PEDIA: Gastritis and Peptic Ulcer Disease Secondary gastritis or ulceration

Lecturer: Dr. Josie Grace Castillo  Aspirin and other NSAIDS

 “Stress” ulceration
GASTRITIS AND PEPTIC ULCER DISEASE  Gastric or duodenal in location
 Occur in assoc. w/severe stress (ex. Systemic
Anatomic/ illness, burns, head injuries), ingestion of drugs
Gland Cell type Secretory products (NSAIDS, alcohol, aspirin) Crohn’s disease
area eosinophilic gastritis
Cardiac Mucous Cells Mucus, Pepsinogen  Life threatening in acute phase but after
Endocrine Cells healing, recovery is complete
Fundus parietal cells HCl
Chief Pepsinogen PRIMARY GASTRITIS (H. PYLORI)
Enterochromaffin cells Histamine,Serotnonin,  H. Pylori is acquired in childhood, before 5 y/o
G cells Gastrin  In absence of treatment, infection is lifelong
Antral G cells Gastrin
D cells Somatostatin MAJOR RISK FACTOR
ECL cells Histamine, Serotonin  Poor socioeconomic conditions
 Unsanitary condition
PUD
 Pathogenesis is multifactorial PREVALENCE:
 Final common pathway  80% in children <10 y/o
 Action of acid and pepsin laden contents of the  Prevalence of infection increases with age
stomach on the gastric and duodenal mucosa and
inability of the mucosal defense systems to allay TRANSMISSION
those effects  Fecal-oral, oral-oral, gastric-oral
 Human stomach- only known reservoir
Protective factors: bicarb, PG, mucous production, BF to  Waterborne transmission
mucosa
Host factors: H pylori, gastric acid, pepsin , NSAID MECHANISM OF DISEASE:
 H. pylori synthesize products that directly or
Gastritits indirectly damage the gastric mucosa
 microscopic evidence of inflammation affecting the  Cause persistent inflammatory response
gastric mucosa  Alter the regulation of acid secretion

Peptic ulcers BACTERIAL VIRULENCE FACTOR

 deep mucosal lesions that disrupt the muscularis  Motility – presence of flagella allows
mucosa coat of the gastric or duodenal wall movement through gastric mucus
 Adherence of organism to gastric mucosa
Peptic erosions alone – specific adhesion- receptor interaction
 superficial mucosal lesions does not penetrate the (?)
muscularis mucosa  Enzyme (urease) and toxin (VacA) production
 Urease protects the organism against gastric
2 FORMS OF GASTRITIS acid
Primary or unexplained  Ammonia generated by urease is toxic to all
 H. Pylori Gastritis mammalian cells and thus may damage the
 Caused by gastric infection w/H pylori (86%) gastric epithelium
 w/chronic and relapsing course
 Idiopathic Ulers HOST INFLAMMATORY RESPONSE
 In 15-20%  Stimulate interleukin-8 production w/c recruits
 No history of NSAID intake, H. Pylori negative and activates neutrophils and leukocytes
 High recurrence rate after discontinuation of  Severity of mucosa injury is directly correlated
PPI w/extent of Neutrophil infiltration
 GASTRIC ACID SECRETION
 Acute infection is associated with transient
hypochlorhydia lasting for several months
 Acute hypochlorhydia facilitate transmission of
infection
 H. pylori gastritis cause an increase in gastrin
release due to depletion of somatostatin-
producing D-cell density
SYMPTOMS
Gastritis
 No evidence that H. pylori gastritis in the
absence of duodenal ulcer disease cause
symptoms in children
Duodenal ulcer disease
 Assoc w/ chronic and recurrent symptoms
 Episodic epigastric pain frequently associated
w/vomiting and nocturnal awakening
 Acute episode of hematemesis may indicate
primary or secondary ulceration
 80% will have symptoms that persist into
adulthood
DIAGNOSIS
Upper GI endoscopy**
 Gold standard diagnosis gastritis and PUD
 Endoscopic appearance of stomach correlates
poorly with the presence or absence of
gastritis
 Histologic evidence of mucosal inflammation is
essential to establish diagnosis of gastritis
 Biopsies of antrum or corpus, duodenum
should be obtained
 Nodularity of antral mucosa associated with H.
pylori gastritis in children
Helicobacter pylori
HISTOLOGY
 Warthin-starry silver stain
 Giemsa stain/Cresyl violet stain
CULTURE
 Routine culture is difficult due to its fastidious
requirements
 Inoculate minced biopsy specimens in blood agar
plates under microaerophilic conditions at 37
degrees celsius
 Visible colonies require 5-7 days of culture
 Organism is identified if (+) urease, catalase,
oxidase and (-) for hippurate hydrolysis, nitrate
reduction
UREASE TEST:
 Rapid test to identify H pylori in antral mucosa
 A specimen placed on urea medium; hydrolysis
of urea leads to color change of the medium
from tan to pink
 Color change occurs in 30 mins – 24 hrs
depending on the # of bacteria present
UREA BREATH TEST (UBT)
 Safe and noninvasive method
 100%sensitive and 92% specific
 Isotopic urea (milk/juice) is ingested by patient; if
H. pylori is present in the stomach, breakdown of
the labeled urea by H. pylori urease results in the
production of labeled CO2 which is measured in
expired air.
 Following treatment, UBT is 100% sensitive and
specific in assessing H. pylori status
 Should not be carried out for at least 1 month
after the completion of treatment.
SEROLOGY
 Infection provokes a specific serum IgG response
 Antibody response takes up to 60 days to
develop.
 Mean antibody levels in young children are
significantly lower than in older children and
adults.
 Maximum antibody titers seen at 7 y/o
 Commercially available serologic tests do not
have sensitivity and specificity to diagnose
H.pylori in children < 12 y/o
STOOL ANTIGEN ENZYME IMMUNOASSAY (HpSA)
 Detect H. pylori antigen in feces
 94% sensitive, 92 % specific for diagnosis of
infection and in the following treatment
TREATMENT
 No evidence demonstrating a link between H.
pylori gastritis and abdominal pain except in
children in whom ulcers are present
 If infection is incidentally diagnosed, it should be
treated
 Treatment regimens are given for 1 week
 Eradication rates: < 90%
 PPI: inhibit gastric secretion, promoting
increased effectiveness of acid-sensitive
antibiotics like clarithromycin
Recommended eradication therapies for H. pylori CLINICAL FEATURES
disease in children  Abdominal pain and upper GI blood loss
1st line Medications Dosage  Massive hemorrhage or intestinal perforation
option  Site and mealtime relationships of abdominal
1 Amoxicillin 50mkday BID x 14 days pain often not present
Clarithromycin 15mkday BID x 14 days  Associated with high mortality
PPI ( Omeprazole) 1mkday BID x 1 month
2 Amoxicillin 50mkday BID x 14 days DIAGNOSIS
Metronidazole 20mkday BID x 14 days  Role of upper GI endoscopy is controversial
PPI 1mkday BID x 1 month  Presumptive diagnosis can be made without
3 Clarithromycin 50mkday BID x 14 days direct visualization of the bleeding lesion
Metronidazole 20mkday BID x 14 days  Endoscopy is useful if the diagnosis is in doubt or
PPI 1mkday BID x 1 month if therapeutic endoscopy is considered
 High risk of perforation
TREATMENT FAILURE  Stress gastritis- multiple areas of florid
 Poor patient compliance inflammation with or without hemorrhage
 Inadequate drug delivery
 Antimicrobial resistance TREATMENT
 Stress gastritis/ulcer
SECONDARY PEPTIC DISEASE  H2-receptor antagonists ( ranitidine/
cimetidine)
STRESS GASTRITIS/ACUTE EROSIVE GASTRITIS  Mucosal protectant ( sucralfate)
 Occurs w/in 24 hrs of onset of a critical illness  Drug-induced gastritis
sepsis, burns, severe head injury, multiple  H2RAs
trauma, Respiratory Failure, coagulopathy  PPIs
 75% asymptomatic
 25% of children in PICU w/macroscopic evidence
of GI bleeding
 Presenting feature: Hematemesis or melena; No
abdominal pain.
 Pathogenesis:
 Local mucosal ischemia w/ impaired blood
flow cause stress erosions
 Increased acid and pepsin secretion
 Decreased gastric somatostatin levels
 Decreased mucus production

DRUGS AND TOXINS:

 Corticosteroids
 Inhibitory effect on local production of PG
and gastric mucus
 NSAIDS
 damage the gastric mucosa directly through
irritant effects
 Inhibit PG synthesis, adversely affecting the
function of normal host mucosal defenses
 Causing focal loss of surface mucus
layers
 Inhibiting mucosal HCO3 secretion
 Decreasing mucosal blood flow
 Alcohol
 Induce gastric erosions and hemorrhage
 PEDIA: Congenital abnormalities of the DIAGNOSIS
stomach and duodenum  Prenatally
Lecturer: Dr. Josie Grace Castillo  Polyhdramnios
 Dilated stomach and narrowed outlet on UTZ
CONGENITAL ABNORMALITIES OF THE STOMACH AND  Abdominal x-ray
DUODENUM  Gaseous gastric distention w/o intestinal gas
 Congenital gastric outlet obstruction  Single bubble appearance**
 Gastric Atresia or Stenosis
 Gastric duplication MANAGEMENT
 Hypertrophic pyloric stenosis  NG suction, fluid resuscitation
 Gastric Volvulus  Antibiotics
 Hypertrophic gastropathy  Surgical treatment:
 Short atretic segment: on w/gastsection of
ATRESIA membr, pyloroplasty
 complete obstruction of the gut either by a  Extensive atretic segments: resection
membranous or fibrous band or complete separation
of the adjacent sections CONGENITAL GASTRIC OUTLET OBSTRUCTION
 Results from pyloric atresia and antral webs
STENOSIS  Cause is unknown
 in complete obstruction caused by intrinsic narrowing
of the intestinal lumen of the gut CLINICAL MANIFESTATIONS
 Nobilious vomiting
GASTRIC ATRESIA OR STENOSIS  Feeding deficiencies
 Results in a blind end in the antrum/pylorus  Abdominal distention during the 1st day of life
 Involves the mucosa and submucosa with normal  Gastric aspirate >20mL at birth
muscle and serosa (diaphragm)  Rupture may occur as early as the 1st 12 hours of life
 Or involves the entire gastroduodenal wall (true
atresia) TREATMENT
 Incidence: 1:100,000  Correction of dehydration and hypochloremic alkalosis
 Unknown cause  Nasogastric decompression
 May be inherited by AR transmission  Surgical or endoscopic repair

