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Pediatric Nursing

I. Pediatric Cardiovascular


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Congenital Heart Defects

A. General concepts

1. Definition: present at birth - consequences are congestive heart failureand hypoxemia

2. Etiology: usually not known - associated with maternal factors:a. infectionb. alcoholismc. age over 40 yearsd. diabetes mellitus, type onee. genetics, chromosomal changes

3. Findings of congenital heart defectsa. child small for ageb. physiological failure to thrivec. exercise intolerance

d. dyspnea while feedinge. squatting positionf. clubbing of fingersg. cyanosis and/or pallor may be associated with poor perfusionh. unusual pulsations

4. Physical consequences of congenital heart defectsa. increased workload; pulmonary hypertension; decreased systemic

output; cyanotic defects


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b. can lead to hypoxemia and polycythemiac. concern: formation of thrombus with embolusd. blood flow patterns may be affected

B. Acyanotic defect - infant/child is "pink" but child may develop cyanosis1. Pathology: hole in the heart's internal wall

a. blood flows from heart's arterial (left) to venous (right) side or a

"left to right shunt", not systemically, but only within heart itselfb. size of defect will determine severity of condition

2. Common types:

C. Cyanotic defect: infant/child is usually "blue", but child may appear pink

1. Pathologya. unoxygenated blood mixes with oxygenated, via a "right to left

shunt"b. decreases oxygenation to the entire systemc. results far more severe than acyanoticd. thrombus formation is always a concern

D. Diagnostics1. EKG: noninvasive, painless, infants and young children may require mild

sedation2. Cardiac catheterization

a. presence of diaper rash may postpone procedureb. preparation depends on level of growth and developmentc. post procedure child may have difficulty complying with keeping

insertion point in correct positionE. Nursing care of the child with a congenital heart defect

1. Emotional, physiological, and psychological interventions
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2. Assisting the child and family to adjust to special needs3. Goals of treatment

a. child will maintain adequate oxygenation and physiologicalstability

b. family will understand signs and symptoms of the condition, andhow to manage each of them

c. child will attain milestones of normal growth and developmentd. when child has surgery, child and family will be prepared, know

prognosis, and know how to give home care afterwarde. improve cardiac functionf. remove accumulated fluidg. decrease cardiac demandsh. improve tissue oxygenation

4. Nursing interventions

a. recognize CHF

FINDINGS OF CONGESTIVE HEART FAILURE

b. monitor height, weight, vital signs, pulses, pulse oximeter, intakeand output

c. medications: digoxin (Lanoxin), furosemide (Lasix) orchlorothiazide (Diuril), ACE inhibitors: Capoten, Vasotec

d. monitor serum potassium levele. recognize and treat pain appropriately: pharmacological and

nonpharmacological interventionsf. maintain a safe environmentg. conserve energy

h. maintain proper nutrition, with small, frequent feedings monitorsodium intake, fluid restriction may be required

i. support and discuss treatment with parentsj. place in proper position - slanting position with head elevated,

older babies in infant seats, occasional knee-chest5. Teaching points

a. inform parents about findings of infectionb. discuss possible behavior changes the child may exhibit
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c. counsel parents about high-risk children requiring antibioticprophylaxis for dental work

Acquired Cardiovascular Disordersoccur after birth as a result of infection, autoimmune responses, environmental or familialtendencies

F. Hyperlipidemia: excessive lipids1. Etiology: dietary, heredity2. Pathophysiology

a. increased lipids and cholesterolb. causes atherosclerosis, leading to coronary heart disease

3. Diagnosis: lab tests: increased LDL, lipids and cholesterol; decreasedHDL

4. Managementa. diet: ADA diet in two steps:

i. < 30 kcal from fat; < ten from saturated fat; < 300 mg/Lcholesterol

ii. < 30 kcal from fat, < seven from saturated fat; < 200 mg/Lcholesterol

b. medications: colestipol (Colestid), niacin (Nicor), cholestyramine(Questran)

5. Nursing interventionsa. encourage screening for at risk children with family historyb. teach dietary guidelines or refer to dietician

G. Bacterial endocarditis: inflammation of the valves of the inner lining of the heart1. Etiology: possible causative agents

a. streptb. staphc. fungi

2. Pathophysiologya. organisms enter blood stream (vascular dissemination)b. form vegetation on endocardium

3. Diagnosticsa. EKG changesb. sedimentation rate evaluatedc. WBC elevatedd. blood cultures

4. Managementa. high doses of antibiotics

5. Nursing interventionsa. monitor for signs of infection

b. provide rest periods6. Teaching points

a. need for long-term IV therapyb. side effects of antibioticsc. high-risk children need prophylactic antibiotic therapy before

dental work or other invasive proceduresII. Pediatric Respiratory

Respiratory Infections

A. General concepts1. Etiology: bacterial, viral; often influenced by age, season, preexisting

disorder, living conditions2. Findings: increased respiratory and heart rate, fever, nausea/vomiting,

nasal discharge and blockage, mucus production, coughing, adventitiouslung sounds

3. Nursing care goalsa. child will not exhibit findings of respiratory distress, will be able to

clear secretions, and remain comfortable with a patent airwayb. child will not spread infection to others


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c. child will ingest adequate fluids, and maintain hydration4. Management

a. medications: antibiotics, antipyreticsb. possible: anti-inflammatory, anti-mucolytics, bronchodilators,

oxygen as needed5. Nursing interventions

a. chest physiotherapyb. provide nutrition and encourage fluids - Jello, soup, puddingsc. promote rest and comfortd. prevent spread of infectione. ease respiratory efforts - warm mist

6. Teaching pointsa. handwashingb. avoid contact with affected children

B. Respiratory failure: inability to maintain adequate oxygenation1. Predisposing factors

a. obstructive anomalies, aspirationb. infections, tumors, anaphylaxis

c. restrictive conditions: respiratory distress, cystic fibrosis,pneumonia, pneumothorax

d. paralytic conditions2. Findings

a. restlessness, mood changesb. changes in LOCc. increasing rates of respiration and pulsed. dyspnea

3. Management

a. frequent observation and physical exams, with pulse oximeterb. correct hypoxemia, maintain ventilation and deliver oxygenc. monitor for side effects and expected outcomes of therapy

C. Airway obstruction and basic life support1. Cardiac arrest is usually due to prolonged hypoxemia secondary to

inadequate ventilation, oxygen or circulation2. When following guidelines for pediatric life support, consider not just the

child's age, but also size. Individual anatomy and development will vary.3. Airway clearance techniques

a. determine conscious versus unconscious childb. for infants and toddlers: back blows and chest thrustsc. for preschool and school-age: modified Heimlich maneuver

("astride")

Infant Respiratory Disorders

D. Respiratory distress syndrome (RDS): "hyaline membrane disease"1. Definition: related to development delay in lung maturation2. Etiology

a. premature infants: usually due to surfactant deficiencyb. newborns: birth asphyxia, multiple gestations, diabetic motherc. older children: trauma, drowning

3. Pathophysiologya. decrease in amount and/or quality of pulmonary surfactantb. in older children, surfactant may be washed out by drowning or

fluid aspirationc. increased alveolar surface tension

d. impaired gas exchange
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e. increased pulmonary resistancef. hypoperfusion

4. Findings

Findings of Respiratory Distress Syndrome

The transition from respiratory-related to systemic related indicates aprogressive severity of the disease

1. Respiratory relateda. ralesb. expiratory gruntingc. nasal flaringd. retractionse. tachypneaf. apnea

2. Systemic related

a. flaccid bodyb. nonresponsivec. hypotensiond. shock
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a. tachypnea, increased respiratory effortb. paradoxic "seesaw" respirationsc. nasal flaringd. substernal retractionse. expiratory grunt, possible apneaf. cyanosis

g. hypoxia5. Diagnostics

a. physical exam, pulse oximeterb. serum: ABG's, glucose, calciumc. chest radiograph confirmation diffuse pattern over both lung

fields that resembles ground glass6. Management:

a. oxygen therapy (possible mechanical ventilation) and chestphysiotherapy to maintain ventilation and oxygenation

b. medications: possible medications: surfactant, prophylacticantibiotics, diuretics, inotropes, methyl-xanthines

7. Nursing interventions:

a. frequent respiratory assessment.b. maintain acid base balance and tissue perfusionc. electrolyte statusd. suction as indicated

8. Teaching points:a. inform parents about equipmentb. positioning of infantc. need for meticulous care by nurses due to subtle changes

possible in infants oxygenation statusE. Bronchopulmonary dysplasia: (BPD), chronic obstructive lung disorder

1. Etiology - at risk:a. infants requiring oxygen and/or lengthy mechanical ventilation

b. infants surviving RDSc. lung immaturity

2. Pathophysiologya. mechanical ventilation presses lung tissueb. bronchial epithelium is damagedc. products of inflammation introduced, alveolar walls become thick,

fibroticd. continued mechanical ventilation affects the growth of new cells

and paralyzes ciliae. lungs develop cystic areas (sacs) and atelectasis (collapsed

alveoli); mucus moves less3. Findings

a. tachycardia and tachypneab. increased work of breathingc. pallor d. cyanosis with activitye. restlessness

