MAJOR SIGNS AND SYMTOMS OF DIGESTIVE

TRACT DISORDERS
1. DYSPHAGIA
A. STRUCTURAL DEFECT non-transfer
- dysphagia
- narrowing within the esophagus
- extrinsic
- foreign body or stricture
B. MOTILITY DISORDERS transfer dysphagia
- oropharyngeal of swallowing
- muscles for ingestion
- neuromuscular disorders (CP)
- GLOBUS
2. REGURGITATION
- PASSIVE effortless movement of stomach
contents into the esophagus and moral
- LES
- GER incompetent or in infants immature
LES
- developmental process / maturity

3. VOMITING
- ACTIVE, highly coordinated reflex process
- increased salivation/involuntary retching
- medullary vomiting center/CTZ/CNS centers
Causes:
MECHANICAL
a. OBSTRUCTIVE - Pyloric stenosis
- Instussuception
- Malrotation
- Atresias/Stenosis
- Adhesive bands
- Hirschsprungs disease
- Imperforate Anus
- Annular Pancreas
b. NON-OBSTRUCTIVE LESIONS
a. GER
b. PARALYTIC ILEUS
c. SEVERE coughing
d. METABOLIC DISORDERS
e. CNS disease
 2. REFLEX
3. NON-SPECIFIC
BILE STAINED VOMITUS obstruction is
below the 2nd part of the duodenum.
CYCLIC VOMITING syndrome with
numerous episodes of vomiting interspersed with
well-intervals.
- 2-5 years old bracket
- equated to be a migraine or a seizure
equivalent.

4. ANOREXIA
- refusal to eat/fussiness about food
 - hunger and satiety centers hypothalamus
- stomach and upper small bowel distention-
SATIATION
- if no ORGANIC CAUSE is discovered,
consider the following:
- slower weight gain between 1-5 years
old
- way of getting attention
- parental neglect, tension between
parents, parent-child conflict, jealousy between
siblings.
- faulty eating habits
- unattractive food
5. CONSTIPATION:
- stool consistency
- stool frequency
- difficulty in passing out stools
- defects in either RECTAL FILLING/RECTAL
EMPTYING
* ineffective COLONIC PERISTALSIS delay in
rectal filling
* STOOL RETENTION lesions in rectal
muscles, sacral SC, a & e fibers, abdominal & pelvic
floor musculature.
6. ABDOMINAL PAIN
- perception
- tolerance
A fibers sharp and localized pain from skin
and muscle
@ fibers dull & poorly localized pain
viscera, peritoneum
VISCERAL pain from dermatomal innervation
of the affected organ
- epigastrium painful stimulus from liver
pancreas biliary tree, stomach, upper bowel
- umbilicus painful stimulus from small
bowel, cecum, appendix or proximal colon
 - suprapubic painful stimulus from dietal
large bowel, urinary tract, pelvic organs.
PARIETAL PAIN more localized and intense
than visceral pain in general most common
provoking stimulus for abdominal pain is TENSION
AND STRETCHING.

7. GASTROINTESTINAL HEMORRHAGE:
- identification of bleeding site
- mucosa of the GI tract
- bleeding varices
 - vascular malformations rare
- small intestine
hematemesis bleeding from esophagus,
stomach, duodenum
hematochezia either a distal bleeding or a
massive hemorrhage above distal ileum (red or
maroon)
melena moderate to mild bleeding above
distal ileum blackened stools of tarry consistency.
-COMPLICATIONS:
non-deficiency anemia, hypotension,
tachycardia, rarely GI symptoms.
ABDOMINAL DISTENTION/ABDOMINAL MASSES
1. decrease tone of the wall musculature
2. increase fluid, gas, solid
ASCITES ascitic fluid in the peritoneal cavity
- both flanks/anteriorly
- transudate decrease protein concentration
- exudate increase protein concentration
(inflammatory conditions, neoplasms)
PNEUMOPERITONEUM tympanitic percussion
noted over solid organs.
- perforated viscus
DIGESTIVE TRACT discreet masses in the
lumen or wall or mesentery
 - fecal masses
- gut wall neoplasms (rare in children)

DIARRHEA:
- decrease consistency, increase frequency in
the passing of stools
- 3 or 7 loose watery stools / day
- consistency rather than frequency, most
important feature
- best defined as excessive loss of fluid and
electrolytes.
- basis of all diarrhea disturbed intestinal
solute transport
voluminous diarrhea disorders from small bowel
absorption
Low volume diarrhea disorders from colonic
absorption

