View large version
Embed image
Transient lower esophageal sphincter relaxations Hypotensive lower esophageal sphincter — Anatomy 80% of population
5% of hernias
Paraesophageal hernias associated with abnormal laxity gastrosplenic and gastrocolic ligaments. Can develop into gastric volvulus as fixed at the GOJ and stomach rolls up into the thorax- usually organoaxial , occasionally mesenteroaxial volvulus.
GORD
Type III hernias Combine I and II. Type IV hiatus hernia - large defect in the phrenoesophageal membrane, allowing other organs to enter hernia sac. 50 to 94% of patients with GORD have a type I hiatal hernia compared to 13 to 59% of normals
-Bleeding from Cameron lesions -Respiratory complica - tions from lung compression Operations: Reduction of the herniated stomach into the abdomen. Herniotomy (excision of the hernia sac). Herniorraphy (closure of the hiatal defect). An antireflux procedure- usually a Nissen’s. Gastropexy (attachment of the stomach subdiaphrag - matically to prevent reherniation) if stomach very mobile after repair. Type II paraoesophageal hernia should always be repaired once identified. Oesophageal acid Clearance This is defined as following reflux, the period that the esophageal pH remains < 4. Normally, c learance started by peristalsis and is completed by titration of the residual acid by swallowed saliva (salivary bicarbonate). Prolongation of esophageal acid clearance occurs in 50% with oesophagitis: Pathophysiology of reflux esophagitis
ATTACK
Transient lower esophageal sphincter relaxations This is the physiological mechanism of belching. The frequency of tLESRs is greatly increased by distension of the stomach or by assuming an upright posture. Hypotensive lower esophageal sphincter LES hypotension is as a result of foods, drugs, or habits leading to GORD. Strain-induced reflux occurs when LES pressure < 4 mmHg. Free reflux seen when LES pressure is within 0 to 4 mmHg of intragastric pressure. Causes of anatomic disruption of the GOJ: Hiatal hernia and diaphragmatic sphincter in which severity of esophagitis correlates with hiatal hernia size. Hiatus hernia assoc. with a reduced threshold for eliciting tLESRs in response to gastric distension, hypotensive LES, and GOJ disruption. BMI and waist circumference which is correlated with intragastric pressure and the gastroesophageal pressure gradient. Obesity which is associated with hiatal hernia/ increased reflux symptoms/ increased frequency of tLESRs and increased proportion of tLESRs associated with acid reflux. Pregnancy and exogenous estrogen which causes heartburn in 30-50 % of pregnancies.
Oesophageal Defence Mechanisms Pepsin, bile acids, trypsin, and food hyperosmolality increases susceptibility of esophageal mucosa to acid injury. At pH 2, pepsin disrupts the histologic integrity of the mucosal barrier, increases hydrogen ion permeability, and causes hemorrhage. Pepsin's ability to cause mucosal injury is pH dependent, with maximal enzyme activity below pH 3. Bile acids less important than as acid and pepsin. Preepithelial defenses include surface mucous and bicarbo - nate that maintain a significant pH gradient between lumen and cell surface. Preepithelial defences are poorly developed in the esophagus; as a result, the pH gradient in the mucus layer is minimal or nil.
H+
Epithelieal Defense: Tight junctions and lipid rich matrix in intercellular space can slow H+ penetration with ion gradients > pH 5. Oesophageal epithelium also extrudes hydrogen ions via a Na/H exchanger; and a Na dependent Cl/HCO3 exchanger. Hydrogen ions are then buffered by extracellular bicarbonate in equilibrium with blood. Blood flow is the main postepithelial defense against acid injury. It increases in response to luminal acid, delivering more bicarbonate to the intercellular space. When the epithelial cells are no longer able to maintain intracellular pH, they lose the ability to volume regulate and cellular edema ensues. Esophageal acid injury also stimulates cell proliferation, which is observed in biopsy specimens as thickening of the basal cell layer of the epithelium. HCO3-
Affects 1. Reduces competence of the GOJ in preventing reflux 2. Compromises oesophageal acid clearance. 3. Lower threshold for tLER’s Anatomy
Reflux event frequency The dominant mechanism varies as a function of disease severity. tLESRs predominate with mild disease. Hiatus hernia and/or a weak sphincter predominate with more severe disease. Impaired osophageal emptying mechanisms: Peristaltic dysfunction, resulting in either failed or hypotensive (<30 mmHg) peristaltic contractions. Peristaltic dysfunction becoming more common with increasing severity of esophagitis. “Re-reflux" associated with hiatal hernias also impairs esophageal emptying. Salivary dysfunction Chronic xerostomia is associated with prolonged esophageal acid exposure and esophagitis. Smoking causes hyposalivation.
Non-Acid Reflux This is the reflux of gastric contents with a pH>4.0. Detection of non-acid reflux done by Multichannel intraluminal impedance and pH testing. This may cause symptoms by distention of the oesophagus rather than by acidity. "Acid reflux" , "Weakly acid" and "Weakly alkaline" are terms used with ph of <4.0, 4-7 and >7 respectvely. Non-acid reflux usually suspected if less than full response to PPI. OESOPHAGEAL
Type 1 Hiatus hernia Type 2 Hiatus herna ( Paraoesop hageal)
Before volulus After volvulus
Mechanism of tLESRs -Integrated motor response involving not only LES relaxation -Crural diaphragmatic inhibition -Oesophageal shortening by contraction of its longitudinal muscle -Contraction of the costal diaphragm -tLESRs are an active, vagally mediated reflex, rather than the result of forceful gastric distention One hypothesis is that a primary determinant of reflux disease is not an increased number of tLESRs, rather an increased proportion of tLESRs that are associated with acid reflux as opposed to only gas venting. Heartburn in pregnancy is due to both mechanical and intrinsic factors that adversely affect lower esophageal sphincter tone.
