gastrointestinal diseases and abnormalities in...

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Gastrointestinal Diseases and Abnormalities in Adult

Marcellus Simadibrata K MD PhD SpPD KGEH

Division Gastroenterology Department of Internal Medicine Faculty of Medicine University of Indonesia

Lecture Module Gastrointestinal May 2007

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Introduction• Gastrointestinal Diseases and Abnormalities:

Upper and Lower• Emergency in Gastroenterology need good

diagnosis and rapid treatment• UPPER GASTROINTESTINAL TRACT: Esophagus-Gaster-Duodenum-Proximal

Jejunum-Treitz ligament• LOWER GASTROINTESTINAL TRACT” Treitz ligament-Distal Jejunum-Ileum-Colon-

Anus

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Diseases of the upper gastrointestinal tract:

• Syndrome of Dyspepsia• Gastroesophageal Reflux Disease(GERD)• Dysphagia• Peptic Ulcer• Upper gastrointestinal bleeding(Hematemesis-

Melena)• Polyp and Cancer of the gaster/duodenum• Cholangitis• Bile duct Stone• Pancreatitis

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Diseases of the lower gastrointestinal tract:

• Diarrhea• Irritable Bowel Syndrome• Collitis Infective-Non Infective• Inflammatory Bowel Disease• Polyp and Cancer of the Colon• Hemoroid

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Syndrome of Dyspepsia

• Definition of Dyspepsia: persistent or recurrent upper abdominal pain or discomfort characterized by postprandial fullness, early satiety, nausea, and bloating.

• Classification: Functional and organic dyspepsia, or ulcer and non ulcer dyspepsia(NUD)

Functional: dysmotility like, ulcer like, non-specific, (reflux like). Functional: no organic diseases.

Organic(with x-ray or endoscopy): peptic ulcer of the gaster-duodenum, cancer gaster-duodenum, severe gastritis-duodenitis.

Nud: no ulcer on x-ray or endoscopy. The reflux like dyspepsia has been already categorized in Gastro-esophageal reflux disesase(GERD).

• Epidemiology: Each year 10-20% of US population seeks medical attention. NUD 2-3 x peptic ulcer disease.

• Etiology & Pathogenesis: Etiology/pathogenesis : Imbalance of the aggravating factors and defensive factors. The aggravating/agresive factor increased and the defensive factors decrease will cause functional and organic /ulcer dyspepsia.

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Aggravating/agresive factors of syndrome dyspepsia:

• Gastric acid • Pepsin• Helicobacter pylori infection• Gastric motor activity: 25-50% patients exhibit postprandial antral

hypomotility or delayed gastric emptying• Psychological factors: anxiety and depression• Diet: foods: spicy/hot, sour, vinnegar, drinks: coffee,

smoking/tobacco, alcohol • Drugs: non-steroidal anti-inflammatory drugs(nsaid), traditional pain

killer drugs, steroids, antibiotics(erythromycin, ampicillin), iron, potassium, digoxin, theophylline.

• Metabolic diseases: diabetes mellitus, hypothoroidism• Hypopotassemia.• Free radicals

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Defensive factors of syndrome dyspepsia:

• Prostaglandin• Mucus• Mucosal blood flow• Surfactant• Bicarbonat• Heat shock protein• Epitel/preepithelial factors• etc

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Clinical features in syndrome dyspepsia

• NUD: 1. ulcerlike: dominant epigasric pain, relieved by antacids or food

2. dysmotility like: epigastric discomfort aggravated by food or associated with early satiety, fullness, nausea, retching, vomiting, or bloating.

3. nonspecific:symptoms does not fit the other categories

(4.reflux like:hrartburn and regurgitation)• Ulcer: the same with NUD

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Physical examination in syndrome dyspepsia

• not specific• epigastric tenderness some times• abdominal mass if advanced gastric

carcinoma

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Findings and diagnostic findings in syndrome dyspepsia:

• routine: blood, stool(occult blood test, parasites), amylase-lypase to exclude pancreatitis, liver function test to excluce liver cirrhosis or obstructive jaundice.

• upper gastrointestinal endoscopy: should be performed if patients older than 45 years or in those with alarm symptoms: weight loss,hemorrhage, dysphagia, vomiting, jaundice or patients who consumed NSAID. Biopsy for histopathological examination of malignancy or helicobacter pylori.

• Double contrast upper gastrointestinal barium radiography• Gastric scintigraphy: gastric gastroparesis/motility• Helicobacter pylori serology examination.• Ultrasound/CT-scan: to exclude gallbladder/biliary

stone/malignancies, pancreatitis.

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Management of Syndrome Dyspepsia:

• Avoid/stop -decrease the aggravating/agresive factors, increase the defensive• Factors.• Young patients < 45 years, no alarm symptoms nor NSAID consumer: empiric

therapy 2-4 weeks. Empiric therapy according the symptoms. Ulcer like: antacids or h2 receptor antagonist or proton pump inhibitor. Dysmotility like: prokinetic or h2 receptor antagonist. Nonspecific: antifatulent antacids, simethicone, antianxiety-depression.

• Peptic ulcer: H2RA or PPI with/without cytoprotector• H2 receptor antagonists: cimetidine 3 x 200 mgday, ranitidine 2 x 150 mg/day,

famotidine 2 x 20 mg/day, roxatidine 2 x 150 mg/day• Proton pump inhibitor: omeprazole 1-2 x 20 mg/day, lansoprazole 1-2 x 30 mg/day,

pantoprazole 1-2 x 40 mg/day, esomeprazole 1-2 x 20 mg/day, rabeprazole 1-2 x 10 mg/day

• Cytoprotector: sucralfate 3-4x500-1000 mg/day, cetraxate 2-3x1/day, misoprostol(exogen prostglandin) 2x1/day, tephrenone 3 x 50 mg/day, rebamipide 3 x 100 mg/day.

• Prokinetic agents: metoclopramide 2-3 x 5-10 mg/day, domperidone 2-3 x 1 tab/day, cisapride 2-3 x 5 mg/day

• Upper GI malignancies: operation(consult to the surgeon).

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DISPEPSIA

Usia < 45 th tanpa Usia > 45 th atau < 45 th dng tandabahayatanda bahaya Riwayat pemakaian OAINS kronik

Riwayat kanker pada keluarga

Terapi empirik dispepsia(-) Terapi Tanda bahaya2 mg: dihentikan muntah hebat

demamhematemesis

Dispepsia(+) anemiaikterus

Serologi(tervalidasi lokal) berat badan turun

Hasil(+) Hasil(-)

Endoskopi

Sarana endoskopi(-)

UBT/HpSA

Hasil(-) Hasil(+) Terapi eradikasi RUJUKinternis, internis plus, gastroenterolgis

Gagal atau dokter anak dengan fasilitasendoskopi

KonsensusKonsensus NasionalNasional PenatalaksanaanPenatalaksanaan InfeksiInfeksi Helicobacter pylori 2003Helicobacter pylori 2003

Skema 1. Penatalaksanaan pasien di pelayanan kesehatan lini pertama

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DISPEPSIAumur > 45 thtanda bahayagagal terapi

Riwayat ulkus peptik + komplikasiPermintaan pasien

Pengguna aspirin/NSAIDGERD

Tidak Ya

UBT/HpSA Endoskopi

Hasil(-) Hasil(+) Rapid urease test Histopatologi

hasil(+) hasil(-)

Terapi simtomatik Terapi eradikasi Terapi simtomatik

Gagal

Reevaluasi diagnostik

Skema 2. Penatalaksanaan pasien dispepsia oleh gastroenterologis/internis dengan fasilitas endoskopi

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GASTROESOPHAGEAL REFLUX DISEASE(GERD)

• DEFINITION of GERD is a pathologic consequences of the effortless movement of gastric contents to the esophagus, including symptoms or signs referable to the esophagus, pharynx, larynx, and respiratory tract.

