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PEDIATRIC NURSING


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NURSING CARE OF THE CHILD WITH

A GASTROINTESTINAL DISORDER


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FLUID, ELECTROLYTE AND ACID-BASE

IMBALANCE FLUID BALANCE

Fluid is distributed in 3 body compartments:

a. Intracellular compartment- 35 to 40% of body wt.

b. Interstitial compartment- 20% of body wt.

c. Intravascular compartment- 5% of body wt.

The INTERSTITIAL AND INTRAVASCULAR FLUID MAKES UP

THE ECF (EXTRACELLULAR FLUID COMPARTMENT).


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Fluid is normally obtained through oral ingestion of fluid and

by the water formed in the metabolic breakdown of food.

Fluid is lost through our urine and feces. Minor losses,

INSENSIBLE LOSSES occur from evaporation.


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DEHYDRATION

A body fluid disturbance where the total output

of fluid exceeds the total amount of intake.


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TYPES OF DEHYDRATION

Are categorized on the basis of osmolality and

depends primarily on the serum sodium

concentration.


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ISOTONIC (ISOSMOTIC OR

ISONATREMIC) DEHYDRATION

The primary form of DHN in children

Water and salt are lost in approximately equal amounts.

There is no osmotic force between the ICF and ECF so the major

loss is form the ECF.

The effect would be:

a. DECREASE in the plasma volume and circulating blood volume

b. It would affect the skin, muscles and kidneys

SHOCK is the greatest threat in children with this type of DHN.

Plasma sodium remains at normal limits between 130 & 150

meq/L.


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HYPOTONIC (HYPOSMOTIC OR

HYPONATREMIC) DEHYDRATION

Electrolyte deficit > water deficit

Plasma concentration of Sodium and chloride will be low.

ICF is more concentrated than the ECF, water moves from the

ECF to the ICF to establish osmotic equilibrium. Shock is a common finding

Can be due to excessive GI loss from vomiting, low intake of

salt associated with extreme losses through therapeutic

diuresis. It can also occur when there is extreme electrolyte loss in

diseases (adrenocortical insufficiency, diabetic acidosis).


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HYPERTONIC (HYPEROSMOTIC OR

HYPERNATREMIC ) DEHYDRATION Water loss> electrolyte loss

Usually caused by a proportionately larger loss of water and a largerintake of electrolytes

It is the most dangerous type of DHN

Fluid shifts from the ICF to the ECF. Plasma Na concentration is > 150 meq/L.

Neurologic disturbances is more apparent such as alteration in LOC,poor ability to focus attention, lethargy, increased muscle tone withhyperreflexia, hyperirritability to stimuli.

May occur in a child with nausea, profuse diarrhea, renal disease

associated with polyuria. RBC and HCT increases because the blood is more concentrated.

Levels of electrolytes (Na, Cl,and bicarbonate) is increased.


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SIGNS AND SYMPTOMS OF

DEHYDRATIONISOTONIC HYPOTONIC HYPERTONIC

Thirst mild moderate Extreme

Skin turgor poor Very poor moderate

Skin consistency dry clammy moderate

Skin temperature cool cool Warm

Urine output decreased Decreased decreased

Activity irritable lethargic Very lethargic

Serum Sodium level normal reduced increased


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DIAGNOSTIC EVALUATION FOR

DEHYDRATION Degree of DHN is described as a percentage:

a. 5% (mild DHN)

b. 10% (moderate DHN)

c. 15% (severe DHN)

Reflecting acute loss in ml/kg. of body wt.

Wt. is the most important determinant of the total percent of body wt.

Other predictors include:

a. Changing LOC

b. Response to stimulic. Prolonged capillary refill

d. Increased HR

e. Sunken eyes and fontanelles


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LEVEL OF DHN MILD MODERATE SEVERE

Wt. loss-infants 5% 10% 15%

Wt. loss- children 3-4% 6-8% 10%

Pulse Normal Slightly increased Very increased

Blood pressure Normal Normal to orthostatic

(>10 MMHG CHANGE)

Orthostatic to shock

Behavior Normal Irritable, more thirsty Hyperirritable to

lethargic

Thirst Slight Moderate Intense

Mucous membrane Normal Dry Parched

Tears Present Decreased Absent, sunken eyes

Anterior fontanel Normal Normal to sunken Sunken

External jugular vein Visible when supine Not visible except with

supraclavicularpressure

Not visible even with

supraclavicularpressure

Skin (less useful in

children >2 y/o)

Capillary refill> 2

seconds

Slowed CRT (2-4

seconds)

Very delayed crt (4

seconds) and tenting;

skin cool, acrocyanotic

or mottled

Urine specific gravity >1.020 >1.020; oliguria Oliguria or anuria


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ACID-BASE IMBALANCE

In the GI system, it occurs because of severe diarrhea or vomiting.

To determine acid-base balance, a key component is pH.

pH denotes whether a solution is acid or alkaline and is determined by the

proportion of Hydrogen ions (H+) ions in relation to Hydroxide (OH-) ions.

A solution is ACID if it contains more H ions than OH ions, it is ALKALINE if

OH ions exceeds H ions.

ABG (Arterial Blood Gas) is used to determine whether the body is

acidotic.

NORMAL VALUES FOR ABG:

pH 7.35 to 7.45

Pco2- 35 to 45 mmhg

HCO3- 22 to 26 meq/L.


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METABOLIC ACIDOSIS

May result from diarrhea.

In diarrhea, Na is lost with the stool which in turn causes the bodyto conserve H+ ions in an attempt to keep the total number of +and ions in the serum balanced.

As a result, the number of H+ ions in the blood INCREASESproportionately over the OH-ions making the child ACIDOTIC.