 Probably results from failure of antrum and pylorus to GASTRIC DUPLICATION

recanalize after transient occlusion by epithelium  Cystic or tubular structures that occur within the walls
during embryogenesis. of the stomach
 Assoc. w/other congenital defects  Occurs most commonly along the greater curvature but
 multiple intestinal atresias can arise from the post. Or ant. Wall/pylorus
 Down syndrome  Account for 2-7% of all GI duplications
 Epidermolysis bullosa  Do not usually communicate with the stomach lumen
 Share a common wall and blood supply
CLINICAL PRESENTATION  Lined w/gastric epithelium
 Onset of symptoms will depend on degree of gastric  Sometimes connected w/stomach or pancreas
outlet obstruction  More common in girls
 Complete obstruction
 Persistent non bilious vomiting  Etiology
 Dehydration  Diverticulization
 Upper abdomen distention  Canalization defects
 Partial  Caudal twinning
 Signs appear in childhood
 FTT  Assoc anomalies seen in 35%
 Upper abdomen discomfort  Intestinal tract duplications
 Vertebral aomalies
  Symptoms present in 1st yr of life, depending on the SYMPTOMS: OCCUR AT 2-8 WKS AFTER BIRTH
size, location, presence/absence of communication  Initial sx: projectile non bilious vomiting
with GIT  Progressive vomiting immediately after feeding (5-10
mins) or delayed until stomach is full
 In younger child  After vomiting, infant is hungry and wants to feed
 Projectile vomiting, wt loss, failure to thrive again
 In older children  Emesis may be blood streaked in the prenece of
 Epigastric pain, abdominal fullness or mass (33%), gastritis
GI bleeding, GI obstruction  Hypochloremic metabolic alkalosis: Due to
progressive loss of fluid, h2 ions and chloride
ABDOMINAL X-RAY:  No weight gain or even weight loss
 Soft tissue mass protruding into the lumen  Icteropyloricsyndrome:
 Extrinsic compression of stomach  Unconjugated hyperbilirubinemia due to
 Filing defect of cyst with barium enhanced enterohepatic resorption of bilirubin
 Ssociated with decreased level of glucuronyl
UTS transferase – 5%
 Inner hyperechoic mucosal and outer hypoechoic
muscle layers PE:
 Gastric distention
CT scan, MRI  Visible peristaltic wave that progresses across the
abdomen after feeding
MANAGEMENT:  Palpable firm, movable ‘olive shaped pyloric’ mass,
 Complete surgical excision about 2 cm in length, easiest palpated after vomiting
 If large, partial excision, partial gastrectomy and cyst located above and right to the umbilicus (23-55%)
gastrostomy  ID pyloric olive:PPV 100%

ABDOMINAL X-RAY
HYPERTROPHIC PYLORIC STENOSIS  Large gastric air bubble with little or no interstitial air
 Most common cause of gastric outlet obstruction in
infancy UTS
 Most frequent indication for surgery during first 6 mos  Recommended
of life  Rapid and non invasive
 1-3/1,000 infants in US, incidence is rising  Lack of radiation
 Males>Females (4:1)>Caucasians  No risk of contrast aspiration
 Rare in asian  Measures length and diameter of pylorus, pyloric
 High transmission rate from affected mother muscle thickness
 Male offspring – 20%  Sensitivity of 95%, PPV 90%
 Female offspring – 10%  Criteria for diagnosis:
 Due to hypertrophy of the circular smooth  Pyloric thickness: 3-4mm
musculature surrounding the pylorus and antrum  Overall pyloric length :15-19mm
 Hyperperistalsis against a closed pyloric canal produces  Pyloric diameter: 10-14 mm
edema and hypertrophy leading to high grade
obstruction UGIS
 Unknown etiology  Elongated pyloric channel (string sign)
 Reduced levels of neuronal Nitric oxide  Bulge of the pyloric muscle into the antrum
synthetase(nNOS) contribute to pylorospasm (Shoulder sign)
 Other causes implicated:  Parallel streaks of barium seen in the narrowed
 Infantile Hypergastrinemia and hyperacidity channel(double tract sign)
 Elevated serum levels of prostaglandin (PGE2,  Proposed algorithm to determine w/c study request
PGF2) - smooth muscle contraction  Based on gastric aspirate vol.
 Cow milk protein allergy
 Early postnatal (3-13 days) exposure to macrolide
antibiotics ( erythromycin)- 8x risk HPS
 Maternal treatment with macrolide antibiotics
during pregnancy and breastfeeding
  After a 1 hour fast, gastric contents are aspirated and CLINICAL MANIFESTATION:
quantified  Nonspecific; suggests high intestinal obstruction
 Aspirate>5 ml: gastric outlet obstruction in > 90% (  In infancy
Request for UTZ initially then UGIS if needed)  Non-bilious vomiting
 Aspirate <5ml: medical cause is suspected in > 90%  Epigastric distention
( Request for UGIS)  In older children:
 Chronic gastric volvulus is more common
TREATMENT:  History of emesis
 Initial  Abdominal pain and distention
 Replacement of fluids and electrolytes  Early satiety
 Correction of alkalosis  Failure to thrive
 Definition:
 Ramstedt pyloromyotomy- longitudinal division DIAGNOSIS
of anterior pyloric muscle from serosa to  Abdominal x-ray: dilated stomach, double fluid level
submucosa with “break” near the LES

PROGNOSIS: MANAGEMENT
 Recurrence in 1-3%  Emergency surgery to prevent gastric ischemia,
 Adhesion and infection 1-5% necrosis, perforation
 Post op vomiting 50%  Reduction of volvulus with gastropexy
 Due to:
 Edema of pylorus at the incision site HYPERTROPHIC GASTROPATHY
 Delayed gastric emptying  Uncommon n children
 GER  Usually transient, benign and self-limited
 Persistent vomiting  May be secondary to CMV infection, HSV, Giardia,H.
 Incomplete pyloromyotomy pylori
 Other cause of obstruction – adhesions  Mechanism: widening of gap junctions between gastric
epithelial cells with resultant loss of fluid and rotein