• EPIDEMIOLOGY of GERD: extremely common, at least once monthly 40% adult americans. 7% report daily heartburn, 1% have erosive esophagitis. Incidence: increases after 40 years, more common in men than women.

• ETIOLOGY AND PATHOGENESIS of GERD: imbalance of aggressive factors and defensive factors. Gastric contents: hydrochloric acid, pepsin, bile salts, and pancreatic enzymes. Anti reflux barriers: lower esophageal sphincter(LES), intra abdominal segment of the esophagus, diphragmatic crura, phrenoesophageal ligament, mucosal rosette, angle of His, Lumenal acid clearance & Tissue resistance

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Pathophysiology of GERD

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CLINICAL FEATURES of GERD

• -Heartburn• -Substernal chest discomfort• -Regurgitation bitter or acid-tasting liquid• -Water brash or hypersalivary• -Solid dysphagia• -Odynophagia• -Oropharynx damage: sorethroat, erache, gingivitis, poor

dentition, and globus.• -Reflux damage of the larynx and respiratory tract:

hoarseness, wheezing, bronchitis, asthma, pneumonia

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FINDINGS ON DIAGNOSTIC TESTING of GERD

• A history of heartburn• Test for reflux: Barium swallow radiography, acid reflux testing, esophageal

pH monitoring, radionuclide 99mTc scintigraphy.• Tests for assessing symptoms: Bernstein’s acid perfusion test, esophageal

pH monitoring, empirical trial of acid –suppressive medications(PPI test)• Tests for assessing esophageal damage: Barium swallow radiography,

upper gastrointestinal endosco py with or without biopsy, esophageal potential difference measurement.

• Tests for assessing disease pathogenesis: acid clearance tests, radionuclide 99mTc scintigraphy, esophageal manometry, gastric acid secretory studies

• Barium swallow or upper gastrointestinal radiography: ulcers, strictures, hiatal hernias, Barretts’s esophagus.

• Upper gastrointestinal endoscopy: gold standard for reflux-induced injury: normal mucosa, erythema, edema, friability, exudate, erosions, ulcers, strictures, Barret’s metaplasia. Histologic of esophagitis : increased height of the esophageal papillae and basal cell hyperplasia.

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Spectrum Of Endoscopic Findings with GERD

Normal esophagus Grade 3 esophagitis

Grade 4 esophagitis Barrett’s esophagus

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MANAGEMENT of GERD• -Lifestyle modification: - Elevation of the head and head of the bed• (to enhance nocturnal esophageal acid clearance)• - Stop/avoid smoking and ethanol/alcohol(deleterious effects on LES pressure,• acid clearance, & epithelial function)• - Reduce meal size and the intake of fat, carminatives and chocolate• (gastric distention)• - Stop/avoid coffee(caffein and decaffeinated), tea, carbonated beverages• (stimulate acid production)• - Stop/avoid tomato juice and citrus products (exacerbatr symptoms—their• osmotic effects)• - Stop drugs/medications can reduce LES pressure: anticholinergics,• theophylline, diazepam, opiates, calciu channel antagonists, b adrenergic• agonists, a-adrenergic antagonists, & progesterone.• Medication therapy:• - Acid suppressive drugs: 1. H2 receptor antagonists(cimetidine, ranitidine, famotidine, nizatidine): • mild-moderate• 2. Proton pump inhibitor(PPI)( omeprazole, lansoprazole, rabeprazole,• pantoprazole, esomeprazole): drug of choice• 3. Prokinetics agents: metoclopramide, domperidone, cisapride• 4. Liquid Antacids: good for mild but have side effects(diarrhea, etc)• Surgical treatment:• failure of medications to prevent stricture formation and the development of pneumonia or airway• compromise: Nissen and Belsey fundoplications and Hill gastropexy.• Endoscopic fundopication: suturing with endoscopic or solution injection with Enteryx

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Management of complications in GERD

• Strictures:Esophageal dilation with Hurst or Savary dilators

• Barrett’s esophagus: endoscopic surveillance every 6 months or 1year

• Hemorrhage: endoscopic treatment or surgery

• Perforation: surgical therapy

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Figure 1. Algorythm of the management of GERD by The American Gastroenterology Association / AGA

GERD symptoms Typical? No Ambulatory pH monitoring Yes Acid supression Yes No Think of other therapy Abnormal? diagnosis YesAsimptomatic stop drug after 6-8 weeks No Yes No Endoscopy Recurrence Symotom Do not continue therapy Esophagitis or No Ambulatory pHBarret’s esophagus? monitoring

Yes No Maximize medical Abnormal therapy

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PEPTIC ULCER DISEASE(PUD)• DEFINITION: Mucosal break in the gaster and duodenum, diameter more

than 0,5 cm. Refractory ulcer if duodenal ulcer 8 weeks of therapy is ineffective or gastric ulcer a lack of response to 12 weeks of treatment.

• INCIDENCE AND EPIDEMIOLOGY: 500.000 new cases per year and 4 million annual recurrences in the United States, 1year point prevalence active PUD is 1.8%, Lifetime prevalence is 11-14% for men and 8-11% for women

• ETIOLOGY AND PATHOGENESIS: Increase risks in genetic factor(first degree relatives in PUD, bloog group O, nonsecretors of blood group antigens, gastrinoms and systemic mastocytosis, genetically linked syndromes(multiple endocrine neoplasia type 1 and familital mastocytosis). Imbalance of aggravating/aggressive factors and defensive factors. Aggravating/aggressive factors: Helicobacter pylori infection, NSAID, stress, nicotine(tobacco), food(vinnegar), free radicals, drugs (corticosteroid, aspirin etc.), alcohol, chemicals. Defensive factors: Mucus, bicarbonate secretion, Mucosal blood flow, prostaglandin, surface active phospholipids etc

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PATHOGENESIS of Gastric mucosal Damage

Figure1. The Balance between aggressive and defensive factors

Aggressive factors Defensive factors Gastric acid Mucosal blood flow Pepsin Epithelial cell surface Bile reflux Prostaglandin Nicotine Phospholipid/surfactan NSAID Mucus Corticosteroid Bicarbonate Helicobacter pylori Motility Free radicals Mucosal impermeability to Stress H+ ion Intracellular pH regulation Growth factor

cited from Daldiyono & Shiessel R et.al.

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CLINICAL FEATURES of PUD

• Abdominal pain 94%: epigastric in location, does not radiate, occurs 2-3 hours postprandially, and relieved by food or antacids. Some time awakens the patient between midnight and 3 AM.

• Some patients have no symptoms• Complications: hemorrhage(melena)(15%),

perforation(7%), penetration, and obstruction(2%).

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FINDINGS ON DIAGNOSTIC TESTING of PUD

• routine blood: hemoglobine, leukocyte• routine stool: occult blood test• Upper gastrointestinal barium radiography: gastric & duodenal ulcer• Upper gastrointestinal endoscopy: gastric & duodenal ulcer, biopsy

for histopathological examination: benign/malignant disease, Helicobacter pylori infection

• Helicobacter pylori testing: serology, culture/CLO test/histopathology examination from upper GI endoscopy examination, C-Urea Breath test, Stool’s H.pylori antigen

• Serum gastrin and gastric acid secretion testing: Serum gastrin measurements are indicated in PUD & endocrine neoplasia(esp.hyperparathyroidism), ulcer distsl to the duodenal bulb, and in refractory ulcers to standard therapy, including H.pylori eradication. Gastric acid secretion testing is indicated for hypergastrinemia in whom a gastrinoma is suspected.

