Health alterations 2015

Child development and impact of hospitalization

Page references

Psychosocial development Erikson stages

 Trust vs. mistrust (birth to 1 year)
 Autonomy vs. shame and doubt (1-3 years)
 Initative vs. guilt (3-6 years)
 Industry vs. inferiority (6-12 years)
 Identity vs. role confusion (12-18 years)

Infancy (birth – 1 year)

 Period of rapid change in systems
 Physical development
o Wide variation
o Height ( by 50% in first 6 months, then ½ inch monthly)
o Weight (doubles by 5 months, triples by 1 year)
o First tooth by 8 months
o Language development and socialization begin (cooing, touching face)
o Play is integral in socialization (look at face, mirrors, interaction)
Erikson: infant
 Erikson: trust vs. mistrust (birth to 1 year)
 Achieving this task is based on the quality of the caregiver-infant relationship and the
care received by the infant. Need to be constant, reliable
 Trust is developed by meeting comfort, feeding, stimulation, and caring needs.
 Mistrust develops if needs are inadequately or inconsistently met, or if needs are
continuously met before being vocalized by the infant. (want baby to self regulate, self
soothing)

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Maintaining health
 Nutrition (breast feeding first year, at 6 months solid foods, bland foods, no fruit and
veggies first has sugar and they love it)
 Sleep and rest (q2-3 hours)
 Dental hygiene (8 months first tooth, dentist at age 1 or 6 months after first tooth, use
wet cloth to clean gums)
 Immunization/SIDS (differs from province to province) (baby sleep in parents’ room first
6 months, NOT IN BED WITH PARENTS) dummy helps with SIDS
 Injury prevention (ingestion, burns, falls)

Toddlerhood (1-3)
 Period of developing independence
 Physical development
o Growth rate slows in 2nd year
o Steady growth pattern
o Food intake decreases (too busy)
o All teeth present by 33 months
Erikson:
 Erikson: autonomy vs. shame and doubt
 Independence is paramount for toddlers, who are attempting to do everything for
themselves.
 Toddlers often use negativism, or negative responses, as they begin to express their
independence. (let them pick out their own cloths, putting on clothes, brushing teeth)
 Maintaining routines and reliability, provides a sense of comfort for toddlers as they
begin to explore the environment beyond those most familiar to them.
Maintaining health
 Nutrition (picky, they decide what they want, should be eating the same as the rest of
the family, finger foods, choking)
 Sleep and activity (11-12 hours and a nap, they wake up afraid)
 Dental health (dentists q6 months)
 Injury prevention (MVA’s car seat not in right, Drowning, burns)

Preschool (3-5)
 Period of slow and steady change
 Physical development
o Height  by 2.5-3 inches/year
o Weight ( by 3-5 lbs. per year {average 32 lbs at 3 yrs, 41 lbs at 5 years})
 Phycological development
o More social development
o Language
o Play

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Erikson
 Erikson: initiative vs. guilt
 Preschoolers become energetic learners, despite not having all of the physical abilities
necessary to be successful at everything.
 Guilt can occur when preschoolers believe they have misbehaved or when they are
unable to accomplish a task. (make up their own game and rules)
 Guiding preschoolers to attempt activities within their capabilities while setting limits is
appropriate.
Maintaining health
 Nutrition: outside influences
 Sleep and activity (need around 12 hours, out growing naps, awake up frequently
because their social)
 Dental health: primary teeth
 Injury prevention (MVAs, ATVs, bicycle injury) buckle it up
 Kids at this age imitate us.

School age (6-12)

Physical development
 Pubertal changes
 Maturation of systems
Psychological Development
 Efficient vocabulary
 Play is structured (best friends)
Erikson:
 Erikson: industry vs. inferiority
 A sense of industry is achieved through the development of skills and knowledge that
allows the child to provide meaningful contributions to society.
 A sense of accomplishment is gained through the ability to cooperate and compete with
others.
 Children should be challenged with tasks that need to be accomplished and be allowed
to work through individual differences in order to complete the tasks.
 Creating systems that reward successful mastery of skills and tasks can create a sense of
inferiority in children unable to complete the tasks or acquire the skills.
 Children should be taught that not everyone will master every skill
 Self esteem, going to be good at one thing and not at another.
Maintaining health
 Nutrition ( balanced diet, parents don’t really know what they are eating. Outside
influences)
 Sleep and activity (individualized)
 Exercise (not have to encourage a lot)
 Dental health (regular q6months, high risk of cavities)
 Injury prevention (MVA need booster seat, drowning) most injuries happen at home or
school
Adolescence (12-19)

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Physical development
 Period of rapid change and growth spurts
 Development of secondary sex characteristics
Erikson
 Erikson: identity vs. role confusion
 Adolescents often try different roles and experiences to develop a sense of personal
identity and come to view themselves as unique individuals.
 Group identity: Adolescents become part of a peer group that greatly influences
behavior.
Health issues and concerns
 Parenting/family adjustment
 Psychosocial adjustment (going through puberty
 Intentional(self harm)/unintentional injury (MVA)
 Sexual behavior (teaching teens how to be safe), STI’s, pregnancy
 Substance abuse (teaching them, they are going to try things)
 Depression, suicide (screening and asking from help)
 Physical, sexual, emotional abuse (if you suspect it report it, see certain injuries that
could be abuse, if they are being abused at higher risk of used substances)
Maintaining health
 Nutrition (greatest need, increase ca for bone growth)
 Sleep and rest (sleep deprived need at least 9 hours of sleep)
 Exercise (not getting enough exercise don’t need to do gym)
 Dental hygiene (don’t have time)
 Injury prevention (MVA but this time they are the driver remember they don’t have the
fast reaction time. Depression STI eating disorders)

Impact of illness and hospitalization

 Period of stress/crisis for child and family
 Change of routine and roles of you as a parent
 Challenges coping mechanisms

The hospitalized child may be faced with:

 Unfamiliar surroundings
 Unfamiliar routine
 Unfamiliar caregivers
 Feelings of fear
 Perception of disease/illness
 Pain ****** Erikson stages
 What do they know about their illness, what is happening?

Children’s reactions are influenced by:

 Age

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 Developmental level
 Previous experience (if they been before)
 Innate coping skills
 Diagnosis
 Support systems parents stay

There are four common stressors

 Separation
 Loss of control
 Bodily injury
 Pain****
Each of these stressors are experienced differently, depending on the
developmental level of the child.

Separation anxiety
Common in 6-30 month olds and involved known phases: some parents can’t stay all the time
while the child is in the hospital
 Protest (if parents say I have to go, hanging on to parent)
 Despair (parent gone, sad mom and dad left me, no concept of time. Inactive,
depression may not talk to nurse. May deteriorate because they are do sad.
 Detachment (parents may come back but will start to talk to nurse.)
 If toddler: they may try to escape to find mom and dad. Know where child is.
Nursing interventions
 Minimize separation
 Primary nursing: having the same nurse
 Rooming-in: having parents stay the whole time
 Support parents: hard having child in hospital
 Establish daily routine: when do you normally give child bath, keep routine as normal as
possible
 Provide continuity from home
Loss of control
 Increases the perception of threat: depends on what is going on,
 Influenced by physical restriction, altered routines, and dependency
 Toddler:Potty trained may have accidents, cling to mom and dad.
 Preschool: use words they know. BP: ‘gonna feel big bear hug’
 School age: going to get board, give them something to do.
 Teens: want info, they are smart, they look at body language. Want to know who can
relate to them

Bodily injury and pian

 Infants...facial expression (before 6 months don’t remember pain) give sugar water or
skin to skin for putting in iv

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 Toddlers…grimace, rocking, aggression (spit in their face, pinch and bite, kick. Less
invasive the bigger the reaction with toddler. Giving a needle tell them its going to hurt.
 Preschoolers….threat of bodily injury (afraid youre going to do something) after giving
needle there is a pinhole, they think they are going to bleed out, watch what you say)
respond to distraction
 School-age…need factual info (be honest with them, they are brave ones in front of their
friends, they can tell you where something hurts, burns vs aching
 Adolescents…threat to body image, stand out from the peer group. They will asks
questions, body langue matching what your saying. Privacy. They think nurses know
everything and they think you know that they are in pain, they don’t need to tell you

Parental reactions to hospitalization

Parents are influenced by:
 Seriousness of the illness/injury/disease
 Previous experiences
 Support systems
 Previous coping abilities
 Additional stressors
 Cultural/religious beliefs
 Familial relationships/roles
 Major stressor to have child in hospital

Parental reactions ranges of reactions… understand where the emotions are coming from
 Disbelief
 Anger
 Guilt (mothers will blame themselves)
 Fear
 Frustration
 Depression

Sibling reactions (this depends on if the sibling is younger or older

 Loneliness
 Fear
 Worry
 Anger *****
 Resentment *****
 Jealously ***** getting all the attention
 Guilt *****

“Normalizing” the Hospital Environment

 Promote freedom of achievement
 Maintain child’s routine, if possible
 Time structuring (do things at same times)

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 Self-care (age appropriate)

 Schoolwork (they have teachers at the janeway)
 Friends and visitors (sleepovers if possible)

Beneficial Effects of Hospitalization

 Recovery from illness
 Increase coping skills
 Master stress and feel competent in coping
 New socialization experiences

Development: neural tube defects

Development: the sequence of physical, psychosocial and cognitive development changes that
take place over the human lifespan
 Occurs as a simultaneous, ongoing interrelationship with three aspects of change:
o Growth

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o Differentiation
o Maturation
 It is a complex process, gradual changes that occur across multiple domains, results in an
individuals functional abilities.
 Increase in complexity, predictable sequence.
 Continues over the lifespan.
 State of health, environment, life experiences may alter development (stagnate,
regress).
 The concept of development has implications for nursing practice across all population
groups and health care settings.

Development and Interrelated Concepts

Neural tube defects

 -Abnormalities that derive from the embryonic neural tube
 -Failure of closure of neural tube
 -4-6 weeks of pregnancy
 -Any part of neural tube may be involved
 Largest group of congenital anomalies
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 Normally the spinal cord and cauda are encased in a protective sheath of bone and
meninges.
 May involve entire length of the neural tube or a small portion
 Incidence
o 4.1 in every 10 000 births

Pathophysiology of NTDs
 Failure of the neural tube to close during the embryo’s early development (3 to 5 weeks)
 Multifactorial etiology
 Genetic mutation in the folate pathways
 Additional factors
o Maternal obesity
o Maternal diabetes mellitus
o Low B12 status
o Maternal hyperthermia
o Use of antiepileptic drugs (AEDs) in pregnancy

Types of NTDs
 Cranioschisis
 Exencephaly
 Anencephaly
 Encephalocele
 Rachischisis or spina bifida
 Meningocele and myelomeningocele

Prevention of NTDs
 -Treatment = prevention
o -Folic acid supplementation: 0.4 mg/day
o -If history of neural tube defects: 4 mg/day
o -Folic acid fortification of food has resulted in decreased incidence.
o -Begin folic acid supplementation at preconception
o -Will prevent 50 to 70% of all cases of NTD

Spina bifida
 Failure of osseous spine to close
 Two types:
1. Spina bifida occulta: not visible externally
2. Spina bifida cystica: visible defect, has a saclike protrusion
 Congenital neural tube defect that affects head and spinal column

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 Most common developmental disorder of the CNS

 Malformation of neural tube can occur anywhere along the spine
 1/ 2000 births

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Spina Bifida Occulta

 -Skin indicators (absent, singly, or in combination)
o Skin depression or dimple
o -Port-wine angiomatous nevus
o -Tufts of dark hair
o -Soft subcutaneous lipomas
Spina Bifida Cystica
 Definition: visible defect with external saclike protrusion
 Two types
o Meningocele
o Myelomeningocele

Meningocele
 Sac contains meninges and spinal fluid but no neural elements
 No neurological deficits
Myelomeningocele
 Neural tube fails to close
 May be anywhere along the spinal column
o Lumbar and lumbosacral areas most common
 May be diagnosed prenatally or at birth
 Sac contains meninges, spinal fluid, and nerves
 Varying and serious degrees of neurological deficit
 Location and magnitude of defect determine nature and extent of impairment
 Not necessarily uniform on both sides of defect

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A: Myelomeningocele with intact sac. B: Myelomeningocele with ruptured sac.

Initial Management of Myelomeningocele

 Prevention of infection
 Assessment of neurological and associated anomalies
 Before surgical closure apply moist nonadherent dressings.
 Inspect sac every 2 to 4 hours.
 Early closure after birth
Nursing care
 Care of myelomeningocele sac
 Prevent complications
 Provide postoperative care
 Support family and educate about home care
 Latex allergy

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Long term management

 Promote mobility
 Promote bowel/bladder function
 Protect skin integrity
 Promote positive self concept/independence
 Monitor for increased ICP

Latex Allergy
 Identified as a serious health hazard when a child with spina bifida experiences
anaphylaxis caused by latex allergy
 Patients with spina bifida are at high risk for latex allergy because of repeated exposure
to latex products from multiple surgeries and repeated urinary catheterizations.
Allergic Reactions to Latex
 -Range from urticaria, wheezing, watery eyes, rash, to anaphylactic shock
 -Reactions tend to increase in severity when latex comes into contact with mucous
membranes, wet skin, the bloodstream, or an airway.
 -Cross-reactions with foods: banana, avocado, kiwi, chestnuts

Cleft lip and Palate cerebral palsy (CP)

Development Review
 reviewed Erikson’s stages of psychosocial development
 We discussed specific risk categories for impaired development
 Introduced the concept of Development and discussed Neural Tube Defects last class

Cleft Lip and/or Cleft Palate

 Facial malformations that occur during embryonic development
 May appear separately or together
 CL- failure of the maxillary and median nasal processes to fuse
 CP- is a midline fissure of the palate that results from failure of the two sides to fuse
 Cleft lip- unliteral or bilateral
 Cleft palate- isolated or associated with cleft lip
 Two of the most common birth defects in Canada

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 Affect 600 newborns every year

 Higher incidence in certain ethnic groups (e.g., indigenous populations)

Etiology
 May be an isolated anomaly or may occur with a recognized syndrome
 May be caused by exposure to teratogens (e.g., alcohol, anticonvulsants, steroids, folic
acid deficiency)
 Genetic and environmental factors (e.g. maternal infection, medications like
antiepileptics)
 Maternal obesity and smoking are possible factors as well

Pathophysiology
 A genetic defect in cell migration that results in a failure of the maxillary and
premaxillary processes to come together between the 3 and 12 week of embryonic
development.
 Often appear together:
o CL and CP are distinct
o Occur at different times
 Merging of the upper lip at the midline is completed between the 7 and 11 weeks of
gestation.
 Fusion of the secondary palate (hard and soft palate) takes place between the 7 and 12
weeks of gestation.
Diagnostic evaluation
 Prenatal Ultrasound
 Apparent at birth: emotional reactions of the parents

Clinical Manifestations
 Recurrent ear infections
 Feeding problems
 Nasal regurgitations during bottle feeding
 Growth retardation
 Misaligned teeth / Poor speech

Nursing Care
 Preoperative care
 Postoperative care
 Long-term care

Feeding Infant With Cleft Lip or Palate

 Issues
 Techniques and interventions

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 Special feeding equipment

 Breastfeeding issues

A: Haberman feeder. B: Mead-Johnson bottle used to feed infant with cleft lip and palate.
C: Pigeon bottle.

Surgical Correction of Cleft Lip

 Closure of lip defect precedes correction of the palate
 Usually preformed at 10 weeks of age (or at 4.5 kg): usually, < 3 months
 Scar massage

Surgical Correction of Cleft Palate

 Typically done at 6 to 12 months of age: before 18 months
 Effect on speech development

Postoperative Care
 Assess for bleeding and respiratory distress
 Ensure adequate hydration/ nutritional support
 Incision site care
 Discharge teaching

Interrelated Concepts
 Development
o Functional Ability
o Family Dynamics
o Culture

Cerebral Palsy (CP)

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 A group of permanent disorders of the development of movement and postures, causing

activity limitations attributed to nonprogressive disturbances that occurred in the
developing fetal or infant brain
 Non-progressive disorder
 Often associated with perceptual, language and intellectual deficits
 Characterized by abnormal muscle tone and coordination
 CP believed to result from existing prenatal brain abnormalities
 15 to 60% of children with CP will also have epilepsy

Etiology of CP
 Prenatal brain abnormalities
o 80% of cases are caused by unknown prenatal factors.
o Intrauterine exposure to chorioamnionitis
o Infants born before 36 weeks have a 100× rate of CP as compared to term
infants.
o Periventricular leukomalacia
o Result of shaken baby syndrome
o Additional factors

Diagnostic Evaluation of CP
 Infants at risk warrant careful assessment during early infancy.
 Neurological examination and history
 Neuroimaging
 Metabolic and genetic testing

Early Warning Signs of CP

 Poor head control and clenched fists after age 3 months
 Stiff or rigid limbs
 Arching back and pushing away
 Floppy tone
 Unable to sit without support at 8 months
 Failure to smile by 3 months
 Lack of interest in surroundings
 Primitive reflexes
 Excessive irritability or crying
 Excessive sleeping
 Lack of interest in surroundings
 Feeding difficulties

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o Frequent gagging or choking with feeds

Types of CP
 Spastic
 Dyskinetic
 Ataxic
 Mixed

Spastic CP
 Hypertonicity
 Persistent primitive reflexes
 Inadequate protective reflexes
 Altered speech quality
 Poor coordination
 Leg scissoring
 Persistent muscle contraction

Dyskenetic/Athetonic CP
 Abnormal, constant, involuntary wormlike movements
 Decreased fine motor skills
 No contractures

Ataxic CP
 Poor equilibrium and muscle coordination
 Unsteady, wide-based gait

Dystonic CP
 Slow, twisting movements of the trunk or extremities
 Drooling, abnormal posture

Dystonic/Mixed CP:
 A combination of spastic and athetonic CP

Clinical Manifestations of CP
 Delay in gross motor development
 Abnormal motor performance
 Alterations in muscle tone
 Abnormal posture
 Reflex abnormalities

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 Associated disabilities

Assessment
 ID high risk infants
 Assess presence of primitive reflexes
 Neurological exam
 Developmental exam

Therapeutic Management
 Surgery to correct deformities
 Medications
 Support nutrition
 Support locomotion/independence
 Optimize motor functioning
 Optimize educational potential
 Prevent complications

Goals of Therapy
 To establish locomotion, communication, and self-help skills
 To gain optimal appearance and integration of motor functions
 To correct associated defects as effectively as possible
 To provide educational opportunities adapted to the child’s capabilities
 To promote socialization experiences

Therapeutic Management
 Ankle foot braces may be worn.
 Orthopedic surgery to correct spastic deformities
 Pharmacological agents to treat pain related to spasms and seizures
 Botulinum toxin A injections
 Dental hygiene
 Physiotherapy, speech therapy, and occupational therapy

Nursing care
 Assist the family in devising and modifying equipment and activities.
 Medication administration
 Safety precautions
 Recreational activities
 Support family

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Nutrition

Gastroesophageal Reflux Disease (GERD)

Regurgitation of stomach contents into esophagus
Predisposing conditions:
 Hiatal hernia
 Incompetent Lower Esophageal Sphincter (LES)
 Impaired esophageal motility
 Decreased gastric emptying
Signs and Symptoms
 Vary from person to person
 Pyrosis
 Wheezing, coughing, dyspnea
 Sore throat
 Choking
 Regurgitation

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Diagnosis
 History and physical
 Endoscopy when patient experiences:
o Dysphagia
o Odynophagia
o Bleeding
o Vomiting
o Weight loss
 Barium swallow
 Esophageal manometry studies
 pH monitoring

Endoscopic procedures
 Inspects internal organs and cavities
 Endoscope – tube with light source
o Rigid
o Flexible
 Before procedure
o Education and consent
o Bleeding disorders
o Prep depends on type of endoscopy
o Baseline labs & Vitals
 Sedation (IV access, resuscitation equipment)

Esophagogastroduodenoscopy (EGD)
 Pre-procedure
o Education & consent
o NPO after MN
o No dentures
o Throat sprayed with xylocaine during procedure & patient sedated
o Monitor labs
 Post-procedure
o *NPO until gag reflex returns* (2-4 hours)
o Sore throat
o Monitor for S/S aspiration
o Vital signs
o Bleeding
o Pain (bloating from air)

