9 gastrointestinal tract

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Functional and organic disorders of gastrointestinal tract (Child/Adolescent) As. Prof., MD, PhD As. Prof., MD, PhD L. Rakovska, L. Rakovska, V.N. Karazin Kharkiv National University The Department of Pediatrics

Transcript of 9 gastrointestinal tract

  1. 1. Functional and organic disorders of gastrointestinal tract (Child/Adolescent) As. Prof., MD, PhDAs. Prof., MD, PhD L. Rakovska,L. Rakovska, V.N. Karazin Kharkiv National University The Department of Pediatrics
  2. 2. Topics for Discussion Definition, classification, etiology, clinical manifestation, diagnostics, treatment and prognosis of most often organic diseases of gastrointestinal tract in children: GERD Peptic ulcer Inflammatory bowel diseases Functional disorders of gastrointestinal tract in children
  3. 3. Most common organic disorders of gastrointestinal tract Esophagus GERD Stomach Chronic gastritis Peptic ulcer Duodenum Chronic duodenitis Peptic ulcer Pancreas Chronic pancreatitis Intestine Ulcerative colitis Crohn disease
  4. 4. Gastroesophageal reflux (GER) is effortless retrograde movement of gastric contents into the esophagus Gastroesophageal reflux disease (GERD) is a digestive disorder that is caused by gastric acid flowing from the stomach into the esophagus.
  5. 5. Is GER normal or patology? GER is considered a normal physiologic process that occurs several times a day in healthy infants, children, and adults. GER is generally associated with transient relaxations of the lower esophageal sphincter (LES) independent of swallowing, which permits gastric contents to enter the esophagus. Episodes of GER in healthy adults tend to occur after meals, last less than 3 min, and cause few or no symptoms.
  6. 6. Etiological and pathogenetic factors of GER reduced tone of the LES transient relaxations of the LES increased intra-abdominal pressure, cough, respiratory difficulty (asthma or cystic fibrosis), and hiatal hernia. esophagitis (which impairs esophageal motility) When esophagitis develops as a result of acid reflux, esophageal motility and LES function are impaired further, creating a cycle of reflux and esophageal injury.
  7. 7. GERD. Clinical symptoms in infants spits up, Sings of esophagitis (irritability, arching, feeding aversion) Apnea, stridor failure to thrive
  8. 8. GERD. Clinical symptoms in older children heartburn, dysphagia, chest pain(?) cough, wheezing, hoarse voice, aspiration pneumonia, recurrent otitis media or sinusitis dental erosions failure to thrive
  9. 9. GERD. Investigations CBC anemia, Serology - hypoalbuminemia secondary to esophageal bleeding and inflammation Barium upper gastrointestinal series (contrast radiography) helps to rule out gastric outlet obstruction, malrotation, or other anatomic contributors to GER. A negative barium study does not rule out GER.
  10. 10. GERD. Investigations (cont.) 24-hour esophageal pH probe monitoring, uses a pH electrode placed transnasally into the distal esophagus, with continuous recording of esophageal pH (less 4). Esophageal impedance monitoring, which records the migration of electrolyte-rich gastric fluid in the esophagus. Endoscopy (biopsy?) is useful to rule out esophagitis, esophageal stricture, and anatomic abnormalities.
  11. 11. Endoscopic image of a normal esophagus (A) and erosive peptic esophagitis (B). // Nelson textbook of Pediatrics 19th ed.
  12. 12. GERD MANAGEMENT 1. Lifestyle modification Thickened feedings Smaller, more frequent feedings Avoidance of tobacco smoke and alcohol Abstaining from caffeine Positional therapy- upright in seat, elevate head of crib or bed Reduces number of episodes, enhances nutrition Can be of some help; be careful not to underfeed child Always a good idea; may help control reflux symptoms Offers some benefit Prone positioning with head up is helpful, but not for young infants due to risk of SIDS For patients with nocturnal GERD.For patients with nocturnal GERD.
  13. 13. GERD MANAGEMENT 2. Pharmacological therapy Acid supressant Proton pump inhibitorProton pump inhibitor (PPI)(PPI) Histamine H2 receptorHistamine H2 receptor antagonistantagonist (H2RA)(H2RA) MetoclopramideMetoclopramide (prokinetic)(prokinetic) Antacids (?)Antacids (?) Effective medicalEffective medical therapy for heartburntherapy for heartburn and esophagitisand esophagitis Reduces heartburn, lessReduces heartburn, less effective for healingeffective for healing esophagitisesophagitis Enhances stomachEnhances stomach emptying and LES toneemptying and LES tone
  14. 14. Peptic ulcer disease Peptic ulcer disease, the end result of inflammation due to an imbalance between cytoprotective and cytotoxic factors in the stomach and duodenum, manifests with varying degrees of gastritis or frank ulceration.