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MANAGEMENT of PUD:• Non pharmacological management: stomach diet, avoid/stop aggressive factors, avoid stress.• Pharmacological management:• H2 receptor antagonist: cimetidine, ranitidine, famotidine, nizatidine, roxatidine• This drug inhibit the H2 receptors, basal, histamine-stimulated, pentagastrin stimulated, and

meal-stimulated acid secretion in a linear, dose dependent manner with a maximal 90% inhibition of vagal and gastrin stimulated acid production and near total inhibition of nocturnal and basal secretion.

• Proton pump inhibitors: Omeprazole, lansoprazole, pantoprazole, rabeprazole, esomeprazole. This drug inhibit H+,K- adenosine triphosphatase activity in the gastric parietal cell canalicular membrane, leading to nearly complete inhibition of basal and stimulated acid secretion. PPI have far greater effects on daytime(meal-stimulated) acid secretion than do H2RA.

• Cytoprotective Agents: Sucralfate, binds to tissue proteins, forming a protective barrier that absorbs bile salts and pepsin. Sucralfate may also stabilize gastric mucus and have trophic effects on the mucosa. Adverse effects of sucralfate: constipation and renal failure. Misoprostol is a prostaglandin E1 analog, inhibits gastric acid secretion, stimulateds bicarbonate and mucus secretion, enhances mucosal blood flow, and inhibits cell turnover. Dose related diarrhea occurs in 10-30% patients and may be associated with crampy discomfort. Women child-bearing potential should be advised of the risk of fetal loss. Bismuth subsalicylate coats ulcer craters, possibly forming a protective layer against the effects of acid and pepsin. Bismuth compounds also stimulate mucosal prostaglandine E2 production, increase bicarbonate secretion, and have anti H-pylori activity. Tephrenone and rebamipide has the ability to increase prosstaglandin production, blood flow, mucus, bicarbonate secretion etc.

• Treatment of H.pylori infection: Triple regimens: PPI + 2 antibiotics(amoxycillin & clarithromycin) 7-14 days

• Treatment and prevention of NSAID related peptic ulcer disease.• Management of refractory ulcers: look for the cause of refractory such as patient noncompliance,

surreptitious NSAID use, tobacco use, untreated Hpylori infection, gastric acid hypersecretion(gastrinoma), and malignancy. Rare causes of chronic ulceration are Crohn’s disease, amyloidosis, sarcoidosis, eosinophilic gastroenteritis, and infections(e.g. tuberculosis, syphilis, cytomegalovirus). Endoscopic follow up is indicated in these situations. High dose proton pump inhibitors omeprazole 40 mg perday or lansoprazole 60 mg/day can heal 90% refractory ulcers after 8 weeks.

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Helicobacter pylori Eradication(KSHPI)• Tripple therapy(1 or 2 weeks):

1. PPI+Amoksisilin+Klaritromisin 2. PPI+Metronidazol+Klaritromisin 3. PPI+Metronidazol+Tetrasiklin (alergy to chlarithromisin)• Quadruppel therapy(1 or 2 weeks):

1. If fail of therapy combination 3 drugs: Bismuth+PPI+Amoksisilin+Klaritromisin Bismuth+PPI+Metronidazol+Klaritromisin 2. Hight resistency areas: PPI+Bismuth+Tetrasiklin+Metronidazol

• PPI 2 x/d; Omeprazol/Esomeprazol 20 mg, Lansoprazol 30 mg, Pantoprazol 40 mg, Rabeprazol 10 mg.• Amoksisilin: 2 x 1000 mg/d, Klaritromisin 2 x 500 mg/d,

Metronidazol 3 x 500 mg/d, Tetrasiklin 4 x 250 mg/d, Bismuth 4 x 120 mg/d.

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DYSPHAGIA• DEFINITION: Dysphagia refers to the sensation of food being

hindered in its passage from the mouth to the stomach. Odynophagia is pain on swallowing. Globus sensation is perception of a lump, tightness, or fullness in the throat that is temporariloy relieved by swallowing.

• CATEGORY: Dysphagia divided into: 1. Those illnesses involving the oral preparation, oral transfer, or pharyngeal phases of swallowing 2. Those conditions involving dysfunction of the esophageal phase

• ETIOLOGY & PATHOGENESIS: The etiology of dysphagia is an abnormality of any of the components of swallowing. The act of swallowing has four components: oral preparation phase, the oral transfer phase, the pharyngeal phase, and the esophageal phase.

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Table 1. Causes of dysphagia• Oropharyngeal dysphagia • Neuromuscular diseases• Cerebrovascular accident• Parkinson’s disease• Wilson’s disease• Amyotrophic lateral sclerosis• Brain stem tumors• Bulbar poliomyelitis• Peripheral neuropathy• Myasthenia gravis• Muscular dystrophies• Polymyositis• Metabolic myopathy• Amyloidosis• Systemic lupus erythemathosus• Local mechanical lesions• Inflammation(pharyngitis, abscess, tuberculosis, radiation, syphilis)• Neoplasm• Congenital webs• Plummer-vinson syndrome • Extrinsic compression(thyromegaly, cervical spine hyperostosis, adenopathy) • Oropharyngealk resection• Upper esophageal sphincter(UES) disorders• Hypertensive UES• Hypotensive UES• Abnormal UES relaxation(cricopharyngeal achalasia, central nervous system, lymphoma,• Oculopharyngeal muscular dystrophy, cricopharyngeal bar, Zenker’s diverticuum, familial• Dysautonomia)Esophageal dysphagia • Motility disorders• Achalasia• Scleroderma• Diffuse esophageal spasm• Nutcracker esophagus• Hypertensive lower esophageal sphincter• Nonspecific esophageal dysmotility• Other rheumatologic conditions• Chagas’ disease• Intrinsic mechanical lesions• Benign stricture(peptic, lye, radiation)• Schatzki’s ring• Carcinoma• Esophageal webs• Esophageal diverticula• Benign tumors• Foreign bodies• Extrinsic mechanical lesions• Vascular compression• Mediastinal abnormalities• Cervical osteoarthritis

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DIAGNOSIS of Dysphagia• Diagnosis is made by history, physical examination & additional testing. • History: distinguish between oropharyngeal or esophageal in location and if it is

structural or neuromuscular in origin. If dysphagia occurs during the act of swallowing and is associated with drooling, choking, coughing, nasal aspiration, or tossing movements of the head, then an oropharyngeal process is probable. Conversely, as esophageal cause is likely if dysphagia occurs seconds after swallowing, if there is associated retrosternal pain, and if regurgitation occurs some time after ingestion. Dysphagia perceived in the retrosternal or subxiphoid are is most consistent with an esophageal source, whereas in cervical dysphagia it is difficult to discriminate between oropharyngeal and esophageal causes. Structural disorders of the esophagus usually cause dysphagia to solids intially, with progression to liquid dysphagia only if lumenal narrowing becomes severe. In contrast, patients with neuromuscular disorders of the esophagus usually complain of both liquid and solid dysphagia from the onset of symptoms.

• Physical examination: The head and neck must be examined for sensory and motor function of the cranial nerves, masses, adenopathy, or spinal deformity. The patient is observed swallowing water so that the coordinated symmetrical action of the facial and cervical musculature can be visualized. The clinician should examine the patient for systemic disease, including the presence of sclerodactily, telangiectasias, and calcinosis seen in scleroderma; neuropathies or muscle weakness characteristics of generalized neuromuscular disease; and hepatomegaly or adenopathy symptomatic of esophageal maloignancy

• Additional testing: Preferred—barium swallow radiography to assess the rapid changes in anatomy on swallowing. Upper endocsopy and biopsy—to check a structural lesion of the oropharynx. UES manometry—detect and characterize disorders of UES relaxation.

