Far Eastern University

Nicanor Reyes Medical Foundation

Institute of Medicine Presence of blood in stool:
• Fresh blood: hematochezia (LGI 4th part of duodenum)
Batch 2020
o MCC: anal fissure
Pediatrics 3A - Upper GIT
• Black: melena
Dr. Devega 2018
o UGI secondary to oxidation of H+
DIARRHEA Presence of fever, convulsions or other problems
• It is essentially a clinical manifestation of altered GI • (e.g. cough, heart, recent measles)
function in DIGESTION, ABSORPTION, or SECRETION Emesis
leading to excessive loss of fluid and electrolytes • Bile stained/bilious: past the 2nd part of the duodenum
• >3x / 24 hrs • Non-bile stained: UGI
• watery stool Type and Quality of fluids and food consumed during the illness
• Most common cause: Rotavirus • ▪ E.g "am" rice that is cooked repeatedly
Drugs or other remedies taken (amoxicillin, erythromycin)
DURATION • Infancy (0-2 y.o), early (1st yr), late (2nd year) Anti-
• Acute motility drugs – not to be given to children
o <14 days, sudden onset • <5 y/o —> bloating, EPS, seizures
• Chronic
o >14 days EPIDEMIOLOGY
o non-infectious in origin: stress, overfeeding, • Increased morbidity and mortality among infants
lactose intolerance, malabsorption, celiac disease < 1 y/o (6-11 months)
• Persistent
o >14 days Reasons for increase morbidity and mortality in < 1 y/o
o infectious in origin, continuation of acute diarrhea 1. Weaning practices begin to set in (< 6 mos)
that wasn’t treated 2. Maternal antibody titer decreases at ~6 mos
o ex. Amoebiasis 3. Infants become exposed to various sources of diarrhea, especially
MECHANISM OF DIARRHEA as motor activity is increased
1. Osmotic
• Ingestion of poorly absorbed solute Risk Factors in diarrheal diseases:
• Fermented in the colon
• Production of SCFA 1. Environment 2. Host
• ↑ osmotic solute load • Fecal contamination of water • Malnutrition
• Lesser volume than secretory diarrhea • Lack of sanitary facilities • Immunologic suppression
• Stops with fasting • Improper food preparation and • Reduced gastric acidity
• Ex, ingestion of lactulose, sorbitol, etc. storage • Decreased intestinal motility
2. Secretory • Poor personal and domestic • Gastric factor
• Often w/ secretagogue hygiene
• Builds to a receptor on the bowel epithelium • Poor weaning practices
• Stimulating intracellular accumulation of cAMP
• Accumulation of free bile acid – hydroxyl fatty acid causes ETIOLOGY
the colonic mucosa to secrete through this mechanism. Infectious
A. Viral
• Ex. Cholera toxin, ileal resection, IBD
3. Diminished Anatomic or functional surface area • Rotavirus (wheel): MCC of viral diarrhea in infants
o Self-limited in 3-5 days; give ORS
• Short bowel syndrome
• Norwalk: MCC in adults
• Celiac disease
• Symptoms:
• Mucosal disease, like rotavirus enteritis
o Non- bloody
4. Altered Motility
o Vomiting
• Hypermotility brought about the presence of thyroid
o Watery
hormones, prostaglandins, and serotonin.
o URTI associated
• Hypomotility as in malnutrition and idiopathic
o Duration of 3-5 days
pseudoobstruction
o Activity of the child is not altered
5. Mucosal Invasion
o Erythematous plaques
• Inflammation, ↓ colonic reabsorption, ↑ motility
• MOA of viral diarrhea: selective infection of the upper
• Salmonella, Shigella, Amebiasis, etc. villi, decreasing the disaccharide activity à decreasing
absorption of CHO
HISTORY:
o Nelsons: rotavirus protein NSP4 acts as a viral
• Duration enterotoxin.
• Consistency B. Bacterial
• Presence of blood in stool • E. coli: MC bacterial cause; 25% of cases
• Fever convulsion, etc o Associated with infantile or travelers diarrhea
o Maybe due to dehydration: disappears after rehydration • Shigella: MC bloody stool due to mucosal invasion
o Acc to doc, you have the most WBC in stool here
Loss of Water via: Consistency:
(Nelson: Minimal WBC in stool at early inf.)
• Vomiting • Watery
• Salmonella: found in rotten foods; do not give antibiotics
• Urination • Stony hard
(esp. chloramphenicol)
• Sweating • Mucoid
• Respiration
Frianeza 1 of 8
 • V. cholera Non-Infectious
o Contaminated food and water 1. Overfeeding / faulty feeding
o Not a common cause of diarrhea among 2y.o 2. GI allergy (protein diarrhea)
o MCC of dehydration 3. Pyscholgical: tension/stress