 Serial UTZ done after surgery CLINICAL MANIFESTATIONS

 Initial swelling of pyloric muscles  Vomiting
 Rapid involution over the next 3 weeks  Anorexia
 Normal pyloric muscle thickness in 6 weeks  Upper abdominal pain
 Conservative management  Diarrhea
 If surgical treatment is not available  Edema (hypoproteinemic protein-losing enteropathy)
 For poor surgical candidates  Ascities
 Nasoduodenal feeding
 Oral or IV atropine sulfate (pyloric muscle
relaxant)  Mean age at diagnosis: 5years old (2 ays – 7 years)
 Illness lasts 2-14 weeks with complete resolution
GASTRIC VOLVULUS
 Stomach is tethered longitudinally by the DIAGNOSIS
gastrohepatic, gastrosplenic and gastrocolic ligaments,  Endoscopy with biopsy
transversely by the gastrophrenic ligament  Tissue CMV PCR is diagnostic
 If any of these attachments is absent or stretched, the  UGIS : thickened gastric folds
stomach may rotate around itself
TREATMENT
TRIAD:
 Supportive
 Sudden onset of severe abdominal pain
 Adequate hydration
 Intractable retching with emesis
 H2 receptor blockade
 Inability to pass a tube into the stomach
 Albumin replacement if with symptomatic
hypoalbuminemia
 CMV (+) Ganciclovir
 H pylori (+) Amoxicillin, Clarithromycin, Omeprazole
 PEDIA: Congenital malformations of the
esophagus
Lecturer: Dr. Josie Grace Castillo
ESOPHAGUS
 Conduit for transport of food from the mouth to the
stomach
 Distinct structure from 4th week of gestation
 At birth, 8-10cms in length
 At 2-3 yo, length doubles
 Adult length: 25 cms
ESOPHAGEAL MOTOR FUNCTION
 Fetal swallowing of pharyngeal contents: 11 weeks
AOG
 Mouthing and sucking movements: 15 weeks AOG
 True sucking (rhythmic sucking and swallowing):34
weeks AOG
 30 sec burst of sucking at 2 mins intervals
coordinated with swallowing
 Polyhydramnios
 Hallmark of lack of normal swallowing or of
esophageal or Upper GI obstruction
FUNCTIONAL REGIONS OF THE ESOPHAGUS
1. Upper esophageal sphincter (UES)
2. Esophageal body
3. Lower esophageal sphincter (LES)
Upper Esophageal Sphincter (UES)
 Zone of high intraluminal pressure lying between the
pharynx and the cervical esophagus
 0.5 – 1 cm in length
 Main functions:
 Provide mot proximal physical barrier of the GIT
against pharyngeal and laryngeal reflux during
esophageal peristalsis
 To avoid entry of air into the GIT during negative
intrathorcic events, i.e. inspiration
 “normal” UES pressure: 8-70mmHg
Esophageal Body
 Begins at caudal edge of cricopharyngeal muscle up
to the esophagogastric junction (EGJ)
 Primary peristalsis
 Reflects peristaltic contraction wave initiated by
swallowing
 Results from a sequential contraction of
esophageal muscle layers moving down the
entire length of the esophagus, appearing shortly
after the pharyngeal contraction travels the UES
 Secondary peristalsis
 Can be elicited at any level of the esophagus in
response to lumnal distention by fluid and air
 Does not involve full swallowing reflex
 Starts at the highest level reached by refluxed
materials into the esophagus
 Contributes to the esophageal clearance of a
bolus not fully cleared by a primary peristaltic
wave
Lower Esophageal Sphincter (LES)
 High-presure zone localized at the esophagogastric
junction (EGJ)
 Regulates flow contets between the esophagus and
stomach
 2-4 m in length in adults
 LES pressure: 20 mmHg
 Main function: create a high-pressure zone for
preventing retrograde movement of gastric contents
into the esophagus
TRACHEOESOPHAGEAL FISTULA AND ATRESIA
 Relut from disruption of the process of elongation &
separation of the trachea and esophagus on the 4th-
10th week AOG
 TEF: due to incomplete fusion of tracheosophageal
septum
 Atresia with or without TEF: failure of recanaliztion of
the esophagus in the embryonic period
 Atresia occurs in 1:4,000 live births, 90% with TEF
 0.5-2%% risk of recurrence among siblings of an
affected child
MATERNAL RISK FACTORS:
 Advanced maternal age
 European ethnicity
 Obesity
 Low socioeconomic status
 Tobacco smoking
 50-70% have associated congenital anomalies
VACTERL SYNDROME
 Vertebral defects (13%)
 Anorectal malformations – imperforate anus (24%)
 Cardiac abnormalities – PDA, septal defects (11-49%)
 TEF
 Renal defects (24%)
 Limb malformations – radial limb dysplasia
PRESENTATION:
 Frothing and bubbling at the nose and mouth at birth
 Episodes of coughing, cyanosis, and respiratory
distress
 Feeding exacerbates these symptoms and precipitate
aspiration
DIAGNOSIS
 Essentially clinical
 Drooling of saliva, periodic episodes of coughing and
cyanosis + history of maternal polyhydramnios
 Early-onset respiratory distress
 Inability to pass an NGT or OGT into the stomach
using large bore tubing
 Plan x-ray: coiled feeding tube in esophageal pouch
and/or air-distended stomach
X-ray
 Radio-opaque tube in-situ can ID lower limits of
esophageal pouch
 Radio-opaque contrast injected through the
catheter will delineate the atretic segment or
locate the fistula
 Gas in the stomach and intestines indicate
presence of TEF
 Detect associated skeletal abnormalities
5 BASIC TYPES OF TEF AND ATRESIA
Type A
 Esophageal atresia with distal TEF
 Upper segment ends blindly and lower segment is
connected to trachea by a fistula
 Most common type seen in 87%
 Symptoms:
 Drooling of saliva
 Coughing after feeding attempts
 Recurrent and periodic bouts of cyanosis and
abdominal distention
 Aspiration pneumonia
Type B
 Esophageal atresia without TEF
 Blind upper and lower segments
 Seen in 8%
 Symptoms similar in Type A but without abdominal
distention
 No gas seen on x-ray of stomach and intestines
Type C
 H-type anomaly
 TEF exists with NO associated atresia
 Seen in 4%
 Symptoms:
 Coughing and choking with liquid feeding but
seldom with solid food
 Recurrent pneumonia
 Diagnosis may be delayed till adulthood
Type D
 Esophageal atresia with proximal TEF
 Upper segment is connected to trachea by fistula
 Seen in 0.5-1%
 Symptoms: choking and cyanosis with feeding
Type E
 Esophageal atresia with proximal and distal TEF
 Seen in 0.5-1%
 Symptoms similar to type D
MANAGEMENT
 Maintain patent airway and prevent aspiration of
secretions
 Continuous aspiration of secretions with a sump
suction tube placed in the upper pouch to prevent
aspiration
 Supine position with head elevated 30-45
 Search for other associated anomalies
 IV fluids, blood-spectrum antibiotics
 Surgical ligation of TEF and primary end-to-end
anastomosis of the esophagus, ideally on the 1st
24HOL, to prevent aspiration and resulting
pneumonitis
 If gap between ends of the esophagus is >3-4cms
 Ligation of fistula and gastrostomy with later
definitive repair
 Esophagus is replaced with some other structure
– gastric, jejuna, or colon interposition as neo-
esophagus
PROGNOSIS
 Primary determinants of survival are coexistent
congenital anomalies & severity of associated
pulmonary disease
 PROGNOSIS (continued...)
 Complications of surgery:
 Anastomotic breakdown & leak – 5-20%
 Refistulation – 1-12%
 Esophageal stricture – 30-50%
 GERD – 30-70%
 Due to poor motility
 Delayed gastric emptying
 Due to altered angle of His due to tension on
the distal esophagus & proximal stomach to
allow for adequate anastomosis
ESOPHAGEAL DYSMOTILITY
I. Upper esophageal and upper esophageal sphincter
dysmotility ( striated muscle)
a. Cricopharyngeal achalasia
b. Cricopharyngeal incoordination
c. Cricopharyngeal spasm
II. Lower esophageal and lower esophageal sphincter
dysfunction (smooth muscle)
a. Achalasia
b. Diffuse esophageal spasm
UPPER ESOPHAGEAL AND UES DYSMOTILITY
Cricopharyngeal achalasia
 Failure of complete relaxation of UES
Cricopharyngeal incoordination
 Full relaxation of UES but incoordination of
relaxation with the pharyngeal contraction
 Self-limited in infancy; remits spontaneously in 1st
yr of life
Cricopharyngeal spasm
 Idiopathic in older children
 Treated by myotomy of UES
 Systemic causes of swallowing dysfunction
 Cerebral palsy
 Arnold chiari malformation
 Cranial nerve defects – transient infantile
paralysis of laryngeal nerve
 Infections – botulism, tetanus, poliomyelitis
 Autoimmune disease – scleroderma, myasthenia
gravis
 Tracheostomy
LES DYSFUNCTION
Achalasia
 Primary esophageal motor disorder
 Functional obstruction of distal esophagus due to
 Loss of LES relaxation
 Loss of esophageal peristalsis
 Unknown etiology
 Possible causes
 Degenerative
 Autoimmune – antibody to Auerbach plexus
 Infectious –Chaga’s dse (Trypanosoma cruzi)
 Allgrove syndrome – achalasia, alacrima,
corticotropin insensitivity
PATHOLOGY
 Selective loss of post-ganglionic inhibitory
neurons (for LES relaxation)
 High basal LES pressure
 Insufficient LES relaxation
 Loss of esophageal peristalsis
CLINICAL MANIFESTATIONS
 Regurgitation and dysphagia for solids and
liquids
 Undernutrition or respiratory symptoms
 Esophagitis – due to retained esophageal food
 Mean age at diagnosis: 8.8 y/o
 Mean duration of symptoms before diagnosis: 23
mos
DIAGNOSTIC TESTS
 Chest x-ray
 Air-fluid level in a dilated esophagus
 Barium fluoroscopy
 Smooth tapering of lower esophagus leading
to a closed LES
 “bird’s beak”
 Manometry
 Most sensitive diagnostic test
 Findings:
 Aperistalsis in distal esophagus
 Incomplete or absent LES relaxation
 High pressure LES
 Low amplitude esophageal body
contractions
TREATMENT
 Pneumatic dilation
 Initial treatment of choice
 Surgical (Heller) myotomy
 Performed with antireflux procedure to
prevent GERD
 Endoscopic injection of LES with Botulinum toxin
 Counter-balances selective loss of inhibitory
neurotransmitters by inhibiting the release
of acetylcholine from nerve terminals
 Effective in 50-65%; repeat injections after 1
yr
 Expensive
 Will require dilation or surgery eventually
 PEDIA: Gastroesophageal reflux disease Frequency of Reflux Increased By
(GERD)  Insufficient LES tone
Lecturer: Dr. Josie Grace Castillo  Abnormal frequency of LES relaxation
 Hiatal herniation
GASTROESOPHAGEAL REFLUX
 Retrograde mov’t of gastric contents across the LES Transient Les Relaxation (TLESR)
into the esophagus  Primary mechanism allowing reflux to occur
 In normal children, episodes of GER may occur after a  Independent of swallowing
meal (~5x within an hour of feeding)  LES pressure is reduced by 0-2mmHg (above gastric);
 Occur in 38% of healthy neonates lasts >10 secs
 Becomes pathologic when episodes are more frequent  Main stimulus: Gastric distention (postprandially,
or persistent, producing esophagitis or respiratory due to air swallowing)
sequelae
Factors Affecting LES Pressure
INFANT REFLUX
 Peaks at 4 mos CATEGORY INCREASE DECREASE
 88% resolve by 12 mos
Diet Proteins Fat
 Manifestations:
Coffee
 Regurgitation (postprandially)
Chocolate,
 Esophagitis (irritability, arching, feeding aversion)
peppermint
 Failure to thrive
Alcohol
 Resolve spontaneously by 12-24 mos
 Respiratory: apnea, stridor Hormones Gastrin Glucagon
Motilin Secretin, CCK
REFLUX IN OLDER CHILDREN Progesterone
 Chronic, waxing and waning pattern Estrogen
 Resolves in 50%, similar to adults
Neural Cisapride Atropine, nicotine
 Manifestations:
transmitter Norepinephrine Salbutamol
 Abdominal and chest pain
s, drugs Acetylcholine Dopamine
 Extraesophageal
Histamine, Theophylline
 Otitis media
serotonin Calcium blockers
 Sinusitis
Cimetidine Opiates
 Vocal cord nodules
 Laryngeal edema
 Asthma Etiopathology
 Transient LES relaxation (TLESR)
GER – passage of gastric contents into the esophagus  Primary mechanism allowing reflux to occur
GERD – present when reflux of gastric contents is the cause  Gastric distention is main stimulus
of troublesome symptoms and/or complications  Postprandial
 Abnormal gastric emptying
GASTROESOPHAGEAL REFLUX  Air swallowing
 LES lumen is closed at rest & opens during deglutition  Other factors:
 LES acts as the main barrier inhibiting reflux of acid  Increased movement, straining
contents from the stomach into the esophagus  Large volume or hyperosmolar meals
 A zone of high resting pressure can be manometrically  Obesity
documented near the region of the LES  Increased respiratory effort (coughing/wheezing)
 Reflux occurs when the opening pressure of the LES
exceeds its closing pressure

