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289 Cards in this Set

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Urinary Tract Infection (S/Sx)
Nausea, vomiting, anorexia, chills, nocturia, urinary frequency, urgency
Suprapubic or lower back pain, bladder spasms, dysuria, burning on urination
Urinary Tract Infection Objective Data for Assessment
Fever
Hematuria; foul-smelling urine; tender, enlarged kidney
Leukocytosis, positive findings for bacteria, WBCs, RBCs, Pyuria, Ultrasound, CT scan, IVP
Normal pH of Urine
5-9
Normal Specific Gravity of Urine
1.001 to 1.035
Normal Protein in Urine
< 20 mg/dL
Normal bilirubin in Urine
Up to 1 mg/dL
What should not be present in urine?
Glucose, Ketones, Hgb, WBCs, RBCs, Casts, Nitrites
UTI: Causes
Escherichia coli most common pathogen
Streptococci
Staphylococcus saprophyticus
Occasionally fungal and parasitic pathogens
Types of UTIs
Recurrent—repeated episodes
Persistent—bacteriuria despite antibiotics
Febrile—typically indicates pyelonephritis
Urosepsis—bacterial illness; urinary pathogens in blood
UTI: Etiology and Pathophysiology
Alteration of defense mechanisms increases risk of UTI
Organisms usually introduced via ascending route from urethra
Less common routes
Bloodstream
Lymphatic system
Pediatric Manifestations of Urinary Tract Infection
Frequency
Fever in some cases
Odiferous urine
Blood or blood-tinged urine
Sometimes no symptoms except generalized sepsis
UTI: Diagnostic Studies
Dipstick
Microscopic urinalysis
Culture
Clean-catch is preferred
U-bag for collection from child
Specimen obtained by catheterization or suprapubic needle aspiration has more accurate results
May be necessary when clean-catch cannot be obtained
UTI Care
Drug Therapy—Antibiotics plus pain relief
Uncomplicated cystitis: short-term course of antibiotics
Complicated UTIs: long-term treatment
Trimethoprim-sulfamethoxazole (TMP-SMX) or nitrofurantoin
Amoxicillin
Cephalexin
Others
Gentamycin, carbenicillin ++
Pyridium
Combination agents (e.g., Urised) used to relieve pain
Hypospadias
Congential anonmaly: Urethral meatus opens on ventral surface of penis
Affects 1 in 250 live male births
Hypospadias Repair
Preferred repair to begin between 6 and 12 months old. May need two stage repair.
Post-op care:
Hospital stay less than 24 hours
Pain control: acetaminophen with codeine
Monitor urinary output – catheter in place initially
Assess amount of incisional edema – compression bio-occlusive dressing
No straddle toys for 2 to 3 weeks
No rough play, sandbox, swimming or tub baths until healed
Diet high in protein and fiber and extra fluids
Types of Renal Failure
Acute renal failure (ARF)
Chronic renal failure (CRF)
Acute Renal Failure
Definition: kidneys suddenly unable to regulate the volume and composition of urine
Not common in children
Principal feature is oliguria:less than .5mL/kg/hour in infants
Associated with azotemia, metabolic acidosis, and electrolyte disturbances
Most common cause of Acute Renal Failure
Most common pathologic cause: transient renal failure resulting from SEVERE DEHYDRATION
What do you assess for in Acute Renal Failure
Assess for hypertension, edema or SOB from possible volume overload due to retained fluid
Normal Urine Output for Neonates
50- 300 cc/day
Normal Urine Output for Infants
300-500 cc/day
Normal Urine Output for Preschooler
500-800 cc/day
Normal Urine Output for School Age
600-1400 cc/day
Normal Urine Output for Adolescents
1000-1500 cc/day
Acute Renal Failure- reversible or not?
yes. it is reversible
What will labs show in Acute Renal Failure?
increased serum BUN and creatine
Therapeutic Management Acute Renal Failure (Tx)
Therapeutic management
Treat underlying cause
Foley to r/o retention
Volume restoration to increase fluid flow to kidneys if dehydrated
Correct fluid and electrolyte imbalances
Diet higher in carbohydrates and fats, lower in protein
Chronic Renal Failure (CRF)
Begins when diseased kidneys cannot maintain normal chemical structure of body fluids
Progressive deterioration over months or years
Can be from any disease that gradually destroys the nephrons (such as chronic pyelonephritis or chronic glomerulonephritis)
Most common cause before age 5 is due to renal and urinary tract congenital malformations
Clinical syndrome called uremia
Less than 25% glomerural filtration
Can have up to 75% of nephrons destroyed and kidneys will still function
Chronic Renal Failure S/Sx
Child appears pale, low energy
May have elevated B/P
Behind on growth chart
Poor appetite, nausea and vomiting as disease progresses
Nephrotic Syndrome
Group of symptoms and not a specific disease
Condition in which the kidneys lose a significant amount of protein in urine
Most common presentation of glomerular injury in children
Characteristics of Nephrotic Syndrome
Proteinuria
Hypoalbuminemia
Hyperlipidemia
Periorbital or Ankle Edema
Weight Gain
Massive urinary protein loss
Decreased Urinary Output
Fatigue, pallor, possible hypertension
Urine is dark and frothy
Nephrotic Syndrome Management
Supportive care
Diet
Low to moderate protein
Sodium restrictions if large amount of edema
Steroids
2 mg/kg divided into BID doses
Prednisone drug of choice (cheapest and safest)
Immunosuppressant therapy (Cytoxan)
Diuretics
Chronic Renal Failure (CRF) Tx
Diet is the most efficient treatment. Limit proteins but leave enough for growth
Diet adequate calories and protein for growth while minimizing demands on kidney. Restrict dietary phosphorus
Treat with dialysis or kidney transplant
Nursing Interventions for Nephrotic Syndrome
Administer Corticosteriods (Prednisone!!!!) as ordered
Educate family that relapses are to be expected
Supportive TX
Diet!!!!: restrict sodium and fluids during edema phase
Diuretics and pain meds sometimes helpful
Elevate or support edematous body parts such as scrotum, abdomen and legs
Monitor for skin breakdown
Nephrotic Syndrome S/Sx
massive edema, weight gain (weigh every day w same amount of clothing), elevated specific gravity, elevated BP, not hungry dark frothy urine, elevated lipids and elevated cholesterol (unknown why)
How do you diagnose Nephrotic Syndrome?
Diagnosed with Renal Biopsy
Side effects of corticosteroids
causes cataracts, stunts growth, cranky kid, look kinda chunky with moon face, striae, raises blood glucose
Glomerulonephritis
Inflammation of glomerular tissues
Glomerulonephritis Symptoms
Generalized edema due to decreased glomerular filtration
Begins with periorbital
Progresses to lower extremities and then to ascites
Key Factors of Glomerulonephritis
HTN due to increased ECF
Oliguria
Hematuria
Bleeding in upper urinary tract → smoky urine
Proteinuria
Increased amount of protein = increase in severity of renal disease
Most common cause of Glomerulonephritis
untreated streptococcal infection

(most are postinfectious)
Acute Poststreptococcal Glomerulonephritis (APSG)
Autoimmune response
Onset 5 to 12 days after other type of infection
Often group A β-hemolytic streptococci
Most common in children 6 to 7 years old
Uncommon in younger than 2 years old
Can occur at any age
Types of Glomerulonephritis
Infection or autoimmune response
Acute Poststreptococcal Glomerulonephritis (APSG) S/Sx
periorbital edema worse in morning, loss of appetite, decreased urinary output, dark colored urine, hx of recent streptococcal infection
Prognosis of Glomerulonephritis
95%—rapid improvement to complete recovery
5% to 15%—chronic glomerulonephritis
1%—irreversible damage
Nursing Management of APSG (Acute post-streptococcal glomerulonephritis)
Administer meds as ordered (antibiotics, possible B/P meds, diuretics, steroids)
Manage edema
Daily weights
Accurate I&O
Daily abdominal girth
Nutrition
Low-sodium, low to moderate protein
Susceptibility to infections
Bed rest is not necessary
Observe for signs of potential renal failure: oliguria, azotemia V.S. changes, weight gain
Types of Trauma
Nonintentional injury
Child abuse injury
Childhood characteristics affecting susceptibility to injuries
-Epiphyseal plate present (may help heal faster, may disrupt growth- stunted or crooked)
-Bones are growing
-Bones more plastic
-Periosteum thicker (also helps shorten healing time)
Prevention of injury
Epiphyseal Injuries
Weakest point of long bones is the cartilage growth plate (epiphyseal plate)
Frequent site of damage during trauma
May affect future bone growth
Treatment may include open reduction and internal fixation to prevent growth disturbances
The Immobilized Child
Immobilization was once thought to be restorative from illness and injury
We know now that immobilization has serious consequences
-Physical
-Social
-Psychologic
Physiologic Effects of Immobilization- Muscular System
Muscular system
Decreased muscle strength and endurance
Atrophy
Loss of joint mobility
Physiologic Effects of Immobilization- Skeletal System
Skeletal system
Bone demineralization
Negative calcium balance
Physiologic Effects of Immobilization- Cardiovascular System
Cardiovascular system
Decreased efficiency of orthostatic neurovascular reflexes
Diminished vasopressor mechanism
Altered distribution of blood volume
Venous stasis
Dependent edema
Physiologic Effects of Immobilization- Respiratory
Respiratory system
Decreased need for oxygen
Diminished vital capacity
Poor abdominal tone and distention
Mechanical or biochemical secretion retention
Loss of respiratory muscle strength
Physiologic Effects of Immobilization- GI System
GI system
Distention caused by poor abdominal muscle tone
Difficulty feeding in prone position
Gravitation effect on feces
Chart BMs!