Barium swallow

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 Pre-procedure
o NPO at least 8 hrs before
o Assess swallowing ability
 Post
o Monitor elimination – BM to pass contrast material
o Monitor for S/S obstruction
o May need cathartics until stool no longer white

Management of GERD
 Lifestyle modifications: Diet, meds, weight, smoking
 Nutritional therapy: diet, avoid aggravating foods. Small and frequent meals
 Medication therapy
o “step-up “approach:
 Antacids
 H2 receptor blocker
 Proton pump inhibitors (PPI)
o “step down” approach
 PPI
 H2 receptor blocker
 Antacids
 Endoscopic therapy
 Surgical therapy

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Medication review
Antacids
 Tums, Maalox, Mylanta
 Neutralize acid
 When taken on empty stomach – reduce acid for short time
 When taken at onset of distress, after eating – reduce acid for longer
 Wait to take other meds for an hour
H2-receptor blockers
 Ranitidine (Zantac), Famotidine (Pepcid)
 Decrease HCL secretion
 Take with meals
Proton pump inhibitors
 Omeprazole (Losec), Rabeprazole (Pariet), Esomeprazole (Nexium)
 Reduces gastric acid secretion
 Read instructions some 1 hr pre meals (e.g esomeprazole)

Complications of untreated GERD

 Esophagitis
 Dysphagia
 Barrett’s esophagus
 Bronchospasm
 Pneumonia
Hiatal Hernia
 Protrusion of stomach into esophagus through opening in diaphragm
 Two types:
o Sliding – most common
o Para-esophageal – “rolling”
Sliding Esophageal and Para-esophageal Hernia

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Signs and symptoms

 Similar to GERD
 Heartburn after meal
 Dysphagia
 Pain when bending or straining
Diagnosis
 Barium swallow, endoscopy
Treatment
 Same as GERD

Gastritis
 Inflammation of stomach mucosa
 breakdown in normal gastric mucosal barrier
Acute
 Hours to days
Chronic

Causes
 Medications (NSAIDs, digitalis, Corticosteroids)
 Diet (alcohol, spicy, irritating foods)
 H-pylori
 Autoimmune component
 Infections

Signs and symptoms of gastritis

 Acute
o Anorexia
o Nausea & vomiting
o Epigastric tenderness
o Feeling full

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o Hemorrhage
 Chronic
o Same as acute
o Vit B12 deficiency
Diagnosis
 History & physical – drug/alcohol use
 Endoscopy with biopsy
 H-pylori testing
 CBC - anemia
 Stool sample – occult blood

Nursing care
Acute
 Eliminate cause
 Supportive care
o If vomiting occurs:
 Bedrest
 NPO
 IV fluids
 Antiemetics
o CF when symptoms subside
o Drug therapy – reduce irritation of gastric mucosa
Chronic
 Evaluate, eliminate cause
o Stop ETOH, H-pylori treatment
 Non-irritating diet – 6 small meals a day
 No smoking
 B12

Peptic Ulcer Disease (PUD)

 Erosion of mucosal wall
 Acute – superficial erosion, minimal inflammation
 Chronic – long duration, erosion of muscular wall
 Gastric
 Duodenal

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 Stress-related

Causes
 H-pylori infection
 Medications
o ASA
o NSAIDs
o Corticosteroids
 Stress
o Burns
o Sepsis
o Trauma
 Diet: caffeine, spicy foods
 ETOH
 Smoking

Signs & Symptoms

 Common to have no symptoms
 Pain
 Weight loss
 Bleeding
o Hematemesis (gastric)

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o Melena (duodenal
 Duodenal
o Burning, cramp
o Occur for weeks-months then may disappear for a time
o 2-4 hours after a meal
 Gastric
o Burning, gaseous pain
o 1-2 hours after meals
 Stress related ulcers
o Acute ulcers after major event

Diagnostic Tests
 Endoscopy
 H-pylori testing
 Barium studies
 Labs
o CBC
o Urinalysis
o Liver enzymes
o Amylase
o Stools

H-Pylori Testing
Non-invasive
 Serum blood tests (IgG)
 Urea breath test
 Stool test
Invasive
 Biopsy of stomach (endoscopic procedure)

Interprofessional Care – PUD

Conservative therapy
 Rest
 Bland diet
 No smoking
 Medications

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o H2 receptor blockers, PPI, antibiotics, Antacids, anticholinergics, cytoprotective

 Stress reduction
Acute
 IV fluids
 NPO
 NG to suction – if complications experienced

H-pylori Treatment
Triple Therapy 7-14 days (first line therapy)
 PPI (proton pump inhibitors) (Prilosec/omeprazole)
 Amoxicillin
 Biaxin (clarithromycin)

Complications of PUD
 Hemorrhage
 Perforation
o Sudden, severe abdominal pain
o Rigid abdomen
o Shallow, rapid resps
o Peritonitis occurs
 Gastric Outlet Obstruction
o Narrowing (scar tissue, inflammation)
o Abdominal discomfort
o Projectile vomiting
o Loud, visible peristalsis
Nursing care
 History & physical – prevent and detect
 Rest
 Diet modifications (may be NPO during acute exacerbation)
o If NPO – NG, intake/output, fluid replacement, mouth care
 Drug therapy
 No smoking
 Long term follow up and care
 Physical & emotional rest

Nutrition
Celiac disease
 Also called gluten-induced enteropathy, gluten-sensitive enteropathy and celiac sprue
 Absence of enzyme in mucosa of small intestine
 Decreased absorptive capacity of intestine, especially foods containing the gluten of
wheat, rye, oats and barley

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Clinical manifestations
 Steatorrhea, diarrhea
 Abdominal distention (and pain)
 Nausea, vomiting, constipation
 Anorexia, FTT (growth failure)
 Muscle wasting
 Headaches
 Brain fog
 Rashes
 Joint pain or numbness (bone pain)
 S/S usually develop at 1-2 yrs of age
 Range of severity of malabsorption

Diagnosis
 Mucosal biopsy
 Symptomatic improvement after initiation of gluten-free diet, return with gluten
challenge
 Lab: fat in stool, anemia, hypoalbuminemia, low serum vitamin D, A, Ca, prolonged
prothrombin time

Therapeutic management
 Dietician
 Gluten-free diet
 Supplemental vitamins and iron
 Encourage corn, rice, soy, potato flour, fresh fruit
 Education of parents

Birthday party
 Cake
 Cookies
 Chips
 Candy
 Chicken Nuggets
 Pizza

Iron deficiency anemia

 Most common type of childhood anemia
 Most common nutritional deficiency in children
 Results from inadequate supply of iron

Etiology and Pathophysiology

 Occurs as a result of blood loss, poor nutritional intake, rapid growth

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 Inadequate iron supply - smaller RBC’s, ↓ quantity of Hgb, ↓ oxygen-carrying capacity

of the blood
 Body stores of iron ↓

Caused by inadequate supply of dietary iron

 Indigenous populations
 Low birth weight, premature infants
 Adolescents are at risk because of rapid growth and tendency toward poor eating habits.

Severity of symptoms related to amt and duration of iron deficiency

Children at risk:
 Premature/multiple-birth infants
 - Infants > 6 months not taking appropriate solid food
 - Children experiencing chronic blood loss

Assessment
 Classic symptoms include pallor, fatigue, and irritability
 Poor muscle development/ growth retardation may occur
 Nail-bed deformities, tachycardia and heart murmurs occur with prolonged anemia
 Lab data: Hgb levels, MCV, serum iron-binding capacity, and ↓ serum ferritin indicate
decreased iron content
 Assess dietary history for nutritional intake

Therapeutic Management
 Correct bleeding if present
 Increase the amount of iron the child is receiving
 Give oral iron supplements - ferrous sulfate
 Folic acid aids in converting iron from ferritin to Hgb
 Implement dietary modifications - high iron, protein, Vitamin C
 Promote rest, protect from infection, monitor cardiac functioning
 Administer PRBC’s slowly
 Restricting large intakes of milk in infants

Child and family education

 Appropriate iron supplement administration
 Side effects of iron
 Dietary sources of iron
 Danger of iron supplement overdose
 Information on conserving energy, preventing trauma

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Cellular Regulation
 refers to all functions carried out within a cell to maintain homeostasis, including its
responses to extracellular signals (e.g., hormones, cytokines, and neurotransmitters) and
the way each cell produces an intracellular response

Cancer in children
 Childhood cancer is the leading cause of death from disease in children ages 1 to 19
years.

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 The incidence of cancer in this age group is approximately 129 / million children
 In Newfoundland and Labrador, we diagnosis approximately 20 new children per year
 Leukemia is the most prevalent type of cancer
 Next is tumors involving the CNS, followed by lymphomas
 Males have a slightly higher percentage of occurrence over females (ratio1.2/1)
 Currently more than 80% of all children with cancer will be cured of their disease. Due to
adults having bad habits, children can have more toxic medications due to good kidneys
and liver.
 This is an increase of 50% over the last 40 years
 The “cure” word is generally reserved for once the child is 5 years off treatment
 If relapse chances of ‘cure’ is cut in half. 80-40-20

Prevention
 There is no known means of preventing childhood cancer

Diagnostic Evaluation
 Complete History. If young do preg history. Family history
 Review of Symptoms. What they have what they are
 Physical Examination. Community health nurse pick it up more than parents
 Laboratory Tests. CBC, differencals (important for cancer) electrolytes
 Imaging Studies
 Biopsy

Treatment of cancer in children

 All children in Newfoundland and Labrador are treated at the Janeway under the care of
three Pediatric Hematologist/Oncologists
 The Janeway is a part of a cooperative group called Children's Oncology Group
o we patriciate in clinical trials which positively influence the outcomes of children
diagnosed with cancer.
o we can assure patients and their families, they are receiving state-of-the-art
therapy
o Treatment usually includes chemotherapy, radiation(put under general), surgery,
bone marrow transplants, & biologic response modifiers.

Types of childhood cancer

Leukemia:
 Childhood leukemia is categorized primarily by the specific blood cell lineage (lymphoid
or myeloid) and the stage of maturity where there is disruption in the cell development
Leukemia: Two forms that are generally identified are: KNOW
 ALL –Acute Lymphoblastic leukemia
 AML – Acute myelogenous leukemia

ALL type of leukemia is further subdivided according to the:

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 morphology (structure = L1, L2, L3),

 immunophenotyping (T or B lymphoid origin)
 Cytogenetic analysis ( Chromosomal number and Structure identified (translocations,
deletions, and rearrangements)
 Children with trisomy 21 have a 20 times greater risk of developing ALL.
 Pathophysiology of cancer- taught in patho, review in textbook

Pathophysiology
 Leukemia is an unrestricted proliferation of immature WBCs in the blood-forming tissues
of the body. The immature WBCs are in circulation
 The liver and spleen are the most severely affected organs.
 Although leukemia is an overproduction of WBCs, often the acute form causes low
leukocyte count.
 Cellular destruction takes place by infiltration and subsequent competition for metabolic
elements

Diagnosis
 Based on history and physical exam/manifestations
 Signs and symptoms: Fever, Low blood counts (neutropenic) (s&s of this)
 Not going out anywhere, wash hands. Prevent infection. Anemic. Thrombocytopenia.
Bleeding (bruising and patiki)
o Peripheral blood smear:
 Immature leukocytes
 Frequently low blood counts
o Lymph node enlargement
o Enlarged liver and spleen
 Need a bone marrow aspiration or biopsy for definitive diagnosis (knocked out to do
this)
 Lumbar puncture to evaluate central nervous system (CNS) involvement (travel into CNS)

Consequences of leukemia
 Anemia from decreased RBCs
 Infection from neutropenia
 Bleeding tendencies from decreased platelet production

Therapeutic management
 Chemotherapeutic agents
o Use precautions in handling and administering chemotherapeutic agents.

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o With or without cranial radiation (chem cant go through blood brain barrier) IT
chemo
o Oral not Im due to risk of bleeding. IVs, chemo can burn so we want central line.
Portacath and double lumin hickmen cath)

Prognosis (not importants)

 Children diagnosed between 2 and 9 years of age have a better outlook than those
diagnosed before age 2 and after 10 years.
 Identified factors for determining prognosis:
o Initial WBC count
o Age at time of diagnosis
o Type of cell involved
o Sex of the child
o Karyotype analysis
Nursing care (IMPORTANT where questions are going to come from)
 Prepare the child and family for procedures. Parents needs to learn to care for new
ports. Everything happening all at once. Pain with cancer, we believe no one should be in
pain, morphine. Childe should not be in pain, N/V. we can take them off them later.
 Pain management
 Prevent complications of myelosuppression.
o Infection (thrombocytopenia, monitor for fever. Teach them how to do temp,
anything more than 38. Need to go right away. Wash hands, isolation, toys that
can be washed down, private room maybe if someone else has leukemia. Restrict
visitors. No live plants or flowers (bugs) wash fruits and veggies, no live vaccine
(no MMR) wait unit counts rise. If infection good diet, but give them what they
want a lot of the time they wont eat
o Hemorrhage. No infection, draw blood work from port. Soft tooth brush. Good
mouth care. NO rectal temp. urine and stool toxic so you need to change diaper.
Make sure they are clean
o Anemia. Not doing anything that could cause injury or bleeding when counts are
low. Let them rest. Get platelets and RBC, but depending on diagnosis and how
low it is, some let it go really low because that’s normal.

 Manage problems of drug toxicity/chemotherapy.

o Nausea and vomiting(give something before chemo starts), anorexia(not hungry,
let them eat whatever whenever), mucosal ulceration (inside of mouth but these
are all the way through the GI tract, magic mix), neuropathy (pain, lots of meds
to give for that), hemorrhagic cystitis, alopecia(shaving head could causes small
cuts), steroid effects(gain weight), mood changes (steroid rage)
 Provide emotional support.
 ALSO will take about saving eggs, it spreads to reproductive organs

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Lymphomas
 Third most common group of malignancies in children and adolescents
 Hodgkin's disease
o A malignancy of the lymphoid system, primarily involving the lymph nodes
o Often metastasizes to spleen, liver, bone marrow, lungs, and other tissues
o More than half of the number of patients with cervical adenopathy will have a
mediastinal mass – causing ?
o Accounts for 5% of cancers in children
o More prevalent in those 15 to 19 years of age
o More prevalent in males
 Survival rates vary according to stage of disease 85 – 95% for Stage I & II and 70-90% for
stage III & IV (NEED TO KNOW)
o Stage I – 1 lymph node region
o Stage II – 2 or more lymph node regions (on same side of diaphragm)
o Stage III - multiple regions on both sides of diaphragm
o Stage IV – Diffuse involvement including liver
 Patients are further subdivided when they have B symptoms present: night sweats, Wt.
loss or fever
Classifications of hodgkin’s disease
 Classification A: asymptomatic
 Classification B: fever, night sweats, unexplained weight loss of 10% or more over
previous 6 months.
 Other systemic symptoms: fever weight loss, night sweats, cough, abdominal discomfort,
anorexia, nausea, pruritus

Non-hodgkin’s lymphoma
 Non-Hodgkin's lymphoma (NHL)
o More prevalent in children less than 14 years of age
 Occurs more frequently in children than does Hodgkin's disease
 Clinical appearance
o Disease usually diffuse rather than nodular
o Cell type undifferentiated or poorly differentiated

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o Dissemination occurs early, often, and rapidly.

o Mediastinal involvement and invasion of meninges are common.
 Non-Hodgkin’s Lymphoma (NHL): a malignancy of the lymphocyte precursors in the
bone marrow and thymus
 NHL:
o -Generally, there is involvement of various areas of the body beyond the lymph
nodes: such as – abdomen, mediastinum, bone marrow, lung, bone and brain
 NHL is categorized into 3 main types:
o small noncleaved - B cell (<25% lymphoblasts in the bone marrow)
o Lymphoblastic -T cell
o Large cell – B cell, T cell, Indeterminant
Diagnostic evaluation
 Lymph node biopsy for diagnosis and staging
 Bone marrow aspiration & lumbar puncture

Therapeutic management
 Radiation
 Chemotherapy (alone or with radiation)
 Prognosis
 Nursing care
o Prepare for diagnostic and operative procedures
o Explain treatment adverse effects
o Child and family support

Normal. Abnormal (heart and lung symotoms)

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Neuroblastoma
 Most common malignant extracranial solid tumor of childhood
 Most tumors develop in the adrenal gland or retroperitoneal sympathetic chain.
o Tumors arise from any area of the sympathetic chain including the adrenal
medulla and sympathetic ganglia
o The most common site of origin is the adrenal gland
o Other sites: head, neck, chest, pelvis
 “Silent tumor”: metastasis may have already occurred before diagnosis is made
o Approximately two thirds will present with metastatic disease to the bone
marrow, lymph nodes, bone skin, or liver
 Accounts for 8-10% of all childhood cancers
 Prognosis for neuroblastoma is 75% for children under the age of 1 and less than 50% for
children older
 Staging for neuroblastoma goes from 1 for localized tumor only; to stage 4 with diffuse
involvement of various organs including bone marrow and bone

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Diagnostic evaluation
 The objective is to locate the primary site and sites of metastasis.
 Signs and symptoms depend on the location and stage of disease.
 Radiological studies, bone marrow evaluation
 MIBG (metaiodobenzylgaunidine) scanning is used to determine involvement of bone,
bone marrow, and soft tissue.

Therapeutic management
 Accurate clinical staging to establish treatment plan
 Surgery to remove tumour and obtain biopsies
 Radiation, chemotherapy
 Stem cell rescue

Prognosis
 In general, the younger the child at diagnosis the better the prognosis.
 May have spontaneous regression as embryonic cells mature and with development of
active immune system

Nursing care
 Similar to that for leukemia
 Psychological and physical preparation for diagnostic and operative procedures
 Prevention of postoperative complications
 Education related to chemotherapy, radiotherapy, and associated adverse effects
 Support parents in dealing with their feelings.

Newfoundland and Labrador foundations

 Foundations raising money here in Newfoundland & Labrador in memory of children lost
but never forgotten:
o Islaview foundation
o Nevaeh’s lemonade stand/angel foundation
o Maggie's legacy
o Kaiden’s Force

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Cellular Regulations
Adult Cancer
Cancer
 Abnormal cell growth & differentiation
 Cells divide without control & can invade other tissues
 Dying cells grow and form new abnormal cells
 Metastasis
o Cancer cells invade surrounding tissues
o Spread to other areas of the body (through lymph & blood vessels)
o Diagnosed when onset of new findings

Prevention and detection

 Early detection & prompt treatment = better prognosis
 Reduce/eliminate smoking & sun exposure
 Balanced diet (having high in fat diet, over time cells can change)
 Regular physical activity
 Healthy body weight
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 Limit alcohol
 Self-examine (important for the decrease of access to health care.)

