Dr GI Joe

Patients presenting with upper gastrointestinal symptoms such as heartburn, chest pain, and dyspepsia represent a common and complex clinical challenge. This protocol provides a structured, evidence-based pathway for the clinician to differentiate between structural diseases like gastroesophageal reflux disease (GERD) and a group of conditions defined by the Rome IV criteria as Disorders of Gut-Brain Interaction (DGBI). A core principle of this protocol is that a functional diagnosis is a positive diagnosis, established through a systematic workup that identifies characteristic symptom patterns after excluding organic pathology. It is not, and should not be considered, a mere diagnosis of exclusion when other tests are negative.

The primary esophagogastric DGBI addressed within this protocol include:

The first step in evaluating any patient with these symptoms is to screen for alarm features that mandate an expedited workup to rule out serious underlying pathology.

For patients without alarm features, proceed to the appropriate diagnostic pathway, beginning with the GERD-spectrum evaluation for those presenting with heartburn or chest pain.

This pathway is strategically designed to systematically determine whether a patient's reflux-like symptoms are caused by pathologic acid reflux (GERD) or by a functional esophageal disorder. This distinction is critical, as it dictates entirely different management strategies. For a patient without alarm features, the initial approach is an empiric trial of acid-suppressive therapy.

The standard initial strategy is an 8-week empiric trial of a once-daily proton-pump inhibitor (PPI). If symptoms persist, the first step is to optimize therapy by escalating to twice-daily (BID) dosing, ensuring the medication is taken 30-60 minutes before meals. If symptoms remain refractory despite this optimization, further diagnostic evaluation is required.

Upper endoscopy is a pivotal diagnostic tool in this pathway. The findings directly determine the next steps in management and diagnosis.

Ambulatory reflux monitoring (via a catheter-based or wireless capsule system) is the definitive test to characterize the relationship between a patient's symptoms and reflux events. The timing of the test relative to PPI therapy is critical and depends on the clinical question.

The results from an OFF-PPI ambulatory reflux study will place the patient into one of three distinct diagnostic categories, each with a unique therapeutic path.

Once a diagnosis of proven GERD is established, the management focus shifts to effective and durable symptom control, which presents its own set of challenges in refractory cases.

For patients with a confirmed diagnosis of GERD (established by LA Grade C/D esophagitis or an abnormal AET), the goal of management is symptom control and healing of the esophageal mucosa. While most patients respond well to standard PPI therapy, a subset will experience persistent symptoms. Management of this cohort demands a systematic approach to optimizing therapy before considering a functional overlap or labeling the condition as truly refractory.

The term "Refractory GERD" is an objective diagnosis, not merely a label for persistent symptoms. The formal definition depends on the patient's baseline findings:

Not all PPIs provide the same degree of acid suppression. Failure to respond to one agent may be due to its lower relative potency. Switching to a more potent agent is a key step in managing refractory symptoms.

When a patient with proven GERD has persistent symptoms, the following steps must be taken:

Only after this rigorous workup confirms the absence of refractory GERD can the clinician confidently pivot to the distinct therapeutic paradigm required for functional esophageal disorders.

The management of functional esophageal disorders, such as Functional Heartburn and Reflux Hypersensitivity, requires a fundamental paradigm shift away from acid suppression and toward therapies that target the underlying mechanisms of visceral hypersensitivity and disordered brain-gut communication.

The foundational step in management is to: Stop unnecessary PPI therapy.

These medications are ineffective for symptoms not driven by pathologic acid and can contribute to polypharmacy and potential side effects. The cornerstone of treatment is the use of central neuromodulators.

Management should follow a stepwise progression, starting with the agents with the strongest evidence base.

In addition to pharmacotherapy, several other modalities can be effective and should be considered as part of a comprehensive treatment plan.

Behavioral Interventions: Cognitive Behavioral Therapy (CBT), gut-directed hypnotherapy, and mindfulness have all demonstrated efficacy in improving symptoms and coping mechanisms in patients with functional GI disorders.

Having established the management framework for functional esophageal disorders, the protocol now addresses the distinct diagnostic and therapeutic challenges presented by dyspeptic symptoms.

Dyspepsia, characterized by symptoms centered in the upper abdomen like epigastric pain, burning, or postprandial distress, requires a distinct diagnostic algorithm from the GERD pathway. The primary goal is to systematically exclude structural and organic diseases before arriving at a positive diagnosis of Functional Dyspepsia (FD) and identifying its clinical subtype.

The initial management strategy for dyspepsia is stratified by patient age and the presence of alarm features.

A diagnosis of Functional Dyspepsia can only be made after a normal EGD and the exclusion of key organic mimics. The following checklist should be completed:

Once FD is diagnosed, it is crucial to subtype it based on the dominant symptom profile, as this directly guides therapy.

This crucial differentiation between an "ulcer-like" pain syndrome and a "motility-like" distress syndrome is the key to selecting the appropriate first-line therapy.

The treatment of Functional Dyspepsia is not one-size-fits-all. Therapy must be targeted to the patient's dominant symptom subtype, reflecting the different underlying pathophysiologies of Epigastric Pain Syndrome (EPS) and Postprandial Distress Syndrome (PDS).

For patients whose primary symptoms are epigastric pain and burning, the therapeutic ladder focuses on acid suppression and neuromodulation.

For patients whose primary symptoms are meal-related fullness and early satiety, the therapeutic ladder focuses on agents that modulate gastric motility and accommodation.

While PDS has a "motility-like" profile, advanced motility testing is not a routine part of the diagnostic workup for most patients with Functional Dyspepsia.

This protocol reiterates that these conditions are positive diagnoses of brain-gut dysregulation, not diagnoses of exclusion. A systematic, criteria-based approach prevents futile cycles of acid suppression and correctly identifies patients who require therapies targeted at the core pathophysiologic mechanisms of visceral hypersensitivity and dysmotility. By carefully differentiating between structural entities like GERD and the various functional syndromes, clinicians can move beyond empiric acid suppression to deploy targeted therapies—including neuromodulators, prokinetics, and behavioral interventions—leading to more effective outcomes for patients with these challenging Disorders of Gut-Brain Interaction.