To correct the acidosis, the body uses 2 BUFFERING SYSTEM.

1. RESPIRATORY BUFFERING SYSTEM

- Attempts to correct imbalance quickly

- H+ ions combine with HCO3- ions to form carbonic acid.

- This CARBONIC acid is broken down into CO2 and water which iseliminated by the lungs during expiration.


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The child breathes rapidly (hyperpnea) to blow off CO2 to prevent itfrom combining with H2O and reforming HCO3.

S/sx.

1. Headache

2. Nausea and vomiting

3. Weakness

4. Apathy

5. Disorientation

6. Tremors7. Convulsions

8. Coma

9. Kussmauls respiration


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NURSING MANAGEMENT FOR

METABOLIC ACIDOSIS

Administer sodium bicarbonate.

Monitor fluid and electrolyte levels

If patient has changes in sensorium, implement safety precautions.

Monitor for arrhytmias


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METABOLIC ALKALOSIS

With vomiting, HCL is lost

INCREASE K loss in diuretic therapy

When CL- ions are lost, the number of H+ ions decrease so the

number of + and charges remains balanced.

The number of H+ ions LOWER than the number of OH- ions

in HCO3, and Ph

To further reduce no. of H+ ions, lungs conserve water and CO2 by

slowing respirations (hypopnea). The excessive CO2 retained by this

maneuver dissolves in the blood as carbonic acid and is converted

into excessive H and HCO3.


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S/sx:

a. Nausea

b. Diarrhea

c. Tingling fingersd. Numbness

e. Bradycardia

f. Respiratory depression

g. Shallow RR with periods of apnea

h. Irregular PR, arrhythmias and muscle twitching due to K and

Ca level.


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NURSING MANAGEMENT

Fluid and Electrolyte replacement

Monitor I and O

Assess for signs of hypokalemia

Seizure precautions

Avoid taking OTC antacids


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CLINICAL MANIFESTATIONS OF GI

DYSFUNCTION IN CHILDREN

1. Failure to thrive- wt. consistently below the 3rd percentile or BMI

below the 5th percentile or a decrease from established growth

pattern.

2. Spitting up or regurgitation- passive transfer of gastric contents

into the esophagus or mouth

3. Vomiting- forceful ejection of gastric contents; is under CNS

control and usually accompanied by nausea

Projectile vomiting- vomiting accompanied by vigorous peristaltic

waves and typically associated with PYLORIC STENOSIS orPYLOROSPASM.

4. Nausea- Unpleasant sensation vaguely referred to the throat or

abdomen


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5. Constipation- delay or difficulty with the passage of stools that ispresent for 2 or more weeks

6. Encopresis- involuntary overflow of incontinent stools causingsoiling or incontinence secondary to fecal retention or impaction

7. Diarrhea- increase in the number of stools with an increased watercontent as a result of alterations of water and electrolyte transportby the GIT.

8. Hypoactive, Hyperactive, or Absent bowel sounds- evidence ofintestinal motility problems that may be caused by inflammation or

obstruction9. Abdominal distention- protuberant contour of the abdomen that

may be caused by delayed gastric emptying, accumulation of gas orstool, inflammation or obstruction


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11. jaundice- yellow discoloration of the skin and sclerae associated

with liver dysfunction

12. dysphagia- difficulty swallowing due to abnormalities in the

neuromuscular function of the pharynx or upper esophageal

sphincter or by the disorders of the esophagus

13. Dysfunctional swallowing- impaired swallowing caused by CNS

defects or structural defects of the oral cavity, pharynx, esophagus

14. Fever- common GI manifestation in children; usually associated

with DHN, infection or inflammation


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DISORDERS OF MOTILITY

1. DIARRHEA

- It is a symptom resulting from disorders involving digestive,

absorptive and secretory functions

- Is caused by abnormal intestinal water and electrolyte transport

- Involves the stomach and intestines (gastroenteritis), small

intestine (enteritis), colon (colitis), colon and intestines

(enterocolitis)

- Is classified as acute or chronic


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ACUTE DIARRHEA

A sudden increase in frequency and a change in consistency of

stools often caused by an infectious agent in the GIT.

It may be associated with URTI or UTI, antibiotic therapy or laxative

use.

Is usually self-limited and subsides without specific tx. If DHN does

not occur.


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CHRONIC DIARRHEA

An increase in stool frequency and increased water content with a

duration of > 14 days.

Often caused by malabsorption syndromes, inflammatory bowel

disease, immune disease, food allergy, lactose intolerance, chronic

nonspecific diarrhea or inadequate mgt. of acute diarrhea.


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DIFFERENCE BETWEEN INFANT NORMAL STOOL

AND DIARRHEAL STOOL

CHARACTERISTIC INFANT NORMAL STOOL DIARRHEAL STOOL

Frequency 1-3 stool Unlimited number

Color Yellow Green

Effort of expulsion Some pushing effort Effortless; may be

explosive

Ph > 7.0 (alkaline) < 7.0 (acidic)

Odor Odorless Sweet or foul smelling

Occult blood (-) (+); blood may be overt

Reducing substances (-) (+)


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ETIOLOGY OF DIARRHEA

Pathogens are spread by fecal-oral route through contaminatedwater or food or from person-person where there is close contact

ROTAVIRUS- is the most important cause of serious gastroenteritisamong children and a significant nosocomial pathogen

Is most severe in children between 3-24 mons. Of age Other agents include:

a. Bacterial agents

- E.coli

- Salmonella groups (nontyphoidal)

- Salmonella typhi

b. Vibrio cholerae

c. Clostridium difficile


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SIGNS AND SYMPTOMS OF DIARRHEA