4. Managementa. oxygen (possible mechanical ventilation)b. medications: diuretics, bronchodilators, anti-inflammatory agents

in gradually decreasing amountsc. diet: increased calorie formulas and hydrationd. provide supplemental oxygen at home as needed

5. Nursing interventions:

a. provide rest periodsb. observe for fluid overload or pulmonary edemac. provide age appropriate toysd. frequent respiratory assessment

F. Apnea: cessation of breathing for over 20 seconds1. Etiologies

a. prematurityb. foreign-body aspiration, drowning, or trauma


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c. incorrect positioningd. gastroesophageal refluxe. infectionsf. seizureg. hypoglycemia

2. Pathophysiology: dependent on type of apnea:

a. central - absence of respiratory effort and air movementb. obstructive - respiratory effort but no air movementc. mixed - first central, then obstructive

3. Findingsa. depend on type (above)b. color changes, hypotonia

4. Diagnostics: laboratory tests, chest x-rays, EEG, ECG,pneumocardiography, upper GI series

5. Managementa. home apnea monitoring and basic life support (BLS) training to

familyb. medications: based on type and underlying condition

Respiratory Conditions

G. Upper respiratory tract infections (URI)

1. Etiology: often acute viral nasopharyngitis, or the "common cold"2. Pathophysiology

a. organism invades mucous membranesb. edema, vasodilation and increased mucus productionc. usually self-limiting


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3. Findings: nasal congestion, sneezing, colored nasal discharge, low gradefever, cough, irritability

4. Management:a. medications: antipyretics, decongestants (oral or nasal),

analgesicsb. cool mist humidifier

c. adequate fluidsd. reste. assess for presence of earache (otitis media), temperature over

38.3 degrees Celsius and refusal to eat - may indicatecomplications

H. Sinusitis

1. Etiology: viral, bacterial, URI, obstructive deformities, cystic fibrosis2. Findings

a. cold that does not improveb. chronic nasal congestion, purulent nasal dischargec. headached. tenderness over sinus arease. halitosis

3. Diagnostics: sinus x-rays, CT4. Management

a. medications1. antibiotics2. antipyretics3. analgesics4. decongestants5. antihistamines

5. Nursing carea. monitor respirationsb. warm mist (possible)


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I. Acute pharyngitis1. Etiology: streptococcus (bacterial); or viral (often accompanies tonsillitis)2. Findings

a. bacteriali. "sicker" with sudden onsetii. very sore throat

iii. high fever iv. headache

b. virali. gradual onsetii. fever iii. cough, rhinitis

3. Diagnosticsa. throat cultureb. rapid strep

4. Managementa. medications: penicillin for strep, possible antipyretics and

analgesics

5. Nursing interventionsa. monitor for complications such as acute rheumatic fever and acute

glomerulonephritisb. monitor fluid intakec. moisture compress to neck cold or warmd. cool liquids or ice chips

J. Tonsillitis1. Etiology: bacterial, viral in association with pharyngitis2. Pathophysiology: infection and inflammation enlarge tonsils; as airway

narrows, it hinders swallowing and breathinga. palatine tonsils usually visible during oral examb. pharyngeal tonsils are also known as the adenoids

3. Findingsa. "kissing tonsils"b. sore throatc. halitosisd. mouth breathing; snores at nighte. fever

4. Diagnostics: history, physical exam, throat culture5. Management

a. supportive: antibiotics, fluids, rest, antipyretics, analgesicsb. surgery: tonsillectomy done after 3 episodes of tonsillitis in one

yearc. adenoidectomy may be done with tonsillectomy, if adenoiditis is

present.6. Nursing interventions

a. assess for frequent swallowing bleeding may be the causeb. assess any vomitusc. place child on sided. medicate for pain as needede. avoid fluids with red or brown colorf. soft foods avoid highly seasoned food

7. Teaching points: teach parentsa. child needs quiet activityb. monitor for bleedingc. antipyretics and analgesics no ASA

d. soft foods as throat is very soreK. Croup syndromes (including laryngitis, tracheitis, epiglottitis)
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Similarities and Differences of Diseases Included in the Croup Syndromes

1. Definition: several airway-blocking infections, common in children

a. signs of croupi. inspiratory stridorii. harsh/brassy cough, barking coughiii. hoarse voice


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iv. respiratory distressb. types, by primary area affected:

i. subglottal area: acute spasmodic croup, laryngitis,laryngotracheobronchitis (LTB), tracheitis

ii. supraglottal area: epiglottitis

2. Etiologya. usually viralb. occasionally bacterial (tracheitis, epiglottitis)

c. younger children with "true croup" (spasmodic croup)d. older children with tracheitis and epiglottitis

3. Pathophysiology: mucosa inflamed; edema narrows the airway4. Findings

a. classic: "barky" harsh cough, stridor, hoarseness,fever, purulentsecretions, dyspnea if severe

b. bacterial: child looks "sicker"c. epiglottitis manifests the four "D's"

i. droolingii. dysphagia (difficulty swallowing)iii. dysphonia (hoarse voice)iv. distressed inspiratory efforts

5. Managementa. viral

i. cool air/mist; fluidsii. if inpatient, nebulized racemic epinephrine and inhaled

steroidsiii. antipyretics

b. bacterial: same as above with antibiotics, possible intubationc. epiglottitis is a medical emergency; tracheotomy may be

necessary6. Nursing interventions

a. teach parent and child signs of impending airway obstructionb. report increased pulse, respirations, retractions, increased

restlessnessc. never attempt to directly visualize epiglottis with tongue depressor;

it could precipitate laryngospasm


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Lower Airway Disorders

L. Bronchiolitis: acute infection at bronchiolar level1. Etiology

a. viral: RSV (respiratory syncytial virus) most commonb. occasionally bacterial

2. Pathophysiologya. virus spreads via direct contactb. enters body via nose or eyec. leads to edema, mucus accumulation and cellular debris which

obstruct bronchioles

d. can progress to atelectasis3. Findings - infection is rare in children older than 2 years of age

a. usually mild URIb. sneezing, productive cough, low-grade fever, rhinorrhea (nasal

discharge), adventitious lung soundsc. otitis media and conjunctivitis may also be present

4. Diagnostics: history, RSV/viral nasal washing, chest x-ray

5. Management depends on severitya. mild: fluids, humidification, rest

b. severe: hospitalization, antiviral, IV fluids, possiblybronchodilators, steroids and mechanical ventilation. Maintaincontact secretion precautions

c. prophylaxis: respiratory syncytial virus immune globulin in highrisk infants

6. Nursing interventionsa. admit each child to single room or with other RSV infected

childrenb. teach handwashing and use of contact precautionsc. assess fluid volume status

7. Teaching pointsa. check immunization schedule. RSV IVIG may interfere with

immune response. No vaccines for 9 months after child receivesthese

M. Pneumonia: inflammation of lung parenchyma


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1. Etiology: usually classified by anatomic distribution or pathogena. most commonly viralb. sometimes bacterialc. sometimes aspiration of foreign substance

2. Pathophysiologya. triggers terminal airways, alveoli infiltrate and cell destruction

b. cellular debris falls into lumenc. bacterial agent can reach circulatory system via pulmonary

lymphaticsd. may occur as a complication of another illness

3. Findingsa. can be abrupt or insidious

b. adventitious lung sounds, fever, malaise, nonproductive cough,restless, lethargic

c. progressing to more severe with retractions, respiratory distress,productive cough

4. Diagnosticsa. increased WBC - chest x-Ray reveals consolidation in lungs or

presence of fluid5. Management - depends on type

a. viral - oxygen, chest physiotherapy, fluidsb. bacterial - antibiotics, oxygen, chest physiotherapy, fluidsc. aspiration - supportive therapy, treatment of secondary

complication riskd. administer pneumococcal vaccine to at risk individuals

6. Nursing interventionsa. frequent assessment of respiratory statusb. cool mist tent - change clothing frequentlyc. cluster nursing care

N. Aspiration of foreign body

1. Etiology: child aspirates solids, liquids, vegetative matter into airpassages, most common in older infants and children up to three years ofage

2. Pathophysiology: most substances become lodged in bronchi, andseverity is determined by location, substance aspirated and extent ofobstruction

3. Findings: sudden coughing, gagging, wheezing, cyanosis, dyspnea, andstridor

4. Diagnostics: chest x-ray, fluoroscopy, bronchoscopy5. Management: direct laryngoscopy or bronchoscopy to remove object,

then supportive therapy6. Nursing interventions

a. recognize signs of FB aspirationb. administer back blows or Heimlich maneuver as indicated