Signs and symptoms (there are 7 warning signs) knowing these signs helps us educate patients
 C - Change in bowel or bladder habits (changes over time)
 A – A sore that doesn’t heal
 U – Unusual bleeding or discharge
 T – Thickening or lump
 I – Indigestion or difficulty swallowing
 O - Obvious change in wart or mole
 N – Nagging cough or hoarseness

Diagnosis
 History & Physical
 Diagnostic study depends on suspected site
 Biopsy – definitive means of cancer diagnosis (guide treatment decisions)

Lung cancer (most preventable cancer)

Risk factors
 Cigarette smoking
 Inhaled carcinogens
Signs and symptoms
 Silent (don’t appear until later on)
 Persistent cough (most common) this and persistent infections
 Persistent pneumonitis (inflammation partnered with infection)
 Chest pain
 Dyspnea
 Anorexia, fatigue, weight loss
 Not enough oxygen exchange causes the three above
Diagnosis
 History & Physical
 Chest x-ray
 CT scan
 Sputum specimens
 Bronchoscopy – biopsy

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If you are a smoker of 50 years and they stop for ten year their chances of cancer decreases by
half.
Bronchoscopy
 Larynx, trachea & bronchi visualized through fibre-optic bronchoscope
 30-45 minutes
 Throat sprayed with local anesthetic
 Bronchoscope inserted through nose or mouth
 NPO until gag reflex returns
 Patient teaching, why are they getting get, how the procedure is done. When doing on
child, increased risk of O2 drop
 Not uncommon to have fever, something was introduced in the lungs that’s not
supposed to be there

Lung Cancer: Collaborative Care

 Surgical resection (want to get it out, lobectomy) phenoectomy (take out whole lung)
 Radiation (shrink the tumor)
 Chemotherapy
 Biological Therapy
 Smoking prevention and cessation – nicotine replacement (if continue to smoke can
cause more trouble with breathing)
 Education: signs and symptoms to report and if they on home O2(sign o2 in use, no
smoking, not near something that makes sparks)
Goals:
 Effective breathing
 Adequate airway clearance
 Adequate oxygenation of tissues
 Pain control
 Realistic attitude towards treatment & prognosis
 Increase in calories needed

Colorectal cancer (malignant disease of colon, rectum or both)

Risk factors

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 Diet (red meat, processed food, junk food)

 Physical inactivity
 Alcohol
 Age (over 50)
 Long-term smoking
 Colorectal polyps (increased)
 Chronic inflammatory bowel disease (the cellular changes can lead to cancer)
Signs and symptoms
 Non-specific (not appear until advanced diagnosis)
 Rectal bleeding (no visible to the naked eye)
 Change in bowel habits (over time)
 Abdominal cramps
 Gas, bloating
 Loss of appetite
 Lethargy
 Sensation of incomplete evacuation
Diagnosis
 History & Physical (diet, history of polyps)
 Fecal occult blood (FOB) (avoid NSAIDs and red meats) or fecal immunochemical test
(FIT) (Same as FOB used for cancer screening, this is the one that gets sent in mail.)
 Colonoscopy (if the above test are positive)
 CT, MRI, Ultrasound (looking for metastasis
Lab values: CBC (anemia) LFTs (liver function tests, looking for metastasis

Colonoscopy
 Prep
o Clear fluids
o Bowel prep (keep taking until it comes out clear)
o NPO
o IV sedation, they put air up to pump of bowel to get a better look, tell patient
that they will have gas afterword)

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Colorectal cancer: collaborative care

 Surgical resection (get rid of the cancerous portion)
 Chemotherapy (Frist to shrink it)
 Radiation
 Health promotion: screening (any adult over the age of 50 FIT test, if positive
colonoscopy will be booked. But I should be false positive)
 Pre/Post-op care
o Positioning
o Ostomy care
o Drain care
o Diet (what can they eat? When can they eat?) chewing gum can help to start the
bowels up again. EARAS
o Bowel movements (what will they look like)
Goals
 Appropriate treatment
 Normal bowel elimination
 QOL appropriate to prognosis
 Pain relief
 Feelings of comfort & wellbeing
 Colon cancer screening program

Breast cancer
Risk factors
 Female
 Advancing age (greater than 50)
 Family history (genetic competent)
 Hormone use (if taking estrogen)
 Personal history of cancer
 Early menarche, late menopause (prolong exposure to hormones)
 Weight gain
 Sedentary lifestyle
 Diet
Signs and symptoms
 Lump
o Hard, irregular shape, non-mobile, non-tender
 Nipple discharge
 Nipple retraction
Diagnosis
 History & Physical
 Mammogram
 Ultrasound

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 Biopsy

Mammography
 X-ray of breast
 10 minutes
 Moderate discomfort (pressure)
Breast screening program withing NL
Cultural considerations, exposing the breast in some cultures can be taboo
Breast Cancer: Collaborative Care
 Surgery
 Radiation
 Chemotherapy
 Hormonal therapy (blocks the estrogen)
 Brachytherapy
Goals
 Patient active participant in decision-making
 Adhere to plan
 Manage adverse effects
 Access support (body image is important)

Sentinel Lymph Node(first node that drains from the tumor) Biopsy (SLNB)
 They used to table the nodes in the axilla, causing lymphedema.

Breast Cancer: Collaborative Care

 Support
 Education
 Pre/Post-op care
o Education

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o Drains
o Positioning of affected arm (elevated, above level of the heart)
o Prevent lymphedema
 No BP/IV/BW/Injections in affected arm
 Increased risk of lymphedema and infection.
 If in other arms used legs or a central line could be put in
o Reduce lymphedema
 Massage
 Elevation
 Compression therapy
 Exercises (ROM)
 Medications

Cervical cancer
Risk factors
 Low socioeconomic status
 Early sexual activity
 Multiple partners
 Infection with HPV
 Immunosuppression
 Smoking

Signs and symptoms

 Asymptomatic
 Unusual discharge, abnormal bleeding
 Pain (late symptom)
 Weight loss
 Anemia
 Cachexia (muscle wasting)

Diagnosis
 History and physical
 PAP test (screening can prevent)

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Cervical Cancer: Collaborative Care

 Vaccines for HPV
 Treatment

Endometrial/Uterine & Ovarian Cancer

Risk factors
 Estrogen
 Age
 Nulliparity
 Obesity
 Smoking
 Family history
 Early menarche, late menopause

Signs and symptoms

 Endometrial/uterine: *abnormal bleeding, pain (late)
 Ovarian
o Pelvic/abdominal pain
o Bloating
o Urinary frequency/urgency
o ↑abd. girth (late)
o Weight loss or gain (late)

Diagnosis
 History & Physical
 Biopsy

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 Pelvic exam
 Ultrasound

Treatment
 Surgery
 Radiation
 Progesterone
 Chemo

Prostate cancer
Risk factors
 Age
 Ethnicity
 Family history
 Diet
 Overweight

Signs and symptoms

 Asymptomatic
 Dysuria
 Hesitancy
 Dribbling
 Urgency
 Hematuria
 Retention (BPH can also cause this)
 Interruption of urinary stream

Diagnosis
 Digital rectal exam
 Biopsy
 PSA are not used to diagnoses but is used during treatment, if they decrease then the
treatment is working

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Prostate Cancer: Collaborative Care

 Curable
 Grading tumor helps decide treatment plan – Gleason Scale
 Active surveillance
 Surgery
 Radiation therapy
 Medication therapy
o Androgen deprivation therapy (↑risk OP and fractures)
 Catheter care (to get urethra open, once the catheter is removed there could be
incontinence
 Signs & symptoms of bladder infection
 Kegel exercises
 They can be given estrogen

Cellular regulation
Cancer treatment and care
Classification of cancer

Tumors classified according to:

 Site (of origin)
 Histological analysis (grading) – I, II, III, IV (tissue in the area, cells found in that are and
how abnormal they are compared to parent cells, grade one would be similar and so on)
 Extent of diagnosis (staging) – 0, 1, 2, 3, 4 (how big it is and if it has spread, 4 is
metastatic)

Benign:
 Usually encapsulated
 Recurrence rare
 Cells appear similar to parent cells
Malignant
 Ability to invade & metastasize
 Cells bear little resemblance to parent cells

TNM Standardization of Clinical Staging (don’t need to know the numbers)

 Tumor size – characteristics, depth of invasion to adjacent tissues or organs
 Node Involvement – extent & location of lymph node involvement
 Metastasis – degree of disease spread to other organs
 T – tumour size and extent of primary tumour

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o T-1: 0-2 centimeters

o T-2: 2-5 centimeters
o T-3: >5 centimeters
o T-4: tumor has broken through the skin or attached to chest wall

 N – node involvement

o N-O: surgeon can’t feel any nodes

o N-1: surgeon feels swollen nodes
o N-2: nodes feel swollen, lumpy
o N-3: swollen nodes located near collarbone

 M – extent of distance metastasis

o M – 0: tested nodes are free of cancer
o M – 1: testing nodes slow cancer cells or micro metastasis

Treatment options
 Based on cell of origin of cancer
 Focuses on:
o Removing or destroying cancer cells
o Preventing continued abnormal cell growth
 Surgical therapy
 Chemotherapy
 Radiation therapy
 Biological therapy

Surgical therapy
Removal of tumour and margin of surrounding tissue
Supportive/palliative surgery
Pre op
 Consent
 NPO
 Baseline Labs
 Urines
 Chest x-ray
 Medications
 Education
Post op
 Pain management
 Infection prevention
 Fluid & electrolytes

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 Monitor bleeding
 Oxygenation
 Education (drains, wound care, etc.)

Chemotherapy
 Cytotoxic medications
 Combination of meds used to enhance cell destruction
 Oral and IV route most common
 Adverse effects:
o Unintentional harm to normal rapidly proliferating cells (mucous membranes – GI
tract, hair follicles, bone marrow)
 CVADS
 IV Pumps

Central Venous Access Devices

 Placed for chemotherapy
 Reduces risk of damage to tissues
 Most common:
o PICC
o Implanted Port (used for long term basis)
o Hickman Catheter
 Nursing care
o Preparing patient for procedure
o Accessing, Dressing changes, Flushing
o Monitoring for complications (infection, embolism, dislodgement, etc.)

Radiation therapy
 Radiation of target tissues, destroying cells
 Localized treatment – only cells within treatment field affected
 Cure, control, palliate
 Simulation is part of process
o Patient on table, images taken, marks placed on skin so field can be reproduced
 External
 Internal brachitherapy (implant something that gives off the radiation)
 Protect skin: no heating pad, ice packs (sensation of the area is heighten) constricting
garments, harsh chemicals
 Internal/implanted radiation (you’re being exposed too)
o Cluster care
o Minimize direct contact with patients

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Nursing care for patient receiving chemo and radiation

 Education: regimen and adverse effects
 Assessment & monitoring for effects
 Management of effects

Fatigue
 Lack of energy, tired, exhausted, more time resting or sleeping
 Adequate nutrition & hydration
 Rest & activity
 Manage pain & anxiety (can give medications, cluster care) yoga can help, heat or cold
application
Anorexia
 No desire to eat (oral issue, nausea)
 Body weight measured at least 2x week
 Small, frequent meals: high protein and calorie
 Nutritional supplements

Bone marrow suppression

 WBC affected in 1 week
 Platelets affected in 2-3 weeks
 RBC affected in 2-3 months
 Neutropenia - ↑risk infection & sepsis
o Most susceptible 7-14 days after chemo
o Monitor WBC (neutrophils)
 <1 to 1.5 x 109/L neutropenic
o Temp – (>38) febrile neutropenia
 Oncologic Emergency
 Private room
 Visitor restrictions
 Blood cultures
 Look for the source of infection, draw from arm, cvad, wound, drain ect.
FIND THAT SOURCE.
 For when they go home, tell them hand washing, wash dishes in hot water,
stay away from anyone that is sick.
 Don’t take any med that will mask a fever
 Anemia
o CBC (Hgb)
o Cluster care
o Rest periods
o Monitor for S&S
 VS
 Fatigue

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 Pallor
 Dizziness
 SOB
 Thrombocytopenia
o CBC (platelets)
o Monitor bleeding
o Prevent bleeding
 Electric razor
 Soft toothbrush
 Prevent injury
Skin reactions
 Erythema (red skin)– radiation therapy
 Alopecia
o Temporary
o Regrows 3-4 weeks after treatment ends

Oral, Oropharyngeal & Esophageal Reactions

 ↓saliva – xerostomia, loss of taste
 Oral care before & after meals & bedtime
o Saline solution, medications (pain, infection)
 Diet
o Soft, non-irritating, high protein, high calorie foods
o Small, frequent meals
o Supplements
 Weight monitored closely

Pulmonary effects
 Pneumonitis (radiation)
o Cough, fever, night sweats
o Bronchodilators, expectorants, bed rest, O2
 Pulmonary edema (chemotherapy)
o Cough, dyspnea, ↑resps, crackles
o High Fowlers, O2, medications, I/O

Gastro-Intestinal Effects
 Nausea, Vomiting, Diarrhea
 Antiemetic medications
o Metoclopramide
o Ondansetron
o Dexamethasone
 S&S dehydration: electrolyte imbalances

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 Nutrition and hydration

Reproductive effects
 Effect on ovary & testes depend on dose and type of treatment
 Testes – highly sensitive to radiation
 Potential infertility
 Pre-treatment harvesting

Pain managements
 “Do you have pain?”
 Pain assessment
 Acute
 Chronic
 Breakthrough
 Medications
 Acupuncture
 Guided imagery
 Heat/cold
 Massage
 Meditation
 Music therapy

Biological and targeted therapy

 Biological agents to modify relationship between host and tumor
o May cause cells to stop growing, block release of hormones, strengthen immune
system
 Flu like symptoms

Bone marrow and stem cell transplantation

 Intensive procedure, many risks

Complications of Cancer: Oncologic Emergencies

◦ Obstructive – tumor obstruction of organ or blood vessel
◦ Superior Vena Cava Syndrome (blood flow is obstructed)

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◦ Facial edema, periorbital edema, distension of neck veins, headache,

seizures
◦ Spinal Cord Compression
◦ Back pain, motor weakness, paresthesia, bowel/bladder function changes
rd
◦ 3 Space Syndrome
◦ ↓BP, ↑HR, ↓output
◦ Intestinal Obstruction
◦ Nausea/vomiting, abdominal pain
◦ Metabolic – from hormones produced by tumor or secondary to treatment
◦ Tumor Lysis Syndrome (when cancer cells die all the substances is released in the
blood and they cant be broken down by liver then they go to kidneys, causing
damage.
◦ Hyperuricemia, hyperphosphatemia, hyperkalemia, hypocalcemia

After midterm 1
Scoliosis
Mobility is a state or quality of being mobile or movable.
 Immobility
 Disuse syndrome
 Deconditioned

Individual risk factors

Traumatic injury
 Brain
 Spinal cord
 Bones, joints, muscles
 Neurological conditions
 Chronic conditions (and/or treatment interventions)

Elements of Musculoskeletal Assessment

History
 Family history (genetics)
 Past medical history (other conditions)
 Current medications (side effects)
 Lifestyle behaviors
 Occupation
 Social environment
 Problem-based history
Common Symptoms Associated with Altered Mobility
 Pain
 Reduced joint movement

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 Reduced sensation or loss of sensation

 Falls
 Fatigue
 Altered gait or imbalance
 Reduced functional ability
Common Diagnostic Tests
Radiographic test
 X-ray
 MRI
 CT scans
 Bone scan
 Bone mineral density
 Myelogram
 Arthrography

Other diagnostic tests

 Arthroscopy
 Electromyography
 General laboratory tests
o Multiple

Clinical Management:
Primary Prevention
 Regular physical activity (4 days a week, 240 minutes)
 Protection against injury (helmet)
 Optimal nutrition
 Fall prevention measures

Clinical Management:
Collaborative Interventions
 General care guidelines for immobilized patient
o Frequent turning, positioning, alignment
o Skin assessment and skin care
o Range of motion
o Deep breathing
o Weight bearing (if possible)
o Measures to optimize elimination
o Nutrition
 Exercise therapy (up and moving as fast as we can) working with physio can OT
o Ambulation
o Joint mobility
o Stretching
o Balance

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 Pharmacological agents
o Anti-inflammatory agents
o Analgesics
o Nutrition supplementation
 Surgical interventions
o Curative(broken leg and then its fixed) versus palliative (not going to cure you but
make the rest of your life better)
 Immobilization
o Casts and splints, braces, traction, sings, shoulder immobilizers, pillows
 Assistive devices
o Crutches, canes, walkers, wheelchairs, prostheses

Scoliosis (peds text)

 Most common spinal deformity
 Complex spinal deformity in three planes, involving:
o Lateral curvature
o Spinal rotation causing rib asymmetry
o Thoracic hypokyphosis
 Classification
o Congenital (diagnosis before birth)
o infantile, juvenile, adolescent
o idiopathic (most common) (just happened, don’t know why)
 Multiple potential causes, most cases are idiopathic
 Generally, becomes noticeable after preadolescent growth spurt
 School screening is controversial.
 The Canadian Pediatric Society does not recommend routine screening.

One shoulder higher than over, hips not aligned

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Severe scoliosis
Lateral curvature of spine

Diagnostic Evaluation
 Observation
o Note any asymmetry of shoulder height, scapular or flank shape or hip height
and alignment. Look at back standing and then get them to bend over to see the
 Standing radiographs to determine degree of curvature
 Risser scale (doc will do, elevate skeletal maturity, are you done growing)
 Cobb technique (math thing, determine about of curve of spine, depending on curve
and age of bones depends on treatment)
 Curve less than 10 degrees considered a postural variation (not concerned)
 Curve less than 25 degrees is mild; no treatment required (mild) If higher going to start
treating, order CTs MRIs
Signs and symptoms (rarely signs and symptoms)
 Asymmetry of shoulder and hip height
 Prominent scapula
 Asymmetry of ribs and flank
 No c/o pain in early stages, after a while the curve is going to hurt, numb legs because of
nerves being pinched
Possible complications
 Decreased lung capacity
 Shorten life span
 Arthritic changes in the spine

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 Neurologic sequelae and paralysis (can leak CPF)

Therapeutic Management
 Team approach to treatment
 Regular clinical & radiological evaluation (even if you don’t have symptoms)
 Bracing & Exercise (mild) does not curve, allows it not to progress. For exercise, want to
build core. Nothing that will put pressure on spine, trampoline, horse back riding.
 Surgical intervention for severe curvature(above 25)(depends on age of child, and spinal
maturity, will not put rods in if not done growing and look at degree of curve
(instrumentation and fusion)
o Harrington rods
o Lugue rods
o Cotrel-Dubousset instrumentation
Spinal fusion

Nursing considerations
 Early assessment of problem (earlier that better
 Pre-op care
o Xray, day before and day of to see if there is any change
o Blood work (CBC with differential, electrolytes, hemoglobin okay, no infection,
type and screen (what type of blood) INR (bleeding times) covid test
o Pregnancy test (routine thing that is done, does not mean they are sexually
active
o Urinalysis
 Post-op care
o Education about pain, PCA’s can be used (parents need to be told what these
PCA’s pumps are, they will freak that you’re giving them drugs
o Lay flat for 24-48 hours. Move with log roll, tell them what that means, we have
to look at incision, look at their skin.
o After 24 hours get them up and moving, let them know that it will hurt when
they do.
 Make sure you keep checking blood work
 Full head to do, they were in the same position for 8 hours, look for skin break down.
 For dressing, if there is blood mark it so when you come back if it is growing
 Monitoring Vitals closely
 Neuro checks (lift hands wiggle fingers, tough toe to see if they can feel it)

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 Family/child education
o Compliance
o care of brace (wear shirt under brace to prevent skin break down, there will be
schedule for wearing times, usually starts with 4 hours and goes up
o exercise regimes (need to happen to strengthen body)
o activity restrictions (hard to tell kids that they cant do something that they really
want to do
o pre-post op care

Figure 53-15. A: Standard thoracolumbosacral (TLSO) brace for idiopathic scoliosis. Note the
colour and design incorporated into the brace to make it more acceptable to children and
adolescents. B: Variation of a standard TLSO that fastens in the back (C) to provide needed
support for the spine curvature.

Mobility (fracture/hip dysplasia)

Fractures
 Common injury in children (the way it is treated in children is different, bones heal fast)
 Methods of treatment are different in pediatrics than in older adults.
 Rare in infants, except with motor vehicle collisions or falls from heights (abuse)
 The distal forearm is most common fracture
 Clavicle is commonly broken bone in childhood, especially in those less than 10 years of
age.
 School age: bike, automobile, skateboard injuries, hockey, soccer

Growth Plate (Physeal) Injuries

 The weakest point of long bones is the cartilage growth plate (epiphyseal plate). (if it is
near growth plate determines treatment)
 Frequent site of damage during trauma
 May affect future bone growth
 Treatment may include open reduction and internal fixation to prevent growth
disturbances.