PATHOGENESIS:
a. SECRETORY diarrhea secretagogue e.g.
cholera toxin
-stools watery, large volume
-persists even on an NPO regimen
b. OSMOTIC diarrhea after ingestion of a poorly
absorbed solute e.g. lactose intolerance
- lesser volume and stops with fasting
c. MOTILITY rapid or delayed transit slowed
motility bacterial overgrowth

Management cornerstone
- F & E therapy
- nutritional rehab. during & after
- antimicrobial use, judicious
GASTROESOPHAGEAL REFLUX (GER) CHALASIA
- incompetent LES excessive and passive reflux
of gastric contents
- free reflux across a dilated sphincter
chronically lax sphincter ESOPHAGITIS
- reflux with N pressure [increase intraabdominal
P-coughing, crying, defecating)
Signs and Symptoms of GER linear relation:
* esophageal epithelium
* gastric contents
85% - excessive vomiting in the 1st week of life
10% - 6th week
60% - at 2 y/o SSx abate without treatment:
(upright posture, eats solid food)
 *ASPIRATION Pneumonia
*GROWTH AND WEIGHT GAIN
end result of GER esophagitis hematemesis IDA if
untreated stricture formation
- repeated pneumonia
- inanition
DIAGNOSIS: careful clinical assessment
: assess response to therapy
- severe or complex cases confirmed by Ba
esophagography under fluoroscopic control
strictures
- severe esophagitis ragged mucosal outline on
x-ray
- esophagoscopy with Biopsy
Treatment :
- young infants prone
- older infants/children-raise head of the bed
- keep child upright
- thickening infants formula with cereal
Metoclopramide 0.15mg/kg/dose QID
- gastric emptying
- esophageal motility
- reduce reflux
Esophagitis antacids
- H2 receptor blockers
- Omeprazole improves esophageal
motility
- depress acid secretion
MEDICAL THERAPY
OPERATIVE THERAPY
STRICTURE FORMATION Antireflux therapy
bougienage
NISSEN FUNDUPLICATION
PERCUTANEOUS GASTROJEJUNOSTOMY

ILEUS
- failure of intestinal peristalsis without evidence of
mechanical obstruction
-gut motility
-often associated with abdominal surgery/infection
-metabolic abnormalities (uremia, hypokalemia,
acidosis)
-VINCRISTINE
-LOPERAMIDE anti motility
- presents with: increasing abdominal distention and
: minimal pain; initially
: early mech. obstruction-hyperactive
bowel sounds
- minimal to absent
plain abdominal radiograph - multiple air-flued
levels
contrast radiograph slow movement of Barium
through a patent lumen
Treatment:
-connection of underlying abnormality
 - NGT decompression for abdominal distention
that is assoc. with pain, relieve vomiting
Prokinetic agents

PEPTIC ULCER DISEASE IN CHILDREN:

-imbalance between CYTOPROTECTIVE &
CYTOTOXIC factors in the stomach and duodenum
- GASTRITIS gastric mucosa
- PEPTIC ULCER muscularis mucosa
- gastric ulcers lesser curvature of the stomach
- duodenal ulcers duodenal bulb
CLASSIFICATIONS OF ULCERS in children:
a. Primary peptic ulcers chronic, duodenal
2. Secondary, peptic ulcer acute, gastric
Primary ulcers assoc. with Helicobacter
pyplori infection
Secondary peptic ulcers - stress [sepsis,
shock intracranial lesion cushings ulcer or
secondary to burn injury (curlings ulcer)
- maybe due to drugs (NSAID)

PATHOGENESIS:
at 3-4 y/o gastric acid secretion
approximates adult values
Excessive acid secretion is associated with:
a. large parietal cell mass
 b. hypersecretion by antral GI cells
c. increase vagal tone increased or sustained
acid secretion in response to meals; increase
secretion during the night.
SECRETAGOGUES: promotes gastric acid production
Ach released by the vagus nerve
Histamine secreted by enterochromaffin
cells
Gastrin released by the G cells of the artrum