MILD DIARRHEA

Fever 38.4 to 39.0C)

Anorexia

Irritable and appear unwell Consist of 2-10 loose watery

bowel movt. Per day

Mucous membrane of the mouth

appears dry

Rapid pulse Skin is warm

Skin turgor not yet decreased

UO is usually normal

SEVERE DIARRHEA

rectal tempt. Is often as highas (39.5 to 40.0C)

PR and RR are weak and rapid

Skin is pale and cool

Infants appear apprehensive,listless and lethargic

Obvious signs of DHN: sunken

eyes, poor skin turgor Stool is liquid green perhaps

mixed with mucus and blood

UO is scanty and concentrated


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Elevated Hct, Hgb and serum

CHON levels

Metabolic acidosis


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THERAPEUTIC MANAGEMENT FOR

DIARRHEA

1. Assess fluid and electrolyte

balance.

2. Rehydration3. Maintenance of fluid thrapy

4. Reintroduction of an

adequate diet.

5. Obtain sample of stool for

stool culture so definite

antibiotic therapy can be

prescribed.

6. If child can drink, institute ORT

(ORAL REHYDRATION

THERAPY).


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NURSING MANAGEMENT FOR

PATIENTS WITH DIARRHEA

1. Promote adequate hydration

and comfort

a. (+) vomiting- NPOtemporarily

b. Wet lips with a moisturizing

jelly if it is dry

c. Give pacifier to promote

comfort

d. (+) fever- do TSB

e. Increase OFI

f. Do not obtain BT in the rectal

area.

g. Assess perianal skin forirritation.

h. Keep perianal area clean and

dry.

i. Change diapers frequently

2. Record I and O strictly.

3. Weigh child daily to assess for

DHN.


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4. Discourage intake of clear fluids,

carbonated drinks and gelatin.

5. Assess V/S, skin turgor, mucousmembranes, and mental status.

Expose slightly reddened intact

skin to air when possible to

promote healing

6. Avoid use of commercial baby

wipes with alcohol on excoriated

skin

7. Observe buttocks and perineum

for skin infection.


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MECONIUM PLUGS

- Caused by meconium that has

reduced water content and areusually evacuated after DRE(digital rectal exam)

MECONIUM ILEUS

- Initial manifestation of cysticfibrosis w/c is the luminalobstruction of the distal smallintestine by abnormalmeconium.

MGT. OF CONSTIPATION

1. In infancy, increase CHO inthe formula.

2. During childhood, the dietmust consist of increasedfiber and fluid.

HIGH FIBER FOODS

a. bread, grains

- Whole grain bread or rolls

- Whole grain cereals

- bran


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- Pancakes, waffles, muffins with

fruit or bran

- Unrefined (brown) riceb. Vegetables

- Raw vegetables especially

broccoli, cabbage, carrots,

cauliflower, celery, lettuce, and

spinach

- Cooked vegetables like asparagus,

brussels sprouts, corn, potatoes,

squash, string beans and turnips

c. Fruits

- Raw fruits especially those with

skins or seeds other than ripebanana or avocado

- Raisins, prunes or dried fruits


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DISORDERS OF THE STOMACH AND

DUODENUMI. GASTROESOPHAGEAL REFLUX(ACHALASIA)

A neuromuscular disturbance

in which the gastroesophageal

(cardiac) sphincter and thelower part of the esophagus

are lax and thus allow easy

regurgitation of gastric

contents into the esophagus.

Usually starts 1 week afterbirth and may be associated

with hiatal hernia.

CAUSES OF GER

Dysfunction of the lower

esophageal sphincter

Delay in gastric emptying

Poor clearance of esophageal acid

Susceptibility of esophageal

mucosa to acid injury

Gastric distention

Increased abdominal pressurebecause of coughing, CNS

disease, hiatal hernia and

gastrostomy placement


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Clinical manifestations andcomplications

SYMPTOMS IN INFANTS

a. Spitting up, regurgitation

b. Excessive crying, irritability,arching of the back, stiffening

c. Wt. loss

d. Failure to thrive

e. Respiratory problems (cough,

wheeze, stridor, gagging,choking with feeding

f. Hematemesis

g. Apnea

SYMPTOMS IN CHILDREN

a. Heartburn

b. Abdominal pain

c. Noncardiac chest pain

d. Chronic cough

e. Dysphagia

f. Nocturnal asthmag. Recurrent pneumonia


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COMPLICATIONS

a. Esophagitis

b. Esophageal stricture

c. Laryngitis

d. Recurrent pneumonia

e. Anemia

f. Barretts esophagus

DIAGNOSTIC EVALUATION

1. Upper GI Series/Barium swallow

- X-ray of upper GI tract

- To detect presence of anatomic

abnormalities

Nx. Interventions

a. NPO post midnight

b. Instruct pt. about the procedure

c. Educate pt. that barium has a thick

consistency and chalky taste.

d. Administer laxative to help expel

barium and prevent fecal impaction


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e. Assess abdomen for distention

f. Observe the stool. Initially it iswhite but returns to normal color

within 72 hrs.

g. Instruct ct. to inform physician ifconstipation and abdominaldistention occur.

2. Scintigraphy

- Detects radioactive substances inthe esophagus after a feeding of acompound and assesses gastricemptying

NX. MGT.

1. Identify symptoms

2. Avoid caffeine, chocolate

and spicy foods that mayweaken the LES.

3. Wt. mgt. in children

4. Monitor Iand O


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HYPERTROPHIC

PYLORIC STENOSIS

PYLORIC SPHINCTER

- It is the opening between the

lower portion of the stomachand beginning portion of the

intestine, the duodenum.