Antireflux Barrier
 LES, supported by crura of diaphragm
 Valvelike function of EGJ
 At risk population for GERD Diagnosis:
 Neuromotor impairment  LOOK FOR REFLUX!
 Prevalence: 50% in populations with IQ <50
 Esophageal anatomic disorders Diagnostic approach
 Repaired TEF  History and PE
 Pulmonary disease  Upper GI series
 Cystic fibrosis  Esophageal pH monitoring
 Prematurity  Endoscopy and biopsy
 Bronchopulmonary dysplasia
 Genetic GER &GERD
 autosomal dominant ( chromosome 13q14 locus HISTORY & PE
GERD1)  Sufficient to reliably diagnose:
 Presence of GER
GASTROESOPHAGEAL REFLUX DISEASE (GERD)  Recognize complications
4 classes of symptomatology  Initiate management
1. REGURGITATION / VOMITING
 Most common Barium contrast radiography
 Infant initially feeds well with effortless UPPER GI SERIES
regurgitation  Not sensitive nor specific enough to diagnose GER
 Regurgitated feeds cause the infant to be  Sensitivity: 29-86%
nauseated, & vomiting is induced  Specificity: 21-83%
2. ASPIRATION  PPV: 80-82%
 Manifest with chronic or recurrent pneumonia,  Limited duration
asthma, apnea / cyanosis, laryngitis  Unable to differentiate physiologic from
 Seen in 46 – 63% of cases pathologic reflux
3. ESOPHAGITIS  Useful for evaluation of anatomic abnormalities
 Presents with iron deficiency anemia due to  Pyloric stenosis
continuous microscopic blood loss from the  Malrotation
chronically inflamed esophagus  Annular pancreas
 May present with hematemesis & melena  Hiatal hernia
 Stricture formation seen in 5% of children with  Esophageal stricture
untreated GERD
 Signs in infants: GASTROESOPHAGEAL REFLUX DISEASE (GERD)
 Irritability Barium swallow / UGIS
 Arching, choking  Reflux demonstrated in 50 – 75%
 Feeding aversion, gagging  Severity of reflux
 Older children would complain of abdominal or Grade 1 – reflux into distal esophagus
chest pain Grade 2 – reflux above the carina
Grade 3 – reflux into the cervical esophagus
Potential Extra-Esophageal Manifestations of GERD Grade 4 – free reflux with widely patent LES
Grade 5 – reflux with aspiration
Ear, Nose &
Pulmonary Others
Throat Esophageal pH monitoring
 Valid and reliable test for ACID reflux but not alkali
• Asthma (non- • Chronic cough • Dental
reflux
seasonal, non- • Laryngitis erosions on
 Measures frequency & duration of acid esophageal
allergic) • Hoarseness lingual
reflux episodes
• Chronic Bronchitis • Globus surface
• Bronchiectasis • Pharyngitis • Non-cardiac  24H pH monitoring
• Pulmonary fibrosis • Sinusitis pain  Provides quantitative & sensitive
• Chronic • Vocal cord • Sleep apnea documentation of acidic reflux episodes
obstructive granuloma  May be used to assess efficacy of acid
pulmonary • Recurrent otitis suppression during treatment
disease media  Sensitivity & specificity NOT well established
• Pneumonia
  Reflux index: percentage of total recording
time esophageal pH<4
 >8% abnormal
 < 5-8% normal
Multichannel intraluminal impedance (MII)
 Measures the movement of fluids, solids and air in
the esophagus
 Can detect extremely small bolus volumes
 Useful in postprandial period or when gastric
contents are non-acidic
 No established normal values
Endoscopy
 Direct visual examination of esophageal mucosa
 Can assess the presence and severity of:
 Esophagitis
 Stricture
 Erosions, ulcers
 Exudates
 Normal appearance of the esophagus during EGD
does not exclude
 Histopathological esophagitis
 Subtle mucosal changes
Esophageal biopsy
 Detect microscopic esophagitis
 Can exclude other causes of esophagitis other than
GER like allergy or infection
Nuclear scintigraphy
 Food or formula labeled with Technetium is
introduced into the stomach
 Scan for evidence of reflux and aspiration
 Evaluates postprandial reflux and demonstrates
reflux independent of gastric pH
 Sensitivity: 15-59%
 Specificity: 83-100%
 Lack of standardized technique & absence of age-
specific normal values limit its use
Empirical antireflux therapy
 Commonly used in adults
 “PPI test”
 Only modest sensitivity & specificity as a dxtic
test of GERD
 In older children & adolescents with symptoms
suggestive of GERD – 4 wk empiric PPI trial is
justified
 Improvement following treatment does not
confirm diagnosis of GERD
 Symptoms may have improved spontaneously
or responded to placebo effect
TREATMENT GOALS
 Relief of symptoms
 Mucosal healing
 Treatment normal
of complications ( esophagitis)
 Maintenance of remission
LIFESTYLE CHANGES IN INFANTS
 Consider 2-4 wks trial of an extensive protein
hydrolysate milk formula
 To exclude soy and cow milk protein allergy
 For breastfed infants, full hypoallergenic diet for
the mother
 Thickened formula decreases visible regurgitation
 1Tbsp cereal/oz milk
 Supine positioning during sleep is generally
recommended
 Correct abnormal feeding techniques, volumes,
frequencies
LIFESTYLE CHANGES IN OLDER CHILDREN AND
ADOLESCENTS
 Left side-lying position and elevation of the head of
the bed to decrease GER symptoms
 Minimizes transient relaxation of LES
 No support for dietary restriction
 But note food or medicines that could decrease
LES pressure and exacerbate GER symptoms
 Avoid caffeine, carbonated drinks, chocolates,
mint
 Avoid acidic and spicy foods
 Reduce weight
 Avoid smoking and alcohol
PHARMACOLOGIC THERAPY
 Antacids, sucralfate
 Histamine 2 receptor antagonist (H2RA)
 Proton pump inhibitor (PPI)
 Prokinetic
THERAPY OPTIONS
Acid-neutralizing agents
 Antacids : 0.5-1ml/kg/dose 3-8x/day
 May bind with calcium & cause aluminum or
magnesium toxicity with chronic use
 Provide rapid but transient relief of symptoms
 Adjunct therapy for pain
Mucosal protective agents
 Sucralfate: 1 gm in 15ml solution QID before meals
 Beneficial for patients with esophagitis, erosions,
ulcerations
Prokinetic agents
CISAPRIDE
 Non-cholinergic, non-antidopminergic agent that
enhances smooth muscle contraction throughout
the entire GIT
 Increases LES pressure & amplitude of the
esophageal peristalsis
 Improves gastric emptying time
 1-1.2mg/kg/day TID before meals
 Major side effect: cardiac arrhythmia
DOMPERIDONE
 Dopamine antagonist
 1.2mg/kg/day TID before meals
METOCLOPRAMIDE
 Dopamine antagonist that increases LES pressure
& rate of esophageal peristalsis & gastric
emptying time
 Major side effect: extra-pyramidal symptoms
Anti-secretory agents
 Effective for treatment of esophagitis
 H2-receptor antagonists (H2RAs)
 Selectively inhibit histamine receptors on
gastric parietal cells
 For mild to moderate reflux esophagitis
 Cimetidine 5-10mg/kg/dose QID
 Ranitidine 4-5mg/kg/day BID or TID
 Famotidine 0.5mg/kg/dose BID or TID
 Limiting factor: rapid tachyphyllaxis
Proton pump inhibitors (PPIs)
 For severe & erosive esophagitis
 Most potent antireflux effect by blocking H-K
aATPase channels in gastric acid secretion
 Superior to H2RAs
 Approved for use in children
 Omeprazole, Lansoprazole, Esomeprazole
 Not recommended for use in infants unless
there is evidence of erosive esophagitis
Empirical Anti-Reflux therapy
 Time-limited trial of high dose PPI (1 month) – cost
effective strategy for diagnosis in older children
and adolescents
 Failure to respond to empirical treatment or
requirement of treatment for prolonged periods
mandates formal diagnostic evaluation
Anti-reflux Surgery (fundoplication)
 Treatment of last resort
 Fundoplication with or without gastrostomy for
feeding
 Indications
 Refractory esophagitis and strictures
 Failed optimal medical therapy
 Dependency on medical therapy over a long
period of time
 Non-compliance with medical therapy
 Life threatening complications
RISKS OF FUNDOPLICATION
 Gas bloat or dysphagia – “too tight”
 Incompetent – “too loose”
 Long term studies suggest that fundoplications
become incompetent
 Reflux recurrence rate
 14% Nissen (tight wrap)
 20% Thal (loose wrap)
COMPLICATIONS OF GERD
Esophageal
ESOPHAGITIS
 Irritability, feeding aversion, arching, gagging
 Chest pain in older children
 Sandifer syndrome
 Rarely, hematemesis, anemia
 Erosive esophagitis:
 Seen in 12%
 M >F, older children, neurologically impaired,
hiatal hernia
SANDIFER’S SYNDROME (TORTICOLLIS)
 Opisthotonus position of head & neck with upper
trunk bent to one side; arching and turning of
head
 This posturing seems to improve esophageal
clearance
 Pronounced during & immediately after meals
 Not observed during sleep
 Specific manifestation of pediatric GERD
STRICTURE FORMATION
 Seen with prolonged and severe esophagitis
 In 5% of children with untreated GERD
 BARRETT ESOPHAGUS Treatment:
 Due to long-standing esophagitis  Dietary restriction
 Metaplastic transformation of normal  Clinical and histologic remission: 70-98%
esophageal squamous epithelium into intestinal  Elimination diet
columnar epithelium  Guided by circumstantial evidence, food
 Precursor of esophageal adenocarcinoma allergy test result
 Seen 5th decade of life  Six food elimination diet
 Milk, soy, wheat, egg, peanuts and tree nuts,
Nutritional seafood
 Failure to thrive due to caloric deficiencies  Elemental diet
 May require enteral (nasogastric, nasojejunal, PEG)  Exclusive amino acid based formula
or parenteral feeding  Topical and systemic steroids
 Budesonide
Extraesophageal : Respiratory (atypical) presentations
RESPIRATORY SYMPTOMS
 Direct contact of refluxed gastric contents with ESOPHAGEAL VARICES
the respiratory tract  Complication of portal hypertension
 Aspiration, laryngeal penetration,  Develops when portal HTN is decompressed through
microaspiration the portosystemic collateral circulation
 Reflexive interaction between the esophagus and  Treatment is directed at the underlying cause
respiratory tract  Hemorrhage from EV’s is the major cause of morbidity
 Bronchospasm, laryngeal closure and mortality due to portal HTN

Apnea and Stridor Presentation:

APNEA  Hematemesis and melena
 Temporal relationship with GERD
 pH-MII studies show that 50% of apnea is due to Treatment
GERD  Endoscopic Rubber band ligation
STRIDOR  Sclerotherapy
 Triggered by GERD only seen in infants
anatomically predisposed toward stridor FOREIGN BODY IN THE ESOPHAGUS
(laryngomalacia, micrognathia)  80% of foreign body ingestion occur in children
 Between 6mos – 3 yrs
 Common items ingested: coins, small toys, food
EOSINOPHILIC ESOPHAGITIS  Lodge in 3 areas
 Esophageal epithelium is infiltrated by eosinophils ,  Level of cricopharyngeus (UES)
>15/hpf  Aortic arch
 Mean age at diagnosis: 7 yrs  Superior to diaphragm at EGJ (LES)
 Mean duration of symptoms: 3 yrs  30% asymptomatic
 Associated with atopic dses, food allergies
Presentations
Manifestations:  Choking, gagging, coughing
 Vomiting  Excessive salivation, dysphagia, food refusal, emesis,
 Feeding problems pain in the neck, throat
 Chest or epigastric pain  Respiratory symptoms: stridor, wheezing, cyanosis,
 Dysphagia with food impaction dyspnea – impinges on larynx, post tracheal wall
 Cervical swelling, erythema, subcutaneous
Laboratories: crepitations - perforation
 Peripheral eosinophilia
 Elevated IgE levels

Endoscopic finding:
 Granular, furrowed, ringed or exudative appearance
of the esophagus
 Evaluation: Treatment
 Chest x-ray AP and lateral views of neck, chest,  Upper GI endoscopy
abdomen  Rapidly IDs extent of tissue damage
 Flat surface of coin is seen on AP view, edge on  Recommended in all symptomatic children
lateral view  Dilution by water or milk as acute treatment
 Reverse is true for coin in the trachea  Contraindicated:
 Radiolucent: plastic, wood, bones, aluminum  Neutralization
 Failure to visualize the object with plain x-ray in a  Induce emesis
symptomatic patient warrants further investigation  Gastric lavage

Treatment:  Treatment depends on severity and extent of

 Endoscopic visualization of the object and mucosa damage
and removal of the object
 Therapeutic endoscopy should be done with an ET Strictures:
tube protecting the airway  More common with circumferential ulcerations
 Urgent removal: disc button batteries, respiratory  Require dilation or surgical resection with colon
symptoms interposition
 Observe up to 24 hrs: Asymptomatic, blunt objects
(coins) Corticosteroids:
 Reduce risk of strictures in more advanced caustic
CAUSTIC INGESTION esophagitis
Alkali ingestion
 70% of accidental ingestions Antibiotics
 Produce severe, deep liquefaction necrosis  Initial treatment of esophagitis to reduce
 Most common: drain decloggers, bleach superinfection in the necrotic tissue bed
 Tasteless, more ingested

Acidic ingestion Endoscopic grading of the severity of esophageal injury

 20% of cases following caustic ingestion
 Produce coagulation necrosis and a thick eschar ENDOSCOPIC APPEARANCE OF
SEVERITY
 Tastes bitter so less is consumed ESOPHAGEAL MUCOSA
 Produce severe gastritis, respiratory symptoms due Grade 0 Normal mucosa
to volatile gas
Grade 1 Erythema
Presentation: Grade 2 Erythema, sloughing, ulceration, exudates
 Vomiting, drooling, refusal to drink (non-circumferential)
 Oral burns Grade 3 Deep mucosal sloughing and ulceration
 Dysphagia, dyspnea, stridor (circumferential)
 Abdominal pain, hematemesis Grade 4 Eschar, full thickness injury and perforation
 Absence of oropharyngeal lesions does not exclude
possibility of significant esophagogastric injury
 Absence of symptoms associated with no or minimal
injury
 Hematemesis, respiratory distress OR presence of at
least 3 symptoms predicts severe lesions
 PEDIA: Small & Large Intestines Disorders Treatment
Lecturer: Roumilla Mendoza, M.D • Naso or orogastric decompression
• Evaluate for associated anomalies
INTESTINES (EMBRYOLOGY)  2-D echo
• Primitive gut – 4th week of gestation  X-ray of chest and spine
• Proliferation of epithelium with obliteration of the • Surgery
lumen followed by recanalization – 6th week of
gestation DUODENAL STENOSIS
• Incomplete duodenal obstruction when a duodenal
INTESTINAL ATRESIA & STENOSIS membrane has a hole through it
• Hallmark: OBSTRUCTION • Can be centrally or eccentrically placed
• Partial/Complete • Accounts for 70% of all intestinal stenosis
• Simple/Strangulating • May present much later in life
• Intrinsic/Extrinsic • (+) association with Down syndrome