PROSTAGLANDINS - decrease gastric acid

production and enhance protective MUCIN
production
MUCOSAL DEFENSE:
- mucous gel
- prostaglandin E2
- epithelium (2nd line barrier)
- secrete chemokines
- secretion of HC03 into the mucous coat
no acid no ulcer
Gastric Ulcer Duodenal Ulcer
1. Rate of gastric emptying 1. Rapid gastric emptying time
contributes to the loss of buffering
capacity of food
2. N or low acid secretion associated 2. Increase in acid and pepsin
with a break in the normal mucosal secretion
barrier to acid and pepsin
MANIFESTATIONS:
Age
hematemesis/melena - 1/2 of patients
epigastric pain school-aged children and
adolescents
feeding difficulty infants and younger children
gastric perforation neonate
vomiting signs of gastric outlet obstruction
dull, aching - children
sharp or burning pain - adults
nocturnal pain common in older children
PRIMARY ULCER
-helicobacter pylori gastritis
-gm (-) s shaped rod that produces, UREASE,
CATALASE OXIDASE
-fecal-oral or oral-oral route
-group 1 carcinogen (WHO)
-diagnosis-histologic/biopsy
-initial upper endoscopy
SECONDARY ULCERS
ASPIRIN/NSAIDS
- mucosal injury
-cyclooxygenase and prostaglandin
-erosive gastropathy
-stomach > duodenum, antrum
 STRESS ULCERS
- within 240 of onset of a critical illness
- gastric erosions
- prophylactic measures-inhibit gastric acid
production
TREATMENT: main goals
1. ulcer healing
2. primary cause elimination
3. relief of symptoms
4. prevention of complications
1st line drugs for gastritis and peptic ulcer
* H2 receptor antagonist
* proton pump inhibitors
Helicobacter pylori antibiotics and PPI
Surgical therapy:
Indicators:
- perforation
- bleeding
- obstruction
PYLORIC STENOSIS
- non-bilious vomiting
- projectile / progressive emesis
- 3rd week of life /1st week/5months
-vomiting
*hyperchloremic metabolic alkalosis
*severe dehydration
*chronic malnutrition
*hypokalemia
Diagnosis:
-2cm firm movable mass; olive shaped
-gastric peristaltic wave
-olive easier to palpate
If dx is doubtful imaging techniques, US, abdominal
- pyloric muscle thickness >4mm.
- over all pyloric length >14mm.
Ba studies:
elongated pyloric channel
bulge of pyloric muscle into the antrum
(shoulder sign)
parallel streaks of Ba seen in the narrowed
channel (double tract sign)
Treatment:
- correct fluid, acid-base, electrolyte losses
- rehydrated and serum HC03 concentration is
<30mcg/dL
alkalosis post operative apnea
-Surgical Tx curative
Ramstedt Pyloromyotomy
(0-0.5% MORTALITY)
MALROTATION
-3mos AOG abdominal rotation and attachment
complete
- incomplete rotation of intestine during fetal
development
- non-rotation-when the bowel fails to rotate
after it returns to the abdominal cavity

Clinic manifestation:
infants (1st week of life) bilious emesis and
acute bowel obstruction
older infants recurrent abdominal pain-colic
older children recurrent abdominal pain or
vomiting or both
 adolescent 25-50% are asymptomatic
symptomatic acute intestinal
obstruction
volvulus associated with malrotation life
threatening complication

Diagnosis:
Radiographic studies
abdominal plain film non-specific
- double bubble signs
Ba enema demonstrates malposition of
cecum
UGIS malposition of the ligament of Treitz
Treatment:
Surgical
Persistent symptoms after repair of
malrotation psuedo-obstruction-like motility
disorder.

MECKELS DIVERTICULUM
- remnant of the embryonic yolk sac also
referred to as omphalomesenteric duct or vitelline
duct
-3-6 cm outpouching of the ileum along the
antimesenteric border approximately 50-75cm from
the ileocecal value.
CLINICAL MANIFESTATIONS:
1ST 2 years of life
majority of symptomatic MD
-ectopic mucosa acid-secreting mucosa
-intermittent painless rectal bleeding (due
to ulceration of adjacent normal ileal
mucosa)
-brick colored stools/currant jelly
-most common mechanism of obstruction -
when the diverticulum acts as a lead point of an
intussusception
-occasionally inflamed diverticulitis Ap
perforation and peritonitis
DIAGNOSIS:
-significant painless rectal bleeding
-confirmation is difficult
-Meckel radionuclide scan-performed after
intravenous infusion of technetium 99m
pertechnetate [dye taken up the mucus-secreting
cells of the ectopic gastric mucosa]
-diagnosis rarely made prior to surgery.