• C. difficile: pseudomembranous colitis 4. Malabsorption: lactose intolerance
o Drug induced: clindamycin, tetracycline, 5. Anatomical defects
ampicillin, gentamycin PRACTICAL DIAGNOSIS OF DIARRHEA – ginawa ko lang bullet J
• C. perfringens, S. aureus, B. cereus
C. Parasitic: Acute diarrhea à MUCOID, BLOODY, LOOSE
• Will not cause dehydration; stool is mucoid, not watery ↓
• E. histolyticai – more of chronic type of diarrhea EInvasive and Enteroadherent
o Dx: recovery of trophozoites with ingested RBCs ↓
o Trophozoite cause symptoms (diarrhea) • Shigella
o Commonly acquired in fresh vegetables (common • Salmonella
daw sa baguio) • EIEC
• Giardia lamblia: MCC among immunocompromised • EPEC
• Ascariasis: does not cause diarrhea but may lead to • E. histolytica
obstruction
D. Fungal
PATHOGENESIS of Infectious Diarrhea: Nelsons
Pathogenesis and severity depends on:
• Preformed toxins: S. aureus, B. cereus
• Secretory toxin: cholera, E.coli, Salmonella, Shigella
• Cytotoxic toxin: Shigella, S. aureus, V. parahaemolyticus, C.
difficile, E.coli, C. jejuni
• Invasiveness and replication on food
1. Non-inflammatory diarrhea
• Enterotoxin production by bacteria
• Translocation of bacteria
• Destruction of villus (surface cells) by viruses
• Adherence of parasites
2. Inflammatory diarrhea
• Bacteria that directly invade the intestine or produce
cytotoxin with consequent fluid, protein and cells AD à MINIMAL or NO MUCUS, no blood, watery/copious
(erythrocytes, leukocytes) that enter the intestinal lumen ↓
SOME VIRUSES, such as rotavirus, target the microvillus tips of the Viral Secretory
enterocytes and can enter the cells by direct invasion or calcium Rotavirus ETEC
dependent endocytosis resulting into villus shortening and loss of Others V. cholerae
microvilli
In toxigenic diarrhea
• Enterotoxin of V. cholera
o Activates adenylyl cyclases (Dr. Devega J)
o Increased mucosal levels of cAMP
o Inhibit electroneuronal NaCl absorption but have
no effect on glucose-stiumlated Na+ absorption
• Enterotoxin of ETEC
o Colonizes and adheres to enterocytes of the small
bowel via surface fimbrae(pili) and
o Activates guanylate cyclase – heat labile toxin
o Increased mucosal levels of cGMP to
o Induces hypersecretion of fluids and electrolytes
into the small intestine ADà NO MUCUS or BLOOD, explosive after taking lactose-
In inflammatory diarrhea (eg. Shigella, Salmonella) containing formula
• Extensive histologic damage, resulting in altered cell ↓
morphology and reduced glucose-stimulated Na+ and Lactose intolerance
electroneutral NaCl absorption ↓
usually accompanies acute infections diarrhea (viral), acidic
Acc to Nelson: stool. Perianal dermatitis
*Shigella causes gastroenteritis via superficial invasion of COLONIC **Lactose intolerance is often seen in viral diarrhea
mucosa, which they invade through M cells located over Peyer **Target is TIPS
patches. (page 1864) **Transient; osmotic diarrhea in mechanism
**Viral diarrhea can lead to a lactulose intolerance
SAMPLEX QUESTION: which organism causes mucoid, bloody and S/Sx: bloating, abdominal pain d/t hypermotilty of bowels,
loos stools by invasion of the intestinal mucosa thus penetrating borborygmi, flatulence, failure to thrive (good appetite but not
the lamina propria setting inflammation in the small intestines? gaining weight)
A. Salmonella B. Shigella C. EIEC D. Campylobacter
Vomiting: forceful expulsion of gastric contents
Regurgitation: effortless expulsion, can be normal
• It is salmonella because according to table 340-6 of Nelson,
Shigella infection affects the COLON while salmonella
Frianeza
up to 6 mos, starts to lessen and stops at 2 years old. 2 of 8
Esophagitis: MC complication of GERD
infection invades both the colon and DISTAL small bowel
Assessing Patients for Dehydration: TYPE B:
• Significant water and electrolyte loss • Treatment:
o 4hours to administer ORS/replace fluid and electrolytes
Types (WHO) o Wt(kg) x 75ml = amount of fluid to replenish given in 4h
Type A: no dehydration o IVF: if unable to tolerate orally
• Passing out of watery stool >3x in 24 hrs but no s/sx of o Admission: only if parents insist
dehydration
Type B: some dehydration
• With some s/sx (loss of electrolytes and fluids)
Type C: severe dehydration
• Severe loss of electrolytes and fluids