No one likes a constipated kid.
Anorexia
Physiologic Effects of Immobilization- Integumentary System
Integumentary system
Decreased circulation and pressure leading to decreased healing capacity
Physiologic Effects of Immobilization- Urinary System
Urinary system
Alteration of gravitational force
Difficulty voiding in supine position
Urinary retention
Impaired ureteral peristalsis
Physiologic Effects of Immobilization- Neurosensory System
Loss of innervation
-If nerve tissue is damaged by pressure
-If circulation to nerve tissue is interrupted
-Effects of improper positioning
Sensory and perceptual deprivation
Psychologic Effects of Immobility
Diminished environmental stimuli
Altered perception of self and environment
Increased feelings of frustration, helplessness, anxiety
Depression, anger, aggressive behavior
Developmental regression
Fractures
Common injury in children
Methods of treatment different in pediatrics than in older adult population
Rare in infants, except with MVC
Clavicle most frequently broken bone in child, especially younger than age 10
School age: bike, sports injuries
Types of Fractures
Compound or open: fractured bone protrudes through the skin
Complicated: bone fragments have damaged other organs or tissue
Comminuted: small fragments of bone are broken from the fractured shaft and lie in surrounding tissue
Greenstick: compressed side of bone bends, but tension side of bone breaks, causing incomplete fracture
Clinical Manifestations of Fracture
Generalized swelling
Pain or tenderness
Diminished functional use
May have bruising, severe muscular rigidity, crepitus
Assessment of Fractures
The Five Ps
Pain and point of tenderness
Pulse—distal to the fracture site
Pallor
Paresthesia—sensation distal to the fracture site
Paralysis—movement distal to the fracture site
Bone Healing and Remodeling for certain ages
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
The Child in Traction
Traction: extended pulling force may be used to:
Provide rest for an extremity
Help prevent or improve contracture deformity
Correct a deformity
Treat a dislocation
Allow position and alignment
Provide immobilization
Reduce muscle spasms (rare in children)
Traction: Essential Components
Traction: forward force produced by attaching weight to distal bone fragment
-Adjust by adding or subtracting weights
Countertraction: backward force provided by body weight
-Increase by elevating foot of bed
Frictional force: provided by patient’s contact with the bed
Types of Traction
Manual traction: applied to the body part by the hand placed distally to the fracture site
Skin traction: pulling mechanisms are attached to the skin with adhesive material or elastic bandage
Skeletal traction: applied directly to skeletal structure by pin, wire, or tongs inserted into or through the diameter of the bone distal to the fracture
Cervical Traction
Tongs inserted through burr holes in skull with weights attached to the hyperextended head
As neck muscles fatigue, vertebral bodies gradually separate so the spinal cord no longer pinched between vertebrae
Halo traction can be applied in some cases
Nursing Considerations for the Kid in Traction
Assessing the patient in traction
Skin care issues
Pain management/comfort
Dis-traction
Process of separating opposing bone to encourage regeneration of new bone in the created space
Can be used when limbs are unequal in length and new bone is needed to elongate the shorter limb
External Fixation
Ilizarov external fixator
Permits limb lengthening by manual distraction
Therapeutic Management of Sports Injuries
Traumatic Injury
Soft tissue injury: injuries to muscles, ligaments, and tendons
-Sports injuries
-Mishaps during play
ICES
-Ice, Compression, Elevation, Support
Alleviate repetitive stress
Rest as primary therapy
-Usually means reduced activity and alternative exercises, not bedrest
Nurse’s Role in Sports for Children and Adolescents
Evaluation for activities
Prevention of injury
Treatment of injuries
Rehabilitation after injuries
Instruction to student and parents
Legg-Calve-Perthes Disease
Self-limited, idiopathic, occurs in children ages 3 to 12, more common in males ages 4 to 8
Avascular necrosis of femoral head
10% to 15% of cases have bilateral hip involvement
Most have delayed bone age
May present with hx of limp, soreness, stiffness or pain in hip or knee worse in early morning and at the end of long day of physical activities
Diagnosed by x-ray
Therapeutic Management of Legg-Calve-Perthes Disease
Treatment goal: keep head of femur in acetabulum
Containment with various appliances and devices such as an abduction cast
Rest, no weight bearing initially to reuce inflammation and restore motion
Surgery in some cases
Home traction in some cases
Pathophysiology of Legg-Calve-Perthes Disease
cause unknown but involves disturbed circulation to the femoral head with ischemic aseptic necrosis
After resolving, may have normal femoral head or may have severe alteration
Prognosis of Legg-Calve-Perthes Disease
Self-limited disease
Outcome has wide variations due to multiple factors. Younger children (under age 5) have better outcomes due to less femoral damage before tx is implemented
Nursing considerations for Legg-Calve- Perthes Disease
Identification of affected children and referral
Teaching care and management. Conservative therapy with braces may continue for 2 to 4 years
Compliance issues with child/family
Slipped Femoral Capital Epiphysis (SFCE)
Spontaneous displacement of the proximal femoral epiphysis in a posterior and inferior direction
Occurs shortly before or during accelerated growth periods or puberty (12-14 yr old males)
Usually idiopathic, multifactorial
Obesity, puberty hormone changes, bone changes
Clinical Manifestations of SFCE
Clinical manifestations
Episode of trauma with acute displacement
Gradual displacement without definite injury
Intermittent displacement (or combination of all)
Suspected with hx of pain in hip, knee or inner thigh in an adolescent
Therapeutic Management of SFCE- Slipped Femoral Capital Epiphysis
internal pinning to keep bone from slipping and close the physeal plate. Corrected as soon as possible after dx (usually within 24 hours)
Nursing Considerations of SFCE
Assess for post surgical complications of fever, drainage, swelling, numbness, color change in limb or contralateral hip pain.
Bedrest initially. Nonweight bearing on affected limb for 2 to 8 weeks
Scoliosis
The most common spinal deformity
Complex spinal deformity
-Lateral curvature
-Spinal rotation causing rib asymmetry
-Thoracic hypokyphosis
May be congenital or develop
Osteomyelitis
Inflammation and infection of bony tissue
May be caused by exogenous or hematogenous sources
Infectious agent invades the bone following penetrating wound, open fracture, contamination in surgery, or secondary extension from an abscess or burn
S/Sx and Diagnosis of Osteomyelitis
Signs and symptoms begin abruptly; resemble symptoms of arthritis and leukemia
Marked leukocytosis
Bone cultures obtained from biopsy or aspirate
Early x-rays may appear normal
Bone scans for diagnosis
Therapeutic Management of Osteomyelitis
May have subacute presentation with walled-off abscess rather than a spreading infection
Prompt, vigorous IV antibiotics for extended period (3 to 4 weeks or up to several months)
Monitor hematologic, renal, hepatic responses to treatment
Nursing Considerations for Osteomyelitis
Complete bedrest and immobility of limb
Pain management concerns
Long-term IV access (for antibiotic administration)
Nutritional considerations
Long-term hospitalization/therapy
Psychosocial needs
Osteogenesis Imperfecta (OI)
A group of heterogeneous inherited disorders of connective tissue
Characterized by excessive fragility and bone defects
Defective periosteal bone formation and reduced cortical thickness of bones
Hyperextensibility of ligaments
Juvenile Rheumatoid Arthritis (JRA)
Also called juvenile chronic arthritis or idiopathic arthritis of childhood
Peak ages: 1 to 3 years and 8 to 10 yea
Actually a heterogenous group of diseases
Pauciarticular onset (involves ≤4 joints)
Polyarticular onset (involves ≥5 joints)
Systemic onset (high fever, rash, hepatosplenomegaly, pericarditis, pleuritis, lymphadenopathy)