7. Teaching pointsa. parents need to know most likely causes to prevent aspiration

1. peanut butter2. balloons3. aluminum tabs from soda cans4. paper clips

O. Long-term respiratory dysfunction: asthma/reactive airway disease1. Definition: chronic inflammatory disorder of the airways, manifested by

periods of exacerbations and remissions; has an allergic component2. Etiology

a. genetic predispositionb. triggers are: allergens, infection, stress, exercise, medical

conditions, medications.c. types: intrinsic, extrinsic, occupational


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3. Pathophysiology

a. trigger leads to an immediate phase reaction (cell activated, withmast cell, eosinophils and histamine released with other mediatorsof inflammation)

b. resulting in bronchoconstriction with additional granulocyteresponse with more inflammatory presence


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c. later phase reaction (additional inflammation andhyperresponsiveness)

d. bronchospasm and obstruction cause most symptoms4. Findings

a. classic: hacking cough, wheeze on expirations, dyspneab. cough may be nonproductive at first, to productive with mucus

c. change in LOC, restlessness5. Diagnostics

a. physical exam, history

b. pulmonary function tests (PFT)c. bronchodilator treatments, chest x-ray, skin testing, CBC with

differentiald. allergy testing

6. Managementa. goals: normal growth and development, patent airway, good

controlb. preventive: allergen control and avoidancec. use of peak flow meter

d. medications1. long term control (preventor) medications: to achieve and

maintain control of inflammation; also called controllers1. corticosteroids - anti-inflammatory2. cromolyn sodium - nonsteroidal anti-inflammatory3. nedocromil - anti-allergic and anti-inflammatory4. long acting beta adregenics (Albuterol) used for

acute exacerbations5. methylxanthines (theophylline) bronchodilator6. leukotriene modifiers (Zileuton) - mediator of

inflammation2. quick relief (rescue) medications to treat acute symptoms

and exacerbations1. short acting beta adrenergics2. anticholinergics3. systemic corticosteroids

7. Acute managementa. use of bronchodilatorsb. steroids (inhaled, IV and/or oral)c. oxygen, IV fluids, possibility of intubation

8. Nursing Interventionsa. monitor child for respiratory distress and/or need for nebulizer

treatments.b. place semi-high Fowlers position

c. stay with child if at all possible - have parent stay during acutephase of illness

d. monitor fluid volume status9. Teaching points

a. child and family must comply with medications and treatmentsb. correct use of metered-dose inhaler (MDI) with a spacerc. risks include overuse of bronchodilators

10. Complicationsa. exercise-induced bronchospasm acute and reversible, usually

stop in 20-30 minutesb. status asthmaticus emergency situation

P. Cystic fibrosis

1. Definition: inherited autosomal recessive trait - abnormal mucus secretionand obstruction

2. Etiologya. genetic originb. basic defect exocrine gland dysfunction

3. Pathophysiologya. mucous glands produce a thick mucoprotein that accumulates

instead of a thin freely flowing secretion


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b. affects respiratory, gastrointestinal and reproductive systems4. Findings

a. gastrointestinal1. meconium ileus2. steatorrhea3. prolapse of rectum

4. failure to growb. respiratory

1. thick tenacious mucus causes patchy atelectasis cough2. barrel-shaped chest3. clubbing of fingers and toes

5. Diagnostics

a. sweat chloride test - iontophoresis - Pilocarpine over 60 mEq/L isdiagnostic of CF

b. chest x-ray: patchy atelectasisc. stool analysis

6. Managementa. CPT

b. medications: bronchodilators, antibiotics (Pseudomonasaeruginosa - Cepacia, and staph aureus)

c. D-Nase - decreases viscosity of mucusd. enzymes administered with meals and snacks to replace

pancreatic enzymes7. Nursing interventions

a. high protein, high caloric well balanced diet, vitamins ADEKshould be added

b. frequent hospitalizations to treat respiratory infectionsc. monitor IV fluids

III. Pediatric Neurology

III. Pediatric Neurology

A. General concepts:1. Assessment of cerebral function:2. Children under 2 unable to respond to directions3. Infants primarily reflexive4. Observe spontaneous and elicited reflex responses having parent

present may be helpful5. Include family history and health history6. Know stage of growth and development and developmental milestones

B. Increased intracranial pressure (ICP)


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a. CAT Scan MRI5. Management

a. principle of maintaining cerebral perfusion pressure (CPP), whichequals mean arterial blood pressure minus ICP

b. medications: osmotic diuretics, antihypertensives, anti-seizure,fentanyl, Versed and Vecuronium may be added

c. maintain patient airway: mechanical ventilation, oxygend. in severe cases, ICP monitor ventricular tap may be required to

relieve accumulated CSFe. minimize external stimuli

6. Nursing interventions:a. observe/monitor LOC, pupillary reaction and vital signs/neuro

signsb. pain management should be monitoredc. nutrition may require tube feeding if long termd. positioning HOB is elevated 15-30 degrees head is maintained

in midline.e. cluster care to allow periods of rest

f. may not bathe child if ICP is unstableg. may need artificial tearsh. support family

C. Hydrocephalus - imbalance in the production and absorption of CSF in theventricles

1. Etiology: congenital, acquired, or idiopathic2. Pathophysiology: depends on type

a. communicating: impaired absorption of CSF within thesubarachoid space

b. noncommunicating: obstruction of the flow of CSF through theventricular system

3. Findingsa. changes from baseline neurological status, and often same as

increased ICP


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b. infant (signs of increased intracranial pressure)I. bulging fontanels, increased head circumference

II. "setting sun" eyes, pupils slow to constrict to lightIII. eats poorlyIV. high-pitched cryV. variable pulse, changes in respirations

c. older child (signs of increased intracranial pressure)I. headaches

II. dizzinessIII. vomiting

IV. diplopia

V. ataxia4. Diagnostics:

a. CT SCAN MRII. sedation may be required

5. Managementa. surgical placement of ventriculoperitoneal (VP) shunt in neonates,

infants and older children placed on unoperated side to prevent

pressure on operative siteb. monitor for increased intracranial pressurec. measure head circumferenced. no scalp vein IV lines

6. Nursing interventions:a. neuro and vital signsb. assess pain level acetaminophen with or without codeinec. observe for abdominal distention for possible catheter

complicationsd. NPO feed after bowel sounds returne. monitor fluid volume statusf. monitor head circumference

g. keep diaper off perineal dressing7. Teaching points

a. teach family signs of infectionI. elevated temperature

II. poor feedingIII. irritabilityIV. altered level of consciousness

b. home careI. no contact sports

II. child should be as active as possible.8. Complications: shunt infection and malfunction

D. Seizures

1. Definition: brief malfunctions of the brain's electrical system that resultfrom cortical neuronal discharge

2. Etiology: cerebral, biochemical, post-traumatic, febrile, idiopathic, mostcommon neurologic dysfunction in children

3. Pathophysiologya. trigger electrical discharges affecting nearby normal cellsb. spreads throughout brain reaching midbrain reticular regionsc. possible generalized seizure with neurological symptoms

4. Findingsa. determined by site of originb. may include altered levels of consciousness, involuntary

movements and changes in perception

c. seizure may be a finite event, with limited manifestationsd. may have an aurae. status epilepticus is continuous seizure lasting more than 30

minutes or a series of seizures from which the child does notregain a premorbid level of consciousness

f. febrile seizures: occur in association with a fever, usually greaterthan 38.8 degrees Celsius (101.8 degrees Fahrenheit)
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g. may be nonrecurrent (acute) such as febrile episode or recurrent(chronic) such as epilepsy

5. Diagnostics goal is to ascertain the type and cause of seizure.a. detailed and accurate historyb. physical exam to include neurological assessmentc. CBC glucose level

d. skull films, CT- MRI EEGE. Epilepsy

1. Definition: chronic seizure disorder with recurrent and unprovokedseizures

2. Etiology: unknown. international classification: partial and generalizeda. partial: limited to a particular local area of the brain

I. most commonI. simple partial with motor signs

II. simple partial with sensory signsIII. complex partial with psychomotor seizures

b. generalized: involves both hemispheres of the brainI. most common

I. tonic-clonic (grand mal)II. absence (petit mal)

3. Pathophysiology: see seizures4. Diagnostics: toxicology screen, ABGs, electrolytes, anticonvulsant drug

level, possible lumbar puncture

5. Management: see seizure precautions, seizure care, postictal carea. supportive:

I. airway suction and oxygenII. safety loosen clothing, place on floor, clear area, and

remove restrictive clothing

b. medications antiepileptic drugs6. Nursing interventions

a. observe seizure protect from injuryI. order of onset

II. movementIII. faceIV. eyesV. respirations


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VI. incontinence of urine or stoolVII. durationVIII. do not restrain

b. assess postictal statusc. stay with child until fully conscious

7. Teaching points

a. long-term care medication regimeb. child can participate in most activities for agec. assess trigger factors -possibly video games with flashing lights if

sensitiveF. Neural tube defects (NTDs)

1. Anencephaly - degeneration of the brain to a spongy form mass with nobony covering

a. most seriousb. both cerebral hemispheres are absentc. condition is incompatible with life beyond a few days