Weight for age: (from Basic Pediatrics Trans)

• > 2 years old: weigh alone
• <6 months old: wt(g) = Age(mos) x 600 + Birthweight
• 6-12 months: wt(g) = Age(mos) x 500 + BW
**Sa mga samplex na nakita ko inaassume na
3000g yung BW (kahit sa EJG)
• 1-6 y/o: Age(yr) x 2 +8
• 7-12 y.o: (Age(yr) x 7 – 5) / 2

TYPE C: SEVERE DEHYDRATION

• Concave/schapoid abdomen, typically seen in severe
dehydration
• Marasmus, very dry lips, very lethargic
• Treatement: Urgent (IV fluids)
o 1st choice: Plain LR (preferred)
§ 100mg/kg in 6hrs (<1yr)
§ 100mg/kg in 3hrs (older)
TYPE A: NO DEHYDRATION o 2nd choice: D5LR
o 3rd choice: Plain NSS
• Watch for signs of dehydration and other symptoms,
o ORS: if IV fluids are unavailable (20ml/kg/hr for
explain to the caregiver to return if the child does not
6hrs via NGT)
improve in 3 days
1st 30 mg/kg Then 70mg/kg
• Or the following:
<1 y/o 1st hr 5 hours
o Passes an excessive amount of stools
o Repeated vomiting Older 30 mins 2.5 hrs
o Becomes very thirsty Key Signs: Other signs:
o Eating/drinking poorly • Lethargic or unconscious • Skin pinch goes down
o Develops fever • Floppy very slowly
o Blood in stool • Unable to drink • Very sunken eyeballs
• Treatment (acc to EJG and samplexes) • Absent tears
o After each loose stools for 2 days VS: ↑ CR ↑RR, hypotension • Very dry mucosa
o Ideal osmolairty for ORS = 240-245
o Do not mix other drinks, just refrigerate
Used when patient is at home: 3 RULES FOR TREATING ACUTE DIARRHEA AT HOME: FLUIDS,
Age Amount of ORS to Amount of ORS to FOOD, FOLLOW-UP
give after each stool provide for at home 1. Give child more fluids than usual to prevent dehydration
(1glass =250ml) -eto yung sagot sa 2. Give the child plenty of food to prevent undernutrition
samplex 3. Watch for signs of dehydration and other problems
< 24 months 50-100 ml 500 ml/day NOTE:
2-10 yrs old 100-200 ml 1000 ml/day • Do not stop bottle/breastfeeding
>10 years As much as wanted 2000 ml/ day • Any food can be given except those high in salt, sugar, fiber,
Method of administration: diluted soup and special formulas
• Use cup and spoon technique (to prevent vomiting and • In malnourished and dehydrated patients, there is a chronic
for follow-up) fluid and electrolyte loss
• Use dropper or syringe (for infants) • Overestimation of rehydration may lead to CHF
• Glass and sip techniques (for adults) • Skin pinch tes for:
• NEVER BOTTLEFEED ORS – wag mo ilagay sa tsupon J o Elasticity/wrinkling of the skin
• If unable to take orally – OGT(NGT?) o Turgor: (+) pallor at the site of pinch rapid return
of the skin to normal
TYPE B: SOME DEHYDRATION o Adults: done in the extremities
o Pediatrics: done in the abdomen
Key signs: Other signs: o Anterior fontanel: depressed during dehydration
• Restlessness • Thirsty
• Irritability • Skin pinch: goes back
• Drink eagerly slowly
• Eyes: Sunken Frianeza 3 of 8
• Tears: Absent
• Mouth and tongue: dry
Risks associated with severe dehydration that might necessistate IV • could potentially prevent a large proportion of cases fro
resuscitation (Nelson pp1869) recurring
• <6 mos • reduces:
• prematurity o mortality by 46%
• chronic illness o hospital admission by 23%
• fever (>38C if less than 3mos OR >39C if 3-36mos) • leads to increased use of ORS and reduction of
• bloody diarrhea inappropriate antibiotic
• persistent emesis <6 months 10 mg / day PO x 10- 14 days
• poor UO 6 months – 2 years old 20 mg / day PO x 10 -14 days
• sunken eyes PREVENTIVE ASPECTS OF DIARRHEA
• depressed level of consciousness • Breastfeeding: best for babies (antibodies)
o Clean breast with cotton with soap and water
Limitations to ORS:
LOW OSMOLALITY WHO ORS: o Put ice on breast after BF to ↑ fullness
1.shock
Glucose 75 mmol/L o Gastroenteritis: rare in BF babies
2.ileus, intussuception
Sodium 75 mEq • Hand washing and proper food storage
3.CHO intolerance (rare)
Chloride 65 mEq (64 sa book) • Balanced diet
4.Severe emesis
Potassium 20 mEq 5.High stool ouput • Clean environment
Total 245 mOsm/L (>10mL/kg/hr) • Immunizations
o Vaccine: German measles - watery stool affects GI, causes
NELSON: immune system to be depressed.
**ORS global standard of care and more effective than home fluids, o Rotavirus vaccine given at a minimum age of 6 weeks.
including decarbonated soda beverages, fruit juices, and tea. These with a minimum interval of 4 weeks between doses.
are not suitable for rehydration or maintenance therapy because The last dose should be administered not later than 32
they have inappropriately high osmolalities and low sodium conc. weeks of age
** Oral rehydration should be given to infants and children
slowly, especially if they have emesis. It can be given initially by a
dropper, teaspoon, or syringe, beginning with as little as 5 mL at a
time. The volume is increased as tolerated.