  15. 15. Peptic ulcer. Etiology Primary: H. pylori Idiopathic ulcer Secondary: Drugs (aspirin and NSAIDs, alcohol) Illnesses (CNS disease, burns, sepsis, multi-organ system failure, chronic lung disease, Crohn disease, cirrhosis) Toxins
  16. 16. PATHOGENIC PROPERTIES OF HELICOBACTER PYLORI Adheres to gastric epithelium Lives within mucous gel layer overlying gastric epithelium Penetrates intercellular junctions Invades gastric glands and canaliculi of parietal cells Produces cytotoxins Induces epithelial cytolysis and disrupts intercellular junctions
  17. 17. PATHOGENIC PROPERTIES OF HELICOBACTER PYLORI Increases permeability of mucous layer to hydrogen ions and pepsin Enables gastric acid and pepsin to create ulcer craters Evades host immune defenses Damages tissue Secretes urease to produce ammonia, which protects it from gastric acid
  18. 18. PU. Pathogenesis Excessive acid secretion (a large parietal cell mass, hypersecretion by antral G cells, and increased vagal tone, resulting in increased acid secretion in response to meals and increased secretion during the night). Disorders of mucosal defense mechanisms
  19. 19. The most important differences between Nonulcer dyspepsia and Peptic Ulcer Disease (clinical symptoms) Nonulcer dyspepsiaNonulcer dyspepsia ChronicChronic gastroduodenitisgastroduodenitis Peptic Ulcer DiseasePeptic Ulcer Disease Upper abdominal locationUpper abdominal location FullnessFullness BloatingBloating NauseaNausea Alarm symptoms:Alarm symptoms: Weight lossWeight loss HematemesisHematemesis Melena, heme-positiveMelena, heme-positive stoolsstools Chronic vomitingChronic vomiting Microcytic anemiaMicrocytic anemia Nocturnal painNocturnal pain Frog position in severe crampy abdominal pain
  20. 20. Investigation for PU Endoscopy-mandatory with alarm symptoms Test for H.pylori CBC, ESR, Amylase, lipase, Abdominal ultrasound
  21. 21. What tests H.pylori are available? Non-invasive Diagnostic Tests Serologic tests Urea breath tests Stool antigen Endoscopic Tests Urease Histology Culture PCR
  22. 22. Helicobacter pylori infection revealed by endoscopy (nodular gastropathy). http://emedicine.medscape.com/article
  23. 23. Helicobacter pyloriassociated peptic ulcer in the duodenal bulb. http://emedicine.medscape.com/article
  24. 24. Treatment of peptic ulcer Diet Acid suppression or neutralization H2-receptor antagonists Proton pump inhibitors (PPI) Cytoprotective Agents
  25. 25. Treatment of H. pylori infection (eradication) Amoxicillin + Metronidazole for 14 days+ PPI for 1 mo or Amoxicillin + Clarythromycin for 14 days + PPI for 1 mo or Clarithromycin + Metronidazole for 14 days +PPI for 1 mo Adapted from Gold BD, Colletti RB, Abbott M, et al: Medical position statement: The North American Society for Pediatric Gastroenterology and Nutrition. Helicobacter pylori infection in children: recommendations for diagnosis and treatment, J Pediatr Gastroenterol Nutr 31:490497, 2000.
  26. 26. Treatment of H. pylori infection (eradication) The sequential treatment regimen (10-day) for the first 5 days PPI + amoxicillin for the remaining 5 days PPI + clarithromycin + metronidazole.
  27. 27. Inflammatory bowel disease (IBD) 2 distinctive disorders of idiopathic chronic intestinal inflammation: Crohn disease Ulcerative colitis.