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Management of Dysphagia• The management depend on the cause.• Neuromuscular disease—myotomy(surgical)• Benign strictures—dilatation by bougienage• Early malignancies –surgically resected• Unresectable malignancies – dilatation, cautery, laser or

stenting• Achalasia—medications(calcium channel antagonists),

botulinum toxin injection into the LES, by endoscopic dilation, and by surgical myotomy.

• Other primary esophageal dysmotilities respond to nitrates, calcium channel antagonist, surgical myotomy.

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UPPER GASTROINTESTINAL BLEEDING(HEMATEMESIS-MELENA)

• DEFINITION: Upper gastrointestinal bleeding/ hematemesis melena refers to bleeding source from the upper gi tract. The blood in stool – tarry stools, the blood vomiting—black tarry vomiting

• EPIDEMIOLOGY: - The frequent cause of upper gi bleeding in Indonesia is rupture of esophageal varices. - The frequent cause of upper gi bleeding in Europe is peptic ulcer.

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DEFINITION• Hematemesis: blood vomiting(black

colour) from upper gastrointestinal tract• Melena: black tarry stool, bleeding from

upper gastrointestinal tract• Hematochezia: fresh bleeding(red colour)

from the anal gastrointestinal tract or massive bleeding from upper gastrointestinal tract

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Causes of upper gastrointestinal hemorrhage with endoscopic examination in Cipto Mangunkusumo

Hospital (1996-1998)Causes Percent(%)Rupture of esophageal varicesMixed causesErosive gastritisPortal hypertensive gastropathyDuodenal ulcerGastric ulcerRupture of gastric varicesDuodenal carcinomaGastric carcinomaErosive esophagitisEsophageal ulcerErosive duodenumGastric polypAngiodysplasi/hemangiomaNo abnormalities

27.222.119.011.75.75.51.81.10,90,70,40.20.20.23.3

Simadibrata M, Rani AA. 11 th Asian Pacific Congress of Gastroenterology and th 8th Asian Pacific Congress of Digestive Endoscopy. HongKong March 10-14, 2000: B64(A212)

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Re-bleeding according to endoscopic stigmata

Endoscopic findings

Incidence(%)

Re-bleeding

(%)

Surgery (%)

Mortality (%)

Clean baseFlat spotAdherent clotNon-bleeding visible vesselActive bleeding

6211811

7

5102243

55

0.561034

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23711

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Cited from Triadafilopoulos, Laine & Peterson.

Red color : bad/poor stigmata

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a. Spurting b. oozing Type I

Forrest Classification of bleeding peptic ulcers

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a. Visible vessel

b. Adherent clot

c. Flat pigmented spot

Type II

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d. Clean base

Type III

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Bad Predictor in upper gastrointestinal bleeding

• Age > 60 years• Other comorbid• Hypotension or shock• Coagulopathy• Bleeding onset in hospital• Transfusion requirement > 6 unit• Fresh bleeding from stomach • Recurrens bleeding from the same lesion

Triadapafilopoulos G. Aliment Pharmacol Ther 2005;22(suppl.3): 53-8

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DIFFERENTIAL DIAGNOSIS/CAUSES OF UPPER GASTROINTESTINAL HEMORRHAGE

• Peptic ulcer disease(duodenal, gastric, stomal)• Gastritis(NSAID, stress, chemotherapy-induced)• Varices(esophageal, gastric, duodenal)• Portal gastropathy• Mallory-Weiss tear• Esophagitis and esophageal ulcers(acid reflux, infection, pillo-

induced, sclerotherapy, radiation-induced)• Neoplasms• Vascular ectasias and angiodysplasias• Watermelon stomach• Aortoenteric fistula• Hematobilia• Hemosuccus pancreaticus• Dieulafoy’s erosion

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WORKUP/DIAGNOSIS of Hematemesis Melena• The first step in the assesment of a patient with upper GI bleeding is to determine the urgency of the clinical condition. So the most

important thing is to give resuscitation.• Then me make the diagnosis upon history, physicalo examination and additional tsting• Resuscitation: Hematemesis, melena or hematochezia usually suggest a major hemorrhage. Pallor, hypotension, and tachycardia are

evidence of substantial blood volume loss(>40%) immediate volume replacement. Postural hypotension > 10 mmHg 205 blood volume reduction, must be replaced immediately. Intravenous access 2 karge-bore catheters, if shock CVP. A nasogastric tube(ngt) is placed. A bright red aspirate =/= clear with lavage indication of emergency upper gi endoscopy(30% mortality), whereas coffee ground-colored materaial permits further assesment in a hemodinamically stable patient. A clear aspirate some pts with duodenal bleeding. Blood samples sent to laboraroty for hematocrit, platelets, hemoglovin, coagulation factors and for blood typing and crossmatching. Significant intravascular volume losses immediately replaced with normal saline while awaiting arrival of blood products. Hemodinamically unstable pts should be intensive care unit

• History: is taken while resuscitation underway. Prior history of peptic disease and dyspeptic symptoms suggest ulcer bleeding. History of NSAID, alcohol, or caustic substances comsuption. Patients with suspected liver disease are treated aggresively, usually undergoing urgent upper endoscopy risk of varices bleeding. Other historical: prior aortic surgery, coagulopathies, known or suspected neoplas, or recent nosebleeds specific diagnoses.

• Physical examination: Cutaneous stigmata of cirrhosis or malignancy may be present. Multiple cutaneous telangiectases hereditary hemorrhagic telangiectasia. Lymphadenopathy, hepatosplenomegaly degree of blood loss. A low hematocrit or microcytic indices chronic blood loss – iron studies or ferritin measurement. Thrombocytopenia results from bone marrow disease, autoimmune disorders, or portal hypertension with splenomegaly. Prolongation of the prothrombin time is seen with liver disease, warfarin use, or malnutrition. In massive upper gi bleeding, azotemia reflects intestinal absorption of the nitrogenous breakdown products of blood coupled with hypovolemic effects, whereas azotemia with elevation in creatinine concentrations suggests renal insufficiency. Abnormal liver chemistry findingscirrhosis with portal hypertension

• Upper gi endoscoopy: Urgent upper endoscopy is indicated in patients with bleeding that does not stop spontaneously or In those patients suspected having cirrhosis or aortoenteric fistulae. If bleeding stopped, endoscopy may be postponed without compromising care. Some patients with uncomplicated courses of illness may be given empirical therapy for presumed peptic disease if both the physician and patient are comfortable without a specific diagnosis. Upper endoscopy is relatively contraindicated in cases which perforation is suspected and is relatively contraindicated in patients with compromised cardiopulmonary status or depressed levels of consciousness. In these circumstances, endotracheal intubation with mechanical ventilation enhance the safety of the technique. Upper Gi barium radiography is not performed in the acute setting with a potentially unstable patient.

• Scintigraphy and angiography: Hemorrhage so brisk(obscure endoscopic visualization) scintigraphis 99mTc-sulfur colloid or 99mTc pertechnetate- labeled erythrocyte scans can localize bleeding to an area of the abdomen if the rate of blood loss exceeds 0.5 ml per minute. Scintigraphy is most commonly used to determine if angiography is feasible and to direct the angiographic search while minimizing the dye load. Angiography is used in cases when endoscopy cannot visualize the lumen because of massive hemorrhage. However, to detect a source of bleeding, the rate of blood loss must exceed 0.5 ml per minute as well. Angiography also may detect vascular ectasia in patients with intermittent hemorrhage who have normal findins on upper endoscopy, and also usesfulo for hemobilia, or hemosuccus pancreaticus.

• Other radiographic studies: for aortoenteric fistula abdominal computed tomographic or magnetic resonance imaging studies-—fter endoscopy excluded other bleeding sources.