2. Spina bifida (SB)a. etiology: incomplete closure of vertebrae and neural tube;

unknown causeb. pathophysiology

I. spina bifida occulta: defect not visible externallyII. spina bifida cystica: visible defect with an external sack-like

protrusionI. meningocele: encases meninges and spinal fluid

but no neural elements; no neurological deficitII. meningomyelocele: contains meninges, spinal fluid,

and nerves; varying neurological deficit

c. findings vary widely to degree of spinal defect - the higher thelocation the more symptoms the infant will have.

d. diagnostics:I. physical exam

II. MRI ultrasound CT- myelographyIII. WBC

e. nursing interventionsI. initial care

I. protect sac from rupturing and drying outII. assess for presence of latex allergyIII. moist sterile nonadherent dressing usually salineIV. fluidsV. no diaper VI. positioning on abdomen

VII. ROMVIII. early surgical closure of lesionIX. avoid rectal temperatures

II. long termI. protect skin integrity

II. maintain bladder and bowel functionIII. support musculoskeletal integrity

f. teaching pointsI. teach parents how to measure head circumference after

closureII. may require VP shuntIII. findings of infection

G. Cerebral palsy (CP)1. Etiology

a. disorders characterized by early onset and impaired movementand posture; non-progressive - missed developmental milestones

b. cause: abnormality in extrapyramidal or pyramidal motor system(cortex, basal ganglia, cerebellum)

c. can occur prenatally, perinatally, or postnatally


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d. may be accompanied by perceptual problems, language deficitsand intellectual involvement

e. usually diagnosed by exclusion2. Pathophysiology

a. classifications: athetoid, spastic, ataxic, mixed

b. associated defects: mental retardation and cognitive impairment,hearing or visual losses, attention deficit disorder (ADD)

c. high metabolic rate, leading to increased calorie expenditure

3. Findingsa. primary disturbances: abnormal muscle tone and coordinationb. spastic movement in one or more extremity

c. athetoid movementsd. primitive reflexes persiste. disturbances in gait, abnormal posturef. impairments in speech and swallowing

4. Diagnostics: physical exam, EEG, CT, MRI5. Management

a. establish locomotion, communication and self-helpb. gain optimal appearance and functionc. correct associated problems as effectively as possible

d. promote socialization6. Nursing interventions

a. early recognition- assess children at riskb. treat what child demonstratesc. ROMd. teach ADL- dressing, feeding, walkinge. incorporate play into treatment plan

7. Teaching pointsa. multi-disciplinary approachb. speech training is begun earlyc. long term problem and a financial concernd. offer support for family resources

H. Down syndrome (trisomy 21)1. Etiology: extra group G chromosome, chromosome 21. Associated with

late maternal age2. Pathophysiology: depends on which region of chromosome 21 was

altereda. distinctive facial featuresb. heart defects

Classification of Cerebral Palsy

1. Athetoid Characterized by slow irregular twisting snakelike movements occurring in the

upper extremities Involuntary movement of oral muscles which may result in drooling and dysarthria

2. Spasticity May involve either one or both sides Impaired fine and gross motor skills Individual's attempts at motion increase the abnormal posturing and overflow of

motion to other parts of body

Hypertonic movements3. Ataxic

Rapid repetitive movements performed poorly Poor integration of movements when individual reaches

4. Mixed Combination of athetosis and spaticity
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c. mental retardation (varies from severe retardation to low averageintelligence)

d. dermatologic changese. incomplete embryogenesis

3. Findingsa. facial features

I. brachycephalyII. flat occiputIII. protruding tongueIV. high-arch palateV. almond shaped eyesVI. low slung ears

b. body featuresI. short, broad hands with simian crease

II. short, broad neckIII. dry skinIV. large space between great toe and second toe

4. Diagnosticsa. physical examsb. chromosome analysis

5. Managementa. supportive: specific to body system affectedb. promotion of developmental progressc. cognitive

6. Nursing interventionsa. treat what the child exhibitsb. assess sight and hearingc. allow extra time when giving instructionsd. support family

7. Teaching pointsa. genetic counselingb. long-term disorderc. financial referrals

Infectious Neurological Disorders

I. Guillain-Barre syndrome - infectious demyelinating polyneuritis1. Etiology: unknown - possible sequela to microbial infection or

administration of vaccines2. Pathophysiology

a. an unknown factor inflames spinal and cranial nervesb. inflammation compresses and demyelinates nerves


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c. nerves conduct impulses poorly resulting in paralysis of musclesinnervated by involved nerves

d. ascending flaccid paralysis3. Findings

a. preceded by mild influenza-like illness or sore throatb. gradual progression of symptoms

i. acute - onset of findingsii. plateau findings remain constantiii. recovery begins to improve and progress to complete

recovery, usually 2 to 3 weeks after onset.c. muscle tenderness, paresthesia usually ascend from feet/legs

upward progressing to total paralysis4. Diagnostics:

a. physical assessment

b. CSF analysisc. EMG findings acute muscle denervation

5. Managementa. short term: supportive and symptomaticb. based on physiologic needs and body system affected: possible

tracheostomy, ventilatory support, IV fluids and plasmapheresisc. long-term: integumentary, musculoskeletal and respiratory

systemsd. medications: IV immunoglobulin and steroids, possible

immunosuppressive agents6. Nursing interventions:

a. assess for progress of disease especially swallowing and

breathingb. neuro and vital signsc. assess skin integrityd. may require tube feedingse. maintain Foleyf. ROMg. support child and family

7. Teaching points


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a. multi-disciplinary approachb. long-term processc. may have residual disability

J. Botulism - acute flaccid paralysis1. Etiology

a. food poisoning from anaerobic bacillus: clostridium botulisum

contaminated foodb. three types: infantile, classic, wound

2. Findingsa. CNS findings usually appear within 12 to 36 hoursb. blurred vision, diplopia, lethargy, vomiting and dysphagia,

weakness, difficulty speaking, life threatening progressiverespiratory paralysis

3. Managementa. supportive: dependent on body system affectedb. protect ventilation, respiration, and provide nutritionc. medications

i. botulism antitoxin

4. Nursing interventionsa. observe for and report signs of neuromuscular weaknessb. child will tire easilyc. assess for swallowing difficulties

5. Teaching pointsa. child must rest during recoveryb. normal bowel elimination may not return for a while; no enemas or

cathartics

K. Reye's syndrome (toxic encephalopathy)1. Etiology: follows a common viral illness, drugs (salicylate association),

toxins, genetics2. Pathophysiology

a. acute noninflammatory encephalopathy and hepatopathy3. Findings

a. related to cerebral edema and fatty changes in liverb. viral upper respiratory infectionc. fever d. severe nausea and vomiting


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e. profoundly impaired consciousnessf. liver dysfunctiong. coma

4. Diagnostics: liver biopsya. ammonia levelsb. possible lumbar puncture

5. Managementa. supportive: dependent on body system affected

b. avoid aspirin and other salicylates in children with viral diseasessuch as influenza orvaricella disease

6. Nursing interventionsa. assess children at riskb. continuously monitor affected childc. neuro and vital signsd. assess IV lines, Foleye. may have N/G tubef. monitor fluid volume status

7. Teaching points

a. keep parents informed about status and equipment.

Traumatic Neurological Conditions

L. Head trauma1. Etiology: force to the scalp, skull, meninges or brain usual causative

agents are falls, motor vehicle crashes and bicycles2. Pathophysiology: elastic pliable skill of infant and young child absorbs

much of direct energya. directly related to force of impact and secondary forces

i. acceleration injury

ii. deceleration injuryb. types: primary and secondaryc. cerebral function depends on oxygen, glucose and blood flow to

brain; cerebral edema and hypoxia can occur quickly3. Findings: neurological status depends on ICP

a. may or may not be consciousb. irritablec. paled. vomitinge. sleepyf. LOC may be alteredg. pupils may be affected

4. Diagnostics: assess for pre-existing disorders, take history of event, CATSCAN, MRI, EEG

5. Management

a. acute

i. control ICP: medications: sedating agents, steroids, anti-convulsants, ventilatory support, positioning, HOB up 30once cervical spine injury is ruled out

ii. long-term rehabilitation possible6. Complications: hemorrhage, infection, cerebral edema and brainstem

herniation through the tentorium

7. Nursing interventions

a. neuro and vital signsb. monitor ICPc. maintain seizure precautionsd. quiet environmente. assess LOCf. level of comfort


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g. observe for rhinorrhea, otorrhea and test for glucose if drainagepresent

8. Teaching points

a. long-term processb. keep parents informed and teach about the equipment

c. teach parent to talk to child but dont ask them to do things like"squeeze my hand"

M. Meningitis: acute inflammation of the meninges and CNS1. Etiology: can be caused by pneumococcal or meningococcal bacteria