- Occurs when the

circumferential of the pyloric

sphincter becomes thickenedresulting in elongation and

narrowing of the pyloric

channel.

It is usually evident at 4-6 wks. Of

age

Exact cause is unknown

There is a genetic predisposition

1stborn children and males are

affected 5x more frequently than

females

More common in full term infants


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CLINICAL MANIFESTATIONS OFHPS

a. Projectile vomiting w/c occur

shortly after feeding

b. Nonbilious vomitus; blood

tinged

c. Infant hungry; avid nurser,

d. No evidence of pain or

discomfort except chronic

hunger

e. Wt. loss

f. DHN

g. Distended upper abdomen

h. Readily palpable olive shaped

mass in the epigastrium just to

the right of the umbilicus

Visible gastric peristaltic waves that

move from L-R across the

epigastrium


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DIAGNOSTIC EVALUATION

a. UTZ

- Will reveal an elongated,

sausage shaped mass with an

elongated pyloric channel

b. Upper GI radiography

c. Decreased serum Na and K

d. Decrease in serum CL levels

e. Increase Ph and bicarbonatef. Elevated BUN

THERAPEUTIC MGT.

1. PYLOROMYOTOMY

- Sxcal relief of pyloric obstruction

- An incision is made in the RUQ2. LAPARAOSCOPY

- Use of a laparoscope


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NX. MGT.

PRE-OPERATIVE CARE

1. Restore hydration and

electrolyte balance

2. Monitor Iand O and urine

specific gravity

3. (+) gastric lavage- ensure

patency of the tube and

measure and record the amount

and type of drainage; position

infant flat on bed or head

slightly elevated

POST-OPERATIVE CARE

1. After 4-6 hrs. start infants on a

small amt. of ORS . If (-)

vomiting, the amt. is increased

orally or breast-feeding is begun.

2. Monitor Iand O

3. Observe for evidence of pain


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HERNIA

Protrusion of a portion of an organ or

organs through an abnormalopening.


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TYPES OF HERNIA

1. Diaphragmatic Hernia

- Protrusion of abdominal organsthrough an opening in thediaphragm

Symptoms:

a. Mild to severe respiratorydistress few hrs. after birth

b. Tachypnea

c. Cyanosis

d. Dyspnea

e. Absent breath sounds inaffected area

f. Impaired CO

g. Possible symptoms of shock

h. Severe acidosis

DX:

- Confirmed by radiographic study,often diagnosed prenatally as early

as 25th

AOGMGT:

1. Correction of acidosis

2. Possible use of intubation

3. GI decompression

4. Prophylactic antibiotic

administration5. Sxcal reduction of hernia and repair

of defect


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3. Abdominal Hernia

-Umbilical-weakness in abdominalwall around umbilicus;incomplete closure of abdominalwall that allows intestinal

contents to protrude through anopening.

Sx:

- Noted by inspection andpalpation of the abdomen

- High incidence in premature andafrican-american infants

- Usuall closes spontaneously by 1-2 y/o.

Mgt:

a. No treatment on small defects

b. Operative repair if persists toage 406 or if defect is > 1.5-2.0cm by age 2.

c. Discourage use of homeremedies ( belly bands, coins)


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Abdominal

Omphalocele- protrusion ofintraabdominal viscera into base ofumbilical cord; sac is covered withperitoneum w/o skin

Sx:- Obvious on inspection

Mgt:

- Sxcal repair of defect

- Preoperative:

a. Gradual reduction of abdominal

contentsb. Prohylactic antibiotic administration

Gastroschisis

- Protrusion of intraabdominalcontents through a defect in theabdominal wall lateral to umbilicalring; no peritoneal sac

Sx:- Obvious on inspection

Mgt:

- Sxcal repair of defect

- Preoperative:

a. Keep sac or viscera moist with saline

soaked padsb. Use overhead warming unit

c. Nasogastric suction

d. NPO


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PEPTIC ULCER DISEASE

It is a shallow excavation formed inthe mucosal wall of the stomach,pylorus or duodenum

In infants, ulcers tend to be gastric; inadolescents they are usuallyduodenal

Etiology:

- Exact cause is unknown

- Increased in persons with blood typeO

- H.Pylori- weakens gastric mucosalbarrier allowing damage to themucosa

- Ulcerogenic drugs

- Smoking

- Alcoholism

- Stressful life events

It is most likely caused by animbalance between the CYTOTOXIC

(DESTRUCTIVE) factors andCYTOPROTECTIVE (DEFENSIVE)factors in the GIT.

DESTRUCTIVE FACTORS:

a. Acid

b. Pepsin

c. ASA and NSAID- inhibitsprostaglandin synthesis

d. Bile acids

e. Infections with H.Pylori


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DEFENSIVE FACTORS:

a. Mucous layer

- Acts to diffuse acid form the

lumen to the gastric mucosal

surfaceb. Local bicarbonate secretion

- Produced by the stomach and

duodenum

- Decreases acidity on epithelial

cells, minimizing effects of lowph

ASSESSMENT:

1. neonate- hematemesis or melena,

respiratory distress, abdominal

distention vomiting if rupture may

occur and if extensive

cardiovascular collapse.2. Toddler- anorexia, vomiting,

bleeding after few weeks

3. Preschool or early school age- pain

w/c may be mild, severe, colicky or

continuous

4. School age and adolescents- pain in

epigastric area before meals

relieved by eating


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Dx:

a. FIBEROPTIC ENDOSCOPY- most

reliable diagnostic test

b. CBC- to detect anemia

c. Stool analysisd. Liver function tests

Mgt:

1. Promote healing of ulcer

through compliance with

medications.