ATRESIA Diagnosis
 Congenitally acquired complete obstruction • Anteroposterior radiograph demonstrate an
STENOSIS enlarged duodenum, which represents duodenal
 Incomplete or partial obstruction stenosis. Air is observed distally
LOCATION
 Duodenum - common JEJUNAL/ILEAL ATRESIA
• Etiology: Intrauterine vascular accidents
DUODENAL ATRESIA • Clinical Manifestations
• Incidence 1/10,000 births  Bilious vomiting/abdominal distention
• 25-40% of intestinal atresias • Diagnosis
• Common in prematures  Abdominal x-rays, UGIS
• May have associated anomalies • Treatment: Surgical
• Down syndrome occures in 20-30%
• Etiology ANOMALIES ASSOCIATED WITH INTESTINAL ATRESIA
 Failure of recanalization of the duodenal lumen  Annular pancreas
 Malrotation
Anatomic Configurations  Ectopic anus
A. Complete membrane obstructing the lumen (most  Gastrochisis
common)  Omphalocele
B. A pouch with a fibrous cord connecting to the  VATER sequence (Vertebral, anal,
distal duodenum tracheoesophageal, and renal anomalies)
C. Blind ending pouch with no connection to the  Congenital heart disease
distal duodenum (least common)  Ileal duplication
 Genetic defects (more common with duodenal
Presentation atresia)
• Hallmark: bilious vomiting, absence of abdominal  Trisomy 21 (Down’s syndrome)
distention absencedefect
 2p- chromosomal of abdominal distention
• Usually noted on the first day of life  13q- chromosomal defect
• Jaundice may be present  5p- chromosomal defect (cri-du-chat)
• Polyhydramnios present in 33-50% of cases
• During prenatal ultrasonography
ANOMALIES OF ROTATION AND FIXATION
Diagnosis Nonrotation
• Abdominal x-ray – double bubble sign  bowel fails to rotate after it returns to the
• Contrast study abdominal cavity
 Arrow shows membrane Malrotation
 Incomplete rotation of the intestine during fetal
development
 Clinical Features (Malrotation) ANOMALIES OF INNERVATION AND MOTILITY
• 90% will present in the first 2 months of life with HIRSCHSPRUNG’S DISEASE
intestinal obstruction • Congenital aganglionic megacolon
• Chronic symptoms present in a few cases • Complete absence of the ENS
• Diagnosis: UGIS, barium enema, ultrasound • Most common cause of lower intestinal obstruction
• Treatment: surgical in neonates
• Significant morbidity may occur in patients who • 1:5,000 live births
develop short bowel syndrome • Infant (usually male, in a ratio of 5:1)
• Can be sporadic or familial
DUPLICATIONS • Association with other congenital defects
• Defects in recanalization • Down syndrome – most common
• Usually symptomatic
• Presents within the 1st year of life Clinical Manifestation
• Diagnosis: ultrasound, Meckel’s scan, CT scan • Soon after birth
• Treatment: Surgical • Little meconium is passed or there is delayed
passage
MECKEL’S DIVERTICULUM • Abdomen is distended
• 3-6 cm outpouching of the ileum within 50-75 cm • Usually empty rectal vault, followed by gush of air
from the ileocecal valve. upon withdrawal of finger
• Arises from the antimesenteric border • 20% of patients will have persistent diarrhea
• Contain all layers of the intestinal wall • Sever constipation and recurrent fecal impactions
• Usually contains an ectopic gastric mucosa are common in older children
• Associated congenital anomalies • Anemia, malnutrition, hypoproteinemia
 Cleft palate, bicornuate uterus, annular pancreas • Resistance to infection can be impaired
• Clinical manifestations • Above symptoms may occur in patients with short
 Painless intermittent lower intestinal bleeding segment aganglionosis
 Intestinal obstruction more common in older
patients Diagnosis
 Can mimic symptoms of acute appendicitis • Rectal Manometry
• Neoplastic transformation has been reported • Rectal Biopsy
• Diagnosis: Meckel radionuclide scan • Barium Enema
 Uses technetium-99 pertechnetate
• Treatment: surgical FUNCTIONAL CONSTIPATION
• Idiopathic
OMPHALOCELE • Fecal withholding
• 2.5/10,000 births • Develops after the passage of painful bowel
• Herniation of the abdominal viscera into the base of movements
the umbilical cord
• Abdominal contents appear normal & is covered with Diagnosis
a membranous sac • Barium Enema
• May be associated with extraintestinal defects
Treatment
GASTROSCHISIS • Patient education
• 1/10,000 births • Relief of impaction
• Abdominal wall defect lateral to the umbilicus • Softening of the stool
• Bowel not covered by a sac, appears abnormal,
thickened & matted
• Extraintestinal defects not common

Treatment
• Surgical repair
• Immediate postoperative morbidity/mortality
higher in omphalocoele
• Long term morbidity/mortality higher in
gastroschisis
 HIRSCHSPRUNG CLASSIFICATION
FUNCTIONAL
DISEASE Low Malformation
Onset > 2 years Birth • Terminal portion of the colon passes through the
Encopresis Common Very rare levator ani
• Can be treated with localized surgery with good
Failure to
Uncommon Possible outcome
thrive
High Malformation
Enterocolitis None Possible • Colon ends in or above the levator muscles
Abdominal • Usually communicates with the urinary tract or
Uncommon Common
distention genital tract
Anal tone Normal Normal • Surgical repair more complex
Rectal exam + stool • Stool
Rectal biopsy Normal - Ganglion cells DIAGNOSIS
• Careful inspection of perineum at birth
Barium enema - Transition Zone + transition zone
• Evaluation of other anomalies
• Sonography
CHRONIC INTESTINAL PSEUDO-OBSTRUCTION
• Primary/secondary MANAGEMENT
Causes • Decompress the gut
• Abnormal myoelectrical activity • Rule out an obstructive uropathy
• Abnormal intestinal neuropathy • Wait 24 hours for fistulas to fill to establish if there is
• Abnormal intestinal myopathy perineal membrane or fistula
Treatment • Surgery: colostomy then repair
• Nutritional support
• Prokinetics? COMPLICATIONS
• Supportive • Fecal incontinence
• Soiling
INTESTINAL NEURONAL DYSPLASIA • Constipation
• May mimic Hirschsprung • Urinary incontinence
• Absent or hypoplasia of sympathetic nerves
• Dysplastic submucosal plexus SUPERIOR MESENTERIC ARTERY SYNDROME
Treatment • Extrinsic compression of the duodenum after rapid
• Same as functional constipation weight loss & in supine position
• Surgery if refractory to treatment • Abdominal X-ray – cut off sign of the duodenum
• Treatment: relief of obstruction
ANORECTAL MALFORMATIONS
• Common ILEUS
• 1:2,000 to 1:5,000 live births • Failure of peristalsis without evidence of mechanical
• High form more common in males obstruction
• 50% occurs isolated defect • Abdominal distention, vomiting, pain
• 50% associated with a wide variety of other defects • X-ray: Air fluid level
 VATER or VACTERL association – most common • Treatment: Correction of the underlying abnormality
ETIOLOGY ADHESIONS
Possible causes • Fibrous bands of tissue causing obstruction after
• Vascular accidents may cause localized defect abdominal surgery
• Defects in mesodermal migration • Can occur as early as 2 weeks post-op
• Diabetes and drug ingestion in mothers
• Treatment
• Occupational exposures in father  Nasogastric decompression
• Hereditary  Antibiotics
 Fluid resuscitation
 Surgery if medical management fails
INTUSSUSCEPTION NECROTIZING ENTEROCOLITIS
• Portion of the alimentary tract telescoped into an • Life threatening emergency of the GIT in the
adjacent segment newborn period
• Common cause of obstruction in 3-6 yrs of age • Various degrees of mucosal or transmural necrosis of
• Male:Female ratio of 4:1 the intestines
• Ileocolic- most common site • Prematurity – greatest risk factor
• Clinical manifestations may be sudden catastrophic
Clinical Manifestations or insidious
• Sudden onset of pain
• Vomiting ALLERGIC GI DISORDER
• No fecal excretion of flatus Mixed IgE & Non-IgE mediated
• Currant jelly stool – 60% • Esophagus
• Stomach
Diagnosis • Small intestines
• Abdominal x-ray Non-IgE mediated
• Ultrasound  Allergic proctocolitis
• Contrast enema (coiled-spring sign)  Food induced-enterocolitis

APPENDICITIS INFLAMMATORY BOWEL DISEASE

• Peak incidence 12-18 years • Crohn’s disease (CD) is a chronic, idiopathic
• Invasion of appendiceal wall by bacteria transmural inflammation which can affect one or
• Delay in diagnosis beyond 36-48 hours- >65% several segments of the digestive tract
perforation rate • Ulcerative Colitis (UC) is a chronic idiopathic
inflammation of the rectum extending continuously
Clinical manifestation over a variable length of the colon from the distal to
• Vague periumbilical pain initially the proximal end.
• Localizes to RLQ in the next 12-24 hours • Intermediate colitis (IC) is reserved for cases of colitis
• anorexia in which findings are not sufficient to allow
differentiation between CD and UC.
Physical Examination
• Direct and rebound tenderness IBD Presentation
• Rovsing sign Symptoms/ Signs CD UC
• Psoas Rectal bleeding ++ ++++
• Obturator internus sign Abdominal pain ++++ +++
Diarrhea ++ ++++
Laboratories Weight loss ++++ ++
• Leukocytosis Growth Failure +++ +
• White or red blood cells in urinalysis Perianal disease ++
Mouth ulcers ++ +
Radiologic studies
Erythema nodosum + +
• Plain abdominal x-ray (sentine loops, colon cut-off
Fevers ++ +
sign)
Anemia +++ +++
• Ultrasound (wall thickness >6mm, luminal
Arthritis + +
distention, lack of compressibility, complex mass,
fecalith)
Diagnostic Approach to IBD
INGUINAL HERNIAS  Suspect the diagnosis
• Persistent patency of proccesus vaginalis  History, exam CBC, ESR, CRP, albumin
• Hernia occurs when intra abdominal contents enter  Exclude other etiologies
the inguinal region  Stool culture, C. difficile, TB skin test
• Treatment: surgical  Classify disease as Crohn’s or UC; determine
disease location in CD
 Upper endoscopy, colonoscopy, UGI/SBFT
 Identify extraintestinal manifestations
 Liver function test, joint, skin, eye exams
 PEDIA: Congenital Abnormalities of the Diagnosis
Stomach • ABDOMINAL X-RAY
 Soft tissue mass protruding into the lumen
CONGENITAL GASTRIC OUTLET OBSTRUCTION  Extrinsic compression of stomach
• Results from pyloric atresia and antral webs  Filling defect of cyst with barium
• Cause is unknown • UTS
• CT SCAN
Clinical Manifestation • MRI
• Nonbilious vomiting
• Feeding difficulties Management:
• Abdominal distention during the 1st day of life • Complete surgical excision
• Gastric aspirate > 20mL at birth • If large : partial excision, Partial gastrectomy and cyst
• Rupture may occur as early as the 1st 12 hrs of life gastrectomy