90% children have negative rheumatic factor
Symptoms may “burn out” and become inactive
Chronic inflammation of synovium with joint effusion, destruction of cartilage, and ankylosis of joints as disease progresses
S/Sx of JRA
Stiffness
Swelling
Loss of mobility in affected joints
Warm to touch, usually without erythema
Tender to touch in some cases
Symptoms increase with stressors
Growth retardation
Diagnosis Of JRA Based on American College of Rheumatology Criteria
Age of onset younger than 16 years
One or more affected joints
Duration of arthritis more than 6 weeks
Exclusion of other forms of arthritis
JRA: Therapeutic Management
No specific cure
Goals of therapy: preserve function, prevent deformities, and relieve symptoms
Iridocyclitis/uveitis
Inflammation of iris and ciliary body
Unique to JRA
Requires treatment by ophthalmologist
Therapy individualized to child
PT, OT
Nutrition, exercise
Splinting devices
Pain management
Systemic Lupus Erythematosus (SLE)
Chronic, multisytem, autoimmune disease of connective tissues and blood vessels
Characterized by inflammation
Symptoms variable and unpredictable
More common in females ages 10 to 19 years
More common in African-American, Asian, and Hispanic children
Familial tendency
Cause unknown
Possible triggers: hormonal imbalance, immune disorders, environmental exposure to drugs, infection, stress, chemical agents
SLE: Clinical Manifestations
Cutaneous lesions, lymphadenopathy
Nausea, vomiting, diarrhea, abdominal pain
Generalized weakness, arthritis, joint pain and stiffness without deformity
Forgetfulness, seizures, paralysis
Pleurisy, pericarditis
Proteinuria and renal failure
SLE: Therapeutic Management
Goals of treatment
-Supportive care
-Pharmacology
Nursing considerations
-Minimize exacerbations
-Therapy compliance
-Body image concerns
What is the second leading cause of death in children ages 1 to 14 years
Childhood cancer
Childhood Cancer statistics
Incidence approximately 129 per million
Leukemia most common pediatric cancer
Next most common are brain tumors and lymphoma
Greatly improved prognosis in past 30 years
Types of Cancers
Leukemia
Lymphoma
Nervous System Tumors
Bone Tumors
Other Solid Tumors
Nursing Assessment:
General Signs & Symptoms of Pediatric Cancer
Fever (because they can't fight off infection as WBC are compromised)
Pain
Swollen Lymph Glands
Bruising (decreased platelets)
Anemia (depression of RBCs in Leukemia)
Abdominal Mass
White Reflex (retinal blastoma)
Diagnostic Evaluation
History
Physical Examination
Biopsy
Imaging
Laboratory Testing
Types of Therapy for Cancer
Surgery
Chemotherapy (via vascular access device)
Radiation
Bone Marrow Transplant
Radiation to Brain for Children
Not done anymore because it caused major learning problems.
Leukemia Definition and two main types
Malignancy of blood forming cells.
RBC, WBC & Platelets and always affected by Leukemia
Acute Lymphoblastic Leukemia = (ALL)
Acute Myeloid Leukemia = (AML)
Three Main Consequences of Leukemia
1. Anemia from decrease in RBC
2. Infection from Neutropenia (decreased WBC)
3. Bleeding tendencies from decrease in platelets (Thrombocytopenia)
Leukemia
Average Age
peak incidence occurs from 3 – 5 years
Leukemia is more common in which gender?
slightly higher in males
Risk Factors for Leukemia
Down Syndrome, exposure to large amounts of
radiation and certain chemicals (benzene)
Pathophysiology of Leukemia
Unrestricted proliferation of Immature WBC it just acts an an energy hog.
It divides but does not mature past blastate and is released. As they increase in number few and few blood cells are made by the marrow.
The leukemic cells such up energy (glucose) and space. When they invade bone marrow, they weaken the bones.
Spleen and liver become filled with leukemic cells.
May get into the brain and cause increased cranial pressure.
Leukemia's Primary Signs and Symptoms
Fatigue
Recurrent Fever of unknown origin *
Infections (not responding to antibiotics)*
Pallor
Bruise/bleeding*
Abdominal pain
Petechiae
Swollen lymph nodes
Hepatosplenomegaly
Testicular mass (12-25 yrs)
Bone & Joint pain
Nosebleeds
Generalized weakness
Nursing Priorities for a Child with Leukemia
Private Room
High calorie, high protein diet- let them choose
Administers anti-emetics way before treatment
Conserve energy
Infection control (wash your damn hands)
Use soft bristled/sponge toothbrush
Avoid impact activities
Don't palpate spleen (because of hepatosplenomegaly)
Diagnostic work up for Leukemia
Complete History & Physical Exam
Lab work (CBC with diff., Complete metabolic panel, uric acid, PT/PTT, Ca+, Phosphate, K+, Sed rate)
CXR
Bone Marrow Aspiration & Biopsy
Lumbar puncture (LP)

Bone Marrow Aspiration is the most definitive test (normal contains less than 5% of immature WBCs. Leukemia has 90% at time of diagnosis
Types of Therapy for Leukemia
Chemotherapy (PO, IV, IM, IT)
Common Types: Vincristine, Asparaginase, Methotrexate,Steroids
Cranial and spinal radiation
Bone marrow transplant
Allogenic (matched sibling, unrelated donor or related cord blood)
Autologous (Pt’s own marrow)
Syngeneic (Identical twin )
PHases of Chemotherapy (for Leukemia)
Induction phase- big blast of chemo to bring about a remission as soon as possible. It’s the highest dose possible for the child. Also potentially the most life-threatening. This is when the child is most vulnerable.
Approx. 90-98% with ALL will go into remission 4-6 wks after treatment has started. Must to another bone marrow aspiration to determine

CNS Prophylaxis- the second phase of treatment. Given in intrathecal route- directly into Spinal column. May be done in outpatient treatment.
The child may then undergo another induction phase.

Maintenance phase- reduce Leukemic cells further. May be in this phase for years.

If the child relapse they go back to the beginning and start induction phase again.

Will do bone marrow transplant when child is constantly relapsing
Lymphomas Definition and Types
Def: malignant solid tumor of the immune system’s cells (Lymphocytes)
Hodgkin’s (HL)
Non-Hodgkin’s (NHL)
Hodgkins Lymphoma S/Sx, Diagnosis and Treatment
Painless, enlarged, firm, non-tender lymph nodes
Night sweats
Weight loss
Fever
Mediastinal mass
Hepatosplenomegaly
Fever of unknown origin
has Reed-Sternberg Cells found in lymph node biopsy. It typically occurs between 15-34 years mostly 15-19 years and then again at age 50. Itchy feeling. Stays confined to lymph nodes. Child will typically undergo surgery where they are opened from sternum to pubic bone to see if it has spread. Staged 1-4. Treatment is based on stages.
Lymphoma Diagnosis and Ages
Diagnosis: by biopsy only

Age:
HL: rare before the age of 5
NHL: incidence peaks at 5-7 years and again at 12-14 years of age
*(60% of lymphomas are NHL)
Non-Hodgkins Lymphoma S/Sx, Diagnosis and Treatment
Non-Hodgkins
Mediastinal mass
Abdominal pain
Nausea/vomiting
Hepatosplenomegaly
Lymphadenopathy
CNS and possible bone marrow involvement
Rapid growing, usually metastatic at diagnosis

NH- spreads early and is more aggressive. There are multiple cell types so it’s more difficult to diagnose. Treatment is aggressive chemo. Child will look sicker
Diagnostic Work Up for Lymphomas
Physical exam
Lab work (same as for leukemia)
CXR
CT: neck, chest, abdomen and pelvis
PET Scan
Bone scan
Bone marrow aspiration and biopsy
Surgical lymph node biopsy
CSF for cytology
Types of Therapy for Lymphomas
Chemotherapy (HL and NHL)
Radiation therapy (HL and NHL)
Bone marrow transplant (HL and NHL)
Surgery (NHL) resection of localized tumor
Brain Tumors
Primary vs. Metastatic
Primary: Arise from normal cells within the brain. Can be benign or malignant.

Metastatic: Originate outside CNS. Always malignant. May present as primary diagnosis or relapse.
Brain Tumor Types
Astrocytoma:
High grade (more aggressive)
Low grade (localized)
Common sites: cerebellum, cerebral hemispheres, hypothalamus
Account for the majority of pediatric brain tumors

Medulloblastoma:
Arises in posterior fossa region, near brain stem
Tendency to spread to other areas of brain and spinal cord
Occur most often in first decade of life
More common in males
Brain Tumors
Presenting symptoms
Headache (new onset, persistent)
Morning Vomiting
Unsteadiness in walking
Clumsiness/Falls
Seizures
Weakness in arms and legs
Visual problems
Mental status changes (lethargy)
Personality/Behavioral changes
Increase head circumference
Loss of bowel and bladder function
Generalized ill feeling
Brain Tumors
Diagnostic work up
Neurological history and exam
CT scan
MRI
CSF cytology
Alfa feto protein (AFP)
Brain Tumors
Type of therapy
Surgery (total resection or debulking)
Chemotherapy (“blood brain barrier” may need to be intrathecal)
Radiation therapy
used for older children (>3 years) or aggressive tumors
Experimental drugs
Neuroblastoma
Neuro “nerves”, Blastoma “cancer affecting immature of developing cells”
Most common tumor in infants younger than 1 (commonly a fetal origin)
Rarely occurs past early school age
Develops in abdomen or adrenal gland
Most patients have widespread disease at diagnosis.
Neuroblastoma
Signs and Symptoms
Fevers
Anemia/fatigue
Wt. loss
mass in neck or abdomen **(crosses midline) causing pain, irritability, distention, respiratory distress.
Bone pain (limp/refusal to walk)
weakness and/or paralysis in lower extremities
Constipation/diarrhea
Neuroblastoma
Diagnostic Workup/Treatment
Renal X-ray
CT/MRI
Bone scan
Bone marrow biopsy
Urine catecholamine's and vanillylmandelic (VMA)

