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.
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.
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.
19.
20. 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
21. 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 loss Weight loss
Hematemesis Hematemesis
Melena, heme-positive Melena, heme-positive
stoolsstools
Chronic vomiting Chronic vomiting
Microcytic anemia Microcytic anemia
Nocturnal pain Nocturnal pain
Frog position in severe crampy
abdominal pain
22. Investigation for PU
Endoscopy-mandatory with alarm
symptoms
Test for H.pylori
CBC, ESR,
Amylase, lipase,
Abdominal ultrasound
28. 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 31:490–497, 2000.
29. 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.
31. Crohn’s 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)
33. Who is affected by Crohn's
disease?
all ages, the age group most often
affected is between 15 years to 35
years.
Males = females
34. 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
35. 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.
36. 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
37. 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
38. Ulcerative colitis
an idiopathic chronic inflammatory
disorder, is localized to the colon
and spares the upper
gastrointestinal (GI) tract.
40. 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.
41. Diagnosis of ulcerative colitis
Flexible sigmoidoscopy
Biopsy for histologic
examination of the colon.
42. Ulcerative colitis. Specimen from
colectomy reveals diffusely hemorrhagic
granular mucosa in a continuous
distribution.
http://emedicine.medscape.com/article
43. 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
44. 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
45. Functional
gastrointestinal disorders
(FGIDs) are defined as a
variable combination of
chronic or recurrent
gastrointestinal symptoms not
explained by structural or
biochemical abnormalities.
46. 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.
47. 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.
48. 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.
50. 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
51. Differential diagnosis
Gastroesophageal reflux
Esophageal achalasia
Gastroparesis
Bulimia nervosa
Obstructive anatomical disorders
That must be excluded by appropriate
diagnostic tests.
52. 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.
53. H1b. Cyclic Vomiting Syndrome
The criteria discussed in the
neonatal/toddler section should also
be used for children and adolescents.
54. 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
55. 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
56. 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
57. 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
59. 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
60. 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.
61. 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
63. 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.
64. 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
65. 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.
66. 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 difficulties 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.
67. The mechanisms by which abnormal
sensation and motility may occur
include the following:
Brain-gut Interactions
Genetic Factors
Altered Bacterial Flora.
68. 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.
69. 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.
70. Infection and Intestinal Inflammation
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
inflammation.
71. Altered Bacterial Flora.
When the normal balance in the
intestine between beneficial 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 benefit
from certain probiotics and antibiotics.
72. 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
73. In children with abdominal
pain-related FGIDs, this
alarm features, signs, and
symptoms absent!!!
77. 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.
78. 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
79. H2a. Functional Dyspepsia
Epidemiology. The prevalence of
dyspepsia varies between 3.5% and
27% depending on gender and
country of origin.
80. 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
81. 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.
83. 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.
84. 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
85. 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.
86. 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
87. 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.
88. 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.
91. 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)
92. 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.
93. 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.
94. 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.
95. 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 10—12 years.
96. 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.
98. 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
99. 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.
100. 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.
101. 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.
102. 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%.
103. 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
104. 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
105. 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.
106. Psychological features. The
symptoms of anxiety, depression, and
somatization described in both
children with recurrent abdominal
pain and their parents.
107. 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
108. H3. Constipation and
Incontinence
H3a. Functional Constipation
The term "functional constipation"
describes all children in whom
constipation does not have an organic
etiology.
109. ` 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.
110. 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
111. 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.
112. 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.
113. 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
114. Treatment.
Polyethylene glycol 1—1,5 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.
115. 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.
116. 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.
117. 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
118. Clinical evaluation. An abdominal
radiograph may sometimes be
obtained to diagnose occult fecal
retention because of incomplete
passage of stool.
119. Treatment
Education, a non accusatory approach;
Regular toilet use with rewards;
Consultation of a mental health
professional
120. Success is not final,
failure is not fatal.
It is the courage to
continue that counts.
Winston Churchill
