Dyspepsia and upper gastrointestinal bleeding Dr. Wayne H.C. Hu 胡興正
25 year old medical student Occasional smoker and drinker. About to take final examinations. 3 week history of epigastric bloating. Worse after meals, early satiety. Appetite fair, lost 0.5 Kg in weight. No night pain. No malaena/ haematemesis. Occasional acid regurgitation.
Findings Physical examination normal apart from mild epigastric tenderness on palpation. CBP, liver and renal function tests normal.
s None s AXR s Helicobacter testing s Endoscopy s Barium meal s Ultrasound abdomen Investigations?
Dyspepsia Very common complaint 19%-30% of population have dyspepsia (Hu( et al 1997) Causes: Peptic ulcer, Erosions, Gastric cancer, Gastroparesis,, Functional dyspepsia, Pancreatic cancer (radiates to back) etc.
Causes of upper abdominal discomfort: Non-GI Abdominal wall pain: worse on movement, sitting up, sharp localised pain Angina: pain related to exertion, may be after meals, radiation to the shoulder and throat Myocardial infarction: Constant severe pain, acute onset
Causes of upper abdominal discomfort: GI tract Acute pancreatitis: radiation to the back, acute onset Biliary colic: right sided, onset 30-60 minutes after meal intake (cholecystokinin( release and gallbladder contraction), relation to fatty foods
Ductal stone: central pain, spontaneous pain or pain after meals, ultrasound or CT may NOT show small stones Easily confused with stomach pain Ductal stone
Causes of upper abdominal discomfort: GI tract Gastric cancer Peptic ulcer Functional dyspepsia Irritable bowel syndrome: better after bowel movement
Dyspepsia 26% 23% 31% 19% 34%
Diagnosis of dyspepsia Make sure the patient has dyspepsia rather than biliary,, large intestinal, cardiac pain etc. Overall,, functional dyspepsia is the commonest cause. Must not miss cancer- fatal if untreated. Duodenal ulcer may respond to empirical treatment with anti-secretive therapy or H. pylori eradication.
Alarm symptoms- suggest organic Weight loss Malaena/ haematemesis Vomiting Dysphagia Anaemia Lymphadenopaathy Abdominal mass/ liver Old age disease
Approach to dyspepsia Exclude alarm symptoms. Endoscopy + other investigations if present. Empirical treatment: antacids, H2 antagonists if young. Endoscopy if alarm symptoms, age over 45, or poor response to empirical treatment.
Approach to dyspepsia?empirical endoscopy: costs similar to empirical treatment in various studies. H. pylori testing and eradication: treats ulcers, functional dyspepsia?benefit. Reflux worsened by H. pylori eradication. Similar benefit to symptoms.
Treatment of functional dyspepsia Disease of relapse and remissions. High placebo response rate may be related to the natural remission of the disease. Antacids etc. good and cheap placebo. Useful as first line treatment.
Treatment of functional dyspepsia Careful explanation and reassurance. Symptomatic relief and attention to co-morbid factors like anxiety, stress etc. Underlying psychiatric disorders: cognitive therapy to modify beliefs, antidepressant, anxiolytic drugs.
Drug treatment: prokinetics Metoclopramide: : not for longterm use. Sedation and extrapyramidal side-effects. effects. Domperidone: : does not cross the blood-brain brain barrier.