  28. 28. Crohns disease is characterized by acute and chronic inflammation of the small and large intestine and structures apart from the bowel (BA Lashner in Inflammatory Bowel Diseases, J Kirsner ed. 5the ed WB Saunders, 2000) Ulcerative colitis is an inflammatory disease of the colon of unknown etiology (PB Miner in Inflammatory Bowel Diseases, J Kirsner ed. 5the ed WB Saunders, 2000)
  29. 29. Pathogenesis of IBD Genetic factors Environmental influences Defective Immune Regulation
  30. 30. Who is affected by Crohn's disease? all ages, the age group most often affected is between 15 years to 35 years. Males = females
  31. 31. Clinical symptoms of Crohn's disease abdominal pain diarrhea rectal bleeding (obvious blood in the stools or black, tar like stools) fever weight loss failure to grow
  32. 32. Crohn's disease (ileitis or enteritis, granulomatous colitis) Although Crohn disease can first appear as a rectal fissure or fistula, the rectum is often spared. Arthritis/arthralgia occurs in a minority (11%) of affected children. Other extraintestinal symptoms include erythema nodosum or pyoderma gangrenosum, liver disease, renal calculi, uveitis, anemia, specific nutrient deficiency, and growth failure.
  33. 33. Diagnosis of Crohn's disease In addition to a complete medical history and physical examination, diagnostic procedures may include: CBC- anemia, leukocytosis Stool culture - to determine a parasite or bacteria Endoscopy (colonoscopy) Biopsy
  34. 34. The colonoscopic images that follow show moderate-to-severe inflammation of the ileum typical of Crohn's disease, and severe colitis with ulceration, friability, and mucopurulent exudate. http://www.consultantlive.com/gastrointestinal-disordershttp://www.consultantlive.com/gastrointestinal-disorders
  35. 35. Ulcerative colitis an idiopathic chronic inflammatory disorder, is localized to the colon and spares the upper gastrointestinal (GI) tract.
  36. 36. Ulcerative Colitis Signs and Symptoms Diarrhea Rectal bleeding Tenesmus Passage of mucus Crampy abdominal pain.
  37. 37. Clinical evaluation Rise in acute-phase reactants: CRP, platelet count, ESR, and a decrease in hemoglobin. Fecal lactoferrin is a highly sensitive and specific marker for detecting intestinal inflammation. Fecal calprotectin levels correlate well with histologic inflammation, predict relapses, and detect ileitis. In severely ill patients, the serum albumin level will fall rather quickly. Leukocytosis may be present but is not a specific indicator of disease activity.
  38. 38. Diagnosis of ulcerative colitis Flexible sigmoidoscopy Biopsy for histologic examination of the colon.
  39. 39. Ulcerative colitis. Specimen from colectomy reveals diffusely hemorrhagic granular mucosa in a continuous distribution. http://emedicine.medscape.com/article
  40. 40. Some Medications Commonly Prescribed for Management of IBD Medication Class Mechanism of action Comments Prednisone Corticosteroid Decreases inflammation Can cause weight gain, bone loss, glucose intolerance, behavioral changes Sulfasalazin e 5-aminosalicylate (sulfapyridine plus aspirin-like compound) Decreases inflammation, helps maintain remission Can cause nausea, headache, diarrhea, abdominal pain Mesalamine olsazine 5-aminosalicylate (mesalamine plus resin coating) Decreases inflammation, helps maintain remission Fewer side effects than sulfasalazine because there is no sulfa component; active ingredient is delivered directly to the ileum and colon
  41. 41. Azathioprine,Azathioprine, 6-MP,6-MP, cyclosporine-cyclosporine- AA ImmunosuppreImmunosuppre ssantssant antimetabolitesantimetabolites SuppressesSuppresses immuneimmune activationactivation Azathioprine and 6-MPAzathioprine and 6-MP are usually combinedare usually combined with a faster-actingwith a faster-acting medication, such asmedication, such as prednisone;prednisone; cyclosporine workscyclosporine works faster but can causefaster but can cause unwanted effectsunwanted effects including trembling,including trembling, confusion, andconfusion, and irregular heart rateirregular heart rate InfliximabInfliximab ImmunomodulImmunomodul atorator Blocks TNF-Blocks TNF- alpha receptoralpha receptor bindingbinding Can cause nausea,Can cause nausea, vomiting, fatiguevomiting, fatigue BudesonideBudesonide Non-systemicNon-systemic corticosteroidcorticosteroid LocalizedLocalized release into therelease into the GI tractGI tract Side effects includeSide effects include headache, respiratoryheadache, respiratory infection, nauseainfection, nausea
  42. 42. Functional gastrointestinal disorders (FGIDs) are defined as a variable combination of chronic or recurrent gastrointestinal symptoms not explained by structural or biochemical abnormalities.
  43. 43. There are no structural abnormalities that can be seen by endoscopy, X- ray, or blood tests. Thus it is identified by the characteristics of the clinical symptoms and infrequently, when needed, limited tests.
