Gastric emptying is a neurohormonally controlled process that occurs after gastric accommodation, in which get digestible solids are pulverized in the stomach into small particles and then emptied into the duodenum through coordinated astral contractions.
Gastroparesis is a condition of delayed gastric emptying in the absence of gastric outlet obstruction.
The prevalence of gastroparesis based on insurance claims in 2018 was 267 per hundred thousand persons.
Gastroparesis results from conditions that affect the functions of extrinsic and intrinsic nerves, pacemakers, and smooth muscle cells of the stomach and pylorus, leading to prolongation of gastric emptying in the presence of antral hypomobility.
Gastroparesis is caused by reduced contractions of the distal stomach with abnormal pyloric relaxation and is more common among females than males with the ratio of 2:1-4:1-4 and typically causes nausea, vomiting, early satiety, bloating, and abdominal pain or discomfort.
Disorders of gastric motility are classified as neuropathic in which reduced frequency of the distal antral contractions, and increased pyloric contractions (diabetic neuropathy, postvagotomy),or myopathic disorders, which involve normal frequency, but decreased amplitude of an and small intestinal contractions (scleroderma, amyloidosis).
Guidelines define the diagnosis as gastric emptying by scintigraphy with more than 10% of gastric retention at four hours in patients with symptoms of gastroparesis without mechanical obstruction based on upper endoscopy or abdominal imaging.
Diabetic gastroparesis may be associated with loss of intrinsic or enteric inhibitory, neurons and pacemaker cells, and loss of intrinsic cholinergic neurons in the stomach.
The carbon 13 spirulina stable isotope breath test is also approved for diagnosing gastroparesis.
Gastroparesis is categorized based on the percentage of gastric retention at four hours: mild 10 to 15%, moderate 16 to 35%, or severe greater than 35%.
The most common causes of gastroparesis are: type 2 diabetes, 51.7%, post surgical effects, 15%, medication induced, 11.8%, idiopathic 11.3%, type 1 diabetes, 5.7%, and 4.5% other.
Other risk factors include neurological disorders like Parkinson’s disease, hypothyroidism, amyloidosis, connective tissue disorders, and viral infections.
Gastric emptying is highly dependent on food characteristics, including volume, caloric density, and chemical composition.
Low calorie liquids are emptied from the stomach passively, whereas high calorie liquids, digestible solids, and indigestible solids require progressively more gastric effort.
When gastric emptying is delayed, the emptying of high fat foods and indigestible solids is affected first; retention of gastric contents correlates with symptoms such as nausea vomiting and abdominal pain.
Gastroparesis is diagnosed when the symptoms correlate with evidence of delayed gastric emptying on scintigraphy.
Delayed gastric emptying secondary to abnormal motility occurs without mechanical outlet obstruction.
Chronic condition with significant morbidity.
Most common in young and middle aged females.
Patients present with nausea, vomiting, early satiety, bloating, abdominal pain, anorexia and weight loss.
Gastric retention of more than 10% of a standard low-fat meal at 4 hours indicates the presence of delayed emptying.
36% of cases are idiopathic and 29% are related to autonomic dysfunction secondary to diabetes.
May affect as many as 50% of patients with long standing diabetes.
The differential diagnosis of gastroparesis includes functional dyspepsia, rumination syndrome, cyclical vomiting, and cannabinoid hyperemesis syndrome.
Treatment:
Treatment includes discontinuation of medications that delay gastric emptying: opioids, cannabis, anticholinergics, GLP-1 receptor angonists optimizing glycemic control in patients with diabetes.
A diet with small particle foods – blended or chopped, that is low in fat and non-digestible fiber and anti-emetics, H1 receptor, antagonists for mild gastroparesis, antiemetics and prokinetics ( metoclopropramide , erythromycin) for moderate gastroparesis and liquid diet with jejunal feedings for severe gastroparesis.
Severe refractory gastroparesis may be retreated with gastric peroral endoscopic myotomy with endoscopic guided incision of the pylorus sphincter muscle, or gastric electrical stimulation implanted into the stomach muscle.
Prokinetic drugs may improve gastrointestinal symptoms.
Metoclopamide is approved for gastroparesis, but due to the risk of tardive dyskinesia only short-term use is recommended.
Severe refractory cases may be benefited from surgery, tube feedings or gastric pacing.
Erythromycin increasingly used in the management of gastroparesis.
Erythromycin is a potent motilin agonist that induces phase III migrating motor complex contractions.
Erythromycin is a potent prokinetic that enhances gastric emptying in healthy volunteers, in patients with gastroparesis caused by diabetes or vagotomy.
Erythromycin is effective both p.o. and intravenously.