Growth and development

 Children susceptible to growth plate injuries
 Injury to the growth plate may impede growth

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o Periosteum thick and vascular in childhood allowing faster healing than in

adulthood
o Young children have a more cartilaginous skeleton - less prone to severe fractures
than adults. You can actually bend a Childs bone 45 degrees before it cracks
Fractures
 Very common in children
 Most common in the long bones
 Two types:
o Complete (tow separate pieces
o Incomplete (fragments holding on keeping bone together)
 Three types of fracture lines:
o Transverse
o Oblique
o Spiral (this one is mostly abuse)
 Types of fractures
o Complete or incomplete: fragments separated versus attached
o Simple or closed: does not produce a break in the skin
o Compound or open: fractured bone protrudes through the skin
o Complicated: bone fragments have damaged other organs or tissues (rib into
lung)
o Comminuted: small fragments of bone are broken from fractured shaft and lie in
surrounding tissue (not causing any problems)

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Clinical manifestations of fractures

 Pain and tenderness (screaming and crying, keep you away from it because it hurts)
 Swelling, bruising
 May or may not be obvious
 decreased use of affected part
 Crepitus ( bone on bone popping, hear bone grading on bone)
 Neurological and vascular damage is, less frequent in children

Bone Healing and Remodeling (don’t need to memories)

 Typically, rapid healing in children
 Neonatal period: 2 to 3 weeks
 Early childhood: 4 weeks
 Later childhood: 6 to 8 weeks
 Adolescence: 8 to 12 weeks
 Stages of bone healing and remodeling
o 1 - Hematoma formation – first 24 hrs
o 2 - Cellular proliferation – 2-3 days
o 3 - Callus formation – 21 days
o 4 - Ossification – 10 weeks
o 5 - Consolidation and remodeling

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Not being testing on

Management and treatment (goals of fracture management) Put back in alignment

 Reduction (open or closed)
 Immobilization
 Restore function
 Prevent further injury
Treatment and procedures
 Casting
 Bracing
 Traction (not as used as much anymore)
 Limb amputations (not used as much anymore, bone grafting)
 Surgical intervention

Casting
 Four categories
o Upper extremity
o Lower extremity
o Spinal and cervical
o Spica casts
 Made from plaster of paris or synthetic materials such as fiberglass or plastic

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Child in a cast
 Cast application techniques
 Nursing care
 Cast care at home
 Cast removal
o Skin care after removal. When cast is taken off will be pale, smaller than other
extremities, it will be covered in gross stuff tell them to take a bath and have it
come off itself. Teenage girls one leg will be hairy.
 Tell families if itchy use hair dryer on cool setting

Nursing
 Facilitate application and removal (have to hold extremity in place
 Positioning
 N/V assessment
 Monitor for complications
 Education and anticipatory guidance (itching, cast care, change in appearance, exercise
regimen)

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Neurovascular Assessment 6 P’s

 Pain
 Pallor
 Pulselessness
 Paresthesia (sensation)
 Paralysis (wiggle fingers)
 Pressure
If yes than there is a problem

Compartment syndrome (anyone with a cast is at risk) cause compression of skin, nerves,
ischemia.
  pressure in a limited space
 Compromises/reduces circulation and function
 Leads to ischemia and neurovascular impairment
 S/S:  sensitivity,  pain, weakness, shiny, taut skin
 Frist take cast off, or cut into muscle to preserve muscle function (greys buddy who
jumped into concert and Bailey had to cut his leg)

The child in traction

 The main prepose of traction is
o Fatigue muscle to reduce spasm for realignment
o Align bone fragments
o Immobilize fracture until realignment is achieved
o Allow for preoperative and postoperative positioning and alignment
 Newer technology has produced orthopedic fixation devices that allow for mobility.
(don’t use traction as much)
Traction: Essential Components (need to know)
 Traction: forward force produced by attaching weight to distal bone fragment
o Adjust by adding or subtracting weights
o Nurses don’t add or take off weight, we just make sure right weights are on it)
 Countertraction: backward force provided by body weight
o Increase by elevating foot of bed
 Frictional force: provided by patient’s contact with the bed
 Sometime use manual traction like pulling shoulder in place
 Skin traction
 Skeletal traction, like in the head
Traction
 Realigns bone fragments
 Reduces muscle spasm
 Treats dislocation
 Pre and post-op positioning and alignment
 Prevents/improves contracture deformity
 Provides rest and comfort

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Types of Traction (General)

 Upper extremity (uncommon in children) don’t see a lot
 Lower extremity (don’t need to know)
o Bryant traction
o Buck extension
o Russell traction
o 90-degree–90-degree traction
o Balanced suspension

Nothing hanging from ropes

No one leaning on ropes
Kids will climb over the bed
SKIN CARE, nothing in bed.
Catheters or bedpans
Need to come up with stuff for kid to do while in bed

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Cervical traction
 A halo brace or halo vest can be applied in some cases.
 Gardner-Wells tongs
 Inserted through burr holes in skull with weights attached to hyperextended head
 As neck muscles fatigue, vertebral bodies gradually separate so that the spinal cord is no
longer pinched between the vertebrae.

Principles of Skeletal Traction

 Counter traction with weights. Make sure that ropes and pullies are aligned. NEVER
REMOVE WEIGHTS
 Make sure all ropes and pulleys are aligned and weights are hanging freely.
 Do not remove weights unless instructed to do so – you do not want to displace the
fracture.
 Traction must be applied at all times.
 Physician order should include amount of weight to be applied.

Nursing Considerations
 Knowledgeable re the purpose and set-up of traction

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 Maintain traction
 Maintain alignment
 Care for skin/skeletal set-up (no need for skin breakdown)
 Prevent skin breakdown (the holes in the head)
 Monitor for infection (deep breaths to prevent phenomena)
 Prevent complications
External fixation
 Above and below facture
 Clean with NS twice a day, its open right down to the bone
 Be caesious
 Depending on the amount of handwear they may go home
 Can get wet but don’t put soap

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Prevention of fractures
 Eat calcium rich foods such as milk (and vit D to absorb)
 Exercise several times a week, muscle strengthening, balance
 Shoes with good traction (for older adult inside)
 Keep rooms free from clutter (clean up toys for children. If there is a rug make sure it is
stuck down)

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Developmental Dysplasia of the Hip

 Broad term that describes a spectrum of disorders related to abnormal development of
the hip
 Femoral head and acetabulum improperly aligned
 10 per 1000 births
 More common in girls
 80% unilateral
 Family history increased risk 5x. genetics, machinal happens in birth, multiple baby
births
Three Forms of DDH
 1) Acetabular Dysplasia - the femoral head fails to exert enough pressure against the
acetabulum (slip out)
 2) Sublaxated - the femoral head is in contact with the acetabulum, but not centered
deeply within
 3) Dislocation - the femoral head is no longer in contact with the acetabulum

Signs/Symptoms
 Asymmetry of gluteal and thigh folds (no folds means dislocation)
 Galeazzi sign (one leg longer than the other) shortened limb
 Limited hip abduction
 Hip instability
o Ortolani (abduct, hear click) or Barlow tests (fingers on greater slip ADD)
o - Trendelenberg sign ( E in picture below) for bigger kids, should be picked up on
newborn exam

Asymmetry of skin fold

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Complications
 Abnormal acetabular development/joint malformation
o Lordosis
o Sciatic nerve injury
o Avascular necrosis of the femoral head
o Soft tissue damage
o Permanent disability

Treatment and Management

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 Depends on severity of dysplasia, time of diagnosis and age of child

 Pavlik harness (new born to 6 months)
 Spica cast (6-18 months) surgery to have it fixed/reduced
 Traction (skin or skeletal) Surgery tha traction (older child)
 Surgical correction
Spica Cast (can do anything a regular child can)

Pavlik Harness needs to be adjusted every weel

Nursing Considerations
 Cast care/brace care
 Positioning (will be able to move, they don’t know they aren’t suppose to move)
 Support bonding (want parents to pick up babies and play with babies)
 Growth and development (give them toys and treat them like normal child)
 Restrict movement
 Skin care (put clothes on below, teach parents to massage skin underneath. They usually
have extra. Some may have to get baths in this)
Tests for fractures
 Hobgoblin, calcium, bilirubin (Fracture of femur)
Fluid and electrolytes elimination

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 Fluid and electrolyte balance is the process of regulating the extracellular fluid volume,
body fluid osmolality, and plasma concentrations of electrolytes.
 Elimination is excretion of waste from the body
 Bowel elimination is passage and dispelling of stool through the intestinal tract by means
of intestinal smooth muscle contraction
 Urinary elimination is passage of urine out of the urinary tract through the urinary
sphincter and urethra
UTI
Causes
 Escherichia coli- most common pathogen due to not cleaning properly
 Streptococci
 Staphylococcus saprophyticus
 Occasionally fungal and parasitic pathogens

Etiology and Pathophysiology

 Physiologic and mechanical defense mechanisms
o Emptying bladder
o Normal antibacterial properties of urine and tract
o Ureterovesical junction competence
o Peristaltic activity
 Alteration of defense mechanisms increases risk
 Organisms usually introduced via ascending route from urethra
 More common in girls than boys
 Contributing factor: urologic instrumentation
 Sexual intercourse promotes “milking” of bacteria from perineum and vagina (education
needs to happens earlier, school age)
 UTIs rarely result from hematogenous route unless prior injury to urinary tract
UTI Classifications
 Upper: renal parenchyma, pelvis, and ureters
 Lower: lower urinary tract
 Recurrent, Persistent and Febrile UTI
 Asymptomatic/Symptomatic Bacteriuria

Nursing Assessment: UTI – detailed history, are you emptying bladder, how much, when was last
BM it can push on bladder. Going to ask if child is irritable

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 Neonate: - Poor feeding, vomiting, FTT, frequent urination (going to be admitted and
IV antibiotics they get dehydrated fast)
 Infants: - Fever, foul-smelling urine, vomiting. Diaper rash that doesn’t going away.
Abd may be distended.
 Older children: Urinary frequency(pee in pants), pain with micturition, abdominal pain,
unusual bedwetting. Flank pain

UTI: Diagnostic Studies

 History and physical
 Microscopic Analysis
o White blood cells / bacteria
 Urine culture
o Clean-catch specimen preferred
o U-bag for collection from child (cotton balls)
o Catheterization or suprapubic aspiration
o Let them run around with no diaper and have cup ready
o If fever will treat with broad spectrum until sample comes back
 Imaging studies if recurrent UTI, may have reflux into kidneys
o Abdominal CT
Nursing Care
 Monitor intake and output
 Encourage frequent voiding (they aren’t going to want to pee so bring something in,
markers and place them backwards on toilet, Ipad)
 Encourage increased fluid intake (want them to pee everything out)
 Medications (make sure they take all medication, education on how to draw up
medication there will be a lot of air bubbles) getting meds into a child is hard. Gonna
want to wait until about half hour or more because it will change taste of stuff. Don’t put
it in fav bring. Purity syrup is good to put the med in.
Child and Family Education
 Teach parents methods to reduce UTI’s: Wipe front to back.
 Void after sex
 Cotton underwear
 Tight clothing avoid
 If constipated don’t strain may need stool softener
 Encourage child to void frequently and drink plenty of fluids
 Teach parents to administer full course of antibiotics

Nephrotic Syndrome (understand the patho)

Affects glomerulus

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 Most common presentation of glomerular injury in children. Normally proteins cant

pass through but with this proteins pass through.
 Characteristics
o Massive proteinuria (hyperalbuminuria)
o Hypoalbuminemia (low in blood)
o Hyperlipidemia
o Edema, ascites
o Hypovolemia
Pathophysiology
 Increased permeability of glomerular membrane allows albumin to pass into the urine
(reduce albumin in blood, lowers osmotic pressure in capillaries) shift in IF and cause
edema.
 Kidneys reabsorb salt and water
 Protein deficiency leads to massive edema
 Decreased immunoglobulins and susceptibility to infection
 Hyperlipidemia occurs secondary to liver stimulation by decreased volume of albumin
 Relapses often occur

Clinical Manifestations (think of the pathway and think of the signs and symptoms of above)

Measure abd laying down

Generalized Edema

Changes in Nephrotic Syndrome

 Glomerular membrane
o Normally impermeable to
large proteins

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o Becomes permeable to proteins, especially albumin

o Albumin lost in urine (hyperalbuminuria)
o Serum albumin decreased (hypoalbuminemia)
o Fluid shifts from plasma to interstitial spaces, leading to hypovolemia
Therapeutic Management
 Supportive care
 Teach about when its coming back. Urine sample at home if 2+ go to hospital. Stay home
suspectable to infection. Hand washing. Going back to school they look different think of
Erikson’s.
 Diet: low salt; sodium restrictions when large amount of edema present. Fluid
restriction. Don’t want drinks left out.
 Corticosteroids
o 2mg/kg body weight divided into BID doses for 6 weeks. By day 7-21 will see a
difference. Needs to be tapered off.
o Prednisone is drug of choice (least expensive and safest)
 Immunosuppressant therapy (cyclophosphamide, chlorambucil, or cyclosporine) if not
responding to steroids
 Diuretic therapy (don’t give they will go into shock) may give albumin IV and treated like
blood product help to shift everything back to blood and then might give Lasix. But they
are watched like a Hawke. So no you don’t give diuretic they are hypovolemic
 Supportive care
 Diet
 Monitor weight, I&O, abdominal girth (weigh diaper)
 Prevent infection (put in isolation they are at high risk of infection)
 Medications: Intravenous albumin, Corticosteroids, Diuretics,
Nursing Care
 Continuous monitoring of intake and output
 Astute assessment…. Skin breakdown. Need to monitor BP and temp
 Address loss of appetite (remember they will not want to eat)
 Possible fluid restriction
 Family support
o Continuous support
o Parent teaching (steroids - weight gain, constipation, roid rage, increase risk for
infection.)
o Up-and-down course of remissions and exacerbations can be stressful.
Home Care
 Discharge-to-home instructions
 Educate parents to detect signs of relapse.
 Follow-up urine, for albumin
o Encourage adequate fluid intake even after infection.
 Explain rationale to enhance adherence to fluid intake.

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Fluid, electrolytes and elimination

Constipation
 An alteration in the frequency, consistency, or ease of passage of stool.
 May be secondary to other disorders
 Idiopathic (functional) constipation - no known cause
 Chronic constipation - may be due to environmental or psychosocial factors. Children
will try to hold their poop

Newborn Period: First meconium should be passed within 24 to 36 hours of life; if not assess
for:
 - Hirschsprung disease(congenital disorder missing nerve cells), hypothyroidism
 - Meconium plug, meconium ileus (CF)
Infancy
 Often related to diet
 Constipation in exclusively breastfed infant almost unknown
o - Infrequent stool may occur because of minimal residue from digested breast
milk
 Formula-fed infants may develop constipation. What they are feeding them, iron
fortified and is hard to break down.

Childhood
 Constipation is often due to environmental changes or control over body functions
 May result from stress. Try to hold their stool. Afraid to go in school. (YOU)

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Management of Constipation
 Glycerin suppositories(it’s the simulation)/ mineral oil
 Take a history, when and how often do they poop, what are they eating
 Alterations in diet: change formula, increase fibre, increase fluid, eliminate binding foods
(whole grains breads raw veggies, beans, raisins prunes, apple, popcorn blueberries
 Establish regular times for defecation (try to relax them)

Nursing Considerations
 Assess bowel patterns (belly soft bowel sounds how often they go), medications(stool
softener, PEG), diet
 Educate parents and child re age-appropriate foods, bowel training, discourage laxatives
(don’t want dependence)
 Offer reassurance

Diarrhea
 Acute diarrhea is a leading cause of illness in children under 5 years of age.
 1.5 to 2.5 million deaths per year worldwide from diarrhea (no clean access to water)
 24% of all deaths in developing countries are related to diarrhea and dehydration
Types of Diarrhea
 Acute- variety of causative organisms
 Acute infectious/infectious gastroenteritis -caused by viral, bacterial & parasitic
pathogens
 Chronic-increased in stool frequency & increased water content for more than 14 days
(IBS) crones and cololytis
 Intractable diarrhea of infancy - no pathogens, longer that 2 weeks
 Chronic nonspecific diarrhea (CNSD)-greater than 2 weeks
Chronic Nonspecific Diarrhea (CNSD)
 AKA (also known as) irritable colon of childhood
 AKA toddlers’ diarrhea
 6 to 54 months of age
 Diarrhea >2 weeks’ duration
 Normal growth/no evidence of malnutrition
 No blood in the stool/no infection
 Poor dietary habits and food sensitivities
 Large stools
 Food sensitivity, going to see the undigested food in stool.
Diarrheal Disturbances
 Gastroenteritis

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 Enteritis
 Colitis
 Enterocolitis
Etiology of Diarrhea
 Most pathogens are spread through the fecal-oral route (day care)
 Risk factors include lack of clean water, poor hygiene, poor sanitation
 Worldwide- most common cause of acute gastroenteritis are infectious agents
o Rotavirus – known to cause a lot of diarrhea, children get vaccine
 Antibiotic therapy – alters normal intestinal flora

Diagnostic Evaluation
 Observation of general appearance and behavior
 History
o Assess severity of symptoms
o Risk of complications
o Other symptoms (fever, vomiting, character of the stool(colour consistency, size),
urine output, dietary habits)
o Include questions on recent travel, contact with animals/birds, treatment with
antibiotics, diet changes, exposure to untreated drinking water, day care
attendance)
o Lab data: for severe dehydration and clients with IV therapy (only do blood work
if we have to)
 Watery, explosive stools suggest glucose intolerance
 Foul smelling, greasy, bulky stools suggest fat malabsorption
 Diarrhea after the introduction of cow’s milk, fruits or cereal may be related to enzyme
deficiency or protein intolerance
 Neutrophils or blood cells in the stool indicate bacterial gastroenteritis or IBD
 Eosinophils suggest protein intolerance or parasitic infection
 Stool cultures: when blood, mucous, leukocytes are present
 CBC, electrolytes, creatinine and BUN- children with moderate-to-severe dehydration
 Hemoglobin, creatine, BUN usually elevated with acute diarrhea

Treatment
 Major Goals in management of acute diarrhea

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o 1) assessment of fluid and electrolyte imbalance

o 2) rehydration
o 3) maintenance fluid therapy
o 4) reintroduction of an adequate diet
 Therapeutic management
o Oral rehydration Therapy (ORT)- more effective, safer, less painful and less costly
than IV rehydration
 Treatment of choice
 Promote and enhance the reabsorption of sodium and water
 If parents use Gatorade it should be diluted with 50% water
o Can give the fluid to young children in 5-10 ml increments every 1-5 minutes. We
do this to see if they keep it down. If they cant keep it down then we do IV
o Continued feeding or early reintroduction of a normal diet has no adverse effects
and actually lessens the severity and duration of the illness and improves weight
gain compared with the gradual reintroduction of foods
 After rehydration, place an appropriate diet (continue to breastfeed, offer
formula, offer normal foods)
o If severe dehydration and shock: IV fluids are initiated (also in cases of
uncontrollable vomiting and those who are unable to drink)
o Antibiotic therapy with acute gastroenteritis is controversial. Sometimes you just
have to wait for everything to get out
o Use of probiotics accompanying antibiotic treatment
Contraindicated
 Caffeinated beverages (also for adults, high in carbs and low in electrolyte’s)
 BRAT diet (stay away from this.)
 Do not keep them on Clear liquids alone (normal diet)
 Stay away from Fluids with high carbohydrate content, low electrolyte content, and high
osmolality
o Sodas, fruit juice, gelatin, broth
Prevention of Diarrhea
 Most diarrhea is spread by the fecal-oral route (personal hygiene, wipe front to back
hand washing, how are we getting rid of poopy wipes and diapers)
 Teach personal hygiene, disposal of soiled diapers
 Clean water supply/protect from contamination
 Careful food preparation (how we even thaw foods, not left out. Clean after cutting
meat)
 Hand washing
 Isolation (if admitted with vomiting and diarrhea)
Vomiting
 Forceful ejection of gastric contents through the mouth
 Often accompanied by nausea and retching
 2 categories: Nonbilious and bilious
 Usually self-limiting and requires no specific treatment

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Therapeutic management- treat the cause, prevent complications from fluid loss (same
as with diarrhea)
o May need antiemetics
Dehydration
 A common body fluid disturbance encountered in the nursing care of infants and
children
 Occurs whenever total output of fluid exceeds the total intake of fluid
 Several causes:
o Insensible losses through the skin & respiratory track
o Lack of oral intake
o Burns
o Diabetic ketoacidosis
o Abnormal losses (vomiting and diarrhea)

Types of dehydration
 Isotonic
o Primary form of dehydration in children
o Electrolyte and water deficits are present in approximately balanced proportions.
Water and Na+ is balanced
o Water and sodium are lost in equal amounts
o No osmotic force between ICF and ECF, major loss is sustained from the ECF
compartment
o Plasma sodium within normal limits between 130-150 mmol/L
 Hypotonic
o Electrolyte deficit exceeds the water deficit, leaving the serum hypotonic
o Water moves from the ECF to the ICF to establish osmotic equilibrium, this
causes increases to the ECF volume loss
o Serum sodium is less than 130mmol/L
 Hypertonic
o Water loss in excess of electrolyte loss.
o Most dangerous type
o Fluids shifts from ICF to the ECF
o Plasma sodium is greater than 150 mmol/L
Degree of Dehydration
 The degree of dehydration has been described as a percentage of body weight
dehydrated:
o Mild- less than 3% in older children or less than 5% in infants
o Moderate- 5%-10% in infants and 3%-6% in older children