Drug treatment: acid suppression H2 antagonists not very useful compared to placebo. Proton pump inhibitors better efficacy especially in those with ulcer symptoms. Useful if there is co-existing reflux. Expensive
Primary Management of New Onset Uninvestigated Dyspepsia Asia-Pacific Region Exclude by history: biliary pain, irritable bowel, reflux DYSPEPSIA If <2-4 weeks: Dietary advise & observe Review current medication Treatment Trial: Anti-secretory therapy or Prokinetic Duration: <2-4weeks NO Failure or Relapse after early response Locally-validated Hp test ( ulcer test ) Positive Eradication therapy Negative Alarm features? Strong fear of serious disease? Chronic NSAID use in therapeutic doses? **Age > 45 years? FUNCTIONAL DYSPEPSIA Dysmotility-like: Prokinetic Ulcer-like: Anti-secretory drug Non-specific: Prokinetic or Anti-secretory Evaluate after 4 weeks YES Negative Investigate: Endoscopy Positive Structural disease e.g. ulcer, cancer, oesophagitis Treat appropriately SUCCESS FAILURE SUCCESS Change to another class of therapy Final evaluation after 8 weeks FAILURE Specialist referral FOLLOW UP FAILURE ** Age cut-off varies with age-specific incidence of gastric cancer in each country (35-55 Yrs) Reference: N. Talley, SK Lam, KL Goh and KM Fock. Management guidelines for uninvestigated and functional dyspepsia in the Asia-Pacific region: First Asian Pacific working party on functional dyspepsia. Journal of Gastroenterology and Hepatology (1998) 13
Primary Management of New Onset Uninvestigated Dyspepsia Asia-Pacific Region DYSPEPSIA Treatment Trial: Anti-secretory therapy or Prokinetic Duration: <2-4weeks NO Alarm features? Strong fear of serious disease? Chronic NSAID use in therapeutic doses? **Age > 45 years? SUCCESS 1
Primary Management of New Onset Uninvestigated Dyspepsia Asia-Pacific Region DYSPEPSIA Treatment Trial: Anti-secretory therapy or Prokinetic Duration: <2-4weeks NO Alarm features? Strong fear of serious disease? Chronic NSAID use in therapeutic doses? **Age > 45 years? Failure or Relapse after early response Locally-validated Hp test ( ulcer test ) Negative Positive Eradication therapy FUNCTIONAL DYSPEPSIA Dysmotility-like: Prokinetic Ulcer-like: Anti-secretory drug Non-specific: Prokinetic or Anti-secretory SUCCESS FAILURE 2
Primary Management of New Onset Uninvestigated Dyspepsia Asia-Pacific Region DYSPEPSIA Alarm features? Strong fear of serious disease? Chronic NSAID use in therapeutic doses? **Age > 45 years? YES Negative Investigate: Endoscopy FUNCTIONAL DYSPEPSIA Dysmotility-like: Prokinetic Ulcer-like: Anti-secretory drug Non-specific: Prokinetic or Anti-secretory Evaluate after 4 weeks SUCCESS SUCCESS Change to another class of therapy Final evaluation after 8 weeks FAILURE 3
Dyspepsia: Pain or discomfort centered in the upper abdomen. Functional dyspepsia: No definite structural or biochemical explanation for the dyspepsia Definitions
Symptoms of functional dyspepsia Epigastric pain syndrome: pain or burning, hunger pain, relief with food, not relieved by bowel movement Postprandial distress syndrome: bloating, gaseousness after meals, early satiety A lot of overlap between groups Associated with reflux and irritable bowel syndrome.
Dyspepsia subgroups Ulcer-like (epigastric pain) 17% 1% 9% Dysmotility-like (postprandial distress) 3% 18% 9% Talley NJ et al.gastroenterology 1993 16% Reflux -like Non-specific 27%
Dyspeptic symptoms Do not reliably distinguish between functional and organic disease. Severe bloating, nausea and vomiting suggests delayed gastric emptying.
Predominant symptom Epigastric pain (ulcer like dyspepsia) Pain most bothersome symptom. Postprandial distress (Dysmotility( like dyspepsia) Unpleasant or troublesome non-painful sensation most bothersome. Associated with fullness, early satiety, bloating, nausea. Unspecified dyspepsia
Treatment response Proton-pump inhibitor response in those with predominant pain. 60 50 40 30 20 Losec 20 Losec 10 Placebo 10 Talley Aliment Pharmacol Ther 1998 0 Pain Dysmotility
Aetiology of functional dyspepsia?? Motility disorder: delayed gastric emptying, failure of fundus to relax after meal. Sensory disorder: hypersensitivity to intragastric balloon distension.
