Gastroparesis(Redirected from Delayed gastric emptying)
Gastroparesis (GP also called delayed gastric emptying) is a medical condition consisting of a paresis (partial paralysis) of the stomach, resulting in food remaining in the stomach for an abnormally long time. Normally, the stomach contracts to move food down into the small intestine for additional digestion. The vagus nerve controls these contractions. Gastroparesis may occur when the vagus nerve is damaged and the muscles of the stomach and intestines do not properly function. Food then moves slowly or stops moving through the digestive tract.
Signs and symptomsEdit
The most common symptoms of gastroparesis are the following:
- Chronic nausea (93%)
- Vomiting (especially of undigested food) (68–84%)
- Abdominal pain (46–90%)
- A feeling of fullness after eating just a few bites (60–86%)
Other symptoms include the following:
- Abdominal bloating
- Body aches (myalgia)
- Erratic blood glucose levels
- Gastroesophageal reflux (GERD)
- Lack of appetite
- Morning nausea
- Muscle weakness
- Night sweats
- Spasms of the stomach wall
- Constipation or infrequent bowel movements
- Weight loss, malnutrition
Vomiting may not occur in all cases, as sufferers may adjust their diets to include only small amounts of food.
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Primary complications of gastroparesis include:
- Fluctuations in blood glucose due to unpredictable digestion times (in diabetic patients)
- General malnutrition due to the symptoms of the disease (which frequently include vomiting and reduced appetite) as well as the dietary changes necessary to manage it. This is especially true for vitamin deficiencies such as scurvy because of inability to tolerate fresh fruits.
- Severe fatigue and weight loss due to calorie deficit
- Intestinal obstruction due to the formation of bezoars (solid masses of undigested food)
- Small intestine bacterial overgrowth is commonly found in patients with gastroparesis.
- Bacterial infection due to overgrowth in undigested food
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 symptoms are almost identical to those of low stomach acid, therefore most doctors will usually recommend trying out supplemental hydrochloric acid before moving on to the invasive procedures required to confirm a damaged nerve.
More than 50% of all gastroparesis cases is idiopathic in nature, with unknown causes. It is however frequently caused by autonomic neuropathy. This may occur in a minority of people with type 1 or type 2 diabetes. In fact, diabetes mellitus has been named as the most common cause of gastroparesis, as high levels of blood glucose may effect chemical changes in the nerves. The vagus nerve becomes damaged by years of high blood glucose or insufficient transport of glucose into cells resulting in gastroparesis.
Gastroparesis has also been associated with connective tissue diseases such as scleroderma and Ehlers–Danlos syndrome, and neurological conditions such as Parkinson's disease. 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. 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. Gastroenteritis, mononucleosis, and other ailments have been anecdotally linked to the onset of the condition, but no systematic study has proven a link.
Gastroparesis sufferers are disproportionately female. One possible explanation for this finding is that women have an inherently slower stomach emptying time than men. A hormonal link has been suggested, as gastroparesis symptoms tend to worsen the week before menstruation when progesterone levels are highest. Neither theory has been proven definitively.
Gastroparesis can be connected to hypochlorhydria and be caused by chloride, sodium and/or zinc deficiency, as these minerals are needed for the stomach to produce adequate levels of gastric acid (HCl) to properly empty itself of a meal.
On the molecular level, it is thought that gastroparesis can be caused by the loss of neuronal nitric oxide expression since the cells in the GI tract secrete nitric oxide. This important signaling molecule has various responsibilities in the GI tract and in muscles throughout the body. When nitric oxide levels are low, the smooth muscle and other organs may not be able to function properly. Other important components of the stomach are the interstitial cells of Cajal (ICC) which act as a pacemaker since they transduce signals from motor neurons to produce an electrical rhythm in the smooth muscle cells. Lower nitric oxide levels also correlate with loss of ICC cells, which can ultimately lead to the loss of function in the smooth muscle in the stomach, as well as in other areas of the gastrointestinal tract.
Gastroparesis can be diagnosed with tests such as barium x-rays, manometry, and gastric emptying scans. For the x-ray, the patient drinks a liquid containing barium after fasting which will show up in the x-ray and the physician is able to see if there is still food in the stomach as well. This can be an easy way to identify whether the patient has delayed emptying of the stomach. The clinical definition for gastroparesis is based solely on the emptying time of the stomach (and not on other symptoms), and severity of symptoms does not necessarily correlate with the severity of gastroparesis. Therefore, some patients may have marked gastroparesis with few, if any, serious complications.
In other cases or if the x-ray is inconclusive, the physician may have the patient eat a meal of beef containing barium so they can watch as it is being digested and see how slowly the digestive tract is moving. This can be helpful for diagnosing patients who are able to digest liquids but not solid foods.
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. Current treatment is limited and includes nutritional modifications, medications to stimulate gastric emptying, drugs that reduce vomiting, and rarely surgical approaches.
Treatment includes dietary changes (low fiber diets) and, in some cases, restrictions on fat and/or solids. Eating smaller meals, spaced two to three hours apart has proved helpful. Avoiding foods that cause the individual problems, such as pain in the abdomen, or constipation, such as rice or beef, will help avoid symptoms.
Metoclopramide, a dopamine D2 receptor antagonist, increases contractility and resting tone within the GI tract to improve gastric emptying. In addition, dopamine antagonist action in the central nervous system prevents nausea and vomiting. Similarly, the dopamine receptor antagonist domperidone is used to treat gastroparesis. Erythromycin is known to improve emptying of the stomach but its effects are temporary due to tachyphylaxis and wane after a few weeks of consistent use.
The antidepressant mirtazapine has proven effective in the treatment of gastroparesis unresponsive to conventional treatment. This is due to its antiemetic and appetite stimulant properties. Mirtazapine acts on the same serotonin receptor (5-HT3) as does the popular anti-emetic ondansetron.
In specific cases where treatment of chronic nausea and vomiting proves resistant to drugs, implantable gastric stimulation may be utilized. A medical device is implanted that applies neurostimulation to the muscles of the lower stomach to reduce the symptoms. This is only done in refractory cases that have failed all medical management (usually at least two years of treatment). Medically refractory gastroparesis may also be treated with a pyloromyotomy, which widens the gastric outlet by cutting the circular pylorus muscle. This can be done laparoscopically or endoscopically.
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. Further studies have been recommended due to the limited sample size of previous studies.
Most cases of postinfectious gastroparesis are self‐limiting, with recovery within 12 months of initial symptoms but some cases last well over 2 years. The condition affects people of all ages, but in children the duration tends to be shorter and the disease course milder. In adolescents and adults, the duration of clinical symptoms can be prolonged.
Postinfectious gastroparesis, which constitutes the majority of idiopathic gastroparesis cases, affects up to 4% of the American population. 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.
There has only been one true epidemiological study of idiopathic gastroparesis which was completed by the Rochester Epidemiology Project. They looked at patients from 1996-2006 who were seeking medical attention instead of a random population sample and found that the prevalence of delayed gastric emptying was four fold 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.
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