Gastroparesis
Gastroparesis | |
---|---|
radioisotope gastric-emptying scan (GES), wireless motility capsule (WMC), serial X-ray after ingesting radiopaque markers (ROM), gastric manometry, esophagogastroduodenoscopy (EGD), and a stable isotope breath test. | |
Treatment | Dietary modifications, medications to stimulate gastric emptying, medications to reduce vomiting,[5] and gastric electrical stimulation.[6] |
Frequency | possibly up to 4%[citation needed] |
Gastroparesis (gastro- from Ancient Greek
Symptoms include nausea, vomiting, abdominal pain, feeling full soon after beginning to eat (early
Diagnosis is via one or more of the following:
Treatment includes dietary modifications, medications to stimulate gastric emptying, medications to reduce vomiting, and surgical approaches.[5] Additionally, gastric electrical stimulation (GES; approved on a humanitarian device exemption) can be used as treatment.[6] Overall survival in gastroparesis patients is significantly lower than survival in the general population.[9] It is associated with poor outcomes.[9]
Signs and symptoms
Gastroparesis has been linked to
Nausea in gastroparesis is usually
Postprandial fullness is an unpleasant feeling of stomach fullness that occurs after eating. Patients might characterize postprandial fullness as a feeling of food remaining in the stomach for an extended period of time. Satiation is a lack of hunger after eating. It is the inverse of hunger and appetite. Early satiety is the disappearance of appetite before nutrient absorption during food ingestion. Early satiation may be described by patients with gastroparesis as a loss of appetite or disappearance of appetite while eating. Early satiety is the sensation of stomach fullness that occurs shortly after beginning to eat and is out of proportion to the meal.[10]
Bloating is a highly subjective feeling of increased abdominal pressure. Bloating without eating should be distinguished from postprandial fullness. It is sometimes, but not always, associated with food consumption.[10]
Complications
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
Individuals with gastroparesis are also more likely to develop gastric bezoars. Bezoars are large masses of foreign substances and food that have become trapped in the GI tract, especially in the stomach.[11] The incidence of bezoar formation in gastroparesis patients has been estimated to be approximately six percent based on a barium study.[16]
There is a strong link between gastroparesis and the development of small intestinal bacterial overgrowth (SIBO). One study examined 50 gastroparesis patients using a glucose breath test and discovered that SIBO was present in 60% of their cohort. Furthermore, longer episodes of gastroparesis symptoms increase the risk of SIBO. Poor gastrointestinal motility and gastric acid production are believed to allow bacteria to colonize the small intestine. Furthermore, many individuals with gastroparesis are treated with acid-suppressive drugs, which significantly impair the GI tract's innate bactericidal activity. SIBO causes small bowel inflammation, impairing absorption and worsening nutritional deficiencies in gastroparesis.[17]
Because of the debilitating symptoms, patients with gastroparesis are at risk of significant nutritional abnormalities. In one study, 305 patients with gastroparesis had their dietary intake and nutritional status evaluated, and the average caloric intake was 1168 kcal/day, which resulted in substantial nutritional deficiencies. Furthermore, 64% of gastroparesis patients consumed a calorie-deficient diet. Additionally, higher symptom scores were inversely proportional to caloric intake.
Other complications include fluctuations in
Causes
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. Patients with cancer may develop gastroparesis because of chemotherapy-induced neuropathy, immunosuppression followed by viral infections involving the GI tract, procedures such as celiac blocks, paraneoplastic neuropathy or myopathy, or after an allogeneic bone marrow transplant via graft-versus-host disease.[3]
Gastroparesis present similar symptoms to slow gastric emptying caused by certain opioid medications, antidepressants, and allergy medications, along with high blood pressure. For patients already with gastroparesis, these can make the condition worse.
Gastroparesis has also been associated with connective tissue diseases such as scleroderma and Ehlers–Danlos syndrome, and neurological conditions such as Parkinson's disease and multiple system atrophy.[24] It may occur as part of a mitochondrial disease. Opioids and anticholinergic medications can cause medication-induced gastroparesis. Chronic gastroparesis can be caused by other types of damage to the vagus nerve, such as abdominal surgery.[25] Heavy cigarette smoking is also a plausible cause since smoking causes damage to the stomach lining. Idiopathic gastroparesis (gastroparesis with no known cause) accounts for a third of all chronic cases; it is thought that many of these cases are due to an autoimmune response triggered by an acute viral infection.[2] Gastroenteritis, mononucleosis, and other ailments have been anecdotally linked to the onset of the condition, but no systematic study has proven a link.[26]
People with gastroparesis are disproportionately female. One possible explanation for this finding is that women have an inherently slower stomach emptying time than men.[27] A hormonal link has been suggested, as gastroparesis symptoms tend to worsen the week before menstruation when progesterone levels are highest.[28] Neither theory has been proven definitively.