Radiolabelled meal ingestion 60 50 40 30 20 Dyspeptics Controls 10 0 Proximal Distal Troncon et al Gut 1994
Air insufflation (400ml) 25 20 15 10 No Pain Pain 5 0 Dyspeptic Control Lemann et al Dig Dis Sci 1991
Aetiology of functional dyspepsia?? Acid secretion??: Probably does not play a role. No difference in basal and stimulated acid output. H. pylori??: Controversial. No difference in prevalence between dyspeptics and non- dyspeptics. However one study showed long- term benefit after eradication; but another multi- centered study showed the opposite.
H. pylori in blood donors 30 25 20 15 10 Hp+ Hp- 5 0 Dyspepsia Nignt pain Pain after meals Reflux Holtmann Dig Dis Sci 1994
Aetiology of functional dyspepsia?? Gastritis: Not a cause of dyspepsia! No difference in non-erosive gastritis among dyspeptics and non-dyspeptics. Gastric and duodenal erosions probably belong to the spectrum of ulcer disease.
Aetiology of functional dyspepsia?? Psychological??: Psychological morbidity very common in patients in specialist clinics (depression, anxiety etc.) Increased symptoms with stress.
Aetiology of functional dyspepsia?? Dyspeptics in the community may not be different psychologically to normals.. Anxiety affects doctor-seeking behaviour.
7 Anxiety and Depression 6 5 Mean Score 4 3 2 Normal Dyspepsia IBS 1 0 Anxiety score p<0.05 Depression score p<0.05 Hu et al 1997
Psychological morbidity determines health seeking 5 4.5 4 3.5 3 2.5 2 1.5 1 0.5 0 Anxiety Deperession Consulter Non-consulter Hu et al 1997
Gastrointestinal Bleeding: Why and how Wayne H.C. Hu Hu 胡興正 Specialist in Gastroenterology and Hepatology
Outline Clinical considerations Investigations of upper GI bleeding Non-variceal bleeding Variceal bleeding
Upper GI bleed: Definition Origin proximal to the ligament of Trietz Present as haematemesis, coffee-ground vomiting, PR bleeding if rapid blood loss
Upper GI bleed: Epidemiology 300,000 admissions annually in USA 5x more common than lower GI bleeding Mortality 7-10% 7 Stable mortality rate over the last 30 years
Management principals Assessment and stabilisation of haemodynamic state Stop the bleeding Treat the underlying abnormality Prevent recurrent bleeding
Assessment History: previous ulcer, aspirin and NSAID intake Examination: haemodynamic state, signs of liver disease
Poor prognostic factors Increasing age Comorbid medical condisions Variceal bleed Fresh blood in vomit or stool Shock Active bleeding at endoscopy Large (>2cm) ulcer Onset of bleeding in hospital Emergency surgery
Minor bleeding Haemodynamic state Loss <10% intravascular volume No haemodynamic change Moderate bleeding Loss 10-20% intravascular volume Postural hypotension
Severe bleed Haemodynamic state Loss>20% intravascular volume Shock and tachycardia
Common Gastric ulcer Duodenal ulcer Mallory-Weiss tear Varices Causes of bleeding
Causes of bleeding Less common Dieulafoy s lesion Gastric antral vascular ectasia Portal hypertensive gastropathy Neoplasia Oesophagitis Gastric erosions
Hereditary haemorrhagic telangiectasia
Endoscopy
Endoscopic evaluation Repeat endoscopy may be indicated: 35% of obscure bleeding have definite source on repeat OGD. At enteroscopy,, lesion that should have been identified at OGD in 28%-75% of patients.
