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289 Cards in this Set
- Front
- Back
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Urinary Tract Infection (S/Sx)
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Nausea, vomiting, anorexia, chills, nocturia, urinary frequency, urgency
Suprapubic or lower back pain, bladder spasms, dysuria, burning on urination |
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Urinary Tract Infection Objective Data for Assessment
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Fever
Hematuria; foul-smelling urine; tender, enlarged kidney Leukocytosis, positive findings for bacteria, WBCs, RBCs, Pyuria, Ultrasound, CT scan, IVP |
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Normal pH of Urine
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5-9
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Normal Specific Gravity of Urine
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1.001 to 1.035
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Normal Protein in Urine
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< 20 mg/dL
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Normal bilirubin in Urine
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Up to 1 mg/dL
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What should not be present in urine?
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Glucose, Ketones, Hgb, WBCs, RBCs, Casts, Nitrites
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UTI: Causes
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Escherichia coli most common pathogen
Streptococci Staphylococcus saprophyticus Occasionally fungal and parasitic pathogens |
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Types of UTIs
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Recurrent—repeated episodes
Persistent—bacteriuria despite antibiotics Febrile—typically indicates pyelonephritis Urosepsis—bacterial illness; urinary pathogens in blood |
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UTI: Etiology and Pathophysiology
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Alteration of defense mechanisms increases risk of UTI
Organisms usually introduced via ascending route from urethra Less common routes Bloodstream Lymphatic system |
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Pediatric Manifestations of Urinary Tract Infection
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Frequency
Fever in some cases Odiferous urine Blood or blood-tinged urine Sometimes no symptoms except generalized sepsis |
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UTI: Diagnostic Studies
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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 |
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UTI Care
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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 |
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Hypospadias
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Congential anonmaly: Urethral meatus opens on ventral surface of penis
Affects 1 in 250 live male births |
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Hypospadias Repair
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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 |
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Types of Renal Failure
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Acute renal failure (ARF)
Chronic renal failure (CRF) |
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Acute Renal Failure
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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 |
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Most common cause of Acute Renal Failure
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Most common pathologic cause: transient renal failure resulting from SEVERE DEHYDRATION
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What do you assess for in Acute Renal Failure
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Assess for hypertension, edema or SOB from possible volume overload due to retained fluid
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Normal Urine Output for Neonates
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50- 300 cc/day
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Normal Urine Output for Infants
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300-500 cc/day
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Normal Urine Output for Preschooler
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500-800 cc/day
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Normal Urine Output for School Age
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600-1400 cc/day
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Normal Urine Output for Adolescents
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1000-1500 cc/day
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Acute Renal Failure- reversible or not?
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yes. it is reversible
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What will labs show in Acute Renal Failure?
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increased serum BUN and creatine
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Therapeutic Management Acute Renal Failure (Tx)
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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 |
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Chronic Renal Failure (CRF)
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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 |
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Chronic Renal Failure S/Sx
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Child appears pale, low energy
May have elevated B/P Behind on growth chart Poor appetite, nausea and vomiting as disease progresses |
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Nephrotic Syndrome
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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 |
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Characteristics of Nephrotic Syndrome
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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 |
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Nephrotic Syndrome Management
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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 |
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Chronic Renal Failure (CRF) Tx
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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 |
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Nursing Interventions for Nephrotic Syndrome
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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 |
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Nephrotic Syndrome S/Sx
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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)
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How do you diagnose Nephrotic Syndrome?