(most serious) or can be caused by a virus.2. Pathophysiology: most common route of infection by vascular

dissemination from an infection elsewherea. organisms then spread into CSF and throughout subarachnoid

spaceb. infective process

i. inflammationii. exudate

iii. WBC accumulationiv. tissue damagev. brain becomes hyperemic and edematous

3. Findingsa. fever b. chillsc. headached. vomitinge. LOC alterationsf. irritableg. nuchal rigidityh. positive Kernig and Brudzinski signs

4. Diagnosticsa. lumbar puncture: definitive diagnostic tool, CSF is tested for gram

stain, blood cell count and presence of glucose and proteincontent

b. sedation of child may be required. Versed, Demerol or Fentanylmay be used

5. Management: treated as bacterial until causative agent is identifieda. bacterial meningitis is an emergencyb. respiratory isolation precautions until causative agent identifiedc. medications: antibiotics

6. Nursing interventionsa. monitor fluid status - IV fluids

b. monitor electrolytesc. neuro and vital signsd. maintain quiet environmente. monitor for seizuresf. assess peripheral vascular collapse if causative agent is

meningococci7. Teaching points

a. immunizations are available to prevent several types

IV. Pediatric EndocrinologyV. The endocrine system

A. Three types of tissues

1. cells that send chemical message via hormones2. target cells in end organ that receive chemical message3. environment: medium through which chemical message travels from the

site of synthesis to area of cellular actionB. Endocrine function

1. endocrine + autonomic systems = neuroendocrine system2. neuroendocrine system: synthesizes and releases chemical substances

that then regulate bodily function: messages are carried by nerve


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b. after puberty, child will be the same as peers

D. SIADH: syndrome of inappropriate antidiuretic hormone1. Definition: hypersecretion of antidiuretic hormone or ADH (vasopressin)2. Etiology: infections, head trauma, or brain tumors3. Pathophysiology

a. kidneys reabsorb too much free water

b. decreased urine output, increased specific gravity (SG), anddecreased serum sodium

4. Findingsa. urine SG > 1.030b. anorexia, nausea, weakness, stomach crampsc. increased weight (edema)d. decreased serum sodium - under 120 mEq/L child becomes

symptomatic - lower sodium levels cause neurological findings5. Management

a. restrict fluids to correct hyponatremiab. correct underlying etiologyc. monitor I & O, electrolytes, neuro status

d. observe for signs of fluid overload6. Nursing Interventions:

a. assess patients at risk for early identificationb. I & O daily weightsc. monitor for signs of fluid overloadd. seizure precautions if sodium level low

E. Hypothyroidism1. Definition: deficiency of thyroid hormone (TH); common childhood

endocrine disorder2. Etiology

a. congenital or acquired deficiency in thyroid hormonesb. thyroid irradiation

3. Pathophysiologya. absent or underdeveloped glandb. decreased triiodothyronine (T3) or thyroxine (T4)

4. Findings: depend on extent of dysfunction and age of child at onseta. lethargy, constipation, feeding problemsb. hypotonia, large tonguec. dry skin, weight gain, puffy eyes, sparse haird. intolerance to colde. slowed growth, developmental delay and/or retardation if T4 low at

birth and thyroid replacement not startedf. if findings develop after two to three years, when brain has grown,

no mental retardation

5. Diagnosticsa. history and physicalb. increased TSHc. decreased serum T3 and T4d. anemiae. decreased BMR (basal metabolic rate)f. increased cholesterol and triglyceridesg. hypoglycemia

6. Managementa. lifelong hormone replacement (levothyroxine)b. restc. protect client from cold

7. Nursing interventionsa. assess children at risk.b. monitor administration of replacement hormone cant be

increased too fastc. allow rest periods or cluster cared. encourage child to exercise when able

8. Teaching pointsa. life-long problem


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b. child needs periodic blood tests to monitor hormone levels.

F. Hyperthyroid: "Graves' disease"1. Definition: hypersecretion of thyroid hormones, causing increased BMR or

hyperactivity of thyroid gland2. Etiology: auto-immune response to TSH (thyroid-stimulating hormone)

receptors; idiopathic; familial

3. Findingsa. increases in: BMR, appetite, nervousness, heart rateb. gradual weight loss despite voracious appetitec. lowered tolerance to heatd. exophthalmos (eyes bulge)

e. myopathyf. personality changes, poor school performance, mood instabilityg. linear growth and bone age acceleratedh. insomniai. increased blood pressure

4. Diagnosticsa. history and physical

b. palpable thyroid enlargement (goiter)c. elevated serum T3 and T4 levelsd. elevated radioactive iodine uptakee. presence of thyroid antibodiesf. decreased TSH levels

5. Managementa. antithyroid therapy - Propylthiouracil or Tapazole to decrease

amount of circulating thyroid hormoneb. surgery (subtotal thyroidectomy) check voice quality after

surgery.6. Nursing interventions

a. assess behavior patterns before and after medication

b. quiet non-stimulating environmentc. administer moisturizing eye drops for child with exophthalmosd. provide nutrition appropriate for activity levele. establish a routine with child and parents

7. Teaching pointsa. side effects of propylthiouracil -sore throat and feverb. child may need to reduce activities for a while

8. Concern: thyrotoxicosis or thyroid storm from sudden release ofhormone: from vigorous palpation or surgery

a. can be a life threatening situationb. findings

1. acute onset of severe irritability

2. vomiting3. diarrhea4. hyperthermia5. hypertension6. tachycardia7. prostration

c. treat with cooling blanketd. propranolol (Inderal), potassium iodine (thyro-block)e. antithyroid drugs

G. Diabetes mellitus - type 11. Definition: deficiency of hormone insulin - most common endocrine

disorder of childhood.

2. Etiology: genetic, auto-immune response; usually with trigger factors ofvirus, bacterium or possible chemical irritant

3. Pathophysiology

a. trigger directs islet cell antibodies against cell surfacesb. antibodies destroy the insulin-secreting Beta cellsc. less insulin means glucose is blocked from entering the cells - the

concentration in bloodstream increases (hyperglycemia)


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d. when glucose level exceeds kidney's threshold (about 180 mg/dl)kidney then "spills" glucose into urine (glycosuria)

e. producing osmotic diureses (polyuria)f. starved for glucoseg. urinary fluid loss causes excessive thirst (polydipsia)

4. Findings

a. hyperglycemia1. the three "polys" of diabetes: polydipsia, polyuria,

polyphagia2. additional findings: fatigue, hunger, weight loss, enuresis

5. Diagnosticsa. fasting blood glucoseb. oral glucose tolerance testc. urine tests for presence of ketones and/or glucosed. glycosylated hemoglobin (A1c) reflects average blood glucose

levels for past 2 to 3 months6. Management

a. medications: insulin (rapid-acting-Lispro, short-acting - regular,

intermediate-acting-NPH). Insulin needs are affected by foodintake, exercise, emotions, growth spurts and illness

b. other: diet, age appropriate activity levels. No special foods - needsufficient calories. Must eat snacks - and meals at the same timeeach day.

c. self-blood glucose monitoringd. insulin pump delivers insulin continuously

7. Concerns: "honeymoon period" and insulin regulation, compliance, sickday management, ketones

8. Complicationsa. DKA (diabetic ketoacidosis) or extreme hyperglycemia (blood

sugar >350 mg/dl)

1. etiology: not enough or no insulin - body chooses alternatesource of energy - fat

2. findings1. fruity breath, decreased level of consciousness2. nausea/vomiting, abdominal pain3. 10 percent dehydration4. increased urine output5. Kussmaul's respirations6. metabolic acidosis

b. management1. place on cardiac monitor2. regular insulin (IV drips and then subcutaneous)

3. frequent monitoring of blood glucose4. frequent monitoring of electrolytes; neuro checks

9. Hypoglycemiaa. etiology: most common cause of insulin therapy and bursts of

physical activity, without additional food or with missed meals -before meals or when insulin is peaking

b. findings1. fatigue2. nervousness3. pallor 4. sweating5. palpitations

6. hunger7. loss of coordination8. seizures9. coma

c. management1. 10 to 15 mg f simple carbohydrate - honey of low fat milk2. followed by complex carbohydrate such as slice of bread

or crackers


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3. occasionally glucagons is prescribed - for home treatment -works in about 10 minutes

10. Nursing interventionsa. assess child frequently neuro and vital signsb. blood glucose levelsc. administer insulin as ordered

d. support child familye. arrange meetings with team members - dietary, PT, and social

worker11. Teaching points

a. family may be overwhelmed with diagnosisb. use teaching aids to facilitate their success - booklets, videosc. illness managementd. insulin should never be omittede. dose may changef. fluid balance is a concern

V. Pediatric Gastrointestinal


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A. Dehydration

1. Definition: occurs when total output of fluid exceeds total intakea. 60% of fluid lost from extracellular fluid (ECF)

b. 40% of fluid lost from intracellular (ICF)c. insensible fluid loss lost through skin, urinary loss, fecal loss,

and respiratory tract2. Differences compared to adults

a. are less able to concentrate urineb. as infants, they have immature kidney and immune regulatory

systemsc. have a higher metabolic rated. have more body surface in relation to body masse. because more of body weight is fluid, children need more fluid and

lose more urine per kilogram of body weight3. Types of dehydration (serum sodium determines type)

a. isotonic: occurs in conditions in which electrolyte and waterdeficits occur in balanced proportions. Primary form of dehydrationin children.

