Motility Disorders and Esophagitis are must-know esophageal pathologies are NOT inherently malignant (cancerous), but may be associated with increased risk for malignancy.
Motility Disorders
- Achalasia – failure of the lower esophageal sphincter (LES) to relax.
- Pathophysiology: ganglion cell and myenteric plexus breakdown, cholinergic nerve predominance leading to persistent contraction of muscle.
- Cancer risk: squamous cell esophageal cancer in those with >10 year history of achalasia.
- Clinically: dysphagia to solids and liquids, regurgitation of bland food; chest pain, weight loss. No response to PPI.
- Best initial test: barium esophagogram (bird’s beak appearance!)
- Confirmatory test: manometry
- EGD may be done to ensure there is no mass obstruction or concomitant pathology (e.g. ulcer, inflammation)
- Mimicking condition: malignant/benign tumors that invade nearby esophageal nerves (pseudoachalasia).
- Consider when patient c/o weight loss and age > 60
- Mimicking condition: malignant/benign tumors that invade nearby esophageal nerves (pseudoachalasia).
- Treatment:
- Pneumatic dilation via upper endoscopy (slightly cheaper)
- Surgical myotomy
- Both aforementioned treatments have similar rates of success!
- Injection of botulinum toxin via EGD has 50% relapse rate at/before 6 months.
- Last line: CCBs (nifedipine) or prolonged-release nitrates.
- Diffuse Esophageal Spasm / Nutcracker Esophagus
- Clinically: chest pain similar to angina and dysphagia.
- Pathophysiology: unknown; concomitant high-amplitude (>30 mm Hg in DES; >220 mmHg in Nutcracker) esophageal muscular contractions.
- Diagnosis: barium esophagogram “corkscrew esophagus“
- Treatment: CCBs, botulinum toxin, hydralazine, and/or anxiolytics.
Esophagitis
- Infectious Esophagitis – bacterial, fungal, parasitic, viral.
- Clinically: painful swallowing and/or dysphagia.
- Candida (albicans) – both immunocompetent and immunocompromised patients
- EGD will show small white raised plaques.
- Treatment: Fluconazole PO
- CMV – immunocompromised patients only.
- EGD with biopsy of ulcer base (CMV base)
- Treatment: Ganciclovir and valganciclovir
- HSV – both immunocompetent and immunocompromised patients
- EGD with biopsy of ulcer edge (HSV edge)
- Treatment: Acyclovir
- Pill Esophagitis
- Direct mucosal irritation and inflammation
- Risk factors: non-peristalsis of esophagus, medications decreasing muscular function (e.g. opioids), diminished salivary output, direct pill damage.
- Clinically: dysphagia, odynophagia, chest pain – can occur a few hours after ingestion or days later.
- Typical offenders:
- Alendronate, ferrous sulfate, mexiletine, tetracycline, doxycycline, quinidine, potassium.
- Worry about stricture progression with:
- Alendronate, NSAIDs, potassium, ferrous sulfate.
- Prevention is key! Simply drink plenty of water/fluids when taking pill and sit UP greater than/equal to 30 minutes.
- Eosinophilic Esophagitis
- Squamous mucosal inflammation secondary to permeation of eosinophils.
- Think of when seeing: atopic man, near middle age, with dysphagia to solid foods and frequent food blockages.
- Associated with asthma, eczema, food allergies.
- Population studies: 54 per 100,000 people in the US.
- Diagnosis: EGD shows longitudinal furrows, stenosis of lumen, leukoplakia and white exudates, and rings. BIOPSY shows eosinophils, >15 eos per HPF.
- Must rule out GERD-induced esophageal eosinophilia via trial of PPI.
- If repeat biopsy shows improvement post-PPI, you’ve diagnosed GERD-associated eosinophilia.
- If no improvement with PPI, it is eosinophilic esophagitis!
- Treatment:
- Diet modification (stop eating foods that agitate esophagus)
- Swallowed aerosolized glucocorticoids – budesonide or fluticasone
- Oral prednisone (if above don’t work)
- Treat any associated strictures with dilation.
- CHRONIC process with high recurrence rate if treatment interruption.
Bibliography
- ACP MKSAP 17: Gastroenterology and Hepatology, pgs. 3-7
- Image source: http://www.wikiwand.com/en/Diffuse_esophageal_spasm