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Diagnosed with Renal Biopsy
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Side effects of corticosteroids
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causes cataracts, stunts growth, cranky kid, look kinda chunky with moon face, striae, raises blood glucose
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Glomerulonephritis
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Inflammation of glomerular tissues
Glomerulonephritis Symptoms Generalized edema due to decreased glomerular filtration Begins with periorbital Progresses to lower extremities and then to ascites |
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Key Factors of Glomerulonephritis
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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 |
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Most common cause of Glomerulonephritis
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untreated streptococcal infection
(most are postinfectious) |
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Acute Poststreptococcal Glomerulonephritis (APSG)
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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 |
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Types of Glomerulonephritis
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Infection or autoimmune response
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Acute Poststreptococcal Glomerulonephritis (APSG) S/Sx
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periorbital edema worse in morning, loss of appetite, decreased urinary output, dark colored urine, hx of recent streptococcal infection
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Prognosis of Glomerulonephritis
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95%—rapid improvement to complete recovery
5% to 15%—chronic glomerulonephritis 1%—irreversible damage |
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Nursing Management of APSG (Acute post-streptococcal glomerulonephritis)
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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 |
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Types of Trauma
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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 |
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Epiphyseal Injuries
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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 |
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The Immobilized Child
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Immobilization was once thought to be restorative from illness and injury
We know now that immobilization has serious consequences -Physical -Social -Psychologic |
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Physiologic Effects of Immobilization- Muscular System
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Muscular system
Decreased muscle strength and endurance Atrophy Loss of joint mobility |
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Physiologic Effects of Immobilization- Skeletal System
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Skeletal system
Bone demineralization Negative calcium balance |
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Physiologic Effects of Immobilization- Cardiovascular System
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Cardiovascular system
Decreased efficiency of orthostatic neurovascular reflexes Diminished vasopressor mechanism Altered distribution of blood volume Venous stasis Dependent edema |
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Physiologic Effects of Immobilization- Respiratory
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Respiratory system
Decreased need for oxygen Diminished vital capacity Poor abdominal tone and distention Mechanical or biochemical secretion retention Loss of respiratory muscle strength |
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Physiologic Effects of Immobilization- GI System
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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 |
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Physiologic Effects of Immobilization- Integumentary System
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Integumentary system
Decreased circulation and pressure leading to decreased healing capacity |
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Physiologic Effects of Immobilization- Urinary System
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Urinary system
Alteration of gravitational force Difficulty voiding in supine position Urinary retention Impaired ureteral peristalsis |
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Physiologic Effects of Immobilization- Neurosensory System
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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 |
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Psychologic Effects of Immobility
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Diminished environmental stimuli
Altered perception of self and environment Increased feelings of frustration, helplessness, anxiety Depression, anger, aggressive behavior Developmental regression |
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Fractures
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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 |
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Types of Fractures
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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 |
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Clinical Manifestations of Fracture
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Generalized swelling
Pain or tenderness Diminished functional use May have bruising, severe muscular rigidity, crepitus |
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Assessment of Fractures
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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 |
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Bone Healing and Remodeling for certain ages
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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 |
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The Child in Traction
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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) |
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Traction: Essential Components
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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 |
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Types of Traction
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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 |
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Cervical Traction
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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 |
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Nursing Considerations for the Kid in Traction
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Assessing the patient in traction
Skin care issues Pain management/comfort |
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Dis-traction
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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 |
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Therapeutic Management of Sports Injuries
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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 |
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Nurse’s Role in Sports for Children and Adolescents
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Evaluation for activities
Prevention of injury Treatment of injuries Rehabilitation after injuries Instruction to student and parents |
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Legg-Calve-Perthes Disease
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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 |
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Therapeutic Management of Legg-Calve-Perthes Disease
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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 |
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Pathophysiology of Legg-Calve-Perthes Disease
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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 |
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Prognosis of Legg-Calve-Perthes Disease
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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 |
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Nursing considerations for Legg-Calve- Perthes Disease
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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 |
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Slipped Femoral Capital Epiphysis (SFCE)
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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 |
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Clinical Manifestations of SFCE
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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 |
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Therapeutic Management of SFCE- Slipped Femoral Capital Epiphysis
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internal pinning to keep bone from slipping and close the physeal plate. Corrected as soon as possible after dx (usually within 24 hours)
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Nursing Considerations of SFCE
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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 |
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Scoliosis
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The most common spinal deformity
Complex spinal deformity -Lateral curvature -Spinal rotation causing rib asymmetry -Thoracic hypokyphosis May be congenital or develop |
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Osteomyelitis
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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 |
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S/Sx and Diagnosis of Osteomyelitis
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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 |
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Therapeutic Management of Osteomyelitis
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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 |
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Nursing Considerations for Osteomyelitis
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Complete bedrest and immobility of limb
Pain management concerns Long-term IV access (for antibiotic administration) Nutritional considerations Long-term hospitalization/therapy Psychosocial needs |
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Osteogenesis Imperfecta (OI)
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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 |
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Juvenile Rheumatoid Arthritis (JRA)
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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 |
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S/Sx of JRA
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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 |
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Diagnosis Of JRA Based on American College of Rheumatology Criteria
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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 |
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JRA: Therapeutic Management
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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 |
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Systemic Lupus Erythematosus (SLE)
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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 |
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SLE: Clinical Manifestations
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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 |
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SLE: Therapeutic Management
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Goals of treatment
-Supportive care -Pharmacology Nursing considerations -Minimize exacerbations -Therapy compliance -Body image concerns |
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What is the second leading cause of death in children ages 1 to 14 years
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Childhood cancer
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Childhood Cancer statistics
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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 |
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Types of Cancers
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Leukemia
Lymphoma Nervous System Tumors Bone Tumors Other Solid Tumors |
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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) |
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Diagnostic Evaluation
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History
Physical Examination Biopsy Imaging Laboratory Testing |
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Types of Therapy for Cancer
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Surgery
Chemotherapy (via vascular access device) Radiation Bone Marrow Transplant |
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Radiation to Brain for Children
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Not done anymore because it caused major learning problems.
