GASTRO INTESTINAL DYSFUNCTION

‘
NAME THE PARTS
1. DEHYDRATION

occurs when ever

the total output
exceeds the total
intake.
COMPARTMENTS:

ECF Compartment- assessed

thru the ff:
Edema, skin turgor, dryness
of mucosa, tension of
fontanelles.
ICF Compartment- not very
accessible, assessed thru:
Headache, seizure, confusion.
PLASMA COMPARTMENT
DEHYDRATION
• Insensible water loss: Skin, lungs, GIT
• Note:
• a. Body Surface Area- infants greater than
adults.
• b. Basal Metabolic Rate- infants has higher than
adults.
• C. Kidney Function-immature in infants.
• d. Fluid Requirement- greater in infants, per KG
BODY WEIGHT.
TYPES OF DEHYDRATION
• a. Isotonic (isonatremic) Dehydration
• - loss of total body water coupled with loss of
sodium of an equal magnitude.(loss of salt and
water)
• - Serum Na+ is normal :135-145 meq/l
• - Serum Osmolality is normal: 280-300 mosm/l
• - no shifting of body water from ICF to ECF.
TYPES OF DEHYDRATION

• b. Hypotonic (hyponatremic) Dehydration

• - loss of sodium ions proportionally greater
than water loss.(Na>water)
• - Serum Na+ is low:< or=130meq/l.
• -Serum Osmolality is low <260 mosm/l.
• - body water shifts from ECF to ICF (Cell
Swell).
TYPES OF DEHYDRATION

• c. Hypertonic (hypernatremic) Dehydration

• - loss of water is greater than salt loss.
(water>Na).
• - serum Na+ is high:>150 meq/l
• - Serum Osm is high:<300 mosm/l
• -body water shifts from ICF to ECF ( cell
shrink).
LAB EVALUATION:

• a. Hct
• b. Urinalysis
• c. Electrolytes:Na, K, Cl
• d. BUN- elevated
• e. Glucose- elevated
NURSING CONSIDERATIONS:

• a. Monitor V/S
• b. I&O
• c. Assess physical signs of DHN,poor skin
turgor,assess fontanels, dry skin.
• d. Assess causative factor.
• e. Administer IV fluids, rehydration.
DISORDERS OF MOTILITY

• a. DIARRHEA- is the excessive loss of fluid

and electrolyte in stool, secondary to
disturbed intestinal solute
transport.Technically limitted to Lower GI
Tract.
• b. Gastro Enteritis- is an inflammation of
the entire (upper and lower) GI Tract.
(vomiting and Diarrhea).
• B. Acute Diarrhea- caused by
infectious agents.
• C. Chronic Persistent Diarrhea-
secondary to infectious agents,
infection of immune compromised
host or residual symptoms due to
intestinal damage.
EPIDEMIOLOGY:
• - Increased susceptibility seen in young
age
• -immune deficiency
• - measles
• - malnutrition,
• - travel diarrhea
• - lack of breast feeding
• - contaminated food or water.
ETIOLOGY:
• Children- viral(Rotavirus)
• - Adult- Noro virus
• - bacterial and parasitic pathogens
SIGNS AND SYMPTOMS:

• a. Frequency and volume of

diarrhea or vomiting.
• b. Time of last voiding.
• C. General appearance of patient.
• d. Abdominal cramps, emesis,
malaise and fever.
DIAGNOSIS: AGE/DIARRHEA
• a. Examine stool for mucus, blood and
leukocytes.
• b. Obtain stool culture early.
• c. Proctosigmoidoscopy- diagnosis for
inflammatory enteritis.
TREATMENT:
• a. Rehydration
• - oral electrolyte solution
• -IV hydration
• b. do not use soda, fruit juices
• c. high sodium replacement (gatorade)
• d. Start BRAT diet.
• e. Antidiarrheal compounds are not indicated
for use in children.
2. VOMITING
• is the forceful ejection of gastric contents through the
mouth.
• - Coordinated process that is under CNS control
accompanied by Nausea and retching
• Causes:
• Acute infectious diseases
• Food intolerance, allergies
• Increase ICP
• Psychogenic problems
• Toxic ingestions in children
VOMITING
• Complications:
• a. Dehydration
• b. Electrolyte disturbance
• c. Malnutrition
• d. Aspiration
• Nursing Management:
• a. Prevent aspirations
• b. Monitor I&O
• c. Nutrition
3. CONSTIPATION
• 3 or more days without passage of stools
• - painful bowel movements
• - Retention of stool
• OBSTIPATION- extremely long interval
between defecation.
• ECOMPRESIS- constipation with fecal
soiling.
CONSTIPATION
• Causes:
• Systemic disorder
• Drugs
• Idiopathic or functional
• Nursing Management: Increase fiber,
Increase OFI, exercise. Avoid meats
STRUCTURAL DEFECTS