Medications for PUD:

1. Antacids- neutralizes gastric acid

2. H2 Receptor antagonists (Famotidine,

Ranitidine)- suppresses gastric acid

production

3. Proton Pump Inhibitors (omeprazole)

- Inhibit Hydrogen ion pump in th

parietal cells thus blocking theproduction of acid

4. Mucosal protective agents (sucralfate,

bismuth containing compounds)

Sucralfate- aluminum containing agent

that forms a protective barrier over

ulcerated mucosa


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Bismuth containing compounds

-inhibit growth of microorganisms

2. Do not use ASA or NSAIDS if an

antipyretic or analgesic is needed,

use ACETAMINOPHEN (TYLENOL).3. Avoid heavily spiced foods such as

pizza or sausage.

4. Avoid carbonated drinks and

beverages.


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HEPATIC DISORDERS


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FUNCTIONS OF THE LIVER

- Liver lies immediately under the

diaphragm on the right side.

1. Essential for the normal

metabolism of CHO, proteinsand fats.

2. Maintains normal blood sugar

level by exchanging glucose to

glycogen and storing it until cells

needs it.

3. Changes glycogen to glucose and

releases it into the blood stream

when needed by the body cells.

4. Aids in the catabolism of fatty acids

and proteins and serves as temporary

space for both fat and protein.

5. By the means of the enzyme,

GLUCORONOSYLTRANSFERASE

converts indirect or unconjugatedbilirubin into direct or conjugated

bilirubin so it can be excreted in bile

and from the body.

6. Manufactures bile- necessary for the

digestion of fat; fibrinogen and

prothrombin, heparin.

7. Produces large amounts of body heat


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8. Destroys RBCs and detoxifies

harmful substances such as

drugs.


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LIVER FUNCTION TESTS

Serum bilirubin INCREASE indirect bilirubin means it is not convertedinto direct bilirubin hence liver function may be

impaired Normal value of total bilirubin in serum is 1.5 mg per

100 ml.

INCREASE direct bilirubin implies obstruction of the

bile duct

Stool and urine

bilirubin

(+) bile pigments in the stool, bile is manufactured and

excreted form the liver

(-) bile pigment, stool is clay colored

(+) bilirubin in urine indicate possible liver dysfunction

Alkaline

phosphatase

An enzyme produced by the liver and bone and

excreted in the bile

INCREASED levels in the blood indicates bile duct

obstruction

Prothrombin time Is associated with blood coagulation.

In chronic liver disease, level of prothrombin falls

severely so PT time is INCREASED.


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Aspartate transaminase (AST; serum

glutamic-oxaloacetic transaminase(SGOT)

an enzyme in the heart and liver

Is released into the bloodstreamwhen there is damage to the organ

blood levels INCREASE by 8 hrs.

after injury; level reaches a peaks in

24-36 hrs. and falls to normal in 4-6

days

Alanine Transaminase (ALT; serumglutamate pyruvate transaminase

(SGPT)

Found mostly in the liverRises for the same reasons as AST

(SGOT)

Lactic dehydrogenase an enzyme in the heart and liver

is increased in INFECTIOUS

MONONUCLEOSIS

Serum albumin Albumin, is a serum CHON

synthesized in the liver

Is DECREASED in acute or chronic

liver disease


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HEPATITIS

Inflammation and infection of the liver

Caused by invasion of the Hepa A, B, C, D, E viruses,

chemical or drug reaction, autoimmune hepatitis,

Wilson's disease, steatohepatitis


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HEPATITIS A

Causative agent: A picornavirus, hepatitis

A virus

Incubation period: 25 days on average

Period of communicability: Highest

during 2 wks. Preceding onset of

symptoms

Mode of transmission: fecal-oral route

Immunity: natural

Active artificial immunity: HAV vaccinePassive artificial immunity: Immune

globulin (IG)

HEPATITIS BCausative agent: A hepadnavirus, hepatitis B

virus

Incubation period: 120 days on average

Period of communicability: later part ofincubation period and during the acutestage

Mode of transmission: principal route-parenteral; least- oral, sexual, any bodyfluid or perinatal transfer- transplacentalblood (last trimester), at delivery or duringbreast-feeding

Immunity: naturalActive artificial immunity: HBV vaccine

Passive artificial immunity: Specific hepa Bimmune serum globulin


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HEPATITIS C, D, E, G

Hepa C is a single strand RNA virusand is primarily transmitted by bloodor blood products, IV use or sexualcontact

Hepa D is a defective RNA virus thatrequires function of the HBV.

Incubation period is 2-8 wks.

Hepa E is eneterally transmitted andtransmission may occur throughfecal-oral route or from contaminated

water

Hepa G is a bllod-borne virus thatmay be transmitted by organtransplantation

Assessment

Headache

Fever

Anorexia

Jaundice

Generalized aching

RUQ pain

Headache

Pruritus

Urine becomes darker in color

Sclerae becomes jaundiced

Stool becomes white or gray


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Lab findings show an INCREASE

AST and ALT

INCREASED bilirubin levels in the

urine

Bile pigments in the stool are

decreased.

Serum bilirubin levels are

increased.

MGT:

1. Strict hand washing.

2. Dispose carefully feces, needles

and syringes.

3. Screen pregnant women for

hepa B surface antigen.

4. Infants born to (+) hepa B

mothers must be given HBIG and

active immunization

5. Increased rest and maintain a

good caloric intake


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FULMINANT HEPATIC FAILURE

Is present when acute, massive

necrosis or sudden impairment of

the liver function occurs leading to

HEPATIC ENCEPHALOPATHY.

