Info
🌱 來自: Huppert’s Notes
Esophagus🚧 施工中
Esophagus
Gastroesophageal reflux disease (GERD)
• Pathophysiology: Decreased lower esophageal sphincter (LES) tone; may also have decreased esophageal motility, gastric outlet obstruction, and/or hiatal hernia
• Clinical features: Heartburn (i.e., burning sensation in the retrosternal area), regurgitation (i.e., perception of refluxed gastric content flowing up into the mouth or hypopharynx)
• Diagnosis: Treat empirically. Typically only perform EGD and/or ambulatory pH monitoring in patients who have refractory or alarm symptoms (e.g., new onset GERD at age >60 yr, dysphagia/odynophagia, weight loss, anorexia, GIB or iron-deficiency anemia, persistent vomiting, or GI malignancy in a first-degree relative)
• Treatment:
- Mild: Lifestyle modifications (e.g., weight loss, eliminate dietary triggers, avoid lying down after eating, use of a wedge pillow)
- Moderate: Add an H2 blocker
- Severe: Switch to a PPI.
• Potential side effects of PPI use: Increased risk of C. diff infection, osteoporosis, vitamin B12 deficiency
• Consider the use of a long-term PPI in patients with refractory symptoms, recurrent GI bleeds, Zollinger-Ellison syndrome, Barrett’s esophagus, severe esophagitis
- Refractory: If no improvement with empiric treatment after 8 weeks, recommend EGD. Surgical options: Laparoscopic fundoplication or bariatric surgery if obesity is contributing.
• Complications: Erosive esophagitis, stricture, Barrett’s esophagus, increased risk of esophageal cancer
Barrett’s esophagus
• Pathophysiology: Normal squamous epithelium that lines the esophagus changes to columnar epithelium with goblet cells like intestinal cells, typically due to repeated exposure to stomach acid from GERD. Can progress to esophageal adenocarcinoma.
• Diagnosis: Guidelines from various societies differ; overall, should consider screening patients with multiple risk factors for adenocarcinoma (male sex, older age, white, chronic GERD, obesity, hiatal hernia, smoking, first-degree relative with GI malignancy).
• Treatment:
- PPI indefinitely
- If no dysplasia present: Surveillance EGD every 3–5 yr
- If low- or high-grade dysplasia present: Remove with radiofrequency ablation, photodynamic therapy, cryotherapy or endoscopic resection. Perform repeat endoscopy for surveillance within 3–12 months (timing based on severity and whether the dysplasia was deemed to be eradicated)
Esophageal motility disorders
• Classification: First differentiate oropharyngeal dysphagia (difficulty initiating a swallow) vs. esophageal dysphagia (sensation of obstruction several seconds after swallowing)
• Clinical features:
- Dysphagia with solids only is often due to a mechanical obstruction
• Intermittent: Esophageal rings or webs (Plummer-Vinson syndrome, Schatzki’s ring), eosinophilic esophagitis
• Progressive with chronic heartburn/GERD, no weight loss: Peptic stricture
• Progressive, age >50 yr, weight loss: Esophageal carcinoma, Zenker’s diverticula
- Dysphagia with solids and liquids is often due to a motility problem
• Intermittent: Esophageal rings
• Intermittent, with chest pain (similar to angina pain): Diffuse esophageal spasm (DES)
• Progressive, with heartburn/GERD and skin tightening: Scleroderma
• Progressive, with regurgitation of food and saliva, weight loss: Achalasia
• Diagnosis:
- Barium swallow. Perform an EGD prior if the patient has a history of radiation, caustic injury, esophageal cancer, or stricture to avoid the risk of perforation
- EGD: Used to detect structural abnormalities
- Esophageal manometry: If the barium swallow and EGD are normal, esophageal manometry may be used to diagnose a motility disorder
• Treatment:
- EGD with dilation of strictures and rings
- Diffuse esophageal spasm: First line, PPI; second line, calcium channel blocker; third line, botulinum injection
- Achalasia: First line, dilation, surgical or endoscopic myotomy of LES; second line, botulinum injection; third line, nitrates
Esophagitis
• Infectious esophagitis: Candida albicans is the most common fungal etiology (treatment: fluconazole or itraconazole). Other etiologies include HSV (treatment: acyclovir) or CMV (treatment: ganciclovir).
• Medication-induced esophagitis: Several hours after taking oral medications (e.g., commonly occurs with alendronate, doxycycline, aspirin). Treatment: Stop offending medication if possible.
• Eosinophilic esophagitis: Typical presentation is an atopic man in mid-30s who presents with dysphagia. Diagnosis: Eosinophils on biopsy plus exclusion of other causes of eosinophils in the esophagus (including infections, medications, connective tissue diseases, esophageal Crohn’s). Treatment: PPI +/− topical steroids (delivered as orodispersible tablet or as an inhaled formulation).
Esophageal hiatal hernia
• Sliding hiatal hernias (type I): Most common type of hiatal hernia (>95%). Causes displacement of the gastroesophageal junction above the diaphragm. Typically due to benign anatomic causes. Associated with an increased risk of GERD. Treatment: No treatment unless symptomatic.
• Paraesophageal hiatal hernia (type II–IV): Less common cause of hiatal hernia (<5%). Type II involves the gastric fundus herniating through a defect in the diaphragm while the GE junction remains below the diaphragm; type III has features of both I and II; type IV involves a diaphragmatic defect large enough to allow other organs to also protrude in the hernia sac (e.g., colon, spleen, pancreas, small intestine). Complications: Volvulus, strangulation, obstruction. Treatment: Elective surgical repair if symptomatic; emergent surgical repair if volvulus, uncontrolled bleeding, obstruction, strangulation, or respiratory compromise.
Other
• Mallory-Weiss tear: Forceful vomiting causes upper GI mucosal tear; classic history is initial non-bloody emesis for several episodes followed by development of hematemesis. Treatment: EGD with thermal coagulation, Hemoclips, or band ligation.
• Boerhaave syndrome: Forceful vomiting causes esophageal transmural tear with chest pain, odynophagia, fever, subcutaneous emphysema, and possibly shock. Diagnosis: Contrast esophagram (with water-soluble gastrografin) or CT chest/abdomen/pelvis. Pleural fluid may reveal low pH, high amylase. Treatment: Admit to the ICU, NPO, IV PPI/antibiotics, drainage of fluid collection; requires thoracic surgery if evidence of clinical deterioration, extension of perforation, or certain complications.