b. hypotonic: occurs in conditions in which electrolyte deficit exceedsthe water deficit

c. hypertonic: occurs in conditions in which water loss exceedselectrolyte loss

4. Pathophysiology


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a. decreased fluids and electrolytes from ECFb. leads to eventual loss of fluid from ICFc. cellular dysfunction, shock

5. Nursing interventionsa. fluid losses must be replacedb. monitor urine output and specific gravity, daily weight

c. fontanels in infantd. electrolyte losses: monitor sodium, potassium, chloride, calciume. acid-base balance disturbance: metabolic acidosis

6. Findings of dehydration

7. Management of pediatric dehydrationa. monitor the 4 first signs and 3 second signs of dehydrationb. administer fluids (oral, NG, IV)

2. Vomiting7. Definition: forceful ejection of gastric contents through the mouth8. Etiology: infection, obstruction, allergy, psychological causes, motion

sickness, neurologic lesions, and inflammatory process9. Pathophysiology

a. cause stimulates emetic center of brainb. mechanism of vomiting involves autonomic nervous system

1. salivation, sweating2. pallor, increased heart rate3. contraction of stomach antrum & duodenum

c. types of vomiting: regurgitation, forceful, projectile10. Management

a. detect and treat the underlying causeb. prevent dehydration, electrolyte loss and acid-base disturbancec. provide anti-emetic medications if needed

11. Nursing interventionsa. assess vomitusb. assess child for dehydrationc. keep child NPOd. position child to avoid aspiration when vomitinge. monitor electrolytesf. encourage child to brush teeth or rinse mouth after vomiting

12. Teaching pointsa. teach parents to start feeding child slowly with clear fluids when

tolerated


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Upper GI Disorders

C. Tracheoesophageal fistula (TEF) and esophageal atresia (EA)1. Definition: failure of esophagus to develop as a continuous passage and

a failure of the trachea and esophagus to separate into distinct structures2. Etiology: congenital, idiopathic, VATER syndrome (combination of

vertebral, anorectal, and renal abnormalities in addition to TEF)3. Pathophysiology: most common

a. TEF proximal esophageal segment terminates in a blind pouchb. distal segment is connected to trachea or primary bronchus

4. Findingsa. coughingb. cyanosis with feedsc. increased oral secretionsd. depend on type of defecte. choking

5. Diagnostics: history, chest and abdominal x-rays6. Management

a. pre-op: airway patency, NPO, IV therapy, place in position leastlikely to cause aspiration

b. prevention of aspiration pneumoniac. surgical emergency

7. Nursing interventionsa. assess each newborn for the malformationb. intermittent suctioningc. position - head of crib elevated 30 degreesd. care of gastrostomy tubee. tube feedings are begun when toleratedf. observe initial oral feeding sterile water

8. Teaching points

a. teach parents the care of the gastrostomy tube and how toadminister feedings

b. findings of respiratory distressc. suctioning techniques if appropriate

D. Gastroesophageal reflux disease: GERD


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1. Definition: transfer of gastric contents in the esophagus2. Etiology: physiological. functional, pathologic very common If GERD

occurs often and findings persist, treat it hiatal hernia and coughing maylead to GERD

3. Diagnostics: history, barium swallow, upper GI series, esophageal pH,manometry studies, endoscopy, scintigraphy detects radioactivematerial in esophagus after feeding of the material and also assessesgastric emptying

4. Managementa. depends on the severity of findingsb. none if child is thriving without findingsc. diet: thicken feeds, decrease caffeine intake, acid foods and

solutions, give small, more frequent feeds with frequent burpingd. position: prone with head of bed elevated or flat prone following

feeding and at night

e. medications H2-receptor antagonists (Tagamet or Pepcid),

proton pump inhibitors (Nexium or Protonix)f. surgery: Nissen fundoplication

5. Nursing interventionsa. monitor feeding position and feeding toleranceb. monitor nutritional statusc. check I & Od. monitor electrolyte levels

6. Teaching pointsa. teach parents to have child avoid caffeine, chocolate, and spicy

foodsb. older children should avoid tobacco and alcoholc. medication administration schedule should be followed to receive

optimal benefitE. Pyloric stenosis

1. Definition: circumferential muscle of the pyloric sphincter becomesthickened resulting in elongation and narrowing of the pyloric channel

2. Etiologya. unknown causeb. hypertrophy, hyperplasia of circular muscles of pylorus

3. Pathophysiologya. trigger irritates mucoid lining of pylorus; edemab. narrowed pylorus resists passing of fluid; chymec. pylorus then enlarges and contracts with more force to attempt

gastric emptying

d. slowly pylorus constricts, and resistance persists until next cycle4. Findings

a. usually begins at two to four weeks of ageb. progressive, projectile, nonbilious vomiting after eating

c. metabolic alkalosisd. movable, palpable, firm, olive-shaped mass in right upper

abdominal quadrante. irritability, crying, hunger

5. Diagnostics: history, abdominal x-ray, upper GI, ultrasound, electrolytes6. Management

a. pre-op: IV fluids, NPO, surgery (pyloromyotomy) also calledFredet-Ramstedt Procedure

b. post-op: small, frequent feedings initially, gradually increasing7. Nursing interventions

a. pre-op1. monitor IV fluids and electrolyte replacement2. document vomiting episodes and stools3. access patency of N/G tube if present4. position child flat or head slightly elevated

b. post-op
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7. Teaching pointsa. dietary modificationsb. bowel routine

G. Diarrhea1. Etiologies: intestinal infections (bacterial, viral, parasitic); food intolerance;

overfeeding; medications; stress; malabsorption; colon disease

2. Pathophysiology:a. causative factor - irritates mucosal liningb. damages microvilli, increases secretion and decreases absorptionc. abnormal intestinal water and electrolyte transportd. increased intestinal water permeability and dehydration in younger

children.

e. possible metabolic acidosisf. can be acute or chronic

3. Findingsa. dehydration (mild, moderate, severe)b. increased stoolingc. increased heart & respiratory rate

d. dry hot skine. dry mucous membranesf. decreased urine, decreased tearing in infants

4. Managementa. goals: restore fluid and electrolyte balance and return bowel to

normal functioningb. fluids: oral rehydration or parenteral rehydrationc. medications: antibiotics, antidiarrheals

H. Celiac disease

1. Definition: gluten-sensitive enteropathy (GSE) = (celiac sprue)2. Etiology: absorption problem with genetic predisposition, possibly immune

abnormality

3. Pathophysiologya. inability to digest gliadin (byproduct of gluten); permanent

intolerance of glutenb. increasing levels of glutamine in the small intestine, toxic to

mucosal cellsc. atrophy of villi and decreased absorptive surface

d. malabsorption of fats, carbohydrates, vitamins and electrolytes


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e. gluten is found in the grain of wheat, barley, rye, and oats4. Findings (most often appears between ages of one and five years)

a. diarrhea (stools: pale and watery, offensive odor)b. abdominal distentionc. failure to thrived. vomiting

e. muscle wastingf. steatorrheag. anorexiah. abdominal pain

5. Diagnosticsa. history (symptoms occur three to six months after infant begins

eating grains)b. serum anti-gliadin antibody (AGA)c. jejunal biopsy - reveals mucosal inflammation, villous atrophy and

crypt hyperplasiad. serologic testing to detect antibodies

6. Management

a. diet: gluten-free with vitamin supplementsb. crisis: IV fluids, steroids

7. Nursing interventionsa. monitor tolerance of new diet weight gainb. monitor episodes of diarrheac. assess for steatorrhead. provide diet high in calories fruits, vegetables low fat

8. Teaching pointsa. gluten free diet restrictionsb. reading food labels

I. Intussusception1. Definition: one of the most frequent causes of intestinal obstruction

between ages of three months and five years2. Etiology: unknown possible hypertrophic response to the virus; is

common in children with cystic fibrosis3. Pathophysiology

a. trigger bowel (proximal segment) telescopes inside itselfcausing obstruction

b. pressure on bowel leads to bleedingc. possible mesenteric ischemiad. edema and possible bowel necrosis, perforation, peritonitis, or

shocke. most common site: ileocecal valve

4. Findings

a. sudden acute abdominal painb. bilious vomitingc. currant jelly stoolsd. sausage-shaped abdominal masse. lethargy

5. Diagnostics: barium enema abdominal x-ray, rectal exam revealsmucus and blood

6. Managementa. priority goal: restore bowel to normal position and function quickly,

and stabilize fluidsb. non-surgical hydrostatic reduction - barium, water-soluble

contrast, air pressure

c. if not successful, surgery7. Nursing interventions

a. monitor fluid statusb. assess painc. monitor for barium excretion and passage of brown stool that

indicates intussusception has resolvedd. usually post operative care if child has surgery

