What is the best course of treatment for a patient with a recent history of enteric virus infection, now presenting with bloating, nausea postprandially (after meals), and decreased appetite?

Post-Infectious Functional Dyspepsia: Treatment Approach

For a patient with bloating, postprandial nausea, and reduced appetite following enteric virus infection, initiate a dietary elimination trial targeting food antigens while simultaneously treating with an antiemetic and considering a tricyclic antidepressant for visceral hypersensitivity. This represents post-infectious functional dyspepsia, where loss of immune tolerance to food antigens drives ongoing symptoms 1.

Pathophysiology After Enteric Infection

The acute viral infection triggers a cascade where previously tolerated food antigens now interact with the immune system, activating eosinophils and mast cells that release histamine and inflammatory mediators 1. This creates:

• Localized intestinal immune activation with mast cell degranulation and histamine release 1
• Visceral hypersensitivity as the primary mechanism for postprandial symptom generation 2
• Enhanced motor and symptomatic responses to normal food intake 2

Children are particularly vulnerable to serious enteric viral infections due to immature immune systems, with peak incidence under 2 years of age, though all pediatric age groups are affected 3.

Exclude Gastroparesis First

Do NOT order gastric emptying studies unless nausea and vomiting are the predominant features 4. Bloating alone should not prompt scintigraphy 4. This patient's symptom complex—bloating with postprandial nausea and reduced appetite—suggests functional dyspepsia with visceral hypersensitivity rather than delayed gastric emptying 4, 1.

First-Line Dietary Intervention

Start with a 2-week elimination diet removing suspected food antigens, as this is the simplest and most cost-effective initial approach 4. Specific targets include:

• Fatty foods, which are most frequently implicated in symptom induction and provoke symptoms more reliably than glucose in laboratory studies 2
• Lactose-containing foods in quantities that may trigger postprandial bloating 5
• Fermentable carbohydrates (beans, cabbage, lentils, brussels sprouts, legumes) to reduce gas production and bloating 5
• Sorbitol and fructose, which contribute to postprandial bloating 5

Dietary interventions work by modulating the food antigen-immune interaction that drives the pathophysiological process 1.

Pharmacological Management

Antiemetic Therapy

Ondansetron 4-8 mg orally before meals is appropriate for postprandial nausea 6. As a 5-HT3 receptor antagonist, it addresses nausea without the prokinetic effects needed only in true gastroparesis 6.

Critical safety considerations:

• Avoid in congenital long QT syndrome 6
• Monitor for serotonin syndrome if combining with other serotonergic drugs 6
• Watch for masking of progressive ileus, particularly after the recent viral infection 6

Neuromodulator for Visceral Hypersensitivity

Initiate a tricyclic antidepressant (e.g., amitriptyline 10-25 mg at bedtime, titrating upward) to reduce visceral hypersensitivity and raise the sensation threshold 4. These agents have dual benefits:

• Anti-histaminergic actions that counteract mast cell mediator release 1
• Central neuromodulation addressing the gut-brain interaction abnormalities 4

This targets the core pathophysiology where food antigens drive intestinal immune activation with systemic effects including nociceptive nerve triggering 1.

Alternative Pharmacological Options

If symptoms persist despite dietary modification and neuromodulation:

• H2-receptor antagonists (e.g., famotidine) act on histamine pathways activated by mast cells 1
• Mast cell stabilizers directly address the immune activation 1
• Proton pump inhibitors may benefit some patients through unclear mechanisms 1

Monitoring and Reassessment

Reassess at 2-4 weeks to determine:

• Response to dietary elimination (if improved, systematically reintroduce foods to identify specific triggers)
• Tolerance and efficacy of antiemetic therapy
• Need for neuromodulator dose adjustment
• Whether symptoms suggest alternative diagnoses requiring investigation 7

Common Pitfalls to Avoid

Do not rush to gastric emptying studies in patients with bloating as the predominant symptom—this leads to unnecessary testing and misdiagnosis of gastroparesis 4. The symptom pattern here (bloating > nausea, reduced appetite rather than vomiting) indicates functional dyspepsia, not gastroparesis 4.

Do not ignore the temporal relationship to the viral infection, as this suggests post-infectious functional dyspepsia where immune tolerance has been lost 1. This context makes dietary antigen elimination particularly relevant 1.

Do not prescribe prokinetics (metoclopramide) without documented delayed gastric emptying, as these carry significant risks including tardive dyskinesia and are only indicated for true gastroparesis 4.

If Symptoms Persist Beyond 4-6 Weeks

Consider:

• Brain-gut behavioral therapies (cognitive behavioral therapy, hypnotherapy) to address central processing abnormalities 4
• Formal food antigen testing with IgG panels, though evidence is limited 1
• Screening for organic causes: hypothyroidism, celiac disease, diabetes 7
• Re-evaluation for bacterial overgrowth as a post-infectious complication 7