Tx:
Surgical resection
Chemotherapy
Stem cell transplant (last resort)
Radiation therapy
Bone tumors
Two Types
Osteosarcoma
Ewing's Sarcoma
Osteosarcoma
Definition
Location
Peak Incidence
Sx & Tx
Malignant tumor of the bone
Most common type of bone cancer in children and teens
Location: either side of knee or upper arm
Peak incidence: during adolescent growth spurts
Symptoms: pain, swelling, occ. fracture at tumor site
Treatment: surgery and chemotherapy
Ewing’s Sarcoma
Location
Peak Incidence
Sx & Tx
Bone tumor that infiltrates surrounding soft tissue
Location: arms, legs, pelvis or chest wall
Peak incidence: between 10 and 20 years of age
Symptoms: pain, swelling at the sites, fever
Treatment: surgery, radiation
and chemotherapy
Wilms Tumor
Definition
Location
Peak Age
Sx & Tx and prognosis
Solid tumor of the kidney

Associated with congenital syndromes
(aniridia, GU abnormalities)

Location: firm flank mass, not crossing midline

Peak age: 2-3

Symptoms: abdominal pain, anorexia, vomiting, hematuria, HTN **Do not palpate abdomen**

Treatment: nephrectomy, chemotherapy and radiation

Prognosis: Favorable survival, depending on histology and grade

HTN is due to pressure on renal artery
If one twin has it, likely that the other will as well.
Rhabdomyosarcoma
Definition
Location
Peak Age
Sx & Tx and prognosis
Aggressive malignant soft tissue tumor

Location: can arise anywhere in body,
most are found in head & neck region

Peak age: under age 6 & teens 15-19

Symptoms: depending on location Eye edema, facial palsies, hematuria, vaginal Bleeding, anatomical deformity, pain, or painless mass and functional impairment

Treatment: biopsy, surgery to remove tumor, chemotherapy, radiation therapy

Prognosis: Survival relating to site and stage
Retinoblastoma
Definition
Location
Peak Age
Sx & Tx and prognosis
Malignant tumor of the retina (single tumor in one eye or multiple tumors in one or both eyes)
Peak age: before 3 years of age
Location: retina
Signs/Symptom: white reflex “cat’s eye”, can be seen in a photograph, poor vision, strabismus, eye pain (pressure of tumor)
Genetic predisposition (parents, siblings should have eye examinations)
Treatment: laser therapy, cryotherapy, radiation, removal of the eye
Prognosis: depends on size and extent of tumor
usually excellent
Infection and Cancer
Reason
S/Sx
Sites
Treatment
Reasons: disease process or immunosuppression related to chemotherapy and radiation therapy

Sources: bacterial viral, fungal, protozoa

Signs: fever (>101F), chills, lethargy, altered LOC, tachycardia, hypotension

Sites: implanted devices (port-a-cath, broviac, VP shunt), mouth, skin, rectal area

Treatment:
blood culture (peripheral & central line),
urine culture (before initiating antibiotics)
Saline bolus and initiation of IV antibiotics
Good and frequent hand washing
Lab work for Children with Cancer
WBC, Hgb, Hct, Platelets
Neutropenia: decreased neutrophil count
Absolute neutrophil count (ANC)
Important in determining medical management of patient

ANC = WBC x (segs % + bands %)

Mild ANC: 1500 – 1900
Moderate ANC: 1000 – 1400
Severe ANC: < 500
Thrombocytopenia Risk of Hemorrhage
in Cancer
Defined as low platelet count

Normal: 150,000 to 450,000 cells/mm2
Mild: > 75,000
Moderate: 50,000 to 74,900
Mod. Severe: 25,000 to 49,900
Severe: < 25,000

Platelet cells help to stop bleeding
Life span of 8-10 days
transfusion of Platelets < 20,000 unless actively
bleeding or surgery or procedure (LP)

Signs and symptoms of bleeding:
bruising, petichiae, epistaxis, prolonged bleeding, heavy
menses
Nursing interventions of Thrombocytopenia
No rectal temperature
No suppositories
Avoid constipation
Avoid NSAIDS/ASA
Transfusion guidelines
Transfuse with platelets
Pheresed products
Type specific
Single/random donor units

Premeds: Tylenol & Benadryl
Nausea/Vomiting in relation to Chemo
Causes:
chemotherapy, radiation therapy, disease process

Types:
anticipatory, acute and delayed

Nursing management:
Prevention is always better than treatment
Pre-medicate !!!!
Give medication on time NOT prn, don’t delay
Environmental odors (no perfume, take lid of food outside the room, good ventilation in room)
Give kids whatever they want to eat, do not force food during the chemo

Common anti-nausea medications: Benadryl & Reglan, Zofran, Ativan
Prevent constipation
Constipation in Kids with Cancer
Medication induced: Vincristine, Pain Medications

Management

Monitor stool frequently
Daily Laxative and/or stool softeners
High fiber diet, increased fluids (1/2 bodyweight in ounces)
Careful abdominal assessment (bloating, firmness, pain)
No rectal manipulation or medications (neutropenia, thrombocytopenia)
Increase activity as tolerated
Provide opportunity and privacy for stooling (older kids)
Diarrhea in Kids with Cancer
Causes
medication, infection (rotavirus, C-diff)

Management
Good history taking of current meds/diet
Stool cultures (WBC, C-diff, Ova & Parasites,
Rotavirus)

Nursing management
Low residue diet
Barrier creams (diaper rash, candida), sitz baths
Fluid & electrolyte replacement therapy
Odor control
Monitor bowel sounds/abdominal girth
Check stool for blood
Altered Nutrition:
Causes
Goals
Meds
Causes
chemotherapy, radiation therapy, disease process
taste alterations, mucositis/esophagitis xerostomia, dysphagia, N/V, electrolyte imbalances, weight changes, cachexia, ascites

Goals of nutritional support
Reverse deficits
Promote normal growth/development
Minimize morbidity and maximize quality of life

Medications/nursing management
Supplemental feedings to prevent weight loss/promote healing
NG tube feedings
TPN
Alimentary Tract Ulcers
Definition & Risk Factors
Mouth sores/ mucositis: inflammation of mucous membranes

Risk factors
Chemotherapy & radiation
Dehydration
Poor oral hygiene
Immunosuppression

Severe ulcerations, require parenteral or enteral nutrition

Remember whatever happens in your mouth (ulcers) also happens in your digestive tract!
Nursing management of mucositis:
Good dental hygiene
Oral care/rinses (without alcohol!)
Pain management
Hydration & nutrition
Infectious disease (prophylaxis/treatment)
Airway protection
Pain management in Kids with Cancer
Very important (around the clock if necessary)
Assess vital signs
Non verbal cues: Irritability, crankiness, restlessness (assess developmental level)
Use age appropriate pain scale (face)
Assess effectiveness of medication (able to play, resting/sleeping)
Parental input/education
Alopecia (Hair Loss) in Kids with Cancer
Hair loss occurs about 2 – 3 weeks after first chemotherapy

High doses of radiation (> 4000 cGy) may cause permanent destruction to hair follicle

No hair loss DOES NOT mean drug’s aren’t working

Not all drugs cause hair loss

Nursing management: prepare patient (body image), wigs, hats, scarves

Don’t forget sunscreen!
Neurological Problems in Kids with Cancer
Posterior Fossa syndrome (After brain tumor removal or de-bulking)
Symptoms
Ataxia (lack of coordination, clumsiness)
Aphasia (mutism, speech disturbances)
Weakness/hemiparesis (one sided paralysis)
Can last days to months usually resolves
*educate parents/kids can be scary for them!
Hemorrhagic Cystitis in Kids with Cancer
Causes: chemotherapy
Signs/symptoms;
Blood in urine, painful urination, frequency, suprapubic pain, bladder spasms

Nursing management:
Encourage fluids,
monitor urine frequently with urine dips
medication prophylaxis (Mesna)
Steroid Effects
Moon face
Weight gain (increased hunger)
Steroid psychosis
Emotional lability
Immunocompromised
Photo/Sun Sensitivity in Kids with Cancer
Management
Sun screen !!!!
Sunburn may cause erythema or 2nd or 3rd degree burn
Education regarding drug culprits (such as MTX)
Encourage use of UV protective sunglasses, clothing, shade
The Childhood Cancer Survivor Late Effects
Definition:
Long-term consequences of treatment
Physical
Emotional
Social
Existing/potential health insurance issues, school and employment issues
Cognitive dysfunction (learning disabilities, attention)

Hearing loss

Cardiac (pericarditis, heart failure,)

Pulmonary dysfunction (radiation induced fibrosis, pneumonitis)

Endocrine (growth hormone deficiency, short stature, early or late puberty, hypothyroidism or failure)
Gonadal failure

Girls: early menopause in 30s r/t ovarian failure, potential sterility

Boys: potential sterility, low testosterone

Secondary malignancies (brain, breast, skin, leukemia’s, lymphoma’s)

Psychosocial issues (body image, school problems., family, employment, insurance, depression, anxiety)
Dental issues (increased cavities, enamel deficiency)

