Dr GI Joe

The initial triage of a patient presenting with esophageal symptoms is a critical determinant of clinical outcomes. A systematic approach, predicated on recognizing distinct symptom patterns and alarm features, is essential for directing the urgency and nature of subsequent investigations. This initial assessment allows for the rapid identification of high-risk scenarios, distinguishing between patients who require immediate intervention and those who can be managed on an outpatient basis.

 | Presenting Symptom/Scenario | Associated Differential Diagnosis
 | Odynophagia (Painful Swallowing) | Infectious Esophagitis (Candida, HSV, CMV), Pill-Induced Injury, Severe Reflux Ulcer
| Dysphagia (Difficulty Swallowing) | Eosinophilic Esophagitis (EoE), Peptic Stricture, Schatzki Ring, Malignancy, Motility Disorder
| Chest Pain / Heartburn | Erosive Esophagitis (GERD), Eosinophilic Esophagitis (EoE)
| Food Impaction | Eosinophilic Esophagitis (EoE) until proven otherwise
| Immunosuppression (e.g., HIV) | Infectious Esophagitis, with Candida being the most common
| Recent New Medication Use | Pill-Induced Esophagitis (Doxycycline, bisphosphonates, KCl, NSAIDs, tetracyclines, clindamycin)

The presence of one or more of the following alarm features warrants an expedited esophagogastroduodenoscopy (EGD) to rule out underlying malignancy or other serious pathology:

The clinical presentation dictates the necessary timeline for endoscopic evaluation.

This structured initial assessment ensures patient safety and directs resources appropriately, leading directly to the next critical step: the endoscopic evaluation.

Esophagogastroduodenoscopy (EGD) serves as the cornerstone for the diagnosis, and often the treatment, of most esophageal disorders. A standardized protocol for performing and documenting the procedure is essential for ensuring diagnostic accuracy, facilitating effective communication among providers, and enabling appropriate risk stratification and long-term management planning.

The indications for performing an EGD can be broadly categorized as diagnostic or therapeutic.

Once a diagnosis is established or suspected during the EGD, management is tailored to the specific disorder identified.

Gastroesophageal reflux disease is a primary driver of esophageal pathology, leading to mucosal inflammation and injury. The Los Angeles (LA) classification is the global standard for grading the severity of erosive esophagitis, which directly informs the intensity of initial therapy and the need for follow-up endoscopy.

 | Grade | Endoscopic Findings
 | A | One or more mucosal breaks ≤5 mm in length, not continuous between tops of mucosal folds.
| B | One or more mucosal breaks >5 mm in length, not continuous between tops of mucosal folds.
| C | Mucosal breaks that are continuous between the tops of two or more mucosal folds but involve <75% of the circumference.
| D | Mucosal breaks that involve ≥75% of the esophageal circumference.

Chronic, poorly controlled GERD is the primary risk factor for the development of Barrett's Esophagus, the most significant long-term complication of the disease.

Barrett's Esophagus is a premalignant condition in which the normal squamous epithelium of the esophagus is replaced by metaplastic columnar epithelium containing intestinal-type goblet cells. Its clinical significance lies in its potential to progress to esophageal adenocarcinoma. Therefore, meticulous diagnosis, risk stratification, and surveillance are paramount.

The extent of Barrett's Esophagus is standardized using the Prague C&M Criteria. The measurement landmark is the gastroesophageal junction (GEJ), identified as the most proximal aspect of the gastric folds.

Measuring both C and M values is clinically essential for accurate risk stratification. Circumferential involvement represents a larger surface area of at-risk mucosa and is a stronger predictor of cancer progression risk than maximal length alone. For example, a patient with C4M4 Barrett's (4 cm of circumferential involvement) has a significantly higher risk of progression than a patient with C1M4 (only 1 cm of circumferential involvement with a 4 cm tongue), even though the maximal length is identical.