  44. 44. G. Functional disorders: neonatesG. Functional disorders: neonates and toddlersand toddlers G1.G1. Infant regurgitation Uncomplicated involuntary return (regurgitation) of stomach contents into the mouth. Common and normal in infants. G2.G2.Infant rumination syndrome Voluntary, habitual regurgitation of recently swallowed stomach contents. Rare. G3.G3.Cyclic vomiting syndrome Recurrent episodes of intense nausea and vomiting lasting hours to days separated by symptom-free intervals lasting weeks to months. G4.G4.Infant colic Long bouts of crying or irritability without obvious cause.
  45. 45. G. Functional disorders:G. Functional disorders: neonates and toddlersneonates and toddlers G5.G5.Functional diarrhea Daily, painless, recurrent passage of 3 or more large, unformed stools for at least 4 weeks in infancy or preschool years. G6.G6.Infant dyschezia Straining and crying with stool passage. G7.G7.Functional constipation Infrequent, painful, hard, or large diameter bowel movements.
  46. 46. H. Functional disorders: children and adolescents H1. Vomiting and aerophagia H1a. Adolescent rumination syndrome H1b. Cyclic vomiting syndrome H1c. Aerophagia H2. Abdominal pain-related FGIDs H2a. Functional dyspepsia H2b. Irritable bowel syndrome H2c. Abdominal migraine H2d. Childhood functional abdominal pain H2dl. Childhood functional abdominal pain syndrome H3. Constipation and incontinence H3a. Functional constipation H3b. Nonretentive fecal incontinence
  47. 47. HI. Vomiting and Aerophagia H1a. Adolescent Rumination Syndrome Epidemiology. Rumination syndrome is most common in male infants and female adolescents. Diagnostic Criteria* Must include all of the following 1. Repeated painless regurgitation and rechewing or expulsion of food that a. begin soon after ingestion of a meal b. do not occur during sleep c. do not respond to standard treatment for gastroesophageal reflux 2. No retching 3. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject's symptoms *Criteria fulfilled at least once per week for at least 2 months before diagnosis
  48. 48. Differential diagnosis Gastroesophageal reflux Esophageal achalasia Gastroparesis Bulimia nervosa Obstructive anatomical disorders That must be excluded by appropriate diagnostic tests.
  49. 49. Treatment. Behavioral therapy Multidisciplinary approach Tricyclic antidepressants Postpyloric feedings, either through nasojejunal or gastrojejunal feeding catheters, may be necessary when weight loss is significant. Rumination appears to serve the purpose of self- stimulation in intellectually handicapped children and may be associated with eating disorders in adolescents.
  50. 50. H1b. Cyclic Vomiting Syndrome The criteria discussed in the neonatal/toddler section should also be used for children and adolescents.
  51. 51. H1b. Diagnostic Criteria for Cyclic Vomiting Syndrome Must include all of the following: 1. Two or more periods of intense nausea and unremitting vomiting or retching lasting hours to days 2. Return to usual state of health lasting weeks to months
  52. 52. TreatmentTreatment and preventionprevention I. Between attacks: Elimination of triggers factors. Sedative, neuroleptic drugs: amitriptyline, sanomigran (pizotifen), phenobarbital, or propranolol may reduce frequency or eliminate episodes
  53. 53. TreatmentTreatment and preventionprevention II. During the prodrome of CVS Oral: Antiemetic medications (ondansetron) Sedative, anxiolytic and antiemetic drugs (longacting benzodiazepine) Acidinhibiting drug agent to protect esophageal mucosa and dental enamel Deep sleep for several hours may prevent the episode
  54. 54. TreatmentTreatment and preventionprevention III. Once an episode starts Intravenous: sedated of patients until the episode ends (diazepam or lorazepam), fluids, electrolytes H2-histamine receptor antagonists
  55. 55. H1c. Aerophagia Epidemiology. Aerophagia has been observed in 8.8% of the institutionalized mentally handicapped population.
  56. 56. Diagnostic Criteria* for Aerophagia Must include at least 2 of the following: 1. Air swallowing 2. Abdominal distention because of intraluminal air 3. Repetitive belching and/or increased flatus *Criteria fulfilled at least once per week for at least 2 months before diagnosis
  57. 57. Differential diagnosis Asthma: excessive air swallowing is often caused by anxiety and may accompany asthma crisis). Motility disorders (chronic intestinal pseudo- obstruction and malabsorption syndromes): in patients with aerophagia, the abdominal distention decreases or resolves during sleep. Hydrogen breath tests can be used to rule out sugar malabsorption and/or bacterial overgrowth.