• ESOPHAGEAL ATRESIA
• TRACHEOESOPHAGEAL FISTULA
• Failed separation of the esophagus and trachea
by a septum
• Forms at 4th week of gestation
• Fatal Outcome if not treated.
• Incidence:1:3000 to 4500 live births
ETIOLOGY: EA /TEF
• - Maternal Polyhydramnios
• - Low birth weight
• - Prematurity
• - VACTERL Syndrome:
• ( Vertebral, Anorectal, Cardiovascular,
Tracheoesophageal, Renal, limb anomalies.)
• Pathophysiology:
• a. Altered embryonic cellular growth.
TYPES OF EA AND TEF:
Type A- Esophageal
Atresia without
assoc. Fistula
-2nd most common
(8%)
-Blind pouch at each
end, widely
separated
-No communication
to the trachea
-Absence of air in
stomach
TYPE B –
Esophageal
Atresia with TEF
-Between proximal
segment of
esophagus and
trachea
-Risk for aspiration
-Absence of air in
stomach
-Rare form (0.8%)
TYPE C-
Esophageal
Atresia with TEF
-Between distal of
Esophagus and
Trachea
-(GROSS-VOGT
Type)
-Stomach distention
with air
-Most common
variety (85%)
TYPE D-
Esophageal
Atresia with
Fistula
-Between both proximal
and distal ends of
esophagus and trachea
-Risk for aspiration, air
in stomach
-Rare form (0.7-7%)
TYPE E- TEF
without
Esophageal
atresia
- Normal trachea and
esophagus
- Connected by a
fistula (H –type)
- Risk of choking and
cyanosis.
- Air in stomach
CLINICAL MANIFESTATIONS:
- Frothy saliva in mouth and nose
- Drooling
- 3 C’s: Coughing, choking, cyanosis
DIAGNOSTICS:

a.3 C’s: Coughing, choking, cyanosis

b.Insertion of NG tube- inability to pass
catheter
c.Radiographic study- to determine the
type
d.Radiopaque catheter is inserted with
dye
e.Bronchoscopic examination to visualize
fistula.
f. History of polyhydramnios (2000ml)
THERAPEUTIC MANAGEMENT
a. Stop oral feeding
b. IV fluids
c. Head upright to prevent aspiration.
d. Suction mouth and pharynx
e. Double lumen catheter placed on upper
esophagus- suction and decompression of air
in stomach (NGT)
f. Antibiotics to prevent pneumonitis.
g. Surgical correction: Thoracotomy with
division and ligation of TEF and end to end
anastomosis.
TRACHEOMALACIA
•weakness of tracheal wall.
- Dilated proximal pouch compresses
the trachea early in fetal life.
NSG MANAGEMENT:
a.Teach parents signs of respiratory
difficulty,
• Esophageal stricture (poor feeding,
dysphagia, drooling, regurgitation of
undigested food)
a.The child is not allowed to swallow big
chunks of food.
b.Give frequent sips of fluid to aid in
swallowing.
c.Inform child to chew food thoroughly.
d.Teach parent about CPR.
STRUCTURAL
DEFECTS:
PYLORIC
STENOSIS
- Occurs when the
circumferencial muscle of
the pyloric spincter
becomes thickened,
resulting in elongation and
narrowing of the pyloric
channel.
- Producing an outlet
obstruction and dilatation,
hypertrophy and
peristalsis of the stomach.
- Develops in first few
weeks of life.
PYLORIC STENOSIS
CLINICAL MANIFESTATIONS
a.Projectile vomiting ( begins 3
weeks of age or 5 mos.)
b.Dehydration
c.Metabolic Alkalosis
d.Failure to thrive
e.Electrolyte imbalance- hypokalemia
and hypochloremia.
Etiology: Unknown
a. genetic predisposition.
b. firstborn and males -5x more
than females.
c. common in full term than
premature infants.
 