HEPATIC ENCEPHALOPATHY- is due

to the livers inability to metabolizeammonia to form urea so it can be

excreted. Ammonia is a CNS

depressant and is produced in the

GIT when CHON is broken down by

bacteria, by the liver and in lesser

amounts by gastric juices and

peripheral tissue metabolism. The

kidneys are another source in the

presence of hypokalemia.

Clinical features:

1. Confusion

2. Drowsiness

3. Disorientation

Treatment:

1. Reduce CHON intake

2. Administer lactulose to prevent

absorption of Ammonia in the

colon

3. Administer nonabsorbableantibiotics such as neomycin to

decrease production of ammonia

by the intestinal bacteria.


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OBSTRUCTION OF THE BILE DUCTS

Occurs in children generally fromcongenital atresia, stenosis orabsence of the duct.

It is a congenital disorder so the chiefsign does not develop until 2 wks. Ofage

Clinical features:

1. Jaundice

2. INCREASE alkaline phosphatase

3. AST is normal in the early phase andbecomes abnormal when liverdamage occurs.

4. absorption of fat soluble vitamins ispoor.

5. Calcium absorption is also poor.

Therapeutic mgt:

1. Appropriate blood work ad liverbiopsy must be done under localanesthesia to rule out hepatitis.

2. Collect duodenal secretions by

endoscopy to assess bile.3. Radionuclide imaging

4. Mucus plug is suspected, pt.may be given MgSO4 (to relaxthe bile duct) or dehydrochoricacid (Decholin) IV to stimulateflow of blie.

5. (+) atresia of bile duct, sxcalcorrection is the tx.


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12. spider angiomas and prominent

blood vessels are seen on the

upper torso

13. Decreased ability to detoxify

substances

14. Decreased CHON synthesis

15. Decreased ability to produce

prothrombin

16. Decreased ability to produce bile

17. Hypoglycemia18. Esophageal varices

19. hypersplenism

THERAPEUTIC MGT:

1. Frequent assessment of liver

status with PE and liver function

tests

2. Mgt. of specific complications3. Liver transplantation


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ESOPHAGEAL VARICES

Or distended veins

Form at the distal end of the

esophagus near the stomach

2ndary to back pressure on the

veins due to increased BP in the

portal circulation.

Its rupture is an E

MGT:

1. Vasopressin or Nitroglycerin may

be given IV to lessenhypertension

2. Injection of sclerosing agent into

veins

3. Iced saline NGT lavage may be

given

4. Insert a SENGSTAKEN-BLAKEMORE

TUBE or a LINTON-NACHLAS

catheter into the stomach to

apply pressure against the

bleeding vessels. Compression

must be reduced for 5-10 minutes

every 6-8 hrs.


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STRUCTURAL DEFECTS

CLEFT LIP OR CLEFT PALATE

Description: failure of soft tissue

and/or bony structure to fuse

during embryonic development ;

may occur separately or together

and involve one or both sides of

the palates midline.

Etiology: caused by fetal insult;

teratogenic factors which include:

1. Drugs

2. Exposre to radiation

3. Exposure to rubella virus

4. Chromosomal abnormalities

Pathophysiology

1. In CLEFT LIP- maxillary

prominence fails to fuse with

medial nasal prominence

between 7th and 8th wk. of

intrauterine life.

2. In CLEFT PALATE- failure of

maxillary bone plate to close

during 7th to 12th weeks of

intrauterine life


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ASSESSMENT:

1. LIP- unilateral or bilateral; extentvaries from a slight notch in thevermillion border to a completeseparation from the floor of the

nose2. PALATE- unilateral or bilateral;

varying degree for the extent ofpalate involvement that isevident upon visual inspection

THERAPEUTIC MGT:

1. Surgery: plastic surgicalcorrection of cleft lip is during 1st

3 mons. Of life; palate correctionarte done at either 12 or 18

m0ns. Or delayed until 4 yrs. Ofage

2. Meds: analgesics to controlpostop pain

3. Use of feeding devices: use ofsoft elongated lambs nipples;

Brecht feeder for infant with alarge cleft palate

4. Speech therapy


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NX. MGT:

1. PRE-OP CARE:

a. Assess feeding requirements

b. Assess nature of defect and its impacton feeding

c. Monitor respiratory status and abilityto suck during feeding

d. Encourage BF if appropriate

e. Initiate feeding w/ special devices asrequired

f. Feed small amounts gradually

g. Burp frequently every 15-30 cc

h. Demonstrate special feeding orsuctioning techniques to parents

2. POST- OP CARE:1. Assess suture line for

drainage, crusting and signs ofinfection

2. Cleft lip repair: cleanse sutureline after feeding and as

ordered; use a cotton tipapplicator moistened withsaline or solution preferred bysurgeon

3. Position infant on back or onside; avoid prone position to

prevent rubbing of surgicalsite on mattress

4. Maintain lip protective devicelogan bow on operative site


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5. Restrain with soft elbow or jacket

restraint; remove one at a time and

periodically to perform ROM

exercises

6. Avoid contact with sharps, straws or

forks near surgical site7. Feed with cup, wide bowl or soup

spoon; if palate repaired avoid

inserting spoon into mouth.

8. Avoid use of oral suction or placing

objects into mouth such as tongue

depressor or oral thermometer

9. Prevent sucking: no pacifiers, use of

straw for oral fluid intake

INFLAMMATORY DISORDERS


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INFLAMMATORY DISORDERS

APPENDICITIS Inflammation of the appendix, a

blind sac connected to the end of

cecum; may lead to perforation,

peritonitis and sepsis if left

untreated.