  58. 58. Treatment Effective reassurance and explanation of symptoms to both parents and child are essential. Eating slowly avoidance of chewing gum or drinking carbonated beverages psychotherapeutic strategies
  59. 59. H2. Abdominal pain-related FGIDs H2a. Functional dyspepsia H2b. Irritable bowel syndrome H2c. Abdominal migraine H2d. Childhood functional abdominal pain H2d1. Childhood functional abdominal pain syndrome
  60. 60. Chronic abdominal pain may be the predominant clinical manifestation of a large number of organic disorders, but in the majority of cases, it is a functional disorder with no anatomic, metabolic, infectious, inflammatory or neoplastic cause to account for it.
  61. 61. What Causes the FGD in child/adolescent? Unknown Biopsychosocial model Abnormal gastrointestinal sensory perception (Visceral sensation) Abnormal gastrointestinal motility Psychological factors Family history (genetic factors) Disordered brain-gut communication Infection Altered gut bacteria Intestinal inflammation
  62. 62. Abnormal Sensation. Two-thirds of patients with FGIDs have increased sensitivity to gut stimuli (visceral hypersensitivity). As a result, normal physiologic activities such as gut contractions may cause pain or discomfort. In other words, persons with these conditions tend to experience pain or discomfort from sensations that go unnoticed by other people.
  63. 63. Abnormal Motility. The gut uses a highly coordinated series of contractions to move food, absorb nutrients, and eliminate waste. In FGI disorders these activities are sometimes altered. Such dysmotility may cause various problems ranging from swallowing difculties to incontinence. For instance, if the movement of food or waste is too rapid diarrhea may develop. If too slow, then bloating or constipation may occur. Likewise, esophageal or intestinal muscle spasms cause pain.
  64. 64. The mechanisms by which abnormal sensation and motility may occur include the following: Brain-gut Interactions Genetic Factors Altered Bacterial Flora.
  65. 65. Brain-gut Interactions. In patients with FGIDs, brain-gut interactions are disordered. Thus, these individuals may abnormally process bowel sensations and consequently experience pain, nausea, and other GI symptoms. Additionally, in patients with FGIDs environmental and psychological stressors may have a greater effect on GI symptoms.
  66. 66. Genetic Factors. Functional GI disorders often run in families. Research suggests that this may be related to underlying genetic factors, such as abnormalities in serotonin transporter genes.
  67. 67. Infection and Intestinal Inammation Among previously asymptomatic patients with a GI infection, between 7% and 31% go on to develop IBS with symptoms that may last for months to even years. In these patients symptoms may be the result of persistent, low-grade intestinal inammation.
  68. 68. Altered Bacterial Flora. When the normal balance in the intestine between benecial and harmful bacteria is changed, it may lead to changes in the function of the GI tract and chronic GI symptoms. Also, certain studies suggest a benet from certain probiotics and antibiotics.
  69. 69. Alarm Symptoms, Signs, and Features in Children and Adolescents with Noncyclic Abdominal Pain-Related FGIDs (Red flags) Pain localized away from the umbilicus Pain interrupting sleep at night Dysphagia Significant vomiting or diarrhea Blood in stool Involuntary weight loss Growth retardation Delayed puberty Extraintestinal symptoms (fever, rash, joint pain, apthous ulcers, urinary symptoms) Abnormal labs: anemia, elevated ESR Family history of inflammatory bowel disease, celiac disease, or peptic ulcer disease
  70. 70. In children with abdominal pain-related FGIDs, this alarm features, signs, and symptoms absent!!!
  71. 71. Organic pain - differential GI tract Chronic constipation Lactose intolerance Parasite infection (Giardia) Excess fructose/sorbitol ingestion Crohns Peptic ulcer Reflux esophagitis Meckels diverticulum Recurrent intussusception Hernia internal, inguinal, abdominal wall Chronic appendicitis
  72. 72. Organic pain differential(cont) Gallbladder and pancreas Cholelithiasis Choledochal cyst Recurrent pancreatitis Genitourinary tract UTI Hydronephrosis Urolithiasis
  73. 73. Organic pain differential (end) Miscellaneous causes Familial Mediterranean fever Sickle cell crisis Lead poisoning HSP Angioneurotic edema Acute intermittent porphyria
  74. 74. Limited screening for organic disease CBC, ESR, CRP for infectious/inflammatory process or anemia UA to exclude UTI Stool tests (coprogram) Giardia antigen if clinical suspicion H.pylori if report early satiety and epigastric pain Abdominal Ultrasound CT if abscess or extraintestinal or retroperitoneal mass suspected. Endoscopy if chronic abdominal pain AND persistent bleeding, weight loss, early satiety with peptic symptoms, anorexia, chest pain or vomiting.