Critical Distinction: An irregular Z-line with columnar tongues extending less than 1 cm above the GEJ is not considered Barrett's Esophagus and does not require surveillance, even if biopsies show intestinal metaplasia. This finding carries an extremely low risk of progression.

 | Segment Length | Surveillance Interval | Annual Cancer Progression Risk
 | Short-Segment (<3 cm) | Every 5 years | 0.07 – 0.2%
 | Long-Segment (≥3 cm) | Every 3 years | 0.3–0.5%

 | Baseline Histology Before Eradication | Post-Eradication Surveillance Schedule
 | Low-Grade Dysplasia (LGD) | EGD at 1 year, 2 years, then every 3 years.
 | High-Grade Dysplasia (HGD) | EGD every 3 months for year 1, every 6 months for year 2, then annually.

From premalignant conditions, we now turn to a distinct inflammatory disorder, Eosinophilic Esophagitis.

Eosinophilic Esophagitis is a chronic, immune/allergen-mediated inflammatory condition characterized by eosinophilic infiltration of the esophageal mucosa. It is a primary cause of dysphagia and food impaction, particularly in younger individuals with a history of atopy. Management is multi-faceted, focusing on reducing inflammation through medication or dietary changes.

The diagnosis of EoE requires biopsies demonstrating ≥15 eosinophils per high-power field (hpf). Three therapeutic options are considered equivalent and first-line:

After initiating first-line therapy, a repeat EGD with biopsies is required in 8-12 weeks to assess for histologic remission (<15 eos/hpf). For patients with disease refractory to initial therapies, the biologic agent dupilumab is an effective option.

Next, we consider esophagitis caused by infectious pathogens.

Infectious esophagitis is a significant cause of morbidity, primarily seen in immunocompromised individuals, such as those with advanced HIV, organ transplant recipients, or patients on chronic immunosuppressive therapy. The endoscopic appearance can be highly suggestive of the causative organism, guiding initial empiric therapy while awaiting histologic confirmation.

 | Pathogen | Typical Endoscopic Appearance | Biopsy Strategy | First-Line Treatment
 | Candida albicans | Adherent white plaques or exudates | Brushings and/or biopsy of plaques | Fluconazole 200-400 mg daily for 14-21 days.
| Herpes Simplex Virus (HSV) | Small, discrete, "punched-out" or volcano-like ulcers | Biopsy the ulcer edge for viral inclusions | Acyclovir 400 mg five times daily or Valacyclovir 1 g three times daily for 7-10 days.
| Cytomegalovirus (CMV) | Large, linear, shallow ulcers, typically in the distal esophagus | Biopsy the ulcer base for viral inclusions | Ganciclovir 5 mg/kg IV every 12 hours, followed by oral Valganciclovir for 14-21 days.

Beyond inflammatory and infectious causes, structural blockages can also impair esophageal function.

Structural abnormalities such as rings and strictures are a common cause of mechanical obstruction, typically presenting with dysphagia to solid foods. The primary management strategy for these conditions is mechanical dilation to restore a sufficient luminal diameter.

A Schatzki ring is a thin, circumferential mucosal diaphragm located at the squamocolumnar junction. It is believed to arise from chronic GERD-related inflammation and fibrosis. The classic presentation is intermittent solid food dysphagia, famously termed "steakhouse syndrome." Management involves mechanical dilation followed by long-term PPI therapy to prevent recurrence.

For patients whose symptoms persist despite an endoscopically normal-appearing esophagus, the investigation must proceed to evaluate for less obvious causes.

A finding of a normal EGD in a patient with persistent dysphagia does not conclude the diagnostic workup. Instead, it shifts the focus away from mucosal and overt structural disease toward more subtle mechanical issues or underlying esophageal motility disorders. A systematic approach is required to identify the correct etiology.

The following algorithm guides the next steps after a non-diagnostic EGD:

Clinical Pearl: In summary, the post-EGD workup for dysphagia is guided by the suspected etiology: pursue a barium esophagram if a subtle structural lesion is suspected, and proceed to high-resolution manometry for a suspected functional/motility disorder.