Etiology:

1. Obstruction of the lumen of the

appendix as a result of fecalith

or hardened feces

2. Other causes are lymphoid

hyperplasia, tumors, fibrotic

stenosis, worms or low fiber diet

pathophysiology:

1. Lumen obstruction causes

blocking of mucous secretion,

blood vessels compressed and

ischemia results.

2. Bacterial invasion and necrosis

subsequently occur

3. Acute inflammation rapidly

progresses to perforation and

peritonitis if left undiagnosed


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ASSESSMENT

1. Appendicitis

a. pain, cramping initially located inperiumbilical area descends to RLQ;most intemse at Mc Burneys point-located midway between theanterior superior iliac crest and theumbilicus

b. Rebound tenderness of abdominalrigidity

c. Low grade fever

d. N/V

e. Constipation or diarrhea

f. Side lying position w/abdominalguarding; legs flexed

2. Peritonitis

a. Fever increases

b. Progressive abdominaldistention

c. increase abdominal pain

d. Rigid guarding of abdomen

e. Tachycardia, tachypnea

f. Pallor, chills and restlessness


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DIAGNOSTIC PROCEDURES:

1. Lab studies:

a. CBC: WBC count increases to15,000-20,000 usually withpolymorphonuclear pyuria

b. U/A- reveals pyuria

2. Diagnostic studies:

a. Abdominal X-ray- revealspresence of fecalith in appendix

b. UTZ- reveals location of abscess

before sx.

THERAPEUTIC MGT:

1. sx.- appendectomy

2. Medications:

a. Analgesics

b. Antibiotics

2. NX. MGT:

a. pre-op care:

1. assess pain and check forrebound tenderness

2. Assess VS, noting for

tachycardia, shallow fastrespirations and fever >100F

3. Keep NPO


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4. Provide comfort measures:

a. Give analgesics

b. Frequent mouth care

c. Right side lying or low to semi-

fowlers position to promotecomfort or localize abscess when

appendix ruptures

d. Report any changes in type, level

or location of pain

e. Provide diversional activity forquiet play

f. Avoid use of laxatives or enemas


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INTUSSUSCEPTION

Telescoping of one portion of bowelinto another portion resulting inobstruction to passage of intestinalcontents.

Etiology: cause is unknown

Children at risk are those with cysticfibrosis, celiac disease andgastroenteritis.

Most common site is the ILEOCECCALVALVE

Pathophysiology:

1. Inflammation and ischemia occur in

the intestinal wall as portions pressagainst each other

2. Eventual tissue necrosis, perforationand peritonitis may occur

ASSESSMENT:

1. Paroxysmal, acute pain inabdomen

2. Vomiting

3. Currant jelly-like stools

4. Cylindrical mass above affectedarea

DX. PROCEDURS:

1. Abdominal x-ray

2. Barium enenma


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THERAPEUTIC MGT:

a. Hydrostatic reduction- bybarium enema

b. Sx. If reduction by bariumenema is not successful or there

is tissue necrosisc. Meds:

1. Antibiotics

2. analgesics

NX. MGT:

1. Assess for findings ofintussusception

2. Maintain patency of NG tube

3. Administer IV fluids as ordered

4. Ensure NG tube is appropriate toage

Newborns and infants- catheter size5 to 6, 8

>6 y/o- 8 to 10

Adolescent- 12 to 16Inform need for sx. If reduction is not

successful

HIRSCHPRUNG DISEASE (CONGENITAL


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HIRSCHPRUNG DISEASE (CONGENITAL

AGANGLIONIC MEGACOLON)

Congenital defect that result in

mechanical obstruction form

inadequate motility of an intestinal

segment

Etiology: may be accompanied by

anomalies of other GI or GUanomalies

Pathophysiology:

1. Absence of ganglion cells in an

intestinal segment results in lack of

peristalsis

2. Bowel proximal to defect dilates

because of a lack of peristalsis

3. Failure of anal sphincter tyo relax;

fecal matter accumulates in

aganglionic segment

ASSESSMENT:

1. Neonatal period

a. Failure to pass meconium w/in

48 hrs. after birth

b. Bile-stained vomitusc. Abdominal distention

2. Early childhood

a. Ribbon-like stools

b. Constipation

c. Foul smelling stools

d. Visible peristalsis

e. Recurrent diarrhea


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DX. PROCEDURES:

1. Barium enema- reveals

narrowed segment of bowel

2. Rectal biopsy- absence of

aganglion cells3. Abdominal x-ray- dilated loops

of intestine

4. Rectal manometry- failure of

internal sphincter to relax

THERAPEUTIC MGT:

a. medications: preoperative

antibiotics

b. Treatments: ENEMA, NGT

placement

c. sx: 2 stage process

1. Temporary colostomy construction

2. Resection of aganglionic segment;

anastomosis of the intact ganglion

segment to the rectum is erformed

during a pull through procedure

3. Colostomy closure is done 3 mons.

Following pull through


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NX. MGT:

1. PRE-OP CARE:

a. Assess wt, I and O, abdominal

girth and fluid and electrolyte

statusb. Offer diet high in calories and

CHON and low in residue

2. POST-OP CARE:

a. Monitor hydration status

including NG, colostomy andindwelling urinary catheter

drainage; IV, NG and oral intake

b. Maintain patency of NG tube

c. Monitor for return of bowel

sounds for 48-72 hrs.

d. Provide instructions regarding

colostomy carte

e. Provide dietary instructionsincluding high residue or normal

diet, adequate fluid intake


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MALABSORPTION SYNDROMES

CELIAC DISEASE (GLUTEN

INDUCED ENTEROPATHY)

- Intolerance to gluten, the CHON

component of BROW (barley, rye,

oat, wheat)