Obesity
musculoskeletal (scoliosis, osteoporosis **avascular necrosis secondary to high dose steroids
Intervention and Follow Up for Late Effects of Childhood Cancer
Annual exam and evaluation at late effects clinic
Neuropsychological testing
Individualized Education Plan/Special Education
Hearing (Audiograms)/Vision evaluations
Dental exams
Screening Echo’s, ECG’s,CXR’s, PFT’s, mammograms
Yearly Lab work
Smoking avoidance
Avoid alcohol and drugs
Counseling/Therapy
Anemia
The most common hematologic disorder of childhood
Decrease in number of RBCs and/or hemoglobin concentration below normal
Decreased oxygen-carrying capacity of blood
Consequences of Anemia
Decrease in oxygen-carrying capacity of blood and decreased amount of oxygen available to tissues
When anemia develops slowly, child adapts
General Therapeutic Management of Anemia
Treat underlying cause
Transfusion after hemorrhage if needed
Nutritional intervention for deficiency anemias
Supportive care
IV fluids to replace intravascular volume
Oxygen
Bed rest
Iron Deficiency Anemia
Caused by inadequate supply of dietary iron
Generally is preventable
Iron-fortified cereals and formulas for infants
Special needs of premature infants
Adolescents at risk due to rapid growth and poor eating habits
Iron Deficiency Anemia
Pathophysiology
Therapeutic Management
Prognosis
Nursing Considerations
Pathophysiology – Iron required for hemoglobin production. Decreased iron contributes toward low hemoglobin levels and therefore reduced oxygen carrying capacity
Therapeutic management- nutrition and iron supplementation
Prognosis – Usually very good. Should see rises in hgb levels within one month
Nursing considerations
Assess for pallor, listlessness, frequent infections and muscular weakness. Can be overweight and anemic
Education regarding administration of oral iron supplements. Nutrition education for family
Sickle Cell Anemia
A hereditary hemoglobinopathy
Ethnicity
Occurs primarily in African-Americans
Occurrence 1 in 375 infants born in U.S.
1 in 12 have sickle cell trait
Occasionally also in people of Mediterranean descent
Also seen in South American, Arabian, and East Indian descent
Pathophysiology of Sickle Cell
Partial or complete replacement of normal Hgb with abnormal hemoglobin S (HgbS)
Hemoglobin in the RBCs takes on an elongated (“sickle”) shape
Sickled cells are rigid and obstruct capillary blood flow
Microscopic obstructions lead to engorgement and tissue ischemia
Hypoxia occurs and causes sickling

Large tissue infarctions occur
Damaged tissues in organs lead to impaired function
Splenic sequestration
May require splenectomy at early age
Results in decreased immunity
Liver, kidney, bones, cardiovascular and neurological changes over time from impairment of blood flow and capillary obstruction
Sickle Cell Crisis
Precipitating Factors
Precipitating factors
Anything that increases the body’s need for oxygen or alters transport of oxygen
Trauma
Infection, fever
Physical and emotional stress
Increased blood viscosity due to dehydration
Hypoxia
From high altitude, poorly pressurized airplanes, hypoventilation, vasoconstriction due to hypothermia
Sickle Cell Crisis
Acute exacerbations that vary in severity and frequency
Types
Vaso-occlusive (VOC) thrombotic
Most common type of crisis—very painful
Stasis of blood with clumping of cells in microcirculation → ischemia → infarction
Signs: fever, pain, tissue engorgement
Prognosis for Sickle Cell Anemia
No cure (except possibly bone marrow transplants)
Supportive care/prevent sickling episodes
Relieve pain, oxygen, antibiotics as ordered, fluids to maintain hydration, relaxation techniques
Frequent bacterial infections may occur due to immunocompromise
Bacterial infection is leading cause of death in young children with sickle cell disease
Strokes in 5% to 10% of children with disease
Result in neurodevelopmental delay, mental retardation
Disease Management of Sickle Cell Anemia
Recognize early infections and get aggressive treatment of infection
Good hand washing is essential
Supplemental folic acid for rbc production. Good nutrition habits
Possibly prophylactic antibiotics from
2 months to 5 year to decrease infections
*Decrease crisis events by maintaining good hydration, avoiding temperature extremes, and avoiding stress and fatigue
*Stay updated on pneumococcal vaccine
Nursing Management for Sickle Cell Anemia
Monitor child’s growth—watch for failure to thrive
Careful multisystem assessment
Assess pain. Teach child and family how to manage pain at home
Observe for presence of inflammation or possible infection. Teach to seek medical care early
Teach child and family how to identify factors that trigger a crisis and decrease those risk factors
Genetic screening and counseling are the primary forms of prevention and should be offered to families at risk
Research is ongoing. Gene therapy may offer a cure in the future
Thalassemia
Inherited blood disorders of hemoglobin synthesis characterized by decrease in synthesis of globin chains leading to decreased production in hgb
Classified by Hgb chain affected and by amount of effect (alpha or beta). Beta form is most common
Autosomal recessive with varying expressivity
Both parents must be carriers to have offspring with thalassemia major disease. Found mostly in persons of Asian, African or Mediterranean descent
Pathophysiology of Thalassemia
Anemia results from defective synthesis of Hgb, structurally impaired RBCs, and shortened life of RBCs
Chronic hypoxia
Headache, irritability, precordial and bone pain, exercise intolerance, anorexia, epistaxis
Detected in infancy or toddlerhood
Pallor, FTT, hepatosplenomegaly, severe anemia (Hgb <6)
Diagnosis and Treatment for a Kid with Thalassemia
Diagnosed by hemoglobin electrophoresis
RBC changes often seen by 6 weeks of age
Child presents with severe anemia, FTT
Medical Management: monthly blood transfusions to maintain normal Hgb levels
Side effect—hemosiderosis
Treat with iron-chelating drugs such as deferoxamine (Desferal)
Binds excess iron for excretion by kidney
Nursing Management for a Kid with Thalassemia
Observe for complications of transfusion
Emotional support to family
Encourage genetic counseling
Parent and patient teaching for self-care
Teach about need to monitor rbc production and for low hgb levels
Assess for pallor, irritability, growth retardation, hepatosplenomegaly (if spleen not yet removed) and abnormal skeletal development
Expect delayed or absent secondary sex characteristics
Child can live well into adulthood with proper clinical management
Bone marrow transplant is potential cure
Aplastic Anemia
All formed elements of the blood are simultaneously depressed: “pancytopenia”
Aplastic Anemia
Etiology
Primary (congenital) – Fanconi syndrome
Secondary (acquired) – irradiation, antibiotics, chemical exposure (benzene containing products), certain cancers in which myeloid elements are infiltrated such as in leukemia or lymphoma, HPV infection, hepatitis, overwhelming infections, or idiopathic
Aplastic Anemia
Diagnostics and Therapeutic Management
Diagnostic evaluation – by bone marrow aspiration
Therapeutic management- failure of bone marrow to carry out blood forming function. Treatment includes immunosuppressive therapy, replacement of bone marrow through transplantation
Aplastic Anemia
Nursing Considerations
Prepare child and family for diagnostic and therapeutic procedures
Prevent complications from pancyotopenia
Support child and family
Hemophilia
A group of hereditary bleeding disorders that result from deficiencies of specific clotting factors
Hemophilia A
Classic hemophilia
Deficiency of factor VIII
Accounts for 80% of cases of hemophilia
Occurrence: 1 in 5000 males
Etiology of Hemophilia A
X-linked recessive trait
Males are affected
Females may be carriers
Degree of bleeding depends on amount of clotting factor and severity of a given injury
Up to one third of cases have no known family history
In these cases disease is caused by a new mutation
Manifestations of Hemophilia
Bleeding tendencies from mild to severe
Symptoms may not occur until 6 months of age
Mobility leads to injuries from falls and accidents
Hemarthrosis
Bleeding into joint spaces of knee, ankle, elbow, leading to impaired mobility
Ecchymosis
Epistaxis
Bleeding after procedures
Minor trauma, tooth extraction, minor surgeries
Large subcutaneous and intramuscular hemorrhages may occur
Bleeding into neck, chest, mouth may compromise airway
Muscle Bleeds: Signs & Symptoms
Soft Tissue Bleeds and Bruising
-No functional impairment
-Tenderness but no severe pain
-No factor needed
Muscle Bleeds: Signs & Symptoms
Iliopsoas bleeds
-Flexed hip
-Pain, inability to extend the leg on the affected side
-Treat with a major dose of factor
Muscle Bleeds: Signs & Symptoms
Thigh/Calf Bleeds
-Pain
-With/without swelling
-Impaired mobility
-Routine factor dose
-Major factor dose if compartment syndrome is suspected
Muscle Bleeds: Signs & Symptoms
Neck Swelling
EMERGENCY!!!!
-Potential airway compromise
-Treat with a MAJOR dose of factor
Muscle Bleeds: Signs & Symptoms
Deltoid/Forearm Bleed and Bruising
-Routine factor dose
-Major dose if a compartment syndrome is suspected
Muscle Bleeds: Signs & Symptoms
Butt-Cheek Bleeds
-Pain
-With/without swelling
-Routine factor side
-Major factor dose if the lef on the affected side exhibits tingling or swelling
Treatment for Joint Bleeds
Routine dose of factor for early onset joint bleeds
Major dose of factor for advanced joint bleeds

