Git Gerd 08.
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Git Gerd 08.



Medical college lectures: GIT 4th year.

Medical college lectures: GIT 4th year.



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Git Gerd 08. Presentation Transcript

  • 1. Gastroesophageal Reflux Disease (GERD)
    • Any symptoms or esophageal mucosal damage,causing discomfort, that results from reflux of gastric acid into the esophagus
    • GERD resulting in heartburn affects 30% of the general population
    • Classic GERD symptoms
      • Heartburn (pyrosis): substernal burning discomfort
      • Regurgitation: bitter, acidic fluid in the mouth when lying down or bending over
  • 2. High Prevalence of Gastroesophageal Reflux Symptoms
  • 3.  
  • 4. Important Reasons to Diagnose and Treat GERD
    • Negative impact on health-related quality of life 1
    • Risk factor for esophageal adenocarcinoma 2
    • Revicki et al. Am J Med 1998;104:252.
    • Lagergren et al. N Engl J Med 1999;340:825.
  • 5. Pathophysiology:
    • Occasional episodes of GERD are common in health.
    • Reflux is normally followed by oesophageal peristaltic waves which efficiently clear the eso, alkaline saliva neutralises residual acid& symptoms do not occur.
    • GERD develops when the oesophageal mucosa is exposed to gastric contents for prolonged periods of time, resulting in symptoms & in a proportion of cases, oesophagitis.
    • Several factors are known to be involved:
  • 6.  
  • 7. 1.AbnormaL LES:
    • In health, LES is tonically contracted, relaxing only during swallowing.
    • Some patients with GERD have reduced LES, permitting reflux when intra-abdominal pressure rises.
    • In others, basal sphincter tone is normal but reflux occurs in response to frequent episodes of inappropriate sphincter relaxation
  • 8. 2.HH:
    • Hiatus hernia causes reflux because:
    • A. The pressure gradient between the abdominal & thoracic cavities, which normally pinches the hiatus, is lost.
    • B. The oblique angle between the cardia& oesophagus disappears.
    • Many patients who have large hiatus hernias develop reflux symptoms, but the relationship between the presence of a HH& symptoms is poor.
    • Hiatus hernia is very common in individuals who have no symptoms& some symptomatic patients have only a very small or no hernia.
    • Nevertheless, almost all patients who develop oesophagitis, Barrett's oesophagus or peptic strictures have a hiatus hernia.
  • 9. 2.HH:
    • Herniation of the stomach through the diaphragm into the chest
    • Occurs in 30% of the population > 50 years
    • Often asymptomatic
    • Heartburn & regurgitation can occur
    • Gastric volvulus may complicate large para-oesophageal hernias
  • 10.  
  • 11. 3.Delayed oesophageal clearance :
    • Defective oesophageal peristaltic activity is commonly found in patients who have oesophagitis.
    • It is a primary abnormality, since it persists after oesophagitis has been healed by PPI.
    • Poor oesophageal clearance leads to increased acid exposure time.
  • 12. 4.Gastric contents
    • Is the most important oesophageal irritant& there is a close relationship between acid exposure time & symptoms.
  • 13. 5. Defective gastric emptying
    • Gastric emptying is delayed in GERD.
    • The reason for this is unknown.
  • 14. 6. Others
    • Recent attention on the importance of duodenogastro-oesophageal reflux, containing bile, pancreatic enzymes&pepsin in addition to acid.
  • 15. 7. Increased inra abd pressure:
    • Pregnancy
    • Obesity: Weight loss may improve symptoms
  • 16. 6. Diet / environmental factors :
    • Dietary fat, chocolate, alcohol , coffee relax LES & provoke symptoms.
    • There is little evidence to incriminate smoking or NSAIDs as a causes.
  • 17. Clinical features
    • The major symptoms are heartburn /regurgitation, often provoked by bending, straining or lying down.
