Esophagitis, Rings, Webs & Diverticula

Approach to dysphagia

Where does it stick? Trouble initiating a swallow, with coughing, choking, or nasal regurgitation, is oropharyngeal (transfer) dysphagia and points to neuromuscular disease such as stroke or myasthenia gravis, or to a Zenker diverticulum. Food that sticks behind the sternum after the swallow is esophageal dysphagia.

Solids versus liquids. Dysphagia to solids only means mechanical narrowing. Intermittent symptoms suggest a ring or eosinophilic esophagitis; steadily progressive symptoms suggest a peptic stricture or carcinoma; an upper web with iron deficiency suggests Plummer-Vinson syndrome. Dysphagia to solids and liquids from the outset means a motility disorder: achalasia (a tight LES that fails to relax, with a bird's-beak taper on barium), diffuse esophageal spasm, or scleroderma.

Eosinophilic esophagitis

Pathogenesis. Eosinophilic esophagitis (EoE) is a chronic, Th2-driven allergic reaction to food antigens. IL-13 induces epithelial eotaxin-3, which recruits eosinophils, and IL-5 sustains them. It is most common in young atopic males with asthma, eczema, allergic rhinitis, or food allergy.

Presentation and findings. Adults present with dysphagia to solids and food impaction; EoE is the leading cause of food bolus impaction in young adults. Children more often show feeding refusal, vomiting, or abdominal pain. Endoscopy reveals stacked concentric rings (trachealization), linear longitudinal furrows, white exudates, and a narrow-caliber esophagus. Biopsies show ≥15 eosinophils per high-power field extending into the proximal and mid esophagus. GERD also brings eosinophils into the mucosa, but fewer and confined to the distal segment. Untreated inflammation fibroses the wall into strictures.

The steroid must be swallowed, not inhaled: the aim is to coat the esophageal mucosa, not the airway.

Infectious, pill, and caustic esophagitis

Infectious esophagitis mainly affects immunosuppressed patients and presents with odynophagia (painful swallowing). Candida is the most common cause. The biopsy site follows the host cell: HSV infects squamous epithelium, so the diagnostic cells lie at the ulcer edge, whereas CMV infects endothelial and stromal cells, so the ulcer base is sampled.

Antiviral logic. Acyclovir needs the HSV thymidine kinase for activation, which CMV lacks; CMV's UL97 kinase activates ganciclovir instead, and foscarnet, which needs no viral kinase, covers resistant strains.

Pill esophagitis. A tablet swallowed with little water or at bedtime can lodge, most often in the mid esophagus where the aortic arch or an enlarged left atrium narrows the lumen, and injure the mucosa directly. Classic culprits are tetracyclines (especially doxycycline), bisphosphonates such as alendronate, NSAIDs and aspirin, potassium chloride, and iron. Patients describe sudden odynophagia or retrosternal pain, and endoscopy shows a discrete ulcer surrounded by normal mucosa. Prevention is a full glass of water and staying upright afterward, at least 30 minutes for bisphosphonates.

Caustic ingestion. Alkali (lye, drain cleaners) saponifies fat and dissolves protein, producing liquefactive necrosis that penetrates deeply and risks perforation and later strictures. Acids cause coagulative necrosis, whose eschar limits depth; they often injure the stomach more than the esophagus. Lye strictures carry a markedly increased risk of esophageal squamous cell carcinoma decades later.

Webs and rings

Plummer-Vinson syndrome. This triad pairs dysphagia from an upper (postcricoid) esophageal web with iron deficiency anemia and atrophic glossitis or angular cheilitis; koilonychia is common, and middle-aged women are typical patients. Webs are thin, eccentric mucosal shelves. The syndrome is premalignant for squamous cell carcinoma of the hypopharynx and upper esophagus. Iron repletion and web dilation relieve the dysphagia.

Schatzki ring. A thin, concentric mucosal ring at the squamocolumnar junction of the distal esophagus, usually sitting above a sliding hiatal hernia. It causes intermittent, non-progressive dysphagia to solids or sudden meat impaction ("steakhouse syndrome"), typically once the lumen is under 13 mm. Dilation plus acid suppression is the treatment.

Webs are upper and eccentric (think Plummer-Vinson and iron deficiency); rings are lower and concentric (think Schatzki and a sliding hernia).

Diverticula

Zenker diverticulum. A pulsion, or false, diverticulum in which mucosa and submucosa herniate posteriorly through Killian triangle, the weak area between the thyropharyngeal and cricopharyngeal parts of the inferior pharyngeal constrictor. The driver is cricopharyngeal (UES) dysfunction: the sphincter relaxes poorly, so each swallow raises hypopharyngeal pressure. Older men are typical. The pouch traps food, producing oropharyngeal dysphagia, gurgling, halitosis, regurgitation of undigested food hours to days later, a soft neck mass, and aspiration pneumonia.

Diagnose a suspected Zenker diverticulum with a barium swallow; blind endoscopy or nasogastric tube placement can perforate the pouch. Treatment is cricopharyngeal myotomy with diverticulectomy or an endoscopic septotomy.

Traction and epiphrenic diverticula. Traction diverticula are true diverticula, containing all wall layers, pulled outward from the mid esophagus near the carina by scarring from mediastinal lymphadenitis such as tuberculosis or histoplasmosis; they are usually asymptomatic. Epiphrenic diverticula are false pulsion pouches just above the LES, generated by high intraluminal pressure in motility disorders such as achalasia or spasm, and may cause nocturnal regurgitation. As a rule, pulsion diverticula are false and traction diverticula are true.

Motility disorders and hiatal hernia

Diffuse esophageal spasm. Also called distal esophageal spasm, it features premature, simultaneous contractions of the distal smooth muscle with normal LES relaxation. Patients have intermittent chest pain that mimics angina and dysphagia to solids and liquids, often triggered by very hot or cold drinks. Barium shows a corkscrew or rosary-bead esophagus, and manometry confirms the diagnosis. Nitrates relieve the pain, which is why it can masquerade as angina, and calcium channel blockers are the usual first-line relaxants.

Scleroderma esophagus. Systemic sclerosis, especially the limited (CREST) form, replaces smooth muscle in the distal two-thirds of the esophagus with fibrosis and atrophy, while the striated upper third is spared. Distal peristalsis disappears and the LES becomes hypotensive, so acid refluxes freely and clears poorly, causing severe erosive esophagitis, peptic strictures, and Barrett esophagus. Raynaud phenomenon, sclerodactyly, and telangiectasias are the accompanying clues.

Sliding hiatal hernia. In about 95% of hiatal hernias, the GE junction and cardia slide above the diaphragm, producing an hourglass stomach on imaging. Loss of the crural pinch promotes GERD, and a Schatzki ring often marks the top of the hernia. Obesity, age, and raised intra-abdominal pressure predispose, and management is that of reflux. Large hernias may bleed slowly from linear erosions where the diaphragm pinches the stomach (Cameron lesions), causing iron deficiency.

Paraesophageal hiatal hernia. In this rolling hernia the GE junction stays in its normal position below the diaphragm while the gastric fundus herniates alongside the esophagus. It causes less reflux but can incarcerate, strangulate, or twist into a gastric volvulus, so symptomatic hernias are repaired surgically. Both hiatal hernias are acquired, unlike the congenital Bochdalek (posterolateral) and Morgagni (anterior) diaphragmatic defects.