May need crutches.
Diagnostics and Clinical Therapy for Hemophilia
Can be diagnosed through amniocentesis
Genetic testing of family members to identify carriers
Diagnosis on basis of history, labs, and exam
Labs: low levels of factor VIII or IX, prolonged PTT
Normal: platelet count, PT, and fibrinogen
Medical Management
DDAVP
IV
Causes 2 to 4 times increase in factor VIII activity
Used for mild hemophilia
Replace missing clotting factors
Transfusions
At home with prompt intervention to decrease complications
Following major or minor hemorrhages
Prognosis for Hemophilia
Historically, most died by age 5 years
Now those with mild to moderate hemophilia live near-normal lives
Gene therapy for the future
Infuse carrier organisms into patient; these act on target cells to promote manufacture of deficient clotting factor
Home Care Interventions for Hemophilia
Close supervision and safe environment
Dental procedures in controlled situation
Shave only with electric razor
Superficial bleeding—apply pressure for at least 15 minutes and ice to vasoconstrict
If significant bleeding occurs, transfuse for factor replacement
Managing Hemarthrosis
During bleeding episodes, elevate and immobilize the joint
Ice
Analgesics
ROM after bleeding stops to prevent contractures
PT
Avoid obesity to minimize joint stress
HIV Infection in Children
Modes of Transmission and Clinical Manifestations
Transmitted to infants around birth or transmitted as a result of high risk behaviors in adolescents
Perinatal transmission accounts for majority of AIDS cases in children
Common Clinical Manifestations
Lymphadenopathy
Hepatosplenomegaly
Oral candidiasis
Chronic or recurrent diarrhea
Failure to thrive
Developmental delay
Parotitis
Diagnosis of HIV
History of fungal infections, repeated bacterial infestations, FTT, prolonged flu-like viral infections, prolonged diarrhea
Passive transfer of maternal HIV-1 antibodies, which may be detectable in the child's bloodstream until 18 months old.
Diagnose HIV infection in children younger than 18 months of age through special blood tests (DNA polymerase chain reaction test) that identify the virus. Virologic assays, including HIV-1 DNA or RNA assays, represent the gold standard for diagnostic testing of infants and children younger than 18 months.
Treatment of HIV
Goals include slowing growth of HIV, promoting normal growth and development, preventing infections, monitoring for cancers, enhance quality of life and prolong survival
Combination of antiviral drug therapies
Immunization against common childhood illnesses
Quality nutritional management for growth and adequate weight gain
Family counseling, education and support
Hypopituitarism: Growth Hormone (GH) Deficiency
Inhibits somatic growth
Primary site of dysfunction appears to be in the hypothalamus
Diagnostic Evaluation of GH Deficiency
Family history
Growth patterns and health history
Definitive diagnosis based on radioimmunoassay of plasma GH levels
Hand x-rays to evaluate growth potential vs. ossification
Endocrine studies to detect deficiencies
Therapeutic Management of GH Deficiency
Biosynthetic growth hormone (injections)
Other hormone replacements as needed
Thyroid extract
Cortisone
Testosterone or estrogens and progesterone
Prognosis of GH Deficiency
GH replacement successful in 80% of affected children
Growth rate of 3.5 to 4 cm/yr before treatment and increase to 8 to 9 cm/yr after treatment
Response varies based on age, length of treatment, frequency of doses, dosage, weight, and GH receptor amount
Nursing Considerations for GH Deficiency
Family members support needs
Child’s body image
Preparing child for daily injections
Treatment very expensive ($10,000 to $50,000 per year)
Pituitary Hyperfunction
Excess GH before closure of the epiphyseal shafts results in overgrowth of long bones
Reach heights of 8 feet or more
Vertical growth and increased muscle
Weight is generally in proportion to height
Pituitary Hyperfunction: Acromegaly
Excess GH after epiphyseal closure is called acromegaly
Typical facial features: Overgrowth of the mandible leads to protrusion of the jaw (prognathism) and malocclusion of teeth. Cartilaginous proliferation of the larynx leads to a deep, husky voice. The tongue is frequently enlarged and furrowed. In long-standing acromegaly, costal cartilage growth leads to a barrel chest.
Therapeutic Management of Pituitary Hyperfunction
Surgical treatment to remove tumor
Radiation and radioactive implants
Hormone replacement therapy after surgery in some cases
Nursing Considerations
Early identification of children with excessive growth rates
Early treatment for improved outcomes
Emotional support
Body image concerns
Precocious Puberty
Defined as sexual development before age 9 in boys or before age 8 in girls
Occurs more frequently in girls
Potential causes
Disorder of the gonads, adrenal glands, or hypothalamic-pituitary gonadal axis
No causative factor in 80% to 90% of girls and 50% boys
Therapeutic Management of Precocious Puberty
Treatment of specific cause if known
May be treated with Lupron
Slows prepubertal growth to normal rates
Treatment is discontinued at age for normal pubertal changes to resume
Psychologic support for child and family
Diabetes Insipidus (DI)
The principal disorder of the posterior pituitary
Results from hyposecretion of ADH
Produces uncontrolled diuresis
Primary causes: familial or idiopathic
Secondary causes: trauma, tumors, CNS infection, aneurysm
Clinical Manifestations of DI
Cardinal signs: polyuria and polydipsia
First sign is often enuresis
Infants: irritability that is relieved with feedings of water but not milk; dehydration often occurs
Therapeutic Management of DI
Instruct parents in difference between diabetes insipidus and diabetes mellitus
Daily hormone replacement of vasopressin
Drug of choice: DDAVP
Nasal spray or IV administration
Requires treatment for life
Nursing Management of DI
Accurate I&O
Observe for signs of fluid overload
Seizure precautions
Administer ADH-antagonizing meds
Disorders of Thyroid Function
Thyroid hormone regulates BMR
Thyroid secretes two types of hormones
Thyroid hormone, which is made up of:
Thyroxin (T4)
Triiodothyronine (T3)
Thyrocalcitonin
May have hypo- or hyperthyroidism
May have disturbance in secretion of TSH
Juvenile Hypothyroidism
Congenital
Congenital hypoplastic thyroid gland
Acquired
Partial or complete thyroidectomy for CA or thyrotoxicosis
Following radiation for Hodgkin or other malignancy
Rarely occurs from dietary insufficiency in U.S.

Part of the blood tests at births

Hypothyroidism
Child can become sluggish and lose mental capabilities and can lead to mental retardation
Clinical Manifestations of Juvenile Hypothyroidism
Decelerated growth
Constipation
Sleepiness
Myxedematous skin changes
Dry skin
Sparse hair
Periorbital edema
Therapeutic Management of Juvenile Hypothyroidism
Oral thyroid hormone replacement
Prompt treatment needed for brain growth in infant
May administer in increasing amounts over 4 to 8 weeks to reach euthyroidism
Compliance with medication regimen is crucial
Hyperthyroidism (Graves Disease)
Most common cause of hyperthyroidism in childhood is Graves disease
Believe caused by serum thyroid-stimulating immunoglobulin, but no specific etiology
Enlarged thyroid gland and exophthalmos
Peak incidence 12 to 14 years old but may be present at birth
Familial association
Graves Disease Management
Therapy is controversial
Goal of therapy: retard rate of hormone secretion
Treatments
Antithyroid drugs (PTU and methimazole)
Subtotal thyroidectomy
Ablation with radioiodine
Nursing Considerations for Graves Disease
Identify children with hyperthyroidism
Alert for signs and symptoms
Child needs quiet environment, rest periods
Help family cope with emotional lability associated with disorder
Dietary requirements to meet the child’s increased metabolic rate
Medications: side effects
Cushing Syndrome
A characteristic group of manifestations caused by excessive circulating free cortisol
May be caused by excessive or prolonged steroid therapy
Condition is reversible once steroids are discontinued
Abrupt withdrawal of steroids may precipitate acute adrenal insufficiency
Etiologies of Cushing Syndrome
Pituitary: excess of ACTH
Adrenal: hypersecretion of glucocorticoids
Ectopic: extrapituitary neoplasm
Iatrogenic: administration of excessive steroids
Food dependent: inappropriate adrenal response to secretion of polypeptide
Cushingoid Appearance
Excessive hair growth
Moon face, red cheeks
Weight gain
Pendulous abdomen with red striae
Poor wound healing
Ecchymoses
Diagnostic Evaluation of Cushing Syndrome
Confirm excess cortisol levels
X-rays: evaluate for osteoporosis and skull films to look for enlargement of sella turcica
Labs
Fasting blood glucose
Serum electrolytes
24-hour urine
Therapeutic management
Surgery
Replacement of growth hormone, ADH, TH, gonadotropins, and steroids
Diabetes Mellitus (DM)
Characterized by a total or partial deficiency of the hormone insulin
The most common endocrine disorder of childhood
Peak incidence in early adolescence
Type 1 Diabetes
Characterized by destruction of beta cells, usually leading to absolute insulin deficiency
Onset typically in childhood and adolescence but can occur at any age
Most DM of childhood is type 1
Maturity-Onset Diabetes of the Young (MODY)
Similar to type 2 DM
May be seen in obese teens
May be controlled with oral hypoglycemic agents and diet modifications
More benign disease but increasing frequency in pediatric population
Etiology Type I DM
Type 1 DM believed to be autoimmune disease arising when a person with a genetic predisposition is exposed to a precipitating event such as a viral infection
Heredity is prominent factor in the etiology
Pathophysiology of DM
With a deficiency of insulin, glucose is unable to enter the cell and remains in blood, causing hyperglycemia
When serum glucose exceeds the renal threshold, glucose spills into urine (glycosuria)
Cells break down protein for conversion to glucose by the liver (glucogenesis)
Ketoacidosis
When glucose is unavailable for cellular metabolism, the body breaks down alternate sources of energy
Ketones released and excess ketones eliminated in urine (ketonuria) or by the lungs (acetone breath)
Ketones in blood are strong acids that lower serum pH and produce ketoacidosis
Kussmaul Respirations
Hyperventilation characteristic of metabolic acidosis resulting from the respiratory system’s attempt to eliminate excess CO2 by increased depth and rate
Diabetic Ketoacidosis (DKA)
Pediatric emergency
Results from progressive deterioration with dehydration, electrolyte imbalance, acidosis, coma, and may cause death
Long-Term Complications of DM
Microvascular complications, especially nephropathy and retinopathy
Macrovascular disease, neuropathy
Therapeutic Management of Type 1 DM
Insulin therapy
Glucose monitoring: goal range
80 to 120 mg/dl
Lab measurement of hemoglobin A1c
Urine testing for ketones
Not routinely used except to test q3h during illness and whenever glucose is ≥240 mg/dl when illness not present