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Leukemia Definition and two main types
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Malignancy of blood forming cells.
RBC, WBC & Platelets and always affected by Leukemia Acute Lymphoblastic Leukemia = (ALL) Acute Myeloid Leukemia = (AML) |
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Three Main Consequences of Leukemia
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1. Anemia from decrease in RBC
2. Infection from Neutropenia (decreased WBC) 3. Bleeding tendencies from decrease in platelets (Thrombocytopenia) |
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Leukemia
Average Age |
peak incidence occurs from 3 – 5 years
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Leukemia is more common in which gender?
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slightly higher in males
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Risk Factors for Leukemia
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Down Syndrome, exposure to large amounts of
radiation and certain chemicals (benzene) |
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Pathophysiology of Leukemia
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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. |
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Leukemia's Primary Signs and Symptoms
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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 |
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Nursing Priorities for a Child with Leukemia
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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) |
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Diagnostic work up for Leukemia
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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 |
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Types of Therapy for Leukemia
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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 ) |
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PHases of Chemotherapy (for Leukemia)
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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 |
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Lymphomas Definition and Types
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Def: malignant solid tumor of the immune system’s cells (Lymphocytes)
Hodgkin’s (HL) Non-Hodgkin’s (NHL) |
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Hodgkins Lymphoma S/Sx, Diagnosis and Treatment
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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. |
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Lymphoma Diagnosis and Ages
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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) |
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Non-Hodgkins Lymphoma S/Sx, Diagnosis and Treatment
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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 |
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Diagnostic Work Up for Lymphomas
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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 |
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Types of Therapy for Lymphomas
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Chemotherapy (HL and NHL)
Radiation therapy (HL and NHL) Bone marrow transplant (HL and NHL) Surgery (NHL) resection of localized tumor |
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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. |
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Brain Tumor Types
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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 |
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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 |
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Brain Tumors
Diagnostic work up |
Neurological history and exam
CT scan MRI CSF cytology Alfa feto protein (AFP) |
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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 |
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Neuroblastoma
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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. |
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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 |
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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 |
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Bone tumors
Two Types |
Osteosarcoma
Ewing's Sarcoma |
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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 |
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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 |
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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. |
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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 |
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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 |
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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 |
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Lab work for Children with Cancer
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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 |
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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 |
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Nursing interventions of Thrombocytopenia
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No rectal temperature
No suppositories Avoid constipation Avoid NSAIDS/ASA |
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Transfusion guidelines
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Transfuse with platelets
Pheresed products Type specific Single/random donor units Premeds: Tylenol & Benadryl |
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Nausea/Vomiting in relation to Chemo
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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 |
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Constipation in Kids with Cancer
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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) |
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Diarrhea in Kids with Cancer
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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 |
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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 |
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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! |
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Nursing management of mucositis:
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Good dental hygiene
Oral care/rinses (without alcohol!) Pain management Hydration & nutrition Infectious disease (prophylaxis/treatment) Airway protection |
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Pain management in Kids with Cancer
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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 |
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Alopecia (Hair Loss) in Kids with Cancer
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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! |
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Neurological Problems in Kids with Cancer
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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! |
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Hemorrhagic Cystitis in Kids with Cancer
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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) |
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Steroid Effects
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Moon face
Weight gain (increased hunger) Steroid psychosis Emotional lability Immunocompromised |
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Photo/Sun Sensitivity in Kids with Cancer
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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 |
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The Childhood Cancer Survivor Late Effects
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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 |
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Intervention and Follow Up for Late Effects of Childhood Cancer
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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 |
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Anemia
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The most common hematologic disorder of childhood
Decrease in number of RBCs and/or hemoglobin concentration below normal Decreased oxygen-carrying capacity of blood |
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Consequences of Anemia
|
Decrease in oxygen-carrying capacity of blood and decreased amount of oxygen available to tissues
When anemia develops slowly, child adapts |
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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 |
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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 |
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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 |
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Sickle Cell Anemia
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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 |
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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 |
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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 |
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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 |
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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 |
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Disease Management of Sickle Cell Anemia
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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 |
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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 |
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Thalassemia
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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 |
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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) |
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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 |
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Nursing Management for a Kid with Thalassemia
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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 |
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Aplastic Anemia
|
All formed elements of the blood are simultaneously depressed: “pancytopenia”
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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 |
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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 |
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Aplastic Anemia
Nursing Considerations |
Prepare child and family for diagnostic and therapeutic procedures
Prevent complications from pancyotopenia Support child and family |
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Hemophilia
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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 |
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Etiology of Hemophilia A
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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 |
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Manifestations of Hemophilia
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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 |
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Muscle Bleeds: Signs & Symptoms
Soft Tissue Bleeds and Bruising |
-No functional impairment
-Tenderness but no severe pain -No factor needed |
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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 |
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Muscle Bleeds: Signs & Symptoms
Thigh/Calf Bleeds |
-Pain
-With/without swelling -Impaired mobility -Routine factor dose -Major factor dose if compartment syndrome is suspected |
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Muscle Bleeds: Signs & Symptoms
Neck Swelling |
EMERGENCY!!!!