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o Severe- more than 10% in infants and more than 6% in older children
Clinical signs of dehydration
 Tachycardia (earliest sign)
 Dry skin
 Dry mucous membranes
 Sunken fontanels
 Signs of circulatory failure (coolness & mottling of extremities)
 Loss of skin elasticity
 Prolonged capillary filling time
 Body weight
 Urine & stool (how much, is it clear is it dark)
 Vital signs
Diagnostic Evaluation
 Physical examination (mucus membranes, tachy, skin cool. Activity level) put them in iso
 Weight
 Lab data
 Urine output (1 ml per kg per hour)
 Urine specific gravity
 Vitals Q15-30 min
Therapeutic Management
 Correct the fluid imbalance (if we know the cause we are going to teat it)
 Treat underlying cause
 If alert, awake and not in danger (i.e. mild dehydration):
o Oral fluid administration
 If the child is unable to ingest sufficient amounts of fluids & electrolytes, parenteral fluid
is initiated
o Solution is based on what is known regarding the type and cause of dehydration
Nursing Care
 Accurate measurement and assessment
o Urine and stools
o Vomitus colour how often how much antiemetics?
o Sweating
o Vital signs
o Skin and mucous membranes (are they dry are the lips cracked)
o Body weight
o Fontanel (infants)
 Lab data (CBC diff electrolytes , remember it effects the kidneys
 Fluid intake

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Elimination, fluid and electrolytes (Ashely’s class)

 Continence/incontinence
 Anuria – absence of urine
 Dysuria – painful urination
 Polyuria – multiple episodes of urination
 Frequency – multiple episodes in short period of time
 Hesitancy – urge is there, but difficulty starting

The kidney: function

 Urine production
 H20 regulation
 Excretes waste
 Electrolyte balance
 Acid-base balance
 BP regulation
 Regulates RBC production
 Synthesis of Vitamin D (calcium & phosphorus regulation)
 Secretes prostaglandins (vasodilator)

Lab Tests for Renal Functions

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Kidney Disease
 Partial or complete impairment of kidney function
o Inability to excrete metabolic waste products & water
o Functional disturbances of all body systems
o GFR & BUN and CR
 Acute (Acute Kidney Injury)
o Rapid loss of function
o Reversible – if detected & treated promptly
o Results in GFR & oliguria (abnormally small amt urine)
 Chronic (Chronic Kidney Disease)
o Progressive, irreversible deterioration in renal function

Acute Kidney Injury (AKI)

 Hours or days
 Potentially reversible
 High mortality rate
 Severe prolonged hypotension, hypovolemia, or nephrotoxic agent
 ↑BUN, Cr & K ±oliguria
 RIFLE Criteria

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Causes of AKI

Acute Tubular Necrosis (ATN)

 Most common cause of AKI
 Due to ischemia, nephrotoxins or sepsis
 3 Phases of ATN
o Initiation Phase – ↑serum creat., ↑BUN, ↓Urine output
o Maintenance Phase – anuric, oliguric, nonoliguric (days-weeks)
o Recovery Phase – BUN, Cr, GFR begin to return to normal
Signs & Symptoms
 Fluid volume excess (↓urine output = fluid retention)
 Metabolic acidosis (acid products of metabolism not excreted)
 Sodium/Potassium imbalance (hyponatremia/hyperkalemia)
 Hematological disorders (anemia)
 Calcium/phosphate imbalance
 Waste product accumulation
 Neurological disorders
Diagnostic Testing
 History & physical
 Urinalysis
 Renal ultrasound
 CT scan
 Bloodwork
o Serum creatinine & BUN
o Serum electrolytes
Interprofessional Care
 Fluid Restriction

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• 600 ml + previous 24 hr fluid loss

 Nutritional Therapy
• Adequate protein, K+, Na+ and Phosphate restrict
 Monitor/Lower Potassium
• Prevent life threatening dysrhythmias (ECG)
 Calcium supplements or phosphate-binding agents
 Enteral/Parenteral nutrition
 Renal Replacement Therapy

Treatment of Hyperkalemia
 Stabilize Myocardium
• ECG changes – Calcium Gluconate IV
 Shift Potassium into cells
• Regular IV insulin + Glucose to prevent hypoglycemia
• Salbutamol
• Sodium Bicarb
 Enhance potassium removal
o Kayexalate
o Loop diuretics
o Dialysis
 Long term treatment
o Dietary K+ restriction
o Limit or stop medications that cause hyperkalemia

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Nursing Assessment

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Nursing care

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 Assessment
o V/S, I&O
o Daily weights
o Edema
o Mental status
 Nephrotoxic drugs
o Smallest dose, shortest time
 Monitor/prevent infection
 Skin Care (edema/toxins)
 Mouth Care
 Psychosocial support
 Education
o Nutrition
o Rest/activity

Chronic Kidney Disease

 Progressive, irreversible loss of kidney function

Determinates of health
 Culture
 Biology and Genetic Endowment

Signs & Symptoms

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 Uremia
 Polyuria
 ↓GFR, ↑serum creatinine & BUN
 Nitrogenous waste buildup
 Altered carb. Metabolism
 ↑triglycerides
 Electrolyte imbalances
 Anemia
 Bleeding tendencies
 Infection
 Fluid retention
o HTN, HF, Pulmonary Edema
o Dyspnea
 GI issues
 Neurological changes
 Bone issues
o Chronic kidney disease-mineral bone disorder
 Pruritus
 Personality & behavioral changes

Diagnostic Testing
 History & physical
 Bloodwork
o BUN, Serum Creatinine, eGFR, electrolytes
 Urine protein-to-creatinine ratio
o First morning void specimen
 Renal ultrasound
o Rule out obstruction and note size of kidneys

Interprofessional Management
Medication Therapy
 Treat Hyperkalemia
 Treat Hypertension
o Lifestyle management and drugs
 Chronic Kidney Disease – Mineral and Bone Disorder
o Limit P, give phosphate binders, vit D supplements
 Treat anemia
o Erythropoiesis-stimulating agents
o Iron supplements, Folic Acid
 Treat Dyslipidemia
o Statins

Complications of Drug Therapy

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 Digoxin, oral glycemic agents, antibiotics, opioid medications

 Avoid NSAIDS
Nutritional Therapy
 Protein Restriction
 Na+ and Fluid Restriction
 K+ Restriction
 Phosphate Restriction
Nursing Care
 Head to toe assessment: sign and symptoms of fluid overload and electrolyte
imbalances
 Daily weights
 Vital signs
 Nutrition (dietician)
 Education (treatment options)
 Respect patient choice

Dialysis
 Hemodialysis
 Peritoneal dialysis
 Continuous renal replacement therapies: slow removal and replacement

Hemodialysis
 3 x week (3-5hr treatment)
 Vascular Access
 AVF – Arteriovenous fistula
o Joins artery to vein
o 4-6 weeks (3 months preferred) to mature before can be used
o Check patency
 Bruit
 Palpable thrill
o Avoid BP, BW, IV, Injections in arm
 Meds taken after dialysis
 Restrict fluid
 Psychosocial support
 Infection (high risk)
 Assess weight pre/post
 Vital signs
o Hypotension

Peritoneal Dialysis
 4+ exchanges every day
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 Warmed to body temp before

 Assess weight pre/post
 Monitor PD output
o Clear, light yellow
o Amount (equal or exceed dialysate)
 Fewer dietary restrictions, greater mobility
 Risk of infection/peritonitis

Urinary Tract Calculi

 1 in 10 Canadians
 50% experience recurrence
 Abnormal stone formed
 Accumulation of mineral salts
 Calculus = stone
 Lithiasis = stone formation
 Stones
o Calcium based (most common)
o Uric Acid
o Cystine
o struvite

Signs & Symptoms

 Depends on place of obstruction
 Abdominal pain (severe)

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 Hematuria
 Renal colic
 Nausea & vomiting
 Cool, moist skin
 Fever chills
Diagnostic Testing
 Urinalysis
 Urine culture
 Retrograde pyelography
 Ultrasound
 Cystoscopy
 X-ray (KUB)
 Blood work – renal function
o BUN, creatinine
Cystoscopy
 Direct visualization of bladder by cystoscope (endoscopic test)
 May be NPO if general anesthesia, if local anesthesia, fluids encouraged
 Meds to prevent bladder spasms given before
 25 minutes
 Drink fluids post-procedure
 Monitor voiding
Interprofessional & Nursing Care
 Pain control: opioids
 Treat infection
 Evaluate cause & prevent development
 Nutritional therapy: prevent new stones, drink adequate fluid
 Lithotripsy
 Surgical therapy
 Strain urine

Glucose Regulation

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4-6mmol/dl

Diabetes Mellitus (DM)

Multisystem disease
 Abnormal insulin production
 Impaired insulin utilization
Prevalence is increasing
 Financial burden

Determinants of Health
 Income and social status: low income and food insecurity (type 2)
 Biology & Genetics: ↑risk Indigenous people, ↑risk new Canadians (Latin American,
Asian, South Asian, African descent)
 Personal Health Practices & Coping Skills: Diet, exercise

Classifications of Diabetes
Canadian Diabetes Association – 11 classifications
 Type 1 diabetes
 Prediabetes (abnormal blood values, not high enough but almost, needs lifestyle
changes)
 Type 2 diabetes
 Secondary diabetes (associated with other conditions or syndromes)
 Gestational diabetes (at an increased risk of developing type 2)

Type one Diabetes

 10% of persons with diabetes

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 Genetic pre-disposition & exposure to virus

 Pancreatic beta cells destroyed (insulin not being produced)
 Onset any age, usually before 30 (between 11 and 13, history of sudden weight loss.
 Thin (history of sudden weight loss) + classic symptoms
 Acute onset of symptoms (pancreas can no longer produce insulin)
 Require insulin

Type two diabetes

 90% of persons with diabetes
 Insulin resistance (tissues do not respond to action of insulin)
 Older than 35 years
 Obese, family history, HTN, cholesterol
 Slow, gradual
 Diet and exercise
 Oral hypoglycemic agents and insulin
Signs and symptoms
 Polyuria
 Polydipsia
 Polyphagia
 Weight loss (seen in types 1)
 Weakness, Fatigue (seen in types 1)
 Type 2 DM: nonspecific – fatigue, recurrent infections, prolonged wound healing, visual
changes, painful peripheral neuropathy in feet
Diagnosis
 History and Physical
BP, EKG, Blood tests (lipids), urines
 Glycated hemoglobin - A1C (>6.5%) (don’t eat after midnight)
 Fasting blood glucose [FBG] (>7.0 mmol/L)
 Random plasma glucose [RPG] (>11.1 mmol/L) any time of the day
 Two-hour plasma glucose level in a 75g Oral glucose tolerance test [OGTT] (>11.1
mmol/L) this is used for gestational diabetes
Interprofessional Care
 Goal: Maintain blood glucose levels near normal
 Patient & family teaching
o Nutritional therapy
o Exercise
o Self-monitoring of blood glucose
o Medication therapy
In types 2 with history of heart problems A1C wants to be <6.5

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Medication Therapy
Insulin
 1-4 injections per day
 Rapid acting (NovoRapid, Humalog)
 Short acting (Novolin ge Toronto, Humulin R)
 Intermediate acting (NPH, Humulin N, Novolin ge NPH)
 Extended long acting (Lantus, Levemir)
 Premixed (Humulin 30/70, Novolin ge 30/70)
Complications
 Allergic reactions
 Lipodystrophy – rotate injection sites
 Somogyi effect (it usually happens at 2 in the morning, wake up and high sugars)
o Low blood glucose during sleep
o Rebound hyperglycemia
Antihyperglycemic agents
 Sulphonylureas
 Meglitinides (Gluconorm)
 Biguanides (Metformin) (hold if going in and using contrast dye)
 α-Glucosidase Inhibitors
 Thiazolidinediones (Actos, Avandia)
 Dipeptidyl Peptidase-4 Inhibitors (Januvia)
 Sodium-Glucose Cotransporter Type 2 Inhibitors (Trulicity)
Nutritional Therapy
 DM nurse educator and a registered dietician
 Individualized to accommodate preferences, culture, lifestyle
 Eat 3 meals/day at regular times
 Limit sugars, sweets & high fat foods
 Eat more high-fiber foods
 Drink water
 Add physical activity
Optimal nutrition
 Protein: 15-20% of energy
 Carbohydrates: 45% to 60% of energy
 Fat: less than 35% of energy, with no more than 9% from saturated fat
 Fibre: 30-50 g/day
Alcohol
 High calorie, no nutritional value
 Hypoglycemia (inhibits glucose production by liver)
 Food should be consumed with alcohol

Glycemic Index (GI)

 How much food increases glucose

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 Food with high GI (potatoes, white bread) will cause sharp rise in blood glucose
 Food with low GI (brown rice) steadily increase glucose over longer time
Carb Counting

Exercise
 Lowers blood sugar
 150 minutes/week
 Slow, gradual increase in exercise (3x per week)
 ↓triglycerides and LDL, BP & improves circulation
 Aids in weight loss
 Lowers cardiovascular risk
 Snack before exercising
Self-Monitoring Blood Glucose (SMBG)
 Patient can make self-management decisions
 At least 3x day for DM1 & at least 1x day for DM2
 Helps normalize glucose
 Reduce risk of long-term complications
 Patient must have:
o Visual acuity
o Fine motor coordination
o Cognitive ability
o Comfort with technology

Education for Self-Management

 How to check blood glucose
 Diligent skin & dental hygiene

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o Regular dental checkups

o Daily assessment of feet
 Medical identification at all times. Medical alert bracelet or necklace
 Supplies at all times
o Medication
o Glucometer
o Snacks (fast-acting carbohydrate)
Nursing Management
Acute illness/surgery
 ress can ↑blood glucose
 Eat regular meals & fluids
 Check blood glucose q4 hours & take medications
 If NPO for surgery, IV fluids with dextrose, insulin and adjustments to regular dosing
 Hold metformin before procedures involving contrast medium (they both go through he
kidneys and could damage them)
 Monitor for hypoglycemia and hyperglycemia
 When sick, insulin should not be held (glucose may increase with stress/illness)
 Patients who take metformin, sulphonylureas, or SGLT2i should not take these meds if ill
& dehydrated (vomiting & diarrhea)
Sick Day Medications (if they can keep anything down and it last for more than 24 hours)
 Rehydrate (water, broth, diet soft drinks) have to try and take something in.
 Hold: Sadmans. They can damage kidneys
o Sulfonylureas
o Ace Inhibitors
o Diuretics
o Metformin
o Angiotensin Receptor Blockers
o Non-Steroidal Anti-Inflammatories
o SGLTZ Inhibitors
o frequency of glucose checks

Glucose regulation part 2

Acute Complications of DM these are considered medical emergency’s… coma, seizures and
death

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 Diabetic Ketoacidosis (DKA)

 Hyperosmolar hyperglycemic state (HHS)
 Hypoglycemia
Diabetic Ketoacidosis (DKA)
 Fats are metabolized in absence of insulin
 Most often Type 1 DM, but may be seen in Type 2 DM (severe illness or stress)
o Hyperglycemia
o Dehydration and electrolyte loss
o Acidosis (ketones are acidic)
 Signs & symptoms:
o Polyuria, polydipsia, dehydration (dry mucous membranes, tachycardia), lethargy,
weakness, nausea & vomiting, abdominal pain, hyperventilation with Kussmaul
respirations (exhalation of excess CO2), acetone breath (sweet, fruity odor teach
family about this)
o Glucose levels vary.
Interprofessional Care
Early stages it can be managed at home if they recognize it.
 History & Physical (focused head to toe)
o Cardiovascular & respiratory status (what’s going on, are they fast breathing,
EKG)
o Mental status (confusion common)
 Blood glucose, CBC, ketones, pH (acidosis), electrolytes(watch for potassium), BUN,
blood gases
 Urinalysis – glucose, ketones
 Fluid imbalance life-threatening (priority is IV access) – IV access is the second thing you
do after assessment & fluid & electrolyte replacement.
 Hydrate first then treat hyperglycemia
 IV insulin (sliding scale drip) monitor Q1hr and adjust insulin
 Insulin and glucose for high potassium. Insulin helps K+ into the cells so it can make a
person become hypokalemia
 If sugars drop of much give dextrose so they don’t bottom out.
 Watch fluids, look at BP, lungs can get fluids. Watch output with min of 30 mls per hour.

Hyperosmolar Hyperglycemic State (HHS) less common then DKA. The difference is the
ketones. They don’t have the acidosis. This is seen more in type 2.
 Life threatening syndrome

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o Insulin produced to prevent DKA but not enough to prevent severe

hyperglycemia, kidneys kick in diuresis and fluid depletion
 Few symptoms initially (blood glucose ↑ before symptoms appear)
 Signs and symptoms:
o Somnolence (drowsy) , coma, seizures, hemiparesis (part of body not working
due to brain not getting glucose it needs), aphasia. Sugars are going to be high.
 Older adult with type 2
o Impaired thirst sensation.
o Very very important because this population is already probably dehydrated
Functional inability to replace fluids
Interprofessional Care
 Medical emergency and high mortality rate
 Immediate IV access & fluids (rehydration)
 IV insulin
 Need more fluid in general than DKA because they were probably already dehydrated

Nursing Management of DKA & HHS

 Monitoring glucose, electrolytes, ketones
 IV fluids
 Insulin therapy
 Renal status
 Cardiopulmonary status
 Level of Consciousness (LOC) cerebral profusion is impaired

Hypoglycemia
 Glucose <4 mmol/L but it is individualized. Know what the clients baseline is and bring it
down slowly.

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 Too much insulin or med, not enough food, excessive exercise or alcohol intake without
food.
 Sudden onset
 Remember Beta blocker BLOCK signs and symptoms of hypo
 Signs & Symptoms. Similar to intoxication
o Diaphoresis (sweating)
o Tremors
o Hunger
o Nervousness
o Anxiety
o Pallor
o Palpitations
Current Nursing and Collaborative Management of Hypoglycemia
Check blood glucose
 If <4 mmol/L – treat
 15 to 20 g of fast-acting carbohydrate
o 3-4 glucose tabs
o 175 mL fruit juice or regular soft drink
o 6 Life Savers candy
 Recheck blood glucose after 15 minutes & repeat, if still <4 mmol/L
 If glucose >4 mmol/L eat snack if meal more than 1 hour away
o Snacks – peanut butter sandwich, cheese & crackers, cereal & milk
 Recheck blood glucose in 45 minutes
 If no improvement with 2-3 doses of carb or patient not alert
o 1mg glucagon IM or Subcut or 3 mg intranasal
o 20 – 50 mL of 50% dextrose IV push (in acute care)
 If LOC after they wake give them a snack so they do not drop again.

Chronic Complications
 Damage to large and small vessels secondary to chronic hyperglycemia
 Macrovascular

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o Cerebro-vascular – at risk for stroke

o Cardiovascular – increased LDL and lead to heart attack
o Peripheral vascular – limbs, ulcers.
 Microvascular
o Retinopathy - eye
o Nephropathy - kidney
o Neuropathy - nerves
o Dermopathy – skin
To prevent we need tight glycemic control
Could be put on heart meds, cholesterol meds to help prevent.
Diabetic Retinopathy
 Microvascular damage to vessels in retina
 Regular exams to monitor for changes (early intervention) only means is maintaining
glucose levels
 Patient may see spots and vision reduced.
 Treatment
o Laser photocoagulation therapy – laser treatment that helps close off newly
formed leasking vessels
o Vitrectomy – drain off excess fluid to reduce pressure
o Intraocular injection of medications – helps decrease pressure
Nephropathy
 Damage to vessels that supply glomeruli. Filter in kidney is damaged
 HTN accelerates progression (aggressive BP management)
o ACE Inhibitors (protective measure)
o ARBs (protective measure)
 Regular screening
o Microalbuminuria (detects kidney damage early)
o Creatinine
o GFR

Nerve damage:
 Sensory neuropathy
o Hands & feet

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o Paresthesias, abnormal sensations, pain, loss of sensation

 Autonomic neuropathy
o All body systems can be affected
o Hypoglycemic unawareness, bowel incontinence, urinary retention, delayed
gastric emptying (nausea, vomiting, reflux), sexual dysfunction.
 Treatment
o Control of blood glucose
o Medications to relieve pain (topical creams, antidepressants, antiseizure
medications)
Complications of foot & lower extremity
 From combination of microvascular & macrovascular diseases
 Sensory neuropathy + peripheral vascular disease
o Loss of sensation – injury (improper footwear, stepping on something)
 Prevent ulcers/injury
o Proper footwear
o Diligent foot (skin & nail) care (education: look at feet)
Integumentary complications & Infection
 Discolored spots on skin – painless
 Increased susceptibility to infection
Age-Related Considerations
 DM prevalence ↑ with age
o ↓Beta-cell function pancreas. So not producing insulin
o ↓ Insulin sensitivity: body doesn’t know how to use
o Altered carbohydrate metabolism: older body doesn’t work the same
o Progressive increase in ↑A1C
o Medications to treat other: this could impair insulin action or cause sugars to
vary.