Nutrition
Exercise
Teach patient and family how to manage hypoglycemic episodes
Illness management
Management of DKA
Patient Education: DM and Insulin Therapy
Nature of the disease
Meal planning
Insulin therapy: types of insulin, duration, onset and peak action, mixing and administration, rotation of injection sites
Insulin pump therapy in some cases
Glucose monitoring
Recognition and treatment of hypoglycemia and hyperglycemia
Management of “minor” illnesses
Record keeping
Hygiene
Family support
Acute care
Possible Nursing Diagnoses for Pediatric Client with DM
Risk for Injury related to insulin deficiency
Risk for Injury related to hypoglycemia
Deficient Knowledge (Diabetes Management) related to care of child with newly diagnosed diabetes mellitus
Common Reasons Behind Burn Injuries in Children
Toddlers: hot water scalds
Older children: flame-related burns
Child abuse
Children with matches or lighters account for 1 in 10 house fires
Three Nursing Assessment Areas for Burn Injury Evaluation
EXTENT of injury described as TBSA (total body surface area)—use age-related charts
DEPTH of injury
1st degree: Superficial
2nd degree: Partial Thickness (epidermis and part of dermis layer)
3rd degree: Full Thickness (entire epidermis, dermis layer and can extend into the subcutaneous layer)
4th degree: full thickness + underlying tissue (full thickness injury plus underlying structures such as bone, muscle and fascia)
SEVERITY of Injury
minor, moderate or major
Estimating Percentage of Body Surface Burned
CHILD
Head: 18%
Anterior Torso: 18%
Posterior Torso: 18%
Arms:9% each
Legs: 14% each
Add 1/2% to each leg for each year over 1
Subtract 1% from head for each year over 1
Estimating Percentage of Body Surface Burned
INFANT
Head:18%
Anterior Torso: 18%
Posterior Torso: 18%
Arms: 9% each
Legs: 14% each

Add 1/2% to each leg for each year over 1
Subtract 1% from head for each year over 1
Severity of Burn Grading System with Appropriate Treatment Based on Severity Scale
MINOR BURNS
Partial Thickness burns covering less than 10% TBSA.
No full thickness burns anywhere on body
No burns on face, hands, feet, perineum, over joints or electrical burns.
No evidence of inhalation injury or body trauma
Treat in outpatient or 1 to 2 day admission in community based hospital
Severity of Burn Grading System with Appropriate Treatment Based on Severity Scale
MODERATE BURNS
Partial thickness burns covering 10 to 20% of TBSA burned
No full thickness burns anywhere on body
Treat by admitting to hospital, preferably one with expertise in burn care
Severity of Burn Grading System with Appropriate Treatment Based on Severity Scale
MAJOR BURNS
Partial thickness burns covering greater than 20% of TBSA
Any time there are any full thickness burns on the body
Best treatment can be found by admitting to a specialized burn treatment center
Burns: Therapeutic Management
Emergency care priorities
Stop the burning process
Assess the victim’s condition
Cover the burn to prevent contamination
Transport child to appropriate level of care
Provide reassurance
First priority: airway maintenance
Fluid replacement therapy: critical in first
24 hours
Nutrition: enhanced metabolic demands
Medication: antibiotics, analgesics, anesthetics for procedural pain
Complications of Burn Injuries
Immediate threat of airway compromise
Profound shock
Infection (local and systemic sepsis)
Inhalation injuries, aspiration, pulmonary edema, pulmonary embolus
Care of Minor Burns
Wound cleansing
Debridement
Controversy: removal of blisters
Dressings
Controversy: cover wound with antimicrobial ointment or use occlusive dressings
Primary excision
Debridement
Topical antimicrobial agents
Biologic skin coverings
Allograft (human cadaver skin)
Xenograft (porcine skin)
Synthetic skin substitutes
Split-thickness skin grafts (sheet or mesh graft)
Rehabilitation After Major Burns
Begins once wound coverage has been achieved
Prevention/management of contractures
Physical/occupational therapy
Multidisciplinary team
Facilitate adaptation of child and family
Increased Intracranial Pressure (ICP)
Early signs and symptoms may be subtle
As pressure increases, signs and symptoms become more pronounced and level of consciousness (LOC) deteriorates

Taught that children are getting too many CT exams, especially under 2. It puts child at greater risk for brain cancer- brain is very susceptible to radiation exposure
For children under than 2:
If no scalp hematoma, loss of consciousness for more than 5 seconds, no palpable skull fracture and acting normally- NO CT

Good Signs-
Normal mental status, no loss of consciousness, no vomiting, no severe headache

Change in LOC is the most sensitive sign of ICP- be precise!
Clinical Manifestations of Increased ICP in Infants
Irritability, poor feeding
High-pitched cry, difficult to soothe
Fontanels: tense, bulging
Cranial sutures: separated
Eyes: setting-sun sign
Scalp veins: distended
Clinical Manifestations of Increased ICP in Children
Headache
Vomiting: with or without nausea
Seizures
Diplopia, blurred vision
Behavioral Signs of Increasing ICP
Irritability, restlessness
Drowsiness, indifference, decrease in physical activity and motor skills
Complaint of fatigue, somnolence
Inability to follow commands, memory loss
Decreased appetite with resulting weight loss
Late Signs of Increasing ICP
Decreased LOC
Decreased motor response to command
Decreased sensory response to painful stimuli
Alterations in pupil size and reactivity
Papilledema
Decerebrate or decorticate posturing
Cheyne-Stokes respirations
Levels of Consciousness (in Descending Order)
Full consciousness
Confusion: impaired decision making
Disorientation: to time and place
Lethargy: sluggish speech
Obtundation: arouses with stimulation
Stupor: responds only to vigorous and repeated stimulation
Coma: no motor or verbal response to noxious stimuli
Persistent vegetative state: permanently lost function of cerebral cortex
Pediatric Glasgow Coma Scale
Three part assessment:
Eyes
Verbal response
Motor response
Score of 15: unaltered LOC
Score of 3: extremely decreased LOC (worst possible score on the scale)

Bottom Score of GCS - 3
Highest Score of GCS- 15
Indications for ICP Monitoring
Glasgow coma scale <7 - less stable
Glasgow coma scale <8 with respiratory distress
Deteriorating neurologic condition
Subjective judgment
Nursing Care for Child with Increased ICP
Patient positioning
Avoid activities that may increase ICP
Eliminate or minimize environmental noise
Suctioning issues
Nutrition and Hydration
IV administration of fluids and parenteral nutrition
Caution with overhydration
Later begin gastric feedings via NG or GT
Patient may continue to have risk of aspiration

Be careful about hydration- do not want to over hydrate. Maybe slightly underhydrated
Respiratory Management for Child with Increased ICP
Airway management is primary concern
Cerebral hypoxia lasting more than 4 minutes or (hours?) may cause irreversible brain damage
CO2 causes vasodilation, increased cerebral blood flow, and increased ICP
May have minimal gag and cough reflexes
Risk of aspiration of secretions
If body is kept cold- the brain damage my be reversible
Nursing Care Needs for Child with Increased ICP
Elimination
Hygienic care
Position and exercise
Stimulation
Family support
Nursing Diagnoses for Child with Increased ICP
Disturbed Sensory Perception related to CNS impairment
Self-Care Deficits related to physical immobility, perceptual and cognitive impairments
Risk for Aspiration related to depressed sensorium, impaired motor function
Risk for Injury related to depressed sensorium
Special Diagnostic Procedures for Child with Increased ICP
Lab tests: glucose, CBC, electrolytes, blood culture if fever; evaluate for toxic substances, liver function
Imaging: CT, MRI, echoencephalography, ultrasound, nuclear brain scan, PET
Lumbar puncture
EEG
X-ray (rule out skull fractures, dislocations; evaluate degenerative changes, suture lines)
Head Injury
Etiology and Pathophysiology
Etiology
Falls
Motor vehicle injuries
Bicycle injuries
Pathophysiology:
Force of intracranial contents cannot be absorbed by the skull and musculoligamentous support of the head
Especially vulnerable to acceleration-deceleration injuries
Subsequent Complications of Head Injuries
Hypoxic brain injury
Increased ICP
Infection
Cerebral edema
Concussion
Transient and reversible
Results from trauma to the head
Instantaneous loss of awareness and responsiveness lasting for minutes to hours
Generally followed by amnesia and confusion
Contusion and Laceration
Terms used to describe visible bruising and tearing of cerebral tissue
Coup: bruising at the point of impact
Contrecoup: bruising at a site far removed from the point of impact
Diagnostic Evaluation for Head Injury
Assessment of ABCs
Vital signs
Neurologic exam: eyes, verbal and motor responses
Special tests: CT, MRI, behavioral assessment

