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Gastroparesis (GP) (gastro- from Ancient Greek γαστήρ gaster, "stomach" and πάρεσις -paresis, "partial paralysis"), 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 symptoms
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
- Erratic blood glucose levels
- Lack of appetite
- Gastroesophageal reflux
- Spasms of the stomach wall
- Weight loss and malnutrition
- Night sweats
- Muscle weakness
- Body aches (myalgia)
Morning nausea may also indicate gastroparesis. Vomiting may not occur in all cases, as sufferers may adjust their diets to include only small amounts of 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.
It is frequently caused by autonomic neuropathy. This may occur in 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. Other possible causes include anorexia nervosa and bulimia nervosa, which may also damage the vagus nerve. 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 also occur as part of a mitochondrial disease.
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 also 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) in order to properly empty itself of a meal.
Gastroparesis can be diagnosed with tests such as x-rays, manometry, and gastric emptying scans. 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.
Treatment includes dietary changes (low-fiber and low residue 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.
The antidepressant mirtazapine has proven effective in the treatment of gastroparesis unresponsive to conventional treatment. This is due to its anti-emetic 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 2 years of treatment).
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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
- Severe fatigue and weight loss due to calorie deficit
- Intestinal obstruction due to the formation of bezoars (solid masses of undigested food)
- Bacterial infection due to overgrowth in undigested food
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- Sildenafil may help diabetic patients
- Rapid improvement in post-infectious gastroparesis symptoms with mirtazapine
- Mirtazapine for Severe Gastroparesis Unresponsive to Conventional Prokinetic Treatment