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
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. 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. 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. 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. 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. 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. GERD. Clinical symptoms in infants spits up, Sings of
esophagitis (irritability, arching, feeding aversion) Apnea,
stridor failure to thrive
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. 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. 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. Endoscopic image of a normal esophagus (A) and erosive
peptic esophagitis (B). // Nelson textbook of Pediatrics 19th
ed.
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. 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. 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. 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. 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. 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. 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. 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. Investigation for PU Endoscopy-mandatory with alarm
symptoms Test for H.pylori CBC, ESR, Amylase, lipase, Abdominal
ultrasound
22. Helicobacter pylori infection revealed by endoscopy
(nodular gastropathy). http://emedicine.medscape.com/article
23. Helicobacter pyloriassociated peptic ulcer in the duodenal
bulb. http://emedicine.medscape.com/article
24. Treatment of peptic ulcer Diet Acid suppression or
neutralization H2-receptor antagonists Proton pump inhibitors (PPI)
Cytoprotective Agents
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. 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.
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)
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. 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. 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. 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. 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. Ulcerative colitis an idiopathic chronic inflammatory
disorder, is localized to the colon and spares the upper
gastrointestinal (GI) tract.
36. Ulcerative Colitis Signs and Symptoms Diarrhea Rectal
bleeding Tenesmus Passage of mucus Crampy abdominal pain.
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. Diagnosis of ulcerative colitis Flexible sigmoidoscopy
Biopsy for histologic examination of the colon.
39. Ulcerative colitis. Specimen from colectomy reveals
diffusely hemorrhagic granular mucosa in a continuous distribution.
http://emedicine.medscape.com/article
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. 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. Functional gastrointestinal disorders (FGIDs) are defined
as a variable combination of chronic or recurrent gastrointestinal
symptoms not explained by structural or biochemical
abnormalities.
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. 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. 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.
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. Differential diagnosis Gastroesophageal reflux Esophageal
achalasia Gastroparesis Bulimia nervosa Obstructive anatomical
disorders That must be excluded by appropriate diagnostic
tests.
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. H1b. Cyclic Vomiting Syndrome The criteria discussed in the
neonatal/toddler section should also be used for children and
adolescents.
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. 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. 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. 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. H1c. Aerophagia Epidemiology. Aerophagia has been observed
in 8.8% of the institutionalized mentally handicapped
population.
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. 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. 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
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. 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. 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. 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. The mechanisms by which abnormal sensation and motility may
occur include the following: Brain-gut Interactions Genetic Factors
Altered Bacterial Flora.
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. 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. 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. 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. 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. In children with abdominal pain-related FGIDs, this alarm
features, signs, and symptoms absent!!!
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. 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. H2a. Functional Dyspepsia Epidemiology. The prevalence of
dyspepsia varies between 3.5% and 27% depending on gender and
country of origin.
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. 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.
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. 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. 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. 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. 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. 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. Psychological features. Anxiety, depression, and multiple
other somatic complaints have been reported by IBS children and
their parents.
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. 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. 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. 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. 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. 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. Clinical evaluation. History Basic metabolic panel An upper
gastrointestinal radiography
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. 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. 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. 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. 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. 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. 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. 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. Psychological features. The symptoms of anxiety,
depression, and somatization described in both children with
recurrent abdominal pain and their parents.
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. H3. Constipation and Incontinence H3a. Functional
Constipation The term "functional constipation" describes all
children in whom constipation does not have an organic
etiology.
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. 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. 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. 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. 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. 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. 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. 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. 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. Clinical evaluation. An abdominal radiograph may sometimes
be obtained to diagnose occult fecal retention because of
incomplete passage of stool.
116. Treatment Education, a non accusatory approach; Regular
toilet use with rewards; Consultation of a mental health
professional
117. Success is not final, failure is not fatal. It is the
courage to continue that counts. Winston Churchill