8. Teaching points


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a. parents may feel guilty they didnt know about childs conditionb. everything moves fastc. child may need hospitalization

J. Hirschsprung's disease1. Definition / etiology: congenital aganglionic megacolon2. Pathophysiology

a. absence of autonomic (parasympathetic) ganglion cells, usually atrectum and part of large intestine

b. intestine does not propel stoolc. stool builds up; colon dilates, constipation results with risk of

intestinal rupture3. Findings

a. newborn: failure to pass stool or merconium in first 24 hours oflife, reluctance to ingest fluids, bile-stained vomitus, distendedabdomen, "ribbon-like" stools - flat, wide, and wavy

b. later: failure to thrive, distended abdomen, constipation, signs offecal impaction

4. Diagnostics: history and physical exam, radiographic barium enema,

rectal biopsy, anorectal manometry reveals absence of ganglion cells5. Management

a. surgical correction: remove aganglionic portionb. temporary ostomy for three to six months, then reanastomose

6. Nursing interventionsa. assess fluid and electrolyte statusb. monitor comfort levelc. assess colostomyd. provide nutrition as orderede. assess N/Gf. make referrals for home care assistance

7. Teaching points

a. colostomy care as child will be dischargedb. parents should be told that toilet training may be difficult

K. Appendicitis

1. Definition: inflammation of vermiform appendix (blind sac at end ofcecum)


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2. Etiologya. virus, hardened fecal material, parasites, foreign bodyb. most common in school-aged children

3. Pathophysiologya. trigger obstruction increased mucus accumulationb. distention, capillary occlusion and engorgement of capillary walls

c. eventually, abscesses and fistula formd. possible perforation leading to peritonitis

4. Findingsa. colicky abdominal pain

1. generalized but usually localizes to lower right quadrant

2. most intense pain at McBurney's pointb. nausea, vomitingc. possible fever and chillsd. decreased bowel soundse. guarding of abdomen - stooped posturef. rebound tenderness

5. Diagnostics: physical exam, laboratory tests (CBC with WBC), MRI,

possible also C Reactive Protein (CRP)a. may order HCG serum human gonadotropin on adolescent

females to rule out ectopic pregnancy6. Management

a. surgical removal (open or laparoscopic)b. IV fluidsc. antibioticsd. analgesics

7. Nursing interventionsa. postoperative

1. monitor IV fluids comfort level2. position in semi Fowlers

3. check drainage tubes if present4. prevent fluids as bowel sounds return if ordered

8. Teaching pointsa. activity level at homeb. when can return to school, if knownc. caution: do not give enemas or cathartics or use heating pad if

suspected appendicitis


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VI. Genitourinary System

A. Common findngs: renal and urinary tract (UT) disorders

Renal Findings:

-Urination (polyuria, oliguria, urgency)-Fluids (increased BP, Edema)

UT Findings:

-2 Clusters G-I (Anorexia, Nausea/vomiting, Thirst/dehydration, Failure to thrive)

-Lower Body (Abdominal & back pain, Painful or frequenturination, Persistent diaper rash)

B. Urinary tract infection

1. Definitiona. bacteria in urine and inflammatory responseb. may involve any structure in urinary system: kidney

(pyelonephritis), ureters, bladder (cystitis) or urethrac. findings will point to locationd. peak age: toddler to preschool age

2. Etiologya. bacterial (E. coli. - 80% of cases), structural defect, physiological


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b. extrinsic (example: Foley catheter, medications)c. improper perineal hygiene

3. Pathophysiologya. organism usually ascends through urethra to bladderb. with a structural defect, urine flows back from ureters into kidney

4. Findings often depend on age

a. under two years: often nonspecific resembling GI disturbancei. failure to thrive, feeding problems, nausea/vomitingii. dysuria, persistent diaper rash, abdominal distention

b. over two yearsi. enuresis, daytime incontinence in toilet-trained, foul

smelling urineii. frequency and urgency, dysuriaiii. possible pyelonephritis: similar signs but with fever, back

pain, and lethargy5. Diagnostics: urine culture and serum testing, radiographic testing6. Management

a. antimicrobials

b. antipyreticsc. analgesicsd. fluids (IV and oral)

7. Nursing interventionsa. careful historyb. check diaper every half-hourc. provide adequate or increased fluid intaked. monitor for irritability

8. Teaching pointsa. hygiene wipe front to back for girlsb. do not delay urinationc. if child is maintained on daily low dose antibiotics giving dose at

bedtime allows medications to remain in bladder overnightC. Enuresis

1. Definition: inability to control bladder functions, often due to maturation;nocturnal, or "bed wetting" very common

2. Etiologya. primary: never dry at night, and due to CNS or psychological

reasonsb. secondary: child has been toilet trained and becomes incontinent

againi. findings as aboveii. due to infection, medications, trauma

3. Diagnostics: history, urine tests, serum culture

4. Managementa. primary

i. have the child participate in activitiesii. limit fluid at night, void before bedtimeiii. imagery, behavioral conditioning - bladder trainingiv. medications

1. tricyclic antidepressant; imipramine (Tofranil)2. desmopressin (DDAVP)

b. secondary: treat underlying cause5. Nursing interventions

a. help parents understand problem and treatment planb. involve child in planning, if age appropriate

6. Teaching pointsa. do not punish child if enuresis occurs

Upper Urinary Tract Disorders

D. Vesicourethral reflux (VUR)1. Definition: retrograde flow of bladder urine into the ureters during voiding2. Etiology


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a. primary (congenital anomaly) - abnormal insertion of ureters intobladder

b. secondary (acquired, usually associated with UTI)3. Pathophysiology

a. bladder refluxb. residual urine from ureters remains in bladder until next void

c. increases chance for and perpetuates infectiond. vesicoureteral reflux grading system: grade 1 to 5

4. Findings: UTI with chronic findings and recurrences5. Diagnostics

a. radiographic studiesb. voiding cystourethrogramc. urine culture

6. Managementa. medications: for grades 1 to 4, low-dose antibiotics; monitorb. surgery: for severe cases, grade 4 or grade 5

7. Nursing interventionsa. adequate or increased fluid intake

b. usual post-op care if child has surgeryc. monitor I & O

8. Teaching pointsa. all children in family should be screened for possible reflux

E. Acute glomerulonephritis (AGN)1. Definition: immune complex disease that occurs after a streptococcal

infection (A B-hemolytic strep)2. Etiology

a. previous acute bacterial infection (pharyngitis, impetigo)b. underlying systemic disorder

3. Pathophysiologya. infection (usually group a b-hemolytic strep) provokes immune

complex responseb. immune complexes trapped in glomerular capillary loopc. activate inflammatory response, which injures capillary wallsd. decrease lumen functions and GFR (glomerular filtration rate)e. decreased filtration of plasma results in excessive acummulation

of water and retention of sodiumf. onset appears after latent period of about ten days

4. Findingsa. oliguriab. edema (periorbital and peripheral)c. hematuria ("smoky" or "tea-colored" urine)d. mild hypertension

e. lethargyf. moderate proteinuriag. loss of appetite

5. Diagnostics: urine testing, serum (antibody, complement, CRP, ESR,WBC), throat culture, history of antecedent strep infection

6. Managementa. no specific treatments; recovery spontanteous and uneventful in

most casesb. supportive with careful regulation of fluid balance; I & O, daily

weightsc. medications: antihypertensives, if neededd. nutrition (low in sodium, protein, potassium)

7. Nursing interventionsa. monitor vital signs, fluid balance, and behaviorb. assess childs appearance presence of edemac. possible institution of seizure precautions if indicatedd. possible fluid restrictione. provide frequent rest periods

8. Teaching pointsa. importance of finishing medications as ordered


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b. findings of recurrenceF. Chronic nephrosis (nephrotic syndrome)

1. Definition: massive proteinuria, hypoalbuminemia, hyperlipemia andedema

2. Etiology: not fully understood - possibly renal lesions or other processesa. types

1. primary (idiopathic nephrosis): restricted to glomerularinjury

2. secondary: develops as part of systemic illness3. Pathophysiology: mainly occurs in children between 2 and 7 years-old

a. glomerular alteration and increased permeability toplasmaproteins, especially albumin

b. plasma protein losses; increased presence in urine, decreaseplasma volume, colloidal osmotic pressure in capillariesdecreases

c. hydrostatic pressure is greater than colloidal osmotic pressureresulting in fluid accumulation in interstitial spaces and bodycavities

d. shift in plasma fluid leads to hypovolemiae. hypovolemia - triggers kidneys to produce renin, and angiotensin

which stimulates the release of aldosterone and increases thereabsorbtion of water and sodium

f. aldosterone increasesg. decreased blood pressure also causes release of ADH leading to

increase in water absorption4. Findings

a. progressive weight gainb. puffiness of facec. generalized edema (insidious)d. periorbital edema

e. loss of appetitef. oliguria - urine smoky brown (resembles tea or cola)g. lethargyh. pallor