Treatment: HYPERTROPHIC PYLORIC STENOSIS

• Correction of dehydration and hypochlorenic • Most common cause of gastric outlet obstruction in
alkalosis infancy
• Nasogastric decompression • Most frequent indication for surgery during the 1st 6
• Surgical endoscopic repair mos. Of life
• 1-3/1,000 infants in US, incidence is rising
GASTRIC DUPLICATION • M>F (4:1), > Caucasians, rare in Asians
• Cystic or tubular structures that occur within the walls • High transmission rate from affected mother
of the stomach  Male offspring- 20%
• Commonly located on the greater curvature  Female offspring- 10%
• Account for 2-7% of all GI duplications  Hypertrophic Pyloric Stenosis
• Do not usually communicate with the stomach lumen
• Share a common blood supply Etiology
• Unknown etiology
Etiology • Reduced levels of neuronal nitric oxide synthetase
• Diverticulization (nNOS) contribute to pylorospasm
• Canalization defects • Other causes implicated:
• Caudal twinning  Infantile hypergastrinemia
 Elevated serum levels of prostaglandin (PGE2,
 Associated anomalies seen in 35% PGF2)- smooth muscle contraction
 Intestinal tract duplication  Early postnatal (3-13 days) exposure to
 Vertebral anomalies macrolide antibiotics (erythromycin- 8x risk HPS)
 Symptoms present in 1st year of life depending on the  Maternal treatment with macrolide antibiotics
size, location, presence/ absence of communication during pregnancy and breastfeeding
with GIT  Cow milk protein allergy
IN YOUNGER CHILDREN • Due to hypertrophy of the circular smooth
• Nonbilious vomiting musculature surrounding the pylorus and antrum
• Weight Loss • Hyperperistalsis against a closed pyloric canal
• Failure to thrive produces edema with subsequent work hypertrophy
IN OLDER CHILDREN leading to high grade obstruction
• Epigastric pain
• Abdominal fullness or mass- 33% Manifestations
• GI bleeding • Symptoms occur at 2-8 wks after birth
• GI Obstruction • Initial symptom: Projectile nonbilious vomiitng
• Progressive vomiting immediately after feeding (5-10
mins.) or delayed until stomach is full
• After vomiting, infant is hungry and wants to feed
again
• Emesis may be blood-streaked in presence of
gastritis.
 • Symptoms: occur at 2-8 wks after birth
 Initial symptom: projectile non-bilious vomiting
 Progressive vomiting immediately after feeding
(5-10 mins) or delayed until stomach is full
 After vomiting, infant is hungry and wants to
feed again
 Emesis may be blood-streaked in presence of
gastritis
HYPOCHLOREMIC METABOLIC ALKALOSIS
• Due to progressive loss of fluid. H2 ions and chloride
• No weight gain or failure to thrive
ICTEROPLYLORIC SYNDROME
• Unconjugated hyperbilirubinemia due to enhanced
enterohepatic resorption of bilirubin
• Associated with decreased levels of glucuronyl
tranferase – 5%
Physical examination
• Gastric distension
• Visible peristaltic wave that progresses across the
abdomen after feeding
• Palpable firm, movable olive-shaped pyloric mass,
about 2 cm in length located above & to the right of
the umbilicus (23-55%)
• Easiest palpated after an episode of vomiting
• ID of pyloric olive: PPV 100%
Abdominal x-ray:
• Large gastric air bubble with little or no intestinal
air
UTS
• Recommended
 Rapid and non-invasive
 Lack of radiation
 NO risk of contrast aspiration
• Measures length & diameter of pylorus, pylorus GASTRIC VOLVULUS
muscle thickness
• Sensitivity of 93%, PPV 90%
• Criteria for diagnosis:
 Pyloric thickness: 3-4 mm
 Overall pyloric length: 15-19 mm
 Pyloric diameter: 10-14 mm
UGIS:
• Elongated pyloric channel (string sign)
• Bulge of the pyloric muscle into the antrum
(Shoulder sign)
• Parallel streaks of barium seen in the narrowed
channel (Double tract sign)
 Proposed algorithm to determine which study to
request
 Based on gastric aspirate volume
 After a 1-hour fast, gastric contents are aspirated &
quantified
 Aspirate >5mL: gastric outlet obstruction in >90%
 Request for UTZ initially then UGIS if needed
 Aspirate <5mL: medical cause is suspected in >
90%
 Request for UGIS
Treatment
• Initial
 Replacement of fluid and electrolytes
 Correction of dehydration
Prognosis
• Recurrence: 1-3%
• Adhesion and infection: 1-5%
• Post-op vomiting: 50%
 Due to:
 Edema of pylorus at the incision site
 Delayed gastric emptying
 GER
• Persistent vomiting
 Incomplete pyloromyotomy
 Other cause of obstruction - adhesions
• Serial UTZ done after surgery
 Initial swelling of pyloric muscles
 Rapid involution over the next 3 weeks
 Normal pyloric muscle thickness in 6 weeks
• Conservative management
 If surgical treatment is not available
 For poor surgical candidates
 Nasoduodenal feeding
 Oral or IV atropine sulfate (pyloric muscle
relaxant)
• Stomach is tethered longitudinally by the
gastrohepatic, gastrosplenic and gastrocolic ligaments;
transversely by the gastrophrenic ligament
• If any of these attachments is absent or stretched, the
stomach may rotate around itself
Clinical manifestation:
• Nonspecific; suggests high intestinal obstruction
• In infancy
 Nonbilious vomiting
 Epigastric distension
 • In older children
 Chronic gastric volvulus is more common
 History of emesis
 Abdominal pain and distension
 Early satiety
 Failure to thrive

Diagnosis:
• Abdominal x-ray
 Dilated stomach
 Double fluid level with “beak” near the LES

Management:
o Emergency surgery be prevent gastric
ischemia, necrosis, perforation
o Reduction of volvulus with gastropexy

HYPERTROPHIC GASTROPATHY
• Uncommon in children
• Usually transient, benign and self- limited
• May be secondary to CMV infection, HSV, Giardia, H.
pylori
• Mechanism: widening of gap junction, between gastric
epithelial cells with resultant loss of fluid and protein

Clinical Manifestations:
• Vomiting
• Anorexia
• Upper abdominal pain
• Diarrhea
• Edema (hypoproteinemic protein- losing
enteropathy)
• Ascites
• Mean age of diagnosis : 5y/o (2 days- 7yrs)
• Illness lasts 2-14 wks with complete resolution

Diagnosis:
• Endoscopic with biopsy
• Tissue CMV PCR is diagnostic
• UGIS
 Thickened gastric folds

Treatment:
• Supportive
 Adequate hydration
 H2 receptor blockade
 Albumin replacement if with symptomatic
hypoalbuminemia
 CMV (+) Ganciclovir
 H. pylori (-) Amoxicillin, Clarithromycin,
Omeprazole
 PEDIA: Liver Imaging Studies
Lecturer: Roumilla Mendoza, M.D • plain radiographs
• Ultrasound
LIVER • CT scan/MRI
• Liver as a metabolic organ • cholangiography
 Endocrine • ERCP
 secretion into sinusuidal system
 Exocrine Liver biopsy
 secretion into the biliary system • percutaneous
• Liver as a filter • wedge biopsy
• Liver as a hematopoietic organ
CHOLESTASIS
Pathologic Manifestations • prolonged elevation of conjugated bilirubin beyond 2
• Inflammation or necrosis weeks of life
• Cholestasis • Direct bilirubin is > 20% of total bilirubin
• Cirrhosis • Direct bilirubin is > 2 mg/dl
• Neonatal Cholestasis
Clinical Manifestations
• Hepatomegaly
 consistency, tenderness, mass, bruit
• Jaundice
 cholestasis (direct hyperbilirubinemia)
• Pruritus
 due to retained salts/acids

SPIDER ANGIOMAS
• central pulsating arterioles with radiating venules

Clinical manifestations:
• Palmar erythema
• clubbing
• Xanthomas
• Portal Hypertension
 ascites BILIARY ATRESIA
 esophageal varices • Progressive Obliteration of the bile ducts
• Encephalopathy • 1:5000- 1:18,000
• Renal dysfynction • Bile duct proliferation (biopsy)
• Hepatopulmonary syndrome • Treatment: Hepato portoenterostomy (Kasai)
• Failure to thrive procedure
• Bleeding tendencies • Most common cause of pediatric cirrhosis

EVALUATION OF LIVER DYSFUNCTION CHOLEDOCHAL CYST

Biochemical tests • Congenital dilatations of the common bile ducts
• AST/ALT- reflects liver cell injury • Progressive biliary obstruction and cirrhosis
• Alkaline phosphatase/GGT- impaired bile flow • Most common: type 1
• Total/Direct/Indirect bilirubin • Diagnosis: Ultrasound, MRC
• Protime- hepatic synthetic function • Treatment: surgical
• Albumin- hepatic synthetic function
• Cholesterol levels IDIOPATHIC NEONATAL HEPATITIS
• Sporadic/familial
• Unknown cause
• Extension giant cell formation (biopsy)
• Prognosis: good
INFECTIOUS NON-ALCOHOLIC FATTY LIVER
• Bacterial • Spectrum
• Viral • Overweight or obese children
 TORCH • most are asymptomatic
 Hepatotropic viruses
 HIV Treatment:
 Enteroviruses • lifestyle modification
 Parvovirus B19 • ursodeoxycholic acid?
• anti-oxidants
GENETICS • metformin
• Alagille syndrome
• Wilson disease GALLBLADDER DISORDERS
 hepatolenticular degeneration
 Autosomal recessive CHOLECYSTITIS
 Kayser-fleischer ring (cornea) • Acute acalculous cholecystitis
 uncommon
• Diagnosis: serum ceruloplasmin level/24 hour urinary  infectious (Strep, Salmonella, Ascaris)
copper, liver biopsy  US: enlarged, thick-walled GB, (-) stone
• Treatment: decrease copper intake, penicillamine • Tx: management of systemic infection
• Prognosis: if untreated: liver failure
ACUTE HYDROPS
METABOLIC • acute noncalculous noninflammatory distension
• Galactosemia • may develop in pateints on long term TPN
 deficiency of galactose-1-phosphate • RUQ pain, fever, jaundice
uridyltransferase (GALT) • US: markedly distended scho-free GB
 Treatment: use of lactose free formula • absence of biliary tree dilatation
• Tx: Conservative
MANAGEMENT OF CHOLESTATIC JAUNDICE:
Nutritional CHOLELITHIASIS (GALLBLADDER STONES)
• totaL caloric intake (125% RDA) • >70% of gallstones are pigment type
• fat soluble vitamins • Found in children with predisposing disorders
• medium chain triglyceride • Symptomatic: surgical
• Asymtomatic: management is controversial
Therapeutic
• choloretics ursodeoxycholic acid- 10-20mg/kg/day FUNCTIONS
• phenobarbital- 3-10 mg/kg/day • Endocrine organ
• Pancreatic islets (insulin, glucagon)
Portal hypertension • Exocrine organ
• diuretics (spironolactone, furosemide) • digestive enzymes
• albumin • bicarbonate
• propanolol
• H2 blockers ANATOMIC ABNORMALITIES
PANCREATIC AGENESIS- rare
FULMINANT LIVER FAILURE Complete
• Severe functional impairment of liver cells • associated with severe neonatal diabetes
• no pre-existing liver disease • death at an early age
• evolving over a period of 8 weeks Partial/dorsal pancreatic agenesis
• hepatic encelopathy as major symptom • often asymptomatic
• Treatment: supportive • may be associated with diseases, congenital heart
disease, recurrent pancreatitis
 ANNULAR PANCREAS
• may be associated with duodenal malformations
• history of maternal polyhydramnios
• present with complete or partial obstruction
• Treatment: Surgery