DIAGNOSTIC EVALUATION:
a. History- non bilious vomiting 30-60 mins.
After feeding becoming increasingly
projectile.
b. P.E-“ OLIVE shape” palpated at the RUQ
c. Ultrasonography-
d. Upper GI series
e. Labs:
- Decrease Na and K due to vomiting
• Decrease serum chloride, increase in
- ph and bicarbonate due to metabolic
alkalosis
- Elevated BUN due to dehydration.
THERAPEUTIC MANAGEMENT:
a. FREDET-RAMSTEDT procedure also known
as PYLOROTOMY.
b. Pre-op care:
- IV fluid to correct metabolic alkalosis and
fluid and electrolyte imbalance.
- Stomach decompression via NGT.
a. Surgery: 24 to 48 hours for corrections
b. Post op care:
- Feeding 4-6 hours after surgery
- Small frequent feeding of water, glucose or
electrolyte solution.
- After 48 hours –normal eating pattern is
reinstated and scheduled.
1.HIRSCHPRUNG DISEASE
(CONGENITAL AGANGLIONIC
MEGACOLON)
- Mechanical obstruction caused by
inadequate motility of part of the
intestine.
- Common in males
- Absence of GANGLION CELLS in
one or more segments of the colon.
- Etiology: Unknown
Clinical
manifestations:
- Absence of
peristalsis
- Accumulation
of intestinal
contents
- Distention of
proximal bowel
to the
defective
megacolon
- Ischemia
DIAGNOSIS:
• Rectal Biopsy- absence of ganglion
cells.
• Treatment: Surgical removal of the
Aganglionic part
- Colostomy
- Endorectal Pull through procedure.
1.GASTROESOPHAGEAL REFLUX
(GER) CHALASIA
- Transfer of gastric contents to the
esophagus
- Dysfunction in lower esophageal
sphincter.
- Transient relaxation of the lower
esophageal sphincter ( TRLES)
- Predispose to aspiration, pneumonia,
apnea, esophagitis, bleeding.
1.GASTROESOPHAGEAL REFLUX
(GER) CHALASIA
Diagnosis:
a.Scintigraphy- radioactive tracer
of the parts of the body.
Treatment:
b.Wait for maturity to happen.
c.Small frequent feeding.
d.Elevated head positioning
e.Cimetidine, ranitidine,
omeprazole, metoclopramide.
SURGICAL PROCEDURE
•Nissen
Fundoplication- upper
part of the stomach is
wrap around in the
lower part of the
esophagus.
• 
1. INTUSSUSCEPTION
- Telescoping of one
portion of the intestine
to another.
- Common in ileocecal
valve
- Common in males, 3
mos to 5 y/o.
- Obstruct passage of
intestinal contents
- Stools with blood and
mucus
- “Currant jelly stools”
DIAGNOSIS:
ACUTE ABDOMINAL PAIN
VOMITING OF BILE
BLOODY STOOLS
PALPABLE ABDOMINAL MASS (SAUSAGE
SHAPE MASS)
ULTRASONOGRAPHY

TREATMENT:
REDUCTION OF BARIUM ENEMA,
EXPLORATORY LAP, AIR PRESSURE OF
CO2
IT’S A SURGICAL EMERGENCY!
INFLAMMATORY
DISORDER