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MANAGEMENT of Hematemesis Melena

• Transfusion of blood products• Medications: peptic ulcer disease/stress gastritis: H2RA, or PPI; varices or portal gastropathy: 0.2-0.4 unit

perminute intravenous vasopressin for patients without cardiovascular contraindications or terlipressin or somatostatin or octreotide 25-50ug per hour reduce variceal bleeding. Angiodysplasia: intravenous or oral estrogens with or without progesterone benefit in recurrent bleeding.

• Therapeutic endoscopy: Urgent endoscopy liver disease, aortoenteric fistula or bleeding does not stop. Before endoscopy, the stomach should be lavaged throug ngt with saline or water to enhance mucosal visualization. If an actively bleeding ulcer is observed – endoscopic therapy using thermal and nonthermal methods efficacious. Thermal methods: bipolar electrocautery, heater probe application and Nd: YAG laser therapy. Non thermal injection technique with vasoconstrictors(e.g. epinephrine) , sclerosants(e.,g. alcohol and ethanolamine), or even saline – good. Stigmata of recent hemorrhage: non bleeding vissible vessel and an adherent clot—thermal or injection therapy. Stress gastritis, NSAID induced gastritis and portal gastropathy(multiple bleeding sites) cannot be controlled endoscopically.

• Emergency upper endoscopy is indicated for management of esophageal varicel hemorrhage. Injection sclerotherapy(sodium morrhuate, ethanolamine) into or adjacent to the bleeding varix is succes 85-95%. Varideal band ligation the same as effective as sclerotherapy. In contrast gastric varices are not amenable to sclerotherapy or banding and require nonendoscopic control.

• Mechanical compression: for patients who fail to respond to endoscopi therapy of variceal hemorrhage—ballon tamponade with a Senstaken-Blakemore tube or Linton-nachlas tube hemostasis in up to 90% of cases, then followed by sclerotherapy or ligation.

• Therapeutic angiography: Good in peptic ulcer hemorrhage refractory to endoscopic control. With absorbable gelatin sponge(gelfoam) or an autologous clot patients who are not candidates for surgery. Intra arterial vasopressin or embolization may be useful in some patients with stress gastritis bleeding, esophageal sources, refractory Mallory – Weiss tears, neoplasms, hemobilia, and hemosuccus pancreaticus. Patients with esoophageal variceal hemorrhage refractory to endoscopic therapy transjugular intrahepatic portosystemic shunt(TIPS) or percutaneous trans hepatic obliteration(PTO).

• Surgery:if endoscopy fails to control the source of bleeding, emergency surgery may be required

46

COMPLICATIONS

• Exsanguination• Death: Mortality 8-10% and 30-40% for

persistent or recurrent bleeding.

48

Algorythm of the Management of Hematemesis Melena Hematemesis Melena Routine blood test & Cross match

Minor bleeding Major bleeding - Observation in general room - Elective endoscopy Resuscitation in High Care Unit - Discharge from hospital soon Endoscopy Sign of bleeding Varices No sign of new bleeding New bleeding/major See other protocol Observation in general Endocopic therapy room

Hemostatic success Fail

Stabil Rebleeding Surgery

H.pylori eradication Repeat endoscopic stop NSAID therapy Fail Success

Palmer KR. Gut 2002;51:iv1-iv6

49

Workup of a patient with acute upper gastrointestinal bleeding(CRC=complete blood count; IV=intravenous; TIPS=transjugular intrahepatic portosystemic shunt)

Vital signsResuscitation CBD, platelets Coagulation factors Type and crossmatch Two large bore IV lines Nasogastric tubeHistory and physicalOther tests as indicated

IV normal salinePacked red blood cellsAnd factors as needed

Empirical trial ofmedications

Urgent upper endoscopy

Efective evaluationWith upper endoscopyOr barium radiography

Therapeutic angiographyOr urgent surgery

Sclerotherapy orVariceal banding

Vasopresin orOctreotide andBalloon tamponade

TIPS or surgery

Cautery orinjection

Therapeutic angiographyOr urgent surgery

Volume loss orHemodynamicInstability

No significant volume lossNo active bleeding

No active bleeding

Active or recurrent bleedingLiver disease or priorAortic surgery

Recurrentbleeding

Remainsstable

Bleeding siteNonvisualized or nor amenableTo the therapeutic endoscopy

Esophagealvarices

Ulcer, vascularabnormality

Therapyfailure

Therapyfailure

Therapyfailure

Yamada T et.al. Handbook of Gastroenterology.Lippincott Raven 1999

50

LOWER GASTROINTESTINAL BLEEDING

• DEFINITION: Lower gastrointestinal bleeding refers to bleeding source from the lower gi tract. The blood in stool – red fresh bloody stools.

51

ETIOLOGY/CAUSES/DIFFERENTIAL DIAGNOSIS LOWER GI BlEEDING

• Diverticulosis• Angiodysplasias• Hemorrhoids• Anal fissures• Neoplasms• Inflammatory bowel disease• Ischemic colitis• Infectious colitis• Radiation induced colitis• Meckel’s diverticulum• Intussusception• Aortoenteric fistula• Solitary rectal ulcera• NSAID-induced cecal ulcers

52

DIAGNOSIS/WORKUP• Resuscitation: correction of volume deficits &

stabilization of hemodynamic variables. If suspected upper gi bleeding ngt, Laboratory studies

• History & Physical examination: GI diseases such as IBD, malignancy(weight loss, anorexia, lymphadenopathy, or palpable masses) etc

• Additional testing: Endoscopy, Scintigraphy & angiography, Other radiologic studies(Barium enema).

53

MANAGEMENT LOWER GI BLEEDING

• Medications: Hemorrhoids, anal fissures & solitary rectl ulcers bulk forming agents, sitz baths & avoidance of straining. Steroid-containing ointment/suppos many cases. Estrogen-progesterone comainations—angiodysplasia. IBD specific anti inflammatory drug. Radiation proctitis intrarectal formalin, sucralfate, steroid, hyperbaric oxygen.

• Therapeutic endoscopy: bipolar cautery, monopolar cautery, heater probe& Nd:YAG laser angiodysplasia, chronic radiation proctocolitis. Polypectomy polyp, colinic malignancy(EMR). Sclerotherapy/ligation/thermal hemorrhoid

• Therapeutic angiography: diverticula&angiodysplasia: intraarterial vasopresin (control 90% hemorrhages), angiographic embolization(13-18% risk of bowel infarction.

• Surgery

54

COMPLICATIONS

• Shock hypovolemia, acute renal failure• Side effects of transfusion

55

Workup of a patient with acute lower gastrointestinal bleeding (CBD=complete blood count; iv=intravenous; AVMs=arteriovenous malforations)

Vital signsResuscitation CBC, platelets Coagulation factors Type and crossmatch Two large bore Iv linesHistory and physicalOther tests as indicatedNasogastric tube if upper GISource not excluded

Iv normal salinePacked red blood cellsAnd factors as needed

Elective evaluationWith colonoscopyOr sigmoidoscopy

Urgent upperendoscopy

Urgent colonoscopyAfter brisk purge orErythrocyte scintigraphyFollowed by angiography

Small intestinalBarium radiographyEnteroscopyMeckel’s scan

Endoscopic cautery or injectionAngiographic embolizationOr vasopressin

Iron supplements Consider:DiagnosisAngiographyIntraoperativeEnteroscoyEmpirical hormonalTherapy for AVMsPartial colectomy

Urgent surgery

Volume loss orHemodynamic Instabiliry

No significant volume lossNo active bleeding

No active bleeding

PosibleUpper GIsource

Active bleedingPresumed lower GI source

No siteidentified

Normal

Bleeding site visualisasi RecurrentBleedingMinimal blood loss

RecurrentBleedingRequiringtransfusions

Treatment failure ofEngoing bleedingWith no source identified


56

Workup of a patient with occult gastrointestinal bleeding (CT=computed tomography)

Colonoscopy

Upper endoscopy

Barium radiographyOf the small intestine

Oral Ironsupplementation

No further diagnosticevaluation

EnteroscopyAngiographyAbdominal CTIntraoperative enteroscopyConsider evaluation for malabsorption

No site identified

No site identified

No site identified

Hemoglobinnormalizes

Anemiapersists


57

Algorhytm for obscure bleeding

American Gastroenterological Association.Gastroenterology January 2000;118:201-21.