PANCREAS DIVISUM
• 5-15% of population
• failure of fusion of the ventral and dorsal anlage
• tail, body and part of the head drain in the small
accessory duct of Santorini
• may result in recurrent pancreatitis if duct of
Wirsung becomes blocked

ECTOPIC PANCREATIC RESTS

• heterotrophic pancreas
• presence of pancreatic tissues within the walls of
intestines and stomach, sometimes in spleen,
omentum or in Meckel’s diverticulum
• Barium studies: umbilicated appearance CONDITIIONS ASSOCIATED WITH ACUTE PANCREATITIS
• Endoscopy: irregular yellow nodule 2-4mm Systemic Diseases
• Treatment: surgical if with bowel obstruction • Infections
• Inflammatory and vasculitic disorders
CONGENITAL ISOLATED DEFECTS  collagen vascular disease
• extremely rare  henoch- schonlein purpura
• can be primary or secondary  hemolytic uremic syndrome
• manifestations may include  kawasaki disease
 failure to thrive  inflammatory bowel disease
 hypoproteinemia • sepsis/shock
 edema
INFECTIOUS AGENTS ASSOCIATED WITH ACUTE
MALIGNANCY PANCREATITIS
CARCINOMA OF EXOCRINE PANCREAS Bacteria
Duct Cell Adenomacarcinoma • Typhoid fever
• most common malignant pancreatic tumor • Verocytotoxin- producing E.coli
• poor prognosis • Mycoplasma
Acinar Cell Carcinoma • Leptospirosis
• malignant Viruses
• usually metastatic at time of diagnosis • Mumps
Pancreatoblastoma • Coxsackie B
• infantile pancreatic carcinoma • Eschovirus
• average age is 4.1 yrs • Influenza A & B
Treatment: surgical resection • Hepatitis A & B
• Epstein Barrchemotherapy
ACUTE PANCREATITIS • Varicella
• acute inflammatory process of the pancreas, with • Rubella
variable involvement of peripancreatic tissues or • Rubeola
remote organ system Parasites
• iniated by inappropriate activation of pancreatic • Malaria
zymogens to active enzymes within the parenchyma • Ascariasis (duct obstruction)
resulting in autodigestion • Clonorchis sinensis (duct obstruction)
• Infectious Agents Associated with Acute
Pancreatitis
 Mechanical/ Structural
• TRAUMA Therapeutic approaches
 Blunt Injury • Nasogastric Decompression
 Child Abuse • Restoration and maintenance of fluids, electrolytes
 ERCP (Endoscopic Retrograde and acid base balance
Cholangiopancreatography) • Adequate analgesia
• PERFORATION : Duodenal ulcer; other  DOC- Meperidine
• ANOMALIES • Nutritional Support
 Pancreas divisum  total parenteral nutrition
 Choledochal Cyst • Antibiotics
 Stenosis  no benefit in uncomplicated cases
 Other anomalies  antibiotic prophylaxis in necrotizing
• OBSTRUCTION pancreatitis
 Stones • H2 Antagonist
 Parasites • Somatostatin
 Tumors  inhibition of pancreatic secretion
 relaxation of sphincter of Oddi
Criteria for Diagnosis  reduce edotoxemia by stimulating RES
• Typical clinical manifestations
• increase serum concentrations of pancreatic Surgery
enzymes ( 3-4 times above upper limits of normal) PROPOSED INDICATIONS
• sonographic or radiologic evidence of pancreatic • uncertainty of diagnosis
inflammation • decompression of obstruction in main
pancreatic duct or distal CBD
Clinical Manifestations • correction of abdominal complications
• abdominal pain (epigastric and steady) • surgical measures to ameliorate the acute
• persistent vomiting phase of the disease
• fever
Complications of Acute Pancreatitis
ACUTE HEMORRHAGIC PANCREATITIS (RARE) LOCAL COMPLICATION
• Life threatening related to SIRS • Pseudocyst
• Cullen sign or Grey Turner sign may be present  serum pancreatic enzymes may remain
elevated
Laboratory Investigations  diagnosis reliably made by USD or CT
 SERUM AMYLASE  frequently resolves without interventions
 most frequently utilized  drainage may be percutaneous, endoscopic
 elevated within hours and remains elevated for or surgical if non-resolving
3-5 days for uncomplicated cases
CHRONIC PANCREATITIS
 SERUM LIPASE • Characterized by recurrent or persisting abdominal
 remains elevated for 8-14 days pain with development of pancreatic exocrine or
 as sensitive as amylase but more specific endocrine insufficiency in some
• Symptoms begin at 10-12yrs
 CBC & PLATELET COUNT • Spontaneous resolution of acute symptoms occur at
 hemoconcentrations and coagulopathy 4-8days
 BLOOD GLUCOSE- hyperglycemia
 SERUM LIPID- hyperlipidemia Treatment
 SERUM ELECTROLYTES- hypocalcemia, • Nutritional Support
hyperkalemia • Adequate analgesia
 BUN, CREATININE- kidney failure • Endoscopic sphincterotomy/biliary stent
 BILIRUBIN- jaundice replacement
 ABG- acidosis • Surgery
 PEDIA: Diarrhea ETIOLOGY
Lecturer: Dr. Josie Grace Castillo • Important infectious diarrheal pathogens

DIARRHEA Viruses Rotavirus

• Frequent passage of loose stools
Bacteria ETEC
• Reflects increased volume of stool water resulting from
EPEC
an increased secretion or decreased absorption
EIEC*
• Stool volume exceeds 200 mL/24 H in adults
Campylobacter jejuni*
• Loose stool weight of >10 mL/kg/24 H in infants and
Shigella*
children
Vibrio cholera
• Acute diarrhea lasts <14 days
• Chronic diarrhea lasts >14 days Protozoa Cryptosporidium
Entamoeba histolytica
PATHOPHYSIOLOGIC MECHANISMS Giardia lamblia
• Osmotic diarrhea
• Secretory diarrhea * Also causes dysentery
• Reduction in anatomic surface area
• Alteration in intestinal motility ACUTE DIARRHEA
• Commonly due to an infectious cause
Osmotic Diarrhea • Risk factors:
• Caused by presence of non-absorbable solutes in the  Environmental contamination
GIT  Increased exposure to enteropathogens
• Stops with fasting  Young age
• Stool pH <5  Immune deficiency
• (+) stool reducing sugar  Measles
• Ex. Lactose intolerance  Malnutrition
Secretory Diarrhea  Vit. A deficiency – mortality risk increased by
• Significant excess secretion compared to absorption 20-24%
• High volume, extremely watery stools  Zinc deficiency – mortality risk increased by 13-
• Diarrhea continues with fasting 21%
• Ex. Cholera and E. coli  Lack of exclusive or predominant breastfeeding

OSMOTIC VS. SECRETORY DIARRHEA PATHOGENESIS OF INFECTIOUS DIARRHEA

Invasion of Mucosa
Osmotic Secretory • Followed by intraepithelial cell multiplication or
diarrhea diarrhea invasion of lamina propia
Volume of Production of Cytotoxins
<200 mL/24H >200 mL/24H
stool • Disrupt cell function via direct alteration of
Response Diarrhea mucosal surface
Diarrhea stops
to fasting continues Production of Enterotoxins
• Alter cellular salt & water balance, yet leave cell
Stool Na <70 mEq/L >70 mEq/L
morphology unchanged
Reducing Adherence to Mucosal Surface
(+) (-)
substances • with resultant flattening of microvilli & disruption
Stool pH <5 >6 of normal cell functioning
 PATHOGENIC MECHANISMS
Invasive Cytotoxic Toxigenic Adherent CLINICAL MANIFESTATIONS
• Related to infecting pathogen and dose/inoculum
• Shigella • Shigella • Shigella • EPEC
• Depends on development of complications:
• Salmonella • EPEC • ETEC • Shiga toxin-
 Dehydration
producing
 Electrolyte imbalance
E. coli
 Nature of infecting pathogen
• Yersinia • Shiga toxin-• Yersinia • EAEC
enterolitica producing enterolitica
Preformed toxin
E. coli
• Ex. Staphylococcus
• Campylobac• Clostridium• Aeromonas• Diffusely
• Rapid onset nausea & vomiting in 6H
ter jejuni difficile adherent E.
• Fever, abdominal cramps, diarrhea in 8-72H
Coli
Enterotoxin Producing
• Vibrio • Vibrio
• Ex. Bacillus cereus, Clostridium perfringens
parahemoly cholera
• Watery diarrhea, abdominal cramps after 8-16H
ticus
incubation period
• EIEC • Rotavirus
Bacterial Dysentery
• Entamoeba
• Ex. Salmonella, Shigella, Camplylobacter, EIEC
histolytica
• Bloody diarrhea, fecal leukocytes, abdominal
cramps, tenesmus, fever
3 TYPES OF ENTERIC INFECTION
• 72-120Hincubation period
Parameter I II III
Mechanism Non- Inflammatory Penetrating DIAGNOSIS
inflammatory (invasion, Clinical Evaluation
(enterotoxin cytotoxin) • Obtain contact and exposure history
or • Assess degree of dehydration & provide rapid
adherent/sup resuscitation & rehydration as required
erficial • Determine etiology for institution of prompt
invasion) antibiotic therapy if indicated
Location Proximal small Colon Distal small  Nausea, vomiting – infection of upper GIT
bowel bowel  Fever – inflammatory diarrhea, dehydration or
Illness Watery Dysentery Enteric fever presence of co-infection (UTI, otitis media)
diarrhea  Severe abdominal pain, tenesmus – infection
Stool exam No fecal WBC Fecal PMN’s Fecal of colon, rectum
mononuclear
leukocytes Stool examination
Examples Vibrio cholera Shigella Salmonella • Fecal leukocytes
ETEC ETEC, EHEC typhi  Indicative of bacterial invasion of colonic
Bacillus cereus Clostridium Yersinia mucosa
Giardia difficile enterocolitica • Stool culture
lamblia Campylobact  Necessary in the following conditions:
Rotavirus er jejuni  Bloody diarrhea with fecal leukocytes
Entamoeba  Outbreaks of diarrhea
histolytica  Immunosupressed children with diarrhea

TREATMENT
• Oral Rehydration Solution (ORS)
• Enteral feeding & diet selection
• Additional therapies
• Antibiotic therapy
ORS Severe Dehydration
• Preferred mode of rehydration & replacement of Give ORS soln (about 5mL/kg/hr) as soon as the
ongoing losses child can drink; usually after 3-4hrs (in infants) or
• Limitations to ORS 1-2 hrs (in children)
 Shock
 Ileus Weight Volume ORS soln/hr
 Intussusception
 Carbohydrate intolerance < 4kgs 15mL
 Severe emesis 4 - <6kgs 25mL
 High stool output (>10 mL/kg/H)
6 - <10kgs 40mL
Diarrhea Treatment Plan C:
10 - <14kgs 60mL
Treat Severe Dehydration Quickly
Can you give IVF immediately? 14 - <19kgs 85mL
YES
• Start IV fluids immediately. If the child can drink, Reassess after 6 hrs (infants) & after 3 hrs
give ORS by mouth while the drip is set up. Give (children). Classify dehydration.
100 ml/kg Ringer’s lactate soln divided as Then choose the appropriate diarrhea treatment
follows: plan to continue treatment.
Age 1st give then give
30 mL/kg in: 70 mL/kg in: Diarrhea Treatment Plan B:
< 12 mos 1 hr * 5 hrs Treat Some Dehydration with ORS
1 – 5 yrs 30 mins* 2 ½ hrs • Give in clinic recommended amt of ORS over 4-hr
* Repeat once if radial pulse is still very weak or period
not detectable • Determine amt of ORS to give during 1st 4 hrs