  75. 75. Recommendation of North American Society for Pediatric Gastroenterology, Hepatology and Nutrition Additional diagnostic evaluation is not required in children without alarm symptoms Testing may be carried out to reassure children and their parents
  76. 76. H2a. Functional Dyspepsia Epidemiology. The prevalence of dyspepsia varies between 3.5% and 27% depending on gender and country of origin.
  77. 77. H2a. Diagnostic Criteria* for Functional Dyspepsia Must include all of the following: 1. Persistent or recurrent pain or discomfort centered in the upper abdomen (above the umbilicus) 2. Not relieved by defecation or associated with the onset of a change in stool frequency or stool form (ie, not IBS) 3. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject's symptoms *Criteria fulfilled at least once per week for at least 2 months before diagnosis
  78. 78. Dyspepsia is usually polysymptomatic. The pain or discomfort can be associated with vomiting, nausea, abdominal fullness, bloating or early satiety. 26% of pediatric subjects has ulcer-like symptoms while 15% manifested dysmotility-like symptoms.
  79. 79. Differential diagnosis of functional dyspepsia Inflammation Gastroesophageal reflux Eosinophilic esophagitis or gastroenteritis Helicobacter pylori gastritis Duodenal ulcer Inflammatory bowel disease Dysmotility Gastroparesis Biliary dyskinesia Pseudo-obstruction Extraintestinal disorders Chronic hepatitis Chronic pancreatitis Chronic cholecystitis Abdominal migraine Psychiatric disorders Ureteropelvic obstruction
  80. 80. Physiological features. Disordered gastric myoelectrical activity, delayed gastric emptying, altered antroduodenal motility, reduced gastric volume response to feeding Rapid gastric emptying associated with slow bowel transit was found in dyspeptic children with bloating as predominant symptom.
  81. 81. Treatment Avoidance of nonsteroidal antiinflammatory agents Avoidance foods that aggravate symptoms (eg, caffeine and spicy and fatty foods) Antisecretory agents (H2 blockers or proton pump inhibitors) are often offered for pain predominant symptoms Prokinetics (metoclopramide, and domperidone and cisapride where available) for symptoms associated with discomfort. Psychological comorbidity should be
  82. 82. H2b. Irritable Bowel Syndrome Epidemiology. According to Rome II criteria, IBS was diagnosed in 0.2% of children (mean age, 52 months) seen by primary care pediatricians and in 22% 45% of children aged 4-18 years presenting to pediatric gastroenterology clinics.
  83. 83. H2b. Diagnostic Criteria* for Irritable Bowel Syndrom Must include all of the following: 1. Abdominal discomfort (an uncomfortable sensation not described as pain) or pain associated with 2 or more of the following at least 25% of the time: a. Improved with defecation b. Onset associated with a change in frequency of stool c. Onset associated with a change in form (appearance) of stool 2. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject's symptoms *Criteria fulfilled at least once per week for at least 2 months before diagnosis
  84. 84. Symptoms that cumulatively support the diagnosis of IBS are (1)abnormal stool frequency (4 or more stools per day and 2 or less stools per week), (2)abnormal stool form (lumpy/hard or loose/watery stool), (3)abnormal stool passage (straining, urgency, or feeling of incomplete evacuation), (4)passage of mucus, (5)bloating or feeling of abdominal distention.
  85. 85. Physiological features. Visceral hypersensitivity has been documented in children with IBS. It may be related to numerous processes, including infection, inflammation, intestinal trauma, or allergy, and may be associated with disordered gut motility. Genetic predisposition, early stressful events, and ineffective patient-coping mechanisms are compounding factors.
  86. 86. Psychological features. Anxiety, depression, and multiple other somatic complaints have been reported by IBS children and their parents.