After midterm 2
Mobility (Ashley class)
Osteoarthrosis

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 Slowly progressive deterioration of articular cartilage, new tissue gets produced

 Degenerative joint disease
 Few experience symptoms until age 50-60 (not a normal part of aging process)
 Risk factors
o Aging
o Known event or condition (trauma or medications)
o Genetic traits
o Obesity
Signs and symptoms
 Pain (mild discomfort to disability) pain increase with movement
 Stiffness (in morning, decreases with movement)
 Tender joints: mostly occur in weight bearing joints (hips and knees)
 Deformity
 Effects joints asymmetrically
Diagnosis
 Based on assessment findings (history and physical)
 Bone scan, CT, MRI
 X-ray – narrowing of joint spaces
 No lab abnormalities specific to OA
 If inflammation is present, lab values will be increased. ESR CRP for at risk or have
Disease Management
 Goal: Improve/manage pain, optimize function, prevent disability.
 Balance between rest and activity (needs to be a balance)
 Heat/cold
 Weight management & Exercise(decreasing stress on joints)
 Complementary & alternative therapy (massage, acupuncture)
 Start with non pharm things but then we go to meds
 Medications (start with lowest dose, because its chronic and it may need to be
increased as time goes on) capsaysin (cream) NSAIDs (hurts stomach)
 Surgical therapy (only when other forms of treatment does not work or disease has
progressed. Arthroscopy, reconstructive (hip or shoulder replacement)

Nursing care (what is the priority?)

 Pain assessment (pain management is very important)
 MSK assessment (we need a baseline so we can compare)
 Psychosocial support (mood, sleep, ability to do ADLs)
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 Health Promotion Education

o Self-management. Want to prevent any further destruction.
o Exercise(swimming and walking)
o Weight loss
o Non pharm treatment for pain in inflammation
 Gentle exercise
 Heat/cold application
 Yoga
 Home modifications (trip hazards, hand rails, night lights, proper footwear, raised toilet)

Osteoporosis
 Bone disorder resulting in low bone density (can go undetected)
 Rate of bone reabsorption exceed formation = fragile bone tissue
 Porous, brittle, fragile bone
 Spine, hips, wrists
 Primary (didn’t develop good bone mass) or Secondary (from long term use of med,
corticosteroid)
Signs and symptoms
 Loss of height (collapsed vertebrae)
 Back pain (first sign to spontaneous fracture)
 Restricted movement
 Fractures (history of)
 Pain on palpation
Diagnosis
 History and Physical Assessment (risk factors?)
 Bone mineral density test (DEXA scan)- low energy X-ray to evaluate bone density in hip
and spine. (Lumbar, radius and neck of femur
Nursing care
 Nutrition
 Calcium supplement + Vitamin D (help absorb the Ca+)
 Exercise (bones need regular stress and strain)
 Prevent fractures
 Medications (biofastomate, give in morning with full glass of water on empty stomach
and stay up right for 30 minutes)
 Education

Fractures

 Closed
 Open
 Complete
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 Incomplete
Clinical manifestation
 Pain
 Loss of function
 Deformity
 Muscle spasms
 Crepitus
 Swelling & discoloration-Neurovascular signs
Diagnosis
 X-ray
Goal
 Realign bone fragments (reduction)
o Closed reduction – non-surgical
o Open reduction - surgical
 Immobilization to maintain realignment
 Restoration of function
Nursing Care
 Healing
 Prevent complications
 Pain relief
 Rehabilitation
 Assessment
o History & physical
o Neurovascular
 Cast care
 Prevent complications
 Ambulation (weight bearing status)
Complications
 Infection
 Compartment syndrome
 Venous thromboembolism (VTE)
 Fat embolism
 Constipation

Osteomyelitis
 Infection of bone (open fracture are at risk)
 Monitor for:
o Pain, erythema and edema
o Fever

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o Elevated WBC and ESR

o Blood cultures
 Treatment
o Long course IV antibiotics
o Surgical debridement
o Analgesics
Compartment Syndrome (decreased compartment size or content)
 The 6 p’s
o Pain
o Pressure
o Paresthesia
o Pallor (prolong cap refill)
o Paralysis
o Pulselessness

Fasciotomy is how we would treat compartment syndrome, going to need skin graph, vac
dressing and antibiotics.

Venous Thromboembolism: DVT, PE

Prevention key
 Early ambulation
 Anti-embolism stocking, SCDs

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 Anticoagulants
 Monitor for manifestations (swollen, red calf, acute SOB with chest pain)
Fat Embolism
 24 to 48 hours after fracture to long bone
 Fat globules released from bone marrow blood vessels
o Dyspnea, resp, O2
o Headache, confusion
o Tachycardia, chest pain
o Late: cutaneous petechiae (discriminates from PE) on the neck
 Prevention is key - immobilization
 Bedrest until fracture is fixed, immobilization. . Body reabsorbs it
 Treat symptoms: O2, fluid replacement (for shock), pain and anti-anxiety meds
Hip fracture
Extra-capsular fracture (outside the cap
 Good blood supply and heal fast, but more soft tissue damage
Intra-capsular fracture
 Damage vascular system more often- avascular necrosis
Complication: Avascular Necrosis Intra capsular facture
 Blood flow disrupted to the site = ischemia, bone necrosis
 Treatment:
o Replacement of damaged bone, get rid of the damage bone, can happen 6 moths
to two years after the fracture. Groin pain, weight baring pain.

Clinical Manifestations
 External rotation of affected leg
 Muscle spasms

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 Shortening of affected extremity

 Severe pain & tenderness
 Surgical treatment
 Internal fixation device. Partial which is replacing the top of the head of the femur or
total to ball and cup are replaced
Nursing Care
 Monitor vital and neurovascular signs, deep breathing, coughing
 Pain management.
 Prevention complications, if not able to go to surgery right away put in traction
 PFO (prepare for operation)
Post op
 Monitoring for complications
 Mobility (want them up and moving)
o Pain management
o Weight bearing status (both the nurse and the client needs to know this)
o Positioning (want to protect the joint)
 Avoid extreme flexion: no crossing legs, elevated toilet seats (don’t want
the hip to bed more than 90 degrees until hip joint has a chance to heal.
Positioning

Inflammation (Ashley)
Cholecystitis & Cholelithiasis (chole = gallbladder)
Cholelithiasis
 Stones in Gallbladder (high vs low stone placement)
 Made of pigments (bile) or fat (cholesterol, more prevalent)

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Cholecystitis
 Inflammation of GB
 Usually associated with cholelithiasis (stones cause the inflammation of GB)
Can be acute or chronic

Cholelithiasis: Signs & Symptoms

 May be silent (many don’t know they gave them)
 Starts with Mild pain goes to Severe Pain
 3-6 hrs following a high fat meal:
o Abdominal distension
o RUQ pain radiating to shoulder (pain in shoulder usually means cardiac, many
symptoms are they same. SO ASSESSMENT DID YOU EAT SOMEHTING FATTY??)
o Severe pain up to an hour, then residual tenderness RUQ
o Tachycardia, diaphoresis, weakness
o Spasms – ‘biliary colic’ (colic is spasms) happens if stones pass through the ducts.
When they move is when the problem happens
 Rule out cardiac cause

Cholecystitis: Signs & Symptoms

 Acute
o Pain & tenderness RUQ

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o Feels like Indigestion and not settling

o N&V
o Restlessness
o Diaphoresis
↑ WBC s & Fever
'
o
o Positive Murphy’s Sign (take hand and touch right upper quad and if they can’t
stand it, it is a positive sign)
 Chronic
o Fat intolerance (most have a altered diet)
o Dyspepsia (indigestion) Bloating, pain
o Heartburn
o Flatulence
Cholelithiasis & Cholecystitis: Complications (Just know there is a number of complications and
they go undetected and untreated)
 Gangrenous cholecystitis
 Subphrenic abscess (bad if it bursts)
 Acute pancreatitis (back up elsewhere)
 Cholangitis – inflammation of the bile ducts
 Biliary cirrhosis (damage to bile duct)
 Fistulas (abnormal connection between body parts)
 Rupture of Gallbladder – peritonitis
 Choledocholithiasis – stone in common bile duct

Clinical Manifestations Caused by Obstructed Bile Flow

 Risk of bleeding – ↓ vit . K ,↓prothrombin
 Clay coloured stools – blockage of flow of bile salts (bile gives stool the colour)
 Dark amber urine – bilirubin in urine (compensation, it goes in the blood and the kidneys
filter it.
 Intolerance of fatty foods (nausea, fullness, anorexia) - no bile in small intestine for fat
digestion
 Obstructive jaundice – no bile flow in duodenum (think about what will happen when
they eat fatty foods if no bile)
 Pruritis (itching) – bile salts in skin
 Steatorrhea (fatty stools) – no bile salts, preventing fat emulsion and digestion

Diagnosis
 History & Physical (Abdominal, what do you eat? Pain after eating? Voiding? Colour?
Stool?)
 Ultrasound (see if there is a stone)

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 ERCP- Endoscope inserted to look at gallbladder, cystic duct, common hepatic duct and
common bile duct (when they have this they may put contrast dye and this can cause
pancreatitis) takes about an hour
 Labs
o Liver enzymes (help support diagnosis)
o WBC (inflammation)
o bilirubin
o Amylase, lipase (when we see these think pancerous
Management
May not do anything
Conservative Therapy
 Cholelithiasis
o Bile acids (medication)– administered to dissolve stones (UDCA) takes 6-12
months for it to work some symptom free I 2-3 months but if they don’t change
diet they will come back
o ERCP – widened to allow stone passage or stones may be retrieved
o Extracorporeal shock-wave lithotripsy (ESWL) - stones fragmented by laser pulse
 Cholecystitis
o Pain management – analgesics and anticholinergics
o Control of possible infection – antibiotics
o Fluid & Electrolyte balance – IV fluids (they may not be able to eat)
o NPO
o NG tube - severe n/v & gastric decompression
Surgical Therapy Want to prevent rupture
 Laparoscopic Cholecystectomy (post op gas pain)
 Open Cholecystectomy
o T-tube in common bile duct – ensures patency of the duct until edema from
trauma of exploring duct subsides (this is a drain)
 Transhepatic Biliary Catheter
o Preop in biliary obstruction and hepatic dysfunction (secondary to obstructive
jaundice)
o Palliative care
o Catheter inserted in common bile duct & duodenum & connected to drainage
bag (bile can flow freely) (this is more for palliation

Nursing Care Post-Op

 V/S
 IV fluids
 Once bowel sound are heard Sips  clear fluids  full fluids

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 Soft diet when bowel sounds return and passing gas

 Splint incision
 Pain management
 Deep breathing coughing q1h; incentive spirometry
 Turn, reposition & ambulate ASAP
 Walking to help move air
 Dressing, Drain Care
 N&V, anorexia
 Complications:
o Bleeding
o Peritonitis (infection) Rigid abdomen is main sign
o Pneumonia (do the deep breathing and coughing)
o Jaundice (obstruction of bile)
Medication Therapy
 Analgesics – Morphine
 Anticholinergics
 Fat-soluble vitamins (A, D, E, K) – chronic gallbladder disease or biliary tract obstruction
 Bile salts – facilitate digestion and vitamin absorption
 Cholestyramine – for pruritis
Nutritional Therapy
 Small, frequent meals
 Low in saturated fats
 High fiber and calcium
 Avoid rapid weight loss – promotes gallstone formation
Education
 Low fat diet
 Medication adherence
 Report:
o Jaundice
o Pruritus
o Dark urine, clay colored stool
o Pain
o N/V
o Abd distension/rigid

 Post op
o Ambulate gradually
o No heavy lifting for 4-6 wks
o Watch infection at site

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o Follow up with family HCP

o Loose stools are common as the body adjusts for a week or so
Pancreatitis
 Inflammation of the pancreas (can cause diabetes)
 Pancreas: converts food into fuel for the body's cells.
 Two key functions:
o Exocrine function – helps digestion
o Endocrine function – regulates blood sugar
 Acute or chronic

Common Causes
 Gallbladder disease
 ETOH
 Trauma
 Infections
 Medications
 Post-op complication
 Post-ERCP pancreatitis
 If they enzymes cant get out it goes back inside and then in the tissue

Acute Pancreatitis
Clinical Manifestations
 Severe Abdominal Pain
o LUQ, mid-epigastrium
o Left and goes around to the back

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o Worse when lying down due to the pancreases stretched

o Aggravated by eating & not relieved by vomiting
 Bowel sounds decreased or absent
 Abdominal distension
 Pt. may flex spine to try to relieve pain (fetal position)
 Hypotension, tachycardia
 Jaundice
 Crackles in lungs (inflammatory chemicals excreted in the blood stream)
 N&V
 Low grade fever
 Ecchymosis (late sign)
 Shock

Complications (don’t have to memorize)

 Pseudocyst – accumulation of fluid, pancreatic enzymes, tissue debris and inflam.
exudates (collection of something that builds up)
o Abdominal pain, palpable mass, N&V, and anorexia
o Usually resolve spontaneously, but can perforate – peritonitis , or may rupture
into stomach or duodenum
o Trt: internal drainage with an anastomosis between pancreatic duct and jejunum
 Abscess – results from infected pseudocyst
o May rupture or perforate adjacent organs
o Upper abdominal pain, abdominal mass, high fever, leukocytosis
o Trt: surgical drainage to prevent sepsis
 Systemic Complications
o Hypotension, tachycardia, pleural effusion, atelectasis, pneumonia, acute
respiratory distress syndrome, coagulation disorders (↑risk for thrombi)
Diagnosis
 Physical exam & history
 Amylase (elevated early, elevated for 24-72 hrs)
 Lipase (ACES or ASES are high is pancreatitis)
 liver enzymes, triglycerides & Glucose

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 Abd. U/S, X-ray, or CT scan

 CT with contrast and MRCP – for detecting complications (pseudocysts and abscess)
(MRI)
Conservative Therapy
 Pain management
o Opioids – Ex: IV morphine
o Antispasmodic agents
o Spasmolytics – nitroglycerin (help to relax)
 Fluid & Electrolyte management
o Ringer’s Lactate (anti inflammatory effect)
 Treatment of Shock
o Plasma or plasma volume expanders (Albumin)
 Reducing Pancreatic Enzyme Secretion (nowhere for them to go)
o ↓ stimulation of pancreas
o NPO
o NG to LCS (low continuous suction)
o Parenteral nutrition (if needed) (sort term) or feeding tube back to food when
levels start to come down)
 Prevent infection
o Inflamed and necrotic pancreatic tissue promotes bacterial growth
o Prophylactic antibiotics (if needed)
Interventional therapy
 ERCP
 Drainage of necrotic tissue

Medication Therapy
 Acute pancreatitis
o Antacids
o Antispasmodics
o Carbonic anhydrase inhibitor

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o Morphine
o Nitroglycerine or papaverine
o PPI’s
 Chronic
o Insulin (they develop diabetes)
o Pancreatin, Pancrelipase (supplements to help digest fats)
Nutritional Therapy
 NPO initially
o enteral or parenteral nutrition may be required
o Nutritional BW
o Care of NG tube
o Oral care
 Small frequent meals (when markers start to come back, high carb)
 High carbohydrate
 No alcohol (make it worse)
 Supplemental fat-soluble vitamins (ADEK vites_
 Watch for pain, increased abd (shift in fluid). girth, elevated amylase & lipase =
intolerance to oral foods (not taking foods well with these symptoms)
Nursing
 Focused head to toe assessment including:
o Vitals
o Pain
o Electrolyte imbalances
o Signs of shock
o Respiratory function
o Abdominal
o Signs of Hypocalcemia (tetany, involuntary contraction of muscles)
o Blood glucose levels
o NG – oral care
o Wound care
Discharge Planning
 Home care referral if necessary
 PT/OT
 No alcohol
 No smoking (tabaco can cause secretion of pancreas enzymes
 Low fat diet
 Monitor for infection, diabetes and steatorrhea (fatty stools, foul smelling)
 Medication compliance
Chronic pancreatitis
Common Causes
 70% associated with alcohol use disorder
 Idiopathic pancreatitis

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 May follow acute pancreatitis (many sessions of acute and it usually long-term
inflammation) chronic follows acute.
 Obstructive vs non-obstructive
o Obstructive associated with biliary disease or Cancer (stones, tumor)
o Non-obstructive associated with inflammation and sclerosis(hardening) (alcohol
most common cause)

Clinical Manifestations
o Abdominal pain (spirts where it gets bad but usually always there)
o Heavy, gnawing feeling, burning and cramp-like
o Not relived with food or antacids
 Malabsorption with weight loss
 Constipation
 Mild jaundice with dark urine
 Steatorrhea (fatty stool)
 Can develop Diabetes Mellitus (secondary)
 Complications(same as acute): pseudocyst, bile duct or duodenal obstruction, pancreatic
ascites or pleural effusion, splenic vein thrombosis, pseudoaneurysms and pancreatic
cancer
Diagnosis
 Based on signs/symptoms, labs, and imaging
 Serum amylase and lipase – may slightly ↑ (ACES ARE HIGH) (acute very elevated
chronic slightly)
 Serum bilirubin and alkaline phosphatase may be ↑
 Mild leukocytosis (WBC increase)
 Stool samples for fecal fat content
 Deficiencies in fat-soluble vitamins (A,D,E,K)
 Diabetes
 ERCP, CT, MRI, MRCP, transabdominal ultrasound, endoscopic ultrasound
Interprofessional Care (they are really sick, in and out of hospital)
 Focus: Prevention of attacks (certain foods, low fat), Pain relief, Control of pancreatic
exocrine and endocrine insufficiency
 Diet – bland & low fat, small frequent meals, avoid fatty, rich stimulating foods, no
alcohol, no smoking
 Pancreatic enzyme replacement
o Pancreatic enzyme products (Pancreatin & Pancrelipase – these are supps)
o Bile salts – facilitate absorption of fat-soluble vitamins & prevent fat loss
o Acid-neutralizing & acid-inhibiting drugs - decrease HCL (help with pain)
 Surgery - biliary disease, obstruction or pseudocyst
Inflammation (Ashely)
Function of the liver
 Glucose metabolism & regulation
 Converts ammonia(protein) into urea

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 Protein metabolism
 Fat metabolism (bile)
 Vitamin & iron storage
 Bile formation
 Bilirubin excretion
 Drug metabolism

Liver disease
 Hepatitis – inflammation of liver cells
o A, B, C, D, E
o Nonalcoholic fatty liver disease & nonalcoholic steatohepatitis
o Alcohol and drug induced hepatitis
o Autoimmune & genetic liver diseases
 The above not detected or treated can cause cirrhosis – permanent injury to liver,
related to chronic inflammation

Nonalcoholic Fatty Liver Disease (NAFLD)

 Patients are presenting with Simple fatty liver with no hepatic inflammation (steatosis)
to Nonalcoholic Steatohepatitis (NASH) (fat buildup present) to severe scarring
(cirrhosis)
 Drink little or no alcohol
 Accumulation of fat in liver cells
 Treatment directed at reduction of risk factors: tx of diabetes, reduction in body weight,
elimination of harmful medications.