Small bowel investigations Enteroscopy Barium meal and follow-through Small bowel enema (enteroclysis( enteroclysis) Capsule endoscopy
Barium studies Ba meal and follow- through less invasive. Small bowel enema require intubation but more sensitive. Difficult to detect small ulcers and bleeding vessels.
Capsule endoscopy 1999: first wireless capsule endoscope used in a human volunteer. Capsule consists of battery, camera, flash and transmitter. 2 pictures/ second transmitted to receiver worn on body.
1. Capsule Ø11 mm 26 mm Ø11 mm SB ESO 20 min operating time: 10 min @ 13.8 FPS 10 min @ 4 FPS Antenna Gilo-4 Gulp-1 Dome Dome Optics PCB Batteries Spacer Cover Optics
Data recorder worn on belt Sensors applied to abdomen with adhesive pads Preparation
Main Screen Minimized View Video Control Localization Suspected blood Indications (to show, first mark first duodenal image landmark) Passage Times (Gastric & small bowel) Marker indicating location in study Captured Thumbnails
Capsule endoscopy findings Angiodysplasia Small bowel ulcer
Double-balloon balloon enteroscopy Therapy possible. Enteroscope advanced either orally or per rectum. Sequential inflation of balloons to aid intubation.
Double-balloon balloon enteroscopy
Technetium red cell scan RBC labelled with 99Tc. Detects bleeding 0.1-0.4ml/min. Positive in 50% of lower GI bleeding. Alternate test usually needed before intervention.
Detects bleeding >0.5ml/min. Positive in 50% of lower GI bleeds overall, 60-70% when actively bleeding. Administration of vasodilators, anticoagulants increase yield. Angiography
Therapy during angiography Vasopressin infusion, embolisation. Blue dye injection into bleeding vessel aids identification during surgery.
Peptic Ulcer
Stigmata Stigmata of bleeding Rebleeding risk Spurting vessel 90-100% Visible vessel 50% Adherent clot 30-35% Oozing from ulcer 10-27% Flat spot <8% Clean base <3%
Spurting vessel
Visible vessel
Flat spots
Clean base
Endoscopic therapy Indicated for active bleeding/ spurting and visible vessel Benefit demonstrated for removing adherent clot and treating underlying lesion Flat spots and slow oozing alone not shown to benefit from treatment
Injection Adrenaline Sclerosant Thermal Endoscopic treatment Non-contact: laser and argon plasma Contact thermal probe BICAP probe Metallic clips
Injection
Laser and argon plasma Heating of tissue protein Contraction of arterial wall Laser therapy require direct path and accurate aiming Argon plasma cogulation useful for mucosal bleeding but not ulcer vessel
Argon plasma coagulator
Heater probe Seals the vessel Firm tamponade needed Endpoint is footprint at site of vessel
Heater probe
Metallic clips Difficult to apply tangentially Effective for arterial bleeding
Second-look endoscopy Repeat endoscopy after initial treatment Repeat treatment if stigmata of bleeding +ve+ Reduction of rebleeding rate
Drug treatment Regular dose H2A does not affect bleeding Continuous high dose PPI infusion may lower acid and stabilise the clot, reduce rebleeding H pylori eradication if positive
Variceal bleeding
Risk of bleeding Larger size (>5mm) Red wale marking Red colour sign Advanced cirrhosis Co-existing gastric varices
Injection sclerotherapy First described in 1939 Injection of substances causing thrombosis, inflammation and fibrosis of varix Cyanoacrylate glue superior for gastric variceal bleeding
Band Ligation Varix approached and sucked into chamber as possible Rubber band released Used for oesophageal varices
Drug therapy Somatostatin/ octreotide Vasopressin Beta blockers May be used as adjuvant to endoscopic haemostasis
Summary GI bleeding sources usually identified by endoscopy Repeat endoscopy may be useful if initially negative Capsule endoscopy and enteroscopy for suspected small bowel lesions Multiple modalities for treatment, comparable efficacy
Summary Sclerotherapy or banding for oesophgeal varices Tissue glue for gastric varices