Gastrocolic Reflex – reflex of hypermotilty

ANTIMICROBIAL AGENTS USED IN THE TREATMENT OF

SPECIFIC CAUSES OF DIARRHEA:

*E. coli – antibiotic only within the 1st 24 hrs; no function afterwards

VIT A SUPPLEMENTATION
S/Sx:
• photophobia: fear of bright light
• bitot’s spot
• Keratomalacia - softening of cornea à
burst à rupture à blindness
• dry skin
• hyperkeratosis pilaris
2 doses, 1 day apart
< 6 mos 50k IU
6-12 mos 100K IU
1-5 years 200K IU
ZINC SUPPLEMENTATION
• reduced duration
• reduced severity of diarrhea

Frianeza 4 of 8
ORAL CAVITY Other complication: Teeth malformation, teeth
• conditions that affect suck and swallow - tooth malposition displacement or missing teeth
• infection: most common condition that affects suck and Cleft palate is more associated
swallow with congenital malformations
o pharyngitis, tonsillitis, fungal elements in the oral like chromosomal abnormalities,
cavity etc.
• 304 weeks AOG – nutritive suck Possible causes (theories)
• 12wk gestation – plain and simple sucking (sucking reflex) - genetics, drugs, syndrome, - maternal drug exposure, part of
– non nutritive suck infection a syndrome-malformation
• 34 wks gestation – nutritional sucking complex, genetic
• 2 months – social smiling Goals of surgery for Cleft PALATE:
• feeding is the immediate problem • fusion of the cleft segments
**Sabi ni doc, etiology of GI malformations are MOSTLY UNKNOWN – • intelligible and pleasant speech
so smart guess daw yan. • reduction of nasal regurgitation
Cleft Lip Cleft Palate • avoidance of injury to the growing maxilla
d/t hypoplasia of the Failure of the palatal shelves Post-operative management:
mesenchymal layer, resulting in to approximate or fuse • gentle aspiration of nasopharynx to minimize the chances
a failure of the medial nasal and of the common complications of atelectasis or pneumonia.
maxillary process to join. • Feed with Mead Johnson bottle
• Arms restrained with elbow cuffs
Asso w/ cranial facial anomalies Assc with CNS anomalies • Fluid or semfluod diet is maintained for 3 wks
Complete – up to nostrils MC in females • Px’s hands, toys and other FB – kept away from surgical site
Incomplete – not up to nostril Ankyloglosia/tounge tie
MC on the left side • Persistence of tissue connecting the mouth and dorsal
MC on males tongue due to persistence of frenulum
MC among Asians and Native • Usually no feeding and speech problems
Americans • If with speech problems – cut connection
Feeding is the immediate Anencephaly
Feeding is the immediate problem • Common in pregnant woman with polyhydramnios
problem o Normal amniotic 500-1000
Not an emergency Corrected usually at >= 10 o Polyhydramnios - >500-2000 (anencephaly, GI obst.)
Can be corrected in 2-3 months mos o Oligohydramnios - <500-1000
when the infant has shown (sa book less than 1year) • CPD (Cephaliopelvic disproportion) - Most common
satisfactory weight gain and is indication to Cessarian Section
free of any oral, respiratory or *persists after surgery • Head > chest circumference
systemic infections **Microcephaly – small head so there is a possible mental
(sa book 3 mos J) retardation
Risk for aspiration pneumonia Complications: otitis media, **Anencephaly – absence of brain tissue
Affects feeding because (-) recurrent deafness,
intraoral pressure excessice tooth decay, Pathophysio by Dr. Devega (yan nasa notes ko)
speech defect - at 12 weeks, patietns starts to swallow AF
- since there is absent brain tissue – there will be no
message coming from the brain to swallow the AF
- results to polyhyrdramnios Frianeza 5 of 8
(sabi sa book swallowing happens as early as 16-20wks)
ESOPHAGUS Radiographic findings:
• Normal length • coiled feeding tube in the esophageal pouch
o 8-10 cm at birth • air distended stomach (TEF)
o doubles in the 1st 2-3 years of life Differentials: stricture, esophageal web (happens in 4th wk of life
o reaches 25 cm (adult size) and in distal third)
o LES pressure is approx. 20mmHg (<10mmHg VACTERL SYNDROME
abnormal) • Vertebral bodies abnormality
Constrictions of the Esophagus • Anal
• Cricopharyngel (cervical) constriction/upper • Cardiac
o By cricopharyngeus muscle / LUS • Tracheo-Esophageal
o Narrowest = 1.5cm • Renal
• Bronchoaortic constriction/body • Limbs/extremities
o By LMB and aortic arch
o 1.6cm B - EA w/o TEF - 2nd most common
• Diaphragmatic EJ (GEj/LES)/lower • flat abdomen – airless schapoid abdomen
o 1.6c – 1.9cm D - EA w/ proximal TEF
Esophageal Achalasia A - EA w/ distal TEF - most common
1. Cricopharyngeal achalasia E - EA w/ proximal and distal TEF
• incomplete relaxation of the UES • distended abdomen
• do cranial MRI to detect Arnold Chiari malformation • chokes and becomes cyanotic while feeding
2. LE achalasia C - TEF w/o EA "H type" - late detection (compatible to life)
• Loss of LES relaxation • refractory bronchospasm
• Dx: Barium swallow – bird’s beak sign • recurrent pneumonias / aspiration pneumonia
• Manometry is the most sensitive diagnostic test
S/Sx EA with TEF EA w/out TEF
• Regurgitation and dysphagia for solids and liquids - distended abdomen - flat abdomen
• May be accompanied by undernutrion or chronic cough, - air in the abdomen - not compatible
misdiagnosed as anorexia and asthma respectively - 85% - radiopaque
**Fistula is most probably located above the bifurcation of the
Esophageal Atreasia trachea.
**Excessive secretion in the oral cavity & nose is the presenting
symptom.