Physiology and mechanism
The symptoms of gastroparesis are best understood in the context of the physiology of gastric emptying (GE). The stomach functions as a reservoir for food and nutritional content, which are broken down to produce chyme. Chyme is then released into the duodenum at a controlled rate to allow for maximum nutrient absorption. 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. The delay of any of the factors in gastric emptying causes disorganization or reduced frequency of antral contractions and thus delayed GE.[29]
On the molecular level, it is thought that gastroparesis can be caused by the loss of neuronal
Pathogenesis of symptoms in diabetic gastroparesis include:
- Loss of gastric neurons containing nitric oxide synthase (NOS) is responsible for defective accommodation reflex, which leads to early satiety and postprandial fullness.[4]
- Impaired electromechanical activity in the myenteric plexus is responsible for delayed gastric emptying, resulting in nausea and vomiting.[4]
- Sensory neuropathy in the gastric wall may be responsible for epigastric pain.[4]
- Abnormal pacemaker activity (tachybradyarrhythmia) may generate a noxious signal transmitted to the CNS to evoke nausea and vomiting.[4]
Diagnosis
Gastroparesis is suspected in patients who have abdominal pain, nausea, vomiting, or bloating, or when these symptoms occur after eating. Once an
Griffith et al. first described GES in 1966,
The stable isotope breath test involves using the stable isotope
The stable isotope breath test is unreliable for individuals with small bowel diseases like
The
Recent studies have also shown that 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.[43] The ability to examine extragastric motility with a single test is another advantage of using WMC in the diagnosis of gastroparesis. This is useful because extragastric impaired motility occurs in more than 40% of those with suspected gastroparesis and gastrointestinal symptoms do not correlate well with the gastrointestinal segment affected. 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.[44]
Antroduodenal manometry involves
Antroduodenal manometry aids in differentiating between
Although transabdominal ultrasonography and magnetic resonance imaging (MRI) have been proposed as noninvasive diagnostic tools for gastroparesis, their use is currently restricted to research.[32]
By measuring changes in the antral area, two-dimensional
Another appealing tool is
Treatment
Treatment includes dietary modifications, medications to stimulate gastric emptying, medications to reduce vomiting, and surgical approaches.[5]
Dietary treatment involves low fiber diets and, in some cases, restrictions on fat or solids. Eating smaller meals, spaced two to three hours apart has proved helpful. Avoiding foods like rice or beef that cause the individual problems such as pain in the abdomen or constipation will help avoid symptoms.[52]
agonist for the treatment of gastroparesis.In specific cases where treatment of chronic nausea and vomiting proves resistant to drugs,
In cases of postinfectious 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.[citation needed]
Outlook
Long-term studies in gastroparesis patients show that it is not a benign disease and has significant
Other research indicates that
Some evidence suggests that postviral gastroparesis has a better prognosis and lasts less time than idiopathic gastroparesis.[64] Cases of post-infectious gastroparesis are self-limiting, with recovery within 12 months of initial symptoms, although some cases last well over 2 years. In children, the duration tends to be shorter and the disease course milder than in adolescents and adults.[5]
Prevalence
Post-infectious gastroparesis, which constitutes the majority of idiopathic gastroparesis cases, affects up to 4% of the American population.[citation needed] Women in their 20s and 30s seem to be susceptible. One study of 146 American gastroparesis patients found the mean age of patients was 34 years with 82% affected being women, while another study found the patients were young or middle aged and up to 90% were women.[5]
There has only been one true epidemiological study of idiopathic gastroparesis which was completed by the Rochester Epidemiology Project.[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.[65]
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Further reading
- Camilleri M, Parkman HP, Shafi MA, Abell TL, Gerson L (January 2013). "Clinical guideline: management of gastroparesis". The American Journal of Gastroenterology. 108 (1): 18–37, quiz 38. PMID 23147521.
- Parkman HP, Fass R, Foxx-Orenstein AE (June 2010). "Treatment of patients with diabetic gastroparesis". Gastroenterology & Hepatology. 6 (6): 1–16. PMID 20733935.
- Kim BJ, Kuo B (January 30, 2019). "Gastroparesis and Functional Dyspepsia: A Blurring Distinction of Pathophysiology and Treatment". Journal of Neurogastroenterology and Motility. 25 (1). The Korean Society of Neurogastroenterology and Motility: 27–35. PMID 30509017.
External links
- Overview from NIDDKNational Institute of Diabetes, Digestive, and Kidney Diseases at NIH