected individuals to consult with health care providers before significant weight loss occurs .
Of note, the renewed Gastroparesis Cardinal Symptom Index (GCSI) classifies distinct forms of the disease according to predominant symptoms and severity of DGE. Such an evaluation may help to choose an appropriate therapy and to make prognostic statements .
Anamnesis and clinical examination will reveal only unspecific symptoms that may point to gastric problems.
In order to evaluate gastric emptying times, scintigraphy is usually applied. 99m Tc-sulfur colloid-bound to solid food is the standard marker to visualize food passage through the stomach. For better comparability of results, a standardized meal consisting of radiolabeled toast, jam, and a low-fat egg substitute should be chosen to administer labeled technetium . DGE may be diagnosed if more than 60% and 10% of that meal remain in the stomach after two and four hours, respectively.
Wireless motility and pH capsules may serve as an alternative to measuring gastric emptying times. After oral ingestion, the capsule will register and report motility and pH values. In DGE patients, motility indices are usually decreased. A 3-fold increase in pH is considered to mark the successful passage from the stomach to the duodenum and should not happen more than five hours after test start.
Breath tests with labeled substrates such as octanoate or spirulina may also be carried out. Only after the substrate is metabolized in the duodenum, the patient will exhale labeled CO2. Sensitivity and specificity of this test are good if duodenal digestion is not pathologically altered.
Of note, DGE symptoms do not necessarily correlate with the extent of delay of gastric emptying.
Upon diagnosis of DGE, further, tests should be applied to identify the underlying condition. Laboratory analyses of blood samples may reveal previously undetected diabetes mellitus and elevated inflammation markers that may point at gastrointestinal or respiratory infections. Electrogastrography may be helpful to detect disturbances in excitation conduction and postprandial reflexes.
Direct DGE therapy consists of dietary adjustments, drug therapy in form of prokinetics and antiemetics and possibly endoscopic or surgical intervention. However, in order to cure DGE, the underlying condition needs to be identified and treated accordingly.
DGE patients should be advised to prefer several small meals instead of few large ones. Fibre and fat intake should be limited. Diabetic DGE patients should furthermore adjust their diet in order to avoid peaks in blood glucose levels.
Metoclopramide is the most commonly prescribed prokinetic and antiemetic drug. Side effects such as tardive dyskinesia may result from the long-term use and are most frequently observed in older women after more than one year of treatment. Similar to metoclopramide, domperidone stimulates gastric motility by inhibiting dopamine receptors and inhibits vomiting. The antibiotic erythromycin also mediates prokinetic effects. However, development of pharmacodynamic tolerance often limits its long-term use. Domperidone, as well as erythromycin, increase the risk of sudden cardiac death. In some cases, the parasympathomimetic drug pyridostigmine is used to stimulate gastrointestinal motility. Sole prokinetic therapy may be supplemented with antiemetic treatment. Antiemetic phenothiazines, neurokinin receptor antagonists as well as mirtazapine may be prescribed to this end.
If conservative treatment does not suffice to alleviate symptoms and improve gastric emptying, implantation of gastric electrical stimulators may be required. Patients suffering from idiopathic DGE, however, rarely respond to this treatment. Pyloric botulinum toxin injection may be an alternative. Here, toxin-mediated muscle relaxation shall accelerate food passage from the stomach into the duodenum, but the effectivity of this method is not yet proven.
Because DGE is a symptom of an underlying disease rather than an independent pathology, prognosis depends on the former.
Blood glucose levels should be controlled better in diabetes mellitus patients suffering from hyperglycemia. Infections of the gastrointestinal and respiratory tract should be treated accordingly. If the cause of DGE can be remedied, gastric emptying times usually normalize.
However, this is not the case when DGE is triggered by permanent nerve damage or other not curable diseases. If the underlying disease progresses, DGE may even aggravate.
DGE is considered a multifactorial disease. A significant share of cases can be associated with diabetes mellitus or postoperative complications, but about two out of three cases are labeled as idiopathic . For diabetes mellitus patients, a positive correlation between increased body weight and DGE incidence has been demonstrated . Thus, obesity may play a role in DGE etiology. Individuals suffering from diabetes mellitus type 1 seem to be more susceptible for DGE than those diagnosed with diabetes mellitus type 2. With regards to DGE, incidence rates and hospitalization times are significantly increased in diabetes mellitus type 1 patients. Surgical interventions that have been associated with DGE are resections of esophageal or gastric neoplasms, surgery due to peptic ulcer disease, gastric partitioning as well as pancreatoduodenectomy. Interestingly, the incidence of DGE after pancreatoduodenectomy seems to correlate with the prevalence of heart failure . Postoperative DGE may be mediated by damage to the vagus nerve. Additionally, it has been speculated that previously experienced conditions such as food poisoning, gastroenteritis or even respiratory infections and lung transplantation predispose for DGE  .
In isolated cases, DGE has been associated with eating disorders, gastric ischemia, Crohn disease and other inflammatory bowel disorders, dysmotility syndromes, pancreatic disease as well as connective tissue disorders, neurologic diseases, hormonal disorders and pregnancy, parasitic infections and paraneoplastic syndrome. DGE may also be of iatrogenic nature and occur in the course of radiation therapy, chemotherapy, and total parenteral nutrition.