1. PEPTIC ULCER DISEASE

- An ulceration of the gastric
and duodenal lining.
- Most common peptic
ulceration: anterior part of
the upper duodenum.
Pathophysiology:
a. Disturbance in acid
secretion and mucosal
protection
b. Increased acidity or
decrease mucusal
resistance, erosion and
ulceration.
Gastric Ulcer
ulcerartion of gastric mucusa,
submucusa and muscularis.
Assessment: (GASTRIC
ULCER)
● Epigastric pain
Characteristics:
● Gnawing, sharp pain in the
mid-epigastrium
● 1-2 hours after eating
● not relieved by food intake
● aggravating the pain
 ● N/V- Most common
● hematemesis
● weight loss
NURSING INTERVENTIONS:
1. Give BLAND diet, small frequent meals
during the active phase of disease.
2. H2 blockers, mucosal barrier protectants and
antacids.
3. Monitor complications: bleeding, perforation
and intractable pain.
4. Stress reduction and relaxation technique.
5. Monitor hydration status,Hct,Hgb.
6. Assist with saline lavage.
7. Prepare Blood Transfusion
• Give VASOPRESSIN- reduce bleeding
1.Prepare for surgery:
• ●Total Gastrectomy, vagotomy,
gastric resection.
• ●Billroth 1- gastrodoudenostomy
• ●Billroth 11- Gastro jejunostomy
• ●Pyloroplasty
DOUDENAL ULCER
•ulceration of duodenal mucosa and
submucosa
•- due to increased acidity.
•Assessment:
•● Pain characteristics:
•-burning pain- mid epigastrium 2-4
hours after eating or during night,
relieve by food intake.
ACUTE
APPENDICITIS
- inflammation of
vermiform
appendix
Causes:
Fecalith, foreign
bodies
- Decrease in
high fiber diet
- Mucous
obstruction
PATHOPHYSIOLOGY:

•● Pressure in lumen
•● Compression of blood vessels and
ischemia
•● ulceration of lining
•● bacterial invasion, necrosis
•● Perforation, rupture (peritonitis)-
complication
•Diagnostics:
a.Increase WBC- 15,000-20,000 inc
neutron.
b.UTZ
c.Pain at MC Burneys point
d.Psoas sign
e.Rovsing sign
•Treatment: Appendectomy
CLEFT LIP
1. failure of maxillary and median nasal process to fuse
(5- ws of intra uterine life.
- The defect ranges from a small notch in the upper lip
to a total separation of the lip and facial structure up
to the floor of the nose.
- Absent teeth and gingival
- Maybe unilateral or bilateral
- Common in males
- Congenital
- Decrease folic acid during pregnancy or caused by
teratogenic drug.
- Flat nose
- S/Sx

- Difficulty in
feeding
- Mouth breathing
(increase air
infection)
 
Treatment:CHEILOPLASTY
- 6-12 weeks of age with revision of scar.
- Surgery readiness:rule of 10
- A. 10 weeks old
- B,10 lbs
- C. wbc <10,000
- D. 10 grms Hgb
-ASAP for modern surgery to prevent
aspiration
- surgery: z plasty- staggered suture line.
-Logan – fine metal device bar placed on top
of lips so as not to loosen sutures.
POST OP:
a.Never on prone position!
b.Put on supine with head with arm or
elbow restraint
c.Prevent tension on suture lines.avoid
crying
d.Feeding with dropper with SAP in
upright position.
e.Clear liquid place at side of mouth.
f. Clear suture line after feeding of sterile
water or called boiled water..
Cleft palate
1. opening the palate
usually on the
midline (midline
fissure of the palate).
- Involved anterior
hard palate, posterior
soft palate or both.
- Common in females
 TREATMENT: PALATOPLASTY

- Repair done before 2-3 years old or

12-1 mos. Before speech
development begins
- Wait for the development of palatal
notch
- 8-9 y/o repair again by palatar
prosthesis (Velopharyngeal flap)
• Pre op feeding:
a.Flange nipple,lambs nipple, brecht
feeder
• Breast feeding method: Palatar
prosthesis in order to breastfeed
POST OP CARE:
a.Position: prone on abdomen side- to
promote natural drainage of secretion.
b.Observe for bleeding or frequent
swallowing.
c.Elbow restraint (use carboard in elbow)
Post op care:

d.Feeding device: bottle, breast, cup,

never use straw9Cause dehiscence due
to pressure in suture line.
e.Feeding allowed after 4-6 hours
f. After 48 hours- blenderized feeding
g.Remove packing after 2-3 days post op.