Dyspepsia is also commonly known as indigestion. It is a common symptom with extensive differential diagnosis and pathophysiology. Can be idiopathic (functional) or with a secondary cause.
Rome IV criteria define dyspepsia as having one or more of the following symptoms
Postprandial fullness (post prandial distress syndrome if no cause)
Early satiety (inability to finish a normal size meal, also classified as postprandial distress syndrome if no cause)
Epigastric pain/burning (classified as epigastric pain syndrome if no cause is identified)
Functional dyspepsia based on the Rome IV criteria is defined as the presence of one or more of the following symptoms plus no evidence of structural disorder from upper endoscopy to explain the symptoms
Uncomfortable postprandial fullness
Uncomfortable early satiation
Epigastric pain or bothersome epigastric burning
Functional dyspepsia or non-ulcer dyspepsia can be subclassified into 2 types of conditions.
Postprandial distress syndrome (PDS)
Epigastric pain syndrome (EPS)
While patients with these symptoms and a negative diagnostic evaluation likely have functional dyspepsia, according to the Rome IV guidelines, the criteria should be fulfilled for the last three months with symptom onset at least six months before diagnosis. Patients with functional dyspepsia must also fulfil criteria for PDS or EPS.
The cause of dyspepsia can be idiopathic (functional) or with a secondary cause (25%). Secondary cause of dyspepsia include:
GERD (reflux disease), Peptic ulcer disease, Gastric cancer, Medication like NSAID induced dyspepsia even without ulcer.
Other infiltrative disease to stomach (chrons’ disease, sarcoidosis, Amyloidosis, Lymphoma)
Functional dyspepsia (Non-ulcer dyspepsia) is when dyspepsia has no cause (idiopathic)
Many mechanisms have been proposed but the pathogenesis of functional dyspepsia is still unclear. Some of the possible mechanism for functional dyspepsia are as follows:
Gastric motility and compliance: Gastric motility disorder has been associated with non-ulcer dyspepsia. Example of disorder motility include: Delayed gastric emptying, Rapid gastric emptying, Antral hypomotility, Gastric dysrhythmias, and Impaired gastric accommodation in response to a meal.
Visceral hypersensitivity: this is characterized by a lowered threshold for pain induction in the presence of normal gastric motility. Both mechanoreceptor dysfunction and aberrant processing of afferent nervous signal input in the spinal cord or brain may play a role in this condition which lead to non-ulcer dyspepsia.
Helicobacter pylori infection: This is because H. pylori may cause altered smooth muscle dysfunction due to the induction of an inflammatory response or by the initiation of an antibody response. Although studies have not found a solid association between H.pylori infection and abnormal gastric motility function in patient with non-ulcer dyspepsia, it is known that the inflammatory response caused by infection of H.pylori can ower the throeshol dof discomfort to gastric distention.
Psychosocial dysfunction: non-ulcer dyspepsia has been shown to be a result from a complex interaction of psychosocial and physiological factors. Non-ulcer dyspepsia has been associated with generalized anxiety disorder (GAD), somatization, and major depression disorder. There is also a higher prevalence of functional gastrointestinal disorders in patients with self-reported history of childhood abuse.
Epigastric pain with normal EGD (diagnosis of exclusion)
Diagnosis of exclusion as the most common cause epigastric pain and symptoms that may look like (GERD, Gastritis, PUD, Gastric cancer) but yet has a negative EGD
Note – PUD is most common cause of upper GI bleeding
Diagnosis of Functional Dyspepsia
As mentioned, non-ulcer dyspepsia is a diagnosis of exclusion. They can only be definitive diagnosed with upper endoscopy when other causes of epigastric pain are ruled out.
The diagnosis of functional (idiopathic or nonulcer) dyspepsia is made from the characteristic clinical history of postprandial fullness, early satiety, or epigastric pain/ burning for the last three months with symptom onset at least six months before diagnosis and the exclusion of other causes of dyspepsia with upper endoscopy and additional testing, if indicated, based on the symptoms.
Gastroesophageal reflux disease can often be confused with functional dyspepsia, as dyspepsia symptoms commonly coexist with heartburn, and some patients with functional dyspepsia respond to PPI therapy. Gastroparesis is rare but can also be confused with functional dyspepsia, as gastric emptying may be slow and symptoms of dyspepsia occur in both disorders; vomiting or weight loss with very slow gastric emptying suggest gastroparesis
When is Upper Endoscopy necessary with suspecting Dyspepsia:
If the patient present with alarming symptoms like (weight loss, anemia, dysphagia, odynophagia) or patient is > 55 year old
Treatment and Management of Dyspepsia
For patient under the age of 45 years old with no alarming symptoms like (weight loss, anemia, dysphagia), they are managed empirically with proton pump inhibitors (PPI) like Protonix. In situations where PPI are not available, Histamine receptor-2 blockers (H2 blocker), liquid antacid can be used instead although they have less efficacy.
Initial therapy for patients with functional dyspepsia is PPI. In addition, if local prevalence of H.pylori is > 10%, there is a need to test for and treat H.pylori if present. If negative should be treated with PPI empirically if local prevalence of H.pylori < 5%. If prevalence is intermediate, your doctor may choose to do either just PPI or with H.pylori tesing inclusive.
If patients’ symptoms are refractory to 8 weeks of PPI, therapeutic trial with tricyclic antidepressant (TCA) should be initiated. Amitriptyline (50 mg), escitalopram (10 mg) are commonly used.
Other treatment if PPI and TCA fail to control symptoms include the following:
Prokinetics like metoclopramide
Fundic relaxant drugs: This is not commonly sued but a small randomized trial have shown that buspirone (10 mg, three times daily for four weeks) can increase gastric accommodation and reduced the overall severity of symptoms of dyspepsia, despite slowing gastric emptying of liquid.
Dietary Modification: Although many food substance and lipid in the duodenum can induce dyspepsia from changes in gastric motility, there is limited data to support dietary modifications. Many doctors will advise the increase intake of fiber.
Psychological therapy (cognitive behavioral therapy, hypnotherapy, or psychotherapy) has benefited selected patients and should be considered for motivated patients who associate symptoms with stressors.