-Potential airway compromise -Treat with a MAJOR dose of factor |
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Muscle Bleeds: Signs & Symptoms
Deltoid/Forearm Bleed and Bruising |
-Routine factor dose
-Major dose if a compartment syndrome is suspected |
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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 |
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Treatment for Joint Bleeds
|
Routine dose of factor for early onset joint bleeds
Major dose of factor for advanced joint bleeds May need crutches. |
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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 |
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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 |
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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 |
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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 |
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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 |
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Diagnosis of HIV
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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. |
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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 |
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Hypopituitarism: Growth Hormone (GH) Deficiency
|
Inhibits somatic growth
Primary site of dysfunction appears to be in the hypothalamus |
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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 |
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Therapeutic Management of GH Deficiency
|
Biosynthetic growth hormone (injections)
Other hormone replacements as needed Thyroid extract Cortisone Testosterone or estrogens and progesterone |
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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 |
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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) |
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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 |
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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. |
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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 |
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Precocious Puberty
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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 |
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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 |
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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 |
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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 |
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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 |
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Nursing Management of DI
|
Accurate I&O
Observe for signs of fluid overload Seizure precautions Administer ADH-antagonizing meds |
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Disorders of Thyroid Function
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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 |
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Juvenile Hypothyroidism
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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 |
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Clinical Manifestations of Juvenile Hypothyroidism
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Decelerated growth
Constipation Sleepiness Myxedematous skin changes Dry skin Sparse hair Periorbital edema |
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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 |
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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 |
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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 |
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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 |
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Cushing Syndrome
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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 |
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Etiologies of Cushing Syndrome
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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 |
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Cushingoid Appearance
|
Excessive hair growth
Moon face, red cheeks Weight gain Pendulous abdomen with red striae Poor wound healing Ecchymoses |
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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 |
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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 |
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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 |
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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 |
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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 |
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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) |
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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 |
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Kussmaul Respirations
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Hyperventilation characteristic of metabolic acidosis resulting from the respiratory system’s attempt to eliminate excess CO2 by increased depth and rate
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Diabetic Ketoacidosis (DKA)
|
Pediatric emergency
Results from progressive deterioration with dehydration, electrolyte imbalance, acidosis, coma, and may cause death |
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Long-Term Complications of DM
|
Microvascular complications, especially nephropathy and retinopathy
Macrovascular disease, neuropathy |
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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 |
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Patient Education: DM and Insulin Therapy
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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 |
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Possible Nursing Diagnoses for Pediatric Client with DM
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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 |
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Common Reasons Behind Burn Injuries in Children
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Toddlers: hot water scalds
Older children: flame-related burns Child abuse Children with matches or lighters account for 1 in 10 house fires |
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Three Nursing Assessment Areas for Burn Injury Evaluation
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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Burns: Therapeutic Management
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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 |
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Complications of Burn Injuries
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Immediate threat of airway compromise
Profound shock Infection (local and systemic sepsis) Inhalation injuries, aspiration, pulmonary edema, pulmonary embolus |
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Care of Minor Burns
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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) |
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Rehabilitation After Major Burns
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Begins once wound coverage has been achieved
Prevention/management of contractures Physical/occupational therapy Multidisciplinary team Facilitate adaptation of child and family |
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Increased Intracranial Pressure (ICP)
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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! |
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Clinical Manifestations of Increased ICP in Infants
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Irritability, poor feeding
High-pitched cry, difficult to soothe Fontanels: tense, bulging Cranial sutures: separated Eyes: setting-sun sign Scalp veins: distended |
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Clinical Manifestations of Increased ICP in Children
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Headache
Vomiting: with or without nausea Seizures Diplopia, blurred vision |
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Behavioral Signs of Increasing ICP
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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 |
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Late Signs of Increasing ICP
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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 |
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Levels of Consciousness (in Descending Order)
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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 |
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Pediatric Glasgow Coma Scale
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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 |
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Indications for ICP Monitoring