58

ACUTE ABDOMEN

• DEFINITION: Acute abdomen refers to any acute intra & extra abdominal disease processes. Many cases require urgent surgical management, although some can be managed nonsurgically.

59

ETIOLOGY/CAUSES/DIFFERENTIAL DIAGNOSIS OF ACUTE ABDOMEN

• Gastrointestinal• Appendisitis• Perforated peptic ulcer• Intestinal ischemia• Diverticulitis• Inflammatory bowel disease• Meckel’s diverticulitis• Pancreaticobiliary tract, liver, spleen• Acute pancreatitis• Calculous cholecystitis• Acalculous cholecystitis• Acute cholangitis• Hepatic abscess• Ruptured hepatic tumor• Splenic rupture• Urinary tract• Renal/ureteral stone• Gynecologic• Ectopic pregnancy• Tuboovarian abscess• Ovarian torsion• Uterine rupture• Ruptured ovarian cyst or follicle• Retroperitoneum• Abdominal aortic aneurysm• Supradiaphragmatic• Pneumothorax• Pulmonary embolus• Acute pericarditis• Empyema

60

WORKUP/DIAGNOSIS ACUTE ABDOMEN

• Diagnosis is made upon history, physical examination and additional testing.• History: Acute appendicitis periumbilical pain, low-grade fever, and anorexia with or

without vomiting then followed by movement of the pain into the right lower quadrant McBurney’s point. Constipation:obstructive conditions, inflammatory disorders produce ileus. Watery diarrhea: gastroenteritis, bloody diarrhea: infectious colitis, inflammatory bowel disease, mesenterial ischemia. Jaundice: hepatic and pancreaticobiliary disease, sepsis. Urinary frequency, dysuria, hematuria, and suprapubic or flank pain : urologic disease.

• Physical examination: appendicitis acute: local peritonitis at McBurney’s point, psoas sign(+). Perforation: general/local peritonitis, disappear of liver percussion dullness. Bruits mesenteric thrombosis. Ectopic pregnancyunilateral adnexal mass with blue cervical discoloration.

• Additional testing: • Initial studies: Blood testing: anemia, leukocytes, or leukopenia, serum electrolytes,

blood urea nitrogen, and creatinine, pregnancy test, peritonitis abdominal radiographs(3 positions abdominal xray) Gas in the biliary tree – fistula or cholangitis. Ileus diffusely dilated loops of the small intestine & colon. Free subdiaphragmatic air 75% patients with ulcer perforation.

• Decision to operate immediately• Imaging studies: CT-scan, ERCP/MRCP

61

MANAGEMENT OF ACUTE ABDOMEN

• Urgent surgery• Conservative management

62

DIARRHEA

• DEFINITION: Stool soft or watery with a daily stool weight of > 200 g(250g). Frequency more than 3 times/day

63

CAUSES/DIFFERENTIAL DIAGNOSIS OF DIARRHEA• High output osmotic• Nonabsorbed solutes• Saline and phosphate laxatives• Sorbitol, fructose, lactulose• Disaccharidase deficiency• Lactase deficiency• Isomaltase-sucrase deficiency• Trehalase deficiency• Small intestinal mucosal disease• Celiac spure• Tropical sprue• Viral gastroenteritis• Whipple’s disease• Amyloidosis• Intestinal ischemia• Lymphoma• Giardiasis• Pancreatic insuffciency• Chronic pancreatitis• Pancreatic carcinoma• Cystic fibrosis• Reduced intestinal surface area• Small intestinal resection• Enteric fistulae• Jejunoileal bypass• Bile salt malabsorption• Bacterial overgrowth• Ileal resection• Crohn’s disease• Defective transport• Congenital chloridorrhea• High-output secretory• Laxatives• Bisacodyl• Phenolphthalein• Ricinoleic acid• Dioctyl sodium sulfosuccinate• Bacterial toxins• Vibrio cholerae• Toxigenic Eschericia coli• Clostridium perfringens• Hormonally induced• Vasoactive intestinal polypeptide• Serotonin• Calcitonin• Glucagon• Gastrin• Substance P• Prostaglandins

• Defective neural control• Diabetic diarrhea• Bile acid diarrhea• Ileal resection• Crohn’s disease• Bacterial overgrowth• Post cholecystectomy• Mucosal inflammation• Collagenous colitis• Lymphocytic c olitis• Villous adenoma• High output injury• Inflammatory bowel disease• Crohn’s disease• Ulcerative colitis• Acute infections• Viruses(rotavirus, Norwalk agent)• Parasites(Giardia, Cryptosporidium,• Cyclospora)• E.coli• Shigella• Salmonella• Campylobacter• Yersinia enterocolitica• Entamoeba histolytica(amebiasis)• Chronic infections• E.histolytica(amebiasis)• Clostridium difficile• Ischemia• Atherosclerosis• Vasculitis• Normal output• Motility disorders• Irritable bowel syndrome• Endocrinopathies• Hyperthyroidism• Proctitis• Ulcerative proctitis• Infectious proctitis• Fecal incontinence• Surgical and obstetrical trauma• Hemorrhoids• Anal fissures• Perianal fistulae• Anal neuropathy(diabetes

64

CLASSIFICATION

• Time: acute less than 15 days chronic more than 15 days

• Organic diseases: Organic and functional• Infective/infectious causes: Infective/infectious

and non-infective/infectious• Stool: soft, watery, bloody or steatorrhea,

bloody , nonsteatorrhea nonbloody• Pathomechanism: osmotic, secretory, increased

motility, mucosal inflammation,

65

DIAGNOSIS OF DIARRHEA• Diagnosis is made upon history, physical examination and additional testing• History: duration of diarrhea, recent travel, sexual practices, ingestion of well water and poorly cooked food and

shellfish, and exposure to high-risk persons in day care centers, hospitals, mental institutions, and nursing homes. The characteristics of the diarrhea causative organism. Watery diarrhea+nausea, little paintoxin producing bacteria. Invasive bacteria pain, bloody diarrhea. Viruses watery diarrhea, pain significant, fever, mild-moderatevomiting. Homosexual men, prostitutes, iv drug abusers diarrhea through oral-fecal transfer. Antibiotic associated colitis recent antibiotic use. Recent initiated medication regimens or inadvertent uses of over the counter preparations antacids containing magnesium, common drugs: antirrhytmias, antihypertensives, diuretics, central nervous system drugs, antiarthritis, cholesterol lowereing medications and theophylline.

• Phycical examination: abdominal tumor/mass, dehydration, fever etc. Hypotension, decreased skin turgor, dry mucous membranes dehydration need intravenous hydration. Emaciation, cheilosis and glossitis severe malabsorption. Dermatitis herpetiformis celiac sprue, pyoderma gangrenosusm inflammatory bowel disease, sclerodactily scleroderma. Arthritis inflammatory bowel disease or Whipple’s disease. Resting tachycardia hyperthyroidism, pulmonic stenosis and tricuspid regurgitation carcinoid syndrome. Peripheral or autonomic neuropathy visceral neuropathy in diabetes and intestinal pseudo-obstruction. Neuropsychiatric findings Whipples disease. Abdominal mass malignancy, Crohn’s disease, diverticulitis. Localized abdominal tenderness inflammatory condition. A digital rectal examination perianal disease with Crohn’s disease, reduced sphincter tone incontinence. Occult or gross fecal blood infectious, inflammatory and neoplastic conditions.