- Symptoms of disorder occur 3-6

mons. Following introduction of

gluten-containing grains into diet

usually before 2 yrs. Of age

ASSESSMENT:

1. Early signs

a. diarrhea; failure to gain wt. following

diarrheal episode

b. Constipation

c. Vomiting

d. Abdominal paine. Steatorrhea

2. Later signs

a. Behavioral changes: irritability, apathy

b. Muscle wasting with loss of

subcutaneous fat

c. Celiac crisis- rare event which requireimmediate medical attention

1. Severe DHN

2. Metabolic acidosis


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Diagnostic procedures:

a. lab. Studies- stool analysis-

reveals steatorrhea

b. Diagnostic studies

1. Jejunal biopsy- reveals atrophyof mucosal cells

2. Serum antigliadin and

antireticulin antibodies (+)

indicative of disorder

3. Sweat test- to rule out cysticfibrosis

Therapeutic mgt:

1. Acute care

a. Assess for findings related to

celiac disease

b. Instruct parents on GLUTENFREE DIET: NO BROW and BROW

containing substances

throughout life.

c. Teach parents to adhere to diet,

prevent stress and infection to

prevent celiac crisis.

INFLAMMATORY BOWEL DISEASE


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INFLAMMATORY BOWEL DISEASE:

ULCERATIVE COLITIS AND CROHNS DISEASE

Involves the development of

ulcers of the mucosa or

submucosa layers of the colon

and rectum.

Both probably represent an

alteration in immune system

response or an autoimmune

processes.

There is an INCREASED IgAa and

IgG on the intestinal mucosa.

Smoking and frequent use of ASAare correlated with Crohns

disease.

Crohns disease is an

inflammation of segments of the

intestine and commonly involves

the terminal ileum.

In ulcerative colitis, the colon and

the rectum are involved, with the

distal colon and rectum most

severely affected.


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ASSESSMENT:

1. Abdominal pain

2. Diarrhea

3. Malnutrition

4. Complications:a. Hemorrhage

b. Bowel perforation

c. Peritonitis

d. Formation of fistulas between

bowel loops

COMPARISON OF CROHNS DISEASE


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COMPARISON OF CROHN S DISEASE

AND ULCERATIVE COLITIS

Comparison factor Ccrohrohns Disease Ulcerative Colitis

Part of bowel affected Ileum Colon and rectum

Nature of lesions Intermittent Continuous

Diarrhea Moderate Severe and bloody

Anorexia Severe Mild

Weight loss Severe Mild

Growth retardation Marked Mild

Anal and perianal lesions Common Rare

Association with carcinoma Rare Common


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Diagnosis:

1. It is established by colonoscopyand barium enema.

COLONOSCOPY- shallow ulcerationsalong the bowel can be seen,

mucosa is friable ( easilyirritated).

2. BIOPSY- for definite diagnosis

* After biopsy- observe BP, PR andassess for occult blood

Therapeutic mgt:

1. Provide an enteral or TPN toallow the bowel to rest and heal.

2. When food is reintroduced afterthe resting period, provide a

HIGH CHON, CHO, VITAMIN diet3. Assess I & O.

4. Administer anti-inflammatorydurg such as prednisone,sulfasalazine, or azathioprinewhich is an immunosuppressive

agent.

5. For ulcerative colitis,cyclosporine may be used.


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Sx: bowel resection to remove a

portion of the bowel (colectomy)

followed by an ileoanal pull

through.

DISORDERS CAUSED BY FOOD VITAMIN AND


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DISORDERS CAUSED BY FOOD, VITAMIN AND

MINERAL DEFICIENCIES

1. KWASHIORKOR

- A disease caused by CHON

deficiency

- Occurs most frequently in

children ages 1-3 yrs.old

- Tends to occur after weaning

ASSESSMENT:

1. Growth failure

2. Severe muscle wasting

3. Dependent edema4. Ascites

5. Irritable and lack interest in the

surroundings

6. Hair shafts develop a striped

appearnce of brown, then white

and so on- a zebra sign.

7. Diarrhea

8. Iron deficiency anemia

9. Hepatomegaly

THERAPEUTIC MGT:

1. High CHON diet


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2. NUTRITIONAL MARASMUS

- Is a disease caused by a

deficiency of all food groups

which is basically a form of

starvation

- Is most common in children < 1

yr. of age

ASSESSMENT:

- Have many of the symptoms as

with Kwashiorkor including

growth failure, muscle wasting,

irritability, IDA and diarrhea.

TX: diet rich in all nutrients


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VITAMIN DEFICIENCY DISORDERSVitamin Cause of deficiency Signs and symptoms

Vitamin A Lack of yellow

vegetables in diet

Tender tongue; cracks

and corners of mouth

Night blindness

Xeropthalmia (dry and

lusterless conjunctivae)

Keratomalacia (necrosisof the cornea with

perforation, loss of

ocular fluid, and

blindness)

Vitamin B1 Most common inchildren who eat

polished rice as dietary

staple

Beriberi (tingling andnumbness of

extremities; heart

palpitations; exhaustion)

Vitamin B1 Diarrhea and vomiting

Aphonia (cry w/o


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sounds)

Anesthesia of feet

Niacin Common in children who

eat corn as dietary staple

Peliagra (dermatitis,

resembles a sunburn)

Diarrhea

Mental confusion

(dementia)

Vitamin C Lack of fresh fruits in the

diet

Scurvy (muscle

tenderness; petechiae)Vitamin D Lack of sunlight Poor muscle tone,

delayed tooth formation

Rickets (poor bone

formation)

Craniotabes (softening of

the skullSwelling at joints

particularly of wrists and

cartilage of ribs

Bowed legs

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