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Glasgow coma scale <7 - less stable
Glasgow coma scale <8 with respiratory distress Deteriorating neurologic condition Subjective judgment |
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Nursing Care for Child with Increased ICP
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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 |
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Respiratory Management for Child with Increased ICP
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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 |
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Nursing Care Needs for Child with Increased ICP
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Elimination
Hygienic care Position and exercise Stimulation Family support |
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Nursing Diagnoses for Child with Increased ICP
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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 |
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Special Diagnostic Procedures for Child with Increased ICP
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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) |
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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 |
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Subsequent Complications of Head Injuries
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Hypoxic brain injury
Increased ICP Infection Cerebral edema |
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Concussion
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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 |
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Contusion and Laceration
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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 |
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Diagnostic Evaluation for Head Injury
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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 |
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Therapeutic Management for Head Injury
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Care in hospital if severe injuries, loss of consciousness for several minutes, prolonged or continued seizures
NPO initially Possible surgical interventions Prognosis |
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Nursing Considerations for Head Injury
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Frequent assessment: vital sign and neurologic checks
Provide analgesia and sedation Careful observation and recording Family support Rehabilitation Prevention |
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Near Drowning
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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 |
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Nursing Considerations for Near Drowning
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Care depends on condition of the child
Helping parents cope with feelings of guilt Parental anxiety related to prognosis PREVENTION OF DROWNING |
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CNS INFECTIONS
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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 |
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Bacterial Meningitis
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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 |
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Transmission of Bacterial Meningitis
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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 |
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Nonbacterial Meningitis (Aseptic Meningitis)
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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 |
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Reye Syndrome (RS)
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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 |
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Reye Syndrome (RS) S & Sx
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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 |
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Reye Syndrome (RS) Tx
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Should be put in ICU and placed on ventilator- major of kids who survive recover completely.
Symptoms management- Monitor Liver, Kidneys and Neuro changes |
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Seizures
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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 |
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Seizures: Signs and Symptoms
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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 |
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Major Causes of Seizures in Children
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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 |
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Absence Seizures
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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 |
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Atonic Seizures
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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 |
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Myoclonic Seizures
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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 |
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Status Epilepticus
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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 |
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Emergency Management for Big Ass Seizures
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High-dose sedatives
Maintain patent airway Prepare for respiratory support |
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Pediatric Diagnosis of Seizure Disorders
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Ascertain type of seizure
History, observation Determine the cause of the event Diagnostics EEG, MRI Labs: glucose, electrolytes, BUN, Ca++ LP |
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Common Pediatric Seizure Triggers
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Changes in dark-light patterns (camera flashes, headlights, rotating fan blades, reflections off snow or water)
Sudden loud noises Extreme temperature changes Dehydration Fatigue |
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Febrile Seizures- Occurance
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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 |
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Febrile Seizures
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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) |
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Febrile Seizures Management/Prevention
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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 |
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Febrile Seizures Treatment
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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 |
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Pharmacologic Management for Seizures
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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 |
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When to discontinue seizure meds
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When seizure free for 2 years
Normal EEG Avoid DC during puberty or when subject to frequent infections Recurrence possible within first year |
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Nursing Interventions for Seizures
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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 |
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Phenobarbital - purpose
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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 |
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Phenytoin (Dilantin)
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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 |
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Fosphenytoin
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May be given with saline or glucose
Rate up to 150 mg/min IV or IM |
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Valproic Acid
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Trade names: Depakote, Depakene
IV or PO IV for status epilepticus S.E.: Hepatotoxicity! |
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Diazepam
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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 |
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Ativan
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Alternative to diazepam
May be preferable to diazepam Longer duration of action Less respiratory distress in children older than 2 years |
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Midazolam (Versed)
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Intranasal route
For acute epileptic seizures Onset 3 to 5 minutes; duration |
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Hypoplastic anemia
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Profound depression of RBCs but normal WBCs and platelet
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What indicates a neurosurgical emergency?
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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. |