• Additional testing: • Acute diarrhea: routine stool examination. complicated and prolonged infection, unresponsive to supportive

care routinestool culture for Salmoneella, shigella, or Campylobacter organisms. Special culture techniques Yersinia, Plesiomonas organisms and enterohemorrhagic E.coli. Stool samples for parasitic disease—ova & parasites: Giardia, Cryptosporidium, E.histolytica or Strongyloidesorganisms. Recent antibiotic use –Stool C.difficile culture aand toxin determination. 20-40% acute infectious diarrhea remain undiagnosed despite laboratory evaluation.

• Chronic diarrhea: Stool examination for leukocytes, fat (Sudan stain) for fat malabsorption, parasites and stool culture. Antibiotic use culture C.difficile. Serum electerolyte, Erythrocyte sedimentation rate systemic inflammatory disease. Serum albumin and globulin reduced malabsorption, malnutrition, or protein losing enteropathy. Additional blood testsfor malnutrition: carotene, iron, folate, vitamin B12, cholesterol, alkaline phosphatase and prothrombin time. Flexibel sigmoidoscopy exclude proctitis, pseudomembranes and melanosis coli due to laxative abuse. Biopsy for normal appearance microscopic and collagenous colitis or irritable bowel syndrome.

66

MANAGEMENT OF DIARRHEA

• Intravenous resuscitation• Agents for mild diarrhea: antidiarrheal, bismuth

subsalicylate, diphenoxylate, codeine.• Antibiotics for acute infectious diarrhea• Therapy for osmotic diarrhea: carbohydrate

malabsorption lactase deficiency or fructose or sorbitol intolerance dietary modification, lactase supplements

• Therapy of secretory diarrhea somatostatin analog(octreotide), parenteral calcitonin, indomethacine.

• Therapy for inflammatory diarrhea anti-inflammatory drugs(aminosalicylate and corticosteroid. Refractory cases azathioprine, 6mercaptourine, methotrexate.

67

Polyp and Cancer of the gaster/duodenum

• Definition: tumor of the gaster/duodenum, benign and malignant(cancer)

• Management: polypectomy per endoscopic or operation

68

Cholangitis• Definition: Infection of the common bile duct due

to obstruction like biliary stone or cholangiocarcinoma or papillary tumor.

• Management: - Antibiotic - ERCP diagnostic and

therapetic(sphincterotomy + stone extraction or stenting)

- Operative: laparoscopic cholecystectomy & stone extraction or laparotomy biliodigestive procedure

69

Bile duct Stone

• Definition: Stone of the common bile duct.• Management: ERCP or operation

70

Pancreatitis• Definition: Inflammation or infection of the

pancreas• Classification: Acute and Chronic• Management: - Fasting - Total parenteral nutrition - Antibiotics - Octreotide or somatostatin - Anti TNF

71

Acute pancreatitis with pancreatic enlargement& Peripancreatic edema & pseudocysts

72

Diagnosis of Acute Pancreatitis

• Clinical Features: abdominal pain, vomiting• Elevation of plasma amylase - lipase recommendation grade A 3 or 4 x normal (must not always rely on this value)• Plain radiograph• Abdominal Ultrasonography: pancreatic swelling(25-50% patients), CBD/gall bladder stones, dilatation of the CBD• Abdominal CT-scan(recommendation grade C)• Abdominal Magnetic Resonance Imaging(MRI)• CBD stones: ERCP & MRCP

73

Severity of Acute pancreatitisSeverity of Acute pancreatitis• Mild ( Edema type ): fat necrosis of the

pancreatic superficial & interstitial edema• Severe( Hemorrhagic-Necrotic type):

diffuse fat necrosis of pancreatic superficial and parenchymal. Necrotic and bleeding of the pancreatic parenchymal.

74

Etiologic factor & Pathogenesis in Acute PancreatitisEtiologic factor & Pathogenesis in Acute PancreatitisEtiologic factor(Biliary, alcoholism, unknown etc)

Initial process(bile reflux, duodenal refux etc)

Initial damage of the pancreas(edema, vascular injury, acinar pancreatic duct rupture)

Digestive enzyme activation Trypsin

Phospholipase A Elastase Lypase Chymotrypsin Kallikrein

Autodigestive

Pancreatic necrosis

Lankisch.Acute Pancreatitis. Springer Verlag 1987

75

Etiology-1• The frequent etiology in UK: gall stone disease(50%), alcohol abuse(20-25%), and idiopathic(25%).• OtherEuropean countries: alcoholism, choledocholithiasis, idiopathic, pancreas trauma, peptic ulcer, pancreatic duct obstruction etc.

76

Etiology-2• Indonesia: Nurman A(MintoHardjo Navy Hospital): Idiopathic(55.3%), Infection(21.3%)(Typhoid fever 3, DHF 5, Leptospirosis 3, Ascaris 5, Acut appendicitis 1, Sepsis 2), Biliary stone(19.1%), Metabolic(2.3%)(Hypertriglyceridemia 1, chronic renal failure 2) Others(2.3%)(Cancer of the head of pancreas 1, pregnancy 1)

Lesmana et.al. (Husada Hospital) from 900 ERCP examinations: gallstone pancreatitis, ascaris

Wijayadi T. (Cipto Mangunkusumo Hospital): Idiopathic, Leptospirosis, Dengue hemorrhagic fever, biliary stone etc.

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Management of Acute Pancreatitis

• Conservative• Surgery

78

Conservative Management-11. Oral fasting, insert nasogastric tube, take out

gastroduodenal contents. Fast unti the amylase-lipase decreased near 2-3 x normal or the clinically acute abdomen has diminished and total gastroduodenal secretion is less than 50 –100 ml/24 hrs.

2. Liver Diet I or Pancreas diet I via ngt 2-3 days then change to liver diet II or pancreas diet II soft porridge 2-3 days. Then change to liver diet III or pancreas diet III rough porridge. Then change to liver diet IV or pancreas diet IV.

3. Partial parenteral Nutrition + electrolyte Total parenteral nutrition after 3-5 days admission

79

Conservative Management-2• Antibiotics• Analgetics: petidine, tramadol, donot give

morphine• Anti pancreatic secretion drug: somatostatin 250

microgr/jam intravena or octreotide 2 x 0,05-0,1 mg subcutaneously

• Anti cytokine/anti platelet activating factor(PAF): lexipafant 100 mg/24 hrs intravena for 7 days

80

Conservative Management-3• Urinastatin: human glucoprotein from

urine: 50000 IU in glucose 5%( or NaCl 0,9%) 250 ml iv in 2hrs, 3 x/day for 3 days, then 50000IU/dayi.

• Additional therapies: solution for shock, albumin, dopamine, hemodialisis, ventilator(PEEP), Calcium , insulin, Endoscopic papilotomy, heparin, antibiotics.

81

Irritable Bowel Syndrome• Definition: Symptoms of lower gastrointestinal

like diarrhea, constipation or combination with abdominal cramps/pain. No organic abnormality found in colonoscopy.

• Management: - Diet rich of fibre - Anti Anxiety-Depression - Constipation: Prokinetic , 5 HT 4 agonist - Diarrhea: Antispasmodic, anticholinergic

82

JAUNDICE(IKTERUS)• Definition: a yellow discoloration of the

sclera, skin and mucous membranes, results from accumulation of bilirubin, a by product of heme metabolism.