Liver cirrhosis (scaring) final stage of liver disease

 Normal liver tissue replaced with fibrosis tissue that interrupt’s function
 Liver is inflamed, common bile duct obstructed (thick bile & pus), infection, scar tissue,
obstructed blood flow through portal regions
 Final stage of chronic liver disease
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Liver Cirrhosis: 3 types

Alcoholic cirrhosis
 Build up of scar tissue around hepatic portal system
 Chronic alcoholism
 Most common type
Post necrotic cirrhosis
 Profuse scar tissue
 Following Acute hepatitis
Biliary cirrhosis
 Scarring around bile duct (go through liver and outside liver)
 Chronic biliary obstruction or infection (gale stones)

Compensated vs Decompensated Liver Cirrhosis

Compensated (body is able to function normally) know they have some scaring but when we
check labs they could be slightly elevated or normal. Could be this way for years
 Liver able to function normally
 LFT’s, albumin, bilirubin and PTT normal
Decompensated (liver can keep up anymore and the signs and symptoms starts) labs will be
abnormal
 Advanced cirrhosis
 One or more complications of liver cirrhosis occurs

Clinical Manifestations
 Abdominal pain (dull, heavy – right upper quad)
 Anorexia (they don’t want to get it hurts)
 Dyspepsia (reflex)
 Nausea & vomiting
 Weakness

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 Muscle loss
 Fatigue
 Slight weight loss…. Weight gain due to fluid
 Hepatomegaly & splenomegaly

Manifestations of Decompensated Cirrhosis

 Jaundice (build of belly in the blood)
 Skin lesions
o Spider angiomas
o Palmer erythema
 Hematological conditions
o Thrombocytopenia
o Leukopenia
o Anemia (decrease RBCs)
o Coagulation disorders (if liver doesn’t produced clotting factors)
 Endocrine disturbances (liver helps with estrogen and testosterone) women (vaginal
bleeding or no period) male (breast tissue)
 Peripheral neuropathy

Clinical manifestations

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Complications
 Portal Hypertension and Esophageal & Gastric Varices
 Peripheral Edema and Ascites
 Hepatic Encephalopathy
 Hepato-Renal Syndrome

Portal Hypertension and Esophageal & Gastric Varices

 Portal vein – Carries blood from digestive organs to liver
 Damaged liver (cirrhosis) causes back up of blood in the portal vein – portal
hypertension
 Blood backs up further and causes varices (stomach & esophagus) & enlarges spleen
 *Bleeding Esophageal Varices are most life-threatening complication of cirrhosis*
 Varices when there is a blockage in the hepatic vein and the blood goes to the smaller
vessels, causes them to burst. Throwing up blood or bloody stool)
 Varices are swollen vessels

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Peripheral Edema and Ascites

 Ascites – accumulation of serous fluid in the peritoneal or abdominal cavity
o Abdominal distension & weight gain
o Decreased urinary output & s/s of dehydration
o Hypokalemia
 Peripheral Edema – can come before, during or after ascites
o Ankle & presacral edema

Hepatic Encephalopathy (accumulation of waste products on the brain)

 Neuropsychiatric manifestation of advanced liver disease
 Caused by build up of waste products (ammonia) in the blood and brain that liver could
not excrete
 Clinical Manifestations:
o Changes in neurological and mental responsiveness
o Asterixis (flapping tremors) Has to do with cerebellum being affected
o Impairments in writing- difficulty moving pen from left to right and
constructional apraxia (inability to construct simple figures
o Hyperventilation (ammonia levels, body is trying to get rid of ammonia
o Hypothermia
o Grimacing
o Grasping reflexes

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Hepato-Renal Syndrome (liver is not filtering, gong to kidney and cause damage)
 Complication of decompensated cirrhosis
 Kidney failure with advancing azotemia, oliguria, and ascites
 Frequently follows diuretic therapy, GI hemorrhage or paracentesis
 Kidney failure can be reversed with liver transplant

Diagnosis
 Lab values
o ↑ AST , ALT , ALP (liver function tests) elevated = issues with liver. When liver
cells are damaged they leak these, causes them to go up.
o ↓ total protein, albumin – lack of hepatic synthesis
o ↑ s erum bilirubin – liver unable to excrete
o Prolonged PTT
 Liver biopsy
o to confirm underlying cause if not clinically evident (caution due to liver being
vascular… clotting)
 Noninvasive Fibrosis Markers
o Transient elastography – noninvasive imaging technique – degree of hepatic
fibrosis measured
o Models of serum markers – blood samples taken to calculate fibrosis score for
predicting degree of liver fibrosis

Interprofessional Care
 Conservative therapy
o Avoidance of alcohol, (ASA, sedatives, & NSAIDS avoid these)
o Rest (in decompensated) (short term can help)
 Ascites (want to get rid of excess fluids)
o Diuretics (watch kidneys)
o Low-sodium diet
o Paracentesis (if indicated) (drain fluid of belly)
o Transjugular Intrahepatic Portosystemic Shunt (invasive, stent in portal vein)
 Esophageal and gastric varices – prevent bleeding (screen for them, do they have it?)
o Endoscopy – to screen for varices
o Variceal size, wall thickness, liver dysfunction
 Beta blocker – reduce portal venous pressure
 If bleeding occurs (medical emergency) ABC’s we want to reduce the pressures
o Airway management
o IV (fluids & blood products) (circulation)
o Drugs – octreotide, vasopressin
o Endoscopic sclerotherapy or band ligation (put band on the weakened part of
vein)
o Balloon Tamponade (last resort) balloon on varices and put pressure

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Disease management
 Hepatic Encephalopathy – reduce ammonia formation
o Lactulose (helps excrete ammonia)
o Antibiotics (rifaximin) - in patients where lactulose alone doesn’t work
o Tx of causes
o Liver transplant - reoccurring hepatic encephalopathy & end-stage liver disease
 Nutritional Therapy
o High calorie, high carbohydrate, moderate to low fat
o Protein restriction only after severe flare of symptoms (due to the ammonia)
o Low sodium – when ascites and edema present
o No alcohol

Nursing Management
 Assessment (look for complications)
 Promote Rest
 Maintain adequate nutrition
 Monitor for jaundice and pruritis (itching)
o Cholestyramine (med that removes bile salts if accumulating)
o Keep nails short and clean (increased risk for bleeding and infection)
 Monitor color of urine and stools
o Dark brown and foamy urine + grey or tan stools when jaundice present
 Edema and ascites
o Monitor I&O
o Daily weights
o Skin care, turn and positioning q2h
o Support abdomen, elevate limbs
 Patients on diuretics
o Monitor serum sodium, potassium, chloride, bicarb, and creatinine
o Monitor for S&S of electrolyte imbalance
 Esophageal Varices
o Monitor for bleeding – hematemesis, melena
 Hepatitis A & B vaccines (if they have some function and don’t want it to get worse)
 Psychosocial support (if it is due to alcohol) stigma
 Hepatic Encephalopathy
o Assess: Level of responsiveness(LOC), sensory and motor abnormalities, fluid and
electrolyte imbalances, acid-base imbalances, effect of treatment measures.
o Q2H neuro assessments
o Monitor for constipation and administer drugs as ordered.
o 2-3 loose bowel movements per day to eliminate toxins

CAGE

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Infection (Ashely)
Tuberculosis
 Infectious disease caused by M. tuberculosis (gram + acid-fast bacillus)
 Primarily involves lungs
 Can also occur in kidneys, bones, adrenal glands, lymph nodes, and meninges (insolation
or to respiratory)
 Reportable communicable disease (need to report to community health, contact tracing)
 Airborne droplet transmission (cough sneeze, speak) latent have TB but not having
symptoms or can transmit. Contagious when symptoms are present

Determinants of Health
 Income & Social Status
 Physical Environments
 Personal Health Practice & Coping Skills
 Culture (higher in the indigenous population)

Clinical Manifestations (elderly present differently)

 Symptom free in early stages
 Fatigue
 Malaise
 Anorexia
 Weight loss
 Low-grade fevers
 Night sweats
 Cough – frequent, productive
 Chest pain – dull or tight
 Hemoptysis (advanced cases)

Complications
 Miliary Tuberculosis necrotic
o Invades bloodstream and spreads to organs. Can invade through a blood vessel
 Pleural Effusion and Empyema (Collection of pus)
 Tuberculosis Pneumonia (unable to clear lungs)
 Other Organ Involvement
o Infected meninges
o Bone and joint tissue
o Infections in Kidneys and adrenal glands, Lymph nodes, Genital tract

Diagnostic Studies
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 History and Physical (SOB, coughing, chest pain, decreased O2

 Tuberculin Skin Testing
 Chest X-ray (only helps to support the diagnosis of TB
 Acid-fast bacilli (AFB) smear (This is how it is diagnosis
o Three consecutive sputum samples (3 positives means TB) come off precautions
when you have three negatives
 Nucleic acid amplification (NAA) (rapid test) less sensitive than cultures
 QuantiFERON-TB Gold In-Tube

Protein derivative of TB
No reaction is negative
It may be false positive
But if positive they are sent for chest X ray and sputum test

Medication Therapy (done out-patient)

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 Anti-TB agents
 First-Line Meds: (know that TB is hard to treat, high chance of resistance, so attack it by
used multiple meds) need to take full course of these medications, make them feel
better and get rid of organism.
 Monitor sputum’s during therapy, after a few weeks there will be a neg result but need
continue meds
 Liver and kidney function
 Direct observation therapy: partner then with someone to make sure they patient takes
all the medication
o Isoniazid (INH)
o Rifampin (RMP)
o Pyazinamide (PZA)
o Ethambutol (EMB)
Nursing Management
 Nursing assessment (respiratory system, nutrition, screen in high-risk groups.)
 Health promotion – screening
 Infection control measures
o Respiratory isolation
 Until patient considered non-infectious (effective med therapy, clinical
improvement, 3 negative smears) Hospital:private room, droplet, neg
pressure room. Home: limit visitors, open window, one room)
 Emotional support (wear mask if they leave their room, wash hands, cover when
coughing/sneezing, air out room)
 Education
o Infection control precautions
o Med adherence
 Canadian lung association
 Early prevention, detection

Viral hepatitis

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Hepatitis
 Inflammation of the liver
 Most common cause is viral infection
 Common types: A, B, C, D, & E
 Other causes of Hepatitis: chemicals, drugs (incl. ETOH), autoimmune diseases,
metabolic disorders and genetic abnormalities
 Most patients managed at home (comorbidity)
 Prevention: Vaccination and Infection Prevention Control

Determinants of Health
 Culture & Ethnicity (indigenous)
 Personal Health Practices & Coping Skills (high risk behavior)
 Gender (baby boomers more at risk, gay, transgenered)

Clinical Manifestations – Acute Phase

 Most may not know they have it
 Anorexia (don’t have desire to eat)
 Nausea & vomiting
 Malaise
 Fever
 Headache
 Low-grade fever
 Arthralgias (joint pain)
 Skin rashes
 Upper right quad. Discomfort
 Jaundice (liver is inflamed)
o Icteric (jaundice)
o Anicteric (no jaundice)

Chronic phase
 Hepatitis B & C
 Many have no symptoms
 Nonspecific symptoms: malaise, fatigue, myalgias, arthralgias, and hepatomegaly
 Untreated – cirrhosis, hepatocarcinoma, liver failure
 Can lead to cancer and then lead to liver failure

Diagnosis
 Viral Serological Tests (blood test)

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o Used to diagnose different types

 Serum Liver Enzymes (elevated, liver damage causes an increase)
o Liver injury
o ↑AST & ALT – liver cell injury
o ↑ ALP & GGT – bile duct injuries
 Liver functions test
o Albumin (gonna get edema, remember water holds on the albumin)
o Serum Bilirubin – twice normal level with jaundice
o Prothrombin Time
o INR
 ↑INR & Serum Bilirubin and ↓Serum Albumin – deteriorating liver function

Hepatitis A
 Fecal-oral route
 Highest risk of transmission before symptoms present (2 weeks before)
 Lifelong immunity after recovery to hep A
 Sources of Infection:
o Fecal oral route
 Ingestion of contaminated food or liquids
 Poor Hygiene
 Contaminated H2O
 Poor sanitary conditions
 Get twinrex before travel
How to prevent
 Good Handwashing
 Vaccination
 Environmental sanitation
 Universal precautions
 Spread through fecal oral route: use you PPE. Contact precautions.
 Usually resolve over time and if they are unwell just treat symptoms

Hepatitis B
 Perinatally (infected mother to infant)

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 Percutaneously (IV drug use, accidental needlestick)

 Sexually
 Permucosal exposure to infectious blood, blood products or other body fluid
 Acute Hep B can spontaneously resolve
o Immunocompromised may not clear infection
 Chronic Hep B – cirrhosis & end-stage liver disease
 Needleless system (we use the lock)
 Identify those at risk and prevent transmission
 Vaccine
 Universal precautions
 Medications For Chronic Hepatitis B (suppress viral load & slow disease progression)
o Interferon
o Nucleos(t)ide analogues
 As a help care provider you could get needle stick. Blood test for you and patient, report
it, emerg immunoglobulin, or vaccine

Hepatitis C
 Percutaneously
 High-risk sexual behavior
 Spontaneous clearance of Hep C – more than 50% the other 50% turn into chronic.
 Chronic Hep C curable with medication therapy
o Direct acting antiviral agents
 Universal precautions
 No vaccine available
 Prevent transmission
 Patients that do hemodialysis are at risk. And increased those who had blood
transfusions before 1992

Hepatitis D
 Cannot survive on its own (requires Hep B to replicate) Has to have Hep B to get hep D
 Acquired the same time or later in a Hep B infection
 Percutaneous transmission
 Cant get rid of it

Hepatitis E
 Fecal-oral route transmission
 Self-limiting hepatitis
 Immunosuppressed individuals may progress to chronic infection
 Recover within a few weeks without treatment.

Interprofessional Care
 Provide relief from discomfort, so they can return back to normal and get liver enzymes
back to normal.
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 What type are we dealing with?

 Meds to treat symptoms
 History and physical exam
 Liver enzymes – ALT, AST
 LFT’s – Albumin, bilirubin, INR
 Hepatitis tests
 Well-balanced diet, vitamins, rest, avoid alcohol and hepatotoxic meds
 Chronic hepatitis
o Medications
o Cyrocsis and then liver failure

Inflammation
Acute appendicitis
 Inflammation of the appendix (blind sac at the end of the cecum).
 Most common emergency abdominal surgery in childhood.

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o Average age 10
 Etiology: cause is obstruction of the lumen of the appendix.
 Patho: acute obstruction, outflow of mucus secretion is blocked and pressure within the
lumen builds. This causes ischemia followed by ulceration of the epithelial lining and
bacterial invasion. Necrosis will follow causing perforation or rupture with fecal and
bacterial contamination of the peritoneal cavity.
o Inflammation will spread rapidly throughout the abdomen (peritonitis). Loss of
extracellular fluid (peritoneum is a major portion of the total body surface area)
leads to electrolyte imbalance and hypovolemic shock.
o The fecal matter or pus is going to go into abd and cause infection within.

Clinical manifestations
 Classic first symptom- periumbilical pain (around belly bottom)
 Nausea
 Abdominal pain – RLQ
 Fever (slight, low grade due to inflammation)
 Vomiting
 Possible anorexia (not want to eat due to pain), diarrhea
 Elevated WBC
 *Perforation can occur within ~48 hours of first sign of pain
o Sudden relief from pain (not for long) The app pushing on tissue, relief of pain
from the app bursting. Pain will come back once the infection in abd starts
o Complications include major abscess, fistula, peritonitis, partial bowel
obstruction

Diagnosis
 - based on history, physical exam & S/S
 - Pain at McBurney’s point
 - Elevated WBC’s

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 Jump: if they scream when feet hit the floor.

 Pain scale (fetal position, facial expression)
 Shift to the left or increased bands. Immature white blood cells
Lab studies
 CBC
 CRP (shows inflammation in body)
 Urinalysis (rule out UTI, remember belly pain)
 Females- serum human gonadotropin (ectopic pregnancy)
 Ultrasound or CT (usually untra, gonna see appendix
Management
 Before perforation
o Rehydration (IV)
o Antibiotics (prophylactic)
o surgical removal of the appendix (laparoscopic) (gas pain, get them up and
moving, the gas will go up in shoulders so helicopter arms)
 Ruptured appendix
o IV administration of fluid & electrolytes
o Antibiotics (IV 7-10 days)
o NPO & NG compression (decompress belly)
o Going to open up at this point
 Going to use suction, and irrigate. If really bad they will use antibiotic
solution)
 May use penrose drain and dry dressing
o Postop care: 3-5 days in
 IV fluids (electrolytes normal)
 Antibiotics
 NG suction (Bowel sounds, passing gas or bowel movements)
 (Irrigation of the peritoneal cavity)
 ?Penrose drain

Inflammatory bowel disease (IBD)

A term used for two forms of chronic intestinal inflammation
 Ulcerative colitis (UC)
 Crohn’s disease (CD)

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Etiology: IBD is not completely understood

 No known cure
Ulcerative Colitis (UC)
 Inflammation of mucosa of distal colon and rectum
o Distal colon and rectum most affected
 Affects the mucosa and submucosa
o Mucous membranes edematous, bleed easily due excoriation of the mucosa
o Underlying serosa remains intact
 Mucosa has multiple ulcerations and polyps
Clinical manifestations
 Bloody mucus, diarrhea, rectal bleeding
o Diarrhea often severe
 Abdominal cramps, hyperactive bowel sounds
 Pain with defecation
 Fever (low grade)
 Anorexia (mild or moderate), anemia (due to bleeding), fatigue
 Amenorrhea (no period)
 Point pain due to inflammation

Crohn’s disease
 May involve various segments of GI tract, from mouth to anus
 Involves all layers of the bowel wall
 With progression, lesions erode through full thickness of intestinal wall
 Ulceration results in adhesions, stiffing of the bowel wall, strictures, fistulas
 Fistulas form between loops of bowel, affect the bowel, bladder, vagina or skin
 Abscesses may occur

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Clinical Manifestations
 Diarrhea (moderate to severe)
 Crampy abdominal pain
 Anorexia may be severe (stop eating all together)
 Weight loss may be severe
 Growth delay may be severe
 Rectal bleeding rare (it effects the whole GI tract)
 Anal and perianal lesions-common
 Fistulas and strictures-common
 Amenorrhea

Going for a scope

 Empty stomach
 Spray
 NPO
 Empty bowels
They will admit a child
 NG tube with go lightly (laxative)
 Bring child to OR and knock them out

Diagnosis

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 Health history (when do pain start, Stool chart)

 Physical Exam: abdominal (bowel sounds), peri-anal and rectal exam, G & D
 Lab: CBC, stool testing, (white blood count, is there infection?)
 Radiography: upper GI (Xray), Ba swallow/enema, abdominal CT
 Endoscopy: sigmoid/colonoscopy with biopsy

Therapeutic management (UC and CD)

 Goals: 1) control the inflammation to reduce or eliminate the symptoms 2) obtain long-
term remission(could be years) 3) promote normal growth and development 4) allow as
normal a lifestyle as possible
 Nutritional support:
o Enteral and parental nutrition (could use IV or picc line depending)
(supplements)
o Well balanced high protein (helps heal), high- calorie
o Supplementation with multivitamins, iron folic acid (due to the weird stuff going
on in the bowels, low absorption)
 Meds: anti-inflammatories, anti-diarrheals(depending on the age and diagnosis the doc
will order this), antibiotics(high risk of infection), analgesics (due to pain), corticosteroids
(decrease inflammation, but this increases risk for infection) remember with corts you
need to taper it off
 Surgical intervention
o UC & CD when medical and nutritional therapies fail to prevent complications
 Colectomy and ileostomy
 Portions of bowel removed
 Supportive care (family)
o Chronic disease (there will be flair ups)
o Manage diet (high protein, high calories)

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o Coping with factors that increase stress & emotional lability (stress causes flare-
ups) or extreme happiness. Stay away from spicey foods. Greasy foods)
o Adjust to a disease with remissions and exacerbations
o Possibility of surgery (multiple times)
o Education services (Crohn’s & Colitis Foundation of Canada) have good info about
foods.

Infection (Nicole)
Tonsillitis and adenoiditis
 Inflammation of tonsils and adenoids:
 Tonsils have roles in immunity: masses of lymphoid tissue
 Etiology: occurs with pharyngitis, causative agent may be viral or bacterial (viral play its
course if bacterial = antibiotics and take full course)
 Take a swab to determine with strep, can do rapid but will be sent down
STREP GOING TO PATICEI
Strep stronger and longer antibiotic

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Tonsillitis
Clinical manifestations- caused by inflammation leads to infection
 Tonsils enlarge from edema
 Kissing tonsils
 Obstruct air or food (difficulty swallowing and breathing) Kids could be breathing
through their mouth or become apneic by 15 seconds
Therapeutic management
 Self-limiting, may need antibiotics
 Stay home, cold foods, Tylenol or fever and rest. If you get it 6 or more times a year or
apneic get referred to ENT
 Tonsillectomy- surgery (recurrent tonsillitis, airway obstruction (apnea)

Preoperative Assessment
 Recent URTI (upper resp infections)
 Elevated temp
 Allergies (meds)
 Hx of bleeding tendencies (back of throat highly vascular)
 Uncontrolled illnesses (Diabetes? Asthmatic?) want to know so we can watch
 Family hx of reaction to anesthetic. Children tend to be nauseous, give gravel before
they wake up.
 Loose teeth. Put them to sleep with mask then when they are asleep put in IV. As soon
as they are out if loose tooth, they take out the tooth. You are the tooth fairy.