It has been estimated that 1 to 2% of the population suffers from DGE at any point in their lives. Because DGE affects significantly more women than men, prevalence rates differ accordingly and have been reported as approximately 4 per 10,000 females but only 1 per 10,000 males  .
The mean age of DGE patients has been calculated to be 41 years . Children may be affected by DGE and interestingly, gender distribution is reversed in this age group. Boys suffer from DGE more often than girls .
More specific data are available regarding a possible correlation between diabetes mellitus and DGE. The 10-year cumulative incidence in patients diagnosed with diabetes mellitus type 1 is more than 5%, in diabetes mellitus type 2 patients it is 1%. This same study reported a 10-year cumulative incidence of 0.2% for the general population . Elsewhere, the prevalence of DGE has been estimated as up to 65% for type 1 and up to 30% for type 2 diabetes mellitus patients. Moreover, diabetes mellitus type 2 patients seem to develop DGE at older ages . Correlations between DGE and diabetic neuropathy as well as diabetic retinopathy have been observed .
Contractions of smooth muscle cells located in distinct layers of the stomach wall are regulated by the enteric nervous system, which, in turn, pertains to the autonomic nervous system. Interstitial cells of Cajal serve as pacemakers. They generate slow wave electrical activity that reaches enteric synapses, trigger neurotransmitter release from enteric nerves and thus activate the aforementioned cascade that leads to muscle contraction. Finally, food passage through the stomach is promoted by tonic contractions of the fundus, phasic contractions of the pyloric antrum and duodenal peristaltic . This complex system leaves a variety of possible points of attack and disorders affecting the autonomic nervous system, the enteric nervous system, the interstitial cells of Cajal or the muscle layers in the walls of stomach or duodenum may result in DGE. Moreover, endocrine regulation of stomach motility seems to be mediated by motilin and ghrelin, two peptides secreted by enteroendocrine cells . Although these processes are not yet completely understood, they may play a role in DGE pathogenesis.
Diabetes Mellitus is also considered as a possible trigger for DGE. Increased blood glucose levels increase gastric emptying times. Hyperglycemia particularly interferes with contractions of the pyloric antrum, an effect that also reduces effectivity of possibly prescribed prokinetic compounds. Also, diabetic neuropathy may impair autonomic and vagus nerve signaling. Nerve damage, most often vagus nerve damage, is also suspected to be the trigger of postoperative DGE. In general, gastric emptying may be delayed by sensory dysfunctions leading to blunted reflexes, reduced contractility or spasms as well as motor disturbances.
There are no specific recommendations to prevent DGE.
Maintenance of physiological blood glucose levels prevents hyperglycemia and because this condition seems to be associated with DGE, this measure may contribute to DGE prevention. Similar recommendations might be given regarding a healthy body weight.
Delayed gastric emptying (DGE) describes the condition of increased retention of food in the stomach. DGE is considered to be a multifactorial disorder that may result from a wide variety of underlying diseases. This is due to the complex network of neurological, hormonal and muscular processes that coordinate and affect gastric emptying. Neuropathies and iatrogenic nerve damage may lead to hypomotility or stomach spasms and thus inhibit gastric emptying. Diabetes mellitus, in contrast, may evoke hyperglycemia and increased blood glucose levels interfere with gastric motility. However, most cases of DGE are deemed idiopathic because they cannot be associated with any condition or event.
DGE patients most frequently present with nausea, vomitus, and stomach pain. DGE therapy should aim at remedying the underlying disease. If the respective pathological condition is reversible, gastric emptying times usually normalize. However, if permanent nerve damage, non-resectable neoplasms such as pancreatic cancer trigger DGE, the prognosis is poor.
Delayed gastric emptying (DGE) refers to a condition where food remains for prolonged times inside the stomach. Passage towards the upper part of the small intestine, the duodenum, is retarded.
Gastric emptying is regulated by a complex network of nerves and muscles. Any damage to this network may result in DGE. Hyperglycemia, for instance, interferes with stomach contractions and is often observed in either undetected or uncontrolled diabetes mellitus. Lesions to nerves may be induced during surgeries. Unfortunately, no precise cause can be detected for the majority of DGE cases.
Nausea, vomitus, and stomach pain are most frequently experienced. Many patients also report bloating and continuous feelings of satiety or even fullness. These sensations may provoke serious attacks of anxiety and depression.
Imaging techniques will probably be applied to diagnose DGE. In this line, patients will eat radiolabeled food that can be traced while it passes through the gastrointestinal tract. This is one method to measure gastric emptying times. An alternative option is the ingestion of a small capsule that constantly measures motility and pH value. Because duodenal pH values are considerably higher than those measured in the stomach, time passed until arrival in the small intestine can be determined.
Because DGE is a symptom of any underlying disease rather than an isolated pathology, this underlying problem needs to be treated in order to cure DGE. The prognosis is significantly less favorable if the causative disease is not curable.
Direct treatment of DGE aims at alleviating the symptoms and usually consists of prokinetic and antiemetic drugs, i.e., a medication that stimulates gastric motility and inhibits vomiting. In this context, metoclopramide or domperidone are most frequently prescribed. These compounds mediate both actions, accelerate gastric emptying and reduce vomiting.