Feeding
• 4 hours after birth → feeding problem
• Insert NGT to check if there is obstruction
• Length of the tube is estimated by measuring nose to ears
to esophagus to abdomen
• Slightly Globular - normal abdomen at birth
• Breathing mostly abdominal no thoracic in newborns
• Most common complication is pneumonia
• most common congenital anomaly in the esophagus
o atresia – failure to develop completely and fuly causing Major principle in Treatment:
complete and total obstruction • establish airway and prevent aspiration pneumonia
o stenosis – narrowing so there is only partial obstruction • IV fluds, antibiotics , NO mechvent
• What is the etiology? **Put in prone position to minimize secretions from distal esophagus
• Theories: genetics, obesity, drugs, advanced maternal age, reaching the trachea and keep on suctioning.
tobacco smoking, low socioeconomic status **Aspiration of gastric contents via a distal fistula causes more
• 90% of EA have TEF damaging pneumonitis than aspiration of pharyngeal secretions
• 90% survival rate from the blind upper pouch.
• 50% non-symptomatic **Then refer for ligation of TEF and anastomosis of esophagus
• 50% with associated congenital malformation >3cm – get a portion of gastric, jejunum or colon to link
S/Sx: - feeding exacerbates the symptoms
• coughing Normal Landmarks of Abdominal X-ray
• cyanaosis • Right diaphragm is higher than Left diaphragm because of
• choking / excessive oral secretions the liver
• vomiting • Magenblaze - air in the stomach
• regurgitation • Haustral markings of colon
• frothy or bubbling of secretions in the mouth and nose • Gas on Sacral area (gas/black) - if without there is a
o secretions can’t pass the mouth and stomach problem
Early signs: • Vertebral column - should have no deviation
• polyhydramnios • Small bowel located centrally
• inability to pass OGT and NGT with early onset respiratory • Stomach distention due to obstruction of pyloric sphincter
distress • Boundary of upper and lower GI - ligament of Treitz (4th
• absence of infant stomach bubble part of duodenum)

Frianeza 6 of 8
Upper GI – vomiting Imaging requested:
Lower GI – distention • UTZ
o Pyloric thicknes of 3-4mm
Acquired Esophageal Disorders: o Pyloric length of 15-19mm
Corrosive substances o Pyloric diameter of 10-14 mm
• Alkali – liquefactive necrosis • Contrast studies
o Most cases (70%) – accidental ingestion o String sign – Elongated pyloric channel
o Drain decolggers are most common o Shoulder sign – Bulge of pyloric muscle into the
• Acidic – coagulation necrosis (eschar formation) antrum
o Severe gastritis o Double tract sign – Parallel streaks of baroum
o Volatile acids – respiratory symptoms seen in the narrowed channel
• Seqelae Differential Diagnosis:
o Esophagitis • GERD
o Necrosis • Adrenal insufficiency (metab acidosis, elevated serum K)
o Perforation • Duodenal stenosis proximal to the ampulla of vater
o Stricture formation • Pyloric spasma
• Upper endoscopy – most efficient means of rapid • Sepsis – refusal to suck
identification of tissue damage and must be undertaken in • Meningitis
all symptomatic children Treatment:
• Dilution by water or milk is recommended as acute • Correcting fluid, acid base and electrolytes before surgery
treatment • Pyloromyotomy
• Contraindicated: • Conservative: nasoduodenal feeding and atropine sulfate
o Gastic lavage
o Induced emesis
o Neutralization
Foreign Bodies
• 6 months – 3 years
• Commonly lodges in the 3 anatomical strictures of the
esophagus
o Cervical esophagus, Broncho-artic &
Diaphragmatic
• Emergency and associated with significant morbidity and
mortality because of potential for perforation and sepsis
• Evaluation starts with plain AP of neck, chest and abdomen
with neck and chest lateral
• Plastic, wood, glass, aluminum and bones may be GASTROESOPHAGEAL REFLUX DISEASE
raduolucent; do endoscopy • Classic presentation:
• Tx – endoscopic removal o 12 month old with excessive regurgitation and
vomiting, poor weight gain, anemia, hematemesis,
HYPERTROPHIC PYLORIC STENOSIS chest pain and dysphagia
• Rare in Asians, common in males, B and O blood type and • Gastroesophageal reflux disease (GERD) is the most
father with pyloric stenosis common esophageal disorder in children of all ages
• What is the etiology? • Physiologic GER is exemplified by the effortless
Clinical Manifestations regurgitation of normal infants.
• Non-bilious vomiting – initial symptom o becomes pathologic GERD in infants and children
o 3wks of age (earliest-1wk; late-5months) who manifest or report bothersome symptoms
o May or may not be projectile because of frequent or persistent GER, producing
o Progressive, occurs after meals esophagitis-related symptoms, or extraesophageal
o After vomiting, infant is hungry again presentations, such as respiratory symptoms or
• Hypochloremic metabolic alkalosis nutritional effects.
o Due to vomiting which leads to progressive loss of Clinical Manifestations
fluid, H+, CL • Infantile reflux manifests more often with regurgitation
• Icteropyloric syndrome (Jaundice) (especially postprandially), signs of esophagitis (irritability,
o MC clinical association arching, choking, gagging, feeding aversion), and resulting
o Unconjugated hyperbilirubinemia is more failure to thrive; symptoms resolve spontaneously in the
common and resolves with surgery majority of infants by 12-24 mo.
• Failure to thrive, dehydration and electrolyte losses • Older children can have regurgitation during the preschool
Diagnosis years; this complaint diminishes somewhat as children age,
• Physical Exam and complaints of abdominal and chest pain supervene in
o Firm, movable, approximately 2cm in length, later childhood and adolescence.
olive shaped, hard, best palpated from the left • Sandifer syndrome - present with food refusal or neck
side, and located above the right of umbilicus contortions (arching, turning of head).
in the midepigastrium beneath the liver’s edge • Otitis media, sinusitis, lymphoid hyperplasia, hoarseness,
o Olive is easiest palpated after an episode of vocal cord nodules, and laryngeal edema haveall been
vomiting associated with GERD.
o Visible peristaltic wave on abdomen
o Abdominal distention Frianeza 7 of 8
o Hyperactive bowel sounds
o Tympanitic on percussion
 Small Bowel Obstruction
• No gas at sacral area
• Presence of air fluid level

