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Gastroesophageal Reflux Disease


The principle barrier to reflux is the lower esophageal sphincter. LES comprise the lower 4cm of esophagus,where resting pressure within the lumen normally exceeds the intragastric pressure. This high intraluminal pressure at LES prevents the GE reflux. The LES is a physiological entity rather than any anatomical structure.

  1. Several factors contribute to the high intraluminal pressure of LES. (AIIMS Nov 98/ PGI Dec 01)
    1. Intrinsic musculature (Longitudinal muscle) of distal esophagus. These muscle fibres differ from those in other areas of the esophagus in that they are in a state of tonic contraction. They normally relax with initation of a swallow and then return to a state of tonic contraction.
    2. Sling fibres of the cardia Q
    3. Crura of the diaphragm
    4. Intraabdominal length of esophgaus
    5. Intraabdominal pressure The intrabdominal pressure compresses the intraabdominal segment of esophagus (ie LES) and is probably the most important factor in preventing the reflux. Q

Sphincter competence is a function of sphincter pressure, sphincter length and the length exposed to intraabdominal pressure.

In case of sliding hernia the gastroesophageal junction shifts to posterior mediastinum. The LES is then exposed
to the low intrathoracic pressure instead of the high intraabdominal pressure. The low intrathoracic pressure is unable to prevent the reflux in sliding hernia.

Other factors apart from LES which prevent the reflux.

  1. The gastro esophageal angle – the oblique entry of esophagus has a valvular effect, in that it closes the when the gastric fundus distends
  2. The folds of mucosa at the cardia helps in closing the LES when intragastric pressure rises. The intrathoracic pressure has no role I preventing reflux. Its too low (ranging from -5 to +5 mm of Hg).
  3. A functional (frequent transient LES relaxation) or mechanical problem of the LES
    (hypotensive LES) is the most common cause of GERD. Certain foods (coffee/TB, alcohol), medications (calcium channel blockers, nitrates, β blockers, Diazepam, Atropine), or hormones (progesterone) can decrease LES pressure. Obesity is a contributing factor. (PGI Dec 02, June 03)
  4. Connective tissue disease which is associated with GER is scleroderma (PGI Dec 99)
  1. Clinical Features
    Typical symptoms include the following: Heartburn/ Regurgitation/ Dysphagia:
  • Atypical
  1. Symptoms include the following:
    1. Cough and/or wheezing/ Hoarseness/ Chest pain:
  2. Imaging Studies:
    1. Barium esophagogram: It is particularly important for patients who experience dysphagia.
    2. Esophagogastroduodenoscopy: It identifies the presence and severity of esophagitis and the possible presence of Barrett esophagus and also excludes the presence of other diseases that can present similarly, such as a peptic ulcer
  3. Other Tests:
    1. Esophageal manometry
    2. This study defines the function of the LES and esophageal body (peristalsis).
    3. Ambulatory 24-hour pH monitoring (Gold standard for GER)Q(PGI June 98)
    4. Radionuclide measurement of gastric emptying
  4. Medical Care:
    Lifestyle modifications include the following:
    1. Lose weight (if overweight). Avoid alcohol, chocolate, citrus juice, and tomato-based products.
      Avoid large meals. Wait 3 hours after a meal before lying down.
    2. Elevate head side of the bed by 8 inches.
  5. Pharmacological therapy
    1. Antacids.
    2. Histamine-2 receptor antagonists.
    3. Proton pump inhibitors: used only when GERD has been objectively documented.
    4. Prokinetic agents
  6. Surgical Care:
    Indications for fundoplication include the following:
    1. Patients with symptoms incompletely controlled by proton pump inhibitor.
    2. The presence of Barrett esophagus is an indication for surgery.
    3. Presence of extraesophageal manifestations of GERD may indicate the need for surgery. These include (1) respiratory manifestations (cough, wheezing, aspiration); (2) ear, nose, and throat manifestations (hoarseness, sore throat, otitis media); and (3) dental manifestations (enamel erosion).
  7. Complications:
    The squamous epithelium responds to acid by summoning lymphocytes and neutrophils to the sub- epithelial layers. The resulting mucosal damage and loss of the surface squamous cells then promotes frank ulceration, fibrosis and stricture formation.

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