5. Diagnostics: history, urine tests will show massive proteinuria, BUN andcreatinine will be elevated, and antistreptolysin O(ASO) titer

6. Management mainly supportive of what child demonstratesa. diet: no added salt but high in potassium and proteinb. medications: corticosteroids, immunosuppressants, diuretics

7. Nursing interventionsa. monitor vital signs and body weight and I&Ob. assess volume and character of urine

c. restrict fluid intaked. seizure precautions if appropriatee. activity should increase as protein in the urine decreasesf. place child in semi-Fowlers or Fowlers to treat periorbital edema

8. Teaching pointsa. how to test urine at home for presence of proteinb. dietary restrictionsc. findings of infection

G. Wilms tumor1. Definition: most common renal and intraabdominal tumor of childhood2. Etiology: probably arises from malignant undifferentiated cluster of cells

favors left kidney

3. Pathophysiologya. cells regenerate an abdominal structure renal function is

impaired4. Findings

a. abdominal mass or swelling firm, nontenderb. fatigue, malaisec. respiratory findings if metastasis

5. Diagnostics


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a. chest and abdominal x-raysb. laboratory tests CBC

6. Managementa. surgical removal possible chemotherapy, actinomycin D and

radiation7. Nursing interventions

a. pre-op - post signs on bed "do not palpate abdomen"b. post-op - assess BP, urine output and pulmonary status

8. Teaching pointsa. support familyb. child should avoid contact sportsc. findings of infection

H. Hemolytic uremic syndrome (HUS)1. Definition: most common acquired renal failure in children

a. acute disorder shows the "triad"1. hemolytic anemia

2. thrombocytopenia3. acute renal failure

b. occurs most often in children under four2. Etiology: unknown; some association with genetics, endotoxins, bacteria

(E. coli., rickettsia, coxsackie), enzyme deficiency, decreasedantioxidants

3. Pathophysiologya. usually follows an acute GI or upper respiratory infection (URI)b. pathogen attaches to GU tractc. GU tract produces toxins that damage capillary wallsd. inflammation - glomerular vessels less capable of filtratione. anemia occurs (due to RBC fragmentation)f. thrombocytopenia (due to platelets trapped in small vessels)

4. Findings

a. prior URIb. rapid onset of pallorc. accompanying hemorrhagic manifestations such as bruising or

rectal bleedingd. triade. hypertension

5. Diagnostics: identify "triad" from history and lab testing6. Management

a. supportiveb. for anemia: transfusions fresh frozen plasma (FFP)c. for renal symptoms: fluids, possible dialysis or peritoneal dialysis

for the child who has been anuric for 24 hours

d. treatment of hypertensione. correction of electrolyte disorders

7. Nursing interventionsa. monitor vital signsb. monitor I&Oc. prepare for dialysisd. monitor laboratory resultse. monitor transfusion response

8. Teaching pointsa. possible renal impairmentb. keep parents informed of treatment plan as everything happens

quickly

I. Acute renal failure1. Definition: sudden, severe loss of function of kidneys, usually reversible2. Etiologies

a. dehydrationb. underlying conditionsc. burns (thermal injuries)d. obstructione. infection


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3. Pathophysiologya. severe reduction in glomerular rateb. an elevated BUNc. decreased tubular reabsorption of sodium from the proximal

tubuled. increase in sodium in distal tubules stimulated renin mechanism

e. decrease renal blood flowf. cortical and tubular necrosis

4. Findingsa. usually related to imbalances in fluids and electrolytesb. often nonspecific (edema, hypertension, decreased feeding,

anorexia, lethargy, pallor, seizures)c. oliguria

5. Diagnosticsa. historyb. I & Oc. laboratory testingd. radiographic (ultrasound, renal scan)

6. Managementa. treatment directed at

1. correcting underlying cause2. managing complications3. supportive therapy

b. acute: fluids, electrolytes, dialysis (peritoneal, hemodialysis),antihypertensives, diuretics

7. Nursing interventionsa. monitor level of dehydration and volume restoration to avoid water

intoxication and hyponatremiab. insert Foleyc. monitor laboratory results

d. assess potassium in food and fluide. monitor vital signs especially blood pressuref. neuro signs, if appropriate

8. Teaching pointsa. nutritional needs and appropriate snacksb. include parents when formulating plan of carec. possible complications: acute and chronic renal damage, infection

and cardiac failureJ. Chronic renal failure (CRF)

1. Definition: progressive deterioration of kidneys so that they can no longermaintain normal chemical structure of body fluids under normal conditions

2. Etiology: immunological injury, congenital anomalies, underlying

disease/condition3. Pathophysiology: irreversible and permanent

a. progressive nephron destructionb. distribution throughout nephron - uremia (urea in blood)c. final stage: end-stage renal disease (ESRD) is irreversible

4. Findingsa. failure to thrive, anorexia, nausea and vomitingb. fluid and electrolyte imbalancesc. hypertension, uremia, anemia, bleeding tendenciesd. increased fatigue on exertione. skin: sallow, muddy appearance

5. Diagnostics: history, physical exam, laboratory testing, radiographic

studies6. Management

a. dialysisb. kidney transplantc. diet: modified (decreased sodium, potassium, phosphorus,

protein; fluid restriction, high calcium)

d. medications: antihypertensives, diuretics, erythropoietin, growthhormone, immunosuppressants (post transplant)


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e. monitor status (for example, laboratory reports)f. give psychological support

7. Nursing interventionsa. monitor body fluid volume and electrolyte balanceb. monitor vital signs, especially blood pressurec. monitor ABGs for metabolic acidosis

d. monitor rate of growth and developmente. assess for findings of infectionf. prepare child and parents for possible dialysis and/or

transplantation8. Teaching points

a. signs of rejection of new kidneyb. need to follow treatment plan and take medications as ordered

9. Concerns: bone demineralization, anemia, failure to thrive, retention ofwastes; transplant concern

Genitalia Problems

K. Cryptorchidism1. Definition: failure of one or both testes to descend normally through

inguinal canal into scrotum2. Etiology/pathophysiology

a. abnormal testes, orb. decrease in the hormonal stimulation necessary for descent

3. Management: wait up to one year for descent, medications (HCG) toassist in descent (older child), or surgery (orchiopexy).

L. Hypospadius1. Definition: urethral meatus below normal placement on glans penis or

anywhere along ventral (underside) surface of penile shaft2. Etiology: idiopathic - related to genetics, environment, hormonal

3. Pathophysiology: incomplete development in utero4. Management: surgical correction (with urinary catheter and stents post-

op), post-op pressure dressing must not be removed by anyone otherthan the health care provider, usually repaired before child goes to school

5. Concerns: stenosis, chordee, body image/self esteemM. Bladder exstrophy

1. Definition: externalization of bladder, splaying at the urethra with failure oftubular formation and diastasis of pelvic bone

2. Etiology: congenital - associated with genital abnormalities3. Pathophysiology

a. failure of abdominal wall and underlying structures, including theventral wall of the bladder, to fuse in utero

b. bladder develops outsidec. the earlier in gestation, the more severe the defect

d. defect almost always associated with epispadias4. Management

a. treament objectives1. preservation of renal function2. attainment of urinary control3. adequate reconstructive repair4. preservation of optimum sexual function

b. pre-op1. prevent organs from drying out, fluids, infection control2. surgery: staged procedure

c. post-op (antibiotics, compression bandage, bed rest)5. Concerns: urinary incontinence, VUR, infection

N. Ambiguous genitalia1. Etiology: abnormalities in chromosomal complement, embryogenesis, or

hormones2. Pathophysiology: interruption in normal development around seven to

eight weeks gestation, when normally male begins differentiating fromfemale


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3. Diagnostics: history, physical exam, tests to determine gender(endoscopy, ultrasound, radiographic contract), genetics lab test,laparotomy, biopsy

4. Concerns: body image/self esteem, family support

VII. Pediatric Musculoskeletal System


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General Concepts:

A. Children's musculoskeletal differences1. Bones are more pliable and porous; bend, buckle, absorb shock2. Tendons and ligaments are more flexible

3. Bones produce callus that speeds healing4. Thicker periosteum, so stronger and more active osteogenesis5. Skull is pliable during infancy; anterior fontanel fuses at 18 months;

posterior fontanel fuses at two months

6. Skeletal maturation completes when epiphysis fuses with diaphysis,which is usually 18 to 21 years of age

B. Immobilization in children1. Affects multiple systems

1. muscular, GI, GU, pulmonary, cardiovascular, integumentary2. psychologic, behavioral, economic

2. Affects normal growth and development3. Pathologic changes occur due to

1. decreased muscle strength and mass, decreased metabolism2. possible bone demineralization3. decreased range of motion and decreased joint movement

4. Concerns1. hydration2. dietary modification3. activity as condition permits4. self care as condition permits
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