    • 'Waterbrash‘: salivation from reflex salivary gland stimulation as acid enters the eso, is often present.
    • A history of weight gain is common.
    • Some patients are woken at night by choking as refluxed fluid irritates the larynx.
    • Others develop odynophagia or dysphagia.
    • A few present with atypical chest pain which may be severe, can mimic angina probably due to reflux-induced oesophageal spasm.
  • 18. Clinical features
    • Classic GERD
    • Extraesophageal/Atypical GERD
    • Complicated GERD
    Clinical Presentations of GERD
  • 19.  
  • 20. Extraesophageal Manifestations of GERD
    • Pulmonary
      • Asthma
      • Aspiration pneumonia
      • Chronic bronchitis
      • Pulmonary fibrosis
    • Other
    • Chest pain
    • Dental erosion
    • ENT
      • Hoarseness
      • Laryngitis
      • Pharyngitis
      • Chronic cough
      • Globus sensation
      • Dysphonia
      • Sinusitis
      • Subglottic stenosis
      • Laryngeal cancer
  • 21. Potential Oral & Laryngopharyngeal Signs Associated with GERD
    • Edema /hyperemia of larynx
    • Vocal cord erythema, polyps, granulomas, ulcers
    • Hyperemia & lymphoid hyperplasia of posterior pharynx
    • Interarytenyoid changes
    • Dental erosion
    • Subglottic stenosis
    • Laryngeal cancer
    Vaezi MF, Hicks DM, Abelson TI, Richter JE. Clin Gastro Hep 2003;1:333-344.
  • 22. Pathophysiology of Extraesophageal GERD
  • 23. Complications: 1. Oesophagitis
    • A range of endoscopic findings, from mild redness to severe. With bleeding, ulceration &stricture formation.
    • There is a poor correlation between symptoms, histological &endoscopic findings.
    • Significant GERD may be present despite normal endoscopy / normal oesophageal histology.
  • 24. Complications: Oesophagitis
  • 25. Complications:2.Barrett's oesophagus
    • ‘ Columnar lined oesophagus'-CLO, is a pre-malignant glandular intestinal metaplasia of the lower oeso, in which the normal squamous lining is replaced by columnar mucosa.
    • Occurs as an adaptive response to chronic GERD,found in 10% undergoing gastroscopy for reflux symptoms.
    • CLO is the major risk factor for oesophageal adenocarcinoma, with a lifetime cancer risk of 10%, more closely related to the severity& duration of reflux rather than the CLO per se.
    • The cancer incidence is estimated at 1/200 patient years (0.5% /year), being low& > 95% with CLO die of causes other than oesophageal cancer.
    • Prevalence is increasing, more in men (especially white) &> 50.
    • It is weakly associated with smoking but not alcohol.
    • E-cadherin polymorphisms, p53 mutations, TGF-β, EGF receptors, COX-2& TNF-α may play roles.
  • 26. Barrett Diagnosis:diagnosis
    • Requires multiple systematic biopsies to maximise the chance of detecting intestinal metaplasia /or dysplasia.
  • 27. Barret:Management
    • Neither PPI nor antireflux surgery will stop progression or induce regression of CLO& treatment is only indicated for symptoms of reflux or complications such as stricture.
    • Endoscopic ablation therapy or photodynamic therapy can induce regression but 'buried islands' of glandular mucosa may persist underneath the squamous epithelium& cancer risk is not eliminated.
    • At present these therapies remain experimental but show promise; they are also used in patients with high-grade dysplasia (HGD) or early malignancy who are not suitable for surgery.
  • 28. Barret: Management
    • Regular endoscopic surveillance can detect dysplasia& malignancy at an early stage & improve 2-year survival but, because most CLO is undetected until cancer develops, surveillance strategies are unlikely to influence the overall mortality rate of oesophageal cancer.
    • Surveillance is expensive &cost-effectiveness conflicting.