• Normal bilirubin level 0.4 + 0.2/dl, >95% unconjugated. Hyperbilirubinemia: total bilirubin level > 1.5 mg/dl, unconjugated level > 1.0 mg/dl, conjugated level > 0.3 mg/dl

83

Unconjugated hyperbilirubinemia

• Hemolysis and ineffective erythropoiesis• Neonatal jaundice• Uridine diphosphate

glucuronosyltransferase deficiencies• Other causes of unconjugated

hyperbilirubinemia

84

Conjugated Hyperbilirubinemia

• Congenital forms• Familial forms• Acquired forms

85

Table 1 Causes of JaundiceUnconjugated hyperbilirubinemia Hemolysis: Glucose-6 phosphate deficiency Pyruvate kinase deficiency Medications Bilirubin overproduction Ineffective erythropoiesis Large hematoma Pulmonary embolism with infarction Neonatal causes Physiologic jaundice Lucey-Driscoll syndrome Breast milk jaundice Uridine diphosphate glucuronosyltransferase deficiencies Gilbert’s syndrome Crigler-Najjar syndromes(I and II) Miscellaneous causes Medications Hypothyroidism ThyrotoxicosisConjugated hyperbilirubinemia Congenital causes Rotor’s syndrome Dubin-Johnson syndrome Choledochal cysts Familial disorders Benign recurrent intrahepatic cholestasis Cholestasis of pregnancy Hepatocellular defects Ethanol abuse Viral infection Cholestatis syndromes Primary biliary cirrhosis Primary sclerosing cholangitis Biliary obstruction Pancreatic disease Systemic disease Infiltrative disorders Postoperative complications Renal disease Sepsis Medications

Yamada T.Handbook ofGastroenterology 1998

86

Workup• History: unconjugated roles of increased production, decreased uptake/ impaired conjugation. Conjugated

intrahepatic or extrahepatic site. Fever, abrupt onset jaundice, right upper quadrant pain, tender hepatomegaly acute disease. Shaking chills, high fever cholangitis or bacterial infection. Low grade fevers and flulike symptoms viral hepatitis. Pain radiating to the back pancreatic disease. Pruritus obstructive jaundice > 3-4 weeks. Weight loss, anorexia, nausea, vomiting nonspecific hyperbilirubinemic disorders. Recent blood transfusions, intravenous drug abuse, and sexual exposure viral hepatitis. Drugs, solvents, ethanol, oral contraceptives produce jaundice by cholestassis or hepatocellular damage. A history of jaundice, prior biliary surgery and previous episodes of jaundice bile duct disease. A family history of jaundice defect in bilirubin transport or conjugation or a heritable liver disease(Wilson’s disease, hemochromatosis, @1antitrypsin deficiency. Pts < 30 yo acute parenchymal disease, > 65 yo risks for stones or malignancy. Men alcoholic liver disease, pancreatic or hepatocellular carcinoma & hemochromatosis. Women primary biliary cirrhosis, gallstones, chronic active hepatitis.

• Physical Examination: asess the cause, severity, chronicity of jaundice. Fever Acute or chronic disease, high fever bacterial process. Cachexia, muscel wasting, palmar erythema, Dupuytren’s contracture, parotid enlargement, xanthelasma, gynecomastia, spider angiomas chronic liver disease. Shrunken, nodular liver with splenomegaly cirrhosis. Massess or lymphadenopathy malignancy. Liver spans >15 cm fatty infiltration, congestion, malignancy or infiltrative disease. Friction rub malignancy. Ascites cirrhosis, malignancy, severe acute hepatitis. Palpable, distended gallbladder malignant biliary obstruction. Asterixis, changes in mental status advanced liver disease.

• Additional Testing: - Laboratory studies: Reticulocyte count, lactate dehydrogenase, haptoglobin levels & peripheral blood smear

hemolysis. If hemolysis(+) specific test of immune mechanisms and test for vitamin B12 deficiency intoxication, thalasemia, sideroblastic anemia. Hemolysis(-), pure unconjugated hyperbilirubinemia Gilbert’s syndrome. Conjugated hyperbilirubinemia in hepatocellular causes vs cholestatis causes aminotransferases level, alkaline phosphatase, total protein, albumin. If alkaline phosphatase normal extrahepatic biliary obstruction unlikely. Aminotransferase elevations of >300 IU/ml uncommon in nonhepatobiliary disease, <300 IU/ml ethanol and most drug induce injury , > 1000IU/ml acute hepatitis, certain drug responses(acetaminophen), ischemic injury. Aspartate aminotransferase(AST) > alanine aminotransferase(ALT) ethanol injury. Viral hepatitis ratio inversed. Elevated globulin levels + hypoalbuminemia cirrhosis. Hypercholesterolemia cholestasis

- Noninvasive Imaging studies: Ultrasound: biliary obstruction(accuracy 77% - 94%) Computed tomography(CT) Radionuclide imaging with 99mTC-labeled iminodiacetic acid --< cycstic duct obstruction Magnetic Resonance Imaging(MRI) , Magnetic Resonance CholangioPancreatography(MRCP) - Invasive Diagnostic studies: Endoscopic retrograde cholangiopancreatography(ERCP) Percutaneous transhepatic cholangiography(PTC) Liver biopsy

87

Management• Depends underlying cause.• Hereditary unconjugated hyperbilirubinemia no therapy• Hemolysis discontinuation offending medication or with

corticosteroid of underlying autoimmune process• Certain hepatocellular diseases respond to specific therapies:

chronic active hepatitis C interferon; phlebotomy for hemochromatosis

• Bile duct obstruction: biliary drainage. Healthy choledocholithiasis laparoscopic cholecystectomy + CBD exploration, removal biliary stones, preoperative ERCP. Elderly pts cannot surgery ERCP + Endoscopic sphincterotomy. ERCP failed surgery. Malignant biliary obstruction drained endoscopically or radiographically , surgical procedure.

88

Complications

• Infants kernicterus• Extrahepatic biliary obstruction

secondary biliary cirrhosis, bacterial cholangitis, hepatic abscess formation.

89

HistoryPhysical examinationLaboratory studies: Aminotransferases Total bilirubin Alkaline phosphatase Albumin

Normal liverBiochemical results

Abnormal liver biochemicalResults showing cholestasis

Total, conjugated, andUnconjugated bilirubin

Specific lab studies: Hepatitis screens AMA, ANA, SMA Ceruloplasmin Ferritin SPEP @1-antitrypsin levels

HemolysisGilbert’s syndromeCrigler-NajjarSyndromes(I and II)

Dubin-JohnsonSyndromeRotor’s syndrome

Consider ultrasound or CT to

Exclude structural disease

Consider liver biopsy

Medical managementVersus observation

UltrasoundOr CT

ERCP orPTC

Relief of biliary obstruction: Surgical Endoscopic Radiologic

Unconjugatedhyperbilirubinemia

Conjugatedhyperbilirubinemia

Suspect intrahepaticcholestasis Suspect

extraheaptic cholestasis

Normal ducts:Still suspectExtrahepaticcholestasis

Normalducts

Dilatedducts

DilatedductsNormalducts

FIGURE 1. Workup of a patient with jaundice. (CT=computed tomography; AMA=antimiitochondrialAntibody; ANA=antinuclear antibody; SMA=anti-smoothe muscle antibody; ERCP=endoscopic retro-Grade cholangiopancreatography; PTC=percutaneous transhepatic cholangiography;SPEP=serumProtein electrophoresis. Yamada T. Handbook of Gastroenterology.

90

HEPATITIS

• Definition: inflammation of the liver • Classification: Acute and Chronic

gastrointestinal diseases and abnormalities in...

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