Dyspepsia, Gastroparesis & Chronic Nausea/Vomiting
Scope the old and the alarming, test-and-treat the rest, and match each vomiting pattern to its fix
Dyspepsia and functional dyspepsia
Definition. Dyspepsia is epigastric pain or burning, bothersome postprandial fullness, or early satiety. Most patients have functional dyspepsia; the main structural causes are peptic ulcer disease (H. pylori, NSAIDs) and, less often, gastric or esophageal cancer.
Alarm features. Unintentional weight loss, progressive dysphagia, odynophagia, persistent vomiting, overt GI bleeding or iron-deficiency anemia, a palpable mass or lymphadenopathy, and a family history of upper GI cancer. Age 60 or older, or any alarm feature, calls for upper endoscopy, because gastric cancer risk rises with age.
- Age ≥60 or alarm featuresEGD to exclude malignancy and ulcer.
- Younger, no alarm featuresStop NSAIDs; test for H. pylori with a urea breath test or stool antigen. If positive, eradicate (for example, bismuth quadruple therapy for 14 days) and confirm cure at least 4 weeks after treatment.
- PPI trial4–8 weeks if H. pylori is negative or symptoms persist after eradication.
- Low-dose tricyclicAmitriptyline or nortriptyline for PPI nonresponders, acting as a central neuromodulator.
- Further optionsProkinetics and psychological therapy such as CBT.
Hold PPIs for 2 weeks and antibiotics or bismuth for 4 weeks before a breath or stool test to avoid false negatives. Serology is not used, because IgG stays positive after cure and cannot distinguish active from past infection.
Functional dyspepsia (Rome IV). One or more of bothersome postprandial fullness, early satiation, epigastric pain, or epigastric burning, with no structural explanation after evaluation (including a normal EGD when performed). Criteria must be met for the last 3 months, with onset at least 6 months earlier. The postprandial distress subtype is meal-induced fullness and satiety; the epigastric pain subtype is pain or burning that need not be meal-related. Treatment follows the same ladder: eradicate H. pylori if present, then PPI, then a low-dose TCA.
Approach to chronic nausea and vomiting
Exclude the mimics first. Before labeling vomiting as gastroparesis or a functional syndrome, look for:
- Pregnancy (always check a pregnancy test in reproductive-age women)
- Drugs: opioids, GLP-1 receptor agonists, digoxin, chemotherapy, anticholinergics
- Metabolic and endocrine causes: hypercalcemia, uremia, adrenal insufficiency, thyroid disease, DKA
- CNS causes: raised intracranial pressure (morning vomiting, headache, papilledema)
- Mechanical obstruction: gastric outlet or small bowel, excluded by EGD or imaging
Laboratory clue. Prolonged vomiting produces a hypokalemic, hypochloremic metabolic alkalosis from loss of gastric acid and secondary aldosterone effects.
Gastroparesis: causes and diagnosis
Definition and causes. Gastroparesis is objectively delayed gastric emptying without mechanical obstruction. Idiopathic and diabetic cases are the most common; diabetic gastroparesis reflects vagal autonomic neuropathy, usually after long-standing disease. Other causes include vagal injury after vagotomy or fundoplication, drugs (opioids, anticholinergics, GLP-1 receptor agonists), and a preceding viral illness, which often improves over months.
Presentation. Early satiety, postprandial fullness, bloating, nausea, and vomiting of undigested food eaten hours earlier; a succussion splash may be heard. In diabetes, delayed and unpredictable absorption produces erratic glucose control, including postprandial hypoglycemia on mealtime insulin.
Diagnosis. Perform EGD first to exclude gastric outlet obstruction (retained food alone does not establish gastroparesis). Then confirm with a 4-hour solid-meal gastric emptying scintigraphy; retention of more than 10% at 4 hours (or more than 60% at 2 hours) is delayed. Stop opioids and prokinetics 48–72 hours before the study, and check glucose on the day of testing, rescheduling if it is above about 275 mg/dL, because hyperglycemia itself slows emptying.
Food returned hours after a meal points to gastric retention; recognizable food returned within minutes, without nausea, points to rumination.
Gastroparesis: treatment
Diet and basics. Small, frequent meals low in fat and insoluble fiber (fat slows emptying and fiber forms bezoars), with more calories taken as liquids or purees. Optimize glycemic control and stop offending drugs, especially opioids and GLP-1 receptor agonists.
| Drug | Mechanism | Use | Key toxicity |
|---|---|---|---|
| Metoclopramide | D2 antagonist, 5-HT4 agonist; prokinetic and antiemetic | Only FDA-approved drug for gastroparesis; limit to 12 weeks | Boxed warning for tardive dyskinesia; dystonia, akathisia, parkinsonism, hyperprolactinemia; avoid in Parkinson disease |
| Erythromycin | Motilin receptor agonist | IV for acute flares or short oral courses | Tachyphylaxis within weeks; QT prolongation; CYP3A4 interactions |
| Domperidone | Peripheral D2 antagonist (little CNS penetration) | Restricted access in the US | QT prolongation |
Involuntary lip smacking or tongue movements on metoclopramide mean tardive dyskinesia: stop the drug. Anticholinergics such as benztropine treat acute dystonia, not tardive dyskinesia.
Refractory disease. Symptomatic antiemetics, gastric per-oral endoscopic pyloromyotomy (G-POEM), gastric electrical stimulation, or a venting gastrostomy with jejunal feeding for patients who cannot maintain nutrition.
Bezoars. Phytobezoars (undigested plant fiber, classically persimmons) form in gastroparesis and after gastric surgery, causing satiety, pain, bleeding, or obstruction. They are fragmented endoscopically, sometimes after softening with cola lavage, with surgery for obstruction. Trichobezoars (hair) occur with trichotillomania and trichophagia; Rapunzel syndrome is a trichobezoar whose tail extends into the small bowel.
Functional vomiting syndromes
| Feature | Cannabinoid hyperemesis | Cyclic vomiting syndrome | Rumination syndrome |
|---|---|---|---|
| Pattern | Stereotyped bouts of intractable vomiting and abdominal pain | Stereotyped acute episodes lasting under a week, well between them | Effortless regurgitation within minutes of every meal |
| Clue | Chronic heavy (usually daily) cannabis use; relief with hot showers or baths | Personal or family history of migraine | No nausea or retching; food rechewed and reswallowed or spit out |
| Episode treatment | Haloperidol or droperidol, topical capsaicin, benzodiazepines | Sumatriptan, ondansetron, sedation in a dark, quiet room | Not episodic; occurs with every meal |
| Long-term | Sustained cannabis cessation (the only cure) | Amitriptyline prophylaxis (topiramate alternative) | Diaphragmatic breathing |
Cannabinoid hyperemesis syndrome. Standard antiemetics such as ondansetron often fail, and opioids or cannabinoids worsen the problem. Hot water and capsaicin both activate TRPV1 receptors, which is the proposed explanation for their relief.
Cyclic vomiting syndrome. Episodes often begin abruptly in the early morning and recur for months to years; migraine is a strong association. Tricyclic prophylaxis reduces episode frequency, and triptans or ondansetron given at the first prodromal symptoms can abort an episode.
Rumination syndrome. An unconscious, learned contraction of the abdominal wall pushes gastric contents back up. The diagnosis is clinical, and high-resolution manometry with impedance can confirm it. Treatment is behavioral: diaphragmatic breathing, which competes with the abdominal contraction. Antiemetics and PPIs do not help.