    • Surveillance is currently recommended every 2-3 years for those without dysplasia & at 6-12-monthly intervals for those with low-grade dysplasia.
    • Oesophagectomy is widely recommended for those with HGD as the resected specimen harbours cancer in up to 40%.
    • Recent data suggest that HGD often remains stable & may not progress to cancer, at least in the medium term.
    • Close follow-up with biopsies every 3 months is an alternative strategy for those with HGD.
  • 29. Complications:3. IDA
    • Occurs as a consequence of chronic, insidious blood loss from long-standing oesophagitis.
    • Almost all such patients have a large hiatus hernia& bleeding can occur from subtle erosions in the neck of the sac ('Cameron lesions
  • 30. Complications: 4.Benign oesophageal stricture
    • Develop as a consequence of long-standing oesophagitis.
    • Most elderly & have poor oesophageal peristaltic activity.
    • Present with dysphagia which is worse for solids than liquids.
    • Bolus obstruction following ingestion of meat causes absolute dysphagia.
    • A history of heartburn is common but not invariable;as in many elderly patients.
    • Diagnosis is made by endoscopy, with biopsies to exclude Cancer.
    • Endoscopic balloon dilatation or bouginage is helpful.
    • Subsequently, long-term therapy with a PPI at full dose should be started to reduce the risk of recurrent oesophagitis & stricture formation.
  • 31. GERD:Investigations
    • Young patients with typical symptoms, without worrying features such as dysphagia, weight loss or anaemia, can be treated empirically without investigation.
    • Investigation is advisable if patients present in middle or late age, if symptoms are atypical or if a complication is suspected.
    • Endoscopy is the investigation of choice, performed to exclude other upper GI diseases & identify complications.
    • A normal endoscopy in a patient with compatible symptoms should not preclude treatment for GERD.
    • Twenty-four-hour pH monitoring is indicated if, despite endoscopy, the diagnosis is not clear.
    • A pH of < 4 for > 6-7% of the study time is diagnostic of GERD.
  • 32.  
  • 33. When to Perform Diagnostic Tests
    • Uncertain diagnosis
    • Atypical symptoms
    • Symptoms associated with complications
    • Inadequate response to therapy
    • Recurrent symptoms
    • Prior to anti-reflux surgery
  • 34. Diagnostic Tests for GERD
    • Barium swallow
    • Endoscopy
    • Ambulatory pH monitoring
    • Esophageal manometry
  • 35. Barium Swallow
    • Useful first diagnostic test for patients with dysphagia
      • Stricture (location, length)
      • Mass (location, length)
      • Bird’s beak
      • Hiatal hernia (size, type)
    • Limitations
      • Detailed mucosal exam for erosive esophagitis, Barrett’s esophagus
  • 36. Endoscopy
    • Indications for endoscopy
      • Alarm symptoms
      • Empiric therapy failure
      • Preoperative evaluation
      • Detection of Barrett’s esophagus
      • Detect grade: LA grading classification system for GERD.
  • 37. The LA Classification system – Grade A reflux esophagitis Stomach Grade A : One (or more) mucosal break, no longer than 5 mm, that does not extend between the tops of two mucosal folds.
  • 38. The LA Classification system – Grade B reflux esophagitis Stomach Grade B : One (or more) mucosal break, more than 5 mm long, that does not extend between the tops of two mucosal folds.
  • 39. The LA Classification system – Grade C reflux esophagitis Stomach Grade C : One (or more) mucosal break that is continuous between the tops of two or more mucosal folds, but which involves less than 75% of the circumference.
  • 40. The LA Classification system – Grade D reflux esophagitis Stomach Grade D : One (or more) mucosal break that involves at least 75% of the esophageal circumference.