NO Age * Up to 4-12 12 mos– 2 – 5 yrs

Give 70 mL/kg of Ringer’s lactate (or if not 4 mos 2 yrs
available, normal saline) over 5 hrs in infants (aged mos
<12mos) & over 2 ½ hrs in children (aged 12mos- Weight < 6- 10- 12-19kgs
5yrs). 6kgs <10kgs <12kgs
Age 12 mos – 5
In mL 200- 400- 700-900 900-1400
Age < 12 mos yrs
Weight 400? 700
Give over 5 hrs Give over 2 ½
hrs *use the child’s age only if you don’t know the wt.
the approximate amt ORS required (in ml) can also
<4 kgs 200mL - be calculated by multiplying the child’s wt (in kg) by
(40mL/hr) 75.
4 - <6kgs 350mL - • If the child wants more ORS than shown, give
(70mL/hr) more.
• For infants under 6 mos who are not breastfed,
6 - <10kgs 550mL 550mL also give 100-200ml clean water during this
(110mL/hr) (220mL/hr) period
10 - <14kgs 850mL 850mL
SHOW THE MOTHER HOW TO GIVE ORS SOLUTION
(170mL/hr) (340mL/hr)
• Give small frequent sips from a cup
14 - <19kgs 1200mL 1200mL • If the child vomits, wait 10 mins. Then
(240mL/hr) (480mL/hr) continue, but more slowly.
• Cont. breastfeeding whenever the child wants
Reassess the child q 1-2hrs. If the hydration
status is not improving, give the IV drip more
rapidly.

**see last page for table on Diarrhea Treatment

Plan C: Treat Severe Dehydration Quickly
 AFTER 4 HRS:
• Reassess the child & classify the child for
dehydration
• Select the appropriate plan to continue
treatment
• Begin feeding the child in the clinic
IF THE MOTHER MUST LEAVE BEFORE
COMPLETING TREATMENT:
• Show her how to prepare ORS soln at home
• Show her how much ORS to give to finish 4-hr
treatment at home
• Give her enough ORS packets to complete
rehydration. Also give her 2 packets as
recommended in Plan A
• Explain the 3 rules of Home Treatment
Diarrhea Treatment Plan A:
Treat Diarrhea at Home
• Counsel the mother on the 3 rules of home
treatment:
1. GIVE EXTRA FLUID (AS MUCH AS THE CHILD WILL
TAKE)
• Breastfeed frequently & for longer at each feed
• If the child is exclusively breastfed, give ORS or
clean water in addition to breast milk
• If the child is not exclusively breastfed, give 1
or more of the ff: ORS soln, food-based fluids
(soup, rice water, yoghurt drinks), or clean
water
• It is especially important to give ORS at home
when:
 The child has been treated with Plan B or
Plan C during this visit
 The child cannot return to a clinic if the
diarrhea gets worse
• Teach the mother how to mix & give ORS
• Show the mother how much fluid to give in
addition to the usual fluid intake:
 Up to 2 yrs – 50-100 mL after each loose
stool
 2yrs – 100-200 mL after each loose stool
• Tell the mother to:
 Give frequent small sips from a cup
 If the child vomits, wait 10 mins. Then
cont, but more slowly
 Cont giving extra fluid until the diarrhea
stops
2. CONTINUE FEEDING
• Continue to breastfeed frequently
• If the child is not breastfed, give the usual milk
• If the child is >6 mos or already taking solid
food:
 Also give cereal or other starchy food
mixed with veggies, meat or fish. Add 1 or
2 tsp of vegetable oil to each serving
 Give freshly prepared foods
 Give fresh fruit juice or mashed banana to
provide Vit. K
 Encourage the child to eat; offer food at
least 6x / day
 Give the same foods after diarrhea stops,
& give an extra meal each day for 2 wks
3. WHEN TO RETURN
• Take the child immediately to the clinic if the
child does not get better in 5 days or develops
any of the following:
 Many watery stools
 Repeated vomiting
 Marked thirst
 Eating or drinking poorly
 Fever
 Blood in the stool
ENTERAL FEEDING AND DIET SELECTION
• Resume breastfeeding or non-diluted milk formula as
soon as possible
• Give complex carbohydrates, lean meats, and fruits
and vegetables
• Avoid fatty foods or foods high in simple sugars
(juice, carbonated soda)
• Dietary aim: provide 100 kcals/kg/day,
• CHON 2-3 g/kg/day
• Withdrawal of milk or replacement with
• lactose-free formula is not necessary
ZINC SUPPLEMENTATION
• Leads to reduced duration & severity of diarrhea
• Infants
 <6 mos: 10 mg/day
 >6 mos: 20 mg/day
• Duration: 10-14 days during and after diarrhea
• Reduces incidence of diarrhea for next 6 mos
 PROBIOTICS Clinical Features of Dehydration According to Severity
• Living organisms or components of cells that have (AAP Recommendations)
beneficial effect on the host
 Ex. Lactobacillus, bifidobacteria, saccharomyces Mild to
Severe
• Favorable affect the host by local and/or immune Manifestations No DHN Moderate
DHN
modulation pathways DHN
 Compete with pathogens for nutrients Normal Slightly Deeply
 Produce bacteriocins which act as local Eyes
sunken sunken
antibiotics
 Produce lactic & acetic acid, which lowers Tears Present Decreased Absent
luminal pH and inhibits pathogen growth
Mouth and Moist Dry Parched
• Therapy has not been standardized
tongue
• Most effective organism has not been identified
Instant Recoil <2 Recoil >2
ANTI-SECRETORY AGENT Skinfold
recoil secs secs
Racecadotril
• Enkephalinase inhibitor Normal Prolonged Prolonged,
Capillary refill
• Reduces stool output minimal
• Dose: 1.5 mg/kg/dose Warm Cool Cold;
Extremities mottled;
Clinical Features of Dehydration According to Severity cyanotic
(AAP Recommendations)
Normal to Decreased Minimal
Urine output
Manifes- Minimal or Mild to Severe decreased
tations No Moderate DHN
dehydration dehydration Treatment Based on Degree of Dehydration (AAP)
Body wt < 3% 3–9% > 9% Degree of Rehydration Replaceme
loss (%) Nutrition
DHN therapy nt of losses
Mental Well, alert Normal, Apathetic, <10 kgs
status* fatigued or Lethargic to BW: 60- Continue
restless, comatose 120ml breastfeeding
Minimal or
Irritable Not applicable ORS/BM Resume age-
no DHN
>10kgsBW: appropriate
Thirst * Normal or Thirsty, eager Drinks 120-240ml normal diet
slightly to drink poorly; ORS/BM
increased unable to
drink Mild to ORS, 50-
Moderate 100ml/kg BW Same Same
Heart Normal Normal to Tachycardia; DHN over 3-4H
rate increased bradycardia
in severe LRS or NSS in
cases 20ml/kg BW IV
until perfusion
Quality of Normal Normal to Weak, & mental
pulses decreased thready or status
impalpable Severe
improves; then Same Same
DHN
Breathing Normal Normal; fast Deep 100ml/kg BW
ORS over 4H or
D5NSS IV at 2x
maintenance
rate
BACTERIAL OVERGROWTH CARBOHYDRATE MALABSORPTION
-11 -13
• 10 to 10 bacterial CFU/gm feces SYMPTOMS:
• Symbiotic relationship with host, providing nutrients • Loose watery diarrhea
and protecting the host from pathogenic organisms • Flatulence
• Excessive amounts of bacteria in host is harmful • Abdominal distention
• Pain
Protective mechanisms:
• Gastric pH  Unabsorbed CHO enters the colon and is fermented by
• Small bowel motility & migrating motor complexes intestinal bacteria, producing organic acids and
• Ileocecal valve hydrogen gas
• Mucosal defenses  Acidic stool pH (<5)
 Mucin and Ig – prevent bacterial overgrowth
LACTASE DEFICIENCY
Risk factors: PRIMARY ADULT TYPE HYPOLACTASIA
• Small bowel obstruction • Physiologic decline in lactase
• Partial bowel obstruction • Varies between ethnic groups; Asians = 40%
• Intestinal pseudoobstruction • Downregulation of lacatase gene as early as 2 yrs old
• Prematurity
• Immunodeficiency SECONDARY LACTOSE INTOLERANCE
• Malnutrition • Follows small bowel mucosal damage
 Rotavirus infection
Diagnosis: • Usually transient
• Small bowel aspirate culture • Improves with mucosal healing in 4-5 days
• Hydrogen breath test • Lactase Deficiency
• Stool exam: +++ fat globules
• Bacterial Overgrowth Diagnosis:
• Hydrogen breath test
Inefficient intraluminal processing of dietary fats with • Small bowel biopsy to measure mucosal lactase
steatorrhea due to: concentration
• Bacterial deconjugation of bile salts • Testing is not mandatory
• Vit. B12 malabsorption • Dietary changes that reduce/eliminate lactose
• Microvillus brush border damage with malabsorption provide relief

Decreased Vit. B12 and Increased Folate levels Treatment:

• Bacterial consumption of Vit. B12, enhanced synthesis • Milk-free diet
of folate • Lactose-free milk or Soy milk for infants
• Lactase tablet preparation
Lactic acidosis • Short Bowel Syndrome (SBS)

Intraluminal factors Causes:

• Intestinal disorders CONGENITAL
 Carbohydrate malabsorption • Multiple atresias
 Excessive carbonated fluid intake • Gastroschisis
 Transport capacity of the SI is exceeded BOWEL RESECTION
 Excessive intake of non-absorbable solutes • NEC
 Ex. Sorbitol, MgOH, Lactulose • Volvulus with or without malrotation
• Long segment Hirschsprung Disease
• Trauma
• Crohn’s disease
SHORT BOWEL SYNDROME (SBS)
• Loss of >50% of small bowel, with or without a portion
of the large intestine can result in symptoms of
generalized malabsorption disorder
• Small bowel length:
 NB: 200-250 cms
 Adult: 300-800 cms
• Anatomic location of resection
 Jejunal resections better tolerated than ileal
resection
 “Ileal brake”
 15 cm bowel + ileocecal value OR 20 cm bowel, no
valve: potential to survive and weaned from TPN

Treatment:
• Repletion of massive water & electrolyte losses as
the bowel initially accommodates to absorb these
losses
• Total parenteral nutrition with slow progression to
continuous enteral feeding
• Use MCT-based protein hydrolysate milk formula
• As intestinal adaptation occurs, bowel mucosa
proliferates and bowel lengthens with growth
• If with large stool output:
 Soluble fiber and anti-diarrheal (Loperamide)

Long-Term Complications:
PARENTERAL NUTRITION
• Catheter infection
• Hepatic cholestasis & cirrhosis
• Gallstones

VITAMIN AND MINERAL DEFICIENCIES

• Vit. B12, Folate, Iron
• Fat-soluble vitamins, Zinc, Copper

BLOODY DIARRHEA, SECONDARY TO FEEDING COLITIS