  87. 87. Differential diagnosis of irritable bowel syndrome Inflammation Ulcerative colitis Crohn disease Infection Parasitic (Lamblia (Giardia) intestinalis Bacterial (Yersinia, Campylobacter, Tuberculosis, Clostridium difficile) Drug induced diarrhea Celiac disease Lactose intolerance Neoplasia (lymphoma)
  88. 88. The most important differential sings DiseaseDisease Functional: irritableFunctional: irritable bowel syndromebowel syndrome InflammatoryInflammatory bowel diseasebowel disease OnsetOnset RecurrentRecurrent RecurrentRecurrent LocationLocation ofof painpain Periumbilical, splenic andPeriumbilical, splenic and hepatic flexureshepatic flexures Depends on site ofDepends on site of involvementinvolvement Pain qPain qualityuality Dull, crampy, intermittent;Dull, crampy, intermittent; duration 2 hrduration 2 hr Dull cramping,Dull cramping, tenesmustenesmus OtherOther symptomssymptoms Family stress, schoolFamily stress, school phobia, diarrhea andphobia, diarrhea and constipation;constipation; hypersensitive to pain fromhypersensitive to pain from distentiondistention Malaise, fever,Malaise, fever, weight loss weight loss hematocheziahematochezia (Rectal bleeding)(Rectal bleeding)
  89. 89. Clinical evaluation. A normal physical examination and growth curve with the absence of alarm signals substantiate a positive diagnosis. Potential triggering events and psychosocial factors are important to explore. Education about mechanisms leading to IBS avoids unnecessary invasive testing.
  90. 90. Treatment. Peppermint oil which relaxes intestinal smooth muscles by decreasing calcium influx into the cells. Citalopram, a selective serotonin reuptake inhibitor Amitriptyline, a tricyclic antidepressant which has anticholinergic as well as analgesic effects, significantly improved symptoms in adolescents with diarrhea-predominant IBS. Anticholinergic agents, dicyclomine and hyoscyamine, block muscarinic effects of acetylcholine on the gastrointestinal tract, relaxing smooth muscles, slowing intestinal motility and decreasing diarrhea. Gut-directed hypnotherapy and cognitive behavioral therapy has also been shown to be beneficial.
  91. 91. H2c. Abdominal Migraine It has been suggested that abdominal migraine, cyclic vomiting syndrome, and migraine headache comprise a continuum of a single disorder, with affected individuals often progressing from one clinical entity to another.
  92. 92. Epidemiology. Abdominal migraine affects 1%-4% of children. It is more common in girls than boys (3:2), with a mean age of onset at 7 years and a peak at 1012 years.
  93. 93. H2c. Diagnostic Criteria* for Abdominal Migraine Must include all of the following: 1. Paroxysmal episodes of intense, acute periumbilical pain that lasts for 1 hour or more 2. Intervening periods of usual health lasting weeks to months 3. The pain interferes with normal activities 4. The pain is associated with 2 or more of the following: a. Anorexia b. Nausea c. Vomiting d. Headache e. Photophobia f. Pallor 5. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process considered that explains the subject's symptoms Criteria fulfilled 2 or more times in the preceding 12 months Supportive criteria include a family history of migraine and a history of motion sickness.
  94. 94. Clinical evaluation. History Basic metabolic panel An upper gastrointestinal radiography
  95. 95. Differential diagnosis of abdominal migraines Gastrointestinal: Obstruction (volvulus) Recurrent pancreatitis Cholelithiasis Ulcerative colitis Crohn disease Rheumatological Familial Mediterranean fever Systemic lupus syndrome Metabolic Acute intermittent porphyria Genitourinary Ureteropelvic obstruction Ovarian torsion The paroxysmal nature of symptoms and the absence of the characteristic abdominal pain between episodes make
  96. 96. Physiological features Episodic dysautonomia, visual evoked responses, mitochondrial DNA mutations that cause deficits in cellular energy production, and heightened hypothalamic stress response that activates the emetic response. A family history of migraines is very common. A recent study confirmed that the mothers and grandmothers of patients with abdominal migraines have twice the prevalence of migraine headaches compared with controls.
  97. 97. Treatment. Potential triggers to be avoided: caffeine-, nitrite-, and amine-containing foods prolonged fasting, emotional arousal, travel, altered sleep patterns, exposure to flickering or glaring lights.
  98. 98. Treatment. Prophylactic therapy includes: amitriptyline, cyproheptadine, phenobarbital or propranolol. These medications have been shown to reduce the frequency as well as severity of episodes in children. Abortive therapy includes: sumatriptan, a serotonin receptor agonist, which substantially decreases frequency, duration, and intensity of attacks ondansetron, a serotonin receptor antagonist, which has a 76% efficacy rate in reducing the severity of vomiting.
  99. 99. H2d. Childhood Functional Abdominal Pain Epidemiology. The prevalence of FAP in 4 18-year-old patients presenting to gastroenterology clinics varied between 0% to 7.5%.