  • 41. Ambulatory 24 hr. pH Monitoring
    • Physiologic study
    • Quantify reflux in proximal/distal esophagus
      • % time pH < 4
      • DeMeester score
    • Symptom correlation
  • 42. Ambulatory 24 hr. pH Monitoring Normal GERD
  • 43. Wireless, Catheter-Free Esophageal pH Monitoring
    • Improved patient comfort / acceptance
    • Continued normal work, activities&diet study
    • Longer reporting periods possible (48 hours)
    • Maintain constant probe position .
    Potential Advantages
  • 44. Esophageal Manometry
    • Assess LES pressure, location / relaxation
      • Assist placement of 24 hr. pH catheter
    • Assess peristalsis
      • Prior to antireflux surgery
    Limited role in GERD
  • 45. Treatment Goals for GERD
    • Eliminate symptoms
    • Heal esophagitis
    • Manage or prevent complications
    • Maintain remission
  • 46. Management: Life-style
    • Weight loss
    • Avoidance of dietary items that worsen symptoms.
    • Elevation of the bed head in those who experience nocturnal symptoms
    • Avoidance of late meals
    • Modify diet
      • Eat more frequent but smaller meals
      • Avoid fatty/fried food, peppermint, chocolate, alcohol, carbonated beverages, coffee and tea.
    • Avoid eating within 2-3 hours of bedtime.
    • Giving up smoking.
  • 47. Management: antacids
    • Proprietary antacids &alginates also provide symptomatic benefit.
    • H2-receptor antagonist drugs also help symptoms without healing oesophagitis.
    • PPI are the treatment of choice for severe symptoms &for complicated reflux disease
    • PPI are better than H2Bs in healing oesophagitis& relieving symptoms.
    • Symptoms almost invariably resolve& oesophagitis heals in the majority of patients.
    • Recurrence of symptoms is common when therapy is stopped& some require life-long treatment at the lowest acceptable dose.
  • 48. Effectiveness of Medical Therapies for GERD Treatment Response Lifestyle modifications/antacids 20 % H 2 -receptor antagonists 50 % Single-dose PPI 80 % Increased-dose PPI up to 100 %
  • 49. Treatment Modifications for Persistent Symptoms
    • Improve compliance
    • Optimize pharmacokinetics
      • Adjust timing of medication to 15 – 30 minutes before meals (as opposed to bedtime)
      • Allows for high blood level to interact with parietal cell proton pump activated by the meal
    • Consider switching to a different PPI as esmo or rebeprazol.
  • 50. GERD is a Chronic Relapsing Condition
    • Esophagitis relapses quickly after cessation of therapy
      • > 50 % relapse within 2 months
      • > 80 % relapse within 6 months
    • Effective maintenance therapy is imperative
    • Prevalence: higher.
    • Severity of symptoms: does not correlate with the degree of mucosal inflammation.
    • Complications: late complications as peptic strictures or bleeding from oesophagitis are more common.
    • Recurrent pneumonia: consider aspiration from occult GERD.
  • 52.  
  • 53. Erosive Esophagitis
  • 54. Peptic Stricture Barium Swallow Endoscopy
  • 55. Esophageal Stricture: Dilating Devices
  • 56. TTS Balloon Dilation of a Peptic Stricture
  • 57. Barrett’s Esophagus
  • 58. Esophageal Cancer Barium Swallow Endoscopy
  • 59.  
  • 60. When to Discuss Anti-Reflux Surgery with Patients
    • Intractable GERD – rare
      • Difficult to manage strictures
      • Severe bleeding from esophagitis
      • Non-healing ulcers
    • GERD requiring long-term PPI-BID in a healthy young patient
    • Persistent regurgitation/aspiration symptoms
    • Not Barrett’s esophagus alone
  • 61. Endoscopic GERD Therapy
    • Endoscopic antireflux therapies
      • Radiofrequency energy delivered to the LES
        • Stretta procedure
      • Suture ligation of the cardia
        • Endoscopic plication
      • Submucosal implantation of inert material in the region of the lower esophageal sphincter
        • Enteryx
  • 62. Time is cruel: