WEEK 14 PART 1
GASTROINTESTINAL DISORDERS OF CHILDREN
ANATOMY AND PHYSIOLOGY
 Digestion and absorption of nutrients
(From the mouth pa lang nag-uumpisa na ang
digestion because nagrerelease na agad ng thialine w/c
starts the digestion of carbohydrates sa mouth baba sa
esophagus to stomach with hydrochloric acid be digested
after 2-3 hours magkakaron ng gastric emptying time then
papdala sa small intestine then maabsorb ng intestinal
villi ang mga nutrients.)
 Perform excretory function (paglalabas ng poops)
 Provide detoxification (liver will detoxificate with the
help of pancreas and Gall bladder)
 Participate in maintaining fluid and electrolyte
balance (retaining the electrolyte balance by means
of absorbing or excreting ng mga kinain)
 Serve a lymphoid function by providing a barrier for
pathogens
DISORDERS OF MOTILITY
HIRSCHPRUNG DISEASE (CONGENITAL
AGANGLIONIC MEGACOLON)
→ Congenital anomaly that results in mechanical obstruction
from inadequate motility of part of the intestine
→ Lack of ganglion cells
PATHOPHYSIOLOGY
For pooping: may mga stretch receptors sa intestine so kapag
napuno na ng poops ang intestine mag-iistretch yung mga
stretch cells tapos magsisend siya ng message sa brain the
PNS activate. PNS will tell the cells on the large intestine para
mag labas ng feces. SO sa CAM wala siyang ganglion cells
means walang pagsasabihan ang PNS para magrelease ng
feces. SNS ang siya ng SNS so nagiging contracted lang siya
sa halip na nagrerelax ara mailabas yung feces.
CLINICAL MANIFESTATION
 Failure to pass meconium within the first 48 hours (two
possible cause: 1st imperforated anus 2nd: lack of ganglion
cells)
 Ribbon-like fouls smelling stools (spaghetti, ribbon,
string, pencil)
 Abdominal distention
 Vomiting
 Constipation
DIAGNOSTIC EVALUATION
 Basing on history and physical examination
 Barium enema – Lower GI Series test with a white liquid
na pinapasok then radiopaque to see the white dye
*barium swallow for Upper GI series
o Normal white poop (after)
o Increase fluid intake (after)
 Anorectal manometry (measures reflex pressure) – may
papasok na probe sa pwet hanggang intestine to check the
pressure of the intestine
o Malakas na pressure (+)
 Rectal biopsy (confirmatory) – titingnan sa microscope
for checking the ganglion cells
THERAPEUTIC MANAGEMENT
 Surgery (two stages)
o 1st – temporary ostomy to relieve
obstruction – puputulin ang panget na
intestine na walang ganglion cells
o 2nd – complete corrective surgery soave
endorectal pull-trough
 Anorectal myomectomy – very short-segment disease
– muscle part lang ang tinatanggal
NURSING MANAGEMENT
 Observation of the passage meconium (early
diagnosis)
 Helping the parents adjust to the congenital disorder
(avoid false reassurance)
 Preparing the parents for the medical-surgical
procedure (avoid false reassurance)
IRRITABLE BOWEL
→ “Spastic colon”
→ Functional gastrointestinal disorder
→ No known cause
 → May appear post-infection or due to food tolerance
(lactose etc.) – autoimmunity that attacks the
intestinal lumen or mucosa

CLINICAL MANIFESTATION
 Alternating Diarrhea and Constipation Kapag tumaas ang intraluminal pressure magiistop ang blood
 Flatulence flow sa appendix then magkakaroon ng inflammatory
 Bloating response. Ang problema kapag di agad na manage ang
 Abdominal distention appendicitis may chance na magrupture yun and yung
 Lower abdominal pain intraluminal content spread in the abdomen and since
maraming bacteria sa intraluminal magcacause siya ng
THERAPEUTIC MANAGEMENT peritonitis and sepsis.
 Environmental modifications Kapag nawala ang pain- rupture
 Stress management CLINICAL MANIFESTATION
 Psychosocial intervention  First symptom: colicky, cramping, abdominal pain
 Antispasmodics (HMDD-buscupan ) in the periumbilical area
 Antidiarrheal (diatabs) – wag lagi kasi baka  Nausea, vomiting, anorexia
magkaroon ng drug tolerance  Blumberg sign: rebound tenderness – ipipress ang
 Simethicone (anti-flatulence) RLQ then saka siya sassakit kapag inaangat yung
 Diet kamay
o High fiber (soluble) – naabsorb ng katawan  Rovsing sign: RLQ tenderness upon palpation of
o Psyllium supplements other quadrants
*kapag nagtatae – kumain ng apple na walang balat  Psoas sign – Ififilex ang(R) hip for testing, then hindi
*kapag constipated – kumain ng apple na may balat siya mafiflex
NURSING MANAGEMENT  Obturator sign – papatayuin or higa then papaikutin
 Family support and education ang legs kapag sumakit ang RLQ (+)
 Collaborate with the family with dietary DIAGNOSTIC EVALUATION
modifications:  Basing on history and physical examination
o Eating slowly  CBC: high WBC - walang infection pero may
o Avoiding carbonated beverages (nakakapautot inflammation
ang carbonated beverages)  Ultrasonography
o Adding fiber to diet  CT scan
o Relieving environmental stress THERAPEUTIC MANAGEMENT
 Surgery- APPENDECTOMY (open or
INFLAMMATORY CONDITIONS laparoscopic)
 Kapag nagrupture(X-laparascopic) winawash ang
ACUTE APPENDICITIS intestine para walang maiwan na fecal debris
→ Inflammation of the vermiform appendix pagkatapos massive antibiotics (metronidazole)
→ Appendix – produces mucus and house of good
bacteria (RLQ- mcBurnysi Point)

NURSING MANAGEMENT
 Assist in establishing diagnosis (physical exam)
 Instruct the child to point a finger on the painful
region
PATHOPHYSIOLOGY  Light palpation will satisfactorily elicit pain
 Wag laging ipalpate
 Pre-op care
 o Avoid hot compress
o Avoid extensive palpation
o Avoid analgesic (cover symptom of
ruptured)
o Avoid enema (increase intraluminal
pressure that might cause rupture)
 Post-op care
o Flat on bed In position
MECKEL DIVERTICULUM
→ Remnant of the fetal omphalomesentric duct that
connects the yolk sac with the primitive midgut
during fetal life
→ Normally the structure obliterates by 7th – 8th of
gestation
→ Mechanisms that causes obstruction: intussusception,
incarceration by hernia, volvulus

CLINICAL MANIFESTATION CLINICAL MANIFESTATION

 Painless, rectal bleeding (due to ulceration)- most  Nonbilous projectile vomiting (sumisirit) (not yellow
common vomitus)
 Dehydration
DIAGNOSTIC EVALUATION  Weight loss (daily weight)
 Based on history and physical examination  Failure to thrive
 Radiographic study  Palpable olive-shaped mass in epigastrium
 Radionuclide scintigraphy (Meckel Scan) –
confirmatory DIAGNOSTIC EVALUATION
 Lab studies- severity of anemia (dahil sa rectal  Basing on history and physical examination
bleeding)  Ultrasonography
o Check for hemoglobin  Upper GI radiography
THERAPEUTIC MANAGEMENT THERAPEUTIC MANAGEMENT
 Severe Hemorrhage: correct hypovolemic shock (IVF  Surgery
and Oxygen) o Pyloromyotomy or Fredet-ramstedt procedure
 Surgery – standard procedure (epigastric ang insertion
 Diverticulitis site)
o Antibiotics NURSING MANAGEMENT
NURSING MANAGEMENT  Careful regulation of fluid therapy
 Pre-OP  Reestablishment of normal feeding patterns
o Frequent monitoring of VS and blood  Encourage the parents to become involved in caring
pressure (possible hypovolemia) for the child
o Keep the child on bed rest  Post-op – Semi fowler position
o Recording the approximate amount of blood INTUSSUSCEPTION
lost in stool
 Post-OP → Telescoping or invagination of the proximal intestinal
o Maintain IVF segment to a more distal segment that results in
o NGT for decompression lymphatic and venous obstruction
o Psychological support
OBSTRUCTIVE DISORDERS

HYPERTROPHIC PYLORIC STENOSIS

→ Occurs when the circumferential muscle of the
pyloric sphincter becomes thickened that produces
outlet obstruction and compensatory dilation
 → Permanent intestinal intolerance to dietary wheat
gliadin and related protein that produces mucosal
lesions in genetically susceptible individuals
*Sa small intestine mayroong microvilli- (sa loob ng
microvilli mayroong artery and vein which absorb
nutrients) and since di na-absorb yung gliadin ma-
accumulate siya sa intestine that destroys intestinal
villi that cause inflammation => prolonged
inflammation cause scarring => di na siya
makakabsorb ng ibang nutrients
→ Also caused by immunological-mediated
enteropathy.

CLINICAL MANIFESTATION
 Sudden onset of crampy abdominal pain
 Inconsolable crying
 Drawing up of knees on the chest
 Bilous vomiting
 Palpable sausage-shaped mass in abdomen
 Currant jelly-like stool (Blood and mucus) (painful)
DIAGNOSTIC EVALUATION
 Based on subjective finding
 Barium enema (highlight the intestine)
 Abdominal radiograph
 Rectal exam (mucus and blood)
THERAPEUTIC MANAGEMENT
 Non-surgical hydrostatic reduction - using enema CLINICAL MANIFESTATION
or air pressure  Failure to thrive
o Not recommended if there are signs of  Chronic diarrhea => prone to dehydration
perforation (pagkabutas ng intestine)  Abdominal distention
 Necrosis  Muscle wasting
 Peritonitis (rigid or board like abdomen)  Anorexia
 Bloating  Irritability
 Surgery – resection of non-viable portion DIAGNOSTIC EVALUATION
o NG decompression
 Presence of antigliadin and antiendomysial
o IVF
immunoglobulin and their disappearance when
o Antibiotic therapy
gluten is removed in the diet
NURSING MANAGEMENT  Villous atrophy and hyperplasia in children who eat a
 Assist in establishing diagnosis diet with gluten - intestine biopsy
 Explain the basic defect to the parents and how its (esophagogastroduodenoscopy)
corrected  Remission of symptoms upon gluten withdrawal

MALABSORPTION DISORDER THERAPEUTIC MANAGEMENT

 Dietary Management
CELIAC DISEASE o Gluten free diet
→ Gluten-sensitive/ gluten-induced enteropathy o Avoid B-R-O-W
 B- arley
 R- ye
  O- at  Maximize speech production and
 W-heat growth of midface
 SUBSTITUTES: rice and corn
NURSING MANAGEMENT
NURSING MANAGEMENT  Feeding:
 Helping the child adhere to dietary regimen  Best accomplished with the infants head in an upright
 Advise parents the necessity of reading all label position
ingredients  Special bottles for feeding
 HIDDEN SOURCE OF GLUTEN:  Check for ear infection or deafness
o Bread  Post-op:
o Cake o Cleft lip: avoid prone position
o Cookies o Cleft palate: prone position or side lying
o Crackers o Elbow restrains (remove at regular
o Donuts intervals)
o Pies o Avoid use of suction, tongue depressor,
o Spaghetti thermometers, spoons, and straws
o Pizza
o Hotdog
o Luncheon meat
o Hamburger
 Due to inflamed bowel the child must avoid high
fiber foods such as nuts, raisins, raw vegetable, raw
fruit with skin, until inflammation subside
CLEFT LIP AND CLEFT PALATE
→ CL results from incomplete fusion of the embryonic
structures surrounding the primitive oral cavity
→ CP occurs when the primary and secondary plates fail
to fuse during embryonic development
ETIOLOGY
 Teratogens ESOPHAGEAL ATREASIA AND
 Inheritance TRACHEOESOPHAGEAL FISTULA
 Drugs (phenytoin, valproic acid, thalidomide, → Failure of the esophagus to develop as a continuous
pesticide dioxin) passage
 Folic acid deficiency → Failure of the trachea and esophagus to separate into
 Maternal smoking and alcohol ingestion distinct structures
CLINICAL MANIFESTATION
CLINICAL MANIFESTATION
 Suspected: Frothy saliva in mouth and nose,
coughing and choking
 Cyanosis- aspiration of milk or saliva
 Abdominal distention
 Recurrent pneumonia

DIAGNOSTIC EVALUATION
 Apparent at birth
 CL diagnosed in utero through ultrasound 14-16th
week
 Palpation of the palate
THERAPEUTIC MANAGEMENT DIAGNOSTIC EVALUATION
 Surgery
o Cleft lip (cheiloplasty)  Radiographic studies (radiopaque insertion in
o Cleft palate (palatoplasty) abdomen)
  Polyhydramnios (2000ml of amniotic fluid) – clue to
a possibility of EA
THERAPEUTIC MANAGEMENT

 Maintain patent airway (side lying and semi fowler)

 Prevent pneumonia
 Gastric decompression
 Supportive therapy
 Surgical repair