  100. 100. Diagnostic Criteria* for Childhood Functional Abdominal Pain Must include all of the following: 1. Episodic or continuous abdominal pain 2. Insufficient criteria for other FGIDs 3. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject's symptoms * Criteria fulfilled at least once per week for at least 2 months before diagnosis
  101. 101. H2dl. Diagnostic Criteria* for Childhood Functional Abdominal Pain Syndrome Must include childhood functional abdominal pain at least 25% of the time and 1 or more of the following: 1. Some loss of daily functioning 2. Additional somatic symptoms such as headache, limb pain, or difficulty sleeping * Criteria fulfilled at least once per week for at least 2 months before diagnosis
  102. 102. Clinical evaluation. CBC count, ESR or C-reactive protein, urinalysis, urine culture. Stool culture, stool examination for ova and parasites, and breath hydrogen testing for carbohydrate malabsorption can be considered in a child with diarrhea. Ultrasound examination of the abdomen can give information about kidneys, gallbladder, and pancreas. Additional tests should only be done when indicated, based on the history and physical examination.
  103. 103. Psychological features. The symptoms of anxiety, depression, and somatization described in both children with recurrent abdominal pain and their parents.
  104. 104. Treatment A biopsychosocial approach should be employed in the treatment of children with FAP. To identify and, if possible, reverse physical and psychological stress factors that may play a role in the onset, severity, exacerbation or maintenance of pain. Reassurance and explanation of possible mechanisms involving the brain-gut interaction, the possible role of psychosocial factors should be explained to the child and
  105. 105. H3. Constipation and Incontinence H3a. Functional Constipation The term "functional constipation" describes all children in whom constipation does not have an organic etiology.
  106. 106. ` Epidemiology. 0,3% and 8% in the pediatric population. It represents 3%5% of general pediatric outpatient visits and up to 25% of pediatric gastroenterology consultations. Peak incidence occurs at the time of toilet training (between 2 and 4 years of age), with an increased prevalence in boys. A positive family history has been found in 28% 50% of constipated children.
  107. 107. H3a. Diagnostic Criteria* for Functional Constipation Must include 2 or more of the following in a child with a developmental age of at least 4 years with insufficient criteria for diagnosis of IBS: 1. Two or fewer defecations in the toilet per week 2. At least 1 episode of fecal incontinence per week 3. History of retentive posturing or excessive volitional stool retention 4. History of painful or hard bowel movements 5. Presence of a large fecal mass in the rectum 6. History of large diameter stools that may obstruct the toilet * Criteria fulfilled at least once per week for at least 2 months before diagnosis
  108. 108. Clinical evaluation. A careful history: the time after birth of the first bowel movement, the time of onset of the problem, characteristics of stools (frequency, consistency, caliber, and volume), the presence of associated symptoms (pain at defecation, abdominal pain, blood on the stool or the toilet paper, and fecal incontinence), stool withholding behavior, urinary problems, and neurologic deficits.
  109. 109. Psychological features. Children presenting with constipation have lower quality of life and exhibit poorer self-esteem. Constipated children display more anxiety related to toilet training.
  110. 110. Differential diagnosis This unprepared single-contrast barium enema demonstrates a transition zone consistent with Hirschsprung disease. Contrast enema of a patient with megasigmoid and impacted stool. http://emedicine.medscape.com/article
  111. 111. Treatment. Polyethylene glycol 11,5 g/kg/d per 3 days is usually effective in treating fecal impaction. Stimulant laxatives for maintenance, stool softeners. Rewards for success in toilet learning are often helpful.
  112. 112. H3b. Nonretentive Fecal Incontinence Nonretentive fecal incontinence represents the repeated, inappropriate passage of stool into a place other than the toilet in a child older than 4 years with no evidence of fecal retention.
  113. 113. H3b. Nonretentive Fecal Incontinence Epidemiology. Fecal incontinence is reported to be 4,1% in the 5-6-year- old age group and 1,6% in the 11 12-year-old age group and has been noted to be more frequent among boys and children from families with lower socioeconomic status.
  114. 114. H3b. Diagnostic Criteria* for Nonretentive Fecal Incontinence Must include all of the following in a child with a developmental age at least 4 years: 1. Defecation into places inappropriate to the social context at least once per month 2. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject's symptoms 3. No evidence of fecal retention * Criteria fulfilled for at least 2 months before diagnosis
  115. 115. Clinical evaluation. An abdominal radiograph may sometimes be obtained to diagnose occult fecal retention because of incomplete passage of stool.
  116. 116. Treatment Education, a non accusatory approach; Regular toilet use with rewards; Consultation of a mental health professional
  117. 117. Success is not final, failure is not fatal. It is the courage to continue that counts. Winston Churchill
  118. 118. Thanks!!!