Types of Intestinal Obstruction

• Partial/ Total
• Intrinsic/ Extrinsic
• Mechanical/ Functional
• Simple/ Strangulating
• Strangulating if with injury of the blood vessel

Classic Signs of intestinal obstruction

• bilious vomiting
• Abdominal distention (epigastric)
• Constipation
• 1st week of life - duodenal atresia/stenosis

Abdominal pain is not part of classics signs

Treatment
• Prevent dehydration
• Correction of fluid acid-base and electrolyte losses
• Surgical referral

DISEASES OF THE DIGESTIVE SYSTEM

COMMON GIT MANIFESTATIONS:
Diagnosis • Anorexia
1. History and PE suffice initially to reach the diagnosis. • Dysphagia
2. Contrast (usually barium) radiographic – poor sensitivity • Regurgitation
and specificity • Vomiting
3. esophageal pH monitoring o Mechanical
4. Endoscopy allows diagnosis of complications § Obstructive – PS, intussuception,
5. intraluminal impedance atresia/stenosis
6. Laryngotracheobronchoscopy evaluates for visible airway § Non-obstructive – GER, ileus
signs that are associated with extraesophageal GERD o Reflex
a. Pepsin in tracheal fluid – marker of reflux- § GUT, CNS, Labyrinthine
associated aspiration of gastric contents • Non-specific
Management o Cyclic vomiting, eating disorders
1. Positioning
• When the infant is awake and observed, prone position CRITERIA FOR CYCLIC VOMITING SYNDROME: (all criteria must
and upright carried position can be used to minimize be met)
reflux. • At least 5 attacks in any interval or a minimum of 3attacks
• Seated, flat supine during post prandial period • Episodic attacks of intense N/V lasting 1 hour to 10 days
provokes GERD and occurring at least 1 week apart
2. Pharmacotherapy • Stereotypical pattern and symptoms in the individual
• Antacids patient
• H2 blockers • Vomiting during the attacks occur >4 times/hour for >1
• PPI – standard of care hour
• Prokinetics (metoclopramide, bethanecol, • Return to baseline health between episodes
erythromycin • Not attributed to another disorder
3. Surgery - fundoplication

**Hanggang ditto lang yung sinabi ni Dr. Devega na basahin and hanggag dito
lang din ppt niya. Nasa trans na libed yung kasunod na nilagay ko bahala na
kayo. Madaming add-on dun sa nameless trans na tinutukoy ni EJG, di ko na
nilagay, kayo na rin bahala kung babasahin niyo yun. Kung may correction
dito, itama niyo nalang. Di ko na naproofread yan.

Sources:
Kliegman, R., Stanton, B., St. Geme, J. W., Schor, N. F., & Behrman, R. E.
(2016). Nelson textbook of pediatrics (Edition 20.). Phialdelphia, PA: Elsevier.
Kara Libed Trans
Nameless trans na tinutukoy ni EJG
EJG
SAMPLEX RATIOS
LECTURE NOTES – yung iba diyan tinanong niya samin so kung gusto niyo
umupo, yan yung ibang hinahanap niya na sagot J
Frianeza 8 of 8