Vitals: Respirations- first effect of change in neuro health. Especially if in brain stem
Therapeutic Management for Head Injury
Care in hospital if severe injuries, loss of consciousness for several minutes, prolonged or continued seizures
NPO initially
Possible surgical interventions
Prognosis
Nursing Considerations for Head Injury
Frequent assessment: vital sign and neurologic checks
Provide analgesia and sedation
Careful observation and recording
Family support
Rehabilitation
Prevention
Near Drowning
Drowning is the second leading cause of accidental death in children
Death occurs from asphyxia while submerged
Can occur with even small quantity of water (even as little as a pail of water)
Near-drowning: survived at least 24 hours after submersion
Colder the submersion the better the outcome
Nursing Considerations for Near Drowning
Care depends on condition of the child
Helping parents cope with feelings of guilt
Parental anxiety related to prognosis
PREVENTION OF DROWNING
CNS INFECTIONS
CNS has limited response to injury
Difficult to distinguish etiology by looking at clinical manifestations
Lab studies required to identify causative agent
Inflammation can affect the meninges, brain, or spinal cord
Bacterial Meningitis
Acute inflammation of the CNS
Decreased incidence following use of Hib vaccine
Can be caused by various bacterial agents
Streptococcus pneumoniae
Group β streptococci
Escherichia coli
Transmission of Bacterial Meningitis
Droplet infection from nasopharyngeal secretions
Appears as extension of other bacterial infection through vascular dissemination
Organisms then spread through CSF
Diagnostics: LP is the definitive diagnostic test
Therapeutic management
Nursing considerations

Happens typically after upper respiratory infection
Symptoms: fever, vomiting, headache in older children, irritability, bulging fontanels, lethargy, photophobia

Seizures in 30% of children, especially if child had fever or cerebral edema

IV antibiotics- priority as a nurse
Nonbacterial Meningitis (Aseptic Meningitis)
Causative agents are principally viruses
Frequently associated with other diseases
Measles, mumps, herpes, leukemia
Onset abrupt or gradual
Manifestations: headache, fever, malaise
Diagnosis and treatment
Prognosis
Reye Syndrome (RS)
A disorder defined as toxic encephalopathy associated with other characteristic organ involvement
Characterized by fever, profoundly impaired consciousness, and disordered hepatic function
Etiology is obscure
Most cases follow a common viral illness
Potential association between aspirin therapy for fever and development of RS

Don’t give aspirin to kids who have had viral illnesses
Reye Syndrome (RS) S & Sx
Develop within a few days to a few weeks after viral illness
Begins with lethargy then n/v
Changes in level of consciousness, irritability, hostility
Within 24 hrs- children have rapid deterioration- hallucinations and decreased level of consciousness
Reye Syndrome (RS) Tx
Should be put in ICU and placed on ventilator- major of kids who survive recover completely.
Symptoms management-
Monitor Liver, Kidneys and Neuro changes
Seizures
Caused by malfunctions of brain’s electrical system
Determined by site of origin
Most common neurologic dysfunction in kids
Occur with wide variety of CNS conditions
Seizures: Signs and Symptoms
Change in LOC
Involuntary movements
Posturing
Changes in perception, behaviors, or sensations
Incidence and Occurrence:
2.3 million Americans affected
Especially children and elderly
More seizures in children younger than 2 years than any other age group
Major Causes of Seizures in Children
Birth injuries (anoxia) or congenital defects of CNS
Acute infections in late infancy and early childhood
In children older than 3 years, usually is idiopathic
Absence Seizures
Formerly called petit mal or “lapses”
Brief loss of consciousness
Minimal or no change in muscle tone
Almost always appear in childhood
(4 to 12 years)

Sudden onset of 20+ events per day
No warning/no aura
Duration 5 to 10 seconds
Motor: lip smacking, twitching of eyes, face, slight hand movements
May drop object; child rarely falls
No incontinence
Often misdiagnosed
Inattention/daydreaming
ADD/ADHD
Atonic Seizures
Sudden momentary loss of muscle tone
Onset usually ages 2 to 5 years
May or may not have loss of consciousness
Sudden fall to ground, often on face
Less severe—head droops forward several times
Myoclonic Seizures
Sudden brief contractions of muscle group
May be single or repetitive
No loss of consciousness
Often occur when falling asleep
May be nonspecific symptom in many CNS disorders
May be mistaken as exaggerated startle reflex
Status Epilepticus
Definition: seizure lasting more than
30 minutes or series of seizures without regaining premorbid LOC
Treatment:
Maintain airway
Establish IV access
Medications
Medications:
Diastat (prefilled rectal syringe)
Versed (intranasal)
IV Ativan or valproic acid
IV loading with phenytoin for ongoing management
Emergency Management for Big Ass Seizures
High-dose sedatives
Maintain patent airway
Prepare for respiratory support
Pediatric Diagnosis of Seizure Disorders
Ascertain type of seizure
History, observation
Determine the cause of the event
Diagnostics
EEG, MRI
Labs: glucose, electrolytes, BUN, Ca++
LP
Common Pediatric Seizure Triggers
Changes in dark-light patterns (camera flashes, headlights, rotating fan blades, reflections off snow or water)
Sudden loud noises
Extreme temperature changes
Dehydration
Fatigue
Febrile Seizures- Occurance
Transient disorder of childhood
Affect approximately 3% of children
Usually occur between ages 6 months and 3 years
Rare after age 5
Twice as frequent in males
Febrile Seizures
Cause ??????
Usually in temperatures higher than 101.8°
Seizure occurs when temperature is rising, not after
Seizure usually over before arriving in emergency department
Febrile Seizure Treatment: fever reduction
Evaluate history (episodic and family)
Seizure control if ongoing
Diazepam (rectal)
Febrile Seizures Management/Prevention
95% to 98% of children with febrile seizures do not have epilepsy or neurologic damage
Management:
Avoid tepid baths—usually ineffective
Vigorous use of antipyretics
Protect child from injury during seizure
Call 911 if seizure lasts more than 5 minutes
Febrile Seizures Treatment
Prophylaxis with medications
If focal or prolonged seizures
If neurologic anomalies
If first-degree relative has seizure history
In child less than 1 year old
If multiple seizures in 2-hour period
Pharmacologic Management for Seizures
Monotherapy is treatment of choice for pediatrics
Gradual increase of dose until seizure control or signs of toxicity
Polypharmacy if uncontrolled with one drug
Monitor therapeutic levels
Increase dosage as child grows
Monitor for known side effects
Avoid abrupt discontinuation—gradual dose reduction
When to discontinue seizure meds
When seizure free for 2 years
Normal EEG
Avoid DC during puberty or when subject to frequent infections
Recurrence possible within first year
Nursing Interventions for Seizures
Observe and document episode
Protect from injury
Stay calm
Remain with child
Privacy if possible
Teach home management of seizures
CPR training for family members
Rectal diazepam available for intractable seizures
Activity restriction on individual basis
Safety devices—helmets, no swimming alone, awareness of school, other caregivers
Phenobarbital - purpose
Febrile seizures, neonatal seizures
Also for other seizures: front-line IV choice if patient does not respond to diazepam
High dosage may require respiratory support
Phenytoin (Dilantin)
For Seizures
PO or slow IV push (<50 mg/min)
Precipitates when mixed with glucose
Side effects: Gingival hyperplasia, ataxia, rashes, acne, hirsutism, osteoporosis

Onset 5 to 30 minutes; duration
12 to 24 hours
Fosphenytoin
May be given with saline or glucose
Rate up to 150 mg/min
IV or IM
Valproic Acid
Trade names: Depakote, Depakene
IV or PO
IV for status epilepticus
S.E.: Hepatotoxicity!
Diazepam
Trade names: Valium IV, Diastat (rectal gel)
Medication of choice for status epilepticus
Rectal gel for home or prehospital management
Onset 3 to 10 minutes; short duration (minutes)
Concurrent loading with phenytoin for sustained control of seizures
Ativan
Alternative to diazepam
May be preferable to diazepam
Longer duration of action
Less respiratory distress in children older than
2 years
Midazolam (Versed)
Intranasal route
For acute epileptic seizures
Onset 3 to 5 minutes; duration
Hypoplastic anemia
Profound depression of RBCs but normal WBCs and platelet
What indicates a neurosurgical emergency?
Observation of an asymmetric pupil or one dilated unreactive pupil in a comatose child.
May require evacuation of an epidural hematoma.


Bleeding from nose or ears needs further evaluation because a watery discharge from the nose that is positive for glucose suggests leaking of spinal fluid from skull fracture.