Spencer C. Knox, MD

Internal Medicine Resident Physician, PGY-3

Tag: esophagus

Esophageal Metaplasia and Neoplasia

Esophageal cancer accounts for a jaw-dropping amount of cancer-related deaths, and is now classified as the 6th-highest cause of death in this group.  In this installment of the study guide series, I will discuss Barrett Esophagus (I learned this entity as Barrett Metaplasia) and esophageal cancer (neoplasia).

 

Barrett Metaplasia

  • Metaplasia:  columnar epithelium replaces the physiologic squamous epithelium in the distal portion of the food pipe.
  • PRE-MALIGNANT CONDITION
    • Cancer risk of 0.5% per year in those who have Barrett Esophagus.
    • Usual pathway (if progresses to ca):  intestinal metaplasia –> low-grade dysplasia –> high-grade dysplasia.
  • NO evidence that routine screening for BE based on GERD symptoms is helpful.
  • Clinically:
    • Think of this in an older obese white male with chronic reflux and a history of chain-smoking.
    • Protective = average wine consumption, fruits/veggies.
    • Barrett Esophagus occurs in the presence or absence of reflux!
  • Diagnosis:
    • Upper endoscopy showing typical intestinal metaplasia of distal esophagus.
      • Salmon-colored mucosa
      • Further classifications:  Short segment (< 3cm) or long segment (> 3cm)
  • Treatment:
    • PPI are useful for reflux symptom improvement, not preventing progression to dysplasia.
    • HIGH-grade dysplasia = destroy bad tissue with radiofrequency ablation or other resection.
  • Surveillance
    • EGD is primary modality.
    • Based on dysplasia grade:
      • none = repeat EGD 3-5 years.
      • low-grade = repeat EGD 6-12 months
      • high-grade = look for focal lesions, which may harbor more progressive disease; repeat EGD q3 months with resection/surgery.

Esophageal Carcinoma

  • Adenocarcinoma is most common type (#1) in US; SCC is also very common.
  • Typically presents in males, aged 50-60’s.
  • 5-year survival rate 15-25%, depending on stage at presentation.
  • Risk factors:
    • Adenocarcinoma = GERD, Barrett metaplasia, tobacco, radiation, male, old age, poor diet.
    • SCC = tobacco and alcohol, direct toxic injury, Zn and selenium deficiency, prior radiation to region, poor population, poor oral hygiene, HPV, nitrosamine exposure (occupational hazards), nonepidermolytic palmoplantar keratoderma.
  • Diagnosis:
    • #1 symptom = SOLID-food dysphagia
    • Weight loss, low appetite, low hemoglobin/hematocrit.
    • EGD is best way to diagnose.
    • Squamous Cell Carcinoma is proximal
    • Adenocarcinoma is distal
    • CT scan is useful to evaluate for metastatic disease; PET used for questionable lesions.
  • Treatment
    • Refer to Oncology, resection versus chemotherapy is stage dependent at time of diagnosis.

Bibliography

  • ACP MKSAP 17:  Gastroenterology and Hepatology, pgs. 9-12
  • Image source:  https://en.wikipedia.org/wiki/Barrett’s_esophagus
    • Intestinal metaplasia consistent with Barrett esophagus (left side of main image) and normal stratified squamous epithelium (right side), Alcian blue stain.

Esophageal Motility and Esophagitis

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
    • 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

Introduction to Esophageal Problems

The very first entry in my GI & Hepatology study outline series will set the stage/define major descriptors of proximal GI (esophageal) symptoms and help with categorizing pathology.

Dysphagia = the sensation that food and/or liquid is not appropriately going through the mouth/throat/esophagus.  Typical symptoms:  “food is getting stuck / impeded.”

  • Oropharyngeal phase – food bolus from mouth into hypopharynx and proximal esophagus
    • “Transfer Dysphagia” – cannot START the swallow maneuver.
    • Symptoms:  coughing, food entering nares, choking; hoarseness and/or dysarthria (neuromuscular weakness/dysfunction)
    • At direct aspiration risk due to inability to clear food/liquid from epiglottis (look for perpetual pulmonary infections)
    • Examples:  cricoid webs, iron deficiency, mass compression, ALS, stroke, dementia, Myasthenia Gravis.
    • Best initial test = modified barium swallow (videofluoroscopy)
      • Test begins with liquid phase, proceeded by solid phase
      • If overall test is normal, symptoms are NOT oropharyngeal in nature.
    • Treatment
      • Dietary modification and swallow exercises (speech language pathology)
  • Esophageal phase – from proximal esophagus to stomach.
    • Symptoms:  lower chest discomfort, can be to solids (mechanical blockage) or liquids (motility issue) or both solids/liquids (motility).
    • Examples:  Achalasia, systemic sclerosis, strictures, cancer, vascular dysphagia, Schatzki ring, or webs
    • Best initial test = upper endoscopy (EGD)

Pyrosis = heartburn, or regurgitation of gastric (acidic) material into esophagus.  #1 GI complaint in the US.  Think about it if symptoms occur 1 hour after eating.  Must first rule out cardiac problems!

Odynophagia = PAIN with swallowing, related to inflammation and mucosal damage.

Globus feeling = symptoms include lump/ball in throat, can be constant when patient is not swallowing.  Consider barium swallow or nasal endoscopy to rule out organic disease.

Bibliography

  • ACP MKSAP 17:  Gastroenterology and Hepatology, pgs. 1-2
  • Image:  F. Netter Anatomy illustration

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