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Postop care (both t&a)

 Side-lying or prone position (drooling a lot and hard to swallow)
 Monitor V/S
 Monitor for bleeding (blood in back of the throat, content swallowing is sign of bleeding
or clear their throat. There is something in the back of the throat. Bright red. When they
come back they will have old blood. Hugh risk for bleed. Admitted for 24 hours. If live
within 30 you can go out. If not admitted for 14 days.
 Small amt fluids when fully awake – avoid red or brown fld, no straw (causes neg
pressure on site and cause bleeding). Start with clear fluids and work the way up.
 Soft foods. For first 24 avoid dairy because it coats throat and thicken saliva. No hard or
spicy foods.
 Relieve throat pain (morphine and around the clock Tylenol
 Home management instructions (drinking lots, no dairy, no spicy or hard foods. Teach
signs and symptoms of bleeding so they can rush back to hospital)

Influenza (virus)
 Caused by 3 orthomyxovirusses
 Spread by direct contact or by articles contaminated by nasopharyngeal secretions
 1-3-day incubation period, infectious for 24 hours before and after the onset of
symptoms

Clinical manifestations – may be mild, moderate or severe (last 4-5 days)

 Dry throat & nasal mucosa, dry cough, hoarseness, flushed face, exhaustion, lack of
energy, fever, chills, joints hurt
o Croup is common especially in infants.
o Complications: pneumonia, secondary infections(ear infection), encephalitis

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Therapeutic management
 Treat symptoms at home
 Uncomplicated- symptomatic treatment (acetaminophen or ibuprofen, fluids, don’t want
to get dehydrated)
 Tamiflu (start within 2 days of symptoms) (children over the age of 1 can get Tamiflu)
Prevention
 Vaccine (yearly, education) these come in different strains, children can get it but have to
be over 6 months old. Frist time they need two. Frist then 4 weeks later to build
immunity and every year after 1 vaccine)
Nursing care
 Relieve symptoms (put on oxygen)

Otitis Media (OM)

 Inflammation of middle ear with or without effusion (build up of fluid on other side of
membrane)
 Causes: Strep pneumoniae or H. Influenza
 Peak incidence: 6 mos.- 2 yrs / 5- 6yrs
 Acute, chronic(get ear infection get antibiotic the two weeks later got it again), or acute
with effusion
 Prevention of recurrence (take full dose and still have symptoms go back and get
another med) Children end up with hearing lose because they didn’t treat the ear
infection right.

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Why is OM more common in infants and small children?

 A child’s eustachian tube is shorter, wider and straighter and more horizontal.

Risk factors/sequelae
 Secondhand smoke (that’s why you cant smoke in car)
 Daycare (germ pool)
 Supine positioning when eating/drinking (the fluid can leak in the tube) Sit up right hold
jaw.
 Possible sequelae: temporary hearing loss, mastoiditis or meningitis

Therapeutic Management
 If bolding fluid behind. Will look red and pus. Babies will pick, and sleep on that side.
Toddlers will try to pop their ears or could be jaw tooth
 Antibiotics, Analgesics, Antipyretics
 Nursing considerations include:
o Relieving pain
o Facilitating drainage
o Preventing complications or recurrence (go to ENT and put tubes in to help the
drainage and pressure. Day surgery, might be giving drops) Can’t go swimming or
if they do put plugs in. any time the head is near water use the plugs. After ENT
will send them for hearing test.
o Support and education of family
Pneumonia
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 Inflammation of the pulmonary parenchyma (can get it in one lode or one lung or both)
 Most frequent in early infancy/childhood, then in young adulthood
 May be primary or secondary disease (can get it you’re already sick)
 Symptoms vary based on etiology agent and patient status

Etiology of Pneumonias
 Bacterial- appear ill (what we will see most)
o Symptoms: high fever, shallow respirations (have the infection of the lungs and it
hurts), cough, chest pain (hurts to breath)
o Treatment: antibiotics (take pull course, give them chasers, if they throw up
within half hour and kept throwing up they will give IV), bedrest, (not going to
want to eat) fluids, antipyretics (fever and pain)
 Viral- occur frequently (RSV, influenza).
o Treatment- symptomatic, promote oxygenation (cool mist can help back big
breaths)) and comfort (antipyretics, fluids)
 Aspiration

Symptoms of pneumonia
 Fever
 Respiratory signs (anything of 60 RR they are NPO)- cough, tachypnea, chest pain
(pressure helps to release pain, when coughing use pillow to brace), retractions (skin
sucked into rids is a sign of resp destress)
 Behavior- irritable, restless
 GI signs- anorexia, vomiting (because breathing so fast)

Therapeutic Management
 Antibiotics and oxygen (it is a medication) (they will get admitted if they need oxygen)
 Close monitoring (every 15 mins or if they are bad one on one)
 Bedrest, hydration (IV) and antipyretics (fever and pain control)
o Prognosis usually good
o Potential complications include, pneumothorax (chest tube), otitis media, pleural
effusion

Aspiration pneumonia
 Risk for child with feeding difficulties (NG, someone is watching incase the tube moves)
 Prevention of aspiration
 Feeding techniques (chin thrust, sitting up straight), positioning
 Avoid these aspiration risks:

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o Oily nose drops

o Talcum powder

Bronchiolitis and RSV (usually occur together)

 Bronchiolitis-acute viral infection (bronchiolar level)
 RSV = respiratory syncytial virus
 Winter – Spring season (November to April) it depends on weather
 Transmission through direct contact. Live on surfaces for 30 minutes
 Bronchiolar mucosa swell, lumina fill with exudate, interstitial pneumonitis (alveoli
inflamed, hyperinflation and air trapping
 Dx: NP swab

Clinical Manifestations
 Initial: rhinnorhea (running nose… like a bath tub draining and gets thicker as they get
worse), pharyngitis, coughing, intermittent fever. Tachypneic
 Progression: increased coughing, wheezing, tachypnea, retractions (resp distress)
 Severe: listlessness, increased tachypnea, apneic spells (blue spells), deteriorating breath
sounds
 See a child and hear wheezes and course breath sounds and its clear. Its bad, there is
less oxygen getting in. retractions getting worse, bad sign

Therapeutic Management
 Cool humidified oxygen (moisten all mucous membrane and keep secretion thin)
o Pulse oximetry
 Fluids
 Airway maintenance (Head tilt chin lift) do assessment wherever they are comfortable
 Isolation (private room)
 Bronchodilators (see if it will help)
Prevention: RSV vaccine (there is criteria)

Nursing care
 Admitted, Separate rooms
 Droplet, contact and routine precautions
 NS nose drops and bulb syringe try and suck out the secretions. Do before feeds so they
can breath. If they become tachypneic stop feeding and put in IV

Croup Syndromes
 Characterized by hoarseness, resonant “barking” or “brassy” cough like a seal,
inspiratory stridor, and varying degrees of respiratory distress resulting from swelling or
obstruction in the region of the larynx.
 Small diameter of the airway (infants and children)
 Most cases are caused by viruses, due to immunization
 Croup syndromes affect larynx, trachea, and bronchi
o Epiglottitis, laryngitis, laryngotracheobronchitis (LTB), tracheitis
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Acute epiglottitis
 A medical emergency
 Usually occurs in children aged 2-5
 Clinical manifestations (onset is abrupt)
o Sore throat, pain, tripod positioning (sitting and leading over mouth open)
o Drooling, difficulty swallowing, Inspiratory stridor, mild hypoxia, distress
o Fever(inflamed epiglottis), irritable, restless, anxious
o Froglike croaking sound on inspiration (not hoarse) (one time we do not look in
throat, changing the tripod position can cut off air)
 Therapeutic management
o Prevention of progressive respiratory obstruction (hypoxia, acidosis, obstruction,
death) let them get in a position where they are comfortable
o Intubation or tracheostomy AT BEDSIDE
 Nursing care (serious and frightening)

Croup Syndromes Acute laryngotracheobronchitis

 Most common of the croup syndromes
 Generally affects children under 5 year, usually preceded by URTIs
 Manifestations
o low grade fever, stridor, seal like cough. Inspiratory stridor
o Suprasternal retractions
o Barky, brassy “seal-like” cough, hoarseness
o Increasing respiratory distress and hypoxia
o Can progress to respiratory acidosis, respiratory failure, and death

Therapeutic management
 Airway management
 Maintain hydration (not eating if they can’t breath), orally or intravenously
 High humidity with cool mist (take child outside in the cold. The cool air will get rid of it)
(hot shower making steam, put head in freezer)
 Nebulizer treatments: epinephrine(open up airway), budesonide (pulmacort) steroid
 Oral steroids nebs or IM, intramuscular dexamethasone
Nursing care (vigilant observation, assessment)

Acute spasmodic laryngitis

 Spasmodic croup (barking cough, stridor, give mist and cool air)
 Paroxysmal attacks of laryngeal obstruction
o Occur chiefly at night

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 Child usually feels well the following day

Bacterial tracheitis
 Infection of mucosa of the upper trachea
 Distinct entity with features of croup and epiglottitis (present the say as LTE but don’t
respond to treatment
 Clinical manifestations similar to LTB but unresponsive to LTB therapy
 Previous URTI with croupy cough, stridor, no drooling, no dysphagia, high fever
 Thick, purulent secretions result in respiratory distress. WBC elevated

Therapeutic management and nursing care

 Antipyretics
 Antibiotics
 May require intubation

Use bubbles to get them to take big breath.

Infection (communicable disease)

Infectious disease transmissible from one person to another
Communicable disease
 Manifestation of communicable disease dependent upon:
o Degree of pathogenicity
o Dose of infectious agent
o Resistance of host
o Correct mode of entry
 All must exist to create risk: just because they are exposed doesn’t mean you will get it
 Exposure does not mean person will become infected
Latent period
 period after infection of a host when infectious agent cannot be transmitted to another
host
Communicable period
 period after an infection when agent can be transmitted to another host
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Incubation period
 time between exposure and first appearance of Sx
Disease period
 time between first appearance of Sx and resolution of Sx
 resolution does not mean agent is destroyed just no more symptoms
Window phase
 period after infection in which antigen is present but no antibodies are detected

Chicken pox
 Agent- varicalla zoster virus
 Incubation period- 2-3 weeks, usually 14-16 days
 Communicability: 1-2 days before eruption of lesions (we don’t know we have it)
 Primarily affects skin
 Transmission
o through droplets (airborne) from mucous membranes
o direct contact with vesicle discharge & contaminated objects (the drainage and
they stick and crust on, if the goo touches you you’re exposed.
o Mouth and underside of toung

Signs and symptoms

 begins with respiratory S&S, malaise and low-grade fever
 Itchy rash with vesicular lesions that cover body
 More severe form in adults
o May cause pneumonia, disseminated infection in adults

Treatment & Preventive Care

 Standard Precautions & handwashing
 Isolation of children from public places until lesions are crusted and dry
 Antihistamines/Diphenhydramine (help with itching) pregnant woman need the vaccine
 Antivirals (acyclovir) for high-risk children (cancer)
 Varicella zoster immune globulin recommended if pregnant and with a substantial
exposure
 Oatmeal bath or cool bath, calamine cream, nails short the scratching causes scaring
 Push down on the pock when itchy and itchy goes away

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Infectious Mononucleosis
 Acute, self-limiting infectious disease
 Common among people younger than 25
 Usually mild, can be severe

Etiology and pathophysiology

 Herpes-like Epstein-Barr virus (don’t really know how its spread)
 Mechanism of spread not proven (believed to be in saliva by direct contact)
 Mildly contagious
 Period of communicability unknown
 Incubation period following exposure is 30-50 days.

Diagnostic tests
 Symptoms may appear from 10 days to 6 weeks after exposure
 Spot test (Monospot) blood work

Clinical manifestations
 Early: headache, malaise, fatigue, chills, low-grade fever, loss of appetite, puffy eyes
 Cardinal features: fever, sore throat, cervical adenopathy (lymph nodes)
 Common features: splenomegaly, palatine petechiae, exudative pharyngitis (sore throat
with pus on tansils), or tonsilitis, macular eruption

Therapeutic management
 No specific treatment
 Self-limiting, and uncomplicated (have to wait it out)
 Sore throat: gargles (salt water), hot drinks(whatever temp the sooths the troat),
lozenges
 Antibiotics are contraindicated (unless beta-hemolytic streptococci are present) that
comes from blood work

Nursing care
 Provide comfort
 Mild analgesic

Bacterial Meningitis
 Acute inflammation of the meninges and cerebrospinal fluid (CSF)

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 Decreased incidence following use of Hib vaccine in all age groups except for children
under 2 months of age
 A medical emergency and needs immediate action (need to find out what type of
bacteria it is so it can be treated)
 Can result in death
 Can be caused by various bacterial agents
o Mainly: Haemophilus influenza type b (HIB B), Streptococcus pneumoniae, group
beta streptococci (GBS) do when mom is going into labor, Neisseria meningitides,
Listeria monocyogenes
 Organisms can enter the blood from the nasopharynx or middle ear
o Also enter through penetrating wounds, skull fractures
 After implanting, the organisms spread into the CSF, infection spreads
 Causes edema(inflammation), going to keep growing then purulent exudate to cover
surface of the brain

Transmission
 Droplet infection from nasopharyngeal secretions
 Appears as extension of other bacterial infection through vascular dissemination
 Organisms then spread through CSF
 Droplet

Serious complications
 septic shock
 seizures (its in the head, at risk for seizures suction)
 hydrocephalus (also spina bifida, they will put in a shunt) (budging fontanelle, vomiting
and headache)
 deafness/blindness
 CP (ICP gets so much can cause brain damage
 Can be fatal

Diagnostic evaluation
 Diagnosis and differentiation based on CSF analysis
 CSF:
o WBC: elevated (infection)
o Protein: elevated (bacteria eats your protein and they create protein and
body makes more)
o Glucose: decreased (any CNS infection alters glucose in the brain)
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o Gram stain/culture: positive (show bacteria)

o Color: turbid or cloudy (should be clear, could see pus)
 Lumbar puncture

Clinical manifestations – children and teens

 Fever/chills (infection)
 Headache, nuchal rigidity (stiff neck, they cant put chin to chest because it hurts so
much) (increase pressure)
 Vomiting (pressure)
 Seizures (Pressure)
 Irritable, agitation (brain covered in pus)
 Photophobia, hallucinations, drowsiness (talk in third person)
 Kernig and Brudzinski signs (positive)
 Petechial or purpuric rash (medical emerg)
 Coma

Clinical manifestation – infant and young children

 Classic picture in above slide, rarely seen in children between 3 months and 2 years
 Fever (inflammation)
 Poor feeding/suck (infection)
 Vomiting
 Seizures (frequent) more prone
 High pitched cry (anything neurological high cry)
 Bulging fontanel
 Irritable

Petechial or purpuric rash

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Kernig Sign (can’t straighten, hamstrings hurt) Brudzinski Sign (Raise head, legs will come up)

Management
ARE THEY ALREADY DIAGNOSIS
First antibiotics beucase you already know they have it
Then isolation
 Diagnostic evaluation: LP is definitive diagnostic test
 Therapeutic management
o Isolation precautions
o Antimicrobial therapy (once it comes back postive, broadspectrum antibiotic, will
need picc line)
o Restrict hydration (don’t over hydrate, the pressure in the brain will alter
hormones so they may not be able to get rid of the fluid. Edema)
o maintain ventilation (airway)
o Management of systemic shock
o Reduction of ICP (trun off lights, reduce noise, reduce visitors, low voices)
o Keep body straight, neck hurts so flat pillow, head of bed at 30 degrees to help
drain the fluid
o Control of seizures and temperature (tylonal)

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o Treatment of complications (suction, airway, medications)

 Medications (antibiotic, antiepilectic, pain meds, fever
 Pain
 Nonspecific measures
 Prognosis
 Nursing care: family support: new baby and mom transmitted it
Once well again going to refer to
 Audiology
 Learning disabilities
 Spastic CP
Monitor
 Nero vitals
 Intake and output
 Care when waling around

Lumbar punture
 Insertion of spinal
 needle into
 subarachnoid space
 between the lower
 lumbar vertebrae.

Nonbacterial (Aseptic) Meningitis

 Inflammation of the meninges from one of a variety of enteroviruses (virus)
 Causative agents are principally viruses; enteroviruses are the most common cause of
viral meningitis.
 Onset is abrupt or gradual.
 S/S in older child usually preceded by nonspecific febrile illness (tonisiles)
 Manifestations: headache, malaise, muscle aches (neck pain), fever, photophobia nausea
and vomiting, and nuchal rigidity. The leg test may not be postive or as bad)
 Treatment is primarily symptomatic.
 Treat at home and just do the nursing
 Only do lumbar if you have the leg signs or the rash

Sepsis
 The body’s extreme response to an infection
o Sepsis is a life-threatening condition that occurs when the body’s response to an
infection injures its own tissues and organs.
 A life-threatening medical emergency

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 Infections can lead to sepsis, most often start in the lung, urinary tract(babies),
skin(scrach to mush at pocks), of gastrointestinal tract.
 Without timely treatment, sepsis can lead to tissue damage, organ failure, and death.
 Sepsis affects 30,000 Canadians each year, and over one-third of these will die if not
treated appropriately.

People at a higer risk of sepsis

 Adults 65 or older and young children
 People with weakened immune systems
 People with chronic medical conditions (e.g., diabetes, lung disease, cancer, kidney
disease)
 People with recent severe illness or hospitalization
 Children younger than one

Signs and symptoms

 High heart rate (weak pulse)
 Low blood pressure
 Confusion or disorientation (not enough O2 to brain)
 Extreme pain or discomfort (infection all over the place)
 Fever and flushed or, shivering, or feeling very cold
 Shortness of breath
 Clammy or sweaty skin (cold or hot)
 Dysfunction in vital organs (brain, heart, kidneys, lungs

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Lactate goes to high go into acidocsis, sign of sepsis

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KNOW THIS: WHAT TO DO FOR SEPIC

 Blood culture
 Antibiotics
 Push fluids (RL)
 If BP still low then start vasopressors

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Pediatric sepsis
 Sepsis in children presents differently from sepsis in adults.
 Children with neuromuscular disorders or cancer are at an increased risk of developing
sepsis.
 Children who have recently undergone surgery must also be closely monitored for signs
of sepsis. (cold shock and HR low or heat shock and HR high)
 Sepsis may present in different ways: either a “cold shock” (a drop in temperature and
heart rate) or a “heat shock” (a high fever and very quick heart rate). Tachpenic
 Due to its added vagueness, it is crucial to seek medical help as soon as you suspect a
child may have developed sepsis.
 Assessment, ask partents

Signs and symptoms

 Cold and clammy hands and feet OR red and flushed skin
 Weak and feeble pulse
 Heart rate either much slower OR much quicker than normal
 Quick breathing
 Confusion, decreased mental capabilities (based on their age and development)

Neonatal sepsis
 Neonatal sepsis occurs in infants less than four weeks old.
 Premature infants and infants with chronic lung disease or congenital heart disease are
at a high risk of developing sepsis.
 Sepsis may occur at early onset (~6 hours after birth) or late onset (up to four weeks
after birth
 Symptoms are variable and hard to spot, so it is important to watch closely for signs of
infection and seek medical attention immediately.

Signs and symptoms

 Diminished spontaneous activity
 Less vigorous sucking, refusal to eat
 Low heart rate
 Respiratory distress
 High fever OR very low temperature
 Jaundice (especially in early onset neonatal sepsis)
 Abdominal distention

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Systemic Inflammatory Response Syndrome (SIRS) Criteria

 The SIRS criteria are used to aid in the diagnosis of sepsis. If a client has 2 or more of the
following SIRS criteria plus a suspected or confirmed infection than they are believed to
have Sepsis.
 Sepsis plus changes in lactic acid (high), blood pressure, and organ dysfunction is severe
sepsis.
 Septic Shock is when a client has severe sepsis and cannot maintain their blood pressure
despite IV fluid resuscitation.

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